FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Jiang, Y
Wu, SH
Shu, XO
Xiang, YB
Ji, BT
Milne, GL
Cai, QY
Zhang, XL
Gao, YT
Zheng, W
Yang, G
AF Jiang, Yu
Wu, Sheng-Hui
Shu, Xiao-Ou
Xiang, Yong-Bing
Ji, Bu-Tian
Milne, Ginger L.
Cai, Qiuyin
Zhang, Xianglan
Gao, Yu-Tang
Zheng, Wei
Yang, Gong
TI Cruciferous Vegetable Intake Is Inversely Correlated with Circulating
Levels of Proinflammatory Markers in Women
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Article
DE Cruciferous vegetables; Inflammation; Oxidative stress; Biomarker.
ID S-TRANSFERASE POLYMORPHISMS; COLORECTAL-CANCER RISK; OXIDATIVE STRESS;
IN-VIVO; DIETARY ISOTHIOCYANATES; CLINICAL-TRIAL; HEALTH; INFLAMMATION;
FRUIT; CONSUMPTION
AB Background Higher intakes of cruciferous vegetables or their constituents have been shown to lower inflammation in animal studies. However, evidence for this antiinflammatory effect of cruciferous vegetable consumption in humans is scarce.
Objective/Design In this crOss-sectional analysis, we evaluated associations of vegetable intake with a panel of inflammatory and oxidative stress markers among 1,005 middle-aged Chinese women. Dietary intake of foods was assessed by a food frequency questionnaire.
Results Multivariable-adjusted circulating concentrations of tumor necrosis factor-a (TNF-alpha), interlukin-1 beta (IL-1 beta), and IL-6 were lower among Women with higher intakes of cruciferous vegetables. The differences in concentrations of inflammatory biomarkers between extreme quintiles of cruciferous vegetable intake were 12.66% for TNF-a (P-trend=0.01), 18.18% for IL-1 beta (P-trend=0.02), and 24.68% for IL-6 (P-trend=0.02). A similar, but less apparent, inverse association was found for intakes of all vegetables combined but not for noncruciferous vegetables. Levels of the urinary oxidative stress markers F-2-isoprostanes and their major metabolite, 2,3-dinor-5,6-dihydro-15-F-2t-IsoP, were not associated with intakes of cruciferous vegetables or all vegetables combined.
Conclusions This study suggests that the previously observed health benefits of cruciferous vegetable consumption may be partly associated with the antiinflammatory effects of these vegetables.
C1 [Jiang, Yu] Changning Ctr Dis Control & Prevent, Div Chron Dis Control & Prevent, Shanghai, Peoples R China.
[Jiang, Yu; Wu, Sheng-Hui; Shu, Xiao-Ou; Cai, Qiuyin; Zhang, Xianglan; Zheng, Wei; Yang, Gong] Vanderbilt Univ, Sch Med, Dept Med, Div Epidemiol, Nashville, TN 37203 USA.
[Milne, Ginger L.] Vanderbilt Univ, Sch Med, Dept Med, Div Clin Pharmacol, Nashville, TN 37203 USA.
[Xiang, Yong-Bing; Gao, Yu-Tang] Shanghai Canc Inst, Shanghai, Peoples R China.
[Ji, Bu-Tian] NCI, Div Canc Epidemiol & Genet, NIH, US Dept HHS, Bethesda, MD 20892 USA.
RP Yang, G (reprint author), Vanderbilt Univ, Med Ctr, Dept Med, Div Epidemiol, 2525 West End Ave,Suite 600 IMPH, Nashville, TN 37203 USA.
EM Gong.Yang@Vanderbilt.edu
RI Milne, Ginger/D-7648-2014
OI Milne, Ginger/0000-0003-3890-151X
FU US National Cancer Institute [RO1CAl22364]; inflammation and oxidative
stress biomarker assays [R37 CA070867]; baseline data collection and
genotyping [NO2-CP-11010-66]; Fogarty International Center [D43
TW008313]; Vanderbilt University Center in Molecular Toxicology [P30
ES000267]; NIH [P30 ES000267]
FX This study was supported by Public Health Service grants from the US
National Cancer Institute, including grant number RO1CAl22364 (to
G.Yang) for the inflammation and oxidative stress biomarker assays, R37
CA070867 (to W.Zheng) for the baseline data collection and genotyping,
and a contract, NO2-CP-11010-66 (to X.-0.Shu) for biospecimen
collection.Y.Jiang was supported by a training grant from the Fogarty
International Center (D43 TW008313 to X.-0.Shu).G.L.Milne acknowledges
support from the Vanderbilt University Center in Molecular Toxicology
(NIH P30 ES000267).
NR 44
TC 12
Z9 12
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
EI 2212-2680
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD MAY
PY 2014
VL 114
IS 5
BP 700
EP 708
DI 10.1016/j.jand.2013.12.019
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AG4XR
UT WOS:000335424200007
PM 24630682
ER
PT J
AU White, SF
Fowler, KA
Sinclair, S
Schechter, JC
Majestic, CM
Pine, DS
Blair, RJ
AF White, Stuart F.
Fowler, Katherine A.
Sinclair, Stephen
Schechter, Julia C.
Majestic, Catherine M.
Pine, Daniel S.
Blair, R. James
TI Disrupted Expected Value Signaling in Youth With Disruptive Behavior
Disorders to Environmental Reinforcers
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE disruptive behavior; conduct disorder; decision making; expected value;
environmental reinforcers
ID CALLOUS-UNEMOTIONAL TRAITS; VENTROMEDIAL PREFRONTAL CORTEX; PSYCHOPATHIC
TRAITS; RESPONSE REVERSAL; CONDUCT DISORDER; CHILDREN; REWARD;
DISSOCIATION; ADOLESCENTS; DYSFUNCTION
AB Objective: Youth with disruptive behavior disorders (DBD), including conduct disorder (CD) and oppositional defiant disorder (ODD), have difficulties in reinforcement-based decision making, the neural basis of which is poorly understood. Studies examining decision making in youth with DBD have revealed reduced reward responses within the ventromedial prefrontal cortex/orbitofrontal cortex (vmPFC/OFC), increased responses to unexpected punishment within the vmPFC and striatum, and reduced use of expected value information in the anterior insula cortex and dorsal anterior cingulate cortex during the avoidance of suboptimal choices. Previous work has used only monetary reinforcement. The current study examined whether dysfunction in youth with DBD during decision making extended to environmental reinforcers. Method: A total of 30 youth (15 healthy youth and 15 youth with DBD) completed a novel reinforcement-learning paradigm using environmental reinforcers (physical threat images, e.g., striking snake image; contamination threat images, e.g., rotting food; appetitive images, e.g., puppies) while undergoing functional magnetic resonance imaging (fMRI). Results: Behaviorally, healthy youth were significantly more likely to avoid physical threat, but not contamination threat, stimuli than youth with DBD. Imaging results revealed that youth with DBD showed significantly reduced use of expected value information in the bilateral caudate, thalamus, and posterior cingulate cortex during the avoidance of suboptimal responses. Conclusions: The current data suggest that youth with DBD show deficits to environmental reinforcers similar to the deficits seen to monetary reinforcers. Importantly, this deficit was unrelated to callous-unemotional (CU) traits, suggesting that caudate impairment may be a common deficit across youth with DBD.
C1 [White, Stuart F.; Fowler, Katherine A.; Sinclair, Stephen; Pine, Daniel S.; Blair, R. James] NIMH, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Schechter, Julia C.; Majestic, Catherine M.] NIMH, Intramural Res Program, Bethesda, MD USA.
RP White, SF (reprint author), 9000 Rockville Pike,Bldg 15k,Room 300C, Bethesda, MD 20892 USA.
EM whitesf@mail.nih.gov
FU Intramural Research Program at NIMH; NIH [1-ZIA-MH00286008,
1-ZIA-MH002781-11]; NIH Combined Neuroscience Institutional Review Board
[05-M0105]
FX This work was supported by the Intramural Research Program at NIMH, NIH
under grant number 1-ZIA-MH00286008 (R J B.) and 1-ZIA-MH002781-11
(D.S.P:). Ethics approval for this study was granted by the NIH Combined
Neuroscience Institutional Review Board under protocol number 05-M0105.
NR 35
TC 14
Z9 14
U1 4
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
EI 1527-5418
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD MAY
PY 2014
VL 53
IS 5
BP 579
EP 588
DI 10.1016/j.jaac.2013.12.023
PG 10
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA AG0HJ
UT WOS:000335096200011
PM 24745957
ER
PT J
AU Gray, GE
Moodie, Z
Metch, B
Gilbert, PB
Bekker, LG
Churchyard, G
Nchabeleng, M
Mlisana, K
Laher, F
Roux, S
Mngadi, K
Innes, C
Mathebula, M
Allen, M
McElrath, MJ
Robertson, M
Kublin, J
Corey, L
AF Gray, Glenda E.
Moodie, Zoe
Metch, Barbara
Gilbert, Peter B.
Bekker, Linda-Gail
Churchyard, Gavin
Nchabeleng, Maphoshane
Mlisana, Koleka
Laher, Fatima
Roux, Surita
Mngadi, Kathryn
Innes, Craig
Mathebula, Matsontso
Allen, Mary
McElrath, M. Julie
Robertson, Michael
Kublin, James
Corey, Lawrence
CA HVTN 503 Phambili Study Team
TI Recombinant adenovirus type 5 HIV gag/pol/nef vaccine in South Africa:
unblinded, long-term follow-up of the phase 2h HVTN 503/Phambili study
SO LANCET INFECTIOUS DISEASES
LA English
DT Article
ID TEST-OF-CONCEPT; SEXUALLY-TRANSMITTED-DISEASES; IMMUNODEFICIENCY-VIRUS;
T-CELLS; IMMUNE-RESPONSES; NONHUMAN-PRIMATES; HEALTHY-ADULTS;
RHESUS-MONKEYS; EFFICACY TRIAL; GENITAL-TRACT
AB Background The HVTN 503/Phambili study, which assessed the efficacy of the Merck Ad5 gag/pol/nef subtype B HIV-1 preventive vaccine in South Africa, was stopped when futility criteria in the Step study (assessing the same vaccine in the Americas, Caribbean, and Australia) were met. Here we report long-term follow-up data.
Methods HVTN 503/Phambili was a double-blind, placebo-controlled, randomised trial that recruited HIV-1 uninfected, sexually active adults aged 18-35 years from five sites in South Africa. Eligible participants were randomly assigned (1:1) by computer-generated random numbers to either vaccine or placebo, stratified by site and sex. Cox proportional hazards models were used to estimate HIV-1 infection in the modified intention-to-treat cohort, all of whom were unmasked early in follow-up. The trial is registered with ClinicalTrials.gov, number NCT00413725 and the South African National Health Research Database, number DOH-27-0207-1539.
Findings Between Jan 24,2007, and Sept 19,2007,801 participants (26-7%) of a planned 3000 were randomly assigned (400 to vaccine, 401 to placebo); 216 (27%) received only one injection, 529 (66%) received only two injections, and 56 (7%) received three injections. At a median follow-up of 42 months (IQR 31-42), 63 vaccine recipients (16%) had HIV-1 infection compared with 37 placebo recipients (9%; adjusted HR 1-70,95% CI 1-13-2-55; 1)=0-01). Risk for HIV-1 infection did not differ according to the number of vaccinations received, sex, circumcision, or adenovirus type 5 (Ads) serostatus. Differences in risk behaviour at baseline or during the study, or annualised dropout rate (7-7% [95% CI 6-2-9-5] for vaccine recipients vs 8-8% [7-1-10-7] for placebo recipients; p=0-40) are unlikely explanations for the increased rate of HIV-1 infections seen in vaccine recipients.
Interpretation The increased risk of HIV-1 acquisition in vaccine recipients, irrespective of number of doses received, warrants further investigation to understand the biological mechanism. We caution against further use of the Ad5 vector for HIV vaccines.
C1 [Gray, Glenda E.; Laher, Fatima] Univ Witwatersrand, Perinatal HIV Res Unit, ZA-1864 Johannesburg, South Africa.
[Gray, Glenda E.] South African Med Res Council, Cape Town, South Africa.
[Moodie, Zoe; Metch, Barbara; Gilbert, Peter B.; McElrath, M. Julie; Kublin, James; Corey, Lawrence] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Bekker, Linda-Gail; Roux, Surita] Univ Cape Town, Desmond Tutu HIV Fdn, ZA-7925 Cape Town, South Africa.
[Churchyard, Gavin] Aurum Inst Hlth Res, Johannesburg, South Africa.
[Nchabeleng, Maphoshane; Mathebula, Matsontso] Univ Limpopo, MEDUNSA HIV Clin Res Unit, Mankweng E, South Africa.
[Mlisana, Koleka; Mngadi, Kathryn] Univ KwaZulu Natal, Ctr AIDS Programme Res S Afr, Durban, South Africa.
[Allen, Mary] NIAID, Vaccine Res Program, Div Aids, NIH, Bethesda, MD 20892 USA.
[Robertson, Michael] Merck & Co Inc, Infect Dis & Vaccines Clin Res, N Wales, PA USA.
RP Gray, GE (reprint author), Univ Witwatersrand, Perinatal HIV Res Unit, POB 114, ZA-1864 Johannesburg, South Africa.
EM gray@pixie.co.za
FU National Institute of Allergy and Infectious Diseases, Merck; South
African Medical Research Council
FX Funding National Institute of Allergy and Infectious Diseases, Merck,
and South African Medical Research Council.
NR 37
TC 42
Z9 42
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1473-3099
EI 1474-4457
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD MAY
PY 2014
VL 14
IS 5
BP 388
EP 396
DI 10.1016/S1473-3099(14)70020-9
PG 9
WC Infectious Diseases
SC Infectious Diseases
GA AG0GF
UT WOS:000335093200023
PM 24560541
ER
PT J
AU del Rosario, MC
Ossowski, V
Knowler, WC
Bogardus, C
Baier, LJ
Hanson, RL
AF del Rosario, Melissa C.
Ossowski, Vicky
Knowler, William C.
Bogardus, Clifton
Baier, Leslie J.
Hanson, Robert L.
TI Potential epigenetic dysregulation of genes associated with MODY and
type 2 diabetes in humans exposed to a diabetic intrauterine
environment: An analysis of genome-wide DNA methylation
SO METABOLISM-CLINICAL AND EXPERIMENTAL
LA English
DT Article
DE In utero; Maternal diabetes; Immunoprecipitation; Microarray
ID PIMA-INDIANS; MELLITUS; PATHOPHYSIOLOGY; ANTIBODIES; OBESITY; LISTS;
YOUNG; ARRAY; RISK
AB Objective. The aim of this study is to investigate the potential role of DNA methylation in mediating the increased risk of developing type 2 diabetes in offspring of mothers who had diabetes during pregnancy.
Materials and Methods. Peripheral blood leukocytes were collected from non-diabetic Pima Indians who were either offspring of diabetic mothers (ODM; n = 14) or offspring of nondiabetic mothers (ONDM; n = 14). The two groups were matched for age, sex, age of mother, and fraction of Pima ethnicity. Differentially methylated regions were determined using a MeDIP-chip assay on an Affymetrix Human Tiling 2.0R Array. Data were analyzed using the model based analysis of tiling arrays (MAT) algorithm, and 4883 regions overlapping with putative promoters, were identified as differentially methylated, having met an empirically derived threshold (nominal p < 0.0077). The list of genes with differentially methylated promoters was subjected to KEGG pathway analysis to determine canonical metabolic pathways enriched by these genes.
Results. Pathway analysis of genes with differentially methylated promoters identified the top 3 enriched pathways as maturity onset diabetes of the young (MODY), type 2 diabetes, and Notch signaling. Several genes in these pathways are known to affect pancreatic development and insulin secretion.
Conclusions. These findings support the hypothesis that epigenetic changes may increase the risk of type 2 diabetes via an effect on beta-cell function in the offspring of mothers with diabetes during pregnancy. Published by Elsevier Inc.
C1 [del Rosario, Melissa C.; Ossowski, Vicky; Knowler, William C.; Bogardus, Clifton; Baier, Leslie J.; Hanson, Robert L.] Natl Inst Diabet & Digest & Kidney Dis, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ 85014 USA.
RP Hanson, RL (reprint author), Natl Inst Diabet & Digest & Kidney Dis, Diabet Epidemiol & Clin Res Sect, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA.
EM rhanson@phx.niddk.nih.gov
RI Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU NIH
FX This research is funded by the NIH intramural research program. MCD was
supported by the NIH Intramural training program.
NR 30
TC 19
Z9 20
U1 0
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0026-0495
EI 1532-8600
J9 METABOLISM
JI Metab.-Clin. Exp.
PD MAY
PY 2014
VL 63
IS 5
BP 654
EP 660
DI 10.1016/j.metabol.2014.01.007
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AG1UC
UT WOS:000335200700008
PM 24582139
ER
PT J
AU Robinson, GW
Kang, K
Yoo, KH
Tang, Y
Zhu, BM
Yamaji, D
Colditz, V
Jang, SJ
Gronostajski, RM
Hennighausen, L
AF Robinson, Gertraud W.
Kang, Keunsoo
Yoo, Kyung Hyun
Tang, Yong
Zhu, Bing-Mei
Yamaji, Daisuke
Colditz, Vera
Jang, Seung Jian
Gronostajski, Richard M.
Hennighausen, Lothar
TI Coregulation of Genetic Programs by the Transcription Factors NFIB and
STAT5
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID NUCLEAR FACTOR-I; WHEY ACIDIC PROTEIN; MOUSE MAMMARY EPITHELIUM; ESTER
LIPASE GENE; TRANSGENIC MICE; WAP GENE; PROGESTERONE-RECEPTOR;
CELL-PROLIFERATION; LUNG MATURATION; DNA-SEQUENCES
AB Mammary-specific genetic programs are activated during pregnancy by the common transcription factor signal transducer and activator of transcription (STAT) 5. More than one third of these genes carry nuclear factor I/B (NFIB) binding motifs that coincide with STAT5 in vivo binding, suggesting functional synergy between these two transcription factors. The role of NFIB in this governance was investigated in mice from which Nfib had been inactivated in mammary stem cells or in differentiating alveolar epithelium. Although NFIB was not required for alveolar expansion, the combined absence of NFIB and STAT5 prevented the formation of functional alveoli. NFIB controlled the expression of mammary-specific and STAT5-regulated genes and chromatin immunoprecipitation- sequencing established STAT5 and NFIB binding at composite regulatory elements containing histone H3 lysine dimethylation enhancer marks and progesterone receptor binding. By integrating previously published chromatin immunoprecipitation-sequencing data sets, the presence of NFIB-STAT5 modules in other cell types was investigated. Notably, genomic sites bound by NFIB in hair follicle stem cells were also occupied by STAT5 in mammary epithelium and coincided with enhancer marks. Many of these genes were under NFIB control in both hair follicle stem cells and mammary alveolar epithelium. We propose that NFIB-STAT5 modules, possibly in conjunction with other transcription factors, control cell-specific genetic programs.
C1 [Robinson, Gertraud W.; Kang, Keunsoo; Yoo, Kyung Hyun; Tang, Yong; Yamaji, Daisuke; Colditz, Vera; Jang, Seung Jian; Hennighausen, Lothar] Natl Inst Diabet & Digest & Kidney Dis, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA.
[Kang, Keunsoo] Dankook Univ, Dept Microbiol, Cheonan 330714, South Korea.
[Tang, Yong] Chengdu Univ Tradit Chinese Med, Chengdu 610072, Peoples R China.
[Zhu, Bing-Mei] Nanjing Univ Tradit Chinese Med, Lab Acupuncture & Med, Nanjing 210046, Jiangsu, Peoples R China.
[Gronostajski, Richard M.] SUNY Buffalo, Dept Biochem, Dev Genom Grp, New York State Ctr Excellence Bioinformat & Life, Buffalo, NY 14203 USA.
RP Hennighausen, L (reprint author), Natl Inst Diabet & Digest & Kidney Dis, NIH, Bldg 8,Room 101, Bethesda, MD 20892 USA.
EM lotharh@mail.nih.gov
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases; National Institutes of Health from the
National Natural Science Funding of China [81273838]; Natural Science
Fund for Colleges and Universities, Department of Education, Jiangsu,
China [11KJA360003]; National Heart, Lung, and Blood Institute; National
Institutes of Health [HL080624]; New York State Stem Cell Science
[C026429]
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health. Funding for B.M. Z. came from the
National Natural Science Funding of China (81273838) and the Natural
Science Fund for Colleges and Universities, Department of Education,
Jiangsu, China (11KJA360003). R. M. G. was supported by the National
Heart, Lung, and Blood Institute, National Institutes of Health (Award
HL080624) and New York State Stem Cell Science (Award C026429).
NR 55
TC 4
Z9 5
U1 0
U2 4
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD MAY
PY 2014
VL 28
IS 5
BP 758
EP 767
DI 10.1210/me.2012-1387
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AG5IK
UT WOS:000335452500014
PM 24678731
ER
PT J
AU Xue, R
Zakharov, MN
Xia, Y
Bhasin, S
Costello, JC
Jasuja, R
AF Xue, Ran
Zakharov, Mikhail N.
Xia, Yu
Bhasin, Shalender
Costello, James C.
Jasuja, Ravi
TI Research Resource: EPSLiM: Ensemble Predictor for Short Linear Motifs in
Nuclear Hormone Receptors
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID PROSTATE-CANCER CELLS; ANDROGEN RECEPTOR; INTRINSIC DISORDER;
COREGULATORS; DOMAIN; BINDING; ACTIVATION; SRC; CLASSIFIER; ANTAGONIST
AB Nuclear receptors (NRs) are a superfamily of transcription factors central to regulating many biological processes, including cell growth, death, metabolism, and immune responses. NR-mediated gene expression can be modulated by coactivators and corepressors through direct physical interaction or protein complexes with functional domains in NRs. One class of these domains includes short linear motifs (SLiMs), which facilitate protein-protein interactions, phosphorylation, and ligand binding primarily in the intrinsically disordered regions (IDRs) of proteins. Across all proteins, the number of known SLiMs is limited due to the difficulty in studying IDRs experimentally. Computational tools provide a systematic and data-driven approach for predicting functional motifs that can be used to prioritize experimental efforts. Accordingly, several tools have been developed based on sequence conservation or biophysical features; however, discrepancies in predictions make it difficult to determine the true candidate SLiMs. In this work, we present the ensemble predictor for short linear motifs (EPSLiM), a novel strategy to prioritize the residues that are most likely to be SLiMs in IDRs. EPSLiM applies a generalized linear model to integrate predictions from individual methodologies. We show that EPSLiM outperforms individual predictors, and we apply our method to NRs. The androgen receptor is an example with an N-terminal domain of 559 disordered amino acids that contains several validated SLiMs important for transcriptional activation. We use the androgen receptor to illustrate the predictive performance of EPSLiM and make the results of all human and mouse NRs publically available through the web service http://epslim.bwh.harvard.edu.
C1 [Xue, Ran; Bhasin, Shalender; Costello, James C.; Jasuja, Ravi] Harvard Univ, Brigham & Womens Hosp, Sch Med,Res Program Mens Hlth Aging & Metab, Boston Claude D Pepper Older Amer Independence Ct, Boston, MA 02115 USA.
[Zakharov, Mikhail N.] NIH, Natl Lib Med, Natl Ctr Bioinformat Technol, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Xia, Yu] McGill Univ, Fac Engn, Dept Bioengn, Montreal, PQ H3A 0C3, Canada.
RP Jasuja, R (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Program Mens Hlth Aging & Metab,Boston Claude D P, Boston, MA 02115 USA.
EM james.costello@ucdenver.edu; rjasuja@partners.org
OI Xia, Yu/0000-0002-5596-5518
FU Evans Foundation; Brigham and Women's Hospital startup funds; National
Institute on Aging [5 R01 AG037193-11]; National Science Foundation
[CCF-1219007]
FX This work was supported by the Evans Foundation (merit award to R.J.),
Brigham and Women's Hospital startup funds (S. B. and R.J.), the
National Institute on Aging (Grant 5 R01 AG037193-11), and the National
Science Foundation (Grant CCF-1219007).
NR 49
TC 1
Z9 1
U1 0
U2 5
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD MAY
PY 2014
VL 28
IS 5
BP 768
EP 777
DI 10.1210/me.2014-1006
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AG5IK
UT WOS:000335452500015
PM 24678734
ER
PT J
AU Sallach, J
Di Pasquale, G
Larchert, F
Niehoff, N
Rubsam, M
Huber, A
Chiorini, J
Almarza, D
Eming, SA
Ulus, H
Nishimura, S
Hacker, UT
Hallek, M
Niessen, CM
Buning, H
AF Sallach, Jessica
Di Pasquale, Giovanni
Larcher, Fernando
Niehoff, Nadine
Ruebsam, Matthias
Huber, Anke
Chiorini, Jay
Almarza, David
Eming, Sabine A.
Ulus, Hikmet
Nishimura, Stephen
Hacker, Ulrich T.
Hallek, Michael
Niessen, Carien M.
Buening, Hildegard
TI Tropism-modified AAV Vectors Overcome Barriers to Successful Cutaneous
Therapy
SO MOLECULAR THERAPY
LA English
DT Article
ID ADENOASSOCIATED VIRUS TYPE-2; HEPARAN-SULFATE PROTEOGLYCAN;
GROWTH-FACTOR RECEPTOR; MOUTH-DISEASE VIRUS; GENE-THERAPY; INTEGRIN
ALPHA-V-BETA-8; HUMAN KERATINOCYTES; VIRAL-VECTORS; EPIDERMAL
MORPHOGENESIS; TRANSDUCTION EFFICIENCY
AB Autologous human keratinocytes (HK) forming sheet grafts are approved as skin substitutes. Genetic engineering of HK represents a promising technique to improve engraftment and survival of transplants. Although efficacious in keratinocyte-directed gene transfer, retro-/lenti-viral vectors may raise safety concerns when applied in regenerative medicine. We therefore optimized adeno-associated viral (AAV) vectors of the serotype 2, characterized by an excellent safety profile, but lacking natural tropism for HK, through capsid engineering. Peptides, selected by AAV peptide display, engaged novel receptors that increased cell entry efficiency by up to 2,500-fold. The novel targeting vectors transduced HK with high efficiency and a remarkable specificity even in mixed cultures of HK and feeder cells. Moreover, differentiated keratinocytes in organotypic airlifted three-dimensional cultures were transduced following topical vector application. By exploiting comparative gene analysis we further succeeded in identifying alpha v beta 8 integrin as a target receptor thus solving a major challenge of directed evolution approaches and describing a promising candidate receptor for cutaneous gene therapy.
C1 [Sallach, Jessica; Niehoff, Nadine; Ruebsam, Matthias; Huber, Anke; Eming, Sabine A.; Hallek, Michael; Niessen, Carien M.; Buening, Hildegard] Univ Cologne, CMMC, D-50931 Cologne, Germany.
[Sallach, Jessica; Huber, Anke; Hallek, Michael; Buening, Hildegard] Univ Hosp Cologne, Dept Internal Med 1, Cologne, Germany.
[Di Pasquale, Giovanni; Chiorini, Jay] Natl Inst Dent & Crania facial Res, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD USA.
[Larcher, Fernando; Almarza, David] Univ Carlos III Madrid UC3M, Ctr Invest Energet Medioambiental Tecnol CIEMAT, Ctr Biomed Res Rare Dis CIBERER U714, Madrid, Spain.
[Niehoff, Nadine; Ruebsam, Matthias; Eming, Sabine A.; Niessen, Carien M.] Univ Carlos III Madrid UC3M, Dept Bioengn, Madrid, Spain.
[Niehoff, Nadine; Ruebsam, Matthias; Eming, Sabine A.; Niessen, Carien M.] Univ Hosp Cologne, Dept Dermatol, Cologne, Germany.
[Eming, Sabine A.; Niessen, Carien M.] Cologne Excellence Ctr Cellular Stress Responses, Cologne, Germany.
[Ulus, Hikmet] Childrens Med Surg, Cologne, Germany.
[Nishimura, Stephen] UCSF, Dept Pathol & Lab Med, San Francisco, CA USA.
[Hacker, Ulrich T.] UCCL, Leipzig, Germany.
RP Buning, H (reprint author), Univ Cologne, CMMC, Robert Koch Str 21, D-50931 Cologne, Germany.
EM hildegard.buening@uk-koeln.de
RI Larcher, Fernando/J-1527-2016
OI Larcher, Fernando/0000-0002-6771-3561
FU Research Priority Program 1230 [SPP1230]; Deutsche
Forschungsgemeinschaft (DFG) [BU1310/12]; Center for Molecular Medicine
Cologne (CMMC) [B1]; Instituto de Salud Carlos III [PI11/01225];
Comunidad de Madrid [S2010/BMD-2359]; CMMC [C1.1]; National Institutes
of Health [HL113032, NS044155]; European Union [LSHBCT-2005-512102]
FX This work was supported by grants from the Research Priority Program
1230 (SPP1230) "Mechanisms of gene vector entry and persistence" of the
Deutsche Forschungsgemeinschaft (DFG) to H.B. (BU1310/12) and from the
Center for Molecular Medicine Cologne (CMMC) to H.B. (B1). F.L. was
supported by grants from Instituto de Salud Carlos III (PI11/01225) and
Comunidad de Madrid (S2010/BMD-2359), S.A.E. by the CMMC (C1.1), S.N. by
the National Institutes of Health (HL113032, NS044155) and M.H. by the
European Union (LSHBCT-2005-512102). We thank Jude Samulski (University
of North Carolina at Chapel Hill, NC) for providing plasmid pXX6,
Vyomesh Patel (Oral & Pharyngeal Cancer Branch, National Institute of
Dental and Craniofacial Research, National Institutes of Health,
Bethesda, MD) for sharing reagents, and Hanna Janicki (University of
Cologne, Germany), and Stephanie Cambier (UCSF, San Francisco, CA) for
technical assistance. The authors declare no conflict of interest.
NR 50
TC 13
Z9 13
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
EI 1525-0024
J9 MOL THER
JI Mol. Ther.
PD MAY
PY 2014
VL 22
IS 5
BP 929
EP 939
DI 10.1038/mt.2014.14
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA AG4WQ
UT WOS:000335421500007
PM 24468915
ER
PT J
AU Doria-Rose, NA
Schramm, CA
Gorman, J
Moore, PL
Bhiman, JN
DeKosky, BJ
Ernandes, MJ
Georgiev, IS
Kim, HJ
Pancera, M
Staupe, RP
Altae-Tran, HR
Bailer, RT
Crooks, ET
Cupo, A
Druz, A
Garrett, NJ
Hoi, KH
Kong, R
Louder, MK
Longo, NS
McKee, K
Nonyane, M
O'Dell, S
Roark, RS
Rudicell, RS
Schmidt, SD
Sheward, DJ
Soto, C
Wibmer, CK
Yang, YP
Zhang, ZH
Mullikin, JC
Binley, JM
Sanders, RW
Wilson, IA
Moore, JP
Ward, AB
Georgiou, G
Williamson, C
Karim, SSA
Morris, L
Kwong, PD
Shapiro, L
Mascola, JR
AF Doria-Rose, Nicole A.
Schramm, Chaim A.
Gorman, Jason
Moore, Penny L.
Bhiman, Jinal N.
DeKosky, Brandon J.
Ernandes, Michael J.
Georgiev, Ivelin S.
Kim, Helen J.
Pancera, Marie
Staupe, Ryan P.
Altae-Tran, Han R.
Bailer, Robert T.
Crooks, Ema T.
Cupo, Albert
Druz, Aliaksandr
Garrett, Nigel J.
Hoi, Kam H.
Kong, Rui
Louder, Mark K.
Longo, Nancy S.
McKee, Krisha
Nonyane, Molati
O'Dell, Sijy
Roark, Ryan S.
Rudicell, Rebecca S.
Schmidt, Stephen D.
Sheward, Daniel J.
Soto, Cinque
Wibmer, Constantinos Kurt
Yang, Yongping
Zhang, Zhenhai
Mullikin, James C.
Binley, James M.
Sanders, Rogier W.
Wilson, Ian A.
Moore, John P.
Ward, Andrew B.
Georgiou, George
Williamson, Carolyn
Karim, Salim S. Abdool
Morris, Lynn
Kwong, Peter D.
Shapiro, Lawrence
Mascola, John R.
CA NISC Comparative Sequencing
TI Developmental pathway for potent V1V2-directed HIV-neutralizing
antibodies
SO NATURE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HUMAN MONOCLONAL-ANTIBODIES;
MAXIMUM-LIKELIHOOD; HIV-1-NEUTRALIZING ANTIBODIES; VACCINE EFFICACY;
STRUCTURAL BASIS; ENVELOPE TRIMER; B-CELLS; INFECTION; BROAD
AB Antibodies capable of neutralizing HIV-1 often target variable regions 1 and 2 (V1V2) of the HIV-1 envelope, but the mechanism of their elicitation has been unclear. Here we define the developmental pathway by which such antibodies are generated and acquire the requisite molecular characteristics for neutralization. Twelve somatically related neutralizing antibodies (CAP256-VRC26.01-12) were isolated from donor CAP256 (from the Centre for the AIDS Programme of Research in South Africa (CAPRISA)); each antibody contained the protruding tyrosine-sulphated, anionic antigen-binding loop (complementarity-determining region (CDR) H3) characteristic of this category of antibodies. Their unmutated ancestor emerged between weeks 30-38 post-infection with a 35-residue CDR H3, and neutralized the virus that superinfected this individual 15 weeks after initial infection. Improved neutralization breadth and potency occurred by week 59 with modest affinity maturation, and was preceded by extensive diversification of the virus population. HIV-1 V1V2-directed neutralizing antibodies can thus develop relatively rapidly through initial selection of B cells with a long CDR H3, and limited subsequent somatic hypermutation. These data provide important insights relevant to HIV-1 vaccine development.
C1 [Doria-Rose, Nicole A.; Gorman, Jason; Ernandes, Michael J.; Georgiev, Ivelin S.; Pancera, Marie; Staupe, Ryan P.; Altae-Tran, Han R.; Bailer, Robert T.; Druz, Aliaksandr; Kong, Rui; Louder, Mark K.; Longo, Nancy S.; McKee, Krisha; O'Dell, Sijy; Roark, Ryan S.; Rudicell, Rebecca S.; Schmidt, Stephen D.; Soto, Cinque; Yang, Yongping; Kwong, Peter D.; Shapiro, Lawrence; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Schramm, Chaim A.; Zhang, Zhenhai; Shapiro, Lawrence] Columbia Univ, Dept Biochem, New York, NY 10032 USA.
[Moore, Penny L.; Bhiman, Jinal N.; Nonyane, Molati; Wibmer, Constantinos Kurt; Morris, Lynn] NHLS, Natl Inst Communicable Dis, Ctr HIV & STIs, ZA-2131 Johannesburg, South Africa.
[Moore, Penny L.; Bhiman, Jinal N.; Wibmer, Constantinos Kurt; Morris, Lynn] Univ Witwatersrand, Fac Hlth Sci, ZA-2050 Johannesburg, South Africa.
[Moore, Penny L.; Garrett, Nigel J.; Williamson, Carolyn; Karim, Salim S. Abdool; Morris, Lynn] Univ KwaZulu Natal, CAPRISA, ZA-4013 Congella, South Africa.
[DeKosky, Brandon J.; Georgiou, George] Univ Texas Austin, Dept Chem Engn, Austin, TX 78712 USA.
[Kim, Helen J.; Wilson, Ian A.; Ward, Andrew B.] Scripps Res Inst, Dept Integrat Struct & Computat Biol, La Jolla, CA 92037 USA.
[Kim, Helen J.; Wilson, Ian A.; Ward, Andrew B.] Scripps Res Inst, Ctr HIV AIDS Vaccine Immunol & Immunogen Discover, La Jolla, CA 92037 USA.
[Kim, Helen J.; Wilson, Ian A.; Ward, Andrew B.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
[Crooks, Ema T.; Binley, James M.] Torrey Pines Inst, San Diego, CA 92037 USA.
[Cupo, Albert; Moore, John P.] Cornell Univ, Weill Med Coll, New York, NY 10065 USA.
[Hoi, Kam H.; Georgiou, George] Univ Texas Austin, Dept Biomed Engn, Austin, TX 78712 USA.
[Sheward, Daniel J.] Univ Cape Town, Inst Infect Dis & Mol Med, Div Med Virol, ZA-7701 Cape Town, South Africa.
[Sheward, Daniel J.] NHLS, ZA-7701 Cape Town, South Africa.
[Mullikin, James C.] NIH, NISC Comparat Sequencing Program, Bethesda, MD 20892 USA.
[Mullikin, James C.] NHGRI, NIH Intramural Sequencing Ctr, NIH, Bethesda, MD 20892 USA.
[Sanders, Rogier W.] Univ Amsterdam, Acad Med Ctr, Dept Med Microbiol, NL-1105 AZ Amsterdam, Netherlands.
[Wilson, Ian A.] Scripps Res Inst, Skaggs Inst Chem Biol, La Jolla, CA 92037 USA.
[Georgiou, George] Univ Texas Austin, Dept Mol Biosci, Austin, TX 78712 USA.
[Karim, Salim S. Abdool] Columbia Univ, Dept Epidemiol, New York, NY 10032 USA.
RP Morris, L (reprint author), NHLS, Natl Inst Communicable Dis, Ctr HIV & STIs, ZA-2131 Johannesburg, South Africa.
EM lynnm@nicd.ac.za; pdkwong@nih.gov; lss8@columbia.edu; jrmascola@nih.gov
RI Schmidt, Stephen/B-5398-2012; Ward, Andrew/F-9203-2014;
OI Ward, Andrew/0000-0001-7153-3769; Moore, Penny/0000-0001-8719-4028; ,
Carolyn/0000-0003-0125-1226; Bhiman, Jinal/0000-0001-6354-4003; Abdool
Karim, Salim/0000-0002-4986-2133; Wibmer, Constantinos
Kurt/0000-0003-2329-2280
FU Vaccine Research Center; NIAID; Fogarty International Center; NHGRI;
NIGMS of the National Institutes of Health, USA; International AIDS
Vaccine Initiative; National Science Foundation; Scripps CHAV-ID; South
African Department of Science and Technology; Wellcome Trust; Hertz
Foundation; Donald D. Harrington Foundation; Poliomyelitis Research
Foundation; National Research Foundation of South Africa; US Department
of Energy, Basic Energy Sciences, Office of Science [W-31-109-Eng-38]
FX We thank the participants in the CAPRISA 002 study for their commitment.
For technical assistance and advice, we thank: K. Mlisana, S. Sibeko, N.
Naicker, the CAPRISA 002 clinical team, N. Samsunder, S. Heeralall, B.
Lambson, M. Madzivhandila, T. Khoza, C. Mitchell Scheepers, E. Turk,
C.-L. Lin, M. Roederer, J. Stuckey, B. Hartman, G. Loots, J. H. Lee, G.
Ippolito, B. Briney, S. Hunicke-Smith and J. Wheeler, and members of the
WCMC HIVRAD Core and the NIH Vaccine Research Center HIMS, HIMC, SBS and
SBIS sections. We thank J. Baalwa, D. Ellenberger, F. Gao, B. Hahn, K.
Hong, J. Kim, F. McCutchan, D. Montefiori, J. Overbaugh, E.
Sanders-Buell, G. Shaw, R. Swanstrom, M. Thomson, S. Tovanabutra and L.
Zhang for contributing the HIV-1Envelope plasmids used in our
neutralizationpanel. Funding was provided by the intramural research
programs of the Vaccine Research Center and NIAID, the Fogarty
International Center, NHGRI, and NIGMS of the National Institutes of
Health, USA; the International AIDS Vaccine Initiative; the National
Science Foundation; Scripps CHAV-ID; the South African Department of
Science and Technology; and fellowships from the Wellcome Trust, Hertz
Foundation, Donald D. Harrington Foundation, Poliomyelitis Research
Foundation and the National Research Foundation of South Africa. Use of
sector 22 (Southeast Region Collaborative Access team) at the Advanced
Photon Source was supported by the US Department of Energy, Basic Energy
Sciences, Office of Science, under contract number W-31-109-Eng-38.
NR 83
TC 213
Z9 217
U1 4
U2 51
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD MAY 1
PY 2014
VL 509
IS 7498
BP 55
EP +
DI 10.1038/nature13036
PG 21
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TM
UT WOS:000335199100038
PM 24590074
ER
PT J
AU Zhang, KH
Zhang, J
Gao, ZG
Zhang, DD
Zhu, L
Han, GW
Moss, SM
Paoletta, S
Kiselev, E
Lu, WZ
Fenalti, G
Zhang, WR
Muller, CE
Yang, HY
Jiang, HL
Cherezov, V
Katritch, V
Jacobson, KA
Stevens, RC
Wu, BL
Zhao, Q
AF Zhang, Kaihua
Zhang, Jin
Gao, Zhan-Guo
Zhang, Dandan
Zhu, Lan
Han, Gye Won
Moss, Steven M.
Paoletta, Silvia
Kiselev, Evgeny
Lu, Weizhen
Fenalti, Gustavo
Zhang, Wenru
Mueller, Christa E.
Yang, Huaiyu
Jiang, Hualiang
Cherezov, Vadim
Katritch, Vsevolod
Jacobson, Kenneth A.
Stevens, Raymond C.
Wu, Beili
Zhao, Qiang
TI Structure of the human P2Y(12) receptor in complex with an
antithrombotic drug
SO NATURE
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; ACTIVE METABOLITE; NUCLEOTIDE RECEPTORS;
CRYSTAL-STRUCTURE; AMINO-ACIDS; ANTAGONISTS; IDENTIFICATION;
CLOPIDOGREL; INHIBITION; ACTIVATION
AB P2Y receptors (P2YRs), a family of purinergic G-protein-coupled receptors (GPCRs), are activated by extracellular nucleotides. There are a total of eight distinct functional P2YRs expressed in human, which are subdivided into P2Y1-like receptors and P2Y(12)-like receptors(1). Their ligands are generally charged molecules with relatively low bioavailability and stability in vivo(2), which limits our understanding of this receptor family. P2Y(12)R regulates platelet activation and thrombus formation(3,4), and several antithrombotic drugs targeting P2Y(12)R-including the prodrugs clopidogrel (Plavix) and prasugrel (Effient) that are metabolized and bind covalently, and the nucleoside analogue ticagrelor (Brilinta) that acts directly on the receptor-have been approved for the prevention of stroke and myocardial infarction. However, limitations of these drugs (for example, a very long half-life of clopidogrel action and a characteristic adverse effect profile of ticagrelor) 5,6 suggest that there is an unfulfilled medical need for developing a new generation of P2Y(12)R inhibitors(7,8). Here we report the 2.6 angstrom resolution crystal structure of human P2Y(12)R in complex with a non-nucleotide reversible antagonist, AZD1283. The structure reveals a distinct straight conformation of helix V, which sets P2Y(12)R apart from all other known class A GPCR structures. With AZD1283 bound, the highly conserved disulphide bridge in GPCRs between helix III and extracellular loop 2 is not observed and appears to be dynamic. Along with the details of the AZD1283-binding site, analysis of the extracellular interface reveals an adjacent ligand-binding region and suggests that both pockets could be required for dinucleotide binding. The structure provides essential insights for the development of improved P2Y(12)R ligands and allosteric modulators as drug candidates.
C1 [Zhang, Kaihua; Zhang, Jin; Zhang, Dandan; Zhu, Lan; Lu, Weizhen; Zhang, Wenru; Wu, Beili; Zhao, Qiang] Chinese Acad Sci, CAS Key Lab Receptor Res, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China.
[Gao, Zhan-Guo; Moss, Steven M.; Paoletta, Silvia; Kiselev, Evgeny; Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Han, Gye Won; Fenalti, Gustavo; Cherezov, Vadim; Katritch, Vsevolod; Stevens, Raymond C.] Scripps Res Inst, Dept Integrat Struct & Computat Biol, La Jolla, CA 92037 USA.
[Mueller, Christa E.] PharmaCtr Bonn, Inst Pharmaceut, D-53121 Bonn, Germany.
[Yang, Huaiyu; Jiang, Hualiang] Chinese Acad Sci, Drug Discovery & Design Ctr, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China.
[Stevens, Raymond C.] ShanghaiTech Univ, iHuman Inst, Shanghai 201203, Peoples R China.
RP Zhao, Q (reprint author), Chinese Acad Sci, CAS Key Lab Receptor Res, Shanghai Inst Mat Med, 555 Zuchongzhi Rd, Shanghai 201203, Peoples R China.
EM zhaoq@simm.ac.cn
RI Jacobson, Kenneth/A-1530-2009; Cherezov, Vadim/L-9812-2013; Katritch,
Vsevolod/Q-8357-2016; Muller, Christa/C-7748-2014; Stevens,
Raymond/K-7272-2015;
OI Jacobson, Kenneth/0000-0001-8104-1493; Cherezov,
Vadim/0000-0002-5265-3914; Muller, Christa/0000-0002-0013-6624; Stevens,
Raymond/0000-0002-4522-8725; Zhang, Kaihua/0000-0003-3734-3624
FU National Basic Research Program of China [2012CB910400, 2012CB518000];
National Institutes of Health (NIH) [R01 AI100604, U54 GM094618];
National Science Foundation of China [31370729, 31170683]; National
Institute of General Medical Sciences Postdoctoral Research Associate
program; NIH National Institute of Diabetes and Digestive and Kidney
Diseases Intramural Research Program
FX This work was supported by National Basic Research Program of China
grants 2012CB910400 and 2012CB518000 (B. W., Q.Z.), National Institutes
of Health (NIH) grants R01 AI100604 (B. W., Q.Z.) and U54 GM094618 (V.
C., V. K., R. C. S.; Target GPCR-87), National Science Foundation of
China grants 31370729 and 31170683 (B. W., Q.Z.), the National Institute
of General Medical Sciences Postdoctoral Research Associate program (E.
K.) and the NIH National Institute of Diabetes and Digestive and Kidney
Diseases Intramural Research Program (K.A.J.). The authors thank
AstraZeneca for their gift of AZD1283, and thank S. Nylander, F.
Giordanetto and H. van Giezen for careful review and scientific feedback
on the manuscript, A. Walker for assistance with manuscript preparation,
and C. Wang and D. Wacker for help on collection of X-ray diffraction
data.
NR 36
TC 102
Z9 108
U1 9
U2 77
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD MAY 1
PY 2014
VL 509
IS 7498
BP 115
EP 118
DI 10.1038/nature13083
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TM
UT WOS:000335199100050
PM 24670650
ER
PT J
AU Zhang, J
Zhang, KH
Gao, ZG
Paoletta, S
Zhang, DD
Han, GW
Li, TT
Ma, LM
Zhang, WR
Muller, CE
Yang, HY
Jiang, HL
Cherezov, V
Katritch, V
Jacobson, KA
Stevens, RC
Wu, BL
Zhao, Q
AF Zhang, Jin
Zhang, Kaihua
Gao, Zhan-Guo
Paoletta, Silvia
Zhang, Dandan
Han, Gye Won
Li, Tingting
Ma, Limin
Zhang, Wenru
Mueller, Christa E.
Yang, Huaiyu
Jiang, Hualiang
Cherezov, Vadim
Katritch, Vsevolod
Jacobson, Kenneth A.
Stevens, Raymond C.
Wu, Beili
Zhao, Qiang
TI Agonist-bound structure of the human P2Y(12) receptor
SO NATURE
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; MUSCARINIC ACETYLCHOLINE-RECEPTOR; RESOLUTION
CRYSTAL-STRUCTURE; A(2A) ADENOSINE RECEPTOR; MEMBRANE-PROTEINS;
IDENTIFICATION; ANTAGONISTS; ACTIVATION; RHODOPSIN; COMPLEX
AB The P2Y(12) receptor (P2Y(12)R), one of eight members of the P2YR family expressed in humans, is one of the most prominent clinical drug targets for inhibition of platelet aggregation. Although mutagenesis and modelling studies of the P2Y(12)R provided useful insights into ligand binding(1-4), the agonist and antagonist recognition and function at the P2Y(12)R remain poorly understood at the molecular level. Here we report the structures of the human P2Y(12)R in complex with the full agonist 2-methylthio-adenosine-5'-diphosphate (2MeSADP, a close analogue of endogenous agonist ADP) at 2.5 angstrom resolution, and the corresponding ATP derivative 2-methylthio-adenosine-5'-triphosphate (2MeSATP) at 3.1 angstrom resolution. These structures, together with the structure of the P2Y(12)R with antagonist ethyl 6-(4-((benzylsulfonyl) carbamoyl)piperidin-1-yl)-5-cyano-2-methylnicotinate (AZD1283)(5), reveal striking conformational changes between nucleotide and non-nucleotide ligand complexes in the extracellular regions. Further analysis of these changes provides insight into a distinct ligand binding landscape inthed-group of class AG-protein-coupled receptors (GPCRs). Agonist and non-nucleotide antagonist adopt different orientations in the P2Y(12)R, with only partially overlapped binding pockets. The agonist-bound P2Y(12)R structure answers long-standing questions surrounding P2Y(12)R-agonist recognition, and reveals interactions with several residues that had not been reported to be involved in agonist binding. As a first example, to our knowledge, of a GPCR in which agonist access to the binding pocket requires large-scale rearrangements in the highly malleable extracellular region, the structural and docking studies will therefore provide invaluable insight into the pharmacology and mechanisms of action of agonists and different classes of antagonists for the P2Y(12)R and potentially for other closely related P2YRs.
C1 [Zhang, Jin; Zhang, Kaihua; Zhang, Dandan; Li, Tingting; Ma, Limin; Zhang, Wenru; Wu, Beili; Zhao, Qiang] Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China.
[Gao, Zhan-Guo; Paoletta, Silvia; Jacobson, Kenneth A.] Natl Inst Diabet & Digest & Kidney Dis, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Han, Gye Won; Cherezov, Vadim; Katritch, Vsevolod; Stevens, Raymond C.] Scripps Res Inst, Dept Integrat Struct & Computat Biol, La Jolla, CA 92037 USA.
[Mueller, Christa E.] Univ Bonn, PharmaCtr Bonn, D-53121 Bonn, Germany.
[Yang, Huaiyu; Jiang, Hualiang] Chinese Acad Sci, Shanghai Inst Mat Med, Drug Discovery & Design Ctr, Shanghai 201203, Peoples R China.
[Stevens, Raymond C.] ShanghaiTech Univ, IHuman Inst, Shanghai 201203, Peoples R China.
RP Wu, BL (reprint author), Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, 555 Zuchongzhi Rd, Shanghai 201203, Peoples R China.
EM beiliwu@simm.ac.cn; zhaoq@simm.ac.cn
RI Jacobson, Kenneth/A-1530-2009; Cherezov, Vadim/L-9812-2013; Katritch,
Vsevolod/Q-8357-2016; Muller, Christa/C-7748-2014; Stevens,
Raymond/K-7272-2015;
OI Jacobson, Kenneth/0000-0001-8104-1493; Cherezov,
Vadim/0000-0002-5265-3914; Muller, Christa/0000-0002-0013-6624; Stevens,
Raymond/0000-0002-4522-8725; Zhang, Kaihua/0000-0003-3734-3624
FU National Basic Research Program of China [2012CB910400, 2012CB518000,
2014CB910400]; National Institutes of Health [R01AI100604, U54
GM094618]; National Science Foundation of China [31370729]; National
Science and Technology Major Project [2013ZX09507001, 2012ZX09301001];
National Institutes of Health NIDDK Intramural Research Program;
National Natural Science Foundation of China [91313000]
FX This work was supported by the National Basic Research Program of China
grants 2012CB910400, 2012CB518000 and 2014CB910400 (B. W., Q.Z.), the
National Institutes of Health grants R01AI100604 (B. W., Q.Z.) and U54
GM094618 (V. C., V. K., R. C. S.; Target GPCR-87), the National Science
Foundation of China grants 31370729 and National Science and Technology
Major Project 2013ZX09507001 and 2012ZX09301001 (B. W., Q.Z.), National
Institutes of Health NIDDK Intramural Research Program (K.A.J.) and the
National Natural Science Foundation of China 91313000 (H.J.). The
authors thank S. Nylander, E. Kiselev and S. Moss for scientific
feedback on the manuscript, A. Walker for assistance with manuscript
preparation and K. Kadyshevskaya for help with figure preparation. The
synchrotron radiation experiments were performed at the BL41XU of
SPring-8 with the approval of the Japan Synchrotron Radiation Research
Institute (JASRI) (proposal no. 2013B1049). We thank the beamline staff
members of the BL41XU for help with X-ray data collection.
NR 34
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U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD MAY 1
PY 2014
VL 509
IS 7498
BP 119
EP 122
DI 10.1038/nature13288
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TM
UT WOS:000335199100051
PM 24784220
ER
PT J
AU Kimmel, SE
French, B
Geller, NL
AF Kimmel, Stephen E.
French, Benjamin
Geller, Nancy L.
CA COAG Investigators
TI Genotype-Guided Dosing of Vitamin K Antagonists REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID ANTICOAGULATION; TRIAL
C1 [Kimmel, Stephen E.; French, Benjamin] Univ Penn, Philadelphia, PA 19104 USA.
[Geller, Nancy L.] NHLBI, Bethesda, MD 20892 USA.
RP Kimmel, SE (reprint author), Univ Penn, Philadelphia, PA 19104 USA.
EM stevek@mail.med.upenn.edu
NR 2
TC 6
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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
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD MAY 1
PY 2014
VL 370
IS 18
BP 1763
EP 1764
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA AG4QM
UT WOS:000335405200023
PM 24785213
ER
PT J
AU Davis, FM
Azimi, I
Faville, RA
Peters, AA
Jalink, K
Putney, JW
Goodhill, GJ
Thompson, EW
Roberts-Thomson, SJ
Monteith, GR
AF Davis, F. M.
Azimi, I.
Faville, R. A.
Peters, A. A.
Jalink, K.
Putney, J. W., Jr.
Goodhill, G. J.
Thompson, E. W.
Roberts-Thomson, S. J.
Monteith, G. R.
TI Induction of epithelial-mesenchymal transition (EMT) in breast cancer
cells is calcium signal dependent
SO ONCOGENE
LA English
DT Article
DE epithelial-mesenchymal transition; calcium; vimentin; STAT3; signal
transduction; breast cancer
ID GENE-EXPRESSION; UP-REGULATION; MIGRATION; TRPM7; PROGRESSION;
METASTASIS; CHANNELS; ACTIVATION; CONTRIBUTES; PHENOTYPE
AB Signals from the tumor microenvironment trigger cancer cells to adopt an invasive phenotype through epithelial-mesenchymal transition (EMT). Relatively little is known regarding key signal transduction pathways that serve as cytosolic bridges between cell surface receptors and nuclear transcription factors to induce EMT. A better understanding of these early EMT events may identify potential targets for the control of metastasis. One rapid intracellular signaling pathway that has not yet been explored during EMT induction is calcium. Here we show that stimuli used to induce EMT produce a transient increase in cytosolic calcium levels in human breast cancer cells. Attenuation of the calcium signal by intracellular calcium chelation significantly reduced epidermal growth factor (EGF)-and hypoxia-induced EMT. Intracellular calcium chelation also inhibited EGF-induced activation of signal transducer and activator of transcription 3 (STAT3), while preserving other signal transduction pathways such as Akt and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. To identify calcium-permeable channels that may regulate EMT induction in breast cancer cells, we performed a targeted siRNA-based screen. We found that transient receptor potential-melastatin- like 7 (TRPM7) channel expression regulated EGF-induced STAT3 phosphorylation and expression of the EMT marker vimentin. Although intracellular calcium chelation almost completely blocked the induction of many EMT markers, including vimentin, Twist and N-cadherin, the effect of TRPM7 silencing was specific for vimentin protein expression and STAT3 phosphorylation. These results indicate that TRPM7 is a partial regulator of EMT in breast cancer cells, and that other calcium-permeable ion channels are also involved in calcium-dependent EMT induction. In summary, this work establishes an important role for the intracellular calcium signal in the induction of EMT in human breast cancer cells. Manipulation of calcium-signaling pathways controlling EMT induction in cancer cells may therefore be an important therapeutic strategy for preventing metastases.
C1 [Davis, F. M.; Azimi, I.; Peters, A. A.; Roberts-Thomson, S. J.; Monteith, G. R.] Univ Queensland, Sch Pharm, Brisbane, Qld 4072, Australia.
[Faville, R. A.; Goodhill, G. J.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4072, Australia.
[Jalink, K.] Netherlands Canc Inst, Div Cell Biol, Amsterdam, Netherlands.
[Putney, J. W., Jr.] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
[Goodhill, G. J.] Univ Queensland, Sch Math & Phys, Brisbane, Qld 4072, Australia.
[Thompson, E. W.] St Vincents Inst, Fitzroy, Vic, Australia.
[Thompson, E. W.] Univ Melbourne, St Vincents Hosp, Dept Surg, Fitzroy, Vic 3065, Australia.
RP Monteith, GR (reprint author), Univ Queensland, Sch Pharm, Brisbane, Qld 4072, Australia.
EM gregm@uq.edu.au
RI Peters, Amelia/E-4254-2010; Roberts-Thomson, Sarah/B-4282-2011;
Thompson, Erik/A-1425-2009; Azimi, Iman/E-2043-2011; Davis,
Felicity/P-1387-2016; Monteith, Gregory/B-1626-2008
OI Roberts-Thomson, Sarah/0000-0001-8202-5786; Thompson,
Erik/0000-0002-9723-4924; Azimi, Iman/0000-0001-9477-9999; Davis,
Felicity/0000-0001-9112-118X; Monteith, Gregory/0000-0002-4345-530X
FU National Health and Medical Research Council (NHMRC) [569645, 1022263];
Intramural Research Program of the US National Institutes of Health,
National Institute of Environmental Health Sciences (NIEHS); NHMRC
Biomedical Postgraduate Scholarship [511262]; UQ Postdoctoral
Fellowship; National Breast Cancer Foundation
FX The research was partially supported by the National Health and Medical
Research Council (NHMRC; project grants 569645 and 1022263) and the
Intramural Research Program of the US National Institutes of Health,
National Institute of Environmental Health Sciences (NIEHS). FD was
funded by an NHMRC Biomedical Postgraduate Scholarship (511262), RF was
funded by a UQ Postdoctoral Fellowship and EWT was funded in part by the
National Breast Cancer Foundation.
NR 53
TC 54
Z9 56
U1 4
U2 38
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD MAY 1
PY 2014
VL 33
IS 18
BP 2307
EP 2316
DI 10.1038/onc.2013.187
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA AG5ID
UT WOS:000335451800004
PM 23686305
ER
PT J
AU Martin, D
Nguyen, Q
Molinolo, A
Gutkind, JS
AF Martin, D.
Nguyen, Q.
Molinolo, A.
Gutkind, J. S.
TI Accumulation of dephosphorylated 4EBP after mTOR inhibition with
rapamycin is sufficient to disrupt paracrine transformation by the KSHV
vGPCR oncogene
SO ONCOGENE
LA English
DT Article
DE Kaposi's sarcoma; mTOR; PI3K; 4EBP; rapamycin; cancer
ID PROTEIN-COUPLED RECEPTOR; KAPOSIS-SARCOMA; MAMMALIAN TARGET;
HERPESVIRUS; CELL; PATHOGENESIS; INFECTION; GROWTH; EXPRESSION;
NEOPLASIA
AB Dysregulation of the PI3K/Akt/mTOR pathway is one of the most frequent events in human cancer. However, the clinical benefits of PI3K/Akt/mTOR inhibitors have not yet achieved their predicted potential in many of the most prevalent human cancers. Of interest, treatment of Kaposi's sarcoma (KS) patients with rapamycin provided the first evidence of the antineoplastic activity of mTOR inhibitors in humans, becoming the standard of care for KS arising in renal transplant patients. Thus, the study of KS may provide a unique opportunity to dissect the contribution of specific mTOR downstream targets to cancer development. The KS associated herpesvirus (KSHV) is the etiological agent for KS, and the KSHV-encoded oncogene viral-G protein-coupled receptor (vGPCR) promotes the potent activation of the PI3K-Akt-mTOR pathway by both direct and paracrine mechanisms. We focused on a direct target of mTOR, EIF4EBP1/2/3 (4EBP), which inhibits the translation of eukaryotic initiation factor 4E (eiF4E)-bound mRNAs. 4EBP phosphorylation by mTOR relieves its inhibitory activity, hence resulting in increased eiF4E-dependent mRNA translation. We developed a paracrine transformation model, recapitulating the cellular composition of KS lesions, in which vGPCR-expressing cells promote the rapid proliferation of endothelial cells, thus expressing KSHV-latent genes by the release of growth factors. Using this model, we show here that the accumulation of dephosphorylated 4EBP in response to rapamycin or by the expression of an mTOR-insensitive mutant of 4EBP1 is sufficient to disrupt the eiF4E function downstream of mTOR to a similar extent than the mTOR catalytic inhibitor Torin2 and to halt KS development. We also provide evidence that eiF4E contributes to paracrine neoplastic, signaling through the release of pro-angiogenic factors that are acting on endothelial cells, expressing KSHV-latent genes. These findings may provide a preclinical platform and the rationale for the development of novel mTOR, inhibiting agents that may selectively disrupt the mTOR-4EBP interaction for the treatment of KS and other tumor lesions, exhibiting hyperactive mTOR pathway function.
C1 [Martin, D.; Nguyen, Q.; Molinolo, A.; Gutkind, J. S.] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Gutkind, JS (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bldg 30 Room 320,30 Convent Dr MSC 4340, Bethesda, MD 20892 USA.
EM sg39v@nih.gov
FU National Institutes of Health Intramural AIDS-Targeted Antiviral
Program; National Institute of Dental and Craniofacial Research
FX This research was supported by the National Institutes of Health
Intramural AIDS-Targeted Antiviral Program and the National Institute of
Dental and Craniofacial Research. We apologize to colleagues whose
primary research papers may not have been cited due to space
constraints.
NR 28
TC 4
Z9 4
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD MAY 1
PY 2014
VL 33
IS 18
BP 2405
EP 2412
DI 10.1038/onc.2013.193
PG 8
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA AG5ID
UT WOS:000335451800013
PM 23708663
ER
PT J
AU Pattanayak, P
Bluemke, DA
AF Pattanayak, Puskar
Bluemke, David A.
TI Cardiac MR Imaging to Probe Tissue Composition of the Heart by Using T1
Mapping
SO RADIOLOGY
LA English
DT Editorial Material
ID CARDIOVASCULAR MAGNETIC-RESONANCE; DIFFUSE MYOCARDIAL FIBROSIS;
SYSTEMIC-SCLEROSIS; CARDIOMYOPATHY; BIOPSY
C1 [Pattanayak, Puskar; Bluemke, David A.] Natl Inst Biomed Imaging & Engn, Dept Radiol & Imaging Sci, NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Bluemke, DA (reprint author), Natl Inst Biomed Imaging & Engn, Dept Radiol & Imaging Sci, NIH, Ctr Clin, 10 Ctr Dr,Room 1C355, Bethesda, MD 20892 USA.
EM bluemked@nih.gov
OI Bluemke, David/0000-0002-8323-8086
NR 15
TC 1
Z9 1
U1 0
U2 2
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD MAY
PY 2014
VL 271
IS 2
BP 320
EP 322
DI 10.1148/radiol.14140287
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AG1CQ
UT WOS:000335153000002
PM 24761952
ER
PT J
AU Zavodni, AEH
Wasserman, BA
McClelland, RL
Gomes, AS
Folsom, AR
Polak, JF
Lima, JAC
Bluemke, DA
AF Zavodni, Anna E. H.
Wasserman, Bruce A.
McClelland, Robyn L.
Gomes, Antoinette S.
Folsom, Aaron R.
Polak, Joseph F.
Lima, Joao A. C.
Bluemke, David A.
TI Carotid Artery Plaque Morphology and Composition in Relation to Incident
Cardiovascular Events: The Multi-Ethnic Study of Atherosclerosis (MESA)
SO RADIOLOGY
LA English
DT Article
ID INTIMA-MEDIA THICKNESS; RISK-ASSESSMENT STRATEGIES; LIPID-LOWERING
THERAPY; LEFT-VENTRICULAR MASS; HIGH-RESOLUTION; IN-VIVO; INTRAPLAQUE
HEMORRHAGE; VULNERABLE PATIENT; PREDICTIVE ABILITY; ROC CURVE
AB Purpose: To determine if carotid plaque morphology and composition with magnetic resonance (MR) imaging can be used to identify asymptomatic subjects at risk for cardiovascular events.
Materials and Methods: Institutional review boards at each site approved the study, and all sites were Health Insurance Portability and Accountability Act (HIPAA) compliant. A total of 946 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) were evaluated with MR imaging and ultrasonography (US). MR imaging was used to define carotid plaque composition and remodeling index (wall area divided by the sum of wall area and lumen area), while US was used to assess carotid wall thickness. Incident cardiovascular events, including myocardial infarction, resuscitated cardiac arrest, angina, stroke, and death, were ascertained for an average of 5.5 years. Multivariable Cox proportional hazards models, C statistics, and net reclassification improvement (NRI) for event prediction were determined.
Results: Cardiovascular events occurred in 59 (6%) of participants. Carotid IMT as well as MR imaging remodeling index, lipid core, and calcium in the internal carotid artery were significant predictors of events in univariate analysis (P < .001 for all). For traditional risk factors, the C statistic for event prediction was 0.696. For MR imaging remodeling index and lipid core, the C statistic was 0.734 and the NRI was 7.4% and 15.8% for participants with and those without cardiovascular events, respectively (P = .02). The NRI for US IMT in addition to traditional risk factors was not significant.
Conclusion: The identification of vulnerable plaque characteristics with MR imaging aids in cardiovascular disease prediction and improves the reclassification of baseline cardiovascular risk. (C) RSNA, 2014
C1 [Zavodni, Anna E. H.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Dept Med Imaging, Toronto, ON, Canada.
[Wasserman, Bruce A.; Lima, Joao A. C.] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
[Lima, Joao A. C.] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[McClelland, Robyn L.] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98195 USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Dept Radiol, Los Angeles, CA 90024 USA.
[Folsom, Aaron R.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Polak, Joseph F.] Tufts Med Ctr, Dept Radiol, Boston, MA USA.
[Bluemke, David A.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
RP Bluemke, DA (reprint author), NIH, Dept Radiol & Imaging Sci, Ctr Clin, 10 Ctr Dr,Bldg 10-1C355, Bethesda, MD 20892 USA.
EM david.bluemke@nih.gov
OI Bluemke, David/0000-0002-8323-8086
FU NHLBI NIH HHS [N01 HC095163, N01HC95159, N01HC95168, R01 HL069905]
NR 35
TC 15
Z9 16
U1 0
U2 5
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD MAY
PY 2014
VL 271
IS 2
BP 381
EP 389
DI 10.1148/radiol.14131020
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AG1CQ
UT WOS:000335153000009
PM 24592924
ER
PT J
AU Todarello, G
Feng, NP
Kolachana, BS
Li, C
Vakkalanka, R
Bertolino, A
Weinberger, DR
Straub, RE
AF Todarello, Giovanna
Feng, Ningping
Kolachana, Bhaskar S.
Li, Chao
Vakkalanka, Radhakrishna
Bertolino, Alessandro
Weinberger, Daniel R.
Straub, Richard E.
TI Incomplete penetrance of NRXN1 deletions in families with schizophrenia
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Copy number variation; CNV; Deletion; NRXN1; Neurexin; Schizophrenia
ID HIDDEN-MARKOV MODEL; SNP GENOTYPING DATA; CHROMOSOMAL-ABNORMALITIES;
CNVS; ASSOCIATION; DISORDERS; SPECTRUM
AB Neurexin 1 (NRXN1) is a presynaptic neuronal adhesion molecule that interacts with postsynaptic neuroligins in both glutamatergic and GABAergic synapses and is important in synaptic formation and function. NRXN1 deletions increase the risk of schizophrenia, so our aims were to explore this in our family sample, to distinguish de novo from inherited mutations, to examine transmission to affected and unaffected siblings and to estimate penetrance. We performed copy number analyses in NRXN1 using data from Illumina BeadArrays from 635 subjects with schizophrenia (276 in genotyped families), 487 of their unaffected parents and 309 unaffected siblings as well as 635 normal controls, all from the CBDB/NIMH Genetic Study of Schizophrenia. Deletions called by software were confirmed by quantitative PCR and comparative genome hybridization. There were deletions in 15 individuals in 11 families, including de novo exonic deletions in one case and one unaffected sibling. We observed no deletions in controls, 7 deletions in cases (1.10%), and an unexpectedly high deletion frequency in parents (n = 5, 1.02%) and siblings (n = 3, 0.97%). Three families showed inheritance from an unaffected parent, and in two families an unaffected parent did not transmit to the affected offspring. Thus we have added to the evidence that NRXN1 deletions are more frequent in patients with schizophrenia than in healthy individuals. However, the presence of de novo deletions in unaffected relatives and transmission from and to unaffected family members demonstrated that while the deletions may well have been necessary for some carriers to develop schizophrenia, they were not always sufficient. (C) 2014 Elsevier B. V. All rights reserved.
C1 [Todarello, Giovanna] Univ Bari, Psychiat Neurosci Grp, Dept Basic Med Sci Neurosci & Sense Organs, Bari, Italy.
[Feng, Ningping; Kolachana, Bhaskar S.; Vakkalanka, Radhakrishna; Weinberger, Daniel R.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Li, Chao; Weinberger, Daniel R.; Straub, Richard E.] Johns Hopkins Univ, Lieber Inst Brain Dev, Baltimore, MD 21205 USA.
[Bertolino, Alessandro] Univ Bari, Dept Basic Med Sci Neurosci & Sense Organs, Bari, Italy.
[Bertolino, Alessandro] Hoffman La Roche Ltd, Pharma Res & Early Dev, Neurosci DTA, Basel, Switzerland.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD 21230 USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD 21230 USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Dept Neurosci, Baltimore, MD 21230 USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Inst Med Genet, Baltimore, MD 21230 USA.
RP Straub, RE (reprint author), Johns Hopkins Univ, Lieber Inst Brain Dev, Med Campus,855 North Wolfe St,Suite 300, Baltimore, MD 21205 USA.
EM richard.straub@libd.org
FU National Institute of Mental Health, NIH
FX This study was supported by direct funding of Intramural Research
Program of the National Institute of Mental Health, NIH to the
Weinberger lab and the Lieber Institute for Brain Development.
NR 27
TC 14
Z9 15
U1 1
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
EI 1573-2509
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD MAY
PY 2014
VL 155
IS 1-3
BP 1
EP 7
DI 10.1016/j.schres.2014.02.023
PG 7
WC Psychiatry
SC Psychiatry
GA AG5EN
UT WOS:000335442200001
PM 24680031
ER
PT J
AU Liu, YM
Shim, E
Nguyen, P
Gibbons, AT
Mitchell, JB
Poirier, MC
AF Liu, Yongmin
Shim, Eunwoo
Phuonggiang Nguyen
Gibbons, Alexander T.
Mitchell, James B.
Poirier, Miriam C.
TI Tempol Protects Cardiomyocytes from Nucleoside Reverse Transcriptase
Inhibitor-Induced Mitochondrial Toxicity
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE mitochondria; antiretroviral therapy; electron microscopy; oxidative
phosphorylation; superoxide; Seahorse extracellular flux analyzer
ID ANTIRETROVIRAL NUCLEOSIDE; PERINATAL EXPOSURE; DYSFUNCTION; ANALOGS;
HEART; DNA
AB Nucleoside reverse transcriptase inhibitors (NRTIs), essential components of combinational therapies used for treatment of human immunodeficiency virus-1, damage heart mitochondria. Here, we have shown mitochondrial compromise in H9c2 rat cardiomyocytes exposed for 16 passages (P) to the NRTIs zidovudine (AZT, 50 mu M) and didanosine (ddI, 50 mu M), and we have demonstrated protection from mitochondrial compromise in cells treated with 200 mu M 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (Tempol) or 200 mu M 1-hydroxy-4-[2-triphenylphosphonio)-acetamido]-2,2,6,6-tetramethylpiperidine (Tempol-H), along with AZT/ddI, for 16P. Exposure to AZT/ddI caused a moderate growth inhibition at P3, P5, P7, and P13, which was not altered by addition of Tempol or Tempol-H. Mitochondrial oxidative phosphorylation capacity was determined as uncoupled oxygen consumption rate (OCR) by Seahorse XF24 Analyzer. At P5, P7, and P13, AZT/ddI-exposed cells showed an OCR reduction of 8.8-57.2% in AZT/ddI-exposed cells, compared with unexposed cells. Addition of Tempol or Tempol-H, along with AZT/ddI, resulted in OCR levels increased by about 300% above the values seen with AZT/ddI alone. The Seahorse data were further supported by electron microscopy (EM) studies in which P16 cells exposed to AZT/ddI/Tempol had less mitochondrial pathology than P16 cells exposed to AZT/ddI. Western blots of P5 cells showed that Tempol and Tempol-H upregulated expression of mitochondrial uncoupling protein-2 (UCP-2). However, Complex I activity that was reduced by AZT/ddI, was not restored in the presence of AZT/ddI/Tempol. Superoxide levels were increased in the presence of AZT/ddI and significantly decreased in cells exposed to AZT/3TC/Tempol at P3, P7, and P10. In conclusion, Tempol protects against NRTI-induced mitochondrial compromise, and UCP-2 plays a role through mild uncoupling.
C1 [Liu, Yongmin; Shim, Eunwoo; Phuonggiang Nguyen; Gibbons, Alexander T.; Poirier, Miriam C.] NCI, Carcinogen DNA Interact Sect, Lab Canc Biol & Genet, CCR,NIH, Bethesda, MD 20892 USA.
[Mitchell, James B.] NCI, Tumor Biol Sect, Radiat Biol Branch, CCR,NIH, Bethesda, MD 20892 USA.
RP Liu, YM (reprint author), NCI, Carcinogen DNA Interact Sect, NIH, Bldg 37,Rm 4032,37 Convent Dr,MSC-4255, Bethesda, MD 20892 USA.
EM yongminl@mail.nih.gov
OI Nguyen, Phuonggiang/0000-0003-1638-1584
FU National Institutes of Health, Center for Cancer Research, National
Cancer Institute
FX Intramural Research Program of the National Institutes of Health, Center
for Cancer Research, National Cancer Institute.
NR 26
TC 4
Z9 4
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD MAY
PY 2014
VL 139
IS 1
BP 133
EP 141
DI 10.1093/toxsci/kfu034
PG 9
WC Toxicology
SC Toxicology
GA AG0ZN
UT WOS:000335144600012
PM 24591154
ER
PT J
AU Chen, SA
Zhou, DJ
Hsin, LY
Kanaya, N
Wong, C
Yip, R
Sakamuru, S
Xia, MH
Yuan, YC
Witt, K
Teng, C
AF Chen, Shiuan
Zhou, Dujin
Hsin, Li-Yu
Kanaya, Noriko
Wong, Cynthie
Yip, Richard
Sakamuru, Srilatha
Xia, Menghang
Yuan, Yate-Ching
Witt, Kristine
Teng, Christina
TI AroER Tri-Screen Is a Biologically Relevant Assay for Endocrine
Disrupting Chemicals Modulating the Activity of Aromatase and/or the
Estrogen Receptor
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE Aromatase-expressing cell line; EDCs; estrogen receptor; high-throughput
screening; MCF-7 cells; qHTS; Tox21
ID BREAST-CANCER CELLS; BISPHENOL-A; MCF-7 CELLS; RNA-SEQ; EXPRESSION;
ESTRADIOL; INHIBITORS; ALPHA; MECHANISMS; TAMOXIFEN
AB Endocrine disrupting chemicals (EDCs) interfere with the biosynthesis, metabolism, and functions of steroid hormones, including estrogens and androgens. Aromatase enzyme converts androgen to estrogen. Thus, EDCs against aromatase significantly impact estrogen- and/or androgen-dependent functions, including the development of breast cancer. The current study aimed to develop a biologically relevant cell-based high-throughput screening assay to identify EDCs that act as aromatase inhibitors (AIs), estrogen receptor (ER) agonists, and/or ER antagonists. The AroER tri-screen assay was developed by stable transfection of ER-positive, aromatase-expressing MCF-7 breast cancer cells with an estrogen responsive element (ERE) driven luciferase reporter plasmid. The AroER tri-screen can identify: estrogenic EDCs, which increase luciferase signal without 17 beta-estradiol (E2); anti-estrogenic EDCs, which inhibit the E2-induced luciferase signal; and AI-like EDCs, which suppress a testosterone-induced luciferase signal. The assay was first optimized in a 96-well plate format and then miniaturized into a 1536-well plate format. The AroER tri-screen was demonstrated to be suitable for high-throughput screening in the 1536-well plate format, with a 6.9-fold signal-to-background ratio, a 5.4% coefficient of variation, and a screening window coefficient (Z-factor) of 0.78. The assay suggested that bisphenol A (BPA) functions mainly as an ER agonist. Results from screening the 446 drugs in the National Institutes of Health Clinical Collection revealed 106 compounds that modulated ER and/or aromatase activities. Among these, two AIs (bifonazole and oxiconazole) and one ER agonist (paroxetine) were confirmed through alternative aromatase and ER activity assays. These findings indicate that AroER tri-screen is a useful high-throughput screening system for identifying ER ligands and aromatase-inhibiting chemicals.
C1 [Chen, Shiuan; Zhou, Dujin; Hsin, Li-Yu; Kanaya, Noriko; Wong, Cynthie; Yip, Richard; Yuan, Yate-Ching] City Hope Natl Med Ctr, Beckman Res Inst, Dept Canc Biol, Duarte, CA 91010 USA.
[Sakamuru, Srilatha; Xia, Menghang] NIH, Natl Ctr Adv Translat Sci, Rockville, MD 20850 USA.
[Witt, Kristine; Teng, Christina] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
RP Chen, SA (reprint author), City Hope Natl Med Ctr, Beckman Res Inst, Dept Canc Biol, Duarte, CA 91010 USA.
EM schen@coh.org
FU CBCRP [17UB-8701]; NTP-NCATS [ES-7020-01]; National Cancer Institute of
the National Institutes of Health [P30CA33572]; National Cancer
Institute of the NIH [P30CA33572]
FX CBCRP (17UB-8701 to S. C.); NTP-NCATS Interagency Agreement
(ES-7020-01); National Cancer Institute of the National Institutes of
Health (P30CA33572). Research reported in this publication included work
performed in the Bioinformatics core, High Throughput Screening core,
and Integrative Genomics core supported by the National Cancer Institute
of the NIH under award number P30CA33572.
NR 41
TC 4
Z9 4
U1 0
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD MAY
PY 2014
VL 139
IS 1
BP 198
EP 209
DI 10.1093/toxsci/kfu023
PG 12
WC Toxicology
SC Toxicology
GA AG0ZN
UT WOS:000335144600016
PM 24496634
ER
PT J
AU Iantorno, M
Weiss, RG
AF Iantorno, Micaela
Weiss, Robert G.
TI Using advanced noninvasive imaging techniques to probe the links between
regional coronary artery endothelial dysfunction and atherosclerosis
SO TRENDS IN CARDIOVASCULAR MEDICINE
LA English
DT Review
ID MAGNETIC-RESONANCE; CARDIOVASCULAR RISK; PHENOTYPIC HETEROGENEITY;
MENTAL STRESS; NITRIC-OXIDE; BLOOD-FLOW; DISEASE; HEART; INFLAMMATION;
PLAQUE
AB Cardiovascular disease remains the number one cause of death in the US annually. The development in recent years of imaging strategies that can identify coronary endothelial dysfunction noninvasively provides new information about the early presence and local spatial heterogeneity of endothelial function in patients with, and those at risk for, coronary artery disease. In this article, we will briefly review the mechanisms relating endothelial function and atherosclerosis, contemporary imaging strategies now able to quantify coronary endothelial function noninvasively, and recent insights on human coronary endothelial function. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Iantorno, Micaela] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Iantorno, Micaela; Weiss, Robert G.] Johns Hopkins Univ Hosp, Dept Med, Div Cardiol, Baltimore, MD 21205 USA.
RP Weiss, RG (reprint author), Johns Hopkins Univ Hosp, Blalock 544,600 N Wolfe St, Baltimore, MD 21287 USA.
EM rweiss@jhmi.edu
FU NHLBI NIH HHS [R01 HL084186]
NR 56
TC 2
Z9 2
U1 0
U2 6
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1050-1738
J9 TRENDS CARDIOVAS MED
JI Trends Cardiovasc. Med.
PD MAY
PY 2014
VL 24
IS 4
BP 149
EP 156
DI 10.1016/j.tcm.2013.10.001
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AG4XJ
UT WOS:000335423400003
PM 24296299
ER
PT J
AU Zhang, YZ
Zhao, DH
Yang, HP
Liu, AJ
Chang, XZ
Hong, DJ
Bonnemann, C
Yuan, Y
Wu, XR
Xiong, H
AF Zhang, Yan-Zhi
Zhao, Dan-Hua
Yang, Hai-Po
Liu, Ai-Jie
Chang, Xing-Zhi
Hong, Dao-Jun
Bonnemann, Carsten
Yuan, Yun
Wu, Xi-Ru
Xiong, Hui
TI Novel collagen VI mutations identified in Chinese patients with Ullrich
congenital muscular dystrophy
SO WORLD JOURNAL OF PEDIATRICS
LA English
DT Article
DE collagen VI; in-frame; missense; triple helical domain; Ullrich
congenital muscular dystrophy
ID MUSCLE; DEFICIENCY; DOMINANT; DISEASES
AB Background: We determined the clinical and molecular genetic characteristics of 8 Chinese patients with Ullrich congenital muscular dystrophy (UCMD).
Methods: Clinical data of probands were collected and muscle biopsies of patients were analyzed. Exons of COL6A1, COL6A2 and COL6A3 were analyzed by direct sequencing. Mutations in COL6A1, COL6A2 and COL6A3 were identified in 8 patients.
Results: Among these mutations, 5 were novel [three in the triple helical domain (THD) and 2 in the second C-terminal (C2) domain]. We also identified five known missense or in-frame deletion mutations in THD and C domains. Immunohistochemical studies on muscle biopsies from patients showed reduced level of collagen VI at the muscle basement membrane and mis-localization of the protein in interstitial and perivascular regions.
Conclusions: The novel mutations we identified underscore the importance of THD and C2 domains in the assembly and function of collagen VI, thereby providing useful information for the genetic counseling of UCMD patients.
C1 [Zhang, Yan-Zhi; Yang, Hai-Po; Liu, Ai-Jie; Chang, Xing-Zhi; Wu, Xi-Ru; Xiong, Hui] Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China.
[Zhao, Dan-Hua; Hong, Dao-Jun; Yuan, Yun] Peking Univ, Hosp 1, Dept Neurol, Beijing 100034, Peoples R China.
[Bonnemann, Carsten] NINDS, Neuromuscular & Neurdgenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
RP Xiong, H (reprint author), Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China.
EM xh_bjbj@163.com
FU Beijing Natural Science Foundation of China [7112133]; National Basic
Research Program of China (973 Program) [2012CB944602]; National Natural
Science Foundation of China [81271400]
FX This work was supported by grants from the Beijing Natural Science
Foundation of China (7112133), the National Basic Research Program of
China (973 Program, 2012CB944602), and the National Natural Science
Foundation of China (81271400).
NR 21
TC 2
Z9 5
U1 0
U2 4
PU ZHEJIANG UNIV SCH MEDICINE
PI HANGZHOU
PA CHILDRENS HOSPITAL, 57 ZHUGAN XIANG, HANGZHOU, 310003, PEOPLES R CHINA
SN 1708-8569
EI 1867-0687
J9 WORLD J PEDIATR
JI World Journal of Pediatrics
PD MAY
PY 2014
VL 10
IS 2
BP 126
EP 132
DI 10.1007/s12519-014-0481-1
PG 7
WC Pediatrics
SC Pediatrics
GA AG4CT
UT WOS:000335367600005
PM 24801232
ER
PT J
AU Bossert, JM
Stern, AL
AF Bossert, Jennifer M.
Stern, Anna L.
TI Role of ventral subiculum in context-induced reinstatement of heroin
seeking in rats
SO ADDICTION BIOLOGY
LA English
DT Article
DE muscimol + baclofen; Conditioned cues; hippocampus; relapse;
reinstatement; drug environment; heroin self-administration
ID MEDIAL PREFRONTAL CORTEX; NUCLEUS-ACCUMBENS SHELL; COCAINE-SEEKING;
INDUCED RELAPSE; DRUG-SEEKING; PROJECTIONS; ORGANIZATION; HIPPOCAMPAL;
BEHAVIOR; INACTIVATION
AB In rats, reexposure to heroin-paired contexts after extinction of lever responding in a different context reinstates heroin seeking. Previous reports indicate that ventral hippocampus/Ca1 region plays a critical role in cocaine-, cue- and context-induced reinstatement of cocaine seeking. Here, we examined whether ventral subiculum, the output region of ventral hippocampus, is involved in context-induced reinstatement of heroin seeking. We found that reversible inactivation of ventral subiculum, but not posterior Ca1, with the gamma-aminobutyric acid agonists muscimol + baclofen decreased context-induced reinstatement of heroin seeking. Our findings, together with previous studies on cocaine seeking, indicate a critical role of ventral subiculum in context-induced relapse across drug classes.
C1 [Bossert, Jennifer M.; Stern, Anna L.] NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA.
RP Bossert, JM (reprint author), NIDA, IRP, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM jbossert@intra.nida.nih.gov
FU National Institute on Drug Abuse (NIH, DHHS)
FX This work was supported by the Intramural Research Program of the
National Institute on Drug Abuse (NIH, DHHS) funds to the Neurobiology
of Relapse Section (PI: Yavin Shaham). We thank Hila Eichenbaum for her
help in conducting the experiments and Yavin Shaham for his help in the
writing of the manuscript.
NR 27
TC 11
Z9 11
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1369-1600
J9 ADDICT BIOL
JI Addict. Biol.
PD MAY
PY 2014
VL 19
IS 3
BP 338
EP 342
DI 10.1111/adb.12015
PG 5
WC Biochemistry & Molecular Biology; Substance Abuse
SC Biochemistry & Molecular Biology; Substance Abuse
GA AF3FS
UT WOS:000334597500003
PM 23231571
ER
PT J
AU Ishiguro, H
Hall, FS
Horiuchi, Y
Sakurai, T
Hishimoto, A
Grumet, M
Uhl, GR
Onaivi, ES
Arinami, T
AF Ishiguro, Hiroki
Hall, Frank S.
Horiuchi, Yasue
Sakurai, Takeshi
Hishimoto, Akitoyo
Grumet, Martin
Uhl, George R.
Onaivi, Emmanuel S.
Arinami, Tadao
TI NrCAM-regulating neural systems and addiction-related behaviors
SO ADDICTION BIOLOGY
LA English
DT Article
DE glutamate; cell adhesion molecule; Behavior
ID MARBLE-BURYING BEHAVIOR; OBSESSIVE-COMPULSIVE DISORDER; NOVELTY-SEEKING
BEHAVIOR; KNOCKOUT MICE; NR-CAM; PERSONALITY PROFILE; NEURITE OUTGROWTH;
PLACE PREFERENCE; COCAINE REWARD; TEMPERAMENT
AB We have previously shown that a haplotype associated with decreased NrCAM expression in brain is protective against addiction vulnerability for polysubstance abuse in humans and that Nrcam knockout mice do not develop conditioned place preferences for morphine, cocaine or amphetamine. In order to gain insight into NrCAM involvement in addiction vulnerability, which may involve specific neural circuits underlying behavioral characteristics relevant to addiction, we evaluated several behavioral phenotypes in Nrcam knockout mice. Consistent with a potential general reduction in motivational function, Nrcam knockout mice demonstrated less curiosity for novel objects and for an unfamiliar conspecific, showed also less anxiety in the zero maze. Nrcam heterozygote knockout mice reduced alcohol preference and buried fewer marbles in home cage. These observations provide further support for a role of NrCAM in substance abuse including alcoholism vulnerability, possibly through its effects on behavioral traits that may affect addiction vulnerability, including novelty seeking, obsessive compulsion and responses to aversive or anxiety-provoking stimuli. Additionally, in order to prove glutamate homeostasis hypothesis of addiction, we analyzed glutamatergic molecules regulated by NRCAM expression. Glutaminase appears to be involved in NrCAM-related molecular pathway in two different tissues from human and mouse. An inhibitor of the enzyme, prolyl-leucyl-glycinamide, treatment produced, at least, some of the phenotypes of mice shown in alcohol preference and in anxiety-like behavior. Thus, NrCAM could affect addiction-related behaviors via at least partially modulation of some glutamatergic pathways and neural function in brain.
C1 [Ishiguro, Hiroki] Univ Yamanashi, Grad Sch Med Sci, Dept Neuropsychiat & Clin Eth, Chuo Ku, Yamanashi 4093898, Japan.
[Ishiguro, Hiroki; Horiuchi, Yasue; Arinami, Tadao] Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Med Genet, Tsukuba, Ibaraki, Japan.
[Hall, Frank S.; Uhl, George R.] NIDA, Mol Neurobiol Branch, IRP, NIH, Baltimore, MD USA.
[Sakurai, Takeshi] Mt Sinai Sch Med, Dept Psychiat, Seaver Autism Ctr, New York, NY USA.
[Sakurai, Takeshi] Mt Sinai Sch Med, Dept Pharmacol, Seaver Autism Ctr, New York, NY USA.
[Sakurai, Takeshi] Mt Sinai Sch Med, Black Family Stem Cell Inst, New York, NY USA.
[Hishimoto, Akitoyo] Kobe Univ, Dept Neuropsychiat, Grad Sch Med Sci, Kobe, Hyogo 657, Japan.
[Grumet, Martin] Rutgers State Univ, WM Keck Ctr Collaborat Neurosci, Piscataway, NJ USA.
[Onaivi, Emmanuel S.] William Paterson Univ, Dept Pharmacol, Wayne, NJ USA.
RP Ishiguro, H (reprint author), Univ Yamanashi, Grad Sch Med Sci, Dept Neuropsychiat & Clin Eth, Chuo Ku, 1110 Shimokato, Yamanashi 4093898, Japan.
EM hishiguro@yamanashi.ac.jp
RI Hall, Frank/C-3036-2013
OI Hall, Frank/0000-0002-0822-4063
FU KAKENHI from the Ministry of Education, Culture, Sports, Science and
Technology (Japan) [20375489, 20659177]; Ministry of Health, Labour and
Welfare [18A-1]; Japan Brain Foundation; National Institute on Drug
Abuse, NIH/DHHS (USA); Seaver Foundation
FX The present study was supported by KAKENHI (20375489 and 20659177) from
the Ministry of Education, Culture, Sports, Science and Technology
(Japan), Research Grant (18A-1) for Nervous and Mental Disorders from
Ministry of Health, Labour and Welfare, and Grant support from the Japan
Brain Foundation. The present study was also supported in part by
intramural funding from the National Institute on Drug Abuse, NIH/DHHS
(USA). Dr. Sakurai is a Seaver fellow and partly supported by the Seaver
Foundation.
NR 57
TC 6
Z9 6
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1369-1600
J9 ADDICT BIOL
JI Addict. Biol.
PD MAY
PY 2014
VL 19
IS 3
BP 343
EP 353
DI 10.1111/j.1369-1600.2012.00469.x
PG 11
WC Biochemistry & Molecular Biology; Substance Abuse
SC Biochemistry & Molecular Biology; Substance Abuse
GA AF3FS
UT WOS:000334597500004
PM 22780223
ER
PT J
AU Litten, RZ
Ryan, M
Falk, D
Fertig, J
AF Litten, Raye Z.
Ryan, Megan
Falk, Daniel
Fertig, Joanne
TI AlcoholMedications Development: Advantages and Caveats of
Government/Academia Collaborating with the Pharmaceutical Industry
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Medications Development; Pharmacotherapy; Collaboration;
Conflict of Interest; Research Bias
ID ALCOHOL DEPENDENCE; CONTROLLED-TRIAL; RISK
AB The process of developing pharmacological treatments for alcohol use disorder is notoriously complex and challenging. The path to market is long, costly, and inefficient. One way of expediting and reducing the drug development process is through collaborationsbuilding partnerships among government, academia, pharmaceutical and biotechnology companies, healthcare organizations and advocacy groups, and the patients (end consumers) themselves. By forging collaborations, particularly with pharmaceutical companies, the alcohol treatment field stands to reap benefits in generating new medications for use in mainstream treatment settings. At the same time, there are certain caveats that should be considered, particularly by academic researchers, before entering into such partnerships. This commentary examines the advantages and caveats of government and academia collaborations with pharmaceutical companies.
C1 [Litten, Raye Z.; Ryan, Megan; Falk, Daniel; Fertig, Joanne] NIAAA, Div Treatment & Recovery Res, Clin Invest Grp NCIG, Bethesda, MD 20892 USA.
RP Litten, RZ (reprint author), NIAAA, Div Treatment & Recovery Res, 5635 Fishers Lane, Bethesda, MD 20892 USA.
EM rlitten@mail.nih.gov
NR 22
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1196
EP 1199
DI 10.1111/acer.12357
PG 4
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200002
PM 24689461
ER
PT J
AU Mitchell, MC
Teigen, EL
Ramchandani, VA
AF Mitchell, Mack C., Jr.
Teigen, Erin L.
Ramchandani, Vijay A.
TI Absorption and Peak Blood Alcohol Concentration After Drinking Beer,
Wine, or Spirits
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Absorption; Pharmacokinetics; Beverage Type Differences; Blood
Alcohol Concentrations; Gastric Emptying Rate
ID ETHANOL; FOOD; PHARMACOKINETICS; METABOLISM
AB BackgroundBoth the amount and the rate of absorption of ethanol (EtOH) from alcoholic beverages are key determinants of the peak blood alcohol concentration (BAC) and exposure of organs other than gut and liver. Previous studies suggest EtOH is absorbed more rapidly in the fasting than in the postprandial state. The concentration of EtOH and the type of beverage may determine gastric emptying/absorption of EtOH.
MethodsThe pharmacokinetics of EtOH were measured in 15 healthy men after consumption of 0.5g of EtOH/kg body weight. During this 3-session crossover study, subjects consumed in separate sessions, beer (5.1% v/v), white wine (12.5% v/v), or vodka/tonic (20% v/v) over 20minutes following an overnight fast. BAC was measured by gas chromatography at multiple points after consumption.
ResultsPeak BAC (C-max) was significantly higher (p<0.001) after vodka/tonic (77.417.0mg/dl) than after wine (61.7 +/- 10.8mg/dl) or beer (50.3 +/- 9.8mg/dl) and was significantly higher (p<0.001) after wine than beer. The time to C-max occurred significantly earlier (p<0.01) after vodka/tonic (36 +/- 10minutes) compared to wine (54 +/- 14 minutes) or beer (62 +/- 23 minutes). Six subjects exceeded a C-max of 80mg/dl after vodka/tonic, but none exceeded this limit after beer or wine. The area under the concentration-time curve (AUC) was significantly greater after drinking vodka/tonic (p<0.001) than after wine or beer. Comparison of AUCs indicated the relative bioavailability of EtOH was lower after drinking beer.
ConclusionsFindings indicate that BAC is higher after drinking vodka/tonic than beer or wine after fasting. A binge pattern is significantly more likely to result in BAC above 80mg/dl after drinking vodka/tonic than beer or wine. Men drinking on an empty stomach should know BAC will vary depending on beverage type and the rate and amount of EtOH.
C1 [Mitchell, Mack C., Jr.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
[Teigen, Erin L.] ABMRF Fdn Alcohol Res, Baltimore, MD USA.
[Ramchandani, Vijay A.] NIAAA, Sect Human Psychopharmacol, Lab Clin & Translat Studies, Bethesda, MD USA.
RP Mitchell, MC (reprint author), Univ Texas Southwestern, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM Mack.Mitchell@utsouthwestern.edu
FU ABMRF/The Foundation for Alcohol Research, Baltimore, Maryland
FX This paper was supported by ABMRF/The Foundation for Alcohol Research,
Baltimore, Maryland.
NR 15
TC 8
Z9 9
U1 5
U2 30
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1200
EP 1204
DI 10.1111/acer.12355
PG 5
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200003
PM 24655007
ER
PT J
AU Yokoyama, A
Yokoyama, T
Brooks, PJ
Mizukami, T
Matsui, T
Kimura, M
Matsushita, S
Higuchi, S
Maruyama, K
AF Yokoyama, Akira
Yokoyama, Tetsuji
Brooks, Philip J.
Mizukami, Takeshi
Matsui, Toshifumi
Kimura, Mitsuru
Matsushita, Sachio
Higuchi, Susumu
Maruyama, Katsuya
TI Macrocytosis, Macrocytic Anemia, and Genetic Polymorphisms of Alcohol
Dehydrogenase-1B and Aldehyde Dehydrogenase-2in Japanese AlcoholicMen
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Acetaldehyde; Alcohol Dehydrogenase; Aldehyde Dehydrogenase; Anemia;
Mean Corpuscular Volume
ID MEAN CORPUSCULAR VOLUME; SQUAMOUS-CELL CARCINOMA; ACETALDEHYDE
CONCENTRATIONS; ALDH2 GENOTYPES; BONE-MARROW; HUMAN-LIVER; MEN; ETHANOL;
RISK; BLOOD
AB BackgroundOxidation of ethanol by alcohol dehydrogenase (ADH) generates acetaldehyde (AcH), which is converted to acetate by aldehyde dehydrogenase-2 (ALDH2). Roughly 40% of East Asians are ALDH2-deficient due to an inactive enzyme encoded by the ALDH2*2 allele. ALDH2-deficient individuals have a dramatically elevated risk of esophageal cancer from alcohol consumption.
MethodsWe investigated the relationship between ALDH2*2, ADH1B*2 (encoding a highly active ADH) and erythrocyte abnormalities, in a population of Japanese alcoholic men (N=1,238).
ResultsMacrocytosis (mean corpuscular volume [MCV] 100fl) and macrocytic anemia (MCV 100fl and hemoglobin <13.5g/dl) were found in 62.4 and 24.1% of the subjects, respectively. Age-adjusted daily alcohol consumption did not differ according to ADH1B and ALDH2 genotypes. However, macrocytosis and macrocytic anemia were strongly associated with the ALDH2*1/*2 genotype multivariate odds ratios (ORs; 95% confidence interval [CI]=2.85 [1.95 to 4.18] and 3.68 [2.64 to 5.15], respectively, versus ALDH2*1/*1). In comparison with the ADH1B*1/*1 and ALDH2*1/*1 genotype combination, the ADH1B*1/*1 and ALDH2*1/*2 genotype combination and the ADH1B*2 allele and ALDH2*1/*2 genotype combination increased stepwise the ORs (95% CI) for macrocytosis (1.65 [0.92 to 2.94] and 4.07 [2.33 to 7.11], respectively, p for difference in OR=0.015) and macrocytic anemia (2.80 [1.52 to 5.15] and 5.32 [3.29 to 8.62], respectively, p for difference in OR=0.045). Genotype effects were more prominent on the risks of the more advanced erythrocyte abnormalities. Older age, cigarette smoking, and low body mass index independently increased the risks of the erythrocyte abnormalities. Consumption of beer, which contains folate, decreased the risks, whereas consumption of alcoholic beverages lacking folate did not.
ConclusionsThese results suggest that the erythrocyte abnormalities in alcoholics are attributable to high AcH exposure as well as to nutritional deficiencies and may be prevented by folate.
C1 [Yokoyama, Akira; Mizukami, Takeshi; Matsui, Toshifumi; Kimura, Mitsuru; Matsushita, Sachio; Higuchi, Susumu; Maruyama, Katsuya] Natl Hosp Org Kurihama Med & Addict Ctr, Yokosuka, Kanagawa 2390841, Japan.
[Yokoyama, Tetsuji] Natl Inst Publ Hlth, Dept Hlth Promot, Saitama, Japan.
[Brooks, Philip J.] NIAAA, Div Metab & Hlth Effects, NIH, Bethesda, MD USA.
[Brooks, Philip J.] NIAAA, Neurogenet Lab, NIH, Bethesda, MD USA.
[Matsui, Toshifumi] Kyorin Univ Hosp, Dept Geriatr Med, Tokyo, Japan.
RP Yokoyama, A (reprint author), Natl Hosp Org Kurihama Med & Addict Ctr, Clin Res Unit, 5-3-1 Nobi, Yokosuka, Kanagawa 2390841, Japan.
EM a_yokoyama@kurihama1.hosp.go.jp
NR 44
TC 8
Z9 8
U1 2
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1237
EP 1246
DI 10.1111/acer.12372
PG 10
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200007
PM 24588059
ER
PT J
AU Vatsalya, V
Momenan, R
Hommer, DW
Ramchandani, VA
AF Vatsalya, Vatsalya
Momenan, Reza
Hommer, Daniel W.
Ramchandani, Vijay A.
TI Cardiac Reactivity During the Ascending Phase of Acute Intravenous
Alcohol Exposure and Association with Subjective Perceptions of
Intoxication in Social Drinkers
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Clamp; Intravenous Infusion; Heart Rate; Heart Rate Variability;
Subjective Perceptions
ID HEART-RATE-VARIABILITY; NERVOUS-SYSTEM; INGESTION; DISEASE; ETHANOL;
RELIABILITY; SENSITIVITY; CHALLENGES; VALIDITY; ADULTS
AB BackgroundThe aim of this study was to characterize cardiac reactivity measures, heart rate (HR), and heart rate variability (HRV), following acute intravenous (IV) alcohol administration and their association with subjective responses in social drinkers.
MethodsTwenty-four subjects (11 females) received IV alcohol infusions to attain and clamp the breath alcohol concentration (BrAC) at 50mg% or placebo in separate sessions. Serial 5-minute cardiac recordings at baseline and during the infusion were analyzed to obtain frequency and time domain cardiac measures. Self-reported subjective perceptions were also obtained at the same time points.
ResultsHR showed significant decreases from baseline, while the HRV measure pNN50 showed steady increases during the ascending phase of alcohol infusion. HR was inversely correlated with pNN50 across time and treatment. There was a significant association of HR with subjective feelings of high, intoxication, feeling drug effects, and liking drug effects across time during the ascending phase.
ConclusionsAcute IV alcohol resulted in decreases in HR and increases in HRV consistent with autonomic parasympathetic activation. The association of these changes with subjective responses suggests that cardiac reactivity may serve as a physiological marker of subjective alcohol effects. This study broadens the understanding of acute cardiovascular effects of alcohol and clinically significant cardiac conditions such as arrhythmia and cardiomyopathy associated with chronic alcohol drinking.
C1 [Vatsalya, Vatsalya; Ramchandani, Vijay A.] NIAAA, Sect Human Psychopharmacol, LCTS, Bethesda, MD 20892 USA.
[Momenan, Reza; Hommer, Daniel W.] NIAAA, Sect Brain Electrophysiol & Imaging, LCTS, Bethesda, MD 20892 USA.
RP Ramchandani, VA (reprint author), NIAAA, Sect Human Psychopharmacol, LCTS, 10 Ctr Dr,Room 2-2352, Bethesda, MD 20892 USA.
EM vijayr@mail.nih.gov
FU NIAAA Division of Intramural Clinical and Biological Research [1Z01
AA000466]
FX This study was supported by the NIAAA Division of Intramural Clinical
and Biological Research (1Z01 AA000466). The authors gratefully
acknowledge the NIH Clinical Center Alcohol Clinic and Day Hospital
staff for clinical support, research staff (Elizabeth Edenberg, Mike
Hoefer, Nina Saxena, Shilpa Kumar, Seth Eappen, Julnar Issa) for data
collection support, and the study volunteers for their participation in
the study.
NR 60
TC 1
Z9 1
U1 2
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1247
EP 1254
DI 10.1111/acer.12377
PG 8
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200008
PM 24655119
ER
PT J
AU Yong, WD
Spence, JP
Eskay, R
Fitz, SD
Damadzic, R
Lai, DB
Foroud, T
Carr, LG
Shekhar, A
Chester, JA
Heilig, M
Liang, TB
AF Yong, Weidong
Spence, John Paul
Eskay, Robert
Fitz, Stephanie D.
Damadzic, Ruslan
Lai, Dongbing
Foroud, Tatiana
Carr, Lucinda G.
Shekhar, Anantha
Chester, Julia A.
Heilig, Markus
Liang, Tiebing
TI dAlcohol-Preferring Rats Show Decreased CorticotropinReleasing Hormone-2
Receptor Expression and Differences in HPA Activation Compared to
Alcohol-Nonpreferring
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcoholism; Corticotropin-Releasing Hormone Type 2 Receptor; Selective
Breeding; Stress; Amygdala
ID ANXIETY-LIKE BEHAVIOR; QUANTITATIVE TRAIT LOCUS; SOCIAL-INTERACTION
TEST; MESSENGER-RNAS; CRF RECEPTORS; GENETIC PREDISPOSITION; DRINKING
BEHAVIOR; RESTRAINT STRESS; ACOUSTIC STARTLE; CENTRAL NUCLEUS
AB BackgroundCorticotropin-releasing hormone (CRH) and urocortins (UCNs) bind to corticotropin-releasing hormone type 2 receptor (CRF2 receptor), a Gs protein-coupled receptor that plays an important role in modulation of anxiety and stress responses. The Crhr2 gene maps to a quantitative trait locus (QTL) for alcohol preference on chromosome 4 previously identified in inbred alcohol-preferring (iP) and-nonpreferring (iNP) F2 rats.
MethodsReal-time polymerase chain reaction was utilized to screen for differences in Crhr2 mRNA expression in the central nervous system (CNS) of male iP and iNP rats. DNA sequence analysis was then performed to screen for polymorphism in Crhr2 in order to identify genetic variation, and luciferase reporter assays were then applied to test their functional significance. Next, binding assays were used to determine whether this polymorphism affected CRF2 receptor binding affinity as well as CRF2 receptor density in the CNS. Finally, social interaction and corticosterone levels were measured in the P and NP rats before and after 30-minute restraint stress.
ResultsCrhr2 mRNA expression studies found lower levels of Crhr2 mRNA in iP rats compared to iNP rats. In addition, DNA sequencing identified polymorphisms in the promoter region, coding region, and 3-untranslated region between the iP and iNP rats. A 7bp insertion in the Crhr2 promoter of iP rats altered expression in vitro as measured by reporter assays, and we found that CRF2 receptor density was lower in the amygdala of iP as compared to iNP rats. Male P rats displayed decreased social interaction and significantly higher corticosterone levels directly following 30-minute restraint when compared to male NP rats.
ConclusionsThis study identified Crhr2 as a candidate gene of interest underlying the chromosome 4 QTL for alcohol consumption that was previously identified in the P and NP model. Crhr2 promoter polymorphism is associated with reduced mRNA expression in certain brain regions, particularly the amygdala, and lowered the density of CRF2 receptor in the amygdala of iP compared to iNP rats. Together, these differences between the animals may contribute to the drinking disparity as well as the anxiety differences of the P and NP rats.
C1 [Yong, Weidong] Chinese Acad Med Sci, Inst Lab Anim Sci, Beijing 100730, Peoples R China.
[Yong, Weidong] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Yong, Weidong] Indiana Univ Sch Med, Dept Pediat, Indianapolis, IN 46202 USA.
[Spence, John Paul; Fitz, Stephanie D.; Shekhar, Anantha] Indiana Univ Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA.
[Eskay, Robert; Damadzic, Ruslan; Heilig, Markus] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Lai, Dongbing; Foroud, Tatiana] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Carr, Lucinda G.; Liang, Tiebing] Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.
[Chester, Julia A.] Purdue Univ, Dept Psychol Sci, W Lafayette, IN 47907 USA.
RP Liang, TB (reprint author), Indiana Univ Sch Med, Dept Med, Clin Bldg,Room 500A,541 Clin Dr, Indianapolis, IN 46202 USA.
EM tliang@iu.edu
FU State High-Tech Program [863-2012AA022403]; National Institute on
Alcohol Abuse and Alcoholism (NIAAA) grants [R01AA10707, P60 AA007611,
AA07611, R01 MH065702]; Indiana Clinical & Translational Institute
through a CTSA award from NIH, NCATS [TR000162]
FX This research was supported by the State High-Tech Program
(863-2012AA022403), the National Institute on Alcohol Abuse and
Alcoholism (NIAAA) grants R01AA10707, P60 AA007611, AA07611, and R01
MH065702. JPS was supported by a predoctoral award from the Indiana
Clinical & Translational Institute through a CTSA award from NIH, NCATS
(TR000162). The authors declare that there are no conflict of interests
of any kind regarding this work.
NR 55
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Z9 7
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1275
EP 1283
DI 10.1111/acer.12379
PG 9
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200011
PM 24611993
ER
PT J
AU Umhau, JC
Schwandt, M
Solomon, MG
Yuan, PX
Nugent, A
Zarate, CA
Drevets, WC
Hall, SD
George, DT
Heilig, M
AF Umhau, John C.
Schwandt, Melanie
Solomon, Matthew G.
Yuan, Peixiong
Nugent, Allison
Zarate, Carlos A.
Drevets, Wayne C.
Hall, Samuel D.
George, David T.
Heilig, Markus
TI Cerebrospinal FluidMonocyte Chemoattractant Protein-1 in Alcoholics:
Support for a NeuroinflammatoryModel of Chronic Alcoholism
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Monocyte Chemoattractant Protein-1; Alcoholism; Inflammation;
Cerebrospinal Fluid; Cytokine
ID MICROGLIAL ACTIVATION; BRAIN; MCP-1; INFLAMMATION; DISEASE; ETHANOL;
NEURODEGENERATION; IMPAIRMENT; RATS; RECRUITMENT
AB BackgroundLiver inflammation in alcoholism has been hypothesized to influence the development of a neuroinflammatory process in the brain characterized by neurodegeneration and altered cognitive function. Monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 (MCP-1/CCL2) elevations have been noted in the alcoholic brain at autopsy and may have a role in this process.
MethodsWe studied cerebrospinal fluid (CSF) levels of MCP-1 as well as interleukin-1 and tumor necrosis factor- in 13 healthy volunteers and 28 alcoholics during weeks 1 and 4 following detoxification. Serum liver enzymes were obtained as markers of alcohol-related liver inflammation.
ResultsCompared to healthy volunteers, MCP-1 levels were significantly higher in alcoholics both on day 4 and day 25 (p<0.0001). Using multiple regression analysis, we found that MCP-1 concentrations were positively associated with the liver enzymes gamma glutamyltransferase (GGT; p=0.03) and aspartate aminotransferase/glutamic oxaloacetic transaminase (AST/GOT; p=0.004).
ConclusionsThese preliminary findings are consistent with the hypothesis that neuroinflammation as indexed by CSF MCP-1 is associated with alcohol-induced liver inflammation, as defined by peripheral concentrations of GGT and AST/GOT.
C1 [Umhau, John C.; Schwandt, Melanie; Solomon, Matthew G.; Hall, Samuel D.; George, David T.; Heilig, Markus] NIAAA, NIH, Bethesda, MD USA.
[Yuan, Peixiong; Nugent, Allison; Zarate, Carlos A.] NIMH, NIH, Bethesda, MD 20892 USA.
[Drevets, Wayne C.] Johnson & Johnson Consumer Prod Inc, Janssen Pharmaceut, Titusville, NJ USA.
RP Umhau, JC (reprint author), Whiteriver Indian Hosp, Whiteriver Serv Unit, US Publ Hlth Serv, 200 W Hosp Dr, Whiteriver, AZ 85941 USA.
EM umhau@jhu.edu
RI Schwandt, Melanie/L-9866-2016;
OI Heilig, Markus/0000-0003-2706-2482; Nugent, Allison/0000-0003-2569-2480
FU Laboratory of Clinical and Translational Studies, National Institute on
Alcohol Abuse and Alcoholism; National Institute of Mental Health, both
of the National Institutes of Health
FX The Laboratory of Clinical and Translational Studies, National Institute
on Alcohol Abuse and Alcoholism, and the National Institute of Mental
Health, both of the National Institutes of Health, supported this study.
Monte Phillips provided invaluable technical assistance.
NR 47
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Z9 7
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1301
EP 1306
DI 10.1111/acer.12367
PG 6
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200014
PM 24689518
ER
PT J
AU Smith, KL
John, CS
Sypek, EI
Ongur, D
Cohen, BM
Barry, SM
Bechtholt, AJ
AF Smith, Karen L.
John, Catherine S.
Sypek, Elizabeth I.
Oenguer, Dost
Cohen, Bruce M.
Barry, Sarah M.
Bechtholt, Anita J.
TI Exploring the Role of Central Astrocytic Glutamate Uptake in Ethanol
Reward inMice
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Ethanol; Astrocyte; Glutamate; Drinking in the Dark; Place Preference
ID CONDITIONED PLACE PREFERENCE; MALE C57BL/6J MICE; KV2.1 POTASSIUM
CHANNELS; ALCOHOL-PREFERRING RATS; NMDA RECEPTOR; METABOTROPIC
GLUTAMATE; STRAIN DIFFERENCES; PREFRONTAL CORTEX; PRELIMBIC CORTEX;
PACKING DENSITY
AB BackgroundAlcoholism is associated with specific brain abnormalities revealed through postmortem studies, including a reduction in glial cell number and dysregulated glutamatergic neurotransmission. Whether these abnormalities contribute to the etiology of alcoholism, are consequences of alcohol use, or both is still unknown.
MethodsWe investigated the role of astrocytic glutamate uptake in ethanol (EtOH) binge drinking in mice, using the drinking in the dark (DID) paradigm by blocking the astrocytic glutamate transporter (GLT-1) with intracerebroventricular (ICV) administration of dihydrokainic acid (DHK). To determine whether astrocytic glutamate uptake regulates the conditioned rewarding effects of EtOH, we examined the effects of ICV DHK on the acquisition and expression of EtOH-induced conditioned place preference.
ResultsBlocking central astrocytic glutamate uptake selectively attenuated EtOH binge drinking behavior in mice. DHK did not alter the acquisition or expression of preference for EtOH-associated cues, indicating that reduced astrocytic glutamate trafficking may decrease binge-like drinking without altering the conditioned rewarding effects of EtOH.
ConclusionsSeveral alternative conclusions are plausible, however, interpreting these data in the context of the human literature, these findings suggest that the reduction of glia in the alcoholic brain may not be a predisposing factor to developing alcoholism and could be a consequence of EtOH toxicity that decreases excessive EtOH intake.
C1 [Smith, Karen L.; John, Catherine S.; Sypek, Elizabeth I.; Oenguer, Dost; Cohen, Bruce M.; Barry, Sarah M.; Bechtholt, Anita J.] Harvard Univ, McLean Hosp, Sch Med, Dept Psychiat, Belmont, MA USA.
[Smith, Karen L.] Boston Univ, Sch Med, Dept Pharmacol & Expt Therapeut, Lab Addict Disorders, Boston, MA 02118 USA.
[Bechtholt, Anita J.] NIAAA, NIH, Bethesda, MD 20892 USA.
RP Bechtholt, AJ (reprint author), NIAAA, NIH, 5635 Fishers Lane,Room 2056, Bethesda, MD 20892 USA.
EM anita.bechtholt@gmail.com
OI sypek, elizabeth/0000-0001-6904-2426
FU NIAAA [R03AA019577]; Shervert Frazier Research Institute; Englehard
Foundation
FX Funding for this work was provided by NIAAA (R03AA019577), AJB; the
Shervert Frazier Research Institute, BMC & DO the Englehard Foundation,
BMC. The authors would like to thank Dr. Uwe Rudolph for logistical
support. Dr. Bechtholt contributed to this article as an employee of
McLean Hospital-Harvard Medical School. The views expressed are her own
and do not necessarily represent the views of the National Institutes of
Health or the United States Government.
NR 53
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U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD MAY
PY 2014
VL 38
IS 5
BP 1307
EP 1314
DI 10.1111/acer.12361
PG 8
WC Substance Abuse
SC Substance Abuse
GA AF4BU
UT WOS:000334657200015
PM 24655029
ER
PT J
AU Murphy, RA
Reinders, I
Register, TC
Ayonayon, HN
Newman, AB
Sattedield, S
Goodpaster, BH
Simonsick, EM
Kritchevsky, SB
Harris, TB
AF Murphy, Rachel A.
Reinders, Ilse
Register, Thomas C.
Ayonayon, Hilsa N.
Newman, Anne B.
Sattedield, Suzanne
Goodpaster, Bret H.
Simonsick, Eleanor M.
Kritchevsky, Stephen B.
Harris, Tamara B.
TI Associations of BMI and adipose tissue area and density with incident
mobility limitation and poor performance in older adults
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID MUSCLE FAT INFILTRATION; BODY-MASS INDEX; PHYSICAL FUNCTION;
SKELETAL-MUSCLE; RISK-FACTORS; CARDIOVASCULAR HEALTH; LIFE EXPECTANCY;
DISABILITY; OBESITY; STRENGTH
AB Background: Obesity is a risk factor for disability, but risk of. specific adipose depots is not completely understood.
Objective: We investigated associations between mobility limitation, performance, and the following adipose measures: body mass index (BMI) and areas and densities of visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and intermuscular adipose tissue (IMAT) in older adults.
Design: This was a prospective population-based study of men (n = 1459) and women (n = 1552) initially aged 70-79 y and free from mobility limitation. BMI was determined from measured height and weight. Adipose tissue area and density in Hounsfield units were measured in the thigh and abdomen by using computed tomography. Mobility limitation was defined as 2 consecutive reports of difficulty walking one-quarter mile or climbing 10 steps during semiannual assessments over 13 y. Poor performance was defined as a gait speed <1 m/s after 9 y of follow-up (n = 1542).
Results: In models adjusted for disability risk factors, BMI, and areas of VAT, abdominal SAT, and IMAT were positively associated with mobility limitation in men and women. In women, thigh SAT area was positively associated with mobility limitation risk, whereas VAT density was inversely associated. Associations were similar for poor performance. BMI and thigh IMAT area (independent of BMI were particularly strong indicators of incident mobility limitation and poor performance. For example, in women, the HR (95% Cl) and OR (95% Cl) associated with an SD increment in BMI for mobility limitation and poor performance were 1.31 (1.21, 1.42) and 1.41 (1.13, 1.76), respectively. In men, the HR (95% Cl) and OR (95% Cl) associated with an SD increment in thigh IMAT for mobility limitation and poor performance were 1.37 (1.27, 1.47) and 1.54 (1.18, 2.02), respectively.
Conclusions: Even into old age, higher BMI is associated with mobility limitation and poor performance. The amount of adipose tissue in abdominal and thigh depots may also convey risk beyond BMI.
C1 [Murphy, Rachel A.; Reinders, Ilse; Harris, Tamara B.] NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, Bethesda, MD 20814 USA.
[Register, Thomas C.] Wake Forest Sch Med, Stiehl Ctr Aging, Sect Comparat Med Pathol, Winston Salem, NC USA.
[Kritchevsky, Stephen B.] Wake Forest Sch Med, Stiehl Ctr Aging, Sect Gerontol & Geriatr, Winston Salem, NC USA.
[Ayonayon, Hilsa N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Sattedield, Suzanne] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Medicine, Memphis, TN 38163 USA.
[Goodpaster, Bret H.] Univ Pittsburgh, Dept Med, Ctr Aging & Populat Hlth, Pittsburgh, PA USA.
[Simonsick, Eleanor M.] NIA, Translat Gerontol Branch, Intramural Res Program, Bethesda, MD 20814 USA.
RP Murphy, RA (reprint author), NIA, Lab Populat Sci, 7201 Wisconsin Ave,3C-309, Bethesda, MD 20814 USA.
EM rachel.murphy@nih.gov
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
FU National Institute on Aging (NIA) [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, R01-AG028050]; National Institute of Nursing Research
[R01-NR-012459]; Intramural Research Program of the NIH, NIA; Banning
Postdoctoral Fellowship
FX Supported by the National Institute on Aging (NIA) (contracts
N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106 and grant R01-AG028050) and
the National Institute of Nursing Research (grant R01-NR-012459); in
part by the Intramural Research Program of the NIH, NIA; and by a
Banning Postdoctoral Fellowship (to RAM).
NR 37
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U1 3
U2 13
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY
PY 2014
VL 99
IS 5
BP 1059
EP 1065
DI 10.3945/ajcn.113.080796
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AF7LD
UT WOS:000334895700014
PM 24522448
ER
PT J
AU Tasevska, N
Park, Y
Jiao, L
Hollenbeck, A
Subar, AF
Potischman, N
AF Tasevska, Natasha
Park, Yikyung
Jiao, Li
Hollenbeck, Albert
Subar, Amy F.
Potischman, Nancy
TI Sugars and risk of mortality in the NIH-AARP Diet and Health Study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID CORONARY-HEART-DISEASE; SWEETENED BEVERAGE CONSUMPTION; FOOD FREQUENCY
QUESTIONNAIRES; TYPE-2 DIABETES-MELLITUS; PANCREATIC-CANCER RISK; MILK
EXTRINSIC SUGARS; FRUCTOSE CORN SYRUP; MIDDLE-AGED WOMEN;
GROWTH-FACTOR-I; GLYCEMIC LOAD
AB Background: Although previous studies have linked intake of sugars with incidence of cancer and other chronic diseases, its association with mortality remains unknown.
Objective: We investigated the association of total sugars, added sugars, total fructose, added fructose, sucrose, and added sucrose with the risk of all-cause, cardiovascular disease, cancer, and other-cause mortality in the NIH-AARP Diet and Health Study.
Design: The participants (n = 353,751), aged 50-71 y, were followed for up to 13 y. Intake of individual sugars over the previous 12 mo was assessed at baseline by using a 124-item NIH Diet History Questionnaire.
Results: In fully adjusted models (fifth quartile compared with first quartile), all-cause mortality was positively associated with the intake of total sugars [HR (95% Cl): 1.13 (1.06, 1.20); P-trend < 0.0001], total fructose [1.10 (1.04, 1.17); P-trend < 0.0001], and added fructose [1.07 (1.01, 1.13); P-trend = 0.065) in women and total fructose [1.06 (1.01, 1.10); P-trend = 0.002] in men. In men, a weak inverse association was found between other-cause mortality and dietary added sugars (P-trend = 0.04), sucrose (P-trend = 0.03), and added sucrose (P-trend = 0.006). Investigation of consumption of sugars by source showed that the positive association with mortality risk was confined only to sugars from beverages, whereas the inverse association was confined to sugars from solid foods.
Conclusions: In this large prospective study, total fructose intake was weakly positively associated with all-cause mortality in both women and men, whereas added sugar, sucrose, and added sucrose intakes were inversely associated with other-cause mortality in men. In our analyses, intake of added sugars was not associated with an increased risk of mortality. The NIFI-AARP Diet and Health Study was registered at clinicaltrials.gov as NCT00340015.
C1 [Tasevska, Natasha; Subar, Amy F.; Potischman, Nancy] NCI, Appl Res Program, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Tasevska, Natasha] Arizona State Univ, Nutr Program, Sch Nutr & Hlth Promot, Phoenix, AZ USA.
[Park, Yikyung; Jiao, Li] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Jiao, Li] Baylor Coll Med, Sect Gastroenterol & Hepatol, Dept Med, Houston, TX 77030 USA.
[Hollenbeck, Albert] AARP, Washington, DC USA.
RP Tasevska, N (reprint author), Arizona State Univ, Sch Nutr & Hlth Promot, Nutr Program, 500 North 3rd St, Phoenix, AZ 85004 USA.
EM natasha.tasevska@asti.edu
OI Park, Yikyung/0000-0002-6281-489X
FU Intramural Research Program of the National Cancer Institute, NIH,
Department of Health and Human Services
FX Supported by the Intramural Research Program of the National Cancer
Institute, NIH, Department of Health and Human Services.
NR 79
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U1 2
U2 23
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY
PY 2014
VL 99
IS 5
BP 1077
EP 1088
DI 10.3945/ajcn.113.069369
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AF7LD
UT WOS:000334895700017
PM 24552754
ER
PT J
AU Kris-Etherton, PM
Pratt, CA
Saltzman, E
Van Horn, L
AF Kris-Etherton, Penny M.
Pratt, Charlotte A.
Saltzman, Edward
Van Horn, Linda
TI Introduction to Nutrition Education in Training Medical and Other Health
Care Professionals
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Editorial Material
C1 [Kris-Etherton, Penny M.] Penn State Univ, Dept Nutr Sci, University Pk, PA 16802 USA.
[Pratt, Charlotte A.] NIH, NHLBI, Bethesda, MD 20892 USA.
[Saltzman, Edward] Tufts Univ, Sch Med, Dept Nutr Sci, Boston, MA 02111 USA.
[Van Horn, Linda] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
RP Kris-Etherton, PM (reprint author), Penn State Univ, Dept Nutr Sci, University Pk, PA 16802 USA.
EM pmk3@psu.edu
NR 6
TC 0
Z9 0
U1 2
U2 8
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY
PY 2014
VL 99
IS 5
BP 1151S
EP 1152S
DI 10.3945/ajcn.113.073494
PG 2
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AF7LD
UT WOS:000334895700029
PM 24670942
ER
PT J
AU Kris-Etherton, PM
Akabas, SR
Bales, CW
Bistrian, B
Braun, L
Edwards, MS
Laur, C
Lenders, CM
Levy, MD
Palmer, CA
Pratt, CA
Ray, S
Rock, CL
Saltzman, E
Seidner, DL
Van Horn, L
AF Kris-Etherton, Penny M.
Akabas, Sharon R.
Bales, Connie W.
Bistrian, Bruce
Braun, Lynne
Edwards, Marilyn S.
Laur, Celia
Lenders, Carine M.
Levy, Matthew D.
Palmer, Carole A.
Pratt, Charlotte A.
Ray, Sumantra
Rock, Cheryl L.
Saltzman, Edward
Seidner, Douglas L.
Van Horn, Linda
TI The need to advance nutrition education in the training of health care
professionals and recommended research to evaluate implementation and
effectiveness
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID LIFE-STYLE INTERVENTION; MEDICAL-EDUCATION; NATIONAL CONSENSUS; CLINICAL
NUTRITION; RISK-FACTORS; WEIGHT-LOSS; DIET; CURRICULUM; OVERWEIGHT;
MANAGEMENT
AB Nutrition is a recognized determinant in 3 (ie, diseases of the heart, malignant neoplasms, cerebrovascular diseases) of the top 4 leading causes of death in the United States. However, many health care providers are not adequately trained to address lifestyle recommendations that include nutrition and physical activity behaviors in a manner that could mitigate disease development or progression. This contributes to a compelling need to markedly improve nutrition education for,health care professionals and to establish curricular standards and requisite nutrition and physical activity competencies in the education, training, and continuing education for health care professionals. This article reports the present status of nutrition and physical activity education for health care professionals, evaluates the current pedagogic models, and underscores the urgent need to realign and synergize these models to reflect evidence-based and outcomes-focused education.
C1 [Kris-Etherton, Penny M.] Penn State Univ, Dept Nutr Sci, University Pk, PA 16802 USA.
[Akabas, Sharon R.] Columbia Univ, Inst Human Nutr, New York, NY 10032 USA.
[Bales, Connie W.] Duke Univ, Med Ctr, Durham, NC USA.
[Bistrian, Bruce] Harvard Univ, Sch Med, Boston, MA USA.
[Braun, Lynne] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Edwards, Marilyn S.] Univ Texas Houston, Sch Med, Houston, TX USA.
[Laur, Celia; Ray, Sumantra] UK Med Res Council, Human Nutr Res Unit, Cambridge, England.
[Lenders, Carine M.] Boston Med Ctr, Div Pediat Nutr, Boston, MA USA.
[Levy, Matthew D.] Medstar Georgetown Univ Hosp, Dept Pediat, Div Primary Care & Gen Pediat, Washington, DC USA.
[Palmer, Carole A.] Tufts Univ, Sch Dent Med, Boston, MA 02111 USA.
[Pratt, Charlotte A.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Rock, Cheryl L.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Saltzman, Edward] Tufts Univ, Sch Med, Dept Nutr Sci, Boston, MA 02111 USA.
[Seidner, Douglas L.] Vanderbilt Univ, Vanderbilt Ctr Human Nutr, Med Ctr, Nashville, TN USA.
[Van Horn, Linda] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
RP Kris-Etherton, PM (reprint author), Penn State Univ, Dept Nutr Sci, 319 Chandlee Lab, University Pk, PA 16802 USA.
EM pmk3@psu.edu
FU Medical Research Council [MC_U105960384]; NIDDK NIH HHS [K23 DK082732,
P30 DK046200, P30 DK058404]
NR 98
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Z9 20
U1 1
U2 25
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY
PY 2014
VL 99
IS 5
BP 1153S
EP 1166S
DI 10.3945/ajcn.113.073502
PG 14
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AF7LD
UT WOS:000334895700030
PM 24717343
ER
PT J
AU Beauchamp, MK
Leveille, SG
Patel, KV
Kiely, DK
Phillips, CL
Bandinelli, S
Ferrucci, L
Guralnik, J
Bean, JF
AF Beauchamp, Marla K.
Leveille, Suzanne G.
Patel, Kushang V.
Kiely, Dan K.
Phillips, Caroline L.
Bandinelli, Stefania
Ferrucci, Luigi
Guralnik, Jack
Bean, Jonathan F.
TI What Physical Attributes Underlie Self- Reported vs. Observed Ability to
Walk 400 m in Later Life?
SO AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION
LA English
DT Article
DE Physical Performance; Rehabilitation; Successful Aging; Mobility
Limitation
ID INCIDENT MOBILITY DISABILITY; LOWER-EXTREMITY FUNCTION; OLDER-ADULTS;
400-METER WALK; SUBSEQUENT DISABILITY; MAINTAINING MOBILITY; MUSCLE
POWER; PERFORMANCE; INCHIANTI; MORTALITY
AB Objective The aims of this study were to evaluate and contrast the physical attributes that are associated with self-reported vs. observed ability to walk 400 m among older adults.
Design Analysis of baseline and 3-yr data from 1026 participants 65 yrs or older in the InCHIANTI (Invecchiare in Chianti) study was conducted. Observed and self-reported ability to walk 400 m at baseline and at 3 yrs were primary outcomes. Predictors included leg speed, leg strength, leg strength symmetry, range of motion, balance, and kyphosis.
Results Balance, leg speed, leg strength, kyphosis, leg strength symmetry, and knee range of motion were associated with self-reported ability to walk 400 m at baseline (P < 0.001, c = 0.85). Balance, leg speed, and knee range of motion were associated with observed 400-m walk (P < 0.001, c = 0.85) at baseline. Prospectively, baseline leg speed and leg strength were predictive of both self-reported (P < 0.001, c = 0.79) and observed (P < 0.001, c = 0.72) ability to walk 400 m at 3 yrs.
Conclusions The profiles of attributes that are associated with self-reported vs. observed walking ability differ. The factor most consistently associated with current and future walking ability is leg speed. These results draw attention to important foci for rehabilitation.
C1 [Beauchamp, Marla K.; Bean, Jonathan F.] Harvard Univ, Sch Med, Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Boston, MA USA.
[Leveille, Suzanne G.] Harvard Univ, Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care,Coll Nursing Hlth Sci, Univ Massachusetts Boston,Med Sch, Boston, MA 02215 USA.
[Patel, Kushang V.] Univ Washington, Dept Anesthesiol & Pain Med, Seattle, WA 98195 USA.
[Kiely, Dan K.] Harvard Univ, Sch Med, Hebrew Senior Life, Inst Aging Res, Boston, MA USA.
[Phillips, Caroline L.] NIA, Lab Epidemiol & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Bandinelli, Stefania] Azienda Sanitaria Firenze, Geriatr Rehabil Unit, Florence, Italy.
[Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
[Guralnik, Jack] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Div Gerontol, Baltimore, MD 21201 USA.
RP Beauchamp, MK (reprint author), Spaulding Cambridge Outpatient Ctr, 1575 Cambridge St, Cambridge, MA 02138 USA.
RI Bean, Jonathan/F-5798-2017
OI Bean, Jonathan/0000-0001-8385-8210
FU Canadian Institutes of Health Research; National Institutes of Health
(NIH) [1K24HD070966-01]; Intramural Research Program of the NIH,
National Institute on Aging
FX Supported by a fellowship from the Canadian Institutes of Health
Research (to M.K.B.) and by a National Institutes of Health (NIH) K24
award (1K24HD070966-01) (to J.F.B.). This research was supported in part
by the Intramural Research Program of the NIH, National Institute on
Aging. Financial disclosure statements have been obtained, and no
conflicts of interest have been reported by the authors or by any
individuals in control of the content of this article.
NR 40
TC 3
Z9 3
U1 4
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0894-9115
EI 1537-7385
J9 AM J PHYS MED REHAB
JI Am. J. Phys. Med. Rehabil.
PD MAY
PY 2014
VL 93
IS 5
BP 396
EP 404
DI 10.1097/PHM.0000000000000034
PG 9
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA AF3GV
UT WOS:000334600700005
PM 24322434
ER
PT J
AU Mai, PL
Vadaparampil, ST
Breen, N
McNeel, TS
Wideroff, L
Graubard, BI
AF Mai, Phuong L.
Vadaparampil, Susan Thomas
Breen, Nancy
McNeel, Timothy S.
Wideroff, Louise
Graubard, Barry I.
TI Awareness of Cancer Susceptibility Genetic Testing The 2000, 2005, and
2010 National Health Interview Surveys
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID HEREDITARY BREAST; OVARIAN-CANCER; RISK-ASSESSMENT; FAMILY-HISTORY;
PHYSICIANS; WOMEN; INFORMATION; RACE/ETHNICITY; ACCULTURATION; HISPANICS
AB Background: Genetic testing for several cancer susceptibility syndromes is clinically available; however, existing data suggest limited population awareness of such tests.
Purpose: To examine awareness regarding cancer genetic testing in the U. S. population aged >= 25 years in the 2000, 2005, and 2010 National Health Interview Surveys.
Methods: The weighted percentages of respondents aware of cancer genetic tests, and percent changes from 2000-2005 and 2005-2010, overall and by demographic, family history, and healthcare factors were calculated. Interactions were used to evaluate the patterns of change in awareness between 2005 and 2010 among subgroups within each factor. To evaluate associations with awareness in 2005 and 2010, percentages were adjusted for covariates using multiple logistic regression. The analysis was performed in 2012.
Results: Awareness decreased from 44.4% to 41.5% (p<0.001) between 2000 and 2005, and increased to 47.0% (p<0.001) in 2010. Awareness increased between 2005 and 2010 in most subgroups, particularly among individuals in the South (p(interaction)=0.03) or with a usual place of care (p(interaction)=0.01). In 2005 and 2010, awareness was positively associated with personal or family cancer history and high perceived cancer risk, and inversely associated with racial/ethnic minorities, age 25-39 or >= 60 years, male gender, lower education and income levels, public or no health insurance, and no provider contact in 12 months.
Conclusions: Despite improvement from 2005 to 2010, <= 50% of the U. S. adult population was aware of cancer genetic testing in 2010. Notably, disparities persist for racial/ethnic minorities and individuals with limited health care access or income. Published by Elseiver Inc. on behalf of American Journal of Preventive Medicine
C1 [Mai, Phuong L.; Graubard, Barry I.] Natl Inst Drug Abuse, Div Canc Epidemiol & Genet, NIH, Bethesda, MD USA.
[Breen, Nancy] Natl Inst Drug Abuse, Appl Res Program, Hlth Serv & Econ Branch, NIH, Bethesda, MD USA.
[Wideroff, Louise] Natl Inst Drug Abuse, NCI, Div Basic Neurosci & Behav Res, NIH, Bethesda, MD USA.
[McNeel, Timothy S.] Informat Management Serv Inc, Calverton, MD USA.
[Vadaparampil, Susan Thomas] Univ S Florida, Coll Med, Moffitt Canc Ctr, Hlth Outcomes & Behav Program, Tampa, FL USA.
[Vadaparampil, Susan Thomas] Univ S Florida, Coll Med, Dept Oncol Sci, Tampa, FL USA.
RP Mai, PL (reprint author), 9609 Med Ctr Dr,RM 6-E540 MSC 9772, Bethesda, MD 20892 USA.
EM maip@mail.nih.gov
FU National Cancer Institute, NIH
FX This research was funded by the Intramural Research Program of the
National Cancer Institute, NIH. We would like to thank all of the
respondents for participating in the surveys.
NR 34
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Z9 14
U1 1
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD MAY
PY 2014
VL 46
IS 5
BP 440
EP 448
DI 10.1016/j.amepre.2014.01.002
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA AF5QQ
UT WOS:000334768400003
PM 24745633
ER
PT J
AU Rudzinski, ER
Anderson, JR
Lyden, ER
Bridge, JA
Barr, FG
Gastier-Foster, JM
Bachmeyer, K
Skapek, SX
Hawkins, DS
Teot, LA
Parham, DM
AF Rudzinski, Erin R.
Anderson, James R.
Lyden, Elizabeth R.
Bridge, Julia A.
Barr, Frederic G.
Gastier-Foster, Julie M.
Bachmeyer, Karen
Skapek, Stephen X.
Hawkins, Douglas S.
Teot, Lisa A.
Parham, David M.
TI Myogenin, AP2 beta, NOS-1, and HMGA2 Are Surrogate Markers of Fusion
Status in Rhabdomyosarcoma A Report From the Soft Tissue Sarcoma
Committee of the Children's Oncology Group
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE rhabdomyosarcoma; immunohistochemistry; fusion status
ID PARAFFIN-EMBEDDED TISSUES; ALVEOLAR RHABDOMYOSARCOMA; EMBRYONAL
RHABDOMYOSARCOMA; INTERGROUP-RHABDOMYOSARCOMA; GENE FUSIONS; EXPRESSION;
CLASSIFICATION; IMMUNOHISTOCHEMISTRY; DIAGNOSIS; SURVIVAL
AB Pediatric rhabdomyosarcoma (RMS) is traditionally classified on the basis of the histologic appearance into alveolar (ARMS) and embryonal (ERMS) subtypes. The majority of ARMS contain a PAX3-FOXO1 or PAX7-FOXO1 gene fusion, but about 20% do not. Intergroup Rhabdomyosarcoma Study stage-matched and group-matched ARMS typically behaves more aggressively than ERMS, but recent studies have shown that it is, in fact, the fusion status that drives the outcome for RMS. Gene expression microarray data indicate that several genes discriminate between fusion-positive and fusion-negative RMS with high specificity. Using tissue microarrays containing a series of both ARMS and ERMS, we identified a panel of 4 immunohistochemical markers-myogenin, AP2 beta, NOS-1, and HMGA2-which can be used as surrogate markers of fusion status in RMS. These antibodies provide an alternative to molecular methods for identification of fusion-positive RMS, particularly in cases in which there is scant or poor-quality material. In addition, these antibodies may be useful in fusion-negative ARMS as an indicator that a variant gene fusion may be present.
C1 [Rudzinski, Erin R.] Seattle Childrens Hosp, Dept Labs, Seattle, WA 98015 USA.
[Hawkins, Douglas S.] Fred Hutchinson Canc Res Ctr, Div Hematol Oncol, Seattle, WA 98104 USA.
[Hawkins, Douglas S.] Univ Washington, Seattle, WA 98195 USA.
[Anderson, James R.; Lyden, Elizabeth R.] Univ Nebraska Med Ctr, Dept Biostat, Omaha, NE USA.
[Bridge, Julia A.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
[Barr, Frederic G.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Gastier-Foster, Julie M.] Ohio State Univ, Coll Med, Dept Pathol, Columbus, OH 43210 USA.
[Gastier-Foster, Julie M.] Ohio State Univ, Coll Med, Dept Pediat, Columbus, OH 43210 USA.
[Skapek, Stephen X.; Hawkins, Douglas S.] Univ Texas SW Med Ctr Dallas, Dept Pediat Hematol Oncol, Dallas, TX 75390 USA.
[Teot, Lisa A.] Childrens Hosp Boston, Dept Pathol, Boston, MA USA.
[Parham, David M.] Univ Oklahoma Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK USA.
RP Rudzinski, ER (reprint author), Seattle Childrens Hosp, Dept Labs, OC-8-720,4800 Sandpoint Way NE, Seattle, WA 98015 USA.
EM erin.rudzinski@seattlechildrens.org
RI Gastier-Foster, Julie/E-3105-2011
FU St. Baldrick's Foundation [179772]; NIH [RC2-CA148216]; NCI
FX Research supported by St. Baldrick's Foundation Childhood Cancer
Research Grant, 179772 (E. R. R.); NIH-RC2-CA148216 (S. X. S., J.A.B.,
F. G. B., J.M.G.-F.). F. G. B. is supported by the Intramural Research
Program of the NCI. The authors have disclosed that they have no
significant relationships with, or financial interest in, any commercial
companies pertaining to this article.
NR 24
TC 13
Z9 13
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD MAY
PY 2014
VL 38
IS 5
BP 654
EP 659
DI 10.1097/PAS.0000000000000195
PG 6
WC Pathology; Surgery
SC Pathology; Surgery
GA AF7ZG
UT WOS:000334933700008
PM 24618610
ER
PT J
AU Schisterman, EF
Mumford, SL
Chen, Z
Browne, RW
Barr, DB
Kim, S
Louis, GMB
AF Schisterman, E. F.
Mumford, S. L.
Chen, Z.
Browne, R. W.
Barr, D. Boyd
Kim, S.
Louis, G. M. Buck
TI Lipid concentrations and semen quality: the LIFE study
SO ANDROLOGY
LA English
DT Article
DE lipoprotein metabolism; epidemiology; semen quality; fecundity
ID CHROMATIN STRUCTURE ASSAY; IN-VITRO FERTILIZATION; HUMAN-FERTILITY;
UNITED-STATES; HUMAN-SPERM; GENERAL-POPULATION; HEALTHY-MEN;
CHOLESTEROL; DECLINE; OBESITY
AB The decline in sperm count rates over the last 50years appears to parallel the rising prevalence of obesity. As lipid levels are strongly associated with obesity, high lipids levels or hyperlipidaemia may thus play an important role in the decline in fertility in addition to other environmental or lifestyle factors. The objective of this population based cohort study was to evaluate the association between men's serum lipid concentrations and semen quality parameters among 501 male partners of couples desiring pregnancy and discontinuing contraception. Each participant provided prospectively up to two semen samples (94% of men provided one or more semen samples, and 77% of men provided a second sample approximately 1month later). Linear mixed effects models were used to estimate the associations between baseline lipid concentrations and semen quality parameters, adjusted for age, body mass index and race. We found that higher levels of serum total cholesterol, free cholesterol and phospholipids were associated with a significantly lower percentage of spermatozoa with intact acrosome and smaller sperm head area and perimeter. Our results suggest that lipid concentrations may affect semen parameters, specifically sperm head morphology, highlighting the importance of cholesterol and lipid homeostasis for male fecundity.
C1 [Schisterman, E. F.; Mumford, S. L.; Chen, Z.; Kim, S.; Louis, G. M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD 20854 USA.
[Browne, R. W.] SUNY Buffalo, Dept Biotech & Clin Lab Sci, Buffalo, NY 14260 USA.
[Barr, D. Boyd] Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth Res, NIH, 6100 Execut Blvd,7B03, Rockville, MD 20854 USA.
EM schistee@mail.nih.gov
OI Schisterman, Enrique/0000-0003-3757-641X; Buck Louis,
Germaine/0000-0002-1774-4490
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) [N01-HD-3-3355, N01-HD-3-3356, N01-HD-3-3358]
FX This work was supported by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD) (contracts #N01-HD-3-3355, N01-HD-3-3356 and N01-HD-3-3358). We
acknowledge the Reproductive Health Assessment Team, Biomonitoring and
Health Assessment Branch, National Institute for Occupational Health and
Safety (NIOSH) for the analysis of semen samples under a Memo of
Understanding with the NICHD.
NR 62
TC 11
Z9 12
U1 0
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-2919
EI 2047-2927
J9 ANDROLOGY-US
JI Andrology
PD MAY
PY 2014
VL 2
IS 3
BP 408
EP 415
DI 10.1111/j.2047-2927.2014.00198.x
PG 8
WC Andrology
SC Endocrinology & Metabolism
GA AF7GC
UT WOS:000334881300016
PM 24596332
ER
PT J
AU Hu, ZY
Lan, KH
He, SS
Swaroop, M
Hu, X
Southall, N
Zheng, W
Liang, TJ
AF Hu, Zongyi
Lan, Keng-Hsin
He, Shanshan
Swaroop, Manju
Hu, Xin
Southall, Noel
Zheng, Wei
Liang, T. Jake
TI Novel Cell-Based Hepatitis C Virus Infection Assay for Quantitative
High-Throughput Screening of Anti-Hepatitis C Virus Compounds (vol 58,
pg 995, 2014)
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Correction
C1 [Hu, Zongyi] Natl Inst Diabet & Digest & Kidney Dis, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
NIH, Natl Ctr Adv Translat Sci, Bethesda, MD USA.
RP Hu, ZY (reprint author), Natl Inst Diabet & Digest & Kidney Dis, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
RI Southall, Noel/H-8991-2012
OI Southall, Noel/0000-0003-4500-880X
NR 1
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
EI 1098-6596
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD MAY
PY 2014
VL 58
IS 5
BP 2995
EP 2995
DI 10.1128/AAC.02529-14
PG 1
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA AE9XF
UT WOS:000334364300072
ER
PT J
AU Hosono, Y
Abe, T
Ishiai, M
Islam, MN
Arakawa, H
Wang, WD
Takeda, S
Ishii, Y
Takata, M
Seki, M
Enomoto, T
AF Hosono, Yoshifumi
Abe, Takuya
Ishiai, Masamichi
Islam, M. Nurul
Arakawa, Hiroshi
Wang, Weidong
Takeda, Shunichi
Ishii, Yutaka
Takata, Minoru
Seki, Masayuki
Enomoto, Takemi
TI Tumor suppressor RecQL5 controls recombination induced by DNA
crosslinking agents
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
LA English
DT Article
DE RecQL5; BRCA2; Fanconi anemia; ICL repair; Rad51 filament; Tumor
suppressor
ID IMMUNOGLOBULIN GENE CONVERSION; FANCONI-ANEMIA; HOMOLOGOUS
RECOMBINATION; VERTEBRATE CELLS; GENOME STABILIZATION; REPAIR PATHWAY;
BREAST-CANCER; HELICASE; REPLICATION; SUSCEPTIBILITY
AB RecQ family DNA helicases function in the maintenance of genome stability. Mice deficient in RecQL5, one of five RecQ helicases, show a cancer predisposition phenotype, suggesting that RecQL5 plays a tumor suppressor role. RecQL5 interacts with Rad51, a key factor in homologous recombination (HR), and displaces Rad51 from Rad51single stranded DNA (ssDNA) filaments in vitro. However, the precise roles of RecQL5 in the cell remain elusive. Here, we present evidence suggesting that RecQL5 is involved in DNA interstrand crosslink (ICL) repair. Chicken DT40 RECQL5 gene knockout (KO) cells showed sensitivity to ICL-inducing agents such as cisplatin (CDDP) and mitomycin C (MMC) and a higher number of chromosome aberrations in the presence of MMC than wild-type cells. The phenotypes of RECQL5 KO cells resembled those of Fanconi anemia gene KO cells. Genetic analysis using corresponding gene knockout cells showed that RecQL5 is involved in the FANCD1 (BRCA2)-dependent ICL repair pathway in which Rad51-55DNA filament formation is promoted by BRCA2. The disappearance but not appearance of Rad51-foci was delayed in RECQL5 KO cells after MMC treatment. Deletion of Rad54, which processes the Rad51-ssDNA filament in HR, in RECQL5 KO cells increased sensitivity to CDDP and further delayed the disappearance of Rad51-foci, suggesting that RecQL5 and Rad54 have different effects on the Rad51-s5DNA filament. Furthermore, the frequency and variation of CDDP-induced gene conversion at the immunoglobulin locus were increased in RECQL5 KO cells. These results suggest that RecQL5 plays a role in regulating the incidence and quality of ICL-induced recombination. (C) 2014 Elsevier B.V. All tights reserved.
C1 [Hosono, Yoshifumi; Seki, Masayuki] Tohoku Pharmaceut Univ, Grad Sch Pharmaceut Sci, Mol Cell Biol Lab, Aoba Ku, Sendai, Miyagi 9818558, Japan.
[Abe, Takuya; Arakawa, Hiroshi] IFOM, FIRC Inst Mol Oncol Fdn, I-20139 Milan, Italy.
[Ishiai, Masamichi; Takata, Minoru] Kyoto Univ, Ctr Radiat Biol, Dept Late Effect Studies, Lab DNA Damage Signaling,Sakyo Ku, Kyoto 6068501, Japan.
[Islam, M. Nurul; Wang, Weidong] NIA, Genet Lab, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
[Islam, M. Nurul] Yale Univ, Sch Med, Dept Mol Biophys & Biochem, New Haven, CT 06520 USA.
[Takeda, Shunichi] Kyoto Univ, Grad Sch Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan.
[Ishii, Yutaka] Shujitsu Univ, Sch Pharm, Naka Ku, Okayama 7038516, Japan.
[Seki, Masayuki] Tohoku Pharmaceut Univ, Dept Biochem, Aoba Ku, Sendai, Miyagi 9818558, Japan.
[Enomoto, Takemi] Musashino Univ, Fac Pharm, Pharmaceut Sci Res Inst, Mol Cell Biol Lab, Nishitokyo, Tokyo 2028585, Japan.
RP Seki, M (reprint author), Tohoku Pharmaceut Univ, Dept Biochem, Aoba Ku, 4-1 Komatsushima 4-Chome, Sendai, Miyagi 9818558, Japan.
EM Leno@musashino-u.ac.jp; t_eno@musashino-u.ac.jp
RI ABE, TAKUYA/A-2861-2015
OI ABE, TAKUYA/0000-0001-5298-082X
FU Ministry of Education, Culture, Sports, Science and Technology of Japan
(NEXT KAKENHI Grant) [22131002]; Japan Society for the Promotion of
Science (JSPS KAKENHI Grant) [23370065, 12J07075]; Intramural Research
Program of the National Institute on Aging, National Institutes of
Health [Z01:AG000657-09]
FX This work was supported by Grants-in-Aid for Scientific Research on
Priority Areas from the Ministry of Education, Culture, Sports, Science
and Technology of Japan (NEXT KAKENHI Grant Number 22131002) and also by
the Japan Society for the Promotion of Science (JSPS KAKENHI Grant
Number 23370065 and 12J07075). This work was supported in part by the
Intramural Research Program of the National Institute on Aging
(Z01:AG000657-09), National Institutes of Health (W.W.).
NR 54
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Z9 2
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-4889
EI 0006-3002
J9 BBA-MOL CELL RES
JI Biochim. Biophys. Acta-Mol. Cell Res.
PD MAY
PY 2014
VL 1843
IS 5
BP 1002
EP 1012
DI 10.1016/j.bbamcr.2014.01.005
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AF1LZ
UT WOS:000334476700018
PM 24418621
ER
PT J
AU Liggett, JL
Zhang, XB
Eling, TE
Baek, SJ
AF Liggett, Jason L.
Zhang, Xiaobo
Eling, Thomas E.
Baek, Seung Joon
TI Anti-tumor activity of non-steroidal anti-inflammatory drugs:
Cyclooxygenase-independent targets
SO CANCER LETTERS
LA English
DT Review
DE NSAIDs; COX; Sulindac sulfide; Tolfenamic acid; NAG-1
ID NF-KAPPA-B; COLON-CANCER CELLS; ENDOPLASMIC-RETICULUM STRESS; ACTIVATING
TRANSCRIPTION FACTOR-3; EPITHELIAL-MESENCHYMAL TRANSITION; FAMILIAL
ADENOMATOUS POLYPOSIS; COX-2 INHIBITOR CELECOXIB; NUCLEAR BETA-CATENIN;
TOLFENAMIC ACID; COLORECTAL-CANCER
AB Non-steroidal anti-inflammatory drugs (NSAIDs) are used extensively for analgesic and antipyretic treatments. In addition, NSAIDs reduce the risk and mortality to several cancers. Their mechanisms in anti-tumorigenesis are not fully understood, but both cyclooxygenase (COX)-dependent and -independent pathways play a role. We and others have been interested in elucidating molecular targets of NSAID-induced apoptosis. In this review, we summarize updated literature regarding cellular and molecular targets modulated by NSAIDs. Among those NSAIDs, sulindac sulfide and tolfenamic acid are emphasized in this review because these two drugs have been well investigated for their anti-tumorigenic activity in many different types of cancer. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Liggett, Jason L.; Baek, Seung Joon] Univ Tennessee, Coll Vet Med, Dept Biomed & Diagnost Sci, Knoxville, TN 37996 USA.
[Zhang, Xiaobo] Northwest A&F Univ, Coll Anim Sci & Technol, Yangling 712100, Shaanxi, Peoples R China.
[Eling, Thomas E.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Baek, SJ (reprint author), Univ Tennessee, Coll Vet Med, Dept Biomed & Diagnost Sci, 2407 River Dr, Knoxville, TN 37996 USA.
EM sbaek2@utk.edu
FU American Cancer Society [CNE-111611]; National Institutes of Health
[R01CA108975]; University of Tennessee, Center of Excellence in
Livestock Diseases and Human Health
FX We apologize to all colleagues whose important work we could not cite
due to space restrictions. The authors thank Misty Bailey for her
critical review. This work was supported by grants from the American
Cancer Society (CNE-111611), National Institutes of Health
(R01CA108975), and the University of Tennessee, Center of Excellence in
Livestock Diseases and Human Health.
NR 103
TC 22
Z9 22
U1 0
U2 25
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD MAY 1
PY 2014
VL 346
IS 2
BP 217
EP 224
DI 10.1016/j.canlet.2014.01.021
PG 8
WC Oncology
SC Oncology
GA AF6JJ
UT WOS:000334820800008
PM 24486220
ER
PT J
AU Yeo, D
Huynh, N
Beutler, JA
Christophi, C
Shulkes, A
Baldwin, GS
Nikfarjam, M
He, H
AF Yeo, Dannel
Nhi Huynh
Beutler, John A.
Christophi, Christopher
Shulkes, Arthur
Baldwin, Graham S.
Nikfarjam, Mehrdad
He, Hong
TI Glaucarubinone and gemcitabine synergistically reduce pancreatic cancer
growth via down-regulation of P21-activated kinases
SO CANCER LETTERS
LA English
DT Article
DE Glaucarubinone; Gemcitabine; Pancreatic cancer; P21-activated kinases
ID PAK4; COMBINATION; INHIBITION; ACTIVATION; RESECTION; MALARIA; DRUGS
AB Pancreatic cancer is one of the most lethal of human malignancies. Nearly 100% cases of pancreatic cancer carry mutations in KRas. P-21-activated kinases (PAKs) are activated by and act downstream of KRas. Glaucarubinone, a natural product first isolated from the seeds of the tree Simarouba glauca, was originally developed as an antimalarial drug, and has more recently been recognised as an anticancer agent. The aims of this study were to determine whether glaucarubinone, alone or in combination with the front-line chemotherapeutic agent gemcitabine, would inhibit the growth of pancreatic cancer cells in vitro or in vivo and the mechanism involved. Growth of the human pancreatic cancer cell lines PANC-1 and MiaPaCa-2 was measured by H-3-thymidine incorporation in vitro, and by volume as xenografts in SCID mice. The expression and activities of the two serine/threonine kinases PAK1 and PAK4, which are key regulators of cancer progression, were measured by Western blotting. Here we report that glaucarubinone decreased proliferation and migration of pancreatic cancer cells in vitro, and reduced their growth as xenografts in vivo. Treatment with glaucarubinone and gemcitabine reduced proliferation in vitro and tumor growth in vivo more than treatment with either glaucarubinone or gemcitabine alone. Treatment with glaucarubinone reduced PAK1 and PAK4 activities, which were further decreased by the combination of glaucarubinone and gemcitabine. These results indicate that glaucarubinone reduced pancreatic cancer cell growth at least in part via inhibition of pathways involving PAKI and PAK4. The synergistic inhibition by glaucarubinone and gemcitabine observed both in vitro and in vivo suggests that glaucarubinone may be a useful adjunct to current regimes of chemotherapy. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Yeo, Dannel; Nhi Huynh; Christophi, Christopher; Shulkes, Arthur; Baldwin, Graham S.; Nikfarjam, Mehrdad; He, Hong] Univ Melbourne, Dept Surg, Austin Hlth, Heidelberg, Vic 3084, Australia.
[Beutler, John A.] NCI, Mol Targets Lab, Frederick, MD 21702 USA.
RP He, H (reprint author), Univ Melbourne, Dept Surg, Austin Hlth, Studley Rd, Heidelberg, Vic 3084, Australia.
EM hong.he@unimelb.edu.au
OI Baldwin, Graham/0000-0002-0944-8747; Nikfarjam,
Mehrdad/0000-0003-4866-276X
FU National Health and Medical Research Council (NHMRC) of Australia
[508908, 1041831, 1020983]; Austin Hospital Medical Research Foundation;
NIH National Cancer Institute Center for Cancer Research; Australian
Rotary Health
FX We thank the Drug Synthesis & Chemistry Branch, NCI, for supplying the
glaucarubinone used in this study, and Hiroshi Maruta for stimulating
discussions. This work was supported by National Health and Medical
Research Council (NHMRC) of Australia Grants 508908 (HH) [27], 1041831
(GB & AS), and 1020983 (GB), by the Austin Hospital Medical Research
Foundation, and by the Intramural Research Program of the NIH National
Cancer Institute Center for Cancer Research. Dannel Yeo is supported by
the Ph.D scholarship from Australian Rotary Health.
NR 28
TC 21
Z9 22
U1 1
U2 14
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD MAY 1
PY 2014
VL 346
IS 2
BP 264
EP 272
DI 10.1016/j.canlet.2014.01.001
PG 9
WC Oncology
SC Oncology
GA AF6JJ
UT WOS:000334820800013
PM 24491405
ER
PT J
AU Ivetac, A
Swift, SE
Boyer, PL
Diaz, A
Naughton, J
Young, JAT
Hughes, SH
McCammon, JA
AF Ivetac, Anthony
Swift, Sara E.
Boyer, Paul L.
Diaz, Arturo
Naughton, John
Young, John A. T.
Hughes, Stephen H.
McCammon, J. Andrew
TI Discovery of Novel Inhibitors of HIV-1 Reverse Transcriptase Through
Virtual Screening of Experimental and Theoretical Ensembles
SO CHEMICAL BIOLOGY & DRUG DESIGN
LA English
DT Article
DE HIV; molecular dynamics; NNRTI; reverse transcriptase; virtual screening
ID IMMUNODEFICIENCY-VIRUS TYPE-1; RELAXED COMPLEX SCHEME; AIDED DRUG
DESIGN; NONNUCLEOSIDE INHIBITORS; RECEPTOR FLEXIBILITY; POTENT;
MECHANISM; DOCKING; DERIVATIVES; SIMULATION
AB Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are potent anti-HIV chemotherapeutics. Although there are FDA-approved NNRTIs, challenges such as the development of resistance have limited their utility. Here, we describe the identification of novel NNRTIs through a combination of computational and experimental approaches. Based on the known plasticity of the NNRTI binding pocket (NNIBP), we adopted an ensemble-based virtual screening strategy: coupling receptor conformations from 10 X-ray crystal structures with 120 snapshots from a total of 480ns of molecular dynamics (MD) trajectories. A screening library of 2864 National Cancer Institute (NCI) compounds was built and docked against the ensembles in a hierarchical fashion. Sixteen diverse compounds were tested for their ability to block HIV infection in human tissue cultures using a luciferase-based reporter assay. Three promising compounds were further characterized, using a HIV-1 RT-based polymerase assay, to determine the specific mechanism of inhibition. We found that 2 of the three compounds inhibited the polymerase activity of RT (with potency similar to the positive control, the FDA-approved drug nevirapine). Through a computational approach, we were able to discover two compounds which inhibit HIV replication and block the activity of RT, thus offering the potential for optimization into mature inhibitors.
C1 [Ivetac, Anthony; Swift, Sara E.; McCammon, J. Andrew] Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA.
[Boyer, Paul L.; Hughes, Stephen H.] NCI, HIV Drug Resistance Program, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Diaz, Arturo; Naughton, John; Young, John A. T.] Salk Inst Biol Studies, Nomis Ctr Immunobiol & Microbial Pathogenesis, La Jolla, CA 92037 USA.
[McCammon, J. Andrew] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA.
[McCammon, J. Andrew] Univ Calif San Diego, Howard Hughes Med Inst, La Jolla, CA 92093 USA.
RP Ivetac, A (reprint author), Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA.
EM aivetac@mccammon.ucsd.edu
FU National Science Foundation, the National Institutes of Health and
Howard Hughes Medical Institute; National Institutes of Health (NIH),
National Cancer Institute, Center for Cancer Research
FX We acknowledge the San Diego Supercomputing Center, the Center for
Theoretical Biological Physics, and the National Biomedical
Computational Resource for computational resources and the National
Science Foundation, the National Institutes of Health and Howard Hughes
Medical Institute for financial support. We also acknowledge the Nomis,
Auen, and Morris Foundations and the James B. Pendleton Charitable Trust
for their support. This study was supported in part by the Intramural
Research Program of the National Institutes of Health (NIH), National
Cancer Institute, Center for Cancer Research. 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.
NR 39
TC 9
Z9 10
U1 0
U2 29
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1747-0277
EI 1747-0285
J9 CHEM BIOL DRUG DES
JI Chem. Biol. Drug Des.
PD MAY
PY 2014
VL 83
IS 5
BP 521
EP 531
DI 10.1111/cbdd.12277
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA AF6XD
UT WOS:000334857000002
PM 24405985
ER
PT J
AU Mueller, GA
Maleki, SJ
Pedersen, LC
AF Mueller, Geoffrey A.
Maleki, Soheila J.
Pedersen, Lars C.
TI The Molecular Basis of Peanut Allergy
SO CURRENT ALLERGY AND ASTHMA REPORTS
LA English
DT Review
DE Peanut allergy; Molecular basis; Peanut allergens; Major allergens;
Minor allergens; Protein structures; Cross-reactivity; Molecular
modifications
ID GLYCATION END-PRODUCTS; ARA H 2; PLANT FOOD ALLERGENS; IGE-BINDING
EPITOPES; CRYSTAL-STRUCTURE; ARACHIS-HYPOGAEA; IMMUNOGLOBULIN-E;
CARBOHYDRATE DETERMINANTS; FUNCTIONAL-ASPECTS; TRYPSIN-INHIBITOR
AB Peanut allergens can trigger a potent and sometimes dangerous immune response in an increasing number of people. The molecular structures of these allergens form the basis for understanding this response. This review describes the currently known peanut allergen structures and discusses how modifications both enzymatic and non-enzymatic affect digestion, innate immune recognition, and IgE interactions. The allergen structures help explain cross-reactivity among allergens from different sources, which is useful in improving patient diagnostics. Surprisingly, it was recently noted that similar short peptide sequences among unrelated peanut allergens could also be a source of cross-reactivity. The molecular features of peanut allergens continue to inform predictions and provide new research directions in the study of allergic disease.
C1 [Mueller, Geoffrey A.; Pedersen, Lars C.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Maleki, Soheila J.] ARS, USDA, So Reg Res Ctr, New Orleans, LA USA.
RP Mueller, GA (reprint author), NIEHS, Struct Biol Lab, 111 TW Alexander Dr,MD-MR-01, Res Triangle Pk, NC 27709 USA.
EM Mueller3@niehs.nih.gov
FU National Institute of Environmental Health Sciences, National Institutes
of Health [Z01-ES102885-01, ZIA-ES102645]
FX The authors wish to thank Drs. Robert London, Michael Fessler, and Jason
Williams for critical readings of the manuscript. This research was
supported by Research Project Number Z01-ES102885-01 and ZIA-ES102645 in
the Intramural Research Program of the National Institute of
Environmental Health Sciences, National Institutes of Health.
NR 81
TC 4
Z9 5
U1 6
U2 38
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1529-7322
EI 1534-6315
J9 CURR ALLERGY ASTHM R
JI Curr. Allergy Asthma Rep.
PD MAY
PY 2014
VL 14
IS 5
AR 429
DI 10.1007/s11882-014-0429-5
PG 9
WC Allergy; Immunology
SC Allergy; Immunology
GA AE7KS
UT WOS:000334177300001
PM 24633613
ER
PT J
AU Taylor, SM
Fairhurst, RM
AF Taylor, Steve M.
Fairhurst, Rick M.
TI Malaria parasites and red cell variants: when a house is not a home
SO CURRENT OPINION IN HEMATOLOGY
LA English
DT Review
DE enzymopathy; hemoglobinopathy; malaria; ovalocytosis; Plasmodium
falciparum erythrocyte membrane protein 1
ID PLASMODIUM-FALCIPARUM MALARIA; INFECTED ERYTHROCYTES; SICKLE HEMOGLOBIN;
TRAIT; RESISTANCE; PROTECTS; MECHANISM; CHILDREN; VIVAX; TRANSMISSION
AB Purpose of reviewMultiple red cell variants are known to confer protection from malaria. Here, we review advances in identifying new variants that modulate malaria risk and in defining molecular mechanisms that mediate malaria protection.Recent findingsNew red cell variants, including an innate variant in the red cell's major Ca2+ pump and the acquired state of iron deficiency, have been associated with protection from clinical falciparum malaria. The polymorphisms hemoglobin C (HbC) and hemoglobin S (HbS) - known to protect carriers from severe falciparum malaria - enhance parasite passage to mosquitoes and may promote malaria transmission. At the molecular level, substantial advances have been made in understanding the impact of HbS and HbC upon the interactions between host microRNAs and Plasmodium falciparum protein translation; remodeling of red cell cytoskeletal components and transport of parasite proteins to the red cell surface; and chronic activation of the human innate immune system, which induces tolerance to blood-stage parasites. Several polymorphisms have now been associated with protection from clinical vivax malaria or reduced Plasmodium vivax density, including Southeast Asian ovalocytosis and two common forms of glucose-6-phosphate dehydrogenase deficiency.SummaryRed cell variants that modulate malaria risk can serve as models to identify clinically relevant mechanisms of pathogenesis, and thus define parasite and host targets for next-generation therapies.
C1 [Taylor, Steve M.] Duke Univ, Med Ctr, Duke Global Hlth Inst, Div Infect Dis & Int Hlth, Durham, NC 27706 USA.
[Taylor, Steve M.] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP Fairhurst, RM (reprint author), NIAID, Lab Malaria & Vector Res, NIH, 12735 Twinbrook Pkwy,Room 3E-10A, Rockville, MD 20852 USA.
EM rfairhurst@niaid.nih.gov
FU NIAID [K08AI100924]; NIAID, NIH
FX S.M.T. is supported by an award from the NIAID, K08AI100924. R. M. F. is
supported by the Intramural Research Program of the NIAID, NIH.
NR 42
TC 9
Z9 10
U1 5
U2 27
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1065-6251
EI 1531-7048
J9 CURR OPIN HEMATOL
JI Curr. Opin. Hematol.
PD MAY
PY 2014
VL 21
IS 3
BP 193
EP 200
DI 10.1097/MOH.0000000000000039
PG 8
WC Hematology
SC Hematology
GA AF8HW
UT WOS:000334957500006
PM 24675047
ER
PT J
AU Muller, BG
van den Bos, W
Pinto, PA
de la Rosette, JJ
AF Muller, Berrend G.
van den Bos, Willemien
Pinto, Peter A.
de la Rosette, Jean J.
TI Imaging modalities in focal therapy: patient selection, treatment
guidance, and follow-up
SO CURRENT OPINION IN UROLOGY
LA English
DT Review
DE focal therapy; MRI; prostate cancer; ultrasonography
ID INTENSITY FOCUSED ULTRASOUND; LOCALIZED PROSTATE-CANCER; TRANSRECTAL
ULTRASOUND; MULTIPARAMETRIC MRI; ACTIVE SURVEILLANCE; BIOPSY;
ULTRASONOGRAPHY; REGISTRATION; ELASTOGRAPHY; MULTICENTER
AB Purpose of reviewFocal therapy for prostate cancer is emerging as a management option between active surveillance and radical treatments. In this article, we present two of the most important imaging modalities in focal therapy, multiparametric MRI (mpMRI) and ultrasonography. We review the recent advances within these two platforms.Recent findingsState-of-the-art imaging in all phases of focal therapy is essential for treatment safety. In patient selection, treatment guidance, and follow-up, different aspects of imaging are important. mpMRI is an imaging technology with high imaging resolution and contrast. This makes it an excellent technology for patient selection and treatment planning and follow-up. Ultrasound has the unique property of real-time image acquisition. This makes it an excellent technology for real-time treatment guidance. There are multiple novelties in these two platforms that have increased the accuracy considerably. Examples in ultrasound are contrast-enhanced ultrasonography, elastography, shear-wave elastography, and histoscanning. In mpMRI, these advantages consist of multiple sequences combined to one image and magnetic resonance thermometry.SummaryStandardization of multiparametric transrectal ultrasound and mpMRI is of paramount importance. For targeted treatment and follow-up, a good negative predictive value of the test is important. There is much to gain from both of these developing fields and imaging accuracy of the two platforms is comparable. Standardization in conduct and interpretation, three-dimensional reconstruction, and fusion of the two platforms can make focal therapy the standard of care for prostate cancer.
C1 [Muller, Berrend G.; van den Bos, Willemien; de la Rosette, Jean J.] AMC Univ Hosp, Dept Urol, Amsterdam, Netherlands.
[Pinto, Peter A.] NCI, Dept Urol, Bethesda, MD 20892 USA.
RP Muller, BG (reprint author), Acad Med Ctr, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM b.g.muller@amc.uva.nl
FU National Institutes of Health (NIH); Cure for Cancer Foundation
FX Disclosures: P.A.P. receives an unrestricted research grant from the
National Institutes of Health (NIH). B. G. M. and W.v.d.B. receive an
unrestricted research grant from the 'Cure for Cancer Foundation'.
NR 45
TC 12
Z9 13
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0963-0643
EI 1473-6586
J9 CURR OPIN UROL
JI Curr. Opin. Urol.
PD MAY
PY 2014
VL 24
IS 3
BP 218
EP 224
DI 10.1097/MOU.0000000000000041
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AF1XB
UT WOS:000334506100003
PM 24637316
ER
PT J
AU Kelly, NR
Shank, LM
Bakalar, JL
Tanofsky-Kraff, M
AF Kelly, Nichole R.
Shank, Lisa M.
Bakalar, Jennifer L.
Tanofsky-Kraff, Marian
TI Pediatric Feeding and Eating Disorders: Current State of Diagnosis and
Treatment
SO CURRENT PSYCHIATRY REPORTS
LA English
DT Article
DE Pediatric; Child; Adolescent; Eating disorder; Feeding disorder; Binge
eating; Loss of control eating; Anorexia nervosa; Bulimia nervosa; Pica;
Rumination; Avoidant/restrictive food intake; Compensatory behavior;
Regurgitation; Weight; Overweight; Obesity
ID RANDOMIZED CONTROLLED-TRIAL; COGNITIVE REMEDIATION THERAPY; FAMILY-BASED
TREATMENT; ANOREXIA-NERVOSA; BULIMIA-NERVOSA; ADOLESCENT GIRLS;
RUMINATION SYNDROME; INCORPORATING DIMENSIONS; BEHAVIORAL TREATMENT;
OVERWEIGHT CHILDREN
AB The Diagnostic and Statistical Manual of Mental Disorders now recognizes six primary feeding and eating disorders including pica, rumination disorder, avoidant/restrictive food intake disorder, anorexia nervosa, bulimia nervosa and binge-eating disorder. Guided by research from the past 3 years, the current review outlines diagnostic criteria for each disorder, their clinical correlates and treatment options. Recent modifications to diagnostic criteria will likely help to improve treatment outcomes and prognosis. Nevertheless, several concerns remain regarding the validity of current diagnostic criteria for youth, including the clinical relevance of the size and frequency of binge eating episodes. Additionally, the lack of randomized controlled trials has led to an overreliance on data from quasi-experimental studies, case series and single case studies that impede development of strong clinical recommendations for treating feeding and eating disorders. Recommendations for future research include identifying empirically supported treatments and prevention programs focused on early markers of pediatric feeding and eating concerns.
C1 [Kelly, Nichole R.; Shank, Lisa M.; Bakalar, Jennifer L.; Tanofsky-Kraff, Marian] Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, DoD, Bethesda, MD 20814 USA.
[Kelly, Nichole R.; Shank, Lisa M.; Bakalar, Jennifer L.; Tanofsky-Kraff, Marian] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Obes, Program Dev Endocrinol & Genet, NIH,DHHS, Bethesda, MD 20814 USA.
RP Tanofsky-Kraff, M (reprint author), Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, DoD, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM nichole.kelly@nih.gov; lisa.shank@usuhs.edu; jennifer.bakalar@usuhs.edu;
marian.tanofsky-kraff@usuhs.edu
NR 120
TC 5
Z9 7
U1 7
U2 36
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3812
EI 1535-1645
J9 CURR PSYCHIAT REP
JI Curr. Psychiatry Rep.
PD MAY
PY 2014
VL 16
IS 5
AR 446
DI 10.1007/s11920-014-0446-z
PG 12
WC Psychiatry
SC Psychiatry
GA AF0XI
UT WOS:000334437700004
PM 24643374
ER
PT J
AU Muranski, P
AF Muranski, Pawel
TI An easy way to make a good anti-tumor chimeric antigen receptor T cell?
SO CYTOTHERAPY
LA English
DT Editorial Material
ID EFFECTOR
C1 [Muranski, Pawel] NHLBI, Stem Cell Allogen Transplantat Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Muranski, P (reprint author), Bldg 10 CRC Rm3E5288,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM muranskp@mail.nih.gov
NR 10
TC 0
Z9 0
U1 0
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1465-3249
EI 1477-2566
J9 CYTOTHERAPY
JI Cytotherapy
PD MAY
PY 2014
VL 16
IS 5
BP 577
EP 578
DI 10.1016/j.jcyt.2014.03.003
PG 2
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology; Hematology; Medicine, Research & Experimental
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
& Experimental Medicine
GA AF5BC
UT WOS:000334728000001
PM 24725890
ER
PT J
AU Estampador, AC
Pomeroy, J
Renstrom, F
Nelson, SM
Mogren, I
Persson, M
Sattar, N
Domellof, M
Franks, PW
AF Estampador, Angela C.
Pomeroy, Jeremy
Renstrom, Frida
Nelson, Scott M.
Mogren, Ingrid
Persson, Margareta
Sattar, Naveed
Domellof, Magnus
Franks, Paul W.
TI Infant Body Composition and Adipokine Concentrations in Relation to
Maternal Gestational Weight Gain
SO DIABETES CARE
LA English
DT Article
ID INSULIN SENSITIVITY; GLUCOSE-TOLERANCE; DIABETES-MELLITUS;
PHYSICAL-ACTIVITY; PREGNANCY; OBESITY; GROWTH; WOMEN; INTERLEUKIN-6;
ADIPOSITY
AB OBJECTIVETo investigate associations of maternal gestational weight gain and body composition and their impact on offspring body composition and adipocytokine, glucose, and insulin concentrations at age 4 months.RESEARCH DESIGN AND METHODSThis was a prospective study including 31 mother-infant pairs (N = 62). Maternal body composition was assessed using doubly labeled water. Infant body composition was assessed at 4 months using air displacement plethysmography, and venous blood was assayed for glucose, insulin, adiponectin, interleukin-6 (IL-6), and leptin concentrations.RESULTSRate of gestational weight gain in midpregnancy was significantly associated with infant fat mass (r = 0.41, P = 0.03); rate of gestational weight in late pregnancy was significantly associated with infant fat-free mass (r = 0.37, P = 0.04). Infant birth weight was also strongly correlated with infant fat-free mass at 4 months (r = 0.63, P = 0.0002). Maternal BMI and maternal fat mass were strongly inversely associated with infant IL-6 concentrations (r = -0.60, P = 0.002 and r = -0.52, P = 0.01, respectively). Infant fat-free mass was inversely related to infant adiponectin concentrations (r = -0.48, P = 0.008) and positively correlated with infant blood glucose adjusted for insulin concentrations (r = 0.42, P = 0.04). No significant associations for leptin were observed.CONCLUSIONSTiming of maternal weight gain differentially impacts body composition of the 4-month-old infant, which in turn appears to affect the infant's glucose and adipokine concentrations.
C1 [Estampador, Angela C.; Pomeroy, Jeremy; Renstrom, Frida; Franks, Paul W.] Lund Univ, Skane Univ Hosp, Dept Clin Sci, Genet & Mol Epidemiol Unit, Malmo, Sweden.
[Pomeroy, Jeremy] NIH, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ USA.
[Renstrom, Frida; Franks, Paul W.] Umea Univ, Dept Publ Hlth & Clin Med, Div Med, Genet Epidemiol & Clin Res Grp, Umea, Sweden.
[Nelson, Scott M.] Univ Glasgow, Fac Med, Glasgow, Lanark, Scotland.
[Mogren, Ingrid; Persson, Margareta] Umea Univ Hosp, Dept Clin Sci, Obstet & Gynecol Unit, S-90185 Umea, Sweden.
[Persson, Margareta] Dalarna Univ, Sch Hlth & Social Studies, Falun, Sweden.
[Sattar, Naveed] Univ Glasgow, Cardiovasc Res Ctr, British Heart Fdn, Glasgow, Lanark, Scotland.
[Domellof, Magnus] Umea Univ, Dept Clin Sci, Pediat Unit, Umea, Sweden.
[Franks, Paul W.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Franks, PW (reprint author), Lund Univ, Skane Univ Hosp, Dept Clin Sci, Genet & Mol Epidemiol Unit, Malmo, Sweden.
EM paul.franks@med.lu.se
RI Domellof, Magnus/E-5307-2011;
OI Domellof, Magnus/0000-0002-0726-7029; Estampador,
Angela/0000-0003-0097-4529; Nelson, Scott/0000-0002-9099-3047; Franks,
Paul/0000-0002-0520-7604; Sattar, Naveed/0000-0002-1604-2593; Mogren,
Ingrid/0000-0003-2985-1135
FU Torsten Foundation; Ragnar Soderberg Foundation; Fredrik and Ingrid
Thurings Foundation; Vasterbotten regional health authority
FX The study was a preparatory project for the LifeGene Study
(www.lifegene.se) and was funded by the Torsten and Ragnar Soderberg
Foundations, the Fredrik and Ingrid Thurings Foundation, and the
Vasterbotten regional health authority (all grants to P.W.F.).
NR 40
TC 5
Z9 5
U1 0
U2 4
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2014
VL 37
IS 5
BP 1432
EP 1438
DI 10.2337/dc13-2265
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AF6QQ
UT WOS:000334840100060
PM 24623025
ER
PT J
AU Cuellar-Rodriguez, J
Connor, D
Murray, P
Gea-Banacloche, J
AF Cuellar-Rodriguez, J.
Connor, D.
Murray, P.
Gea-Banacloche, J.
CA Natl Inst Hlth NIH
TI Discrepant results from sampling different lumens of multilumen
catheters: the case for sampling all lumens
SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES
LA English
DT Article
ID PEDIATRIC ONCOLOGY PATIENTS; BLOOD-STREAM INFECTION; CENTRAL VENOUS
CATHETERS; CLINICAL UTILITY; CULTURES DRAWN; VOLUME; DIAGNOSIS;
SENSITIVITY; GUIDELINES; CANCER
AB It is unclear whether blood culture samples should be obtained through one or multiple catheter lumens. We measured how frequently drawing blood cultures from all the lumens from a multilumen catheter resulted in discordant results and how often these caused medical interventions. We performed a retrospective review of the microbiology database of the National Institutes of Health (NIH) Clinical Center. Most patients were immunocompromised. All blood cultures obtained from May 1, 2007 to April 30, 2009 were reviewed. We analyzed all positive blood cultures (i.e., positivity of any of the blood cultures drawn through the catheter lumens) when simultaneous samples from different lumens were obtained, and reviewed the medical charts of those in which blood cultures from different lumens had discordant results (i.e., not all lumens revealed the same organism). We also analyzed how often the discordant results lead to a medical intervention, defined as a change of antimicrobials and/or removal of the catheter. There were 405 episodes of positive blood cultures, in which simultaneous samples of different lumens of a multilumen catheter were obtained. Eighty-five episodes (21 %) were considered to be contaminants and excluded. We analyzed 320 episodes of positive blood cultures in 153 patients; 173 episodes (54.1 %) had discordant results. In 77 % of the 173 episodes, the discordant isolate led to a medical intervention. In immunocompromised patients, sampling all the lumens of a multilumen catheter results in more positive blood cultures, and many of these result in medical interventions. When evaluating bloodstream infection in patients with multilumen catheters, sampling all lumens should be strongly considered.
C1 [Cuellar-Rodriguez, J.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Connor, D.] Univ Pittsburgh, Sch Med, Dept Med & Biomed Informat, Pittsburgh, PA 15261 USA.
[Murray, P.] BD Diagnost, Sparks, MD 21152 USA.
[Gea-Banacloche, J.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
RP Gea-Banacloche, J (reprint author), NCI, Expt Transplantat & Immunol Branch, 10 Ctr Dr,Bldg 10,Room CRC 3-3130, Bethesda, MD 20892 USA.
EM banacloj@mail.nih.gov
NR 21
TC 1
Z9 1
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0934-9723
EI 1435-4373
J9 EUR J CLIN MICROBIOL
JI Eur. J. Clin. Microbiol. Infect. Dis.
PD MAY
PY 2014
VL 33
IS 5
BP 831
EP 835
DI 10.1007/s10096-013-2021-7
PG 5
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA AF8AV
UT WOS:000334938300019
PM 24297770
ER
PT J
AU van Duyvenvoorde, HA
Lui, JC
Kant, SG
Oostdijk, W
Gijsbers, ACJ
Hoffer, MJV
Karperien, M
Walenkamp, MJE
Noordam, C
Voorhoeve, PG
Mericq, V
Pereira, AM
Claahsen-van de Grinten, HL
van Gool, SA
Breuning, MH
Losekoot, M
Baron, J
Ruivenkamp, CAL
Wit, JM
AF van Duyvenvoorde, Hermine A.
Lui, Julian C.
Kant, Sarina G.
Oostdijk, Wilma
Gijsbers, Antoinet C. J.
Hoffer, Mariette J. V.
Karperien, Marcel
Walenkamp, Marie J. E.
Noordam, Cees
Voorhoeve, Paul G.
Mericq, Veronica
Pereira, Alberto M.
Claahsen-van de Grinten, Hedi L.
van Gool, Sandy A.
Breuning, Martijn H.
Losekoot, Monique
Baron, Jeffrey
Ruivenkamp, Claudia A. L.
Wit, Jan M.
TI Copy number variants in patients with short stature
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE short stature; small for gestational age; idiopathic short stature;
growth; copy number variations (CNV); single-nucleotide polymorphism
(SNP) array
ID IDIOPATHIC SHORT STATURE; GENOME-WIDE ASSOCIATION; FOR-GESTATIONAL-AGE;
FACTOR-I RECEPTOR; HETEROZYGOUS EXPRESSION; GROWTH-RETARDATION; SHORT
CHILDREN; HUMAN HEIGHT; GENE; MUTATION
AB Height is a highly heritable and classic polygenic trait. Recent genome-wide association studies (GWAS) have revealed that at least 180 genetic variants influence adult height. However, these variants explain only about 10% of the phenotypic variation in height. Genetic analysis of short individuals can lead to the discovery of novel rare gene defects with a large effect on growth. In an effort to identify novel genes associated with short stature, genome-wide analysis for copy number variants (CNVs), using single-nucleotide polymorphism arrays, in 162 patients (149 families) with short stature was performed. Segregation analysis was performed if possible, and genes in CNVs were compared with information from GWAS, gene expression in rodents' growth plates and published information. CNVs were detected in 40 families. In six families, a known cause of short stature was found (SHOX deletion or duplication, IGF1R deletion), in two combined with a de novo potentially pathogenic CNV. Thirty-three families had one or more potentially pathogenic CNVs (n = 40). In 24 of these families, segregation analysis could be performed, identifying three de novo CNVs and nine CNVs segregating with short stature. Four were located near loci associated with height in GWAS (ADAMTS17, TULP4, PRKG2/BMP3 and PAPPA). Besides six CNVs known to be causative for short stature, 40 CNVs with possible pathogenicity were identified. Segregation studies and bioinformatics analysis suggested various potential candidate genes. published online 25 September 2013
C1 [van Duyvenvoorde, Hermine A.; Oostdijk, Wilma; van Gool, Sandy A.; Wit, Jan M.] Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands.
[van Duyvenvoorde, Hermine A.; Pereira, Alberto M.] Leiden Univ, Med Ctr, Dept Endocrinol & Metab Dis, NL-2300 RC Leiden, Netherlands.
[van Duyvenvoorde, Hermine A.; Kant, Sarina G.; Gijsbers, Antoinet C. J.; Hoffer, Mariette J. V.; Breuning, Martijn H.; Losekoot, Monique; Ruivenkamp, Claudia A. L.] Leiden Univ, Med Ctr, Dept Clin Genet, NL-2300 RC Leiden, Netherlands.
[Lui, Julian C.; Baron, Jeffrey] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Dev, Bethesda, MD USA.
[Karperien, Marcel] Univ Twente, MIRA Inst Biomed Technol & Tech Med, Dept Dev BioEngn, NL-7500 AE Enschede, Netherlands.
[Walenkamp, Marie J. E.] Vrije Univ Amsterdam Med Ctr, Dept Pediat, Amsterdam, Netherlands.
[Noordam, Cees; Claahsen-van de Grinten, Hedi L.] Radboud Univ Nijmegen, Med Ctr, Dept Pediat, NL-6525 ED Nijmegen, Netherlands.
[Voorhoeve, Paul G.] Canisius Wilhelmina Hosp, Dept Pediat, Nijmegen, Netherlands.
[Mericq, Veronica] Univ Chile, Inst Maternal & Child Dis, Santiago, Chile.
RP van Duyvenvoorde, HA (reprint author), Leiden Univ, Med Ctr, Dept Clin Genet, S6-P,POB 9600, NL-2300 RC Leiden, Netherlands.
EM H.A.van_Duyvenvoorde@lumc.nl
RI Noordam, C./H-8077-2014; Lui, Chun Kin Julian/E-2253-2012; Kant,
Sarina/F-8596-2010;
OI Mericq, Veronica/0000-0003-2287-0181
FU Novo Nordisk
FX Dr Oostdijk received grant support from Novo Nordisk. Dr Walenkamp has
served on an advisory board for Ipsen and has received speaker
honorariums from Ferring, Ipsen and Pfizer. Professor Dr Wit has served
on advisory boards for Tercica, Ipsen, Pfizer, Prolor, Teva and
Biopartners, and has received speaker honorariums from Pfizer, Lilly,
Ipsen and Ferring. The remaining authors declare no conflict of
interest.
NR 44
TC 18
Z9 19
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD MAY
PY 2014
VL 22
IS 5
BP 602
EP 609
DI 10.1038/ejhg.2013.203
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AF3GS
UT WOS:000334600400008
PM 24065112
ER
PT J
AU Bohlega, S
Al-Ajlan, H
Al-Saif, A
AF Bohlega, Saeed
Al-Ajlan, Huda
Al-Saif, Amr
TI Mutation of fibulin-1 causes a novel syndrome involving the central
nervous system and connective tissues
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE FBLN1; fibulins; homozygosity mapping; exome sequencing;
neurodegenerative disease
ID EPIDERMAL-GROWTH-FACTOR; MACULAR DEGENERATION; CUTIS LAXA; GENE; REGIONS
AB Fibulin-1 is an extracellular matrix protein that has an important role in the structure of elastic fibers and basement membranes of various tissues. Using homozygosity mapping and exome sequencing, we discovered a missense mutation, p.(Cys397Phe), in fibulin-1 in three patients from a consanguineous family presented with a novel syndrome of syndactyly, undescended testes, delayed motor milestones, mental retardation and signs of brain atrophy. The mutation discovered segregated with the phenotype and was not found in 374 population-matched alleles. The affected cysteine is highly conserved across vertebrates and its mutation is predicted to abolish a disulfide bond that defines the tertiary structure of fibulin-1. Our findings emphasize the crucial role fibulin-1 has in development of the central nervous system and various connective tissues. published online 2 October 2013
C1 [Bohlega, Saeed] King Faisal Specialist Hosp & Res Ctr, Dept Neurosci, Riyadh 11211, Saudi Arabia.
[Al-Ajlan, Huda; Al-Saif, Amr] King Faisal Specialist Hosp & Res Ctr, Dept Genet, Riyadh 11211, Saudi Arabia.
[Al-Saif, Amr] NIH, Neurogenet Lab, Bethesda, MD 20892 USA.
RP Al-Saif, A (reprint author), NIH, Neurogenet Lab, 35 Convent Dr Rm 1a1015, Bethesda, MD 20892 USA.
EM amr.al-saif@nih.gov
NR 16
TC 0
Z9 1
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD MAY
PY 2014
VL 22
IS 5
BP 640
EP 643
DI 10.1038/ejhg.2013.210
PG 4
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AF3GS
UT WOS:000334600400013
PM 24084572
ER
PT J
AU Rousseau, J
Gioia, R
Layrolle, P
Lieubeau, B
Heymann, D
Rossi, A
Marini, JC
Trichet, V
Forlino, A
AF Rousseau, Julie
Gioia, Roberta
Layrolle, Pierre
Lieubeau, Blandine
Heymann, Dominique
Rossi, Antonio
Marini, Joan C.
Trichet, Valerie
Forlino, Antonella
TI Allele-specific Col1a1 silencing reduces mutant collagen in fibroblasts
from Brtl mouse, a model for classical osteogenesis imperfecta
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE allele-specific Col1a1 silencing; siRNA; shRNA; osteogenesis imperfecta;
lentiviral vector
ID IN-UTERO TRANSPLANTATION; MURINE MODEL; PRECLINICAL MODELS; LENTIVIRAL
VECTOR; MAMMALIAN-CELLS; RNAI; EXPRESSION; BONE; THERAPY; LETHAL
AB Gene silencing approaches have the potential to become a powerful curative tool for a variety of monogenic diseases caused by gain-of-function mutations. Classical osteogenesis imperfecta (OI), a dominantly inherited bone dysplasia, is characterized in its more severe forms by synthesis of structurally abnormal type I collagen, which exerts a negative effect on extracellular matrix. Specific suppression of the mutant (Mut) allele would convert severe OI forms to the mild type caused by a quantitative defect in normal collagen. Here, we describe the in vitro and ex vivo investigation of a small interfering RNA (siRNA) approach to allele-specific gene silencing using Mut Col1a1 from the Brtl mouse, a well-characterized model for classical human OI. A human embryonic kidney cell line, which expresses the firefly luciferase gene, combined with either wild-type or Mut Brtl Col1a1 exon 23 sequences, was used for the first screening. The siRNAs selected based on their specificity and the corresponding short hairpin RNAs (shRNAs) subcloned in a lentiviral vector were evaluated ex vivo in Brtl fibroblasts for their effect on collagen transcripts and protein. A preferential reduction of the Mut allele of up to 52% was associated with about 40% decrease of the Mut protein, with no alteration of cell proliferation. Interestingly, a downregulation of HSP47, a specific collagen chaperone known to be upregulated in some OI cases, was detected. Our data support further testing of shRNAs and their delivery by lentivirus as a strategy to specifically suppress the Mut allele in mesenchymal stem cells of OI patients for autologous transplantation. published online 11 September 2013
C1 [Rousseau, Julie; Layrolle, Pierre; Heymann, Dominique; Trichet, Valerie] INSERM, UMR 957, Nantes, France.
[Rousseau, Julie; Layrolle, Pierre; Heymann, Dominique; Trichet, Valerie] Univ Nantes, Nantes Atlantique Univ, Fac Med, Lab Physiopathol Resorpt Osseuse & Therapie Tumeu, Nantes, France.
[Gioia, Roberta; Rossi, Antonio; Forlino, Antonella] Univ Pavia, Dept Mol Med, Biochem Unit, I-27100 Pavia, Italy.
[Lieubeau, Blandine] INRA USC707, Nantes, France.
[Lieubeau, Blandine] Oniris Univ Nantes, EA IECM 4644, LUNAM Univ, Nantes, France.
[Marini, Joan C.] NICHD, Bone & Extracellular Matrix Branch, NIH, Bethesda, MD USA.
RP Forlino, A (reprint author), Univ Pavia, Dept Mol Med, Biochem Unit, Via Taramelli 3b, I-27100 Pavia, Italy.
EM aforlino@unipv.it
RI Forlino, Antonella/H-5385-2015; Rossi, Antonio/E-9935-2012; Layrolle,
Pierre/K-9257-2015; Trichet, Valerie/L-1553-2015
OI Forlino, Antonella/0000-0002-6385-1182; Layrolle,
Pierre/0000-0001-9800-5210;
FU Region des Pays de la Loire [JG/ND/RECH N 660]; Agence Nationale de la
Recherche [N R07196NS]; AFM TELETHON [N.16017]; [PRIN20094C2H2M];
[Cariplo 2011-0270]; Fondazione Telethon
FX This study was supported by the Region des Pays de la Loire (JG/ND/RECH
N 660, to JR), the Agence Nationale de la Recherche 2007 Project N
R07196NS, PRIN20094C2H2M to AR, Cariplo 2011-0270 to AF and AFM TELETHON
N.16017 to AF and VT.
NR 46
TC 3
Z9 3
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD MAY
PY 2014
VL 22
IS 5
BP 667
EP 674
DI 10.1038/ejhg.2013.198
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AF3GS
UT WOS:000334600400017
PM 24022296
ER
PT J
AU Zhang, H
Shi, JX
Liang, FM
Wheeler, W
Stolzenberg-Solomon, R
Yu, K
AF Zhang, Han
Shi, Jianxin
Liang, Faming
Wheeler, William
Stolzenberg-Solomon, Rachael
Yu, Kai
TI A fast multilocus test with adaptive SNP selection for large-scale
genetic-association studies
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE genome-wide association study; cis-regulating meQTLs mapping; multilocus
test; variable selection; multiple comparisons; pathway analysis
ID GENOME-WIDE ASSOCIATION; DISTANCE-BASED REGRESSION; PANCREATIC-CANCER; P
VALUES; SUSCEPTIBILITY; METHYLATION; ADJUSTMENT; VARIANTS; PATTERNS;
DISEASES
AB As increasing evidence suggests that multiple correlated genetic variants could jointly influence the outcome, a multilocus test that aggregates association evidence across multiple genetic markers in a considered gene or a genomic region may be more powerful than a single-marker test for detecting susceptibility loci. We propose a multilocus test, AdaJoint, which adopts a variable selection procedure to identify a subset of genetic markers that jointly show the strongest association signal, and defines the test statistic based on the selected genetic markers. The P-value from the AdaJoint test is evaluated by a computationally efficient algorithm that effectively adjusts for multiple-comparison, and is hundreds of times faster than the standard permutation method. Simulation studies demonstrate that AdaJoint has the most robust performance among several commonly used multilocus tests. We perform multilocus analysis of over 26 000 genes/regions on two genome-wide association studies of pancreatic cancer. Compared with its competitors, AdaJoint identifies a much stronger association between the gene CLPTM1L and pancreatic cancer risk (6.0 x 10(-8)), with the signal optimally captured by two correlated single-nucleotide polymorphisms (SNPs). Finally, we show AdaJoint as a powerful tool for mapping cis-regulating methylation quantitative trait loci on normal breast tissues, and find many CpG sites whose methylation levels are jointly regulated by multiple SNPs nearby. published online 11 September 2013
C1 [Zhang, Han; Shi, Jianxin; Stolzenberg-Solomon, Rachael; Yu, Kai] NCI, Div Canc Epidemiol & Genet, Biostat Branch, Rockville, MD 20850 USA.
[Liang, Faming] Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA.
[Wheeler, William] Informat Management Serv Inc, Silver Spring, MD USA.
RP Yu, K (reprint author), NCI, Div Canc Epidemiol & Genet, Biostat Branch, 9609 Med Ctr Dr,Room 7E630, Rockville, MD 20850 USA.
EM yuka@mail.nih.gov
RI Zhang, Han/K-2118-2016
OI Zhang, Han/0000-0001-7977-9616
FU Intramural Program of the National Institutes of Health; National Cancer
Institute; National Science Foundation [DMS-0607755, CMMI-0926803]; King
Abdullah University of Science and Technology [KUS-C1-016-04]
FX We thank three anonymous referees for their helpful comments. This study
utilized the high-performance computational capabilities of the Biowulf
Linux cluster at the National Institutes of Health, Bethesda, MD.
(http://biowulf.nih.gov). The work of H Zhang, J Shi, R
Stolzenberg-Solomon and K Yu were supported by the Intramural Program of
the National Institutes of Health and the National Cancer Institute. The
work of F Liang was supported in part by the National Science Foundation
(DMS-0607755, CMMI-0926803); and the award (KUS-C1-016-04) made by the
King Abdullah University of Science and Technology.
NR 36
TC 5
Z9 5
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD MAY
PY 2014
VL 22
IS 5
BP 696
EP 702
DI 10.1038/ejhg.2013.201
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AF3GS
UT WOS:000334600400021
PM 24022295
ER
PT J
AU Gopalan, N
Andrade, BB
Swaminathan, S
AF Gopalan, Narendran
Andrade, Bruno Bezerril
Swaminathan, Soumya
TI Tuberculosis-immune reconstitution inflammatory syndrome in HIV: from
pathogenesis to prediction
SO EXPERT REVIEW OF CLINICAL IMMUNOLOGY
LA English
DT Review
DE HAART; HIV; paradoxical reaction; TB; IRIS; ART; biomarkers for IRIS
ID CD4(+) T-CELLS; ACTIVE ANTIRETROVIRAL THERAPY; INFECTED PATIENTS;
RISK-FACTORS; RESTORATION DISEASE; MYCOBACTERIAL INFECTIONS;
HIV-1-INFECTED PATIENTS; SYNDROME IRIS; SOUTH-AFRICA; ACTIVATION
AB Tuberculosis-immune reconstitution inflammatory syndrome (TB-IRIS) is an exaggerated, dysregulated immune response against dead or viable antigens of Mycobacterium tuberculosis that frequently occurs after initiation of antiretroviral therapy despite an effective suppression of HIV viremia. Scientific advances in IRIS pathogenesis have led researchers and clinicians to postulate risk factors that could possibly predict this syndrome, in an attempt to reduce the incidence and the severity of IRIS, with appropriate anti-inflammatory therapy. This review is a summary of the available literature on pathogenic mechanisms involved from the macro to the micro level, the clinical spectrum, available predictors and the scope of these biomarkers to function as specific therapeutic targets, that could effectively modulate or ameliorate this syndrome in future.
C1 [Gopalan, Narendran; Swaminathan, Soumya] Natl Inst Res TB, Madras 600031, Tamil Nadu, India.
[Andrade, Bruno Bezerril] NIAID, Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Swaminathan, S (reprint author), Natl Inst Res TB, 1 Mayor Sathyamoorthy Rd, Madras 600031, Tamil Nadu, India.
EM doctorsoumya@yahoo.com
RI Andrade, Bruno/J-9111-2012
OI Andrade, Bruno/0000-0001-6833-3811
NR 79
TC 4
Z9 5
U1 0
U2 5
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1744-666X
EI 1744-8409
J9 EXPERT REV CLIN IMMU
JI Expert Rev. Clin. Immunol.
PD MAY
PY 2014
VL 10
IS 5
BP 631
EP 645
DI 10.1586/1744666X.2014.892828
PG 15
WC Immunology
SC Immunology
GA AF2AG
UT WOS:000334514400007
PM 24580108
ER
PT J
AU Liangpunsakul, S
Kleiner, DE
AF Liangpunsakul, Suthat
Kleiner, David E.
TI The Alcoholic Hepatitis Histologic Score: Structured Prognostic Biopsy
Evaluation Comes to Alcoholic Hepatitis
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID LIVER-BIOPSY; MORTALITY; DIAGNOSIS
C1 [Liangpunsakul, Suthat] Indiana Univ, Med Ctr, Dept Med, Div Gastroenterol & Hepatol, Indianapolis, IN USA.
[Liangpunsakul, Suthat] Richard L Roudebush Vet Adm Med Ctr, Indianapolis, IN USA.
[Kleiner, David E.] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Liangpunsakul, S (reprint author), Indiana Univ Sch Med, Div Gastroenterol & Hepatol, 550 N Univ Blvd,4100, Indianapolis, IN 46202 USA.
EM sliangpu@iupui.edu
NR 16
TC 2
Z9 2
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 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD MAY
PY 2014
VL 146
IS 5
BP 1156
EP 1158
DI 10.1053/j.gastro.2014.03.016
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AF1XQ
UT WOS:000334507600010
PM 24680970
ER
PT J
AU Manna, SK
Tanaka, N
Krausz, KW
Haznadar, M
Xue, X
Matsubara, T
Bowman, ED
Fearon, ER
Harris, CC
Shah, YM
Gonzalez, FJ
AF Manna, Soumen K.
Tanaka, Naoki
Krausz, Kristopher W.
Haznadar, Majda
Xue, Xiang
Matsubara, Tsutomu
Bowman, Elise D.
Fearon, Eric R.
Harris, Curtis C.
Shah, Yatrik M.
Gonzalez, Frank J.
TI Biomarkers of Coordinate Metabolic Reprogramming in Colorectal Tumors in
Mice and Humans
SO GASTROENTEROLOGY
LA English
DT Article
DE Azoxymethane; Apc(Min/+); ColorectalCancer; Metabolomics; Cancer
Biomarker; Metabolic Reprogramming
ID FATTY-ACID OXIDATION; MOUSE MODEL; ARGININE METHYLATION; CANCER;
CARCINOMA; CELLS; PROLIFERATION; PROGRESSION; INHIBITION; REGULATOR
AB BACKGROUND & AIMS: There are no robust noninvasive methods for colorectal cancer screening and diagnosis. Metabolomic and gene expression analyses of urine and tissue samples from mice and humans were used to identify markers of colorectal carcinogenesis. METHODS: Mass spectrometry-based metabolomic analysis of urine and tissues from wild-type C57BL/6J and Apc(Min/+) mice, as well as from mice with azoxymethane-induced tumors, was employed in tandem with gene expression analysis. Metabolic profiling was also performed on colon tumor and adjacent nontumor tissues from 39 patients. The effects of beta-catenin activity on metabolic profiles were assessed in mice with colon-specific disruption of Apc. RESULTS: Thirteen markers were found in urine associated with development of colorectal tumors in Apc(Min/+) mice. Metabolites related to polyamine metabolism, nucleic acid metabolism, and methylation, identified tumor-bearing mice with 100% accuracy, and also accurately identified mice with polyps. Changes in gene expression in tumor samples from mice revealed that derangement of metabolites were a reflection of coordinate metabolic reprogramming in tumor tissue. Similar changes in urinary metabolites were observed in mice with azoxymethane-induced tumors and in mice with colon-specific activation of b-catenin. The metabolic alterations indicated by markers in urine, therefore, appear to occur during early stages of tumorigenesis, when cancer cells are proliferating. In tissues from patients, tumors had stage-dependent increases in 17 metabolites associated with the same metabolic pathways identified in mice. Ten metabolites that were increased in tumor tissues, compared with nontumor tissues (proline, threonine, glutamic acid, arginine, N1-acetylspermidine, xanthine, uracil, betaine, symmetric dimethylarginine, and asymmetric-dimethylarginine), were also increased in urine from tumor-bearing mice. CONCLUSIONS: Gene expression and metabolomic profiles of urine and tissue samples from mice with colorectal tumors and of colorectal tumor samples from patients revealed pathways associated with derangement of specific metabolic pathways that are indicative of early-stage tumor development. These urine and tissue markers might be used in early detection of colorectal cancer.
C1 [Manna, Soumen K.; Tanaka, Naoki; Krausz, Kristopher W.; Matsubara, Tsutomu; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Haznadar, Majda; Bowman, Elise D.; Harris, Curtis C.] NCI, Lab Human Carcinogenesis, Ctr Canc Res, Bethesda, MD 20892 USA.
[Xue, Xiang; Shah, Yatrik M.] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA.
[Fearon, Eric R.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Fearon, Eric R.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
[Fearon, Eric R.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
RP Gonzalez, FJ (reprint author), Ctr Canc Res, Lab Metab, 31 Ctr Dr, Bethesda, MD 20892 USA.
EM gonzalef@mail.nih.gov
RI Xue, Xiang/P-9071-2014
OI Xue, Xiang/0000-0003-4704-1814
FU National Cancer Institute Intramural Research Program; Office of Dietary
Supplement Research; National Institutes of Health [CA148828, DK095201]
FX This work is funded by the National Cancer Institute Intramural Research
Program (FJG), Office of Dietary Supplement Research (SKM), and National
Institutes of Health (CA148828 and DK095201) (YMS).
NR 34
TC 18
Z9 19
U1 2
U2 40
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD MAY
PY 2014
VL 146
IS 5
BP 1313
EP 1324
DI 10.1053/j.gastro.2014.01.017
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AF1XQ
UT WOS:000334507600032
PM 24440673
ER
PT J
AU Kang, W
Sung, PS
Park, SH
Yoon, S
Chang, DY
Kim, S
Han, KH
Kim, JK
Rehermann, B
Chwae, YJ
Shin, EC
AF Kang, Wonseok
Sung, Pil Soo
Park, Su-Hyung
Yoon, Sarah
Chang, Dong-Yeop
Kim, Seungtaek
Han, Kwang Hyub
Kim, Ja Kyung
Rehermann, Barbara
Chwae, Yong-Joon
Shin, Eui-Cheol
TI Hepatitis C Virus Attenuates Interferon-Induced Major Histocompatibility
Complex Class I Expression and Decreases CD8(+) T Cell Effector
Functions
SO GASTROENTEROLOGY
LA English
DT Article
DE JFH-1; Antigen Presentation; Immune Evasion; Adaptive Immune Response
ID NATURAL-KILLER-CELLS; PROTEIN-KINASE; IMMUNE-RESPONSES; ENVELOPE
PROTEIN; CORE PROTEIN; INFECTION; DETERMINANTS; PERSISTENCE; INHIBITION;
CLEARANCE
AB BACKGROUND & AIMS: Major histocompatibility complex (MHC) class I-restricted CD8(+) T cells are required for clearance of hepatitis C virus (HCV) infection. MHC class I expression is up-regulated by type I and II interferons (IFNs). However, little is known about the effects of HCV infection on IFN-induced expression of MHC class I. METHODS: We used the HCV cell culture system (HCVcc) with the genotype 2a Japanese fulminant hepatitis-1 strain to investigate IFN-induced expression of MHC class I and its regulatory mechanisms. HCVcc-infected Huh-7.5 cells were analyzed by flow cytometry, metabolic labeling, immunoprecipitation, and immunoblotting analyses. Protein kinase R (PKR) was knocked down with lentiviruses that express small hairpin RNAs. The functional effects of MHC class I regulation by HCV were demonstrated in co-culture studies, using HCV-specific CD8(+) T cells. RESULTS: Although the baseline level of MHC class I was not affected by HCV infection, IFN-induced expression of MHC class I was notably attenuated in HCV-infected cells. This was associated with replicating HCV RNA, not with viral protein. HCV infection reduced IFN-induced synthesis of MHC class I protein and induced phosphorylation of PKR and eIF2 alpha. IFN-induced MHC class I expression was restored by small hairpin RNA-mediated knockdown of PKR in HCV-infected cells. Co-culture of HCV-specific CD8(+) T cells and HCV-infected cells that expressed HLA-A2 demonstrated that HCV infection reduced the effector functions of HCV-specific CD8(+) T cells; these functions were restored by small hairpin RNA-mediated knockdown of PKR. CONCLUSIONS: IFN-induced expression of MHC class I is attenuated in HCV-infected cells by activation of PKR, which reduces the effector functions of HCV-specific CD8(+) T cells. This appears to be an important mechanism by which HCV circumvents antiviral adaptive immune responses.
C1 [Kang, Wonseok; Sung, Pil Soo; Chang, Dong-Yeop; Shin, Eui-Cheol] Korea Adv Inst Sci & Technol, Lab Immunol & Infect Dis, Grad Sch Med Sci & Engn, Taejon 305701, South Korea.
[Kang, Wonseok; Kim, Seungtaek; Han, Kwang Hyub; Kim, Ja Kyung] Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea.
[Park, Su-Hyung; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Yoon, Sarah; Chwae, Yong-Joon] Ajou Univ, Sch Med, Dept Microbiol, Suwon 441749, South Korea.
RP Shin, EC (reprint author), Korea Adv Inst Sci & Technol, Lab Immunol & Infect Dis, Grad Sch Med Sci & Engn, 291 Daehak Ro, Taejon 305701, South Korea.
EM ecshin@kaist.ac.kr
RI Park, Su-Hyung/N-3514-2014; Shin, Eui-Cheol/C-1690-2011
FU National Research Foundation of Korea; Ministry of Science, ICT & Future
Planning of Korea [20100030075, 2012-M3C1A1-048860]; Korea Advanced
Institute of Science and Technology Future Systems Healthcare Project
from the Ministry of Science, ICT & Future Planning of Korea; Yonsei
Liver Blood Bank (YLBB); Sanofi-Aventis Korea; Intramural Research
Program of the National Institutes of Health, The National Institute of
Diabetes and Digestive and Kidney Diseases
FX This research was supported by the National Research Foundation of
Korea, funded by the Ministry of Science, ICT & Future Planning of Korea
(20100030075 and 2012-M3C1A1-048860). This work was partly supported by
the Korea Advanced Institute of Science and Technology Future Systems
Healthcare Project from the Ministry of Science, ICT & Future Planning
of Korea. This study was also supported by the Yonsei Liver Blood Bank
(YLBB), in part by a grant from Sanofi-Aventis Korea. This research was
supported in part by the Intramural Research Program of the National
Institutes of Health, The National Institute of Diabetes and Digestive
and Kidney Diseases. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 32
TC 13
Z9 15
U1 0
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 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD MAY
PY 2014
VL 146
IS 5
BP 1351
EP +
DI 10.1053/j.gastro.2014.01.054
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AF1XQ
UT WOS:000334507600035
PM 24486950
ER
PT J
AU Cheng, I
Kocarnik, JM
Dumitrescu, L
Lindor, NM
Chang-Claude, J
Avery, CL
Caberto, CP
Love, SA
Slattery, ML
Chan, AT
Baron, JA
Hindorff, LA
Park, SL
Schumacher, FR
Hoffmeister, M
Kraft, P
Butler, AM
Duggan, DJ
Hou, LF
Carlson, CS
Monroe, KR
Lin, Y
Carty, CL
Mann, S
Ma, J
Giovannucci, EL
Fuchs, CS
Newcomb, PA
Jenkins, MA
Hopper, JL
Haile, RW
Conti, DV
Campbell, PT
Potter, JD
Caan, BJ
Schoen, RE
Hayes, RB
Chanock, SJ
Berndt, SI
Kuery, S
Bezieau, S
Ambite, JL
Kumaraguruparan, G
Richardson, DM
Goodloe, RJ
Dilks, HH
Baker, P
Zanke, BW
Lemire, M
Gallinger, S
Hsu, L
Jiao, S
Harrison, TA
Seminara, D
Haiman, CA
Kooperberg, C
Wilkens, LR
Hutter, CM
White, E
Crawford, DC
Heiss, G
Hudson, TJ
Brenner, H
Bush, WS
Casey, G
Le Marchand, L
Peters, U
AF Cheng, Iona
Kocarnik, Jonathan M.
Dumitrescu, Logan
Lindor, Noralane M.
Chang-Claude, Jenny
Avery, Christy L.
Caberto, Christian P.
Love, Shelly-Ann
Slattery, Martha L.
Chan, Andrew T.
Baron, John A.
Hindorff, Lucia A.
Park, Sungshim Lani
Schumacher, Fredrick R.
Hoffmeister, Michael
Kraft, Peter
Butler, Anne M.
Duggan, David J.
Hou, Lifang
Carlson, Chris S.
Monroe, Kristine R.
Lin, Yi
Carty, Cara L.
Mann, Sue
Ma, Jing
Giovannucci, Edward L.
Fuchs, Charles S.
Newcomb, Polly A.
Jenkins, Mark A.
Hopper, John L.
Haile, Robert W.
Conti, David V.
Campbell, Peter T.
Potter, John D.
Caan, Bette J.
Schoen, Robert E.
Hayes, Richard B.
Chanock, Stephen J.
Berndt, Sonja I.
Kuery, Sebastien
Bezieau, Stephane
Ambite, Jose Luis
Kumaraguruparan, Gowri
Richardson, Danielle M.
Goodloe, Robert J.
Dilks, Holli H.
Baker, Paxton
Zanke, Brent W.
Lemire, Mathieu
Gallinger, Steven
Hsu, Li
Jiao, Shuo
Harrison, Tabitha A.
Seminara, Daniela
Haiman, Christopher A.
Kooperberg, Charles
Wilkens, Lynne R.
Hutter, Carolyn M.
White, Emily
Crawford, Dana C.
Heiss, Gerardo
Hudson, Thomas J.
Brenner, Hermann
Bush, William S.
Casey, Graham
Le Marchand, Loic
Peters, Ulrike
TI Pleiotropic effects of genetic risk variants for other cancers on
colorectal cancer risk: PAGE, GECCO and CCFR consortia
SO GUT
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; PROSTATE-CANCER;
CHROMOSOME 8Q24; MULTIPLE LOCI; COLON-CANCER; BREAST-CANCER; IDENTIFIES
5; DESIGN; METAANALYSIS
AB Objective Genome-wide association studies have identified a large number of single nucleotide polymorphisms (SNPs) associated with a wide array of cancer sites. Several of these variants demonstrate associations with multiple cancers, suggesting pleiotropic effects and shared biological mechanisms across some cancers. We hypothesised that SNPs previously associated with other cancers may additionally be associated with colorectal cancer. In a large-scale study, we examined 171 SNPs previously associated with 18 different cancers for their associations with colorectal cancer.
Design We examined 13 338 colorectal cancer cases and 40 967 controls from three consortia: Population Architecture using Genomics and Epidemiology (PAGE), Genetic Epidemiology of Colorectal Cancer (GECCO), and the Colon Cancer Family Registry (CCFR). Study-specific logistic regression results, adjusted for age, sex, principal components of genetic ancestry, and/or study specific factors (as relevant) were combined using fixed-effect meta-analyses to evaluate the association between each SNP and colorectal cancer risk. A Bonferroni-corrected p value of 2.92x10(-4) was used to determine statistical significance of the associations.
Results Two correlated SNPs-rs10090154 and rs4242382-in Region 1 of chromosome 8q24, a prostate cancer susceptibility region, demonstrated statistically significant associations with colorectal cancer risk. The most significant association was observed with rs4242382 (meta-analysis OR=1.12; 95% CI 1.07 to 1.18; p = 1.74x10(-5)), which also demonstrated similar associations across racial/ethnic populations and anatomical sub-sites.
Conclusions This is the first study to clearly demonstrate Region 1 of chromosome 8q24 as a susceptibility locus for colorectal cancer; thus, adding colorectal cancer to the list of cancer sites linked to this particular multicancer risk region at 8q24.
C1 [Cheng, Iona] Canc Prevent Inst Calif, Fremont, CA 94538 USA.
[Kocarnik, Jonathan M.; Carlson, Chris S.; Lin, Yi; Carty, Cara L.; Mann, Sue; Newcomb, Polly A.; Potter, John D.; Hsu, Li; Jiao, Shuo; Harrison, Tabitha A.; Kooperberg, Charles; Hutter, Carolyn M.; White, Emily; Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Dumitrescu, Logan; Crawford, Dana C.] Vanderbilt Univ, Dept Mol Physiol, Nashville, TN 37235 USA.
[Dumitrescu, Logan; Crawford, Dana C.] Vanderbilt Univ, Dept Biophys, Nashville, TN 37235 USA.
[Dumitrescu, Logan; Goodloe, Robert J.; Dilks, Holli H.; Baker, Paxton; Crawford, Dana C.; Bush, William S.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN 37235 USA.
[Lindor, Noralane M.; Richardson, Danielle M.] Mayo Clin Arizona, Dept Hlth Sci Res, Scottsdale, AZ 85260 USA.
[Chang-Claude, Jenny] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Avery, Christy L.; Love, Shelly-Ann; Butler, Anne M.; Heiss, Gerardo] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Caberto, Christian P.; Park, Sungshim Lani; Wilkens, Lynne R.; Le Marchand, Loic] Univ Hawaii, Ctr Canc, Epidemiol Program, Honolulu, HI 96822 USA.
[Slattery, Martha L.] Univ Utah, Hlth Sci Ctr, Dept Internal Med, Salt Lake City, UT USA.
[Chan, Andrew T.; Ma, Jing; Giovannucci, Edward L.; Fuchs, Charles S.] Brigham & Womens Hosp & Harvard, Dept Med, Channing Div Network Med, Boston, MA USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Baron, John A.] Univ N Carolina, Sch Med, Dept Med, Chapel Hill, NC USA.
[Hindorff, Lucia A.] NHGRI, Off Populat Genom, NIH, Bethesda, MD 20892 USA.
[Schumacher, Fredrick R.; Monroe, Kristine R.; Conti, David V.; Haiman, Christopher A.; Casey, Graham] Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Hoffmeister, Michael; Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
[Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Duggan, David J.] Translat Genom Res Inst, Div Genet Basis Human Dis, Phoenix, AZ USA.
[Hou, Lifang] Northwestern Univ, Dept Prevent Med, Chicago, IL 60611 USA.
[Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Fuchs, Charles S.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Jenkins, Mark A.; Hopper, John L.] Univ Melbourne, Sch Populat Hlth, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia.
[Haile, Robert W.] Stanford Canc Inst, Palo Alto, CA USA.
[Campbell, Peter T.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Potter, John D.] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
[Caan, Bette J.] Kaiser Permanente Med Care Program, Div Res, Oakland, CA 94611 USA.
[Schoen, Robert E.] Univ Pittsburgh, Med Ctr, Dept Med & Epidemiol, Pittsburgh, PA 15260 USA.
[Hayes, Richard B.] NYU, Sch Med, Div Epidemiol, Dept Environm Med, New York, NY USA.
[Chanock, Stephen J.; Berndt, Sonja I.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Kuery, Sebastien; Bezieau, Stephane] CHU Nantes, Serv Genet Med, F-44035 Nantes 01, France.
[Ambite, Jose Luis; Kumaraguruparan, Gowri] Univ So Calif, Informat Sci Inst, Marinadel Rey, CA USA.
[Dilks, Holli H.] Vanderbilt Univ, Vanderbilt Technol Adv Genom, Nashville, TN 37235 USA.
[Zanke, Brent W.] Ottawa Hosp Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada.
[Lemire, Mathieu; Hudson, Thomas J.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Gallinger, Steven] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Gallinger, Steven] Mt Sinai Hosp, Dept Surg, Toronto, ON M5G 1X5, Canada.
[Hsu, Li] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Seminara, Daniela] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Hutter, Carolyn M.; White, Emily; Peters, Ulrike] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Hudson, Thomas J.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
[Hudson, Thomas J.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Brenner, Hermann] Germany German Canc Consortium DKTK, Heidelberg, Germany.
[Bush, William S.] Vanderbilt Univ, Dept Biomed Informat, Nashville, TN 37235 USA.
RP Cheng, I (reprint author), Canc Prevent Inst Calif, 2201 Walnut Ave,Suite 300, Fremont, CA 94538 USA.
EM iona.cheng@cpic.org; jkocarni@fhcrc.org
RI KURY, Sebastien/G-5971-2015; Hoffmeister, Michael/B-5745-2012; Bezieau,
stephane/G-5621-2015; Jenkins, Mark/P-7803-2015; Brenner,
Hermann/B-4627-2017;
OI KURY, Sebastien/0000-0001-5497-0465; Hoffmeister,
Michael/0000-0002-8307-3197; Bezieau, stephane/0000-0003-0095-1319;
Jenkins, Mark/0000-0002-8964-6160; Brenner, Hermann/0000-0002-6129-1572;
Bush, William/0000-0002-9729-6519; Potter, John/0000-0001-5439-1500;
Hayes, Richard/0000-0002-0918-661X
FU National Human Genome Research Institute (NHGRI); CALiCo [U01HG004803];
EAGLE [U01HG004798]; MEC [U01HG004802]; WHI [U01HG004790]; Coordinating
Center [U01HG004801]; NHGRI ARRA supplements; NHGRI PAGE program
[U01HG004803, U01HG004802, U01HG004790, U01HG004798-01]; NHGRI ARRA
supplement; Vanderbilt CTSA from NCATS/NIH [UL1 TR000445]; NHGRI PAGE
program (NHGRI ARRA supplement); National Cancer Institute [R37CA54281,
R01 CA63464, P01CA33619, U01CA136792, U01CA98758]; National Heart, Lung,
and Blood Institute, National Institutes of Health, US Department of
Health and Human Services [HHSN268201100046C, HHSN268201100001C,
HHSN268201100002C, HHSN268201100003C, HHSN268201100004C,
HHSN271201100004C]; Atherosclerosis Risk in Communities (ARIC); National
Heart, Lung, and Blood Institute contracts [HHSN268201100005C,
HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
HHSN268201100009C, HHSN268201100010C, HHSN268201100011C,
HHSN268201100012C]; National Human Genome Research Institute
[U01HG004402]; National Institutes of Health [HHSN268200625226C];
National Institutes of Health; NIH Roadmap for Medical Research;
National Institutes of Mental Health; [R01HL087641]; [R01HL59367];
[R01HL086694]; [UL1RR025005]
FX PAGE: (a) The Population Architecture Using Genomics and Epidemiology
(PAGE) program is funded by the National Human Genome Research Institute
(NHGRI), supported by U01HG004803 (CALiCo), U01HG004798 (EAGLE),
U01HG004802 (MEC), U01HG004790 (WHI) and U01HG004801 (Coordinating
Center), and their respective NHGRI ARRA supplements. The contents of
this paper are solely the responsibility of the authors and do not
necessarily represent the official views of the NIH. The complete list
of PAGE members can be found at http://www.pagestudy.org. (b) The data
and materials included in this report result from collaboration between
the following studies: The 'Epidemiologic Architecture for Genes Linked
to Environment (EAGLE)' is funded through the NHGRI PAGE program
(U01HG004798-01 and its NHGRI ARRA supplement). The dataset(s) used for
the analyses described were obtained from Vanderbilt University Medical
Center's BioVU which is supported by institutional funding and by the
Vanderbilt CTSA grant UL1 TR000445 from NCATS/NIH. The Vanderbilt
University Center for Human Genetics Research, Computational Genomics
Core provided computational and/or analytical support for this work. The
Multiethnic Cohort study (MEC) characterisation of epidemiological
architecture is funded through the NHGRI PAGE program (U01HG004802 and
its NHGRI ARRA supplement). The MEC study is funded through the National
Cancer Institute (R37CA54281, R01 CA63464, P01CA33619, U01CA136792 and
U01CA98758). Funding support for the 'Epidemiology of putative genetic
variants: The Women's Health Initiative' study is provided through the
NHGRI PAGE program (U01HG004790 and its NHGRI ARRA supplement). The WHI
program is funded by the National Heart, Lung, and Blood Institute,
National Institutes of Health, US Department of Health and Human
Services through contracts HHSN268201100046C, HHSN268201100001C,
HHSN268201100002C, HHSN268201100003C, HHSN268201100004C and
HHSN271201100004C. The authors thank the WHI investigators and staff for
their dedication, and the study participants for making the program
possible. A full listing of WHI investigators can be found at:
http://www.whiscience.org/publications/WHI_investigators_shortlist.pdf.
Funding support for the Genetic Epidemiology of Causal Variants Across
the Life Course (CALiCo) program was provided through the NHGRI PAGE
program (U01HG004803 and its NHGRI ARRA supplement). The following study
contributed to this manuscript and is funded by the following agencies:
The Atherosclerosis Risk in Communities (ARIC) Study is carried out as a
collaborative study supported by National Heart, Lung, and Blood
Institute contracts (HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
HHSN268201100010C, HHSN268201100011C and HHSN268201100012C),
R01HL087641, R01HL59367 and R01HL086694; National Human Genome Research
Institute contract U01HG004402; and National Institutes of Health
contract HHSN268200625226C. The authors thank the staff and participants
of the ARIC study for their important contributions. Infrastructure was
partly supported by Grant Number UL1RR025005, a component of the
National Institutes of Health and NIH Roadmap for Medical Research.
Assistance with phenotype harmonisation, SNP selection and annotation,
data cleaning, data management, integration and dissemination, and
general study coordination was provided by the PAGE Coordinating Center
(U01HG004801-01 and its NHGRI ARRA supplement). The National Institutes
of Mental Health also contributes to the support for the Coordinating
Center.; The PAGE consortium thanks the staff and participants of all
PAGE studies for their important contributions.
NR 70
TC 14
Z9 14
U1 2
U2 13
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD MAY
PY 2014
VL 63
IS 5
BP 800
EP 807
DI 10.1136/gutjnl-2013-305189
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AF0GX
UT WOS:000334393400016
PM 23935004
ER
PT J
AU Giangrande, P
Seitz, R
Behr-Gross, ME
Berger, K
Hilger, A
Klein, H
Schramm, W
Mannucci, PM
AF Giangrande, P.
Seitz, R.
Behr-Gross, M. E.
Berger, K.
Hilger, A.
Klein, H.
Schramm, W.
Mannucci, P. M.
TI Kreuth III: European consensus proposals for treatment of haemophilia
with coagulation factor concentrates
SO HAEMOPHILIA
LA English
DT Article
DE treatment; factor VIII; prophylaxis; guidelines; haemophilia
ID CARE
AB This report summarizes recommendations relating to haemophilia therapy arising from discussions among experts from 36 European countries during the Kreuth III meeting in April 2013. To optimize the organization of haemophilia care nationally, it is recommended that a formal body be established in each country to include the relevant clinicians, national haemophilia patient organization, health ministry, paying authority and (if appropriate) regulatory authorities. The minimum factor VIII consumption level in a country should be 3I.U. per capita. Decisions on whether to adopt a new product should not be based solely on cost. Prophylaxis for children with severe haemophilia is already recognized as the optimum therapy. Ongoing prophylaxis for individual adults should also be provided when required based on clinical decision making by the clinician in consultation with the patient. Children with inhibitors who have failed, or who are not suitable for, immune tolerance therapy should be offered prophylaxis with bypassing agents. Single factor concentrates should be used as therapy wherever possible in patients with rare bleeding disorders. Orphan drug designation for a factor concentrate should not be used to hinder the development, licencing and marketing of other products for the same condition which have demonstrably different protein modification or enhancement.
C1 [Giangrande, P.] Oxford Haemophilia & Thrombosis Ctr, Oxford, England.
[Giangrande, P.] European Haemophilia Consortium, Brussels, Belgium.
[Seitz, R.; Hilger, A.] Paul Ehrlich Inst, Langen, Germany.
[Behr-Gross, M. E.] European Directorate Qual Med & HealthCare EDQM, Strasbourg, France.
[Berger, K.] Univ Hosp Munich, Munich, Germany.
[Klein, H.] NIH, Bethesda, MD 20892 USA.
[Schramm, W.] Rudolf Marx Stiftung, Munich, Germany.
[Mannucci, P. M.] Fdn IRCCS Ca Granda Osped Maggiore, Milan, Italy.
RP Giangrande, P (reprint author), Churchill Hosp, Oxford Haemophilia & Thrombosis Ctr, Oxford OX3 7LE, England.
EM paul.giangrande@ndm.ox.ac.uk
FU Paul Ehrlich Institut (PEI), Langen, Germany;
Ludwig-Maximillian-University (LMU) Munchen, Germany; European
Directorate for the Quality of Medicines & HealthCare (EDQM), Council of
Europe, Strasbourg, France; Rudolf-Marx-Stiftung
FX The Kreuth III initiative was co-sponsored by the Paul Ehrlich Institut
(PEI), Langen, Germany, the Ludwig-Maximillian-University (LMU) Munchen,
Germany and the European Directorate for the Quality of Medicines &
HealthCare (EDQM), Council of Europe, Strasbourg, France. Financial
support was granted by the Rudolf-Marx-Stiftung.
NR 9
TC 10
Z9 10
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1351-8216
EI 1365-2516
J9 HAEMOPHILIA
JI Haemophilia
PD MAY
PY 2014
VL 20
IS 3
BP 322
EP 325
DI 10.1111/hae.12440
PG 4
WC Hematology
SC Hematology
GA AE9RQ
UT WOS:000334346900016
PM 24731129
ER
PT J
AU Earp, MA
Kelemen, LE
Magliocco, AM
Swenerton, KD
Chenevix-Trench, G
Lu, Y
Hein, A
Ekici, AB
Beckmann, MW
Fasching, PA
Lambrechts, D
Despierre, E
Vergote, I
Lambrechts, S
Doherty, JA
Rossing, MA
Chang-Claude, J
Rudolph, A
Friel, G
Moysich, KB
Odunsi, K
Sucheston-Campbell, L
Lurie, G
Goodman, MT
Carney, ME
Thompson, PJ
Runnebaum, IB
Durst, M
Hillemanns, P
Dork, T
Antonenkova, N
Bogdanova, N
Leminen, A
Nevanlinna, H
Pelttari, LM
Butzow, R
Bunker, CH
Modugno, F
Edwards, RP
Ness, RB
du Bois, A
Heitz, F
Schwaab, I
Harter, P
Karlan, BY
Walsh, C
Lester, J
Jensen, A
Kjaer, SK
Hogdall, CK
Hogdall, E
Lundvall, L
Sellers, TA
Fridley, BL
Goode, EL
Cunningham, JM
Vierkant, RA
Giles, GG
Baglietto, L
Severi, G
Southey, MC
Liang, D
Wu, XF
Lu, K
Hildebrandt, MAT
Levine, DA
Bisogna, M
Schildkraut, JM
Iversen, ES
Weber, RP
Berchuck, A
Cramer, DW
Terry, KL
Poole, EM
Tworoger, SS
Bandera, EV
Chandran, U
Orlow, I
Olson, SH
Wik, E
Salvesen, HB
Bjorge, L
Halle, MK
van Altena, AM
Aben, KKH
Kiemeney, LA
Massuger, LFAG
Pejovic, T
Bean, YT
Cybulski, C
Gronwald, J
Lubinski, J
Wentzensen, N
Brinton, LA
Lissowska, J
Garcia-Closas, M
Dicks, E
Dennis, J
Easton, DF
Song, HL
Tyrer, JP
Pharoah, PDP
Eccles, D
Campbell, IG
Whittemore, AS
McGuire, V
Sieh, W
Rothstein, JH
Flanagan, JM
Paul, J
Brown, R
Phelan, CM
Risch, HA
McLaughlin, JR
Narod, SA
Ziogas, A
Anton-Culver, H
Gentry-Maharaj, A
Menon, U
Gayther, SA
Ramus, SJ
Wu, AH
Pearce, CL
Pike, MC
Dansonka-Mieszkowska, A
Rzepecka, IK
Szafron, LM
Kupryjanczyk, J
Cook, LS
Le, ND
Brooks-Wilson, A
AF Earp, Madalene A.
Kelemen, Linda E.
Magliocco, Anthony M.
Swenerton, Kenneth D.
Chenevix-Trench, Georgia
Lu, Yi
Hein, Alexander
Ekici, Arif B.
Beckmann, Matthias W.
Fasching, Peter A.
Lambrechts, Diether
Despierre, Evelyn
Vergote, Ignace
Lambrechts, Sandrina
Doherty, Jennifer A.
Rossing, Mary Anne
Chang-Claude, Jenny
Rudolph, Anja
Friel, Grace
Moysich, Kirsten B.
Odunsi, Kunle
Sucheston-Campbell, Lara
Lurie, Galina
Goodman, Marc T.
Carney, Michael E.
Thompson, Pamela J.
Runnebaum, Ingo B.
Duerst, Matthias
Hillemanns, Peter
Doerk, Thilo
Antonenkova, Natalia
Bogdanova, Natalia
Leminen, Arto
Nevanlinna, Heli
Pelttari, Liisa M.
Butzow, Ralf
Bunker, Clareann H.
Modugno, Francesmary
Edwards, Robert P.
Ness, Roberta B.
du Bois, Andreas
Heitz, Florian
Schwaab, Ira
Harter, Philipp
Karlan, Beth Y.
Walsh, Christine
Lester, Jenny
Jensen, Allan
Kjaer, Susanne K.
Hogdall, Claus K.
Hogdall, Estrid
Lundvall, Lene
Sellers, Thomas A.
Fridley, Brooke L.
Goode, Ellen L.
Cunningham, Julie M.
Vierkant, Robert A.
Giles, Graham G.
Baglietto, Laura
Severi, Gianluca
Southey, Melissa C.
Liang, Dong
Wu, Xifeng
Lu, Karen
Hildebrandt, Michelle A. T.
Levine, Douglas A.
Bisogna, Maria
Schildkraut, Joellen M.
Iversen, Edwin S.
Weber, Rachel Palmieri
Berchuck, Andrew
Cramer, Daniel W.
Terry, Kathryn L.
Poole, Elizabeth M.
Tworoger, Shelley S.
Bandera, Elisa V.
Chandran, Urmila
Orlow, Irene
Olson, Sara H.
Wik, Elisabeth
Salvesen, Helga B.
Bjorge, Line
Halle, Mari K.
van Altena, Anne M.
Aben, Katja K. H.
Kiemeney, Lambertus A.
Massuger, Leon F. A. G.
Pejovic, Tanja
Bean, Yukie T.
Cybulski, Cezary
Gronwald, Jacek
Lubinski, Jan
Wentzensen, Nicolas
Brinton, Louise A.
Lissowska, Jolanta
Garcia-Closas, Montserrat
Dicks, Ed
Dennis, Joe
Easton, Douglas F.
Song, Honglin
Tyrer, Jonathan P.
Pharoah, Paul D. P.
Eccles, Diana
Campbell, Ian G.
Whittemore, Alice S.
McGuire, Valerie
Sieh, Weiva
Rothstein, Joseph H.
Flanagan, James M.
Paul, James
Brown, Robert
Phelan, Catherine M.
Risch, Harvey A.
McLaughlin, John R.
Narod, Steven A.
Ziogas, Argyrios
Anton-Culver, Hoda
Gentry-Maharaj, Aleksandra
Menon, Usha
Gayther, Simon A.
Ramus, Susan J.
Wu, Anna H.
Pearce, Celeste L.
Pike, Malcolm C.
Dansonka-Mieszkowska, Agnieszka
Rzepecka, Iwona K.
Szafron, Lukasz M.
Kupryjanczyk, Jolanta
Cook, Linda S.
Le, Nhu D.
Brooks-Wilson, Angela
CA Australian Canc Study
Australian Ovarian Canc Study Grp
Ovarian Canc Assoc Consortium
TI Genome-wide association study of subtype-specific epithelial ovarian
cancer risk alleles using pooled DNA
SO HUMAN GENETICS
LA English
DT Article
ID CLEAR-CELL CARCINOMA; GRADE SEROUS CARCINOMA; MICROSATELLITE
INSTABILITY; MOLECULAR CHARACTERIZATION; SUSCEPTIBILITY LOCUS;
MUTATIONS; VARIANTS; GENE; IDENTIFICATION; ENDOMETRIOSIS
AB Epithelial ovarian cancer (EOC) is a heterogeneous cancer with both genetic and environmental risk factors. Variants influencing the risk of developing the less-common EOC subtypes have not been fully investigated. We performed a genome-wide association study (GWAS) of EOC according to subtype by pooling genomic DNA from 545 cases and 398 controls of European descent, and testing for allelic associations. We evaluated for replication 188 variants from the GWAS [56 variants for mucinous, 55 for endometrioid and clear cell, 53 for low-malignant potential (LMP) serous, and 24 for invasive serous EOC], selected using pre-defined criteria. Genotypes from 13,188 cases and 23,164 controls of European descent were used to perform unconditional logistic regression under the log-additive genetic model; odds ratios (OR) and 95 % confidence intervals are reported. Nine variants tagging six loci were associated with subtype-specific EOC risk at P < 0.05, and had an OR that agreed in direction of effect with the GWAS results. Several of these variants are in or near genes with a biological rationale for conferring EOC risk, including ZFP36L1 and RAD51B for mucinous EOC (rs17106154, OR = 1.17, P = 0.029, n = 1,483 cases), GRB10 for endometrioid and clear cell EOC (rs2190503, P = 0.014, n = 2,903 cases), and C22orf26/BPIL2 for LMP serous EOC (rs9609538, OR = 0.86, P = 0.0043, n = 892 cases). In analyses that included the 75 GWAS samples, the association between rs9609538 (OR = 0.84, P = 0.0007) and LMP serous EOC risk remained statistically significant at P < 0.0012 adjusted for multiple testing. Replication in additional samples will be important to verify these results for the less-common EOC subtypes.
C1 [Earp, Madalene A.; Brooks-Wilson, Angela] BC Canc Agcy, Canadas Michael Smith Genome Sci Ctr, Vancouver, BC V5Z 1L3, Canada.
[Kelemen, Linda E.; Cook, Linda S.] Alberta Hlth Serv Canc Care, Dept Populat Hlth Res, Calgary, AB, Canada.
[Kelemen, Linda E.] Univ Calgary, Dept Med Genet, Calgary, AB, Canada.
[Kelemen, Linda E.] Univ Calgary, Dept Oncol, Calgary, AB, Canada.
[Magliocco, Anthony M.] Univ S Florida, H Lee Moffitt Canc Ctr, Dept Anat Pathol, Tampa, FL 33682 USA.
[Swenerton, Kenneth D.] Univ British Columbia, Dept Med, Vancouver, BC, Canada.
[Chenevix-Trench, Georgia; Lu, Yi; Australian Canc Study] QIMR Berghofer Med Res Inst, Herston, Qld, Australia.
[Campbell, Ian G.; Australian Ovarian Canc Study Grp] Peter MacCallum Canc Ctr, Div Res, Melbourne, Vic, Australia.
[Hein, Alexander; Beckmann, Matthias W.; Fasching, Peter A.] Univ Erlangen Nurnberg, Ctr Comprehens Canc, Dept Gynecol & Obstet, Univ Hosp Erlangen, D-91054 Erlangen, Germany.
[Ekici, Arif B.] Univ Erlangen Nurnberg, Inst Human Genet, Erlangen, Germany.
[Fasching, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA.
[Lambrechts, Diether] VIB, Vesalius Res Ctr, Louvain, Belgium.
[Lambrechts, Diether] Univ Louvain, Dept Oncol, Lab Translat Genet, Louvain, Belgium.
[Despierre, Evelyn; Vergote, Ignace; Lambrechts, Sandrina] Leuven Canc Inst, Dept Obstet & Gynaecol, Div Gynecol Oncol, Louvain, Belgium.
[Doherty, Jennifer A.] Geisel Sch Med Dartmouth, Epidemiol & Biostat Sect, Lebanon, NH USA.
[Doherty, Jennifer A.; Rossing, Mary Anne] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA USA.
[Rossing, Mary Anne] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Chang-Claude, Jenny; Rudolph, Anja] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Friel, Grace; Moysich, Kirsten B.; Odunsi, Kunle; Sucheston-Campbell, Lara] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Lurie, Galina; Carney, Michael E.] Univ Hawaii, Canc Epidemiol Program, Ctr Canc, Honolulu, HI 96822 USA.
[Goodman, Marc T.; Thompson, Pamela J.] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Runnebaum, Ingo B.; Duerst, Matthias] Univ Jena, Dept Obstet & Gynaecol, Jena Univ Hosp, Jena, Germany.
[Hillemanns, Peter] Hannover Med Sch, Clin Obstet, Hannover, Germany.
[Hillemanns, Peter] Hannover Med Sch, Clin Gynaecol, Hannover, Germany.
[Doerk, Thilo; Bogdanova, Natalia] Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
[Antonenkova, Natalia] Aleksandrov Byelorussian Inst Oncol & Med Radiol, Minsk, Byelarus.
[Leminen, Arto; Nevanlinna, Heli; Pelttari, Liisa M.; Butzow, Ralf] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland.
[Butzow, Ralf] Univ Helsinki, Cent Hosp, Dept Pathol, Helsinki, Finland.
[Bunker, Clareann H.; Modugno, Francesmary] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Modugno, Francesmary; Edwards, Robert P.] Univ Pittsburgh, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA USA.
[Modugno, Francesmary; Edwards, Robert P.] Univ Pittsburgh, Womens Canc Res Ctr, Magee Womens Res Inst, Inst Canc, Pittsburgh, PA USA.
[Ness, Roberta B.] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
[du Bois, Andreas; Heitz, Florian; Harter, Philipp] Huyssens Stiftung Knappschaft GmbH, Kliniken Essen Mitte Evang, Dept Gynecol & Gynecol Oncol, Essen, Germany.
[du Bois, Andreas; Heitz, Florian; Harter, Philipp] Dr Horst Schmidt Kliniken Wiesbaden, Dept Gynecol & Gynecol Oncol, Wiesbaden, Germany.
[Schwaab, Ira] Inst Human Genet & Anthropol, Wiesbaden, Germany.
[Karlan, Beth Y.; Walsh, Christine; Lester, Jenny] Cedars Sinai Med Ctr, Womens Canc Program, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Jensen, Allan; Kjaer, Susanne K.; Hogdall, Estrid] Danish Canc Soc, Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark.
[Kjaer, Susanne K.; Hogdall, Claus K.; Lundvall, Lene] Copenhagen Univ Hosp, Rigshosp, Dept Gynecol, Copenhagen, Denmark.
[Hogdall, Estrid] Univ Copenhagen, Herlev Hosp, Mol Unit, Dept Pathol, Copenhagen, Denmark.
[Sellers, Thomas A.; Phelan, Catherine M.] Univ S Florida, H Lee Moffitt Canc Ctr, Div Populat Sci, Dept Canc Epidemiol, Tampa, FL 33682 USA.
[Fridley, Brooke L.] Univ Kansas, Med Ctr, Dept Biostat, Kansas City, KS 66103 USA.
[Goode, Ellen L.] Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
[Cunningham, Julie M.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Vierkant, Robert A.] Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN USA.
[Giles, Graham G.; Baglietto, Laura; Severi, Gianluca] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[Giles, Graham G.; Baglietto, Laura; Severi, Gianluca] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia.
[Southey, Melissa C.; Campbell, Ian G.] Univ Melbourne, Dept Pathol, Melbourne, Vic, Australia.
[Liang, Dong] Texas So Univ, Coll Pharm & Hlth Sci, Houston, TX 77004 USA.
[Wu, Xifeng; Hildebrandt, Michelle A. T.] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Lu, Karen] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA.
[Levine, Douglas A.; Bisogna, Maria] Mem Sloan Kettering Canc Ctr, Dept Surg, Gynecol Serv, New York, NY 10021 USA.
[Schildkraut, Joellen M.; Weber, Rachel Palmieri] Duke Univ, Med Ctr, Dept Community & Family Med, Durham, NC 27710 USA.
[Schildkraut, Joellen M.; Iversen, Edwin S.] Duke Canc Inst, Durham, NC USA.
[Iversen, Edwin S.] Duke Univ, Dept Stat Sci, Durham, NC USA.
[Berchuck, Andrew] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
[Cramer, Daniel W.; Terry, Kathryn L.] Brigham & Womens Hosp, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA.
[Cramer, Daniel W.; Terry, Kathryn L.; Poole, Elizabeth M.; Tworoger, Shelley S.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Poole, Elizabeth M.; Tworoger, Shelley S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Div Network Med, Boston, MA 02115 USA.
[Bandera, Elisa V.; Chandran, Urmila] Rutgers Canc Inst New Jersey, New Brunswick, NJ USA.
[Orlow, Irene; Olson, Sara H.; Pike, Malcolm C.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Wik, Elisabeth] Haukeland Hosp, Dept Pathol, N-5021 Bergen, Norway.
[Wik, Elisabeth; Salvesen, Helga B.; Bjorge, Line; Halle, Mari K.] Univ Bergen, Dept Clin Sci, Ctr Canc Biomarkers, Bergen, Norway.
[Salvesen, Helga B.; Bjorge, Line; Halle, Mari K.] Haukeland Hosp, Dept Gynecol & Obstet, N-5021 Bergen, Norway.
[van Altena, Anne M.; Massuger, Leon F. A. G.] Radboud Univ Nijmegen, Dept Gynecol, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Aben, Katja K. H.; Kiemeney, Lambertus A.] Radboud Univ Nijmegen, Dept Hlth Evidence, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Aben, Katja K. H.] Comprehens Canc Ctr Netherlands, Utrecht, Netherlands.
[Kiemeney, Lambertus A.] Radboud Univ Nijmegen, Dept Urol, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Pejovic, Tanja; Bean, Yukie T.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Pejovic, Tanja; Bean, Yukie T.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Cybulski, Cezary; Gronwald, Jacek; Lubinski, Jan] Pomeranian Med Univ, Int Hereditary Canc Ctr, Dept Genet & Pathol, Szczecin, Poland.
[Wentzensen, Nicolas; Brinton, Louise A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Inst Oncol, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Garcia-Closas, Montserrat] Inst Canc Res, Div Genet & Epidemiol, Sutton, Surrey, England.
[Garcia-Closas, Montserrat] Breakthrough Breast Canc Res Ctr, London, England.
[Dicks, Ed; Song, Honglin; Tyrer, Jonathan P.; Pharoah, Paul D. P.] Univ Cambridge, Dept Oncol, Cambridge, England.
[Dennis, Joe; Easton, Douglas F.; Pharoah, Paul D. P.] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Eccles, Diana] Univ Southampton, Fac Med, Southampton Univ Hosp, Southampton SO9 5NH, Hants, England.
[Campbell, Ian G.] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Parkville, Vic 3052, Australia.
[Whittemore, Alice S.; McGuire, Valerie; Sieh, Weiva; Rothstein, Joseph H.] Stanford Univ, Sch Med, Dept Hlth Res & Policy, Palo Alto, CA 94304 USA.
[Flanagan, James M.; Brown, Robert] Univ London Imperial Coll Sci Technol & Med, Dept Surg & Canc, London, England.
[Paul, James] Beatson West Scotland Canc Ctr, Glasgow, Lanark, Scotland.
[Risch, Harvey A.] Yale Univ, Sch Publ Hlth, Dept Chron Dis Epidemiol, New Haven, CT USA.
[McLaughlin, John R.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Prosserman Ctr Hlth Res, Toronto, ON M5G 1X5, Canada.
[Narod, Steven A.] Univ Toronto, Womens Coll Res Inst, Toronto, ON, Canada.
[Ziogas, Argyrios; Anton-Culver, Hoda] Univ Calif Irvine, Sch Med, Dept Epidemiol, Ctr Canc Genet Res & Prevent, Irvine, CA 92717 USA.
[Gentry-Maharaj, Aleksandra; Menon, Usha] UCL, Gynaecol Canc Res Ctr, Elizabeth Garrett Anderson Inst Womens Hlth, London, England.
[Gayther, Simon A.; Ramus, Susan J.; Wu, Anna H.; Pearce, Celeste L.; Pike, Malcolm C.] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Dansonka-Mieszkowska, Agnieszka; Rzepecka, Iwona K.; Szafron, Lukasz M.; Kupryjanczyk, Jolanta] Maria Sklodowska Curie Mem Canc Ctr, Inst Oncol, Dept Pathol, Warsaw, Poland.
[Cook, Linda S.] Univ New Mexico, Dept Internal Med, Div Epidemiol & Biostat, Albuquerque, NM 87131 USA.
[Cook, Linda S.] Univ Calgary, Fac Med, Dept Community Hlth Sci, Calgary, AB, Canada.
[Le, Nhu D.] BC Canc Agcy, Vancouver, BC V5Z 1L3, Canada.
[Brooks-Wilson, Angela] Simon Fraser Univ, Dept Biomed Physiol & Kinesiol, Burnaby, BC V5A 1S6, Canada.
RP Earp, MA (reprint author), BC Canc Agcy, Canadas Michael Smith Genome Sci Ctr, 675 West 10th Ave, Vancouver, BC V5Z 1L3, Canada.
EM mearp@bcgsc.ca; abrooks-wilson@bcgsc.ca
RI Whittemore, Alice/F-9925-2014; Brooks-Wilson, Angela/E-9399-2012;
Garcia-Closas, Montserrat /F-3871-2015; Brinton, Louise/G-7486-2015;
Hein, Alexander/F-6999-2010; van Altena, Anne/B-9824-2016; Dork,
Thilo/J-8620-2012; Aben, Katja/G-9686-2016; Bandera, Elisa/M-4169-2014;
Massuger, Leon/H-8072-2014; Kiemeney, Lambertus/D-3357-2009; Fridley,
Brooke/D-8315-2015; Bowtell, David/H-1007-2016; Gronwald,
Jacek/A-4576-2017; Bjorge, Line/C-1307-2017; salvesen,
Helga/C-1187-2017;
OI Brooks-Wilson, Angela/0000-0003-1009-6408; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562; Hein,
Alexander/0000-0003-2601-3398; Aben, Katja/0000-0002-0214-2147; Bandera,
Elisa/0000-0002-8789-2755; Kiemeney, Lambertus/0000-0002-2368-1326;
Fridley, Brooke/0000-0001-7739-7956; Bowtell, David/0000-0001-9089-7525;
Gronwald, Jacek/0000-0002-3643-2871; Bjorge, Line/0000-0002-0240-2770;
salvesen, Helga/0000-0002-4438-8831; Dennis, Joe/0000-0003-4591-1214;
Halle, Mari/0000-0002-2660-8271; Nevanlinna, Heli/0000-0002-0916-2976;
Tworoger, Shelley/0000-0002-6986-7046; Kjaer,
Susanne/0000-0002-8347-1398; Ramus, Susan/0000-0003-0005-7798;
Lissowska, Jolanta/0000-0003-2695-5799; Orlow,
Irene/0000-0001-6234-6961; Giles, Graham/0000-0003-4946-9099
FU Canadian Institutes of Health Research [MOP-86727, MOP-84340];
WorkSafeBC 14; OvCaRe: BC's Ovarian Cancer Research Team; American
Cancer Society [CRTG-00-196-01-CCE]; California Cancer Research Program
[00-01389 V-20170, N01-CN25403, 2II0200]; Cancer Council Victoria;
Cancer Council Queensland; Cancer Council New South Wales; Cancer
Council South Australia; Cancer Council Tasmania; Cancer Foundation of
Western Australia; Cancer Institute of New Jersey; Cancer Research UK
[C490/A6187, C490/A10119, C490/A10124, C536/A13086, C536/A6689]; Celma
Mastry Ovarian Cancer Foundation; Danish Cancer Society [94-222-52];
ELAN Program of the University of Erlangen-Nuremberg; Eve Appeal (Oak
Foundation); Fred C. and Katherine B. Andersen Foundation; German Cancer
Research Center; German Federal Ministry of Education and Research of
Germany, Program of Clinical Biomedical Research [01 GB 9401]; Helsinki
University Central Hospital Research Fund; Helse Vest; Imperial
Experimental Cancer Research Centre [C1312/A15589]; L & S Milken
Foundation; the Lon V. Smith Foundation [LVS-39420]; Mayo Foundation;
Mermaid I project; Minnesota Ovarian Cancer Alliance; National Health
and Medical Research Council of Australia [199600, 209057, 251533,
396414, 400281, 504715]; Nationaal Kankerplan of Belgium; Norwegian
Cancer Society; Norwegian Research Council; OHSU Foundation; Polish
Ministry of Science and Higher Education [4 PO5C 028 14, 2 PO5A 068 27];
Pomeranian Medical University; Radboud University Medical Center;
Roswell Park Cancer Institute Alliance Foundation; Royal Marsden
Hospital; Rudolf-Bartling Foundation; Sigrid Juselius Foundation; state
of Baden-Wurttemberg through Medical Faculty of the University of Ulm
[P.685]; UK National Institute for Health Research Biomedical Research
Centres at the University of Cambridge; University College London
Hospitals; US Army Medical Research and Material Command
[DAMD17-98-1-8659, DAMD17-01-1-0729, DAMD17-02-1-0666, DAMD17-02-1-0669,
W81XWH-10-1-0280]; Department of Defense Ovarian Cancer Research Program
[W81XWH-07-1-0449]; US National Cancer Institute [K07-CA095666,
K22-CA138563, N01-CN55424, N01-PC067010, N01-PC035137, P01-CA017054,
P01-CA087696, P30-CA15083, P50-CA105009, P50-CA136393, R01-CA014089,
R01-CA016056, R01-CA017054, R01-CA049449, R01-CA050385, R01-CA054419,
R01-CA058598, R01-CA058860, R01-CA061107]; US National Institutes of
Health/National Center for Research Resources/General Clinical Research
Center [MO1-RR000056]; US Public Health Service [PSA-042205]; US
National Cancer Institute. [R01-CA063678, R01-CA063682, R01-CA064277,
R01-CA067262, R01-CA071766, R01-CA074850, R01-CA076016, R01-CA080742,
R01-CA080978, R01-CA083918, R01-CA087538, R01-CA092044]; The US National
Cancer Institute [R01-CA061132, R01-095023, R01-CA106414, R01CA122443,
R01-CA112523, R01-CA114343, R01-CA126841, R01CA136924, R01-CA149429,
R03-CA113148, R03-CA115195, R37CA070867, R37-CA70867, U01-CA069417,
U01-CA071966]
FX Funding of constituent studies: This project was funded through grants
from the Canadian Institutes of Health Research (MOP-86727, MOP-84340);
WorkSafeBC 14, and OvCaRe: BC's Ovarian Cancer Research Team. Funding of
the constituent studies was provided by the American Cancer Society
(CRTG-00-196-01-CCE); the California Cancer Research Program (00-01389
V-20170, N01-CN25403, 2II0200); Cancer Council Victoria; Cancer Council
Queensland; Cancer Council New South Wales; Cancer Council South
Australia; Cancer Council Tasmania; Cancer Foundation of Western
Australia; the Cancer Institute of New Jersey; Cancer Research UK
(C490/A6187, C490/A10119, C490/A10124, C536/A13086, C536/A6689); the
Celma Mastry Ovarian Cancer Foundation; the Danish Cancer Society
(94-222-52); the ELAN Program of the University of Erlangen-Nuremberg;
the Eve Appeal (Oak Foundation); the Fred C. and Katherine B. Andersen
Foundation; the German Cancer Research Center; the German Federal
Ministry of Education and Research of Germany, Program of Clinical
Biomedical Research (01 GB 9401); the Helsinki University Central
Hospital Research Fund; Helse Vest; Imperial Experimental Cancer
Research Centre (C1312/A15589); the L & S Milken Foundation; the Lon V.
Smith Foundation (LVS-39420); the Mayo Foundation; the Mermaid I
project; the Minnesota Ovarian Cancer Alliance; the National Health and
Medical Research Council of Australia (199600, 209057, 251533, 396414,
400281, and 504715); Nationaal Kankerplan of Belgium; the Norwegian
Cancer Society; the Norwegian Research Council; the OHSU Foundation; the
Polish Ministry of Science and Higher Education (4 PO5C 028 14, 2 PO5A
068 27); Pomeranian Medical University; Radboud University Medical
Center; the Roswell Park Cancer Institute Alliance Foundation; the Royal
Marsden Hospital; the Rudolf-Bartling Foundation; the Sigrid Juselius
Foundation; the state of Baden-Wurttemberg through Medical Faculty of
the University of Ulm (P.685); the UK National Institute for Health
Research Biomedical Research Centres at the University of Cambridge and
the University College London Hospitals; the US Army Medical Research
and Material Command (DAMD17-98-1-8659, DAMD17-01-1-0729,
DAMD17-02-1-0666, DAMD17-02-1-0669, W81XWH-10-1-0280); the Department of
Defense Ovarian Cancer Research Program (W81XWH-07-1-0449); the US
National Cancer Institute (K07-CA095666, K22-CA138563, N01-CN55424,
N01-PC067010, N01-PC035137, P01-CA017054, P01-CA087696, P30-CA15083,
P50-CA105009, P50-CA136393, R01-CA014089, R01-CA016056, R01-CA017054,
R01-CA049449, R01-CA050385, R01-CA054419, R01-CA058598, R01-CA058860,
R01-CA061107, R01-CA061132, R01-CA063678, R01-CA063682, R01-CA064277,
R01-CA067262, R01-CA071766, R01-CA074850, R01-CA076016, R01-CA080742,
R01-CA080978, R01-CA083918, R01-CA087538, R01-CA092044, R01-095023,
R01-CA106414, R01CA122443, R01-CA112523, R01-CA114343, R01-CA126841,
R01CA136924, R01-CA149429, R03-CA113148, R03-CA115195, R37CA070867,
R37-CA70867, U01-CA069417, U01-CA071966 and Intramural research funds);
the US National Institutes of Health/National Center for Research
Resources/General Clinical Research Center (MO1-RR000056); and the US
Public Health Service (PSA-042205).
NR 52
TC 6
Z9 6
U1 0
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
EI 1432-1203
J9 HUM GENET
JI Hum. Genet.
PD MAY
PY 2014
VL 133
IS 5
BP 481
EP 497
DI 10.1007/s00439-013-1383-3
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA AF2CJ
UT WOS:000334519900002
PM 24190013
ER
PT J
AU Cook, MB
Wang, ZM
Yeboah, ED
Tettey, Y
Biritwum, RB
Adjei, AA
Tay, E
Truelove, A
Niwa, S
Chung, CC
Chokkalingam, AP
Chu, LW
Yeager, M
Hutchinson, A
Yu, K
Rand, KA
Haiman, CA
Hoover, RN
Hsing, AW
Chanock, SJ
AF Cook, Michael Blaise
Wang, Zhaoming
Yeboah, Edward D.
Tettey, Yao
Biritwum, Richard B.
Adjei, Andrew A.
Tay, Evelyn
Truelove, Ann
Niwa, Shelley
Chung, Charles C.
Chokkalingam, Annand P.
Chu, Lisa W.
Yeager, Meredith
Hutchinson, Amy
Yu, Kai
Rand, Kristin A.
Haiman, Christopher A.
Hoover, Robert N.
Hsing, Ann W.
Chanock, Stephen J.
CA African Ancestry Prostate Canc GWA
TI A genome-wide association study of prostate cancer in West African men
SO HUMAN GENETICS
LA English
DT Article
ID POPULATION-STRUCTURE; JAPANESE POPULATION; SUSCEPTIBILITY; REPLICATION;
ADMIXTURE; DISEASE; LOCI; ANNOTATION; AMERICANS; VARIANTS
AB Age-adjusted mortality rates for prostate cancer are higher for African-American men compared with those of European ancestry. Recent data suggest that West African men also have elevated risk for prostate cancer relative to European men. Genetic susceptibility to prostate cancer could account for part of this difference. We conducted a genome-wide association study (GWAS) of prostate cancer in West African men in the Ghana Prostate Study. Association testing was performed using multivariable logistic regression adjusted for age and genetic ancestry for 474 prostate cancer cases and 458 population-based controls on the Illumina HumanOmni-5 Quad BeadChip. The most promising association was at 10p14 within an intron of a long non-coding RNA (lncRNA RP11-543F8.2) 360 kb centromeric of GATA3 (p = 1.29E-7). In sub-analyses, SNPs at 5q31.3 were associated with high Gleason score (a parts per thousand yen7) cancers, the strongest of which was a missense SNP in PCDHA1 (rs34575154, p = 3.66E-8), and SNPs at Xq28 (rs985081, p = 8.66E-9) and 6q21 (rs2185710, p = 5.95E-8) were associated with low Gleason score (< 7) cancers. We sought to validate our findings in silico in the African Ancestry Prostate Cancer GWAS Consortium, but only one SNP, at 10p14, replicated at p < 0.05. Of the 90 prostate cancer loci reported from studies of men of European, Asian or African-American ancestry, we were able to test 81 in the Ghana Prostate Study, and 10 of these replicated at p < 0.05. Further genetic studies of prostate cancer in West African men are needed to confirm our promising susceptibility loci.
C1 [Cook, Michael Blaise; Wang, Zhaoming; Chung, Charles C.; Yeager, Meredith; Hutchinson, Amy; Yu, Kai; Hoover, Robert N.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Wang, Zhaoming; Yeager, Meredith; Hutchinson, Amy] SAIC Frederick Inc, Canc Genom Res Lab, NCI DCEG, Frederick, MD USA.
[Yeboah, Edward D.; Tettey, Yao; Biritwum, Richard B.; Adjei, Andrew A.; Tay, Evelyn] Korle Bu Teaching Hosp, Accra, Ghana.
[Yeboah, Edward D.; Tettey, Yao; Biritwum, Richard B.; Adjei, Andrew A.; Tay, Evelyn] Univ Ghana, Sch Med, Accra, Ghana.
[Truelove, Ann; Niwa, Shelley] WESTAT Corp, Rockville, MD 20850 USA.
[Chokkalingam, Annand P.; Hsing, Ann W.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Chu, Lisa W.] Canc Prevent Inst Calif, Fremont, CA 94538 USA.
[Rand, Kristin A.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Hsing, Ann W.] Stanford Univ, Stanford Canc Inst, Stanford, CA 94305 USA.
RP Cook, MB (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 9609 Med Ctr Dr,Rm 7-E106,MSC 9774, Bethesda, MD 20892 USA.
EM cookmich@mail.nih.gov
RI Cook, Michael/A-5641-2009
OI Cook, Michael/0000-0002-0533-7302
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health; Intramural Program of the National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services [HHSN261200800001E]
FX The authors thank Ms. Vicky Okyne for her expert help in coordinating
the study; consultants/resident urologists, pathologists, nurses, and
interviewers of Korle-Bu Hospital and University of Ghana Medical School
for their assistance with subject enrollment, screening, and clinical
examination; the study participants for their contribution toward a
better understanding of prostate disease; A. DeMarzo and G. Netto of
Johns Hopkins University for pathology review; Ms. Violet Devairakkam,
Ms. Norma Kim, and Mr. John Heinrich of Research Triangle Institute
(RTI) for their expert study management; Prof. Rosalind A. Eeles and her
team for crosschecking published prostate cancer loci specified in Table
3; and members of the African Ancestry Prostate Cancer GWAS Consortium
for looking-up our most promising associations from our African GWAS.
This research was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health. Intramural
Program of the National Cancer Institute, National Institutes of Health,
Department of Health and Human Services including Contract No.
HHSN261200800001E.
NR 56
TC 13
Z9 13
U1 1
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
EI 1432-1203
J9 HUM GENET
JI Hum. Genet.
PD MAY
PY 2014
VL 133
IS 5
BP 509
EP 521
DI 10.1007/s00439-013-1387-z
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA AF2CJ
UT WOS:000334519900004
PM 24185611
ER
PT J
AU Zou, YQ
Zwolanek, D
Izu, YY
Gandhy, S
Schreiber, G
Brockmann, K
Devoto, M
Tian, ZZ
Hu, Y
Veit, G
Meier, M
Stetefeld, J
Hicks, D
Straub, V
Voermans, NC
Birk, DE
Barton, ER
Koch, M
Bonnemann, CG
AF Zou, Yaqun
Zwolanek, Daniela
Izu, Yayoi
Gandhy, Shreya
Schreiber, Gudrun
Brockmann, Knut
Devoto, Marcella
Tian, Zuozhen
Hu, Ying
Veit, Guido
Meier, Markus
Stetefeld, Joerg
Hicks, Debbie
Straub, Volker
Voermans, Nicol C.
Birk, David E.
Barton, Elisabeth R.
Koch, Manuel
Boennemann, Carsten G.
TI Recessive and dominant mutations in COL12A1 cause a novel EDS/myopathy
overlap syndrome in humans and mice
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID CONGENITAL MUSCULAR-DYSTROPHY; TISSUE-SPECIFIC EXPRESSION;
EHLERS-DANLOS-SYNDROME; COLLAGEN-XII; CONNECTIVE-TISSUE; TENASCIN-X;
SOLEUS MUSCLE; DIFFERENTIAL EXPRESSION; EMBRYONIC-DEVELOPMENT;
POSTNATAL-DEVELOPMENT
AB Collagen VI-related myopathies are disorders of connective tissue presenting with an overlap phenotype combining clinical involvement from the muscle and from the connective tissue. Not all patients displaying related overlap phenotypes between muscle and connective tissue have mutations in collagen VI. Here, we report a homozygous recessive loss of function mutation and a de novo dominant mutation in collagen XII (COL12A1) as underlying a novel overlap syndrome involving muscle and connective tissue. Two siblings homozygous for a loss of function mutation showed widespread joint hyperlaxity combined with weakness precluding independent ambulation, while the patient with the de novo missense mutation was more mildly affected, showing improvement including the acquisition of walking. A mouse model with inactivation of the Col12a1 gene showed decreased grip strength, a delay in fiber-type transition and a deficiency in passive force generation while the muscle seems more resistant to eccentric contraction induced force drop, indicating a role for a matrix-based passive force-transducing elastic element in the generation of the weakness. This new muscle connective tissue overlap syndrome expands on the emerging importance of the muscle extracellular matrix in the pathogenesis of muscle disease.
C1 [Zou, Yaqun; Gandhy, Shreya; Hu, Ying; Boennemann, Carsten G.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
[Zwolanek, Daniela; Koch, Manuel] Univ Cologne, Ctr Biochem, Ctr Mol Med Cologne, Med Fac,Inst Dent Res & Oral Musculoskeletal Biol, D-50931 Cologne, Germany.
[Izu, Yayoi; Veit, Guido; Birk, David E.] Univ S Florida, Dept Mol Pharmacol & Physiol, Tampa, FL USA.
[Schreiber, Gudrun] Clin Ctr Pediat Neurol, Kassel, Germany.
[Brockmann, Knut] Univ Med Ctr, Interdisciplinary Pediat Ctr Children Dev Disabil, Gottingen, Germany.
[Devoto, Marcella] Childrens Hosp Philadelphia, Div Human Genet, Philadelphia, PA 19104 USA.
[Devoto, Marcella] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA.
[Devoto, Marcella] Univ Penn, Perelman Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Devoto, Marcella] Univ Roma La Sapienza, Dept Mol Med, Rome, Italy.
[Tian, Zuozhen; Barton, Elisabeth R.] Univ Penn, Sch Dent Med, Dept Anat & Cell Biol, Philadelphia, PA 19104 USA.
[Meier, Markus; Stetefeld, Joerg] Univ Manitoba, Dept Chem Microbiol Biochem & Med Genet, Winnipeg, MB R3T 2N2, Canada.
[Hicks, Debbie; Straub, Volker] Newcastle Univ, Inst Med Genet, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Voermans, Nicol C.] Radboud Univ Nijmegen, Nijmegen Med Ctr, Dept Neurol, Nijmegen, Netherlands.
RP Bonnemann, CG (reprint author), NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Porter Neurosci Res Ctr, 35 Convent Dr,Bldg 35,Room 2A-116, Bethesda, MD 20892 USA.
EM manuel.koch@uni-koeln.de; carsten.bonnemann@nih.gov
RI Veit, Guido/C-9596-2009; Birk, David/I-4072-2012; Voermans,
N.C./L-4724-2015;
OI Veit, Guido/0000-0002-6758-2696; Birk, David/0000-0002-4865-9088;
Stetefeld, Joerg/0000-0003-1478-3248
FU NINDS/NIH intramural research funds; MDA-USA; Deutsche
Forschungsgemeinschaft [SFB 829]; Koln Fortune Programme of the Medical
Faculty; Paul Wellstone Muscular Dystrophy Cooperative Research Center
[U54 AR052646]; Heart and Stroke Foundation Canada; Canada Research
Chair Program; NIAMS/NIH [AR044745]
FX Work in C.G.B.'s lab is supported by NINDS/NIH intramural research
funds. The work was started with support of a grant of the MDA-USA to
C.G.B. Supported by the Deutsche Forschungsgemeinschaft SFB 829 grant A2
(M.K.) and by the Koln Fortune Programme of the Medical Faculty (M.K.).
Work in in E.R.B.'s lab was supported by a Paul Wellstone Muscular
Dystrophy Cooperative Research Center (U54 AR052646). J.S. was supported
by the Heart and Stroke Foundation Canada and the Canada Research Chair
Program. D.B. was supported by NIAMS/NIH AR044745.
NR 63
TC 17
Z9 18
U1 0
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD MAY 1
PY 2014
VL 23
IS 9
BP 2339
EP 2352
DI 10.1093/hmg/ddt627
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AE9VL
UT WOS:000334359100009
PM 24334604
ER
PT J
AU Hicks, D
Farsani, GT
Laval, S
Collins, J
Sarkozy, A
Martoni, E
Shah, A
Zou, YQ
Koch, M
Bonnemann, CG
Roberts, M
Lochmuller, H
Bushby, K
Straub, V
AF Hicks, Debbie
Farsani, Golara Torabi
Laval, Steven
Collins, James
Sarkozy, Anna
Martoni, Elena
Shah, Ashoke
Zou, Yaqun
Koch, Manuel
Boennemann, Carsten G.
Roberts, Mark
Lochmueller, Hanns
Bushby, Kate
Straub, Volker
TI Mutations in the collagen XII gene define a new form of extracellular
matrix-related myopathy
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID CONGENITAL MUSCULAR-DYSTROPHY; EHLERS-DANLOS-SYNDROME;
AUTOSOMAL-DOMINANT MYOPATHY; TENASCIN-X DEFICIENCY; BETHLEM MYOPATHY;
GLYCINE MUTATIONS; SUPPORT OVERLAP; VI; CONTRACTURES; SEQUENCE
AB Bethlem myopathy (BM) [MIM 158810] is a slowly progressive muscle disease characterized by contractures and proximal weakness, which can be caused by mutations in one of the collagen VI genes (COL6A1, COL6A2 and COL6A3). However, there may be additional causal genes to identify as in 50 of BM cases no mutations in the COL6 genes are identified. In a cohort of 24 patients with a BM-like phenotype, we first sequenced 12 candidate genes based on their function, including genes for known binding partners of collagen VI, and those enzymes involved in its correct post-translational modification, assembly and secretion. Proceeding to whole-exome sequencing (WES), we identified mutations in the COL12A1 gene, a member of the FACIT collagens (fibril-associated collagens with interrupted triple helices) in five individuals from two families. Both families showed dominant inheritance with a clinical phenotype resembling classical BM. Family 1 had a single-base substitution that led to the replacement of one glycine residue in the triple-helical domain, breaking the Gly-X-Y repeating pattern, and Family 2 had a missense mutation, which created a mutant protein with an unpaired cysteine residue. Abnormality at the protein level was confirmed in both families by the intracellular retention of collagen XII in patient dermal fibroblasts. The mutation in Family 2 leads to the up-regulation of genes associated with the unfolded protein response (UPR) pathway and swollen, dysmorphic rough-ER. We conclude that the spectrum of causative genes in extracellular matrix (ECM)-related myopathies be extended to include COL12A1.
C1 [Hicks, Debbie; Farsani, Golara Torabi; Laval, Steven; Sarkozy, Anna; Shah, Ashoke; Lochmueller, Hanns; Bushby, Kate; Straub, Volker] Inst Med Genet, MRC, Ctr Neuromuscular Dis Newcastle, Newcastle Upon Tyne, Tyne & Wear, England.
[Collins, James] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Martoni, Elena] Univ Ferrara, Dept Expt & Diagnost Med, I-44100 Ferrara, Italy.
[Zou, Yaqun; Boennemann, Carsten G.] NINDS, NIH, Bethesda, MD 20892 USA.
[Koch, Manuel] Univ Cologne, Ctr Biochem, Inst Dent Res & Oral Musculoskeletal Biol, D-50931 Cologne, Germany.
[Roberts, Mark] Hope Hosp, Dept Neurol, Salford M6 8HD, Lancs, England.
[Roberts, Mark] Hope Hosp, Dept Neuropathol, Salford M6 8HD, Lancs, England.
RP Straub, V (reprint author), Newcastle Univ, Inst Med Genet, Cent Pkwy, Newcastle Upon Tyne NE1 3BZ, Tyne & Wear, England.
EM volker.straub@ncl.ac.uk
OI Lochmuller, Hanns/0000-0003-2324-8001
FU European Community [2012-305121]; 'Integrated European -omics research
project for diagnosis and therapy in rare neuromuscular and
neurodegenerative diseases (NEUROMICS); European Union [305444];
Newcastle University Faculty of Medical Sciences Fellowship; National
Commissioning Group (NCST)
FX This work was supported by the European Community's Seventh Framework
Programme (FP7/2007-2013) (grant number: 2012-305121), 'Integrated
European -omics research project for diagnosis and therapy in rare
neuromuscular and neurodegenerative diseases (NEUROMICS) and European
Union Seventh Framework Programme (FP7/2007-2013) under grant agreement
No. 305444 (RD-Connect). D.H. is supported by a Newcastle University
Faculty of Medical Sciences Fellowship. Diagnostic facilities at the
Newcastle Muscle Centre is supported by the National Commissioning Group
(NCST) for rare neuromuscular disorders. The Institute of Genetic
Medicine in Newcastle is part of the MRC Centre for Neuromuscular
Diseases. Newcastle University is a partner organization of the
TREAT-NMD Alliance.
NR 46
TC 16
Z9 17
U1 0
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD MAY 1
PY 2014
VL 23
IS 9
BP 2353
EP 2363
DI 10.1093/hmg/ddt637
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AE9VL
UT WOS:000334359100010
PM 24334769
ER
PT J
AU Perry, JRB
Hsu, YH
Chasman, DI
Johnson, AD
Elks, C
Albrecht, E
Andrulis, IL
Beesley, J
Berenson, GS
Bergmann, S
Bojesen, SE
Bolla, MK
Brown, J
Buring, JE
Campbell, H
Chang-Claude, J
Chenevix-Trench, G
Corre, T
Couch, FJ
Cox, A
Czene, K
D'adamo, AP
Davies, G
Deary, IJ
Dennis, J
Easton, DF
Engelhardt, EG
Eriksson, JG
Esko, T
Fasching, PA
Figueroa, JD
Flyger, H
Fraser, A
Garcia-Closas, M
Gasparini, P
Gieger, C
Giles, G
Guenel, P
Hagg, S
Hall, P
Hayward, C
Hopper, J
Ingelsson, E
Kardia, LR
Kasiman, K
Knight, JA
Lahti, J
Lawlor, DA
Magnusson, PKE
Margolin, S
Marsh, JA
Metspalu, A
Olson, JE
Pennell, CE
Polasek, O
Rahman, I
Ridker, PM
Robino, A
Rudan, I
Rudolph, A
Salumets, A
Schmidt, MK
Schoemaker, MJ
Smith, EN
Smith, JA
Southey, M
Stockl, D
Swerdlow, AJ
Thompson, DJ
Truong, T
Ulivi, S
Waldenberger, M
Wang, Q
Wild, S
Wilson, JF
Wright, AF
Zgaga, L
Ong, KK
Murabito, JM
Karasik, D
Murray, A
AF Perry, John R. B.
Hsu, Yi-Hsiang
Chasman, Daniel I.
Johnson, Andrew D.
Elks, Cathy
Albrecht, Eva
Andrulis, Irene L.
Beesley, Jonathan
Berenson, Gerald S.
Bergmann, Sven
Bojesen, Stig E.
Bolla, Manjeet K.
Brown, Judith
Buring, Julie E.
Campbell, Harry
Chang-Claude, Jenny
Chenevix-Trench, Georgia
Corre, Tanguy
Couch, Fergus J.
Cox, Angela
Czene, Kamila
D'adamo, Adamo Pio
Davies, Gail
Deary, Ian J.
Dennis, Joe
Easton, Douglas F.
Engelhardt, Ellen G.
Eriksson, Johan G.
Esko, Tonu
Fasching, Peter A.
Figueroa, Jonine D.
Flyger, Henrik
Fraser, Abigail
Garcia-Closas, Montse
Gasparini, Paolo
Gieger, Christian
Giles, Graham
Guenel, Pascal
Haegg, Sara
Hall, Per
Hayward, Caroline
Hopper, John
Ingelsson, Erik
Kardia, L. R.
Kasiman, Katherine
Knight, Julia A.
Lahti, Jari
Lawlor, Debbie A.
Magnusson, Patrik K. E.
Margolin, Sara
Marsh, Julie A.
Metspalu, Andres
Olson, Janet E.
Pennell, Craig E.
Polasek, Ozren
Rahman, Iffat
Ridker, Paul M.
Robino, Antonietta
Rudan, Igor
Rudolph, Anja
Salumets, Andres
Schmidt, Marjanka K.
Schoemaker, Minouk J.
Smith, Erin N.
Smith, Jennifer A.
Southey, Melissa
Stoeckl, Doris
Swerdlow, Anthony J.
Thompson, Deborah J.
Truong, Therese
Ulivi, Sheila
Waldenberger, Melanie
Wang, Qin
Wild, Sarah
Wilson, James F.
Wright, Alan F.
Zgaga, Lina
Ong, Ken K.
Murabito, Joanne M.
Karasik, David
Murray, Anna
CA kConFab Investigators
ReproGen Consortium
TI DNA mismatch repair gene MSH6 implicated in determining age at natural
menopause
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID SECULAR TRENDS; PREMATURE MENOPAUSE; REPRODUCTIVE LIFE; MENARCHE; WOMEN;
CANCER; BRCA1; ASSOCIATION; MUTATIONS; COHORT
AB The length of female reproductive lifespan is associated with multiple adverse outcomes, including breast cancer, cardiovascular disease and infertility. The biological processes that govern the timing of the beginning and end of reproductive life are not well understood. Genetic variants are known to contribute to 50 of the variation in both age at menarche and menopause, but to date the known genes explain 15 of the genetic component. We have used genome-wide association in a bivariate meta-analysis of both traits to identify genes involved in determining reproductive lifespan. We observed significant genetic correlation between the two traits using genome-wide complex trait analysis. However, we found no robust statistical evidence for individual variants with an effect on both traits. A novel association with age at menopause was detected for a variant rs1800932 in the mismatch repair gene MSH6 (P 1.9 10(9)), which was also associated with altered expression levels of MSH6 mRNA in multiple tissues. This study contributes to the growing evidence that DNA repair processes play a key role in ovarian ageing and could be an important therapeutic target for infertility.
C1 [Perry, John R. B.; Murray, Anna] Univ Exeter, Sch Med, Exeter, Devon, England.
[Perry, John R. B.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Perry, John R. B.] Kings Coll London, Dept Twin Res & Genet Epidemiol, London WC2R 2LS, England.
[Perry, John R. B.; Elks, Cathy; Ong, Ken K.] Addenbrookes Hosp, MRC, Epidemiol Unit, Cambridge, England.
[Hsu, Yi-Hsiang; Karasik, David] Hebrew SeniorLife Inst Aging Res, Boston, MA USA.
[Hsu, Yi-Hsiang; Chasman, Daniel I.; Buring, Julie E.; Ridker, Paul M.; Karasik, David] Harvard Univ, Sch Med, Boston, MA USA.
[Hsu, Yi-Hsiang] Harvard Univ, Sch Publ Hlth, Mol & Integrat Physiol Sci Program, Boston, MA 02115 USA.
[Chasman, Daniel I.; Buring, Julie E.; Ridker, Paul M.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02215 USA.
[Johnson, Andrew D.; Murabito, Joanne M.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Johnson, Andrew D.] NHLBI, Cardiovasc Epidemiol & Human Genom Branch, Bethesda, MD 20892 USA.
[Albrecht, Eva; Gieger, Christian] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Genet Epidemiol, Neuherberg, Germany.
[Stoeckl, Doris; Waldenberger, Melanie] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 2, Neuherberg, Germany.
[Waldenberger, Melanie] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, Neuherberg, Germany.
[Andrulis, Irene L.; Knight, Julia A.] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada.
[Andrulis, Irene L.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
[Beesley, Jonathan; Chenevix-Trench, Georgia] Queensland Inst Med Res, Dept Genet, Brisbane, Qld 4006, Australia.
[Berenson, Gerald S.] Tulane Univ, Dept Epidemiol, New Orleans, LA 70118 USA.
[Bergmann, Sven; Corre, Tanguy] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
[Bergmann, Sven; Corre, Tanguy] Swiss Inst Bioinformat, Lausanne, Switzerland.
[Bojesen, Stig E.] Copenhagen Univ Hosp, Herlev Hosp, Dept Clin Biochem, Copenhagen, Denmark.
[Bojesen, Stig E.] Copenhagen Univ Hosp, Herlev Hosp, Copenhagen Gen Populat Study, Copenhagen, Denmark.
[Flyger, Henrik] Copenhagen Univ Hosp, Herlev Hosp, Dept Breast Surg, Copenhagen, Denmark.
[Bolla, Manjeet K.; Brown, Judith; Dennis, Joe; Easton, Douglas F.; Thompson, Deborah J.; Wang, Qin] Univ Cambridge, Ctr Canc Genet Epidemiol, Cambridge, England.
[Bolla, Manjeet K.; Brown, Judith; Dennis, Joe; Easton, Douglas F.; Thompson, Deborah J.; Wang, Qin] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Ong, Ken K.] Univ Cambridge, Dept Paediat, Cambridge, England.
[Campbell, Harry; Rudan, Igor; Wild, Sarah; Wilson, James F.; Zgaga, Lina] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh EH8 9AG, Midlothian, Scotland.
[Chang-Claude, Jenny; Rudolph, Anja] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Couch, Fergus J.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Couch, Fergus J.; Olson, Janet E.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Cox, Angela] Univ Sheffield, Dept Oncol, CR UK YCR Sheffield Canc Res Ctr, Sheffield S10 2TN, S Yorkshire, England.
[Czene, Kamila; Haegg, Sara; Hall, Per; Kasiman, Katherine; Magnusson, Patrik K. E.; Rahman, Iffat] Karolinska Inst, Stockholm, Sweden.
[Margolin, Sara] Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden.
[D'adamo, Adamo Pio; Gasparini, Paolo; Robino, Antonietta] Univ Trieste, Inst Maternal & Child Hlth, IRCCS Burlo Garofolo, Trieste, Italy.
[Davies, Gail; Deary, Ian J.] Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh EH8 9AG, Midlothian, Scotland.
[Davies, Gail; Deary, Ian J.] Univ Edinburgh, Dept Psychol, Edinburgh EH8 9AG, Midlothian, Scotland.
[Davies, Gail; Wright, Alan F.] Univ Edinburgh, Inst Genet & Mol Med, MRC, Human Genet Unit, Edinburgh, Midlothian, Scotland.
[Engelhardt, Ellen G.; Schmidt, Marjanka K.] Netherlands Canc Inst, Div Psychosocial Res & Epidemiol, Amsterdam, Netherlands.
[Schmidt, Marjanka K.] Netherlands Canc Inst, Div Mol Pathol, Amsterdam, Netherlands.
[Eriksson, Johan G.] Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland.
[Eriksson, Johan G.] Natl Inst Hlth & Welf, Helsinki, Finland.
[Eriksson, Johan G.; Lahti, Jari] Folkhalsan Res Ctr, Helsinki, Finland.
[Eriksson, Johan G.] Univ Cent Hosp, Unit Gen Practice, Helsinki, Finland.
[Eriksson, Johan G.] Vasa Cent Hosp, Vaasa, Finland.
[Esko, Tonu] Childrens Hosp, Div Endocrinol, Boston, MA 02115 USA.
[Esko, Tonu] Broad Inst, Cambridge, MA USA.
[Esko, Tonu; Metspalu, Andres] Univ Tartu, Estonian Genome Ctr, EE-51010 Tartu, Estonia.
[Fasching, Peter A.] Univ Erlangen Nurnberg, Univ Hosp Erlangen, Dept Gynecol & Obstet, D-91054 Erlangen, Germany.
[Figueroa, Jonine D.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Fraser, Abigail; Lawlor, Debbie A.] Univ Bristol, Sch Social & Community Med, MRC Ctr Causal Anal Translat Epidemiol, Bristol, Avon, England.
[Garcia-Closas, Montse; Schoemaker, Minouk J.; Swerdlow, Anthony J.] Inst Canc Res, Div Breast Canc Res, London, England.
[Garcia-Closas, Montse; Schoemaker, Minouk J.; Swerdlow, Anthony J.] Inst Canc Res, Div Genet & Epidemiol, London, England.
[Garcia-Closas, Montse; Schoemaker, Minouk J.; Swerdlow, Anthony J.] Inst Canc Res, Breakthrough Breast Canc Res Ctr, London, England.
[Giles, Graham; Hopper, John] Univ Melbourne, Melbourne Sch Populat Hlth, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia.
[Giles, Graham] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[Guenel, Pascal; Truong, Therese] INSERM, U1018, Villejuif, France.
[Haegg, Sara; Ingelsson, Erik] Uppsala Univ, Dept Med Sci, Mol Epidemiol & Sci Life Lab, Uppsala, Sweden.
[Hayward, Caroline] Univ Edinburgh, Western Gen Hosp, Inst Genet & Mol Med, Edinburgh EH4 2XU, Midlothian, Scotland.
[kConFab Investigators] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Kardia, L. R.; Smith, Jennifer A.] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Lahti, Jari] Univ Helsinki, Inst Behav Sci, Helsinki, Finland.
[Marsh, Julie A.; Pennell, Craig E.] Univ Western Australia, Sch Womens & Infants Hlth, Nedlands, WA 6009, Australia.
[Polasek, Ozren] Univ Split, Fac Med, Dept Publ Hlth, Split, Croatia.
[Salumets, Andres] Univ Tartu, Dept Obstet & Gynecol, EE-51014 Tartu, Estonia.
[Salumets, Andres] Competence Ctr Reprod Med & Biol, EE-50410 Tartu, Estonia.
[Smith, Erin N.] Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 USA.
[Smith, Erin N.] Univ Calif San Diego, Rady Childrens Hosp, La Jolla, CA 92093 USA.
[Southey, Melissa] Univ Melbourne, Dept Pathol, Genet Epidemiol Lab, Melbourne, Vic, Australia.
[Stoeckl, Doris] Univ Munich, Dept Obstet & Gynaecol, Munich, Germany.
[Ulivi, Sheila] IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy.
[Murabito, Joanne M.] Boston Univ, Sch Med, Dept Med, Gen Internal Med Sect, Boston, MA 02118 USA.
RP Perry, JRB (reprint author), Univ Exeter, Sch Med, Exeter, Devon, England.
EM john.perry@mrc-epid.cam.ac.uk; A.Murray@exeter.ac.uk
RI Johnson, Andrew/G-6520-2013; Magnusson, Patrik/C-4458-2017;
Waldenberger, Melanie/B-5355-2014; Rudan, Igor/I-1467-2012; d'Adamo,
Adamo Pio/G-4064-2011; Stockl, Doris/B-5352-2014; Knight,
Julia/A-6843-2012; Andrulis, Irene/E-7267-2013; Hayward,
Caroline/M-8818-2016; Visser, Jenny /F-8156-2011; Garcia-Closas,
Montserrat /F-3871-2015; Salumets, Andres/J-2278-2015; Wilson, James
F/A-5704-2009; Polasek, Ozren/B-6002-2011
OI MARONGIU, MARA/0000-0002-7321-2384; Murray, Anna/0000-0002-2351-2522;
Schoemaker, Minouk/0000-0001-8403-2234; Czene,
Kamila/0000-0002-3233-5695; Marsh, Julie/0000-0001-8984-6907; Gieger,
Christian/0000-0001-6986-9554; Karasik, David/0000-0002-8826-0530; Cox,
Angela/0000-0002-5138-1099; Fraser, Abigail/0000-0002-7741-9470; Lawlor,
Debbie A/0000-0002-6793-2262; Eriksson, Johan/0000-0002-2516-2060;
Giles, Graham/0000-0003-4946-9099; Smith, Jennifer/0000-0002-3575-5468;
Lahti, Jari/0000-0002-4310-5297; Zgaga, Lina/0000-0003-4089-9703;
Waldenberger, Melanie/0000-0003-0583-5093; Rudan,
Igor/0000-0001-6993-6884; d'Adamo, Adamo Pio/0000-0001-9367-4909;
Hayward, Caroline/0000-0002-9405-9550; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Salumets, Andres/0000-0002-1251-8160; Wilson,
James F/0000-0001-5751-9178; Polasek, Ozren/0000-0002-5765-1862
FU UK Medical Research Council [G0600705, 0701594]; Wellcome Trust
FX J.R.B.P is a Sir Henry Wellcome Postdoctoral Research Fellow
(092447/Z/10/Z). D.A.L. and A.F. work in a centre that receives
infrastructure funding from the UK Medical Research Council (G0600705)
and A.F. is funded by a UK Medical Research Council Post-doctoral
research fellowship (0701594). Further information on funding for
individual studies is provided in supplementary information. Funding to
pay the Open Access publication charges for this article was provided by
the Wellcome Trust.
NR 38
TC 17
Z9 17
U1 3
U2 24
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD MAY 1
PY 2014
VL 23
IS 9
BP 2490
EP 2497
DI 10.1093/hmg/ddt620
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AE9VL
UT WOS:000334359100022
PM 24357391
ER
PT J
AU Yoneyama, S
Guo, YR
Lanktree, MB
Barnes, MR
Elbers, CC
Karczewski, KJ
Padmanabhan, S
Bauer, F
Baumert, J
Beitelshees, A
Berenson, GS
Boer, JMA
Burke, G
Cade, B
Chen, W
Cooper-Dehoff, RM
Gaunt, TR
Gieger, C
Gong, Y
Gorski, M
Heard-Costa, N
Johnson, T
Lamonte, MJ
Mcdonough, C
Monda, KL
Onland-Moret, NC
Nelson, CP
O'Connell, JR
Ordovas, J
Peter, I
Peters, A
Shaffer, J
Shen, HQ
Smith, E
Speilotes, L
Thomas, F
Thorand, B
Verschuren, WMM
Anand, SS
Dominiczak, A
Davidson, KW
Hegele, RA
Heid, I
Hofker, MH
Huggins, GS
Illig, T
Johnson, JA
Kirkland, S
Konig, W
Langaee, TY
Mccaffery, J
Melander, O
Mitchell, BD
Munroe, P
Murray, SS
Papanicolaou, G
Redline, S
Reilly, M
Samani, NJ
Schork, NJ
Van der Schouw, YT
Shimbo, D
Shuldiner, AR
Tobin, MD
Wijmenga, C
Yusuf, S
Hakonarson, H
Lange, LA
Demerath, EW
Fox, CS
North, KE
Reiner, AP
Keating, B
Taylor, KC
AF Yoneyama, Sachiko
Guo, Yiran
Lanktree, Matthew B.
Barnes, Michael R.
Elbers, Clara C.
Karczewski, Konrad J.
Padmanabhan, Sandosh
Bauer, Florianne
Baumert, Jens
Beitelshees, Amber
Berenson, Gerald S.
Boer, Jolanda M. A.
Burke, Gregory
Cade, Brian
Chen, Wei
Cooper-Dehoff, Rhonda M.
Gaunt, Tom R.
Gieger, Christian
Gong, Yan
Gorski, Mathias
Heard-Costa, Nancy
Johnson, Toby
Lamonte, Michael J.
Mcdonough, Caitrin
Monda, Keri L.
Onland-Moret, N. Charlotte
Nelson, Christopher P.
O'Connell, Jeffrey R.
Ordovas, Jose
Peter, Inga
Peters, Annette
Shaffer, Jonathan
Shen, Haiqinq
Smith, Erin
Speilotes, Liz
Thomas, Fridtjof
Thorand, Barbara
Verschuren, W. M. Monique
Anand, Sonia S.
Dominiczak, Anna
Davidson, Karina W.
Hegele, Robert A.
Heid, Iris
Hofker, Marten H.
Huggins, Gordon S.
Illig, Thomas
Johnson, Julie A.
Kirkland, Susan
Koenig, Wolfgang
Langaee, Taimour Y.
Mccaffery, Jeanne
Melander, Olle
Mitchell, Braxton D.
Munroe, Patricia
Murray, Sarah S.
Papanicolaou, George
Redline, Susan
Reilly, Muredach
Samani, Nilesh J.
Schork, Nicholas J.
Van der Schouw, Yvonne T.
Shimbo, Daichi
Shuldiner, Alan R.
Tobin, Martin D.
Wijmenga, Cisca
Yusuf, Salim
Hakonarson, Hakon
Lange, Leslie A.
Demerath, Ellen W.
Fox, Caroline S.
North, Kari E.
Reiner, Alex P.
Keating, Brendan
Taylor, Kira C.
CA Look AHEAD Res Grp
GIANT Consortium
CARe IBC Consortium
TI Gene-centric meta-analyses for central adiposity traits in up to 57 412
individuals of European descent confirm known loci and reveal several
novel associations
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; BODY-MASS INDEX; CARDIOVASCULAR-DISEASE RISK;
WAIST-HIP RATIO; INSULIN-RESISTANCE; METABOLIC SYNDROME; ABDOMINAL
OBESITY; DRUGGABLE GENOME; BLOOD-PRESSURE; IDENTIFIES 13
AB Waist circumference (WC) and waist-to-hip ratio (WHR) are surrogate measures of central adiposity that are associated with adverse cardiovascular events, type 2 diabetes and cancer independent of body mass index (BMI). WC and WHR are highly heritable with multiple susceptibility loci identified to date. We assessed the association between SNPs and BMI-adjusted WC and WHR and unadjusted WC in up to 57 412 individuals of European descent from 22 cohorts collaborating with the NHLBIs Candidate Gene Association Resource (CARe) project. The study population consisted of women and men aged 2080 years. Study participants were genotyped using the ITMAT/Broad/CARE array, which includes 50 000 cosmopolitan tagged SNPs across 2100 cardiovascular-related genes. Each trait was modeled as a function of age, study site and principal components to control for population stratification, and we conducted a fixed-effects meta-analysis. No new loci for WC were observed. For WHR analyses, three novel loci were significantly associated (P 2.4 10(6)). Previously unreported rs2811337-G near TMCC1 was associated with increased WHR ( SE, 0.048 0.008, P 7.7 10(9)) as was rs7302703-G in HOXC10 ( 0.044 0.008, P 2.9 10(7)) and rs936108-C in PEMT ( 0.035 0.007, P 1.9 10(6)). Sex-stratified analyses revealed two additional novel signals among females only, rs12076073-A in SHC1 ( 0.10 0.02, P 1.9 10(6)) and rs1037575-A in ATBDB4 ( 0.046 0.01, P 2.2 10(6)), supporting an already established sexual dimorphism of central adiposity-related genetic variants. Functional analysis using ENCODE and eQTL databases revealed that several of these loci are in regulatory regions or regions with differential expression in adipose tissue.
C1 [Yoneyama, Sachiko; Monda, Keri L.; North, Kari E.] Univ N Carolina, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27599 USA.
[Lange, Leslie A.] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
[Guo, Yiran; Hakonarson, Hakon; Keating, Brendan] Childrens Hosp Philadelphia, Ctr Appl Genom, Abramson Res Ctr, Philadelphia, PA 19104 USA.
[Guo, Yiran] BGI Shenzhen, Shenzhen 518083, Peoples R China.
[Lanktree, Matthew B.] McMaster Univ, Dept Med, Hamilton, ON L8S 4L8, Canada.
[Anand, Sonia S.; Yusuf, Salim] McMaster Univ, Dept Med, Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON L8S 4L8, Canada.
[Anand, Sonia S.; Yusuf, Salim] McMaster Univ, Dept Clin Epidemiol, Populat Genom Program, Hamilton, ON L8S 4L8, Canada.
[Barnes, Michael R.] Queen Mary Univ London, Natl Inst Hlth Biomed Res Unit, London EC1M 6BQ, England.
[Johnson, Toby; Munroe, Patricia] Queen Mary Univ London, London EC1M 6BQ, England.
[Johnson, Toby; Munroe, Patricia] Queen Mary Univ London, Genome Ctr, William Harvey Res Inst, Barts, London EC1M 6BQ, England.
[Barnes, Michael R.] Queen Mary Univ London, London Sch Med, London EC1M 6BQ, England.
[Johnson, Toby; Munroe, Patricia] Queen Mary Univ London, London Sch Med & Dent, London EC1M 6BQ, England.
[Elbers, Clara C.; Bauer, Florianne; Onland-Moret, N. Charlotte; Van der Schouw, Yvonne T.] UMC Utrecht, Julius Ctr Hlth Sci & Primary Care, NL-3508 GA Utrecht, Netherlands.
[Karczewski, Konrad J.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Padmanabhan, Sandosh] Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow G12 8QQ, Lanark, Scotland.
[Dominiczak, Anna] Univ Glasgow, Coll Med Vet & Life Sci, Glasgow G12 8QQ, Lanark, Scotland.
[Baumert, Jens; Peters, Annette; Thorand, Barbara] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 2, D-85764 Neuherberg, Germany.
[Gieger, Christian; Heid, Iris] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Genet Epidemiol, D-85764 Neuherberg, Germany.
[Illig, Thomas] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, D-85764 Neuherberg, Germany.
[Beitelshees, Amber; Mitchell, Braxton D.] Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[O'Connell, Jeffrey R.; Shen, Haiqinq; Shuldiner, Alan R.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[Shuldiner, Alan R.] Univ Maryland, Sch Med, Program Personalized & Genom Med, Baltimore, MD 21201 USA.
[Berenson, Gerald S.; Chen, Wei] Tulane Univ, Dept Epidemiol, New Orleans, LA 70112 USA.
[Boer, Jolanda M. A.; Verschuren, W. M. Monique] Natl Inst Publ Hlth & Environm, Ctr Nutr Prevent & Hlth Serv, NL-3720 BA Bilthoven, Netherlands.
[Burke, Gregory] Wake Forest Univ, Sch Med, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
[Look AHEAD Res Grp] Wake Forest Univ, Sch Med, Look AHEAD Coordinating Ctr, Winston Salem, NC 27157 USA.
[Cade, Brian; Redline, Susan] Harvard Univ, Sch Med, Div Sleep Med, Boston, MA 02115 USA.
[Cade, Brian; Redline, Susan] Brigham & Womens Hosp, Dept Med, Div Sleep Med, Boston, MA 02115 USA.
[Cooper-Dehoff, Rhonda M.; Gong, Yan; Mcdonough, Caitrin; Johnson, Julie A.; Langaee, Taimour Y.] Univ Florida, Dept Pharmacotherapy & Translat Res, Gainesville, FL 32610 USA.
[Cooper-Dehoff, Rhonda M.; Gong, Yan; Mcdonough, Caitrin; Johnson, Julie A.; Langaee, Taimour Y.] Univ Florida, Ctr Pharmacogen, Gainesville, FL 32610 USA.
[Gaunt, Tom R.] MRC Integrat Epidemiol Unit, Sch Social & Community Med, Bristol BS8 2BN, Avon, England.
[Gorski, Mathias; Heid, Iris] Univ Regensburg, Inst Epidemiol & Prevent Med, Dept Genet Epidemiol, D-93053 Regensburg, Germany.
[Gorski, Mathias] Univ Med Ctr Regensburg, Dept Internal Med 2, D-93053 Regensburg, Germany.
[Heard-Costa, Nancy] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Fox, Caroline S.] Boston Univ, Sch Med, Framingham Heart Study, Boston, MA 02118 USA.
[Lamonte, Michael J.] SUNY Buffalo, Sch Publ Hlth & Hlth Profess, Dept Social & Prevent Med, Buffalo, NY 14214 USA.
[Monda, Keri L.] Amgen Inc, Ctr Observat Res, Thousand Oaks, CA 91320 USA.
[Nelson, Christopher P.; Samani, Nilesh J.] Univ Leicester, Dept Cardiovasc Sci, Leicester LE3 9QP, Leics, England.
[Nelson, Christopher P.; Samani, Nilesh J.] Glenfield Hosp, Leicester NIHR Biomed Res Unit Cardiovasc Dis, Leicester LE3 9QP, Leics, England.
[Ordovas, Jose] Tufts Univ, Nutr & Genom Lab, Boston, MA 02111 USA.
[Peter, Inga] Mt Sinai, Icahn Sch Med, Dept Genet & Genom Sci, New York, NY 10029 USA.
[Shaffer, Jonathan; Davidson, Karina W.; Shimbo, Daichi] Columbia Univ, Med Ctr, Ctr Behav Cardiovasc Hlth, Div Gen Med, New York, NY 10032 USA.
[Smith, Erin] Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA.
[Smith, Erin] Univ Calif San Diego, Sch Med, Radys Childrens Hosp, La Jolla, CA 92093 USA.
[Speilotes, Liz] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Speilotes, Liz] Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Speilotes, Liz] Univ Michigan, Ctr Computat Med & Bioinformat, Ann Arbor, MI 48109 USA.
[Speilotes, Liz] Broad Inst, Cambridge, MA 02141 USA.
[Thomas, Fridtjof] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Memphis, TN 38163 USA.
[Hegele, Robert A.] Univ Western Ontario, Schulich Sch Med & Dent, Robarts Res Inst, London, ON N6A 5C1, Canada.
[Hofker, Marten H.] Univ Groningen, Univ Med Ctr Groningen, Dept Mol Genet, NL-9700 AB Groningen, Netherlands.
[Huggins, Gordon S.] Tufts Med Ctr, Mol Cardiol Res Inst, Ctr Translat Genom, Boston, MA 02111 USA.
[Illig, Thomas] Hannover Med Sch, Hannover Unified Biobank, D-30625 Hannover, Germany.
[Kirkland, Susan] Dalhousie Univ, Dept Community Hlth & Epidemiol, Halifax, NS, Canada.
[Koenig, Wolfgang] Univ Ulm, Med Ctr, Dept Internal Med 2, D-89081 Ulm, Germany.
[Mccaffery, Jeanne] Miriam Hosp, Weight Control & Diabet Res Ctr, Providence, RI 02906 USA.
[Mccaffery, Jeanne] Brown Univ, Warren Alpert Sch Med, Providence, RI 02906 USA.
[Melander, Olle] Lund Univ, Dept Clin Sci Hypertens & Cardiovasc Dis, SE-20502 Malmo, Sweden.
[Murray, Sarah S.; Schork, Nicholas J.] Scripps Hlth, Scripps Res Inst, La Jolla, CA 92037 USA.
[Papanicolaou, George] NHLBI, Div Prevent & Populat Sci, NIH, Bethesda, MD 20824 USA.
[Reilly, Muredach] Univ Penn, Med Ctr, Cardiovasc Inst, Philadelphia, PA 19104 USA.
[Schork, Nicholas J.] Scripps Translat Sci Inst, La Jolla, CA 92037 USA.
[Shuldiner, Alan R.] Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21201 USA.
[Tobin, Martin D.] Univ Leicester, Dept Hlth Sci, Leicester LE1 7RH, Leics, England.
[Tobin, Martin D.] Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England.
[Wijmenga, Cisca] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, NL-9700 RB Groningen, Netherlands.
[Demerath, Ellen W.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
[North, Kari E.] Carolina Ctr Genome Sci, Chapel Hill, NC 27599 USA.
[Reiner, Alex P.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Taylor, Kira C.] Univ Louisville, Sch Publ Hlth & Informat Sci, Dept Epidemiol & Populat Hlth, Louisville, KY 40202 USA.
RP Taylor, KC (reprint author), Univ Louisville, Sch Publ Hlth & Informat Sci, Dept Epidemiol & Populat Hlth, Louisville, KY 40202 USA.
EM kctayl04@louisville.edu
RI van der Schouw, Yvonne/F-8327-2014; Gaunt, Tom/O-3918-2014; Guo,
Yiran/H-4120-2011; Onland-Moret, N. Charlotte/G-9185-2011; Hegele,
Robert/G-3301-2011; Thorand, Barbara/B-5349-2014; Peters,
Annette/A-6117-2011; Wijmenga, Cisca/D-2173-2009; Padmanabhan,
Sandosh/S-3963-2016
OI Padmanabhan, Sandosh/0000-0003-3869-5808; Gieger,
Christian/0000-0001-6986-9554; Mitchell, Braxton/0000-0003-4920-4744;
Lanktree, Matthew/0000-0002-5750-6286; Wijmenga,
Cisca/0000-0002-5635-1614; Johnson, Toby/0000-0002-5998-3270; van der
Schouw, Yvonne/0000-0002-4605-435X; Gaunt, Tom/0000-0003-0924-3247;
Karczewski, Konrad/0000-0003-2878-4671; Guo, Yiran/0000-0002-6549-8589;
Thorand, Barbara/0000-0002-8416-6440;
FU British Heart Foundation [RG/07/005/23633, SP/08/005/25115,
PG/07/131/24254]; Medical Research Council [G0902313, MC_UU_12013/8];
NCATS NIH HHS [UL1 TR000064]; NCRR NIH HHS [UL1 RR025774, UL1-RR-024156,
UL1RR025005]; NHGRI NIH HHS [U01 HG007416, U01HG004402]; NHLBI NIH HHS
[HL080295, K24 HL084034, N01 HC55222, N01-HC-48047, N01-HC-48048,
N01-HC-48049, N01-HC-48050, N01-HC-65226, N01-HC-95095, N01-HC-95159,
N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164,
N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169,
N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086,
R01 HL088119, R01HL086694, R01HL087641, R01HL59367, U01 HL72515]; NIA
NIH HHS [AG023629, R01 AG016592]; NICHD NIH HHS [HD-061437, HD-062783];
NIDDK NIH HHS [P30 DK017047, P30 DK072488, U01 DK057131, U01 DK057136];
NIEHS NIH HHS [R01 ES021724]; NIGMS NIH HHS [U01 GM074492, U01 GM074518]
NR 68
TC 11
Z9 11
U1 1
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD MAY 1
PY 2014
VL 23
IS 9
BP 2498
EP 2510
DI 10.1093/hmg/ddt626
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AE9VL
UT WOS:000334359100023
PM 24345515
ER
PT J
AU Lynch, CD
Sundaram, R
Maisog, JM
Sweeney, AM
Louis, GMB
AF Lynch, C. D.
Sundaram, R.
Maisog, J. M.
Sweeney, A. M.
Louis, G. M. Buck
TI Preconception stress increases the risk of infertility: results from a
couple-based prospective cohort studyuthe LIFE study
SO HUMAN REPRODUCTION
LA English
DT Article
DE infertility; fecundity; stress; cortisol; alpha-amylase
ID SALIVARY ALPHA-AMYLASE; HUMAN-REPRODUCTION; PREGNANCY RATES; CORTISOL;
CONCEPTION; ADOPTION; IMPACT; PROBABILITIES; INTERVENTION; DETERMINANTS
AB Are womens stress levels prospectively associated with fecundity and infertility?
Higher levels of stress as measured by salivary alpha-amylase are associated with a longer time-to-pregnancy (TTP) and an increased risk of infertility.
Data suggest that stress and reproduction are interrelated; however, the directionality of that association is unclear.
In 20052009, we enrolled 501 couples in a prospective cohort study with preconception enrollment at two research sites (Michigan and Texas, USA). Couples were followed for up to 12 months as they tried to conceive and through pregnancy if it occurred. A total of 401 (80) couples completed the study protocol and 373 (93) had complete data available for this analysis.
Enrolled women collected saliva the morning following enrollment and then the morning following their first observed study menses for the measurement of cortisol and alpha-amylase, which are biomarkers of stress. TTP was measured in cycles. Covariate data were captured on both a baseline questionnaire and daily journals.
Among the 401 (80) women who completed the protocol, 347 (87) became pregnant and 54 (13) did not. After adjustment for female age, race, income, and use of alcohol, caffeine and cigarettes while trying to conceive, women in the highest tertile of alpha-amylase exhibited a 29 reduction in fecundity (longer TTP) compared with women in the lowest tertile [fecundability odds ratios (FORs) 0.71; 95 confidence interval (CI) (0.51, 1.00); P 0.05]. This reduction in fecundity translated into a 2-fold increased risk of infertility among these women [relative risk (RR) 2.07; 95 CI (1.04, 4.11)]. In contrast, we found no association between salivary cortisol and fecundability.
Due to fiscal and logistical concerns, we were unable to collect repeated saliva samples and perceived stress questionnaire data throughout the duration of follow-up. Therefore, we were unable to examine whether stress levels increased as women continued to fail to get pregnant. Our ability to control for potential confounders using time-varying data from the daily journals, however, minimizes residual confounding.
This is the first US study to demonstrate a prospective association between salivary stress biomarkers and TTP, and the first in the world to observe an association with infertility.
This study was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (contracts N01-HD-3-3355, N01-HD-3-3356, N01-HD-3358). There are no conflicts of interest to declare.
Not applicable.
C1 [Lynch, C. D.] Ohio State Univ, Coll Med, Columbus, OH 43210 USA.
[Sundaram, R.; Maisog, J. M.; Louis, G. M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD 20852 USA.
[Sweeney, A. M.] Texas A&M Hlth Sci Ctr, Dept Epidemiol & Biostat, College Stn, TX 77843 USA.
RP Lynch, CD (reprint author), Ohio State Univ, Coll Med, 395 W 12th Ave,Room 580, Columbus, OH 43210 USA.
EM courtney.lynch@osumc.edu
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development [N01-HD-3-3355,
N01-HD-3-3356, N01-HD-3358]
FX This study was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (contracts #N01-HD-3-3355, N01-HD-3-3356, N01-HD-3358).
NR 44
TC 24
Z9 24
U1 2
U2 18
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0268-1161
EI 1460-2350
J9 HUM REPROD
JI Hum. Reprod.
PD MAY
PY 2014
VL 29
IS 5
BP 1067
EP 1075
DI 10.1093/humrep/deu032
PG 9
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AF7UX
UT WOS:000334921400018
PM 24664130
ER
PT J
AU Henneberger, PK
Liang, XM
London, SJ
Umbach, DM
Sandler, DP
Hoppin, JA
AF Henneberger, Paul K.
Liang, Xiaoming
London, Stephanie J.
Umbach, David M.
Sandler, Dale P.
Hoppin, Jane A.
TI Exacerbation of symptoms in agricultural pesticide applicators with
asthma
SO INTERNATIONAL ARCHIVES OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH
LA English
DT Article
DE Asthma; Asthma exacerbation; Work-related; Agriculture; Pesticides
ID WORK-RELATED ASTHMA; HEALTH; EXPOSURE; FARMERS; PREDICTORS; STATEMENT;
DIAGNOSIS; SELECTION; OUTCOMES; WHEEZE
AB Exacerbation is a critical event in asthma management. We investigated whether exacerbation of symptoms is associated with farming exposures among agricultural pesticide applicators with asthma.
Participants were pesticide applicators with active asthma (wheezing and breathing problems in past 12 months) who completed enrollment questionnaires for the Agricultural Health Study (AHS). Exacerbation of asthma was defined as having visited a hospital emergency room or doctor for an episode of wheezing or whistling in the past 12 months. Exposures of interest were using 36 specific pesticides in the past 12 months and conducting various agricultural activities. Adjusted odds ratios (ORs) were estimated by logistic regression while controlling for potential confounders.
The 926 AHS adult pesticide applicators with active asthma included 202 (22 %) with exacerbation. Inverse associations with exacerbation were observed for two herbicides [glyphosate, odds ratio (OR) = 0.5, 95 % confidence interval (CI) 0.3, 0.8, and paraquat, OR = 0.3, 95 % CI 0.1, 0.9] and several agricultural activities (repairing engines, grinding metal, driving diesel tractors, and performing veterinary procedures). Only asthma cases with allergies (i.e., doctor-diagnosed hay fever or eczema, 46 %) had positive exacerbation-pesticide associations, with OR = 2.1 (95 % CI 1.1, 4.1) for the herbicide pendimethalin and OR = 10.2 (95 % CI 1.9, 55) for the insecticide aldicarb.
The inverse associations with two pesticides and specific farm activities are consistent with the possibility that asthma cases prone to exacerbation may avoid exposures that trigger symptoms. Although limited by small sample size and a cross-sectional design, our study suggests that use of specific pesticides may contribute to exacerbation of asthma among individuals with allergies.
C1 [Henneberger, Paul K.; Liang, Xiaoming] NIOSH, Div Resp Dis Studies, Morgantown, WV 26505 USA.
[London, Stephanie J.; Sandler, Dale P.; Hoppin, Jane A.] NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Umbach, David M.] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
RP Henneberger, PK (reprint author), NIOSH, Div Resp Dis Studies, MS 2800,1095 Willowdale Rd, Morgantown, WV 26505 USA.
EM pkh0@cdc.gov
OI Sandler, Dale/0000-0002-6776-0018; London, Stephanie/0000-0003-4911-5290
FU National Institute for Occupational Safety and Health; Intramural
Research Program of the National Institutes of Health, National
Institute of Environmental Health Sciences [Z01-ES049030]; National
Institutes of Health, National Cancer Institute [Z01-CP010119]
FX The authors thank the Agricultural Health Study participants, the staff
of the Iowa and North Carolina field stations (Ellen Heywood, Margaret
Hayslip), and the Agricultural Health Study coordinating center (Ben
Laimon, Marsha Dunn, Kate Torres, Stanley Legum). This work was
supported by the National Institute for Occupational Safety and Health
and the Intramural Research Program of the National Institutes of
Health, National Institute of Environmental Health Sciences
(Z01-ES049030) and the National Institutes of Health, National Cancer
Institute (Z01-CP010119).
NR 29
TC 10
Z9 10
U1 2
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-0131
EI 1432-1246
J9 INT ARCH OCC ENV HEA
JI Int. Arch. Occup. Environ. Health
PD MAY
PY 2014
VL 87
IS 4
BP 423
EP 432
DI 10.1007/s00420-013-0881-x
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AF7ZF
UT WOS:000334933600009
PM 23670403
ER
PT J
AU Grady, C
Wiener, L
Abdoler, E
Trauernicht, E
Zadeh, S
Diekema, DS
Wilfond, BS
Wendler, D
AF Grady, Christine
Wiener, Lori
Abdoler, Emily
Trauernicht, Emily
Zadeh, Sima
Diekema, Douglas S.
Wilfond, Benjamin S.
Wendler, David
TI Assent in Research: The Voices of Adolescents
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Adolescents; Clinical research; Assent
ID PEDIATRIC RESEARCH; DECISION-MAKING; CHILDREN; PARTICIPATION
AB Purpose: Adolescents join clinical research after investigators obtain their positive agreement or "assent." Although intended to respect adolescents, little is known about the views of adolescents or their parents regarding assent or research enrollment decisions. This study aimed to better understand perspectives of adolescent research participants and their parents about assent and parental permission.
Methods: Structured interviews were conducted with 13-through 17-year-old teens, enrolled in clinical research at the National Institutes of Health or Seattle Children's Hospital, and separately with one parent.
Results: One hundred and seventy-seven adolescenteparent pairs were interviewed. Teens were well distributed by age and gender, represented a wide variety of research and illnesses ranging in severity from mild to life threatening; 20% were healthy volunteers. Teens and parents were generally satisfied with the assent/permission process. Normally, they made the enrollment decision together and teens wanted parents' input and support. About 25% of teens reported pressure to enroll, not only from parents or relatives but also from doctors/nurses/research teams. Only 2% of teens preferred not to sign a consent form.
Conclusions: Despite some differing views about how decisions should be made, the current assent/permission process is perceived as satisfactorily respectful by most teens in research. Many teens want to sign consent forms, and teens' signatures should generally be sought. Flexible guidance allows research teams and Institutional Review Boards to customize the assent process for teens in particular studies in order to facilitate an appropriate balance between giving teens a voice reflective of their emerging independence and enabling supportive collaboration with parents. Published by Elsevier Inc. on behalf of Society for Adolescent Health and Medicine.
C1 [Grady, Christine; Wendler, David] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
[Wiener, Lori; Zadeh, Sima] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Abdoler, Emily] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Trauernicht, Emily] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Diekema, Douglas S.; Wilfond, Benjamin S.] Seattle Childrens Res Inst, Treuman Katz Ctr Pediat Bioeth, Seattle, WA USA.
RP Grady, C (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM cgrady@nih.gov
FU National Institutes of Health (NIH) Office of Evaluation; NIH Clinical
Center Department of Bioethics; Intramural Research Program, National
Cancer Institute, Center for Cancer Research; Institute for
Translational Health Sciences [UL1TR000423]
FX This research was supported by National Institutes of Health (NIH)
Office of Evaluation, the NIH Clinical Center Department of Bioethics,
the Intramural Research Program, National Cancer Institute, Center for
Cancer Research, and the Institute for Translational Health Sciences
(UL1TR000423).
NR 19
TC 5
Z9 5
U1 1
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
EI 1879-1972
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD MAY
PY 2014
VL 54
IS 5
BP 515
EP 520
DI 10.1016/j.jadohealth.2014.02.005
PG 6
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA AF1XG
UT WOS:000334506600004
PM 24630932
ER
PT J
AU Barzilay, JI
Buzkova, P
Zieman, SJ
Kizer, JR
Djousse, L
Ix, JH
Tracy, RP
Siscovick, DS
Cauley, JA
Mukamal, KJ
AF Barzilay, Joshua I.
Buzkova, Petra
Zieman, Susan J.
Kizer, Jorge R.
Djousse, Luc
Ix, Joachim H.
Tracy, Russell P.
Siscovick, David S.
Cauley, Jane A.
Mukamal, Kenneth J.
TI Circulating Levels of Carboxy-Methyl-Lysine ( CML) Are Associated With
Hip Fracture Risk: The Cardiovascular Health Study
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE CARBOXY-METHYL-LYSINE; HIP FRACTURE RISK; BONE QUALITY; CARDIOVASCULAR
HEALTH STUDY; BONE MINERAL DENSITY
ID GLYCATION END-PRODUCTS; COLLAGEN CROSS-LINKS; POSTMENOPAUSAL WOMEN;
VERTEBRAL FRACTURES; PENTOSIDINE; SERUM; OSTEOPOROSIS; BONE
AB Advanced glycation end products (AGE) in bone tissue are associated with impaired biomechanical properties and increased fracture risk. Here we examine whether serum levels of the AGE carboxy-methyl-lysine (CML) are associated with risk of hip fracture. We followed 3373 participants from the Cardiovascular Health Study (age 78 years; range, 68-102 years; 39.8% male) for a median of 9.22 years (range, 0.01-12.07 years). Rates of incident hip fracture were calculated by quartiles of baseline CML levels, and hazard ratios were adjusted for covariates associated with hip fracture risk. A subcohort of 1315 participants had bone mineral density (BMD) measurement. There were 348 hip fractures during follow-up, with incidence rates of hip fracture by CML quartiles of 0.94, 1.34, 1.18, and 1.69 per 100 participant-years. The unadjusted hazard ratio of hip fracture increased with each 1 SD increase (189ng/mL) of CML level (hazard ratio, 1.27; 95% confidence interval [CI], 1.16-1.40]; p<0.001). Sequential adjustment for age, gender, race/ethnicity, body mass index (BMI), smoking, alcohol consumption, prevalent coronary heart disease (CHD), energy expenditure, and estimated glomerular filtration rate (based on cystatin C), moderately attenuated the hazard ratio for fracture (1.17; 95% CI, 1.05-1.31; p=0.006). In the cohort with BMD testing, total hip BMD was not significantly associated with CML levels. We conclude that increasing levels of CML are associated with hip fracture risk in older adults, independent of hip BMD. These results implicate AGE in the pathogenesis of hip fractures. (c) 2014 American Society for Bone and Mineral Research.
C1 [Barzilay, Joshua I.] Kaiser Permanente Georgia, Div Endocrinol, Atlanta, GA USA.
[Barzilay, Joshua I.] Emory Sch Med, Div Endocrinol, Atlanta, GA USA.
[Buzkova, Petra] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Zieman, Susan J.] NIA, Geriatr Branch Off, NIH, Bethesda, MD 20892 USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Med, Div Epidemiol & Populat Hlth, Bronx, NY USA.
[Djousse, Luc] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Djousse, Luc] Harvard Univ, Sch Med, Boston, MA USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Nephrol, San Diego VA Healthcare Syst, San Diego, CA 92103 USA.
[Tracy, Russell P.] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA.
[Tracy, Russell P.] Univ Vermont, Coll Med, Dept Biochem, Burlington, VT 05405 USA.
[Siscovick, David S.] Univ Washington, Dept Med, Seattle, WA USA.
[Cauley, Jane A.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
RP Barzilay, JI (reprint author), Kaiser Permanente Georgia, 3650 Steve Reynolds Blvd, Duluth, GA 30096 USA.
EM Joshua.barzilay@kp.org
RI Cauley, Jane/N-4836-2015; Djousse, Luc/F-5033-2017
OI Cauley, Jane/0000-0003-0752-4408; Djousse, Luc/0000-0002-9902-3047
FU National Heart, Lung, and Blood Institute (NHLBI) [HHSN268201200036C,
HHSN268200800007C, N01 HC55222, N01HC85079, N01HC85080, N01HC85081,
N01HC85082, N01HC85083, N01HC85086, HL094555, HL080295]; National
Institute on Aging (NIA) [AG023629]
FX This research was supported by contracts HHSN268201200036C,
HHSN268200800007C, N01 HC55222, N01HC85079, N01HC85080, N01HC85081,
N01HC85082, N01HC85083, N01HC85086, and grants HL094555 and HL080295
from the National Heart, Lung, and Blood Institute (NHLBI), with
additional contribution from the National Institute of Neurological
Disorders and Stroke (NINDS). Additional support was provided by
AG023629 from the National Institute on Aging (NIA). A full list of
principal CHS investigators and institutions can be found at
CHS-NHLBI.org.
NR 24
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U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0884-0431
EI 1523-4681
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD MAY
PY 2014
VL 29
IS 5
BP 1061
EP 1066
DI 10.1002/jbmr.2123
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AF4CJ
UT WOS:000334658700005
PM 24877243
ER
PT J
AU Iglesias, AI
Mihaescu, R
Ioannidis, JPA
Khoury, MJ
Little, J
van Duijn, CM
Janssens, ACJW
AF Iglesias, Adriana I.
Mihaescu, Raluca
Ioannidis, John P. A.
Khoury, Muin J.
Little, Julian
van Duijn, Cornelia M.
Janssens, A. Cecile J. W.
TI Scientific reporting is suboptimal for aspects that characterize genetic
risk prediction studies: a review of published articles based on the
Genetic RIsk Prediction Studies statement
SO JOURNAL OF CLINICAL EPIDEMIOLOGY
LA English
DT Review
DE Genetic; Risk prediction; GRIPS; Reporting guideline; Epidemiology;
Review
ID RANDOMIZED CONTROLLED-TRIALS; SINGLE NUCLEOTIDE POLYMORPHISMS;
CORONARY-ARTERY-DISEASE; TYPE-2 DIABETES RISK; BEFORE-AND-AFTER;
DIAGNOSTIC-ACCURACY; PROSPECTIVE COHORT; PERSONALIZED MEDICINE; CLINICAL
INFORMATION; STROBE STATEMENT
AB Objectives: Our main objective was to raise awareness of the areas that need improvements in the reporting of genetic risk prediction articles for future publications, based on the Genetic Risk Prediction Studies (GRIPS) statement.
Study Design and Setting: We evaluated studies that developed or validated a prediction model based on multiple DNA variants, using empirical data, and were published in 2010. A data extraction form based on the 25 items of the GRIPS statement was created and piloted.
Results: Forty-two studies met our inclusion criteria. Overall, more than half of the evaluated items (34 of 62) were reported in at least 85% of included articles. Seventy-seven percentage of the articles were identified as genetic risk prediction studies through title assessment, but only 31% used the keywords recommended by GRIPS in the title or abstract. Seventy-four percentage mentioned which allele was the risk variant. Overall, only 10% of the articles reported all essential items needed to perform external validation of the risk model.
Conclusion: Completeness of reporting in genetic risk prediction studies is adequate for general elements of study design but is suboptimal for several aspects that characterize genetic risk prediction studies such as description of the model construction. Improvements in the transparency of reporting of these aspects would facilitate the identification, replication, and application of genetic risk prediction models. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Iglesias, Adriana I.; Mihaescu, Raluca; van Duijn, Cornelia M.] Erasmus Univ, Dept Epidemiol, Med Ctr, NL-3015 GE Rotterdam, Netherlands.
[Ioannidis, John P. A.] Stanford Univ, Stanford Prevent Res Ctr, Dept Med, Sch Med, Stanford, CA 94305 USA.
[Ioannidis, John P. A.] Stanford Univ, Stanford Prevent Res Ctr, Dept Hlth Res & Policy, Sch Med, Stanford, CA 94305 USA.
[Ioannidis, John P. A.] Stanford Univ, Dept Stat, Sch Humanities & Sci, Stanford, CA 94305 USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA 30333 USA.
[Khoury, Muin J.] NCI, Epidemiol & Genom Res Program, Bethesda, MD 20892 USA.
[Little, Julian] Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON K1H 8M5, Canada.
[Janssens, A. Cecile J. W.] Emory Univ, Dept Epidemiol, Atlanta, GA 30322 USA.
RP Janssens, ACJW (reprint author), Emory Univ, Dept Epidemiol, Atlanta, GA 30322 USA.
EM cecile.janssens@emory.edu
OI Janssens, A Cecile/0000-0002-6153-4976
FU ERACOL program; Centre for Medical Systems Biology [CMSB 1-2]; ENGAGE
Consortium [HEALTH-F4-2007-201413]; Netherlands Organization for
Scientific Research (NWO)
FX A.I.I. was a recipient of the ERACOL program, which gives her the
opportunity to perform this research in the Netherlands. J.L. holds a
Tier 1 Canada Research Chair in Human Genome Epidemiology. C.M.v.D. was
supported by the Centre for Medical Systems Biology (CMSB 1-2) and the
ENGAGE Consortium, grant agreement HEALTH-F4-2007-201413. A.C.J.W.J. was
supported by a Vidi grant from the Netherlands Organization for
Scientific Research (NWO).
NR 70
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Z9 2
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0895-4356
EI 1878-5921
J9 J CLIN EPIDEMIOL
JI J. Clin. Epidemiol.
PD MAY
PY 2014
VL 67
IS 5
BP 487
EP 499
DI 10.1016/j.jclinepi.2013.10.006
PG 13
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA AF8OG
UT WOS:000334974900002
PM 24411311
ER
PT J
AU Bevans, M
Wehrlen, L
Castro, K
Prince, P
Shelburne, N
Soeken, K
Zabora, J
Wallen, GR
AF Bevans, Margaret
Wehrlen, Leslie
Castro, Kathleen
Prince, Patricia
Shelburne, Nonniekaye
Soeken, Karen
Zabora, James
Wallen, Gwenyth R.
TI A problem-solving education intervention in caregivers and patients
during allogeneic hematopoietic stem cell transplantation
SO JOURNAL OF HEALTH PSYCHOLOGY
LA English
DT Article
DE intervention; behavioral medicine; anxiety; distress; coping; cancer;
health behavior; family
ID RANDOMIZED CLINICAL-TRIAL; ADULT CANCER-PATIENTS; QUALITY-OF-LIFE;
FAMILY CAREGIVERS; SELF-EFFICACY; PSYCHOLOGICAL DISTRESS; BREAST-CANCER;
CARE; DEMENTIA; METAANALYSIS
AB The aim of this study was to determine the effect of problem-solving education on self-efficacy and distress in informal caregivers of allogeneic hematopoietic stem cell transplantation patients. Patient/caregiver teams attended three 1-hour problem-solving education sessions to help cope with problems during hematopoietic stem cell transplantation. Primary measures included the Cancer Self-Efficacy Scale-transplant and Brief Symptom Inventory-18. Active caregivers reported improvements in self-efficacy (p < 0.05) and distress (p < 0.01) post-problem-solving education; caregiver responders also reported better health outcomes such as fatigue. The effect of problem-solving education on self-efficacy and distress in hematopoietic stem cell transplantation caregivers supports its inclusion in future interventions to meet the multifaceted needs of this population.
C1 [Bevans, Margaret; Wehrlen, Leslie; Prince, Patricia; Wallen, Gwenyth R.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Castro, Kathleen; Shelburne, Nonniekaye] NCI, Bethesda, MD 20892 USA.
[Soeken, Karen] Univ Maryland, College Pk, MD 20742 USA.
[Zabora, James] Inova Hlth Syst, Alexandria, VA USA.
RP Bevans, M (reprint author), NIH, Ctr Clin, 10 Ctr Dr,Room 2B13, Bethesda, MD 20892 USA.
EM mbevans@cc.nih.gov
FU Intramural NIH HHS [ZIA CL001150-05]
NR 50
TC 7
Z9 7
U1 2
U2 7
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1359-1053
EI 1461-7277
J9 J HEALTH PSYCHOL
JI J. Health Psychol.
PD MAY
PY 2014
VL 19
IS 5
BP 602
EP 617
DI 10.1177/1359105313475902
PG 16
WC Psychology, Clinical
SC Psychology
GA AF6KS
UT WOS:000334824600002
PM 23471761
ER
PT J
AU Kitano, H
Chung, JY
Ylaya, K
Conway, C
Takikita, M
Fukuoka, J
Doki, Y
Hanaoka, J
Hewitt, SM
AF Kitano, Haruhisa
Chung, Joon-Yong
Ylaya, Kris
Conway, Catherine
Takikita, Mikiko
Fukuoka, Junya
Doki, Yoshinori
Hanaoka, Jun
Hewitt, Stephen M.
TI Profiling of Phospho-AKT, Phospho-mTOR, Phospho-MAPK and EGFR in
Non-small Cell Lung Cancer
SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
LA English
DT Article
DE AKT; mTOR; Tissue microarray; Non-small cell lung cancer; Image
analysis; MAPK; Survival analysis; Immunohistochemistry; EGFR
ID GROWTH-FACTOR RECEPTOR; PREDICTS POOR-PROGNOSIS; ORAL MEK INHIBITOR;
SIGNALING PATHWAYS; MAMMALIAN TARGET; BREAST-CANCER; PHASE-II;
EXPRESSION; KINASE; PI3K
AB Activation of numerous pathways has been documented in non-small cell lung cancer (NSCLC). Epidermal growth factor receptor (EGFR) has emerged as a common therapeutic target. The mitogen-activated protein kinase (MAPK) and AKT signaling pathways are downstream of EGFR and deregulated via genetic and epigenetic mechanisms in many human cancers. We evaluated selected markers in the EGFR pathway with reference to outcome. Tissues from 220 cases of NSCLC patients presented in a tissue microarray were assayed with immunohistochemistry for phosphorylated AKT, phosphorylated MAPK, phosphorylated mTOR, and EGFR and then quantified by automated image analysis. Individually, the biomarkers did not predict. Combined as ratios, p-mTOR/p-AKT, and p-MAPK/EGFR function as prognostic markers of survival (p=0.008 and p=0.029, respectively), however, no significance was found after adjustment (p=0.221, p=0.103). The sum of these ratios demonstrates a stronger correlation with survival (p<0.001) and remained statistically significant after adjustment (p=0.026). The algebraic combination of biomarkers offer the capacity to understand factors that predict outcome better than current approaches of evaluating biomarkers individually or in pairs. Our results show the sum of p-mTOR/p-AKT and p-MAPK/EGFR is a potential predictive marker of survival in NSCLC patients.
C1 [Kitano, Haruhisa; Chung, Joon-Yong; Ylaya, Kris; Conway, Catherine; Hewitt, Stephen M.] NCI, Tissue Array Res Program, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Kitano, Haruhisa; Fukuoka, Junya] Toyama Univ Hosp, Pathol Lab, Toyama, Japan.
[Doki, Yoshinori] Toyama Univ, Dept Surg 1, Toyama 930, Japan.
[Kitano, Haruhisa; Hanaoka, Jun] Shiga Univ Med Sci, Dept Surg, Otsu, Shiga 52021, Japan.
RP Hewitt, SM (reprint author), NCI, Tissue Array Res Program, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM genejock@helix.nih.gov
OI Hewitt, Stephen/0000-0001-8283-1788; Chung,
Joon-Yong/0000-0001-5041-5982
FU NIH, National Cancer Institute, Center for Cancer Research
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This
research was supported in part by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 66
TC 10
Z9 10
U1 0
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0022-1554
EI 1551-5044
J9 J HISTOCHEM CYTOCHEM
JI J. Histochem. Cytochem.
PD MAY
PY 2014
VL 62
IS 5
BP 335
EP 346
DI 10.1369/0022155414523022
PG 12
WC Cell Biology
SC Cell Biology
GA AG0FK
UT WOS:000335090500002
PM 24487999
ER
PT J
AU Rajagopalan, S
Long, EO
AF Rajagopalan, Sumati
Long, Eric O.
TI Comment on "Killer Ig- like Receptor 2DL4 Does Not Mediate NK Cell
IFN-gamma Responses to Soluble HLA-G Preparations"
SO JOURNAL OF IMMUNOLOGY
LA English
DT Letter
C1 [Rajagopalan, Sumati; Long, Eric O.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
RP Rajagopalan, S (reprint author), NIAID, Immunogenet Lab, NIH, 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM sumi@nih.gov
FU Intramural NIH HHS [ZIA AI001119-06]
NR 4
TC 3
Z9 4
U1 1
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
IS 9
BP 4003
EP 4003
DI 10.4049/jimmunol.1400430
PG 1
WC Immunology
SC Immunology
GA AF4HO
UT WOS:000334672800001
PM 24748631
ER
PT J
AU Ma, N
Xing, C
Xiao, H
He, YD
Han, GC
Chen, GJ
Hou, CM
Marrero, B
Wang, YJ
Zhang, SQ
Shen, BF
Li, Y
Wang, RX
AF Ma, Ning
Xing, Chen
Xiao, He
He, Youdi
Han, Gencheng
Chen, Guojiang
Hou, Chunmei
Marrero, Bernadette
Wang, Yujuan
Zhang, Shengquan
Shen, Beifen
Li, Yan
Wang, Renxi
TI BAFF Suppresses IL-15 Expression in B Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; MEMORY T-CELLS; EXPERIMENTAL AUTOIMMUNE
ENCEPHALOMYELITIS; PLASMA-CELLS; RHEUMATOID-ARTHRITIS; MICE; DISEASE;
INTERLEUKIN-15; BCMA; TRANSCRIPTION
AB Clinical trials have shown that BAFF inhibitors do not reduce memory B cell levels but can reduce the number of mature B cells. It remains uncertain whether BAFF affects memory-maintaining cytokines such as IL-15. We found that BAFF suppressed IL-15 expression in B cells from lupus-like or experimental allergic encephalomyelitis mice. When BAFF was blocked with atacicept-IgG, IL-15 expression was upregulated in lupus-like or experimental allergic encephalomyelitis mice. Finally, we showed that BAFF suppressed IL-15 expression in transitional 2 B cells by reducing Foxo1 expression and inducing Foxo1 phosphorylation. This study suggests that BAFF suppresses IL-15 expression in autoimmune diseases, and this opens up the possible opportunity for the clinical application of BAFF-and IL-15-specific therapeutic agents.
C1 [Ma, Ning; Xing, Chen; Xiao, He; Han, Gencheng; Chen, Guojiang; Hou, Chunmei; Shen, Beifen; Li, Yan; Wang, Renxi] Inst Basic Med Sci, Immunol Lab, Beijing 100850, Peoples R China.
[Ma, Ning] Jilin Univ, Hosp 1, Dept Rheumatol, Changchun 130021, Peoples R China.
[He, Youdi] Capital Med Univ, Beijing Chaoyang Hosp, Dept Neurol, Beijing 100020, Peoples R China.
[Marrero, Bernadette] NEI, Mol Immunol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Wang, Yujuan] NEI, Immunopathol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Zhang, Shengquan] Anhui Med Univ, Dept Biochem & Mol Biol, Hefei 230032, Peoples R China.
RP Wang, RX (reprint author), Inst Basic Med Sci, Immunol Lab, POB 130,3 Taiping Rd 27, Beijing 100850, Peoples R China.
EM liyan62033@gmail.com; wang_renxi@yahoo.com
RI wang, yujuan/C-8428-2016
FU National Basic Research Program 973 [2013CB530506]; Beijing Natural
Science Foundation [7132139]
FX This work was supported by National Basic Research Program 973 Grant
2013CB530506 and Beijing Natural Science Foundation Grant 7132139.
NR 40
TC 7
Z9 7
U1 0
U2 8
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
IS 9
BP 4192
EP 4201
DI 10.4049/jimmunol.1302132
PG 10
WC Immunology
SC Immunology
GA AF4HO
UT WOS:000334672800025
PM 24670802
ER
PT J
AU Swiecki, M
Wang, YM
Riboldi, E
Kim, AHJ
Dzutsev, A
Gilfillan, S
Vermi, W
Ruedl, C
Trinchieri, G
Colonna, M
AF Swiecki, Melissa
Wang, Yaming
Riboldi, Elena
Kim, Alfred H. J.
Dzutsev, Amiran
Gilfillan, Susan
Vermi, William
Ruedl, Christiane
Trinchieri, Giorgio
Colonna, Marco
TI Cell Depletion in Mice That Express Diphtheria Toxin Receptor under the
Control of SiglecH Encompasses More Than Plasmacytoid Dendritic Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MARGINAL ZONE MACROPHAGES; C-TYPE LECTIN; IN-VIVO;
INTERFERON-ALPHA/BETA; IMMUNE-RESPONSES; VIRAL-INFECTION; CUTTING EDGE;
SIGN-R1; SPLEEN; MONOCYTOGENES
AB Plasmacytoid dendritic cells (pDC) produce IFN-I in response to viruses and are routinely identified in mice by SiglecH expression. SiglecH is a sialic acid-binding Ig-like lectin that has an immunomodulatory role during viral infections. In this study, we evaluated the impact of SiglecH deficiency on cytokine responses in the presence and absence of pDC. We found that lack of SiglecH enhanced IFN-I responses to viral infection, regardless of whether pDC were depleted. We also examined the expression pattern of SiglecH and observed that it was expressed by specialized macrophages and progenitors of classical dendritic cells and pDC. Accordingly, marginal zone macrophages and pDC precursors were eliminated in newly generated SiglecH-diphtheria toxin receptor (DTR)-transgenic (Tg) mice but not in CLEC4C-DTR-Tg mice after diphtheria toxin (DT) treatment. Using two bacterial models, we found that SiglecH-DTR-Tg mice injected with DT had altered bacterial uptake and were more susceptible to lethal Listeria monocytogenes infection than were DT-treated CLEC4C-DTR-Tg mice. Taken together, our findings suggest that lack of SiglecH may affect cytokine responses by cell types other than pDC during viral infections, perhaps by altering viral distribution or burden, and that cell depletion in SiglecH-DTR-Tg mice encompasses more than pDC.
C1 [Swiecki, Melissa; Wang, Yaming; Gilfillan, Susan; Vermi, William; Colonna, Marco] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Riboldi, Elena; Dzutsev, Amiran; Trinchieri, Giorgio] NCI, Expt Immunol Lab, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
[Riboldi, Elena] Univ Piemonte Orientale A Avagadro, Dept Pharmaceut Sci, I-28100 Novara, Italy.
[Kim, Alfred H. J.] Washington Univ, Sch Med, Dept Internal Med, Div Rheumatol, St Louis, MO 63110 USA.
[Vermi, William] Univ Brescia, Sch Med, Sect Pathol, Dept Mol & Translat Med, I-25123 Brescia, Italy.
[Ruedl, Christiane] Nanyang Technol Univ, Div Mol & Cell Biol, Sch Biol Sci, Singapore 637551, Singapore.
RP Colonna, M (reprint author), Washington Univ, BJC Inst Hlth, 425 South Euclid Ave,Campus Box 8118, St Louis, MO 63110 USA.
EM mcolonna@pathology.wustl.edu
RI Kim, Alfred/F-5699-2013;
OI Kim, Alfred/0000-0003-4074-0516; Colonna, Marco/0000-0001-5222-4987
FU NHLBI NIH HHS [2T32HL007317-31, T32 HL007317]; NIDDK NIH HHS
[1K01DK095972-01A1, K01 DK095972]
NR 40
TC 14
Z9 14
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
IS 9
BP 4409
EP 4416
DI 10.4049/jimmunol.1303135
PG 8
WC Immunology
SC Immunology
GA AF4HO
UT WOS:000334672800046
PM 24683186
ER
PT J
AU Romero, R
Kadar, N
Miranda, J
Korzeniewski, SJ
Schwartz, AG
Chaemsaithong, P
Rogers, W
Soto, E
Gotsch, F
Yeo, L
Hassan, SS
Chaiworapongsa, T
AF Romero, Roberto
Kadar, Nicholas
Miranda, Jezid
Korzeniewski, Steven J.
Schwartz, Alyse G.
Chaemsaithong, Piya
Rogers, Wade
Soto, Eleazar
Gotsch, Francesca
Yeo, Lami
Hassan, Sonia S.
Chaiworapongsa, Tinnakorn
TI The diagnostic performance of the Mass Restricted (MR) score in the
identification of microbial invasion of the amniotic cavity or
intra-amniotic inflammation is not superior to amniotic fluid
interleukin-6
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE Biomarker; chorioamnionitis; IL-6; MMP-8; pregnancy; preterm birth;
preterm labor; proteomics; reproducibility
ID PRETERM PREMATURE RUPTURE; TUMOR-NECROSIS-FACTOR;
POLYMERASE-CHAIN-REACTION; CERVICAL-VAGINAL FLUID; BIRTH-WEIGHT INFANTS;
BLOOD-CELL COUNT; ACTIVATING PEPTIDE-1 INTERLEUKIN-8; COMPREHENSIVE
PROTEOMIC ANALYSIS; UMBILICAL-CORD INFLAMMATION; LEUKOCYTE
ESTERASE-ACTIVITY
AB Objective: Intra-amniotic infection/inflammation are major causes of spontaneous preterm labor and delivery. However, diagnosis of intra-amniotic infection is challenging because most are subclinical and amniotic fluid (AF) cultures take several days before results are available. Several tests have been proposed for the rapid diagnosis of microbial invasion of the amniotic cavity (MIAC) or intra-amniotic inflammation. The aim of this study was to examine the diagnostic performance of the AF Mass Restricted (MR) score in comparison with interleukin-6 (IL-6) and matrix metalloproteinase-8 (MMP-8) for the identification of MIAC or inflammation.
Methods: AF samples were collected from patients with singleton gestations and symptoms of preterm labor (n - 100). Intra-amniotic inflammation was defined as 4100 white blood cells/mm(3) (WBCs) in AF; MIAC was defined as a positive AF culture. AF IL-6 and MMP-8 were determined using ELISA. The MR score was obtained using the Surface-Enhanced Laser Desorption Ionization Time of Flight (SELDI-TOF) mass spectrometry. Sensitivity and specificity were calculated and logistic regression models were fit to construct receiver-operating characteristic (ROC) curves for the identification of each outcome. The McNemar's test and paired sample non-parametric statistical techniques were used to test for differences in diagnostic performance metrics.
Results: (1) The prevalence of MIAC and intra-amniotic inflammation was 34% (34/100) and 40% (40/100), respectively; (2) there were no significant differences in sensitivity of the three tests under study (MR score, IL-6 or MMP-8) in the identification of either MIAC or intra-amniotic inflammation (using the following cutoffs: MR score >2, IL-6 > 11.4 ng/mL, and MMP-8>23 ng/mL); (3) there was no significant difference in the sensitivity among the three tests for the same outcomes when the false positive rate was fixed at 15%; (4) the specificity for IL-6 was not significantly different from that of the MR score in identifying either MIAC or intra-amniotic inflammation when using previously reported thresholds; and (5) there were no significant differences in the area under the ROC curve when comparing the MR score, IL-6 or MMP-8 in the identification of these outcomes.
Conclusions: IL-6 and the MR score have equivalent diagnostic performance in the identification of MIAC or intra-amniotic inflammation. Selection from among these three tests (MR score, IL-6 and MMP-8) for diagnostic purposes should be based on factors such as availability, reproducibility, and cost. The MR score requires a protein chip and a SELDI-TOF instrument which are not widely available or considered "state of the art". In contrast, immunoassays for IL-6 can be performed in the majority of clinical laboratories.
C1 [Romero, Roberto; Kadar, Nicholas; Miranda, Jezid; Korzeniewski, Steven J.; Schwartz, Alyse G.; Chaemsaithong, Piya; Soto, Eleazar; Gotsch, Francesca; Yeo, Lami; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Bethesda, MD USA.
[Romero, Roberto; Kadar, Nicholas; Miranda, Jezid; Korzeniewski, Steven J.; Schwartz, Alyse G.; Chaemsaithong, Piya; Soto, Eleazar; Gotsch, Francesca; Yeo, Lami; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Detroit, MI USA.
[Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Miranda, Jezid; Korzeniewski, Steven J.; Schwartz, Alyse G.; Chaemsaithong, Piya; Soto, Eleazar; Yeo, Lami; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Rogers, Wade] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA USA.
[Gotsch, Francesca] Azienda Osped Univ, Integrata Verona, Verona, Italy.
RP Romero, R (reprint author), NICHD, Perinatol Res Branch, NIH, DHHS,Hutzel Womens Hosp, 3990 John R St, Detroit, MI 48201 USA.
EM romeror@mail.nih.gov
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver, National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services (NICHD/NIH); NICHD; NIH [HHSN275201300006C]
FX This research was supported, in part, by the Perinatology Research
Branch, Division of Intramural Research, Eunice Kennedy Shriver,
National Institute of Child Health and Human Development, National
Institutes of Health, Department of Health and Human Services
(NICHD/NIH); and, in part, with Federal funds from NICHD, NIH under
Contract No. HHSN275201300006C.
NR 271
TC 22
Z9 23
U1 1
U2 5
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1476-7058
EI 1476-4954
J9 J MATERN-FETAL NEO M
JI J. Matern.-Fetal Neonatal Med.
PD MAY
PY 2014
VL 27
IS 8
BP 757
EP 769
DI 10.3109/14767058.2013.844123
PG 13
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AF5FG
UT WOS:000334738800001
PM 24028673
ER
PT J
AU Romero, R
Yoon, BH
Chaemsaithong, P
Cortez, J
Park, CW
Gonzalez, R
Behnke, E
Hassan, SS
Chaiworapongsa, T
Yeo, L
AF Romero, Roberto
Yoon, Bo Hyun
Chaemsaithong, Piya
Cortez, Josef
Park, Chan-Wook
Gonzalez, Rogelio
Behnke, Ernesto
Hassan, Sonia S.
Chaiworapongsa, Tinnakorn
Yeo, Lami
TI Bacteria and endotoxin in meconium-stained amniotic fluid at term: could
intra-amniotic infection cause meconium passage?
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE Amniotic fluid glucose; white blood cell; fetal bowel function; fetal
defecation; fetal diarrhea; interleukin-6; intrauterine
inflammation/infection; Limulus amebocyte lysate (LAL)
ID PRETERM PREMATURE RUPTURE; TUMOR-NECROSIS-FACTOR; IN-UTERO DEFECATION;
POLYMERASE-CHAIN-REACTION; ACID-BASE STATUS; ACTIVATING PEPTIDE-1
INTERLEUKIN-8; SYSTEMIC INFLAMMATORY RESPONSE; HUMAN PRENATAL
DEVELOPMENT; DELIVERY ROOM MANAGEMENT; DRUG-DEPENDENT MOTHERS
AB Background: Meconium-stained amniotic fluid (MSAF) is a common occurrence among women in spontaneous labor at term, and has been associated with adverse outcomes in both mother and neonate. MSAF is a risk factor for microbial invasion of the amniotic cavity (MIAC) and preterm birth among women with preterm labor and intact membranes. We now report the frequency of MIAC and the presence of bacterial endotoxin in the amniotic fluid of patients with MSAF at term.
Materials and methods: We conducted a cross-sectional study including women in presumed preterm labor because of uncertain dates who underwent amniocentesis, and were later determined to be at term (n = 108). Patients were allocated into two groups: (1) MSAF (n = 66) and (2) clear amniotic fluid (n = 42). The presence of bacteria was determined by microbiologic techniques, and endotoxin was detected using the Limulus amebocyte lysate (LAL) gel clot assay. Statistical analyses were performed to test for normality and bivariate comparisons.
Results: Bacteria were more frequently present in patients with MSAF compared to those with clear amniotic fluid [19.6% (13/66) versus 4.7% (2/42); p<0.05]. The microorganisms were Gram-negative rods (n = 7), Ureaplasma urealyticum (n = 4), Gram-positive rods (n = 2) and Mycoplasma hominis (n = 1). The LAL gel clot assay was positive in 46.9% (31/66) of patients with MSAF, and in 4.7% (2/42) of those with clear amniotic fluid (p < 0.001). After heat treatment, the frequency of a positive LAL gel clot assay remained higher in the MSAF group [18.1% (12/66) versus 2.3% (1/42), p<0.05]. Median amniotic fluid IL-6 concentration (ng/mL) was higher [1.3 (0.7-1.9) versus 0.6 (0.3-1.2), p=0.04], and median amniotic fluid glucose concentration (mg/dL) was lower [6 (0-8.9) versus 9 (7.4-12.6), p<0.001] in the MSAF group, than in those with clear amniotic fluid.
Conclusion: MSAF at term was associated with an increased incidence of MIAC. The index of suspicion for an infection-related process in postpartum women and their neonates should be increased in the presence of MSAF.
C1 [Romero, Roberto; Yoon, Bo Hyun; Chaemsaithong, Piya; Cortez, Josef; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn; Yeo, Lami] NICHD, Perinatol Res Branch, NIH, DHHS, Bethesda, MD USA.
[Romero, Roberto; Yoon, Bo Hyun; Chaemsaithong, Piya; Cortez, Josef; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn; Yeo, Lami] NICHD, Perinatol Res Branch, NIH, DHHS, Detroit, MI USA.
[Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Yoon, Bo Hyun; Park, Chan-Wook] Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, Seoul, South Korea.
[Chaemsaithong, Piya; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn; Yeo, Lami] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
[Cortez, Josef] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Gonzalez, Rogelio] Pontificia Univ Catolica Chile, Ctr Perinatal Diag & Res CEDIP, Hosp Dr Sotero del Rio, Puente Alto, Chile.
[Behnke, Ernesto] Hosp Dr Sotero del Rio, Dept Obstet & Gynecol, Ctr Perinatal Diag & Res CEDIP, Santiago, Chile.
RP Romero, R (reprint author), Wayne State Univ, Perinatol Res Branch, NICHD, NIH,DHHS,Hutzel Womens Hosp, 3990 John R,Box 4, Detroit, MI 48201 USA.
EM romeror@mail.nih.gov
FU Walter Scott Foundation for Medical Research; Perinatology Research
Branch, Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health, Department of Health and Human Services (NICHD/NIH); NICHD/NIH
[HHSN275201300006C]
FX This research was supported, in part, by a grant from the Walter Scott
Foundation for Medical Research and by the Perinatology Research Branch,
Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health, Department of Health and Human Services (NICHD/NIH); and in
part, with Federal funds from NICHD/NIH under Contract No.
HHSN275201300006C.
NR 272
TC 8
Z9 8
U1 0
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1476-7058
EI 1476-4954
J9 J MATERN-FETAL NEO M
JI J. Matern.-Fetal Neonatal Med.
PD MAY
PY 2014
VL 27
IS 8
BP 775
EP 788
DI 10.3109/14767058.2013.844124
PG 14
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AF5FG
UT WOS:000334738800003
PM 24028637
ER
PT J
AU Wan, RQ
Weigand, LA
Bateman, R
Griffioen, K
Mendelowitz, D
Mattson, MP
AF Wan, Ruiqian
Weigand, Letitia A.
Bateman, Ryan
Griffioen, Kathleen
Mendelowitz, David
Mattson, Mark P.
TI Evidence that BDNF regulates heart rate by a mechanism involving
increased brainstem parasympathetic neuron excitability
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE BDNF; GABA; glutamate; nucleus ambiguus; parasympathetic; vagus nerve
ID CARDIAC VAGAL NEURONS; NEUROTROPHIC FACTOR; NUCLEUS AMBIGUUS; SYNAPTIC
PLASTICITY; DIETARY RESTRICTION; HETEROZYGOUS MICE; BLOOD-PRESSURE;
EXERCISE; RECEPTOR; TRKB
AB Autonomic control of heart rate is mediated by cardioinhibitory parasympathetic cholinergic neurons located in the brainstem and stimulatory sympathetic noradrenergic neurons. During embryonic development the survival and cholinergic phenotype of brainstem autonomic neurons is promoted by brain-derived neurotrophic factor (BDNF). We now provide evidence that BDNF regulates heart rate by a mechanism involving increased brainstem cardioinhibitory parasympathetic activity. Mice with a BDNF haploinsufficiency exhibit elevated resting heart rate, and infusion of BDNF intracerebroventricularly reduces heart rate in both wild-type and BDNF+/- mice. The atropine-induced elevation of heart rate is diminished in BDNF+/- mice and is restored by BDNF infusion, whereas the atenolol-induced decrease in heart rate is unaffected by BDNF levels, suggesting that BDNF signaling enhances parasympathetic tone which is diminished with BDNF haploinsufficiency. Whole-cell recordings from pre-motor cholinergic cardioinhibitory vagal neurons in the nucleus ambiguus indicate that BDNF haploinsufficiency reduces cardioinhibitory vagal neuron activity by increased inhibitory GABAergic and diminished excitatory glutamatergic neurotransmission to these neurons. Our findings reveal a previously unknown role for BDNF in the control of heart rate by a mechanism involving increased activation of brainstem cholinergic parasympathetic neurons
Mice with reduced BDNF levels exhibit elevated heart rate, and infusion of BDNF into the brain normalizes heart rate by a mechanism involving increased brainstem cardioinhibitory parasympathetic activity. Recordings from pre-motor cholinergic cardioinhibitory vagal neurons (CVNs) in the nucleus ambiguus indicate that BDNF increases CVN activity by increasing excitatory glutamatergic and decreasing inhibitory GABAergic neurotransmission to these neurons. Perhaps factors that increase parasympathetic tone (e.g., exercise) reduce resting heart rate, in part, by a BDNF-mediated mechanism.
C1 [Wan, Ruiqian; Griffioen, Kathleen; Mattson, Mark P.] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Weigand, Letitia A.; Bateman, Ryan; Mendelowitz, David] George Washington Univ, Dept Physiol & Pharmacol, Washington, DC 20037 USA.
[Mattson, Mark P.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM dmendel@gwu.edu; mark.mattson@nih.gov
FU National Institute on Aging Intramural Research Program; NIH [HL49965,
HL59895, HL72006]; Glenn Foundation for Medical Research
FX This research was supported by the National Institute on Aging
Intramural Research Program, by NIH grants HL49965, HL59895, and HL72006
to D. M., and by a grant to M. P. M. from the Glenn Foundation for
Medical Research. The authors declare that they have no conflicts of
interest.
NR 48
TC 12
Z9 12
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD MAY
PY 2014
VL 129
IS 4
BP 573
EP 580
DI 10.1111/jnc.12656
PG 8
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AF4RC
UT WOS:000334700600002
PM 24475741
ER
PT J
AU Traynor, BJ
AF Traynor, Bryan J.
TI A roadmap for genetic testing in ALS
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Editorial Material
ID HEXANUCLEOTIDE REPEAT EXPANSION; AMYOTROPHIC-LATERAL-SCLEROSIS; C9ORF72;
FTD
C1 NIA, Neuromuscular Dis Res Unit, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Traynor, BJ (reprint author), NIA, Neuromuscular Dis Res Unit, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
EM traynorb@mail.nih.gov
FU Intramural NIH HHS [ZIA AG000933-02]; NIA NIH HHS [Z01-AG000949-02, Z01
AG000949]
NR 6
TC 2
Z9 2
U1 0
U2 2
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
EI 1468-330X
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD MAY
PY 2014
VL 85
IS 5
BP 476
EP 476
DI 10.1136/jnnp-2013-305726
PG 1
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA AF3NA
UT WOS:000334617800004
PM 23868946
ER
PT J
AU Tucci, A
Liu, YT
Preza, E
Pitceathly, RDS
Chalasani, A
Plagnol, V
Land, JM
Trabzuni, D
Ryten, M
Jaunmuktane, Z
Reilly, MM
Brandner, S
Hargreaves, I
Hardy, J
Singleton, AB
Abramov, AY
Houlden, H
AF Tucci, Arianna
Liu, Yo-Tsen
Preza, Elisabeth
Pitceathly, Robert D. S.
Chalasani, Annapurna
Plagnol, Vincent
Land, John M.
Trabzuni, Daniah
Ryten, Mina
Jaunmuktane, Zane
Reilly, Mary M.
Brandner, Sebastian
Hargreaves, Iain
Hardy, John
Singleton, Andrew B.
Abramov, Andrey Y.
Houlden, Henry
CA UKBEC
TI Novel C12orf65 mutations in patients with axonal neuropathy and optic
atrophy
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Article
ID MARIE-TOOTH DISEASE; SENSORY NEUROPATHY; HEREDITARY MOTOR; PERIPHERAL
NEUROPATHY; EXPRESSION; BRAIN; C12ORF65; DONATION; OPA1; VI
AB Objective Charcot-Marie Tooth disease (CMT) forms a clinically and genetically heterogeneous group of disorders. Although a number of disease genes have been identified for CMT, the gene discovery for some complex form of CMT has lagged behind. The association of neuropathy and optic atrophy (also known as CMT type 6) has been described with autosomaldominant, recessive and X-linked modes of inheritance. Mutations in Mitofusin 2 have been found to cause dominant forms of CMT6. Phosphoribosylpyrophosphate synthetase-I mutations cause X-linked CMT6, but until now, mutations in the recessive forms of disease have never been identified.
Methods We here describe a family with three affected individuals who inherited in an autosomal recessive fashion a childhood onset neuropathy and optic atrophy. Using homozygosity mapping in the family and exome sequencing in two affected individuals we identified a novel protein-truncating mutation in the C12orf65 gene, which encodes for a protein involved in mitochondrial translation. Using a variety of methods we investigated the possibility of mitochondrial impairment in the patients cell lines.
Results We described a large consanguineous family with neuropathy and optic atrophy carrying a loss of function mutation in the C12orf65 gene. We report mitochondrial impairment in the patients cell lines, followed by multiple lines of evidence which include decrease of complex V activity and stability (blue native gel assay), decrease in mitochondrial respiration rate and reduction of mitochondrial membrane potential.
Conclusions This work describes a mutation in the C12orf65 gene that causes recessive form of CMT6 and confirms the role of mitochondrial dysfunction in this complex axonal neuropathy.
C1 [Tucci, Arianna; Liu, Yo-Tsen; Preza, Elisabeth; Pitceathly, Robert D. S.; Trabzuni, Daniah; Ryten, Mina; Reilly, Mary M.; Hardy, John; Abramov, Andrey Y.; Houlden, Henry] UCL Inst Neurol, Dept Mol Neurosci, London, England.
[Tucci, Arianna; Liu, Yo-Tsen; Preza, Elisabeth; Pitceathly, Robert D. S.; Trabzuni, Daniah; Ryten, Mina; Reilly, Mary M.; Hardy, John; Abramov, Andrey Y.; Houlden, Henry] UCL Inst Neurol, Reta Lila Weston Res Labs, London, England.
[Tucci, Arianna; Liu, Yo-Tsen; Preza, Elisabeth; Pitceathly, Robert D. S.; Chalasani, Annapurna; Land, John M.; Trabzuni, Daniah; Ryten, Mina; Reilly, Mary M.; Hargreaves, Iain; Hardy, John; Abramov, Andrey Y.; Houlden, Henry] Natl Hosp Neurol & Neurosurg, London WC1N 3BG, England.
[Liu, Yo-Tsen; Pitceathly, Robert D. S.; Reilly, Mary M.; Houlden, Henry] UCL Inst Neurol, MRC Ctr Neuromuscular Dis, London, England.
[Liu, Yo-Tsen] Taipei Vet Gen Hosp, Sect Epilepsy, Dept Neurol, Neurol Inst, Taipei, Taiwan.
[Liu, Yo-Tsen] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan.
[Chalasani, Annapurna; Land, John M.; Hargreaves, Iain] UCL Inst Neurol, Neurometab Unit, London, England.
[Plagnol, Vincent] UGI, London, England.
[Trabzuni, Daniah] King Faisal Specialist Hosp & Res Ctr, Dept Genet, Riyadh 11211, Saudi Arabia.
[Jaunmuktane, Zane; Brandner, Sebastian] Natl Hosp Neurol & Neurosurg, Div Neuropathol, London WC1N 3BG, England.
[Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Houlden, H (reprint author), UCL, Inst Neurol, Dept Mol Neurosci, Queen Sq, London WC1N 3BG, England.
EM h.houlden@ion.ucl.ac.uk
RI Hardy, John/C-2451-2009; Houlden, Henry/C-1532-2008; Singleton,
Andrew/C-3010-2009; Abramov, Andrey/H-9053-2012; Trabzuni,
Daniah/C-4034-2012;
OI Houlden, Henry/0000-0002-2866-7777; Abramov, Andrey/0000-0002-7646-7235;
Trabzuni, Daniah/0000-0003-4826-9570; Plagnol,
Vincent/0000-0002-5597-9215
FU Wellcome Trust/MRC Joint Call in Neurodegeneration award [WT089698];
NORD; Dystonia Medical Research Foundation (DMRF); Brain Research Trust
(BRT); National Institute for Health Research (NIHR) UCLH/UCL
Comprehensive Biomedical Research Centre; MRC through the MRC Sudden
Death Brain Bank; National Institute of Neurological Disorders and
Stroke (National Brain and Tissue Resource for Parkinson's Disease and
Related Disorders) [U24 NS072026]; National Institute on Aging (Arizona
Alzheimer's Disease Core Center) [P30 AG19610]; Arizona Department of
Health Services [211002]; Arizona Biomedical Research Commission [4001,
0011, 05-901, 1001]; Michael J. Fox Foundation for Parkinson's Research;
[G0901254]; [G0802462]
FX This work was supported in part by the Wellcome Trust/MRC Joint Call in
Neurodegeneration award (WT089698) to the UK Parkinson's Disease
Consortium (UKPDC) whose members are from the UCL/Institute of
Neurology, the University of Sheffield and the MRC Protein
Phosphorylation Unit at the University of Dundee. This study was also
supported by NORD, The Dystonia Medical Research Foundation (DMRF), The
Brain Research Trust (BRT) and the National Institute for Health
Research (NIHR) UCLH/UCL Comprehensive Biomedical Research Centre.
Expression data were provided by the UK Human Brain Expression
Consortium (UKBEC), which comprises John A. Hardy, Mina Ryten, Daniah
Trabzuni, Michael Weale, Adaikalavan Ramasamy and Colin Smith. UKBEC
members are affiliated with the UCL Institute of Neurology (JAH, MR, and
DT), King's College London (MW and AR) and the University of Edinburgh
(CS). This work was supported by the MRC through the MRC Sudden Death
Brain Bank (CS) and by a Project Grant (G0901254 to JH and MW) and
Training Fellowship (G0802462 to MR). The Brain and Body Donation
Program is supported by the National Institute of Neurological Disorders
and Stroke (U24 NS072026 National Brain and Tissue Resource for
Parkinson's Disease and Related Disorders), the National Institute on
Aging (P30 AG19610 Arizona Alzheimer's Disease Core Center), the Arizona
Department of Health Services (contract 211002, Arizona Alzheimer's
Research Center), the Arizona Biomedical Research Commission (contracts
4001, 0011, 05-901 and 1001 to the Arizona Parkinson's Disease
Consortium) and the Michael J. Fox Foundation for Parkinson's Research.
NR 26
TC 9
Z9 9
U1 0
U2 6
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
EI 1468-330X
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD MAY
PY 2014
VL 85
IS 5
BP 486
EP 492
DI 10.1136/jnnp-2013-306387
PG 7
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA AF3NA
UT WOS:000334617800007
PM 24198383
ER
PT J
AU Hiranita, T
Wilkinson, DS
Hong, WMC
Zou, MF
Kopajtic, TA
Soto, PL
Lupica, CR
Newman, AH
Katz, JL
AF Hiranita, Takato
Wilkinson, Derek S.
Hong, Weimin C.
Zou, Mu-Fa
Kopajtic, Theresa A.
Soto, Paul L.
Lupica, Carl R.
Newman, Amy H.
Katz, Jonathan L.
TI 2-Isoxazol-3-Phenyltropane Derivatives of Cocaine: Molecular and
Atypical System Effects at the Dopamine Transporter
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID MONOAMINE UPTAKE INHIBITORS; CANNABINOID CB1 RECEPTOR; BEHAVIORAL
PHARMACOLOGY; IN-VIVO; MESOLIMBIC DOPAMINE; BENZTROPINE ANALOGS;
LOCOMOTOR-ACTIVITY; NONHUMAN-PRIMATES; STIMULANT ACTIONS;
SQUIRREL-MONKEYS
AB The present study examined RTI-371 [3 beta-(4-methylphenyl)-2 beta[3-(4-chlorophenyl)-isoxazol-5-yl]tropane], a phenyltropane cocaine analog with effects distinct from cocaine, and assessed potential mechanisms for those effects by comparison with its constitutional isomer, RTI-336 [3b-(4-chlorophenyl)-2b-[3-(4methylphenyl)-isoxazol-5-yl]tropane]. In mice, RTI-371 was less effective than cocaine and RTI-336 in stimulating locomotion, and incompletely substituted (similar to 60% maximum at 5 minutes or 1 hour after injection) in a cocaine (10 mg/kg i.p.)/saline discrimination procedure; RTI-336 completely substituted. In contrast to RTI336, RTI-371 was not self-administered, and its pretreatment (1.0-10 mg/kg i.p.) dose-dependently decreased maximal cocaine self-administration more potently than food-maintained responding. RTI-336 pretreatment dose-dependently left-shifted the cocaine self-administration dose-effect curve. Both RTI-336 and RTI-371 displaced [H-3]WIN35,428 [[H-3](2)-3 beta-(4-fluorophenyl)-tropan-2 beta-carboxylic acid methyl ester tartrate] binding to striatal dopamine transporters (DATs) with Ki values of 10.8 and 7.81 nM, respectively, and had lower affinities at serotonin or norepinephrine transporters, or muscarinic and s receptors. The relative low affinity at these sites suggests the DAT as the primary target of RTI-371 with minimal contributions from these other targets. In biochemical assays probing the outward-facing DAT conformation, both RTI-371 and RTI-336 had effects similar to cocaine, suggesting little contribution of DAT conformation to the unique pharmacology of RTI-371. The locomotor-stimulant effects of RTI-371 (3.0-30 mg/kg i.p.) were comparable in wildtype and knockout cannabinoid CB1 receptor (CB1R) mice, indicating that previously reported CB1 allosteric effects do not decrease cocaine-like effects of RTI-371. DAT occupancy in vivo was most rapid with cocaine and least with RTI-371. The slow apparent association rate may allow compensatory actions that in turn dampen cocaine-like stimulation, and give RTI-371 its unique pharmacologic profile.
C1 [Hiranita, Takato; Wilkinson, Derek S.; Kopajtic, Theresa A.; Katz, Jonathan L.] NIDA, Psychobiol Sect, Intramural Res Program, Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
[Hong, Weimin C.] NIDA, Cellular Pathobiol Sect, Intramural Res Program, Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
[Zou, Mu-Fa; Newman, Amy H.] NIDA, Med Chem Sect, Intramural Res Program, Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
[Lupica, Carl R.] NIDA, Electrophysiol Sect, Intramural Res Program, Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
[Soto, Paul L.] Texas Tech Univ, Coll Educ, Lubbock, TX 79409 USA.
RP Katz, JL (reprint author), NIDA, Psychobiol Sect, 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
FU Intramural Research Program of the National Institutes of Health
[National Institute on Drug Abuse]
FX This work was supported by the Intramural Research Program of the
National Institutes of Health [National Institute on Drug Abuse].
NR 47
TC 5
Z9 5
U1 1
U2 6
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
EI 1521-0103
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD MAY
PY 2014
VL 349
IS 2
BP 297
EP 309
DI 10.1124/jpet.113.212738
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AF2BT
UT WOS:000334518300014
PM 24518035
ER
PT J
AU Sheehan, FT
Brochard, S
Behnam, AJ
Alter, KE
AF Sheehan, Frances T.
Brochard, Sylvain
Behnam, Abrahm J.
Alter, Katharine E.
TI Three-dimensional humeral morphologic alterations and atrophy associated
with obstetrical brachial plexus palsy
SO JOURNAL OF SHOULDER AND ELBOW SURGERY
LA English
DT Article
DE Reliability; magnetic resonance imaging; shape; retroversion; version;
inclination
ID BIRTH PALSY; HEAD RETROVERSION; GLENOHUMERAL JOINT; SHOULDER FUNCTION;
EXTERNAL ROTATION; BICIPITAL GROOVE; BASEBALL PLAYERS; GLENOID VERSION;
FOLLOW-UP; RELIABILITY
AB Background: Obstetrical brachial plexus palsy (OBPP) is a common birth injury, resulting in severe functional losses. Yet, little is known about how OBPP affects the 3-dimensional (3D) humeral morphology. Thus, the purpose of this study was to measure the 3D humeral architecture in children with unilateral OBPP.
Methods: Thirteen individuals (4 female and 9 male patients; mean age, 11.8 +/- 3.3 years; mean Mallet score, 15.1 +/- 3.0) participated in this institutional review board approved study. A 3D T1-weighted gradient-recalled echo magnetic resonance image set was acquired for both upper limbs (involved and noninvolved). Humeral size, version, and inclination were quantified from 3D humeral models derived from these images.
Results: The involved humeral head was significantly less retroverted and in declination (medial humeral head pointed anteriorly and inferiorly) relative to the noninvolved side. Osseous atrophy was present in all 3 dimensions and affected the entire humerus. The inter-rater reliability was excellent (intraclass correlation coefficient, 0.96-1.00).
Discussion: This study showed that both humeral atrophy and bone shape deformities associated with OBPP are not limited to the axial plane but are 3D phenomena. Incorporating information related to these multi-planar, 3D humeral deformities into surgical planning could potentially improve functional outcomes after surgery. The documented reduction in retroversion is an osseous adaptation, which may help maintain glenohumeral congruency by partially compensating for the internal rotation of the arm. The humeral head declination is a novel finding and may be an important factor to consider when one is developing OBPP management strategies because it has been shown to lead to significant supraspinatus inefficiencies and increased required elevation forces. (C) 2014 Journal of Shoulder and Elbow Surgery Board of Trustees.
C1 [Sheehan, Frances T.; Brochard, Sylvain; Behnam, Abrahm J.; Alter, Katharine E.] NIH, Funct & Appl Biomech Sect, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Brochard, Sylvain] Univ Hosp Brest, Dept Rehabil Med, Brest, France.
[Brochard, Sylvain] INSERM U1101, LaTIM, Brest, France.
[Behnam, Abrahm J.] Virginia Commonwealth Univ, Sch Med, Richmond, VA USA.
[Alter, Katharine E.] Mt Washington Pediat Hosp, Baltimore, MD USA.
RP Sheehan, FT (reprint author), NIH, Bldg 10,CRC Room 1-1469,10 Ctr Dr,MSC 1604, Bethesda, MD 20892 USA.
EM fsheehan@cc.nih.gov
RI sheehan, frances/B-6962-2009
FU Radiology Department, at the Clinical Center of the National Institutes
of Health
FX We thank Diane Damiano, PhD, Christopher Hollingsworth, Lindsay
Curatalo, Christopher Stanley, and Lori Ohlrich for her help and support
in the work. In addition, we thank the Radiology Department, headed by
Dr David Bluemke, at the Clinical Center of the National Institutes of
Health, for its support of this work.
NR 56
TC 6
Z9 6
U1 0
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1058-2746
J9 J SHOULDER ELB SURG
JI J. Shoulder Elbow Surg.
PD MAY
PY 2014
VL 23
IS 5
BP 708
EP 719
DI 10.1016/j.jse.2013.08.014
PG 12
WC Orthopedics; Sport Sciences; Surgery
SC Orthopedics; Sport Sciences; Surgery
GA AF5RZ
UT WOS:000334771900019
PM 24291045
ER
PT J
AU Sadowski, SM
Weisbrod, AB
Ellis, R
Patel, D
Alimchandani, M
Quezado, M
Millo, C
Venzon, DJ
Nilubol, N
Linehan, WM
Kebebew, E
AF Sadowski, Samira M.
Weisbrod, Allison B.
Ellis, Ryan
Patel, Dhaval
Alimchandani, Meghna
Quezado, Martha
Millo, Corina
Venzon, David J.
Nilubol, Naris
Linehan, W. Marston
Kebebew, Electron
TI Prospective Evaluation of the Clinical Utility of 18-Fluorodeoxyglucose
PET CT Scanning in Patients with Von Hippel-Lindaue-Associated
Pancreatic Lesions
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; CELL LUNG-CANCER; NEUROENDOCRINE TUMORS;
ENDOCRINE TUMORS; DISEASE
AB BACKGROUND: The natural history of pancreatic neuroendocrine neoplasms (PNENs) in patients with Von Hippel-Lindau (VHL) disease is poorly defined. Management of patients with PNENs is challenging because there are no reliable preoperative criteria to detect malignant lesions, and the majority of resected tumors are found to be benign. The aim of this study was to determine whether 18-fluorodeoxyglucose-positron emission tomography ((18)FDG-PET) uptake predicts growth and detects malignant VHL-associated PNENs.
STUDY DESIGN: We performed a prospective study of 197 patients with VHL-associated pancreatic lesions. Clinical and imaging characteristics were analyzed to study the associations between FDG-PET uptake, tumor growth, and the development of metastatic disease.
RESULTS: One hundred nine of 197 patients had solid pancreatic lesions and underwent both CT and (18)FDG-PET scanning, which identified 165 and 144 lesions, respectively. Metastatic disease was detected by (18)FDG-PET in 3 patients in whom it was not detected by CT scan and suggested non- neoplastic disease in 3 patients. Maximum standardized uptake values (SUV) on (18)FDG-PET correlated with tumor size on CT (r = 0.47, p < 0.0001), and an increase in SUVmax was associated with tumor growth (r = 0.36, p < 0.0062). No association was seen between (18)FDG-PET uptake and age, VHL genotype, or serum chromogranin A levels.
CONCLUSIONS: Scanning with FDG-PET identifies metastatic disease not detected by CT scan and avoids resection of non-PNEN lesions that have no malignant potential in patients with VHL-associated PNENs. It should be considered as a valuable functional imaging modality in the clinical management of patients with VHL-associated PNENs. (C) 2014 by the American College of Surgeons
C1 [Sadowski, Samira M.; Weisbrod, Allison B.; Ellis, Ryan; Patel, Dhaval; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Alimchandani, Meghna; Quezado, Martha] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Millo, Corina] NCI, Positron Emiss Tomog Dept, NIH, Bethesda, MD 20892 USA.
[Venzon, David J.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Linehan, W. Marston] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Sadowski, SM (reprint author), NCI, Endocrine Oncol Branch, NIH, Clin Res Ctr, Bldg 10 CRC,Room 3W-5840, Bethesda, MD 20892 USA.
EM samira.sadowskiveuthey@nih.gov
FU intramural research program of the Center for Cancer Research; National
Cancer Institute; National Institutes of Health
FX This research was supported by the intramural research program of the
Center for Cancer Research, National Cancer Institute, National
Institutes of Health.
NR 31
TC 5
Z9 5
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1072-7515
EI 1879-1190
J9 J AM COLL SURGEONS
JI J. Am. Coll. Surg.
PD MAY
PY 2014
VL 218
IS 5
BP 997
EP 1003
DI 10.1016/j.jamcollsurg.2014.01.004
PG 7
WC Surgery
SC Surgery
GA AF2ZS
UT WOS:000334581600016
PM 24661849
ER
PT J
AU Kayaalp, M
Browne, AC
Callaghan, FM
Dodd, ZA
Divita, G
Ozturk, S
McDonald, CJ
AF Kayaalp, Mehmet
Browne, Allen C.
Callaghan, Fiona M.
Dodd, Zeyno A.
Divita, Guy
Ozturk, Selcuk
McDonald, Clement J.
TI The pattern of name tokens in narrative clinical text and a comparison
of five systems for redacting them
SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION
LA English
DT Article
ID AUTOMATIC DE-IDENTIFICATION; MEDICAL-RECORDS; HEALTH
AB Objective To understand the factors that influence success in scrubbing personal names from narrative text.
Materials and methods We developed a scrubber, the NLM Name Scrubber (NLM-NS), to redact personal names from narrative clinical reports, hand tagged words in a set of gold standard narrative reports as personal names or not, and measured the scrubbing success of NLM-NS and that of four other scrubbing/name recognition tools (MIST, MITdeid, LingPipe, and ANNIE/GATE) against the gold standard reports. We ran three comparisons which used increasingly larger name lists.
Results The test reports contained more than 1 million words, of which 2388 were patient and 20 160 were provider name tokens. NLM-NS failed to scrub only 2 of the 2388 instances of patient name tokens. Its sensitivity was 0.999 on both patient and provider name tokens and missed fewer instances of patient name tokens in all comparisons with other scrubbers. MIST produced the best all token specificity and F-measure for name instances in our most relevant study (study 2), with values of 0.997 and 0.938, respectively. In that same comparison, NLM-NS was second best, with values of 0.986 and 0.748, respectively, and MITdeid was a close third, with values of 0.985 and 0.796 respectively. With the addition of the Clinical Center name list to their native name lists, Ling Pipe, MITdeid, MIST, and ANNIE/GATE all improved substantially. MITdeid and Ling Pipe gained the most-reaching patient name sensitivity of 0.995 (F-measure=0.705) and 0.989 (F-measure=0.386), respectively.
Discussion The privacy risk due to two name tokens missed by NLM-NS was statistically negligible, since neither individual could be distinguished among more than 150 000 people listed in the US Social Security Registry.
Conclusions The nature and size of name lists have substantial influences on scrubbing success. The use of very large name lists with frequency statistics accounts for much of NLM-NS scrubbing success.
C1 [Kayaalp, Mehmet; Browne, Allen C.; Callaghan, Fiona M.; Dodd, Zeyno A.; Divita, Guy; Ozturk, Selcuk; McDonald, Clement J.] NIH, Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD 20894 USA.
RP McDonald, CJ (reprint author), NIH, Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, 8600 Rockville Pike,Bldg 38A-Room 7N707, Bethesda, MD 20894 USA.
EM ClemMcDonald@mail.nih.gov
FU National Institutes of Health, National Library of Medicine
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Library of Medicine.
NR 25
TC 0
Z9 0
U1 0
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1067-5027
EI 1527-974X
J9 J AM MED INFORM ASSN
JI J. Am. Med. Inf. Assoc.
PD MAY
PY 2014
VL 21
IS 3
BP 423
EP 431
DI 10.1136/amiajnl-2013-001689
PG 9
WC Computer Science, Information Systems; Computer Science,
Interdisciplinary Applications; Health Care Sciences & Services;
Information Science & Library Science; Medical Informatics
SC Computer Science; Health Care Sciences & Services; Information Science &
Library Science; Medical Informatics
GA AF3KR
UT WOS:000334611600006
PM 24026308
ER
PT J
AU Goldspiel, BR
Flegel, WA
DiPatrizio, G
Sissung, T
Adams, SD
Penzak, SR
Biesecker, LG
Fleisher, TA
Patel, JJ
Herion, D
Figg, WD
Lertora, JJL
McKeeby, JW
AF Goldspiel, Barry R.
Flegel, Willy A.
DiPatrizio, Gary
Sissung, Tristan
Adams, Sharon D.
Penzak, Scott R.
Biesecker, Leslie G.
Fleisher, Thomas A.
Patel, Jharana J.
Herion, David
Figg, William D.
Lertora, Juan J. L.
McKeeby, Jon W.
TI Integrating pharmacogenetic information and clinical decision support
into the electronic health record
SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION
LA English
DT Article
ID IMPLEMENTATION CONSORTIUM GUIDELINES; THIOPURINE METHYLTRANSFERASE
GENOTYPE; HLA-B GENOTYPE; PERSONALIZED MEDICINE; HYPERSENSITIVITY;
ABACAVIR; UPDATE
AB Pharmacogenetics (PG) examines gene variations for drug disposition, response, or toxicity. At the National Institutes of Health Clinical Center (NIH CC), a multidepartment Pharmacogenetics Testing Implementation Committee (PGTIC) was established to develop clinical decision support (CDS) algorithms for abacavir, carbamazepine, and allopurinol, medications for which human leukocyte antigen (HLA) variants predict severe hypersensitivity reactions. Providing PG CDS in the electronic health record (EHR) during order entry could prevent adverse drug events. Medical Logic Module (MLM) programming was used to implement PG CDS in our EHR. The MLM checks to see if an HLA sequence-based gene test is ordered. A message regarding test status (result present, absent, pending, or test not ordered) is displayed on the order form, and the MLM determines if the prescriber can place the order, place it but require an over-ride reason, or be blocked from placing the order. Since implementation, more than 725 medication orders have been placed for over 230 patients by 154 different prescribers for the three drugs included in our PG program. Prescribers commonly used an over-ride reason when placing the order mainly because patients had been receiving the drug without reaction before implementation of the CDS program. Successful incorporation of PG CDS into the NIH CC EHR required a coordinated, interdisciplinary effort to ensure smooth activation and a positive effect on patient care. Prescribers have adapted to using the CDS and have ordered PG testing as a direct result of the implementation.
C1 [Goldspiel, Barry R.; Penzak, Scott R.; Patel, Jharana J.] NIH, Ctr Clin, Dept Pharm, Bethesda, MD 20892 USA.
[Flegel, Willy A.; Adams, Sharon D.] NIH, Ctr Clin, Dept Transfus Med, Bethesda, MD 20892 USA.
[DiPatrizio, Gary; Herion, David; McKeeby, Jon W.] NIH, Ctr Clin, Dept Clin Res Informat, Bethesda, MD 20892 USA.
[Sissung, Tristan; Figg, William D.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Biesecker, Leslie G.] NHGRI, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Fleisher, Thomas A.] NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA.
[Lertora, Juan J. L.] NIH, Ctr Clin, Clin Pharmacol Program, Bethesda, MD 20892 USA.
RP Goldspiel, BR (reprint author), NIH, Ctr Clin, Dept Pharm, Bldg 10,Room 1C240,MSC 1196, Bethesda, MD 20892 USA.
EM bgoldspiel@nih.gov
RI Figg Sr, William/M-2411-2016
NR 25
TC 16
Z9 16
U1 1
U2 17
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1067-5027
EI 1527-974X
J9 J AM MED INFORM ASSN
JI J. Am. Med. Inf. Assoc.
PD MAY
PY 2014
VL 21
IS 3
BP 522
EP 528
DI 10.1136/amiajnl-2013-001873
PG 7
WC Computer Science, Information Systems; Computer Science,
Interdisciplinary Applications; Health Care Sciences & Services;
Information Science & Library Science; Medical Informatics
SC Computer Science; Health Care Sciences & Services; Information Science &
Library Science; Medical Informatics
GA AF3KR
UT WOS:000334611600019
PM 24302286
ER
PT J
AU Hong, CW
Amalou, H
Xu, S
Turkbey, B
Yan, PK
Kruecker, J
Pinto, PA
Choyke, PL
Wood, BJ
AF Hong, Cheng William
Amalou, Hayet
Xu, Sheng
Turkbey, Bans
Yan, Pingkun
Kruecker, Jochen
Pinto, Peter A.
Choyke, Peter L.
Wood, Bradford J.
TI Prostate Biopsy for the Interventional Radiologist
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Review
ID TRANSRECTAL ULTRASOUND BIOPSY; IMPROVE CANCER-DETECTION; SYSTEMATIC
BIOPSY; ANTIGEN LEVELS; FUSION BIOPSY; TARGETED BIOPSY; NEEDLE BIOPSIES;
GLEASON SCORE; GUIDED BIOPSY; COLOR
AB Prostate biopsies are usually performed by urologists in the office setting using transrectal ultrasound (US) guidance. The current standard of care involves obtaining 10-14 Cores from different anatomic sections. Biopsies are usually not directed into a specific lesion because most prostate cancers are not visible on transrectal US. Color Doppler, US contrast agents, elastography, magnetic resonance (MR) imaging, and MR imaging/US fusion are proposed as imaging methods to guide prostate biopsies. Prostate MR imaging and fusion biopsy create opportunities for diagnostic and interventional radiologists to play an increasingly important role in the screening, evaluation, diagnosis, targeted biopsy, surveillance, and focal therapy of patients with prostate cancer.
C1 [Hong, Cheng William; Amalou, Hayet; Xu, Sheng; Yan, Pingkun; Kruecker, Jochen; Wood, Bradford J.] NCI, Ctr Intervent Oncol, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Turkbey, Bans; Choyke, Peter L.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Pinto, Peter A.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Yan, Pingkun; Kruecker, Jochen] Philips Res North Amer, Briarcliff Manor, NY USA.
RP Wood, BJ (reprint author), NCI, Ctr Intervent Oncol, Ctr Clin, NIH, 10 Ctr Dr MSC 1182, Bethesda, MD 20892 USA.
EM bwood@nih.gov
FU Center for Interventional Oncology; National Cancer Institute; National
Institutes of Health (NIH); Pfizer Inc; The Leona M. and Harry B.
Helmsley Charitable Trust; Howard Hughes Medical Institute
FX This work was supported by the Center for Interventional Oncology, the
National Cancer Institute, and the Intramural Research Program of the
National Institutes of Health (NIH). NIH and Philips Research North
America have a Cooperative Research and Development Agreement. This
research was made possible through the NIH Medical Research Scholars
Program, a public-private partnership supported jointly by the NIH and
generous contributions to the Foundation for the NIH from Pfizer Inc,
The Leona M. and Harry B. Helmsley Charitable Trust, and the Howard
Hughes Medical Institute as well as other private donors. For a complete
list, please visit the Foundation website at
http://www.fnih.org/work/programs-development/medical-research-scholars-
program. The content of this publication does not reflect the views, or
policies of the Department of Health and Human Services, and mention of
trade names, commercial products, or organizations does not imply
endorsement by the U.S. Government.
NR 60
TC 3
Z9 3
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
EI 1535-7732
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD MAY
PY 2014
VL 25
IS 5
BP 675
EP 684
DI 10.1016/j.jvir.2013.12.568
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA AF7LI
UT WOS:000334896200002
PM 24581731
ER
PT J
AU Amalou, H
Negussie, AH
Ranjan, A
Chow, L
Xu, S
Kroeger, C
Neeman, Z
O'Grady, NP
Wood, BJ
AF Amalou, Hayet
Negussie, Ayele H.
Ranjan, Ashish
Chow, Lucy
Xu, Sheng
Kroeger, Craig
Neeman, Ziv
O'Grady, Naomi P.
Wood, Bradford J.
TI Electrically Conductive Catheter Inhibits Bacterial Colonization
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID CENTRAL VENOUS CATHETERS; BLOOD-STREAM INFECTIONS; CANDIDA-ALBICANS
BIOFILMS; CSF SHUNT INFECTIONS; IN-VITRO; ESCHERICHIA-COLI;
DOUBLE-BLIND; PREVENTION; RESISTANCE; EFFICACY
AB Purpose: To design, prototype, and assess a custom vascular access catheter for its ability to inhibit bacterial colonization in vitro and to optimize electric parameters for efficacy and safe translation.
Materials and Methods: A vascular access catheter with conductive elements was designed and custom fabricated with two electrodes at the tip, separated by a nonconductive segment. The catheter was colonized with Staphylococcus aureus and incubated at predetermined current levels (4-8 mu A) and durations (4-24 h). Catheters were compared using bacterial counts and scanning electron microscopy (SEM).
Results: Bacteria colony-forming units were reduced significantly (P < .05) by > 90% (91.7%-100%) in all uninterrupted treatment arms that included electric current (4 mu A or 8 mu A) of at least 8 hours' duration. Qualitative analysis using SEM revealed that the treated catheter exposed to electric current had markedly less bacteria compared with the untreated catheter.
Conclusions: This catheter with elements inhibits bacterial colonization in vitro when very small electric current (4-8 mu A) is applied across the tip for 8-24 hours. In vivo validation is requisite to future translation to the clinical setting.
C1 [Amalou, Hayet; Negussie, Ayele H.; Ranjan, Ashish; Chow, Lucy; Xu, Sheng; Neeman, Ziv; Wood, Bradford J.] Ctr Clin, Ctr Intervent Oncol, Bethesda, MD 20892 USA.
[O'Grady, Naomi P.] NCI, Bethesda, MD 20892 USA.
[O'Grady, Naomi P.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Kroeger, Craig] VitalDyne Inc, Cokato, MN USA.
[Neeman, Ziv] Radiol Associates, Philadelphia, PA USA.
RP Wood, BJ (reprint author), Ctr Clin, Ctr Intervent Oncol, Bldg 10,MSC 1182, Bethesda, MD 20892 USA.
EM bwood@nih.gov
FU Intramural Research Program of the National Institutes of Health (NIH);
NIH Center for Interventional Oncology; NIH [Z1A CL040015-04 DRD]
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health (NIH), NIH Center for Interventional
Oncology, and NIH Grant No. Z1A CL040015-04 DRD. The NIH and VitalDyne,
Inc, may have intellectual property in the field.
NR 35
TC 1
Z9 1
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
EI 1535-7732
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD MAY
PY 2014
VL 25
IS 5
BP 797
EP 802
DI 10.1016/j.jvir.2014.01.032
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA AF7LI
UT WOS:000334896200019
PM 24745908
ER
PT J
AU Evans, LH
Boi, S
Malik, F
Wehrly, K
Peterson, KE
Chesebro, B
AF Evans, Leonard H.
Boi, Stefano
Malik, Frank
Wehrly, Kathy
Peterson, Karin E.
Chesebro, Bruce
TI Analysis of two monoclonal antibodies reactive with envelope proteins of
murine retroviruses: One pan specific antibody and one specific for
Moloney leukemia virus
SO JOURNAL OF VIROLOGICAL METHODS
LA English
DT Article
DE Monoclonal antibodies; Retroviruses; Env protein; Moloney MuLV;
Amphotropic MuLV
ID FOCUS-FORMING VIRUSES; CELL-LINES; GENE-TRANSFER; ERYTHROLEUKEMIA-CELLS;
POLYTROPIC MULVS; SU PROTEIN; C-VIRUS; FRIEND; MICE; RECOMBINANT
AB Many monoclonal antibodies (MAbs) reactive with various proteins of murine leukemia viruses (MuLVs) have been developed. In this report two additional MAbs with differing and unusual specificities are described. MAb 573 is reactive with the envelope protein of all MuLVs tested including viruses in the ecotropic, xenotropic, polytropic and amphotropic classes. Notably, MAb 573 is one of only two reported MAbs that react with the envelope protein of amphotropic MuLVs. This MAb appears to recognize a conformational epitope within the envelope protein, as it reacts strongly with live virus and live infected cells, but does not react with formalin-fixed or alcohol-fixed infected cells or denatured viral envelope protein in immunoblots. In contrast, Mab 538 reacts only with an epitope unique to the envelope protein of the Moloney (Mo-) strain of MuLV, a prototypic ecotropic MuLV that is the basis for many retroviral tools used in molecular biology. MAb 538 can react with live cells and viruses, or detergent denatured or fixed envelope protein. The derivation of these antibodies as well as their characterization with regard to their isotype, range of reactivity with different MuLVs and utility in different immunological procedures are described in this study. Published by Elsevier B.V.
C1 [Evans, Leonard H.; Boi, Stefano; Malik, Frank; Wehrly, Kathy; Peterson, Karin E.; Chesebro, Bruce] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT 59840 USA.
[Boi, Stefano] Univ Cagliari, Dept Biomed Sci, I-09042 Monserrato, CA, Italy.
RP Evans, LH (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT 59840 USA.
EM levans@niaid.nih.gov
RI Peterson, Karin/D-1492-2016
OI Peterson, Karin/0000-0003-4177-7249
FU NIH, NIAID; Department of Biomedical Sciences, University of Cagliari,
Monserrato (CA), Italy
FX This research was supported by the Intramural Research Program of the
NIH, NIAID and the Department of Biomedical Sciences, University of
Cagliari, 09042 Monserrato (CA), Italy. The authors wish to think
Rebecca Linwood, Sue Priola, and Kim Hasenkrug for helpful discussions
and Aaron Carmody for flow cytometic analysis.
NR 53
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-0934
EI 1879-0984
J9 J VIROL METHODS
JI J. Virol. Methods
PD MAY
PY 2014
VL 200
BP 47
EP 53
DI 10.1016/j.jviromet.2014.02.006
PG 7
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Virology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Virology
GA AF8QX
UT WOS:000334981800009
PM 24556162
ER
PT J
AU Cogger, VC
Mitchell, SJ
Warren, A
de Cabo, R
Le Couteur, DG
AF Cogger, Victoria C.
Mitchell, Sarah J.
Warren, Alessandra
de Cabo, Rafael
Le Couteur, David G.
TI Age-Related Loss of Responsiveness to 2,5-Dimethoxy-4-Iodoamphetamine in
Liver Sinusoidal Endothelial Cells
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Liver endothelium; Fenestrations; 2,5-Dimethoxy-4-iodoamphetamine
ID GROWTH-FACTOR; RAT-LIVER; PARTIAL-HEPATECTOMY; SIEVE;
PSEUDOCAPILLARIZATION; INCREASES; FENESTRATIONS; PERMEABILITY;
REGENERATION; FAILURE
AB Age-related pseudocapillarization of the liver sinusoidal endothelium is associated with impaired lipid and drug metabolism and the development of disease. 2,5-Dimethoxy-4-iodoamphetamine is a serotonin receptor 2 agonist that has been shown to have beneficial effects on the liver sinusoidal endothelium in the setting of partial hepatectomy. Here, we have assessed whether 2,5-dimethoxy-4-iodoamphetamine influences ultrastructure of the sinusoidal endothelium in normal 7-and 24-month-old C57Bl6 mice. Following 48 hours of 2,5-dimethoxy-4-iodoamphetamine administration, we found that the liver endothelium in the young, but not in the old, mice had increased porosity compared with controls. This effect appeared to be modulated by increased fenestration size rather than a change in fenestration number. 2,5-Dimethoxy-4-iodoamphetamine is a useful manipulator of fenestration size in the young liver and could be harnessed in the search for therapeutic interventions for pseudocapillarization.
C1 [Cogger, Victoria C.; Warren, Alessandra; Le Couteur, David G.] Concord Hosp, ANZAC Res Inst, Concord, NSW, Australia.
[Cogger, Victoria C.; Warren, Alessandra; Le Couteur, David G.] Univ Sydney, Sydney, NSW 2006, Australia.
[Cogger, Victoria C.; Warren, Alessandra; Le Couteur, David G.] Univ Sydney, Charles Perkins Ctr, Sydney, NSW 2006, Australia.
[Mitchell, Sarah J.; de Cabo, Rafael] NIA, Expt Gerontol Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Mitchell, Sarah J.] Univ Sydney, Kolling Res Inst, Sydney, NSW 2006, Australia.
[Mitchell, Sarah J.] Royal N Shore Hosp, Sydney, NSW, Australia.
RP Cogger, VC (reprint author), ANZAC Res Inst, Gate 3 Hosp Rd Concord RG Hosp, Concord, NSW 2139, Australia.
EM victoria.cogger@sydney.edu.au
RI de Cabo, Rafael/J-5230-2016;
OI de Cabo, Rafael/0000-0002-3354-2442; , rafael/0000-0003-2830-5693
FU National Institutes of Aging, National Institutes of Health; Ageing and
Alzheimer's Research Fund of the Concord Hospital; National Medical
Health and Research Council of Australia [RGMS ID 2010-01671]
FX This study was supported in part by the Intramural Research Program of
the National Institutes of Aging, National Institutes of Health, and the
Ageing and Alzheimer's Research Fund of the Concord Hospital. National
Medical Health and Research Council of Australia CJ Martin Early Career
Fellowship (RGMS ID 2010-01671 to S.J.M.).
NR 27
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 514
EP 518
DI 10.1093/gerona/glt124
PG 5
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000003
PM 23974079
ER
PT J
AU Elbers, CC
Garcia, ME
Kimura, M
Cummings, SR
Nalls, MA
Newman, AB
Park, V
Sanders, JL
Tranah, GJ
Tishkoff, SA
Harris, TB
Aviv, A
AF Elbers, Clara C.
Garcia, Melissa E.
Kimura, Masayuki
Cummings, Steven R.
Nalls, Mike A.
Newman, Anne B.
Park, Vicki
Sanders, Jason L.
Tranah, Gregory J.
Tishkoff, Sarah A.
Harris, Tamara B.
Aviv, Abraham
TI Comparison Between Southern Blots and qPCR Analysis of Leukocyte
Telomere Length in the Health ABC Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Leukocyte telomere length; Quantitative PCR; Southern blots
ID POPULATION-BASED COHORT; BODY-COMPOSITION; ASSOCIATION; HUMANS; ADULTS
AB Only a few studies, primarily limited to small samples, have examined the relationship between leukocyte telomere length (LTL) data generated by Southern blots, expressed in kilobases, versus quantitative PCR data, expressed in the telomere product/a single gene product (T/S). In the present study, we compared LTL data generated by the two methods in 681 elderly participants (50% African Americans, 50% of European origin, 49.2% women, mean age 73.72.9 years) in the Health Aging and Body Composition Study. The correlation between the data generated by the two methods was modest (R-2 .27). Both methods captured the age effect on LTL and the longer LTL in women than in men. However, only the Southern blot method showed a significantly longer LTL in African Americans than in European decent individuals, which might be attributed to the larger measurement error of the quantitative PCRbased method than the Southern blots.
C1 [Elbers, Clara C.; Tishkoff, Sarah A.] Univ Penn, Dept Biol & Genet, Philadelphia, PA 19104 USA.
[Garcia, Melissa E.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Kimura, Masayuki; Aviv, Abraham] Rutgers, New Jersey Med Sch, Ctr Human Dev & Aging, Newark, NJ USA.
[Nalls, Mike A.] NIA, Neurogenet Lab, Intramural Res Program, Bethesda, MD 20892 USA.
[Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Grad Sch Publ Hlth, Pittsburgh, PA 15260 USA.
[Newman, Anne B.; Sanders, Jason L.] Univ Pittsburgh, Dept Med, Sch Med, Pittsburgh, PA 15260 USA.
[Park, Vicki] Univ Tennessee, Ctr Hlth Sci, Dept Pediat, Memphis, TN 38163 USA.
[Park, Vicki] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[Sanders, Jason L.] Univ Pittsburgh, Sch Med, Med Scientist Training Program, Pittsburgh, PA 15260 USA.
[Tranah, Gregory J.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
RP Elbers, CC (reprint author), Univ Penn, Dept Biol & Genet, Philadelphia, PA 19104 USA.
EM celbers@mail.med.upenn.edu
RI Newman, Anne B./C-6408-2013
OI Newman, Anne B./0000-0002-0106-1150
FU Netherlands Organization for Scientific Research (NWO); NIH
[R01AG030678, R01HD071180]
FX CCE was supported by a Rubicon grant from the Netherlands Organization
for Scientific Research (NWO). AA's NIH research support for this work
includes R01AG030678 and R01HD071180.
NR 20
TC 20
Z9 20
U1 2
U2 14
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 527
EP 531
DI 10.1093/gerona/glt121
PG 5
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000005
PM 23946336
ER
PT J
AU Cai, H
Daimon, CM
Cong, WN
Wang, R
Chirdon, P
de Cabo, R
Sevigny, J
Maudsley, S
Martin, B
AF Cai, Huan
Daimon, Caitlin M.
Cong, Wei-na
Wang, Rui
Chirdon, Patrick
de Cabo, Rafael
Sevigny, Jean
Maudsley, Stuart
Martin, Bronwen
TI Longitudinal Analysis of Calorie Restriction on Rat Taste Bud Morphology
and Expression of Sweet Taste Modulators
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Taste buds; Sweet taste; Calorie restriction; T1r3; Aging
ID DIETARY ENERGY-INTAKE; CIRCUMVALLATE PAPILLAE; WEIGHT-LOSS; FOOD
CRAVINGS; CATALYTIC PROPERTIES; OXIDATIVE STRESS; ALPHA-GUSTDUCIN; UMAMI
TASTE; LIFE-SPAN; FAT DIET
AB Calorie restriction (CR) is a lifestyle intervention employed to reduce body weight and improve metabolic functions primarily via reduction of ingested carbohydrates and fats. Taste perception is highly related to functional metabolic status and body adiposity. We have previously shown that sweet taste perception diminishes with age; however, relatively little is known about the effects of various lengths of CR upon taste cell morphology and function. We investigated the effects of CR on taste bud morphology and expression of sweet tasterelated modulators in 5-, 17-, and 30-month-old rats. In ad libitum (AL) and CR rats, we consistently found the following parameters altered significantly with advancing age: reduction of taste bud size and taste cell numbers per taste bud and reduced expression of sonic hedgehog, type 1 taste receptor 3 (T1r3), -gustducin, and glucagon-like peptide-1 (GLP-1). In the oldest rats, CR affected a significant reduction of tongue T1r3, GLP-1, and -gustducin expression compared with age-matched AL rats. Leptin receptor immunopositive cells were elevated in 17- and 30-month-old CR rats compared with age-matched AL rats. These alterations of sweet tasterelated modulators, specifically during advanced aging, suggest that sweet taste perception may be altered in response to different lengths of CR.
C1 [Cai, Huan; Daimon, Caitlin M.; Cong, Wei-na; Wang, Rui; Chirdon, Patrick; Martin, Bronwen] NIA, Metab Unit, Clin Invest Lab, NIH, Baltimore, MD 21224 USA.
[de Cabo, Rafael] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Sevigny, Jean] CHU Quebec, Ctr Rech, Ctr Rech Rhumatol & Immunol, Quebec City, PQ, Canada.
[Sevigny, Jean] Univ Laval, Fac Med, Dept Microbiol Infectiol & Immunol, Quebec City, PQ G1K 7P4, Canada.
[Maudsley, Stuart] NIA, Receptor Pharmacol Unit, Neurosci Lab, NIH, Baltimore, MD 21224 USA.
RP Martin, B (reprint author), NIA, Metab Unit, Clin Invest Lab, NIH, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM martinbro@mail.nih.gov
RI Cai, Huan/B-6578-2016; de Cabo, Rafael/J-5230-2016;
OI Cai, Huan/0000-0001-7731-8891; de Cabo, Rafael/0000-0002-3354-2442;
Sevigny, Jean/0000-0003-2922-1600; , rafael/0000-0003-2830-5693
FU National Institute on Aging, National Institutes of Health [AG000916-01]
FX This work was supported entirely by the Intramural Research Program of
the National Institute on Aging, National Institutes of Health
(AG000916-01).
NR 77
TC 5
Z9 5
U1 2
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 532
EP 544
DI 10.1093/gerona/glt129
PG 13
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000006
PM 24077597
ER
PT J
AU Studenski, SA
Peters, KW
Alley, DE
Cawthon, PM
McLean, RR
Harris, TB
Ferrucci, L
Guralnik, JM
Fragala, MS
Kenny, AM
Kiel, DP
Kritchevsky, SB
Shardell, MD
Dam, TTL
Vassileva, MT
AF Studenski, Stephanie A.
Peters, Katherine W.
Alley, Dawn E.
Cawthon, Peggy M.
McLean, Robert R.
Harris, Tamara B.
Ferrucci, Luigi
Guralnik, Jack M.
Fragala, Maren S.
Kenny, Anne M.
Kiel, Douglas P.
Kritchevsky, Stephen B.
Shardell, Michelle D.
Dam, Thuy-Tien L.
Vassileva, Maria T.
TI The FNIH Sarcopenia Project: Rationale, Study Description, Conference
Recommendations, and Final Estimates
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Aging; Sarcopenia; Muscle; Outcomes; Weakness
ID LOWER-EXTREMITY FUNCTION; BONE-MINERAL DENSITY; LEG MUSCLE MASS;
BODY-COMPOSITION; GAIT SPEED; OSTEOPOROTIC FRACTURES; PHYSICAL
PERFORMANCE; OLDER-ADULTS; WHITE WOMEN; STRENGTH
AB Low muscle mass and weakness are common and potentially disabling in older adults, but in order to become recognized as a clinical condition, criteria for diagnosis should be based on clinically relevant thresholds and independently validated. The Foundation for the National Institutes of Health Biomarkers Consortium Sarcopenia Project used an evidence-based approach to develop these criteria. Initial findings were presented at a conference in May 2012, which generated recommendations that guided additional analyses to determine final recommended criteria. Details of the Project and its findings are presented in four accompanying manuscripts.
The Foundation for the National Institutes of Health Sarcopenia Project used data from nine sources of community-dwelling older persons: Age, Gene/Environment Susceptibility-Reykjavik Study, Boston Puerto Rican Health Study, a series of six clinical trials, Framingham Heart Study, Health, Aging, and Body Composition, Invecchiare in Chianti, Osteoporotic Fractures in Men Study, Rancho Bernardo Study, and Study of Osteoporotic Fractures. Feedback from conference attendees was obtained via surveys and breakout groups.
The pooled sample included 26,625 participants (57% women, mean age in men 75.2 [6.1 SD] and in women 78.6 [5.9] years). Conference attendees emphasized the importance of evaluating the influence of body mass on cutpoints. Based on the analyses presented in this series, the final recommended cutpoints for weakness are grip strength < 26kg for men and < 16kg for women, and for low lean mass, appendicular lean mass adjusted for body mass index < 0.789 for men and < 0.512 for women.
These evidence-based cutpoints, based on a large and diverse population, may help identify participants for clinical trials and should be evaluated among populations with high rates of functional limitations.
C1 [Studenski, Stephanie A.] Univ Pittsburgh, Dept Internal Med, Sch Med, Pittsburgh, PA 15260 USA.
[Peters, Katherine W.; Cawthon, Peggy M.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Alley, Dawn E.; Guralnik, Jack M.; Shardell, Michelle D.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[McLean, Robert R.; Kiel, Douglas P.] Hebrew Senior Life, Inst Aging Res, Boston, MA USA.
[McLean, Robert R.; Kiel, Douglas P.] Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Med, Sch Med, Boston, MA 02215 USA.
[Harris, Tamara B.; Ferrucci, Luigi] NIA, Intramural Res Program, NIH, Baltimore, MD 21225 USA.
[Fragala, Maren S.] Univ Cent Florida, Coll Educ & Human Performance, Orlando, FL 32816 USA.
[Kenny, Anne M.] Univ Connecticut, Ctr Hlth, Ctr Aging, Farmington, CT USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Sch Med, Sticht Ctr Aging, Winston Salem, NC 27109 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Sch Med, Dept Internal Med, Winston Salem, NC 27109 USA.
[Dam, Thuy-Tien L.] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Vassileva, Maria T.] Fdn Natl Inst Hlth, Biomarkers Consortium, Bethesda, MD USA.
RP Studenski, SA (reprint author), NIA, Baltimore Longitudinal Study Aging, 3001 S Hanover St,Fifth Floor, Baltimore, MD 21225 USA.
EM studenskisa@mail.nih.gov
OI Kiel, Douglas/0000-0001-8474-0310
FU National Institute on Aging [1U13AG041583, P30 AG024827]; Food and Drug
Administration; Foundation for the National Institutes of Health; Abbott
Nutrition; Amgen; Eli Lilly; Merck; Novartis; Dairy Research Institute
FX Funding support for the conference and the work of the consortium was
provided by the National Institute on Aging (1U13AG041583 and P30
AG024827), the Food and Drug Administration, and through grants from the
Foundation for the National Institutes of Health, made possible by
funding from Abbott Nutrition, Amgen, Eli Lilly, Merck, Novartis, and
The Dairy Research Institute.
NR 40
TC 155
Z9 156
U1 4
U2 23
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 547
EP 558
DI 10.1093/gerona/glu010
PG 12
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000007
PM 24737557
ER
PT J
AU Alley, DE
Shardell, MD
Peters, KW
McLean, RR
Dam, TTL
Kenny, AM
Fragala, MS
Harris, TB
Kiel, DP
Guralnik, JM
Ferrucci, L
Kritchevsky, SB
Studenski, SA
Vassileva, MT
Cawthon, PM
AF Alley, Dawn E.
Shardell, Michelle D.
Peters, Katherine W.
McLean, Robert R.
Dam, Thuy-Tien L.
Kenny, Anne M.
Fragala, Maren S.
Harris, Tamara B.
Kiel, Douglas P.
Guralnik, Jack M.
Ferrucci, Luigi
Kritchevsky, Stephen B.
Studenski, Stephanie A.
Vassileva, Maria T.
Cawthon, Peggy M.
TI Grip Strength Cutpoints for the Identification of Clinically Relevant
Weakness
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Muscle; Sarcopenia; Grip strength; Physical function; Gait speed
ID BONE-MINERAL DENSITY; OLDER-ADULTS; MUSCLE STRENGTH; PHYSICAL
PERFORMANCE; BODY-COMPOSITION; WOMENS HEALTH; WHITE WOMEN; MOBILITY;
INCHIANTI; RISK
AB Weakness is common and contributes to disability, but no consensus exists regarding a strength cutpoint to identify persons at high risk. This analysis, conducted as part of the Foundation for the National Institutes of Health Sarcopenia Project, sought to identify cutpoints that distinguish weakness associated with mobility impairment, defined as gait speed less than 0.8 m/s.
In pooled cross-sectional data (9,897 men and 10,950 women), Classification and Regression Tree analysis was used to derive cutpoints for grip strength associated with mobility impairment.
In men, a grip strength of 2632 kg was classified as intermediate and less than 26 kg as weak; 11% of men were intermediate and 5% were weak. Compared with men with normal strength, odds ratios for mobility impairment were 3.63 (95% CI: 3.014.38) and 7.62 (95% CI 6.139.49), respectively. In women, a grip strength of 1620 kg was classified as intermediate and less than 16 kg as weak; 25% of women were intermediate and 18% were weak. Compared with women with normal strength, odds ratios for mobility impairment were 2.44 (95% CI 2.202.71) and 4.42 (95% CI 3.944.97), respectively. Weakness based on these cutpoints was associated with mobility impairment across subgroups based on age, body mass index, height, and disease status. Notably, in women, grip strength divided by body mass index provided better fit relative to grip strength alone, but fit was not sufficiently improved to merit different measures by gender and use of a more complex measure.
Cutpoints for weakness derived from this large, diverse sample of older adults may be useful to identify populations who may benefit from interventions to improve muscle strength and function.
C1 [Alley, Dawn E.; Shardell, Michelle D.; Guralnik, Jack M.] Univ Maryland, Dept Epidemiol & Publ Hlth, Sch Med, Baltimore, MD 21201 USA.
[Peters, Katherine W.; Cawthon, Peggy M.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[McLean, Robert R.; Kiel, Douglas P.] Beth Israel Deaconess Med Ctr, Div Gerontol, Boston, MA 02215 USA.
[McLean, Robert R.; Kiel, Douglas P.] Harvard Univ, Sch Med, Boston, MA USA.
[McLean, Robert R.; Kiel, Douglas P.] Hebrew Senior Life Inst Aging Res, Inst Aging Res, Boston, MA USA.
[Dam, Thuy-Tien L.] Columbia Univ, Dept Med, New York, NY USA.
[Kenny, Anne M.; Fragala, Maren S.] Univ Connecticut, Ctr Hlth, Ctr Aging, Farmington, CT USA.
[Fragala, Maren S.] Univ Cent Florida, Orlando, FL 32816 USA.
[Harris, Tamara B.] NIA, Bethesda, MD 20892 USA.
[Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Sticht Ctr Aging, Winston Salem, NC 27109 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Dept Internal Med, Winston Salem, NC 27109 USA.
[Studenski, Stephanie A.] Univ Pittsburgh, Dept Internal Med, Pittsburgh, PA 15260 USA.
[Studenski, Stephanie A.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Vassileva, Maria T.] Fdn NIH Biomarkers Consortium, Bethesda, MD USA.
RP Alley, DE (reprint author), Univ Maryland, Sch Med, 660 W Redwood St 221B, Baltimore, MD 21201 USA.
EM dalley@epi.umaryland.edu
OI Kiel, Douglas/0000-0001-8474-0310
FU National Institute on Aging [1U13AG041583, P30 AG024827]; Food and Drug
Administration; Foundation for the NIH; Abbott Nutrition; Amgen; Eli
Lilly; Merck; Novartis; Dairy Research Institute; NIH, National
Institute on Aging
FX Funding support for the conference and the work of the consortium was
provided by the National Institute on Aging (1U13AG041583 and P30
AG024827), the Food and Drug Administration, and through grants from the
Foundation for the NIH, made possible by funding from Abbott Nutrition,
Amgen, Eli Lilly, Merck, Novartis, and The Dairy Research Institute.
This research was supported in part by the Intramural Research Program
of the NIH, National Institute on Aging. Additional acknowledgements for
each contributing cohort and members of the FNIH Sarcopenia Project can
be found in an online supplement.
NR 34
TC 65
Z9 67
U1 2
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 559
EP 566
DI 10.1093/gerona/glu011
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000008
PM 24737558
ER
PT J
AU Cawthon, PM
Peters, KW
Shardell, MD
McLean, RR
Dam, TTL
Kenny, AM
Fragala, MS
Harris, TB
Kiel, DP
Guralnik, JM
Ferrucci, L
Kritchevsky, SB
Vassileva, MT
Studenski, SA
Alley, DE
AF Cawthon, Peggy M.
Peters, Katherine W.
Shardell, Michelle D.
McLean, Robert R.
Dam, Thuy-Tien L.
Kenny, Anne M.
Fragala, Maren S.
Harris, Tamara B.
Kiel, Douglas P.
Guralnik, Jack M.
Ferrucci, Luigi
Kritchevsky, Stephen B.
Vassileva, Maria T.
Studenski, Stephanie A.
Alley, Dawn E.
TI Cutpoints for Low Appendicular Lean Mass That Identify Older Adults With
Clinically Significant Weakness
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Muscle; Sarcopenia; Cutpoints
ID BONE-MINERAL DENSITY; ALTERNATIVE DEFINITIONS; PHYSICAL FUNCTION; MUSCLE
STRENGTH; WHITE WOMEN; MEN; SARCOPENIA; HEALTH; RISK; PERFORMANCE
AB Low lean mass is potentially clinically important in older persons, but criteria have not been empirically validated. As part of the FNIH (Foundation for the National Institutes of Health) Sarcopenia Project, this analysis sought to identify cutpoints in lean mass by dual-energy x-ray absorptiometry that discriminate the presence or absence of weakness (defined in a previous report in the series as grip strength < 26kg in men and < 16kg in women).
In pooled cross-sectional data stratified by sex (7,582 men and 3,688 women), classification and regression tree (CART) analysis was used to derive cutpoints for appendicular lean body mass (ALM) that best discriminated the presence or absence of weakness. Mixed-effects logistic regression was used to quantify the strength of the association between lean mass category and weakness.
In primary analyses, CART models identified cutpoints for low lean mass (ALM < 19.75kg in men and < 15.02kg in women). Sensitivity analyses using ALM divided by body mass index (BMI: ALM(BMI)) identified a secondary definition (ALM(BMI) < 0.789 in men and ALM(BMI) < 0.512 in women). As expected, after accounting for study and age, low lean mass (compared with higher lean mass) was associated with weakness by both the primary (men, odds ratio [OR]: 6.9 [95% CI: 5.4, 8.9]; women, OR: 3.6 [95% CI: 2.9, 4.3]) and secondary definitions (men, OR: 4.3 [95% CI: 3.4, 5.5]; women, OR: 2.2 [95% CI: 1.8, 2.8]).
ALM cutpoints derived from a large, diverse sample of older adults identified lean mass thresholds below which older adults had a higher likelihood of weakness.
C1 [Cawthon, Peggy M.; Peters, Katherine W.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA.
[Shardell, Michelle D.; Guralnik, Jack M.; Alley, Dawn E.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, College Pk, MD 20742 USA.
[McLean, Robert R.; Kiel, Douglas P.] Beth Israel Deaconess Med Ctr, Div Gerontol, Boston, MA 02215 USA.
[McLean, Robert R.; Kiel, Douglas P.] Harvard Univ, Sch Med, Boston, MA USA.
[Dam, Thuy-Tien L.] Columbia Univ, Dept Med, New York, NY USA.
[Kenny, Anne M.; Fragala, Maren S.] Univ Connecticut, Ctr Hlth, Ctr Aging, Farmington, CT USA.
[Fragala, Maren S.] Univ Cent Florida, Orlando, FL 32816 USA.
[Harris, Tamara B.; Ferrucci, Luigi] NIA, Bethesda, MD 20892 USA.
[Kiel, Douglas P.] Hebrew Senior Life Inst Aging Res, Inst Aging Res, Boston, MA USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Sticht Ctr Aging, Winston Salem, NC 27109 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Dept Internal Med, Winston Salem, NC 27109 USA.
[Vassileva, Maria T.] Fdn NIH Biomarkers Consortium, Bethesda, MD USA.
[Studenski, Stephanie A.] Univ Pittsburgh, Dept Internal Med, Pittsburgh, PA 15260 USA.
[Studenski, Stephanie A.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
RP Cawthon, PM (reprint author), Calif Pacific Med Ctr, Res Inst, 185 Berry St,Suite 5700, San Francisco, CA 94107 USA.
EM pcawthon@sfcc-cpmc.net
OI Kiel, Douglas/0000-0001-8474-0310
FU National Institute on Aging [1U13AG041583, P30 AG024827]; Food and Drug
Administration; Foundation of the NIH; Abbott Nutrition; Amgen; Eli
Lilly; Merck; Novartis; Dairy Research Institute
FX Support for the conference and the consortium was provided by the
National Institute on Aging (1U13AG041583 and P30 AG024827), the Food
and Drug Administration, and through a grant from the Foundation of the
NIH, supported by funds from Abbott Nutrition, Amgen, Eli Lilly, Merck,
Novartis, and The Dairy Research Institute.
NR 27
TC 51
Z9 51
U1 0
U2 13
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 567
EP 575
DI 10.1093/gerona/glu023
PG 9
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000009
PM 24737559
ER
PT J
AU McLean, RR
Shardell, MD
Alley, DE
Cawthon, PM
Fragala, MS
Harris, TB
Kenny, AM
Peters, KW
Ferrucci, L
Guralnik, JM
Kritchevsky, SB
Kiel, DP
Vassileva, MT
Xue, QL
Perera, S
Studenski, SA
Dam, TTL
AF McLean, Robert R.
Shardell, Michelle D.
Alley, Dawn E.
Cawthon, Peggy M.
Fragala, Maren S.
Harris, Tamara B.
Kenny, Anne M.
Peters, Katherine W.
Ferrucci, Luigi
Guralnik, Jack M.
Kritchevsky, Stephen B.
Kiel, Douglas P.
Vassileva, Maria T.
Xue, Qian-Li
Perera, Subashan
Studenski, Stephanie A.
Dam, Thuy-Tien L.
TI Criteria for Clinically Relevant Weakness and Low Lean Mass and Their
Longitudinal Association With Incident Mobility Impairment and
Mortality: The Foundation for the National Institutes of Health (FNIH)
Sarcopenia Project
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Muscle; Sarcopenia; Mobility; Impairment
ID LOWER-EXTREMITY FUNCTION; OSTEOPOROTIC FRACTURES; BODY-COMPOSITION;
MUSCLE STRENGTH; OLDER PERSONS; WHITE WOMEN; MEN; EPIDEMIOLOGY; RISK;
PERFORMANCE
AB This analysis sought to determine the associations of the Foundation for the National Institutes of Health Sarcopenia Project criteria for weakness and low lean mass with likelihood for mobility impairment (gait speed 0.8 m/s) and mortality. Providing validity for these criteria is essential for research and clinical evaluation.
Among 4,411 men and 1,869 women pooled from 6 cohort studies, 3-year likelihood for incident mobility impairment and mortality over 10 years were determined for individuals with weakness, low lean mass, and for those having both. Weakness was defined as low grip strength (< 26kg men and < 16kg women) and low grip strength-to-body mass index (BMI; kg/m(2)) ratio (< 1.00 men and < 0.56 women). Low lean mass (dual-energy x-ray absorptiometry) was categorized as low appendicular lean mass (ALM; < 19.75kg men and < 15.02kg women) and low ALM-to-BMI ratio (< 0.789 men and < 0.512 women).
Low grip strength (men: odds ratio [OR] 2.31, 95% confidence interval [CI] 1.343.99; women: OR 1.99, 95% CI 1.233.21), low grip strength-to-BMI ratio (men: OR 3.28, 95% CI 1.925.59; women: OR 2.54, 95% CI 1.105.83) and low ALM-to-BMI ratio (men: OR 1.58, 95% CI 1.122.25; women: OR 1.81, 95% CI 1.142.87), but not low ALM, were associated with increased likelihood for incident mobility impairment. Weakness increased likelihood of mobility impairment regardless of low lean mass. Mortality risk patterns were inconsistent.
These findings support our cut-points for low grip strength and low ALM-to-BMI ratio as candidate criteria for clinically relevant weakness and low lean mass. Further validation in other populations and for alternate relevant outcomes is needed.
C1 [McLean, Robert R.; Kiel, Douglas P.] Hebrew SeniorLife Inst Aging Res, Boston, MA 02131 USA.
[McLean, Robert R.; Kiel, Douglas P.] Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Med, Sch Med, Boston, MA 02215 USA.
[Shardell, Michelle D.; Alley, Dawn E.; Guralnik, Jack M.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[Cawthon, Peggy M.; Peters, Katherine W.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Fragala, Maren S.; Kenny, Anne M.] Univ Connecticut, Ctr Hlth, Ctr Aging, Farmington, CT USA.
[Fragala, Maren S.] Univ Cent Florida, Orlando, FL 32816 USA.
[Harris, Tamara B.; Ferrucci, Luigi] NIA, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Sch Med, Sticht Ctr Aging, Winston Salem, NC 27109 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Sch Med, Dept Internal Med, Winston Salem, NC 27109 USA.
[Vassileva, Maria T.] Fdn Natl Inst Hlth, Biomarkers Consortium, Bethesda, MD USA.
[Xue, Qian-Li] Johns Hopkins Univ, Sch Med, Dept Med, Div Geriatr Med & Gerontol, Baltimore, MD 21205 USA.
[Xue, Qian-Li] Johns Hopkins Univ, Ctr Aging & Hlth, Baltimore, MD USA.
[Perera, Subashan; Studenski, Stephanie A.] Univ Pittsburgh, Dept Internal Med, Sch Med, Pittsburgh, PA 15260 USA.
[Studenski, Stephanie A.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Dam, Thuy-Tien L.] Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA.
RP McLean, RR (reprint author), Hebrew SeniorLife Inst Aging Res, 1200 Ctr St, Boston, MA 02131 USA.
EM rmclean@hsl.harvard.edu
OI Kiel, Douglas/0000-0001-8474-0310
FU National Institute on Aging [1U13AG041583, P30 AG024827]; Food and Drug
Administration; Foundation for the National Institutes of Health; Abbott
Nutrition; Amgen; Eli Lilly; Merck; Novartis; Dairy Research Institute
FX Funding support for the conference and the work of the consortium was
provided by the National Institute on Aging (1U13AG041583 and P30
AG024827), the Food and Drug Administration and through grants from the
Foundation for the National Institutes of Health, made possible by
funding from Abbott Nutrition, Amgen, Eli Lilly, Merck, Novartis, and
The Dairy Research Institute.
NR 33
TC 82
Z9 83
U1 4
U2 13
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 576
EP 583
DI 10.1093/gerona/glu012
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000010
PM 24737560
ER
PT J
AU Dam, TT
Peters, KW
Fragala, M
Cawthon, PM
Harris, TB
McLean, R
Shardell, M
Alley, DE
Kenny, A
Ferrucci, L
Guralnik, J
Kiel, DP
Kritchevsky, S
Vassileva, MT
Studenski, S
AF Dam, Thuy-Tien
Peters, Katherine W.
Fragala, Maren
Cawthon, Peggy M.
Harris, Tamara B.
McLean, Robert
Shardell, Michelle
Alley, Dawn E.
Kenny, Anne
Ferrucci, Luigi
Guralnik, Jack
Kiel, Douglas P.
Kritchevsky, Steve
Vassileva, Maria T.
Studenski, Stephanie
TI An Evidence-Based Comparison of Operational Criteria for the Presence of
Sarcopenia
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Muscle; Sarcopenia; Lean mass
ID LOWER-EXTREMITY FUNCTION; BONE-MINERAL DENSITY; OLDER MEN; OSTEOPOROTIC
FRACTURES; PHYSICAL PERFORMANCE; WHITE WOMEN; GAIT SPEED; MUSCLE; RISK;
EPIDEMIOLOGY
AB Several consensus groups have previously published operational criteria for sarcopenia, incorporating lean mass with strength and/or physical performance. The purpose of this manuscript is to describe the prevalence, agreement, and discrepancies between the Foundation for the National Institutes of Health (FNIH) criteria with other operational definitions for sarcopenia.
The FNIH Sarcopenia Project used data from nine studies including: Age, Gene and Environment Susceptibility-Reykjavik Study; Boston Puerto Rican Health Study; a series of six clinical trials from the University of Connecticut; Framingham Heart Study; Health, Aging, and Body Composition Study; Invecchiare in Chianti; Osteoporotic Fractures in Men Study; Rancho Bernardo Study; and Study of Osteoporotic Fractures. Participants included in these analyses were aged 65 and older and had measures of body mass index, appendicular lean mass, grip strength, and gait speed.
The prevalence of sarcopenia and agreement proportions was higher in women than men. The lowest prevalence was observed with the FNIH criteria (1.3% men and 2.3% women) compared with the International Working Group and the European Working Group for Sarcopenia in Older Persons (5.1% and 5.3% in men and 11.8% and 13.3% in women, respectively). The positive percent agreements between the FNIH criteria and other criteria were low, ranging from 7% to 32% in men and 5% to 19% in women. However, the negative percent agreement were high (all > 95%).
The FNIH criteria result in a more conservative operational definition of sarcopenia, and the prevalence was lower compared with other proposed criteria. Agreement for diagnosing sarcopenia was low, but agreement for ruling out sarcopenia was very high. Consensus on the operational criteria for the diagnosis of sarcopenia is much needed to characterize populations for study and to identify adults for treatment.
C1 [Dam, Thuy-Tien] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Peters, Katherine W.; Cawthon, Peggy M.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Fragala, Maren] Univ Cent Florida, Dept Educ & Human Sci, Orlando, FL 32816 USA.
[Harris, Tamara B.; Ferrucci, Luigi] NIA, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[McLean, Robert; Kiel, Douglas P.] Hebrew Senior Life, Inst Aging Res, Boston, MA USA.
[McLean, Robert; Kiel, Douglas P.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[McLean, Robert; Kiel, Douglas P.] Harvard Univ, Sch Med, Boston, MA USA.
[Shardell, Michelle; Alley, Dawn E.; Guralnik, Jack] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[Kenny, Anne] Univ Connecticut, Ctr Hlth, Ctr Aging, Farmington, CT USA.
[Kritchevsky, Steve] Wake Forest Univ, Sch Med, Sticht Ctr Aging, Winston Salem, NC 27109 USA.
[Kritchevsky, Steve] Wake Forest Univ, Sch Med, Dept Internal Med, Winston Salem, NC 27109 USA.
[Vassileva, Maria T.] Fdn Natl Inst Hlth, Biomarkers Consortium, Bethesda, MD USA.
[Studenski, Stephanie] Univ Pittsburgh, Dept Med, Sch Med, Pittsburgh, PA 15260 USA.
RP Dam, TT (reprint author), Columbia Univ, 5141 Broadway Ave,3 Field West,Room 13, New York, NY 10034 USA.
EM td2265@columbia.edu
OI Kiel, Douglas/0000-0001-8474-0310
FU National Institute on Aging [U13AG04158, P30 AG024827, K23 AG040168];
Food and Drug Administration; Foundation of the National Institute of
Health (FNIH); Abbot Nutrition; Amgen; Eli Lilly; Merck; Novartis; Dairy
Research Institute; NIH, National Institute on Aging
FX Funding support for the conference and the work of the consortium was
provided by the National Institute on Aging (U13AG04158 and P30
AG024827), the Food and Drug Administration, and through grants from the
Foundation of the National Institute of Health (FNIH) made possible by
funding from Abbot Nutrition, Amgen, Eli Lilly, Merck, Novartis, and the
Dairy Research Institute. This research was supported in part by the
Intramural Program of the NIH, National Institute on Aging. Additional
acknowledgments for each contributing cohort and members of the FNIH
Sarcopenia Project can be found in an online supplement. Dr. Dam was
supported by the National Institute on Aging through grant number K23
AG040168.
NR 36
TC 81
Z9 83
U1 2
U2 16
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 584
EP 590
DI 10.1093/gerona/glu013
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000011
PM 24737561
ER
PT J
AU Correa-de-Araujo, R
Hadley, E
AF Correa-de-Araujo, Rosaly
Hadley, Evan
TI Skeletal Muscle Function Deficit: A New Terminology to Embrace the
Evolving Concepts of Sarcopenia and Age-Related Muscle Dysfunction
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Sarcopenia; Skeletal muscle; Muscle weakness; Muscle strength; Muscle
function; Skeletal muscle function deficit; Deficit
ID OLDER PERSONS; CONSENSUS; MEXICO
AB Concerns remain as to the best terminology to embrace sarcopenias evolving conceptualization. Many of these concerns stem from the fact that age-related decrements in muscle performance associated with physical impairment are only partially explained by decreases in muscle mass and that other pathophysiologic factors contribute to age-related impairments in muscle performance.
Review of literature on the evolving conceptualization of sarcopenia since its early definition in 1989 and concerns with terminology.
Early definitions of sarcopenia were based solely on muscle mass in relationship to the range of muscle within a reference population. Subsequent definitions added performance criteria to muscle mass alone. The Foundation for the National Institutes of Health Sarcopenia Project identified criteria for clinically relevant low muscle strength (weakness) and low lean mass. Progress on the sarcopenias evolving definitions has not been accompanied by recommendations on specific terminologies that address the lack of sufficient specificity from the use of an anatomic term to define a functional condition with numerous now known nonanatomic contributory factors. Skeletal Muscle Function Deficit is a broader construct that accommodates a set of diagnoses that includes both sarcopenia and other age-related muscle dysfunctions.
Skeletal Muscle Function Deficit is proposed as a new terminology to embrace the evolving conceptualization of sarcopenia and other age-related muscle dysfunctions. It comprises a variety of contributory etiologies and has the potential to provide a framework for developing diagnostic categories that are useful for both clinical practice and research.
C1 [Correa-de-Araujo, Rosaly; Hadley, Evan] NIA, US Dept Hlth & Human Serv, Div Geriatr & Clin Gerontol, NIH, Bethesda, MD 20892 USA.
RP Correa-de-Araujo, R (reprint author), NIA, US Dept Hlth & Human Serv, Div Geriatr & Clin Gerontol, NIH, 7201 Wisconsin Ave, Bethesda, MD 20892 USA.
EM Rosaly.correa-de-araujo@nih.gov
NR 15
TC 23
Z9 23
U1 1
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2014
VL 69
IS 5
BP 591
EP 594
DI 10.1093/gerona/glt208
PG 4
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AF5EY
UT WOS:000334738000012
PM 24737562
ER
PT J
AU Ahn, K
Gotay, N
Andersen, TM
Anvari, AA
Gochman, P
Lee, Y
Sanders, S
Guha, S
Darvasi, A
Glessner, JT
Hakonarson, H
Lencz, T
State, MW
Shugart, YY
Rapoport, JL
AF Ahn, K.
Gotay, N.
Andersen, T. M.
Anvari, A. A.
Gochman, P.
Lee, Y.
Sanders, S.
Guha, S.
Darvasi, A.
Glessner, J. T.
Hakonarson, H.
Lencz, T.
State, M. W.
Shugart, Y. Y.
Rapoport, J. L.
TI High rate of disease-related copy number variations in childhood onset
schizophrenia
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE CNV; genetics; neurodevelopment; schizophrenia
ID AUTISM SPECTRUM DISORDERS; HIDDEN-MARKOV MODEL; SNP GENOTYPING DATA;
RECURRENT MICRODELETIONS; DEVELOPMENTAL DELAY; INCREASE RISK;
DOUBLE-BLIND; DELETIONS; VARIANTS; 16P11.2
AB Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking array of prepsychotic developmental disorders and abnormalities in brain development. Because of the well-known phenotypic variability associated with pathogenic CNVs, we conducted whole genome genotyping to detect CNVs and then focused on a group of 46 rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID. We evaluated 126 COS probands, 69 of which also had a healthy full sibling. When COS probands were compared with their matched related controls, significantly more affected individuals carried disease-related CNVs (P = 0.017). Moreover, COS probands showed a higher rate than that found in AOS probands (P < 0.0001). A total of 15 (11.9%) subjects exhibited at least one such CNV and four of these subjects (26.7%) had two. Five of 15 (4.0% of the sample) had a 2.5-3Mb deletion mapping to 22q11.2, a rate higher than that reported for adult onset (0.3-1%) (P < 0.001) or autism spectrum disorder and, indeed, the highest rate reported for any clinical population to date. For one COS subject, a duplication found at 22q13.3 had previously only been associated with autism, and for four patients CNVs at 8q11.2, 10q22.3, 16p11.2 and 17q21.3 had only previously been associated with ID. Taken together, these findings support the well-known pleiotropic effects of these CNVs suggesting shared abnormalities early in brain development. Clinically, broad CNV-based population screening is needed to assess their overall clinical burden.
C1 [Ahn, K.; Gotay, N.; Andersen, T. M.; Anvari, A. A.; Gochman, P.; Lee, Y.; Rapoport, J. L.] NIMH, Childhood Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Sanders, S.; State, M. W.] Yale Univ, Sch Med, Dept Genet, Program Neurogenet,Child Study Ctr,Dept Psychiat, New Haven, CT 06510 USA.
[Guha, S.; Lencz, T.] Zucker Hillside Hosp, Glen Oaks, NY USA.
[Darvasi, A.] Hebrew Univ Jerusalem, Inst Life Sci, Dept Genet, IL-91904 Jerusalem, Israel.
[Glessner, J. T.; Hakonarson, H.] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
[Shugart, Y. Y.] NIMH, Unit Stat Genom, NIH, Bethesda, MD 20892 USA.
RP Rapoport, JL (reprint author), NIMH, Childhood Psychiat Branch, NIH, 10 Ctr Dr,Room 3N202,MSC 1600, Bethesda, MD 20892 USA.
EM rapoporj@mail.nih.gov
RI Lencz, Todd/J-3418-2014;
OI Lencz, Todd/0000-0001-8586-338X; Guha, Saurav/0000-0002-0620-5408;
Sanders, Stephan/0000-0001-9112-5148
FU Intramural NIH HHS [Z01 MH002581-17]
NR 50
TC 28
Z9 28
U1 4
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD MAY
PY 2014
VL 19
IS 5
BP 568
EP 572
DI 10.1038/mp.2013.59
PG 5
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA AF7VY
UT WOS:000334924300009
PM 23689535
ER
PT J
AU Zhang, F
Fuss, IJ
Yang, Z
Strober, W
AF Zhang, F.
Fuss, I. J.
Yang, Z.
Strober, W.
TI Transcription of ROR gamma t in developing Th17 cells is regulated by
E-proteins
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID LYMPHOCYTE DEVELOPMENT; DIFFERENTIATION; T(H)17; ID3; LINEAGE; RECEPTOR;
DISTINCT; IL-21; BETA; E2A
AB In the present study we investigated the molecular mechanisms regulating the expression of RAR-related orphan receptor gamma t (ROR gamma t), the central factor controlling interleukin (IL)-17 transcription and Th17 differentiation. In key studies, we found that cells from mice with major deletions of E-protein transcription factors, E2A and HEB, display greatly reduced ROR gamma t/IL-17 expression and that E-protein-deficient mice exhibit greatly diminished IL-17-dependent inflammation in experimental allergic encephalitis models. In additional studies, we unexpectedly found that cells from mice with deletion of Id3, a protein that inhibits E-protein binding to DNA, display diminished ROR gamma t/IL-17 expression and mice deficient in this protein exhibit decreased Th17-mediated inflammation in a cell-transfer colitis model. The explanation of these initially paradoxical findings came from studies showing that Id3 deficiency leads to increased IL-4-induced GATA-3 expression, the latter a negative regulator of ROR gamma t transcription; thus, increased Id3 expression likely has a net positive effect on ROR gamma t expression via its inhibition of IL-4 production. Finally, we found that both E-proteins and Id3 are upregulated in tandem by the cytokines that induce Th17 differentiation, transforming growth factor-beta, and IL-6, implying that these transcription factors are critical regulators of Th17 induction.
C1 [Zhang, F.; Fuss, I. J.; Yang, Z.; Strober, W.] NIAID, Mucosal Immun Sect, Lab Host Def, NIH, Bethesda, MD 20892 USA.
RP Zhang, F (reprint author), NIAID, Mucosal Immun Sect, Lab Host Def, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM zhangfp@im.ac.cn; Wstrober@niaid.nih.go
FU Intramural NIH HHS [Z01 AI000354-25]
NR 27
TC 8
Z9 9
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
EI 1935-3456
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD MAY
PY 2014
VL 7
IS 3
BP 521
EP 532
DI 10.1038/mi.2013.69
PG 12
WC Immunology
SC Immunology
GA AF7VT
UT WOS:000334923700008
PM 24064669
ER
PT J
AU Prodger, JL
Hirbod, T
Kigozi, G
Nalugoda, F
Reynolds, SJ
Galiwango, R
Shahabi, K
Serwadda, D
Wawer, MJ
Gray, RH
Kaul, R
AF Prodger, J. L.
Hirbod, T.
Kigozi, G.
Nalugoda, F.
Reynolds, S. J.
Galiwango, R.
Shahabi, K.
Serwadda, D.
Wawer, M. J.
Gray, R. H.
Kaul, R.
CA Rakai Genital Immunology Res Grp
TI Immune correlates of HIV exposure without infection in foreskins of men
from Rakai, Uganda
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID COMMERCIAL SEX WORKERS; T-CELL-ACTIVATION; FEMALE GENITAL-TRACT; MALE
CIRCUMCISION; IMMUNOGLOBULIN-A; UNINFECTED INDIVIDUALS; MUCOSAL;
ACQUISITION; EXPRESSION; IGA
AB Human immunodeficiency virus (HIV) susceptibility is heterogenous, with some HIV-exposed but seronegative (HESN) individuals remaining uninfected despite repeated exposure. Previous studies in the cervix have shown that reduced HIV susceptibility may be mediated by immune alterations in the genital mucosa. However, immune correlates of HIV exposure without infection have not been investigated in the foreskin. We collected sub-preputial swabs and foreskin tissue from HESN (n = 20) and unexposed control (n = 57) men undergoing elective circumcision. Blinded investigators assayed swabs for HIV-neutralizing IgA, innate antimicrobial peptides, and cytokine levels. Functional T-cell subsets from foreskin tissue were assessed by flow cytometry. HESN foreskins had elevated alpha-defensins (3,027 vs. 1,795pg ml(-1), P = 0.011) and HIV-neutralizing IgA(50.0 vs. 13.5% of men, P = 0.019). Foreskin tissue from HESN men contained a higher density of CD3 T cells (151.9 vs. 69.9 cells mm(-2), P = 0.018), but a lower proportion of these was Th17 cells (6.12 vs. 8.04% of CD4 T cells, P = 0.007), and fewer produced tumor necrosis factor a (TNF alpha) (34.3 vs. 41.8% of CD4 T cells, P = 0.037; 36.9 vs. 45.7% of CD8 T cells, P = 0.004). A decrease in the relative abundance of susceptible CD4 T cells and local TNFa production, in combination with HIV-neutralizing IgA and alpha-defensins, may represent a protective immune milieu at a site of HIV exposure.
C1 [Prodger, J. L.; Shahabi, K.; Kaul, R.] Univ Toronto, Dept Med, Toronto, ON, Canada.
[Hirbod, T.] Dept Med, Solna, Sweden.
[Hirbod, T.] Karolinska Inst, Ctr Mol Med, Stockholm, Sweden.
[Kigozi, G.; Nalugoda, F.; Reynolds, S. J.; Galiwango, R.; Serwadda, D.; Wawer, M. J.; Gray, R. H.; Kaul, R.] Rakai Hlth Sci Program, Kalisizo, Uganda.
[Reynolds, S. J.] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Reynolds, S. J.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Serwadda, D.] Makerere Univ, Inst Publ Hlth, Kampala, Uganda.
[Wawer, M. J.; Gray, R. H.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
RP Prodger, JL (reprint author), Univ Toronto, Dept Med, Toronto, ON, Canada.
EM jessica.prodger@utoronto.ca
FU Bill and Melinda Gates Foundation [22006.03]; National Institutes of
Health [R01AI087409-01A1, UO1AI51171, 1UO1AI075115-O1A1]; Division of
Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health
FX We would like to acknowledge STTARR at the Toronto MaRS Discovery
District for assistance with CD3 image analysis and Mariethe Ehnlund at
the Karolinska Institute for technical assistance. Funding was provided
by the Bill and Melinda Gates Foundation, grant number 22006.03, and
R01AI087409-01A1, UO1AI51171, and 1UO1AI075115-O1A1 from the National
Institutes of Health. The study was supported in part by the Division of
Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 49
TC 14
Z9 14
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
EI 1935-3456
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD MAY
PY 2014
VL 7
IS 3
BP 634
EP 644
DI 10.1038/mi.2013.83
PG 11
WC Immunology
SC Immunology
GA AF7VT
UT WOS:000334923700018
PM 24150258
ER
PT J
AU Suwara, MI
Green, NJ
Borthwick, LA
Mann, J
Mayer-Barber, KD
Barron, L
Corris, PA
Farrow, SN
Wynn, TA
Fisher, AJ
Mann, DA
AF Suwara, M. I.
Green, N. J.
Borthwick, L. A.
Mann, J.
Mayer-Barber, K. D.
Barron, L.
Corris, P. A.
Farrow, S. N.
Wynn, T. A.
Fisher, A. J.
Mann, D. A.
TI IL-1 alpha released from damaged epithelial cells is sufficient and
essential to trigger inflammatory responses in human lung fibroblasts
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID BRONCHIOLITIS OBLITERANS SYNDROME; IDIOPATHIC PULMONARY-FIBROSIS;
ENDOPLASMIC-RETICULUM STRESS; INJURY; COPD; PATHOGENESIS; INHIBITION;
MECHANISMS; APOPTOSIS; PATHWAY
AB Activation of the innate immune system plays a key role in exacerbations of chronic lung disease, yet the potential role of lung fibroblasts in innate immunity and the identity of epithelial danger signals (alarmins) that may contribute to this process are unclear. The objective of the study was to identify lung epithelial-derived alarmins released during endoplasmic reticulum stress (ER stress) and oxidative stress and evaluate their potential to induce innate immune responses in lung fibroblasts. We found that treatment of primary human lung fibroblasts (PHLFs) with conditioned media from damaged lung epithelial cells significantly upregulated interleukin IL-6, IL-8, monocyte chemotactic protein-1, and granulocyte macrophage colony-stimulating factor expression (P<0.05). This effect was reduced with anti-IL-1 alpha or IL-1Ra but not anti-IL-1 beta antibody. Costimulation with a Toll-like receptor 3 ligand, polyinosinic-polycytidylic acid (poly I:C), significantly accentuated the IL-1 alpha-induced inflammatory phenotype in PHLFs, and this effect was blocked with inhibitor of nuclear factor kappa-B kinase subunit beta and TGF beta-activated kinase-1 inhibitors. Finally, Il1r1-/- and Il1a -/- mice exhibit reduced bronchoalveolar lavage (BAL) neutrophilia and collagen deposition in response to bleomycin treatment. We conclude that IL-1 alpha plays a pivotal role in triggering proinflammatory responses in fibroblasts and this process is accentuated in the presence of double-stranded RNA. This mechanism may be important in the repeated cycles of injury and exacerbation in chronic lung disease.
C1 [Suwara, M. I.; Green, N. J.; Borthwick, L. A.; Mann, J.; Corris, P. A.; Fisher, A. J.; Mann, D. A.] Newcastle Univ, Inst Cellular Med, Tissue Fibrosis & Repair Grp, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Mayer-Barber, K. D.; Barron, L.; Wynn, T. A.] NIAID, Immunopathogenesis Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Farrow, S. N.] GlaxoSmithKline, Resp Therapy Area, Stevenage, Herts, England.
RP Mann, DA (reprint author), Newcastle Univ, Inst Cellular Med, Tissue Fibrosis & Repair Grp, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
EM A.J.Fisher@newcastle.ac.uk; derek.mann@ncl.ac.uk
FU National Institute for Health Research Newcastle Biomedical Research
Centre based at Newcastle Hospitals Foundation Trust; Newcastle
University; Biotechnology and Biological Sciences Research Council;
GlaxoSmithKline; Wellcome Trust [WT086755MA]; MRC [MR/K001949/1];
European Union
FX The Research was supported by the National Institute for Health Research
Newcastle Biomedical Research Centre based at Newcastle Hospitals
Foundation Trust and Newcastle University. This work was also supported
by research grants from the Biotechnology and Biological Sciences
Research Council and GlaxoSmithKline. Work in the laboratory of D. A. M.
is also funded by a Wellcome Trust grant (WT086755MA) and MRC grant
(MR/K001949/1). L. A. B. was funded by a European Union FP7 Marie Curie
fellowship. A.J.F. was supported by a GlaxoSmithKline clinical
fellowship award.
NR 28
TC 38
Z9 40
U1 2
U2 14
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
EI 1935-3456
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD MAY
PY 2014
VL 7
IS 3
BP 684
EP 693
DI 10.1038/mi.2013.87
PG 10
WC Immunology
SC Immunology
GA AF7VT
UT WOS:000334923700022
PM 24172847
ER
PT J
AU Huh, SY
Min, JH
Kim, W
Kim, SH
Kim, HJ
Kim, BJ
Kim, BJ
Lee, KH
AF Huh, So-Young
Min, Ju-Hong
Kim, Woojun
Kim, Su-Hyun
Kim, Ho Jin
Kim, Byung-Jo
Kim, Byoung Joon
Lee, Kwang Ho
TI The usefulness of brain MRI at onset in the differentiation of multiple
sclerosis and seropositive neuromyelitis optica spectrum disorders
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Article
DE aquaporin-4; brain; onset; MRI; multiple sclerosis; Neuromyelitis optica
ID CLINICALLY ISOLATED SYNDROMES; DIAGNOSTIC-CRITERIA; NATALIZUMAB THERAPY;
FINGOLIMOD FTY720; ABNORMALITIES; MULTICENTER; AQUAPORIN-4; LESIONS; MS;
ENHANCEMENT
AB Background:
Although neuromyelitis optica (NMO) is a central nervous system (CNS) autoimmune disease distinct from multiple sclerosis (MS). NMO and NMO spectrum disorder (NMOSD) sometimes show asymptomatic lesions on brain magnetic resonance imaging (MRI) at onset, and even present with symptomatic brain involvement.
Objectives:
We investigated whether brain MRI at onset can be helpful for the differentiation of MS and NMOSD.
Methods:
We retrospectively analyzed initial brain MRIs, performed within three months of onset, in patients with MS (n = 51) and anti-aquaporin4-antibody-positive patients with NMOSD (n = 67).
Results:
NMOSD patients met the Paty (37%) and Barkhof (13%) criteria, and the criteria of the European Magnetic Imaging in MS (MAGNIMS) study group (9%), for MS. Ovoid lesions perpendicular to the lateral ventricle, isolated juxtacortical lesions in U-fibers and isolated ovoid/round cortical lesions were found only in MS patients, whereas longitudinal corticospinal tract lesions, extensive hemispheric lesions, periependymal lesions surrounding the lateral ventricle and cervicomedullary lesions were found only in NMOSD patients.
Conclusions:
Our study suggests that it is difficult to differentiate MS from NMOSD by the fulfillment of the MRI criteria for MS on brain MRI at onset; however, the characteristic morphology of brain lesions is highly useful for the early differentiation of the two disorders.
C1 [Huh, So-Young] Kosin Univ, Gospel Hosp, Coll Med, Dept Neurol, Pusan, South Korea.
[Huh, So-Young; Kim, Woojun; Kim, Su-Hyun; Kim, Ho Jin] Natl Canc Ctr, Dept Neurol, Bethesda, MD USA.
[Min, Ju-Hong; Kim, Byoung Joon; Lee, Kwang Ho] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Neurol, Seoul 135710, South Korea.
[Kim, Woojun] Catholic Univ Korea, Dept Neurol, Seoul, South Korea.
Univ Korea Hosp, Dept Neurol, Seoul, South Korea.
RP Min, JH (reprint author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Neurol, 50 Ilwon Dong, Seoul 135710, South Korea.
EM juhongm@gmail.com
RI Kim, Byung Jo/A-5943-2012
OI Kim, Byung Jo/0000-0002-0445-7185
FU Korea Healthcare technology R&D Project, Ministry for Health, Welfare
and Family Affairs, Republic of Korea [A080588-28]; Samsung Medical
Center [SMR112102, CRO112042]
FX This work was supported by a grant of the Korea Healthcare technology
R&D Project, Ministry for Health, Welfare and Family Affairs, Republic
of Korea (A080588-28) and was also by grants of Samsung Medical Center
(SMR112102 and CRO112042).
NR 37
TC 17
Z9 21
U1 0
U2 9
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
EI 1477-0970
J9 MULT SCLER J
JI Mult. Scler. J.
PD MAY
PY 2014
VL 20
IS 6
BP 695
EP 704
DI 10.1177/1352458513506953
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AF7AN
UT WOS:000334865900008
PM 24072726
ER
PT J
AU Sacks, DL
AF Sacks, David L.
TI Vaccines against tropical parasitic diseases: a persisting answer to a
persisting problem
SO NATURE IMMUNOLOGY
LA English
DT Article
ID LONG-TERM IMMUNITY; T-CELL IMMUNITY; PROTECTIVE IMMUNITY; IRRADIATED
SPOROZOITES; LEISHMANIA-MAJOR; MALARIA; MEMORY; IMMUNIZATION; CD8(+);
MAINTENANCE
C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Sacks, DL (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM dsacks@niaid.nih.gov
FU Intramural NIH HHS [Z01 AI000494-21]
NR 25
TC 15
Z9 15
U1 0
U2 16
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
EI 1529-2916
J9 NAT IMMUNOL
JI Nat. Immunol.
PD MAY
PY 2014
VL 15
IS 5
BP 403
EP 405
DI 10.1038/ni.2853
PG 3
WC Immunology
SC Immunology
GA AF4FU
UT WOS:000334667900001
PM 24747701
ER
PT J
AU Heikamp, EB
Patel, CH
Collins, S
Waickman, A
Oh, MH
Sun, IH
Illei, P
Sharma, A
Naray-Fejes-Toth, A
Fejes-Toth, G
Misra-Sen, J
Horton, MR
Powell, JD
AF Heikamp, Emily B.
Patel, Chirag H.
Collins, Sam
Waickman, Adam
Oh, Min-Hee
Sun, Im-Hong
Illei, Peter
Sharma, Archna
Naray-Fejes-Toth, Aniko
Fejes-Toth, Geza
Misra-Sen, Jyoti
Horton, Maureen R.
Powell, Jonathan D.
TI The AGC kinase SGK1 regulates T(H)1 and T(H)2 differentiation downstream
of the mTORC2 complex
SO NATURE IMMUNOLOGY
LA English
DT Article
ID SELECTIVE ACTIVATION; UBIQUITIN LIGASE; T-CELLS; PHOSPHORYLATION;
RICTOR; MICE; INFLAMMATION; EXPRESSION; CHANNEL; ASTHMA
AB SGK1 is an AGC kinase that regulates the expression of membrane sodium channels in renal tubular cells in a manner dependent on the metabolic checkpoint kinase complex mTORC2. We hypothesized that SGK1 might represent an additional mTORC2dependent regulator of the differentiation and function of T cells. Here we found that after activation by mTORC2, SGK1 promoted T helper type 2 (T(H)2) differentiation by negatively regulating degradation of the transcription factor JunB mediated by the E3 ligase Nedd4-2. Simultaneously, SGK1 repressed the production of interferon-gamma (IFN-gamma) by controlling expression of the long isoform of the transcription factor TCF-1. Consistent with those findings, mice with selective deletion of SGK1 in T cells were resistant to experimentally induced asthma, generated substantial IFN-g in response to viral infection and more readily rejected tumors.
C1 [Heikamp, Emily B.; Patel, Chirag H.; Waickman, Adam; Sun, Im-Hong; Powell, Jonathan D.] Johns Hopkins Univ Sch Med, Dept Oncol, Sidney Kimmel Comprehens Canc Res Ctr, Baltimore, MD 21218 USA.
[Collins, Sam; Oh, Min-Hee; Horton, Maureen R.] Johns Hopkins Univ Sch Med, Dept Med, Baltimore, MD USA.
[Illei, Peter] Johns Hopkins Univ Sch Med, Dept Pathol, Baltimore, MD USA.
[Sharma, Archna; Misra-Sen, Jyoti] NIA, Immune Cells & Inflammat Sect, Immunol Lab, NIH, Baltimore, MD 21224 USA.
[Naray-Fejes-Toth, Aniko; Fejes-Toth, Geza] Dartmouth Med Sch, Dept Physiol, Lebanon, NH USA.
RP Powell, JD (reprint author), Johns Hopkins Univ Sch Med, Dept Oncol, Sidney Kimmel Comprehens Canc Res Ctr, Baltimore, MD 21218 USA.
EM poweljo@jhmi.edu
RI Heikamp, Emily/K-7158-2016; Sharma, Archna/R-9377-2016
OI Heikamp, Emily/0000-0002-4591-4477; Sharma, Archna/0000-0003-4745-0220
FU US National Institutes of Health [R01 AI77610, NHLBI P01HL010342, NHLBI
R21HL111783, DK 41481, DK 58898]; American Asthma Foundation (J.D.P.);
Intramural Research Program of the NIH; National Institute on Aging
(J.M.S.); FAMRI Center of Excellence [108595]; American Medical
Association (E.B.H.)
FX We thank D. Pardoll, C. Gamper and members of the Powell Lab for
discussions, and the Magnuson laboratory for Rictor-/-mice.
Supported by the US National Institutes of Health (R01 AI77610 to
J.D.P., NHLBI P01HL010342 and NHLBI R21HL111783 to M.R.H., DK 41481 to
A.N.-F.-T. and DK 58898 to G.F.-T.), the American Asthma Foundation
(J.D.P.), the Intramural Research Program of the NIH, National Institute
on Aging (J.M.S.), the FAMRI Center of Excellence 108595 (M.R.H.) and
the American Medical Association (E.B.H.).
NR 41
TC 46
Z9 47
U1 0
U2 13
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
EI 1529-2916
J9 NAT IMMUNOL
JI Nat. Immunol.
PD MAY
PY 2014
VL 15
IS 5
BP 457
EP +
DI 10.1038/ni.2867
PG 10
WC Immunology
SC Immunology
GA AF4FU
UT WOS:000334667900011
PM 24705297
ER
PT J
AU Caprioli, D
Calu, D
Shaham, Y
AF Caprioli, Daniele
Calu, Donna
Shaham, Yavin
TI Loss of phasic dopamine: a new addiction marker?
SO NATURE NEUROSCIENCE
LA English
DT Editorial Material
ID DRUG-ADDICTION; COCAINE USE; STRIATUM; BEHAVIOR; REWARD
AB A study finds that the loss of phasic dopamine signal in ventral, but not dorsal, striatum predicts escalation of cocaine self-administration. We discuss the study's implications for addiction theory and treatment.
C1 [Caprioli, Daniele; Calu, Donna; Shaham, Yavin] NIDA, Behav Neurosci Res Branch, Intramural Res Program, US Natl Inst Hlth,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
RP Caprioli, D (reprint author), NIDA, Behav Neurosci Res Branch, Intramural Res Program, US Natl Inst Hlth,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
EM yshaham@intra.nida.nih.gov
RI shaham, yavin/G-1306-2014;
OI Calu, Donna/0000-0003-2377-9494
FU Intramural NIH HHS [ZIA DA000434-14]
NR 16
TC 4
Z9 4
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
EI 1546-1726
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD MAY
PY 2014
VL 17
IS 5
BP 644
EP 646
DI 10.1038/nn.3699
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA AF9DS
UT WOS:000335016200004
PM 24883455
ER
PT J
AU Johnson, JO
Pioro, EP
Boehringer, A
Chia, R
Feit, H
Renton, AE
Pliner, HA
Abramzon, Y
Marangi, G
Winborn, BJ
Gibbs, JR
Nalls, MA
Morgan, S
Shoai, M
Hardy, J
Pittman, A
Orrell, RW
Malaspina, A
Sidle, KC
Fratta, P
Harms, MB
Baloh, RH
Pestronk, A
Weihl, CC
Rogaeva, E
Zinman, L
Drory, VE
Borghero, G
Mora, G
Calvo, A
Rothstein, JD
Drepper, C
Sendtner, M
Singleton, AB
Taylor, JP
Cookson, MR
Restagno, G
Sabatelli, M
Bowser, R
Chio, A
Traynor, BJ
AF Johnson, Janel O.
Pioro, Erik P.
Boehringer, Ashley
Chia, Ruth
Feit, Howard
Renton, Alan E.
Pliner, Hannah A.
Abramzon, Yevgeniya
Marangi, Giuseppe
Winborn, Brett J.
Gibbs, J. Raphael
Nalls, Michael A.
Morgan, Sarah
Shoai, Maryam
Hardy, John
Pittman, Alan
Orrell, Richard W.
Malaspina, Andrea
Sidle, Katie C.
Fratta, Pietro
Harms, Matthew B.
Baloh, Robert H.
Pestronk, Alan
Weihl, Conrad C.
Rogaeva, Ekaterina
Zinman, Lorne
Drory, Vivian E.
Borghero, Giuseppe
Mora, Gabriele
Calvo, Andrea
Rothstein, Jeffrey D.
Drepper, Carsten
Sendtner, Michael
Singleton, Andrew B.
Taylor, J. Paul
Cookson, Mark R.
Restagno, Gabriella
Sabatelli, Mario
Bowser, Robert
Chio, Adriano
Traynor, Bryan J.
CA ITALSGEN
TI Mutations in the Matrin 3 gene cause familial amyotrophic lateral
sclerosis
SO NATURE NEUROSCIENCE
LA English
DT Article
ID DOMINANT DISTAL MYOPATHY; NUCLEAR-MATRIX; PROTEIN; ALS; COMPLEXES
AB MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Using exome sequencing, we identified mutations in MATR3 in ALS kindreds. We also observed MATR3 pathology in ALS-affected spinal cords with and without MATR3 mutations. Our data provide more evidence supporting the role of aberrant RNA processing in motor neuron degeneration.
C1 [Johnson, Janel O.; Renton, Alan E.; Pliner, Hannah A.; Abramzon, Yevgeniya; Marangi, Giuseppe; Traynor, Bryan J.] NIA, Neuromuscular Dis Res Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Pioro, Erik P.] Cleveland Clin, Neurol Inst, Neuromuscular Ctr, Dept Neurol, Cleveland, OH 44106 USA.
[Boehringer, Ashley; Bowser, Robert] Barrow Neurol Inst, Div Neurol, Phoenix, AZ 85013 USA.
[Chia, Ruth; Cookson, Mark R.] NIA, Cell Biol & Gene Express Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Feit, Howard] Henry Ford Hosp, Dept Neurol, Detroit, MI 48202 USA.
[Marangi, Giuseppe] Univ Cattolica Sacro Cuore, Inst Med Genet, I-00168 Rome, Italy.
[Winborn, Brett J.; Taylor, J. Paul] St Jude Childrens Res Hosp, Dept Cell & Mol Biol, Memphis, TN 38105 USA.
[Gibbs, J. Raphael] NIA, Computat Biol Core, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Gibbs, J. Raphael; Morgan, Sarah; Shoai, Maryam; Hardy, John; Pittman, Alan] UCL, Inst Neurol, Dept Mol Neurosci, London, England.
[Gibbs, J. Raphael; Morgan, Sarah; Shoai, Maryam; Hardy, John; Pittman, Alan] UCL, Inst Neurol, Reta Lila Weston Labs, London, England.
[Nalls, Michael A.; Singleton, Andrew B.] NIA, Mol Genet Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Orrell, Richard W.] UCL, Inst Neurol, Dept Clin Neurosci, London, England.
[Malaspina, Andrea] Queen Mary Univ London, North East London & Essex Reg Motor Neuron Dis Ca, Blizard Inst, Ctr Neurosci & Trauma, London, England.
[Fratta, Pietro] UCL, Dept Neurodegenerat Dis, London, England.
[Harms, Matthew B.; Pestronk, Alan; Weihl, Conrad C.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Baloh, Robert H.] Cedars Sinai Med Ctr, Dept Neurol, Los Angeles, CA 90048 USA.
[Rogaeva, Ekaterina] Univ Toronto, Dept Med, Div Neurol, Tanz Ctr Res Neurodegenerat Dis, Toronto, ON, Canada.
[Zinman, Lorne] Univ Toronto, Sunnybrook Hlth Sci Ctr, Dept Internal Med, Div Neurol, Toronto, ON, Canada.
[Drory, Vivian E.] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Dept Neurol, IL-69978 Tel Aviv, Israel.
[Borghero, Giuseppe] Azienda Univ Osped Cagliari, Dept Neurol, Cagliari, Italy.
[Borghero, Giuseppe] Univ Cagliari, Cagliari, Italy.
[Mora, Gabriele] Salvatore Maugeri Fdn, ALS Ctr, Milan, Italy.
[Calvo, Andrea; Chio, Adriano] Univ Turin, Rita Levi Montalcini Dept Neurosci, Turin, Italy.
[Rothstein, Jeffrey D.; Traynor, Bryan J.] Johns Hopkins Univ, Dept Neurol, Brain Sci Inst, Baltimore, MD 21218 USA.
[Drepper, Carsten; Sendtner, Michael] Univ Wurzburg, Inst Clin Neurobiol, D-97070 Wurzburg, Germany.
[Drepper, Carsten] Univ Wurzburg, Dept Child & Adolescent Psychiat, D-97070 Wurzburg, Germany.
[Restagno, Gabriella] Azienda Sanit Osped Osped Infantile Regina Marghe, Dept Clin Pathol, Mol Genet Unit, Turin, Italy.
[Sabatelli, Mario] Catholic Univ, Neurol Inst, Rome, Italy.
[Sabatelli, Mario] Insieme Contro Malattie Motoneurone Assoc ALS Res, Rome, Italy.
RP Traynor, BJ (reprint author), NIA, Neuromuscular Dis Res Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
EM traynorb@mail.nih.gov
RI Conforti, Francesca Luisa/K-8877-2016; Hardy, John/C-2451-2009;
Singleton, Andrew/C-3010-2009; Pittman, Alan/D-6231-2012; Pliner,
Hannah/F-3608-2015; MANDRIOLI, JESSICA/K-7235-2016; Battistini,
Stefania/N-2596-2015; QUATTRONE, Aldo/A-6734-2016; Calvo,
Andrea/K-4141-2016; LOGROSCINO, GIANCARLO/K-5148-2016; Spataro,
Rossella/B-3656-2016; Lunetta, Christian/K-9214-2016; Sendtner,
Michael/J-1542-2012
OI Fratta, Pietro/0000-0002-8762-8188; Sabatelli,
Mario/0000-0001-6635-4985; Conforti, Francesca
Luisa/0000-0001-8364-1783; Chio, Adriano/0000-0001-9579-5341; Simone,
Isabella Laura/0000-0002-7429-3091; Gambardella ,
Antonio/0000-0001-7384-3074; Morgan, Sarah/0000-0002-1734-4710; Pliner,
Hannah/0000-0003-1484-6501; MANDRIOLI, JESSICA/0000-0002-9244-9782;
Battistini, Stefania/0000-0003-2887-7624; QUATTRONE,
Aldo/0000-0003-2001-957X; Calvo, Andrea/0000-0002-5122-7243; LOGROSCINO,
GIANCARLO/0000-0003-0423-3242; Spataro, Rossella/0000-0002-8910-3131;
Lunetta, Christian/0000-0002-4788-1875; Sendtner,
Michael/0000-0002-4737-2974
FU Intramural Research Programs of the US National Institutes of Health
(NIH); National Institute on Aging [Z01-AG000949-02]; NINDS; Packard
Center for ALS Research at Johns Hopkins; ALS Association; Ontario
Research Fund; UK MND Association [11/6075]; Medical Research Council
(MRC) UK; Wellcome Trust/MRC Joint Call in Neurodegeneration Award
[WT089698]; MRC Neuromuscular Centre; UK National Institute for Health
Research Biomedical Research Unit; Biomedical Research Centre; MRC/Motor
Neuron Disease Association Lady Edith Wolfson fellowship; AriSLA-Italian
Research Foundation for Amyotrophic Lateral Sclerosis; Italian Health
Ministry; Fondazione Vialli e Mauro Onlus; Federazione Italiana Giuoco
Calcio; Compagnia di San Paolo; European Community [259867]; EuroMOTOR;
German Federal Ministry of Education and Research (BMBF); German Network
for Motoneuron Disease [TP4]; NIH [NS061867]; Adelis Foundation
FX DNA samples for this study were obtained in part from the National
Institute of Neurological Disorders and Stroke (NINDS) repository at the
Coriell Cell Repositories (http://www. coriell. org/). We thank the
patients and research subjects who contributed samples for this study.
This work was supported in part by the Intramural Research Programs of
the US National Institutes of Health (NIH), National Institute on Aging
(Z01-AG000949-02) and NINDS. The work was also supported by the Packard
Center for ALS Research at Johns Hopkins (B.J.T.), ALS Association
(B.J.T., A. Chio), Ontario Research Fund (E.R.), UK MND Association (J.
H., R.W.O. grant 11/6075), Medical Research Council (MRC) UK (J. H.),
Wellcome Trust/MRC Joint Call in Neurodegeneration Award (J. H., grant
WT089698), MRC Neuromuscular Centre (J.H.), UK National Institute for
Health Research Biomedical Research Unit (J.H.), Biomedical Research
Centre (A. Pittman), MRC/Motor Neuron Disease Association Lady Edith
Wolfson fellowship (P.F.), AriSLA-Italian Research Foundation for
Amyotrophic Lateral Sclerosis (A. Chio, B.J.T.), Italian Health Ministry
(Ricerca Sanitaria Finalizzata 2007, A. Chio), Fondazione Vialli e Mauro
Onlus (A. Chio), Federazione Italiana Giuoco Calcio (A. Chio, M.
Sabatelli, B.J.T.), Compagnia di San Paolo (A. Chio, G.R.), Adelis
Foundation (V.E.D.), European Community's Health Seventh Framework
Programme (FP7/2007-2013) under grant agreements 259867 (A. Chio, M.
Sendtner, C.D.), EuroMOTOR (M. Sendtner), German Federal Ministry of
Education and Research (BMBF) (M. Sendtner), German Network for
Motoneuron Disease (M. Sendtner, grant TP4) and NIH grant NS061867
(R.B.).
NR 17
TC 101
Z9 105
U1 8
U2 46
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
EI 1546-1726
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD MAY
PY 2014
VL 17
IS 5
BP 664
EP +
DI 10.1038/nn.3688
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA AF9DS
UT WOS:000335016200008
PM 24686783
ER
PT J
AU Widemann, BC
Dombi, E
Gillespie, A
Wolters, PL
Belasco, J
Goldman, S
Korf, BR
Solomon, J
Martin, S
Salzer, W
Fox, E
Patronas, N
Kieran, MW
Perentesis, JP
Reddy, A
Wright, JJ
Kim, A
Steinberg, SM
Balis, FM
AF Widemann, Brigitte C.
Dombi, Eva
Gillespie, Andrea
Wolters, Pamela L.
Belasco, Jean
Goldman, Stewart
Korf, Bruce R.
Solomon, Jeffrey
Martin, Staci
Salzer, Wanda
Fox, Elizabeth
Patronas, Nicholas
Kieran, Mark W.
Perentesis, John P.
Reddy, Alyssa
Wright, John J.
Kim, AeRang
Steinberg, Seth M.
Balis, Frank M.
TI Phase 2 randomized, flexible crossover, double-blinded,
placebo-controlled trial of the farnesyltransferase inhibitor tipifarnib
in children and young adults with neurofibromatosis type 1 and
progressive plexiform neurofibromas
SO NEURO-ONCOLOGY
LA English
DT Article
DE neurofibromatosis type 1; phase 2 trial; plexiform neurofibroma; RAS
signaling; trial design
ID NERVE SHEATH TUMORS; SOLID TUMORS; I TRIAL; MAMMALIAN TARGET;
TRANSFERASE INHIBITORS; RAS; RAPAMYCIN; NF1; GUIDELINES; MANAGEMENT
AB RAS is dysregulated in neurofibromatosis type 1 (NF1) related plexiform neurofibromas (PNs). The activity of tipifarnib, which blocks RAS signaling by inhibiting its farnesylation, was tested in children and young adults with NF1 and progressive PNs.
Patients aged 325 years with NF1-related PNs and imaging evidence of tumor progression were randomized in a double-blinded fashion to receive tipifarnib (200 mg/m(2) orally every 12 h) or placebo (phase A) and crossed over to the opposite treatment arm at the time of tumor progression (phase B). PN volumes were measured with MRI, and progression was defined as 20 volume increase. Time to progression (TTP) in phase A was the primary endpoint, and the trial was powered to detect whether tipifarnib doubled TTP compared with placebo. Toxicity, response, and quality of life were also monitored.
Sixty-two patients were enrolled. Tipifarnib and placebo were well tolerated. On phase A, the median TTP was 10.6 months on the placebo arm and 19.2 months on the tipifarnib arm (P .12; 1-sided). Quality of life improved significantly compared with baseline on the tipifarnib arm but not on the placebo arm. Volumetric tumor measurement detected tumor progression earlier than conventional 2-dimensional (WHO) and 1-dimensional (RECIST) methods.
Tipifarnib was well tolerated but did not significantly prolong TTP of PNs compared with placebo. The randomized, flexible crossover design and volumetric PN assessment provided a feasible and efficient means of assessing the efficacy of tipifarnib. The placebo arm serves as an historical control group for phase 2 single-arm trials directed at progressive PNs.
C1 [Widemann, Brigitte C.; Dombi, Eva; Gillespie, Andrea; Wolters, Pamela L.; Martin, Staci; Fox, Elizabeth; Balis, Frank M.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Wright, John J.] NCI, Canc Therapy Evaluat Program, Invest Drug Branch, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
[Patronas, Nicholas] NIH, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
[Belasco, Jean; Fox, Elizabeth; Balis, Frank M.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Goldman, Stewart] Ann & Robert H Lurie Childrens Hosp, Chicago, IL USA.
[Korf, Bruce R.] Univ Alabama Birmingham, Dept Genet, South Birmingham, AL USA.
[Solomon, Jeffrey] Expert Image Anal LC, Potomac, MD USA.
[Kieran, Mark W.] Dana Farber Childrens Hosp, Ctr Canc, Boston, MA USA.
[Perentesis, John P.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Kim, AeRang] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Salzer, Wanda] US Army, Med Res & Mat Command, Ft Detrick, MD USA.
[Reddy, Alyssa] Childrens Hosp Alabama, Birmingham, AL USA.
RP Widemann, BC (reprint author), NCI, Pediat Oncol Branch, 10 Ctr Dr,Bldg 10 CRC,Room 1-5750,MSC 1101, Bethesda, MD 20892 USA.
EM widemanb@mail.nih.gov
OI Kieran, Mark/0000-0003-2184-7692
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research; Department of Defense [MIPR 1LCDN91152]
FX This research was supported (in part) by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute, Center
for Cancer Research, and by a Clinical Trial Award (MIPR 1LCDN91152)
from the Department of Defense.
NR 41
TC 20
Z9 22
U1 3
U2 9
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
EI 1523-5866
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD MAY
PY 2014
VL 16
IS 5
BP 707
EP 718
DI 10.1093/neuonc/nou004
PG 12
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA AF5HU
UT WOS:000334745400011
PM 24500418
ER
PT J
AU Baumann, MH
Bulling, S
Benaderet, TS
Saha, K
Ayestas, MA
Partilla, JS
Ali, SF
Stockner, T
Rothman, RB
Sandtner, W
Sitte, HH
AF Baumann, Michael H.
Bulling, Simon
Benaderet, Tova S.
Saha, Kusumika
Ayestas, Mario A.
Partilla, John S.
Ali, Syed F.
Stockner, Thomas
Rothman, Richard B.
Sandtner, Walter
Sitte, Harald H.
TI Evidence for a Role of Transporter-Mediated Currents in the Depletion of
Brain Serotonin Induced by Serotonin Transporter Substrates
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE serotonin (5-HT) release; 5-HT depletion; 5-HT transporter (SERT); SERT
substrate; SERT-mediated current
ID INCREASES EXTRACELLULAR SEROTONIN; PRIMARY PULMONARY-HYPERTENSION;
VALVULAR HEART-DISEASE; RAT-BRAIN; D-FENFLURAMINE; P-CHLOROAMPHETAMINE;
IN-VIVO; 3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA; SUBSTITUTED
AMPHETAMINES; NEUROTOXICITY PROFILES
AB Serotonin (5-HT) transporter (SERT) substrates like fenfluramine and 3,4-methylenedioxymethamphetamine cause long-term depletion of brain 5-HT, while certain other substrates do not. The 5-HT deficits produced by SERT substrates are dependent upon transporter proteins, but the exact mechanisms responsible are unclear. Here, we compared the pharmacology of several SERT substrates: fenfluramine, d-fenfluramine, 1-(m-chlorophenyl)piperazine (mCPP) and 1-(m-trifluoromethylphenyl)piperainze (TFMPP), to establish relationships between acute drug mechanisms and the propensity for long-term 5-HT depletions. In vivo microdialysis was carried out in rat nucleus accumbens to examine acute 5-HT release and long-term depletion in the same subjects. In vitro assays were performed to measure efflux of [H-3]5-HT in rat brain synaptosomes and transporter-mediated ionic currents in SERT-expressing Xenopus oocytes. When administered repeatedly to rats (6 mg/kg, i.p., four doses), all drugs produce large sustained elevations in extracellular 5-HT (>5-fold) with minimal effects on dopamine. Importantly, 2 weeks after dosing, only rats exposed to fenfluramine and d-fenfluramine display depletion of brain 5-HT. All test drugs evoke fluoxetine-sensitive efflux of [H-3]5-HT from synaptosomes, but d-fenfluramine and its bioactive metabolite d-norfenfluramine induce significantly greater SERT-mediated currents than phenylpiperazines. Our data confirm that drug-induced 5-HT release probably does not mediate 5-HT depletion. However, the magnitude of transporter-mediated inward current may be a critical factor in the cascade of events leading to 5-HT deficits. This hypothesis warrants further study, especially given the growing popularity of designer drugs that target SERT.
C1 [Baumann, Michael H.; Benaderet, Tova S.; Ayestas, Mario A.; Partilla, John S.; Rothman, Richard B.] NIDA, Med Chem Sect, Intramural Res Program, NIH, Baltimore, MD USA.
[Bulling, Simon; Saha, Kusumika; Stockner, Thomas; Sandtner, Walter; Sitte, Harald H.] Med Univ Vienna, Inst Pharmacol, Ctr Physiol & Pharmacol, A-1090 Vienna, Austria.
[Ali, Syed F.] US FDA, Natl Ctr Toxicol Res, Div Neurotoxicol, Neurochem Lab, Jefferson, AR 72079 USA.
RP Sitte, HH (reprint author), Med Univ Vienna, Inst Pharmacol, Ctr Physiol & Pharmacol, Waehringerstr 13 A, A-1090 Vienna, Austria.
EM harald.sitte@meduniwien.ac.at
RI Stockner, Thomas/A-9509-2014;
OI Stockner, Thomas/0000-0002-7071-8283; Sitte, Harald/0000-0002-1339-7444
FU Intramural Research Program of the NIDA; NIH; Austrian Research Fund/FWF
[F3506, W1232]; [DA000523-05]
FX This research was supported by the Intramural Research Program of the
NIDA, NIH, DA000523-05 to MHB and the Austrian Research Fund/FWF grants
F3506 and W1232 to HHS. We are indebted to Klaus Schicker for valuable
comments on the manuscript.
NR 69
TC 9
Z9 9
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD MAY
PY 2014
VL 39
IS 6
BP 1355
EP 1365
DI 10.1038/npp.2013.331
PG 11
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AF2RV
UT WOS:000334560600007
PM 24287719
ER
PT J
AU Grant, PJ
Joseph, LA
Farmer, CA
Luckenbaugh, DA
Lougee, LC
Zarate, CA
Swedo, SE
AF Grant, Paul J.
Joseph, Lisa A.
Farmer, Cristan A.
Luckenbaugh, David A.
Lougee, Lorraine C.
Zarate, Carlos A., Jr.
Swedo, Susan E.
TI 12-Week, Placebo-Controlled Trial of Add-on Riluzole in the Treatment of
Childhood-Onset Obsessive-Compulsive Disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE mood/anxiety/stress disorders; psychiatry and behavioral sciences;
clinical pharmacology/clinical trials; psychopharmacology; riluzole;
obsessive-compulsive disorder
ID OF-THE-LITERATURE; AUTISTIC DISORDER; CHILDREN; ADOLESCENTS;
METAANALYSIS; RELIABILITY; VALIDITY; SCALE; PHARMACOTHERAPY; SCHEDULE
AB Many children with childhood-onset obsessive compulsive disorder (OCD) fail to respond adequately to standard therapies. Evidence from preclinical and clinical studies suggests that the glutamatergic neurotransmitter system might be an alternative treatment target. This study examined the efficacy of riluzole, a glutamatergic modulator, as an adjunctive therapy for children with treatment-resistant OCD. In a 12-week, double-blind, placebo-controlled study, 60 treatment-resistant children and adolescents (mean age=14.5 +/- 2.4 years), with moderate to severe OCD (mean Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS)=28.2 +/- 3.7), 17 of whom also had concomitant autism spectrum disorder, were randomized to receive riluzole (final dose of 100 mg/day) or placebo in addition to the existing treatment regimen. Fifty-nine subjects completed the randomized trial. Primary outcome measures were changes on the CY-BOCS, the Clinical Global Impressions Scale, and the Children's Global Assessment Scale. Riluzole was fairly well tolerated, although it was associated with one case of pancreatitis and five instances of slight increases in transaminases. All subjects showed significant reductions in CY-BOCS scores during treatment; however, there was no significant difference between placebo and riluzole on any of the primary or secondary outcome measures. The study failed to demonstrate superiority of riluzole over placebo as an adjunctive treatment for children with childhood-onset OCD. However, future studies may show benefits for less treatment-refractory children with fewer concomitant medications.
C1 [Grant, Paul J.; Joseph, Lisa A.; Farmer, Cristan A.; Lougee, Lorraine C.; Swedo, Susan E.] NIMH, Pediat & Dev Neurosci Branch, NIH, Bethesda, MD 20892 USA.
[Luckenbaugh, David A.; Zarate, Carlos A., Jr.] NIMH, Expt Therapeut & Pathophysiol Branch, NIH, Bethesda, MD 20892 USA.
RP Swedo, SE (reprint author), NIMH, Pediat & Dev Neurosci Branch, NIH, 10 Ctr Dr MSC 1255,Bldg 10,Room 1C250, Bethesda, MD 20892 USA.
EM swedos@mail.nih.gov
FU Intramural Program of the National Institute of Mental Health (NIMH) of
the National Institutes of Health (NIH) [1ZIAMH002913]
FX This research (protocol 05-M-0225) was supported by the Intramural
Program of the National Institute of Mental Health (NIMH) of the
National Institutes of Health (NIH; Grant # 1ZIAMH002913).
ClinicalTrials.gov identifier NCF00251303.
NR 32
TC 8
Z9 10
U1 6
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD MAY
PY 2014
VL 39
IS 6
BP 1453
EP 1459
DI 10.1038/npp.2013.343
PG 7
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AF2RV
UT WOS:000334560600016
PM 24356715
ER
PT J
AU Ginexi, EM
Riley, W
Atienza, AA
Mabry, PL
AF Ginexi, Elizabeth M.
Riley, William
Atienza, Audie A.
Mabry, Patricia L.
TI The Promise of Intensive Longitudinal Data Capture for Behavioral Health
Research
SO NICOTINE & TOBACCO RESEARCH
LA English
DT Editorial Material
ID ECOLOGICAL MOMENTARY ASSESSMENT; CESSATION; QUITTERS; SMOKERS
AB Advances in technology and the associated cultural norms, especially the advent of the smartphone, offer an unprecedented opportunity to collect data on relevant health behaviors and experiences unobtrusively at a greater frequency and in greater volumes than ever before. This special issue will acquaint the readership of Nicotine and Tobacco Research with the potential for intensive longitudinal data and will illustrate some innovative analytic techniques for addressing research questions associated with this type of complex data. This introductory article will provide a brief history of the analytic techniques for intensive longitudinal data and will point to some resources that support and enable the use of these techniques.
C1 [Ginexi, Elizabeth M.; Riley, William; Atienza, Audie A.] NCI, NIH, Bethesda, MD 20892 USA.
[Mabry, Patricia L.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Ginexi, EM (reprint author), NCI, Div Canc Control & Populat Sci, Behav Res Program, Room 3E564,MSC 9761,9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM lginexi@mail.nih.gov
NR 18
TC 3
Z9 3
U1 3
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1462-2203
EI 1469-994X
J9 NICOTINE TOB RES
JI Nicotine Tob. Res.
PD MAY
PY 2014
VL 16
SU 2
BP S73
EP S75
DI 10.1093/ntr/ntt273
PG 3
WC Substance Abuse; Public, Environmental & Occupational Health
SC Substance Abuse; Public, Environmental & Occupational Health
GA AF4JS
UT WOS:000334678700002
PM 24711629
ER
PT J
AU Fakhry, C
Psyrri, A
Chaturvedhi, A
AF Fakhry, Carole
Psyrri, Amanda
Chaturvedhi, Anil
TI HPV and head and neck cancers: State-of-the-science
SO ORAL ONCOLOGY
LA English
DT Editorial Material
ID SQUAMOUS-CELL CARCINOMAS; HUMAN-PAPILLOMAVIRUS; OROPHARYNGEAL CANCER;
UNITED-STATES; RETINOBLASTOMA PROTEIN; ORAL-CAVITY; RISK-FACTOR;
PHENOTYPE; INFECTION; PROFILES
C1 [Fakhry, Carole] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Psyrri, Amanda] Attikon Univ Hosp, Athens, Greece.
[Chaturvedhi, Anil] NCI, Bethesda, MD 20892 USA.
RP Fakhry, C (reprint author), Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
NR 39
TC 9
Z9 9
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD MAY
PY 2014
VL 50
IS 5
BP 353
EP 355
DI 10.1016/j.oraloncology.2014.03.010
PG 3
WC Oncology; Dentistry, Oral Surgery & Medicine
SC Oncology; Dentistry, Oral Surgery & Medicine
GA AF3AK
UT WOS:000334583600007
PM 24726207
ER
PT J
AU Chen, B
Yoon, JS
Hu, BR
Basta, M
AF Chen, Bo
Yoon, Jeong Seon
Hu, Bingren
Basta, Milan
TI High-dose intravenous immunoglobulin exerts neuroprotective effect in
the rat model of neonatal asphyxia
SO PEDIATRIC RESEARCH
LA English
DT Article
ID ISCHEMIC-STROKE; IMMUNE DAMAGE; BRAIN-INJURY; CELL-DEATH; ACTIVATION;
PROTECTS; SYSTEM
AB BACKGROUND: Neonatal asphyxia is one of the leading causes of death in newborn and permanent neurological disabilities in surviving children. The underlying hypoxic-ischemic (HI) injury triggers an inflammatory response lading to neuronal damage. Here, we tested the hypothesis that high-dose intravenous immunoglobulin (IVIG) could exert immunomodulatory effect in rat pups subjected to HI injury.
METHODS: HI injury was induced in 7-d-old pups by ligating the common carotid artery followed by exposure to 8% oxygen for 2 h. Brain infarction was evaluated by imaging stained coronal brain sections. Neurological deficits were assessed in weeks 1 through 4 after HI. Western blotting and immunohistochemistry were used to assess complement fragment deposition in the brain tissue.
RESULTS: Treatment with IVIG at 2 g/kg significantly and in a dose-responsive manner reduced brain infarction size as well as mortality and neurological deficits caused by HI. Anatomical and functional improvements in IVIG-treated pups correlated with decreased deposition of C3b complement fragments in the injured brain hemisphere.
CONCLUSION: IVIG significantly improved the outcome of HI injury in rat pups and could potentially be used for the treatment of human neonatal asphyxia to target proinflammatory complement fragments.
C1 [Chen, Bo; Hu, Bingren] Univ Maryland, Sch Med, Dept Anesthesiol, Shock Trauma & Anesthesiol Res Ctr, Baltimore, MD 21201 USA.
[Yoon, Jeong Seon] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Basta, Milan] BioVisions Inc, Potomac, MD 20854 USA.
RP Basta, M (reprint author), BioVisions Inc, Potomac, MD 20854 USA.
EM basta.milan@gmail.com
OI Basta, Milan/0000-0001-5958-9241
FU Investigator Initiated Study (IIS) Award from Baxter Healthcare
(Westlake Village, CA)
FX This study was supported by Investigator Initiated Study (IIS) Award
from Baxter Healthcare (Westlake Village, CA).
NR 20
TC 1
Z9 1
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0031-3998
EI 1530-0447
J9 PEDIATR RES
JI Pediatr. Res.
PD MAY
PY 2014
VL 75
IS 5
BP 612
EP 617
DI 10.1038/pr2014.12
PG 6
WC Pediatrics
SC Pediatrics
GA AF6JL
UT WOS:000334821200005
PM 24488088
ER
PT J
AU Newburg, DS
Grave, G
AF Newburg, David S.
Grave, Gilman
TI Recent advances in human milk glycobiology
SO PEDIATRIC RESEARCH
LA English
DT Editorial Material
ID TANDEM MASS-SPECTROMETRY; LIQUID-CHROMATOGRAPHY; FED INFANTS;
OLIGOSACCHARIDES; MICROARRAYS; LIBRARY; GLYCOME
C1 [Newburg, David S.] Boston Coll, Dept Biol, Chestnut Hill, MA 02167 USA.
[Grave, Gilman] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Growth & Nutr Branch, NIH, Bethesda, MD USA.
RP Newburg, DS (reprint author), Boston Coll, Dept Biol, Chestnut Hill, MA 02167 USA.
EM david.newburg@bc.edu
FU NIAID NIH HHS [U01 AI075563, AI075563]; NICHD NIH HHS [HD013021,
HD059140, HD061930, P01 HD013021, R01 HD059140, R01 HD061930]
NR 31
TC 10
Z9 11
U1 0
U2 24
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0031-3998
EI 1530-0447
J9 PEDIATR RES
JI Pediatr. Res.
PD MAY
PY 2014
VL 75
IS 5
BP 675
EP 679
DI 10.1038/pr.2014.24
PG 5
WC Pediatrics
SC Pediatrics
GA AF6JL
UT WOS:000334821200015
PM 24522101
ER
PT J
AU Widemann, BC
Schwartz, S
Jayaprakash, N
Christensen, R
Pui, CH
Chauhan, N
Daugherty, C
King, TR
Rush, JE
Howard, SC
AF Widemann, Brigitte C.
Schwartz, Stefan
Jayaprakash, Nalini
Christensen, Robbin
Pui, Ching-Hon
Chauhan, Nikhil
Daugherty, Claire
King, Thomas R.
Rush, Janet E.
Howard, Scott C.
TI Efficacy of Glucarpidase (Carboxypeptidase G2) in Patients with Acute
Kidney Injury After High-Dose Methotrexate Therapy
SO PHARMACOTHERAPY
LA English
DT Article
DE glucarpidase; acute kidney injury; carboxypeptidase; methotrexate
ID INDUCED RENAL DYSFUNCTION; HIGH-FLUX HEMODIALYSIS; LEUCOVORIN RESCUE;
CANCER-PATIENTS; NEPHROTOXICITY; TOXICITY; THYMIDINE; ACID;
PHARMACOKINETICS; PHARMACOLOGY
AB Study Objective
Because the incidence rate of renal impairment is 2-10% for patients treated with high-dose methotrexate and renal impairment develops in 0-12.4% of patients treated for osteosarcoma, we sought to evaluate the efficacy of glucarpidase, a recently approved drug that rapidly hydrolyzes methotrexate to inactive metabolites, which allows for nonrenal clearance in patients with delayed renal methotrexate elimination.
Design
Pooled analysis of efficacy data from four multicenter single-arm compassionate-use clinical trials using protocols from 1993 to 2007.
Patients
Of 476 patients with renal toxicity and delayed methotrexate elimination who were treated with intravenous glucarpidase for rescue after high-dose methotrexate, 169 patients had at least one preglucarpidase (baseline) plasma methotrexate concentration greater than 1 mu mol/L and one postglucarpidase methotrexate concentration measurement by high-performance liquid chromatography and were included in the efficacy analysis; renal recovery was assessed in 436 patients who had at least one recorded preglucarpidase and postglucarpidase serum creatinine concentration measurement.
Measurements and Main Results
Efficacy was defined as rapid and sustained clinically important reduction (RSCIR) in plasma methotrexate concentration, with a concentration of 1 mu mol/L or lower at all postglucarpidase determinations. Median age of efficacy-evaluable patients was 20years (range 5weeks-84years). Osteosarcoma (36%), non-Hodgkin lymphoma (27%), and acute lymphoblastic leukemia (20%) were the most frequent underlying diagnoses. Median preglucarpidase serum methotrexate was 11.7 mu mol/L. At the first (median 15minutes) through the last (median 40hours) postglucarpidase measurement, plasma methotrexate concentrations demonstrated consistent 99% median reduction. RSCIR was achieved by 83 (59%) of 140 patients. A total of 64% of patients with renal impairment greater than or equal to Common Terminology Criteria for Adverse Events grade 2 recovered to grade 0 or 1 at a median of 12.5days after glucarpidase administration.
Conclusion
Glucarpidase caused a clinically important 99% or greater sustained reduction of serum methotrexate levels and provided noninvasive rescue from methotrexate toxicity in renally impaired patients.
C1 [Widemann, Brigitte C.; Jayaprakash, Nalini] NCI, Bethesda, MD 20892 USA.
[Schwartz, Stefan] Charite, D-13353 Berlin, Germany.
[Christensen, Robbin; Pui, Ching-Hon; Howard, Scott C.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Chauhan, Nikhil; Daugherty, Claire; King, Thomas R.; Rush, Janet E.] BTG Int Inc, W Conshohocken, PA 19428 USA.
RP King, TR (reprint author), BTG Int Inc, Five Tower Bridge,Suite 800,300 Barr Harbor Dr, W Conshohocken, PA 19428 USA.
EM thomas.king@btgplc.com
FU BTG International Inc.
FX Preparation of this manuscript for publication from the authors'
original creation was sponsored by BTG International Inc.
NR 34
TC 9
Z9 9
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-0008
EI 1875-9114
J9 PHARMACOTHERAPY
JI Pharmacotherapy
PD MAY
PY 2014
VL 34
IS 5
BP 427
EP 439
DI 10.1002/phar.1360
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AF7VX
UT WOS:000334924200005
PM 24132809
ER
PT J
AU Masaki, T
Wang, Y
DiGiovanna, JJ
Khan, SG
Raffeld, M
Beltaifa, S
Hornyak, TJ
Darling, TN
Lee, CCR
Kraemer, KH
AF Masaki, Taro
Wang, Yun
DiGiovanna, John J.
Khan, Sikandar G.
Raffeld, Mark
Beltaifa, Senda
Hornyak, Thomas J.
Darling, Thomas N.
Lee, Chyi-Chia R.
Kraemer, Kenneth H.
TI High frequency of PTEN mutations in nevi and melanomas from xeroderma
pigmentosum patients
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Article
DE xeroderma pigmentosum; melanoma; PTEN; nevi; mTOR; DNA repair; UV
carcinogenesis
ID DNA-POLYMERASE-IOTA; MALIGNANT-MELANOMA; CUTANEOUS MELANOMA; METASTATIC
MELANOMA; SKIN CARCINOGENESIS; GENETIC ALTERATIONS; DISTINCT SUBTYPES;
MELANOCYTIC NEVI; MTOR PATHWAY; BRAF
AB We examined nevi and melanomas in 10 xeroderma pigmentosum (XP) patients with defective DNA repair. The lesions had a lentiginous appearance with markedly increased numbers of melanocytes. Using laser capture microdissection, we performed DNA sequencing of 18 benign and atypical nevi and 75 melanomas (melanoma in situ and invasive melanomas). The nevi had a similar high frequency of PTEN mutations as melanomas [61% (11/18) versus 53% (39/73)]. Both had a very high proportion of UV-type mutations (occurring at adjacent pyrimidines) [91% (10/11) versus 92% (36/39)]. In contrast to melanomas in the general population, the frequency of BRAF mutations (11%, 7/61), NRAS mutations (21%, 13/62), and KIT mutations (21%, 6/28) in XP melanomas was lower than for PTEN. Phospho-S6 immunostaining indicated activation of the mTOR pathway in the atypical nevi and melanomas. Thus, the clinical and histological appearances and the molecular pathology of these UV-related XP nevi and melanomas were different from nevi and melanomas in the general population.
C1 [Masaki, Taro; Wang, Yun; DiGiovanna, John J.; Khan, Sikandar G.; Hornyak, Thomas J.; Kraemer, Kenneth H.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Masaki, Taro] Kobe Univ, Grad Sch Med, Div Dermatol, Kobe, Hyogo 657, Japan.
[Wang, Yun] Peking Univ First Hosp, Dept Dermatol, Beijing, Peoples R China.
[Raffeld, Mark; Beltaifa, Senda; Lee, Chyi-Chia R.] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Hornyak, Thomas J.] Univ Maryland Med Ctr, Dept Dermatol, Baltimore, MD USA.
[Darling, Thomas N.] Uniformed Serv Univ Hlth Sci, Dept Dermatol, Bethesda, MD 20814 USA.
RP Kraemer, KH (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA.
EM kraemerk@nih.gov
OI Darling, Thomas/0000-0002-5161-1974
NR 48
TC 12
Z9 12
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1755-1471
EI 1755-148X
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD MAY
PY 2014
VL 27
IS 3
BP 454
EP 464
DI 10.1111/pcmr.12226
PG 11
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA AE7IM
UT WOS:000334170900016
PM 24483290
ER
PT J
AU Gutierrez, N
Eromobor, I
Petrie, RJ
Vedula, P
Cruz, L
Rodriguez, AJ
AF Gutierrez, Natasha
Eromobor, Itua
Petrie, Ryan J.
Vedula, Pavan
Cruz, Lissette
Rodriguez, Alexis J.
TI The beta-actin mRNA zipcode regulates epithelial adherens junction
assembly but not maintenance
SO RNA-A PUBLICATION OF THE RNA SOCIETY
LA English
DT Article
DE RhoA and Src signaling; actin cytoskeleton regulation; actin mRNA
zipcodes; adherens junction assembly; translation regulation
ID CELL-CELL ADHESION; BREAST-CANCER CELLS; E-CADHERIN; MAMMALIAN-CELLS;
RATE CONSTANTS; LIVING CELLS; CONTACTS; LOCALIZATION; DYNAMICS; RAC
AB Epithelial cell-cell contact stimulates actin cytoskeleton remodeling to down-regulate branched filament polymerization-driven lamellar protrusion and subsequently to assemble linear actin filaments required for E-cadherin anchoring during adherens junction complex assembly. In this manuscript, we demonstrate that de novo protein synthesis, the beta-actin 3 ' UTR, and the beta-actin mRNA zipcode are required for epithelial adherens junction complex assembly but not maintenance. Specifically, we demonstrate that perturbing cell-cell contact-localized beta-actin monomer synthesis causes epithelial adherens junction assembly defects. Consequently, inhibiting beta-actin mRNA zipcode/ZBP1 interactions with beta-actin mRNA zipcode antisense oligonucleotides, to intentionally delocalize beta-actin monomer synthesis, is sufficient to perturb adherens junction assembly following epithelial cell-cell contact. Additionally, we demonstrate active RhoA, the signal required to drive zipcode-mediated beta-actin mRNA targeting, is localized at epithelial cell-cell contact sites in a beta-actin mRNA zipcode-dependent manner. Moreover, chemically inhibiting Src kinase activity prevents the local stimulation of beta-actin monomer synthesis at cell-cell contact sites while inhibiting epithelial adherens junction assembly. Together, these data demonstrate that epithelial cell-cell contact stimulates beta-actin mRNA zipcode-mediated monomer synthesis to spatially regulate actin filament remodeling, thereby controlling adherens junction assembly to modulate cell and tissue adhesion.
C1 [Gutierrez, Natasha; Eromobor, Itua; Vedula, Pavan; Cruz, Lissette; Rodriguez, Alexis J.] Rutgers State Univ, Dept Biol Sci, Newark, NJ 07102 USA.
[Petrie, Ryan J.] NIH, Natl Inst Dent & Craniofacial Res, Bethesda, MD 20892 USA.
RP Rodriguez, AJ (reprint author), Rutgers State Univ, Dept Biol Sci, Newark, NJ 07102 USA.
EM ajrod@andromeda.rutgers.edu
FU NSF [0088668]; NIH [R25 60825-06]; Rutgers Research Exchange Program
FX This work was supported by NSF # 0088668, NSF # 0538554, and NIH R25
60825-06 to N.G. and L.C., and the Rutgers Research Exchange Program to
A.J.R.
NR 42
TC 2
Z9 2
U1 0
U2 9
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1355-8382
EI 1469-9001
J9 RNA
JI RNA-Publ. RNA Soc.
PD MAY
PY 2014
VL 20
IS 5
BP 689
EP 701
DI 10.1261/rna.043208.113
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AF4JJ
UT WOS:000334677800010
PM 24681968
ER
PT J
AU Yin, F
Battiwalla, M
Ito, S
Feng, XM
Chinian, F
Melenhorst, JJ
Koklanaris, E
Sabatino, M
Stroncek, D
Samsel, L
Klotz, J
Hensel, NF
Robey, PG
Barrett, AJ
AF Yin, Fang
Battiwalla, Minoo
Ito, Sawa
Feng, Xingmin
Chinian, Fariba
Melenhorst, Jan Joseph
Koklanaris, Eleftheria
Sabatino, Marianna
Stroncek, David
Samsel, Leigh
Klotz, Jeffrey
Hensel, Nancy F.
Robey, Pamela G.
Barrett, A. John
TI Bone Marrow Mesenchymal Stromal Cells to Treat Tissue Damage in
Allogeneic Stem Cell Transplant Recipients: Correlation of Biological
Markers with Clinical Responses
SO STEM CELLS
LA English
DT Article
DE Allogeneic stem cell transplantation; Graft-versus-host disease;
Biomarkers; Mesenchymal stromal cell
ID VERSUS-HOST-DISEASE; BIOMARKERS; THERAPY; BLOOD; DONOR
AB Bone marrow mesenchymal stromal cells (BMSCs) have been used to treat acute graft-versus-host disease (GVHD) and other complications following allogeneic hematopoietic stem cell transplantation (SCT). We conducted a phase I trial using third party, early passage BMSCs for patients with steroid-refractory GVHD, tissue injury, or marrow failure following SCT to investigate safety and efficacy. To identify mechanisms of BMSC immunomodulation and tissue repair, patients were serially monitored for plasma GVHD biomarkers, cytokines, and lymphocyte phenotype. Ten subjects were infused a fixed dose of 2 x 10(6) BMSCs/kg intravenously weekly for three doses. There was no treatment-related toxicity (primary endpoint). Eight subjects were evaluable for response at 4 weeks after the last infusion. Five of the seven patients with steroid-refractory acute GVHD achieved a complete response, two of two patients with tissue injury (pneumomediastinum/pneumothorax) achieved resolution but there was no response in two subjects with delayed marrow failure. Rapid reductions in inflammatory cytokines were observed. Clinical responses correlated with a fall in biomarkers (Reg 3 alpha, CK18, and Elafin) relevant for the site of GVHD or tissue injury. The GVHD complete responders survived significantly longer and had higher baseline absolute lymphocyte and central memory CD4 and CD8 counts. Cytokine changes also segregated with survival. These results confirm that BMSCs are associated with rapid clinical and biomarker responses in GVHD and tissue injury. However, BMSCs were ineffective in patients with prolonged GVHD with lower lymphocyte counts, which suggest that effective GVHD control by BMSCs requires a relatively intact immune system. Stem Cells 2014;32:1278-1288
C1 [Yin, Fang; Battiwalla, Minoo; Ito, Sawa; Feng, Xingmin; Chinian, Fariba; Melenhorst, Jan Joseph; Koklanaris, Eleftheria; Klotz, Jeffrey; Hensel, Nancy F.; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Melenhorst, Jan Joseph] Univ Penn, Dept Pathol & Lab Med, Abramson Canc Ctr, Perelman Sch Med, Philadelphia, PA USA.
[Sabatino, Marianna; Stroncek, David] NIH, Cell Proc Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Samsel, Leigh] NHLBI, Flow Cytometry Core, NIH, Bethesda, MD 20892 USA.
[Robey, Pamela G.] NIDCR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA.
RP Barrett, AJ (reprint author), NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
EM barrettjj@nhlbi.nih.gov
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
FU Intramural Research Program of the National Heart Lung and Blood
Institute; Intramural Research Program of the Clinical Center;
Intramural Research Program of the National Institute of Dental and
Craniofacial Research, NIH
FX This research was supported by the Intramural Research Programs of the
National Heart Lung and Blood Institute, the Clinical Center and the
National Institute of Dental and Craniofacial Research, NIH.
NR 17
TC 21
Z9 22
U1 0
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD MAY
PY 2014
VL 32
IS 5
BP 1278
EP 1288
DI 10.1002/stem.1638
PG 11
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA AF3FP
UT WOS:000334597200021
PM 24452962
ER
PT J
AU Humeniuk, R
Koller, R
Bies, J
Aplan, P
Wolff, L
AF Humeniuk, Rita
Koller, Richard
Bies, Juraj
Aplan, Peter
Wolff, Linda
TI Brief Report: Loss of p15Ink4b Accelerates Development of Myeloid
Neoplasms in Nup98-HoxD13 Transgenic Mice
SO STEM CELLS
LA English
DT Article
DE p15Ink4b; Myeloproliferative disease; Acute myelogenous leukemia;
Myelodysplastic syndromes; Nup98-HoxD13; Transgenic mouse
ID TUMOR-SUPPRESSOR; MYELODYSPLASTIC SYNDROMES; BETHESDA PROPOSALS;
LEUKEMIA; INACTIVATION; METHYLATION; HYPERMETHYLATION; CLASSIFICATION;
P15(INK4B); P15
AB Homeostasis of hematopoietic stem and progenitor cells is a tightly regulated process. The disturbance of the balance in the hematopoietic progenitor pool can result in favorable conditions for development of diseases such as myelodysplastic syndromes and leukemia. It has been shown recently that mice lacking p15Ink4b have skewed differentiation of common myeloid progenitors toward the myeloid lineage at the expense of erythroid progenitors. The lack of p15INK4B expression in human leukemic blasts has been linked to poor prognosis and increased risk of myelodysplastic syndromes transformation to acute myeloid leukemia. However, the role of p15Ink4b in disease development is just beginning to be elucidated. This study examines the collaboration of the loss of p15Ink4b with Nup98-HoxD13 translocation in the development of hematological malignancies in a mouse model. Here, we report that loss of p15Ink4b collaborates with Nup98-HoxD13 transgene in the development of predominantly myeloid neoplasms, namely acute myeloid leukemia, myeloproliferative disease, and myelodysplastic syndromes. This mouse model could be a very valuable tool for studying p15Ink4b function in tumorigenesis as well as preclinical drug testing. Stem Cells 2014;32:1361-1366
C1 [Humeniuk, Rita; Koller, Richard; Bies, Juraj; Aplan, Peter; Wolff, Linda] NCI, NIH, Bethesda, MD 20892 USA.
RP Wolff, L (reprint author), 37 Convent Dr, Bethesda, MD 20892 USA.
EM wolffl@mail.nih.gov
RI Aplan, Peter/K-9064-2016
NR 17
TC 3
Z9 3
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD MAY
PY 2014
VL 32
IS 5
BP 1361
EP 1366
DI 10.1002/stem.1635
PG 6
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA AF3FP
UT WOS:000334597200028
PM 24449168
ER
PT J
AU Iniguez, SD
Riggs, LM
Nieto, SJ
Dayrit, G
Zamora, NN
Shawhan, KL
Cruz, B
Warren, BL
AF Iniguez, Sergio D.
Riggs, Lace M.
Nieto, Steven J.
Dayrit, Genesis
Zamora, Norma N.
Shawhan, Kristi L.
Cruz, Bryan
Warren, Brandon L.
TI Social defeat stress induces a depression-like phenotype in adolescent
male c57BL/6 mice
SO STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS
LA English
DT Article
DE Anhedonia; animal model; anxiety; bullying; depression; forced swim
test; juvenile; mood disorders
ID UNPREDICTABLE MILD STRESS; ANIMAL-MODELS; MOOD DISORDERS; ADULTHOOD;
ANXIETY; BEHAVIOR; RATS; BRAIN; ANTIDEPRESSANT; PREFERENCE
AB Exposure to stress is highly correlated with the emergence of mood-related illnesses. Because major depressive disorder often emerges in adolescence, we assessed the effects of social defeat stress on responses to depressive-like behaviors in juvenile mice. To do this, postnatal day (PD) 35 male c57BL/6 mice were exposed to 10 days of social defeat stress (PD35-44), while control mice were handled daily. Twenty-four hours after the last episode of defeat (PD45), separate groups of mice were tested in the social interaction, forced swimming, sucrose preference, and elevated plus-maze behavioral assays (n = 7-12 per group). Also, we examined body weight gain across days of social defeat and levels of blood serum corticosterone 40 min after the last episode of defeat stress. Our data indicates that defeated mice exhibited a depressive-like phenotype as inferred from increased social avoidance, increased immobility in the forced swim test, and reduced sucrose preference (a measure of anhedonia), when compared to non-defeated controls. Defeated mice also displayed an anxiogenic-like phenotype when tested on the elevated plus-maze. Lastly, stressed mice displayed lower body weight gain, along with increased blood serum corticosterone levels, when compared to non-stressed controls. Overall, we show that in adolescent male c57BL/6 mice, social defeat stress induces a depression-and anxiety-like phenotype 24 h after the last episode of stress. These data suggest that the social defeat paradigm may be used to examine the etiology of stress-induced mood-related disorders during adolescence.
C1 [Iniguez, Sergio D.; Riggs, Lace M.; Nieto, Steven J.; Dayrit, Genesis; Zamora, Norma N.; Shawhan, Kristi L.; Cruz, Bryan] Calif State Univ San Bernardino, Dept Psychol, San Bernardino, CA 92407 USA.
[Warren, Brandon L.] NIDA, Intramural Res Program, NIH, Baltimore, MD USA.
RP Iniguez, SD (reprint author), Calif State Univ San Bernardino, Dept Psychol, 5500 Univ Pkwy, San Bernardino, CA 92407 USA.
EM iniguez@csusb.edu
RI Iniguez, Sergio/J-2410-2015
FU National Institutes of Health (NIH); National Institute on Drug Abuse
[R24DA033877]; California State University Program for Education and
Research in Biotechnology grant; Associated Students Incorporated grants
from CSUSB
FX The National Institutes of Health (NIH) provided funding for this study.
The NIH had no involvement in the design of the study, data collection
process, or interpretation of the results. The funding sources did not
play any role in writing the research manuscript or the decision to
submit the paper for publication. This work was supported by a grant
from the National Institute on Drug Abuse (R24DA033877 to SDI), a
California State University Program for Education and Research in
Biotechnology grant (to SDI), and the Associated Students Incorporated
grants from CSUSB (to LMR, SJN, GD, NNZ, KLS, and BC).
NR 56
TC 23
Z9 23
U1 2
U2 25
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1025-3890
EI 1607-8888
J9 STRESS
JI Stress
PD MAY
PY 2014
VL 17
IS 3
BP 247
EP 255
DI 10.3109/10253890.2014.910650
PG 9
WC Behavioral Sciences; Endocrinology & Metabolism; Neurosciences
SC Behavioral Sciences; Endocrinology & Metabolism; Neurosciences &
Neurology
GA AF8BQ
UT WOS:000334940500006
PM 24689732
ER
PT J
AU Al-Awadi, AR
Al-Kuhlani, A
Breman, JG
Doumbo, O
Eberhard, ML
Guiguemde, RT
Magnussen, P
Molyneux, DH
Nadim, A
AF Al-Awadi, Abdul R.
Al-Kuhlani, Abdulhakim
Breman, Joel G.
Doumbo, Ogobara
Eberhard, Mark L.
Guiguemde, Robert T.
Magnussen, Pascal
Molyneux, David H.
Nadim, Abolhassan
TI Guinea worm (Dracunculiasis) eradication: update on progress and endgame
challenges
SO TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Editorial Material
DE Dracunculiasis; Dracunculus medinensis Guinea worm; Eradication
ID INSIGNIS NEMATODA; DRACUNCULOIDEA; CERTIFICATION; DISEASE
AB The International Commission for the Certification of Dracunculiasis Eradication (ICCDE) met in December to review progress towards eradication. The status of the programme was presented by WHO and The Carter Center, Atlanta. The Commission received reports from international certification teams that Cote dIvoire, Niger and Nigeria were free of transmission and should be certified, while four countries, namely Chad, Ethiopia, Mali and South Sudan, remained endemic. The Commission certified that Somalia and South Africa were free of transmission. During 2013, there was a decline of about 78 in the numbers of cases reported in South Sudan. A report of the perplexing dracunculiasis epidemiology in Chad was also discussed, where dogs have been found to be infected with Dracunculus medinensis.
C1 [Al-Awadi, Abdul R.] Islamic Org Med Sci, Sulibikhat 90803, Kuwait.
[Al-Kuhlani, Abdulhakim] Minist Publ Hlth & Populat, Sect PHC, Sanaa, Yemen.
[Breman, Joel G.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Doumbo, Ogobara] Univ Mali, Fac Med, Dept Epidemiol Affect Parasitaires, Bamako, Mali.
[Eberhard, Mark L.] Ctr Dis Control & Prevent, Div Parasit Dis & Malaria, Atlanta, GA 30333 USA.
[Guiguemde, Robert T.] Univ Bobo Dioulasso, Burkina Natl Acad Sci, Bobo Dioulasso 01, Burkina Faso.
[Magnussen, Pascal] Univ Copenhagen, Inst Vet Dis, Biol Sect Parasitol & Aquat Dis, DK-1781 Frederiksberg C, Denmark.
[Molyneux, David H.] Univ Liverpool, Liverpool Sch Trop Med, Liverpool L3 5QA, Merseyside, England.
RP Molyneux, DH (reprint author), Univ Liverpool, Liverpool Sch Trop Med, Pembroke Pl, Liverpool L3 5QA, Merseyside, England.
EM david.molyneux@liv.ac.uk
NR 11
TC 12
Z9 12
U1 11
U2 45
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0035-9203
EI 1878-3503
J9 T ROY SOC TROP MED H
JI Trans. Roy. Soc. Trop. Med. Hyg.
PD MAY
PY 2014
VL 108
IS 5
BP 249
EP 251
DI 10.1093/trstmh/tru039
PG 3
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA AF5LE
UT WOS:000334754200002
PM 24699360
ER
PT J
AU Post, RM
Leverich, GS
Kupka, R
Keck, P
McElroy, S
Altshuler, L
Frye, MA
Luckenbaugh, DA
Rowe, M
Grunze, H
Suppes, T
Nolen, WA
AF Post, R. M.
Leverich, G. S.
Kupka, R.
Keck, P., Jr.
McElroy, S.
Altshuler, L.
Frye, M. A.
Luckenbaugh, D. A.
Rowe, M.
Grunze, H.
Suppes, T.
Nolen, W. A.
TI Increased parental history of bipolar disorder in the United States:
association with early age of onset
SO ACTA PSYCHIATRICA SCANDINAVICA
LA English
DT Article
DE assortative mating; bipolar disorder; childhood onset bipolar disorder;
genetics
ID ASTERISK-D-CHILD; MATERNAL DEPRESSION; MENTAL-DISORDERS; OUTPATIENTS;
RISK; RATINGS
AB Objective
Early-onset bipolar (BP) disorder and other poor prognosis characteristics are more prevalent in patients from the United States than from the Netherlands and Germany (abbreviated as Europe). We explored the impact of parental loading for affective illness on onset and other characteristics of BP disorder.
Method
Parental history for unipolar (UP) and bipolar (BP) depression and course of illness characteristics were obtained from self-report in adults (average age 42) with BP disorder. Illness characteristics were examined by chi(2) and multinomial logistic regression in relationship to the degree of parental loading: i) both parents negative; ii) one UP disorder; iii) one with BP disorder; and iv) both affected.
Results
After controlling for many poor prognosis factors, compared with those from Europe, patients from the United States had more iii) one parent with BP disorder and iv) both parents affected. An early age of onset of BP disorder was independently associated with this increased parental loading for affective disorder.
Conclusion
Parental history of BP disorder and both parents with a mood disorder were more common in the United States than Europe and were associated with an early onset of bipolar disorder and other poor prognosis characteristics. These findings deserve replication and exploration of the potential mechanisms involved and their therapeutic implications.
C1 [Post, R. M.; Leverich, G. S.; Rowe, M.] Bipolar Collaborat Network, Bethesda, MD 20814 USA.
[Post, R. M.] George Washington Univ, Dept Psychiat & Behav Sci, Washington, DC USA.
[Kupka, R.] Vrije Univ Amsterdam, Dept Psychiat, Med Ctr, Amsterdam, Netherlands.
[Keck, P., Jr.] Univ Cincinnati, Coll Med, Dept Psychiat & Behav Neurosci, Cincinnati, OH USA.
[Keck, P., Jr.; McElroy, S.] Lindner Ctr HOPE, Mason, OH USA.
[McElroy, S.] Univ Cincinnati, Coll Med, Biol Psychiat Program, Cincinnati, OH USA.
[Altshuler, L.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Altshuler, L.] VA Greater Los Angeles Healthcare Syst, Dept Psychiat, West Los Angeles Healthcare Ctr, Los Angeles, CA USA.
[Frye, M. A.] Mayo Clin, Dept Psychiat, Rochester, MI USA.
[Luckenbaugh, D. A.] NIMH, NIH, Bethesda, MD 20892 USA.
[Grunze, H.] Newcastle Univ, Inst Neurosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Suppes, T.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.
[Suppes, T.] VA Palo Alto Hlth Care Syst, Palo Alto, CA USA.
[Nolen, W. A.] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands.
RP Post, RM (reprint author), Bipolar Collaborat Network, 5415 W Cedar Lane 201B, Bethesda, MD 20814 USA.
EM robert.post@speakeasy.net
OI Grunze, Heinz/0000-0003-4712-8979
FU AstraZeneca; Alkermes; Cephalon; GlaxoSmithKline; Eli Lilly; Marriott
Foundation; National Institute of Mental Health; National Institute of
Drug Abuse; Orexigen; Pfizer Inc.; Shire; Abbott; Bristol-Myers Squibb;
Forest; Jazz; Takeda; Johnson & Johnson Pharmaceutical Research
Development; Sepracor; Takeda Pharmaceuticals North America, Inc.; H.
Lundbeck A/S; Sunovion Pharmaceuticals Inc.; Pfizer; Astra-Zeneca; Bial;
Janssen-Cilag; Sanofi-Aventis; Servier; United BioSource Corporation;
Netherlands Organization for Health Research and Development; European
Union; Stanley Medical Research Institute; Wyeth
FX Dr. Kupka has received research grants from AstraZeneca and honoraria
from Eli Lilly, Janssen-Cilag, Bristol-Myers Squibb, and AstraZeneca.;
Dr. Keck is employed by the University of Cincinnati College of Medicine
and University of Cincinnati Physicians. Dr. Keck is a principal or
coinvestigator on research studies sponsored by Alkermes, AstraZeneca,
Cephalon, GlaxoSmithKline, Eli Lilly, Marriott Foundation, the National
Institute of Mental Health, the National Institute of Drug Abuse,
Orexigen, Pfizer Inc., and Shire, and has been reimbursed for consulting
to, in the past 2 years, Bristol-Myers-Squibb, Teva, Otsuka, Forest,
Merck, Sunovion, Alkermes, and Shire. Dr. Keck is also inventor on US
Patent No. 6,387,956: Shapira NA, Goldsmith TD, Keck PE Jr (University
of Cincinnati), Methods of Treating Obsessive-Compulsive Spectrum
Disorder Comprises the Step of Administering an Effective Amount of
Tramadol to an Individual; filed March 25, 1999; approved May 14, 2002.;
Dr. McElroy is a consultant to or member of the scientific advisory
boards of Eli Lilly and Schering-Plough and is a principal or
coinvestigator on research studies sponsored by Abbott, AstraZeneca,
Bristol-Myers Squibb, Cephalon, Eli Lilly, Forest, GlaxoSmithKline,
Jazz, the Marriott Foundation, the National Institute of Mental Health,
Orexigen, Shire, and Takeda. Dr. McElroy is also inventor on US Patent
No. 6,323,236, Use of Sulfamate Derivatives for Treating Impulse Control
Disorders, and, along with the patent's assignee, the University of
Cincinnati, has received payments from Johnson & Johnson Pharmaceutical
Research & Development, which has exclusive rights under the patent.;
Dr. Altshuler has received past funding from Sepracor (advisory board
honoraria, January 2010), and Eli Lilly (consultant, September 2010) and
past and potential future funding from Takeda Pharmaceuticals North
America, Inc., and H. Lundbeck A/S (advisory board honoraria, October
2012) and Sunovion Pharmaceuticals Inc. (advisory board honoraria,
January 2013).; Dr. Frye has received grant support from Pfizer (drug
supply: varenicline), has been a consultant to Cephalon, Dainippon
Sumitomo, Ortho McNeil/Janssen, Johnson & Johnson, Schering-Plough, and
Pfizer, and has participated in supported CME activities for
AstraZeneca, Bristol-Myers Squibb, Eli Lilly, GlaxoSmithKline, Otsuka,
Pfizer, and Schering-Plough.; Dr. Grunze has received grant/research
support, consulting fees, and honoraria within the last 3 years from
Astra-Zeneca, Bial, Bristol-Myers Squibb, Eli Lilly, Lundbeck,
Janssen-Cilag, Sanofi-Aventis, Servier, United BioSource Corporation.;
Dr. Nolen has received grants from The Netherlands Organization for
Health Research and Development, the European Union, The Stanley Medical
Research Institute, AstraZeneca, Eli Lilly, GlaxoSmithKline, and Wyeth;
has received honoraria or speaker's fees from AstraZeneca, Eli Lilly,
Pfizer, Servier, and Wyeth; and has served on the advisory boards of
AstraZeneca, Cyberonics, Pfizer, and Servier.
NR 25
TC 19
Z9 19
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0001-690X
EI 1600-0447
J9 ACTA PSYCHIAT SCAND
JI Acta Psychiatr. Scand.
PD MAY
PY 2014
VL 129
IS 5
SI SI
BP 375
EP 382
DI 10.1111/acps.12208
PG 8
WC Psychiatry
SC Psychiatry
GA AE8AP
UT WOS:000334221600006
PM 24138298
ER
PT J
AU Barranger, JA
Brady, RO
Grabowski, GA
Mankin, H
Mistry, PK
Weinreb, NJ
AF Barranger, John A.
Brady, Roscoe O.
Grabowski, Gregory A.
Mankin, Henry
Mistry, Pramod K.
Weinreb, Neal J.
TI Position statement: National Gaucher Foundation Medical Advisory Board,
January 7, 2014
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Editorial Material
ID ENZYME REPLACEMENT THERAPY; VELAGLUCERASE ALPHA; SKELETAL
MANIFESTATIONS; TALIGLUCERASE ALPHA; DISEASE PATIENTS; TYPE-1;
IMIGLUCERASE; EXPERIENCE; GLUCOCEREBROSIDASE; IMPROVEMENT
C1 [Barranger, John A.] Lysosomal Storage Dis Clin Care Network, Pittsburgh, PA USA.
[Brady, Roscoe O.] NIH, Bethesda, MD 20892 USA.
[Grabowski, Gregory A.] Synageva BioPharma, Lexington, MA USA.
[Mankin, Henry] Massachusetts Gen Hosp, Dept Orthoped Surg, Boston, MA 02114 USA.
[Mistry, Pramod K.] Yale Univ, Sch Med, New Haven, CT USA.
[Weinreb, Neal J.] Univ Res Fdn Lysosomal Storage Dis, Coral Springs, FL USA.
RP Weinreb, NJ (reprint author), 8170 Royal Palm Blvd, Coral Springs, FL 33065 USA.
EM boneal@winning.com
NR 31
TC 2
Z9 2
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD MAY
PY 2014
VL 89
IS 5
BP 457
EP 458
DI 10.1002/ajh.23687
PG 2
WC Hematology
SC Hematology
GA AE9MN
UT WOS:000334332000002
PM 24488939
ER
PT J
AU Scheinberg, P
Townsley, D
Dumitriu, B
Scheinberg, P
Weinstein, B
Rios, O
Wu, CO
Young, NS
AF Scheinberg, Phillip
Townsley, Danielle
Dumitriu, Bogdan
Scheinberg, Priscila
Weinstein, Barbara
Rios, Olga
Wu, Colin O.
Young, Neal S.
TI Horse antithymocyte globulin as salvage therapy after rabbit
antithymocyte globulin for severe aplastic anemia
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID COLONY-STIMULATING FACTOR; HIGH-DOSE CYCLOPHOSPHAMIDE; ANTI-THYMOCYTE
GLOBULIN; IMMUNOSUPPRESSIVE THERAPY; CYCLOSPORINE; CHILDREN; ATG
AB The effectiveness of salvage therapy for aplastic anemia patients unresponsive to initial rabbit antithymocyte globulin (r-ATG) or cyclophosphamide is not known. We investigated the administration of standard horse ATG (h-ATG) plus cyclosporine (CsA) in patients who were refractory to initial r-ATG/CsA (n = 19) or cyclophosphamide/CsA (n = 6) (registered at as NCT00944749). The primary endpoint was hematologic response at 3 months and was defined as no longer meeting the criteria for severe aplastic anemia. Of the 19 patients who received r-ATG as initial therapy, 4 (21%) achieved a hematologic response by 3 months, and of the 6 patients who received cyclophosphamide, only 1 (17%) responded by 6 months. Among the responders there were no cases of relapse, and in nonresponders 2 patients evolved to monosomy 7. The overall survival for the cohort at 3 years was 68% (95% CI, 50-91%). These results suggest that only a minority can be successfully salvaged after receiving as first therapy either r-ATG or cyclophosphamide. Although h-ATG may be utilized in the salvage setting, the overall response rate probably will be lower than when h-ATG is used as initial treatment. Am. J. Hematol. 89:467-469, 2014. (c) Published 2014.
C1 [Scheinberg, Phillip; Townsley, Danielle; Dumitriu, Bogdan; Scheinberg, Priscila; Weinstein, Barbara; Rios, Olga; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Scheinberg, Phillip] Beneficencia Portuguesa, Hosp Sao Jose, Ctr Oncol, Hematol Serv, Sao Paulo, Brazil.
[Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP Scheinberg, P (reprint author), Rua Martiniano de Carvalho, BR-01321001 Sao Paulo, Brazil.
EM scheinbp@gmail.com
OI Scheinberg, Phillip/0000-0002-9047-4538
FU NIH, National Heart, Lung, and Blood Institute
FX This research was supported by the Intramural Research Program of the
NIH, National Heart, Lung, and Blood Institute.
NR 20
TC 7
Z9 7
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD MAY
PY 2014
VL 89
IS 5
BP 467
EP 469
DI 10.1002/ajh.23669
PG 3
WC Hematology
SC Hematology
GA AE9MN
UT WOS:000334332000004
PM 24415649
ER
PT J
AU Prasad, V
Shea, N
AF Prasad, Vinay
Shea, Neal
TI Open Access Publication, Journal Policy, and Scientific Community Reply
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Prasad, Vinay] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Shea, Neal] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
RP Prasad, V (reprint author), NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
NR 2
TC 2
Z9 2
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9343
EI 1555-7162
J9 AM J MED
JI Am. J. Med.
PD MAY
PY 2014
VL 127
IS 5
DI 10.1016/j.amjmed.2014.01.030
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA AF1XL
UT WOS:000334507100008
PM 24560327
ER
PT J
AU Terrault, N
Reddy, KR
Poordad, F
Curry, M
Schiano, T
Johl, J
Shaikh, O
Dove, L
Shetty, K
Millis, M
Schiff, E
Regenstein, F
Barnes, D
Barin, B
Peters, M
Roland, M
Stock, P
AF Terrault, N.
Reddy, K. R.
Poordad, F.
Curry, M.
Schiano, T.
Johl, J.
Shaikh, O.
Dove, L.
Shetty, K.
Millis, M.
Schiff, E.
Regenstein, F.
Barnes, D.
Barin, B.
Peters, M.
Roland, M.
Stock, P.
CA HIVTR Investigators
TI Peginterferon and Ribavirin for Treatment of Recurrent Hepatitis C
Disease in HCV- HIV Coinfected Liver Transplant Recipients
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Sustained virologic response; histologic response; antiviral therapy
ID HUMAN-IMMUNODEFICIENCY-VIRUS; MULTICENTER EXPERIENCE;
PEGYLATED-INTERFERON; PLUS RIBAVIRIN; SURVIVAL; EFFICACY; SAFETY
AB Achievement of a sustained virologic response (SVR) with antiviral therapy significantly improves graft survival in hepatitis C virus (HCV) monoinfected liver transplant (LT) patients. Risks and benefits of HCV therapy in HCV-human immunodeficiency virus (HIV) coinfected LT recipients are not well established. Among 89 HCV-HIV LT recipients in the HIVTR cohort, 39 (23% Black, 79% genotype 1, 83% fibrosis stage1) were treated with peginterferon-a2a or a2b plus ribavirin for a median 363 days (14-1373). On intent-to-treat basis, 22% (95% CI: 10-39) and 14% (95% CI: 5-30) achieved an end-of-treatment response (EOTR) and SVR, respectively. By per-protocol analysis (completed 48 weeks of therapydose reductions), 42% and 26% had EOTR and SVR, respectively. Severe adverse events occurred in 85%, with 26% hospitalized with infections and 13% developing acute rejection. Early discontinuations and dose reductions occurred in 38% and 82%, respectively, despite use of growth factors in 85%. Eighteen of 39 treated patients (46%) subsequently died/had graft loss, with 10 (26%) attributed to recurrent HCV. In conclusion, SVR rates are low and tolerability is poor in HCV-HIV coinfected transplant recipients treated with peginterferon and ribavirin. These results highlight the critical need for better tolerated and more efficacious HCV therapies for HCV-HIV coinfected transplant recipients.
The authors show that treatment of HCV-HIV coinfected transplant recipients with peginterferon and ribavirin yielded sustained virology responses in only 14% and with high rates of dose reductions (85%), early discontinuation (38%), and severe adverse events (85%).
C1 [Terrault, N.; Peters, M.; Roland, M.] Univ Calif San Francisco, Dept Med, Div Gastroenterol & Hepatol, San Francisco, CA 94143 USA.
[Reddy, K. R.] Univ Penn, Dept Med, Div Gastoenterol & Hepatol, Philadelphia, PA 19104 USA.
[Poordad, F.] Univ Texas Hlth Sci Ctr San Antonio, Texas Liver Inst, Univ Transplant Ctr, San Antonio, TX 78229 USA.
[Curry, M.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Schiano, T.] Mt Sinai SOM, Div Liver Dis, Dept Med, New York, NY USA.
[Johl, J.] NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA.
[Shaikh, O.] Univ Pittsburgh, Dept Med, Div Gastroenterol Hepatol & Nutr, Pittsburgh, PA USA.
[Dove, L.] Columbia Univ, Dept Med, New York, NY USA.
[Shetty, K.] Georgetown Univ, Dept Surg, Washington, DC USA.
[Millis, M.] Univ Chicago, Dept Surg, Chicago, IL 60637 USA.
[Schiff, E.] Univ Miami, Dept Med, Div Hepatol, Miami, FL USA.
[Regenstein, F.] Tulane Univ, Dept Med, New Orleans, LA 70118 USA.
[Barnes, D.] Cleveland Clin, Dept Gastroenterol & Hepatol, Cleveland, OH 44106 USA.
[Barin, B.] EMMES Corp, Rockville, MD USA.
[Stock, P.] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
RP Terrault, N (reprint author), Univ Calif San Francisco, Dept Med, Div Gastroenterol & Hepatol, San Francisco, CA 94143 USA.
EM norah.terrault@ucsf.edu
FU solid organ transplantation in HIV: Multi-Site Study [AI052748];
National Institute of Allergy and Infectious Diseases
FX This work was supported by the solid organ transplantation in HIV:
Multi-Site Study (AI052748) funded by the National Institute of Allergy
and Infectious Diseases. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institute of Allergy and Infectious Diseases or the National
Institutes of Health. We want to thank Rodney Rogers from the University
of California, San Francisco for this expert coordination of the study
consortium. We want to thank all of the solid organ transplantation in
HIV: Multi-Site Study investigators and coordinators for their hard work
and dedication to the study and subjects. A complete list can be found
in the online materials for this article.
NR 14
TC 12
Z9 12
U1 0
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
EI 1600-6143
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD MAY
PY 2014
VL 14
IS 5
BP 1129
EP 1135
DI 10.1111/ajt.12668
PG 7
WC Surgery; Transplantation
SC Surgery; Transplantation
GA AF0LG
UT WOS:000334404900018
PM 24636466
ER
PT J
AU Wirth, EK
Bharathi, BS
Hatfield, D
Conrad, M
Brielmeier, M
Schweizer, U
AF Wirth, Eva K.
Bharathi, B. Suman
Hatfield, Dolph
Conrad, Marcus
Brielmeier, Markus
Schweizer, Ulrich
TI Cerebellar Hypoplasia in Mice Lacking Selenoprotein Biosynthesis in
Neurons
SO BIOLOGICAL TRACE ELEMENT RESEARCH
LA English
DT Article
DE Selenium; Brain; Gpx4; Cell death; Proliferation
ID PROGRESSIVE CEREBELLOCEREBRAL ATROPHY; APOLIPOPROTEIN-E RECEPTOR-2;
NEUROLOGICAL DYSFUNCTION; BRAIN SELENIUM; CELL-DEATH; MOUSE; GENE;
SELENOCYSTEINE; EXPRESSION; DELETION
AB Selenium exerts many, if not most, of its physiological functions as a selenocysteine moiety in proteins. Selenoproteins are involved in many biochemical processes including regulation of cellular redox state, calcium homeostasis, protein biosynthesis, and degradation. A neurodevelopmental syndrome called progressive cerebello-cortical atrophy (PCCA) is caused by mutations in the selenocysteine synthase gene, SEPSECS, demonstrating that selenoproteins are essential for human brain development. While we have shown that selenoproteins are required for correct hippocampal and cortical interneuron development, little is known about the functions of selenoproteins in the cerebellum. Therefore, we have abrogated neuronal selenoprotein biosynthesis by conditional deletion of the gene encoding selenocysteyl tRNA([Ser]Sec) (gene symbol Trsp). Enzymatic activity of cellular glutathione peroxidase and cytosolic thioredoxin reductase is reduced in cerebellar extracts from Trsp-mutant mice. These mice grow slowly and fail to gain postural control or to coordinate their movements. Histological analysis reveals marked cerebellar hypoplasia, associated with Purkinje cell death and decreased granule cell proliferation. Purkinje cell death occurs along parasagittal stripes as observed in other models of Purkinje cell loss. Neuron-specific inactivation of glutathione peroxidase 4 (Gpx4) used the same Cre driver phenocopies tRNA([Ser]Sec) mutants in several aspects: cerebellar hypoplasia, stripe-like Purkinje cell loss, and reduced granule cell proliferation. Parvalbumin-expressing GABAergic interneurons (stellate and/or basket cells) are virtually absent in tRNA([Ser]Sec)-mutant mice, while some remained in Gpx4-mutant mice. Our data show that selenoproteins are specifically required in postmitotic neurons of the developing cerebellum, thus providing a rational explanation for cerebellar hypoplasia as occurring in PCCA patients.
C1 [Wirth, Eva K.; Bharathi, B. Suman; Schweizer, Ulrich] Charite, Inst Expt Endokrinol, D-13353 Berlin, Germany.
[Hatfield, Dolph] NIH, Mouse Canc Genet Program, Ctr Canc Res, Bethesda, MD 20892 USA.
[Conrad, Marcus] Helmholtz Zentrum Munchen, Inst Dev Genet, D-85764 Munich, Germany.
[Brielmeier, Markus] Helmholtz Zentrum Munchen, Abt Vergleichende Med, D-85764 Neuherberg, Germany.
[Schweizer, Ulrich] Univ Bonn, Inst Biochem & Mol Biol, D-53115 Bonn, Germany.
RP Schweizer, U (reprint author), Univ Bonn, Inst Biochem & Mol Biol, Nussallee 11, D-53115 Bonn, Germany.
EM uschweiz@uni-bonn.de
RI Brielmeier, Markus/M-7352-2014;
OI Brielmeier, Markus/0000-0002-8715-869X; Wirth, Eva
Katrin/0000-0002-0491-9941; Conrad, Marcus/0000-0003-1140-5612;
Schweizer, Ulrich/0000-0003-1380-4780
FU Deutsche Forschungsgemeinschaft DFG [Schw914/2-1];
Charite-Universitatsmedizin Berlin
FX The authors thank Silke Kappler for technical assistance and Dr. Richard
Hawkes for zebrin II antibody. The study was funded by Deutsche
Forschungsgemeinschaft DFG Schw914/2-1 and Charite-Universitatsmedizin
Berlin.
NR 28
TC 14
Z9 14
U1 0
U2 9
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0163-4984
EI 1559-0720
J9 BIOL TRACE ELEM RES
JI Biol. Trace Elem. Res.
PD MAY
PY 2014
VL 158
IS 2
BP 203
EP 210
DI 10.1007/s12011-014-9920-z
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA AF1US
UT WOS:000334500000010
PM 24599700
ER
PT J
AU Hoang, AN
Agarwal, PK
Walton-Diaz, A
Wood, CG
Metwalli, AR
Kassouf, W
Brown, GA
Black, PC
Urbauer, DL
Grossman, HB
Dinney, CPN
Kamat, AM
AF Hoang, Anthony N.
Agarwal, Piyush K.
Walton-Diaz, Annerleim
Wood, Christopher G.
Metwalli, Adam R.
Kassouf, Wassim
Brown, Gordon A.
Black, Peter C.
Urbauer, Diana L.
Grossman, H. Barton
Dinney, Colin P. N.
Kamat, Ashish M.
TI Clinical significance of ureteric 'skip lesions' at the time of radical
cystectomy: the M.D. Anderson experience and literature review
SO BJU INTERNATIONAL
LA English
DT Article
DE ureteral margin; cystectomy; bladder cancer; ureteral urothelial
carcinoma; upper tract recurrence
ID FROZEN-SECTION ANALYSIS; TRANSITIONAL-CELL CARCINOMA; BLADDER-CANCER;
IN-SITU; MARGINS; INVOLVEMENT
AB Objective
To assess the incidence and clinical significance of 'skip lesions' that are present in proximal but not in distal ureteric sections, which are occasionally found during the pathological examination of ureteric margins during radical cystectomy (RC).
Patients and Methods
We identified 660 patients who underwent a RC and had at least two permanent margins for a given ureter.
In all, 1173 ureters were analysed and classified as follows: 'normal' (no tumour, reactive atypia, mild or moderate dysplasia) or 'abnormal' (severe dysplasia, carcinoma in situ (CIS), or tumour).
Transitions from 'normal' distal pathology to 'abnormal' on proximal section(s) determined frequency of skip lesions.
Fisher's exact test and the log-rank test were used to study correlations.
Results
Ureteric skip lesions were found in 4.8% patients (2.9% ureters).
Pathology of skip lesions was CIS in 55.9%, transitional cell carcinoma in 23.5% and severe dysplasia in 20.6%.
Skip lesions were associated with lymphovascular invasion (34.4% vs 13.7%, P = 0.004) and advanced pT stage (P = 0.007).
On multivariate analysis, skip lesions correlated with lower median overall survival (OS) (inestimable vs 8.2 years, P = 0.014) in patients with pT0 or pTa disease and a trend towards lower OS (2.7 vs 8.8 years, P = 0.066) in pTis disease.
Concordance between frozen distal margin and permanent proximal margin varied; sensitivity was 80% in those without and 20% in those with skip lesions.
Conclusions
The presence of a ureteric skip lesion may be associated with lower survival in patients with pT0, pTa or pTis urothelial carcinoma.
Thus, while uncommon, ureteric skip lesions should be reported in pathological findings.
C1 [Hoang, Anthony N.; Agarwal, Piyush K.; Walton-Diaz, Annerleim; Metwalli, Adam R.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Wood, Christopher G.; Kassouf, Wassim; Brown, Gordon A.; Black, Peter C.; Grossman, H. Barton; Dinney, Colin P. N.; Kamat, Ashish M.] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA.
[Urbauer, Diana L.] Univ Texas MD Anderson Canc Ctr, Div Quantitat Sci, Houston, TX 77030 USA.
RP Kamat, AM (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Urol, Unit 1373, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM akamat@mdanderson.org
OI Agarwal, Piyush/0000-0002-6042-6834
FU M. D. Anderson Cancer Center Bladder SPORE [5P50CA091846-03]; Department
of Urology T32 Training Grant
FX This research was supported by the M. D. Anderson Cancer Center Bladder
SPORE (5P50CA091846-03) and a Department of Urology T32 Training Grant
NR 12
TC 6
Z9 6
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-4096
EI 1464-410X
J9 BJU INT
JI BJU Int.
PD MAY
PY 2014
VL 113
IS 5B
SI SI
BP E28
EP E33
DI 10.1111/bju.12344
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA AF4LA
UT WOS:000334682300003
PM 24053608
ER
PT J
AU Lai, GY
Giovannucci, EL
Pollak, MN
Peskoe, SB
Stampfer, MJ
Willett, WC
Platz, EA
AF Lai, Gabriel Y.
Giovannucci, Edward L.
Pollak, Michael N.
Peskoe, Sarah B.
Stampfer, Meir J.
Willett, Walter C.
Platz, Elizabeth A.
TI Association of C-peptide and leptin with prostate cancer incidence in
the Health Professionals Follow-up Study
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Prostate cancer; C-peptide; Leptin; Nested case-control study; Risk
ID PROSPECTIVE RISK-FACTOR; GROWTH-FACTOR-I; INSULIN-RESISTANCE;
DIABETES-MELLITUS; SUBSEQUENT RISK; PLASMA LEPTIN; PSA ERA; OBESITY;
ADIPONECTIN; BIOMARKERS
AB Hyperinsulinemia is hypothesized to influence prostate cancer risk. Thus, we evaluated the association of circulating C-peptide, which is a marker of insulin secretion, and leptin, which is secreted in response to insulin and influences insulin sensitivity, with prostate cancer risk.
We identified prostate cancer cases (n = 1,314) diagnosed a mean of 5.4 years after blood draw and matched controls (n = 1,314) in the Health Professionals Follow-up Study. Plasma C-peptide and leptin concentrations were measured by ELISA. Odds ratios (ORs) and 95 % confidence intervals (CI) were estimated taking into account the matching factors age and history of a PSA test before blood draw and further adjusting for body mass index, diabetes, and other factors.
Neither C-peptide (quartile [Q]4 vs. Q1: OR 1.05, 95 % CI 0.82-1.34, p-trend = 0.95) nor leptin (Q4 vs. Q1: OR 0.85, 95 % CI 0.65-1.12, p-trend = 0.14) was associated with prostate cancer risk. Further, neither was associated with risk of advanced or lethal disease (n = 156 cases; C-peptide: Q4 vs. Q1, OR 1.18, 95 % CI 0.69-2.03, p-trend = 0.78; leptin: Q4 vs. Q1, OR 0.74, 95 % CI 0.41-1.36, p-trend = 0.34).
In this large prospective study, circulating C-peptide and leptin concentrations were not clearly associated with risk of prostate cancer overall or aggressive disease. Well into the PSA era, our findings do not appear to be supportive of the hypothesis that hyperinsulinemia influences risk of total or aggressive prostate cancer.
C1 [Lai, Gabriel Y.; Peskoe, Sarah B.; Platz, Elizabeth A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Bethesda, MD 21205 USA.
[Lai, Gabriel Y.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Bethesda, MD 20892 USA.
[Giovannucci, Edward L.; Stampfer, Meir J.; Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Giovannucci, Edward L.; Stampfer, Meir J.; Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, Edward L.; Stampfer, Meir J.; Willett, Walter C.] Harvard Univ, Sch Med, Dept Med, Channing Div Network Med, Boston, MA USA.
[Giovannucci, Edward L.; Stampfer, Meir J.; Willett, Walter C.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Pollak, Michael N.] McGill Univ, Dept Oncol, Montreal, PQ, Canada.
[Pollak, Michael N.] McGill Univ, Jewish Gen Hosp, Lady David Inst Med Res, Montreal, PQ H3T 1E2, Canada.
[Platz, Elizabeth A.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Platz, Elizabeth A.] James Buchanan Brady Urol Inst, Baltimore, MD USA.
[Platz, Elizabeth A.] Johns Hopkins Sch Med, Dept Urol, Baltimore, MD USA.
RP Platz, EA (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Rm E6132,615 N Wolfe St, Bethesda, MD 21205 USA.
EM eplatz@jhsph.edu
FU National Cancer Institute, National Institutes of Health, Department of
Health and Human Services [R01 CA55075, R01 CA141298, R01 CA133891, T32
CA009314]
FX We would like to thank the participants and staff of the Health
Professionals Follow-up Study for their valuable contributions as well
as the following state cancer registries for their help: AL, AZ, AR, CA,
CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ,
NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. In addition,
this study was approved by the Connecticut Department of Public Health
(DPH) Human Investigations Committee. Certain data used in this
publication were obtained from the DPH. The authors assume full
responsibility for analyses and interpretation of these data. We also
thank Yuzhen Tao in the Dr. Pollak's laboratory for running the assays.
This work was funded by Public Health Service research Grants R01
CA55075, R01 CA141298, and R01 CA133891 from the National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services. Gabriel Lai was supported by a National Research Service Award
T32 CA009314 from the National Cancer Institute, National Institutes of
Health, Department of Health and Human Services. The content is solely
the responsibility of the authors and does not necessarily represent the
official views of the National Cancer Institute or the National
Institutes of Health.
NR 36
TC 9
Z9 9
U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
EI 1573-7225
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD MAY
PY 2014
VL 25
IS 5
BP 625
EP 632
DI 10.1007/s10552-014-0369-3
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AF0MU
UT WOS:000334409500009
PM 24664287
ER
PT J
AU Rieder, D
Ploner, C
Krogsdam, AM
Stocker, G
Fischer, M
Scheideler, M
Dani, C
Amri, EZ
Mueller, WG
McNally, JG
Trajanoski, Z
AF Rieder, Dietmar
Ploner, Christian
Krogsdam, Anne M.
Stocker, Gernot
Fischer, Maria
Scheideler, Marcel
Dani, Christian
Amri, Ez-Zoubir
Mueller, Waltraud G.
McNally, James G.
Trajanoski, Zlatko
TI Co-expressed genes prepositioned in spatial neighborhoods stochastically
associate with SC35 speckles and RNA polymerase II factories
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Article
DE Nuclear organization; Spatial gene positioning; Splicing speckles;
Transcription factories
ID TRANSCRIPTION FACTORIES; CHROMATIN-STRUCTURE; DROSOPHILA GENOME; NUCLEAR
SPECKLES; HUMAN-CELLS; ORGANIZATION; CLUSTERS; DOMAINS; ELONGATION;
EXPRESSION
AB Chromosomally separated, co-expressed genes can be in spatial proximity, but there is still debate about how this nuclear organization is achieved. Proposed mechanisms include global genome organization, preferential positioning of chromosome territories, or gene-gene sharing of various nuclear bodies. To investigate this question, we selected a set of genes that were co-expressed upon differentiation of human multipotent stem cells. We applied a novel multi-dimensional analysis procedure which revealed that prior to gene expression, the relative position of these genes was conserved in nuclei. Upon stem cell differentiation and concomitant gene expression, we found that co-expressed genes were closer together. In addition, we found that genes in the same 1-mu m-diameter neighborhood associated with either the same splicing speckle or to a lesser extent with the same transcription factory. Dispersal of speckles by overexpression of the serine-arginine (SR) protein kinase cdc2-like kinase Clk2 led to a significant drop in the number of genes in shared neighborhoods. We demonstrate quantitatively that the frequencies of speckle and factory sharing can be explained by assuming stochastic selection of a nuclear body within a restricted sub-volume defined by the original global gene positioning present prior to gene expression. We conclude that the spatial organization of these genes is a two-step process in which transcription-induced association with nuclear bodies enhances and refines a pre-existing global organization.
C1 [Rieder, Dietmar; Krogsdam, Anne M.; Stocker, Gernot; Fischer, Maria; Trajanoski, Zlatko] Med Univ Innsbruck, Div Bioinformat, Bioctr, A-6020 Innsbruck, Austria.
[Ploner, Christian] Med Univ Innsbruck, Dept Plast Reconstruct & Aesthet Surg, A-6020 Innsbruck, Austria.
[Scheideler, Marcel] Graz Univ Technol, Inst Genom & Bioinformat, A-8010 Graz, Austria.
[Dani, Christian; Amri, Ez-Zoubir] Univ Nice Sophia Antipolis, CNRS, Inst Dev Biol & Canc, Fac Med, F-06189 Nice, France.
[Mueller, Waltraud G.; McNally, James G.] NCI, NIH, Lab Receptor Biol & Gene Express, Bethesda, MD USA.
RP Trajanoski, Z (reprint author), Med Univ Innsbruck, Div Bioinformat, Bioctr, Innrain 80, A-6020 Innsbruck, Austria.
EM zlatko.trajanoski@i-med.ac.at
RI DANI, Christian/G-3639-2014;
OI Dani, Christian/0000-0003-3228-0230; amri, Ez-Zoubir/0000-0001-8426-5396
FU Austrian Federal Ministry for Science and Research; Austrian Science
Funds
FX This work was supported by the Austrian Federal Ministry for Science and
Research, Project GEN-AU BIN and the Austrian Science Funds, Projects
SFB Lipotoxicity and SFB Cell proliferation and cell death in tumors. We
thank Martina Wick, Claudia Neuhold, and Nicole Golob for support in the
lab, and Hubert Hackl for statistical advice and valuable comments.
NR 68
TC 14
Z9 14
U1 0
U2 7
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
EI 1420-9071
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD MAY
PY 2014
VL 71
IS 9
BP 1741
EP 1759
DI 10.1007/s00018-013-1465-3
PG 19
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AF0RM
UT WOS:000334421700011
PM 24026398
ER
PT J
AU Wirth, CC
Glushakova, S
Scheuermayer, M
Repnik, U
Garg, S
Schaack, D
Kachman, MM
Weissbach, T
Zimmerberg, J
Dandekar, T
Griffiths, G
Chitnis, CE
Singh, S
Fischer, R
Pradel, G
AF Wirth, Christine C.
Glushakova, Svetlana
Scheuermayer, Matthias
Repnik, Urska
Garg, Swati
Schaack, Dominik
Kachman, Marika M.
Weissbach, Tim
Zimmerberg, Joshua
Dandekar, Thomas
Griffiths, Gareth
Chitnis, Chetan E.
Singh, Shailja
Fischer, Rainer
Pradel, Gabriele
TI Perforin-like protein PPLP2 permeabilizes the red blood cell membrane
during egress of Plasmodium falciparum gametocytes
SO CELLULAR MICROBIOLOGY
LA English
DT Article
ID MALARIA PARASITE RELEASE; INFECTED ERYTHROCYTES; PORE FORMATION;
OSMIOPHILIC BODIES; XANTHURENIC ACID; MOSQUITO MIDGUT; HOST;
TRANSMISSION; COMPLEMENT; GENE
AB Egress of malaria parasites from the host cell requires the concerted rupture of its enveloping membranes. Hence, we investigated the role of the plasmodial perforin-like protein PPLP2 in the egress of Plasmodium falciparum from erythrocytes. PPLP2 is expressed in blood stage schizonts and mature gametocytes. The protein localizes in vesicular structures, which in activated gametocytes discharge PPLP2 in a calcium-dependent manner. PPLP2 comprises a MACPF domain and recombinant PPLP2 has haemolytic activities towards erythrocytes. PPLP2-deficient [PPLP2(-)] merozoites show normal egress dynamics during the erythrocytic replication cycle, but activated PPLP2(-) gametocytes were unable to leave erythrocytes and stayed trapped within these cells. While the parasitophorous vacuole membrane ruptured normally, the activated PPLP2(-) gametocytes were unable to permeabilize the erythrocyte membrane and to release the erythrocyte cytoplasm. In consequence, transmission of PPLP2(-) parasites to the Anopheles vector was reduced. Pore-forming equinatoxin II rescued both PPLP2(-) gametocyte exflagellation and parasite transmission. The pore sealant Tetronic 90R4, on the other hand, caused trapping of activated wild-type gametocytes within the enveloping erythrocytes, thus mimicking the PPLP2(-) loss-of-function phenotype. We propose that the haemolytic activity of PPLP2 is essential for gametocyte egress due to permeabilization of the erythrocyte membrane and depletion of the erythrocyte cytoplasm.
C1 [Wirth, Christine C.; Weissbach, Tim; Fischer, Rainer; Pradel, Gabriele] Rhein Westfal TH Aachen, Inst Mol Biotechnol, D-52074 Aachen, Germany.
[Glushakova, Svetlana; Kachman, Marika M.; Zimmerberg, Joshua] Eunice Kennedy Schriver Natl Inst Child Hlth & Hu, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Scheuermayer, Matthias] Univ Wurzburg, Res Ctr Infect Dis, D-97080 Wurzburg, Germany.
[Repnik, Urska; Griffiths, Gareth] Univ Oslo, Dept Biosci, N-0316 Oslo, Norway.
[Garg, Swati; Chitnis, Chetan E.; Singh, Shailja] Int Ctr Genet Engn & Biotechnol ICGEB, Malaria Grp, New Delhi 110067, India.
[Schaack, Dominik; Dandekar, Thomas] Univ Wurzburg, Dept Bioinformat, D-97074 Wurzburg, Germany.
[Singh, Shailja] Shiv Nadar Univ, Dept Life Sci, Tehsil Dadri 203207, Gautam Budh Nag, India.
[Fischer, Rainer; Pradel, Gabriele] Fraunhofer Inst Mol Biol & Appl Ecol, D-50274 Aachen, Germany.
RP Pradel, G (reprint author), Rhein Westfal TH Aachen, Inst Mol Biotechnol, Worringerweg 1, D-52074 Aachen, Germany.
EM gabriele.pradel@molbiotech.rwth-aachen.de
RI WeiSSbach, Tim/L-1575-2015; Dandekar, Thomas/A-4431-2017
OI Dandekar, Thomas/0000-0003-1886-7625
FU Deutsche Forschungsgemeinschaft [SPP1580]
FX We thank Inga Siden-Kiamos (FORTH Institute of Molecular Biology and
Biotechnology Crete) for helpful discussions. We are grateful to Gregor
Anderluh (University of Ljubljana) for providing equinatoxin II, to
Pietro Alano (Istituto Superiore di Sanita Rome) for providing parasite
line Pfg377(-) and to Kim Williamson (Loyola University Chicago) for
providing vector pIH. We further thank the team of Georg Krohne
(University of Wurzburg) and the Electron Microscopy Unit for Biological
Sciences (University of Oslo) for support with the electron
microscopy-related work. The authors acknowledge funding by the priority
programme SPP1580 of the Deutsche Forschungsgemeinschaft (G.P. and
G.G.).
NR 73
TC 24
Z9 24
U1 1
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-5814
EI 1462-5822
J9 CELL MICROBIOL
JI Cell Microbiol.
PD MAY
PY 2014
VL 16
IS 5
SI SI
BP 709
EP 733
DI 10.1111/cmi.12288
PG 25
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA AE9IF
UT WOS:000334320800011
PM 24602217
ER
PT J
AU Ippolito, E
Farsetti, P
Boyce, AM
Corsi, A
De Maio, F
Collins, MT
AF Ippolito, Ernesto
Farsetti, Pasquale
Boyce, Alison M.
Corsi, Alessandro
De Maio, Fernando
Collins, Michael T.
TI Radiographic Classification of Coronal Plane Femoral Deformities in
Polyostotic Fibrous Dysplasia
SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH
LA English
DT Article
ID MCCUNE-ALBRIGHT SYNDROME; MECHANICAL AXIS DEVIATION; STIMULATORY
G-PROTEIN; ACTIVATING MUTATIONS; NATURAL-HISTORY; PROXIMAL PART;
LOWER-LIMBS; BONE; FEMUR; ABNORMALITIES
AB Fibrous dysplasia of bone is a skeletal dysplasia with a propensity to affect the femur in its polyostotic form, leading to deformity, fracture, and pain. The proximal femur is most commonly involved with a tendency to distal progression, thereby producing the typical shepherd's crook deformity. However, there are few data on the spectrum and progression of femoral deformities in polyostotic fibrous dysplasia.
The purposes of this study were (1) to develop a radiographic classification for polyostotic fibrous dysplasia; (2) to test this classification's intra- and interobserver reliability; and (3) to characterize the radiographic progression of polyostotic fibrous dysplasia in a population of patients with the condition who were treated with a variety of approaches at several centers.
We retrospectively reviewed radiographs of 127 femurs from 84 adult patients affected by polyostotic fibrous dysplasia. Fifty-nine femurs had undergone one or more operations. The radiographs were evaluated in the coronal plane for neck-shaft angle and angular deformities along the whole femoral shaft down to the distal epiphysis. Four observers evaluated each film two times at intervals; intra- and interobserver reliability testing was performed using the kappa statistic. Eighty-nine femurs (70%) were available for followup to evaluate for progression at a mean of 10 years (range, 6-20 years).
Six reproducible patterns of deformity were identified in both untreated and operated femurs: type 1 (24%), normal neck-shaft angle with altered shape of the proximal femur; type 2 (6%), isolated coxa valga with neck-shaft angle > 140A degrees; type 3 (7%), isolated coxa vara with neck-shaft angle < 120A degrees; type 4 (20%), lateral bowing of the proximal half of the femur associated with normal neck-shaft angle; type 5 (14%), like in type 4 but associated with coxa valga; and type 6 (29%), like in type 4 but associated with coxa vara. Interobserver and intraoberver kappa values were excellent, ranging from 0.83 to 0.87. In 46 of the 89 femurs (52%) for which longitudinal radiographic documentation was available, there was progressive worsening of the original deformity, although the pattern remained the same; types 1 and 2 tended not to progress, whereas types 3 to 6 did.
A reproducible radiographic classification of polyostotic fibrous dysplasia-associated femoral deformities is proposed, which can serve as a tool for assessing and treating these deformities. After reviewing the radiographs of 127 femurs, we identified six reproducible patterns of femoral deformities.
Level III, diagnostic study. See Guidelines for Authors for a complete description of levels of evidence.
C1 [Ippolito, Ernesto; Farsetti, Pasquale; De Maio, Fernando] Univ Roma Tor Vergata, Dept Orthopaed Surg, PTV, I-00133 Rome, Italy.
[Boyce, Alison M.; Collins, Michael T.] NIH, Bethesda, MD 20892 USA.
[Corsi, Alessandro] Univ Roma La Sapienza, Dept Mol Med, I-00185 Rome, Italy.
RP Ippolito, E (reprint author), Univ Roma Tor Vergata, Dept Orthopaed Surg, PTV, Viale Oxford 81, I-00133 Rome, Italy.
EM ippolito@med.uniroma2.it
NR 23
TC 9
Z9 9
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0009-921X
EI 1528-1132
J9 CLIN ORTHOP RELAT R
JI Clin. Orthop. Rel. Res.
PD MAY
PY 2014
VL 472
IS 5
BP 1558
EP 1567
DI 10.1007/s11999-013-3380-1
PG 10
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA AE7LV
UT WOS:000334180400032
PM 24249535
ER
PT J
AU Kennard, BD
Brown, LT
Hawkins, L
Risi, A
Radcliffe, J
Emslie, GJ
Mayes, TL
King, JD
Foxwell, AA
Buyukdura, J
Bethel, J
Naar-King, S
Xu, JH
Lee, SS
Garvie, P
London, C
Tanney, M
Thornton, S
AF Kennard, Beth D.
Brown, Larry T.
Hawkins, Linda
Risi, Andrea
Radcliffe, Jerilynn
Emslie, Graham J.
Mayes, Taryn L.
King, Jessica D.
Foxwell, Aleksandra A.
Buyukdura, Jeylan
Bethel, James
Naar-King, Sylvie
Xu, Jiahong
Lee, Sonia S.
Garvie, Patricia
London, Carla
Tanney, Mary
Thornton, Sarah
CA Adolescent Trials Network HIV AIDS
TI Development and Implementation of Health and Wellness CBI for
Individuals With Depression and HIV
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Article
DE cognitive behavioral therapy; major depressive disorder; HIV; adherence;
health
ID COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CONTROLLED-TRIAL; MEDICATION
ADHERENCE; ADOLESCENT DEPRESSION; QUICK INVENTORY; CHILDREN;
PSYCHOTHERAPY; DISORDERS; SYMPTOMATOLOGY; MANAGEMENT
AB Rates of depression are reported to be between 22% to 33% in adults with HIV, which is double that of the general population. Depression negatively affects treatment adherence and health outcomes of those with medical illnesses. Further, it has been shown in adults that reducing depression may improve both adherence and health outcomes. To address the issues of depression, and nonadherence, Health and Wellness (H&W) cognitive behavioral therapy (CBT) and medication management (MM) treatment strategies have been developed specifically for youth living with both HIV and depression. H&W CBT is based on other studies with uninfected youth and upon research on adults with HIV. H&W CBT uses problem solving, motivational interviewing and cognitive-behavioral strategies to decrease adherence obstacles and increase wellness. The intervention is delivered in 14 planned sessions over a 6-month period, with three different stages of CBT. This paper summarizes the feasibility and acceptability data from an open depression trial with 8 participants, 16 to 24 years of age, diagnosed with HIV and with a Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) diagnosis of depression, conducted at two treatment sites in the Adolescent Trials Network (ATN). Both therapists and subjects completed a Session Evaluation Form (SPF) after each session, and results were strongly favorable. Results from The Quick Inventory of Depressive Symptomatology Clinician (QEDS-C) also showed noteworthy improvement in depression severity. A clinical case vignette illustrates treatment response. Further research will examine the use of H&W CBT in a larger trial of youth diagnosed with both HIV and depression.
C1 [Kennard, Beth D.; Emslie, Graham J.; Mayes, Taryn L.; King, Jessica D.; Foxwell, Aleksandra A.; Buyukdura, Jeylan] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Brown, Larry T.] Brown Univ, Rhode Isl Hosp, Providence, RI 02912 USA.
[Hawkins, Linda; Radcliffe, Jerilynn; Tanney, Mary] Childrens Hosp Philadelphia, Philadelphia, PA USA.
[Hawkins, Linda; Radcliffe, Jerilynn; Tanney, Mary] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Risi, Andrea] Univ S Florida, Silver Child Dev Ctr, Tampa, FL 33620 USA.
[Bethel, James; Xu, Jiahong; Thornton, Sarah] WESTAT Corp, Rockville, MD 20850 USA.
[Naar-King, Sylvie] Wayne State Univ, Detroit, MI 48202 USA.
[Lee, Sonia S.] NICHHD, Pediat Adolescent & Maternal AIDS Branch, Bethesda, MD 20892 USA.
[Garvie, Patricia; London, Carla] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
RP Kennard, BD (reprint author), Univ Texas SW Med Ctr Dallas, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM beth.kennard@utsouthwestern.edu
FU NICHD NIH HHS [U01 HD040533, U01 HD040474, U01 HD040481]
NR 31
TC 6
Z9 6
U1 1
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
EI 1878-187X
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD MAY
PY 2014
VL 21
IS 2
BP 237
EP 246
PG 10
WC Psychology, Clinical
SC Psychology
GA AE7AZ
UT WOS:000334150400013
PM 24795524
ER
PT J
AU Verkoczy, L
Diaz, M
AF Verkoczy, Laurent
Diaz, Marilyn
TI Autoreactivity in HIV-1 broadly neutralizing antibodies: implications
for their function and induction by vaccination
SO CURRENT OPINION IN HIV AND AIDS
LA English
DT Review
DE immune tolerance; autoreactivity; polyreactivity; broadly neutralizing
antibodies; somatic hypermutation
ID B-CELL RESPONSES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; MEMBRANE-PROXIMAL
REGION; MONOCLONAL-ANTIBODIES; ANTIRETROVIRAL THERAPY; POTENT
NEUTRALIZATION; ENVELOPE PROTEIN; IMMUNOGEN DESIGN; STRUCTURAL BASIS;
KNOCKIN MICE
AB Purpose of review
This review discusses progress in understanding the impact of immune tolerance on inducing broadly neutralizing antibodies (bnAbs), and how such knowledge can be incorporated into novel immunization approaches.
Recent findings
Over 120 bnAbs have now been isolated, all of which bear unusual features associated with host tolerance controls, but paradoxically may also be required for their function. Evidence that poly/autoreactivity of membrane proximal external region bnAbs can invoke such controls has been demonstrated by knock-in technology, highlighting its potential for studying the impact of tolerance in the generation of bnAb lineages to distinct HIV-1 envelope targets. The requirement for extensive affinity maturation in developing neutralization breadth/potency during infection is being examined, and similar studies in the setting of immunization will be aided by testing novel vaccine approaches in knock-in models that either selectively express reverted V(D)J rearrangements, or unrearranged germline segments, from which bnAb lineages originate.
It is increasingly apparent that immune tolerance, sometimes invoked by self-reactivity that overlaps with bnAb epitope specificity, adds to a formidable set of roadblocks impeding bnAb induction. The path to an effective HIV-1 vaccine may thus benefit from a deeper understanding of host controls, including categorizing those that are unique or common at distinct bnAb targets, and ranking those most feasible to overcome by immunization. Ultimately, such emerging information will be critical to incorporate into new vaccine approaches that can be tested in human trials.
C1 [Verkoczy, Laurent] Duke Univ, Med Ctr, Duke Human Vaccine Inst, Durham, NC 27710 USA.
[Diaz, Marilyn] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Verkoczy, L (reprint author), Duke Univ, Med Ctr, Duke Human Vaccine Inst, 2 Genome Court,3015 MSRBII Bldg, Durham, NC 27710 USA.
EM laurent.verkoczy@duke.edu
FU NIH, National Institute of Environmental Health Sciences, Division of
Intramural Research [Z01 ES101603]; Center for HIV/AIDS Vaccine
Immunogen-Discovery (CHAVI-ID) [UM1 AI100645]; NIH [R01 AI087202];
Collaboration for AIDS Discovery Vaccine Development Center grant from
the Bill and Melinda Gates Foundation
FX This work was supported by NIH, National Institute of Environmental
Health Sciences, Division of Intramural Research project Z01 ES101603,
the Center for HIV/AIDS Vaccine Immunogen-Discovery (CHAVI-ID) grant UM1
AI100645, NIH grant R01 AI087202 and a Collaboration for AIDS Discovery
Vaccine Development Center grant from the Bill and Melinda Gates
Foundation.
NR 108
TC 18
Z9 19
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1746-630X
EI 1746-6318
J9 CURR OPIN HIV AIDS
JI Curr. Opin. HIV AIDS
PD MAY
PY 2014
VL 9
IS 3
BP 224
EP 234
DI 10.1097/COH.0000000000000049
PG 11
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AE9BM
UT WOS:000334298900005
PM 24714565
ER
PT J
AU Petrovas, C
Koup, RA
AF Petrovas, Constantinos
Koup, Richard A.
TI T follicular helper cells and HIV/SIV-specific antibody responses
SO CURRENT OPINION IN HIV AND AIDS
LA English
DT Article
DE simian immunodeficiency virus; T follicular helper cells; antibodies;
HIV
ID GERMINAL CENTER B; HIV-INFECTION; VIRAL-INFECTION; DENDRITIC CELLS; TFH
CELLS; DIFFERENTIATION; ANTIGEN; EFFECTOR; GENERATION; EXPRESSION
AB Purpose of review
Here, we describe recent data on the characterization of follicular helper CD4 T cells (Tfh) and the dynamics of Tfh-B-cell interactions in HIV and simian immunodeficiency virus (SIV) infection and discuss important aspects of these interactions that need to be addressed in order to design more effective vaccines that elicit broadly neutralizing antibodies.
Recent findings
Mouse, nonhuman primate (NHP) and human Tfh cells share phenotypic, functional and molecular programs, which are regulated by local signals and spatiotemporal parameters. Chronic HIV/SIV infection results in accumulation of Tfh, germinal center B cells and circulating virus-specific immunoglobulins in some individuals. However, most HIV/SIV-infected individuals do not mount broadly neutralizing antibodies, pointing to functional defects in Tfh cells in chronic HIV/SIV infection. The susceptibility of particular CD4 T-cell populations to HIV/SIV infection within lymph nodes notably impacts upon the dynamics of Tfh-germinal center B-cell interactions. Some circulating CD4 T cells share certain characteristics with Tfh cells, however, their direct origin from germinal center Tfh cells is not clear.
There are many ways in which HIV and SIV influence the complex signals and mechanisms regulating the development of Tfh cells and their interactions with germinal center B cells. Understanding the biology of Tfh cells will be necessary to appropriately recruit these cells during vaccination with the goal of stimulating a more broad and potent neutralizing antibody response.
C1 [Petrovas, Constantinos; Koup, Richard A.] NIAID, Immunol Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Koup, RA (reprint author), NIAID, Vaccine Res Ctr, NIH, 40 Convent Dr, Bethesda, MD 20892 USA.
EM rkoup@mail.nih.gov
FU Intramural Research Program of the Vaccine Research Center, NIAID,
National Institutes of Health; Bill and Melinda Gates Foundation
[OPP1032325]
FX This research was supported by the Intramural Research Program of the
Vaccine Research Center, NIAID, National Institutes of Health and CAVD
grant #OPP1032325 from the Bill and Melinda Gates Foundation.
NR 70
TC 11
Z9 11
U1 0
U2 23
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1746-630X
EI 1746-6318
J9 CURR OPIN HIV AIDS
JI Curr. Opin. HIV AIDS
PD MAY
PY 2014
VL 9
IS 3
BP 235
EP 241
DI 10.1097/COH.0000000000000053
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AE9BM
UT WOS:000334298900006
PM 24670319
ER
PT J
AU Ueda, Y
Nishimura, J
Murakami, Y
Kajigaya, S
Kinoshita, T
Kanakura, Y
Young, NS
AF Ueda, Yasutaka
Nishimura, Jun-ichi
Murakami, Yoshiko
Kajigaya, Sachiko
Kinoshita, Taroh
Kanakura, Yuzuru
Young, Neal S.
TI Paroxysmal nocturnal hemoglobinuria with copy number-neutral 6pLOH in
GPI (+) but not in GPI (-) granulocytes
SO EUROPEAN JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE array comparative genomic hybridization; bone marrow failure syndromes;
clonal evolution; loss of heterozygosity; paroxysmal nocturnal
hemoglobinuria
ID NATURAL-KILLER-CELLS; JAPANESE PATIENTS; MUTATION; ALLELES
AB Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired bone marrow disorder caused by expansion of a clone of hematopoietic cells lacking glycosylphosphatidylinositol (GPI)-anchored membrane proteins. Multiple lines of evidence suggest immune attack on normal hematopoietic stem cells provides a selective growth advantage to PNH clones. Recently, frequent loss of HLA alleles associated with copy number-neutral loss of heterozygosity in chromosome 6p (CN-6pLOH) in aplastic anemia (AA) patients was reported, suggesting that AA hematopoiesis 'escaped' from immune attack by loss of HLA alleles. We report here the first case of CN-6pLOH in a Japanese PNH patient only in GPI-anchored protein positive (59%) granulocytes, but not in GPI-anchored protein negative (41%) granulocytes. CN-6pLOH resulted in loss of the alleles A*02:06-DRB1*15:01-DQB1*06:02, which have been reported to be dominant in Japanese PNH patients. Our patient had maintained nearly normal blood count for several years. Our case supports the hypothesis that a hostile immune environment drives selection of resistant hematopoietic cell clones and indicates that clonal evolution may occur also in normal phenotype (non-PNH) cells in some cases.
C1 [Ueda, Yasutaka; Kajigaya, Sachiko; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Nishimura, Jun-ichi; Kanakura, Yuzuru] Osaka Univ, Grad Sch Med, Dept Hematol & Oncol, Osaka, Japan.
[Murakami, Yoshiko; Kinoshita, Taroh] Osaka Univ, Microbial Dis Res Inst, Dept Immunoregulat, Osaka, Japan.
[Murakami, Yoshiko; Kinoshita, Taroh] Osaka Univ, WPI Immunol Frontier Res Ctr, Dept Immunoglycobiol, Osaka, Japan.
RP Ueda, Y (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10-CRC,Rm 3E-5216,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ueday2@nhlbi.nih.gov
RI Kinoshita, Taroh/C-7353-2009
FU NIH; NHLBI; Ministry of Education, Culture, Sports, Science and
Technology of Japan
FX This research was supported by the Intramural Research Program of the
NIH, the NHLBI, and in part by a Grant-in-Aid for Scientific Research
from the Ministry of Education, Culture, Sports, Science and Technology
of Japan. The authors thank Satoru Hayashi for excellent technical
assistance.
NR 13
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-4441
EI 1600-0609
J9 EUR J HAEMATOL
JI Eur. J. Haematol.
PD MAY
PY 2014
VL 92
IS 5
BP 450
EP 453
DI 10.1111/ejh.12253
PG 4
WC Hematology
SC Hematology
GA AE8QX
UT WOS:000334267500012
PM 24931618
ER
PT J
AU Cistaro, A
Pagani, M
Montuschi, A
Calvo, A
Moglia, C
Canosa, A
Restagno, G
Brunetti, M
Traynor, B
Nobili, F
Carrara, G
Fania, P
Lopiano, L
Valentini, M
Chio, A
AF Cistaro, Angelina
Pagani, Marco
Montuschi, Anna
Calvo, Andrea
Moglia, Cristina
Canosa, Antonio
Restagno, Gabriella
Brunetti, Maura
Traynor, Bryan J.
Nobili, Flavio
Carrara, Giovanna
Fania, Piercarlo
Lopiano, Leonardo
Valentini, M. Consuelo
Chio, Adriano
TI The metabolic signature of C9ORF72-related ALS: FDG PET comparison with
nonmutated patients
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Amyotrophic lateral sclerosis; C9ORF72 gene; FDG PET
ID AMYOTROPHIC-LATERAL-SCLEROSIS; HEXANUCLEOTIDE REPEAT EXPANSION;
POSITRON-EMISSION-TOMOGRAPHY; ANTERIOR CINGULATE CORTEX; FRONTOTEMPORAL
DEMENTIA; ALZHEIMERS-DISEASE; CLINICAL CHARACTERISTICS; C9ORF72;
SCHIZOPHRENIA; CRITERIA
AB Recently, a GGGGCC hexanucleotide repeat expansion in the C9ORF72 gene, located on chromosome 9p21 has been demonstrated to be the commonest cause of familial amyotrophic lateral sclerosis (ALS) and to account for 5 to 10 % of apparently sporadic ALS. Relatively little is known about the brain metabolism profile of patients carrying the expansion. Our aim was to identify the [F-18]FDG PET profile in ALS patients with the C9ORF72 expansion (C9ORF72-ALS).
Fifteen C9ORF72-ALS patients were compared with 12 patients with ALS and comorbid frontotemporal dementia (FTD) without the C9ORF72 expansion (ALS-FTD) and 30 cognitively normal patients with ALS without mutations of ALS-related genes (sALS). The three groups were then cross-matched to 40 neurologically normal controls. All patients underwent FDG PET within 4 months of diagnosis.
The C9ORF72-ALS patients compared with the sALS patients showed significant hypometabolism in the anterior and posterior cingulate cortex, insula, caudate and thalamus, the left frontal and superior temporal cortex, and hypermetabolism in the midbrain, bilateral occipital cortex, globus pallidus and left inferior temporal cortex. The ALS-FTD patients compared with the sALS patients showed more limited hypometabolic areas, including the orbitofrontal, prefrontal, anterior cingulate and insular cortex, and hypermetabolic areas, including the bilateral occipital cortex, the left precentral and postcentral cortex and superior temporal gyrus. The C9ORF72-ALS patients compared with the ALS-FTD patients showed hypometabolism in the left temporal cortex.
ALS patients with the C9ORF72 hexanucleotide repeat expansion had a more widespread central nervous system involvement than ALS patients without genetic mutations, with or without comorbid FTD, consistent with their more severe clinical picture.
C1 [Cistaro, Angelina; Fania, Piercarlo] IRMET SpA, Positron Emiss Tomog Ctr, Turin, Italy.
[Pagani, Marco] CNR, Inst Cognit Sci & Technol, Rome, Italy.
[Pagani, Marco] Karolinska Hosp, Dept Nucl Med, S-10401 Stockholm, Sweden.
[Montuschi, Anna; Calvo, Andrea; Moglia, Cristina; Canosa, Antonio; Lopiano, Leonardo; Chio, Adriano] Univ Turin, Rita Levi Montalcini Dept Neurosci, Turin, Italy.
[Calvo, Andrea; Lopiano, Leonardo; Chio, Adriano] Neurosci Inst Turin, Turin, Italy.
[Restagno, Gabriella; Brunetti, Maura] Azienda Osped Citta Salute & Sci, Dept Clin Pathol, Mol Genet Unit, Turin, Italy.
[Traynor, Bryan J.] NIA, Neuromuscular Dis Res Unit, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Nobili, Flavio] Univ Genoa, Dept Neurosci Ophthalmol & Genet, Clin Neurophysiol Unit, Genoa, Italy.
[Carrara, Giovanna; Valentini, M. Consuelo] Azienda Osped Citta Salute & Sci, Dept Neuroradiol, Turin, Italy.
[Chio, Adriano] ALS Ctr, Rita Levi Montalcini Dept Neurosci, I-10126 Turin, Italy.
RP Chio, A (reprint author), ALS Ctr, Rita Levi Montalcini Dept Neurosci, I-10126 Turin, Italy.
EM achio@usa.net
RI Calvo, Andrea/K-4141-2016; Moglia, Cristina/K-4142-2016;
OI Calvo, Andrea/0000-0002-5122-7243; Moglia, Cristina/0000-0001-7377-7222;
Chio, Adriano/0000-0001-9579-5341
FU Compagnia di San Paolo, Programma Neuroscienze; Ministero della Salute
(Ricerca Sanitaria Finalizzata) [RF-2010-2309849]; European Community
[259867]; Intramural Research Programmes of the National Institutes of
Health (NIH); National Institute on Aging [Z01-AG000949-02]
FX We thank the patients and the neurologically normal controls for their
collaboration in this study. This work was supported in part by
Compagnia di San Paolo, Programma Neuroscienze 2008-2009 (to M. Consuelo
Valentini and A. Calvo), Ministero della Salute (Ricerca Sanitaria
Finalizzata, 2010, grant RF-2010-2309849) (to A. Chio) European
Community's Health Seventh Framework Programme (FP7/2007-2013 under
grant agreement 259867) (to A. Chio); The Intramural Research Programmes
of the National Institutes of Health (NIH); National Institute on Aging
(Z01-AG000949-02) (to Bryan J. Traynor).
NR 41
TC 20
Z9 23
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
EI 1619-7089
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD MAY
PY 2014
VL 41
IS 5
BP 844
EP 852
DI 10.1007/s00259-013-2667-5
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AF0QA
UT WOS:000334417900005
PM 24445987
ER
PT J
AU Romagnuolo, J
Cotton, PB
Durkalski, V
Pauls, Q
Brawman-Mintzer, O
Drossman, DA
Mauldin, P
Orrell, K
Williams, AW
Fogel, EL
Tarnasky, PR
Aliperti, G
Freeman, ML
Kozarek, RA
Jamidar, PA
Wilcox, CM
Serrano, J
Elta, GH
AF Romagnuolo, Joseph
Cotton, Peter B.
Durkalski, Valerie
Pauls, Qi
Brawman-Mintzer, Olga
Drossman, Douglas A.
Mauldin, Patrick
Orrell, Kyle
Williams, April W.
Fogel, Evan L.
Tarnasky, Paul R.
Aliperti, Giuseppe
Freeman, Martin L.
Kozarek, Richard A.
Jamidar, Priya A.
Wilcox, C. Mel
Serrano, Jose
Elta, Grace H.
TI Can patient and pain characteristics predict manometric sphincter of
Oddi dysfunction in patients with clinically suspected sphincter of Oddi
dysfunction?
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID FINDINGS TYPE-I; ENDOSCOPIC SPHINCTEROTOMY; BOTULINUM TOXIN; RECURRENT
PANCREATITIS; BILIARY SPHINCTER; CHOLECYSTECTOMY; PRESENTATIONS;
SCINTIGRAPHY; INJECTION; EFFICACY
AB Background: Biliopancreatic-type postcholecystectomy pain, without significant abnormalities on imaging and laboratory test results, has been categorized as "suspected" sphincter of Oddi dysfunction (SOD) type III. Clinical predictors of "manometric" SOD are important to avoid unnecessary ERCP, but are unknown.
Objective: To assess which clinical factors are associated with abnormal sphincter of Oddi manometry (SOM).
Design: Prospective, cross-sectional.
Setting: Tertiary.
Patients: A total of 214 patients with suspected SOD type III underwent ERCP and pancreatic SOM (pSOM; 85% dual SOM), at 7 U. S. centers (from August 2008 to March 2012) as part of a randomized trial.
Interventions: Pain and gallbladder descriptors, psychosocial/functional disorder questionnaires.
Main Outcome Measurements: Abnormal SOM findings. Univariate and multivariate analyses assessed associations between clinical characteristics and outcome.
Results: The cohort was 92% female with a mean age of 38 years. Baseline pancreatic enzymes were increased in 5%; 9% had minor liver enzyme abnormalities. Pain was in the right upper quadrant (RUQ) in 90% (48% also epigastric); 51% reported daily abdominal discomfort. Fifty-six took narcotics an average of 33 days (of the past 90 days). Less than 10% experienced depression or anxiety. Functional disorders were common. At ERCP, 64% had abnormal pSOM findings (34% both sphincters, 21% biliary normal), 36% had normal pSOM findings, and 75% had at least abnormal 1 sphincter. Demographic factors, gallbladder pathology, increased pancreatobiliary enzymes, functional disorders, and pain patterns did not predict abnormal SOM findings. Anxiety, depression, and poorer coping were more common in patients with normal SOM findings (not significant on multivariate analysis).
Limitations: Generalizability.
Conclusions: Patient and pain factors and psychological comorbidity do not predict SOM results at ERCP in suspected type III SOD. (Clinical Trial registration number: NCT00688662.)
C1 [Romagnuolo, Joseph; Cotton, Peter B.; Durkalski, Valerie; Pauls, Qi; Brawman-Mintzer, Olga; Mauldin, Patrick; Williams, April W.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Drossman, Douglas A.] Univ N Carolina, Chapel Hill, NC USA.
[Orrell, Kyle; Tarnasky, Paul R.] Digest Hlth Associates Texas, Dallas, TX USA.
[Fogel, Evan L.] Indiana Univ, Indianapolis, IN 46204 USA.
[Aliperti, Giuseppe] Midwest Therapeut Endoscopy, St Louis, MO USA.
[Freeman, Martin L.] Univ Minnesota, Minneapolis, MN USA.
[Kozarek, Richard A.] Virginia Mason, Seattle, WA USA.
[Jamidar, Priya A.] Yale Univ, New Haven, CT USA.
[Wilcox, C. Mel] Univ Alabama Birmingham, Birmingham, AL USA.
[Serrano, Jose] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
[Elta, Grace H.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Romagnuolo, J (reprint author), Med Univ S Carolina, Div Gastroenterol & Hepatol, 25 Courtenay Dr,ART 7100A, Charleston, SC 29425 USA.
EM romagnuo@musc.edu
FU NIDDK [U01 DK074739]
FX All authors disclosed no financial relationships relevant to this
publication. Supported by NIDDK grant U01 DK074739.
NR 26
TC 4
Z9 4
U1 3
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
EI 1097-6779
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD MAY
PY 2014
VL 79
IS 5
BP 765
EP 772
DI 10.1016/j.gie.2013.11.037
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AE9BQ
UT WOS:000334299300014
PM 24472759
ER
PT J
AU Segars, JH
Parrott, EC
Nagel, JD
Guo, XC
Gao, XH
Birnbaum, LS
Pinn, VW
Dixon, D
AF Segars, James H.
Parrott, Estella C.
Nagel, Joan D.
Guo, Xiaoxiao Catherine
Gao, Xiaohua
Birnbaum, Linda S.
Pinn, Vivian W.
Dixon, Darlene
TI Proceedings from the Third National Institutes of Health International
Congress on Advances in Uterine Leiomyoma Research: comprehensive
review, conference summary and future recommendations
SO HUMAN REPRODUCTION UPDATE
LA English
DT Review
DE NIH conference summary and comprehensive review; uterine leiomyoma;
fibroids; clinical treatment; basic research; conference recommendations
ID PROGESTERONE-RECEPTOR MODULATOR; GONADOTROPIN-RELEASING-HORMONE;
SMOOTH-MUSCLE-CELLS; RANDOMIZED-CONTROLLED-TRIAL; FOCUSED ULTRASOUND
SURGERY; ENDOTHELIAL GROWTH-FACTOR; BLACK WOMENS HEALTH;
REPRODUCTIVE-TRACT LEIOMYOMATA; TYROSINE KINASE INHIBITOR;
FUMARATE-HYDRATASE GENE
AB Uterine fibroids are the most common gynecologic tumors in women of reproductive age yet the etiology and pathogenesis of these lesions remain poorly understood. Age, African ancestry, nulliparity and obesity have been identified as predisposing factors for uterine fibroids. Symptomatic tumors can cause excessive uterine bleeding, bladder dysfunction and pelvic pain, as well as associated reproductive disorders such as infertility, miscarriage and other adverse pregnancy outcomes. Currently, there are limited noninvasive therapies for fibroids and no early intervention or prevention strategies are readily available. This review summarizes the advances in basic, applied and translational uterine fibroid research, in addition to current and proposed approaches to clinical management as presented at the Advances in Uterine Leiomyoma Research: 3rd NIH International Congress. Congress recommendations and a review of the fibroid literature are also reported.
This review is a report of meeting proceedings, the resulting recommendations and a literature review of the subject.
The research data presented highlights the complexity of uterine fibroids and the convergence of ethnicity, race, genetics, epigenetics and environmental factors, including lifestyle and possible socioeconomic parameters on disease manifestation. The data presented suggest it is likely that the majority of women with uterine fibroids will have normal pregnancy outcomes; however, additional research is warranted. As an alternative to surgery, an effective long-term medical treatment for uterine fibroids should reduce heavy uterine bleeding and fibroid/uterine volume without excessive side effects. This goal has not been achieved and current treatments reduce symptoms only temporarily; however, a multi-disciplined approach to understanding the molecular origins and pathogenesis of uterine fibroids, as presented in this report, makes our quest for identifying novel targets for noninvasive, possibly nonsystemic and effective long-term treatment very promising.
The Congress facilitated the exchange of scientific information among members of the uterine leiomyoma research and health-care communities. While advances in research have deepened our knowledge of the pathobiology of fibroids, their etiology still remains incompletely understood. Further needs exist for determination of risk factors and initiation of preventive measures for fibroids, in addition to continued development of new medical and minimally invasive options for treatment.
C1 [Segars, James H.; Guo, Xiaoxiao Catherine] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, DHHS, Bethesda, MD 20892 USA.
[Parrott, Estella C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Gynecol Hlth & Dis Branch, NIH, DHHS, Bethesda, MD 20892 USA.
[Nagel, Joan D.; Pinn, Vivian W.] NIH, Off Res Womens Hlth, Off Director, DHHS, Bethesda, MD 20892 USA.
[Gao, Xiaohua; Dixon, Darlene] NIEHS, Natl Toxicol Program NTP Lab, NTP, NIH,DHHS, Res Triangle Pk, NC 27709 USA.
[Birnbaum, Linda S.] NIEHS, Off Director, NTP, NIH,DHHS, Res Triangle Pk, NC 27709 USA.
RP Dixon, D (reprint author), NIEHS, Natl Toxicol Program NTP Lab, NTP, NIH,DHHS, POB 12233, Res Triangle Pk, NC 27709 USA.
EM dixon@niehs.nih.gov
FU Intramural Research Program of the NIEHS; NTP, NIH; Office of Research
on Women's Health, NIH; Reproductive Sciences Branch; Intramural
Research Program in Reproductive and Adult Endocrinology, NICHD, NIH
FX The Congress was supported, in part, by the Intramural Research Program
of the NIEHS and NTP, NIH; the Office of Research on Women's Health, NIH
and the Reproductive Sciences Branch and the Intramural Research Program
in Reproductive and Adult Endocrinology, NICHD, NIH.
NR 293
TC 27
Z9 29
U1 2
U2 22
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1355-4786
EI 1460-2369
J9 HUM REPROD UPDATE
JI Hum. Reprod. Update
PD MAY-JUN
PY 2014
VL 20
IS 3
BP 309
EP 333
DI 10.1093/humupd/dmt058
PG 25
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AF4IP
UT WOS:000334675600001
PM 24401287
ER
PT J
AU Vera, DM
Hora, RA
Murillo, A
Wong, JF
Torre, AJ
Wang, D
Boulay, D
Hancock, K
Katz, JM
Ramos, M
Loayza, L
Quispe, J
Reaves, EJ
Bausch, DG
Chowell, G
Montgomery, JM
AF Vera, Delphis M.
Hora, Ricardo A.
Murillo, Anarina
Wong, Juan F.
Torre, Armando J.
Wang, David
Boulay, Darbi
Hancock, Kathy
Katz, Jacqueline M.
Ramos, Mariana
Loayza, Luis
Quispe, Jose
Reaves, Erik J.
Bausch, Daniel G.
Chowell, Gerardo
Montgomery, Joel M.
TI Assessing the impact of public health interventions on the transmission
of pandemic H1N1 influenza a virus aboard a Peruvian navy ship
SO INFLUENZA AND OTHER RESPIRATORY VIRUSES
LA English
DT Article
DE Disease outbreak; influenza; military personnel; Peru; ships;
transmission
ID SEROLOGIC ASSAYS; OUTBREAK; VESSEL
AB Background Limited data exist on transmission dynamics and effectiveness of control measures for influenza in confined settings.
Objectives To investigate the transmission dynamics of a 2009 pandemic H1N1 influenza A outbreak aboard a Peruvian Navy ship and quantify the effectiveness of the implemented control measures.
Methods We used surveillance data and a simple stochastic epidemic model to characterize and evaluate the effectiveness of control interventions implemented during an outbreak of 2009 pandemic H1N1 influenza A aboard a Peruvian Navy ship.
Results The serological attack rate for the outbreak was 49.1%, with younger cadets and low-ranking officers at greater risk of infection than older, higher-ranking officers. Our transmission model yielded a good fit to the daily time series of new influenza cases by date of symptom onset. We estimated a reduction of 54.4% in the reproduction number during the period of intense control interventions.
Conclusion Our results indicate that the patient isolation strategy and other control measures put in place during the outbreak reduced the infectiousness of isolated individuals by 86.7%. Our findings support that early implementation of control interventions can limit the spread of influenza epidemics in confined settings.
C1 [Vera, Delphis M.; Hora, Ricardo A.; Wong, Juan F.; Torre, Armando J.; Ramos, Mariana; Reaves, Erik J.; Bausch, Daniel G.] US Naval Med Res Unit 6, Lima, Peru.
[Murillo, Anarina; Chowell, Gerardo] Arizona State Univ, Tempe, AZ USA.
[Wang, David; Boulay, Darbi; Hancock, Kathy; Katz, Jacqueline M.; Montgomery, Joel M.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Loayza, Luis; Quispe, Jose] Peruvian Navy, Lima, Peru.
[Bausch, Daniel G.] Tulane Univ, New Orleans, LA 70118 USA.
[Chowell, Gerardo] NIH, Bethesda, MD 20892 USA.
RP Vera, DM (reprint author), US Naval Med Res Unit 6, 3230 Lima Pl, Washington, DC 20521 USA.
EM delphisv@gmail.com
FU Grant GEIS [I0308_11_LI]; [847705.82000.25GB.B0016]
FX This work was supported and funded by work unit No.
847705.82000.25GB.B0016 and Grant GEIS I0308_11_LI entitled
"Transmission dynamics of influenza outbreaks in military ships:
Assessing the efficacy of control measures."
NR 29
TC 6
Z9 6
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1750-2640
EI 1750-2659
J9 INFLUENZA OTHER RESP
JI Influenza Other Respir. Viruses
PD MAY
PY 2014
VL 8
IS 3
BP 353
EP 359
DI 10.1111/irv.12240
PG 7
WC Infectious Diseases; Virology
SC Infectious Diseases; Virology
GA AE6PS
UT WOS:000334116600011
PM 24506160
ER
PT J
AU Katz, SI
AF Katz, Stephen I.
TI Unity in Action
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Editorial Material
ID INVESTIGATIVE DERMATOLOGY
C1 NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Katz, SI (reprint author), NIAMSD, NIH, Bldg 31,Room 4C32,31 Ctr Dr, Bethesda, MD 20892 USA.
EM katzs@mail.nih.gov
NR 5
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
IS 5
BP 1184
EP 1186
DI 10.1038/jid.2014.135
PG 3
WC Dermatology
SC Dermatology
GA AF2VJ
UT WOS:000334570300002
PM 24732327
ER
PT J
AU Pos, Z
Spivey, TL
Liu, H
Sommariva, M
Chen, JG
Wunderlich, JR
Parisi, G
Tomei, S
Ayotte, BD
Stroncek, DF
Malek, JA
Robbins, PF
Rivoltini, L
Maio, M
Chouchane, L
Wang, E
Marincola, FM
AF Pos, Zoltan
Spivey, Tara L.
Liu, Hui
Sommariva, Michele
Chen, Jinguo
Wunderlich, John R.
Parisi, Giulia
Tomei, Sara
Ayotte, Ben D.
Stroncek, David F.
Malek, Joel A.
Robbins, Paul F.
Rivoltini, Licia
Maio, Michele
Chouchane, Lotfi
Wang, Ena
Marincola, Francesco M.
TI Longitudinal Study of Recurrent Metastatic Melanoma Cell Lines
Underscores the Individuality of Cancer Biology
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID GENETIC-HETEROGENEITY; COPY NUMBER; EVOLUTION; BREAST; MUTATIONS;
AMPLIFICATION; CARCINOMA; DELETIONS; TUMORS; TRIAL
AB Recurrent metastatic melanoma provides a unique opportunity to analyze disease evolution in metastatic cancer. Here, we followed up eight patients with an unusually prolonged history of metastatic melanoma, who developed a total of 26 recurrences over several years. Cell lines derived from each metastasis were analyzed by comparative genomic hybridization and global transcript analysis. We observed that conserved, patient-specific characteristics remain stable in recurrent metastatic melanoma even after years and several recurrences. Differences among individual patients exceeded within-patient lesion variability, both at the DNA copy number (P<0.001) and RNA gene expression level (P<0.001). Conserved patient-specific traits included expression of several cancer/testis antigens and the c-kit proto-oncogene throughout multiple recurrences. Interestingly, subsequent recurrences of different patients did not display consistent or convergent changes toward a more aggressive disease phenotype. Finally, sequential recurrences of the same patient did not descend progressively from each other, as irreversible mutations such as homozygous deletions were frequently not inherited from previous metastases. This study suggests that the late evolution of metastatic melanoma, which markedly turns an indolent disease into a lethal phase, is prone to preserve case-specific traits over multiple recurrences and occurs through a series of random events that do not follow a consistent stepwise process.
C1 [Pos, Zoltan; Spivey, Tara L.; Liu, Hui; Sommariva, Michele; Chen, Jinguo; Wang, Ena; Marincola, Francesco M.] NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Pos, Zoltan] Semmelweis Univ, Hungarian Acad Sci, Lendulet Expt & Translat Immun Res Grp, H-1085 Budapest, Hungary.
[Pos, Zoltan] Semmelweis Univ, Dept Genet Cell & Immunobiol, H-1085 Budapest, Hungary.
[Spivey, Tara L.] NIH, Clin Res Training Program CRTP, Bethesda, MD 20892 USA.
[Spivey, Tara L.] Rush Univ, Med Ctr, Dept Gen Surg, Chicago, IL 60612 USA.
[Sommariva, Michele] Univ Milan, Dept Biomed Sci Hlth, Milan, Italy.
[Wunderlich, John R.; Robbins, Paul F.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Parisi, Giulia; Maio, Michele] Ctr Riferimento Oncol, Canc Bioimmunotherapy Unit, Avian, Italy.
[Tomei, Sara; Malek, Joel A.] Weill Cornell Med Coll Qatar, Dept Genet Med, Doha, Qatar.
[Ayotte, Ben D.] No Michigan Univ, Dept Biol, Marquette, MI 49855 USA.
[Stroncek, David F.] NIH, Cell Proc Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD USA.
[Rivoltini, Licia] Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
[Chouchane, Lotfi] Weill Cornell Med Coll Qatar, Doha, Qatar.
[Marincola, Francesco M.] Sidra Med & Res Ctr, Res Branch, Doha, Qatar.
RP Marincola, FM (reprint author), Sidra Med & Res Ctr, Res Branch, Doha, Qatar.
EM fmarincola@sidra.org
RI Pos, Zoltan/C-3623-2014; Sommariva, Michele/C-1174-2017;
OI Pos, Zoltan/0000-0002-2574-7616; Sommariva, Michele/0000-0002-7622-0996;
coral, sandra/0000-0002-1308-3082; Rivoltini, Licia/0000-0002-2409-6225
FU Associazione Italiana per la Ricerca sul Cancro [IG 11746]; Regione
Toscana "Regional Health Research Program"; Hungarian Academy of
Sciences "Lendulet" [LP2012-49/2012]
FX The study was supported in part by Associazione Italiana per la Ricerca
sul Cancro, IG 11746, Regione Toscana "Regional Health Research Program
2009," and the Hungarian Academy of Sciences "Lendulet" Grant
LP2012-49/2012.
NR 36
TC 0
Z9 0
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
IS 5
BP 1389
EP 1396
DI 10.1038/jid.2013.495
PG 8
WC Dermatology
SC Dermatology
GA AF2VJ
UT WOS:000334570300030
PM 24270663
ER
PT J
AU Okiyama, N
Sugihara, T
Yokozeki, H
Kohsaka, H
AF Okiyama, N.
Sugihara, T.
Yokozeki, H.
Kohsaka, H.
TI Murine models of autoimmune myositis
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT 3rd International Conference on Cutaneous Lupus Erythematosus
CY MAY 06-08, 2013
CL Edinburgh, SCOTLAND
C1 [Okiyama, N.; Sugihara, T.; Kohsaka, H.] Tokyo Med & Dent Univ, Dept Med & Rheumatol, Tokyo, Japan.
[Okiyama, N.; Yokozeki, H.] Tokyo Med & Dent Univ, Dept Dermatol, Tokyo, Japan.
[Okiyama, N.] NCI, Dermatol Branch, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
IS 5
BP 1488
EP 1488
PG 1
WC Dermatology
SC Dermatology
GA AF2VJ
UT WOS:000334570300076
ER
PT J
AU Barsell, AB
Allawh, R
Xiong, M
Tamura, D
Collins, M
Steinberg, SM
Khan, SG
Hill, S
Kraemer, KH
DiGiovanna, II
AF Barsell, A. B.
Allawh, R.
Xiong, M.
Tamura, D.
Collins, M.
Steinberg, S. M.
Khan, S. G.
Hill, S.
Kraemer, K. H.
DiGiovanna, I. I.
TI Bone abnormalities in trichothiodystrophy: Central osteosclerosis is a
prognostic marker for increased risk of early death
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Barsell, A. B.; Allawh, R.; Xiong, M.; Tamura, D.; Steinberg, S. M.; Khan, S. G.; Kraemer, K. H.; DiGiovanna, I. I.] NCI, Bethesda, MD 20892 USA.
[Barsell, A. B.; Allawh, R.] George Wash Univ Sch Med, Washington, DC USA.
[Xiong, M.] Brown Univ Sch Med, Providence, RI USA.
[Hill, S.] NIH, Bethesda, MD 20892 USA.
[Collins, M.] NICDR, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 428
BP S75
EP S75
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400427
ER
PT J
AU Cataisson, C
Salcedo, R
Shibuya, K
Naik, S
Wright, L
Trinchieri, G
Yuspa, SH
AF Cataisson, C.
Salcedo, R.
Shibuya, K.
Naik, S.
Wright, L.
Trinchieri, G.
Yuspa, S. H.
TI MyD88 signaling in both keratinocytes and T-cells contribute to skin
carcinogenesis
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Cataisson, C.; Shibuya, K.; Wright, L.; Yuspa, S. H.] NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Naik, S.] NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA.
[Salcedo, R.; Trinchieri, G.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 186
BP S32
EP S32
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400187
ER
PT J
AU Glatz, M
Stone, K
Milner, JD
Kong, HH
AF Glatz, M.
Stone, K.
Milner, J. D.
Kong, H. H.
TI Altered skin microbial communities associated with wet wrap therapy for
severe eczema
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Glatz, M.; Kong, H. H.] NCI, Dermatol Branch, CCR, NIH, Bethesda, MD 20892 USA.
[Stone, K.; Milner, J. D.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 623
BP S109
EP S109
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400621
ER
PT J
AU Harden, JL
Lewis, SM
Pierson, KC
Suarez-Farinas, M
Lentini, T
Ortenzio, F
Zaba, LC
Goldbach-Mansky, R
Bowcock, AM
Lowes, MA
AF Harden, J. L.
Lewis, S. M.
Pierson, K. C.
Suarez-Farinas, M.
Lentini, T.
Ortenzio, F.
Zaba, L. C.
Goldbach-Mansky, R.
Bowcock, A. M.
Lowes, M. A.
TI CARD14 expression in dermal endothelial cells in psoriasis
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Harden, J. L.; Lewis, S. M.; Pierson, K. C.; Suarez-Farinas, M.; Lentini, T.; Ortenzio, F.; Zaba, L. C.; Lowes, M. A.] Rockefeller Univ, Lab Investigat Dermatol, New York, NY 10021 USA.
[Suarez-Farinas, M.] Rockefeller Univ, Ctr Clin & Translat Sci, New York, NY 10021 USA.
[Goldbach-Mansky, R.] NIAMS, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD USA.
[Bowcock, A. M.] Univ London Imperial Coll Sci Technol & Med, London, England.
RI Suarez-Farinas, Mayte/I-3558-2012
OI Suarez-Farinas, Mayte/0000-0001-8712-3553
NR 0
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 119
BP S21
EP S21
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400120
ER
PT J
AU Heller, ER
Khan, SG
Tamura, D
DiGiovanna, JJ
Kraemer, KH
AF Heller, E. R.
Khan, S. G.
Tamura, D.
DiGiovanna, J. J.
Kraemer, K. H.
TI Mutations in TTDN1 are associated with a unique trichothiodystrophy
phenotype
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Heller, E. R.; Khan, S. G.; Tamura, D.; DiGiovanna, J. J.; Kraemer, K. H.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 432
BP S75
EP S75
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400431
ER
PT J
AU Kim, J
Duverger, O
Hwang, J
Morasso, M
AF Kim, J.
Duverger, O.
Hwang, J.
Morasso, M.
TI Impact of DIx3 deficiency in isthmus/infundibulum for hair shaft
development
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Kim, J.; Duverger, O.; Hwang, J.; Morasso, M.] NIAMS, Skin Biol Lab, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 244
BP S42
EP S42
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400244
ER
PT J
AU Kim, J
Ogawa, Y
Siebenlist, U
Udey, MC
Morass, M
AF Kim, J.
Ogawa, Y.
Siebenlist, U.
Udey, M. C.
Morass, M.
TI IL-17A regulates inflammation in Dlx3-deficient murine skin
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Kim, J.; Morass, M.] NIAMS, Skin Biol Lab, NIH, Bethesda, MD USA.
[Ogawa, Y.; Udey, M. C.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Siebenlist, U.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 121
BP S21
EP S21
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400122
ER
PT J
AU Klover, P
Thangapazham, R
Kato, J
Wang, J
Li, S
Anderson, SA
Hoffmann, V
McCart, E
Nathan, N
Moss, J
Darling, TN
AF Klover, P.
Thangapazham, R.
Kato, J.
Wang, J.
Li, S.
Anderson, S. A.
Hoffmann, V.
McCart, E.
Nathan, N.
Moss, J.
Darling, T. N.
TI Sirolimus normalizes skin and dramatically reduces internal tumors in a
mouse model of tuberous sclerosis complex (TSC)
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Klover, P.; Thangapazham, R.; Wang, J.; Li, S.; McCart, E.; Nathan, N.; Darling, T. N.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Kato, J.; Nathan, N.; Moss, J.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Anderson, S. A.; Hoffmann, V.] NIH, Diagnost & Res Serv Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 454
BP S79
EP S79
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400453
ER
PT J
AU Kuschal, C
DiGiovanna, JJ
Tamura, D
Khan, SG
Edelman, D
Meltzer, P
Soppet, D
Stephens, R
Kraemer, KH
AF Kuschal, C.
DiGiovanna, J. J.
Tamura, D.
Khan, S. G.
Edelman, D.
Meltzer, P.
Soppet, D.
Stephens, R.
Kraemer, K. H.
TI Identification of novel susceptibility genes in trichothiodystrophy and
xeroderma pigmentosum patients by use of exome sequencing
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Kuschal, C.; DiGiovanna, J. J.; Tamura, D.; Khan, S. G.; Kraemer, K. H.] NCI, Derm Br, Bethesda, MD 20892 USA.
[Edelman, D.; Meltzer, P.] NCI, Genet Br, Bethesda, MD 20892 USA.
[Soppet, D.; Stephens, R.] NCI, Adv Biomed Comp Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 187
BP S32
EP S32
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400188
ER
PT J
AU Lessard, JC
Kalinin, A
Stepp, M
Morasso, M
AF Lessard, J. C.
Kalinin, A.
Stepp, M.
Morasso, M.
TI A role for the calcium-binding protein Calm4 in cell migration and wound
healing
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Lessard, J. C.; Kalinin, A.; Morasso, M.] NIAMS, Skin Biol Lab, NIH, Bethesda, MD USA.
[Stepp, M.] George Washington Univ, Sch Med, Dept Anat & Cell Biol, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 766
BP S134
EP S134
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400763
ER
PT J
AU Li, L
Flower, B
Yuspa, SH
AF Li, L.
Flower, B.
Yuspa, S. H.
TI IKK16 inhibits activation NF-kappa B and reduces expression of
proinflammatory chemokines in keratinocytes
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Li, L.; Flower, B.; Yuspa, S. H.] NCI, LCBG, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 136
BP S23
EP S23
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400137
ER
PT J
AU Lim, YH
Ovejero, D
Sugarman, J
Eichenfield, L
Levy, M
Collins, M
Choate, KA
AF Lim, Y. H.
Ovejero, D.
Sugarman, J.
Eichenfield, L.
Levy, M.
Collins, M.
Choate, K. A.
TI Somatic activating mutations in HRAS and NRAS cause cutaneous skeletal
hypophosphatemic syndrome
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Lim, Y. H.; Choate, K. A.] Yale Univ, Sch Med, New Haven, CT USA.
[Ovejero, D.; Collins, M.] NIDCR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA.
[Sugarman, J.] UCSF, San Francisco, CA USA.
[Eichenfield, L.] Univ Calif San Diego, San Diego, CA USA.
[Levy, M.] Dell Childrens Med Ctr, Austin, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 467
BP S81
EP S81
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400466
ER
PT J
AU Mascia, F
Schloemann, D
Michalowski, A
Yuspa, S
AF Mascia, F.
Schloemann, D.
Michalowski, A.
Yuspa, S.
TI Transcriptional snapshot of the early consequences of EGFR ablation in
the epidermis
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Mascia, F.; Schloemann, D.; Michalowski, A.; Yuspa, S.] NCI, LCBG, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 129
BP S22
EP S22
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400130
ER
PT J
AU Naik, HB
Steinberg, SM
Kong, HH
Cowen, EW
AF Naik, H. B.
Steinberg, S. M.
Kong, H. H.
Cowen, E. W.
TI Botulinum toxin improves quality of life and may ameliorate pain
associated with cutaneous leiomyomas
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Naik, H. B.; Steinberg, S. M.; Kong, H. H.; Cowen, E. W.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 533
BP S93
EP S93
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400532
ER
PT J
AU Nakrani, R
Glatz, M
Booher, C
Steinberg, SM
Kong, HH
AF Nakrani, R.
Glatz, M.
Booher, C.
Steinberg, S. M.
Kong, H. H.
TI Subjective component of SCORAD provides unique information when
assessing atopic dermatitis
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Nakrani, R.; Glatz, M.; Booher, C.; Steinberg, S. M.; Kong, H. H.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 326
BP S56
EP S56
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400325
ER
PT J
AU Okiyama, N
Katz, SI
AF Okiyama, N.
Katz, S. I.
TI Programmed cell death1 (PD-1) regulates the effector function of
autoimmune CD8 T cells via the ligands expressed on target epidermal
cells
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Okiyama, N.; Katz, S. I.] NCI, Dermatol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 018
BP S3
EP S3
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400019
ER
PT J
AU Ouchi, T
Udey, MC
AF Ouchi, T.
Udey, M. C.
TI EpCAM expressed by epidermal Langerhans cells modulates topical
immunization to proteins
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Ouchi, T.; Udey, M. C.] NCI, Dermatol Branch, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 021
BP S4
EP S4
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400022
ER
PT J
AU Palazzo, E
Kellett, MD
Gormley, A
Bible, PW
Pietroni, V
Radoja, N
Blumenberg, M
Kim, J
Cataisson, C
Morasso, M
AF Palazzo, E.
Kellett, M. D.
Gormley, A.
Bible, P. W.
Pietroni, V.
Radoja, N.
Blumenberg, M.
Kim, J.
Cataisson, C.
Morasso, M.
TI DIx3-PKC interplay drives skin differentiation by controlling cell cycle
in keratinocytes
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Palazzo, E.; Kellett, M. D.; Gormley, A.; Bible, P. W.; Pietroni, V.; Radoja, N.; Kim, J.; Morasso, M.] NIAMS, Skin Biol Lab, NIH, Bethesda, MD USA.
[Cataisson, C.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Blumenberg, M.] NYU, Dept Dermatol, New York, NY 10016 USA.
RI Palazzo, Elisabetta/J-5287-2016
OI Palazzo, Elisabetta/0000-0002-0812-5524
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 380
BP S66
EP S66
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400379
ER
PT J
AU Sargen, MR
Kanetsky, PA
Newton-Bishop, J
Hayward, N
Mann, G
Gruis, N
Tucker, M
Goldstein, A
Bianchi-Scarra, G
Puig, S
Elder, DE
AF Sargen, M. R.
Kanetsky, P. A.
Newton-Bishop, J.
Hayward, N.
Mann, G.
Gruis, N.
Tucker, M.
Goldstein, A.
Bianchi-Scarra, G.
Puig, S.
Elder, D. E.
TI Histological features of superficial spreading melanoma are associated
with and predictive of CDKN2A germline mutations
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Sargen, M. R.; Elder, D. E.] Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Sargen, M. R.; Kanetsky, P. A.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Newton-Bishop, J.] Univ Leeds, Leeds, W Yorkshire, England.
[Hayward, N.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
[Mann, G.] Westmead Millennium Inst, Sydney, NSW, Australia.
[Gruis, N.] Leiden Univ, Med Ctr, Leiden, Netherlands.
[Tucker, M.; Goldstein, A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Bianchi-Scarra, G.] Univ Genoa, Genoa, Italy.
[Puig, S.] Univ Hosp Clin Barcelona, Barcelona, Spain.
RI Tucker, Margaret/B-4297-2015; hayward, nicholas/C-1367-2015
OI hayward, nicholas/0000-0003-4760-1033
NR 0
TC 0
Z9 0
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 690
BP S121
EP S121
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400688
ER
PT J
AU Tsuji, G
Okiyama, N
Villarroel, V
Katz, SI
AF Tsuji, G.
Okiyama, N.
Villarroel, V.
Katz, S. I.
TI Epigenetic modulation via histone deacetylase (HDAC) 6 inhibition
impairs CD8 T cell functions during skin inflammation
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Tsuji, G.; Okiyama, N.; Villarroel, V.; Katz, S. I.] NCI, Derm Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 020
BP S4
EP S4
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400021
ER
PT J
AU Xiao, Y
Williams, JS
Brownell, I
AF Xiao, Y.
Williams, J. S.
Brownell, I.
TI Sonic hedgehog signaling is essential for touch dome Merkel cell
development
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Xiao, Y.; Williams, J. S.; Brownell, I.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 277
BP S47
EP S47
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400276
ER
PT J
AU Xiao, Y
Williams, JS
Brownell, I
AF Xiao, Y.
Williams, J. S.
Brownell, I.
TI Hedgehog signaling creates a perineural stem cell niche essential for
maintaining sensory touch domes in skin
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Xiao, Y.; Williams, J. S.; Brownell, I.] NCI, Dermatol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 246
BP S42
EP S42
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400246
ER
PT J
AU Zuo, RC
Kuzmina, Z
Naik, HB
Pavletic, SZ
Cowen, EW
AF Zuo, R. C.
Kuzmina, Z.
Naik, H. B.
Pavletic, S. Z.
Cowen, E. W.
TI Serum autoantibodies and cutaneous autoimmunity in chronic
graft-versus-host disease
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology (SID)
CY MAY 07-10, 2014
CL Albuquerque, NM
SP Soc Invest Dermatol
C1 [Zuo, R. C.; Kuzmina, Z.; Naik, H. B.; Pavletic, S. Z.; Cowen, E. W.] NCI CCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2014
VL 134
SU 1
MA 068
BP S12
EP S12
PG 1
WC Dermatology
SC Dermatology
GA AF2RT
UT WOS:000334560400069
ER
PT J
AU Miyagi, E
Kao, S
Yedavalli, V
Strebel, K
AF Miyagi, Eri
Kao, Sandra
Yedavalli, Venkat
Strebel, Klaus
TI CBF beta Enhances De Novo Protein Biosynthesis of Its Binding Partners
HIV-1 Vif and RUNX1 and Potentiates the Vif-Induced Degradation of
APOBEC3G
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1 VIF; ANTIVIRAL ACTIVITY; VIRAL
INFECTIVITY; ENZYME APOBEC3G; IDENTIFICATION; DOMAIN; GAG;
TRANSCRIPTION; PROTEASOME
AB Vif is a lentiviral accessory protein that regulates viral infectivity in part by inducing proteasomal degradation of APOBEC3G (A3G). Recently, CBF beta was found to facilitate Vif-dependent degradation of A3G. However, the exact role of CBF beta remains unclear. Several studies noted reduced Vif expression in CBF beta knockdown cells while others saw no significant impact of CBF beta on Vif stability. Here, we confirmed that CBF beta increases Vif steady-state levels. CBF beta affected expression of neither viral Gag nor Vpu protein, indicating that CBF beta regulates Vif expression posttranscriptionally. Kinetic studies revealed effects of CBF beta on both metabolic stability and the rate of Vif biosynthesis. These effects were dependent on the ability of CBF beta to interact with Vif. Importantly, at comparable Vif levels, CBF beta further enhanced A3G degradation, suggesting that CBF beta facilitates A3G degradation by increasing the levels of Vif and by independently augmenting the ability of Vif to target A3G for degradation. CBF beta also increased expression of RUNX1 by enhancing RUNX1 biosynthesis. Unlike Vif, however, CBF beta had no detectable effect on RUNX1 metabolic stability. We propose that CBF beta acts as a chaperone to stabilize Vif during and after synthesis and to facilitate interaction of Vif with cellular cofactors required for the efficient degradation of A3G.
C1 [Miyagi, Eri; Kao, Sandra; Yedavalli, Venkat; Strebel, Klaus] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Strebel, K (reprint author), NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
EM kstrebel@nih.gov
FU NIH, NIAID
FX This work was supported by the Intramural Research Program of the NIH,
NIAID, to K.S.
NR 65
TC 6
Z9 6
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2014
VL 88
IS 9
BP 4839
EP 4852
DI 10.1128/JVI.03359-13
PG 14
WC Virology
SC Virology
GA AE9TT
UT WOS:000334353900021
PM 24522927
ER
PT J
AU Tabler, CO
Lucera, MB
Haqqani, AA
McDonald, DJ
Migueles, SA
Connors, M
Tilton, JC
AF Tabler, Caroline O.
Lucera, Mark B.
Haqqani, Aiman A.
McDonald, David J.
Migueles, Stephen A.
Connors, Mark
Tilton, John C.
TI CD4(+) Memory Stem Cells Are Infected by HIV-1 in a Manner Regulated in
Part by SAMHD1 Expression
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; T-CELLS; ANTIRETROVIRAL THERAPY; 2
SUBSETS; NAIVE; LYMPHOCYTES; ENTRY; DIFFERENTIATION; IDENTIFICATION;
PERSISTENCE
AB CD4(+) and CD8(+) memory T cells with stem cell-like properties (TSCM cells) have been identified in mice, humans, and nonhuman primates and are being investigated for antitumor and antiviral vaccines and immunotherapies. Whether CD4(+) TSCM cells are infected by human immunodeficiency virus (HIV) was investigated by using a combination HIV reporter virus system in vitro and by direct staining for HIV p24 antigen ex vivo. A proportion of TSCM cells were found to express the HIV coreceptors CCR5 and CXCR4 and were infected by HIV both in vitro and in vivo. Analysis of viral outcome following fusion using the combination reporter virus system revealed that TSCM cells can become productively or latently infected, although the vast majority of TSCM cells are abortively infected. Knockdown of the HIV restriction factor SAMHD1 using Vpx-containing simian immunodeficiency virus (SIV) virion-like particles enhanced the productive infection of TSCM cells, indicating that SAMHD1 contributes to abortive infection in these cells. These results demonstrate that CD4(+) TSCM cells are targets for HIV infection, that they become productively or latently infected at low levels, and that SAMHD1 expression promotes abortive infection of this important memory cell subset.
C1 [Tabler, Caroline O.; Lucera, Mark B.; Haqqani, Aiman A.; Tilton, John C.] Case Western Reserve Univ, Case Ctr Prote & Bioinformat, Cleveland, OH 44106 USA.
[McDonald, David J.] Case Western Reserve Univ, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA.
[Migueles, Stephen A.; Connors, Mark] NIAID, HIV Specif Immun Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Tilton, JC (reprint author), Case Western Reserve Univ, Case Ctr Prote & Bioinformat, Cleveland, OH 44106 USA.
EM jct63@case.edu
FU Case Western Reserve University/University Hospitals Center for AIDS
Research (NIH) [P30 AI036219]; Foundation for AIDS Research (amfAR)
[108257-51-RGRL]
FX This work was supported by the Case Western Reserve
University/University Hospitals Center for AIDS Research (NIH grant P30
AI036219) and by Foundation for AIDS Research (amfAR) research grant
108257-51-RGRL.
NR 48
TC 9
Z9 11
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2014
VL 88
IS 9
BP 4976
EP 4986
DI 10.1128/JVI.00324-14
PG 11
WC Virology
SC Virology
GA AE9TT
UT WOS:000334353900032
PM 24554663
ER
PT J
AU Marshall, LJ
Ferenczy, MW
Daley, EL
Jensen, PN
Ryschkewitsch, CF
Major, EO
AF Marshall, Leslie J.
Ferenczy, Michael W.
Daley, Elizabeth L.
Jensen, Peter N.
Ryschkewitsch, Caroline F.
Major, Eugene O.
TI Lymphocyte Gene Expression and JC Virus Noncoding Control Region
Sequences Are Linked with the Risk of Progressive Multifocal
Leukoencephalopathy
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HEMATOPOIETIC PROGENITOR CELLS; SPI-B; MULTIPLE-SCLEROSIS; TRANSCRIPTION
FACTOR; HUMAN BRAIN; REGULATORY REGION; BINDING SITES; NATALIZUMAB;
VARIANTS; PROTEIN
AB Progressive multifocal leukoencephalopathy (PML)-derived noncoding control region (NCCR) sequences permitted greater early viral gene expression than kidney-associated NCCR sequences. This was driven in part by binding of the transcription factor Spi-B to unique PML-associated Spi-B binding sites. Spi-B is upregulated in developing B cells in response to natalizumab therapy, a known risk factor for PML. Naturally occurring JCV sequence variation, together with drug treatment-induced cellular changes, may synergize to create an environment leading to an increased risk of PML.
C1 [Marshall, Leslie J.; Ferenczy, Michael W.; Daley, Elizabeth L.; Jensen, Peter N.; Ryschkewitsch, Caroline F.; Major, Eugene O.] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
RP Ferenczy, MW (reprint author), NINDS, Lab Mol Med & Neurosci, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM michael.ferenczy@.nih.gov; majorg@ninds.nih.gov
FU NIH Office of AIDS Research; Division of Intramural Research of the
NINDS
FX M.W.F. was supported in part by the Intramural AIDS Research Fellowship
from the NIH Office of AIDS Research. The LMMN is supported by the
Division of Intramural Research of the NINDS.
NR 30
TC 18
Z9 18
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2014
VL 88
IS 9
BP 5177
EP 5183
DI 10.1128/JVI.03221-13
PG 7
WC Virology
SC Virology
GA AE9TT
UT WOS:000334353900049
PM 24554653
ER
PT J
AU Wieland, SF
Asabe, S
Engle, RE
Purcell, RH
Chisari, FV
AF Wieland, S. F.
Asabe, S.
Engle, R. E.
Purcell, R. H.
Chisari, F. V.
TI Limited Hepatitis B Virus Replication Space in the Chronically Hepatitis
C Virus-Infected Liver
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TRANSGENIC MICE; GENOMIC ANALYSIS; VIRAL CLEARANCE; HOST RESPONSE; HUH-7
CELLS; CHIMPANZEES; INTERFERON; EXPRESSION; COINFECTION; DISEASE
AB We compared the kinetics and magnitude of hepatitis B virus (HBV) infection in hepatitis C virus (HCV)-naive and chronically HCV-infected chimpanzees in whose livers type I interferon-stimulated gene (ISG) expression is strongly induced. HBV infection was delayed and attenuated in the HCV-infected animals, and the number of HBV-infected hepatocytes was drastically reduced. These results suggest that establishment of HBV infection and its replication space is limited by the antiviral effects of type I interferon in the chronically HCV-infected liver.
C1 [Wieland, S. F.; Asabe, S.; Chisari, F. V.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Engle, R. E.; Purcell, R. H.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Wieland, SF (reprint author), Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
EM swieland@scripps.edu
OI Chisari, Francis/0000-0002-4832-1044
FU NIH [N01-AI-52705, N01-AI-45180, N01-CO-56000]; Intramural Research
Program of the NIAID, NIH; Sam and Rose Stein Charitable Trust;
[AI20001]; [CA76403]
FX This study was supported by grants AI20001 and CA76403, by contracts
N01-AI-52705, N01-AI-45180, and N01-CO-56000 from the NIH, by the
Intramural Research Program of the NIAID, NIH, and by the Sam and Rose
Stein Charitable Trust.
NR 30
TC 4
Z9 4
U1 0
U2 4
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2014
VL 88
IS 9
BP 5184
EP 5188
DI 10.1128/JVI.03553-13
PG 5
WC Virology
SC Virology
GA AE9TT
UT WOS:000334353900050
PM 24522924
ER
PT J
AU Joedicke, JJ
Zelinskyy, G
Dittmer, U
Hasenkrug, KJ
AF Joedicke, Jara J.
Zelinskyy, Gennadiy
Dittmer, Ulf
Hasenkrug, Kim J.
TI CD8(+) T Cells Are Essential for Controlling Acute Friend Retrovirus
Infection in C57BL/6 Mice
SO JOURNAL OF VIROLOGY
LA English
DT Letter
ID ABSENCE
C1 [Joedicke, Jara J.; Zelinskyy, Gennadiy; Dittmer, Ulf] Univ Duisburg Essen, Univ Hosp Essen, Inst Virol, Essen, Germany.
[Hasenkrug, Kim J.] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Hasenkrug, KJ (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
EM khasenkrug@nih.gov
NR 9
TC 2
Z9 2
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2014
VL 88
IS 9
BP 5200
EP 5201
DI 10.1128/JVI.00312-14
PG 2
WC Virology
SC Virology
GA AE9TT
UT WOS:000334353900053
PM 24707025
ER
PT J
AU Lesma, G
Sacchetti, A
Bai, RL
Basso, G
Bortolozzi, R
Hamel, E
Silvani, A
Vaiana, N
Viola, G
AF Lesma, Giordano
Sacchetti, Alessandro
Bai, Rouli
Basso, Giuseppe
Bortolozzi, Roberta
Hamel, Ernest
Silvani, Alessandra
Vaiana, Nadia
Viola, Giampietro
TI Hemiasterlin analogues incorporating an aromatic, and heterocyclic type
C-terminus: design, synthesis and biological evaluation
SO MOLECULAR DIVERSITY
LA English
DT Article
DE Hemiasterlin; Antimitotic peptides; Tubulin; Cytotoxicity; Dynamic
resolution
ID SPONGE PRODUCT HEMIASTERLIN; CYTOTOXIC PEPTIDES; TRIPEPTIDE
HEMIASTERLIN; MICROTUBULE INHIBITORS; ANTIMICROTUBULE AGENT; TUBULIN
INHIBITORS; NATURAL-PRODUCTS; P-GLYCOPROTEIN; BINDING-SITE; HTI-286
AB A representative series of structural analogs of the antimitotic tripeptides hemiasterlins have been designed and synthesized, as potential inhibitors of tubulin polymerization. Relying also on a computational approach, we aimed to explore unknown extensive changes at the C-fragment, by incorporating the conformationally required double bond into five- and six-membered rings. Key steps of the synthetic strategy are a dynamic resolution affording the A-fragment in 97 % ee and the preparation of six new cyclic C fragments, all potentially able to interact with tubulin by means of H bonds. Unexpectedly, biological evaluation of these analogs did not provide evidences neither for cytotoxic effect nor for inhibition of tubulin polymerization.
C1 [Lesma, Giordano; Silvani, Alessandra; Vaiana, Nadia] Univ Milan, Dipartimento Chim, I-20133 Milan, Italy.
[Sacchetti, Alessandro] Politecn Milan, Dipartimento Chim Mat & Ing Chim Giulio Natta, I-20133 Milan, Italy.
[Bai, Rouli; Hamel, Ernest] NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,Frederick Natl Lab Canc, Frederick, MD 21702 USA.
[Basso, Giuseppe; Bortolozzi, Roberta; Viola, Giampietro] Univ Padua, Dipartimento Salute Donna & Bambino, I-35128 Padua, Italy.
RP Silvani, A (reprint author), Univ Milan, Dipartimento Chim, Via Golgi 19, I-20133 Milan, Italy.
EM alessandro.sacchetti@polimi.it; hamele@dc37a.nci.nih.gov;
alessandra.silvani@unimi.it; giampietro.viola.1@unipd.it
RI Viola, Giampietro/I-4095-2012; Bortolozzi, Roberta/D-4950-2015; silvani,
alessandra/B-3742-2013; Lesma, Giordano/P-1516-2016;
OI Viola, Giampietro/0000-0001-9329-165X; Bortolozzi,
Roberta/0000-0002-3357-4815; silvani, alessandra/0000-0002-0397-2636;
Lesma, Giordano/0000-0002-3897-0008; BASSO,
GIUSEPPE/0000-0002-2634-9302; sacchetti, alessandro/0000-0002-4830-0825
FU Intramural NIH HHS [Z99 CA999999]
NR 38
TC 2
Z9 2
U1 1
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1381-1991
EI 1573-501X
J9 MOL DIVERS
JI Mol. Divers.
PD MAY
PY 2014
VL 18
IS 2
BP 357
EP 373
DI 10.1007/s11030-014-9507-9
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry,
Medicinal; Chemistry, Multidisciplinary
SC Biochemistry & Molecular Biology; Chemistry; Pharmacology & Pharmacy
GA AE8WC
UT WOS:000334282700010
PM 24500310
ER
PT J
AU Kang, PB
Gooch, CL
McDermott, MP
Darras, BT
Finkel, RS
Yang, ML
Sproule, DM
Chung, WK
Kaufmann, P
de Vivo, DC
AF Kang, Peter B.
Gooch, Clifton L.
McDermott, Michael P.
Darras, Basil T.
Finkel, Richard S.
Yang, Michele L.
Sproule, Douglas M.
Chung, Wendy K.
Kaufmann, Petra
de Vivo, Darryl C.
CA Muscle Study Grp
Pediat Neuromuscular Clinical Res
TI THE MOTOR NEURON RESPONSE TO SMN1 DEFICIENCY IN SPINAL MUSCULAR ATROPHY
SO MUSCLE & NERVE
LA English
DT Article
DE compound motor action potential; electrophysiology; motor neuron
disease; motor unit number estimation; spinal muscular atrophy
ID PLACEBO-CONTROLLED TRIAL; ADULT ZEBRAFISH; DOUBLE-BLIND; CHILDREN;
INJURY; SCALE; CORD; SMA; REGENERATION; DISEASES
AB Introduction: The purpose of this study was to measure and analyze motor unit number estimation (MUNE) values longitudinally in spinal muscular atrophy (SMA). Methods: Sixty-two children with SMA types 2 and 3 were observed prospectively for up to 42 months. Longitudinal electrophysiological data were collected, including compound motor action potential (CMAP), single motor unit action potential (SMUP), and MUNE. Results: Significant motor neuron loss and compensatory collateral reinnervation were noted at baseline. Over time, there was a significant mean increase in MUNE (4.92 units/year, P=0.009), a mean decrease in SMUP amplitude (-6.32 V/year, P=0.10), and stable CMAP amplitude. Conclusions: The unexpected longitudinal results differ from findings in amyotrophic lateral sclerosis studies, perhaps indicating that compensatory processes in SMA involve new motor unit development. A better understanding of the mechanisms of motor unit decline and compensation in SMA is important for assessing novel therapeutic strategies and for providing key insights into disease pathophysiology. Muscle Nerve49: 636-644, 2014
C1 [Kang, Peter B.; Darras, Basil T.] Childrens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Kang, Peter B.; Darras, Basil T.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Gooch, Clifton L.; Sproule, Douglas M.; Kaufmann, Petra; de Vivo, Darryl C.] Columbia Univ, Dept Neurol, New York, NY USA.
[Gooch, Clifton L.] Univ S Florida, Dept Neurol, Coll Med, Tampa, FL 33620 USA.
[McDermott, Michael P.] Univ Rochester, Dept Biostat & Computat Biol, Rochester, NY USA.
[McDermott, Michael P.] Univ Rochester, Dept Neurol, Rochester, NY USA.
[Finkel, Richard S.; Yang, Michele L.] Childrens Hosp Philadelphia, Div Neurol, Philadelphia, PA 19104 USA.
[Finkel, Richard S.] Nemours Childrens Hosp, Div Neurol, Orlando, FL USA.
[Yang, Michele L.] Childrens Hosp Colorado, Div Neurol, Aurora, CO USA.
[Chung, Wendy K.] Columbia Univ, Dept Pediat, New York, NY 10027 USA.
[Chung, Wendy K.] Columbia Univ, Dept Med, New York, NY USA.
[Kaufmann, Petra] NINDS, Bethesda, MD 20892 USA.
RP Kang, PB (reprint author), Childrens Hosp, Dept Neurol, 300 Longwood Ave, Boston, MA 02115 USA.
EM pbkang@ufl.edu
RI Gooch, Clifton/M-1874-2016
OI Gooch, Clifton/0000-0002-2210-2038
FU Spinal Muscular Atrophy Foundation; CTSA from NCRR/NIH [UL1 RR024156,
UL1-RR-024134]; NSADA K12 program (NINDS training grant); Harvard
University [UL1 RR025755-01]; Harvard Catalyst Clinical and
Translational Science Center, from NCRR/NIH
FX This study was funded by the Spinal Muscular Atrophy Foundation.
Additional clinical research support was provided to Columbia University
through the CTSA (UL1 RR024156) from NCRR/NIH and the NSADA K12 program
(NINDS training grant); to The Children's Hospital of Philadelphia
through the CTSA (UL1-RR-024134) from NCRR/NIH; and to Harvard
University (UL1 RR025755-01), Harvard Catalyst Clinical and
Translational Science Center, from NCRR/NIH.
NR 32
TC 10
Z9 10
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0148-639X
EI 1097-4598
J9 MUSCLE NERVE
JI Muscle Nerve
PD MAY
PY 2014
VL 49
IS 5
BP 636
EP 644
DI 10.1002/mus.23967
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AF0TK
UT WOS:000334426800003
PM 23893312
ER
PT J
AU Mendez, ML
Romero, AI
Rajal, VB
Castro, EF
Calvo, JI
Palacio, L
Hernandez, A
AF Mendez, Mercedes L.
Romero, Analia I.
Rajal, Veronica B.
Castro, Elza F.
Calvo, Jose I.
Palacio, Laura
Hernandez, Antonio
TI Properties of polyethersulfone ultrafiltration membranes modified with
polyethylene glycols
SO POLYMER ENGINEERING AND SCIENCE
LA English
DT Article
ID PHASE-INVERSION MEMBRANES; LIQUID DISPLACEMENT POROSIMETRY; NATURAL
ORGANIC-MATTER; MOLECULAR-WEIGHT; UF MEMBRANES; POLYSULFONE MEMBRANES;
STRUCTURAL-PROPERTIES; ASYMMETRIC MEMBRANES; SURFACE MODIFICATION;
TRANSPORT-PROPERTIES
AB Polyethersulfone ultrafiltration membranes have been prepared using polyethylene glycols (PEGs) of 400, 1000, and 10,000 gmol, as additive with dimethylacetamide as solvent. Infrared analysis proves that PEG leaves almost completely the surface of the membranes after 24 h of water immersion. Scanning electron microscopy, contact angle, and liquid-liquid displacement porometry have been used to characterize the membrane morphology, surface hydrophilicity and porous structure. The relative flux reduction factor, flux, retention-of PEG (20,000 and 35,000 g/mol) and bovine serum albumin (67,000 g/mol)-and pure water permeability have been measured for the membranes. Results show that the addition of PEG increases slightly hydrophilicity and decreases pore size and narrows the corresponding pore size distribution while thickening the skin layer, in spite of the fast disappearance of the added PEG form the membrane surface. The resulting flux and pure water permeability are higher when middle size PEGs are added but decrease again when very high molecular weight (MW) PEGs are added. Retention decreases initially for increasing MWs of PEG although for very long PEG chains (MW of 10,000 g/mol) retention increases again. After filtration, the membranes with PEG added showed a lower relative flux reduction that decreases for increasing MW of the added PEGs. (c) 2013 Society of Plastics Engineers. POLYM. ENG. SCI., 54:1211-1221, 2014. (c) 2013 Society of Plastics Engineers
C1 [Mendez, Mercedes L.; Romero, Analia I.; Rajal, Veronica B.; Castro, Elza F.] UNSa, Fac Ingn, Inst Invest Ind Quim, RA-4400 Salta, Argentina.
[Rajal, Veronica B.] Univ Calif Davis, Fogarty Int Ctr, Davis, CA 95616 USA.
[Calvo, Jose I.; Palacio, Laura; Hernandez, Antonio] Univ Valladolid, SMAP, E-47071 Valladolid, Spain.
RP Hernandez, A (reprint author), Univ Valladolid, SMAP, Paseo Belen 7,Campus Miguel Delibes, E-47071 Valladolid, Spain.
EM tonhg@termo.uva.es
RI Hernandez, Antonio/B-4622-2012; Palacio, Laura/I-7552-2014
OI Hernandez, Antonio/0000-0002-2475-5681; Palacio,
Laura/0000-0001-9886-9553
FU ANPCyT [PICTO 36716]; CIUNSa [1469/0]; Junta de Castilla y Leon
[VA324A11nd GR18]
FX Contract grant sponsor: ANPCyT; contract grant number: PICTO 36716;
contract grant sponsor: CIUNSa; contract grant number: 1469/0; contract
grant sponsor: Junta de Castilla y Leon (to Spanish authors); contract
grant numbers: VA324A11nd GR18.
NR 50
TC 3
Z9 4
U1 2
U2 27
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0032-3888
EI 1548-2634
J9 POLYM ENG SCI
JI Polym. Eng. Sci.
PD MAY
PY 2014
VL 54
IS 5
BP 1211
EP 1221
DI 10.1002/pen.23637
PG 11
WC Engineering, Chemical; Polymer Science
SC Engineering; Polymer Science
GA AF0ID
UT WOS:000334396600025
ER
PT J
AU Baker, CM
Best, RB
AF Baker, Christopher M.
Best, Robert B.
TI Insights into the binding of intrinsically disordered proteins from
molecular dynamics simulation
SO WILEY INTERDISCIPLINARY REVIEWS-COMPUTATIONAL MOLECULAR SCIENCE
LA English
DT Review
ID IMPLICIT SOLVENT MODELS; ENERGY LANDSCAPE THEORY; EMPIRICAL
FORCE-FIELDS; FLY-CASTING MECHANISM; TRANSITION-STATE; CONFORMATIONAL
SELECTION; INDUCED FIT; FOLDING SIMULATIONS; INTERMOLECULAR
INTERACTIONS; UNSTRUCTURED PROTEINS
AB Intrinsically disordered proteins (IDPs) are a class of protein that, in the native state, possess no well-defined secondary or tertiary structure, existing instead as dynamic ensembles of conformations. They are biologically important, with approximately 20% of all eukaryotic proteins disordered, and found at the heart of many biochemical networks. To fulfil their biological roles, many IDPs need to bind to proteins and/or nucleic acids. And although unstructured in solution, IDPs typically fold into a well-defined three-dimensional structure upon interaction with a binding partner. The flexibility and structural diversity inherent to IDPs makes this coupled folding and binding difficult to study at atomic resolution by experiment alone, and computer simulation currently offers perhaps the best opportunity to understand this process. But simulation of coupled folding and binding is itself extremely challenging; these molecules are large and highly flexible, and their binding partners, such as DNA or cyclins, are also often large. Therefore, their study requires either simplified representations, advanced enhanced sampling schemes, or both. It is not always clear that existing simulation techniques, optimized for studying folded proteins, are well suited to IDPs. In this article, we examine the progress that has been made in the study of coupled folding and binding using molecular dynamics simulation. We summarize what has been learnt, and examine the state of the art in terms of both methodologies and models. We also consider the lessons to be learnt from advances in other areas of simulation and highlight the issues that remain of be addressed.
C1 [Baker, Christopher M.] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
[Best, Robert B.] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Best, RB (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM robertbe@helix.nih.gov
RI Best, Robert/H-7588-2016
OI Best, Robert/0000-0002-7893-3543
FU FEBS Return to Europe Fellowship; Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health (NIH)
FX C.M.B. is supported by a FEBS Return to Europe Fellowship. R.B.B. is
supported by the Intramural Research Program of the National Institute
of Diabetes and Digestive and Kidney Diseases, National Institutes of
Health (NIH).
NR 172
TC 21
Z9 21
U1 9
U2 84
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1759-0876
EI 1759-0884
J9 WIRES COMPUT MOL SCI
JI Wiley Interdiscip. Rev.-Comput. Mol. Sci.
PD MAY
PY 2014
VL 4
IS 3
BP 182
EP 198
DI 10.1002/wcms.1167
PG 17
WC Chemistry, Multidisciplinary; Mathematical & Computational Biology
SC Chemistry; Mathematical & Computational Biology
GA AF2DG
UT WOS:000334522200002
ER
PT J
AU Baron, SL
Steege, AL
Hughes, JT
Beard, SD
AF Baron, Sherry L.
Steege, Andrea L.
Hughes, Joseph T., Jr.
Beard, Sharon D.
TI Introduction to a special issue: Eliminating health and safety
inequities at work
SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE
LA English
DT Editorial Material
C1 [Baron, Sherry L.] CUNY, Queens Coll, Ctr Biol Nat Syst, Flushing, NY USA.
[Steege, Andrea L.] Ctr Dis Control & Prevent, Natl Inst Occupat Safety & Hlth, Div Surveillance Hazard Evaluat & Field Studies, Cincinnati, OH USA.
[Hughes, Joseph T., Jr.; Beard, Sharon D.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Baron, SL (reprint author), Queens Coll Remsen 311,65-30 Kissena Blvd, Flushing, NY 11367 USA.
EM sbaron@qc.cuny.edu
RI Steege, Andrea/H-8900-2016
OI Steege, Andrea/0000-0001-5665-2559
NR 6
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0271-3586
EI 1097-0274
J9 AM J IND MED
JI Am. J. Ind. Med.
PD MAY
PY 2014
VL 57
IS 5
SI SI
BP 493
EP 494
DI 10.1002/ajim.22321
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AE4NM
UT WOS:000333959200001
PM 24687420
ER
PT J
AU Baron, SL
Beard, S
Davis, LK
Delp, L
Forst, L
Kidd-Taylor, A
Liebman, AK
Linnan, L
Punnett, L
Welch, LS
AF Baron, Sherry L.
Beard, Sharon
Davis, Letitia K.
Delp, Linda
Forst, Linda
Kidd-Taylor, Andrea
Liebman, Amy K.
Linnan, Laura
Punnett, Laura
Welch, Laura S.
TI Promoting integrated approaches to reducing health inequities among
low-income workers: Applying a social ecological framework
SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE
LA English
DT Review
DE total worker health; disparities; low-income workers; health inequities
ID BODY-MASS INDEX; FRANCISCOS CHINATOWN RESTAURANTS; RANDOMIZED
CONTROLLED-TRIAL; TIME PHYSICAL-ACTIVITY; PARTICIPATORY RESEARCH;
OCCUPATIONAL-HEALTH; RISK-FACTORS; ENVIRONMENTAL-HEALTH;
SOCIOECONOMIC-STATUS; BLOOD-PRESSURE
AB Background Nearly one of every three workers in the United States is low-income. Low-income populations have a lower life expectancy and greater rates of chronic diseases compared to those with higher incomes. Low- income workers face hazards in their workplaces as well as in their communities. Developing integrated public health programs that address these combined health hazards, especially the interaction of occupational and non-occupational risk factors, can promote greater health equity. Methods We apply a social-ecological perspective in considering ways to improve the health of the low-income working population through integrated health protection and health promotion programs initiated in four different settings: the worksite, state and local health departments, community health centers, and community-based organizations. Results Examples of successful approaches to developing integrated programs are presented in each of these settings. These examples illustrate several complementary venues for public health programs that consider the complex interplay between work-related and non work-related factors, that integrate health protection with health promotion and that are delivered at multiple levels to improve health for low-income workers. Conclusions Whether at the workplace or in the community, employers, workers, labor and community advocates, in partnership with public health practitioners, can deliver comprehensive and integrated health protection and health promotion programs. Recommendations for improved research, training, and coordination among health departments, health practitioners, worksites and community organizations are proposed. Am. J. Ind. Med. 57:539-556, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Baron, Sherry L.] NIOSH, Div Surveillance Hazard Evaluat & Field Studies, Cincinnati, OH 45226 USA.
[Beard, Sharon] NIEHS, Worker Educ & Training Branch, Res Triangle Pk, NC 27709 USA.
[Davis, Letitia K.] Massachusetts Dept Publ Hlth, Occupat Hlth Surveillance Program, Boston, MA USA.
[Delp, Linda] Univ Calif Los Angeles, Labor Occupat Safety & Hlth Program, Los Angeles, CA USA.
[Forst, Linda] Univ Illinois, Sch Publ Hlth, Chicago, IL USA.
[Kidd-Taylor, Andrea] Morgan State Univ, Dept Hlth Policy & Management, Baltimore, MD 21239 USA.
[Liebman, Amy K.] Migrant Clin Network, Environm & Occupat Hlth Initiat, Quantico, VA USA.
[Linnan, Laura] Univ N Carolina, Gillings Sch Publ Hlth, Chapel Hill, NC USA.
[Punnett, Laura] Univ Massachusetts Lowell, Dept Work Environm, Lowell, MA USA.
[Punnett, Laura] Univ Massachusetts Lowell, Ctr Women & Work, Lowell, MA USA.
[Welch, Laura S.] CPWR Ctr Construct Res & Training, Silver Spring, MD USA.
RP Baron, SL (reprint author), NIOSH, 4676 Columbia Pkwy R-17, Cincinnati, OH 45226 USA.
EM slb8@cdc.gov
FU Intramural NIH HHS [Z99 ES999999]; NIEHS NIH HHS [U45 ES006173]
NR 124
TC 21
Z9 21
U1 7
U2 48
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0271-3586
EI 1097-0274
J9 AM J IND MED
JI Am. J. Ind. Med.
PD MAY
PY 2014
VL 57
IS 5
SI SI
BP 539
EP 556
DI 10.1002/ajim.22174
PG 18
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AE4NM
UT WOS:000333959200005
PM 23532780
ER
PT J
AU Lee, D
Schroeder, JR
Karschner, EL
Goodwin, RS
Hirvonen, J
Gorelick, DA
Huestis, MA
AF Lee, Dayong
Schroeder, Jennifer R.
Karschner, Erin L.
Goodwin, Robert S.
Hirvonen, Jussi
Gorelick, David A.
Huestis, Marilyn A.
TI Cannabis withdrawal in chronic, frequent cannabis smokers during
sustained abstinence within a closed residential environment
SO AMERICAN JOURNAL ON ADDICTIONS
LA English
DT Article
ID 2-DIMENSIONAL GAS-CHROMATOGRAPHY; ADULTS SEEKING TREATMENT; ORAL FLUID;
SIMULTANEOUS QUANTIFICATION; MARIJUANA DEPENDENCE; MASS-SPECTROMETRY;
WHOLE-BLOOD; SYMPTOMS; QUESTIONNAIRE; INPATIENT
AB Objectives
Chronic, frequent cannabis smokers may experience residual and offset effects, withdrawal, and craving when abstaining from the drug. We characterized the prevalence, duration, and intensity of these effects in chronic frequent cannabis smokers during abstinence on a closed research unit.
Methods
Non-treatment-seeking participants (N = 29 on admission, 66% and 34% remaining after 2 and 4 weeks) provided subjective effects data. A battery of five instruments was computer-administered daily to measure psychological, sensory, and physical symptoms associated with cannabinoid intoxication and withdrawal. Plasma and oral fluid specimens were concurrently collected and analyzed for cannabinoids. Outcome variables were evaluated as change from admission (Day 0) with regression models.
Results
Most abstinence effects, including irritability and anxiety were greatest on Days 0-3 and decreased thereafter. Cannabis craving significantly decreased over time, whereas decreased appetite began to normalize on Day 4. Strange dreams and difficulty getting to sleep increased over time, suggesting intrinsic sleep problems in chronic cannabis smokers. Symptoms likely induced by residual drug effects were at maximum intensity on admission and positively correlated with plasma and oral fluid cannabinoid concentrations on admission but not afterward; these symptoms showed overall prevalence higher than cannabis withdrawal symptoms.
Conclusions
The combined influence of residual/offset drug effects, withdrawal, and craving was observed in chronic cannabis smokers during monitored abstinence. Abstinence symptoms were generally more intense in the initial phase, implying importance of early intervention in cannabis quit attempts. Sleep disturbance persisting for an extended period suggests that hypnotic medications could be beneficial in treating cannabis dependence. (Am J Addict 2014;23:234-242)
C1 [Lee, Dayong; Karschner, Erin L.; Goodwin, Robert S.; Gorelick, David A.; Huestis, Marilyn A.] NIDA, NIH, Baltimore, MD 21224 USA.
[Schroeder, Jennifer R.] NIDA, Off Clin Director, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Hirvonen, Jussi] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
RP Huestis, MA (reprint author), NIDA, IRP, NIH, Biomed Res Ctr, 251 Bayview Blvd Suite 200,Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU Intramural NIH HHS [ZIA DA000412-12, ZIA DA000412-13, ZIA DA000413-12,
ZIA DA000413-13]; NIDA NIH HHS [R01 DA025044]
NR 35
TC 9
Z9 9
U1 4
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1055-0496
EI 1521-0391
J9 AM J ADDICTION
JI Am. J. Addict.
PD MAY
PY 2014
VL 23
IS 3
BP 234
EP 242
DI 10.1111/j.1521-0391.2014.12088.x
PG 9
WC Substance Abuse
SC Substance Abuse
GA AF0RD
UT WOS:000334420800006
PM 24724880
ER
PT J
AU Gomar, JJ
Gordon, ML
Dickinson, D
Kingsley, PB
Ulug, AM
Keehlisen, L
Huet, S
Buthorn, JJ
Koppel, J
Christen, E
Conejero-Goldberg, C
Davies, P
Goldberg, TE
AF Gomar, Jesus J.
Gordon, Marc L.
Dickinson, Dwight
Kingsley, Peter B.
Ulug, Aziz M.
Keehlisen, Lynda
Huet, Sarah
Buthorn, Justin J.
Koppel, Jeremy
Christen, Erica
Conejero-Goldberg, Concepcion
Davies, Peter
Goldberg, Terry E.
TI APOE Genotype Modulates Proton Magnetic Resonance Spectroscopy
Metabolites in the Aging Brain
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Aging; APOE genotype; cognitive function; neurodegeneration; proton
magnetic resonance spectroscopy; structural equation modeling
ID MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; N-ACETYLASPARTATE;
EPSILON-4 ALLELE; H-1 MRS; DEMENTIA; RISK; GENE; NEUROBIOLOGY
AB Background: Proton magnetic resonance spectroscopy (H-1-MRS) studies on healthy aging have reported inconsistent findings and have not systematically taken into account the possible modulatory effect of APOE genotype. We aimed to quantify brain metabolite changes in healthy subjects in relation to age and the presence of the APOE E4 genetic risk factor for Alzheimer's disease. Additionally, we examined these measures in relation to cognition.
Methods: We studied a cohort of 112 normal adults between 50 and 86 years old who were genotyped for APOE genetic polymorphism. Measurements of H-1-MRS metabolites were obtained in the posterior cingulate and precuneus region. Measures of general cognitive functioning, memory, executive function, semantic fluency, and speed of processing were also obtained.
Results: General linear model analysis demonstrated that older APOE E4 carriers had significantly higher choline/creatine and myoinositol/creatine ratios than APOE E3 homozygotes. Structural equation modeling resulted in a model with an excellent goodness of fit and in which the APOE x age interaction and APOE status each had a significant effect on H-1-MRS metabolites (choline/creatine and myo-inositol/creatine). Furthermore, the APOE x age variable modulation of cognition was mediated by H-1-MRS metabolites.
Conclusions: In a healthy aging normal population, choline/creatine and myo-inositol/creatine ratios were significantly increased in APOE E4 carriers, suggesting the presence of neuroinflammatory processes and greater membrane turnover in older carriers. Structural equation modeling analysis confirmed these possible neurodegenerative markers and also indicated the mediator role of these metabolites on cognitive performance among older APOE E4 carriers.
C1 [Gomar, Jesus J.; Gordon, Marc L.; Keehlisen, Lynda; Huet, Sarah; Buthorn, Justin J.; Koppel, Jeremy; Christen, Erica; Conejero-Goldberg, Concepcion; Davies, Peter; Goldberg, Terry E.] Feinstein Inst Med Res, Litwin Zucker Res Ctr, Manhasset, NY 11030 USA.
[Gomar, Jesus J.] FIDMAG Hermanas Hosp, St Boi De Llobregat, Spain.
[Gordon, Marc L.; Ulug, Aziz M.; Koppel, Jeremy; Davies, Peter; Goldberg, Terry E.] Hofstra North Shore Long Isl Jewish Sch Med, Hempstead, NY USA.
[Dickinson, Dwight] NIMH, NIH, Bethesda, MD 20892 USA.
[Kingsley, Peter B.] N Shore Univ Hosp, Dept Radiol, Manhasset, NY USA.
[Ulug, Aziz M.] Feinstein Inst Med Res, Susan & Leonard Feinstein Ctr Neurosci, Manhasset, NY 11030 USA.
RP Goldberg, TE (reprint author), Feinstein Inst Med Res, Litwin Zucker Res Ctr, 350 Community Dr, Manhasset, NY 11030 USA.
EM tgoldber@nshs.edu
RI Ulug, Aziz/F-6592-2011;
OI Ulug, Aziz/0000-0002-2315-0322; Gomar, Jesus/0000-0002-6995-4270
FU Litwin-Zucker Research Center of the Feinstein Institute for Medical
Research (North Shore-Long Island Jewish Health System); National
Institutes of Health [RO1 AG038734]; Baxter; Eli Lilly; Forest Research
Institute; Genentech; Merck; Applied Neurosolutions
FX This study was supported by the Litwin-Zucker Research Center of the
Feinstein Institute for Medical Research (North Shore-Long Island Jewish
Health System) and National Institutes of Health (RO1 AG038734 to TEG).;
Dr. Gordon has received research support from Baxter, Eli Lilly, Forest
Research Institute, Genentech, and Merck and honoraria for consulting
from Accera, Eli Lilly, GE Healthcare, and Noven Pharmaceuticals. Dr.
Davies has received research support from and served as a consultant to
Applied Neurosolutions. Dr. Goldberg receives royalties for the use of
the Brief Assessment of Cognition in Schizophrenia in clinical trials.
All other authors report no biomedical financial interests or potential
conflicts of interest.
NR 41
TC 8
Z9 8
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2014
VL 75
IS 9
BP 686
EP 692
DI 10.1016/j.biopsych.2013.05.022
PG 7
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA AE6KY
UT WOS:000334102400005
PM 23831342
ER
PT J
AU Muse, J
Emery, M
Sambataro, F
Lemaitre, H
Tan, HY
Chen, Q
Kolachana, BS
Das, S
Callicott, JH
Weinberger, DR
Mattay, VS
AF Muse, John
Emery, Matthew
Sambataro, Fabio
Lemaitre, Herve
Tan, Hao-Yang
Chen, Qiang
Kolachana, Bhaskar S.
Das, Saumitra
Callicott, Joseph H.
Weinberger, Daniel R.
Mattay, Venkata S.
TI WWC1 Genotype Modulates Age-Related Decline in Episodic Memory Function
Across the Adult Life Span
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Aging; episodic memory (EM); hippocampus; KIBRA; long-term potentiation
(LTP); single nucleotide polymorphism (SNP); WWC1
ID KIBRA GENE VARIANTS; COGNITIVE FUNCTIONS; DECLARATIVE MEMORY; IMAGING
GENETICS; WORKING-MEMORY; ARCHITECTURE; ASSOCIATION; PERFORMANCE
AB Background: Episodic memory (EM) declines with age and the rate of decline is variable across individuals. A single nucleotide polymorphism (rs17070145) in the WWC1 gene that encodes the KIBRA protein critical for long-term potentiation and memory consolidation has previously been associated with EM performance, as well as differences in hippocampal engagement during EM tasks using functional magnetic resonance imaging (fMRI). In the current study, we explore the effect of this polymorphism on EM-related activity and cognitive performance across the adult life span using fMRI.
Methods: Two hundred thirty-two healthy, Caucasian subjects (18-89 years) completed a battery of cognitive tests, as well as an EM task during an fMRI scan.
Results: WWC1 T carriers had significantly better delayed recall performance than CC individuals (p=.006). The relationship between increasing age and recall scores (immediate and delayed) was also significantly different between WWC1 genotype groups (p=.01). In addition to the age-related decline in hippocampal formation (HF) activation (p<.05; false discovery rate(small volume correction-HF-region of interest)), we observed an age by WWC1 genotype interaction on HF activation during encoding and retrieval. The CC group showed a significant negative association between HF activity and increasing age, while no such association was observed in the T carrier group (left HF p=.04; r-z correlation difference during encoding and retrieval; right HF p=.0008; r-z correlation difference during retrieval).
Conclusions: Our results show a dynamic relationship between rs17070145 polymorphism and increasing age on neuronal activity in the hippocampal region.
C1 [Muse, John; Emery, Matthew; Sambataro, Fabio; Lemaitre, Herve; Tan, Hao-Yang; Chen, Qiang; Kolachana, Bhaskar S.; Das, Saumitra; Callicott, Joseph H.; Weinberger, Daniel R.; Mattay, Venkata S.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Muse, John; Tan, Hao-Yang; Chen, Qiang; Weinberger, Daniel R.; Mattay, Venkata S.] Johns Hopkins Univ, Lieber Inst Brain Dev, Baltimore, MD USA.
[Weinberger, Daniel R.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Weinberger, Daniel R.] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA.
[Weinberger, Daniel R.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
[Weinberger, Daniel R.] Johns Hopkins Univ, Sch Med, Inst Med Genet, Baltimore, MD USA.
RP Mattay, VS (reprint author), Lieber Inst Brain Dev, 855 North Wolfe St,Suite 300,3rd Floor, Baltimore, MD 21205 USA.
EM anand.mattay@libd.org
RI Sambataro, Fabio/E-3426-2010;
OI Sambataro, Fabio/0000-0003-2102-416X; Lemaitre,
Herve/0000-0002-5952-076X
FU Division of Intramural Research Programs, National Institute of Mental
Health, National Institutes of Health, Bethesda, Maryland; Lieber
institute of Brain Development, Baltimore, Maryland
FX This work was supported by the Division of Intramural Research Programs,
National Institute of Mental Health, National Institutes of Health,
Bethesda, Maryland, and The Lieber institute of Brain Development,
Baltimore, Maryland.
NR 22
TC 8
Z9 8
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2014
VL 75
IS 9
BP 693
EP 700
DI 10.1016/j.biopsych.2013.09.036
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA AE6KY
UT WOS:000334102400006
PM 24290728
ER
PT J
AU Khincha, PP
Wentzensen, IM
Giri, N
Alter, BP
Savage, SA
AF Khincha, Payal P.
Wentzensen, Ingrid M.
Giri, Neelam
Alter, Blanche P.
Savage, Sharon A.
TI Response to androgen therapy in patients with dyskeratosis congenita
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE telomere; dyskeratosis congenita; androgen
ID TELOMERE BIOLOGY DISORDERS; BONE-MARROW FAILURE; APLASTIC-ANEMIA;
COMPONENT 1; LENGTH; MUTATIONS; STEROIDS; CANCER; CTC1
AB Dyskeratosis congenita (DC) is an inherited bone marrow failure syndrome and telomere biology disorder characterized by dysplastic nails, reticular skin pigmentation and oral leucoplakia. Androgens are a standard therapeutic option for bone marrow failure in those patients with DC who are unable to undergo haematopoietic stem cell transplantation, but there are no systematic data on its use in those patients. We evaluated haematological response and side effects of androgen therapy in 16 patients with DC in our observational cohort study. Untreated DC patients served as controls. Seventy percent of treated DC patients had a haematological response with red blood cell and/or platelet transfusion independence. The expected age-related decline in telomere length was noted in androgen-treated patients. All treated DC patients had at least one significant lipid abnormality. Additional treatment-related findings included a significant decrease in thyroid binding globulin, accelerated growth in pre-pubertal children and splenic peliosis in two patients. Liver enzymes were elevated in both androgen-treated and untreated patients, suggesting underlying liver involvement in DC. This study suggests that androgen therapy can be effectively used to treat bone marrow failure in DC, but that side effects need to be closely monitored.
C1 [Khincha, Payal P.; Wentzensen, Ingrid M.; Giri, Neelam; Alter, Blanche P.; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20850 USA.
[Khincha, Payal P.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Wentzensen, Ingrid M.] Johns Hopkins Univ Hosp, McKusick Nathans Inst Genet Med, Baltimore, MD 21287 USA.
RP Savage, SA (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E 454, Bethesda, MD 20850 USA.
EM savagesh@mail.nih.gov
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
FU NIH [N02-CP-11019, N02-CP-65504, N02-CP-65501]; National Cancer
Institute, National Institutes of Health
FX We thank the patients, their families, and the referring clinicians for
their valuable contributions to this study. Lisa Leathwood, RN, and
Maureen Risch, RN, Westat, Inc. (NIH contracts N02-CP-11019,
N02-CP-65504, and N02-CP-65501) provided outstanding study support. This
work and the research of Drs. Khincha, Wentzensen, Giri, Alter and
Savage were supported by the Intramural Research Program of the National
Cancer Institute, National Institutes of Health. We thank Charleen
Adams, NCI, for help with FA-related data abstraction and Dr. Mark H.
Greene, NCI, for his helpful comments.
NR 29
TC 9
Z9 10
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD MAY
PY 2014
VL 165
IS 3
BP 349
EP 357
DI 10.1111/bjh.12748
PG 9
WC Hematology
SC Hematology
GA AE5LR
UT WOS:000334031000010
PM 24666134
ER
PT J
AU Harmacek, L
Watkins-Chow, DE
Chen, JF
Jones, KL
Pavan, WJ
Salbaum, JM
Niswander, L
AF Harmacek, Laura
Watkins-Chow, Dawn E.
Chen, Jianfu
Jones, Kenneth L.
Pavan, William J.
Salbaum, J. Michael
Niswander, Lee
TI A unique missense allele of BAF155, a core BAF chromatin remodeling
complex protein, causes neural tube closure defects in mice
SO DEVELOPMENTAL NEUROBIOLOGY
LA English
DT Article
DE neural tube defect; apoptosis; proliferation; Baf155msp3; epigenetic
regulation
ID DIFFERENTIAL EXPRESSION ANALYSIS; MAMMALIAN SWI/SNF COMPLEXES; MOUSE
MYELENCEPHALIC BLEBS; PROTEASOMAL DEGRADATION; DNA METHYLTRANSFERASES;
EMBRYONIC LETHALITY; BINDING PROTEIN; GENE-EXPRESSION; CELL; NEURULATION
AB Failure of embryonic neural tube closure results in the second most common class of birth defects known as neural tube defects (NTDs). While NTDs are likely the result of complex multigenic dysfunction, it is not known whether polymorphisms in epigenetic regulators may be risk factors for NTDs. Here we characterized Baf155(msp3), a unique ENU-induced allele in mice. Homozygous Baf155(mps3) embryos exhibit highly penetrant exencephaly, allowing us to investigate the roles of an assembled, but malfunctional BAF chromatin remodeling complex in vivo at the time of neural tube closure. Evidence of defects in proliferation and apoptosis were found within the neural tube. RNA-Seq analysis revealed that surprisingly few genes showed altered expression in Baf155 mutant neural tissue, given the broad epigenetic role of the BAF complex, but included genes involved in neural development and cell survival. Moreover, gene expression changes between individual mutants were variable even though the NTD was consistently observed. This suggests that inconsistent gene regulation contributes to failed neural tube closure. These results shed light on the role of the BAF complex in the process of neural tube closure and highlight the importance of studying missense alleles to understand epigenetic regulation during critical phases of development. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol 74: 483-497, 2014
C1 [Harmacek, Laura; Chen, Jianfu; Niswander, Lee] Univ Colorado, Howard Hughes Med Inst, Dept Pediat, Childrens Hosp Colorado, Aurora, CO 80045 USA.
[Harmacek, Laura; Chen, Jianfu; Niswander, Lee] Univ Colorado, Howard Hughes Med Inst, Grad Program Mol Biol, Childrens Hosp Colorado, Aurora, CO 80045 USA.
[Watkins-Chow, Dawn E.; Pavan, William J.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Jones, Kenneth L.] Univ Colorado, Dept Biochem & Mol Genet, Aurora, CO 80045 USA.
[Salbaum, J. Michael] Pennington Biomed Res Ctr, Dept Regulat Gene Express, Baton Rouge, LA 70808 USA.
RP Niswander, L (reprint author), Univ Colorado, Howard Hughes Med Inst, Dept Pediat, Childrens Hosp Colorado, Anschutz Med Campus, Aurora, CO 80045 USA.
EM lee.niswander@ucdenver.edu
RI Niswander, Lee/D-3976-2013;
OI Watkins-Chow, Dawn/0000-0002-4355-0868
FU Department of Pediatrics, a Cancer Center Support [P30CA046934];
Bioinformatics Shared Resource; CCTSI
FX Contract grant sponsor: Department of Pediatrics, a Cancer Center
Support; contract grant number: P30CA046934.; Contract grant sponsor:
the Bioinformatics Shared Resource, and the CCTSI.
NR 61
TC 5
Z9 5
U1 2
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1932-8451
EI 1932-846X
J9 DEV NEUROBIOL
JI Dev. Neurobiol.
PD MAY
PY 2014
VL 74
IS 5
BP 483
EP 497
DI 10.1002/dneu.22142
PG 15
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA AE4ZR
UT WOS:000333998100001
PM 24170322
ER
PT J
AU Germain, RN
Gerner, MY
Kastenmuller, W
Laemmermann, T
Torabi-Parizi, P
Honda, T
Egen, JG
AF Germain, R. N.
Gerner, M. Y.
Kastenmueller, W.
Laemmermann, T.
Torabi-Parizi, P.
Honda, T.
Egen, J. G.
TI Probing myeloid cell localization and function using dynamic intravital
and highly multiplex static imaging methods
SO EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Meeting Abstract
C1 [Germain, R. N.; Gerner, M. Y.; Kastenmueller, W.; Laemmermann, T.; Torabi-Parizi, P.; Honda, T.; Egen, J. G.] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2972
EI 1365-2362
J9 EUR J CLIN INVEST
JI Eur. J. Clin. Invest.
PD MAY
PY 2014
VL 44
SU 1
SI SI
BP 13
EP 13
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA AE6DN
UT WOS:000334080900035
ER
PT J
AU Fassl, SK
Holzinger, D
Vogl, T
Gattorno, M
Omenetti, A
Chae, JJ
Aksentijevich, I
Roth, J
Austermann, J
AF Fassl, S. K.
Holzinger, D.
Vogl, T.
Gattorno, M.
Omenetti, A.
Chae, J. J.
Aksentijevich, I.
Roth, J.
Austermann, J.
TI The molecular link between PSTPIP and MRP8/14 secretion in
PSTPIP1-associated myeloid-related-proteinaemia inflammatory syndrome
(PAMI)
SO EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Meeting Abstract
C1 [Fassl, S. K.; Holzinger, D.; Vogl, T.; Roth, J.; Austermann, J.] Univ Munster, Inst Immunol, D-48149 Munster, Germany.
[Holzinger, D.] Univ Childrens Hosp Muenster, Dept Paediat Rheumatol & Immunol, Munster, Germany.
[Gattorno, M.; Omenetti, A.] G Gaslini Sci Inst, Div Pediat 2, Genoa, Italy.
[Chae, J. J.; Aksentijevich, I.] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2972
EI 1365-2362
J9 EUR J CLIN INVEST
JI Eur. J. Clin. Invest.
PD MAY
PY 2014
VL 44
SU 1
SI SI
BP 23
EP 23
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA AE6DN
UT WOS:000334080900065
ER
PT J
AU Surewaard, BGJ
Nijland, R
Otto, M
van Strijp, JAG
Kubes, P
AF Surewaard, B. G. J.
Nijland, R.
Otto, M.
van Strijp, J. A. G.
Kubes, P.
TI Staphylococcal PSMs contribute to survival and killing post-phagocytosis
SO EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Meeting Abstract
C1 [Surewaard, B. G. J.; Nijland, R.; van Strijp, J. A. G.] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Surewaard, B. G. J.; Kubes, P.] Univ Calgary, Dept Physiol & Pharmacol, Calvin Phoebe & Joan Snyder Inst Chron Dis, Calgary, AB T2N 1N4, Canada.
[Otto, M.] NIH, Lab Human Bacterial Pathogenesis, Hamilton, MT USA.
RI van Strijp, Jos/J-9549-2014
OI van Strijp, Jos/0000-0001-6253-0830
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2972
EI 1365-2362
J9 EUR J CLIN INVEST
JI Eur. J. Clin. Invest.
PD MAY
PY 2014
VL 44
SU 1
SI SI
BP 33
EP 33
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA AE6DN
UT WOS:000334080900092
ER
PT J
AU Lee, NR
Raznahan, A
Wallace, GL
Alexander-Bloch, A
Clasen, LS
Lerch, JP
Giedd, JN
AF Lee, Nancy Raitano
Raznahan, Armin
Wallace, Gregory L.
Alexander-Bloch, Aaron
Clasen, Liv S.
Lerch, Jason P.
Giedd, Jay N.
TI Anatomical coupling among distributed cortical regions in youth varies
as a function of individual differences in vocabulary abilities
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE cerebral cortex; child; language; adolescent; magnetic resonance
imaging; brain; semantics; cognition
ID AUTOMATED 3-D EXTRACTION; ALZHEIMERS-DISEASE; CEREBRAL-CORTEX; MRI DATA;
BRAIN; THICKNESS; CHILDREN; LANGUAGE; INTELLIGENCE; ACQUISITION
AB Patient lesion and functional magnetic resonance imaging (fMRI) studies have provided convincing evidence that a distributed brain network subserves word knowledge. However, little is known about the structural correlates of this network within the context of typical development and whether anatomical coupling in linguistically relevant regions of cortex varies as a function of vocabulary skill. Here we investigate the association between vocabulary and anatomical coupling in 235 typically developing youth (ages 6-19 years) using structural MRI. The study's primary aim was to evaluate whether higher vocabulary performance was associated with greater vertex-level cortical thickness covariation in distributed regions of cortex known to be associated with word knowledge. Results indicate that better vocabulary skills are associated with greater anatomical coupling in several linguistically relevant regions of cortex, including the left inferior parietal (temporal-parietal junction), inferior temporal, middle frontal, and superior frontal gyri and the right inferior frontal and precentral gyri. Furthermore, in high vocabulary scorers, stronger coupling is found among these regions. Thus, complementing patient and fMRI studies, this is the first investigation to highlight the relevance of anatomical covariance within the cortex to vocabulary skills in typically developing youth, further elucidating the distributed nature of neural systems subserving word knowledge. Hum Brain Mapp 35:1885-1895, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Lee, Nancy Raitano; Raznahan, Armin; Wallace, Gregory L.; Alexander-Bloch, Aaron; Clasen, Liv S.; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Lerch, Jason P.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Lerch, Jason P.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
RP Lee, NR (reprint author), NIMH, NIH, 10 Ctr Dr,Bldg 10,4C110,MSC 1367, Bethesda, MD 20892 USA.
EM lnancy@mail.nih.gov
RI Giedd, Jay/J-9644-2015; Lee, Nancy/M-7492-2016;
OI 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 Institutes of Health, National Institute of Mental Health
FX Contract grant sponsor: National Institutes of Health, National
Institute of Mental Health (Intramural Research Program)
NR 43
TC 9
Z9 9
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD MAY
PY 2014
VL 35
IS 5
BP 1885
EP 1895
DI 10.1002/hbm.22299
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AE5FB
UT WOS:000334012100007
PM 23728856
ER
PT J
AU White, SF
Brislin, SJ
Sinclair, S
Blair, JR
AF White, Stuart F.
Brislin, Sarah J.
Sinclair, Stephen
Blair, James R.
TI Punishing unfairness: Rewarding or the organization of a reactively
aggressive response?
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE functional MRI; aggression; altruistic punishment; cognitive
neuroscience; reactive aggression
ID VENTROMEDIAL PREFRONTAL CORTEX; ANTERIOR CINGULATE CORTEX; ALTRUISTIC
PUNISHMENT; NEURAL BASIS; FUNCTIONAL MRI; BASAL GANGLIA; STROOP TASK;
SELECTION; CONFLICT; BRAIN
AB Objectives
The neural correlates of human cooperative behavior remain poorly understood. Previous work has suggested that increases in striatal activation while punishing unfair offers represents reward signaling. However, other regions are also implicated when punishing others, for example dorsomedial frontal cortex (dmFC), anterior insula cortex (AIC), and periaqueductal gray (PAG). Moreover, the response of other regions implicated in signaling reward, for example ventromedial prefrontal cortex (vmPFC) or posterior cingulate cortex (PCC), has not been systematically examined. Experimental Design: Functional magnetic resonance imaging utilizing parametric modulation was conducted on 21 healthy adults participating in a social exchange paradigm. Principal Observations: Participants showed significant positive modulation of activity as a function of delivered punishment in caudate, dmFC, AIC, and PAG; that is, higher punishments by participants of unsatisfactory offers were associated with increasing activity within these regions. However, participants showed significant negative modulation of activity as a function of delivered punishment in vmPFC and PCC; increases in punishment level by participants were associated with decreases in activity within these regions. Conclusions: The current data question whether caudate activity when punishing unfair offers should be considered to indicate the reward value of this punishment. Instead, this activity, in conjunction with activity within dmFC, AIC, and PAG, may represent the organization of an untypical, punishing response that represents a reactive aggressive response to provocation. Notably, an inverse, regulatory relationship between vmPFC and PAG activity has been previously implicated in the context of another stimulus for reactive aggression; looming threat (Mobbs et al. [2007]: Science 317:1079-1083). Hum Brain Mapp 35:2137-2147, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [White, Stuart F.; Sinclair, Stephen; Blair, James R.] NIMH, Sect Affect Cognit Neurosci, Bethesda, MD 20892 USA.
[Brislin, Sarah J.] Florida State Univ, Dept Psychol, Tallahassee, FL 32306 USA.
RP White, SF (reprint author), NIMH, Sect Affect Cognit Neurosci, 9000 Rockville Pike,Bldg 15k,Room 300C, Bethesda, MD 20892 USA.
EM whitesf@mail.nih.gov
FU National Institute of Mental Health, National Institutes of Health
[1-ZIA-MH002860-08]
FX Contract grant sponsor: The Intramural Research Program of the National
Institute of Mental Health, National Institutes of Health; Contract
grant number: 1-ZIA-MH002860-08.
NR 52
TC 13
Z9 13
U1 7
U2 23
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD MAY
PY 2014
VL 35
IS 5
BP 2137
EP 2147
DI 10.1002/hbm.22316
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AE5FB
UT WOS:000334012100024
PM 23868733
ER
PT J
AU Bianciardi, M
van Gelderen, P
Duyn, JH
AF Bianciardi, Marta
van Gelderen, Peter
Duyn, Jeff H.
TI Investigation of BOLD fMRI resonance frequency shifts and quantitative
susceptibility changes at 7 T
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE fractional oxygen saturation; BOLD fMRI resonance frequency shifts; BOLD
fMRI quantitative susceptibility changes; BOLD fMRI phase signal changes
ID IN-VIVO; OXYGEN-METABOLISM; BLOOD; PHASE; MRI; SIGNAL; FLUCTUATIONS;
ACTIVATION; COMPLEX; NOISE
AB Although blood oxygenation level dependent (BOLD) functional magnetic resonance imaging (fMRI) experiments of brain activity generally rely on the magnitude of the signal, they also provide frequency information that can be derived from the phase of the signal. However, because of confounding effects of instrumental and physiological origin, BOLD related frequency information is difficult to extract and therefore rarely used. Here, we explored the use of high field (7 T) and dedicated signal processing methods to extract frequency information and use it to quantify and interpret blood oxygenation and blood volume changes. We found that optimized preprocessing improves detection of task-evoked and spontaneous changes in phase signals and resonance frequency shifts over large areas of the cortex with sensitivity comparable to that of magnitude signals. Moreover, our results suggest the feasibility of mapping BOLD quantitative susceptibility changes in at least part of the activated area and its largest draining veins. Comparison with magnitude data suggests that the observed susceptibility changes originate from neuronal activity through induced blood volume and oxygenation changes in pial and intracortical veins. Further, from frequency shifts and susceptibility values, we estimated that, relative to baseline, the fractional oxygen saturation in large vessels increased by 0.02-0.05 during stimulation, which is consistent to previously published estimates. Together, these findings demonstrate that valuable information can be derived from fMRI imaging of BOLD frequency shifts and quantitative susceptibility changes. Hum Brain Mapp 35:2191-2205, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Bianciardi, Marta; van Gelderen, Peter; Duyn, Jeff H.] NINDS, Adv MRI Sect, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
[Bianciardi, Marta] Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Bianciardi, Marta] Harvard Univ, Sch Med, Boston, MA USA.
RP Bianciardi, M (reprint author), NINDS, AMRI, LFMI, NIH, Bldg 10,Rm B1D 723A MSC 1065, Bethesda, MD 20892 USA.
EM bianciardim@mail.nih.gov
FU National Institutes of Health; National Institute of Neurological
Disorders and Stroke
FX Contract grant sponsor: Intramural Research Program of the National
Institutes of Health; Contract grant sponsor: National Institute of
Neurological Disorders and Stroke.
NR 34
TC 8
Z9 8
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD MAY
PY 2014
VL 35
IS 5
BP 2191
EP 2205
DI 10.1002/hbm.22320
PG 15
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AE5FB
UT WOS:000334012100028
PM 23897623
ER
PT J
AU Grainger, JR
Askenase, MH
Guimont-Desrochers, F
da Fonseca, DM
Belkaid, Y
AF Grainger, John R.
Askenase, Michael H.
Guimont-Desrochers, Fanny
da Fonseca, Denise Morais
Belkaid, Yasmine
TI Contextual functions of antigen-presenting cells in the gastrointestinal
tract
SO IMMUNOLOGICAL REVIEWS
LA English
DT Review
DE mucosal; macrophage; antigen-presenting cell; commensal; monocyte;
pathogen; immune regulation; dendritic cell; Treg
ID REGULATORY T-CELLS; GROWTH-FACTOR-BETA; CLASSICAL DENDRITIC CELLS;
EFFACING BACTERIAL PATHOGENS; INTESTINAL LAMINA PROPRIA; RETINOIC-ACID;
TOXOPLASMA-GONDII; INFLAMMATORY MONOCYTES; IMMUNE-SYSTEM; ORAL TOLERANCE
AB The immune system of the gastrointestinal tract must be tightly regulated to limit pathologic responses toward innocuous antigens while simultaneously allowing for rapid development of effector responses against invading pathogens. Highly specialized antigen-presenting cell (APC) subsets present in the gut play a dominant role in balancing these seemingly disparate functions. In this review, we discuss new findings associated with the function of gut APCs and particularly the contextual role of these cells in both establishing tolerance to orally acquired antigens in the steady state and regulating acute inflammation during infection.
C1 [Grainger, John R.; Askenase, Michael H.; Guimont-Desrochers, Fanny; da Fonseca, Denise Morais; Belkaid, Yasmine] NIAID, Program Barrier Immun & Repair, Mucosal Immunol Sect, Lab Parasit Dis,NIH, Bethesda, MD 20892 USA.
[Askenase, Michael H.] Univ Penn, Immunol Grad Grp, Philadelphia, PA 19104 USA.
[da Fonseca, Denise Morais] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Biochem & Immunol, BR-14049 Ribeirao Preto, Brazil.
RP Belkaid, Y (reprint author), NIAID, Program Barrier Immun & Repair, Mucosal Immunol Sect, Lab Parasit Dis,NIH, 4 Ctr Dr, Bethesda, MD 20892 USA.
EM ybelkaid@niaid.nih.gov
OI Grainger, John/0000-0002-4052-5923
FU Intramural NIH HHS [ZIA AI001132-03]
NR 142
TC 14
Z9 14
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-2896
EI 1600-065X
J9 IMMUNOL REV
JI Immunol. Rev.
PD MAY
PY 2014
VL 259
IS 1
BP 75
EP 87
DI 10.1111/imr.12167
PG 13
WC Immunology
SC Immunology
GA AE5PR
UT WOS:000334041600006
PM 24712460
ER
PT J
AU Shevach, EM
Thornton, AM
AF Shevach, Ethan M.
Thornton, Angela M.
TI tTregs, pTregs, and iTregs: similarities and differences
SO IMMUNOLOGICAL REVIEWS
LA English
DT Review
DE stability; IL-10; Helios; infectious tolerance; Treg cells;
organ-specific autoimmunity
ID REGULATORY T-CELLS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
TRANSCRIPTION FACTOR FOXP3; LATENT TGF-BETA; MHC CLASS-II; DENDRITIC
CELLS; CUTTING EDGE; IN-VIVO; SURFACE EXPRESSION; REG CELLS
AB Foxp3(+) T-regulatory cells (Tregs) are primarily generated in the thymus (tTreg), but also may be generated extrathymically at peripheral sites (pTreg), or induced in cell culture (iTreg) in the presence of transforming growth factor beta (TGF beta). A major unresolved issue is how these different populations of Tregs exert their suppressive function in vivo. We have developed novel systems in which the function of Tregs can be evaluated in vivo in normal mice. Our studies demonstrate that one prominent mechanism of action of polyclonal tTregs is to inhibit T-effector cell trafficking to the target organ, while antigen-specific iTregs primarily prevent T-cell priming by acting on antigen-presenting dendritic cells (DCs). Interleukin-10 (IL-10) plays an important role in the suppressive function of antigen-specific iTregs by controlling the expression of MARCH1 and CD83 on the DC. Activated tTregs may mediate infectious tolerance by delivery of cell surface-expressed TGF beta to naive responder T cells to generate pTregs. Manipulation of Treg function will require the ability to differentiate tTregs from pTregs and iTregs. The expression of the transcription factor Helios has proven to be a useful marker for the identification of stable tTregs in both mouse and human.
C1 [Shevach, Ethan M.; Thornton, Angela M.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Shevach, EM (reprint author), NIAID, Immunol Lab, NIH, Blg 10,RM 11N315, Bethesda, MD 20892 USA.
EM eshevach@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases
FX The studies described in this review were supported by funds from the
Intramural Program of the National Institute of Allergy and Infectious
Diseases. The authors would like to thank all members of the Cellular
Immunology Section who contributed to these studies. The authors have no
conflicts of interest to declare.
NR 67
TC 87
Z9 90
U1 10
U2 38
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-2896
EI 1600-065X
J9 IMMUNOL REV
JI Immunol. Rev.
PD MAY
PY 2014
VL 259
IS 1
BP 88
EP 102
DI 10.1111/imr.12160
PG 15
WC Immunology
SC Immunology
GA AE5PR
UT WOS:000334041600007
PM 24712461
ER
PT J
AU Safdar, N
Anderson, DJ
Braun, BI
Carling, P
Cohen, S
Donskey, C
Drees, M
Harris, A
Henderson, DK
Huang, SS
Juthani-Mehta, M
Lautenbach, E
Linkin, DR
Meddings, J
Miller, LG
Milstone, A
Morgan, D
Sengupta, S
Varman, M
Yokoe, D
Zerr, DM
AF Safdar, Nasia
Anderson, Deverick J.
Braun, Barbara I.
Carling, Philip
Cohen, Stuart
Donskey, Curtis
Drees, Marci
Harris, Anthony
Henderson, David K.
Huang, Susan S.
Juthani-Mehta, Manisha
Lautenbach, Ebbing
Linkin, Darren R.
Meddings, Jennifer
Miller, Loren G.
Milstone, Aaron
Morgan, Daniel
Sengupta, Sharmila
Varman, Meera
Yokoe, Deborah
Zerr, Danielle M.
CA Soc Healthcare Epidemiology Amer
TI The Evolving Landscape of Healthcare-Associated Infections: Recent
Advances in Prevention and a Road Map for Research
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
ID SURGICAL-SITE INFECTIONS; VENTILATOR-ASSOCIATED PNEUMONIA; RANDOMIZED
CONTROLLED-TRIAL; CARBAPENEMASE-PRODUCING ENTEROBACTERIACEAE;
CATHETER-RELATED INFECTIONS; GENTAMICIN-COLLAGEN SPONGE;
URINARY-TRACT-INFECTIONS; BLOOD-STREAM INFECTION; CRITICALLY-ILL ADULTS;
INTENSIVE-CARE
AB This white paper identifies knowledge gaps and new challenges in healthcare epidemiology research, assesses the progress made toward addressing research priorities, provides the Society for Healthcare Epidemiology of America (SHEA) Research Committee's recommendations for high-priority research topics, and proposes a road map for making progress toward these goals. It updates the 2010 SHEA Research Committee document, "Charting the Course for the Future of Science in Healthcare Epidemiology: Results of a Survey of the Membership of SHEA," which called for a national approach to healthcare-associated infections (HAIs) and a prioritized research agenda. This paper highlights recent studies that have advanced our understanding of HAIs, the establishment of the SHEA Research Network as a collaborative infrastructure to address research questions, prevention initiatives at state and national levels, changes in reporting and payment requirements, and new patterns in antimicrobial resistance.
C1 [Safdar, Nasia] Univ Wisconsin, Div Infect Dis, William S Middleton Mem Vet Hosp, Madison, WI USA.
[Anderson, Deverick J.] Duke Univ, Med Ctr, Dept Infect Dis, Durham, NC USA.
[Braun, Barbara I.] Joint Commiss, Oak Brook Terrace, IL USA.
[Carling, Philip] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Cohen, Stuart] Univ Calif Davis, Div Infect Dis, Sch Med Hosp Epidemiol & Infect Prevent, Sacramento, CA 95817 USA.
[Donskey, Curtis] Louis Stokes Cleveland Vet Affairs Med Ctr, Cleveland, OH USA.
[Drees, Marci] Christiana Care Hlth Syst, Newark, DE USA.
[Harris, Anthony] Univ Maryland, Sch Med, EPH Genom Epidemiol & Clin Outcomes, Baltimore, MD 21201 USA.
[Henderson, David K.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Huang, Susan S.] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
[Juthani-Mehta, Manisha] Yale Univ, Sch Med, Infect Dis Sect, New Haven, CT USA.
[Lautenbach, Ebbing] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Linkin, Darren R.] Univ Penn, Philadelphia, PA 19104 USA.
[Meddings, Jennifer] Univ Michigan, Ann Arbor, MI 48109 USA.
[Miller, Loren G.] Harbor UCLA Med Ctr, Div Infect Dis, Torrance, CA 90509 USA.
[Milstone, Aaron] Johns Hopkins Univ, Baltimore, MD USA.
[Morgan, Daniel] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Morgan, Daniel] Vet Affairs Maryland Healthcare Syst, Baltimore, MD USA.
[Sengupta, Sharmila] BLK Super Specialty Hosp, Dept Microbiol, Delhi, India.
[Varman, Meera] Creighton Univ, Med Ctr, Omaha, NE USA.
[Yokoe, Deborah] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Yokoe, Deborah] Harvard Univ, Sch Med, Boston, MA USA.
[Zerr, Danielle M.] Univ Washington, Dept Pediat, Seattle, WA 98195 USA.
[Zerr, Danielle M.] Seattle Childrens Res Inst, Seattle, WA USA.
RP Safdar, N (reprint author), 600 Highland Ave,H4-574, Madison, WI 53792 USA.
EM ns2@medicine.wisc.edu
FU US Department of Veterans Affairs (VA); National Institutes of Health
(NIH) [AG40669]; Centers for Disease Control and Prevention (CDC), Duke
University/Duke Infection Control Outreach Network [U54CK000164];
NIH/National Institute of Allergy and Infectious Diseases (NIAID) Duke
University [K23AI095357]; CDC/Duke University [U54CK000172-01]; The
Joint Commission: Agency for Healthcare Research and Quality (AHRQ)
[1R13HS022174-0112]; CDC National Institute for Occupational Safety and
Health National Personal Protective Technology Laboratory; AHRQ; CDC;
state of Pennsylvania; Doris Duke Charitable Foundation; University of
Pennsylvania; Pennsylvania Department of Health; VA National Center for
Patient Safety; NIH/National Institute of Nursing Research; CDC [1U54
CK000172-01]; NIH/NIAID; NIH/National Cancer Institute
FX Potential conflicts of interest. N.S. reports research grants and/or
contracts from the US Department of Veterans Affairs (VA) and the
National Institutes of Health (NIH; AG40669). D.J.A. reports a financial
relationship with UpToDate Online, a company involved in treatment of
subjects, and having received research grants or contracts from the
Centers for Disease Control and Prevention (CDC), Duke University/Duke
Infection Control Outreach Network (U54CK000164), NIH/National Institute
of Allergy and Infectious Diseases (NIAID) Duke University
(K23AI095357), and CDC/Duke University (U54CK000172-01). B.I.B. reports
having received research grants or contracts from The Joint Commission:
Agency for Healthcare Research and Quality (AHRQ; 1R13HS022174-0112) and
the CDC National Institute for Occupational Safety and Health National
Personal Protective Technology Laboratory. P.C. reports being an advisor
or consultant for Ecolab and holding patents, copyrights, or licenses
from Steris. S.C. reports having received research grants or contracts
from Viropharma, Merck, and Cubist for clinical trials in C. difficile
infection. A.H. reports financial involvement with companies involved in
the treatment of subjects and having served in an advisory or consultant
role for Premier, Cubist, and UpToDate. S.S.H. reports leading a
clinical trial in which participating hospitals receive contributed
product from Sage. E.L. reports having received research grants or
contracts from AHRQ, the CDC, and the state of Pennsylvania. D.R.L.
reports having received research grants/contracts from Doris Duke
Charitable Foundation, the University of Pennsylvania, and the
Pennsylvania Department of Health. J.M. reports having received research
grants or contracts from AHRQ, VA National Center for Patient Safety,
and the NIH/National Institute of Nursing Research. L.G.M. reports
having received research grant or contracts from Merck Harbor-UCLA and
Cerexa and honoraria from Durata. A.M. reports a financial relationship
with Sage Products, a company involved in the treatment of subjects, and
past research support and research grants or contracts from the NIH.
D.M. reports serving in an advisory or consultant role for Welch-Allyn.
D.Y. reports having received research grants or contracts from the CDC
(1U54 CK000172-01). D.M.Z. reports having received research grants or
contracts from the NIH/NIAID and the NIH/National Cancer Institute. All
other authors report no conflicts of interest relevant to this article.
NR 77
TC 7
Z9 7
U1 1
U2 10
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0899-823X
EI 1559-6834
J9 INFECT CONT HOSP EP
JI Infect. Control Hosp. Epidemiol.
PD MAY 1
PY 2014
VL 35
IS 5
BP 480
EP 493
DI 10.1086/675821
PG 14
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA AE4EI
UT WOS:000333933900004
PM 24709716
ER
PT J
AU Leaver, CA
AF Leaver, Cynthia A.
TI Visiting Again? Subjective Well-Being of Children in Elementary School
and Repeated Visits to School Health Nurses
SO JOURNAL OF SCHOOL HEALTH
LA English
DT Article
DE school nurse; student somatic complaints; predictors of school nurse
visits; academic achievement
ID MODEL; ADOLESCENTS; COMPLAINTS; YOUTH
AB BACKGROUND
Children with vague complaints are without chronic illness, and who repeatedly visit the school nurse may be at risk for limited academic success. This study compares student reports of subjective well-being between children who do and do not repeatedly visit the school nurse with vague complaints.
METHODS
Children in grades 4 through 6 completed the School Well-Being Profile-American English (SWBP-AE), a questionnaire with 4 well-being subscales: health status, school environment, social relationships, and school as a means of self-fulfillment. School nurses extracted data on clinic visits from clinic records. Logistic regression explored associations between well-being subscales and repeated visits to the school nurse.
RESULTS
Of the 320 students participating in the study, 33 (12.04%) students made repeated visits to the school nurse. Perception of health status (OR = 2.072; 95% CI = 1.037, 4.163) was the only significant (p < .05) predictor of repeated visits to the nurse.
CONCLUSION
Children with poor perception of their health status are more likely to repeatedly visit the school nurse. Children's perceptions of their school environment, social relationships, or school as a means of self-fulfillment are not statistically significant predictors of repeated visits to the school nurse.
C1 NINR, NIH, Div Intramural Res, Bethesda, MD 20892 USA.
RP Leaver, CA (reprint author), NINR, NIH, Div Intramural Res, 10 Ctr Dr,2-1339, Bethesda, MD 20892 USA.
EM caleaver@cox.net
FU Bravewell Collaborative
FX The author would like to acknowledge the following individuals who have
made significant contributions to the scientific content or technical
support to this research project: Mary Paterson, RN, PhD, Ordinary
Professor, The Catholic University of America, Washington, DC, Gwenyth
R. Wallen, RN, PhD, Chief, Nursing Research and Translational Science,
National Institutes of Health, Clinical Center, Bethesda Maryland, and
Joan Austin, PhD, RN, FAAN, Consultant, National Institutes of Health,
National Institute of Nursing Research. This research was completed
while the author was a PhD student at The Catholic University of
America, School of Nursing, Washington, DC. The author is currently a
postdoctoral fellow at the National Institute of Nursing Research,
National Institutes of Health sponsored by the Bravewell Collaborative.
NR 29
TC 1
Z9 1
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4391
EI 1746-1561
J9 J SCHOOL HEALTH
JI J. Sch. Health
PD MAY
PY 2014
VL 84
IS 5
BP 294
EP 301
DI 10.1111/josh.12150
PG 8
WC Education & Educational Research; Education, Scientific Disciplines;
Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Education & Educational Research; Health Care Sciences & Services;
Public, Environmental & Occupational Health
GA AE4QD
UT WOS:000333966800002
PM 24707923
ER
PT J
AU Longchamps, RJ
Abey, SK
Martino, AC
Henderson, WA
AF Longchamps, R. J.
Abey, S. K.
Martino, A. C.
Henderson, W. A.
TI Letter: apoptosis and hepatic fibrosis in chronic hepatitis B - authors'
reply
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Letter
ID FIBROGENESIS; PATHOGENESIS
C1 [Longchamps, R. J.; Abey, S. K.; Martino, A. C.; Henderson, W. A.] NINR, Digest Disorder Unit, Biobehav Branch, Div Intramural Res,Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA.
RP Longchamps, RJ (reprint author), NINR, Digest Disorder Unit, Biobehav Branch, Div Intramural Res,Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA.
EM hendersw@mail.nih.gov
FU Intramural NIH HHS [Z99 NR999999, ZIA NR000018-01, ZIA NR000018-02, ZIA
NR000018-03, ZIA NR000018-04, ZIA NR000018-05]; NINR NIH HHS [ZIA
NR000018]
NR 6
TC 3
Z9 3
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD MAY
PY 2014
VL 39
IS 9
BP 997
EP 997
DI 10.1111/apt.12715
PG 1
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA AD8ZA
UT WOS:000333553000016
PM 24689349
ER
PT J
AU Chen, F
Wang, Z
Bhattacharyya, T
AF Chen, Foster
Wang, Zhong
Bhattacharyya, Timothy
TI Absence of femoral cortical thickening in long-term bisphosphonate
users: Implications for atypical femur fractures
SO BONE
LA English
DT Article
DE Atypical femur fracture; Osteoporosis
ID ASYMPTOMATIC PATIENTS; THERAPY
AB The radiographs of patients on long term bisphosphonates with atypical femur fractures demonstrate markedly thick cortices at the site of the fracture. We conducted a prospective clinical study to determine if cortical thickening is increased in long term bisphosphonate users. We recruited 43 patients who had taken bisphosphonates for more than 5 years. A group of 45 healthy volunteers and 12 patients recently diagnosed with osteoporosis served as controls. We measured the cortical thickening as the ratio of femoral cortical thickness to diameter of the femur, and looked for cortical beaking.
No difference in the cortical thickness ratio was observed between long term bisphosphonate users and osteoporotic controls (0.53 vs. 0.54, p = 0.659). No cases of cortical beaking were seen and no increase in thigh pain was observed. The power of the study was 95% to detect a 10% difference in cortical thickness ratio. We conclude that long term bisphosphonate use does not produce a generalized increase in subtrochanteric femoral cortical thickening in the majority of patients. (C) 2014 Published by Elsevier Inc.
C1 [Chen, Foster; Wang, Zhong; Bhattacharyya, Timothy] NIAMSD, Clin & Invest Orthopaed Surg Unit, Unit Intramural Res Program, Bethesda, MD 20892 USA.
RP Bhattacharyya, T (reprint author), NIAMS, Clin & Invest Orthopaed Surg Sect, Off Clin Director, 10 Ctr Dr,Bldg 10 CRC Room 4-2339, Bethesda, MD 20892 USA.
EM Timothy.bhattacharyya@nih.gov
FU Intramural NIH HHS [Z99 AR999999]
NR 9
TC 11
Z9 11
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 8756-3282
EI 1873-2763
J9 BONE
JI Bone
PD MAY
PY 2014
VL 62
BP 64
EP 66
DI 10.1016/j.bone.2014.01.011
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AD6NU
UT WOS:000333378300009
PM 24468718
ER
PT J
AU Ellingson, MS
Wick, MJ
White, WM
Raymond, KM
Saenger, AK
Pichurin, PN
Wassif, CA
Porter, FD
Babovic-Vuksanovic, D
AF Ellingson, M. S.
Wick, M. J.
White, W. M.
Raymond, K. M.
Saenger, A. K.
Pichurin, P. N.
Wassif, C. A.
Porter, F. D.
Babovic-Vuksanovic, D.
TI Pregnancy in an individual with mild Smith-Lemli-Opitz syndrome
SO CLINICAL GENETICS
LA English
DT Letter
ID CHOLESTEROL
C1 [Ellingson, M. S.; Wick, M. J.; Pichurin, P. N.; Babovic-Vuksanovic, D.] Mayo Clin, Dept Med Genet, Rochester, MN 55902 USA.
[Wick, M. J.; White, W. M.] Mayo Clin, Dept Obstet, Rochester, MN 55902 USA.
[Raymond, K. M.; Saenger, A. K.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55902 USA.
[Wassif, C. A.; Porter, F. D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Babovic-Vuksanovic, D (reprint author), Mayo Clin, Dept Med Genet, 200 First St SW, Rochester, MN 55902 USA.
EM dbabovic@mayo.edu
OI Wassif, Christopher/0000-0002-2524-1420
FU Intramural NIH HHS [ZIA HD008825-06]
NR 4
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9163
EI 1399-0004
J9 CLIN GENET
JI Clin. Genet.
PD MAY
PY 2014
VL 85
IS 5
BP 495
EP 497
DI 10.1111/cge.12209
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA AD8UH
UT WOS:000333540700016
PM 23790112
ER
PT J
AU Gamaletsou, MN
Rammaert, B
Bueno, MA
Moriyama, B
Sipsas, NV
Kontoyiannis, DP
Roilides, E
Zeller, V
Prinapori, R
Taj-Aldeen, SJ
Brause, B
Lortholary, O
Walsh, TJ
AF Gamaletsou, Maria N.
Rammaert, Blandine
Bueno, Marimelle A.
Moriyama, Brad
Sipsas, Nikolaos V.
Kontoyiannis, Dimitrios P.
Roilides, Emmanuel
Zeller, Valerie
Prinapori, Roberta
Taj-Aldeen, Saad J.
Brause, Barry
Lortholary, Olivier
Walsh, Thomas J.
TI Aspergillus osteomyelitis: Epidemiology, clinical manifestations,
management, and outcome
SO JOURNAL OF INFECTION
LA English
DT Article
DE Aspergillus; Osteomyelitis
ID CHRONIC GRANULOMATOUS-DISEASE; ACQUIRED-IMMUNODEFICIENCY-SYNDROME;
OF-THE-LITERATURE; RENAL-TRANSPLANT RECIPIENT; INVASIVE EXTERNAL OTITIS;
CONTIGUOUS VERTEBRAL OSTEOMYELITIS; STERNAL WOUND INFECTIONS; AORTIC
BYPASS GRAFT; EPIDURAL ABSCESS; FUNGAL-INFECTION
AB Background: The epidemiology, pathogenesis, diagnosis, and management of Aspergillus osteomyelitis are not well understood.
Methods: Protocol-defined cases of Aspergillus osteomyelitis published in the English literature were reviewed for comorbidities, microbiology, mechanisms of infection, clinical manifestations, radiological findings, inflammatory biomarkers, antifungal therapy, and outcome.
Results: Among 180 evaluable patients, 127 (71%) were males. Possible predisposing medical conditions in 103 (57%) included pharmacological immunosuppression, primary immunodeficiency, and neutropenia. Seventy-three others (41%) had prior open fracture, trauma or surgery. Eighty (44%) followed a hematogenous mechanism, 58 (32%) contiguous infections, and 42 (23%) direct inoculation. Aspergillus osteomyelitis was the first manifestation of aspergillosis in 77%. Pain and tenderness were present in 80%. The most frequently infected sites were vertebrae (46%), cranium (23%), ribs (16%), and long bones (13%). Patients with vertebral Aspergillus osteomyelitis had more previous orthopedic surgery (19% vs 0%; P = 0.02), while those with cranial osteomyelitis had more diabetes mellitus (32% vs 8%; P = 0.002) and prior head/neck surgery (12% vs 0%; P = 0.02). Radiologic findings included osteolysis, soft-tissue extension, and uptake on T2-weighted images. Vertebral body Aspergillus osteomyelitis was complicated by spinal-cord compression in 47% and neurological deficits in 41%. Forty-four patients (24%) received only antifungal therapy, while 121 (67%) were managed with surgery and antifungal therapy. Overall mortality was 25%. Median duration of therapy was 90 days (range, 10-772 days). There were fewer relapses in patients managed with surgery plus antifungal therapy in comparison to those managed with antifungal therapy alone (8% vs 30%; P = 0.006).
Conclusions: Aspergillus osteomyelitis is a debilitating infection affecting both immunocompromised and immunocompetent patients. The most common sites are vertebrae, ribs, and cranium. Based upon this comprehensive review, management of Aspergillus osteomyelitis optimally includes antifungal therapy and selective surgery to avoid relapse and to achieve a complete response. (C) 2013 The British Infection Association. Published by Elsevier Ltd. All rights reserved.
C1 [Gamaletsou, Maria N.; Bueno, Marimelle A.; Brause, Barry; Walsh, Thomas J.] Cornell Univ, Weill Cornell Med Ctr, New York, NY 10021 USA.
[Gamaletsou, Maria N.; Sipsas, Nikolaos V.] Univ Athens, Athens 11528, Greece.
[Gamaletsou, Maria N.; Rammaert, Blandine; Sipsas, Nikolaos V.; Roilides, Emmanuel; Brause, Barry; Lortholary, Olivier; Walsh, Thomas J.] Hosp Special Surg, Ctr Osteoarticular Mycoses, New York, NY 10021 USA.
[Gamaletsou, Maria N.; Rammaert, Blandine; Sipsas, Nikolaos V.; Roilides, Emmanuel; Brause, Barry; Lortholary, Olivier; Walsh, Thomas J.] Int Osteoarticular Mycoses Study Consortium, New York, NY USA.
[Rammaert, Blandine; Lortholary, Olivier] Univ Paris 05, Sorbonne Paris Cite, Serv Malad Infect & Trop,Ctr Infectiol Necker Pas, Hop Necker Enfants Malad,APHP,Inst Imagine, Paris, France.
[Rammaert, Blandine; Lortholary, Olivier] Inst Pasteur, Unite Mycol Mol, Paris, France.
[Moriyama, Brad] NIH, Dept Pharm, Ctr Clin, Bethesda, MD 20892 USA.
[Kontoyiannis, Dimitrios P.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Roilides, Emmanuel] Aristotle Univ Thessaloniki, Fac Med, Sch Hlth Sci, Infect Dis Unit,Dept Pediat 3, GR-54006 Thessaloniki, Greece.
[Roilides, Emmanuel] Hippokrateion Hosp, Thessaloniki, Greece.
[Zeller, Valerie] Grp Hosp Diaconesses Croix St Simon, Osteoarticular Reference Ctr, Paris, France.
[Prinapori, Roberta] Univ Genoa, San Martino Genoa Hosp, Dept Infect Dis, Genoa, Italy.
[Taj-Aldeen, Saad J.] Hamad Med Corp, Dept Lab Med & Pathol, Mycol Unit, Doha, Qatar.
RP Walsh, TJ (reprint author), Weill Cornell Med Ctr, Transplantat Oncol Infect Dis Program, 1300 York Ave,Rm A421, New York, NY 10065 USA.
EM thw2003@med.cornell.edu
FU National and Kapodistrian University of Athens; National Institutes of
Health through an MD Anderson Cancer Center Support Grant [CA016672];
Save Our Sick Children Foundation Scholar Award; Sharpe Family
Foundation Scholar Award in Pediatric Infectious Diseases
FX This work was supported by the Special Account for Research Funds (to
M.N.G., N.V.S.) of the National and Kapodistrian University of Athens;
National Institutes of Health through an MD Anderson Cancer Center
Support Grant (CA016672); Save Our Sick Children Foundation Scholar
Award and the Sharpe Family Foundation Scholar Award in Pediatric
Infectious Diseases (T.J.W.)
NR 169
TC 16
Z9 16
U1 1
U2 11
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0163-4453
EI 1532-2742
J9 J INFECTION
JI J. Infect.
PD MAY
PY 2014
VL 68
IS 5
BP 478
EP 493
DI 10.1016/j.jinf.2013.12.008
PG 16
WC Infectious Diseases
SC Infectious Diseases
GA AE1XJ
UT WOS:000333766200009
PM 24378282
ER
PT J
AU Louis, GMB
Hediger, ML
Bell, EM
Kus, CA
Sundaram, R
McLain, AC
Yeung, E
Hills, EA
Thoma, ME
Druschel, CM
AF Louis, Germaine M. Buck
Hediger, Mary L.
Bell, Erin M.
Kus, Christopher A.
Sundaram, Rajeshwari
McLain, Alexander C.
Yeung, Edwina
Hills, Elaine A.
Thoma, Marie E.
Druschel, Charlotte M.
TI Methodology for Establishing a Population-Based Birth Cohort Focusing on
Couple Fertility and Children's Development, the Upstate KIDS Study
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article
DE infertility; in vitro fertilization; children; fecundity; assisted
reproductive technologies
ID ASSISTED REPRODUCTIVE TECHNOLOGY; IN-VITRO FERTILIZATION; TERM HEALTH
OUTCOMES; UNITED-STATES; STAGES QUESTIONNAIRES; INFERTILITY TREATMENT;
PERINATAL OUTCOMES; CERTIFICATE DATA; MEDICAL HOME; VALIDITY
AB Background
Critical data gaps remain regarding infertility treatment and child development. We assessed the utility of a birth certificate registry for developing a population cohort aimed at answering such questions.
Methods
We utilised the Upstate New York livebirth registry (n = 201 063) to select births conceived with (n = 4024) infertility treatment or exposed infants, who were then frequency-matched by residence to a random sample of infants conceived without (n = 14 455) treatment or unexposed infants, 2008-10. Mothers were recruited at 2-4 months postpartum and queried about their reproductive histories, including infertility treatment for comparison with birth certificate data. Overall, 1297 (32%) mothers of exposed and 3692 of unexposed (26%) infants enrolled.
Results
Twins represented 22% of each infant group. The percentage of infants conceived with/without infertility treatment was similar whether derived from the birth registry or maternal report: 71% none, 16% drugs or intrauterine insemination, and 14% assisted reproductive technologies (ART). Concordant reporting between the two data sources was 93% for no treatment, 88% for ART, and 83% for fertility drugs, but differed by plurality. Exposed infants had slightly (P < 0.01) earlier gestations than unexposed infants (38.3 +/- 2.8 and 38.7 +/- 2.7 weeks, respectively) based upon birth certificates but not maternal report (38.7 +/- 2.7 and 38.7 +/- 2.9, respectively). Conversely, mean birthweight was comparable using birth certificates (3157 +/- 704 and 3194 +/- 679 g, respectively), but differed using maternal report (3167 +/- 692 and 3224 +/- 661, respectively P < 0.05).
Conclusions
The birth certificate registry is a suitable sampling framework as measured by concordance with maternally reported infertility treatment. Future efforts should address the impact of factors associated with discordant reporting on research findings.
C1 [Louis, Germaine M. Buck; Hediger, Mary L.; Sundaram, Rajeshwari; Yeung, Edwina; Thoma, Marie E.] Div Intramural Populat Hlth Res, Rockville, MD USA.
[Bell, Erin M.] SUNY Albany, Sch Publ Hlth, Dept Environm Hlth Sci, Albany, NY 12222 USA.
[Bell, Erin M.; Hills, Elaine A.; Druschel, Charlotte M.] SUNY Albany, Sch Publ Hlth, Dept Epidemiol & Biostat, Albany, NY 12222 USA.
[Kus, Christopher A.] New York State Dept Hlth, Div Family Hlth, Albany, NY USA.
[Hills, Elaine A.; Druschel, Charlotte M.] New York State Dept Hlth, Congenital Malformat Registry, Albany, NY USA.
[McLain, Alexander C.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
RP Louis, GMB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, 6100 Execut Blvd,Room 7B03, Rockville, MD 20852 USA.
EM louisg@mail.nih.gov
RI Yeung, Edwina/F-5992-2015;
OI Yeung, Edwina/0000-0002-3851-2613; McLain,
Alexander/0000-0002-5475-0670; Sundaram, Rajeshwari/0000-0002-6918-5002;
Buck Louis, Germaine/0000-0002-1774-4490
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HHSN267200700019C, HHSN275201200005C]
FX Funded by the Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development (contracts
HHSN267200700019C; HHSN275201200005C). The authors thank Kira Leishear
and Patricia Moyer for their statistical programming assistance, and
John Piddock and Larry Schoen for their assistance with vital
registries.
NR 44
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Z9 15
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
EI 1365-3016
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD MAY
PY 2014
VL 28
IS 3
BP 191
EP 202
DI 10.1111/ppe.12121
PG 12
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA AE2KH
UT WOS:000333801300003
ER
PT J
AU Stenberg, N
Bresnahan, M
Gunnes, N
Hirtz, D
Hornig, M
Lie, KK
Lipkin, WI
Lord, C
Magnus, P
Reichborn-Kjennerud, T
Schjolberg, S
Suren, P
Susser, E
Svendsen, BK
von Tetzchner, S
Oyen, AS
Stoltenberg, C
AF Stenberg, Nina
Bresnahan, Michaeline
Gunnes, Nina
Hirtz, Deborah
Hornig, Mady
Lie, Kari Kveim
Lipkin, W. Ian
Lord, Catherine
Magnus, Per
Reichborn-Kjennerud, Ted
Schjolberg, Synnve
Suren, Pal
Susser, Ezra
Svendsen, Britt Kveim
von Tetzchner, Stephen
Oyen, Anne-Siri
Stoltenberg, Camilla
TI Identifying Children with Autism Spectrum Disorder at 18 Months in a
General Population Sample
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article
DE Norwegian Mother and Child Cohort Study; early identification; Autism
Birth Cohort Study; longitudinal studies; M-CHAT; autism spectrum
disorders
ID PERVASIVE DEVELOPMENTAL DISORDERS; MODIFIED CHECKLIST; SCREENING
INSTRUMENT; EARLY RECOGNITION; TODDLERS; AGE; DIAGNOSIS; COHORT; 1ST;
SIGNS
AB Background
Previous research on clinical and high-risk samples suggests that signs of autism spectrum disorder (ASD) can be detected between 1 and 2 years of age. We investigated signs of ASD at 18 months in a population-based sample and the association with later ASD diagnosis.
Methods
The study sample includes 52 026 children born 2003 through 2008 and is a subset of children that participated in the Norwegian Mother and Child Cohort (MoBa), a population-based longitudinal study, and the Autism Birth Cohort (ABC), a sub-study on ASD. Parents completed all 23 items from the Modified Checklist for Autism in Toddlers (M-CHAT) at 18 months.
Results
The M-CHAT 6-critical-item criterion and the 23-item criterion had a specificity of 97.9% and 92.7% and a sensitivity of 20.8% and 34.1%, respectively. In the 173 children diagnosed with ASD to date, 60 children (34.7%) scored above the cut-off on either of the screening criteria. The items with the highest likelihood ratios were 'interest in other children', 'show objects to others' and 'response to name'.
Conclusion
Even though one-third of the children who later received an ASD diagnosis were identified through M-CHAT items, the majority scored below cut-off on the screening criteria at 18 months. The results imply that it might not be possible to detect all children with ASD at this age.
C1 [Stenberg, Nina; Gunnes, Nina; Lie, Kari Kveim; Magnus, Per; Reichborn-Kjennerud, Ted; Schjolberg, Synnve; Suren, Pal; Oyen, Anne-Siri; Stoltenberg, Camilla] Norwegian Inst Publ Hlth, N-0403 Oslo, Norway.
[Bresnahan, Michaeline; Hornig, Mady; Lipkin, W. Ian; Susser, Ezra] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
[von Tetzchner, Stephen] Univ Oslo, Inst Psychol, Oslo, Norway.
[Susser, Ezra] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Hornig, Mady; Lipkin, W. Ian] Columbia Univ, Ctr Infect & Immun, New York, NY USA.
[Svendsen, Britt Kveim; Oyen, Anne-Siri] Lovisenberg Hosp, Nic Waals Inst, Oslo, Norway.
[Hirtz, Deborah] NINDS, NIH, Bethesda, MD 20892 USA.
[Lord, Catherine] New York Presbyterian Hosp, Weill Cornell Med Coll, Inst Brain Dev, New York, NY USA.
[Lord, Catherine] Columbia Univ, Med Ctr, New York, NY USA.
[Stoltenberg, Camilla] Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway.
[Reichborn-Kjennerud, Ted] Univ Oslo, Inst Psychiat, Oslo, Norway.
RP Stenberg, N (reprint author), Norwegian Inst Publ Hlth, POB 4404 Nydalen, N-0403 Oslo, Norway.
EM nist@fhi.no
FU Norwegian Ministry of Health and Care Services; Norwegian Ministry of
Education and Research; Research Council of Norway/FUGE [151918];
National Institute of Neurological Disorders and Stroke (NIH/NINDS),
Bethesda, MD, USA [NS47537]; National Institute of Environmental Health
Sciences (NIH/NIEHS), Research Triangle Park, NC, USA [NO-ES-75558];
National Institute of Neurological Disorders and Stroke, (NIH/NINDS),
Bethesda, MD, USA [NS47537]; Norwegian Research Council [196452]
FX The authors would like to acknowledge and thank all participating
families. The Norwegian Mother and Child Cohort Study is funded by the
Norwegian Ministry of Health and Care Services, the Norwegian Ministry
of Education and Research, the Research Council of Norway/FUGE (grant
no. 151918), the National Institute of Neurological Disorders and Stroke
(NIH/NINDS), Bethesda, MD, USA (grant no. NS47537) and the National
Institute of Environmental Health Sciences (NIH/NIEHS), Research
Triangle Park, NC, USA (contract no. NO-ES-75558). The Autism Birth
Cohort study is funded by the National Institute of Neurological
Disorders and Stroke, (NIH/NINDS), Bethesda, MD, USA (grant no.
NS47537). The present study was supported by a grant from the Norwegian
Research Council (grant no. 196452).
NR 42
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U1 4
U2 26
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
EI 1365-3016
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD MAY
PY 2014
VL 28
IS 3
BP 255
EP 262
DI 10.1111/ppe.12114
PG 8
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA AE2KH
UT WOS:000333801300009
PM 24547686
ER
PT J
AU Schisterman, EF
AF Schisterman, Enrique F.
CA EAGeR Team
TI A randomised trial to evaluate the effects of low-dose aspirin in
gestation and reproduction: Design and baseline characteristics (vol 27,
pg 598, 2013)
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Correction
C1 [Schisterman, Enrique F.; EAGeR Team] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Rockville, MD 20854 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, 6100 Execut Blvd,7B03, Rockville, MD 20854 USA.
EM schistee@mail.nih.gov
OI Schisterman, Enrique/0000-0003-3757-641X
NR 1
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
EI 1365-3016
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD MAY
PY 2014
VL 28
IS 3
BP 275
EP 275
DI 10.1111/ppe.12122
PG 1
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA AE2KH
UT WOS:000333801300012
ER
PT J
AU Saleem, KS
Miller, B
Price, JL
AF Saleem, Kadharbatcha S.
Miller, Brad
Price, Joseph L.
TI Subdivisions and Connectional Networks of the Lateral Prefrontal Cortex
in the Macaque Monkey
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE LPFC; VLPFC; DPFC; CLPFC; OMPFC; OPFC; MPFC; superior temporal gyrus;
parietal cortex; inferior temporal cortex; superior temporal sulcus;
insula; connections
ID SUPERIOR TEMPORAL SULCUS; FRONTAL EYE FIELD; COMPARATIVE
CYTOARCHITECTONIC ANALYSIS; EFFERENT ASSOCIATION PATHWAYS; PRIMATE
ORBITOFRONTAL CORTEX; MOTION-SENSITIVE CELLS; DEEP BRAIN-STIMULATION;
REWARD-GUIDED BEHAVIOR; RHESUS-MONKEY; CORTICAL PROJECTIONS
AB Neuroanatomical studies have long indicated that corticocortical connections are organized in networks that relate distinct sets of areas. Such networks have been emphasized by development of functional imaging methods for correlating activity across the cortex. Previously, two networks were recognized in the orbitomedial prefrontal cortex, the orbital and medial networks (OPFC and MPFC, respectively). In this study, three additional networks are proposed for the lateral prefrontal cortex: 1) a ventrolateral network (VLPFC) in and ventral to the principal sulcus; 2) a dorsal network (DPFC) in and dorsal to the principal sulcus and in the frontal pole; 3) a caudolateral network (CLPFC) in and rostral to the arcuate sulcus and the caudal principal sulcus. The connections of the first two networks are described here. Areas in each network are connected primarily with other areas in the same network, with overlaps around the principal sulcus. The VLPFC and DPFC are also connected with the OPFC and MPFC, respectively. Outside the prefrontal cortex, the VLPFC connects with specific areas related to somatic/visceral sensation and vision, in the frontoparietal operculum, insula, ventral bank/fundus of the superior temporal sulcus, inferior temporal gyrus, and inferior parietal cortex. In contrast, the DPFC connects with the rostral superior temporal gyrus, dorsal bank of the superior temporal sulcus, parahippocampal cortex, and posterior cingulate and retrosplenial cortex. Area 45a, in caudal VLPFC, is unique, having connections with all the networks. Its extrinsic connections resemble those of the DPFC. In addition, it has connections with both auditory belt/parabelt areas, and visual related areas. J. Comp. Neurol. 522:1641-1690, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Saleem, Kadharbatcha S.; Miller, Brad; Price, Joseph L.] Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA.
[Saleem, Kadharbatcha S.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
RP Saleem, KS (reprint author), NIMH, Neuropsychol Lab, 49 Convent Dr,Bldg 49,1B80 MSc 4415, Bethesda, MD 20892 USA.
EM saleemks@mail.nih.gov
OI Saleem, Kadharbatcha S/0000-0002-4450-9234
FU National Institutes of Health [MH70941]; McDonnell Center for Higher
Brain Function; National Institute of Mental Health Intramural Research
Program
FX Grant sponsor: National Institutes of Health; Grant number: MH70941;
Grant sponsor: McDonnell Center for Higher Brain Function; Grant
sponsor: National Institute of Mental Health Intramural Research
Program.
NR 155
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Z9 29
U1 5
U2 22
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9967
EI 1096-9861
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD MAY 1
PY 2014
VL 522
IS 7
BP 1641
EP 1690
DI 10.1002/cne.23498
PG 50
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA AD0HY
UT WOS:000332916300010
PM 24214159
ER
PT J
AU Dauter, Z
Wlodawer, A
Minor, W
Jaskolski, M
Rupp, B
AF Dauter, Zbigniew
Wlodawer, Alexander
Minor, Wladek
Jaskolski, Mariusz
Rupp, Bernhard
TI Avoidable errors in deposited macromolecular structures: an impediment
to efficient data mining
SO IUCRJ
LA English
DT Article
DE macromolecular crystallography; model validation; Protein Data Bank
ID PROTEIN DATA-BANK; VALIDATION TASK-FORCE; CRYSTAL-STRUCTURE;
CRYSTALLOGRAPHIC ANALYSIS; POWDER DIFFRACTION; DATA QUALITY; UNIT-CELL;
Z-DNA; RESOLUTION; BINDING
AB Whereas the vast majority of the more than 85 000 crystal structures of macromolecules currently deposited in the Protein Data Bank are of high quality, some suffer from a variety of imperfections. Although this fact has been pointed out in the past, it is still worth periodic updates so that the metadata obtained by global analysis of the available crystal structures, as well as the utilization of the individual structures for tasks such as drug design, should be based on only the most reliable data. Here, selected abnormal deposited structures have been analysed based on the Bayesian reasoning that the correctness of a model must be judged against both the primary evidence as well as prior knowledge. These structures, as well as information gained from the corresponding publications (if available), have emphasized some of the most prevalent types of common problems. The errors are often perfect illustrations of the nature of human cognition, which is frequently influenced by preconceptions that may lead to fanciful results in the absence of proper validation. Common errors can be traced to negligence and a lack of rigorous verification of the models against electron density, creation of non-parsimonious models, generation of improbable numbers, application of incorrect symmetry, illogical presentation of the results, or violation of the rules of chemistry and physics. Paying more attention to such problems, not only in the final validation stages but during the structure-determination process as well, is necessary not only in order to maintain the highest possible quality of the structural repositories and databases but most of all to provide a solid basis for subsequent studies, including large-scale data-mining projects. For many scientists PDB deposition is a rather infrequent event, so the need for proper training and supervision is emphasized, as well as the need for constant alertness of reason and critical judgment as absolutely necessary safeguarding measures against such problems. Ways of identifying more problematic structures are suggested so that their users may be properly alerted to their possible shortcomings.
C1 [Dauter, Zbigniew] NCI, Synchrotron Radiat Res Sect, Macromol Crystallog Lab, Argonne Natl Lab, Argonne, IL 60439 USA.
[Wlodawer, Alexander] NCI, Prot Struct Sect, Macromol Crystallog Lab, Frederick, MD 21702 USA.
[Minor, Wladek] Univ Virginia, Dept Mol Physiol & Biol Phys, Charlottesville, VA 22908 USA.
[Minor, Wladek] Midwest Ctr Struct Genom, Argonne, IL USA.
[Minor, Wladek] New York Struct Genom Consortium, New York, NY USA.
[Minor, Wladek] Ctr Struct Genom Infect Dis, Seattle, WA USA.
[Minor, Wladek] Enzyme Funct Initiat, Urbana, IL USA.
[Jaskolski, Mariusz] Adam Mickiewicz Univ, Fac Chem, Dept Crystallog, Poznan, Poland.
[Jaskolski, Mariusz] Polish Acad Sci, Inst Bioorgan Chem, Ctr Biocrystallog Res, Poznan, Poland.
[Rupp, Bernhard] KK Hofkristallamt, Vista, CA 92084 USA.
[Rupp, Bernhard] Med Univ Innsbruck, Dept Genet Epidemiol, A-6020 Innsbruck, Austria.
RP Dauter, Z (reprint author), NCI, Synchrotron Radiat Res Sect, Macromol Crystallog Lab, Argonne Natl Lab, Argonne, IL 60439 USA.
EM dauter@anl.gov
OI Minor, Wladek/0000-0001-7075-7090
FU NIH, National Cancer Institute, Center for Cancer Research; European
Union [PIIF-GA-2011-300025]; National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Department of Health
and Human Services [HHSN272201200026C]; NIH [GM094662, GM093342,
GM053163, GM094585]
FX The authors wish to thank Szymon Krzywda, Mirek Gilski, Ivan Shabalin
and Marcin Cymborowski for help in the preparation of some of the data
used as examples. This work was supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research (ZD and AW). BR acknowledges support from the European
Union under a FP7 Marie Curie People Action, grant PIIF-GA-2011-300025
(SAXCESS). WM was supported by federal funds from the National Institute
of Allergy and Infectious Diseases, National Institutes of Health,
Department of Health and Human Services under Contract No.
HHSN272201200026C and by NIH grants GM094662, GM093342, GM053163 and
GM094585.
NR 84
TC 29
Z9 29
U1 2
U2 12
PU INT UNION CRYSTALLOGRAPHY
PI CHESTER
PA 2 ABBEY SQ, CHESTER, CH1 2HU, ENGLAND
SN 2052-2525
J9 IUCRJ
JI IUCrJ
PD MAY
PY 2014
VL 1
BP 179
EP 193
DI 10.1107/S2052252514005442
PN 3
PG 15
WC Chemistry, Multidisciplinary; Crystallography; Materials Science,
Multidisciplinary
SC Chemistry; Crystallography; Materials Science
GA CL3QA
UT WOS:000356864000007
PM 25075337
ER
PT J
AU Ehsani, JP
Bingham, CR
Ionides, E
Childers, D
AF Ehsani, Johnathon P.
Bingham, C. Raymond
Ionides, Edward
Childers, David
TI The Impact of Michigan's Text Messaging Restriction on Motor Vehicle
Crashes
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Motor vehicle crashes; Texting; Restriction; Law; Distraction;
Adolescent driver
AB Purpose: The purpose of this study was to determine the effects of Michigan's universal text messaging restriction (effective July 2010) across different age groups of drivers and crash severities.
Methods: Changes in monthly crash rates and crash trends per 10,000 licensed drivers aged 16, 17, 18, 19, 20-24, and 25-50 years were estimated using time series analysis for three levels of crash severity: (1) fatal/disabling injury; (2) nondisabling injury; and (3) possible injury/property damage only (PDO) crashes for the period 2005-2012. Analyses were adjusted for crash rates of drivers' aged 65-99 years, Michigan's unemployment rate, and gasoline prices.
Results: After the introduction of the texting restriction, significant increases were observed in crash rates and monthly trends in fatal/disabling injury crashes and nondisabling injury crashes, and significant decreases in possible injury/PDO crashes. The magnitude of the effects where significant changes were observed was small.
Conclusions: The introduction of the texting restriction was not associated with a reduction in crash rates or trends in severe crash types. On the contrary, small increases in the most severe crash types (fatal/disabling and nondisabling injury) and small decreases in the least severe crash types (possible injury/PDO) were observed. These findings extend the literature on the effects of cell phone restrictions by examining the effects of the restriction on newly licensed adolescent drivers and adult drivers separately by crash severity. Published by Elsevier Inc. on behalf of Society for Adolescent Health and Medicine.
C1 [Ehsani, Johnathon P.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hlth Behav Branch, Div Intramural Populat Hlth Res, Bethesda, MD USA.
[Bingham, C. Raymond] Univ Michigan, Transportat Res Inst, Young Driver Behav & Injury Prevent Grp, Ann Arbor, MI 48109 USA.
[Bingham, C. Raymond] Univ Michigan, Sch Publ Hlth, Dept Hlth Behav & Hlth Educ, Ann Arbor, MI 48109 USA.
[Ionides, Edward] Univ Michigan, Dept Stat, Coll Literature Sci & Arts, Ann Arbor, MI 48109 USA.
[Childers, David] Univ Michigan, Ctr Stat Consultat & Res, Ann Arbor, MI 48109 USA.
RP Ehsani, JP (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
EM johnathon.ehsani@nih.gov
FU University of Michigan Injury Center; National Center for Injury
Prevention and Control of the Centers for Disease Control and Prevention
FX The University of Michigan Injury Center and the National Center for
Injury Prevention and Control of the Centers for Disease Control and
Prevention provided support for this research.
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
EI 1879-1972
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD MAY
PY 2014
VL 54
IS 5
SU S
BP S68
EP S74
DI 10.1016/j.jadohealth.2014.01.003
PG 7
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA V43TA
UT WOS:000209702500010
PM 24759444
ER
PT J
AU Falk, EB
Cascio, CN
O'Donnell, MB
Carp, J
Tinney, FJ
Bingham, CR
Shope, JT
Ouimet, MC
Pradhan, AK
Simons-Morton, BG
AF Falk, Emily B.
Cascio, Christopher N.
O'Donnell, Matthew Brook
Carp, Joshua
Tinney, Francis J., Jr.
Bingham, C. Raymond
Shope, Jean T.
Ouimet, Marie Claude
Pradhan, Anuj K.
Simons-Morton, Bruce G.
TI Neural Responses to Exclusion Predict Susceptibility to Social Influence
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Adolescent behavior; Risk taking; Driving; Social exclusion; Social
influence; Peer influence; Social pain; Mentalizing; fMRI; Neuroimaging
AB Purpose: Social influence is prominent across the lifespan, but sensitivity to influence is especially high during adolescence and is often associated with increased risk taking. Such risk taking can have dire consequences. For example, in American adolescents, traffic-related crashes are leading causes of nonfatal injury and death. Neural measures may be especially useful in understanding the basic mechanisms of adolescents' vulnerability to peer influence.
Methods: We examined neural responses to social exclusion as potential predictors of risk taking in the presence of peers in recently licensed adolescent drivers. Risk taking was assessed in a driving simulator session occurring approximately 1 week after the neuroimaging session.
Results: Increased activity in neural systems associated with the distress of social exclusion and mentalizing during an exclusion episode predicted increased risk taking in the presence of a peer (controlling for solo risk behavior) during a driving simulator session outside the neuroimaging laboratory 1 week later. These neural measures predicted risky driving behavior above and beyond self-reports of susceptibility to peer pressure and distress during exclusion.
Conclusions: These results address the neural bases of social influence and risk taking; contribute to our understanding of social and emotional function in the adolescent brain; and link neural activity in specific, hypothesized, regions to risk-relevant outcomes beyond the neuroimaging laboratory. Results of this investigation are discussed in terms of the mechanisms underlying risk taking in adolescents and the public health implications for adolescent driving. (C) 2014 Society for Adolescent Health and Medicine.
C1 [Falk, Emily B.; Cascio, Christopher N.; O'Donnell, Matthew Brook] Univ Penn, Annenberg Sch Commun, 3620 Walnut St, Philadelphia, PA 19104 USA.
[Carp, Joshua] Univ Michigan, Dept Psychol, Ann Arbor, MI USA.
[Tinney, Francis J., Jr.] Univ Michigan, Inst Social Res, Ann Arbor, MI USA.
[Bingham, C. Raymond; Shope, Jean T.; Pradhan, Anuj K.] Univ Michigan, UMTRI, Ann Arbor, MI 48109 USA.
[Ouimet, Marie Claude] Univ Sherbrooke, Fac Med & Hlth Sci, Longueuil, PQ, Canada.
[Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hlth Behav Branch, Bethesda, MD USA.
RP Falk, EB (reprint author), Univ Penn, Annenberg Sch Commun, 3620 Walnut St, Philadelphia, PA 19104 USA.
EM falk@asc.upenn.edu
OI Pradhan, Anuj/0000-0002-7612-4208; Simons-Morton,
Bruce/0000-0003-1099-6617
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HHSN275201000007 C]; University of Michigan Injury Center
Pilot Grant
FX The research was supported by the intramural research program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development contract # HHSN275201000007 C (PI: Bingham) and the
University of Michigan Injury Center Pilot Grant (PI: Falk).
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
EI 1879-1972
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD MAY
PY 2014
VL 54
IS 5
SU S
BP S22
EP S31
DI 10.1016/j.jadohealth.2013.12.035
PG 10
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA V43TA
UT WOS:000209702500005
PM 24759437
ER
PT J
AU Pradhan, AK
Li, KG
Bingham, CR
Simons-Morton, BG
Ouimet, MC
Shope, JT
AF Pradhan, Anuj K.
Li, Kaigang
Bingham, C. Raymond
Simons-Morton, Bruce G.
Ouimet, Marie Claude
Shope, Jean T.
TI Peer Passenger Influences on Male Adolescent Drivers' Visual Scanning
Behavior During Simulated Driving
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Adolescent driver; Peer passenger; Driving simulation; Eye tracking;
Distraction
AB Purpose: There is a higher likelihood of crashes and fatalities when an adolescent drives with peer passengers, especially for male drivers and male passengers. Simulated driving of male adolescent drivers with male peer passengers was studied to examine passenger influences on distraction and inattention.
Methods: Male adolescents drove in a high-fidelity driving simulator with a male confederate who posed either as a risk-accepting passenger or as a risk-averse passenger. Drivers' eye movements were recorded. The visual scanning behavior of the drivers was compared when driving alone with when driving with a passenger and when driving with a risk-accepting passenger with a risk-averse passenger.
Results: The visual scanning of a driver significantly narrowed horizontally and vertically when driving with a peer passenger. There were no significant differences in the times the drivers' eyes were off the forward roadway when driving with a passenger versus when driving alone. Some significant correlations were found between personality characteristics and the outcome measures.
Conclusions: The presence of a male peer passenger was associated with a reduction in the visual scanning range of male adolescent drivers. This reduction could be a result of potential cognitive load imposed on the driver due to the presence of a passenger and the real or perceived normative influences or expectations from the passenger. (C) 2014 Society for Adolescent Health and Medicine.
C1 [Pradhan, Anuj K.; Bingham, C. Raymond; Shope, Jean T.] Univ Michigan, Transportat Res Inst, 2901 Baxter Rd, Ann Arbor, MI 48109 USA.
[Li, Kaigang; Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Bethesda, MD USA.
[Ouimet, Marie Claude] Univ Sherbrooke, Sherbrooke, PQ J1K 2R1, Canada.
RP Pradhan, AK (reprint author), Univ Michigan, Transportat Res Inst, 2901 Baxter Rd, Ann Arbor, MI 48109 USA.
EM anujkp@umich.edu
OI Pradhan, Anuj/0000-0002-7612-4208; Simons-Morton,
Bruce/0000-0003-1099-6617
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development [HHSN275201000007C]
FX This research was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, contract # HHSN275201000007C.
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
EI 1879-1972
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD MAY
PY 2014
VL 54
IS 5
SU S
BP S42
EP S49
DI 10.1016/j.jadohealth.2014.01.004
PG 8
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA V43TA
UT WOS:000209702500007
PM 24759440
ER
PT J
AU Simons-Morton, BG
Guo, F
Klauer, SG
Ehsani, JP
Pradhan, AK
AF Simons-Morton, Bruce G.
Guo, Feng
Klauer, Sheila G.
Ehsani, Johnathon P.
Pradhan, Anuj K.
TI Keep Your Eyes on the Road: Young Driver Crash Risk Increases According
to Duration of Distraction
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Adolescents; Risk taking; Cell phone use; Secondary task; Teenage
driver; Naturalistic driving methods
AB Purpose: Secondary task engagement that distracts the driver is a contributing factor to motor vehicle crashes among adults. However, the association between eye glance duration and crash risk with novice teenage drivers has not been determined.
Methods: Vehicles of 42 newly licensed teenage drivers were instrumented with cameras, accelerometers, Global Positioning System(s) (GPS), and other devices. Data were collected continuously for 18 months. Crashes and near crashes (CNCs) were identified by examining highly elevated gravitational force events. Video footage of the 6 seconds prior to each CNC and randomly sampled non-CNC road segments were coded for the duration of eye glances off the forward roadway and the presence of secondary task engagement. The likelihood (odds ratios) of CNC due to eye glance behavior was calculated by comparing the prevalence of secondary task engagement and duration of eyes off road prior to CNC with the prevalence and duration of eyes off road during non-CNC road segments.
Results: Crash risk increased with the duration of single longest glance during all secondary tasks (OR = 3.8 for > 2 s) and wireless secondary task engagement (OR = 5.5 for > 2 s). Single longest glance provided a more consistent estimate of crash risk than total time eyes off the forward roadway.
Conclusions: Those eye glances away from the forward roadway involving secondary tasks increased the likelihood of CNC. The longer the duration of eye glance away from the road the greater the risk, regardless of type of secondary task. Education and policy discouraging secondary task engagement, particularly for prolonged periods, is warranted. (C) 2014 Society for Adolescent Health and Medicine.
C1 [Simons-Morton, Bruce G.; Ehsani, Johnathon P.; Pradhan, Anuj K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Bethesda, MD 20892 USA.
[Guo, Feng; Klauer, Sheila G.] Virginia Tech Univ, Virginia Tech Transportat Inst, Blacksburg, VA USA.
RP Simons-Morton, BG (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Div Intramural Populat Hlth Res, 6100 Execut Blvd,Room 7B13M, Bethesda, MD 20892 USA.
EM mortonb@mail.nih.gov
OI Pradhan, Anuj/0000-0002-7612-4208
FU Foundation for Advancing Alcohol Responsibility
FX Publication of this article was supported by the Foundation for
Advancing Alcohol Responsibility. The opinions or views expressed in
this paper are those of the authors and do not necessarily represent the
official position of the Foundation for Advancing Alcohol
Responsibility.
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
EI 1879-1972
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD MAY
PY 2014
VL 54
IS 5
SU S
BP S61
EP S67
DI 10.1016/j.jadohealth.2013.11.021
PG 7
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA V43TA
UT WOS:000209702500009
PM 24759443
ER
PT J
AU Adkins, E
Wang, XL
Sproule, T
Christianson, G
Park, GJ
Carter, G
Morse, H
Roopenian, D
AF Adkins, Elisabeth
Wang, Xulong
Sproule, Thomas
Christianson, Gregory
Park, Giljun
Carter, Gregory
Morse, Herbert
Roopenian, Derry
TI A novel population of interleukin 21-producing pre-follicular T helper
cells develop spontaneously in young naive mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Adkins, Elisabeth; Wang, Xulong; Sproule, Thomas; Christianson, Gregory; Park, Giljun; Carter, Gregory; Roopenian, Derry] Jackson Lab, Bar Harbor, ME 04609 USA.
[Adkins, Elisabeth; Roopenian, Derry] Tufts Univ, Sackler Sch Grad Biomed Sci, Genet, Boston, MA 02111 USA.
[Morse, Herbert] NIAID, Virol & Cellular Immunol Sect, Immunogenet Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM3P.743
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000124
ER
PT J
AU Azzam, K
Madenspacher, J
Lai, LH
Gowdy, K
Clayton, N
Cunningham, W
Janardhan, K
Taylor, G
Fessler, M
AF Azzam, Kathleen
Madenspacher, Jennifer
Lai, Lihua
Gowdy, Kymberly
Clayton, Natasha
Cunningham, Willie
Janardhan, Kyathanahalli
Taylor, Gregory
Fessler, Michael
TI Irgm1 regulates the pulmonary innate immune response
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Azzam, Kathleen; Madenspacher, Jennifer; Lai, Lihua; Gowdy, Kymberly; Fessler, Michael] NIEHS, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
[Clayton, Natasha; Cunningham, Willie; Janardhan, Kyathanahalli] NIEHS, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
[Taylor, Gregory] Durham VA Med Ctr, Geriatr Res Educ & Clin Ctr, Durham, NC USA.
NR 0
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U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA MUC5P.864
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005045
ER
PT J
AU Baseler, W
O'Connor, G
McVicar, D
AF Baseler, Walter
O'Connor, Geraldine
McVicar, Daniel
TI Mitochondrial-mediated inflammasome activation controls production of
Hepatoma-derived IL-1 beta
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Baseler, Walter; O'Connor, Geraldine; McVicar, Daniel] NCI, Canc Inflammat Program, Frederick, MD 21701 USA.
NR 0
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U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM7P.942
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000160
ER
PT J
AU Basu, S
Bowen, B
Sheyach, E
AF Basu, Samik
Bowen, Britany
Sheyach, Ethan
TI Foxp3-mediated inhibition of Akt inhibits Glut1 expression in human T
regulatory cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Basu, Samik; Bowen, Britany; Sheyach, Ethan] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA14P.203
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005190
ER
PT J
AU Berkower, I
Virnik, K
Hockenbury, M
Rosati, M
Alicea, C
Valentin, A
Pavlakis, G
Felber, B
AF Berkower, Ira
Virnik, Konstantin
Hockenbury, Max
Rosati, Margherita
Alicea, Candido
Valentin, Antonio
Pavlakis, George
Felber, Barbara
TI Live attenuated rubella vectors express HIV Env and SIV Gag antigens in
the context of an acute infection and elicit high antibody titers,
memory B cells, and Gag specific CD8+T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Berkower, Ira; Virnik, Konstantin; Hockenbury, Max] US FDA, Ctr Biol, Bethesda, MD 20014 USA.
[Rosati, Margherita; Alicea, Candido; Valentin, Antonio; Pavlakis, George; Felber, Barbara] NCI, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VIR5P.1033
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005023
ER
PT J
AU Biragyn, A
Bodogai, M
Lee-Chang, C
AF Biragyn, Arya
Bodogai, Monica
Lee-Chang, Catalina
TI The central role of tumor-evoked Bregs in breast cancer metastasis as
inducers of metastasis-promoting Tregs and myeloid-derived suppressive
cells.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Biragyn, Arya; Bodogai, Monica; Lee-Chang, Catalina] NIA, Baltimore, MD 21224 USA.
RI Lee-Chang, Catalina/A-5580-2015
OI Lee-Chang, Catalina/0000-0002-7675-2124
NR 0
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U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM4P.903
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004043
ER
PT J
AU Boelte, K
Sen, S
Priel, DL
Lau, K
Cardone, M
Yoshimura, T
Barb, J
Joehanes, R
Accame, D
Teer, J
Singh, L
Adams, L
Zhang, XQ
Chowdhury, S
Johnson, A
Green, E
Mullikin, J
Kolodgie, F
Virmani, R
O'Donnell, C
Munson, P
Trinchieri, G
Kuhns, D
Biesecker, L
McVicar, D
AF Boelte, Kimberly
Sen, Shurjo
Priel, Debra Long
Lau, Karen
Cardone, Marco
Yoshimura, Teizo
Barb, Jennifer
Joehanes, Roby
Accame, David
Teer, Jamie
Singh, Larry
Adams, Lila
Zhang, XiaoQing
Chowdhury, Soma
Johnson, Andrew
Green, Eric
Mullikin, James
Kolodgie, Frank
Virmani, Renu
O'Donnell, Christopher
Munson, Peter
Trinchieri, Giorgio
Kuhns, Douglas
Biesecker, Leslie
McVicar, Daniel
TI TREML4 expression by myeloid cells may play a role in coronary artery
disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Boelte, Kimberly; Cardone, Marco; Yoshimura, Teizo; Trinchieri, Giorgio; McVicar, Daniel] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Sen, Shurjo; Accame, David; Singh, Larry; Green, Eric; Mullikin, James; Biesecker, Leslie] NHGRI, NIH, Bethesda, MD 20892 USA.
[Johnson, Andrew; O'Donnell, Christopher] NHLBI, NIH, Bethesda, MD 20892 USA.
[Chowdhury, Soma] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA.
[Adams, Lila; Zhang, XiaoQing; Kolodgie, Frank; Virmani, Renu] CVPath Inst, Gaithersburg, MD USA.
[Teer, Jamie] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Barb, Jennifer; Joehanes, Roby; Munson, Peter] NIH, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Priel, Debra Long; Lau, Karen; Kuhns, Douglas] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM1P.308
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000235
ER
PT J
AU Bolanos, RB
Sharma, A
Sultana, D
Chen, QH
Heller, N
Sen, J
AF Bolanos, Rosa Berga
Sharma, Archna
Sultana, Dil
Chen, Qinghua
Heller, Nicola
Sen, Jyoti
TI T Cell Factor-1 and beta-catenin specifically and critically control the
generation and function of T helper 2-type natural killer T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Bolanos, Rosa Berga; Sharma, Archna; Sultana, Dil; Chen, Qinghua; Sen, Jyoti] NIA, Immune Cells & Inflammat Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Heller, Nicola] Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA.
RI Sharma, Archna/R-9377-2016
OI Sharma, Archna/0000-0003-4745-0220
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM7P.725
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005222
ER
PT J
AU Bowen, S
Sharrow, S
Hodes, R
AF Bowen, Steven
Sharrow, Susan
Hodes, Richard
TI Hybrid V gamma-C beta TCR chains support T cell development and an
immunocompetent T cell repertoire
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Bowen, Steven; Sharrow, Susan; Hodes, Richard] NIH, Expt Immunol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM7P.713
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005230
ER
PT J
AU Chang, CL
Bodogai, M
Moritoh, K
Croft, M
Gress, R
Ferrucci, L
Hakim, F
Biragyn, A
AF Chang, Catalina Lee
Bodogai, Monica
Moritoh, Kanako
Croft, Michael
Gress, Ronald
Ferrucci, Luigi
Hakim, Fran
Biragyn, Arya
TI A novel aging-associate B-cell subset controls antitumor CD8+T-cell
response
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Chang, Catalina Lee; Bodogai, Monica; Moritoh, Kanako; Biragyn, Arya] NIH, Immunoregulat Sect, Lab Mol Biol & Immunol, Baltimore, MD USA.
[Croft, Michael] La Jolla Inst Allergy & Immunol, Div Immune Regulat, La Jolla, CA USA.
[Gress, Ronald] NCI, Translat Surg Pathol, NIH, Bethesda, MD 20892 USA.
[Ferrucci, Luigi] NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA.
[Hakim, Fran] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC3P.469
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004167
ER
PT J
AU Chen, GB
Solokina, A
Li, HF
Truong, T
Oelke, M
Wersto, R
Schneck, J
Leng, S
Weng, NP
AF Chen, Guobing
Solokina, Arina
Li, Huifen
Truong, Thai
Oelke, Mathias
Wersto, Robert
Schneck, Jonathan
Leng, Sean
Weng, Nan-ping
TI Different competency of CMV-pp65 or Flu-M1 specific CD8+T cells in naive
and central memory population in healthy human adults
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Chen, Guobing; Solokina, Arina; Truong, Thai; Wersto, Robert; Weng, Nan-ping] NIA, Baltimore, MD 21224 USA.
[Li, Huifen; Oelke, Mathias; Schneck, Jonathan; Leng, Sean] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RI Chen, Guobing/D-9572-2012
OI Chen, Guobing/0000-0002-2401-6168
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TRAN3P.885
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006145
ER
PT J
AU Chen, J
Feigenbaum, L
Awasthi, P
Butcher, D
Anver, M
Golubeva, Y
Bamford, R
Zhang, XJ
St Claire, M
Thomas, C
Discepolo, V
Jabri, B
Waldmann, T
AF Chen, Jing
Feigenbaum, Lionel
Awasthi, Parirokh
Butcher, Donna
Anver, Miriam
Golubeva, Yelena
Bamford, Richard
Zhang, XiaoJie
St Claire, Mark
Thomas, Craig
Discepolo, Valentina
Jabri, Bana
Waldmann, Thomas
TI Increased expression of IL-15 and IL-15Ra in the islets of patients with
T1D
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Chen, Jing; Waldmann, Thomas] NCI, Metab Branch, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel; Awasthi, Parirokh; Butcher, Donna; Anver, Miriam; Golubeva, Yelena] SAIC, Lab Anim Sci Program, Frederick, MD USA.
[Bamford, Richard] Transponics, Jacobus, PA USA.
[Zhang, XiaoJie; St Claire, Mark] NIDDK, Lab Anim Sci Sect, Bethesda, MD 20892 USA.
[Thomas, Craig] NHGRI, NIHchem Genom Ctr, Rockville, MD USA.
[Discepolo, Valentina; Jabri, Bana] Univ Chicago, Dept Pediat, Chicago, IL 60637 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR3P.217
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001158
ER
PT J
AU Chen, X
Xiao, HT
Howard, OMZ
Oppenheim, J
AF Chen, Xin
Xiao, Haitao
Howard, O. M. Zack
Oppenheim, Joost
TI TNFR2 expression by CD4 effector T cells is required to induce
full-fledged experimental colitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Chen, Xin] Leidos Biomed Resaerch Inc, Basic Sci Program, Frederick, MD USA.
[Chen, Xin; Xiao, Haitao; Howard, O. M. Zack; Oppenheim, Joost] NCI, Lab Mol Immunoregulat, Frederick, MD 21701 USA.
[Xiao, Haitao] Hong Kong Baptist Univ, Sch Chinese Med, Hong Kong, Hong Kong, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR3P.204
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001147
ER
PT J
AU Chiang, YP
Hodes, R
AF Chiang, Yungping
Hodes, Richard
TI Lck is essential in the non-canonical T cell receptor CR signaling
pathway regulated pressed by Cbl during T cell development
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Chiang, Yungping; Hodes, Richard] NCI, EIB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM7P.727
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005229
ER
PT J
AU Chong, WP
Chen, J
Silver, P
Caspi, R
AF Chong, Wai Po
Chen, Jun
Silver, Phyllis
Caspi, Rachel
TI Reciprocal interaction between NK cells and DCs regulates the Th17
response by controlling the innate IFN-gamma/IL-27 axis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Chong, Wai Po; Chen, Jun; Silver, Phyllis; Caspi, Rachel] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA13P.124
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005169
ER
PT J
AU Coligan, J
Tian, LJ
Margulies, D
Krzewski, K
Murakami, Y
AF Coligan, John
Tian, Linjie
Margulies, David
Krzewski, Konrad
Murakami, Yousuke
TI Mouse CD300b (CLM-7) regulates the phagocytosis of apoptotic cells via
phosphatidylserine recognition.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Coligan, John; Tian, Linjie; Krzewski, Konrad; Murakami, Yousuke] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Margulies, David] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA4P.215
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002199
ER
PT J
AU Cruse, G
Music, S
Bradding, P
Beaven, M
Metcalfe, D
AF Cruse, Glenn
Music, Stephen
Bradding, Peter
Beaven, Michael
Metcalfe, Dean
TI MS4A4 regulates KIT receptor trafficking, signaling and function in mast
cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Cruse, Glenn; Music, Stephen; Metcalfe, Dean] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Bradding, Peter] Univ Leicester, Infect Immun & Inflammat, Leicester, Leics, England.
[Beaven, Michael] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HYP3P.343
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003122
ER
PT J
AU Cruz, A
Ramaswamy, M
Sengupta, P
Lippincott-Schwartz, J
Siegel, R
AF Cruz, Anthony
Ramaswamy, Madhu
Sengupta, Prabhudda
Lippincott-Schwartz, Jennifer
Siegel, Richard
TI Palmitoylation is required for Fas receptor clustering and cell death in
CD4(+) T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Cruz, Anthony; Ramaswamy, Madhu; Siegel, Richard] NIAMS, NIH, Bethesda, MD USA.
[Sengupta, Prabhudda; Lippincott-Schwartz, Jennifer] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM7P.722
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005236
ER
PT J
AU Dambuza, I
Yu, CR
Wang, RX
Kim, SY
Mahdi, R
Dolinska, M
Sergeev, Y
Wingfield, P
Egwuagu, C
AF Dambuza, Ivy
Yu, Cheng-Rong
Wang, Ren-Xi
Kim, Sung-Ye
Mahdi, Rashid
Dolinska, Monika
Sergeev, Yuri
Wingfield, Paul
Egwuagu, Charles
TI IL-12p35 single chain subunit antagonizes IL-6 mediated STAT1 and STAT3
activation and prevents expansion of Th17 cells in experimental
autoimmune uveitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Dambuza, Ivy; Yu, Cheng-Rong; Wang, Ren-Xi; Kim, Sung-Ye; Mahdi, Rashid; Dolinska, Monika; Sergeev, Yuri; Egwuagu, Charles] NEI, Bethesda, MD 20892 USA.
[Wingfield, Paul] NIAMS, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR1P.246
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003014
ER
PT J
AU Edwards, J
Thornton, A
Shevach, E
AF Edwards, Justin
Thornton, Angela
Shevach, Ethan
TI Integrin beta 8 is a marker of mouse regulatory T-cells (Treg) and is
required for processing of latent TGF-beta 1 from the GARP/latent
TGF-beta 1 complex
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Edwards, Justin; Thornton, Angela; Shevach, Ethan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC4P.483
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005039
ER
PT J
AU Ferdinand, J
Meylan, F
Siegel, R
Al-Shamkhani, A
AF Ferdinand, John
Meylan, Francoise
Siegel, Richard
Al-Shamkhani, Aymen
TI The biological function of membrane versus soluble TL1A
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Ferdinand, John; Al-Shamkhani, Aymen] Univ Southampton, Canc Sci Div, Fac Med, Southampton, Hants, England.
[Ferdinand, John; Meylan, Francoise; Siegel, Richard] NIAMS, Immunoregulat Sect, Autoimmun Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR3P.205
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001154
ER
PT J
AU Filardy, A
He, JP
Silyeira, D
Kelsall, B
AF Filardy, Alessandra
He, JianPing
Silyeira, Danielle
Kelsall, Brian
TI Poor expression and activation of the NLRP3 inflammasome in resident but
not inflammatory colonic monocytes/macrophages
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Filardy, Alessandra; He, JianPing; Silyeira, Danielle; Kelsall, Brian] NIAID, Mucosal Immunobiol Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA MUC2P.831
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001187
ER
PT J
AU Frey, B
Sui, YJ
Wang, YC
Hogg, A
Yu, B
Berman, P
Berzofsky, J
AF Frey, Blake
Sui, Yongjun
Wang, Yichuan
Hogg, Alison
Yu, Bin
Berman, Phillip
Berzofsky, Jay
TI Modulating cathepsin cleavage sites in HIV gp 120 envelope protein
alters the cellular immune response.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Frey, Blake; Sui, Yongjun; Wang, Yichuan; Hogg, Alison; Berzofsky, Jay] NCI, Bethesda, MD 20892 USA.
[Yu, Bin; Berman, Phillip] Univ Calif Santa Cruz, Biomol Engn, Santa Cruz, CA 95064 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC7P.989
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002054
ER
PT J
AU Fujihara, C
Williams, J
Jeon, H
Hodes, R
AF Fujihara, Chiharu
Williams, Joy
Jeon, Hyein
Hodes, Richard
TI Cognate CD40-CD40L interaction is important for maintenance of thymic B
cells.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Fujihara, Chiharu; Williams, Joy; Jeon, Hyein; Hodes, Richard] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRM8P.705
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003240
ER
PT J
AU Ghosh, A
De, S
Bell, J
Weber, B
Wood, W
Becker, K
Sen, J
Bhandoola, A
Sen, R
AF Ghosh, Amalendu
De, Supriyo
Bell, Jeremiah
Weber, Brittany
Wood, William
Becker, Kevin
Sen, Jyoti
Bhandoola, Avinash
Sen, Ranjan
TI Generation and resolution of bivalent chromatin during hematopoiesis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Ghosh, Amalendu; De, Supriyo; Wood, William; Becker, Kevin; Sen, Jyoti; Sen, Ranjan] NIA, LMBI, Baltimore, MD 21224 USA.
[Bell, Jeremiah; Weber, Brittany; Bhandoola, Avinash] Univ Penn, Sch Med, Dept Pathol, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HEM2P.259
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001086
ER
PT J
AU Hart, G
Wei, CW
Chida, A
Crompton, P
Sanz, I
Pierce, S
AF Hart, Geoffrey
Wei, Chungwen
Chida, Asiya
Crompton, Peter
Sanz, Ignacio
Pierce, Susan
TI A B cell riddle: a new tool to study the link between malaria and
Burkitt's Lymphoma
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Hart, Geoffrey; Crompton, Peter; Pierce, Susan] NIAID, NIH, Rockville, MD USA.
[Wei, Chungwen; Chida, Asiya; Sanz, Ignacio] Emory Univ, Atlanta, GA 30322 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM5P.935
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003073
ER
PT J
AU Hataye, J
Casazza, J
Ambrozak, D
Boritz, E
Yamamoto, T
Douek, D
Koup, R
AF Hataye, Jason
Casazza, Joseph
Ambrozak, David
Boritz, Eli
Yamamoto, Takuya
Douek, Daniel
Koup, Richard
TI A scalable RNA RT-PCR based assay to quantify latency disruption in
HIV-1 infected cells from patients on antiretroviral therapy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Hataye, Jason; Casazza, Joseph; Ambrozak, David; Boritz, Eli; Yamamoto, Takuya; Douek, Daniel; Koup, Richard] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VIR1P.1001
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005006
ER
PT J
AU Hathcock, K
Padilia-Nash, H
Camps, J
Triner, D
Shin, DM
Maul, R
Gearhart, P
Morse, H
Ried, T
Hodes, R
AF Hathcock, Karen
Padilia-Nash, Hesed
Camps, Jordi
Triner, Daniel
Shin, Dong-Mi
Maul, Robert
Gearhart, Patricia
Morse, Herbert
Ried, Thomas
Hodes, Richard
TI ATM-deficiency in the absence of T cells promotes the development of B
cell lymphomas with dependence on NF-kappa B
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Hathcock, Karen; Padilia-Nash, Hesed; Camps, Jordi; Triner, Daniel; Shin, Dong-Mi; Maul, Robert; Gearhart, Patricia; Morse, Herbert; Ried, Thomas; Hodes, Richard] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM7P.927
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000153
ER
PT J
AU Hayashi, T
Hu, YQ
Furukawa, K
Ohishi, W
Geyer, S
Weng, NP
Hayashi, I
Yoshida, K
Kajimura, J
Kyoizumi, S
Kusunoki, Y
Nakachi, K
AF Hayashi, Tomonori
Hu, Yiqun
Furukawa, Kyoji
Ohishi, Waka
Geyer, Susan
Weng, Nan-ping
Hayashi, Ikue
Yoshida, Kengo
Kajimura, Junko
Kyoizumi, Seishi
Kusunoki, Yoichiro
Nakachi, Kei
TI The association of ROS levels in blood cells with age, past radiation
exposure, and IL6R gene polymorphisms
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Hayashi, Tomonori; Hu, Yiqun; Hayashi, Ikue; Yoshida, Kengo; Kajimura, Junko; Kyoizumi, Seishi; Kusunoki, Yoichiro; Nakachi, Kei] Radiat Effects Res Fdn, Dept Radiobiol Mol Epidemiol, Hiroshima, Japan.
[Furukawa, Kyoji] Radiat Effects Res Fdn, Dept Stat, Hiroshima, Japan.
[Ohishi, Waka] Radiat Effects Res Fdn, Dept Clin Studies, Hiroshima, Japan.
[Geyer, Susan] Ohio State Univ, Dept Internal Med, Div Hematol, Columbus, OH 43210 USA.
[Weng, Nan-ping] NIA, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
[Hayashi, Ikue] Hiroshima Univ, Fac Dent, Hiroshima, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR3P.211
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001164
ER
PT J
AU Herz, J
McGavern, D
AF Herz, Jasmin
McGavern, Dorian
TI Therapeutic clearance of the virally infected nervous system via
noncytopathic T cell interactions with resident myeloid cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Herz, Jasmin; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC6P.945
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000071
ER
PT J
AU Highfill, S
Smith, J
Long, A
Cui, YZ
Orentas, R
Mackail, C
AF Highfill, Steven
Smith, Jillian
Long, Adrienne
Cui, Yongzhi
Orentas, Rimas
Mackail, Crystal
TI Neutralization of murine myeloid suppressor cells enhances the efficacy
of GD2-specific CAR T cells directed against human sarcoma in a
xenograft model
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Highfill, Steven; Smith, Jillian; Long, Adrienne; Cui, Yongzhi; Orentas, Rimas; Mackail, Crystal] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC11P1010
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000083
ER
PT J
AU Hodge, D
Berthet, C
Coppola, V
Kastenmuller, W
Buschman, M
Shirota, H
Schaughency, P
Anver, M
Della Reynolds,
Sanford, M
Kaldis, P
Young, H
AF Hodge, Deborah
Berthet, Cyril
Coppola, Vincenzo
Kastenmueller, Wolfgang
Buschman, Matthew
Shirota, Hidekazu
Schaughency, Paul
Anver, Miriam
Reynolds, Della
Sanford, Michael
Kaldis, Philipp
Young, Howard
TI Autoimmunity in interferon-gamma AU-rich element deleted-mice is
associated with loss of marginal zone B cells and macrophages.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Hodge, Deborah; Reynolds, Della; Sanford, Michael; Young, Howard] NCI, Frederick, MD 21701 USA.
[Berthet, Cyril] Oncodesign, Dijon, France.
[Coppola, Vincenzo] Ohio State Univ, Immunol & Med Genet, Columbus, OH 43210 USA.
[Buschman, Matthew] Univ Calif San Diego, San Diego, CA 92103 USA.
[Anver, Miriam] Leidos Biomed Res, Frederick, MD USA.
[Kaldis, Philipp] Agcy Sci Technol & Res, Singapore, Singapore.
[Kastenmueller, Wolfgang] Univ Bonn, Bonn, Germany.
[Shirota, Hidekazu] Tohoku Univ Hosp, Sendai, Miyagi, Japan.
[Schaughency, Paul] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA15P.217
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002247
ER
PT J
AU Indramohan, M
Break, T
Witter, A
Berg, R
AF Indramohan, Mohanalaxmi
Break, Timothy
Witter, Alexandra
Berg, Rance
TI The role of IL-23 in regulating the function of phagocytic cells during
Listeria monocytogenes infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Indramohan, Mohanalaxmi; Witter, Alexandra; Berg, Rance] Univ North Texas, Hlth Sci Ctr, Cell Biol & Immunol, Ft Worth, TX USA.
[Break, Timothy] NIAID, Fungal Pathogenesis Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA MPF3P.822
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002174
ER
PT J
AU Jain, S
Adkins, E
McPhee, C
Christianson, G
Sproule, T
Shin, DM
Roopenian, D
Morse, H
AF Jain, Shweta
Adkins, Elisabeth
McPhee, Caroline
Christianson, Gregory
Sproule, Thomas
Shin, Dong-Mi
Roopenian, Derry
Morse, Herbert
TI Intricate interplay of cytokines determine the progression of SLE-like
disease in BXSB.Yaa mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Jain, Shweta; Shin, Dong-Mi; Morse, Herbert] NIAID, Lab Immunogenet, NIH, Rockville, MD USA.
[Adkins, Elisabeth; McPhee, Caroline; Christianson, Gregory; Sproule, Thomas; Roopenian, Derry] Jackson Labs, Bar Harbor, ME USA.
[Shin, Dong-Mi] Seoul Natl Univ, Dept Food & Nutr, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA12P.104
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002142
ER
PT J
AU Janelsins, B
Datta, S
AF Janelsins, Brian
Datta, Sandip
TI Altered inactivation of commensal LPS due to acyloxyacyl hydrolase
deficiency in colonic dendritic cells impairs mucosal Th17 immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Janelsins, Brian; Datta, Sandip] NIAID, Bacterial Pathogenesis Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA MUC4P.825
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003206
ER
PT J
AU Jeon, H
Williams, J
Hodes, R
AF Jeon, Hyein
Williams, Joy
Hodes, Richard
TI Cell types important for fostering normal thymic medullary epithelial
cell development
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Jeon, Hyein; Williams, Joy; Hodes, Richard] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HEM4P.242
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005113
ER
PT J
AU Jones, J
Brandmaier, A
Umetsu, S
Bu, X
Umetsu, D
DeKruyff, R
Freeman, G
AF Jones, Jennifer
Brandmaier, Andrew
Umetsu, Sarah
Bu, Xia
Umetsu, Dale
DeKruyff, Rosemarie
Freeman, Gordon
TI Evolutionary origins and structural analysis of phosphatidylserine
binding by the TIM gene family
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Jones, Jennifer; Brandmaier, Andrew] NCI, NIH, Bethesda, MD 20892 USA.
[Bu, Xia; Freeman, Gordon] DFCI, Boston, MA USA.
[Umetsu, Sarah] UCSF, San Francisco, CA USA.
[Umetsu, Dale; DeKruyff, Rosemarie] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CAM5P.244
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002110
ER
PT J
AU Kamiyama, R
Yoshimi, R
Tsukahara, T
Ueda, A
Takeno, M
Ozato, K
Ishigatsubo, Y
AF Kamiyama, Reikou
Yoshimi, Ryusuke
Tsukahara, Toshinori
Ueda, Atsuhisa
Takeno, Mitsuhiro
Ozato, Keiko
Ishigatsubo, Yoshiyuki
TI The dysfunction of the E3 ubiquitin ligase TRIM21 in systemic lupus
erythematosus
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kamiyama, Reikou; Yoshimi, Ryusuke; Tsukahara, Toshinori; Ueda, Atsuhisa; Takeno, Mitsuhiro; Ishigatsubo, Yoshiyuki] Yokohama City Univ, Grad Sch Med, Dept Internal Med & Clin Immunol, Yokohama, Kanagawa, Japan.
[Ozato, Keiko] NICHHD, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM7P.301
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000209
ER
PT J
AU Kapnick, S
Schwartzberg, P
AF Kapnick, Senta
Schwartzberg, Pamela
TI Investigating the role of inducible T cell kinase in CD8+T-lymphocyte
cytolytic effector function
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kapnick, Senta; Schwartzberg, Pamela] NHGRI, GDRB, NIH, Bethesda, MD 20892 USA.
[Kapnick, Senta] Johns Hopkins Univ, CMDB, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM8P.343
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002019
ER
PT J
AU Kato, S
Terabe, M
Berzofsky, J
AF Kato, Shingo
Terabe, Masaki
Berzofsky, Jay
TI Liver sulfatide-reactive type II NKT cells recognize endogenous
phospholipids
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kato, Shingo; Terabe, Masaki; Berzofsky, Jay] NCI, Mol Immunogenet & Vaccine Res Sect, Vaccine Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INC9P.445
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003045
ER
PT J
AU Kim, JW
Subedi, K
Wersto, R
Zhao, KJ
Peng, WQ
Weng, NP
AF Kim, Jiewan
Subedi, Kalpana
Wersto, Robert
Zhao, Keji
Peng, Weiqun
Weng, Nan-ping
TI The role of genes with bivalent chromatin in memory CD8 T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kim, Jiewan; Subedi, Kalpana; Wersto, Robert; Weng, Nan-ping] NIA, LMBI, NIH, Baltimore, MD 21224 USA.
[Zhao, Keji] NHLBI, Lab Epigenome Biol, NIH, Bethesda, MD 20892 USA.
[Peng, Weiqun] George Washington Univ, Dept Phys, Washington, DC 20052 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRM4P.496
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004017
ER
PT J
AU Kines, R
Cuburu, N
Kobayashi, H
MacDougall, J
de los Pinos, E
Schiller, J
AF Kines, Rhonda
Cuburu, Nicolas
Kobayashi, Hisataka
MacDougall, John
de los Pinos, Elisabet
Schiller, John
TI HPV based photodynamic therapy: a new approach for anti-cancer therapy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kines, Rhonda; MacDougall, John; de los Pinos, Elisabet] Aura Biosci, Cambridge, MA USA.
[Kines, Rhonda; Cuburu, Nicolas; Schiller, John] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
[Kobayashi, Hisataka] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC12P1019
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002012
ER
PT J
AU Kovacs, S
Sheikh, V
Rupert, A
Thompson, W
Estes, J
Sandler, N
Roby, G
Freeman, A
Sereti, I
AF Kovacs, Stephen
Sheikh, Virginia
Rupert, Adam
Thompson, William
Estes, Jacob
Sandler, Netanya
Roby, Gregg
Freeman, Alexandra
Sereti, Irini
TI Evidence of T cell lymphopenia in the colonic mucosa in idiopathic CD4
lymphocytopenia patients
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kovacs, Stephen] Leidos Biomed Res Inc, Lab Immunoregulat, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Sheikh, Virginia; Thompson, William; Roby, Gregg; Freeman, Alexandra; Sereti, Irini] NIAID, NIH, Bethesda, MD 20892 USA.
[Rupert, Adam] Leidos Biomed Res Inc, AIDS Monitoring Lab, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Estes, Jacob] Leidos Biomed Res Inc, Retroviral Immunopathol Sect, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Sandler, Netanya] Univ Texas Med Branch, Infect Dis Sect, Galveston, TX 77555 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HEM4P.250
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003021
ER
PT J
AU Kwong, B
McGavern, D
Lazarevic, V
AF Kwong, Brandon
McGavern, Dorian
Lazarevic, Vanja
TI Pathogenicity of autoreactive Th17 cells is dependent on T-bet
expression in non-T-helper cells in experimental autoimmune
encephalomyelitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kwong, Brandon; Lazarevic, Vanja] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[McGavern, Dorian] NINDS, Viral Immunol & Intravital Imaging Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA13P.117
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005162
ER
PT J
AU Lazarevic, V
Wang, Y
Godec, J
Ben-Aissa, K
Cui, K
Zhao, K
Pucsek, A
Weaver, C
Yagi, R
AF Lazarevic, Vanja
Wang, Yan
Godec, Jernej
Ben-Aissa, Khadija
Cui, Kairong
Zhao, Keji
Pucsek, Alexandra
Weaver, Casey
Yagi, Ryoji
TI T-bet and Runx transcription factors are required for the ontogeny of
pathogenic IFN gamma-producing Th17 cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Lazarevic, Vanja; Wang, Yan; Ben-Aissa, Khadija] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Godec, Jernej] Harvard Med Sch, Dept Microbiol & Immunobiol, Boston, MA USA.
[Cui, Kairong; Zhao, Keji] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Pucsek, Alexandra] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Weaver, Casey] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA.
[Yagi, Ryoji] Chiba Univ, Dept Immunol, Chiba, Japan.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM3P.729
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000122
ER
PT J
AU Le Saout, C
Hasley, R
Imamichi, H
Tcheung, L
Hu, Z
Luckey, M
Park, JH
Durum, S
Smith, M
Rupert, A
Sneller, M
Lane, HC
Catalfamo, M
AF Le Saout, Cecile
Hasley, Rebecca
Imamichi, Hiromi
Tcheung, Lueng
Hu, Zonghui
Luckey, Megan
Park, Jung-Hyun
Durum, Scott
Smith, Mindy
Rupert, Adam
Sneller, Michael
Lane, H. Clifford
Catalfamo, Marta
TI IL-7/Lymphopenia enhanced Type-I IFN response by modulating STAT-1
levels: its impact in CD4 T cell homeostasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Le Saout, Cecile; Hasley, Rebecca; Imamichi, Hiromi; Tcheung, Lueng; Smith, Mindy; Sneller, Michael; Lane, H. Clifford; Catalfamo, Marta] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Hu, Zonghui] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Luckey, Megan; Park, Jung-Hyun] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Durum, Scott] NCI, Lab Immunoregulat, NIH, Bethesda, MD 20892 USA.
[Rupert, Adam] SAIC, AIDS Monitoring Labs, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM8P.338
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002045
ER
PT J
AU Leger, AS
Karauzum, H
Datta, S
Caspi, R
AF Leger, Anthony St.
Karauzum, Hatice
Datta, Sandip
Caspi, Rachel
TI A new model to study mucosal immunity at the ocular surface
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Leger, Anthony St.; Caspi, Rachel] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Karauzum, Hatice; Datta, Sandip] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA MUC7P.758
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004147
ER
PT J
AU Lerman, Y
Sarangi, P
Hyun, YM
Lim, K
Falkner, K
Pietropaoli, A
Kim, M
AF Lerman, Yelena
Sarangi, Pranita
Hyun, Young-Min
Lim, Kihong
Falkner, Kathleen
Pietropaoli, Anthony
Kim, Minsoo
TI Exacerbated tissue homing of neutrophils during sepsis and TLR2-induced
cytokine production are regulated by integrin alpha 3 beta 1.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Lerman, Yelena; Sarangi, Pranita; Hyun, Young-Min; Lim, Kihong; Falkner, Kathleen; Pietropaoli, Anthony; Kim, Minsoo] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
[Sarangi, Pranita] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CAM5P.230
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002114
ER
PT J
AU Li, WQ
Xiao, Z
Ravichandran, S
Luke, B
Collins, J
Durum, S
AF Li, Wenqing
Xiao, Zhen
Ravichandran, Sarangan
Luke, Brian
Collins, Jack
Durum, Scott
TI Role of lysine dimethylation in Bcl-2 function and T cell activation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Li, Wenqing; Durum, Scott] NCI, Canc & Inflammat Program, CCR, NIH, Frederick, MD 21701 USA.
[Xiao, Zhen] NCI, Lab Prote & Alalyt Technol, SAIC Frederick Inc, NIH, Frederick, MD 21701 USA.
[Ravichandran, Sarangan; Luke, Brian; Collins, Jack] NCI, Adv Biomed Comp Ctr, Informat Syst Program, SAIC Frederick Inc,NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM4P.744
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005136
ER
PT J
AU Ligons, D
Sato, N
Park, JH
AF Ligons, Davinna
Sato, Noriko
Park, Jung-Hyun
TI CD103 downregulation marks memory-phenotype CD8 T cells and excludes
them from the gut
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Ligons, Davinna; Park, Jung-Hyun] NCI, Expt Immunol Branch, Bethesda, MD 20892 USA.
[Sato, Noriko] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CAM1P.231
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003098
ER
PT J
AU Lin, B
Fraser, L
AF Lin, Bin
Fraser, Lain
TI Investigating the mechanism of TLR signaling crosstalk in mouse
macrophages
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Lin, Bin; Fraser, Lain] NIAID, Signaling Syst Unit, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRM5P.702
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004228
ER
PT J
AU Liu, Q
Li, ZZ
Gao, JL
Wan, WZ
McDermott, D
Murphy, P
AF Liu, Qian
Li, Zhanzhuo
Gao, Ji-Liang
Wan, Wuzhou
McDermott, David
Murphy, Philip
TI CXCR4 antagonist AMD3100 mobilizes leukocytes from bone marrow and
thymus to blood in mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Liu, Qian; Li, Zhanzhuo; Gao, Ji-Liang; Wan, Wuzhou; McDermott, David; Murphy, Philip] NIAID, Lab Mol Immunol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HEM2P.265
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001088
ER
PT J
AU Liu, Y
Biancotto, A
Huang, Y
Gadina, M
McCoy, JP
Goldbach-Mansky, R
AF Liu, Yin
Biancotto, Angelique
Huang, Yan
Gadina, Massimo
McCoy, John Philip
Goldbach-Mansky, Rapheala
TI Proteasome defects in candle patients' cells lead to IFN production in
both hemopoietic and non-hemopoietic cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Liu, Yin; Huang, Yan; Goldbach-Mansky, Rapheala] NIAMS, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD USA.
[Biancotto, Angelique; McCoy, John Philip] NHLBI, NIH, Bethesda, MD 20892 USA.
[Gadina, Massimo] NIAMS, Off Sci & Technol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INM6P.416
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002090
ER
PT J
AU Lu, YC
Yao, X
Crystal, J
Li, Y
El-Gamil, M
Gross, C
Davis, L
Dudley, M
Yang, J
Samuels, Y
Rosenberg, S
Robbins, P
AF Lu, Yong-Chen
Yao, Xin
Crystal, Jessica
Li, Yong
El-Gamil, Mona
Gross, Colin
Davis, Lindy
Dudley, Mark
Yang, James
Samuels, Yardena
Rosenberg, Steven
Robbins, Paul
TI Efficient identification of mutated cancer antigens recognized by T
cells associated with durable tumor regressions
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Lu, Yong-Chen; Yao, Xin; Crystal, Jessica; Li, Yong; El-Gamil, Mona; Gross, Colin; Davis, Lindy; Dudley, Mark; Yang, James; Rosenberg, Steven; Robbins, Paul] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Samuels, Yardena] Weizmann Inst Sci, Mol Cell Biol, Rehovot, Israel.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM2P.878
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001226
ER
PT J
AU Lucas, C
Lenardo, M
AF Lucas, Carrie
Lenardo, Michael
TI Activating mutations in p110 delta cause human immunodeficiency and
reveal important roles of PI3K in T cell senescence and homeostatic cell
death
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Lucas, Carrie; Lenardo, Michael] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Lucas, Carrie] NIGMS, Postdoctoral Res Associate PRAT Program, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM2P.334
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001073
ER
PT J
AU Malhotra, D
Linehan, J
Jenkins, M
AF Malhotra, Deepali
Linehan, Jon
Jenkins, Marc
TI Self-tolerance in the polyclonal CD4+T cell repertoire
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Malhotra, Deepali; Jenkins, Marc] Univ Minnesota, Ctr Immunol, Microbiol, Minneapolis, MN USA.
[Linehan, Jon] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA8P.132
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005177
ER
PT J
AU McBerry, C
Sakai, S
Kauffman, K
Barber, D
AF McBerry, Cortez
Sakai, Shunsuke
Kauffman, Keith
Barber, Daniel
TI inhibits Th1 responses during cryptococcus neoformans infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [McBerry, Cortez; Sakai, Shunsuke; Kauffman, Keith; Barber, Daniel] NIH, Parasit Dis Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC2P.452
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002239
ER
PT J
AU McVicar, D
Howard, OMZ
Sublesk, J
Quigley, L
Yang, YF
Rayman, P
Rini, B
Linehan, WM
Sayers, T
Finke, J
Stappenbeck, T
Ford, J
AF McVicar, Daniel
Howard, O. M. Zack
Sublesk, Jeff
Quigley, Laura
Yang, Youfeng
Rayman, Patricia
Rini, Brian
Linehan, W. Marston
Sayers, Thomas
Finke, James
Stappenbeck, Thaddeus
Ford, Jill
TI The myeloid receptor TREM2 exacerbates DSS-induced colitis and promotes
colitis-associated cancer
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [McVicar, Daniel; Howard, O. M. Zack; Sublesk, Jeff; Quigley, Laura; Ford, Jill] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Yang, Youfeng; Linehan, W. Marston] NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Rayman, Patricia] Cleveland Clin, Dept Immunol, Cleveland, OH 44106 USA.
[Rini, Brian] Cleveland Clin, Dept Solid Tumor Oncol, Cleveland, OH 44106 USA.
[Stappenbeck, Thaddeus] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM4P.916
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004047
ER
PT J
AU Metidji, A
Shevach, E
AF Metidji, Amina
Shevach, Ethan
TI Type I IFNs modulate T effector (Teff) and T regulatory (Treg) cell
function during experimental autoimmune encephalomyelitis (EAE)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Metidji, Amina; Shevach, Ethan] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC4P.485
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005042
ER
PT J
AU Mistry, P
Laird, M
Schwarz, R
Greene, S
Dyson, T
Jabre, S
Snyder, G
Deredge, D
Chauhan, J
Wintrode, P
Xiao, T
Sundberg, E
Fletcher, S
Toshchakov, V
MacKerell, A
Vogel, S
AF Mistry, Pragnesh
Laird, Michelle
Schwarz, Ryan
Greene, Shannon
Dyson, Tristan
Jabre, Sandra
Snyder, Greg
Deredge, Daniel
Chauhan, Jamal
Wintrode, Patrick
Xiao, Tsan
Sundberg, Eric
Fletcher, Steven
Toshchakov, Vladimir
MacKerell, Alexander
Vogel, Stefanie
TI Inhibition of TLR2 signaling by small molecule inhibitors targeting a
novel putative pocket within the TLR2 TIR domain
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Mistry, Pragnesh; Laird, Michelle; Schwarz, Ryan; Dyson, Tristan; Jabre, Sandra; Snyder, Greg; Sundberg, Eric; Toshchakov, Vladimir; Vogel, Stefanie] Univ Maryland, Microbiol & Immunol, Baltimore, MD 21201 USA.
[Greene, Shannon; Deredge, Daniel; Chauhan, Jamal; Wintrode, Patrick; Fletcher, Steven; MacKerell, Alexander] Univ Maryland, Pharmaceut Sci, Baltimore, MD 21201 USA.
[Xiao, Tsan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INM9P.448
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006104
ER
PT J
AU Morozov, G
Zhao, HY
Mage, M
Boyd, L
Schuck, P
Natarajan, K
Margulies, D
AF Morozov, Giora
Zhao, Huaying
Mage, Michael
Boyd, Lisa
Schuck, Peter
Natarajan, Kannan
Margulies, David
TI Tapasin-related protein TAPBPR interacts directly with peptide-free
MHC-I/beta 2-microgolbulin complexes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Morozov, Giora; Mage, Michael; Boyd, Lisa; Natarajan, Kannan; Margulies, David] NIAID, Lab Immunol, NIH, Bethesda, MD 20892 USA.
[Zhao, Huaying; Schuck, Peter] NIBIB, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA APP3P.101
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000014
ER
PT J
AU Moseman, E
Heydari, S
Zinselmeyer, B
McGavern, D
AF Moseman, E.
Heydari, Sara
Zinselmeyer, Bernd
McGavern, Dorian
TI Adoptive B cell immunotherapy accelerates control of chronic viral
infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Moseman, E.; Heydari, Sara; Zinselmeyer, Bernd; McGavern, Dorian] NINDS, Viral Immunol & Intravital Imaging Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC6P.947
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000057
ER
PT J
AU Nakano, H
Moran, T
Bortner, C
Cook, D
AF Nakano, Hideki
Moran, Timothy
Bortner, Carl
Cook, Donald
TI Responsiveness to anaphylatoxin C5a delineates hematopoietic lineage of
pulmonary dendritic cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Nakano, Hideki; Moran, Timothy; Cook, Donald] NIEHS, Resp Biol, Res Triangle Pk, NC 27709 USA.
[Bortner, Carl] NIEHS, Signal Transduct, Res Triangle Pk, NC 27709 USA.
[Moran, Timothy] Duke Univ, Med Ctr, Pediat, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HYP6P.257
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002212
ER
PT J
AU Nundel, K
Mande, P
Shaffer, A
Sindhava, V
Cancro, M
Marshak-Rothstein, A
AF Nundel, Kerstin
Mande, Purvi
Shaffer, Art
Sindhava, Vishal
Cancro, Michael
Marshak-Rothstein, Ann
TI Distinct roles for TLR7 and TLR9 in regulation of B cell signal strength
and differentiation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Nundel, Kerstin; Mande, Purvi; Marshak-Rothstein, Ann] UMass Med Sch, Worcester, MA USA.
[Shaffer, Art] NIH, Bethesda, MD 20892 USA.
[Sindhava, Vishal; Cancro, Michael] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM6P.766
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000086
ER
PT J
AU Pandiyan, P
Zheng, LX
Bhaskaran, N
Weinberg, A
AF Pandiyan, Pushpa
Zheng, Lixin
Bhaskaran, Natarajan
Weinberg, Aaron
TI Differential effects of TLR-2 ligands on CD4+CD25+Foxp3+regulatory cells
depending on inflammatory cytokine milieu
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Pandiyan, Pushpa; Bhaskaran, Natarajan; Weinberg, Aaron] Case Western Reserve Univ, Dept Biol Sci, Cleveland, OH 44106 USA.
[Zheng, Lixin] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC4P.489
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005032
ER
PT J
AU Park, JY
Keller, H
Sato, N
Park, JH
AF Park, Joo-Young
Keller, Hilary
Sato, Noriko
Park, Jung-Hyun
TI NKT cells require IL-7, not IL-15, for survival and homeostasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Park, Joo-Young; Keller, Hilary; Sato, Noriko; Park, Jung-Hyun] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM4P.761
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005128
ER
PT J
AU Park, JH
Feigenbaum, L
Luckey, M
AF Park, Jung-Hyun
Feigenbaum, Lionel
Luckey, Megan
TI Overexpression of suppressor of cytokine signaling-4 impairs T cell
development and homeostasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Park, Jung-Hyun; Luckey, Megan] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel] NCI, Lab Anim Sci Program, Frederick CRDC, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM7P.723
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005227
ER
PT J
AU Penaloza-MacMaster, P
Barber, D
Wherry, J
Provine, N
Teigler, J
Blackmore, S
Borducchi, E
Bronson, R
Barouch, D
AF Penaloza-MacMaster, Pablo
Barber, Daniel
Wherry, John
Provine, Nicholas
Teigler, Jeffrey
Blackmore, Steven
Borducchi, Erica
Bronson, Roderick
Barouch, Dan
TI Vaccine induced immunopathology mediated by memory CD4 T cells following
chronic viral infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Penaloza-MacMaster, Pablo; Provine, Nicholas; Teigler, Jeffrey; Blackmore, Steven; Borducchi, Erica; Barouch, Dan] Harvard Univ, BIDMC, Boston, MA 02115 USA.
[Barber, Daniel] NIAID, Lab Parasit Dis, Bethesda, MD 20892 USA.
[Wherry, John] Univ Penn, Dept Microbiol 3, Philadelphia, PA 19104 USA.
[Wherry, John] Univ Penn, Inst Immunol, Philadelphia, PA 19104 USA.
[Bronson, Roderick] Harvard Med Sch, Mouse Histopathol Core, Boston, MA USA.
[Barouch, Dan] Ragon Inst MGH MIT & Harvard, MGH MIT & Harvard, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VIR7P.1054
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000021
ER
PT J
AU Perez-Diez, A
Liu, XD
Sheikh, V
Sereti, I
AF Perez-Diez, Ainhoa
Liu, Xiangdong
Sheikh, Virginia
Sereti, Irini
TI Use of humanized mouse models for the study of idiopathic CD4
lymphocytopenia
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Perez-Diez, Ainhoa; Liu, Xiangdong; Sheikh, Virginia; Sereti, Irini] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM7P.313
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000183
ER
PT J
AU Petrovas, C
Paris, R
Koup, R
AF Petrovas, Constantinos
Paris, Robert
Koup, Richard
TI Activated PD-1highCD127highCD27highCD45RAlowCD4 T cell phenotype is
associated with increased susceptibility to HIV infection rather than
exhaustion.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Petrovas, Constantinos; Paris, Robert; Koup, Richard] NIAID, VRC, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM8P.339
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002034
ER
PT J
AU Richard, A
Tan, CY
Hawley, E
Gomez-Rodriguez, J
Goswami, R
Yang, XP
Cruz, A
Penumetcha, P
Hayes, E
Pelletier, M
Gabay, O
Walsh, M
Ferdinand, J
Keane-Myers, A
Choi, Y
O'Shea, J
Al-Shamkhani, A
Kaplan, M
Gery, I
Siegel, R
Meylan, F
AF Richard, Arianne
Tan, Cuiyan
Hawley, Eric
Gomez-Rodriguez, Julio
Goswami, Ritobrata
Yang, Xiangping
Cruz, Anthony
Penumetcha, Pallavi
Hayes, Erika
Pelletier, Martin
Gabay, Odile
Walsh, Matthew
Ferdinand, John
Keane-Myers, Andrea
Choi, Yongwon
O'Shea, John
Al-Shamkhani, Aymen
Kaplan, Mark
Gery, Igal
Siegel, Richard
Meylan, Francoise
TI The TNF family member TL1A promotes Th9 differentiation and Th9-mediated
immunopathology
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Richard, Arianne; Hawley, Eric; Cruz, Anthony; Penumetcha, Pallavi; Hayes, Erika; Pelletier, Martin; Gabay, Odile; Ferdinand, John; Siegel, Richard; Meylan, Francoise] NIAMS, Immunoregulat Sect, Autoimmun Branch, NIH, Bethesda, MD USA.
[Tan, Cuiyan; Gery, Igal] NEI, Expt Immunol Sect, NIH, Bethesda, MD 20892 USA.
[Gomez-Rodriguez, Julio] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Goswami, Ritobrata; Kaplan, Mark] Indiana Univ Sch Med, Dept Pediat & Microbiol & Immunol, Indianapolis, IN 46202 USA.
[Yang, Xiangping; O'Shea, John] NIAMS, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD USA.
[Walsh, Matthew; Choi, Yongwon] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA USA.
[Ferdinand, John; Al-Shamkhani, Aymen] Univ Southampton, Fac Med, Canc Sci Div, Southampton, Hants, England.
[Keane-Myers, Andrea] Naval Med Res Ctr, Biol Def Res Directorate, Ft Detrick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM3P.733
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000127
ER
PT J
AU Robertson, F
Lu, XJ
Terabe, M
Berzofsky, J
AF Robertson, Faith
Lu, Xiuju
Terabe, Masaki
Berzofsky, Jay
TI Type II NKT cells play a role in the regulation of CD4 T cell subsets
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Robertson, Faith; Lu, Xiuju; Terabe, Masaki; Berzofsky, Jay] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM8P.730
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003050
ER
PT J
AU Robins, H
Muraro, P
Malhotra, S
Howell, M
Phippard, D
Desmarais, C
Sousa, ADA
Griffith, L
Lim, N
Nash, R
Turka, L
AF Robins, Harlan
Muraro, Paolo
Malhotra, Sachin
Howell, Michael
Phippard, Deborah
Desmarais, Cindy
Sousa, Alessandra de Paula Alves
Griffith, Linda
Lim, Noha
Nash, Richard
Turka, Laurence
TI T cell repertoire renewal following autologous stem cell transplantation
for multiple sclerosis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Robins, Harlan] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Muraro, Paolo; Sousa, Alessandra de Paula Alves] Imperial Coll, Div Brain Sci, Dept Med, London, England.
[Malhotra, Sachin; Howell, Michael; Phippard, Deborah; Lim, Noha; Turka, Laurence] Immune Tolerance Network, Bethesda, MD USA.
[Griffith, Linda] NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
[Nash, Richard] PSL, Colorado Blood Ctr Inst, Denver, CO USA.
[Turka, Laurence] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Turka, Laurence] Harvard Med Sch, Boston, MA USA.
[Robins, Harlan; Desmarais, Cindy] Adapt Biotechnol, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA THER3P.879
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001242
ER
PT J
AU Rus, V
Tegla, C
Nguyen, V
Cudrici, C
Badea, T
Rus, H
AF Rus, Violeta
Tegla, Cosmin
Vinh Nguyen
Cudrici, Cornelia
Badea, Tudor
Rus, Horea
TI RGC-32 is essential for TGF-beta mediated Th17 cell differentiation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Rus, Violeta; Vinh Nguyen] Univ Maryland, Med, Baltimore, MD 21201 USA.
[Tegla, Cosmin; Rus, Horea] Univ Maryland, Neurol, Baltimore, MD 21201 USA.
[Rus, Violeta; Tegla, Cosmin; Vinh Nguyen; Rus, Horea] VAMHCS, Res Serv, Baltimore, MD USA.
[Badea, Tudor] NEI, Retinal Circuit Dev & Genet Unit, NIH, Bethesda, MD 20892 USA.
[Cudrici, Cornelia] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM3P.728
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000121
ER
PT J
AU Sadegh-Nasseri, S
Kim, A
Hartman, I
Cuidad, MT
Song, NB
Boronina, T
Caspi, R
Jaraquemada, D
AF Sadegh-Nasseri, Scheherazade
Kim, AeRyon
Hartman, Isamu
Teresa Cuidad, M.
Song, Nianbin
Boronina, Tatiana
Caspi, Rachel
Jaraquemada, Dolores
TI Multiple paths to immunodominance: dominant epitopes are captured by MHC
II prior, or post antigen proteolysis, and are enriched by HLA-DM
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Sadegh-Nasseri, Scheherazade; Kim, AeRyon; Hartman, Isamu; Song, Nianbin] Johns Hopkins Univ, Pathol, Baltimore, MD USA.
[Boronina, Tatiana] Johns Hopkins Univ, Dept Biol Chem, Baltimore, MD USA.
[Teresa Cuidad, M.; Jaraquemada, Dolores] Univ Autonoma Barcelona, Cell Biol Physiol & Immunol, Barcelona, Spain.
[Caspi, Rachel] NIH, Immunol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA APP2P.103
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001145
ER
PT J
AU Sagar, D
Masih, S
Schell, T
Jacobson, S
Wigdahi, B
Khan, Z
Jain, P
AF Sagar, Divya
Masih, Shet
Schell, Todd
Jacobson, Steven
Wigdahi, Brian
Khan, Zafar
Jain, Pooja
TI In vivo immunogenicity of Tax 11-19 epitope in HLA-A2/DTR transgenic
mice: implication for dendritic cell-based anti-HTLV-1 vaccine
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Sagar, Divya; Masih, Shet; Wigdahi, Brian; Khan, Zafar; Jain, Pooja] Drexel Univ, Coll Med, Microbiol & Immunol, Doylestown, PA USA.
[Schell, Todd] Penn State Univ, Microbiol & Immunol, Hershey, PA USA.
[Jacobson, Steven] NIH, Viral Immunol Sect, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC12P1020
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002008
ER
PT J
AU Sckisel, G
Bouchlaka, M
Mirsoian, A
Sungur, C
Soulika, A
Wiltrout, R
Blazar, B
Murphy, W
AF Sckisel, Gail
Bouchlaka, Myriam
Mirsoian, Annie
Sungur, Can
Soulika, Athena
Wiltrout, Robert
Blazar, Bruce
Murphy, William
TI Cytokine-based cancer immunotherapy impairs primary T cell immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Sckisel, Gail; Mirsoian, Annie; Sungur, Can; Murphy, William] Univ Calif Davis, Sch Med, Dermatol, Sacramento, CA 95817 USA.
[Bouchlaka, Myriam] Univ Nevada, Microbiol & Immunol, Reno, NV 89557 USA.
[Soulika, Athena] Shriners Hosp Children Northern Calif, Inst Pediat Regenerat Med, Sacramento, CA USA.
[Wiltrout, Robert] NCI, Canc & Inflammat Program, Bethesda, MD 20892 USA.
[Blazar, Bruce] Univ Minnesota, Pediat, Minneapolis, MN USA.
[Murphy, William] Univ Calif Davis, Internal Med, Davis, CA 95616 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC3P.942
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004192
ER
PT J
AU Serti, E
Werner, J
Chattergoon, M
Cox, A
Lohmann, V
Rehermann, B
AF Serti, Elisavet
Werner, Jens
Chattergoon, Michael
Cox, Andrea
Lohmann, Volker
Rehermann, Barbara
TI Monocytes sense hepatitis C virus-replicating cells and induce natural
killer cell antiviral activity in an IL-18-mediated manner
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Serti, Elisavet; Werner, Jens; Rehermann, Barbara] NIDDK, Immunl Sect, Liver Dis Branch, NIH,DHHS, Bethesda, MD 20892 USA.
[Chattergoon, Michael; Cox, Andrea] Johns Hopkins Sch Med, Div Infect Dis, Baltimore, MD USA.
[Lohmann, Volker] Heidelberg Univ, Dept Infect Dis, Mol Virol, Heidelberg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INC8P.437
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001029
ER
PT J
AU Sgourakis, N
Natarajan, K
Margulies, D
Bax, A
AF Sgourakis, Nikolaos
Natarajan, Kannan
Margulies, David
Bax, Ad
TI A structural approach to the study of viral immune evasion mechanisms
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Sgourakis, Nikolaos; Bax, Ad] NIDDK, NIH, Bethesda, MD 20892 USA.
[Natarajan, Kannan; Margulies, David] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TECH1P.850
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006008
ER
PT J
AU Siebeniist, U
Claudio, E
Ha, HL
AF Siebeniist, Ulrich
Claudio, Estefania
Ha, Hye-Lin
TI Critical target cell-specific roles for IL-17 family
cytokines/CIKS-mediated signaling in mouse models of skin and lung
inflammation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Siebeniist, Ulrich; Claudio, Estefania; Ha, Hye-Lin] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR6P.276
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006056
ER
PT J
AU Singh, A
Zhang, YQ
Wood, W
Becker, K
Sen, R
AF Singh, Amit
Zhang, Yongqing
Wood, William
Becker, Kevin
Sen, Ranjan
TI First mitotic division programs naive B cell for successive cell
divisions
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Singh, Amit; Sen, Ranjan] NIA, LMBI, NIH, Baltimore, MD 21224 USA.
[Zhang, Yongqing; Wood, William; Becker, Kevin] NIA, Lab Genet, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM6P.778
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000097
ER
PT J
AU Singh, S
Zhang, H
Tsang, H
Gardina, P
Myers, T
Farber, J
AF Singh, Satya
Zhang, Howard
Tsang, Hsinyi
Gardina, Paul
Myers, Timothy
Farber, Joshua
TI PLZF supports the acquisition and maintenance of the Th17 phenotype in
human cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Singh, Satya; Zhang, Howard; Tsang, Hsinyi; Farber, Joshua] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Gardina, Paul; Myers, Timothy] NIAID, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR5P.250
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003186
ER
PT J
AU Singh, TP
Zhang, H
Farber, J
AF Singh, Tej Pratap
Zhang, Howard
Farber, Joshua
TI Blood monocytes expressing CCR6 and monocyte-derived dendritic cells in
dermis and epidermis are critical for IL-23-induced psoriasis-like
inflammation in mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Singh, Tej Pratap; Zhang, Howard; Farber, Joshua] NIAID, Inflammat Biol Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CAM5P.238
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002104
ER
PT J
AU Skarzynski, M
Vire, B
Thomas, J
Nelson, C
David, A
Aue, G
Burke, T
Rader, C
Wiestner, A
AF Skarzynski, Martin
Vire, Berengere
Thomas, Joshua
Nelson, Christopher
David, Alexandre
Aue, Georg
Burke, Terrence
Rader, Christoph
Wiestner, Adrian
TI Novel IgM-derived antibody-drug conjugate selectively kills chronic
lymphocytic leukemia cells through binding of Fc mu-receptor leading to
rapid internalization and intracellular cytotoxic payload delivery
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Skarzynski, Martin; Vire, Berengere; Aue, Georg; Wiestner, Adrian] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
[Thomas, Joshua; Nelson, Christopher; Burke, Terrence] NCI, Chem Biol Lab, Mol Discovery Program, Frederick Natl Lab Canc Res, Frederick, MD 21701 USA.
[David, Alexandre] NIAID, Lab Viral Dis, Bethesda, MD 20892 USA.
[Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Rader, Christoph] Scripps Florida, Scripps Res Inst, Dept Canc Biol, Jupiter, FL USA.
[Rader, Christoph] Scripps Florida, Scripps Res Inst, Dept Mol Therapeut, Jupiter, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC3P.953
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004199
ER
PT J
AU Slota, C
Weng, NP
AF Slota, Christina
Weng, Nan-ping
TI The effect of norepinephrine on CD8 T cell subsets in healthy human
adults
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Slota, Christina; Weng, Nan-ping] NIA IRP, Lab Mol Biol & Immunol, Baltimore, MD USA.
[Slota, Christina] Univ Penn, Nursing, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR3P.215
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001166
ER
PT J
AU Smith, C
Vivekanandan-Giri, A
Pennathur, S
Kaplan, M
AF Smith, Carolyne
Vivekanandan-Giri, Anuradha
Pennathur, Subramaniam
Kaplan, Mariana
TI Neutrophil extracellular traps as a source of high density lipoprotein
oxidation in lupus related cardiovascular disease.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Smith, Carolyne; Kaplan, Mariana] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Vivekanandan-Giri, Anuradha; Pennathur, Subramaniam] Univ Michigan, Dept Internal Med, Div Nephrol, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM1P.312
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000225
ER
PT J
AU Snyder, G
Deredge, D
Waldhuber, A
Fresquez, T
Smith, P
Duerr, S
Cirl, C
Jiang, J
Jennings, W
Luchetti, T
Snyder, N
Sundberg, E
Wintrode, P
Miethke, T
Xiao, T
AF Snyder, Greg
Deredge, Daniel
Waldhuber, Anna
Fresquez, Theresa
Smith, Patrick
Duerr, Suri
Cirl, Christine
Jiang, Jiansheng
Jennings, William
Luchetti, Timothy
Snyder, Nathaniel
Sundberg, Eric
Wintrode, Patrick
Miethke, Thomas
Xiao, Tsan
TI Development of microbial-derived inhibitory peptides using structural
studies of microbial TIR proteins TcpB, TcpC and host adapters TIRAP and
MyD88.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Snyder, Greg; Sundberg, Eric] Univ Maryland, Sch Med, Dept Med, Inst Human Virol, Baltimore, MD 21201 USA.
[Snyder, Greg; Fresquez, Theresa; Smith, Patrick; Jiang, Jiansheng; Jennings, William; Luchetti, Timothy; Snyder, Nathaniel; Xiao, Tsan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Deredge, Daniel; Wintrode, Patrick] Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, Baltimore, MD 21201 USA.
[Waldhuber, Anna; Duerr, Suri; Cirl, Christine; Miethke, Thomas] Heidelberg Univ, Med Fac Mannheim, Inst Med Microbiol & Hyg, Mannheim, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INM9P.449
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006108
ER
PT J
AU Sommers, C
Rouquette-Jazdanian, A
Li, WM
Nguyen, P
Kortum, R
Samelson, L
AF Sommers, Connie
Rouquette-Jazdanian, Alexandre
Li, WenMei
Nguyen, Phan
Kortum, Robert
Samelson, Lawrence
TI miR-155 regulates lymphocyte homeostasis in LAT mutant mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Sommers, Connie; Rouquette-Jazdanian, Alexandre; Li, WenMei; Nguyen, Phan; Kortum, Robert; Samelson, Lawrence] NCI, LCMB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM4P.749
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005125
ER
PT J
AU Song, W
Seeley-Fallen, M
Onabajo, O
Tan, TH
Upadhyaya, A
AF Song, Wenxia
Seeley-Fallen, Margaret
Onabajo, Olusegun
Tan, Tse-Hua
Upadhyaya, Arpita
TI Actin-binding protein 1 links B-cell receptor to negative signaling
pathways
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Song, Wenxia; Seeley-Fallen, Margaret] Univ Maryland, Cell Biol & Mol Genet, College Pk, MD 20742 USA.
[Onabajo, Olusegun] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Tan, Tse-Hua] Baylor Coll Med, Dept Microbiol & Immunol, Houston, TX 77030 USA.
[Upadhyaya, Arpita] Univ Maryland, Dept Phys, College Pk, MD 20742 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC3P.462
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004166
ER
PT J
AU Stagliano, K
Zhu, ZQ
Hurwitz, A
AF Stagliano, Katherine
Zhu, Ziqiang
Hurwitz, Arthur
TI Very low avidity endogenous memory CD8+T cells control tumor growth
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Stagliano, Katherine; Zhu, Ziqiang; Hurwitz, Arthur] NCI, Canc Inflammat Program, Frederick, MD 21701 USA.
[Stagliano, Katherine; Hurwitz, Arthur] George Washington Univ, Inst Biomed Sci, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM2P.893
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001210
ER
PT J
AU Swanson, P
McGavern, D
AF Swanson, Phillip
McGavern, Dorian
TI CNS stromal cells modulate antiviral CD8 T cell immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Swanson, Phillip; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VIR4P.1009
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001059
ER
PT J
AU Tarbell, K
Price, J
Rahir, G
Beauchamp, N
Zhao, YG
Doog, M
AF Tarbell, Kristin
Price, Jeffrey
Rahir, Gwendoline
Beauchamp, Nicole
Zhao, Yongge
Doog, Matthew
TI In autoimmune-prone NOD mice, altered DC subsets induce aberrant
activation of CD4 T cells, yet DCIR2+DCs can still induce tolerance.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Tarbell, Kristin; Price, Jeffrey; Rahir, Gwendoline; Beauchamp, Nicole; Zhao, Yongge; Doog, Matthew] NIDDK, Immune Tolerance Sect, DEOB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA15P.218
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002243
ER
PT J
AU Taylor, K
Woods, T
Peterson, K
AF Taylor, Katherine
Woods, Tyson
Peterson, Karin
TI Innate immune-induced neuronal cell apoptosis via a SARM1 mediated
mechanism in the absence of viral replication.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Taylor, Katherine; Woods, Tyson; Peterson, Karin] NIAID, Lab Persistent Viral Dis, Rocky Mt Labs, NIH, Hamilton, MT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INM9P.451
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006102
ER
PT J
AU Terabe, M
Robertson, F
Mizra, A
Berzofsky, J
AF Terabe, Masaki
Robertson, Faith
Mizra, Amer
Berzofsky, Jay
TI Effect of blocking different TGF-beta isoforms on tumor immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Terabe, Masaki; Robertson, Faith; Berzofsky, Jay] NCI, NIH, Bethesda, MD 20892 USA.
[Mizra, Amer] Xoma US LLC, Barkeley, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA TUM5P.937
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003076
ER
PT J
AU Thomas, L
Long, E
AF Thomas, Louis
Long, Eric
TI Actin confinement of activating receptors does not dictate natural
killer cell licensing
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Thomas, Louis; Long, Eric] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INM2P.431
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006124
ER
PT J
AU Tian, LJ
Choi, SC
Murakami, Y
Allen, J
Morse, H
Qi, CF
Krzewski, K
Coligan, J
AF Tian, Linjie
Choi, Seung-Chul
Murakami, Yousuke
Allen, Joselyn
Morse, Herbert
Qi, Chen-Feng
Krzewski, Konrad
Coligan, John
TI p85a recruitment by the CD300f phosphatidylserine receptor mediates
apoptotic cell clearance required for autoimmunity suppression
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Tian, Linjie; Choi, Seung-Chul; Murakami, Yousuke; Allen, Joselyn; Morse, Herbert; Qi, Chen-Feng; Krzewski, Konrad; Coligan, John] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA4P.222
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002203
ER
PT J
AU Tilahun, M
Revilleza, MJ
Mans, J
Natarajan, K
Margulies, D
AF Tilahun, Mulualem
Revilleza, Maria Jamela
Mans, Janet
Natarajan, Kannan
Margulies, David
TI Mouse cytomegalovirus glycoprotein m153 binds a dendritic cell-surface
ligand
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Tilahun, Mulualem; Revilleza, Maria Jamela; Natarajan, Kannan; Margulies, David] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Mans, Janet] Univ Pretoria, Dept Med Virol, Pretoria, South Africa.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VIR5P.1026
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005024
ER
PT J
AU Ujiie, H
Shevach, E
AF Ujiie, Hideyuki
Shevach, Ethan
TI gamma delta T cells protect TCR alpha deficient mice from the
autoimmunity induced by scurfy lymphocytes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Ujiie, Hideyuki; Shevach, Ethan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA13P.118
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005164
ER
PT J
AU van Panhuys, N
Klauschen, F
Germain, R
AF van Panhuys, Nicholas
Klauschen, Frederick
Germain, Ronald
TI TCR strength of signal is upstream of and dominates over cytokine
effects in controlling CD4+T cell polarization in vivo
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [van Panhuys, Nicholas; Germain, Ronald] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
[Klauschen, Frederick] Charlie Univ Hosp, Inst Pathol, Berlin, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC2P.449
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002233
ER
PT J
AU Wang, JM
Xiang, Y
Huang, JQ
Gong, WH
Yoshimura, T
Tessarollo, L
Li, YY
Chen, KQ
AF Wang, Ji Ming
Xiang, Yi
Huang, Jiaqiang
Gong, Wanghua
Yoshimura, Teizo
Tessarollo, Lino
Li, Yingying
Chen, Keqiang
TI Fpr2 and its endogenous ligand CRAMP promote dendritic cell maturation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Wang, Ji Ming; Xiang, Yi; Huang, Jiaqiang; Yoshimura, Teizo; Tessarollo, Lino; Chen, Keqiang] NCI, Lab Mol Immunoregulat, Frederick, MD 21701 USA.
[Gong, Wanghua] Leidos, Lab Mol Immunoregulat, Frederick, MD USA.
[Li, Yingying] Chinese Acad Sci, Shanghai, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRC5P.461
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004092
ER
PT J
AU Wang, ZY
Sun, G
Faucette, A
Unger, B
Hong, P
Yao, FY
Guterman, J
Mathiarasu, A
Deng, J
Tang, XN
Bluth, M
Armant, D
Lum, L
Siddiqui, M
Chen, K
AF Wang, Zhao-Yuan
Sun, Guang
Faucette, Azure
Unger, Benjamin
Hong, Peng
Yao, Fayi
Guterman, Jacqueline
Mathiarasu, Aditya
Deng, Jie
Tang, Xiangna
Bluth, Martin
Armant, D.
Lum, Lawrence
Siddiqui, Maq
Chen, Kang
TI A HEXIM1-AIRE transcriptional counterbalance in trophoblasts regulates
maternal-fetal mucosal immunity in pregnancy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Wang, Zhao-Yuan; Faucette, Azure; Unger, Benjamin; Yao, Fayi; Guterman, Jacqueline; Mathiarasu, Aditya; Deng, Jie; Tang, Xiangna; Armant, D.; Chen, Kang] Wayne State Univ, Obstet & Gynecol, Detroit, MI USA.
[Wang, Zhao-Yuan; Faucette, Azure; Unger, Benjamin; Yao, Fayi; Mathiarasu, Aditya; Tang, Xiangna; Chen, Kang] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Detroit, MI USA.
[Sun, Guang] Republ Polytech, Sch Appl Sci, Singapore, Singapore.
[Hong, Peng; Siddiqui, Maq] Suny Downstate Med Ctr, Cell Biol, Brooklyn, NY USA.
[Hong, Peng; Siddiqui, Maq] VA New York Harbor Healthcare Syst, New York, NY USA.
[Bluth, Martin] Wayne State Univ, Pathol, Detroit, MI USA.
[Bluth, Martin; Lum, Lawrence; Chen, Kang] Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
[Armant, D.] Wayne State Univ, Anat & Cell Biol, Detroit, MI USA.
[Armant, D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Lum, Lawrence] Wayne State Univ, Med, Detroit, MI USA.
[Lum, Lawrence; Chen, Kang] Wayne State Univ, Immunol & Microbiol, Detroit, MI USA.
[Chen, Kang] NIAID, MIST, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765004161
ER
PT J
AU Watanabe, M
Moon, KD
Vacchio, M
Hathcock, K
Hodes, R
AF Watanabe, Masashi
Moon, Kyung Duk
Vacchio, Melanie
Hathcock, Karen
Hodes, Richard
TI Down-modulation of tumor suppressor p53 by T cell receptor signaling is
critical for antigen-specific T cell responses
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Watanabe, Masashi; Moon, Kyung Duk; Vacchio, Melanie; Hathcock, Karen; Hodes, Richard] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRM10P.737
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005082
ER
PT J
AU Weindel, C
Richey, L
Bolland, S
Huber, B
AF Weindel, Chi
Richey, Lauren
Bolland, Silvia
Huber, Brigitte
TI B cell autophagy mediates TLR7-dependent SLE and controls extramedullary
hematopoiesis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Weindel, Chi; Huber, Brigitte] Tufts Univ, Sackler Sch Grad Biomed Sci, Boston, MA 02111 USA.
[Richey, Lauren] Tufts Univ, Div Lab Anim Med, Boston, MA 02111 USA.
[Bolland, Silvia] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Huber, Brigitte] Tufts Univ, Sch Med, Dept Integrat Physiol & Pathobiol, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA4P.217
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002196
ER
PT J
AU Weiskopf, D
Angelo, M
Bangs, D
Sidney, J
de Silva, A
Lindow, J
Durbin, A
Whitehead, S
Kirkpatrick, B
Sette, A
AF Weiskopf, Daniela
Angelo, Michael
Bangs, Derek
Sidney, John
de Silva, Aruna
Lindow, Janet
Durbin, Anna
Whitehead, Stephen
Kirkpatrick, Beth
Sette, Alessandro
TI HLA restricted CD8+T cell responses following vaccination with
monovalent and tetravalent dengue live attenuated vaccines
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Weiskopf, Daniela; Sette, Alessandro] La Jolla Inst Allergy & Immunol, Div Vaccine Discovery, La Jolla, CA USA.
[Weiskopf, Daniela] Genetech Res Inst, Colombo, Sri Lanka.
[Lindow, Janet; Kirkpatrick, Beth] Univ Vermont, Coll Med, Burlington, VT USA.
[Durbin, Anna] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Whitehead, Stephen] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC7P.983
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002051
ER
PT J
AU Weng, NP
Shi, A
Li, HM
Hiroi, T
Zhang, YQ
Chen, GB
Metter, J
Ferrucci, L
AF Weng, Nan-ping
Shi, Alvin
Li, Hoi-Ming
Hiroi, Toyoko
Zhang, Yongqing
Chen, Guobing
Metter, Jeffrey
Ferrucci, Luigi
TI Analysis of human TCR beta repertoire by a RARE-sequencing method
reveals distinct features of TCR beta diversity and distribution and
their alterations with age
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Weng, Nan-ping; Shi, Alvin; Li, Hoi-Ming; Hiroi, Toyoko; Chen, Guobing] NIA, LMBI, NIH, Baltimore, MD 21224 USA.
[Zhang, Yongqing] NIA, Gene Express & Genom Unit, NIH, Baltimore, MD 21224 USA.
[Metter, Jeffrey; Ferrucci, Luigi] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
RI Chen, Guobing/D-9572-2012
OI Chen, Guobing/0000-0002-2401-6168
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRM10P.758
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005099
ER
PT J
AU Wessel, A
Hsu, A
Goldbach-Mansky, R
Zilberman-Rudenko, J
Siegel, R
Hanson, E
AF Wessel, Alex
Hsu, Amy
Goldbach-Mansky, Rapheala
Zilberman-Rudenko, Jevgenia
Siegel, Richard
Hanson, Eric
TI Inflammatory disease due to selectively impaired NF-kB activation and
type I interferon response resulting from a de novo human NEMO
hypomorphic mutation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Wessel, Alex; Goldbach-Mansky, Rapheala; Zilberman-Rudenko, Jevgenia; Siegel, Richard; Hanson, Eric] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Zilberman-Rudenko, Jevgenia] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Hsu, Amy] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA HUM2P.333
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765001072
ER
PT J
AU Whibley, N
Mamo, A
Conti, H
Traggiai, E
Kolbinger, F
Vogel, B
Kammueller, M
Siebenlist, U
Iwakura, Y
Gaffen, S
AF Whibley, Natasha
Mamo, Anna
Conti, Heather
Traggiai, Elisabetta
Kolbinger, Frank
Vogel, Beate
Kammueller, Michael
Siebenlist, Ulrich
Iwakura, Yoichiro
Gaffen, Sarah
TI Differential requirements of IL-17 family cytokines in host defense
against oral candidiasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Whibley, Natasha; Mamo, Anna; Conti, Heather; Gaffen, Sarah] Univ Pittsburgh, Rheumatol & Clin Immunol, Pittsburgh, PA USA.
[Traggiai, Elisabetta; Kolbinger, Frank; Vogel, Beate; Kammueller, Michael] Novartis Inst Biomed Res, Basel, Switzerland.
[Siebenlist, Ulrich] NIAID, NIH, Bethesda, MD 20892 USA.
[Iwakura, Yoichiro] Tokyo Univ Sci, Chiba, Japan.
RI Iwakura, Yoichiro/E-5457-2011
OI Iwakura, Yoichiro/0000-0002-9934-5775
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA CCR6P.272
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765006046
ER
PT J
AU Xiao, T
Jin, TC
Chuenchor, W
Ravilious, G
Jiang, JS
Smith, P
AF Xiao, Tsan
Jin, Tengchuan
Chuenchor, Watchalee
Ravilious, Geoffrey
Jiang, Jiansheng
Smith, Patrick
TI DNA sensing by innate immune receptors
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Xiao, Tsan; Jin, Tengchuan; Chuenchor, Watchalee; Ravilious, Geoffrey; Jiang, Jiansheng; Smith, Patrick] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA INM6P.408
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002086
ER
PT J
AU Yang, G
Liu, MF
Wiehe, K
Nicely, N
Haynes, B
Mascola, J
Bjorkman, P
Kelsoe, G
AF Yang, Guang
Liu, Mengfei
Wiehe, Kevin
Nicely, Nathan
Haynes, Barton
Mascola, John
Bjorkman, Pamela
Kelsoe, Garnett
TI HIV broadly neutrizing antibodies and immunological tolerance
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Yang, Guang; Liu, Mengfei; Haynes, Barton; Kelsoe, Garnett] Duke Univ, Immunol, Durham, NC USA.
[Wiehe, Kevin; Nicely, Nathan; Haynes, Barton; Kelsoe, Garnett] Duke Univ, Duke Human Vaccine Inst, Durham, NC USA.
[Mascola, John] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Bjorkman, Pamela] CALTECH, Div Biol, Pasadena, CA 91125 USA.
[Bjorkman, Pamela] CALTECH, Howard Hughes Med Inst, Pasadena, CA 91125 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC7P.988
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002078
ER
PT J
AU Yang, YJ
Gordon, S
Doster, M
Liyanage, N
Chang, J
Williams, C
Agy, M
Mclain, R
Agricola, B
Law, L
Franchini, G
Palermo, R
Katze, M
AF Yang, Yajie
Gordon, Shari
Doster, Melvin
Liyanage, Namal
Chang, Jean
Williams, Chris
Agy, Michael
Mclain, Randy
Agricola, Brian
Law, Lynn
Franchini, Genoveffa
Palermo, Robert
Katze, Michael
TI A systems biology approach revealed distinct host responses between
ALVAC-SIV and NYVAC-SIV vaccines during an evaluation of immunogenicity
in rheusus macaques
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Yang, Yajie; Chang, Jean; Williams, Chris; Law, Lynn; Palermo, Robert; Katze, Michael] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Gordon, Shari; Doster, Melvin; Liyanage, Namal; Franchini, Genoveffa] NCI, Anim Models & Retroviral Vaccine Sect, Bethesda, MD 20892 USA.
[Agy, Michael; Mclain, Randy; Agricola, Brian; Palermo, Robert; Katze, Michael] Univ Washington, Washington Natl Primate Res Ctr, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC7P.992
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765002062
ER
PT J
AU Yin, ZJ
Gildersleeve, J
Finn, MG
Huang, XF
AF Yin, Zhaojun
Gildersleeve, Jeffrey
Finn, M. G.
Huang, Xuefei
TI Developing bacteriophage Q beta as versatile carrier for
anti-carbohydrate cancer vaccine: influence of antigen design on
antibody responses
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Yin, Zhaojun; Huang, Xuefei] Michigan State Univ, Chem, E Lansing, MI 48824 USA.
[Finn, M. G.] Georgia Inst Technol, Chem & Biochem, Atlanta, GA 30332 USA.
[Gildersleeve, Jeffrey] NCI, Biol Chem Lab, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA VAC8P.998
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003079
ER
PT J
AU Yoon, JH
Wang, HS
Morse, H
AF Yoon, Jeong Heon
Wang, Hongsheng
Morse, Herbert
TI ENPP1-positive B cells and activation in human peripheral blood
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Yoon, Jeong Heon; Wang, Hongsheng; Morse, Herbert] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA LYM6P.772
PG 2
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765000088
ER
PT J
AU Zanotti, K
Gearhart, P
AF Zanotti, Kimberly
Gearhart, Patricia
TI ATAD5 deficiency decreases B cell division and Igh recombination
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Zanotti, Kimberly; Gearhart, Patricia] NIA, Lab Mol Biol & Immunol, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA IRM8P.700
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765003247
ER
PT J
AU Zarate-Blades, C
Horai, R
Chen, J
Silver, P
Dillenburg-Pilla, P
Yamane, H
Chan, CC
Honda, K
Caspi, R
AF Zarate-Blades, Carlos
Horai, Reiko
Chen, Jun
Silver, Phyllis
Dillenburg-Pilla, Patricia
Yamane, Hidehiro
Chan, Chi-Chao
Honda, Kenya
Caspi, Rachel
TI Activation of autoreactive T cells by endogenous microflora induces
spontaneous autoimmunity in the immunologically privileged retina
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Zarate-Blades, Carlos; Horai, Reiko; Chen, Jun; Silver, Phyllis; Chan, Chi-Chao; Caspi, Rachel] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Dillenburg-Pilla, Patricia] NIH, OPCB, Bethesda, MD 20892 USA.
[Yamane, Hidehiro] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Honda, Kenya] RIKEN IMS RCAI, Yokohama, Kanagawa, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2014
VL 192
SU 1
MA BA8P.130
PG 1
WC Immunology
SC Immunology
GA V44RB
UT WOS:000209765005175
ER
PT J
AU Ahlman, M
Dave, J
Sadek, A
Mehta, N
Bluemke, D
AF Ahlman, Mark
Dave, Jenny
Sadek, Ahmed
Mehta, Nehal
Bluemke, David
TI Vascular uptake of F-18-fluorodeoxyglucose (FDG) correlates with blood,
liver, splenic, and myocardial uptake
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Ahlman, Mark; Bluemke, David] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Dave, Jenny; Sadek, Ahmed; Mehta, Nehal] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1748
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102414
ER
PT J
AU Bagci, U
Xu, ZY
Mollura, D
AF Bagci, Ulas
Xu, Ziyue
Mollura, Daniel
TI Recent advances in PET, PET-CT, and MRI-PET image segmentation
techniques
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Bagci, Ulas; Xu, Ziyue; Mollura, Daniel] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1280
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101444
ER
PT J
AU Bhatt, G
Wu, XY
Li, XF
Rai, S
Civelek, AC
AF Bhatt, Geetika
Wu, Xiaoyong
Li, Xiao-Feng
Rai, Shesh
Civelek, A. Cahid
TI Three hour solid gastric emptying accurately predicts the 4-h result: Is
4-h measurement necessary?
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Bhatt, Geetika; Wu, Xiaoyong; Li, Xiao-Feng; Rai, Shesh] Univ Louisville, Louisville, KY 40292 USA.
[Civelek, A. Cahid] NIH, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1962
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438104123
ER
PT J
AU Bhatt, G
Wu, XY
Li, XF
Rai, S
Civelek, AC
AF Bhatt, Geetika
Wu, Xiaoyong
Li, Xiao-Feng
Rai, Shesh
Civelek, A. Cahid
TI Three hour solid gastric emptying accurately predicts the 4-h result: Is
4-h measurement necessary?
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Bhatt, Geetika; Wu, Xiaoyong; Li, Xiao-Feng; Rai, Shesh] Univ Louisville, Louisville, KY 40292 USA.
[Civelek, A. Cahid] NIH, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1962
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438103133
ER
PT J
AU Bhatt, G
Li, XF
Civelek, AC
AF Bhatt, Geetika
Li, Xiao-Feng
Civelek, A. Cahid
TI 131I Thyroid cancer therapy in chronically bedridden & dialysis patients
with severe renal failure: Challenges and solutions for determining the
optimum therapy dose and how to minimize radiation dose to caregivers
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Civelek, A. Cahid] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Bhatt, Geetika; Li, Xiao-Feng] Univ Louisville, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1365
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102031
ER
PT J
AU Crandall, J
Shankar, L
Wahl, R
AF Crandall, John
Shankar, Lalitha
Wahl, Richard
TI Phase II single-arm trial comparing the use of FLT PET/CT to standard
computed tomography to assess the treatment response of neoadjuvant
docetaxel and cisplatin in stage IB-IIIA resectable non-small cell lung
cancer
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Crandall, John; Wahl, Richard] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Shankar, Lalitha] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1609
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102275
ER
PT J
AU Dickstein, L
Zanotti-Fregonara, P
Dustin, I
Hong, J
Liow, JS
Pike, V
Zoghbi, S
Rallis-Frutos, D
Innis, R
Theodore, W
AF Dickstein, Leah
Zanotti-Fregonara, Paolo
Dustin, Irene
Hong, Jinsoo
Liow, Jeih-San
Pike, Victor
Zoghbi, Sami
Rallis-Frutos, Denise
Innis, Robert
Theodore, William
TI Comparison of [11C]DPA-713 and [11C]PBR28 to measure translocator
protein in epilepsy
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Dickstein, Leah; Zanotti-Fregonara, Paolo; Dustin, Irene; Hong, Jinsoo; Liow, Jeih-San; Pike, Victor; Zoghbi, Sami; Rallis-Frutos, Denise; Innis, Robert; Theodore, William] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 417
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100418
ER
PT J
AU Dormish, P
Chen, C
Maass-Moreno, R
AF Dormish, Phil
Chen, Clara
Maass-Moreno, Roberto
TI Validation of a SUV-based correction for internal exposure dosimetry
using Monte Carlo simulations
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Chen, Clara; Maass-Moreno, Roberto] NIH, Radiol, Bethesda, MD 20892 USA.
[Dormish, Phil] Univ Virginia, Biomed Engn, Charlottesville, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 99
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100100
ER
PT J
AU Feng, T
Ahlman, M
Tsui, B
Guo, LH
Guttman, M
McVeigh, E
Bluemke, D
AF Feng, Tao
Ahlman, Mark
Tsui, Benjamin
Guo, Liheng
Guttman, Mike
McVeigh, Elliot
Bluemke, David
TI Hybrid MR-guided and PET-guided motion correction of PET images in
simultaneous PET/MR
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Feng, Tao; Tsui, Benjamin; Guo, Liheng; Guttman, Mike; McVeigh, Elliot] Johns Hopkins Univ, Baltimore, MD USA.
[Ahlman, Mark; Bluemke, David] NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 646
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101141
ER
PT J
AU Fujita, M
Hines, C
Zoghbi, S
Rallis-Frutos, D
Xu, R
Pike, V
Drevets, W
Zarate, C
Innis, R
AF Fujita, Masahiro
Hines, Christina
Zoghbi, Sami
Rallis-Frutos, Denise
Xu, Rong
Pike, Victor
Drevets, Wayne
Zarate, Carlos
Innis, Robert
TI Cyclic AMP cascade in major depressive disorder imaged with
C-11-(R)-rolipram - Downregulation in unmedicated patients and
normalization by antidepressant treatment
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Fujita, Masahiro; Hines, Christina; Zoghbi, Sami; Rallis-Frutos, Denise; Xu, Rong; Pike, Victor; Innis, Robert] NIMH, Mol Imaging Br, Bethesda, MD 20892 USA.
[Zarate, Carlos] NIMH, Exp Therap & Pathophysiol, Bethesda, MD 20892 USA.
[Drevets, Wayne] Johnson & Johnson, New Brunswick, NJ USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 81
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100082
ER
PT J
AU Guo, LH
Ahlman, M
Feng, T
Guttman, M
McVeigh, E
Bluemke, D
Tsui, B
Herzka, D
AF Guo, Liheng
Ahlman, Mark
Feng, Tao
Guttman, Michael
McVeigh, Elliot
Bluemke, David
Tsui, Benjamin
Herzka, Daniel
TI Real-time 3D MR respiratory motion acquisition for simultaneous PET/MR
imaging
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Guo, Liheng; McVeigh, Elliot; Herzka, Daniel] Johns Hopkins Univ, Biomed Engn, Baltimore, MD USA.
[Feng, Tao; Tsui, Benjamin] Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD USA.
[Ahlman, Mark; Bluemke, David] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Guttman, Michael] Johns Hopkins Univ, Sch Med, Cardiol, Baltimore, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 644
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101139
ER
PT J
AU Hirvonen, J
Zanotti-Fregonara, P
Gorelick, D
Rallis-Frutos, D
Morse, C
Zoghbi, S
Pike, V
Huestis, M
Innis, R
AF Hirvonen, Jussi
Zanotti-Fregonara, Paolo
Gorelick, David
Rallis-Frutos, Denise
Morse, Cheryl
Zoghbi, Sami
Pike, Victor
Huestis, Marilyn
Innis, Robert
TI Decreased brain cannabinoid CB1 receptor binding in tobacco smokers
examined with positron emission tomography
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Hirvonen, Jussi; Zanotti-Fregonara, Paolo; Rallis-Frutos, Denise; Morse, Cheryl; Zoghbi, Sami; Pike, Victor; Innis, Robert] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Gorelick, David; Huestis, Marilyn] NIDA, Chem & Drug Metab Sect, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 84
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100085
ER
PT J
AU Hurtle, B
Cai, LS
Qu, BX
Diaz-Arrastia, R
Innis, R
Pike, V
AF Hurtle, Bryan
Cai, Lisheng
Qu, Bao-Xi
Diaz-Arrastia, Ramon
Innis, Robert
Pike, Victor
TI Ligand-based virtual screening identifies novel leads for candidate PET
radioligands for neurofibrillary tangles and amyloid plaques
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Hurtle, Bryan; Cai, Lisheng; Innis, Robert; Pike, Victor] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Qu, Bao-Xi; Diaz-Arrastia, Ramon] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 551
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101046
ER
PT J
AU Ikawa, M
Lyoo, CH
Jenko, K
Morse, C
Zoghbi, S
Pike, V
McMahon, F
Turner, R
Innis, R
Kreisl, W
AF Ikawa, Masamichi
Lyoo, Chul Hyoung
Jenko, Kimberly
Morse, Cheryl
Zoghbi, Sami
Pike, Victor
McMahon, Francis
Turner, Raymond
Innis, Robert
Kreisl, William
TI Ratio measure of C-11-PBR28 binding allows noninvasive quantification of
neuroinflammation in Alzheimer's disease
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Ikawa, Masamichi; Lyoo, Chul Hyoung; Jenko, Kimberly; Morse, Cheryl; Zoghbi, Sami; Pike, Victor; McMahon, Francis; Innis, Robert; Kreisl, William] NIMH, Bethesda, MD 20892 USA.
[Turner, Raymond] Georgetown Univ, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1826
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102492
ER
PT J
AU Kim, JS
Kim, I
Lee, SJ
Kim, H
Davies-Venn, C
Won, S
Niu, G
Chen, XY
Paik, C
Bluemke, D
AF Kim, Jin Su
Kim, Insook
Lee, Sung-Jin
Kim, Heejung
Davies-Venn, Cynthia
Won, Samuel
Niu, Gang
Chen, Xiaoyuan
Paik, Chang
Bluemke, David
TI Longitudinal analysis of PET imaging with Cu-64-labeled collagen
specific peptides for the detection of collagen in myocardial fibrosis
in rats
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Kim, Jin Su; Lee, Sung-Jin; Kim, Heejung; Paik, Chang] NIH, NMD, RAD&IS, CC, Bethesda, MD 20892 USA.
[Kim, Insook] Leidos Inc, ADRD, Frederick, MD USA.
[Davies-Venn, Cynthia; Won, Samuel; Bluemke, David] NIH, RAD&IS, CC, Bethesda, MD 20892 USA.
[Niu, Gang; Chen, Xiaoyuan] NIBIB, LOMIN, NIH, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 408
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100409
ER
PT J
AU Kobayashi, M
Zanotti-Fregonara, P
Dickstein, L
Zoghbi, S
Lohith, T
Rallis-Frutos, D
Telu, S
Pike, V
Fujita, M
Innis, R
AF Kobayashi, Masato
Zanotti-Fregonara, Paolo
Dickstein, Leah
Zoghbi, Sami
Lohith, Talakad
Rallis-Frutos, Denise
Telu, Sanjay
Pike, Victor
Fujita, Masahiro
Innis, Robert
TI Influence of polymorphism rs6971 on [C-11]DPA-713 imaging in human brain
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Kobayashi, Masato; Zanotti-Fregonara, Paolo; Dickstein, Leah; Zoghbi, Sami; Lohith, Talakad; Rallis-Frutos, Denise; Telu, Sanjay; Pike, Victor; Fujita, Masahiro; Innis, Robert] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 322
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100323
ER
PT J
AU Kreisl, W
Bhatia, R
Morse, C
Zoghbi, S
Shetty, HU
Liow, JS
Pike, V
Innis, R
AF Kreisl, William
Bhatia, Ritwik
Morse, Cheryl
Zoghbi, Sami
Shetty, H. Umesha
Liow, Jeih-San
Pike, Victor
Innis, Robert
TI Increased P-gp inhibition at the human blood brain barrier can be safely
achieved and reliably measured by performing PET during peak plasma
concentrations of tariquidar
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Kreisl, William; Bhatia, Ritwik; Morse, Cheryl; Zoghbi, Sami; Shetty, H. Umesha; Liow, Jeih-San; Pike, Victor; Innis, Robert] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1801
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102467
ER
PT J
AU Lee, D
Thada, S
Guo, J
Hall, K
Barker, W
Hammoud, D
AF Lee, Dianne
Thada, Shanthalaxmi
Guo, Juen
Hall, Kevin
Barker, William
Hammoud, Dima
TI Quantitative comparison of motion correction methods in HRRT brain
imaging
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lee, Dianne; Hammoud, Dima] NIH, Ctr Infect Dis Imaging Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Thada, Shanthalaxmi; Barker, William] NIH, PET Dept, Bethesda, MD 20892 USA.
[Guo, Juen; Hall, Kevin] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2111
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438104272
ER
PT J
AU Lee, D
Thada, S
Guo, JE
Hall, K
Barker, W
Hammoud, D
AF Lee, Dianne
Thada, Shanthalaxmi
Guo, Juen
Hall, Kevin
Barker, William
Hammoud, Dima
TI Quantitative comparison of motion correction methods in HRRT brain
imaging
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lee, Dianne; Hammoud, Dima] NIH, Ctr Infect Dis Imaging Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Thada, Shanthalaxmi; Barker, William] NIH, PET Dept, Bethesda, MD 20892 USA.
[Guo, Juen; Hall, Kevin] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2111
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438103282
ER
PT J
AU Lee, D
Reid, W
Ibrahim, W
Peterson, K
Lentz, M
Jagoda, E
Hammoud, D
AF Lee, Dianne
Reid, William
Ibrahim, Wael
Peterson, Kristin
Lentz, Margaret
Jagoda, Elaine
Hammoud, Dima
TI Decreased striatal D2/3 receptors in HIV-1 transgenic rat seen with
[18F]Fallypride-PET
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lee, Dianne; Reid, William; Ibrahim, Wael; Peterson, Kristin; Lentz, Margaret; Hammoud, Dima] NIH, Ctr Infect Dis Imaging Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Jagoda, Elaine] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 29
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100030
ER
PT J
AU Lee, SJ
Kim, JS
Kim, I
Yao, ZS
Lee, JH
Pastan, I
Paik, C
AF Lee, Sung-Jin
Kim, Jin Su
Kim, Insook
Yao, Zhengsheng
Lee, Jae-Ho
Pastan, Ira
Paik, Chang
TI Serial fractional doses of mAb B3 and paclitaxel improve accumulation
and penetration of B3 due to apoptosis of tumor cells
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lee, Sung-Jin; Kim, Jin Su; Yao, Zhengsheng; Lee, Jae-Ho; Paik, Chang] NIH, NMD, RAD&IS, CC, Bethesda, MD 20892 USA.
[Kim, Insook] Leidos Inc, ADRD, Frederick, MD USA.
[Pastan, Ira] NCI, LMB, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1376
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102042
ER
PT J
AU Lindenberg, L
Adler, S
Thomas, A
Maltzman, J
Wallin, B
Mena, E
Kurdziel, K
Paik, C
Choyke, P
Hassan, R
AF Lindenberg, Liza
Adler, Stephen
Thomas, Anish
Maltzman, Julia
Wallin, Bruce
Mena, Esther
Kurdziel, Karen
Paik, Chang
Choyke, Peter
Hassan, Raffit
TI Initial clinical experience of 111In radiolabelled amatuximab in
patients with mesothelin-expressing cancers
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lindenberg, Liza; Mena, Esther; Kurdziel, Karen; Choyke, Peter] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
[Maltzman, Julia; Wallin, Bruce] Morphotek Inc, Exton, PA USA.
[Thomas, Anish; Hassan, Raffit] NCI, Mol Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Adler, Stephen] NCI, Mol Imaging Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Paik, Chang] NIH, Radiopharmaceut Lab, Div Nucl Med, Dept Radiol & Imaging Sci,Clin Ctr, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1138
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101302
ER
PT J
AU Lohith, T
Tsujikawa, T
Zoghbi, S
Jaaro-Peled, H
Kimura, Y
Morse, C
Pike, V
Sawa, A
Innis, R
Fujita, M
AF Lohith, Talakad
Tsujikawa, Tetsuya
Zoghbi, Sami
Jaaro-Peled, Hanna
Kimura, Yasuyuki
Morse, Cheryl
Pike, Victor
Sawa, Akira
Innis, Robert
Fujita, Masahiro
TI PET imaging of increased C-11-(R)-rolipram binding in Disc1 transgenic
mouse brain suggesting regulation of cAMP cascade by DISC1
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lohith, Talakad; Tsujikawa, Tetsuya; Zoghbi, Sami; Kimura, Yasuyuki; Morse, Cheryl; Pike, Victor; Innis, Robert; Fujita, Masahiro] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Jaaro-Peled, Hanna; Sawa, Akira] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 469
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100470
ER
PT J
AU Lohith, T
Fabrice, S
Zoghbi, S
Morse, C
Pike, V
Innis, R
Fujita, M
AF Lohith, Talakad
Fabrice, Simeon
Zoghbi, Sami
Morse, Cheryl
Pike, Victor
Innis, Robert
Fujita, Masahiro
TI Potential utility of C-11-FPEB as a PET ligand for imaging metabotropic
glutamate receptor 5 (mGluR5) in human brain
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Lohith, Talakad; Fabrice, Simeon; Zoghbi, Sami; Morse, Cheryl; Pike, Victor; Innis, Robert; Fujita, Masahiro] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 360
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100361
ER
PT J
AU Mansoor, A
Bagci, U
Mollura, D
AF Mansoor, Awais
Bagci, Ulas
Mollura, Daniel
TI Noise adaptive multi-resolution technique to accurately denoise PET,
MRI-PET, and PET-CT images
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Mansoor, Awais; Bagci, Ulas; Mollura, Daniel] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2050
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438104211
ER
PT J
AU Mansoor, A
Bagci, U
Mollura, D
AF Mansoor, Awais
Bagci, Ulas
Mollura, Daniel
TI Noise adaptive multi-resolution technique to accurately denoise PET,
MRI-PET, and PET-CT images
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Mansoor, Awais; Bagci, Ulas; Mollura, Daniel] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2050
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438103221
ER
PT J
AU Reynolds, J
Maass-Moreno, R
AF Reynolds, James
Maass-Moreno, Roberto
TI Comparison of SULmax and PERCIST SULpeak across patients and scanners
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Reynolds, James; Maass-Moreno, Roberto] NIH, Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2069
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438104230
ER
PT J
AU Reynolds, J
Maass-Moreno, R
AF Reynolds, James
Maass-Moreno, Roberto
TI Comparison of SULmax and PERCIST SULpeak across patients and scanners
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Reynolds, James; Maass-Moreno, Roberto] NIH, Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2069
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438103240
ER
PT J
AU Sadek, A
Ahlman, M
Dave, J
Hasan, J
Krishnamoorthy, P
Rose, S
Weiner, E
Herscovitch, P
Bluemke, D
Mehta, N
AF Sadek, Ahmed
Ahlman, Mark
Dave, Jenny
Hasan, Josh
Krishnamoorthy, Parasuram
Rose, Shawn
Weiner, Elizabeth
Herscovitch, Peter
Bluemke, David
Mehta, Nehal
TI Detection of vascular inflammation by PET/MRI as compared to PET/CT
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Sadek, Ahmed; Dave, Jenny; Hasan, Josh; Rose, Shawn; Weiner, Elizabeth; Mehta, Nehal] NHLBI, NIH, Bethesda, MD 20892 USA.
[Krishnamoorthy, Parasuram] Englewood Hosp, Englewood, NJ USA.
[Herscovitch, Peter] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Ahlman, Mark; Bluemke, David] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1778
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102444
ER
PT J
AU Sail, D
Matsumoto, S
Vasalatiy, O
Cherukuri, M
Mitchell, J
AF Sail, Deepak
Matsumoto, Shingo
Vasalatiy, Olga
Cherukuri, Murali
Mitchell, James
TI Synthesis of novel fully deuterated 13C labeled 5,5-dimethyl
pyrroline-N-oxide as spin trap agent
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Sail, Deepak; Vasalatiy, Olga] NIH, Imaging Probe Dev Ctr, Rockville, MD USA.
[Matsumoto, Shingo; Cherukuri, Murali; Mitchell, James] NCI, Radiat Biol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1205
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101369
ER
PT J
AU Sato, N
Wu, HT
Griffiths, G
Choyke, P
AF Sato, Noriko
Wu, Haitao
Griffiths, Gary
Choyke, Peter
TI Generation and use of long-lasting cell labeling agent for positron
emission tomography (PET) imaging
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Sato, Noriko; Griffiths, Gary; Choyke, Peter] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
[Wu, Haitao] NHLBI, Imaging Probe Dev Ctr, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 273
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100274
ER
PT J
AU Satz, S
Baum, R
Kulkarni, H
Narasimhan, D
Mueller, D
Brechbiel, M
Kim, YS
AF Satz, Stanley
Baum, Richard
Kulkarni, Harshad
Narasimhan, Danthi
Mueller, Dirk
Brechbiel, Martin
Kim, Young-Seung
TI First clinical application of a non-cyclic peptidomimetic theranostic
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Satz, Stanley] Adv Imaging Projects Inc, Lake Worth, FL USA.
[Baum, Richard; Kulkarni, Harshad; Mueller, Dirk] Bad Berka Clin, Nucl Med, Bad Berka, Germany.
[Narasimhan, Danthi; Brechbiel, Martin; Kim, Young-Seung] NCI, Rockville, MD USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1193
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101357
ER
PT J
AU Singh, P
Cai, LS
Morse, C
Gladding, R
Fujita, M
Innis, R
Pike, V
AF Singh, Prachi
Cai, Lisheng
Morse, Cheryl
Gladding, Robert
Fujita, Masahiro
Innis, Robert
Pike, Victor
TI Radiosynthesis of [11C]sotrastaurin and evaluation as a PET radioligand
for imaging brain PKC in monkey
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Singh, Prachi; Cai, Lisheng; Morse, Cheryl; Gladding, Robert; Fujita, Masahiro; Innis, Robert; Pike, Victor] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1114
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101278
ER
PT J
AU Suzuki, A
Leland, P
Kobayashi, H
Choyke, P
Jagoda, E
Inoue, T
Joshi, B
Puri, R
AF Suzuki, Akiko
Leland, Pamela
Kobayashi, Hisataka
Choyke, Peter
Jagoda, Elaine
Inoue, Tomio
Joshi, Bharat
Puri, Raj
TI Evaluation of intracranial distribution of interleukin-13 receptor
directed immunotoxin after convection enhanced delivery by SPECT/CT in a
human brain tumor mouse model
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Suzuki, Akiko; Leland, Pamela; Joshi, Bharat; Puri, Raj] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA.
[Kobayashi, Hisataka; Choyke, Peter; Jagoda, Elaine] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
[Inoue, Tomio] Yokohama City Univ, Radiol, Yokohama, Kanagawa 232, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1027
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438101191
ER
PT J
AU Talbott, S
Bhatt, G
Li, XF
Civelek, AC
AF Talbott, Sabrina
Bhatt, Geetika
Li, Xiao-Feng
Civelek, A. Cahid
TI Dose related decreased image quality of CT doesn't degrade the
diagnostic quality of PET-CT
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Civelek, A. Cahid] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Talbott, Sabrina; Bhatt, Geetika; Li, Xiao-Feng] Univ Louisville, Radiol & Med, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 423
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100424
ER
PT J
AU Wang, Y
Yue, XY
Kiesewetter, D
Lu, J
Teng, GJ
Niu, G
Chen, XY
AF Wang, Yu
Yue, Xuyi
Kiesewetter, Dale
Lu, Jie
Teng, Gaojun
Niu, Gang
Chen, Xiaoyuan
TI Reduced TSPO expression after AMD3100 treatment in mouse stroke model: A
PET study with [18F]DPA-714
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Wang, Yu; Yue, Xuyi; Kiesewetter, Dale; Lu, Jie; Niu, Gang; Chen, Xiaoyuan] NIBIB, NIH, Bethesda, MD USA.
[Teng, Gaojun] SEU, Dept Radiol, Nanjing, Jiangsu, Peoples R China.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 1799
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438102465
ER
PT J
AU Wang, Z
Wang, Y
Niu, G
Chen, XY
AF Wang, Zhe
Wang, Yu
Niu, Gang
Chen, Xiaoyuan
TI Spatiotemporal molecular imaging of dynamic differentiation of
transplanted neural stem cells in traumatic brain injury
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Wang, Zhe; Wang, Yu; Niu, Gang; Chen, Xiaoyuan] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 472
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100473
ER
PT J
AU Xu, ZY
Bagci, U
Mollura, D
AF Xu, Ziyue
Bagci, Ulas
Mollura, Daniel
TI Diffusion based enhancement of PET images for improved diagnostic
measurements in clinical nuclear medicine
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Xu, Ziyue; Bagci, Ulas; Mollura, Daniel] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2051
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438104212
ER
PT J
AU Xu, ZY
Bagci, U
Mollura, D
AF Xu, Ziyue
Bagci, Ulas
Mollura, Daniel
TI Diffusion based enhancement of PET images for improved diagnostic
measurements in clinical nuclear medicine
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Xu, Ziyue; Bagci, Ulas; Mollura, Daniel] NIH, Radiol & Imaging Sci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 2051
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438103222
ER
PT J
AU Zanotti-Fregonara, P
Zoghbi, S
Liow, JS
Xu, R
Rallis-Frutos, D
Pike, V
Innis, R
AF Zanotti-Fregonara, Paolo
Zoghbi, Sami
Liow, Jeih-San
Xu, Rong
Rallis-Frutos, Denise
Pike, Victor
Innis, Robert
TI [18F]FIMX is a promising tracer to quantify metabotropic glutamate
receptor 1 (mGluR1) in human brain
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Zanotti-Fregonara, Paolo; Zoghbi, Sami; Liow, Jeih-San; Xu, Rong; Rallis-Frutos, Denise; Pike, Victor; Innis, Robert] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 359
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100360
ER
PT J
AU Zanotti-Fregonara, P
Lyoo, CH
Zoghbi, S
Liow, JS
Xu, R
Pike, V
Zarate, C
Fujita, M
Innis, R
AF Zanotti-Fregonara, Paolo
Lyoo, Chul Hyoung
Zoghbi, Sami
Liow, Jeih-San
Xu, Rong
Pike, Victor
Zarate, Carlos
Fujita, Masahiro
Innis, Robert
TI Image-derived input function derived from a supervised clustering
algorithm: Methodology and validation in a clinical protocol using
[11C](R)-rolipram
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging
(SNMMI)
CY JUN 07-11, 2014
CL St Louis, MO
SP Soc Nucl Med & Mol Imaging
C1 [Zanotti-Fregonara, Paolo; Lyoo, Chul Hyoung; Zoghbi, Sami; Liow, Jeih-San; Xu, Rong; Pike, Victor; Zarate, Carlos; Fujita, Masahiro; Innis, Robert] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY
PY 2014
VL 55
SU 1
MA 316
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CR6FA
UT WOS:000361438100317
ER
PT J
AU Massey, PR
Cowen, EW
Okman, JS
Wilkerson, J
AF Massey, Paul R.
Cowen, Edward W.
Okman, Jonathan S.
Wilkerson, Julia
TI VEGF inhibitors have distinct cutaneous and systemic toxicity profiles:
A metaanalysis and review of the literature
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Meeting Abstract
CT 72nd Annual Meeting of the American-Academy-of-Dermatology
CY MAR 21-25, 2014
CL Denver, CO
SP Amer Acad Dermatol
C1 [Massey, Paul R.; Okman, Jonathan S.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Cowen, Edward W.; Wilkerson, Julia] NCI, Bethesda, MD 20892 USA.
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 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD MAY
PY 2014
VL 70
IS 5
SU 1
MA P8285
BP AB120
EP AB120
PG 1
WC Dermatology
SC Dermatology
GA CQ4OI
UT WOS:000360583900473
ER
PT J
AU Hou, Y
Ghosh, P
Wan, RQ
Ouyang, X
Cheng, HP
Mattson, MP
Cheng, AW
AF Hou, Yan
Ghosh, Paritosh
Wan, Ruiqian
Ouyang, Xin
Cheng, Heping
Mattson, Mark P.
Cheng, Aiwu
TI Permeability transition pore-mediated mitochondrial superoxide flashes
mediate an early inhibitory effect of amyloid beta1-42 on neural
progenitor cell proliferation
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Alzheimer's disease; Amyloid beta-peptide; ERK; Mitochondrial
permeability transition pore; Neurogenesis; SOD
ID ADULT HIPPOCAMPAL NEUROGENESIS; FAMILIAL ALZHEIMERS-DISEASE; TRANSGENIC
MOUSE MODEL; ISCHEMIC BRAIN-INJURY; PRECURSOR PROTEIN; OXIDATIVE STRESS;
A-BETA; STEM-CELLS; ENVIRONMENTAL ENRICHMENT; IMPAIRED NEUROGENESIS
AB Cellular damage by reactive oxygen species and altered neurogenesis are implicated in the etiology of AD and the pathogenic actions of amyloid beta-peptide (A beta); the underlying mechanisms and the early oxidative intracellular events triggered by A beta are not established. In the present study, we found that mouse embryonic cortical neural progenitor cells exhibit intermittent spontaneous mitochondrial superoxide (SO) flashes that require transient opening of mitochondrial permeability transition pores (mPTPs). The incidence of mitochondria SO flash activity in neural progenitor cells (NPCs) increased during the first 6-24 hours of exposure to aggregating amyloid beta-peptide (A beta 1-42), indicating an increase in transient mPTP opening. Subsequently, the SO flash frequency progressively decreased and ceased between 48 and 72 hours of exposure to A beta 1-42, during which time global cellular reactive oxygen species increased, mitochondrial membrane potential decreased, cytochrome C was released from mitochondria and the cells degenerated. Inhibition of mPTPs and selective reduction in mitochondrial SO flashes significantly ameliorated the negative effects of A beta 1-42 on NPC proliferation and survival. Our findings suggest that mPTP-mediated bursts of mitochondrial SO production is a relatively early and pivotal event in the adverse effects of A beta 1-42 on NPCs. If a beta inhibits NPC proliferation in the brains of AD patients by a similar mechanism, then interventions that inhibit mPTP-mediated superoxide flashes would be expected to protect NPCs against the adverse effects of A beta. Published by Elsevier Inc.
C1 [Hou, Yan; Wan, Ruiqian; Ouyang, Xin; Mattson, Mark P.; Cheng, Aiwu] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Ghosh, Paritosh] NIA, Immunol Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Cheng, Heping] Peking Univ, Inst Mol Med, Beijing 100871, Peoples R China.
[Cheng, Heping] Peking Univ, Natl Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China.
[Mattson, Mark P.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov; chengai@mail.nih.gov
FU Intramural Research Program of the National Institute on Aging; Glenn
Foundation for Medical Research; National Natural Science Foundation;
National Basic Research Program of China [2011CB809100]
FX This work was supported by the Intramural Research Program of the
National Institute on Aging, by the Glenn Foundation for Medical
Research, and by the National Natural Science Foundation and National
Basic Research Program of China (2011CB809100).
NR 89
TC 16
Z9 16
U1 0
U2 20
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD MAY
PY 2014
VL 35
IS 5
BP 975
EP 989
DI 10.1016/j.neurobiolaging.2013.11.002
PG 15
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AC2DO
UT WOS:000332308300004
PM 24325797
ER
PT J
AU Rothman, SM
Griffioen, KJ
Fishbein, KW
Spencer, RG
Makrogiannis, S
Cong, WN
Martin, B
Mattson, MP
AF Rothman, Sarah M.
Griffioen, Kathleen J.
Fishbein, Kenneth W.
Spencer, Richard G.
Makrogiannis, Sokratis
Cong, Wei-na
Martin, Bronwen
Mattson, Mark P.
TI Metabolic abnormalities and hypoleptinemia in alpha-synuclein A53T
mutant mice
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Parkinson's disease; Energy metabolism; Leptin; Insulin; Body fat
ID PARKINSONS-DISEASE PATIENTS; IMPAIRED GLUCOSE-TOLERANCE; WEIGHT-LOSS;
SLEEP DISTURBANCES; JAPANESE-AMERICANS; VISCERAL ADIPOSITY;
INSULIN-RESISTANCE; ENERGY-EXPENDITURE; LEPTIN RECEPTOR; PLASMA LEPTIN
AB Parkinson's disease (PD) patients frequently display loss of body fat mass and increased energy expenditure, and several studies have outlined a relationship between these metabolic abnormalities and disease severity, yet energy metabolism is largely unstudied in mouse models of PD. Here we characterize metabolic and physiologic responses to a high calorie diet (HCD) in mice expressing in neurons a mutant form of human a-synuclein (A53T) that causes dominantly inherited familial forms of the disease. A53T (SNCA) and wild type (WT) littermate mice were placed on a HCD for 12 weeks and evaluated for weight gain, food intake, body fat, blood plasma leptin, hunger, glucose tolerance, and energy expenditure. Results were compared with both SNCA and WT mice on a control diet. Despite consuming similar amounts of food, WT mice gained up to 66% of their original body weight on a HCD, whereas SNCA mice gained only 17%. Further, after 12 weeks on a HCD, magnetic resonance imaging analysis revealed that WT mice had significantly greater total and visceral body fat compared with SNCA mice (p < 0.007). At the age of 24 weeks SNCA mice displayed significantly increased hunger compared with WT (p < 0.03). At the age of 36 weeks, SNCA mice displayed significant hypoleptinemia compared with WT, both on a normal diet and a HCD (p < 0.03). The HCD induced insulin insensitivity in WT, but not SNCA mice, as indicated by an oral glucose tolerance test. Finally, SNCA mice displayed greater energy expenditure compared with WT, as measured in a Comprehensive Laboratory Animal Monitoring System, after 12 weeks on a HCD. Thus, SNCA mice are resistant to HCD-induced obesity and insulin resistance and display reduced body fat, increased hunger, hypoleptinemia and increased energy expenditure. Our findings reveal a profile of metabolic dysfunction in a mouse model of PD that is similar to that of human PD patients, thus providing evidence that alpha-synuclein pathology is sufficient to drive such metabolic abnormalities and providing an animal model for discovery of the underlying mechanisms and potential therapeutic interventions. Published by Elsevier Inc.
C1 [Rothman, Sarah M.; Griffioen, Kathleen J.; Mattson, Mark P.] NIA, Neurosci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Fishbein, Kenneth W.; Spencer, Richard G.] NIA, Magnet Resonance Imaging & Spect Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Makrogiannis, Sokratis] NIA, Longitudinal Studies Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Cong, Wei-na; Martin, Bronwen] NIA, Lab Clin Invest, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mark.mattson@nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the National Institutes of Health, National Institute on Aging. The
authors thank Catherine Crews and Charles Reitz for assistance with
management of the mouse colonies.
NR 43
TC 3
Z9 3
U1 1
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD MAY
PY 2014
VL 35
IS 5
BP 1153
EP 1161
DI 10.1016/j.neurobiolaging.2013.10.088
PG 9
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AC2DO
UT WOS:000332308300022
PM 24239384
ER
PT J
AU Periwal, V
Gaillard, JR
Needleman, L
Doria, C
AF Periwal, V.
Gaillard, J. R.
Needleman, L.
Doria, C.
TI Mathematical Model of Liver Regeneration in Human Live Donors
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID LIVING-DONOR; TRANSPLANTATION; RAT
AB Liver regeneration after injury occurs in many mammals. Rat liver regenerates after partial hepatectomy over a period of 2 weeks while human liver regeneration takes several months. Notwithstanding this enormous difference in time-scales, with new data from five human live liver transplant donors, we show that a mathematical model of rat liver regeneration can be transferred to human, with all biochemical interactions and signaling unchanged. Only six phenomenological parameters need change, and three of these parameter changes are rescalings of rate constants by the ratio of human lifespan to rat lifespan. Data from three donor subjects with approximately equal resections were used to fit the three parameters and the data from the other two donor subjects was used to independently verify the fit. J. Cell. Physiol. 229: 599-606, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Periwal, V.; Gaillard, J. R.] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20814 USA.
[Needleman, L.; Doria, C.] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
RP Periwal, V (reprint author), NIDDK, Math Cell Modeling Sect, NIH, Bldg 12A,Room 4007,12 S Dr, Bethesda, MD 20814 USA.
EM vipulp@mail.nih.gov
FU National Institutes of Health, NIDDK
FX Contract grant sponsor: National Institutes of Health, NIDDK.
NR 16
TC 6
Z9 6
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD MAY
PY 2014
VL 229
IS 5
BP 599
EP 606
DI 10.1002/jcp.24482
PG 8
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA AA4JX
UT WOS:000331063000009
PM 24446196
ER
PT J
AU Lee, KS
Park, JE
Kang, YH
Kim, TS
Bang, JK
AF Lee, Kyung S.
Park, Jung-Eun
Kang, Young Hwi
Kim, Tae-Sung
Bang, Jeong K.
TI Mechanisms Underlying Plk1 Polo-Box Domain-Mediated Biological Processes
and Their Physiological Significance
SO MOLECULES AND CELLS
LA English
DT Review
DE non-self-priming; self-priming; Plk1; polo-box domain
ID KINASE 1; PROTEIN-KINASE; SUBCELLULAR-LOCALIZATION; SPINDLE CHECKPOINT;
MITOTIC FUNCTIONS; STRUCTURAL BASIS; CANCER-THERAPY; PHOSPHORYLATION;
POLO-LIKE-KINASE-1; CYTOKINESIS
AB Mammalian polo-like kinase 1 (Plk1) has been studied intensively as a key regulator of various cell cycle events that are critical for proper M-phase progression. The polo-box domain (PBD) present in Plk1's C-terminal noncatalytic region has been shown to play a central role in targeting the N-terminal kinase domain of Plk1 to specific subcellular locations. Subsequent studies reveal that PBD binds to a phosphorylated motif generated by one of the two mechanisms - self-priming by Plk1 itself or non-self-priming by a Pro-directed kinase, such as Cdc2. Here, we comparatively review the differences in the biochemical steps of these mechanisms and discuss their physiological significance. Considering the diverse functions of Plk1 during the cell cycle, a better understanding of how the catalytic activity of Plk1 functions in concert with its cis-acting PBD and how this coordinated process is intricately regulated to promote Plk1 functions will be important for providing new insights into different mechanisms underlying various Plk1-mediated biological events that occur at the multiple stages of the cell cycle.
C1 [Lee, Kyung S.; Park, Jung-Eun; Kim, Tae-Sung] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
[Kang, Young Hwi] Ewha Womans Univ, Dept Life Sci, Immune & Vasc Cell Network Res Ctr, Seoul 120750, South Korea.
[Kang, Young Hwi] Ewha Womans Univ, Program GT5, Seoul 120750, South Korea.
[Bang, Jeong K.] Korea Basic Sci Inst, Div Magnet Resonance, Ochang 363883, South Korea.
RP Lee, KS (reprint author), NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
EM kyunglee@mail.nih.gov
FU National Cancer Institute; Korea Basic Science Institute [T33418]
FX We are grateful to all the past and present members of the Lee
laboratory for stimulating discussions about self-priming and
non-self-priming mechanisms for PBD binding. This work was supported in
part by a National Cancer Institute intramural grant (K.S.L.) and Korea
Basic Science Institute's research grant T33418 (J.K.B).
NR 50
TC 4
Z9 4
U1 0
U2 4
PU KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
PI SEOUL
PA 635-4, YUCKSAM-DONG, GANGNAM-GU, SEOUL 135-703, SOUTH KOREA
SN 1016-8478
EI 0219-1032
J9 MOL CELLS
JI Mol. Cells
PD APR 30
PY 2014
VL 37
IS 4
BP 286
EP 294
DI 10.14348/molcells.2014.0002
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AQ1RZ
UT WOS:000342560000002
PM 24722413
ER
PT J
AU Schrack, JA
Zipunnikov, V
Goldsmith, J
Bandeen-Roche, K
Crainiceanu, CM
Ferrucci, L
AF Schrack, Jennifer A.
Zipunnikov, Vadim
Goldsmith, Jeff
Bandeen-Roche, Karen
Crainiceanu, Ciprian M.
Ferrucci, Luigi
TI Estimating Energy Expenditure from Heart Rate in Older Adults: A Case
for Calibration
SO PLOS ONE
LA English
DT Article
ID DOUBLY LABELED WATER; PHYSICAL-ACTIVITY QUESTIONNAIRES; ACCELEROMETRY;
FITNESS
AB Background: Accurate measurement of free-living energy expenditure is vital to understanding changes in energy metabolism with aging. The efficacy of heart rate as a surrogate for energy expenditure is rooted in the assumption of a linear function between heart rate and energy expenditure, but its validity and reliability in older adults remains unclear.
Objective: To assess the validity and reliability of the linear function between heart rate and energy expenditure in older adults using different levels of calibration.
Design: Heart rate and energy expenditure were assessed across five levels of exertion in 290 adults participating in the Baltimore Longitudinal Study of Aging. Correlation and random effects regression analyses assessed the linearity of the relationship between heart rate and energy expenditure and cross-validation models assessed predictive performance.
Results: Heart rate and energy expenditure were highly correlated (r = 0.98) and linear regardless of age or sex. Intra-person variability was low but inter-person variability was high, with substantial heterogeneity of the random intercept (s.d. = 0.372) despite similar slopes. Cross-validation models indicated individual calibration data substantially improves accuracy predictions of energy expenditure from heart rate, reducing the potential for considerable measurement bias. Although using five calibration measures provided the greatest reduction in the standard deviation of prediction errors (1.08 kcals/min), substantial improvement was also noted with two (0.75 kcals/min).
Conclusion: These findings indicate standard regression equations may be used to make population-level inferences when estimating energy expenditure from heart rate in older adults but caution should be exercised when making inferences at the individual level without proper calibration.
C1 [Schrack, Jennifer A.; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Schrack, Jennifer A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Zipunnikov, Vadim; Goldsmith, Jeff; Bandeen-Roche, Karen; Crainiceanu, Ciprian M.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
[Schrack, Jennifer A.; Bandeen-Roche, Karen] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
RP Schrack, JA (reprint author), NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
EM jschrack@jhsph.edu
FU National Institutes of Health, National Institute on Aging
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Aging. Data for
these analyses were obtained from the Baltimore Longitudinal Study of
Aging, a study performed by the National Institute on Aging. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 25
TC 5
Z9 5
U1 0
U2 5
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 APR 30
PY 2014
VL 9
IS 4
AR e93520
DI 10.1371/journal.pone.0093520
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AL1WP
UT WOS:000338917300004
PM 24787146
ER
PT J
AU Tomasi, D
Volkow, ND
AF Tomasi, Dardo
Volkow, Nora D.
TI Mapping Small-World Properties through Development in the Human Brain:
Disruption in Schizophrenia
SO PLOS ONE
LA English
DT Article
ID FUNCTIONAL CONNECTIVITY MRI; HUMAN CEREBRAL-CORTEX; RESTING-STATE;
1ST-DEGREE RELATIVES; ALZHEIMERS-DISEASE; DEFAULT NETWORK; CORTICAL
HUBS; LOW-FREQUENCY; TEST-RETEST; ORGANIZATION
AB Evidence from imaging studies suggests that the human brain has a small-world network topology that might be disrupted in certain brain disorders. However, current methodology is based on global graph theory measures, such as clustering, C, characteristic path length, L, and small-worldness, S, that lack spatial specificity and are insufficient to identify regional brain abnormalities. Here we propose novel ultra-fast methodology for mapping local properties of brain network topology such as local C, L and S (lC, lL and lS) in the human brain at 3-mm isotropic resolution from 'resting-state' magnetic resonance imaging data. Test-retest datasets from 40 healthy children/adolescents were used to demonstrate the overall good reliability of the measures across sessions and computational parameters (intraclass correlation >0.5 for lC and lL) and their low variability across subjects (< 29%). Whereas regions with high local functional connectivity density (lFCD; local degree) in posterior parietal and occipital cortices demonstrated high lC and short lL, subcortical regions (globus pallidus, thalamus, hippocampus and amygdala), cerebellum (lobes and vermis), cingulum and temporal cortex also had high, lS, demonstrating stronger small-world topology than other hubs. Children/adolescents had stronger lFCD, higher lC and longer lL in most cortical regions and thalamus than 74 healthy adults, consistent with pruning of functional connectivity during maturation. In contrast, lFCD, lC and lL were weaker in thalamus and midbrain, and lL was shorter in frontal cortical regions and cerebellum for 69 schizophrenia patients than for 74 healthy controls, suggesting exaggerated pruning of connectivity in schizophrenia. Follow up correlation analyses for seeds in thalamus and midbrain uncovered lower positive connectivity of these regions in thalamus, putamen, cerebellum and frontal cortex (cingulum, orbitofrontal, inferior frontal) and lower negative connectivity in auditory, visual, motor, premotor and somatosensory cortices for schizophrenia patients than for controls, consistent with prior findings of thalamic disconnection in schizophrenia.
C1 [Tomasi, Dardo; Volkow, Nora D.] NIAAA, Bethesda, MD 20892 USA.
[Volkow, Nora D.] NIDA, Bethesda, MD 20892 USA.
RP Tomasi, D (reprint author), NIAAA, Bethesda, MD 20892 USA.
EM tomasidg@mail.nih.gov
RI Tomasi, Dardo/J-2127-2015
FU National Institutes of Alcohol Abuse and Alcoholism [2RO1AA09481]
FX This work was accomplished with support from the National Institutes of
Alcohol Abuse and Alcoholism (2RO1AA09481). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 74
TC 11
Z9 13
U1 6
U2 20
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 APR 30
PY 2014
VL 9
IS 4
AR e96176
DI 10.1371/journal.pone.0096176
PG 17
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AL1WP
UT WOS:000338917300030
PM 24788815
ER
PT J
AU Johnen, VM
Buch, ER
Neubert, FX
AF Johnen, Vanessa M.
Buch, Ethan R.
Neubert, Franz-Xaver
TI Can Cortical Stimulation of Inferior Frontal Cortex Enhance Proactive
Control?
SO JOURNAL OF NEUROSCIENCE
LA English
DT Editorial Material
ID PLASTICITY; BRAIN
C1 [Johnen, Vanessa M.; Neubert, Franz-Xaver] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England.
[Johnen, Vanessa M.; Neubert, Franz-Xaver] Univ Oxford, John Radcliffe Hosp, Ctr Funct Magnet Resonance Imaging Brain, Oxford OX3 9DU, England.
[Buch, Ethan R.] NINDS, Human Cort Physiol & Neurorehabil Sect, NIH, Bethesda, MD 20814 USA.
[Buch, Ethan R.] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
RP Johnen, VM (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England.
EM vanessa.johnen@psy.ox.ac.uk
NR 11
TC 0
Z9 0
U1 0
U2 3
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 APR 30
PY 2014
VL 34
IS 18
BP 6125
EP 6127
DI 10.1523/JNEUROSCI.0590-14.2014
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA AH2AA
UT WOS:000335921900001
PM 24790182
ER
PT J
AU Mehta, B
Ke, JB
Zhang, L
Baden, AD
Markowitz, AL
Nayak, S
Briggman, KL
Zenisek, D
Singer, JH
AF Mehta, Bhupesh
Ke, Jiang-Bin
Zhang, Lei
Baden, Alexander D.
Markowitz, Alexander L.
Nayak, Subhashree
Briggman, Kevin L.
Zenisek, David
Singer, Joshua H.
TI Global Ca2+ Signaling Drives Ribbon-Independent Synaptic Transmission at
Rod Bipolar Cell Synapses
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE exocytosis; retina; ribbon; vesicle
ID INNER PLEXIFORM LAYER; AII AMACRINE CELLS; NEUROTRANSMITTER RELEASE;
MOUSE RETINA; TRANSMITTER RELEASE; RABBIT RETINA; HAIR-CELLS;
PRESYNAPTIC CALCIUM; GLUTAMATE RELEASE; MULTIVESICULAR RELEASE
AB Ribbon-type presynaptic active zones are a hallmark of excitatory retinal synapses, and the ribbon organelle is thought to serve as the organizing point of the presynaptic active zone. Imaging of exocytosis from isolated retinal neurons, however, has revealed ectopic release (i.e., release away from ribbons) in significant quantities. Here, we demonstrate in an in vitro mouse retinal slice preparation that ribbon-independent release from rod bipolar cells activates postsynaptic AMPARs on AII amacrine cells. This form of release appears to draw on a unique, ribbon-independent, vesicle pool. Experimental, anatomical, and computational analyses indicate that it is elicited by a significant, global elevation of intraterminal [Ca2+] arising following local buffer saturation. Our observations support the conclusion that ribbon-independent release provides a read-out of the average behavior of all of the active zones in a rod bipolar cell's terminal.
C1 [Mehta, Bhupesh; Zenisek, David] Yale Univ, Dept Cellular & Mol Physiol, New Haven, CT 06520 USA.
[Mehta, Bhupesh; Zenisek, David] Yale Univ, Dept Ophthalmol & Visual Sci, New Haven, CT 06520 USA.
[Ke, Jiang-Bin; Zhang, Lei; Baden, Alexander D.; Markowitz, Alexander L.; Nayak, Subhashree; Singer, Joshua H.] Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
[Briggman, Kevin L.] NINDS, Circuit Dynam & Connect Unit, NIH, Bethesda, MD 20892 USA.
RP Zenisek, D (reprint author), Dept Cellular & Mol Physiol, POB 208026,333 Cedar St, New Haven, CT 06520 USA.
EM david.zenisek@yale.edu; jhsinger@umd.edu
FU Intramural Research Program of the National Institutes of Health;
National Institute of Neurological Disorders and Stroke; Howard Hughes
Medical Institute through the Precollege and Undergraduate Science
Education Program; [EY017836]; [014990]
FX We thank J. Jiang for technical support; S. Ali, A. Ayala, P. Ghorbani,
C. Hahn, J. Masison, A. Merrihew, N. Park, K. Sistani, and M. Yi for
assistance with EM reconstruction; Victor Matveev for his help with
CalC; and Greg Sullivan for access to the computing resources of the UMD
Particle Astrophysics group. Supported by EY017836 to J.H.S.; by 014990
to D.Z.; and by the Intramural Research Program of the National
Institutes of Health, National Institute of Neurological Disorders and
Stroke (K.L.B.). S.N. received support from a grant to the University of
Maryland from the Howard Hughes Medical Institute through the Precollege
and Undergraduate Science Education Program.
NR 93
TC 9
Z9 9
U1 0
U2 5
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 30
PY 2014
VL 34
IS 18
BP 6233
EP 6244
DI 10.1523/JNEUROSCI.5324-13.2014
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA AH2AA
UT WOS:000335921900013
PM 24790194
ER
PT J
AU Kamhawi, S
Oliveira, F
Valenzuela, JG
AF Kamhawi, Shaden
Oliveira, Fabiano
Valenzuela, Jesus G.
TI Using Humans to Make a Human Leishmaniasis Vaccine
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
ID VISCERAL LEISHMANIASIS; MODEL
AB The cellular immune response to peptide pools from conserved Leishmania antigens in leishmaniasis-immune individuals identified epitopes for a human DNA vaccine (Das et al., this issue).
C1 [Kamhawi, Shaden; Oliveira, Fabiano; Valenzuela, Jesus G.] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP Valenzuela, JG (reprint author), NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
EM jvalenzuela@niaid.nih.gov
RI Oliveira, Fabiano/B-4251-2009
OI Oliveira, Fabiano/0000-0002-7924-8038
NR 10
TC 4
Z9 4
U1 1
U2 4
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD APR 30
PY 2014
VL 6
IS 234
AR 234fs18
DI 10.1126/scitranslmed.3009118
PG 3
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA AG6GC
UT WOS:000335516100008
PM 24786322
ER
PT J
AU Gill, J
Lee, H
Barr, T
Baxter, T
Heinzelmann, M
Rak, H
Mysliwiec, V
AF Gill, Jessica
Lee, Hyunhwa
Barr, Taura
Baxter, Tristin
Heinzelmann, Morgan
Rak, Hannah
Mysliwiec, Vincent
TI Lower health related quality of life in US military personnel is
associated with service-related disorders and inflammation
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE IL-6; Post-traumatic stress disorder; Depression; Traumatic brain injury
ID TRAUMATIC BRAIN-INJURY; POSTTRAUMATIC-STRESS-DISORDER; SELF-RATED
HEALTH; MENTAL-HEALTH; CARDIOVASCULAR EVENTS; PTSD; DEPRESSION;
MORTALITY; VETERANS; DEPLOYMENT
AB Military personnel who have combat exposures are at increased risk for the service-related disorders of post-traumatic stress disorder (PTSD), depression, sleep disturbances and decreased health related quality of life (HRQOL). Those with a traumatic brain injury (TBI) are at even greater risk. Inflammation is associated with these disorders and may underlie the risk for health declines. We evaluated 110 recently deployed, military personnel presenting with sleep disturbances for service-related disorders (TBI, PTSD, and depression) as well as HRQOL. ANOVA models were used to examine differences among military personnel with two or more service-related disorders (high comorbid group), or one or no disorders (low comorbid group). Logistic regression models were used to determine associations among interleukin-6 (IL-6) to HRQOL and service-related disorders. Approximately one-third of the sample had two or more service-related disorders. HRQOL was lower and IL-6 concentrations were higher in military personnel with PTSD or depression, with the most profound differences in those with more service-related disorders, regardless of sleep disorder. Having symptoms of depression and PTSD resulted in a 3.5-fold risk to be in the lower quartile of HRQOL and the highest quartile of IL-6. In a linear regression model, 41% of the relationship between HRQOL and IL-6 concentrations was mediated by PTSD and depression. Military personnel with PTSD and depression are at high risk for lower HRQOL, and higher IL-6 concentrations. Comprehensive treatment is required to address co-occurring service-related disorders in military personnel to promote health and well-being. (C) 2014 Published by Elsevier Ireland Ltd.
C1 [Gill, Jessica; Lee, Hyunhwa; Heinzelmann, Morgan; Rak, Hannah] NINR, NIH, Bethesda, MD 20892 USA.
[Barr, Taura] W Virginia Univ, Morgantown, WV 26506 USA.
[Baxter, Tristin; Mysliwiec, Vincent] Madigan Army Med Ctr, Tacoma, WA 98431 USA.
RP Gill, J (reprint author), NINR, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM gillj@mail.nih.gov
FU Center for Neuroscience and Regenerative Medicine [60855]
FX This study was funded, in part, by the Center for Neuroscience and
Regenerative Medicine (Grant 60855). The opinions and assertions in this
manuscript are those of the authors and do not necessarily represent
those of the Department of the Army, Department of Defense, U.S.
Government, or the Center for Neuroscience and Regenerative Medicine.
NR 53
TC 10
Z9 10
U1 7
U2 17
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 APR 30
PY 2014
VL 216
IS 1
BP 116
EP 122
DI 10.1016/j.psychres.2014.01.046
PG 7
WC Psychiatry
SC Psychiatry
GA AE6XL
UT WOS:000334141200018
PM 24559851
ER
PT J
AU Nagy, Z
Kovacs, I
Torol, M
Toth, D
Vereb, G
Buzas, K
Juhasz, I
Blumberg, PM
Biro, T
Czifra, G
AF Nagy, Zsuzsanna
Kovacs, Ilona
Toeroel, Miklos
Toth, Dezso
Vereb, Gyoergy
Buzas, Krisztina
Juhasz, Istvan
Blumberg, Peter M.
Biro, Tamas
Czifra, Gabriella
TI Function of RasGRP3 in the formation and progression of human breast
cancer
SO MOLECULAR CANCER
LA English
DT Article
DE Ras activator; RasGRP3; Human breast cancer; Chemotherapeutic
resistance; Tamoxifen; Trastuzumab; Tumorigenesis; EGF; IGF-I; Signaling
pathways
ID GROWTH-FACTOR-I; ACTIVATED PROTEIN-KINASE; NUCLEOTIDE EXCHANGE FACTOR;
ESTROGEN-RECEPTOR; DYNEIN LIGHT-CHAIN-1; TRASTUZUMAB HERCEPTIN;
ENDOCRINE RESISTANCE; SIGNAL-TRANSDUCTION; PHORBOL ESTERS; RAS
ACTIVATION
AB Introduction: Ras guanine nucleotide exchange factors (RasGEFs) mediate the activation of the Ras signaling pathway that is over activated in many human cancers. The RasGRP3, an activator of H-Ras and R-Ras protein exerts oncogenic effects and the overexpression of the protein is observed in numerous malignant cancer types. Here, we investigated the putative alteration of expression and potential function of RasGRP3 in the formation and progression of human breast cancer.
Methods: The RasGRP3 and phosphoRasGRP3 expressions were examined in human invasive ductal adenocarcinoma derived samples and cell lines (BT-474, JIMT-1, MCF7, SK-BR-3, MDA-MB-453, T-47D) both in mRNA (Q-PCR) and protein (Western blot; immunohistochemistry) levels. To explore the biological function of the protein, RasGRP3 knockdown cultures were established. To assess the role of RasGRP3 in the viability of cells, annexin-V/PI staining and MitoProbe (TM) DilC1 (5) assay were performed. To clarify the function of the protein in cell proliferation and in the development of chemotherapeutic resistance, CyQuant assay was performed. To observe the RasGRP3 function in tumor formation, the Severe combined immunodeficiency (SCID) mouse model was used. To investigate the role of the protein in Ras-related signaling Q-PCR and Western blot experiments were performed.
Results: RasGRP3 expression was elevated in human breast tumor tissue samples as well as in multiple human breast cancer cell lines. Down-regulation of RasGRP3 expression in breast cancer cells decreased cell proliferation, induced apoptosis in MCF7 cells, and sensitized T-47D cells to the action of drugs Tamoxifen and trastuzumab (Herceptin). Gene silencing of RasGRP3 reduced tumor formation in mouse xenografts as well. Inhibition of RasGRP3 expression also reduced Akt, ERK1/2 and estrogen receptor alpha phosphorylation downstream from IGF-I insulin like growth factor-I (IGF-I) or epidermal growth factor (EGF) stimulation confirming the functional role of RasGRP3 in the altered behavior of these cells.
Conclusions: Taken together, our results suggest that the Ras activator RasGRP3 may have a role in the pathological behavior of breast cancer cells and may constitute a therapeutic target for human breast cancer.
C1 [Nagy, Zsuzsanna; Biro, Tamas; Czifra, Gabriella] Univ Debrecen, DE MTA Lendulet Cellular Physiol Res Grp, Dept Physiol, Res Ctr Mol Med,Med & Hlth Sci Ctr, H-4032 Debrecen, Hungary.
[Kovacs, Ilona; Toeroel, Miklos] Gyula Kenezy Hosp, Dept Pathol, Debrecen, Hungary.
[Toth, Dezso] Gyula Kenazy Hosp, Dept Surg, Debrecen, Hungary.
[Vereb, Gyoergy] Univ Debrecen, Med & Hlth Sci Ctr, Fac Med, Dept Biophys & Cell Biol, H-4032 Debrecen, Hungary.
[Buzas, Krisztina] Hungarian Acad Sci, Biol Res Ctr, Inst Biochem, H-6701 Szeged, Hungary.
[Juhasz, Istvan] Univ Debrecen, Med & Hlth Sci Ctr, Dept Dermatol, H-4032 Debrecen, Hungary.
[Blumberg, Peter M.] NCI, Canc Biol Lab, Bethesda, MD 20892 USA.
[Blumberg, Peter M.] NCI, Genet Ctr Canc Res, Bethesda, MD 20892 USA.
RP Czifra, G (reprint author), Univ Debrecen, DE MTA Lendulet Cellular Physiol Res Grp, Dept Physiol, Res Ctr Mol Med,Med & Hlth Sci Ctr, Nagyerdei Krt 98,POB 22, H-4032 Debrecen, Hungary.
EM czifrag@gmail.com
RI Vereb, Gyorgy/A-4241-2008
OI Vereb, Gyorgy/0000-0003-2157-3265
FU Hungarian research grants [TAMOP-4.2.2.A-11/1/KONV-2012-0025, "Lendulet"
LP003/2011]; University of Debrecen [RH/885/2013];
[TAMOP-4.2.2./B-10/1-2010-0024]
FX The authors thank Dr. Peter Nagy (University of Debrecen) for providing
human breast cancer cell lines; Laboratory of Cancer Biology and
Genetics (Center for Cancer Research, National Cancer Institute) for
providing human prostate cancer cell line PC-3, Dr. Laszlo Simon
(University of Debrecen) for assistance with SCID mice experiment. This
study was supported by Hungarian research grants
TAMOP-4.2.2.A-11/1/KONV-2012-0025. and "Lendulet" LP003/2011 and by the
University of Debrecen (RH/885/2013). Zs. Nagy is a recipient of the
TAMOP-4.2.2./B-10/1-2010-0024. Predoctoral Research Scholarship.
NR 73
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Z9 1
U1 5
U2 17
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD APR 29
PY 2014
VL 13
AR 96
DI 10.1186/1476-4598-13-96
PG 17
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA AK2IV
UT WOS:000338243600001
PM 24779681
ER
PT J
AU Krupovic, M
Bamford, DH
Koonin, EV
AF Krupovic, Mart
Bamford, Dennis H.
Koonin, Eugene V.
TI Conservation of major and minor jelly-roll capsid proteins in Polinton
(Maverick) transposons suggests that they are bona fide viruses
SO BIOLOGY DIRECT
LA English
DT Article
DE Polintons; Mavericks; Transposable elements; Double jelly-roll fold;
Capsid proteins; Virus evolution
ID STRANDED-DNA VIRUSES; GENETIC ELEMENTS; EVOLUTION; EUKARYOTES;
VIROPHAGE; GENOMICS; RECONSTRUCTION; TRANSPOVIRONS; ADENOVIRUS;
MECHANISM
AB Polintons (also known as Mavericks) and Tlr elements of Tetrahymena thermophila represent two families of large DNA transposons widespread in eukaryotes. Here, we show that both Polintons and Tlr elements encode two key virion proteins, the major capsid protein with the double jelly-roll fold and the minor capsid protein, known as the penton, with the single jelly-roll topology. This observation along with the previously noted conservation of the genes for viral genome packaging ATPase and adenovirus-like protease strongly suggests that Polintons and Tlr elements combine features of bona fide viruses and transposons. We propose the name ` Polintoviruses' to denote these putative viruses that could have played a central role in the evolution of several groups of DNA viruses of eukaryotes.
C1 [Krupovic, Mart] Inst Pasteur, Dept Microbiol, Unite Biol Mol Gene Chez Extremophiles, F-75015 Paris, France.
[Bamford, Dennis H.] Univ Helsinki, Dept Biosci, Viikki Bioctr 2, FIN-00014 Helsinki, Finland.
[Bamford, Dennis H.] Univ Helsinki, Inst Biotechnol, Viikki Bioctr 2, FIN-00014 Helsinki, Finland.
[Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Krupovic, M (reprint author), Inst Pasteur, Dept Microbiol, Unite Biol Mol Gene Chez Extremophiles, F-75015 Paris, France.
EM krupovic@pasteur.fr; koonin@ncbi.nlm.nih.gov
RI Krupovic, Mart/I-4209-2012;
OI Krupovic, Mart/0000-0001-5486-0098; Bamford, Dennis/0000-0002-6438-8118
FU European Molecular Biology Organization [ASTF 82-2014]; Academy of
Finland [271413, 272853, 255342, 256518]; University of Helsinki; EU
ESFRI Instruct Centre; US Department of Health and Human Services
FX MK was partly supported by the European Molecular Biology Organization
(ASTF 82-2014).; DHB is supported by the Academy of Finland (grants
271413 and 272853 as well as Academy Professor funding grants 255342 and
256518). DHB is also grateful to the University of Helsinki for the
support to EU ESFRI Instruct Centre. EVK is supported by intramural
funds of the US Department of Health and Human Services (to the National
Library of Medicine).
NR 40
TC 23
Z9 24
U1 1
U2 8
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 APR 29
PY 2014
VL 9
AR 6
DI 10.1186/1745-6150-9-6
PG 7
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AI3LF
UT WOS:000336762200001
PM 24773695
ER
PT J
AU Chen, J
Miller, BF
Furano, AV
AF Chen, Jia
Miller, Brendan F.
Furano, Anthony V.
TI Repair of naturally occurring mismatches can induce mutations in
flanking DNA
SO ELIFE
LA English
DT Article
ID BASE EXCISION-REPAIR; SHUTTLE VECTOR PLASMID; MAMMALIAN-CELLS; SOMATIC
HYPERMUTATION; HUMAN CANCERS; POSTREPLICATION REPAIR; POLYMERASE-ETA;
BREAST-CANCER; MUTL-ALPHA; STRAND
AB 'Normal' genomic DNA contains hundreds of mismatches that are generated daily by the spontaneous deamination of C (U/G) and methyl-C (T/G). Thus, a mutagenic effect of their repair could constitute a serious genetic burden. We show here that while mismatches introduced into human cells on an SV40-based episome were invariably repaired, this process induced mutations in flanking DNA at a significantly higher rate than no mismatch controls. Most mutations involved the C of TpC, the substrate of some single strand-specific APOBEC cytidine deaminases, similar to the mutations that can typify the 'mutator phenotype' of numerous tumors. siRNA knockdowns and chromatin immunoprecipitation showed that TpC preferring APOBECs mediate the mutagenesis, and siRNA knockdowns showed that both the base excision and mismatch repair pathways are involved. That naturally occurring mispairs can be converted to mutators, represents an heretofore unsuspected source of genetic changes that could underlie disease, aging, and evolutionary change.
C1 [Chen, Jia; Miller, Brendan F.; Furano, Anthony V.] NIDDK, Sect Genom Struct & Funct, Lab Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Furano, AV (reprint author), NIDDK, Sect Genom Struct & Funct, Lab Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
EM avf@helix.nih.gov
FU Intramural Research Program of the NIH
FX Intramural Research Program of the NIH Anthony V Furano
NR 73
TC 14
Z9 14
U1 0
U2 11
PU ELIFE SCIENCES PUBLICATIONS LTD
PI CAMBRIDGE
PA SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND
SN 2050-084X
J9 ELIFE
JI eLife
PD APR 29
PY 2014
VL 3
AR e02001
DI 10.7554/eLife.02001
PG 27
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AH1UP
UT WOS:000335907000003
PM 24843013
ER
PT J
AU Nyante, SJ
Gierach, GL
Dallal, CM
Freedman, ND
Park, Y
Danforth, KN
Hollenbeck, AR
Brinton, LA
AF Nyante, S. J.
Gierach, G. L.
Dallal, C. M.
Freedman, N. D.
Park, Y.
Danforth, K. N.
Hollenbeck, A. R.
Brinton, L. A.
TI Cigarette smoking and postmenopausal breast cancer risk in a prospective
cohort
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE smoking; menarche; family history of breast cancer; breast cancer risk;
cohort study
ID NIH-AARP DIET; ALCOHOL-CONSUMPTION; HORMONE-RECEPTOR; PASSIVE SMOKING;
ACTIVE SMOKING; DNA-ADDUCTS; FOLLOW-UP; WOMEN; HEALTH; ASSOCIATION
AB Background: The relationship between cigarette smoking and breast cancer risk has been inconsistent, potentially due to modification by other factors or confounding.
Methods: We examined smoking and breast cancer risk in a prospective cohort of 186 150 female AARP (formerly American Association of Retired Persons) members, ages 50-71 years, who joined the study in 1995-96 by responding to a questionnaire. Through 2006, 7481 breast cancers were diagnosed. Multivariable-adjusted hazard ratios (HRs) were estimated, overall and stratified by breast cancer risk factors, using Cox proportional hazards regression. Multiplicative interactions were evaluated using the likelihood ratio test.
Results: Increased breast cancer risk was associated with current (HR 1.19, 95% confidence interval (CI) 1.10-1.28) and former (HR 1.07, CI 1.01-1.13) smoking. The current smoking association was stronger among women without (HR 1.24, CI 1.15-1.35) as compared to those with a family history of breast cancer (HR 0.94, CI 0.78-1.13) (P-interaction=0.03). The current smoking association was also stronger among those with later (>= 15 years: HR 1.52, CI 1.20-1.94) as compared with earlier (<= 12 years: HR 1.14, CI 1.03-1.27; 13-14 years: HR 1.18, CI 1.05-1.32) ages at menarche (P-interaction=0.03).
Conclusions: Risk was elevated in smokers, particularly in those without a family history or late menarche. Research into smoking's effects on the genome and breast development may clarify these relationships.
C1 [Nyante, S. J.; Gierach, G. L.; Freedman, N. D.; Park, Y.; Brinton, L. A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Dallal, C. M.] Univ Maryland, Sch Publ Hlth, Dept Epidemiol & Biostat, College Pk, MD 20742 USA.
[Danforth, K. N.] Kaiser Permanente So Calif, Dept Res & Evaluat, Pasadena, CA 91101 USA.
[Hollenbeck, A. R.] AARP Res Ctr, Strateg Issues Res, Washington, DC 20049 USA.
RP Nyante, SJ (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM sarah.nyante@nih.gov
RI Brinton, Louise/G-7486-2015; Freedman, Neal/B-9741-2015; Gierach,
Gretchen/E-1817-2016;
OI Brinton, Louise/0000-0003-3853-8562; Freedman, Neal/0000-0003-0074-1098;
Gierach, Gretchen/0000-0002-0165-5522; Park, Yikyung/0000-0002-6281-489X
FU Intramural Research Program of the National Cancer Institute at the
National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Cancer Institute at the National Institutes of Health. Cancer
incidence data from the Atlanta metropolitan area were collected by the
Georgia Center for Cancer Statistics, Department of Epidemiology,
Rollins School of Public Health, Emory University. Cancer incidence data
from California were collected by the California Department of Health
Services, Cancer Surveillance Section. Cancer incidence data from the
Detroit metropolitan area were collected by the Michigan Cancer
Surveillance Program, Community Health Administration, State of
Michigan. The Florida cancer incidence data used in this report were
collected by the Florida Cancer Data System (FCDC) under contract with
the Florida Department of Health (FDOH). Cancer incidence data from
Louisiana were collected by the Louisiana Tumour Registry, Louisiana
State University Medical Center in New Orleans. Cancer incidence data
from New Jersey were collected by the New Jersey State Cancer Registry,
Cancer Epidemiology Services, New Jersey State Department of Health and
Senior Services. Cancer incidence data from North Carolina were
collected by the North Carolina Central Cancer Registry. Cancer
incidence data from Pennsylvania were supplied by the Division of Health
Statistics and Research, Pennsylvania Department of Health, Harrisburg,
Pennsylvania. Cancer incidence data from Arizona were collected by the
Arizona Cancer Registry, Division of Public Health Services, Arizona
Department of Health Services. Cancer incidence data from Texas were
collected by the Texas Cancer Registry, Cancer Epidemiology and
Surveillance Branch, Texas Department of State Health Services. We are
indebted to the participants in the NIH-AARP Diet and Health Study for
their outstanding cooperation. We also thank Sigurd Hermansen and Kerry
Grace Morrissey from Westat for study outcomes ascertainment and
management and Leslie Carroll at Information Management Services for
data support and analysis.
NR 45
TC 11
Z9 11
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 29
PY 2014
VL 110
IS 9
BP 2339
EP 2347
DI 10.1038/bjc.2014.132
PG 9
WC Oncology
SC Oncology
GA AG6XQ
UT WOS:000335562800022
PM 24642621
ER
PT J
AU Petrick, JL
Wyss, AB
Butler, AM
Cummings, C
Sun, X
Poole, C
Smith, JS
Olshan, AF
AF Petrick, J. L.
Wyss, A. B.
Butler, A. M.
Cummings, C.
Sun, X.
Poole, C.
Smith, J. S.
Olshan, A. F.
TI Prevalence of human papillomavirus among oesophageal squamous cell
carcinoma cases: systematic review and meta-analysis
SO BRITISH JOURNAL OF CANCER
LA English
DT Review
ID POLYMERASE-CHAIN-REACTION; GENITAL HUMAN PAPILLOMAVIRUSES; RISK
HUMAN-PAPILLOMAVIRUS; REPUBLIC-OF-CHINA; ENVIRONMENTAL SURFACES; CANCER
INCIDENCE; VIRAL LOAD; INFECTION; HPV; DNA
AB Background: Oncogenic human papillomavirus (HPV) has been hypothesised as a risk factor for oesophageal squamous cell carcinoma (OSCC), but aetiological research has been limited by the varying methodology used for establishing HPV prevalence. The aims of this systematic review and meta-analysis were to estimate the prevalence of HPV DNA detected in OSCC tumours and the influence of study characteristics.
Methods: Study-level estimates of overall and type-specific HPV prevalence were meta-analysed to obtain random-effects summary estimates.
Results: This analysis included 124 studies with a total of 13 832 OSCC cases. The average HPV prevalence (95% confidence interval) among OSCC cases was 0.277 (0.234, 0.320) by polymerase chain reaction; 0.243 (0.159, 0.326) by in situ hybridisation; 0.304 (0.185, 0.423) by immunohistochemistry; 0.322 (0.154, 0.490) by L1 serology; and 0.176 (0.061, 0.292) by Southern/slot/dot blot. The highest HPV prevalence was found in Africa and Asia, notably among Chinese studies from provinces with high OSCC incidence rates.
Conclusions: Future research should focus on quantifying HPV in OSCC cases using strict quality control measures, as well as determining the association between HPV and OSCC incidence by conducting large, population-based case-control studies. Such studies will provide a richer understanding of the role of HPV in OSCC aetiology.
C1 [Petrick, J. L.; Wyss, A. B.; Butler, A. M.; Cummings, C.; Sun, X.; Poole, C.; Smith, J. S.; Olshan, A. F.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Wyss, A. B.] NIEHS, Epidemiol Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
[Smith, J. S.; Olshan, A. F.] Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Olshan, A. F.] Univ N Carolina, Sch Med, Chapel Hill, NC 27599 USA.
RP Petrick, JL (reprint author), Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
EM jessica.petrick@unc.edu
FU National Institutes of Health (NIH); National Cancer Institute
[T32CA009330-25]; National Institutes of Environmental Health and
Susceptibility [T32ES007018]; Intramural Research Programme of the NIH,
National Institute of Environmental Health Sciences
FX We are grateful to Anne Rositch for her advice on meta-analytic methods
and Hazel Nichols for her feedback on the manuscript. Additionally, we
are grateful to Hilda Razzaghi and Csaba Marosvari for their help in
translating a Persian and Hungarian article, respectively. We would also
like to acknowledge the efforts of the contacted study authors for
providing additional data to this meta-analysis. This was supported by
the National Institutes of Health (NIH), National Cancer Institute
(T32CA009330-25) and the National Institutes of Environmental Health and
Susceptibility (T32ES007018), as well as in part by the Intramural
Research Programme of the NIH, National Institute of Environmental
Health Sciences.
NR 77
TC 11
Z9 12
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 29
PY 2014
VL 110
IS 9
BP 2369
EP 2377
DI 10.1038/bjc.2014.96
PG 9
WC Oncology
SC Oncology
GA AG6XQ
UT WOS:000335562800026
PM 24619077
ER
PT J
AU Ardeljan, D
Wang, Y
Park, S
Shen, D
Chu, XK
Yu, CR
Abu-Asab, M
Tuo, J
Eberhart, CG
Olsen, TW
Mullins, RF
White, G
Wadsworth, S
Scaria, A
Chan, CC
AF Ardeljan, Daniel
Wang, Yujuan
Park, Stanley
Shen, Defen
Chu, Xi Kathy
Yu, Cheng-Rong
Abu-Asab, Mones
Tuo, Jingsheng
Eberhart, Charles G.
Olsen, Timothy W.
Mullins, Robert F.
White, Gary
Wadsworth, Sam
Scaria, Abraham
Chan, Chi-Chao
TI Interleukin-17 Retinotoxicity Is Prevented by Gene Transfer of a Soluble
Interleukin-17 Receptor Acting as a Cytokine Blocker: Implications for
Age-Related Macular Degeneration
SO PLOS ONE
LA English
DT Article
ID NLRP3 INFLAMMASOME; PIGMENT EPITHELIUM; THERAPEUTIC LEVELS; MICE; IL-17;
CELLS; NEOVASCULARIZATION; COMPLEMENT; ACTIVATION; EXPRESSION
AB Age-related macular degeneration (AMD) is a common yet complex retinal degeneration that causes irreversible central blindness in the elderly. Pathology is widely believed to follow loss of retinal pigment epithelium (RPE) and photoreceptor degeneration. Here we report aberrant expression of interleukin-17A (IL17A) and the receptor IL17RC in the macula of AMD patients. In vitro, IL17A induces RPE cell death characterized by the accumulation of cytoplasmic lipids and autophagosomes with subsequent activation of pro-apoptotic Caspase-3 and Caspase-9. This pathology is reduced by siRNA knockdown of IL17RC. IL17-dependent retinal degeneration in a mouse model of focal retinal degeneration can be prevented by gene therapy with adeno-associated virus vector encoding soluble IL17 receptor. This intervention rescues RPE and photoreceptors in a MAPK-dependent process. The IL17 pathway plays a key role in RPE and photoreceptor degeneration and could hold therapeutic potential in AMD.
C1 [Ardeljan, Daniel; Wang, Yujuan; Park, Stanley; Shen, Defen; Chu, Xi Kathy; Tuo, Jingsheng; Chan, Chi-Chao] NEI, Immunopathol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Ardeljan, Daniel] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Wang, Yujuan] Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, Guangzhou 510275, Guangdong, Peoples R China.
[Park, Stanley] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Yu, Cheng-Rong] NEI, Mol Immunol Sect, Immunol Lab, NIH, Bethesda, MD USA.
[Abu-Asab, Mones] NEI, Histol Core, Immunol Lab, NIH, Bethesda, MD USA.
[Eberhart, Charles G.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
[Olsen, Timothy W.] Emory Univ, Dept Ophthalmol, Atlanta, GA 30322 USA.
[Mullins, Robert F.] Univ Iowa, Carver Coll Med, Dept Ophthalmol & Visual Sci, Iowa City, IA USA.
[White, Gary; Wadsworth, Sam; Scaria, Abraham] Genzyme Corp, Framingham, MA 01701 USA.
RP Chan, CC (reprint author), NEI, Immunopathol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
RI wang, yujuan/C-8428-2016
FU National Eye Institute Intramural Research Program; Genzyme
FX The National Eye Institute Intramural Research Program & Genzyme funded
the work. The funder Genzyme provided support in the form of salaries
for authors GW, SW, and AS, but did not have any additional role in the
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 47
TC 17
Z9 17
U1 1
U2 12
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 APR 29
PY 2014
VL 9
IS 4
AR e95900
DI 10.1371/journal.pone.0095900
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG6CA
UT WOS:000335504900011
PM 24780906
ER
PT J
AU Sweeney, EM
Vogelstein, JT
Cuzzocreo, JL
Calabresi, PA
Reich, DS
Crainiceanu, CM
Shinohara, RT
AF Sweeney, Elizabeth M.
Vogelstein, Joshua T.
Cuzzocreo, Jennifer L.
Calabresi, Peter A.
Reich, Daniel S.
Crainiceanu, Ciprian M.
Shinohara, Russell T.
TI A Comparison of Supervised Machine Learning Algorithms and Feature
Vectors for MS Lesion Segmentation Using Multimodal Structural MRI
SO PLOS ONE
LA English
DT Article
ID MULTIPLE-SCLEROSIS LESIONS; WHITE-MATTER LESIONS; OF-THE-ART; BRAIN MRI;
IMAGES; CLASSIFICATION; SCIENCE
AB Machine learning is a popular method for mining and analyzing large collections of medical data. We focus on a particular problem from medical research, supervised multiple sclerosis (MS) lesion segmentation in structural magnetic resonance imaging (MRI). We examine the extent to which the choice of machine learning or classification algorithm and feature extraction function impacts the performance of lesion segmentation methods. As quantitative measures derived from structural MRI are important clinical tools for research into the pathophysiology and natural history of MS, the development of automated lesion segmentation methods is an active research field. Yet, little is known about what drives performance of these methods. We evaluate the performance of automated MS lesion segmentation methods, which consist of a supervised classification algorithm composed with a feature extraction function. These feature extraction functions act on the observed T1-weighted (T1-w), T2-weighted (T2-w) and fluid-attenuated inversion recovery (FLAIR) MRI voxel intensities. Each MRI study has a manual lesion segmentation that we use to train and validate the supervised classification algorithms. Our main finding is that the differences in predictive performance are due more to differences in the feature vectors, rather than the machine learning or classification algorithms. Features that incorporate information from neighboring voxels in the brain were found to increase performance substantially. For lesion segmentation, we conclude that it is better to use simple, interpretable, and fast algorithms, such as logistic regression, linear discriminant analysis, and quadratic discriminant analysis, and to develop the features to improve performance.
C1 [Sweeney, Elizabeth M.; Reich, Daniel S.; Crainiceanu, Ciprian M.] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
[Sweeney, Elizabeth M.; Reich, Daniel S.] NINDS, Translat Neuroradiol Unit, Neuroimmunol Branch, NIH, Bethesda, MD USA.
[Vogelstein, Joshua T.] Duke Univ, Dept Stat Sci, Durham, NC USA.
[Vogelstein, Joshua T.] Child Mind Inst, Ctr Developing Brain, New York, NY USA.
[Cuzzocreo, Jennifer L.; Reich, Daniel S.] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
[Calabresi, Peter A.; Reich, Daniel S.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Shinohara, Russell T.] Univ Penn, Ctr Clin Epidemiol & Biostat, Perelman Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
RP Sweeney, EM (reprint author), Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
EM emsweene@jhsph.edu
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
FU NINDS [R01 NS070906, RO1 NS08521]
FX This research was partially supported by the Intramural Research Program
of NINDS and NINDS R01 NS070906 and NINDS RO1 NS08521. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 61
TC 3
Z9 3
U1 0
U2 12
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 APR 29
PY 2014
VL 9
IS 4
AR e95753
DI 10.1371/journal.pone.0095753
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG6CA
UT WOS:000335504900009
PM 24781953
ER
PT J
AU Kellis, M
Wold, B
Snyder, MP
Bernstein, BE
Kundaje, A
Marinov, GK
Ward, LD
Birney, E
Crawford, GE
Dekker, J
Dunham, I
Elnitski, LL
Farnham, PJ
Feingold, EA
Gerstein, M
Giddings, MC
Gilbert, DM
Gingeras, TR
Green, ED
Guigo, R
Hubbard, T
Kent, J
Lieb, JD
Myers, RM
Pazin, MJ
Ren, B
Stamatoyannopoulos, JA
Weng, ZP
White, KP
Hardison, RC
AF Kellis, Manolis
Wold, Barbara
Snyder, Michael P.
Bernstein, Bradley E.
Kundaje, Anshul
Marinov, Georgi K.
Ward, Lucas D.
Birney, Ewan
Crawford, Gregory E.
Dekker, Job
Dunham, Ian
Elnitski, Laura L.
Farnham, Peggy J.
Feingold, Elise A.
Gerstein, Mark
Giddings, Morgan C.
Gilbert, David M.
Gingeras, Thomas R.
Green, Eric D.
Guigo, Roderic
Hubbard, Tim
Kent, Jim
Lieb, Jason D.
Myers, Richard M.
Pazin, Michael J.
Ren, Bing
Stamatoyannopoulos, John A.
Weng, Zhiping
White, Kevin P.
Hardison, Ross C.
TI Defining functional DNA elements in the human genome
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID PARALLEL REPORTER ASSAY; GENE-EXPRESSION; CHROMATIN IMMUNOPRECIPITATION;
REGULATORY ELEMENTS; HUMAN-CELLS; JUNK DNA; SYSTEMATIC DISSECTION;
PURIFYING SELECTION; ADAPTIVE EVOLUTION; MAMMALIAN GENOME
AB With the completion of the human genome sequence, attention turned to identifying and annotating its functional DNA elements. As a complement to genetic and comparative genomics approaches, the Encyclopedia of DNA Elements Project was launched to contribute maps of RNA transcripts, transcriptional regulator binding sites, and chromatin states in many cell types. The resulting genome-wide data reveal sites of biochemical activity with high positional resolution and cell type specificity that facilitate studies of gene regulation and interpretation of noncoding variants associated with human disease. However, the biochemically active regions cover a much larger fraction of the genome than do evolutionarily conserved regions, raising the question of whether nonconserved but biochemically active regions are truly functional. Here, we review the strengths and limitations of biochemical, evolutionary, and genetic approaches for defining functional DNA segments, potential sources for the observed differences in estimated genomic coverage, and the biological implications of these discrepancies. We also analyze the relationship between signal intensity, genomic coverage, and evolutionary conservation. Our results reinforce the principle that each approach provides complementary information and that we need to use combinations of all three to elucidate genome function in human biology and disease.
C1 [Kellis, Manolis; Kundaje, Anshul; Ward, Lucas D.] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
[Kellis, Manolis; Bernstein, Bradley E.; Kundaje, Anshul; Ward, Lucas D.] Broad Inst, Cambridge, MA 02139 USA.
[Wold, Barbara; Marinov, Georgi K.] CALTECH, Div Biol & Biol Engn, Pasadena, CA 91125 USA.
[Snyder, Michael P.] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
[Bernstein, Bradley E.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Bernstein, Bradley E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Birney, Ewan; Dunham, Ian] European Bioinformat Inst, European Mol Biol Lab, Cambridge CB10 1SD, England.
[Crawford, Gregory E.] Duke Univ, Durham, NC 27708 USA.
[Dekker, Job; Weng, Zhiping] Univ Massachusetts, Sch Med, Program Syst Biol, Worcester, MA 01605 USA.
[Ward, Lucas D.; Elnitski, Laura L.; Feingold, Elise A.; Green, Eric D.; Pazin, Michael J.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Farnham, Peggy J.] Univ So Calif, Los Angeles, CA 90089 USA.
[Gerstein, Mark] Yale Univ, Program Computat Biol & Bioinformat, New Haven, CT 06520 USA.
[Giddings, Morgan C.] Mkt Your Sci LLC, Boise, ID 83702 USA.
[Gilbert, David M.] Florida State Univ, Dept Biol Sci, Tallahassee, FL 32306 USA.
[Gingeras, Thomas R.] Cold Spring Harbor Lab, Funct Genom Grp, Cold Spring Harbor, NY 11724 USA.
[Guigo, Roderic] Ctr Genome Regulat, Bioinformat & Genom Program, E-08003 Barcelona, Catalonia, Spain.
[Hubbard, Tim] Kings Coll London, Cambridge CB10 1SD, England.
[Hubbard, Tim] Wellcome Trust Sanger Inst, Cambridge CB10 1SD, England.
[Kent, Jim] Univ Calif Santa Cruz, Santa Cruz, CA 95064 USA.
[Lieb, Jason D.] Princeton Univ, Lewis Sigler Inst, Princeton, NJ 08544 USA.
[Myers, Richard M.] HudsonAlpha Inst Biotechnol, Huntsville, AL 35806 USA.
[Ren, Bing] Univ Calif San Diego, Ludwig Inst Canc Res, La Jolla, CA 92093 USA.
[Stamatoyannopoulos, John A.] Univ Washington, Seattle, WA 98195 USA.
[White, Kevin P.] Univ Chicago, Chicago, IL 60637 USA.
[Hardison, Ross C.] Penn State Univ, University Pk, PA 16802 USA.
RP Kellis, M (reprint author), MIT, Comp Sci & Artificial Intelligence Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM manoli@mit.edu; rch8@psu.edu
RI Guigo, Roderic/D-1303-2010; Hubbard, Tim/C-2567-2008;
OI Guigo, Roderic/0000-0002-5738-4477; Hubbard, Tim/0000-0002-1767-9318;
Gingeras, Thomas/0000-0001-9106-3573; Farnham,
Peggy/0000-0003-4469-7914; Dunham, Ian/0000-0003-2525-5598; Birney,
Ewan/0000-0001-8314-8497; Pazin, Michael/0000-0002-7561-3640
FU NCI NIH HHS [P30 CA008748, P30 CA045508]; NHGRI NIH HHS [R01 HG003143,
R01 HG004037, U41 HG007234, U54 HG006996, U54 HG006997]; NIA NIH HHS
[R01 AG016379]; NIGMS NIH HHS [R01 GM083337]
NR 117
TC 164
Z9 167
U1 30
U2 124
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 APR 29
PY 2014
VL 111
IS 17
BP 6131
EP 6138
DI 10.1073/pnas.1318948111
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TL
UT WOS:000335199000025
PM 24753594
ER
PT J
AU Heinecke, JL
Ridnour, LA
Cheng, RYS
Switzer, CH
Lizardo, MM
Khanna, C
Glynn, SA
Hussain, SP
Young, HA
Ambs, S
Wink, DA
AF Heinecke, Julie L.
Ridnour, Lisa A.
Cheng, Robert Y. S.
Switzer, Christopher H.
Lizardo, Michael M.
Khanna, Chand
Glynn, Sharon A.
Hussain, S. Perwez
Young, Howard A.
Ambs, Stefan
Wink, David A.
TI Tumor microenvironment-based feed-forward regulation of NOS2 in breast
cancer progression
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID NITRIC-OXIDE SYNTHASE; PREDICTS POOR SURVIVAL; MELANOMA PATIENTS;
CELL-LINE; HYPOXIA; EXPRESSION; INDUCTION; ESTROGEN; GENE; RESISTANCE
AB Inflammation is widely recognized as an inducer of cancer progression. The inflammation-associated enzyme, inducible nitric oxide synthase (NOS2), has emerged as a candidate oncogene in estrogen receptor (ER)-negative breast cancer, and its increased expression is associated with disease aggressiveness and poor survival. Although these observations implicate NOS2 as an attractive therapeutic target, the mechanisms of both NOS2 induction in tumors and nitric oxide (NO)-driven cancer progression are not fully understood. To enhance ourmechanistic understanding of NOS2 induction in tumors and its role in tumor biology, we used stimulants of NOS2 expression in ER-and ER+ breast cancer cells and examined downstream NO-dependent effects. Herein, we show that up-regulation of NOS2 occurs in response to hypoxia, serum withdrawal, IFN-gamma, and exogenous NO, consistent with a feed-forward regulation of NO production by the tumor microenvironment in breast cancer biology. Moreover, we found that key indicators of an aggressive cancer phenotype including increased S100 calcium binding protein A8, IL-6, IL-8, and tissue inhibitor matrix metalloproteinase- 1 are up-regulated by these NOS2 stimulants, whereas inhibition of NOS2 in MDA-MB-231 breast cancer cells suppressed these markers. Moreover, NO altered cellular migration and chemoresistance of MDA-MB-231 cells to Taxol. Most notably, MDA-MB231 tumor xenographs and cell metastases from the fat pad to the brainwere significantly suppressed by NOS2 inhibition in nude mice. In summary, these results link elevated NOS2 to signals from the tumor microenvironment that arise with cancer progression and show that NO production regulates chemoresistance and metastasis of breast cancer cells.
C1 [Heinecke, Julie L.; Ridnour, Lisa A.; Cheng, Robert Y. S.; Switzer, Christopher H.; Wink, David A.] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
[Lizardo, Michael M.; Khanna, Chand] NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Hussain, S. Perwez; Ambs, Stefan] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Glynn, Sharon A.] Natl Univ Ireland, Prostate Canc Inst, Galway, Ireland.
[Young, Howard A.] NCI, Expt Immunol Lab, NIH, Frederick, MD 21702 USA.
RP Wink, DA (reprint author), NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
EM wink@mail.nih.gov
RI Glynn, Sharon/D-7136-2013
OI Glynn, Sharon/0000-0003-1459-2580
FU Intramural Research Program of the US National Institutes of Health;
National Cancer Institute; Center for Cancer Research
FX The work was supported by the Intramural Research Program of the US
National Institutes of Health, National Cancer Institute, and Center for
Cancer Research.
NR 37
TC 32
Z9 32
U1 2
U2 17
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 APR 29
PY 2014
VL 111
IS 17
BP 6323
EP 6328
DI 10.1073/pnas.1401799111
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TL
UT WOS:000335199000057
PM 24733928
ER
PT J
AU Dmitrieva, NI
Burg, MB
AF Dmitrieva, Natalia I.
Burg, Maurice B.
TI Secretion of von Willebrand factor by endothelial cells links sodium to
hypercoagulability and thrombosis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE blood clotting; HUVEC; osmotic stress
ID DEEP-VEIN THROMBOSIS; PLASMA SODIUM; HYPERNATREMIC DEHYDRATION;
ATHEROSCLEROSIS RISK; DISEASE; ABNORMALITIES; COMMUNITIES; VASOPRESSIN;
HEMOSTASIS; THERAPY
AB Hypercoagulability increases risk of thrombi that cause cardiovascular events. Here we identify plasma sodium concentration as a factor that modulates blood coagulability by affecting the production of von Willebrand factor (vWF), a key initiator of the clotting cascade. We find that elevation of salt over a range from the lower end of what is normal in blood to the level of severe hypernatremia reversibly increases vWF mRNA in endothelial cells in culture and the rate of vWF secretion from them. The high NaCl increases expression of tonicity-regulated transcription factor NFAT5 and its binding to promoter of vWF gene, suggesting involvement of hypertonic signaling in vWF up-regulation. To elevate NaCl in vivo, we modeled mild dehydration, subjecting mice to water restriction (WR) by feeding them with gel food containing 30% water. Such WR elevates blood sodium from 145.1 +/- 0.5 to 150.2 +/- 1.3 mmol/L and activates hypertonic signaling, evidenced from increased expression of NFAT5 in tissues. WR increases vWF mRNA in liver and lung and raises vWF protein in blood. Immunostaining of liver revealed increased production of vWF protein by endothelium and increased number of microthrombi inside capillaries. WR also increases blood level of D-dimer, indicative of ongoing coagulation and thrombolysis. Multivariate regression analysis of clinical data from the Atherosclerosis Risk in Communities Study demonstrated that serum sodium significantly contributes to prediction of plasma vWF and risk of stroke. The results indicate that elevation of extracellular sodium within the physiological range raises vWF sufficiently to increase coagulability and risk of thrombosis.
C1 [Dmitrieva, Natalia I.; Burg, Maurice B.] NHLBI, Renal Cellular & Mol Biol Sect, NIH, Bethesda, MD 20892 USA.
RP Dmitrieva, NI (reprint author), NHLBI, Renal Cellular & Mol Biol Sect, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM dmitrien@nhlbi.nih.gov; maurice_burg@nih.gov
RI Dmitrieva, Natalia/A-2924-2013
OI Dmitrieva, Natalia/0000-0001-8074-6950
FU Intramural Program of NHLBI
FX We thank Daniil A. Kitchaev for writing Python script for CMYK yellow
channel extraction from immunohistochemistry images, Daniela Malide and
Christian Combs at the National Heart, Lung, and Blood Institute (NHLBI)
Light Microscopy Core facility for help with microscopy, Leigh Samsel at
NHLBI Flow Cytometry Core Facility for help with Luminex analysis, and
Eric S. Leifer at the NHLBI Office of Biostatistics Research for expert
advice on the clinical data analysis. This manuscript was prepared using
Atherosclerosis Risk in Communities research materials obtained from the
NHLBI Biologic Specimen and Data Repository Information Coordinating
Center. The study was supported by the Intramural Program of NHLBI.
NR 50
TC 10
Z9 10
U1 0
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 29
PY 2014
VL 111
IS 17
BP 6485
EP 6490
DI 10.1073/pnas.1404809111
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TL
UT WOS:000335199000084
PM 24733925
ER
PT J
AU Campbell, CT
Gulley, JL
Oyelaran, O
Hodge, JW
Schlom, J
Gildersleeve, JC
AF Campbell, Christopher T.
Gulley, James L.
Oyelaran, Oyindasola
Hodge, James W.
Schlom, Jeffrey
Gildersleeve, Jeffrey C.
TI Humoral response to a viral glycan correlates with survival on
PROSTVAC-VF
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE glycan array; Forssman antigen
ID RESISTANT PROSTATE-CANCER; MELANOMA-CELL VACCINE; BLOOD-GROUP; SERUM
ANTIBODIES; FORSSMAN ANTIGEN; CLINICAL-TRIALS; DENDRITIC CELLS;
IMMUNOTHERAPY; MICROARRAY; MITOXANTRONE
AB Therapeutic cancer vaccines can be effective for treating patients, but clinical responses vary considerably from patient to patient. Early indicators of a favorable response are crucial for making individualized treatment decisions and advancing vaccine design, but no validated biomarkers are currently available. In this study, we used glycan microarrays to profile antiglycan antibody responses induced by PROSTVAC-VF, a poxvirus-based cancer vaccine currently in phase III clinical trials. Although the vaccine is designed to induce T-cell responses to prostate-specific antigen, we demonstrate that this vaccine also induces humoral responses to a carbohydrate on the poxvirus, the Forssman disaccharide (GalNAc alpha 1-3GalNAc beta). These responses had a statistically significant correlation with overall survival in two independent sample sets (P = 0.015 and 0.008) comprising more than 100 patients. Additionally, anti-Forssman humoral responses correlated with clinical outcome in a separate study of PROSTVAC-VF combined with a radiopharmaceutical (Quadramet). Studies on control subjects demonstrated that the survival correlation was specific to the vaccine. The results provide evidence that antiglycan antibody responses may serve as early biomarkers of a favorable response to PROSTVAC-VF and offer unique insights for improving vaccine design.
C1 [Campbell, Christopher T.; Oyelaran, Oyindasola; Gildersleeve, Jeffrey C.] NCI, Biol Chem Lab, NIH, Frederick, MD 21702 USA.
[Gulley, James L.; Hodge, James W.; Schlom, Jeffrey] NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Gildersleeve, JC (reprint author), NCI, Biol Chem Lab, NIH, Frederick, MD 21702 USA.
EM gildersj@mail.nih.gov
RI Gildersleeve, Jeffrey/N-3392-2014; Hodge, James/D-5518-2015; Gulley,
James/K-4139-2016
OI Hodge, James/0000-0001-5282-3154; Gulley, James/0000-0002-6569-2912
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute; Pharmacology Research Associate Program of
the National Institute of General Medical Sciences
FX We thank Kevin Camphausen for providing sera from nonvaccinated patients
with prostate cancer and Professor Tom Tolbert (University of Kansas),
Professor Lai-Xi Wang (University of Maryland), and Dr. Joseph Barchi
(National Cancer Institute) for contributing glycans for the array. This
research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute. C.T.C.
received fellowship funding from the Pharmacology Research Associate
Program of the National Institute of General Medical Sciences.
NR 63
TC 18
Z9 18
U1 0
U2 10
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 29
PY 2014
VL 111
IS 17
BP E1749
EP E1758
DI 10.1073/pnas.1314722111
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG1TL
UT WOS:000335199000013
PM 24733910
ER
PT J
AU Chapman, S
McDermott, DH
Shen, K
Jang, MK
McBride, AA
AF Chapman, Sandra
McDermott, David H.
Shen, Kui
Jang, Moon Kyoo
McBride, Alison A.
TI The effect of Rho kinase inhibition on long-term keratinocyte
proliferation is rapid and conditional
SO STEM CELL RESEARCH & THERAPY
LA English
DT Article
ID REPROGRAMMED CELLS; EPITHELIAL-CELLS; STEM-CELLS; GROWTH;
DIFFERENTIATION; MULTIPLICATION; Y-27632
AB Introduction: We previously demonstrated that the lifespan of primary human keratinocytes could be extended indefinitely by culture in the presence of the Rho kinase (ROCK) inhibitor Y-27632. This technique has proven to be very useful in diverse areas of basic and clinical research.
Methods: In this follow-up study we determine whether the continual presence of Y-27632 is required for sustained proliferation. We also test whether different ROCK inhibitors can be used for this technique and whether it can also promote indefinite proliferation of animal keratinocytes. We measure keratinocyte gene expression, proliferation, behaviour and lifespan in the presence and absence of Y-27632.
Results: We demonstrate that the extension of lifespan observed by culture of keratinocytes in the presence of fibroblast feeders and a ROCK inhibitor is reversible and that cells senesce gradually when the inhibitor is removed from the medium. Conversely, keratinocytes that are close to the end of their replicative life span can be revived by ROCK inhibition. We demonstrate that different inhibitors of ROCK can also efficiently extend the lifespan of human keratinocytes and that ROCK inhibition extends the lifespan of animal keratinocytes derived from mouse and bovine epithelia. Gene expression analysis of human epidermal keratinocytes cells grown in the presence of Y-27632 demonstrates that ROCK inhibition primarily inhibits keratinocyte differentiation. Live-imaging of keratinocytes cultured with ROCK inhibitors show that the effect of ROCK inhibition on cellular proliferation is immediate and ROCK inhibited cells proliferate rapidly without differentiation or stratification.
Conclusions: ROCK inhibition rapidly and conditionally induces indefinite proliferation of keratinocytes. This method has far-reaching applications for basic research, as well as for regenerative and personalized medicine.
C1 [Chapman, Sandra; Jang, Moon Kyoo; McBride, Alison A.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[McDermott, David H.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Shen, Kui] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
RP McBride, AA (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM amcbride@nih.gov
RI Shen, Kui/E-2764-2015;
OI McDermott, David/0000-0001-6978-0867; McBride,
Alison/0000-0001-5607-5157
FU NIAID, NIH
FX We thank Wendy Weinberg for mouse keratinocytes and Wesley Stepp for
human foreskin keratinocytes. This work was funded by the Intramural
Research Program of the NIAID, NIH. The opinions expressed herein are
solely those of the authors, and use of trade or product names does not
imply endorsement of the United States Government.
NR 28
TC 9
Z9 9
U1 0
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1757-6512
J9 STEM CELL RES THER
JI Stem Cell Res. Ther.
PD APR 28
PY 2014
VL 5
AR 60
DI 10.1186/scrt449
PG 11
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA AI9KK
UT WOS:000337251300001
PM 24774536
ER
PT J
AU Reece, KM
Richardson, ED
Cook, KM
Campbell, TJ
Pisle, ST
Holly, AJ
Venzon, DJ
Liewehr, DJ
Chau, CH
Price, DK
Figg, WD
AF Reece, Kelie M.
Richardson, Emily D.
Cook, Kristina M.
Campbell, Tessa J.
Pisle, Stephen T.
Holly, Alesia J.
Venzon, David J.
Liewehr, David J.
Chau, Cindy H.
Price, Douglas K.
Figg, William D.
TI Epidithiodiketopiperazines (ETPs) exhibit in vitro antiangiogenic and in
vivo antitumor activity by disrupting the HIF-1 alpha/p300 complex in a
preclinical model of prostate cancer
SO MOLECULAR CANCER
LA English
DT Article
DE Hypoxia; HIF-1 alpha; p300; ETPs; Angiogenesis; VEGF
ID HYPOXIA-INDUCIBLE FACTOR-1; TRANSCRIPTIONAL REGULATION; ANGIOGENESIS
INHIBITORS; THERAPY; GROWTH; GENE; FARNESYLTRANSFERASE; GLIOTOXIN;
TARGET; HIF-1
AB The downstream targets of hypoxia inducible factor-1 alpha (HIF-1 alpha) play an important role in tumor progression and angiogenesis. Therefore, inhibition of HIF-mediated transcription has potential in the treatment of cancer. One attractive strategy for inhibiting HIF activity is the disruption of the HIF-1 alpha/p300 complex, as p300 is a crucial coactivator of hypoxia-inducible transcription. Several members of the epidithiodiketopiperazine (ETP) family of natural products have been shown to disrupt the HIF-1 alpha/p300 complex in vitro; namely, gliotoxin, chaetocin, and chetomin. Here, we further characterized the molecular mechanisms underlying the antiangiogenic and antitumor effects of these ETPs using a preclinical model of prostate cancer. In the rat aortic ring angiogenesis assay, gliotoxin, chaetocin, and chetomin significantly inhibited microvessel outgrowth at a GI(50) of 151, 8, and 20 nM, respectively. In vitro co-immunoprecipitation studies in prostate cancer cell extracts demonstrated that these compounds disrupted the HIF-1 alpha/p300 complex. The downstream effects of inhibiting the HIF-1 alpha/p300 interaction were evaluated by determining HIF-1 alpha target gene expression at the mRNA and protein levels. Dose-dependent decreases in levels of secreted VEGF were detected by ELISA in the culture media of treated cells, and the subsequent downregulation of VEGFA, LDHA, and ENO1 HIF-1 alpha target genes were confirmed by semi-quantitative real-time PCR. Finally, treatment with ETPs in mice bearing prostate tumor xenografts resulted in significant inhibition of tumor growth. These results suggest that directly targeting the HIF-1 alpha/p300 complex with ETPs may be an effective approach for inhibiting angiogenesis and tumor growth.
C1 [Reece, Kelie M.; Richardson, Emily D.; Cook, Kristina M.; Campbell, Tessa J.; Chau, Cindy H.; Price, Douglas K.; Figg, William D.] NCI, Mol Pharmacol Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Holly, Alesia J.; Figg, William D.] NCI, Clin Pharmacol Core, Ctr Canc Res, Bethesda, MD 20892 USA.
[Venzon, David J.; Liewehr, David J.] NCI, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Pisle, Stephen T.] SAIC Frederick, Frederick Natl Lab Canc Res, Clin Pharmacol Program, Ft Detrick, MD 21702 USA.
[Figg, William D.] NIH, NCI, Bethesda, MD 20892 USA.
RP Figg, WD (reprint author), NCI, Mol Pharmacol Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
EM figgw@helix.nih.gov
RI Figg Sr, William/M-2411-2016
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Bethesda, MD, USA; National Cancer Institute,
National Institutes of Health [HHSN261200800001E]
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health, National Cancer Institute, Bethesda,
MD, USA. This project has been funded in whole or in part with federal
funds from the National Cancer Institute, National Institutes of Health,
under Contract No. HHSN261200800001E (STP).
NR 36
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Z9 19
U1 2
U2 20
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD APR 28
PY 2014
VL 13
AR 91
DI 10.1186/1476-4598-13-91
PG 12
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA AH3ZR
UT WOS:000336065500001
PM 24775564
ER
PT J
AU Moreland, RT
Nguyen, AD
Ryan, JF
Schnitzler, CE
Koch, BJ
Siewert, K
Wolfsberg, TG
Baxevanis, AD
AF Moreland, R. Travis
Nguyen, Anh-Dao
Ryan, Joseph F.
Schnitzler, Christine E.
Koch, Bernard J.
Siewert, Katherine
Wolfsberg, Tyra G.
Baxevanis, Andreas D.
TI A customized Web portal for the genome of the ctenophore Mnemiopsis
leidyi
SO BMC GENOMICS
LA English
DT Article
DE Mnemiopsis leidyi; Genome browser; Customized Web portal; Gene wiki
ID DATABASE; SIMILARITY; EVOLUTION; SERVER; GENES; SCALE; TOOL
AB Background: Mnemiopsis leidyi is a ctenophore native to the coastal waters of the western Atlantic Ocean. A number of studies on Mnemiopsis have led to a better understanding of many key biological processes, and these studies have contributed to the emergence of Mnemiopsis as an important model for evolutionary and developmental studies. Recently, we sequenced, assembled, annotated, and performed a preliminary analysis on the 150-megabase genome of the ctenophore, Mnemiopsis. This sequencing effort has produced the first set of whole-genome sequencing data on any ctenophore species and is amongst the first wave of projects to sequence an animal genome de novo solely using next-generation sequencing technologies.
Description: The Mnemiopsis Genome Project Portal (http://research.nhgri.nih.gov/mnemiopsis/) is intended both as a resource for obtaining genomic information on Mnemiopsis through an intuitive and easy-to-use interface and as a model for developing customized Web portals that enable access to genomic data. The scope of data available through this Portal goes well beyond the sequence data available through GenBank, providing key biological information not available elsewhere, such as pathway and protein domain analyses; it also features a customized genome browser for data visualization.
Conclusions: We expect that the availability of these data will allow investigators to advance their own research projects aimed at understanding phylogenetic diversity and the evolution of proteins that play a fundamental role in metazoan development. The overall approach taken in the development of this Web site can serve as a viable model for disseminating data from whole-genome sequencing projects, framed in a way that best-serves the specific needs of the scientific community.
C1 [Moreland, R. Travis; Nguyen, Anh-Dao; Ryan, Joseph F.; Schnitzler, Christine E.; Koch, Bernard J.; Siewert, Katherine; Wolfsberg, Tyra G.; Baxevanis, Andreas D.] NHGRI, Genome Technol Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Ryan, Joseph F.] Univ Florida, Whitney Lab Marine Biosci, St Augustine, FL 32080 USA.
RP Baxevanis, AD (reprint author), NHGRI, Genome Technol Branch, Div Intramural Res, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM andy@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Human Genome Research Institute, National Institutes of Health.
We would like to thank Steven Bond, Mark Fredriksen, Derek Gildea, and
Evan Maxwell for their thoughtful, constructive comments during the
development of the Portal. We also thank Steven Bond, Derek Gildea, and
Evan Maxwell for their critical reading of the manuscript.
NR 28
TC 2
Z9 2
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD APR 28
PY 2014
VL 15
AR 316
DI 10.1186/1471-2164-15-316
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA AH1EY
UT WOS:000335863800001
PM 24773765
ER
PT J
AU Hales, CM
Seyfried, NT
Dammer, EB
Duong, D
Yi, H
Gearing, M
Troncoso, JC
Mufson, EJ
Thambisetty, M
Levey, AI
Lah, JJ
AF Hales, Chadwick M.
Seyfried, Nicholas T.
Dammer, Eric B.
Duong, Duc
Yi, Hong
Gearing, Marla
Troncoso, Juan C.
Mufson, Elliott J.
Thambisetty, Madhav
Levey, Allan I.
Lah, James J.
TI U1 small nuclear ribonucleoproteins (snRNPs) aggregate in Alzheimer's
disease due to autosomal dominant genetic mutations and trisomy 21
SO MOLECULAR NEURODEGENERATION
LA English
DT Article
DE Spliceosome; snRNP; Alzheimer's disease; Down syndrome; U1-70k; SmD;
Presenilin; Amyloid precursor protein
ID PAIRED HELICAL FILAMENTS; ELECTRON-MICROSCOPY; SPLICEOSOME; CORTEX
AB Background: We recently identified U1 small nuclear ribonucleoprotein (snRNP) tangle-like aggregates and RNA splicing abnormalities in sporadic Alzheimer's disease (AD). However little is known about snRNP biology in early onset AD due to autosomal dominant genetic mutations or trisomy 21 in Down syndrome. Therefore we investigated snRNP biochemical and pathologic features in these disorders.
Findings: We performed quantitative proteomics and immunohistochemistry in postmortem brain from genetic AD cases. Electron microscopy was used to characterize ultrastructural features of pathologic aggregates. U1-70k and other snRNPs were biochemically enriched in the insoluble fraction of human brain from subjects with presenilin 1 (PS1) mutations. Aggregates of U1 snRNP-immunoreactivity formed cytoplasmic tangle-like structures in cortex of AD subjects with PS1 and amyloid precursor protein (APP) mutations as well as trisomy 21. Ultrastructural analysis with electron microscopy in an APP mutation case demonstrated snRNP immunogold labeling of paired helical filaments (PHF).
Conclusions: These studies identify U1 snRNP pathologic changes in brain of early onset genetic forms of AD. Since dominant genetic mutations and trisomy 21 result in dysfunctional amyloid processing, the findings suggest that aberrant beta-amyloid processing may influence U1 snRNP aggregate formation.
C1 [Hales, Chadwick M.; Levey, Allan I.; Lah, James J.] Emory Univ, Dept Neurol, Sch Med, Atlanta, GA 30322 USA.
[Hales, Chadwick M.; Seyfried, Nicholas T.; Dammer, Eric B.; Duong, Duc; Levey, Allan I.; Lah, James J.] Emory Univ, Ctr Neurodegenerat Dis, Atlanta, GA 30322 USA.
[Seyfried, Nicholas T.; Dammer, Eric B.] Emory Univ, Dept Biochem, Sch Med, Atlanta, GA 30322 USA.
[Yi, Hong] Emory Univ, Robert P Apkarian Integrated Electron Microscopy, Atlanta, GA 30322 USA.
[Gearing, Marla] Emory Univ, Dept Pathol, Sch Med, Atlanta, GA 30322 USA.
[Troncoso, Juan C.] Johns Hopkins Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Troncoso, Juan C.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Mufson, Elliott J.] Rush Univ, Dept Neurol Sci, Chicago, IL 60612 USA.
[Thambisetty, Madhav] NIA, NIH, Bethesda, MD 20892 USA.
RP Lah, JJ (reprint author), Emory Univ, Dept Neurol, Sch Med, Atlanta, GA 30322 USA.
EM jlah@emory.edu
OI Dammer, Eric/0000-0003-2947-7606
FU Robert P. Apkarian Integrated Electron Microscopy Core of Emory
University; Clinical Research Training Fellowship from the American
Brain Foundation; Emory Alzheimer's Disease Research Center
[NIA-AG025688, NIAP01AG14449]; Emory Neuroscience NINDS Core Facility
[P30NS055077]; University of Washington ADRC [NIA-P50-AG05136];
Alzheimer's Association New Investigator Research Award
[NIRG-12-242297]; NIA intramural Research Program of the National
Institutes of Health
FX This research project was supported in part by the Robert P. Apkarian
Integrated Electron Microscopy Core of Emory University. Clinical
Research Training Fellowship from the American Brain Foundation (CMH).
Emory Alzheimer's Disease Research Center-NIA-AG025688 (AIL),
NIAP01AG14449 (JJL, EJM), Emory Neuroscience NINDS Core
Facility-P30NS055077, University of Washington ADRC-NIA-P50-AG05136 and
an Alzheimer's Association New Investigator Research Award
(NIRG-12-242297) to NTS. This work was supported in part by the NIA
intramural Research Program of the National Institutes of Health. We are
grateful for pathological specimens provided by MG, JCT and Thomas
Montine M.D, Ph.D.
NR 25
TC 4
Z9 4
U1 2
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1326
J9 MOL NEURODEGENER
JI Mol. Neurodegener.
PD APR 28
PY 2014
VL 9
AR 15
DI 10.1186/1750-1326-9-15
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA AG7MT
UT WOS:000335602900001
PM 24773620
ER
PT J
AU Wang, ZQ
Fan, M
Candas, D
Zhang, TQ
Qin, LL
Eldridge, A
Wachsmann-Hogiu, S
Ahmed, KM
Chromy, BA
Nantajit, D
Duru, N
He, FC
Chen, M
Finkel, T
Weinstein, LS
Li, JJ
AF Wang, Zhaoqing
Fan, Ming
Candas, Demet
Zhang, Tie-Qiao
Qin, Lili
Eldridge, Angela
Wachsmann-Hogiu, Sebastian
Ahmed, Kazi M.
Chromy, Brett A.
Nantajit, Danupon
Duru, Nadire
He, Fuchu
Chen, Min
Finkel, Toren
Weinstein, Lee S.
Li, Jian Jian
TI Cyclin B1/Cdk1 Coordinates Mitochondrial Respiration for Cell-Cycle G2/M
Progression
SO DEVELOPMENTAL CELL
LA English
DT Article
ID LEUKEMIC HL-60 CELLS; COMPLEX-I; MITOTIC PHOSPHORYLATION; S-PHASE;
PROTEIN; CDC2; B1; MECHANISMS; CHECKPOINT; MITOSIS
AB A substantial amount of mitochondrial energy is required for cell-cycle progression. The mechanisms underlying the coordination of the mitochondrial respiration with cell-cycle progression, especially the G2/M transition, remain to be elucidated. Here, we show that a fraction of cyclin B1/Cdk1 proteins localizes to the matrix of mitochondria and phosphorylates a cluster of mitochondrial proteins, including the complex I (CI) subunits in the respiratory chain. Cyclin B1/Cdk1-mediated CI phosphorylation enhances CI activity, whereas deficiency of such phosphorylation in each of the relevant CI subunits results in impairment of CI function. Mitochondria-targeted cyclin B1/Cdk1 increases mitochondrial respiration with enhanced oxygen consumption and ATP generation, which provides cells with efficient bioenergy for G2/M transition and shortens overall cell-cycle time. Thus, cyclin B1/Cdk1-mediated phosphorylation of mitochondrial substrates allows cells to sense and respond to increased energy demand for G2/M transition and, subsequently, to upregulate mitochondrial respiration for successful cell-cycle progression.
C1 [Wang, Zhaoqing; Fan, Ming; Candas, Demet; Qin, Lili; Nantajit, Danupon; Duru, Nadire; Li, Jian Jian] Univ Calif Davis, Dept Radiat Oncol, Sacramento, CA 95817 USA.
[Zhang, Tie-Qiao; Wachsmann-Hogiu, Sebastian] Univ Calif Davis, Ctr Biophoton Sci & Technol, Sacramento, CA 95817 USA.
[Ahmed, Kazi M.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Dept Canc & DNA Damage Response, Life Sci Div, Berkeley, CA 94720 USA.
[Eldridge, Angela; Chromy, Brett A.] Univ Calif Davis, Dept Pathol & Lab Med, Sacramento, CA 95817 USA.
[He, Fuchu] Beijing Prote Res Ctr, State Key Lab Prote, Beijing 102206, Peoples R China.
[Chen, Min; Weinstein, Lee S.] NIDDK, Signal Transduct Sect, NIH, Bethesda, MD 20892 USA.
[Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Li, Jian Jian] Univ Calif Davis, Sch Med, NCI Designated Comprehens Canc Ctr, Sacramento, CA 95817 USA.
RP Li, JJ (reprint author), Univ Calif Davis, Dept Radiat Oncol, Sacramento, CA 95817 USA.
EM jijli@ucdavis.edu
FU NIH [CA133402, CA152313]; Department of Energy Office of Science
[DE-SC0001271]; NIH Intramural Research Program of NIDDK
FX We thank Grate Adamson at Electron Microscopy Laboratory, University of
California Davis School of Medicine, for technical assistance in
mitochondrial analysis and Haiying Hang at Institute of Biophysics,
Chinese Academy of Sciences, for analysis of cell-cycle data. This work
was supported by NIH grants CA133402 and CA152313 and Department of
Energy Office of Science DE-SC0001271 (to J.L.) and the NIH Intramural
Research Program of NIDDK (to L.S.W. and T.F.).
NR 47
TC 35
Z9 37
U1 7
U2 22
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
EI 1878-1551
J9 DEV CELL
JI Dev. Cell
PD APR 28
PY 2014
VL 29
IS 2
BP 217
EP 232
DI 10.1016/j.devcel.2014.03.012
PG 16
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA AG4XA
UT WOS:000335422500011
PM 24746669
ER
PT J
AU Kane, LA
Lazarou, M
Fogel, AI
Li, Y
Yamano, K
Sarraf, SA
Banerjee, S
Youle, RJ
AF Kane, Lesley A.
Lazarou, Michael
Fogel, Adam I.
Li, Yan
Yamano, Koji
Sarraf, Shireen A.
Banerjee, Soojay
Youle, Richard J.
TI PINK1 phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase
activity
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID MITOCHONDRIAL DEPOLARIZATION; DAMAGED MITOCHONDRIA; SIGNALING NETWORKS;
MITOPHAGY; RECRUITMENT; PROTEASOME; MEMBRANE; BINDING; PHOSPHOPEPTIDES;
TRANSLOCATION
AB PINK1 kinase activates the E3 ubiquitin ligase Parkin to induce selective autophagy of damaged mitochondria. However, it has been unclear how PINK1 activates and recruits Parkin to mitochondria. Although PINK1 phosphorylates Parkin, other PINK1 substrates appear to activate Parkin, as the mutation of all serine and threonine residues conserved between Drosophila and human, including Parkin 565, did not wholly impair Parkin translocation to mitochondria. Using mass spectrometry, we discovered that endogenous PINK1 phosphorylated ubiquitin at serine 65, homologous to the site phosphorylated by PINK1 in Parkin's ubiquitin-like domain. Recombinant TcPINK1 directly phosphorylated ubiquitin and phosphoubiquitin activated Parkin E3 ubiquitin ligase activity in cell-free assays. In cells, the phosphomimetic ubiquitin mutant S65D bound and activated Parkin. Furthermore, expression of ubiquitin S65A, a mutant that cannot be phosphorylated by PINK1, inhibited Parkin translocation to damaged mitochondria. These results explain a feed-forward mechanism of PINK1-mediated initiation of Parkin E3 ligase activity.
C1 [Kane, Lesley A.; Lazarou, Michael; Fogel, Adam I.; Yamano, Koji; Sarraf, Shireen A.; Banerjee, Soojay; Youle, Richard J.] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20824 USA.
[Li, Yan] NINDS, Prot Peptide Sequencing Facil, NIH, Bethesda, MD 20824 USA.
RP Youle, RJ (reprint author), NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20824 USA.
EM youler@ninds.nih.gov
OI Lazarou, Michael/0000-0003-2150-5545
FU National Institute of Neurological Disorders and Stroke intramural
program
FX This work was supported by the National Institute of Neurological
Disorders and Stroke intramural program.
NR 42
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Z9 222
U1 4
U2 37
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD APR 28
PY 2014
VL 205
IS 2
BP 143
EP 153
DI 10.1083/jcb.201402104
PG 11
WC Cell Biology
SC Cell Biology
GA AG3DT
UT WOS:000335296700004
PM 24751536
ER
PT J
AU Watanabe, J
Hattori, M
Berriman, M
Lehane, MJ
Hall, N
Solano, P
Aksoy, S
Hide, W
Toure, Y
Attardo, GM
Darby, AC
Toyoda, A
Hertz-Fowler, C
Larkin, DM
Cotton, JA
Watanabe, J
Sanders, MJ
Swain, MT
Hattori, M
Berriman, M
Quail, MA
Inoue, N
Ravel, S
Taylor, TD
Srivastava, TP
Sharma, V
Warren, W
Wilson, RK
Suzuki, Y
Lawson, D
Hughes, DST
Megy, K
Masiga, DK
Mireji, PO
Attardo, GM
Hansen, IA
Van den Abbeele, J
Benoit, JB
Bourtzis, K
Lehane, MJ
Aksoy, S
Masiga, DK
Obiero, GFO
Robertson, HM
Jones, JW
Zhou, JJ
Field, LM
Friedrich, M
Mireji, PO
Nyanjom, SRG
Telleria, EL
Caljon, G
Van den Abbeele, J
Ribeiro, JMC
Acosta-Serrano, A
Benoit, JB
Ooi, CP
Rose, C
Price, DP
Haines, LR
Lehane, MJ
Christoffels, A
Sim, C
Pham, DQD
Denlinger, DL
Geiser, DL
Omedo, IA
Benoit, JB
Winzerling, JJ
Peyton, JT
Marucha, KK
Jonas, M
Meuti, ME
Rawlings, ND
Mireji, PO
Zhang, QR
Macharia, RW
Michalkova, V
Dashti, ZJS
Baumann, AA
Gade, G
Marco, HG
Hansen, IA
Caers, J
Schoofs, L
Riehle, MA
Hu, WQ
Tu, ZJ
Tarone, AM
Malacrida, AR
Kibet, CK
Benoit, JB
Scolari, F
Attardo, GM
Koekemoer, JJO
Willis, J
Gomulski, LM
Falchetto, M
Scott, MJ
Fu, SH
Sze, SH
Luiz, T
Weiss, B
Walshe, DP
Wang, JW
Benoit, JB
Attardo, GM
Wamalwa, M
Mwangi, S
Aksoy, S
Ramphul, UN
Snyder, AK
Brelsfoard, CL
Thomas, GH
Tsiamis, G
Bourtzis, K
Arensburger, P
Rio, RVM
Macdonald, SJ
Panji, S
Kruger, A
Christoffels, A
Benkahla, A
Balyeidhusa, ASP
Msangi, A
Ooi, CP
Okoro, CK
Masiga, DK
Stephens, D
Walshe, DP
Stanley, EJ
Mpondo, F
Wamwiri, F
Mramba, F
Attardo, GM
Siwo, G
Obiero, GFO
Githinji, G
Harkins, G
Murilla, G
Lehvaslaiho, H
Malele, I
Koekemoer, JJO
Auma, JE
Kinyua, JK
Ouma, J
Watanabe, J
Megy, K
Okedi, L
Manga, L
Jonas, M
Wamalwa, M
Aslett, M
Koffi, M
Berriman, M
Lehane, MJ
Gaunt, MW
Makgamathe, M
Hall, N
Mulder, N
Manangwa, O
Abila, PP
Wincker, P
Mireji, PO
Gregory, R
Rio, RVM
Bateta, R
Sakate, R
Aksoy, S
Ommeh, S
Lehane, S
Nyanjom, SRG
Imanishi, T
Taylor, TD
Osamor, VC
Sharma, V
Hide, W
Kawahara, Y
Benoit, JB
AF Watanabe, Junichi
Hattori, Masahira
Berriman, Matthew
Lehane, Michael J.
Hall, Neil
Solano, Philippe
Aksoy, Serap
Hide, Winston
Toure, Yeya
Attardo, Geoffrey M.
Darby, Alistair C.
Toyoda, Atsushi
Hertz-Fowler, Christiane
Larkin, Denis M.
Cotton, James A.
Watanabe, Junichi
Sanders, Mandy J.
Swain, Martin T.
Hattori, Masahira
Berriman, Matthew
Quail, Michael A.
Inoue, Noboru
Ravel, Sophie
Taylor, Todd D.
Srivastava, Tulika P.
Sharma, Vineet
Warren, Wesley
Wilson, Richard K.
Suzuki, Yutaka
Lawson, Daniel
Hughes, Daniel S. T.
Megy, Karyn
Masiga, Daniel K.
Mireji, Paul O.
Attardo, Geoffrey M.
Hansen, Imma A.
Van den Abbeele, Jan
Benoit, Joshua B.
Bourtzis, Kostas
Lehane, Michael J.
Aksoy, Serap
Masiga, Daniel K.
Obiero, George F. O.
Robertson, Hugh M.
Jones, Jeffery W.
Zhou, Jing-Jiang
Field, Linda M.
Friedrich, Markus
Mireji, Paul O.
Nyanjom, Steven R. G.
Telleria, Erich L.
Caljon, Guy
Van den Abbeele, Jan
Ribeiro, Jose M. C.
Acosta-Serrano, Alvaro
Benoit, Joshua B.
Ooi, Cher-Pheng
Rose, Clair
Price, David P.
Haines, Lee R.
Lehane, Michael J.
Christoffels, Alan
Sim, Cheolho
Pham, Daphne Q. D.
Denlinger, David L.
Geiser, Dawn L.
Omedo, Irene A.
Benoit, Joshua B.
Winzerling, Joy J.
Peyton, Justin T.
Marucha, Kevin K.
Jonas, Mario
Meuti, Megan E.
Rawlings, Neil D.
Mireji, Paul O.
Zhang, Qirui
Macharia, Rosaline W.
Michalkova, Veronika
Dashti, Zahra Jalali Sefid
Baumann, Aaron A.
Gaede, Gerd
Marco, Heather G.
Hansen, Immo A.
Caers, Jelle
Schoofs, Liliane
Riehle, Michael A.
Hu, Wanqi
Tu, Zhijian
Tarone, Aaron M.
Malacrida, Anna R.
Kibet, Caleb K.
Benoit, Joshua B.
Scolari, Francesca
Attardo, Geoffrey M.
Koekemoer, Jacobus J. O.
Willis, Judith
Gomulski, Ludvik M.
Falchetto, Marco
Scott, Maxwell J.
Fu, Shuhua
Sze, Sing-Hoi
Luiz, Thiago
Weiss, Brian
Walshe, Deirdre P.
Wang, Jingwen
Benoit, Joshua B.
Attardo, Geoffrey M.
Wamalwa, Mark
Mwangi, Sarah
Aksoy, Serap
Ramphul, Urvashi N.
Snyder, Anna K.
Brelsfoard, Corey L.
Thomas, Gavin H.
Tsiamis, George
Bourtzis, Kostas
Arensburger, Peter
Rio, Rita V. M.
Macdonald, Sandy J.
Panji, Sumir
Kruger, Adele
Christoffels, Alan
Benkahla, Alia
Balyeidhusa, Apollo S. P.
Msangi, Atway
Ooi, Cher-Pheng
Okoro, Chinyere K.
Masiga, Daniel K.
Stephens, Dawn
Walshe, Deirdre P.
Stanley, Eleanor J.
Mpondo, Feziwe
Wamwiri, Florence
Mramba, Furaha
Attardo, Geoffrey M.
Siwo, Geoffrey
Obiero, George F. O.
Githinji, George
Harkins, Gordon
Murilla, Grace
Lehvaeslaiho, Heikki
Malele, Imna
Koekemoer, Jacobus J. O.
Auma, Joanna E.
Kinyua, Johnson K.
Ouma, Johnson
Watanabe, Junichi
Megy, Karyn
Okedi, Loyce
Manga, Lucien
Jonas, Mario
Wamalwa, Mark
Aslett, Martin
Koffi, Mathurin
Berriman, Matthew
Lehane, Michael J.
Gaunt, Michael W.
Makgamathe, Mmule
Hall, Neil
Mulder, Nicola
Manangwa, Oliver
Abila, Patrick P.
Wincker, Patrick
Mireji, Paul O.
Gregory, Richard
Rio, Rita V. M.
Bateta, Rosemary
Sakate, Ryuichi
Aksoy, Serap
Ommeh, Sheila
Lehane, Stella
Nyanjom, Steven R. G.
Imanishi, Tadashi
Taylor, Todd D.
Osamor, Victor C.
Sharma, Vineet
Hide, Winston
Kawahara, Yoshihiro
Benoit, Joshua B.
CA IGGI
TI Genome Sequence of the Tsetse Fly (Glossina morsitans): Vector of
African Trypanosomiasis
SO SCIENCE
LA English
DT Article
ID PERITROPHIC MATRIX; IMMUNE-RESPONSES; AQUAPORINS; PROTEINS; DIPTERA;
FLIES
AB Tsetse flies are the sole vectors of human African trypanosomiasis throughout sub-Saharan Africa. Both sexes of adult tsetse feed exclusively on blood and contribute to disease transmission. Notable differences between tsetse and other disease vectors include obligate microbial symbioses, viviparous reproduction, and lactation. Here, we describe the sequence and annotation of the 366-megabase Glossina morsitans morsitans genome. Analysis of the genome and the 12,308 predicted protein-encoding genes led to multiple discoveries, including chromosomal integrations of bacterial (Wolbachia) genome sequences, a family of lactation-specific proteins, reduced complement of host pathogen recognition proteins, and reduced olfaction/ chemosensory associated genes. These genome data provide a foundation for research into trypanosomiasis prevention and yield important insights with broad implications for multiple aspects of tsetse biology.
C1 [Lehvaeslaiho, Heikki] KAUST, Thuwal 239556900, Saudi Arabia.
[Arensburger, Peter] Calif State Polytech Univ Pomona, Dept Biol Sci, Pomona, CA 91768 USA.
[Bourtzis, Kostas] Alexander Fleming Biomed Sci Res Ctr, Biomed Sci Res Ctr, Vari 16672, Greece.
[Wincker, Patrick] CEA, F-91507 Evry, France.
[Macharia, Rosaline W.] Univ Nairobi, Ctr Biotechnol & Bioinformat, Nairobi 00100, Kenya.
[Suzuki, Yutaka] Univ Tokyo, Grad Sch Frontier Sci, Dept Computat Biol, Ctr Om & Bioinformat, Kashiwa, Chiba 2778561, Japan.
[Toyoda, Atsushi] Natl Inst Genet, Comparat Genom Lab, Mishima, Shizuoka 4118540, Japan.
[Panji, Sumir; Mulder, Nicola] Univ Cape Town, Fac Hlth Sci, IIDMM, Computat Biol Grp, ZA-7925 Cape Town, South Africa.
[Fu, Shuhua] Texas A&M Univ, Dept Biochem & Biophys, College Stn, TX 77843 USA.
[Marucha, Kevin K.; Bateta, Rosemary] Egerton Univ, Dept Biochem & Mol Biol, Njoro, Kenya.
[Kinyua, Johnson K.] JKUAT, Dept Biochem, Nairobi, Kenya.
[Hu, Wanqi; Tu, Zhijian] Virginia Polytech Inst & State Univ, Dept Biochem, Blacksburg, VA 24061 USA.
[Zhou, Jing-Jiang; Field, Linda M.] Rothamsted Res, Dept Biol Chem & Crop Protect, Harpenden AL5 2JQ, Herts, England.
[Benoit, Joshua B.] Univ Cincinnati, McMicken Coll Arts & Sci, Dept Biol Sci, Cincinnati, OH 45221 USA.
[Gaede, Gerd; Marco, Heather G.] Univ Cape Town, Dept Biol Sci, ZA-7700 Rondebosch, South Africa.
[Pham, Daphne Q. D.] Univ Wisconsin Parkside, Dept Biol Sci, Kenosha, WI 53144 USA.
[Jones, Jeffery W.; Friedrich, Markus] Wayne State Univ, Dept Biol Sci, Detroit, MI 48202 USA.
[Malacrida, Anna R.; Scolari, Francesca; Gomulski, Ludvik M.; Falchetto, Marco] Univ Pavia, Dept Biol & Biotechnol, I-27100 Pavia, Italy.
[Sim, Cheolho] Baylor Univ, Dept Biol, Waco, TX 76798 USA.
[Caers, Jelle; Schoofs, Liliane] Katholieke Univ Leuven, Dept Biol, B-3000 Louvain, Belgium.
[Hansen, Imma A.; Price, David P.; Hansen, Immo A.] New Mexico State Univ, Dept Biol, Las Cruces, NM 88003 USA.
[Thomas, Gavin H.; Macdonald, Sandy J.] Univ York, Dept Biol, York Y010 5DD, N Yorkshire, England.
[Snyder, Anna K.; Rio, Rita V. M.] W Virginia Univ, Dept Biol, Morgantown, WV 26506 USA.
[Van den Abbeele, Jan; Caljon, Guy] Inst Trop Med Antwerp, Dept Biomed Sci, B-2000 Antwerp, Belgium.
[Willis, Judith] Univ Georgia, Dept Cellular Biol, Athens, GA 30602 USA.
[Omedo, Irene A.] CGMRC, KEMRI Wellcome Trust Programme, Dept Clin Res, Kilifi, Kenya.
[Osamor, Victor C.] Covenant Univ, Coll Sci & Technol, Dept Comp & Informat Sci, Ota, Ogun State, Nigeria.
[Sze, Sing-Hoi] Texas A&M Univ, Dept Biochem & Biophys, Dept Comp Sci & Engn, College Stn, TX 77843 USA.
[Scott, Maxwell J.] N Carolina State Univ, Dept Entomol, Raleigh, NC 27695 USA.
[Tarone, Aaron M.] Texas A&M Univ, Dept Entomol, College Stn, TX 77843 USA.
[Denlinger, David L.; Zhang, Qirui] Ohio State Univ, Dept Entomol, Aronoff Lab 400, Columbus, OH 43210 USA.
[Riehle, Michael A.] Univ Arizona, Dept Entomol, Tucson, AZ 85721 USA.
[Robertson, Hugh M.] Univ Illinois, Dept Entomol, Urbana, IL 61801 USA.
Joint FAO IAEA Programme Nucl Tech Food & Agr, Insect Pest Control Lab, A-1220 Vienna, Austria.
[Tsiamis, George] Univ Patras, Dept Environm & Nat Resources Management, Agrinion 30100, Greece.
[Telleria, Erich L.; Michalkova, Veronika; Luiz, Thiago; Weiss, Brian; Wang, Jingwen] Yale Univ, Sch Publ Hlth, Dept Epidemiol Microbial Dis, New Haven, CT 06520 USA.
[Peyton, Justin T.] Ohio State Univ, Dept Ecol Evolut & Organismal Biol, Aronoff Lab 300, Columbus, OH 43210 USA.
[Brelsfoard, Corey L.] St Catharine Coll, Dept Nat Sci, St Catharine, KY 40061 USA.
[Winzerling, Joy J.] Univ Arizona, Coll Agr & Life Sci, Dept Nutr Sci, Career Serv, Tucson, AZ 85721 USA.
[Winzerling, Joy J.] Univ Arizona, Coll Agr & Life Sci, Dept Nutr Sci, Acad Serv, Tucson, AZ 85721 USA.
[Geiser, Dawn L.] Univ Arizona, Dept Nutr Sci, Tucson, AZ 85721 USA.
[Gaunt, Michael W.] Univ London London Sch Hyg & Trop Med, Dept Pathogen Mol Biol, London WC1E 7HT, England.
[Acosta-Serrano, Alvaro; Rose, Clair] Univ Liverpool, Liverpool Sch Trop Med, Dept Parasitol, Liverpool L3 5QA, Merseyside, England.
[Acosta-Serrano, Alvaro; Haines, Lee R.; Walshe, Deirdre P.; Ramphul, Urvashi N.; Lehane, Stella] Univ Liverpool, Liverpool Sch Trop Med, Dept Vector Biol, Liverpool L3 5QA, Merseyside, England.
[Koekemoer, Jacobus J. O.] Onderstepoort Vet Inst, Entomol Sect, ZA-110 Onderstepoort, South Africa.
[Siwo, Geoffrey] Univ Notre Dame, Dept Biol Sci, Eck Inst Global Hlth, Notre Dame, IN 46556 USA.
Univ Pretoria, Dept Vet Trop Dis, ZA-110 Onderstepoort, South Africa.
[Lawson, Daniel; Hughes, Daniel S. T.; Stanley, Eleanor J.] European Bioinformat Inst EMBL EBI, European Mol Biol Labs, Cambridge CB10 1SA, Cambs, England.
[Benkahla, Alia] Inst Pasteur Tunis, Lab Med Parasitol Biotechnol & Biomol, Grp Bioinformat & Modeling, Tunis 1002, Tunisia.
[Solano, Philippe; Koffi, Mathurin] CIRDES Bobo Dioulasso, UMR IRD CIRAD INTERTRYP 177, IRD, Bobo Dioulasso, Burkina Faso.
[Ravel, Sophie] LRCT Campus Int Baillarguet, UMR IRD CIRAD INTERTRYP 177, IRD, Montpellier, France.
[Larkin, Denis M.; Swain, Martin T.] Aberystwyth Univ, Inst Biol Environm & Rural Sci, Aberystwyth SY23 3FG, Ceredigion, Wales.
[Ommeh, Sheila] JKUAT, Biotechnol Res Inst, Nairobi, Kenya.
[Darby, Alistair C.; Gregory, Richard] Univ Liverpool, Inst Integrat Biol, Liverpool L69 7ZB, Merseyside, England.
[Michalkova, Veronika] Slovak Acad Sci, Inst Zool, Bratislava 84506, Slovakia.
[Sakate, Ryuichi; Imanishi, Tadashi; Kawahara, Yoshihiro] Natl Inst Adv Ind Sci & Technol, Biol Informat Res Ctr, Integrated Database Team, Koto Ku, Tokyo 1350064, Japan.
[Wamwiri, Florence; Murilla, Grace; Auma, Joanna E.; Ouma, Johnson] Kenya Agr Res Inst, Trypanosomiasis Res Ctr, Kikuyu 902, Kenya.
[Ribeiro, Jose M. C.] NIAID, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
[Stephens, Dawn; Makgamathe, Mmule] Technol Innovat Agcy, Natl Genom Platform, ZA-4058 Durban, South Africa.
[Balyeidhusa, Apollo S. P.] Makerere Univ, Dept Biochem & Sports Sci, Kampala, Uganda.
[Rawlings, Neil D.] EMBL European Bioinformat Inst, Wellcome Trust Sanger Inst, Bateman Grp, Cambridge CB10 1SA, Cambs, England.
[Obiero, George F. O.; Kibet, Caleb K.] Int Ctr Insect Physiol & Ecol, Mol Biol & Bioinformat Unit, Nairobi, Kenya.
[Okedi, Loyce; Abila, Patrick P.] Natl Livestock Resources Res Inst NaLIRRI, Tororo, Uganda.
[Inoue, Noboru] Obihiro Univ Agr & Vet Med, Natl Res Ctr Protozoan Dis, Obihiro, Hokkaido 0808555, Japan.
[Hertz-Fowler, Christiane; Cotton, James A.; Sanders, Mandy J.; Quail, Michael A.; Aslett, Martin] Wellcome Trust Sanger Inst, Parasite Genom Grp, Cambridge CB10 1SA, Cambs, England.
[Baumann, Aaron A.] Howard Hughes Med Inst, Riddiford Lab, Ashburn, VA 20147 USA.
[Srivastava, Tulika P.; Sharma, Vineet; Sharma, Vineet] RIKEN Ctr Integrat Med Sci, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan.
[Christoffels, Alan; Macharia, Rosaline W.; Dashti, Zahra Jalali Sefid; Wamalwa, Mark; Mwangi, Sarah; Panji, Sumir; Kruger, Adele; Mpondo, Feziwe; Harkins, Gordon] Univ Western Cape, South African MRC Bioinformat Unit, South African Natl Bioinformat Inst, ZA-7530 Bellville, South Africa.
[Toure, Yeya] WHO, Special Programme Res & Training Trop Dis TDR, CH-1211 Geneva 27, Switzerland.
[Warren, Wesley; Wilson, Richard K.] Washington Univ, Sch Med, Genome Inst, St Louis, MO 63110 USA.
[Msangi, Atway; Mramba, Furaha; Malele, Imna; Manangwa, Oliver] TTRI, Tanga, Tanzania.
[Ouma, Johnson] Vector Hlth Int, Arusha, Tanzania.
[Okoro, Chinyere K.] Wellcome Trust Sanger Inst, Cambridge CB10 1SA, Cambs, England.
[Manga, Lucien] WHO, WHO Reg Off Africa, Brazzaville, Congo.
[Srivastava, Tulika P.] Indian Inst Technol, Sch Basic Sci, Mandi 175001, Himachal Prades, India.
[Githinji, George] CGMRC, KEMRI Wellcome Trust Programme, Dept Parasite Vector & Human Biol, Kilifi, Kenya.
[Watanabe, Junichi] Univ Tokyo, Inst Med Sci, Minato Ku, Tokyo 1088639, Japan.
Kenyatta Univ, Dept Biochem & Biotechnol, Nairobi, Kenya.
[Sharma, Vineet; Sharma, Vineet] Indian Inst Sci Educ & Res, Dept Biol Sci, Bhopal 462066, Madhya Pradesh, India.
King Abdulaziz Univ, Fac Sci, Jeddah 21589, Saudi Arabia.
Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02461 USA.
[Kawahara, Yoshihiro] Natl Inst Agrobiol Sci, Agrogen Res Ctr, Bioinformat Res Unit, Tsukuba, Ibaraki 3058602, Japan.
RP Aksoy, S (reprint author), Yale Univ, Sch Publ Hlth, Dept Epidemiol Microbial Dis, 60 Coll St, New Haven, CT 06520 USA.
EM geoffrey.attardo@yale.edu; mb4@sanger.ac.uk; serap.aksoy@yale.edu
RI Rawlings, Neil/M-5566-2013; Darby, Alistair/I-6485-2012; Zhang,
Qirui/C-6579-2011; Cotton, James/B-8806-2008; Telleria,
Erich/F-1580-2015; Thomas, Gavin/E-5753-2011; Taylor, Todd/A-7121-2009;
Ribeiro, Jose/J-7011-2015; Acosta-Serrano, Alvaro/L-5503-2015; scolari,
francesca/L-9233-2015; Hattori, Masahira/C-6958-2016; Silva,
Thiago/L-7699-2016; Caljon, Guy/E-1310-2017; Faculty of, Sciences,
KAU/E-7305-2017;
OI solano, philippe/0000-0002-4351-3506; Macdonald,
Sandy/0000-0002-4112-0987; Lawson, Daniel/0000-0001-7765-983X; Rawlings,
Neil/0000-0001-5557-7665; Masiga, Daniel/0000-0001-7513-0887;
christoffels, alan/0000-0002-0420-2916; Baumann,
Aaron/0000-0002-7410-8482; Darby, Alistair/0000-0002-3786-6209; Zhang,
Qirui/0000-0002-2749-9740; Cotton, James/0000-0001-5475-3583; Thomas,
Gavin/0000-0002-9763-1313; Taylor, Todd/0000-0003-4247-6253;
Acosta-Serrano, Alvaro/0000-0002-2576-7959; scolari,
francesca/0000-0003-3085-9038; Hattori, Masahira/0000-0001-9467-0344;
Silva, Thiago/0000-0002-8520-5405; Caljon, Guy/0000-0002-4870-3202;
Hide, Winston/0000-0002-8621-3271; Tarone, Aaron/0000-0003-0965-7634;
Hall, Neil/0000-0003-2808-0009; Geiser, Dawn/0000-0002-6004-8407; Aksoy,
Serap/0000-0001-9941-143X; Ribeiro, Jose/0000-0002-9107-0818; Scott,
Maxwell/0000-0001-6536-4735
FU Wellcome Trust [085775/Z/08/Z, 098051]; World Health Organization (WHO)
Special Programme for Research and Training in Tropical Diseases (TDR)
[A90088]; Ambrose Monell Foundation; Food and Agriculture
Organization/International Atomic Energy Agency Coordinated Research
Program "Improving SIT for Tsetse Flies through Research on their
Symbionts"; European Union Cooperation in Science and Technology (COST)
Action [FA0701]; Ministry of Education, Culture, Sports, Science, and
Technology of Japan
FX The public release and future updates of the genome sequence and
associated information are hosted at VectorBase (www.vectorbase.org).
The genome sequence can also be found at GenBank under the accession no.
CCAG010000000. The Glossina morsitans genome project was funded by the
Wellcome Trust (grants 085775/Z/08/Z and 098051) and World Health
Organization (WHO) Special Programme for Research and Training in
Tropical Diseases (TDR) (project no. A90088) and the Ambrose Monell
Foundation. Authors also acknowledge support by the Food and Agriculture
Organization/International Atomic Energy Agency Coordinated Research
Program "Improving SIT for Tsetse Flies through Research on their
Symbionts," the European Union Cooperation in Science and Technology
(COST) Action FA0701 "Arthropod Symbiosis: From Fundamental Studies to
Pest and Disease Management," and a grant-in-aid for Scientific Research
on Priority Areas "Comprehensive Genomics" from the Ministry of
Education, Culture, Sports, Science, and Technology of Japan (to M. H.).
BAC libraries were generated through National Institute of Allergy and
Infectious Diseases resources, and sequencing was supported by RIKEN
Japan. We thank the staff in the library construction, sequence
production, and informatics support groups at the Wellcome Trust Sanger
Institute.
NR 38
TC 64
Z9 64
U1 9
U2 72
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD APR 25
PY 2014
VL 344
IS 6182
BP 380
EP 386
DI 10.1126/science.1249656
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF7BG
UT WOS:000334867800033
ER
PT J
AU Habicht, KL
Singh, NS
Khadeer, MA
Shimmo, R
Wainer, IW
Moaddel, R
AF Habicht, K-L.
Singh, N. S.
Khadeer, M. A.
Shimmo, R.
Wainer, I. W.
Moaddel, R.
TI Characterization of a multiple endogenously expressed adenosine
triphosphate-binding cassette transporters using nuclear and cellular
membrane affinity chromatography columns
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 20th International Symposium on Electro- and Liquid Phase-Separation
Techniques (ITP)
CY OCT 06-09, 2013
CL Puerto de la Cruz, SPAIN
DE Breast cancer resistant protein; Bioaffinity chromatography; Frontal
chromatography; Glioblastoma
ID STATIONARY-PHASE; PROTEINS; CELLS
AB Glioblastoma multiforme is an aggressive form of human astrocytoma, with poor prognosis due to multidrug resistance to a number of anticancer drugs. The observed multi-drug resistance is primarily due to the efflux activity of ATP-Binding Cassette (ABC) efflux transporters such as Pgp, MRP1 and BCRP. The expression of these transporters has been demonstrated in nuclear and cellular membranes of the LN-229 human glioblastoma cell line. Nuclear membrane and cellular membrane fragments from LN-229 cells were immobilized on the IAM stationary phase to create nuclear and cellular membrane affinity chromatography columns, (NMAC(LN-229)) and (CMAC(LN-229)), respectively. Pgp, MRP1 and BCRP transporters co-immobilized on both columns were characterized and compared by establishing the binding affinities for estrone-3-sulfate (3.8 vs. 3.7 mu M), verapamil (0.6 vs. 0.7 mu M) and prazosin (0.099 vs. 0.03311 mu M) on each column and no significant differences were observed. Since the marker ligands had overlapping selectivities, the selective characterization of each transporter was carried out by saturation of the binding sites of the non-targeted transporters. The addition of verapamil (Pgp and MRP1 substrate) to the mobile phase allowed the comparative screening of eight compounds at the nuclear and cellular BCRP using etoposide as the marker ligand. AZT increased the retention of etoposide (+15%), a positive allosteric interaction, on the CMAC(LN-229) column and decreased it (-5%) on the NMAC(LN-229), while the opposite effect was produced by rhodamine. The results indicate that there are differences between the cellular and nuclear membrane expressed BCRP and that NMAC and CMAC columns can be used to probe these differences. Published by Elsevier B.V.
C1 [Habicht, K-L.; Singh, N. S.; Khadeer, M. A.; Wainer, I. W.; Moaddel, R.] NIA, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
[Habicht, K-L.; Shimmo, R.] Tallinn Univ, Inst Math & Nat Sci, Dept Nat Sci, EE-10120 Tallinn, Estonia.
RP Moaddel, R (reprint author), NIA, Bioanalyt & Drug Discovery Unit, Clin Invest Lab, NIH, Suite 100,8B131 Biomed Res Ctr,251 Bayview Boul, Baltimore, MD 21224 USA.
EM moaddelru@grc.nia.nih.gov
RI Singh, Nagendra/K-8966-2015
FU Intramural NIH HHS [Z99 AG999999]
NR 15
TC 6
Z9 6
U1 4
U2 22
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
EI 1873-3778
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD APR 25
PY 2014
VL 1339
BP 80
EP 85
DI 10.1016/j.chroma.2014.02.076
PG 6
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA AG1UG
UT WOS:000335201100010
PM 24642394
ER
PT J
AU Szu, SC
Klugman, KP
Hunt, S
AF Szu, Shousun C.
Klugman, Keith P.
Hunt, Steven
TI Re-examination of immune response and estimation of anti-Vi IgG
protective threshold against typhoid fever-based on the efficacy trial
of Vi conjugate in young children
SO VACCINE
LA English
DT Article
DE Vi antibody protective threshold against typhoid fever Vi conjugate
efficacy trial
ID CAPSULAR POLYSACCHARIDE VACCINE; SALMONELLA-TYPHI; IMMUNIZATION;
IMMUNOGENICITY; PERSISTENCE; ANTIBODIES
AB Background: The capsular polysaccharide of Salmonella enterica serovar Typhi, Vi antigen, is an essential virulence factor and a protective antigen. Similar to other polysaccharide vaccines, the protective action of Vi, both to the polysaccharide alone or when presented as a conjugate, is mediated by serum IgG Vi antibodies. The evaluation of Vi capsular polysaccharide based vaccines to prevent typhoid fever would be significantly facilitated by the identification of a "protective level" of serum antibodies to Vi antigen.
Methods: The protective level of anti-Vi IgG against typhoid fever was derived from the protective efficacy and immune response of a Vi-rEPA conjugate vaccine efficacy trial. The estimation was derived by two methods: correlation of the percent efficacy and the antibody distribution profile in the vaccine group at a given period of observation, and use of the relative ratio of anti-Vi IgG levels between the vaccine and placebo groups greater or equal to the Relative Risk of typhoid fever used in the efficacy determination.
Results: Both methods predicted a similar range of a minimum protective level of anti-Vi IgG between 1.4 and 2.0 mu g/ml (short term threshold). When applying a protective threshold of 10 mu g/ml at 6 months post immunization, an IgG level in excess of 1.4 mu g/ml was achieved by 90% of children at 46 months post immunization, consistent with an 89% level of protection over the duration of the study. We thus suggest that the proportion of children with Vi IgG > 10 mu g/ml (long term threshold) 6 months after immunization may reflect the proportion protected over at least a 4 year period.
Conclusion: The current assignment of an anti-Vi IgG protective level may be of value when evaluating vaccine performance of future Vi conjugate vaccines. Published by Elsevier Ltd.
C1 [Szu, Shousun C.; Hunt, Steven] NICHHD, NIH, Bethesda, MD 20892 USA.
[Klugman, Keith P.] Emory Univ, Rollins Sch Publ Hlth, Dept Global Hlth, Atlanta, GA 30322 USA.
RP Szu, SC (reprint author), NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM szus@mail.nih.gov
OI Hunt, Steven/0000-0003-3533-0627
FU Intramural Research Program; Eunice Kennedy Shriver National Institute
of Child Health and Human Development; National Institutes of Health;
Bill and Melinda Gates Foundation
FX This work was supported by the Intramural Research Program, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health and a grant from the Bill and
Melinda Gates Foundation. The findings and conclusions contained within
are those of the authors and do not necessarily reflect positions or
policies of the National Institutes of Health or the Bill and Melinda
Gates Foundation.
NR 25
TC 5
Z9 5
U1 0
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD APR 25
PY 2014
VL 32
IS 20
BP 2359
EP 2363
DI 10.1016/j.vaccine.2014.02.050
PG 5
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA AG0JA
UT WOS:000335100600015
PM 24630869
ER
PT J
AU Tao-Cheng, JH
Thein, S
Yang, Y
Reese, TS
Gallant, PE
AF Tao-Cheng, J. -H.
Thein, S.
Yang, Y.
Reese, T. S.
Gallant, P. E.
TI HOMER IS CONCENTRATED AT THE POSTSYNAPTIC DENSITY AND DOES NOT
REDISTRIBUTE AFTER ACUTE SYNAPTIC STIMULATION
SO NEUROSCIENCE
LA English
DT Article
DE synapse; shanks; CaMKII; electron microscopy; PSD; mGluR.
ID METABOTROPIC GLUTAMATE RECEPTORS; CEREBELLAR GRANULE CELLS;
HIPPOCAMPAL-NEURONS; SUBTHALAMIC NUCLEUS; FAMILY PROTEINS; MOUSE-BRAIN;
SYNAPSES; LOCALIZATION; MECHANISMS; EXPRESSION
AB Homer is a postsynaptic density (PSD) scaffold protein that is involved in synaptic plasticity, calcium signaling and neurological disorders. Here, we use pre-embedding immunogold electron microscopy to illustrate the differential localization of three Homer gene products (Homer 1, 2, and 3) in different regions of the mouse brain. In cross-sectioned PSDs, Homer occupies a layer similar to 30-100 nm from the postsynaptic membrane lying just beyond the dense material that defines the PSD core (similar to 30-nm-thick). Homer is evenly distributed within the PSD area along the lateral axis, but not at the peri-PSD locations within 60 nm from the edge of the PSD, where type I-metabotropic glutamate receptors (mGluR1 and 5) are concentrated. This distribution of Homer matches that of Shank, another major PSD scaffold protein, but differs from those of other two major binding partners of Homer, type I mGluR and IP3 receptors. Many PSD proteins rapidly redistribute upon acute (2 min) stimulation. To determine whether Homer distribution is affected by acute stimulation, we examined its distribution in dissociated hippocampal cultures under different conditions. Both the pattern and density of label for Homer 1, the isoform that is ubiquitous in hippocampus, remained unchanged under high K+ depolarization (90 mM for 2-5 min), N-methyl-D-asparic acid (NMDA) treatment (50 mu M for 2 min), and calcium-free conditions (EGTA at 1 mM for 2 min). In contrast, Shank and calcium/calmodulin-dependent kinase II (CaMKII) accumulate at the PSD upon NMDA treatment, and CaMKII is excluded from the PSD complex under low calcium conditions. (C) 2014 Published by Elsevier Ltd. on behalf of IBRO.
C1 [Tao-Cheng, J. -H.] NINDS, EM Facil, NIH, Bethesda, MD 20892 USA.
[Thein, S.; Yang, Y.; Reese, T. S.; Gallant, P. E.] NINDS, Neurobiol Lab, NIH, Bethesda, MD 20892 USA.
RP Tao-Cheng, JH (reprint author), 49 Convent Dr,Room 3A50, Bethesda, MD 20892 USA.
EM chengs@ninds.nih.gov
FU NIH, NINDS
FX We thank Christine A. Winters for hippocampal neuronal cultures,
Virginia Crocker and Rita Azzam for expert EM technical support, Dr.
Ayse Dosemeci for helpful discussions and critical reading of the
manuscript. Supported by the Intramural Research Program of the NIH,
NINDS.
NR 42
TC 6
Z9 6
U1 0
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
EI 1873-7544
J9 NEUROSCIENCE
JI Neuroscience
PD APR 25
PY 2014
VL 266
BP 80
EP 90
DI 10.1016/j.neuroscience.2014.01.066
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA AE8VO
UT WOS:000334281200008
PM 24530450
ER
PT J
AU Sadat, MA
Moir, S
Chun, TW
Lusso, P
Kaplan, G
Wolfe, L
Memoli, MJ
He, M
Vega, H
Kim, LJY
Huang, Y
Hussein, N
Nievas, E
Mitchell, R
Garofalo, M
Louie, A
Ireland, DC
Grunes, C
Cimbro, R
Patel, V
Holzapfel, G
Salahuddin, D
Bristol, T
Adams, D
Marciano, BE
Hegde, M
Li, YX
Calvo, KR
Stoddard, J
Justement, JS
Jacques, J
Priel, DAL
Murray, D
Sun, P
Kuhns, DB
Boerkoel, CF
Chiorini, JA
Di Pasquale, G
Verthelyi, D
Rosenzweig, SD
AF Sadat, Mohammed A.
Moir, Susan
Chun, Tae-Wook
Lusso, Paolo
Kaplan, Gerardo
Wolfe, Lynne
Memoli, Matthew J.
He, Miao
Vega, Hugo
Kim, Leo J. Y.
Huang, Yan
Hussein, Nadia
Nievas, Elma
Mitchell, Raquel
Garofalo, Mary
Louie, Aaron
Ireland, Derek C.
Grunes, Claire
Cimbro, Raffaello
Patel, Vyomesh
Holzapfel, Genevieve
Salahuddin, Daniel
Bristol, Tyler
Adams, David
Marciano, Beatriz E.
Hegde, Madhuri
Li, Yuxing
Calvo, Katherine R.
Stoddard, Jennifer
Justement, J. Shawn
Jacques, Jerome
Priel, Debra A. Long
Murray, Danielle
Sun, Peter
Kuhns, Douglas B.
Boerkoel, Cornelius F.
Chiorini, John A.
Di Pasquale, Giovanni
Verthelyi, Daniela
Rosenzweig, Sergio D.
TI Glycosylation, Hypogammaglobulinemia, and Resistance to Viral Infections
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID ANTIRETROVIRAL THERAPY; OTITIS-MEDIA; HIV; BIOSYNTHESIS; RESERVOIR;
CHILDREN; EFFICACY; ENTRY; CD4
AB Genetic defects in MOGS, the gene encoding mannosyl-oligosaccharide glucosidase (the first enzyme in the processing pathway of N-linked oligosaccharide), cause the rare congenital disorder of glycosylation type IIb (CDG-IIb), also known as MOGS-CDG. MOGS is expressed in the endoplasmic reticulum and is involved in the trimming of N-glycans. We evaluated two siblings with CDG-IIb who presented with multiple neurologic complications and a paradoxical immunologic phenotype characterized by severe hypogammaglobulinemia but limited clinical evidence of an infectious diathesis. A shortened immunoglobulin half-life was determined to be the mechanism underlying the hypogammaglobulinemia. Impaired viral replication and cellular entry may explain a decreased susceptibility to infections.
C1 [Sadat, Mohammed A.; Hussein, Nadia; Nievas, Elma; Mitchell, Raquel; Garofalo, Mary; Rosenzweig, Sergio D.] NIAID, Infect Dis Susceptibil Unit, Lab Host Def, NIH, Bethesda, MD 20892 USA.
[Moir, Susan; Chun, Tae-Wook; Lusso, Paolo; Kim, Leo J. Y.; Louie, Aaron; Cimbro, Raffaello; Justement, J. Shawn; Murray, Danielle] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Memoli, Matthew J.; Bristol, Tyler] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Marciano, Beatriz E.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Holzapfel, Genevieve; Salahuddin, Daniel; Sun, Peter] NIAID, Lab Immunogenet, NIH, Bethesda, MD 20892 USA.
[Rosenzweig, Sergio D.] NIAID, Primary Immunodeficiency Clin, NIH, Bethesda, MD 20892 USA.
[Wolfe, Lynne; Vega, Hugo; Huang, Yan; Adams, David; Boerkoel, Cornelius F.] Natl Human Res Genome Inst, Undiagnosed Dis Program, NIH, Bethesda, MD USA.
[Calvo, Katherine R.; Stoddard, Jennifer] Natl Inst Dent & Craniofacial Res, Dept Lab Med, Clin Ctr, NIH, Bethesda, MD USA.
[Patel, Vyomesh] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
[Chiorini, John A.; Di Pasquale, Giovanni] Natl Inst Dent & Craniofacial Res, Adeno Associated Virus Biol Sect, NIH, Bethesda, MD USA.
[Kaplan, Gerardo; Jacques, Jerome] Ctr Biol Evaluat & Res, Silver Spring, MD USA.
[Ireland, Derek C.; Grunes, Claire; Verthelyi, Daniela] Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Priel, Debra A. Long; Kuhns, Douglas B.] US FDA, Clin Serv Program, Silver Spring, MD USA.
[Priel, Debra A. Long; Kuhns, Douglas B.] Frederick Natl Lab Canc Res, SAIC Frederick, Frederick, MD USA.
[He, Miao; Hegde, Madhuri] Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA USA.
[Li, Yuxing] Ctr Neutralizing Antibodies TSRI, IAVI Int AIDS Vaccine Initiat, La Jolla, CA USA.
[Li, Yuxing] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA USA.
RP Rosenzweig, SD (reprint author), CC, Serv Immunol, DLM, 10 Ctr Dr,Bldg 10 2C410F, Bethesda, MD 20892 USA.
EM srosenzweig@cc.nih.gov
OI Calvo, Katherine/0000-0002-0771-4191; Cimbro,
Raffaello/0000-0002-6251-5160
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute [HHSN261200800001E]
FX Supported by the Intramural Research Program of the National Institutes
of Health and by a grant from the National Cancer Institute
(HHSN261200800001E).
NR 22
TC 21
Z9 21
U1 1
U2 7
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 24
PY 2014
VL 370
IS 17
BP 1615
EP 1625
DI 10.1056/NEJMoa1302846
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA AH4TG
UT WOS:000336120500008
PM 24716661
ER
PT J
AU Brzezniak, C
Szabo, E
AF Brzezniak, Christina
Szabo, Eva
TI Sunitinib-Associated Hair Depigmentation
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Brzezniak, Christina] Walter Reed Natl Mil Med Ctr, Bethesda, MD 20889 USA.
[Szabo, Eva] NIH, Bethesda, MD 20892 USA.
RP Brzezniak, C (reprint author), Walter Reed Natl Mil Med Ctr, Bethesda, MD 20889 USA.
EM christina.e.brzezniak.mil@health.mil
NR 0
TC 4
Z9 4
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 24
PY 2014
VL 370
IS 17
BP E27
EP E27
DI 10.1056/NEJMicm1309906
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA AH4TG
UT WOS:000336120500001
PM 24758639
ER
PT J
AU Schnitzler, CE
Simmons, DK
Pang, K
Martindale, MQ
Baxevanis, AD
AF Schnitzler, Christine E.
Simmons, David K.
Pang, Kevin
Martindale, Mark Q.
Baxevanis, Andreas D.
TI Expression of multiple Sox genes through embryonic development in the
ctenophore Mnemiopsis leidyi is spatially restricted to zones of cell
proliferation
SO EVODEVO
LA English
DT Article
DE Sox; Ctenophore; Lobate; Mnemiopsis leidyi; Cell proliferation; Stem
cell
ID MIXED MODELS; STEM-CELLS; FAMILY; MECHANISMS; EVOLUTION; METAZOAN;
PROTEINS; MCCRADYI; SPECIFICATION; REGULATORS
AB Background: The Sox genes, a family of transcription factors characterized by the presence of a high mobility group (HMG) box domain, are among the central groups of developmental regulators in the animal kingdom. They are indispensable in progenitor cell fate determination, and various Sox family members are involved in managing the critical balance between stem cells and differentiating cells. There are 20 mammalian Sox genes that are divided into five major groups (B, C, D, E, and F). True Sox genes have been identified in all animal lineages but not outside Metazoa, indicating that this gene family arose at the origin of the animals. Whole-genome sequencing of the lobate ctenophore Mnemiopsis leidyi allowed us to examine the full complement and expression of the Sox gene family in this early-branching animal lineage.
Results: Our phylogenetic analyses of the Sox gene family were generally in agreement with previous studies and placed five of the six Mnemiopsis Sox genes into one of the major Sox groups: SoxB (MleSox1), SoxC (MleSox2), SoxE (MleSox3, MleSox4), and SoxF (MleSox5), with one unclassified gene (MleSox6). We investigated the expression of five out of six Mnemiopsis Sox genes during early development. Expression patterns determined through in situ hybridization generally revealed spatially restricted Sox expression patterns in somatic cells within zones of cell proliferation, as determined by EdU staining. These zones were located in the apical sense organ, upper tentacle bulbs, and developing comb rows in Mnemiopsis, and coincide with similar zones identified in the cydippid ctenophore Pleurobrachia.
Conclusions: Our results are consistent with the established role of multiple Sox genes in the maintenance of stem cell pools. Both similarities and differences in juvenile cydippid stage expression patterns between Mnemiopsis Sox genes and their orthologs from Pleurobrachia highlight the importance of using multiple species to characterize the evolution of development within a given phylum. In light of recent phylogenetic evidence that Ctenophora is the earliest-branching animal lineage, our results are consistent with the hypothesis that the ancient primary function of Sox family genes was to regulate the maintenance of stem cells and function in cell fate determination.
C1 [Schnitzler, Christine E.; Baxevanis, Andreas D.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
[Simmons, David K.; Martindale, Mark Q.] Univ Florida, Whitney Lab Marine Biosci, St Augustine, FL USA.
[Pang, Kevin] Univ Bergen, Sars Int Ctr Marine Mol Biol, Bergen, Norway.
RP Baxevanis, AD (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
EM andy@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health; NSF; NASA
FX This work was supported in part by the Intramural Research Program of
the National Human Genome Research Institute, National Institutes of
Health. This work was also supported by grants from NSF and NASA to MQM.
The authors would like to thank Joe Ryan and Adam Reitzel for their
helpful comments on the manuscript. We also thank two anonymous
reviewers for their comments, which improved the manuscript.
NR 56
TC 14
Z9 14
U1 0
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2041-9139
J9 EVODEVO
JI EvoDevo
PD APR 24
PY 2014
VL 5
AR 15
DI 10.1186/2041-9139-5-15
PG 17
WC Evolutionary Biology; Developmental Biology
SC Evolutionary Biology; Developmental Biology
GA AG6MF
UT WOS:000335532000001
PM 24834317
ER
PT J
AU Turtzo, LC
Lescher, J
Janes, L
Dean, DD
Budde, MD
Frank, JA
AF Turtzo, L. Christine
Lescher, Jacob
Janes, Lindsay
Dean, Dana D.
Budde, Matthew D.
Frank, Joseph A.
TI Macrophagic and microglial responses after focal traumatic brain injury
in the female rat
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
DE Controlled cortical impact; Inflammation; Macrophage; Microglia; MRI;
Rat; Traumatic brain injury
ID TUMOR-ASSOCIATED MACROPHAGES; SPINAL-CORD-INJURY; CYTOKINE EXPRESSION;
NERVOUS-SYSTEM; ESTROUS-CYCLE; PROGESTERONE; ACTIVATION; RECOVERY;
NEUROINFLAMMATION; POLARIZATION
AB Background: After central nervous system injury, inflammatory macrophages (M1) predominate over anti-inflammatory macrophages (M2). The temporal profile of M1/M2 phenotypes in macrophages and microglia after traumatic brain injury (TBI) in rats is unknown. We subjected female rats to severe controlled cortical impact (CCI) and examined the postinjury M1/M2 time course in their brains.
Methods: The motor cortex (2.5 mm left laterally and 1.0 mm anteriorly from the bregma) of anesthetized female Wistar rats (ages 8 to 10 weeks; N = 72) underwent histologically moderate to severe CCI with a 5-mm impactor tip. Separate cohorts of rats had their brains dissociated into cells for flow cytometry, perfusion-fixed for immunohistochemistry (IHC) and ex vivo magnetic resonance imaging or flash-frozen for RNA and protein analysis. For each analytical method used, separate postinjury times were included for 24 hours; 3 or 5 days; or 1, 2, 4 or 8 weeks.
Results: By IHC, we found that the macrophagic and microglial responses peaked at 5 to 7 days post-TBI with characteristics of mixed populations of M1 and M2 phenotypes. Upon flow cytometry examination of immunological cells isolated from brain tissue, we observed that peak M2-associated staining occurred at 5 days post-TBI. Chemokine analysis by multiplex assay showed statistically significant increases in macrophage inflammatory protein 1 alpha and keratinocyte chemoattractant/growth-related oncogene on the ipsilateral side within the first 24 hours after injury relative to controls and to the contralateral side. Quantitative RT-PCR analysis demonstrated expression of both M1- and M2-associated markers, which peaked at 5 days post-TBI.
Conclusions: The responses of macrophagic and microglial cells to histologically severe CCI in the female rat are maximal between days 3 and 7 postinjury. The response to injury is a mixture of M1 and M2 phenotypes.
C1 [Turtzo, L. Christine; Lescher, Jacob; Janes, Lindsay; Frank, Joseph A.] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
[Turtzo, L. Christine; Lescher, Jacob; Janes, Lindsay; Dean, Dana D.; Budde, Matthew D.; Frank, Joseph A.] NIH, Frank Lab, Bethesda, MD 20814 USA.
[Frank, Joseph A.] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20814 USA.
[Dean, Dana D.] Baylor Univ, Dept Environm Sci, Waco, TX 76798 USA.
[Budde, Matthew D.] Med Coll Wisconsin, Dept Neurosurg, Milwaukee, WI 53226 USA.
RP Turtzo, LC (reprint author), Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM turtzolc@mail.nih.gov
FU US Department of Defense Center for Neuroscience and Regenerative
Medicine under Henry M. Jackson Foundation for the Advancement of
Military Medicine award [300604-13.01-60855]; National Institutes of
Health Intramural Research Program
FX These studies were supported by the US Department of Defense Center for
Neuroscience and Regenerative Medicine under Henry M. Jackson Foundation
for the Advancement of Military Medicine award 300604-13.01-60855 and by
the National Institutes of Health Intramural Research Program. We would
also like to thank Aneeka Chaudhry, Tiziana Coppola and Eric Gold for
their invaluable technical assistance with these studies.
NR 57
TC 36
Z9 36
U1 2
U2 16
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD APR 24
PY 2014
VL 11
AR 82
DI 10.1186/1742-2094-11-82
PG 14
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA AG6IW
UT WOS:000335523300001
PM 24761998
ER
PT J
AU Rogatsky, I
Adelman, K
AF Rogatsky, Inez
Adelman, Karen
TI Preparing the First Responders: Building the Inflammatory Transcriptome
from the Ground Up
SO MOLECULAR CELL
LA English
DT Review
ID RNA-POLYMERASE-II; NF-KAPPA-B; BROMODOMAIN PROTEIN BRD4; P-TEFB;
GENE-EXPRESSION; PROINFLAMMATORY GENES; ELONGATION-FACTORS; BINDING
MOTIFS; CPG ISLANDS; IN-VITRO
AB In cells of the immune system, inflammatory stimuli trigger highly coordinated cascades of gene activation that are precisely calibrated to the nature and strength of the stimulus. Herein, we describe the forces that control inflammatory gene transcription and highlight that many critical determinants of responsiveness are established prior to challenge. We discuss key steps in the transcription cycle that are regulated during gene activation and the importance of the underlying enhancer landscape. Further, we illustrate how the diversity in regulatory strategies employed at inflammatory genes provides novel opportunities for therapeutic intervention.
C1 [Rogatsky, Inez] Hosp Special Surg, Div Res, New York, NY 10021 USA.
[Rogatsky, Inez] David Rosensweig Genom Ctr, New York, NY 10021 USA.
[Rogatsky, Inez] Weill Cornell Grad Sch Med Sci, Grad Program Immunol & Microbial Pathogenesis, New York, NY 10021 USA.
[Adelman, Karen] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Adelman, K (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
EM adelmank@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences [Z01 ES101987]; NIH NIAID; HSS David
Rosensweig Genomics Center
FX We thank L. Ivashkiv (HSS), C. Glass (UCSD), and S. Smale (UCLA) for
comments on the manuscript and Y. Chinenov (HSS) for help with figures.
This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences to K.A. (Z01
ES101987), and grants from the NIH NIAID and the HSS David Rosensweig
Genomics Center to I.R.
NR 83
TC 11
Z9 12
U1 0
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
EI 1097-4164
J9 MOL CELL
JI Mol. Cell
PD APR 24
PY 2014
VL 54
IS 2
BP 245
EP 254
DI 10.1016/j.molcel.2014.03.038
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AF8TA
UT WOS:000334987300008
PM 24766888
ER
PT J
AU Costi, R
Metifiot, M
Chung, S
Crucitti, GC
Maddali, K
Pescatori, L
Messore, A
Madia, VN
Pupo, G
Scipione, L
Tortorella, S
Di Leva, FS
Cosconati, S
Marinelli, L
Novellino, E
Le Grice, SFJ
Corona, A
Pommier, Y
Marchand, C
Di Santo, R
AF Costi, Roberta
Metifiot, Mathieu
Chung, Suhman
Crucitti, Giuliana Cuzzucoli
Maddali, Kasthuraiah
Pescatori, Luca
Messore, Antonella
Madia, Valentina Noemi
Pupo, Giovanni
Scipione, Luigi
Tortorella, Silvano
Di Leva, Francesco Saverio
Cosconati, Sandro
Marinelli, Luciana
Novellino, Ettore
Le Grice, Stuart F. J.
Corona, Angela
Pommier, Yves
Marchand, Christophe
Di Santo, Roberto
TI Basic Quinolinonyl Diketo Acid Derivatives as Inhibitors of HIV
Integrase and their Activity against RNase H Function of Reverse
Transcriptase
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID VIRUS TYPE-1 INTEGRASE; DUAL INHIBITORS; RIBONUCLEASE-H;
CRYSTAL-STRUCTURES; CATALYTIC DOMAIN; STRUCTURAL BASIS;
BIOLOGICAL-ACTIVITIES; STRAND TRANSFER; RNA/DNA HYBRID; BINDING-SITE
AB A series of antiviral basic quinolinonyl diketo acid derivatives were developed as inhibitors of HIV-1 IN. Compounds 12d,f,i inhibited HIV-1 IN with IC50 values below 100 nM for strand transfer and showed a 2 order of magnitude selectivity over 3'-processing. These strand transfer selective inhibitors also inhibited HIV-1 RNase H with low micromolar potencies. Molecular modeling studies based on both the HIV-1 IN and RNase H catalytic core domains provided new structural insights for the future development of these compounds as dual HIV-1 IN and RNase H inhibitors.
C1 [Costi, Roberta; Crucitti, Giuliana Cuzzucoli; Pescatori, Luca; Messore, Antonella; Madia, Valentina Noemi; Pupo, Giovanni; Scipione, Luigi; Tortorella, Silvano; Di Santo, Roberto] Univ Roma La Sapienza, Dipartimento Chim & Tecnol Farmaco, Ist Pasteur Fdn Cenci Bolognetti, I-00185 Rome, Italy.
[Metifiot, Mathieu; Maddali, Kasthuraiah; Pommier, Yves; Marchand, Christophe] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Chung, Suhman; Le Grice, Stuart F. J.] NCI, RT Biochem Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Di Leva, Francesco Saverio; Marinelli, Luciana; Novellino, Ettore] Univ Naples Federico II, Dipartimento Farm, I-80131 Naples, Italy.
[Cosconati, Sandro] Univ Naples 2, DiSTABiF, I-81100 Caserta, Italy.
[Corona, Angela] Univ Cagliari, Dept Life & Environm Sci, I-09124 Cagliari, Italy.
RP Costi, R (reprint author), Univ Roma La Sapienza, Dipartimento Chim & Tecnol Farmaco, Ist Pasteur Fdn Cenci Bolognetti, Ple Aldo Moro 5, I-00185 Rome, Italy.
EM roberta.costi@uniroma1.it; marchand@nih.gov
RI Corona, Angela/G-7327-2014; Pescatori, Luca/H-5917-2016;
OI Corona, Angela/0000-0002-6630-8636; Pescatori, Luca/0000-0003-4734-7856;
TORTORELLA, Silvano/0000-0002-3279-9182; COSTI,
Roberta/0000-0002-1314-9029; Marinelli, Luciana/0000-0002-4084-8044; Di
Santo, Roberto/0000-0002-4279-7666; Cosconati,
Sandro/0000-0002-8900-0968; scipione, luigi/0000-0002-2006-7005; Madia,
Valentina Noemi/0000-0002-5724-612X
FU Italian MIUR [ISS 40H4, PAIN (2010W2KM5L_002)]; FP7 CHAARM project; NIH
Intramural Research Program, Center for Cancer Research, National Cancer
Institute; NIH grants from the AIDS Intramural Targeted Program (IATAP)
FX We thank the Italian MIUR for financial support, ISS 40H4, PAIN
2010-2011 (2010W2KM5L_002). R. Di Santo and R. Costi thank the FP7
CHAARM project for support. This work was also supported by the NIH
Intramural Research Program, Center for Cancer Research, National Cancer
Institute, and by NIH grants from the AIDS Intramural Targeted Program
(IATAP).
NR 79
TC 14
Z9 15
U1 0
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD APR 24
PY 2014
VL 57
IS 8
BP 3223
EP 3234
DI 10.1021/jm5001503
PG 12
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA AG0OD
UT WOS:000335113900005
PM 24684270
ER
PT J
AU Xiao, JB
Free, RB
Barnaeva, E
Conroy, JL
Doyle, T
Miller, B
Bryant-Genevier, M
Taylor, MK
Hu, X
Dulcey, AE
Southall, N
Ferrer, M
Titus, S
Zheng, W
Sibley, DR
Marugan, JJ
AF Xiao, Jingbo
Free, R. Benjamin
Barnaeva, Elena
Conroy, Jennie L.
Doyle, Trevor
Miller, Brittney
Bryant-Genevier, Marthe
Taylor, Mercedes K.
Hu, Xin
Dulcey, Andres E.
Southall, Noel
Ferrer, Marc
Titus, Steve
Zheng, Wei
Sibley, David R.
Marugan, Juan J.
TI Discovery, Optimization, and Characterization of Novel D-2 Dopamine
Receptor Selective Antagonists
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID INDUCED WEIGHT-GAIN; D3 RECEPTOR; HIGH-AFFINITY; BINDING; SCHIZOPHRENIA;
PHARMACOLOGY; ANALOGS; BIOLOGY; POTENT
AB The D2 dopamine receptor (D2 DAR) is one of the most validated drug targets for neuropsychiatric and endocrine disorders. However, clinically approved drugs targeting 02 DAR display poor selectivity between the D2 and other receptors, especially the D3 DAR This lack of selectivity may lead to undesirable side effects. Here we describe the chemical and pharmacological characterization of a novel 02 DAR antagonist series with excellent D2 versus D1, D3, D4, and D5 receptor selectivity. The final probe 65 was obtained through a quantitative high-throughput screening campaign, followed by medicinal chemistry optimization, to yield a selective molecule with good in vitro physical properties, metabolic stability, and in vivo pharmacokinetics. The optimized molecule may be a useful in vivo probe for studying D2 DAR signal modulation and could also serve as a lead compound for the development of D2 DAR-selective druglike molecules for the treatment of multiple neuropsychiatric and endocrine disorders.
C1 [Xiao, Jingbo; Barnaeva, Elena; Bryant-Genevier, Marthe; Taylor, Mercedes K.; Hu, Xin; Dulcey, Andres E.; Southall, Noel; Ferrer, Marc; Titus, Steve; Zheng, Wei; Marugan, Juan J.] NIH, Chem Genom Ctr, Natl Ctr Adv Translat Sci, Rockville, MD 20850 USA.
[Free, R. Benjamin; Conroy, Jennie L.; Doyle, Trevor; Miller, Brittney; Sibley, David R.] NINDS, Mol Neuropharmacol Sect, NIH, Bethesda, MD 20892 USA.
RP Marugan, JJ (reprint author), NIH, Chem Genom Ctr, Natl Ctr Adv Translat Sci, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
EM maruganj@mail.nih.gov
RI Southall, Noel/H-8991-2012; Zheng, Wei/J-8889-2014
OI Southall, Noel/0000-0003-4500-880X; Zheng, Wei/0000-0003-1034-0757
FU Molecular Libraries Initiative of the NIH Roadmap for Medical Research
[U54MH084681, R21NS064831]; Intramural Research Program of the National
Center for Advancing Translational Sciences; National Institute of
Neurological Disorders and Stroke, National Institutes of Health
FX We thank Paul Shinn, Danielle van Leer, William Leister, Chris LeClair,
and Heather Baker for assistance with compound purification, HRMS
analysis, and compound management. We also thank Drs. Arnold L.
Rheingold and Curtis Moore at the University of California, San Diego
for the X-ray analysis of compounds (R)-59 and 65. This research was
supported by the Molecular Libraries Initiative of the NIH Roadmap for
Medical Research (Grants U54MH084681 and R21NS064831 to D.R.S.) and the
Intramural Research Program of the National Center for Advancing
Translational Sciences and National Institute of Neurological Disorders
and Stroke, National Institutes of Health.
NR 29
TC 6
Z9 6
U1 1
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD APR 24
PY 2014
VL 57
IS 8
BP 3450
EP 3463
DI 10.1021/jm500126s
PG 14
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA AG0OD
UT WOS:000335113900021
PM 24666157
ER
PT J
AU MacArthur, DG
Manolio, TA
Dimmock, DP
Rehm, HL
Shendure, J
Abecasis, GR
Adams, DR
Altman, RB
Antonarakis, SE
Ashley, EA
Barrett, JC
Biesecker, LG
Conrad, DF
Cooper, GM
Cox, NJ
Daly, MJ
Gerstein, MB
Goldstein, DB
Hirschhorn, JN
Leal, SM
Pennacchio, LA
Stamatoyannopoulos, JA
Sunyaev, SR
Valle, D
Voight, BF
Winckler, W
Gunter, C
AF MacArthur, D. G.
Manolio, T. A.
Dimmock, D. P.
Rehm, H. L.
Shendure, J.
Abecasis, G. R.
Adams, D. R.
Altman, R. B.
Antonarakis, S. E.
Ashley, E. A.
Barrett, J. C.
Biesecker, L. G.
Conrad, D. F.
Cooper, G. M.
Cox, N. J.
Daly, M. J.
Gerstein, M. B.
Goldstein, D. B.
Hirschhorn, J. N.
Leal, S. M.
Pennacchio, L. A.
Stamatoyannopoulos, J. A.
Sunyaev, S. R.
Valle, D.
Voight, B. F.
Winckler, W.
Gunter, C.
TI Guidelines for investigating causality of sequence variants in human
disease
SO NATURE
LA English
DT Article
ID DE-NOVO MUTATIONS; AUTISM SPECTRUM DISORDERS; PROTEIN-CODING GENES;
HUMAN GENOME; INTELLECTUAL DISABILITY; COMPLEX TRAITS; RARE VARIANTS;
ASSOCIATION; POPULATION; PHENOTYPE
AB The discovery of rare genetic variants is accelerating, and clear guidelines for distinguishing disease-causing sequence variants from the many potentially functional variants present in any human genome are urgently needed. Without rigorous standards we risk an acceleration of false-positive reports of causality, which would impede the translation of genomic research findings into the clinical diagnostic setting and hinder biological understanding of disease. Here we discuss the key challenges of assessing sequence variants in human disease, integrating both gene-level and variant-level support for causality. We propose guidelines for summarizing confidence in variant pathogenicity and highlight several areas that require further resource development.
C1 [MacArthur, D. G.; Daly, M. J.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[MacArthur, D. G.; Daly, M. J.; Hirschhorn, J. N.; Winckler, W.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[Manolio, T. A.] NHGRI, Div Genom Med, Bethesda, MD 20892 USA.
[Dimmock, D. P.] Med Coll Wisconsin, Dept Pediat, Div Genet, Milwaukee, WI 53226 USA.
[Rehm, H. L.] Partners Healthcare Ctr Personalized Genet Med, Mol Med Lab, Cambridge, MA 02139 USA.
[Rehm, H. L.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Shendure, J.] Univ Washington, Dept Genome Sci, Seattle, WA 98115 USA.
[Abecasis, G. R.] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Adams, D. R.] NIH, NIH Undiagnosed Dis Program, Off Rare Dis Res, Bethesda, MD 20892 USA.
[Adams, D. R.] NHGRI, Bethesda, MD 20892 USA.
[Adams, D. R.] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Altman, R. B.] Stanford Univ, Dept Bioengn, Stanford, CA 94305 USA.
[Altman, R. B.] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
[Antonarakis, S. E.] Univ Geneva, Sch Med, Dept Med Genet, CH-1211 Geneva, Switzerland.
[Antonarakis, S. E.] iGE3 Inst Genet & Genom Geneva, CH-1211 Geneva, Switzerland.
[Ashley, E. A.] Stanford Univ, Sch Med, Ctr Inherited Cardiovasc Dis, Stanford, CA 94305 USA.
[Barrett, J. C.] Wellcome Trust Sanger Inst, Cambridge CB10 1HH, England.
[Biesecker, L. G.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Conrad, D. F.] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA.
[Conrad, D. F.] Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA.
[Conrad, D. F.] Washington Univ, Sch Med, Dept Immunol, St Louis, MO 63110 USA.
[Cooper, G. M.; Gunter, C.] HudsonAlpha Inst Biotechnol, Huntsville, AL 35806 USA.
[Cox, N. J.] Univ Chicago, Dept Med, Med Genet Sect, Chicago, IL 60637 USA.
[Gerstein, M. B.] Yale Univ, Program Computat Biol & Bioinformat, New Haven, CT 06520 USA.
[Gerstein, M. B.] Yale Univ, Dept Comp Sci, New Haven, CT 06520 USA.
[Gerstein, M. B.] Yale Univ, Dept Mol Biophys, New Haven, CT 06520 USA.
[Gerstein, M. B.] Yale Univ, Dept Biochem, New Haven, CT 06520 USA.
[Goldstein, D. B.] Duke Univ, Sch Med, Ctr Human Genome Variat, Durham, NC 27708 USA.
[Hirschhorn, J. N.] Childrens Hosp, Div Genet, Boston, MA 02115 USA.
[Hirschhorn, J. N.] Childrens Hosp, Div Endocrinol, Boston, MA 02115 USA.
[Leal, S. M.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Pennacchio, L. A.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Genom Div, Berkeley, CA 94720 USA.
[Pennacchio, L. A.] US DOE, Joint Genome Inst, Walnut Creek, CA 94598 USA.
[Stamatoyannopoulos, J. A.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Sunyaev, S. R.] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA.
[Sunyaev, S. R.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Valle, D.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD 21287 USA.
[Voight, B. F.] Univ Penn, Perelman Sch Med, Dept Pharmacol, Philadelphia, PA 19104 USA.
[Voight, B. F.] Univ Penn, Perelman Sch Med, Dept Genet, Philadelphia, PA 19104 USA.
RP MacArthur, DG (reprint author), Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
EM macarthur@atgu.mgh.harvard.edu; drchrisgunter@gmail.com
RI Antonarakis, Stylianos/N-8866-2014; Dimmock, David/I-7913-2015;
OI Antonarakis, Stylianos/0000-0001-8907-5823; Dimmock,
David/0000-0001-6690-2523; Gunter, Chris/0000-0001-9369-7537; Barrett,
Jeffrey/0000-0002-1152-370X; Shendure, Jay/0000-0002-1516-1865
FU NHGRI NIH HHS [R01 HG007022, U54 HG006997]; NHLBI NIH HHS [R01
HL117626]; NIDDK NIH HHS [P30 DK020595]; NIMH NIH HHS [R01 MH101810]
NR 60
TC 324
Z9 329
U1 8
U2 80
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD APR 24
PY 2014
VL 508
IS 7497
BP 469
EP 476
DI 10.1038/nature13127
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF5GI
UT WOS:000334741600026
PM 24759409
ER
PT J
AU Zhang, YE
Li, H
Zhao, G
Sun, AJ
Zong, NC
Li, ZF
Zhu, HM
Zou, YZ
Yang, XD
Ge, JB
AF Zhang, Youen
Li, Hua
Zhao, Gang
Sun, Aijun
Zong, Nobel C.
Li, Zhaofeng
Zhu, Hongming
Zou, Yunzeng
Yang, Xiangdong
Ge, Junbo
TI Hydrogen Sulfide Attenuates the Recruitment of CD11b(+)Gr-1(+) Myeloid
Cells and Regulates Bax/Bcl-2 Signaling in Myocardial Ischemia Injury
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CYSTATHIONINE GAMMA-LYASE; REPERFUSION INJURY; SUPPRESSOR-CELLS;
HEART-FAILURE; ISCHEMIA/REPERFUSION INJURY; INFLAMMATORY RESPONSE;
DENDRITIC CELLS; INFARCTION; MICE; INFILTRATION
AB Hydrogen sulfide, an endogenous signaling molecule, plays an important role in the physiology and pathophysiology of the cardiovascular system. Using a mouse model of myocardial infarction, we investigated the anti-inflammatory and anti-apoptotic effects of the H2S donor sodium hydrosulfide (NaHS). The results demonstrated that the administration of NaHS improved survival, preserved left ventricular function, limited infarct size, and improved H2S levels in cardiac tissue to attenuate the recruitment of CD11b(+)Gr-1(+) myeloid cells and to regulate the Bax/Bcl-2 pathway. Furthermore, the cardioprotective effects of NaHS were enhanced by inhibiting the migration of CD11b(+)Gr-1(+) myeloid cells from the spleen into the blood and by attenuating post-infarction inflammation. These observations suggest that the novel mechanism underlying the cardioprotective function of H2S is secondary to a combination of attenuation the recruitment of CD11b(+)Gr-1(+) myeloid cells and regulation of the Bax/Bcl-2 apoptotic signaling.
C1 [Zhang, Youen; Li, Hua; Zhao, Gang; Sun, Aijun; Li, Zhaofeng; Zou, Yunzeng; Yang, Xiangdong; Ge, Junbo] Fudan Univ, Zhongshan Hosp, Shanghai Inst Cardiovasc Dis, Shanghai 200032, Peoples R China.
[Li, Hua; Zong, Nobel C.; Zhu, Hongming] Univ Calif Los Angeles, Sch Med, Dept Physiol, Los Angeles, CA 90095 USA.
[Li, Hua; Zong, Nobel C.; Zhu, Hongming] Univ Calif Los Angeles, Sch Med, Dept Med CVRL, Los Angeles, CA 90095 USA.
[Sun, Aijun; Zou, Yunzeng; Ge, Junbo] Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.
[Zong, Nobel C.] Univ Calif Los Angeles, Sch Med, NHLBI Prote Ctr, NHLBI Prote Program, Los Angeles, CA 90095 USA.
RP Yang, XD (reprint author), Fudan Univ, Zhongshan Hosp, Shanghai Inst Cardiovasc Dis, Shanghai 200032, Peoples R China.
EM yang.xiangdong@zs-hospital.sh.cn; ge.junbo@zs-hospital.sh.cn
FU State Key Development Program for Basic Research of China
[2011CB503905]; National Key Technology Support Program [2011BAI11B10];
Major Program of the National Natural Science Foundation of China
[81230007]; Shanghai Pujiang Program [12PJ1401700]
FX This study was supported by the State Key Development Program for Basic
Research of China (No. 2011CB503905), the National Key Technology
Support Program (No.2011BAI11B10), the Major Program of the National
Natural Science Foundation of China (No.81230007), and the Shanghai
Pujiang Program (12PJ1401700).
NR 35
TC 7
Z9 8
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 24
PY 2014
VL 4
AR 4774
DI 10.1038/srep04774
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF6RC
UT WOS:000334841300007
PM 24758901
ER
PT J
AU Minakshi, R
Padhan, K
AF Minakshi, Rinki
Padhan, Kartika
TI The YXXempty set motif within the severe acute respiratory syndrome
coronavirus (SARS-CoV) 3a protein is crucial for its intracellular
transport
SO VIROLOGY JOURNAL
LA English
DT Article
ID LIPID DROPLETS; ENDOPLASMIC-RETICULUM; TRANSMEMBRANE PROTEINS;
STRUCTURAL PROTEIN; PLASMA-MEMBRANE; HONG-KONG; CAVEOLIN; CELLS; EXPORT;
IDENTIFICATION
AB Background: The SARS coronavirus (SARS-CoV) 3a protein functions as an ion channel, induces apoptosis and is important for viral pathogenesis. It is expressed on the cell surface and contains a tyrosine-based sorting motif and a di-acidic motif, which may be crucial for its intracellular trafficking. However the role of these motifs is not fully understood in the case of 3a protein.
Methods: The subcellular distribution of the 3a protein was studied by immunofluorescence staining of cells transfected with wild type and mutant constructs along with markers for different intracellular compartments. Semi-quantitative RT-PCR was performed to estimate the mRNA where as western blotting was carried out to detect protein levels of wild type and mutant 3a proteins. In vitro transcription-translation was performed to estimate cell free protein synthesis.
Results: While the wild type 3a protein is efficiently transported to the plasma membrane, the protein with mutations in the tyrosine and valine residues within the YXXV motif (Delta YXXempty set) accumulated in the Golgi compartment. However the 3a protein with mutations within the EXD di-acidic motif (Delta EXD) showed an intracellular distribution similar to the wild type protein. Increased retention of the Delta YXXempty set protein in the Golgi compartment also increased its association with lipid droplets. The Delta YXXempty set protein also expressed at significantly lower levels compared to the wild type 3a protein, which was reversed with Brefeldin A and Aprotinin.
Conclusions: The data suggest that the YXXempty set motif of the SARS-CoV 3a protein is necessary for Golgi to plasma membrane transport, in the absence of which the protein is targeted to lysosomal degradation compartment via lipid droplets.
C1 [Minakshi, Rinki; Padhan, Kartika] Int Ctr Genet Engn & Biotechnol, New Delhi, India.
[Padhan, Kartika] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
RP Padhan, K (reprint author), Int Ctr Genet Engn & Biotechnol, New Delhi, India.
EM kartikpadhan@gmail.com
FU CSIR (India)
FX We thank Dr. Shahid Jameel for generously providing us lab space and
reagents to conduct the experiments. We also thank Dr. Manjula Kalia and
Charu Tanwar for their help with confocal microscopy. A Senior Research
Fellowship to K. P. from CSIR (India) is gratefully acknowledged.
NR 44
TC 1
Z9 1
U1 0
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1743-422X
J9 VIROL J
JI Virol. J.
PD APR 24
PY 2014
VL 11
AR 75
DI 10.1186/1743-422X-11-75
PG 10
WC Virology
SC Virology
GA AG1NJ
UT WOS:000335182000001
PM 24762043
ER
PT J
AU Erdem, AL
Jaszczur, M
Bertram, JG
Woodgate, R
Cox, MM
Goodman, MF
AF Erdem, Aysen L.
Jaszczur, Malgorzata
Bertram, Jeffrey G.
Woodgate, Roger
Cox, Michael M.
Goodman, Myron F.
TI DNA polymerase V activity is autoregulated by a novel intrinsic
DNA-dependent ATPase
SO ELIFE
LA English
DT Article
ID UMUD MUTAGENESIS PROTEIN; SINGLE-STRANDED-DNA; ESCHERICHIA-COLI; RECA
PROTEIN; IN-VITRO; BIOCHEMICAL BASIS; SOS MUTAGENESIS; BINDING PROTEIN;
PURIFICATION; CLEAVAGE
AB Escherichia coli DNA polymerase V (pol V), a heterotrimeric complex composed of UmuD'C-2, is marginally active. ATP and RecA play essential roles in the activation of pol V for DNA synthesis including translesion synthesis (TLS). We have established three features of the roles of ATP and RecA. 1) RecA-activated DNA polymerase V (pol V Mut), is a DNA-dependent ATPase; 2) bound ATP is required for DNA synthesis; 3) pol V Mut function is regulated by ATP, with ATP required to bind primer/template (p/t) DNA and ATP hydrolysis triggering dissociation from the DNA. Pol V Mut formed with an ATPase-deficient RecA E38K/K72R mutant hydrolyzes ATP rapidly, establishing the DNA-dependent ATPase as an intrinsic property of pol V Mut distinct from the ATP hydrolytic activity of RecA when bound to single-stranded (ss) DNA as a nucleoprotein filament (RecA*). No similar ATPase activity or autoregulatory mechanism has previously been found for a DNA polymerase.
C1 [Erdem, Aysen L.; Jaszczur, Malgorzata; Bertram, Jeffrey G.; Goodman, Myron F.] Univ So Calif, Dept Biol Sci, Los Angeles, CA 90089 USA.
[Erdem, Aysen L.; Jaszczur, Malgorzata; Bertram, Jeffrey G.; Goodman, Myron F.] Univ So Calif, Dept Chem, Los Angeles, CA 90089 USA.
[Woodgate, Roger] NICHHD, Lab Genom Integr, NIH, Bethesda, MD 20892 USA.
[Cox, Michael M.] Univ Wisconsin, Dept Biochem, Madison, WI 53706 USA.
RP Erdem, AL (reprint author), Univ So Calif, Dept Biol Sci, Univ Pk, Los Angeles, CA 90089 USA.
FU NIEHS NIH HHS [ES012259, R01 ES012259]; NIGMS NIH HHS [R01 GM032335,
GM32335, GM21422]
NR 32
TC 7
Z9 7
U1 3
U2 3
PU ELIFE SCIENCES PUBLICATIONS LTD
PI CAMBRIDGE
PA SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND
SN 2050-084X
J9 ELIFE
JI eLife
PD APR 24
PY 2014
VL 3
AR e02384
DI 10.7554/eLife.02384
PG 29
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AF7VO
UT WOS:000334923200008
PM 24843026
ER
PT J
AU Fritsch, B
Reis, J
Gasior, M
Kaminski, RM
Rogawski, MA
AF Fritsch, Brita
Reis, Janine
Gasior, Maciej
Kaminski, Rafal M.
Rogawski, Michael A.
TI Role of GluK1 Kainate Receptors in Seizures, Epileptic Discharges, and
Epileptogenesis
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE ATPA; BLA; epilepsy; kainate receptor; kindling; seizure
ID MEDIATED SYNAPTIC-TRANSMISSION; BASOLATERAL AMYGDALA; PHARMACOLOGICAL
CHARACTERIZATION; HIPPOCAMPAL INTERNEURONS; ELECTRICAL-STIMULATION;
TONIC INHIBITION; GRANULE CELLS; IN-VITRO; GLUR5; EXPRESSION
AB Kainate receptors containing the GluK1 subunit have an impact on excitatory and inhibitory neurotransmission in brain regions, such as the amygdala and hippocampus, which are relevant to seizures and epilepsy. Here we used 2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid (ATPA), a potent and selective agonist of kainate receptors that include the GluK1 subunit, in conjunction with mice deficient in GluK1 and GluK2 kainate receptor subunits to assess the role of GluK1 kainate receptors in provoking seizures and in kindling epileptogenesis. We found that systemic ATPA, acting specifically via GluK1 kainate receptors, causes locomotor arrest and forelimb extension (a unique behavioral characteristic of GluK1 activation) and induces myoclonic behavioral seizures and electrographic seizure discharges in the BLA and hippocampus. In contrast, the proconvulsant activity of systemic AMPA, kainate, and pentylenetetrazol is not mediated by GluK1 kainate receptors, and deletion of these receptors does not elevate the threshold for seizures in the 6 Hz model. ATPA also specifically activates epileptiform discharges in BLA slices in vitro via GluK1 kainate receptors. Olfactory bulb kindling developed similarly in wild-type, GluK1, and GluK2 knock-out mice, demonstrating that GluK1 kainate receptors are not required for epileptogenesis or seizure expression in this model. We conclude that selective activation of kainate receptors containing the GluK1 subunit can trigger seizures, but these receptors are not necessary for seizure generation in models commonly used to identify therapeutic agents for the treatment of epilepsy.
C1 [Fritsch, Brita; Reis, Janine; Gasior, Maciej; Kaminski, Rafal M.; Rogawski, Michael A.] NINDS, Epilepsy Res Sect, NIH, Bethesda, MD 20892 USA.
[Fritsch, Brita; Reis, Janine] Univ Hosp, Dept Neurol, D-79106 Freiburg, Germany.
[Rogawski, Michael A.] Univ Calif Davis, Sch Med, Dept Neurol, Sacramento, CA 95817 USA.
[Rogawski, Michael A.] Univ Calif Davis, Ctr Neurosci, Sacramento, CA 95817 USA.
RP Rogawski, MA (reprint author), Univ Calif Davis, Dept Neurol, 4860 Y St,Suite 3700, Sacramento, CA 95817 USA.
EM rogawski@ucdavis.edu
RI Rogawski, Michael/B-6353-2009
OI Rogawski, Michael/0000-0002-3296-8193
FU National Institute of Neurological Disorders and Stroke (NINDS) of the
National Institutes of Health [NS072094, NS079292]; NINDS Intramural
Research Program
FX This work was supported by the National Institute of Neurological
Disorders and Stroke (NINDS) of the National Institutes of Health
(NS072094, NS079292) and by the NINDS Intramural Research Program. B.F.
was a fellow of the NINDS Intramural Research Program. We thank Wayne D.
Yonekawa and Megan Lyle Desai for assistance with experiments, and David
Ide and Danny Trang for technical support.
NR 45
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U1 1
U2 13
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 APR 23
PY 2014
VL 34
IS 17
BP 5765
EP 5775
DI 10.1523/JNEUROSCI.5307-13.2014
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA AF7XP
UT WOS:000334929100005
PM 24760837
ER
PT J
AU Pecina, M
Martinez-Jauand, M
Love, T
Heffernan, J
Montoya, P
Hodgkinson, C
Stohler, CS
Goldman, D
Zubieta, JK
AF Pecina, Marta
Martinez-Jauand, Mercedes
Love, Tiffany
Heffernan, Joseph
Montoya, Pedro
Hodgkinson, Colin
Stohler, Christian S.
Goldman, David
Zubieta, Jon-Kar
TI Valence-Specific Effects of BDNF Val(66)Met Polymorphism on Dopaminergic
Stress and Reward Processing in Humans
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE BDNF Val66Met; dopamine; nucleus accumbens; pain; reward; stress
ID ACTIVITY-DEPENDENT SECRETION; NEUROTROPHIC FACTOR; IN-VIVO;
INDIVIDUAL-DIFFERENCES; PSYCHOLOGICAL STRESS; CONTINUOUS-INFUSION;
CORTICAL-NEURONS; MOOD DISORDERS; SOCIAL DEFEAT; WILD-TYPE
AB Brain-derived neurotrophic factor (BDNF) levels in dopaminergic (DA) cells within the ventral tegmental area (VTA)/nucleus accumbens (NAc) circuitry appear to be a candidate mechanism for the neuroadaptive changes that follow stress and reward responses in animal models. However, the role of the BDNF gene variants in responses to salient cues through DA neurotransmission in humans remains unexplored. Here, we studied the effect of the common functional BDNF Val(66)Met (rs6265) polymorphism on rewarding experiences in the striatum and DA-mediated responses to stress. Seventy-two healthy controls were genotyped for the BDNF Val(66)Met polymorphism and underwent the monetary incentive delay task during an functional magnetic resonance imaging (fMRI) session. Forty-nine of them also underwent a sustained pain challenge with and without placebo administration with potential analgesic properties during PET measures of DA D-2/3-receptor-mediated neurotransmission. Neuroimaging results revealed a significant effect of BDNF (Met(66) carriers > Val/Val) on brain responses during the anticipation of monetary losses, baseline D-2/3 receptor availability, and pain-stress-induced DA release in the NAc. Conversely, BDNF Met(66) carriers showed no activation in response to monetary gains and a blunted DA response to the analgesic placebo in the NAc. These results provide initial human evidence regarding the effect of the BDNF Val(66)Met polymorphism on DA-mediated responses to stress, its cognitive regulation by positive expectations, and the anticipatory responses to monetary gains and losses in the VTA-NAc pathway. Our results are of relevance to the neurobiology of stress and reward interactions and the pathophysiology of stress-related disorders.
C1 [Pecina, Marta; Love, Tiffany; Zubieta, Jon-Kar] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA.
[Pecina, Marta; Love, Tiffany; Heffernan, Joseph; Zubieta, Jon-Kar] Univ Michigan, Mol & Behav Neurosci Inst, Dept Radiol, Ann Arbor, MI 48109 USA.
[Martinez-Jauand, Mercedes; Montoya, Pedro] Inst Univ Invest Ciencies Salut IUNICS, Res Inst Hlth Sci, Palma de Mallorca 07122, Spain.
[Stohler, Christian S.] Columbia Univ, Coll Dent Med, New York, NY 10032 USA.
[Hodgkinson, Colin; Goldman, David] NIAAA, Rockville, MD 20852 USA.
RP Zubieta, JK (reprint author), Univ Michigan, Mol & Behav Neurosci Inst, 205 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.
EM Zubieta@umich.edu
RI Goldman, David/F-9772-2010; Montoya, Pedro/A-4666-2009;
OI Goldman, David/0000-0002-1724-5405; Montoya, Pedro/0000-0001-8652-948X;
Love, Tiffany/0000-0001-9299-3190
FU National Institutes of Health-National Institute of Drug Abuse [R01 DA
022520, R01 DA 027494]; Phil F. Jenkins Foundation; Spanish Ministry of
Education [AP2008-03742]; Spanish Ministry of Science and Innovation and
European (Regional Development Fund) [PSI2010-19372]
FX This work was supported by The National Institutes of Health-National
Institute of Drug Abuse (Grants R01 DA 022520 and R01 DA 027494 to
J.K.Z.), the Phil F. Jenkins Foundation, the Spanish Ministry of
Education (Grant AP2008-03742 to M.M.-J.), and the Spanish Ministry of
Science and Innovation and European (Regional Development Fund Grant
PSI2010-19372 to P. M.). We thank the technologists of the PET Center
and the fMRI laboratory at the University of Michigan.
NR 69
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U1 2
U2 10
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 APR 23
PY 2014
VL 34
IS 17
BP 5874
EP 5881
DI 10.1523/JNEUROSCI.2152-13.2014
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA AF7XP
UT WOS:000334929100015
PM 24760847
ER
PT J
AU Yu, T
Calvo, L
Anta, B
Lopez-Benito, S
Lopez-Bellido, R
Vicente-Garcia, C
Tessarollo, L
Rodriguez, RE
Arevalo, JC
AF Yu, Tao
Calvo, Laura
Anta, Begona
Lopez-Benito, Saray
Lopez-Bellido, Roger
Vicente-Garcia, Cristina
Tessarollo, Lino
Rodriguez, Raquel E.
Arevalo, Juan C.
TI In Vivo Regulation of NGF-Mediated Functions by Nedd4-2 Ubiquitination
of TrkA
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE neurotrophins; pain; TrkA neurotrophin receptor; ubiquitination
ID NERVE GROWTH-FACTOR; ADULT SENSORY NEURONS; CONGENITAL INSENSITIVITY;
NEUROTROPHIN RECEPTORS; TYROSINE KINASE; PAIN; PROTOONCOGENE;
ANHIDROSIS; MUTATIONS; PROTEIN
AB Trk neurotrophin receptor ubiquitination in response to ligand activation regulates signaling, trafficking, and degradation of the receptors. However, the in vivo consequences of Trk ubiquitination remain to be addressed. We have developed a mouse model with a mutation in the TrkA neurotrophin receptor (P782S) that results in reduced ubiquitination due to a lack of binding to the E3 ubiquitin ligase, Nedd4-2. In vivo analyses of TrkAP782S indicate that defective ubiquitination of the TrkA mutant results in an altered trafficking and degradation of the receptor that affects the survival of sensory neurons. The dorsal root ganglia from the TrkAP782S knock-in mice display an increased number of neurons expressing CGRP and substance P. Moreover, the mutant mice show enhanced sensitivity to thermal and inflammatory pain. Our results indicate that the ubiquitination of the TrkA neurotrophin receptor plays a critical role in NGF-mediated functions, such as neuronal survival and sensitivity to pain.
C1 [Yu, Tao; Calvo, Laura; Anta, Begona; Lopez-Benito, Saray; Vicente-Garcia, Cristina; Arevalo, Juan C.] Univ Salamanca, Inst Neurociencias Castilla & Leon INCyL, Dept Cell Biol & Pathol, Salamanca 37007, Spain.
[Lopez-Bellido, Roger; Rodriguez, Raquel E.] Univ Salamanca, Inst Neurociencias Castilla & Leon INCyL, Dept Biochem & Mol Biol, Salamanca 37007, Spain.
[Tessarollo, Lino] NCI, Neural Dev Grp, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Yu, Tao; Calvo, Laura; Anta, Begona; Lopez-Benito, Saray; Lopez-Bellido, Roger; Vicente-Garcia, Cristina; Rodriguez, Raquel E.; Arevalo, Juan C.] Inst Biomed Res Salamanca, Salamanca 37007, Spain.
RP Arevalo, JC (reprint author), Univ Salamanca, INCyL, C Pintor Fernando Gallego 1, Salamanca 37007, Spain.
EM arevalojc@usal.es
RI ArAvalo, Juan Carlos/J-8154-2014;
OI ArAvalo, Juan Carlos/0000-0003-1994-3095; Rodriguez Rodriguez,
Raquel/0000-0003-1805-3066
FU Ministerio de Ciencia e Innovacion [BFU2008-00162]; Ministerio de
Economia y Competitividad [BFU2011-22898]; Marie Curie International
Reintegration Grant within the VII European Community Framework
Programme by Conserjeria de Educacion [SA074A08]; Conserjeria de Sanidad
de Junta Castilla y Leon; Intramural Research Program of the NCI, Center
for Cancer Research, NIH; NARSAD
FX This work was supported by Ministerio de Ciencia e Innovacion Grant
BFU2008-00162, by Ministerio de Economia y Competitividad
(BFU2011-22898), by a Marie Curie International Reintegration Grant
within the VII European Community Framework Programme by Conserjeria de
Educacion (SA074A08), and Conserjeria de Sanidad de Junta Castilla y
Leon (J.C.A.). J.C.A. was a "Ramon y Cajal" Investigator from the
University of Salamanca and NARSAD 2009 Young Investigator Awardee. L.T.
was supported by the Intramural Research Program of the NCI, Center for
Cancer Research, NIH. We thank Dionisio Martin-Zanca, Louis Reichardt,
and Moses Chao for the anti-203 Trk, RTA, and p75 antibodies,
respectively; Moses Chao and Francis Lee for critical review of the
paper and helpful discussions; Lino Tessarollo for sharing unpublished
results; and Synphen Wu and Nicholas Skinner for corrections to the
paper.
NR 37
TC 12
Z9 12
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 APR 23
PY 2014
VL 34
IS 17
BP 6098
EP 6106
DI 10.1523/JNEUROSCI.4271-13.2014
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA AF7XP
UT WOS:000334929100037
PM 24760869
ER
PT J
AU Mire, CE
Geisbert, JB
Agans, KN
Satterfield, BA
Versteeg, KM
Fritz, EA
Feldmann, H
Hensley, LE
Geisbert, TW
AF Mire, Chad E.
Geisbert, Joan B.
Agans, Krystle N.
Satterfield, Benjamin A.
Versteeg, Krista M.
Fritz, Elizabeth A.
Feldmann, Heinz
Hensley, Lisa E.
Geisbert, Thomas W.
TI Durability of a Vesicular Stomatitis Virus-Based Marburg Virus Vaccine
in Nonhuman Primates
SO PLOS ONE
LA English
DT Article
ID ATTENUATED RECOMBINANT VACCINE; EBOLA-VIRUS; HEMORRHAGIC-FEVER;
IMMUNE-RESPONSES; IMMUNIZATION; PROTECTION; CHALLENGE; VECTORS; LIVE;
GLYCOPROTEINS
AB The filoviruses, Marburg virus (MARV) and Ebola virus, causes severe hemorrhagic fever with high mortality in humans and nonhuman primates. A promising filovirus vaccine under development is based on a recombinant vesicular stomatitis virus (rVSV) that expresses individual filovirus glycoproteins (GPs) in place of the VSV glycoprotein (G). These vaccines have shown 100% efficacy against filovirus infection in nonhuman primates when challenge occurs 28-35 days after a single injection immunization. Here, we examined the ability of a rVSV MARV-GP vaccine to provide protection when challenge occurs more than a year after vaccination. Cynomolgus macaques were immunized with rVSV-MARV-GP and challenged with MARV approximately 14 months after vaccination. Immunization resulted in the vaccine cohort of six animals having anti-MARV GP IgG throughout the pre-challenge period. Following MARV challenge none of the vaccinated animals showed any signs of clinical disease or viremia and all were completely protected from MARV infection. Two unvaccinated control animals exhibited signs consistent with MARV infection and both succumbed. Importantly, these data are the first to show 100% protective efficacy against any high dose filovirus challenge beyond 8 weeks after final vaccination. These findings demonstrate the durability of VSV-based filovirus vaccines.
C1 [Mire, Chad E.; Geisbert, Joan B.; Agans, Krystle N.; Satterfield, Benjamin A.; Versteeg, Krista M.; Fritz, Elizabeth A.; Geisbert, Thomas W.] Univ Texas Med Branch, Galveston Natl Lab, Galveston, TX 77555 USA.
[Mire, Chad E.; Geisbert, Joan B.; Agans, Krystle N.; Satterfield, Benjamin A.; Versteeg, Krista M.; Fritz, Elizabeth A.; Geisbert, Thomas W.] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA.
[Feldmann, Heinz] NIAID, Virol Lab, Div Intramural Res, NIH, Hamilton, MT USA.
[Hensley, Lisa E.] NIAID, Integrated Res Facil Ft Detrick, Div Clin Res, NIH, Frederick, MD USA.
RP Geisbert, TW (reprint author), Univ Texas Med Branch, Galveston Natl Lab, Galveston, TX 77555 USA.
EM twgeisbe@utmb.edu
OI Satterfield, Benjamin/0000-0002-7798-0938
FU US Army Medical Research Acquisition Activity [WX81XWH-10-2-0050];
Department of Health and Human Services, NIH [AI098817]
FX This work was supported by an award from the US Army Medical Research
Acquisition Activity to TG (award number WX81XWH-10-2-0050). Some
non-animal portions of the work were also supported by the Department of
Health and Human Services, NIH, grant AI098817 to Dr. John Eldridge and
TWG. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 33
TC 19
Z9 21
U1 1
U2 14
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 APR 23
PY 2014
VL 9
IS 4
AR e94355
DI 10.1371/journal.pone.0094355
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG3EI
UT WOS:000335298200015
PM 24759889
ER
PT J
AU Wall, M
McDermott, MP
Kieburtz, KD
Corbett, JJ
Feldon, SE
Friedman, DI
Katz, DM
Keltner, JL
Schron, EB
Kupersmith, MJ
AF Wall, Michael
McDermott, Michael P.
Kieburtz, Karl D.
Corbett, James J.
Feldon, Steven E.
Friedman, Deborah I.
Katz, David M.
Keltner, John L.
Schron, Eleanor B.
Kupersmith, Mark J.
CA NORDIC Idiopathic Intracranial
TI Effect of Acetazolamide on Visual Function in Patients With Idiopathic
Intracranial Hypertension and Mild Visual Loss The Idiopathic
Intracranial Hypertension Treatment Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID PSEUDOTUMOR CEREBRI; PRESSURE; VALIDATION; DIAGNOSIS; SHUNT
AB IMPORTANCE Acetazolamide is commonly used to treat idiopathic intracranial hypertension (IIH), but there is insufficient information to establish an evidence base for its use.
OBJECTIVE To determine whether acetazolamide is beneficial in improving vision when added to a low-sodium weight reduction diet in patients with IIH and mild visual loss.
DESIGN, SETTING, AND PARTICIPANTS Multicenter, randomized, double-masked, placebo-controlled study of acetazolamide in 165 participants with IIH and mild visual loss who received a low-sodium weight-reduction diet. Participants were enrolled at 38 academic and private practice sites in North America from March 2010 to November 2012 and followed up for 6 months (last visit in June 2013). All participants met the modified Dandy criteria for IIH and had a perimetric mean deviation (PMD) between -2 dB and -7 dB. The mean age was 29 years and all but 4 participants were women.
INTERVENTIONS Low-sodium weight-reduction diet plus the maximally tolerated dosage of acetazolamide (up to 4 g/d) or matching placebo for 6 months.
MAIN OUTCOMES AND MEASURES The planned primary outcome variable was the change in PMD from baseline to month 6 in the most affected eye, as measured by Humphrey Field Analyzer. Perimetric mean deviation is a measure of global visual field loss (mean deviation from age-corrected normal values), with a range of 2 to -32 dB; larger negative values indicate greater vision loss. Secondary outcome variables included changes in papilledema grade, quality of life (Visual Function Questionnaire 25 [VFQ-25] and 36-Item Short Form Health Survey), headache disability, and weight at month 6.
RESULTS The mean improvement in PMD was greater with acetazolamide (1.43 dB, from -3.53 dB at baseline to -2.10dB at month 6; n = 86) than with placebo (0.71 dB, from -3.53 dB to -2.82 dB; n = 79); the difference was 0.71 dB (95% CI, 0to 1.43 dB; P = .050). Mean improvements in papilledema grade (acetazolamide: -1.31, from 2.76 to 1.45; placebo: -0.61, from 2.76 to 2.15; treatment effect, -0.70; 95% CI, -0.99 to -0.41; P < .001) and vision-related quality of life as measured by the National Eye Institute VFQ-25 (acetazolamide: 8.33, from 82.97 to 91.30; placebo: 1.98, from 82.97 to 84.95; treatment effect, 6.35; 95% CI, 2.22 to 10.47; P = .003) and its 10-item neuro-ophthalmic supplement (acetazolamide: 9.82, from 75.45 to 85.27; placebo: 1.59, from 75.45 to 77.04; treatment effect, 8.23; 95% CI, 3.89 to 12.56; P < .001) were also observed with acetazolamide. Participants assigned to acetazolamide also experienced a reduction in weight (acetazolamide: -7.50 kg, from 107.72 kg to 100.22 kg; placebo: -3.45 kg, from 107.72 kg to 104.27 kg; treatment effect, -4.05 kg, 95% CI, -6.27 to -1.83 kg; P < .001).
CONCLUSIONS AND RELEVANCE In patients with IIH and mild visual loss, the use of acetazolamide with a low-sodium weight-reduction diet compared with diet alone resulted in modest improvement in visual field function. The clinical importance of this improvement remains to be determined.
C1 [Wall, Michael] Univ Iowa, Iowa City, IA USA.
[McDermott, Michael P.; Kieburtz, Karl D.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Corbett, James J.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Feldon, Steven E.] Univ Rochester, Inst Eye, Rochester, NY USA.
[Friedman, Deborah I.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Katz, David M.] Bethesda Neurol LLC, Bethesda, MD USA.
[Keltner, John L.] Univ Calif Davis, Med Ctr, Davis, CA USA.
[Schron, Eleanor B.] NEI, Bethesda, MD 20892 USA.
[Kupersmith, Mark J.] St Lukes Roosevelt Hosp, New York, NY 10025 USA.
RP Wall, M (reprint author), Univ Iowa Hosp & Clin, Dept Neurol, 200 Hawkins Dr, Iowa City, IA 52242 USA.
EM michael-wall@uiowa.edu
OI Bruce, Beau/0000-0003-3003-2962; Subramanian, Prem/0000-0001-5824-8322
FU National Eye Institute (NEI) [1U10EY017281-01A1, 1U10EY017387-01A1,
3U10EY017281-01A1S1, 1U10EY017387-01A1S1]
FX This work was supported by National Eye Institute (NEI) grants
1U10EY017281-01A1, DCBC 1U10EY017387-01A1, ARRA for NORDIC
3U10EY017281-01A1S1, and DCBC 1U10EY017387-01A1S1, and supplements for
NORDIC 3U10EY017281-01A1S2.
NR 25
TC 60
Z9 61
U1 0
U2 12
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD APR 23
PY 2014
VL 311
IS 16
BP 1641
EP 1651
DI 10.1001/jama.2014.3312
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA AF4OU
UT WOS:000334693900024
ER
PT J
AU Bachran, C
Gupta, PK
Bachran, S
Leysath, CE
Hoover, B
Fattah, RJ
Leppla, SH
AF Bachran, Christopher
Gupta, Pradeep K.
Bachran, Silke
Leysath, Clinton E.
Hoover, Benjamin
Fattah, Rasem J.
Leppla, Stephen H.
TI Reductive Methylation and Mutation of an Anthrax Toxin Fusion Protein
Modulates its Stability and Cytotoxicity
SO SCIENTIFIC REPORTS
LA English
DT Article
ID LETHAL FACTOR; DIPHTHERIA-TOXIN; PROTECTIVE ANTIGEN; LYSINE RESIDUES;
TRANSLOCATION; TUMOR; IMMUNOTOXIN; POTENCY; DOMAINS; BINDING
AB We characterized an anti-cancer fusion protein consisting of anthrax lethal factor (LF) and the catalytic domain of Pseudomonas exotoxin A by (i) mutating the N-terminal amino acids and by (ii) reductive methylation to dimethylate all lysines. Dimethylation of lysines was achieved quantitatively and specifically without affecting binding of the fusion protein to PA or decreasing the enzymatic activity of the catalytic moiety. Ubiquitination in vitro was drastically decreased for both the N-terminally mutated and dimethylated variants, and both appeared to be slightly more stable in the cytosol of treated cells. The dimethylated variant showed greatly reduced neutralization by antibodies to LF. The two described modifications offer unique advantages such as increased cytotoxic activity and diminished antibody recognition, and thus may be applicable to other therapeutic proteins that act in the cytosol of cells.
C1 [Bachran, Christopher; Gupta, Pradeep K.; Bachran, Silke; Leysath, Clinton E.; Hoover, Benjamin; Fattah, Rasem J.; Leppla, Stephen H.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Leppla, SH (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM sleppla@niaid.nih.gov
FU Intramural Research Program of the NIH, National Institute of Allergy
and Infectious Diseases (NIAID), Bethesda, MD, USA
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Allergy and Infectious Diseases (NIAID),
Bethesda, MD, USA. The authors thank J. Eric Anderson for mass
spectrometric analysis of the proteins described here.
NR 34
TC 6
Z9 6
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 23
PY 2014
VL 4
AR 4754
DI 10.1038/srep04754
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF6PH
UT WOS:000334836500001
PM 24755540
ER
PT J
AU Hackett, TA
de la Mothe, LA
Camalier, CR
Falchier, A
Lakatos, P
Kajikawa, Y
Schroeder, CE
AF Hackett, Troy A.
de la Mothe, Lisa A.
Camalier, Corrie R.
Falchier, Arnaud
Lakatos, Peter
Kajikawa, Yoshinao
Schroeder, Charles E.
TI Feedforward and feedback projections of caudal belt and parabelt areas
of auditory cortex: refining the hierarchical model
SO FRONTIERS IN NEUROSCIENCE
LA English
DT Article
DE connections; brain; monkey; functional organization; laminar;
architecture; anatomy; laminar
ID SUPERIOR TEMPORAL SULCUS; CORTICO-CORTICAL CONNECTIONS; OLD-WORLD
MONKEYS; RHESUS-MONKEY; MACAQUE MONKEY; MULTISENSORY CONVERGENCE;
ASSOCIATION CORTEX; PREFRONTAL CORTEX; MARMOSET MONKEYS; VISUAL AREAS
AB Our working model of the primate auditory cortex recognizes three major regions (core, belt, parabelt), subdivided into thirteen areas. The connections between areas are topographically ordered in a manner consistent with information flow along two major anatomical axes: core-belt-parabelt and caudal-rostral. Remarkably, most of the connections supporting this model were revealed using retrograde tracing techniques. Little is known about laminar circuitry, as anterograde tracing of axon terminations has rarely been used. The purpose of the present study was to examine the laminar projections of three areas of auditory cortex, pursuant to analysis of all areas. The selected areas were: middle lateral belt (MU; caudomedial belt (CM); and caudal parabelt (CPB). Injections of anterograde tracers yielded data consistent with major features of our model, and also new findings that compel modifications. Results supporting the model were: (1) feedforward projection from ML and CM terminated in CPB; (2) feedforward projections from ML and CPB terminated in rostral areas of the belt and parabelt; and (3) feedback projections typified inputs to the core region from belt and parabelt. At odds with the model was the convergence of feedforward inputs into rostral medial belt from ML and CPB. This was unexpected since CPB is at a higher stage of the processing hierarchy, with mainly feedback projections to all other belt areas. Lastly, extending the model, feedforward projections from CM, ML, and CPB overlapped in the temporal parietal occipital area (TPO) in the superior temporal sulcus, indicating significant auditory influence on sensory processing in this region. The combined results refine our working model and highlight the need to complete studies of the laminar inputs to all areas of auditory cortex. Their documentation is essential for developing informed hypotheses about the neurophysiological influences of inputs to each layer and area.
C1 [Hackett, Troy A.; Camalier, Corrie R.] Vanderbilt Univ, Sch Med, Dept Hearing & Speech Sci, Nashville, TN 37232 USA.
[de la Mothe, Lisa A.] Tennessee State Univ, Dept Psychol, Nashville, TN 37203 USA.
[Camalier, Corrie R.] NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA.
[Falchier, Arnaud; Lakatos, Peter; Kajikawa, Yoshinao; Schroeder, Charles E.] Nathan S Kline Inst Psychiat Res, Cognit Neurosci & Schizophrenia Program, Orangeburg, NY 10962 USA.
[Falchier, Arnaud; Lakatos, Peter; Kajikawa, Yoshinao; Schroeder, Charles E.] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
RP Hackett, TA (reprint author), Vanderbilt Univ, Sch Med, Dept Hearing & Speech Sci, 465 21st Ave South MRB-3 Suite 7110, Nashville, TN 37232 USA.
EM troy.a.hackett@vanderbilt.edu
FU NIH [R01DC04318, R01DC011490]; [R21DC012918]
FX The authors gratefully acknowledge the support of NIH grants R01DC04318
to Troy A. Hackett, R01DC011490 to Charles E. Schroeder, and R21DC012918
to Yoshinao Kajikawa.
NR 91
TC 9
Z9 9
U1 2
U2 3
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-453X
J9 FRONT NEUROSCI-SWITZ
JI Front. Neurosci.
PD APR 22
PY 2014
VL 8
AR UNSP 72
DI 10.3389/fnins.2014.00072
PG 21
WC Neurosciences
SC Neurosciences & Neurology
GA AW7UD
UT WOS:000346468800001
PM 24795550
ER
PT J
AU Adomas, AB
Grimm, SA
Malone, C
Takaku, M
Sims, JK
Wade, PA
AF Adomas, Aleksandra B.
Grimm, Sara A.
Malone, Christine
Takaku, Motoki
Sims, Jennifer K.
Wade, Paul A.
TI Breast tumor specific mutation in GATA3 affects physiological mechanisms
regulating transcription factor turnover
SO BMC CANCER
LA English
DT Article
DE Breast cancer; ChIP-seq; GATA3; Mutation; Transcription factor
ID ESTROGEN-RECEPTOR; GENE-EXPRESSION; CANCER METASTASIS; ALPHA EXPRESSION;
MAMMARY-GLAND; HDR SYNDROME; ER-ALPHA; DIFFERENTIATION; BINDING; GENOME
AB Background: The transcription factor GATA3 is a favorable prognostic indicator in estrogen receptor-a (ERa)-positive breast tumors in which it participates with ERa and FOXA1 in a complex transcriptional regulatory program driving tumor growth. GATA3 mutations are frequent in breast cancer and have been classified as driver mutations. To elucidate the contribution(s) of GATA3 alterations to cancer, we studied two breast cancer cell lines, MCF7, which carries a heterozygous frameshift mutation in the second zinc finger of GATA3, and T47D, wild-type at this locus.
Methods: Immunofluorescence staining and subcellular fractionation were employed to verify cellular localization of GATA3 in T47D and MCF7 cells. To test protein stability, cells were treated with translation inhibitor, cycloheximide or proteasome inhibitor, MG132, and GATA3 abundance was measured over time using immunoblot. GATA3 turn-over in response to hormone was determined by treating the cells with estradiol or ERa agonist, ICI 182,780. DNA binding ability of recombinant GATA3 was evaluated using electrophoretic mobility shift assay and heparin chromatography. Genomic location of GATA3 in MCF7 and T47D cells was assessed by chromatin immunoprecipitation coupled with next-generation sequencing (ChIP-seq).
Results: GATA3 localized in the nucleus in T47D and MCF7 cells, regardless of the mutation status. The truncated protein in MCF7 had impaired interaction with chromatin and was easily released from the nucleus. Recombinant mutant GATA3 was able to bind DNA to a lesser degree than the wild-type protein. Heterozygosity for the truncating mutation conferred protection from regulated turnover of GATA3, ERa and FOXA1 following estrogen stimulation in MCF7 cells. Thus, mutant GATA3 uncoupled protein-level regulation of master regulatory transcription factors from hormone action. Consistent with increased protein stability, ChIP-seq profiling identified greater genome-wide accumulation of GATA3 in MCF7 cells bearing the mutation, albeit with a similar distribution across the genome, comparing to T47D cells.
Conclusions: We propose that this specific, cancer-derived mutation in GATA3 deregulates physiologic protein turnover, stabilizes GATA3 binding across the genome and modulates the response of breast cancer cells to estrogen signaling.
C1 [Adomas, Aleksandra B.; Malone, Christine; Takaku, Motoki; Sims, Jennifer K.; Wade, Paul A.] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
[Grimm, Sara A.] NIEHS, Div Intramural Res, Res Triangle Pk, NC 27709 USA.
RP Wade, PA (reprint author), NIEHS, Mol Carcinogenesis Lab, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM wadep2@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences.
NR 41
TC 12
Z9 12
U1 1
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD APR 22
PY 2014
VL 14
AR 278
DI 10.1186/1471-2407-14-278
PG 14
WC Oncology
SC Oncology
GA AG2QD
UT WOS:000335260300004
PM 24758297
ER
PT J
AU Makarev, E
Gorivodsky, M
AF Makarev, Evgeny
Gorivodsky, Marat
TI Islet1 and Its Co-Factor Ldb1 Are Expressed in Quiescent Cells of Mouse
Intestinal Epithelium
SO PLOS ONE
LA English
DT Article
ID LIM-HOMEODOMAIN PROTEINS; STEM-CELL; PROGENITOR CELLS; HOMEOBOX GENES;
DIFFERENTIATION; LGR5; MARKERS; ISL1; IDENTIFICATION; REQUIREMENT
AB Islet1 belongs to Lim homeobox (Lhx) gene family which encodes transcription factors that have been conserved in evolution. They form complexes with other transcriptional regulators, among them obligatory co-factors encoded by Ldb genes. Isl1 (Islet1), Lhx and Ldb1 genes play a crucial role in organ patterning, cell fate determination and cell differentiation in both embryonic and adult tissues. In this study we analyzed expression pattern of Isl1 and its co-factor Ldb1 in small intestine. We also studied the biological role of Ldb1 in gut endoderm. Quantitative PCR analysis revealed a relatively high level of expression of Lhx1, Isl1, Isl2, Lmx1a, Ldb1 and Ldb2 mRNAs in the gut tissue as compared to the level of less abundant detectable Lmx1b mRNA. Immunohistochemical studies demonstrated a unique pattern of Ldb1 and Islet1 proteins in the crypt compartment. Ldb1 is produced at a low level in majority of crypt cells; but, its abundant expression was demonstrated for some single cells. Islet1 is also expressed in single cells of the crypt. Double staining experiments with Ldb1 and Isl1 antibodies showed that both genes are co-expressed in certain cells of the crypt. Further analysis revealed the Ldb1-expressing cells in the gut are both of endodermal and mesodermal origin. Proliferation studies using antibodies to phospho-histone H3 and Ki-67 antigens, as well as long-term BrdU labeling, showed that cells prominently expressing Ldb1/Islet1 are quiescent but do not belong to any known terminally differentiated cell lineages. They may represent a group of stem-like cells in the crypt. Further experiments by cell lineage tracing should be performed to better characterize this cell population. Functional studies of mice with Ldb1 gene ablated in gut endoderm revealed no specific role of Ldb1 in that tissue.
C1 [Makarev, Evgeny; Gorivodsky, Marat] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mammalian Mol Genet, Lab Mammalian Genes & Dev, Bethesda, MD 20892 USA.
RP Gorivodsky, M (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mammalian Mol Genet, Lab Mammalian Genes & Dev, Bethesda, MD 20892 USA.
EM lvmarat@yahoo.com
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, NIH
FX This work was supported by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, NIH. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 41
TC 2
Z9 2
U1 0
U2 0
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 APR 22
PY 2014
VL 9
IS 4
AR e95256
DI 10.1371/journal.pone.0095256
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2IS
UT WOS:000335240300034
PM 24755910
ER
PT J
AU Le Pichon, CE
Chesler, AT
AF Le Pichon, Claire E.
Chesler, Alexander T.
TI The functional and anatomical dissection of somatosensory subpopulations
using mouse genetics
SO FRONTIERS IN NEUROANATOMY
LA English
DT Review
DE somatosensation; pain; nociception; TRP channel; touch; thermodetection;
itch; sensory neuron
ID NOCICEPTIVE SENSORY NEURONS; LONG-TERM DEPRESSION; CAPSAICIN RECEPTOR;
VESICULAR GLUTAMATE; MOLECULAR-MECHANISMS; BEHAVIORAL-RESPONSES;
TRANSGENIC MICE; ITCH SENSATION; CUTANEOUS WARM; COLD SENSATION
AB The word somatosensation comes from joining the Greek word for body (soma) with a word for perception (sensation). Somatosensory neurons comprise the largest sensory system in mammals and have nerve endings coursing throughout the skin, viscera, muscle, and bone. Their cell bodies reside in a chain of ganglia adjacent to the dorsal spinal cord (the dorsal root ganglia) and at the base of the skull (the trigeminal ganglia). While the neuronal cell bodies are intermingled within the ganglia, the somatosensory system is in reality composed of numerous sub-systems, each specialized to detect distinct stimuli, such as temperature and touch. Historically, somatosensory neurons have been classified using a diverse host of anatomical and physiological parameters, such as the size of the cell body, degree of myelination, histological labeling with markers, specialization of the nerve endings, projection patterns in the spinal cord and brainstem, receptive tuning, and conduction velocity of their action potentials. While useful, the picture that emerged was one of heterogeneity, with many markers at least partially overlapping. More recently, by capitalizing on advances in molecular techniques, researchers have identified specific ion channels and sensory receptors expressed in subsets of sensory neurons. These studies have proved invaluable as they allow genetic access to small subsets of neurons for further molecular dissection. Data being generated from transgenic mice favor a model whereby an array of dedicated neurons is responsible for selectively encoding different modalities. Here we review the current knowledge of the different sensory neuron subtypes in the mouse, the markers used to study them, and the neurogenetic strategies used to define their anatomical projections and functional roles.
C1 [Le Pichon, Claire E.] NINDS, NIH, Bethesda, MD 20892 USA.
[Chesler, Alexander T.] NIH, Intramural Pain Program, Sect Sensory Cells & Circuits, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
RP Chesler, AT (reprint author), NIH, Intramural Pain Program, Sect Sensory Cells & Circuits, Natl Ctr Complementary & Alternat Med, Bldg 35A,1E450,35 Convent Dr, Bethesda, MD 20892 USA.
EM alexander.chesler@nih.gov
FU NIH Intramural program for Pain in NCCAM; NIH/NINDS
FX We would like to thank Catherine Bushnell (NIH/NCCAM), Mark Pitcher
(NIH/NCCAM), Mark Hoon (NIH/NIDCR), Alexander Jackson (University of
Connecticut), and Anna-Lisa Lucido (The Jackson Laboratory) for their
helpful comments on our manuscript. We are particular grateful to Mark
Hoon (NIH/NIDCR), Danial Cavanaugh (University of Pennsylvania), Allan
Basbaum (UCSF), and Gregory Scherrer (Stanford University) for
generously sharing their data and providing images. This work was funded
by the NIH Intramural program for Pain in NCCAM as well as NIH/NINDS.
NR 92
TC 23
Z9 23
U1 1
U2 18
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5129
J9 FRONT NEUROANAT
JI Front. Neuroanat.
PD APR 22
PY 2014
VL 8
AR 21
DI 10.3389/fnana.2014.00021
PG 18
WC Anatomy & Morphology; Neurosciences
SC Anatomy & Morphology; Neurosciences & Neurology
GA AF8VQ
UT WOS:000334994100001
PM 24795573
ER
PT J
AU Li, X
Marchant, NJ
Shaham, Y
AF Li, Xuan
Marchant, Nathan J.
Shaham, Yavin
TI Opposing roles of cotransmission of dynorphin and hypocretin on reward
and motivation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Editorial Material
ID OREXIN; NEURONS; NEUROPEPTIDES; RECEPTORS; PEPTIDES; BEHAVIOR; SYSTEMS;
STRESS
C1 [Li, Xuan; Marchant, Nathan J.; Shaham, Yavin] Natl Inst Drug Abuse, Behav Neurosci Res Branch, Intramural Res Program, Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
RP Li, X (reprint author), Natl Inst Drug Abuse, Behav Neurosci Res Branch, Intramural Res Program, Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
EM anna.li@nih.gov; yshaham@intra.nida.nih.gov
RI shaham, yavin/G-1306-2014;
OI Marchant, Nathan/0000-0001-8269-0532
FU Intramural NIH HHS
NR 17
TC 5
Z9 5
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 APR 22
PY 2014
VL 111
IS 16
BP 5765
EP 5766
DI 10.1073/pnas.1403603111
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF4OV
UT WOS:000334694000022
PM 24706899
ER
PT J
AU Alberts, B
Kirschner, MW
Tilghman, S
Varmus, H
AF Alberts, Bruce
Kirschner, Marc W.
Tilghman, Shirley
Varmus, Harold
TI Rescuing US biomedical research from its systemic flaws
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE graduate education; postdoctoral education; federal funding; peer review
AB The long-held but erroneous assumption of never-ending rapid growth in biomedical science has created an unsustainable hypercompetitive system that is discouraging even the most outstanding prospective students from entering our profession-and making it difficult for seasoned investigators to produce their best work. This is a recipe for long-term decline, and the problems cannot be solved with simplistic approaches. Instead, it is time to confront the dangers at hand and rethink some fundamental features of the US biomedical research ecosystem.
C1 [Alberts, Bruce] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94158 USA.
[Kirschner, Marc W.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
[Tilghman, Shirley] Princeton Univ, Dept Mol Biol, Princeton, NJ 08540 USA.
[Varmus, Harold] NCI, Bethesda, MD 20892 USA.
RP Tilghman, S (reprint author), Princeton Univ, Dept Mol Biol, Princeton, NJ 08540 USA.
EM smt@princeton.edu
NR 20
TC 163
Z9 164
U1 4
U2 49
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 APR 22
PY 2014
VL 111
IS 16
BP 5773
EP 5777
DI 10.1073/pnas.1404402111
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF4OV
UT WOS:000334694000025
PM 24733905
ER
PT J
AU Yu, WS
Briones, V
Lister, R
McIntosh, C
Han, YX
Lee, EY
Ren, JK
Terashima, M
Leighty, RM
Ecker, JR
Muegge, K
AF Yu, Weishi
Briones, Victorino
Lister, Ryan
McIntosh, Carl
Han, Yixing
Lee, Eunice Y.
Ren, Jianke
Terashima, Minoru
Leighty, Robert M.
Ecker, Joseph R.
Muegge, Kathrin
TI CG hypomethylation in Lsh(-/-) mouse embryonic fibroblasts is associated
with de novo H3K4me1 formation and altered cellular plasticity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID DNA METHYLATION; STEM-CELLS; HISTONE METHYLTRANSFERASE; CYTOSINE
METHYLATION; TRANSCRIPTION FACTOR; CPG METHYLATION; FAMILY-MEMBER;
BINDING-SITE; GENE; LSH
AB DNA methylation patterns are established in early embryogenesis and are critical for cellular differentiation. To investigate the role of CG methylation in potential enhancer formation, we assessed H3K4me1 modification in murine embryonic fibroblasts (MEFs) derived from the DNA methylation mutant Lsh(-/-) mice. We report here de novo formation of putative enhancer elements at CG hypomethylated sites that can be dynamically altered. We found a subset of differentially enriched H3K4me1 regions clustered at neuronal lineage genes and overlapping with known cis-regulatory elements present in brain tissue. Reprogramming of Lsh(-/-) MEFs into induced pluripotent stem (iPS) cells leads to increased neuronal lineage gene expression of premarked genes and enhanced differentiation potential of Lsh(-/-) iPS cells toward the neuronal lineage pathway compared with WT iPS cells in vitro and in vivo. The state of CG hypomethylation and H3K4me1 enrichment is partially maintained in Lsh(-/-) iPS cells. The acquisition of H3K27ac and activity of sub-cloned fragments in an enhancer reporter assay indicate functional activity of several of de novo H3K4me1-marked sequences. Our results suggest a functional link of H3K4me1 enrichment at CG hypomethylated sites, enhancer formation, and cellular plasticity.
C1 [Yu, Weishi; Briones, Victorino; Han, Yixing; Lee, Eunice Y.; Ren, Jianke; Terashima, Minoru; Muegge, Kathrin] NCI, Mouse Canc & Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Lister, Ryan; Ecker, Joseph R.] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA.
[Lister, Ryan; Ecker, Joseph R.] Salk Inst Biol Studies, Genome Anal Lab, La Jolla, CA 92037 USA.
[McIntosh, Carl] NCI, Basic Sci Program, Ctr Canc Res Genet Core, Frederick, MD 21702 USA.
[Leighty, Robert M.] NCI, Data Management Serv Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Muegge, Kathrin] Frederick Natl Lab, Leidos Biomed Res Inc, Basic Sci Program, Frederick, MD 21702 USA.
RP Muegge, K (reprint author), NCI, Mouse Canc & Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
EM Kathrin.Muegge@nih.gov
RI Lister, Ryan/B-5168-2012; Ecker, Joseph/B-9144-2008
OI Lister, Ryan/0000-0001-6637-7239; Ecker, Joseph/0000-0001-5799-5895
FU National Cancer Institute, National Institutes of Health
[HHSN26120080001E]; National Institutes of Health, National Cancer
Institute, Center for Cancer Research
FX We thank Dr. Lino Tessarolo and Dr. Michael Bustin for helpful
suggestions on the manuscript. This project has been funded in whole or
in part with federal funds from the National Cancer Institute, National
Institutes of Health (Contract HHSN26120080001E). 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 by the Intramural Research
Program of the National Institutes of Health, National Cancer Institute,
Center for Cancer Research.
NR 40
TC 7
Z9 7
U1 0
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 APR 22
PY 2014
VL 111
IS 16
BP 5890
EP 5895
DI 10.1073/pnas.1320945111
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF4OV
UT WOS:000334694000045
PM 24711395
ER
PT J
AU Park, JS
Rhau, B
Hermann, A
McNally, KA
Zhou, C
Gong, D
Weiner, OD
Conklin, BR
Onuffer, J
Lim, WA
AF Park, Jason S.
Rhau, Benjamin
Hermann, Aynur
McNally, Krista A.
Zhou, Carmen
Gong, Delquin
Weiner, Orion D.
Conklin, Bruce R.
Onuffer, James
Lim, Wendell A.
TI Synthetic control of mammalian-cell motility by engineering chemotaxis
to an orthogonal bioinert chemical signal
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE GPCR; cellular therapeutics; synthetic biology
ID TUMOR-INFILTRATING LYMPHOCYTES; RECEIVING ADOPTIVE IMMUNOTHERAPY; NEURAL
STEM-CELLS; T-CELLS; COLORECTAL-CANCER; CLINICAL-APPLICATIONS;
METASTATIC MELANOMA; EXPRESSION; MIGRATION; RECEPTOR
AB Directed migration of diverse cell types plays a critical role in biological processes ranging from development and morphogenesis to immune response, wound healing, and regeneration. However, techniques to direct, manipulate, and study cell migration in vitro and in vivo in a specific and facile manner are currently limited. We conceived of a strategy to achieve direct control over cell migration to arbitrary user-defined locations, independent of native chemotaxis receptors. Here, we show that genetic modification of cells with an engineered G protein-coupled receptor allows us to redirect their migration to a bioinert drug-like small molecule, clozapine-N-oxide (CNO). The engineered receptor and small-molecule ligand form an orthogonal pair: The receptor does not respond to native ligands, and the inert drug does not bind to native cells. CNO-responsive migration can be engineered into a variety of cell types, including neutrophils, T lymphocytes, keratinocytes, and endothelial cells. The engineered cells migrate up a gradient of the drug CNO and transmigrate through endothelial monolayers. Finally, we demonstrate that T lymphocytes modified with the engineered receptor can specifically migrate in vivo to CNO-releasing beads implanted in a live mouse. This technology provides a generalizable genetic tool to systematically perturb and control cell migration both in vitro and in vivo. In the future, this type of migration control could be a valuable module for engineering therapeutic cellular devices.
C1 [Park, Jason S.; Rhau, Benjamin; Hermann, Aynur; McNally, Krista A.; Zhou, Carmen; Conklin, Bruce R.; Onuffer, James; Lim, Wendell A.] Univ Calif San Francisco, Nanomed Dev Ctr, NIH, Dept Mol & Cellular Pharmacol, San Francisco, CA 94158 USA.
[Park, Jason S.; Rhau, Benjamin; Hermann, Aynur; McNally, Krista A.; Zhou, Carmen; Gong, Delquin; Weiner, Orion D.; Conklin, Bruce R.; Onuffer, James; Lim, Wendell A.] Univ Calif San Francisco, Nanomed Dev Ctr, NIH, Cell Prop Lab, San Francisco, CA 94158 USA.
[Park, Jason S.; Conklin, Bruce R.] Gladstone Inst Cardiovasc Dis, San Francisco, CA 94158 USA.
[Gong, Delquin; Weiner, Orion D.; Conklin, Bruce R.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA.
[Gong, Delquin; Weiner, Orion D.; Conklin, Bruce R.] Univ Calif San Francisco, Dept Biochem, San Francisco, CA 94143 USA.
[Conklin, Bruce R.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94158 USA.
[Lim, Wendell A.] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
RP Lim, WA (reprint author), Univ Calif San Francisco, Nanomed Dev Ctr, NIH, Dept Mol & Cellular Pharmacol, San Francisco, CA 94158 USA.
EM wendell.lim@ucsf.edu
RI Weiner, Orion/F-2576-2011
OI Weiner, Orion/0000-0002-1778-6543
FU National Institutes of Health (NIH) [R01 HL60664-07]; NIH Nanomedicine
Development Center [PN2EY016546]; NIH [P50 GM08187]; National Science
Foundation Synthetic Biology Engineering Research Center, NIH [R01
GM084040]; California Institute for Regenerative Medicine fellowship
[TG2-01153]; Howard Hughes Medical Institute; Gladstone Institutes
FX We thank the University of California, San Francisco (UCSF) Preclinical
Therapeutics Core Facility (especially Byron Hann, Don Hom, Donghui
Wang, and Paul Phojanakong) for mouse experimental support and helpful
discussions. We also acknowledge the 2009 UCSF International Genetically
Engineered Machine (iGEM) competition team (especially Katja Kolar, Ryan
Liang, Cathy Liu, Hansi Liu, Jackie Tam, and Eric Wong) for their work
on HL-60 neutrophil chemotaxis experiments and molecular cloning. This
work was supported by National Institutes of Health (NIH) Grant R01
HL60664-07 (to B. R. C.), pilot study funds from the Gladstone
Institutes, NIH Nanomedicine Development Center Grant PN2EY016546 (The
Cell Propulsion Laboratory: Center for Synthetic Signaling and Motility
Systems Engineering) (to W. A. L.), NIH Grant P50 GM08187 (to W. A. L.),
the National Science Foundation Synthetic Biology Engineering Research
Center, NIH Grant R01 GM084040 (to O.D.W.), a California Institute for
Regenerative Medicine fellowship (Grant TG2-01153) (to J.S.P.), and the
Howard Hughes Medical Institute (W.A.L.).
NR 55
TC 24
Z9 24
U1 3
U2 22
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 APR 22
PY 2014
VL 111
IS 16
BP 5896
EP 5901
DI 10.1073/pnas.1402087111
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF4OV
UT WOS:000334694000046
PM 24711398
ER
PT J
AU Cinghu, S
Yellaboina, S
Freudenberg, JM
Ghosh, S
Zheng, XF
Oldfield, AJ
Lackford, BL
Zaykin, DV
Hu, G
Jothi, R
AF Cinghu, Senthilkumar
Yellaboina, Sailu
Freudenberg, Johannes M.
Ghosh, Swati
Zheng, Xiaofeng
Oldfield, Andrew J.
Lackford, Brad L.
Zaykin, Dmitri V.
Hu, Guang
Jothi, Raja
TI Integrative framework for identification of key cell identity genes
uncovers determinants of ES cell identity and homeostasis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE pluripotency; RNA-binding protein; transcription; ROS; computational
biology
ID EMBRYONIC STEM-CELLS; CHROMATIN REMODELING COMPLEX; RNAI SCREEN;
SELF-RENEWAL; DNA-DAMAGE; TRANSCRIPTIONAL NETWORK; NANOG EXPRESSION;
MESSENGER-RNAS; PLURIPOTENCY; P53
AB Identification of genes associated with specific biological phenotypes is a fundamental step toward understanding the molecular basis underlying development and pathogenesis. Although RNAi-based high-throughput screens are routinely used for this task, false discovery and sensitivity remain a challenge. Here we describe a computational framework for systematic integration of published gene expression data to identify genes defining a phenotype of interest. We applied our approach to rank-order all genes based on their likelihood of determining ES cell (ESC) identity. RNAi-mediated loss-of-function experiments on top-ranked genes unearthed many novel determinants of ESC identity, thus validating the derived gene ranks to serve as a rich and valuable resource for those working to uncover novel ESC regulators. Underscoring the value of our gene ranks, functional studies of our top-hit Nucleolin (Ncl), abundant in stem and cancer cells, revealed Ncl's essential role in the maintenance of ESC homeostasis by shielding against differentiation-inducing redox imbalance-induced oxidative stress. Notably, we report a conceptually novel mechanism involving a Nucleolin-dependent Nanog-p53 bistable switch regulating the homeostatic balance between self-renewal and differentiation in ESCs. Our findings connect the dots on a previously unknown regulatory circuitry involving genes associated with traits in both ESCs and cancer and might have profound implications for understanding cell fate decisions in cancer stem cells. The proposed computational framework, by helping to prioritize and preselect candidate genes for tests using complex and expensive genetic screens, provides a powerful yet inexpensive means for identification of key cell identity genes.
C1 [Cinghu, Senthilkumar; Yellaboina, Sailu; Freudenberg, Johannes M.; Ghosh, Swati; Oldfield, Andrew J.; Jothi, Raja] NIEHS, Syst Biol Sect, NIH, Res Triangle Pk, NC 27709 USA.
[Zheng, Xiaofeng; Lackford, Brad L.; Hu, Guang] NIEHS, Stem Cell Biol Sect, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Yellaboina, Sailu; Zaykin, Dmitri V.; Jothi, Raja] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Yellaboina, Sailu] CR Rao Adv Inst Math Stat & Comp Sci, Hyderabad 500046, Andhra Pradesh, India.
RP Hu, G (reprint author), NIEHS, Stem Cell Biol Sect, Mol Carcinogenesis Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM hug4@niehs.nih.gov; jothi@mail.nih.gov
RI Jothi, Raja/G-3780-2015; Hu, Guang/E-7474-2016
OI Hu, Guang/0000-0003-0437-4723
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [1ZIAES102625,
1ZIAES10274, 1ZIAES101866]; Department of Science and Technology, India
(DST-CMS GoI Project) [SR/S4/MS: 516/07]
FX We thank K. Adelman and P. A. Wade for valuable suggestions and K.
Adelman, T. K. Archer, A. Barski, M. B. Fessler, T. A. Kunkel, L. Ho,
and P. A. Wade for critical comments on the manuscript. We thank H.
Kinyamu and J. Yang for guidance on RNA-IP experiments and NIEHS
Microarray, Confocal Microscopy, Flow Cytometry, Viral, and Protein
cores for support. Nanog and p21 luciferase vectors are kind gifts from
J. Huang (National Cancer Institute) and M. Resnick (National Institute
of Environmental Health Sciences), respectively. This work was supported
by Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences Grants 1ZIAES102625
(to R.J.), 1ZIAES10274 (to G.H.), and 1ZIAES101866 (to D.V.Z.), and the
Department of Science and Technology, India (DST-CMS GoI Project
SR/S4/MS: 516/07, to S.Y.).
NR 64
TC 7
Z9 7
U1 0
U2 13
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 APR 22
PY 2014
VL 111
IS 16
BP E1581
EP E1590
DI 10.1073/pnas.1318598111
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF4OV
UT WOS:000334694000007
PM 24711389
ER
PT J
AU Al-Herz, W
Bousfiha, A
Casanova, JL
Chatila, T
Conley, ME
Cunningham-Rundles, C
Etzioni, A
Franco, JL
Gaspar, HB
Holland, SM
Klein, C
Nonoyama, S
Ochs, HD
Oksenhendler, E
Picard, C
Puck, JM
Sullivan, K
Tang, MLK
AF Al-Herz, Waleed
Bousfiha, Aziz
Casanova, Jean-Laurent
Chatila, Talal
Conley, Mary Ellen
Cunningham-Rundles, Charlotte
Etzioni, Amos
Franco, Jose Luis
Gaspar, H. Bobby
Holland, Steven M.
Klein, Christoph
Nonoyama, Shigeaki
Ochs, Hans D.
Oksenhendler, Erik
Picard, Capucine
Puck, Jennifer M.
Sullivan, Kate
Tang, Mimi L. K.
TI Primary immunodeficiency diseases: an update on the classification from
the International Union of Immunological Societies Expert Committee for
Primary Immunodeficiency
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE primary immunodeficiencies; IUIS; classification; genetic defects;
genotype
AB We report the updated classification of primary immunodeficiencies (PIDs) compiled by the Expert Committee of the International Union of Immunological Societies. In comparison to the previous version, more than 30 new gene defects are reported in this updated version. In addition, we have added a table of acquired defects that are phenocopies of PIDs. For each disorder, the key clinical and laboratory features are provided. This classification is the most up-to-date catalog of all known PIDs and acts as a current reference of the knowledge of these conditions and is an important aid for the molecular diagnosis of patients with these rare diseases.
C1 [Al-Herz, Waleed] Kuwait Univ, Dept Pediat, Kuwait, Kuwait.
[Al-Herz, Waleed] Al Sabah Hosp, Dept Pediat, Allergy & Clin Immunol Unit, Kuwait, Kuwait.
[Bousfiha, Aziz] King Hassan II Univ, Ibn Rochd Med Sch, Casablanca Childrens Hosp, Clin Immunol Unit, Casablanca, Morocco.
[Casanova, Jean-Laurent; Conley, Mary Ellen] Rockefeller Univ, Rockefeller Branch, St Giles Lab Human Genet Infect Dis, New York, NY 10021 USA.
[Casanova, Jean-Laurent; Picard, Capucine] Univ Paris 05, Lab Human Genet Infect Dis, Necker Med Sch, Necker Branch,INSERM,Imagine Inst,UMR1163, Paris, France.
[Chatila, Talal] Childrens Hosp Boston, Div Immunol, Boston, MA USA.
[Cunningham-Rundles, Charlotte] Mt Sinai Sch Med, Dept Med & Pediat, New York, NY USA.
[Etzioni, Amos] Technion Israel Inst Technol, Meyer Childrens Hosp, Haifa, Israel.
[Franco, Jose Luis] Univ Antioquia, Grp Primary Immunodeficiencies, Medellin, Colombia.
[Gaspar, H. Bobby] UCL Inst Child Hlth, London WC1N 1EH, England.
[Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Klein, Christoph] Univ Munich, Dr von Hauner Childrens Hosp, Munich, Germany.
[Nonoyama, Shigeaki] Natl Def Med Coll, Dept Pediat, Saitama, Japan.
[Ochs, Hans D.] Univ Washington, Dept Pediat, Seattle Childrens Res Inst, Seattle, WA 98195 USA.
[Oksenhendler, Erik] Hop St Louis, AP HP, Dept Clin Immunol, Paris, France.
[Oksenhendler, Erik] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
[Picard, Capucine] Hop Necker Enfants Malad, AP HP, CEDI, Paris, France.
[Puck, Jennifer M.] Univ Calif San Francisco, Dept Pediat, UCSF Benioff Childrens Hosp, San Francisco, CA USA.
[Sullivan, Kate] Childrens Hosp Philadelphia, Dept Pediat, Div Allergy Immunol, Philadelphia, PA 19104 USA.
[Tang, Mimi L. K.] Murdoch Childrens Res Inst, Melbourne, Vic, Australia.
[Tang, Mimi L. K.] Univ Melbourne, Dept Paediat, Melbourne, Vic, Australia.
[Tang, Mimi L. K.] Royal Childrens Hosp, Dept Allergy & Immunol, Melbourne, Vic, Australia.
RP Gaspar, HB (reprint author), UCL Inst Child Hlth, Mol Immunol Unit, 30 Guilford St, London WC1N 1EH, England.
EM h.gaspar@ucl.ac.uk
OI Picard, Capucine/0000-0001-8788-5056
FU NIAID NIH HHS [P01 AI061093, R01 AI105776, R18 AI048693]
NR 0
TC 195
Z9 205
U1 1
U2 14
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD APR 22
PY 2014
VL 5
AR 162
DI 10.3389/fimmu.2014.00162
PG 33
WC Immunology
SC Immunology
GA CH6GK
UT WOS:000354134300001
PM 24795713
ER
PT J
AU Henry, SC
Schmidt, EA
Fessler, MB
Taylor, GA
AF Henry, Stanley C.
Schmidt, Elyse A.
Fessler, Michael B.
Taylor, Gregory A.
TI Palmitoylation of the Immunity Related GTPase, Irgm1: Impact on Membrane
Localization and Ability to Promote Mitochondrial Fission
SO PLOS ONE
LA English
DT Article
ID CELL-AUTONOMOUS IMMUNITY; TOXOPLASMA-GONDII; PROTEIN PALMITOYLATION;
RESISTANCE MECHANISM; HOST-RESISTANCE; MOUSE CELLS; LRG-47; MACROPHAGES;
AUTOPHAGY; MICE
AB The Immunity-Related GTPases (IRG) are a family of large GTPases that mediate innate immune responses. Irgm1 is particularly critical for immunity to bacteria and protozoa, and for inflammatory homeostasis in the intestine. Although precise functions for Irgm1 have not been identified, prior studies have suggested roles in autophagy/mitophagy, phagosome remodeling, cell motility, and regulating the activity of other IRG proteins. These functions ostensibly hinge on the ability of Irgm1 to localize to intracellular membranes, such as those of the Golgi apparatus and mitochondria. Previously, it has been shown that an amphipathic helix, the alpha K helix, in the C-terminal portion of the protein partially mediates membrane binding. However, in absence of alpha K, there is still substantial binding of Irgm1 to cellular membranes, suggesting the presence of other membrane binding motifs. In the current work, an additional membrane localization motif was found in the form of palmitoylation at a cluster of cysteines near the alpha K. An Irgm1 mutant possessing alanine to cysteine substitutions at these amino acids demonstrated little residual palmitoylation, yet it displayed only a small decrease in localization to the Golgi and mitochondria. In contrast, a mutant containing the palmitoylation mutations in combination with mutations disrupting the amphipathic character of the alpha K displayed a complete loss of apparent localization to the Golgi and mitochondria, as well as an overall loss of association with cellular membranes in general. Additionally, Irgm1 was found to promote mitochondrial fission, and this function was undermined in Irgm1 mutants lacking the palmitoylation domain, and to a greater extent in those lacking the alpha K, or the alpha K and palmitoylation domains combined. Our data suggest that palmitoylation together with the alpha K helix firmly anchor Irgm1 in the Golgi and mitochondria, thus facilitating function of the protein.
C1 [Henry, Stanley C.; Taylor, Gregory A.] VA Med Ctr, Geriatr Res Educ & Clin Ctr, Durham, NC 27705 USA.
[Schmidt, Elyse A.; Taylor, Gregory A.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Schmidt, Elyse A.; Taylor, Gregory A.] Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC USA.
[Schmidt, Elyse A.; Taylor, Gregory A.] Duke Univ, Med Ctr, Dept Immunol, Div Geriatr, Durham, NC USA.
[Schmidt, Elyse A.; Taylor, Gregory A.] Duke Univ, Med Ctr, Ctr Study Aging & Human Dev, Durham, NC 27710 USA.
[Fessler, Michael B.] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
RP Taylor, GA (reprint author), VA Med Ctr, Geriatr Res Educ & Clin Ctr, Durham, NC 27705 USA.
EM gregory.taylor@duke.edu
FU National Institutes of Health [AI57831]; VA Merit Review grant; National
Institute of Environmental Health Sciences, NIH [Z01 ES102005]
FX This work was supported by National Institutes of Health grant AI57831
(GAT), a VA Merit Review grant (GAT), and by the Intramural Research
Program of the National Institute of Environmental Health Sciences, NIH,
Z01 ES102005 (MBF). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 44
TC 9
Z9 9
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 APR 21
PY 2014
VL 9
IS 4
AR e95021
DI 10.1371/journal.pone.0095021
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2DX
UT WOS:000335227400024
PM 24751652
ER
PT J
AU Kim, MH
Rebbert, ML
Ro, H
Won, M
Dawid, IB
AF Kim, Mi Ha
Rebbert, Martha L.
Ro, Hyunju
Won, Minho
Dawid, Igor B.
TI Cell Adhesion in Zebrafish Embryos Is Modulated by March8
SO PLOS ONE
LA English
DT Article
ID E3 UBIQUITIN LIGASE; E-CADHERIN; CLASS-II; XENOPUS EMBRYOS;
DOWN-REGULATION; B-CELLS; C-MIR; EXPRESSION; MOVEMENTS; PROTEIN
AB March8 is a member of a family of transmembrane E3 ubiquitin ligases that have been studied mostly for their role in the immune system. We find that March8 is expressed in the zebrafish egg and early embryo, suggesting a role in development. Both knock-down and overexpression of March8 leads to abnormal development. The phenotype of zebrafish embryos and Xenopus animal explants overexpressing March8 implicates impairment of cell adhesion as a cause of the effect. In zebrafish embryos and in cultured cells, overexpression of March8 leads to a reduction in the surface levels of E-cadherin, a major cell-cell adhesion molecule. Experiments in cell culture further show that E-cadherin can be ubiquitinated by March8. On the basis of these observations we suggest that March8 functions in the embryo to modulate the strength of cell adhesion by regulating the localization of E-cadherin.
C1 [Kim, Mi Ha; Rebbert, Martha L.; Ro, Hyunju; Won, Minho; Dawid, Igor B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Dawid, IB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
EM idawid@nih.gov
FU National Institute for Child Health and Human Development
FX This research has been funded by the intramural research program of the
National Institute for Child Health and Human Development. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 47
TC 1
Z9 1
U1 1
U2 2
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 APR 21
PY 2014
VL 9
IS 4
AR e94873
DI 10.1371/journal.pone.0094873
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2DX
UT WOS:000335227400020
PM 24752240
ER
PT J
AU Yu, XZ
Strub, MP
Barnard, TJ
Noinaj, N
Piszczek, G
Buchanan, SK
Taraska, JW
AF Yu, Xiaozhen
Strub, Marie-Paule
Barnard, Travis J.
Noinaj, Nicholas
Piszczek, Grzegorz
Buchanan, Susan K.
Taraska, Justin W.
TI An Engineered Palette of Metal Ion Quenchable Fluorescent Proteins
SO PLOS ONE
LA English
DT Article
ID ENERGY-TRANSFER; CALCIUM INDICATORS; BINDING PROTEINS; STRUCTURAL BASIS;
ZINC; PREDICTION; CHEMISTRY; SITES; CELLS; FRET
AB Many fluorescent proteins have been created to act as genetically encoded biosensors. With these sensors, changes in fluorescence report on chemical states in living cells. Transition metal ions such as copper, nickel, and zinc are crucial in many physiological and pathophysiological pathways. Here, we engineered a spectral series of optimized transition metal ion-binding fluorescent proteins that respond to metals with large changes in fluorescence intensity. These proteins can act as metal biosensors or imaging probes whose fluorescence can be tuned by metals. Each protein is uniquely modulated by four different metals (Cu2+, Ni2+, Co2+, and Zn2+). Crystallography revealed the geometry and location of metal binding to the engineered sites. When attached to the extracellular terminal of a membrane protein VAMP2, dimeric pairs of the sensors could be used in cells as ratiometric probes for transition metal ions. Thus, these engineered fluorescent proteins act as sensitive transition metal ion-responsive genetically encoded probes that span the visible spectrum.
C1 [Yu, Xiaozhen; Strub, Marie-Paule; Taraska, Justin W.] NHLBI, Lab Mol Biophys, NIH, Bethesda, MD 20892 USA.
[Barnard, Travis J.; Noinaj, Nicholas; Buchanan, Susan K.] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Piszczek, Grzegorz] NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
RP Taraska, JW (reprint author), NHLBI, Lab Mol Biophys, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM justin.taraska@nih.gov
RI Taraska, Justin/H-8876-2016
OI Taraska, Justin/0000-0001-5355-9535
FU National Heart Lung and Blood Institute; National Institute Diabetes and
Digestive and Kidney Diseases; National Cancer Institute [Y1-CO1020];
National Institute of General Medical Sciences [Y1-GM-1104]; U.S.
Department of Energy, Basic Energy Sciences, Office of Science [DE-
AC02- 06CH11357]
FX J.W.T. is supported by the intramural research program of the National
Heart Lung and Blood Institute, and S.K.B. is supported by the National
Institute Diabetes and Digestive and Kidney Diseases. GM/CA at the APS
has been funded in whole or in part with Federal funds from the National
Cancer Institute (Y1-CO1020) and the National Institute of General
Medical Sciences (Y1-GM-1104). Use of the Advanced Photon Source was
supported by the U. S. Department of Energy, Basic Energy Sciences,
Office of Science, under contract DE- AC02- 06CH11357. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 51
TC 4
Z9 4
U1 3
U2 18
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 APR 21
PY 2014
VL 9
IS 4
AR e95808
DI 10.1371/journal.pone.0095808
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2DX
UT WOS:000335227400133
PM 24752441
ER
PT J
AU Brzeska, H
Pridham, K
Chery, G
Titus, MA
Korn, ED
AF Brzeska, Hanna
Pridham, Kevin
Chery, Godefroy
Titus, Margaret A.
Korn, Edward D.
TI The Association of Myosin IB with Actin Waves in Dictyostelium Requires
Both the Plasma Membrane-Binding Site and Actin-Binding Region in the
Myosin Tail
SO PLOS ONE
LA English
DT Article
ID ACANTHAMOEBA MYOSIN; FLUORESCENT PROTEIN; CELL LOCOMOTION; F-ACTIN;
DISCOIDEUM; DYNAMICS; PHOSPHORYLATION; MUTANTS; TRANSFORMATION;
ORGANIZATION
AB F-actin structures and their distribution are important determinants of the dynamic shapes and functions of eukaryotic cells. Actin waves are F-actin formations that move along the ventral cell membrane driven by actin polymerization. Dictyostelium myosin IB is associated with actin waves but its role in the wave is unknown. Myosin IB is a monomeric, non-filamentous myosin with a globular head that binds to F-actin and has motor activity, and a non-helical tail comprising a basic region, a glycine-proline-glutamine-rich region and an SH3-domain. The basic region binds to acidic phospholipids in the plasma membrane through a short basic-hydrophobic site and the Gly-Pro-Gln region binds F-actin. In the current work we found that both the basic-hydrophobic site in the basic region and the Gly-Pro-Gln region of the tail are required for the association of myosin IB with actin waves. This is the first evidence that the Gly-Pro-Gln region is required for localization of myosin IB to a specific actin structure in situ. The head is not required for myosin IB association with actin waves but binding of the head to F-actin strengthens the association of myosin IB with waves and stabilizes waves. Neither the SH3-domain nor motor activity is required for association of myosin IB with actin waves. We conclude that myosin IB contributes to anchoring actin waves to the plasma membranes by binding of the basic-hydrophobic site to acidic phospholipids in the plasma membrane and binding of the Gly-Pro-Gln region to F-actin in the wave.
C1 [Brzeska, Hanna; Pridham, Kevin; Chery, Godefroy; Korn, Edward D.] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Titus, Margaret A.] Univ Minnesota, Dept Genet Cell Biol & Dev, Minneapolis, MN USA.
RP Brzeska, H (reprint author), NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
EM brzeskah@mail.nih.gov
FU National Institutes of Health (NIH) intramural program
FX Research was funded by National Institutes of Health (NIH) intramural
program. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 55
TC 5
Z9 5
U1 0
U2 6
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 APR 18
PY 2014
VL 9
IS 4
AR e94306
DI 10.1371/journal.pone.0094306
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2DP
UT WOS:000335226500023
PM 24747353
ER
PT J
AU Pawar, SA
Shao, LJ
Chang, JH
Wang, WZ
Pathak, R
Zhu, XY
Wang, JR
Hendrickson, H
Boerma, M
Sterneck, E
Zhou, DH
Hauer-Jensen, M
AF Pawar, Snehalata A.
Shao, Lijian
Chang, Jianhui
Wang, Wenze
Pathak, Rupak
Zhu, Xiaoyan
Wang, Junru
Hendrickson, Howard
Boerma, Marjan
Sterneck, Esta
Zhou, Daohong
Hauer-Jensen, Martin
TI C/EBP delta Deficiency Sensitizes Mice to Ionizing Radiation-Induced
Hematopoietic and Intestinal Injury
SO PLOS ONE
LA English
DT Article
ID BINDING-PROTEIN-DELTA; BONE-MARROW INJURY; TOTAL-BODY IRRADIATION;
DNA-DAMAGE RESPONSE; STEM-CELLS; IN-VIVO; GASTROINTESTINAL-SYNDROME;
SELECTIVELY PROTECTS; PLASMA CITRULLINE; CELLULAR-RESPONSE
AB Knowledge of the mechanisms involved in the radiation response is critical for developing interventions to mitigate radiation-induced injury to normal tissues. Exposure to radiation leads to increased oxidative stress, DNA-damage, genomic instability and inflammation. The transcription factor CCAAT/enhancer binding protein delta (Cebpd; C/EBP delta is implicated in regulation of these same processes, but its role in radiation response is not known. We investigated the role of C/EBP delta in radiation-induced hematopoietic and intestinal injury using a Cebpd knockout mouse model. Cebpd-/- mice showed increased lethality at 7.4 and 8.5 Gy total-body irradiation (TBI), compared to Cebpd+/+ mice. Two weeks after a 6 Gy dose of TBI, Cebpd-/- mice showed decreased recovery of white blood cells, neutrophils, platelets, myeloid cells and bone marrow mononuclear cells, decreased colony-forming ability of bone marrow progenitor cells, and increased apoptosis of hematopoietic progenitor and stem cells compared to Cebpd+/+ controls. Cebpd-/- mice exhibited a significant dose-dependent decrease in intestinal crypt survival and in plasma citrulline levels compared to Cebpd+/+ mice after exposure to radiation. This was accompanied by significantly decreased expression of gamma-H2AX in Cebpd-/- intestinal crypts and villi at 1 h post-TBI, increased mitotic index at 24 h post-TBI, and increase in apoptosis in intestinal crypts and stromal cells of Cebpd-/- compared to Cebpd+/+ mice at 4 h post-irradiation. This study uncovers a novel biological function for C/EBP delta in promoting the response to radiation-induced DNA-damage and in protecting hematopoietic and intestinal tissues from radiation-induced injury.
C1 [Pawar, Snehalata A.; Shao, Lijian; Chang, Jianhui; Wang, Wenze; Pathak, Rupak; Zhu, Xiaoyan; Wang, Junru; Boerma, Marjan; Zhou, Daohong; Hauer-Jensen, Martin] Univ Arkansas Med Sci, Div Radiat Hlth, Dept Pharmaceut Sci, Little Rock, AR 72205 USA.
[Hendrickson, Howard] Univ Arkansas Med Sci, Dept Pharmaceut Sci, Little Rock, AR 72205 USA.
[Sterneck, Esta] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
[Hauer-Jensen, Martin] Cent Arkansas Vet Healthcare Syst, Surg Serv, Little Rock, AR USA.
RP Pawar, SA (reprint author), Univ Arkansas Med Sci, Div Radiat Hlth, Dept Pharmaceut Sci, Little Rock, AR 72205 USA.
EM SAPawar@uams.edu
FU Arkansas Bioscience Institute; UAMS Medical Research Endowment Funds;
Center for Microbial Pathogenesis and Host Inflammatory Responses COBRE
Grant [1P20GM103625]; Edward P. Evan's Foundation; NIH, National Cancer
Institute; Veterans Administration
FX Grant support by Arkansas Bioscience Institute (SAP), UAMS Medical
Research Endowment Funds (SAP), Center for Microbial Pathogenesis and
Host Inflammatory Responses COBRE Grant 1P20GM103625 (SAP) and the
Edward P. Evan's Foundation (DZ, MHJ), Veterans Administration (MHJ) is
gratefully acknowledged. ES is supported by the Intramural Research
Program of the NIH, National Cancer Institute. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 61
TC 4
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U1 2
U2 6
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 APR 18
PY 2014
VL 9
IS 4
AR e94967
DI 10.1371/journal.pone.0094967
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2DP
UT WOS:000335226500047
PM 24747529
ER
PT J
AU Szabova, L
Bupp, S
Kamal, M
Householder, DB
Hernandez, L
Schlomer, JJ
Baran, ML
Yi, M
Stephens, RM
Annunziata, CM
Martin, PL
Van Dyke, TA
Ohler, ZW
Difilippantonio, S
AF Szabova, Ludmila
Bupp, Sujata
Kamal, Muhaymin
Householder, Deborah B.
Hernandez, Lidia
Schlomer, Jerome J.
Baran, Maureen L.
Yi, Ming
Stephens, Robert M.
Annunziata, Christina M.
Martin, Philip L.
Van Dyke, Terry A.
Ohler, Zoe Weaver
Difilippantonio, Simone
TI Pathway-Specific Engineered Mouse Allograft Models Functionally
Recapitulate Human Serous Epithelial Ovarian Cancer
SO PLOS ONE
LA English
DT Article
ID ADP-RIBOSE POLYMERASE; MAMMARY-TUMORS; CELL-LINES; POLY(ADP-RIBOSE)
POLYMERASE-1; BREAST-CANCER; BRCA1; CHEMOTHERAPY; INHIBITOR; MUTATIONS;
THERAPY
AB The high mortality rate from ovarian cancers can be attributed to late-stage diagnosis and lack of effective treatment. Despite enormous effort to develop better targeted therapies, platinum-based chemotherapy still remains the standard of care for ovarian cancer patients, and resistance occurs at a high rate. One of the rate limiting factors for translation of new drug discoveries into clinical treatments has been the lack of suitable preclinical cancer models with high predictive value. We previously generated genetically engineered mouse (GEM) models based on perturbation of Tp53 and Rb with or without Brca1 or Brca2 that develop serous epithelial ovarian cancer (SEOC) closely resembling the human disease on histologic and molecular levels. Here, we describe an adaptation of these GEM models to orthotopic allografts that uniformly develop tumors with short latency and are ideally suited for routine preclinical studies. Ovarian tumors deficient in Brca1 respond to treatment with cisplatin and olaparib, a PARP inhibitor, whereas Brca1-wild type tumors are non-responsive to treatment, recapitulating the relative sensitivities observed in patients. These mouse models provide the opportunity for evaluation of effective therapeutics, including prediction of differential responses in Brca1-wild type and Brca1-deficient tumors and development of relevant biomarkers.
C1 [Szabova, Ludmila; Bupp, Sujata; Kamal, Muhaymin; Householder, Deborah B.; Schlomer, Jerome J.; Baran, Maureen L.; Martin, Philip L.; Van Dyke, Terry A.; Ohler, Zoe Weaver; Difilippantonio, Simone] Leidos Biomedical Res Inc, Frederick Natl Lab Canc Res, Ctr Adv Preclin Res, Frederick, MD USA.
[Hernandez, Lidia; Annunziata, Christina M.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Yi, Ming; Stephens, Robert M.] Leidos Biomedical Res Inc, Frederick Natl Lab Canc Res, Adv Biomed Comp Ctr, Frederick, MD USA.
[Van Dyke, Terry A.] Frederick Natl Lab Canc Res, Mouse Canc Genet Program, Frederick, MD USA.
RP Szabova, L (reprint author), Leidos Biomedical Res Inc, Frederick Natl Lab Canc Res, Ctr Adv Preclin Res, Frederick, MD USA.
EM lszabova@mail.nih.gov
RI Annunziata, Christina/L-3219-2016
OI Annunziata, Christina/0000-0003-2033-6532
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This project has been funded in whole with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
number 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 U.S. Government. The
funder had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 47
TC 3
Z9 3
U1 0
U2 2
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 APR 18
PY 2014
VL 9
IS 4
AR e95649
DI 10.1371/journal.pone.0095649
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG2DP
UT WOS:000335226500133
PM 24748377
ER
PT J
AU Fields, RD
AF Fields, R. Douglas
TI Myelin-More than Insulation
SO SCIENCE
LA English
DT Editorial Material
ID CORTEX
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Fields, RD (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bldg 35,Room 2A211,MSC 3713, Bethesda, MD 20892 USA.
EM fieldsd@mail.nih.gov
FU Intramural NIH HHS [Z01 HD000713-13]
NR 12
TC 7
Z9 7
U1 0
U2 18
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD APR 18
PY 2014
VL 344
IS 6181
BP 264
EP 266
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AF1LD
UT WOS:000334474500024
PM 24744365
ER
PT J
AU Mailankody, S
Prasad, V
AF Mailankody, Sham
Prasad, Vinay
TI Comparative Effectiveness Questions in Oncology
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID INCREASED SURVIVAL; PROSTATE-CANCER
C1 [Mailankody, Sham; Prasad, Vinay] NCI, Med Oncol Serv, Bethesda, MD 20892 USA.
RP Mailankody, S (reprint author), NCI, Med Oncol Serv, Bethesda, MD 20892 USA.
NR 5
TC 15
Z9 15
U1 0
U2 5
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 17
PY 2014
VL 370
IS 16
BP 1478
EP 1481
DI 10.1056/NEJMp1400104
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA AF3HE
UT WOS:000334601600004
PM 24738667
ER
PT J
AU Hoofnagle, JH
Sherker, AH
AF Hoofnagle, Jay H.
Sherker, Averell H.
TI Therapy for Hepatitis C - The Costs of Success
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID UNITED-STATES; INTERFERON; INFECTION
AB Welcomed and exciting results from three large, controlled trials of different regimens of oral antiviral agents for chronic hepatitis C, genotype 1, have now been published in the Journal.(1)-(3) The regimens all included the combination of ledipasvir and sofosbuvir, two new direct-acting antiviral agents with potent activity against hepatitis C virus (HCV). The two drugs were given as a single tablet once daily for 8, 12, or 24 weeks, with or without ribavirin. The results were consistent and striking: the various regimens yielded rates of sustained virologic response of 93% to 99%. The combination of ledipasvir and sofosbuvir ...
C1 [Hoofnagle, Jay H.; Sherker, Averell H.] NIDDK, Liver Dis Res Branch, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
RP Hoofnagle, JH (reprint author), NIDDK, Liver Dis Res Branch, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
NR 13
TC 75
Z9 76
U1 0
U2 4
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 17
PY 2014
VL 370
IS 16
BP 1552
EP 1553
DI 10.1056/NEJMe1401508
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA AF3HE
UT WOS:000334601600013
PM 24725236
ER
PT J
AU Klauer, SG
Guo, F
Simons-Morton, BG
AF Klauer, Sheila G.
Guo, Feng
Simons-Morton, Bruce G.
TI Distracted Driving and Crash Risk REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Klauer, Sheila G.; Guo, Feng] Virginia Tech, Transportat Inst, Blacksburg, VA 24061 USA.
[Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Klauer, SG (reprint author), Virginia Tech, Transportat Inst, Blacksburg, VA 24061 USA.
EM cklauer@vtti.vt.edu
NR 3
TC 0
Z9 0
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
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 17
PY 2014
VL 370
IS 16
BP 1565
EP 1566
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA AF3HE
UT WOS:000334601600026
PM 24738680
ER
PT J
AU Savage, SA
AF Savage, Sharon A.
TI Genomic clues to ethnic differences in ALL
SO BLOOD
LA English
DT Editorial Material
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHILDHOOD LEUKEMIA; KIR GENES; CHILDREN;
SURVIVAL
C1 NCI, Bethesda, MD 20892 USA.
RP Savage, SA (reprint author), NCI, Bethesda, MD 20892 USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 10
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 17
PY 2014
VL 123
IS 16
BP 2440
EP 2442
DI 10.1182/blood-2014-02-557330
PG 5
WC Hematology
SC Hematology
GA AH1PX
UT WOS:000335894500003
PM 24744246
ER
PT J
AU Wayne, AS
FitzGerald, DJ
Kreitman, RJ
Pastan, I
AF Wayne, Alan S.
FitzGerald, David J.
Kreitman, Robert J.
Pastan, Ira
TI Immunotoxins for leukemia
SO BLOOD
LA English
DT Review
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; HAIRY-CELL LEUKEMIA; CHRONIC
LYMPHOCYTIC-LEUKEMIA; PHASE-I TRIAL; RECOMBINANT IMMUNOTOXIN; ANTI-CD22
IMMUNOTOXIN; HEMATOLOGIC MALIGNANCIES; PSEUDOMONAS EXOTOXIN; VASCULAR
LEAK; MOXETUMOMAB PASUDOTOX
AB Unconjugated monoclonal antibodies that target hematopoietic differentiation antigens have been developed to treat hematologic malignancies. Although some of these have activity against chronic lymphocytic leukemia and hairy cell leukemia, in general, monoclonal antibodies have limited efficacy as single agents in the treatment of leukemia. To increase their potency, the binding domains of monoclonal antibodies can be attached to protein toxins. Such compounds, termed immunotoxins, are delivered to the interior of leukemia cells based on antibody specificity for cell surface target antigens. Recombinant immunotoxins have been shown to be highly cytotoxic to leukemic blasts in vitro, in xenograft model systems, and in early-phase clinical trials in humans. These agents will likely play an increasing role in the treatment of leukemia.
C1 [Wayne, Alan S.] Univ So Calif, Keck Sch Med,Norris Comprehens Canc Ctr, Div Hematol Oncol & Blood & Marrow Transplantat, Childrens Ctr Canc & Blood Dis,Childrens Hosp Los, Los Angeles, CA 90033 USA.
[Wayne, Alan S.; FitzGerald, David J.; Kreitman, Robert J.; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Wayne, AS (reprint author), Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, 4650 Sunset Blvd,Mailstop 54, Los Angeles, CA 90027 USA.
EM awayne@chla.usc.edu
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research; National Cancer Institute; MedImmune, LLC.
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health, National Cancer Institute, Center for
Cancer Research. Research support for development of some of the
immunotoxins described was provided through a Cooperative Research and
Development Agreement between the National Cancer Institute and
MedImmune, LLC.
NR 77
TC 43
Z9 43
U1 1
U2 16
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 17
PY 2014
VL 123
IS 16
BP 2470
EP 2477
DI 10.1182/blood-2014-01-492256
PG 8
WC Hematology
SC Hematology
GA AH1PX
UT WOS:000335894500012
PM 24578503
ER
PT J
AU Bild, DE
McClelland, R
Kaufman, JD
Blumenthal, R
Burke, GL
Carr, JJ
Post, WS
Register, TC
Shea, S
Szklo, M
AF Bild, Diane E.
McClelland, Robyn
Kaufman, Joel D.
Blumenthal, Roger
Burke, Gregory L.
Carr, J. Jeffrey
Post, Wendy S.
Register, Thomas C.
Shea, Steven
Szklo, Moyses
TI Ten-Year Trends in Coronary Calcification in Individuals without
Clinical Cardiovascular Disease in the Multi-Ethnic Study of
Atherosclerosis
SO PLOS ONE
LA English
DT Article
ID DENSITY-LIPOPROTEIN-CHOLESTEROL; ARTERY RISK DEVELOPMENT; HEART-DISEASE;
YOUNG-ADULTS; MYOCARDIAL-INFARCTION; UNITED-STATES; CARDIA; REGRESSION;
CALCIUM; MESA
AB Background: Coronary heart disease (CHD) incidence has declined significantly in the US, as have levels of major coronary risk factors, including LDL-cholesterol, hypertension and smoking, but whether trends in subclinical atherosclerosis mirror these trends is not known.
Methods and Findings: To describe recent secular trends in subclinical atherosclerosis as measured by serial evaluations of coronary artery calcification (CAC) prevalence in a population over 10 years, we measured CAC using computed tomography (CT) and CHD risk factors in five serial cross-sectional samples of men and women from four race/ethnic groups, aged 55-84 and without clinical cardiovascular disease, who were members of Multi-Ethnic Study of Atherosclerosis (MESA) cohort from 2000 to 2012. Sample sizes ranged from 1062 to 4837. After adjusting for age, gender, and CT scanner, the prevalence of CAC increased across exams among African Americans, whose prevalence of CAC was 52.4% in 2000-02, 50.4% in 2003-04, 60.0% is 2005-06, 57.4% in 2007-08, and 61.3% in 2010-12 (p for trend <0.001). The trend was strongest among African Americans aged 55-64 [prevalence ratio for 2010-12 vs. 2000-02, 1.59 (95% confidence interval 1.06, 2.39); p = 0.005 for trend across exams]. There were no consistent trends in any other ethnic group. Risk factors generally improved in the cohort, and adjustment for risk factors did not change trends in CAC prevalence.
Conclusions: There was a significant secular trend towards increased prevalence of CAC over 10 years among African Americans and no change in three other ethnic groups. Trends did not reflect concurrent general improvement in risk factors. The trend towards a higher prevalence of CAC in African Americans suggests that CHD risk in this population is not improving relative to other groups.
C1 [Bild, Diane E.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[McClelland, Robyn] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Kaufman, Joel D.] Univ Washington, Dept Environm & Occupat Hlth Sci, Seattle, WA 98195 USA.
[Blumenthal, Roger; Post, Wendy S.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Post, Wendy S.; Szklo, Moyses] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Burke, Gregory L.; Register, Thomas C.] Wake Forest Sch Med, Winston Salem, NC USA.
[Carr, J. Jeffrey] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
[Shea, Steven] Columbia Univ, New York, NY USA.
RP Bild, DE (reprint author), NHLBI, Div Cardiovasc Sci, Bldg 10, Bethesda, MD 20892 USA.
EM dbild@pcori.org
RI Kaufman, Joel/B-5761-2008; Carr, John/A-1938-2012
OI Kaufman, Joel/0000-0003-4174-9037; Carr, John/0000-0002-4398-8237
FU NCATS NIH HHS [UL1-TR-000040]; NCRR NIH HHS [UL1-RR-025005]
NR 33
TC 6
Z9 6
U1 0
U2 5
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 APR 17
PY 2014
VL 9
IS 4
AR e94916
DI 10.1371/journal.pone.0094916
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG3IK
UT WOS:000335309100050
PM 24743658
ER
PT J
AU Guo, XG
Park, Y
Freedman, ND
Sinha, R
Hollenbeck, AR
Blair, A
Chen, HL
AF Guo, Xuguang
Park, Yikyung
Freedman, Neal D.
Sinha, Rashmi
Hollenbeck, Albert R.
Blair, Aaron
Chen, Honglei
TI Sweetened Beverages, Coffee, and Tea and Depression Risk among Older US
Adults
SO PLOS ONE
LA English
DT Article
ID HEALTH-AMERICAN-ASSOCIATION; RETIRED-PERSONS DIET; CAFFEINE INTAKE;
DECAFFEINATED COFFEE; NATIONAL-INSTITUTES; PARKINSON-DISEASE;
MENTAL-HEALTH; WEIGHT-GAIN; SOFT DRINK; CONSUMPTION
AB Sweetened beverages, coffee, and tea are the most consumed non-alcoholic beverages and may have important health consequences. We prospectively evaluated the consumption of various types of beverages assessed in 1995-1996 in relation to self-reported depression diagnosis after 2000 among 263,923 participants of the NIH-AARP Diet and Health Study. Odds ratios (OR) and 95% confidence intervals (CI) were derived from multivariate logistic regressions. The OR (95% CI) comparing >= 4 cans/cups per day with none were 1.30 (95% CI: 1.17-1.44) for soft drinks, 1.38 (1.15-1.65) for fruit drinks, and 0.91 (0.84-0.98) for coffee (all P for trend < 0.0001). Null associations were observed for iced-tea and hot tea. In stratified analyses by drinkers of primarily diet versus regular beverages, the ORs were 1.31 (1.16-1.47) for diet versus 1.22 (1.03-1.45) for regular soft drinks, 1.51 (1.18-1.92) for diet versus 1.08 (0.79-1.46) for regular fruit drinks, and 1.25 (1.10-1.41) for diet versus 0.94 (0.83-1.08) for regular sweetened iced-tea. Finally, compared to nondrinkers, drinking coffee or tea without any sweetener was associated with a lower risk for depression, adding artificial sweeteners, but not sugar or honey, was associated with higher risks. Frequent consumption of sweetened beverages, especially diet drinks, may increase depression risk among older adults, whereas coffee consumption may lower the risk.
C1 [Guo, Xuguang] Westat Corp, Dept Hlth Studies, Res Triangle Pk, NC USA.
[Park, Yikyung; Freedman, Neal D.; Sinha, Rashmi] NCI, Nutr Epidemiol Branch, Rockville, MD USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
[Blair, Aaron] NCI, Occupat & Environm Epidemiol Branch, Rockville, MD USA.
[Chen, Honglei] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Chen, HL (reprint author), NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
EM chenh2@niehs.nih.gov
RI Sinha, Rashmi/G-7446-2015; Freedman, Neal/B-9741-2015;
OI Sinha, Rashmi/0000-0002-2466-7462; Freedman, Neal/0000-0003-0074-1098;
Chen, Honglei/0000-0003-3446-7779; Park, Yikyung/0000-0002-6281-489X
FU National Institute of Environmental Health Sciences; National Cancer
Institute
FX The work reported in this manuscript was supported by the intramural
research funding from the National Institute of Environmental Health
Sciences and 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 38
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U1 4
U2 38
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 APR 17
PY 2014
VL 9
IS 4
AR e94715
DI 10.1371/journal.pone.0094715
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AG3IK
UT WOS:000335309100042
PM 24743309
ER
PT J
AU Killeen, GF
Seyoum, A
Gimnig, JE
Stevenson, JC
Drakeley, CJ
Chitnis, N
AF Killeen, Gerry F.
Seyoum, Aklilu
Gimnig, John E.
Stevenson, Jennifer C.
Drakeley, Christopher J.
Chitnis, Nakul
TI Made-to-measure malaria vector control strategies: rational design based
on insecticide properties and coverage of blood resources for mosquitoes
SO MALARIA JOURNAL
LA English
DT Review
DE Plasmodium; Anopheles; Vector control; Mosquito; Malaria; Target product
profile
ID TREATED NETS; BEHAVIORAL RESILIENCE; ANOPHELES-ARABIENSIS; HUMAN
EXPOSURE; TRANSMISSION; POPULATIONS; PREVENTION; RESISTANCE; IMPACT;
TRIAL
AB Eliminating malaria from highly endemic settings will require unprecedented levels of vector control. To suppress mosquito populations, vector control products targeting their blood hosts must attain high biological coverage of all available sources, rather than merely high demographic coverage of a targeted resource subset, such as humans while asleep indoors. Beyond defining biological coverage in a measurable way, the proportion of blood meals obtained from humans and the proportion of bites upon unprotected humans occurring indoors also suggest optimal target product profiles for delivering insecticides to humans or livestock. For vectors that feed only occasionally upon humans, preferred animal hosts may be optimal targets for mosquito-toxic insecticides, and vapour-phase insecticides optimized to maximize repellency, rather than toxicity, may be ideal for directly protecting people against indoor and outdoor exposure. However, for vectors that primarily feed upon people, repellent vapour-phase insecticides may be inferior to toxic ones and may undermine the impact of contact insecticides applied to human sleeping spaces, houses or clothing if combined in the same time and place. These concepts are also applicable to other mosquito-borne anthroponoses so that diverse target species could be simultaneously controlled with integrated vector management programmes. Measurements of these two crucial mosquito behavioural parameters should now be integrated into programmatically funded, longitudinal, national-scale entomological monitoring systems to inform selection of available technologies and investment in developing new ones.
C1 [Killeen, Gerry F.] Ifakara Hlth Inst, Environm Hlth & Ecol Sci Themat Grp, Morogoro, Tanzania.
[Killeen, Gerry F.; Seyoum, Aklilu] Univ Liverpool, Liverpool Sch Trop Med, Vector Biol Dept, Liverpool L3 5QA, Merseyside, England.
[Gimnig, John E.] Ctr Dis Control & Prevent, Div Parasit Dis & Malaria, Atlanta, GA 30333 USA.
[Stevenson, Jennifer C.; Drakeley, Christopher J.] London Sch Hyg & Trop Med, Fac Infect & Trop Dis, Dept Immunol & Infect, London WC1E 7HT, England.
[Stevenson, Jennifer C.] Johns Hopkins Bloomberg Sch Publ Hlth, Johns Hopkins Malaria Res Inst, Baltimore, MD 21205 USA.
[Chitnis, Nakul] Swiss Trop & Publ Hlth Inst, Dept Epidemiol & Publ Hlth, Basel, Switzerland.
[Chitnis, Nakul] Univ Basel, Basel, Switzerland.
[Chitnis, Nakul] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Killeen, GF (reprint author), Ifakara Hlth Inst, Environm Hlth & Ecol Sci Themat Grp, Morogoro, Tanzania.
EM gkilleen@ihi.or.tz
RI Smith, Thomas/B-5569-2015; Chitnis, Nakul/B-3105-2013
OI Smith, Thomas/0000-0002-3650-9381;
FU Bill & Melinda Gates Foundation [45114, 52644, OPP1032350]
FX We thank Dr K Aultman for stimulating discussions that led to this
manuscript, Dr T Burkot and Dr D Malone for comments upon an early
draft, and two anonymous reviewers whose insightful comments
significantly improved the final text and figures. This work was funded
by the Bill & Melinda Gates Foundation (award numbers 45114, 52644 and
OPP1032350).
NR 65
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U1 0
U2 21
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1475-2875
J9 MALARIA J
JI Malar. J.
PD APR 16
PY 2014
VL 13
AR 146
DI 10.1186/1475-2875-13-146
PG 9
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA AL8AA
UT WOS:000339357700001
PM 24739261
ER
PT J
AU Alstott, J
Madnick, S
Velu, C
AF Alstott, Jeff
Madnick, Stuart
Velu, Chander
TI Homophily and the Speed of Social Mobilization: The Effect of Acquired
and Ascribed Traits
SO PLOS ONE
LA English
DT Article
ID NETWORKS; IDENTITY; SEARCH; COMMUNICATION; BEHAVIOR; GROWTH
AB Large-scale mobilization of individuals across social networks is becoming increasingly prevalent in society. However, little is known about what affects the speed of social mobilization. Here we use a framed field experiment to identify and measure properties of individuals and their relationships that predict mobilization speed. We ran a global social mobilization contest and recorded personal traits of the participants and those they recruited. We studied the effects of ascribed traits (gender, age) and acquired traits (geography, and information source) on the speed of mobilization. We found that homophily, a preference for interacting with other individuals with similar traits, had a mixed role in social mobilization. Homophily was present for acquired traits, in which mobilization speed was faster when the recuiter and recruit had the same trait compared to different traits. In contrast, we did not find support for homophily for the ascribed traits. Instead, those traits had other, non-homophily effects: Females mobilized other females faster than males mobilized other males. Younger recruiters mobilized others faster, and older recruits mobilized slower. Recruits also mobilized faster when they first heard about the contest directly from the contest organization, and decreased in speed when hearing from less personal source types (e. g. family vs. media). These findings show that social mobilization includes dynamics that are unlike other, more passive forms of social activity propagation. These findings suggest relevant factors for engineering social mobilization tasks for increased speed.
C1 [Alstott, Jeff] NIMH, Sect Crit Brain Dynam, Bethesda, MD 20892 USA.
[Alstott, Jeff] Univ Cambridge, Dept Expt Psychol, Behav & Clin Neurosci Inst, Cambridge CB2 3EB, England.
[Alstott, Jeff] Univ Cambridge, Dept Psychiat, Behav & Clin Neurosci Inst, Cambridge, England.
[Madnick, Stuart] MIT, Informat Technol Grp, Sloan Sch Management, Cambridge, MA 02139 USA.
[Madnick, Stuart] MIT, Sch Engn, Engn Syst Div, Cambridge, MA 02139 USA.
[Velu, Chander] Univ Cambridge, Dept Engn, Inst Mfg, Cambridge CB2 1PZ, England.
RP Madnick, S (reprint author), MIT, Informat Technol Grp, Sloan Sch Management, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM smadnick@mit.edu
FU NIH-Oxford-Cambridge Scholarship Program; John Norris Maguire
Professorship in Information Technologies Chair account; Langley Castle
Hotel
FX The authors were partially funded by the NIH-Oxford-Cambridge
Scholarship Program and by the John Norris Maguire Professorship in
Information Technologies Chair account. Langley Castle Hotel funded the
awards for the contest used in this study and gathered the data. Other
than this, the funders had no role in the subsequent study design, data
analysis, decision to publish, or preparation of the manuscript.
NR 38
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U1 2
U2 18
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 APR 16
PY 2014
VL 9
IS 4
AR e95140
DI 10.1371/journal.pone.0095140
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AI4VW
UT WOS:000336863900109
PM 24740123
ER
PT J
AU Yin, HF
Jin, CF
Fang, XY
Miao, Q
Zhao, YY
Chen, ZQ
Su, ZA
Ye, PP
Wang, Y
Yin, JF
AF Yin, Houfa
Jin, Chongfei
Fang, Xiaoyun
Miao, Qi
Zhao, Yingying
Chen, Zhiqing
Su, Zhaoan
Ye, Panpan
Wang, Yao
Yin, Jinfu
TI Molecular Analysis and Phenotypic Study in 14 Chinese Families with
Bietti Crystalline Dystrophy
SO PLOS ONE
LA English
DT Article
ID CORNEO-RETINAL DYSTROPHY; CHOROIDAL NEOVASCULARIZATION; FUNDUS
DYSTROPHY; CYP4V2 MUTATIONS; RETINOPATHY; GENE; TIMP3
AB Purpose: To investigate the clinical features and cytochrome P450 family 4 subfamily V polypeptide 2 (CYP4V2) gene mutations in 14 Chinese families with Bietti crystalline dystrophy (BCD).
Methods: Seventeen patients from 14 unrelated Chinese families with BCD were recruited for complete clinical ophthalmic examination and genetic study. The 11 exons of CYP4V2 were amplified from genomic DNA of all patients and their family members by polymerase chain reaction (PCR) and then sequenced. Exons of TIMP3 were also sequenced in BCD patient associated with choroidal neovascularization (CNV). One hundred and seventy unrelated healthy Chinese subjects were screened for mutations in CYP4V2.
Results: All 17 patients with BCD had mutations in CYP4V2; one of these mutations was novel (c.219T>A, p.F73L) and four other mutations had been reported. The p.F73L mutation was a commonly detected mutation in our study (seven out of 34 alleles), either in the homozygous state or in the heterozygous state. Among the patients, considerable phenotypic variability was detected, both within and between families. Screening of TIMP3 did not find any mutation in the BCD patient associated with CNV.
Conclusion: The novel CYP4V2 c.219T>A (p.F73L) mutation may be another recurrent mutation in Chinese patients with BCD. Our study expands the mutation spectrum of CYP4V2 and characterizes novel genotype-phenotype associations in Chinese patients with BCD.
C1 [Yin, Houfa; Jin, Chongfei; Fang, Xiaoyun; Miao, Qi; Zhao, Yingying; Chen, Zhiqing; Su, Zhaoan; Ye, Panpan; Wang, Yao; Yin, Jinfu] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Ctr Eye, Hangzhou 310003, Zhejiang, Peoples R China.
[Yin, Houfa; Fang, Xiaoyun; Miao, Qi; Zhao, Yingying; Chen, Zhiqing; Su, Zhaoan; Ye, Panpan; Wang, Yao; Yin, Jinfu] Zhejiang Prov Key Lab Ophthalmol, Hangzhou, Zhejiang, Peoples R China.
[Jin, Chongfei] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
RP Fang, XY (reprint author), Zhejiang Univ, Sch Med, Affiliated Hosp 2, Ctr Eye, Hangzhou 310003, Zhejiang, Peoples R China.
EM xiaoyun.fang88@gmail.com
FU Qianjiang Talents Project of Zhejiang province [2010R10067]; Zhejiang
Key Innovation Team Project of China [2009R50039]; Zhejiang Key
Laboratory Fund of China [2011E10006]; National Natural Science
Foundation of China [81100640]; Public Welfare Technology Project of
Science Technology Department of Zhejiang Province [2012C23068]
FX This work was supported by the Qianjiang Talents Project of Zhejiang
province (Grant No. 2010R10067), Zhejiang Key Innovation Team Project of
China (Grant No. 2009R50039), Zhejiang Key Laboratory Fund of China
(Grant No. 2011E10006), National Natural Science Foundation of China
(Grant No. 81100640) and Public Welfare Technology Project of Science
Technology Department of Zhejiang Province (Grant No. 2012C23068). The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 36
TC 8
Z9 8
U1 0
U2 5
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 APR 16
PY 2014
VL 9
IS 4
AR e94960
DI 10.1371/journal.pone.0094960
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AI4VW
UT WOS:000336863900088
PM 24739949
ER
PT J
AU Kwon, HS
Nakaya, N
Abu-Asab, M
Kim, HS
Tomarev, SI
AF Kwon, Heung Sun
Nakaya, Naoki
Abu-Asab, Mones
Kim, Hong Sug
Tomarev, Stanislav I.
TI Myocilin Is Involved in NgR1/Lingo-1-Mediated Oligodendrocyte
Differentiation and Myelination of the Optic Nerve
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE astrocyte; differentiation; Lingo-1; myelin; myocilin; oligodendrocyte
ID OPEN-ANGLE GLAUCOMA; GLUCOCORTICOID RESPONSE PROTEIN; HUMAN TRABECULAR
MESHWORK; MOUSE MODEL; ER STRESS; EXPRESSION; GENE; LINGO-1;
IDENTIFICATION; GLYCOPROTEIN
AB Myocilin is a secreted glycoprotein that belongs to a family of olfactomedin domain-containing proteins. Although myocilin is detected in several ocular and nonocular tissues, the only reported human pathology related to mutations in the MYOCILIN gene is primary open-angle glaucoma. Functions of myocilin are poorly understood. Here we demonstrate that myocilin is a mediator of oligodendrocyte differentiation and is involved in the myelination of the optic nerve in mice. Myocilin is expressed and secreted by optic nerve astrocytes. Differentiation of optic nerve oligodendrocytes is delayed in Myocilin-null mice. Optic nerves of Myocilin-null mice contain reduced levels of several myelin-associated proteins including myelin basic protein, myelin proteolipid protein, and 2 ' 3 ' -cyclic nucleotide 3 ' -phosphodiesterase compared with those of wild-type littermates. This leads to reduced myelin sheath thickness of optic nerve axons in Myocilin-null mice compared with wild-type littermates, and this difference is more pronounced at early postnatal stages compared with adult mice. Myocilin also affects differentiation of oligodendrocyte precursors in vitro. Its addition to primary cultures of differentiating oligodendrocyte precursors increases levels of tested markers of oligodendrocyte differentiation and stimulates elongation of oligodendrocyte processes. Myocilin stimulation of oligodendrocyte differentiation occurs through the NgR1/Lingo-1 receptor complex. Myocilin physically interacts with Lingo-1 and may be considered as a Lingo-1 ligand. Myocilin-induced elongation of oligodendrocyte processes may be mediated by activation of FYN and suppression of RhoA GTPase.
C1 [Kwon, Heung Sun; Nakaya, Naoki; Tomarev, Stanislav I.] NEI, Lab Retinal Cell & Mol Biol, Retinal Gangl Cell Biol Sect, NIH, Bethesda, MD 20892 USA.
[Abu-Asab, Mones] NEI, Histol Core, NIH, Bethesda, MD 20892 USA.
[Kim, Hong Sug] NCI, Neuro Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Tomarev, SI (reprint author), NEI, NIH, Bldg 6,Room 212,6 Ctr Dr, Bethesda, MD 20892 USA.
EM tomarevs@nei.nih.gov
FU National Eye Institute, National Institutes of Health
FX This work was supported by the Intramural Research Programs of the
National Eye Institute, National Institutes of Health. We thank Drs.
Haohua Qian for help with flash visual evoked potentials recording and
Thomas V. Johnson for critical reading of this manuscript.
NR 48
TC 12
Z9 12
U1 0
U2 7
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 APR 16
PY 2014
VL 34
IS 16
BP 5539
EP 5551
DI 10.1523/JNEUROSCI.4731-13.2014
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA AF7WN
UT WOS:000334926000015
PM 24741044
ER
PT J
AU Starke, RM
Chalouhi, N
Jabbour, PM
Tjoumakaris, SI
Gonzalez, LF
Rosenwasser, RH
Wada, K
Shimada, K
Hasan, DM
Greig, NH
Owens, GK
Dumont, AS
AF Starke, Robert M.
Chalouhi, Nohra
Jabbour, Pascal M.
Tjoumakaris, Stavropoula I.
Gonzalez, L. Fernando
Rosenwasser, Robert H.
Wada, Kosuke
Shimada, Kenji
Hasan, David M.
Greig, Nigel H.
Owens, Gary K.
Dumont, Aaron S.
TI Critical role of TNF-alpha in cerebral aneurysm formation and
progression to rupture
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
DE Cerebral; Aneurysm; Rupture; Subarachnoid hemorrhage; TNF-alpha; Tumor
necrosis factor
ID SMOOTH-MUSCLE-CELLS; INTRACRANIAL ANEURYSMS; MATRIX METALLOPROTEINASES;
PHENOTYPIC MODULATION; MICE; ATHEROSCLEROSIS; RATS; NEUROINFLAMMATION;
HYPERTENSION; INFLAMMATION
AB Background: Alterations in TNF-alpha expression have been associated with cerebral aneurysms, but a direct role in formation, progression, and rupture has not been established.
Methods: Cerebral aneurysms were induced through hypertension and a single stereotactic injection of elastase into the basal cistern in mice. To test the role of TNF-alpha in aneurysm formation, aneurysms were induced in TNF-alpha knockout mice and mice pretreated with the synthesized TNF-alpha inhibitor 3,6' dithiothalidomide (DTH). To assess the role of TNF-alpha in aneurysm progression and rupture, DTH was started 6 days after aneurysm induction. TNF-alpha expression was assessed through real-time PCR and immunofluorescence staining.
Results: TNF-alpha knockout mice and those pre-treated with DTH had significantly decreased incidence of aneurysm formation and rupture as compared to sham mice. As compared with sham mice, TNF-alpha protein and mRNA expression was not significantly different in TNF-alpha knockout mice or those pre-treated with DTH, but was elevated in unruptured and furthermore in ruptured aneurysms. Subarachnoid hemorrhage (SAH) occurred between 7 and 21 days following aneurysm induction. To ensure aneurysm formation preceded rupture, additional mice underwent induction and sacrifice after 7 days. Seventy-five percent had aneurysm formation without evidence of SAH. Initiation of DTH treatment 6 days after aneurysm induction did not alter the incidence of aneurysm formation, but resulted in aneurysmal stabilization and a significant decrease in rupture.
Conclusions: These data suggest a critical role of TNF-alpha in the formation and rupture of aneurysms in a model of cerebral aneurysm formation. Inhibitors of TNF-alpha could be beneficial in preventing aneurysmal progression and rupture.
C1 [Starke, Robert M.; Chalouhi, Nohra; Jabbour, Pascal M.; Tjoumakaris, Stavropoula I.; Gonzalez, L. Fernando; Rosenwasser, Robert H.; Dumont, Aaron S.] Thomas Jefferson Univ, Dept Neurol Surg, Joseph & Marie Field Cerebrovasc Res Lab, Div Neurovasc & Endovasc Surg, Philadelphia, PA 19107 USA.
[Starke, Robert M.] Univ Virginia, Dept Neurol Surg, Charlottesville, VA 22908 USA.
[Wada, Kosuke; Shimada, Kenji] Univ Calif San Francisco, Ctr Cerebrovasc Res, San Francisco, CA 94143 USA.
[Hasan, David M.] Univ Iowa, Dept Neurosurg, Cedar Rapids, IA USA.
[Greig, Nigel H.] NIA, NIH, Translat Gerontol Branch, Intramural Res Program, Washington, DC USA.
[Owens, Gary K.] Univ Virginia, Dept Mol Physiol & Biophys, Robert M Berne Cardiovasc Res Ctr, Charlottesville, VA USA.
[Dumont, Aaron S.] Tulane Univ, Dept Neurol Surg, New Orleans, LA 70118 USA.
RP Starke, RM (reprint author), Thomas Jefferson Univ, Dept Neurol Surg, Joseph & Marie Field Cerebrovasc Res Lab, Div Neurovasc & Endovasc Surg, Philadelphia, PA 19107 USA.
EM bobby.starke@gmail.com
FU National Institutes of Health (NIH) [K08NS067072, R03NS079227-01A1,
K08NS082363-01A1, R01 HL57353, R01 HL098538, R01 HL087867]; NIH
FX This work was supported by National Institutes of Health (NIH) grants
K08NS067072 to AD, R03NS079227-01A1 and K08NS082363-01A1 to DH, and R01
HL57353, R01 HL098538, and R01 HL087867 to GO. NG is supported by the
Intramural Research Program of the NIH.
NR 35
TC 23
Z9 25
U1 2
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD APR 16
PY 2014
VL 11
AR 77
DI 10.1186/1742-2094-11-77
PG 10
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA AF8GX
UT WOS:000334954900003
PM 24739142
ER
PT J
AU Rinaldi, C
Bott, LC
Fischbeck, KH
AF Rinaldi, Carlo
Bott, Laura C.
Fischbeck, Kenneth H.
TI Muscle Matters in Kennedy's Disease
SO NEURON
LA English
DT Editorial Material
ID BULBAR MUSCULAR-ATROPHY; ANDROGEN RECEPTOR; MOUSE MODEL; OVEREXPRESSION;
PATHOLOGY; PROTEIN
AB Polyglutamine expansion in the androgen receptor causes Kennedy's disease. Two recent reports, Cortes et al. (2014) in this issue of Neuron and Lieberman et al. (2014) in Cell Reports, raise the possibility that targeting expression of the mutant protein in skeletal muscle, instead of the nervous system, may mitigate manifestations of this disorder.
C1 [Rinaldi, Carlo; Bott, Laura C.; Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Bott, Laura C.] Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden.
RP Fischbeck, KH (reprint author), NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
EM kf@ninds.nih.gov
FU Intramural NIH HHS [ZIA NS003038-07]
NR 16
TC 3
Z9 3
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD APR 16
PY 2014
VL 82
IS 2
BP 251
EP 253
DI 10.1016/j.neuron.2014.04.005
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA AF1XI
UT WOS:000334506800001
PM 24742452
ER
PT J
AU Lackford, B
Yao, CG
Charles, GM
Weng, LJ
Zheng, XF
Choi, EA
Xie, XH
Wan, J
Xing, Y
Freudenberg, JM
Yang, PY
Jothi, R
Hu, G
Shi, YS
AF Lackford, Brad
Yao, Chengguo
Charles, Georgette M.
Weng, Lingjie
Zheng, Xiaofeng
Choi, Eun-A
Xie, Xiaohui
Wan, Ji
Xing, Yi
Freudenberg, Johannes M.
Yang, Pengyi
Jothi, Raja
Hu, Guang
Shi, Yongsheng
TI Fip1 regulates mRNA alternative polyadenylation to promote stem cell
self-renewal
SO EMBO JOURNAL
LA English
DT Article
DE alternative polyadenylation; stem cell; reprogramming; mRNA processing
ID 3' UNTRANSLATED REGIONS; GENOME-WIDE ANALYSIS; EMBRYONIC-DEVELOPMENT;
PROCESSING COMPLEX; CLEAVAGE; PLURIPOTENCY; REVEALS; SITES;
DIFFERENTIATION; EXPRESSION
AB Synopsis
image
Alternative polyadenylation is an emerging key post-transcriptional regulatory mechanism. The essential role for mRNA 3 ' end processing factor Fip1 in stem cell self-renewal and pluripotency reveals the importance of poly(A) site choice.
mRNA alternative polyadenylation is critical for stem cell self-renewal and pluripotency
Fip1 is a key regulator of mRNA alternative polyadenylation
The direction of alternative polyadenylation switch is controlled by Fip1 binding and the distance between alternative poly(A) sites
Abstract
mRNA alternative polyadenylation (APA) plays a critical role in post-transcriptional gene control and is highly regulated during development and disease. However, the regulatory mechanisms and functional consequences of APA remain poorly understood. Here, we show that an mRNA 3 ' processing factor, Fip1, is essential for embryonic stem cell (ESC) self-renewal and somatic cell reprogramming. Fip1 promotes stem cell maintenance, in part, by activating the ESC-specific APA profiles to ensure the optimal expression of a specific set of genes, including critical self-renewal factors. Fip1 expression and the Fip1-dependent APA program change during ESC differentiation and are restored to an ESC-like state during somatic reprogramming. Mechanistically, we provide evidence that the specificity of Fip1-mediated APA regulation depends on multiple factors, including Fip1-RNA interactions and the distance between APA sites. Together, our data highlight the role for post-transcriptional control in stem cell self-renewal, provide mechanistic insight on APA regulation in development, and establish an important function for APA in cell fate specification.
C1 [Lackford, Brad; Charles, Georgette M.; Zheng, Xiaofeng; Freudenberg, Johannes M.; Yang, Pengyi; Jothi, Raja; Hu, Guang] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
[Yao, Chengguo; Choi, Eun-A; Shi, Yongsheng] Univ Calif Irvine, Sch Med, Dept Microbiol & Mol Genet, Irvine, CA 92717 USA.
[Weng, Lingjie; Xie, Xiaohui] Univ Calif Irvine, Inst Genom & Bioinformat, Irvine, CA USA.
[Weng, Lingjie; Xie, Xiaohui] Univ Calif Irvine, Dept Comp Sci, Irvine, CA USA.
[Wan, Ji; Xing, Yi] Univ Iowa, Interdept Grad Program Genet, Iowa City, IA USA.
[Wan, Ji; Xing, Yi] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA.
[Xing, Yi] Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA USA.
RP Hu, G (reprint author), NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
EM hug4@niehs.nih.gov; yongshes@uci.edu
RI Wan, Ji/K-1344-2014; Jothi, Raja/G-3780-2015; Hu, Guang/E-7474-2016;
OI Hu, Guang/0000-0003-0437-4723; Yang, Pengyi/0000-0003-1098-3138
FU National Institute of Environmental Health Sciences; National Institutes
of Health Intramural Research Program [1ZIAES102745-02,
1ZIAES102625-03]; NIH [GM090056, GM088342]; American Cancer Society
[RSG-12-186]; National Science Foundation [DBI-084621]; Edward
Mallinckrodt Jr. Foundation
FX We thank Drs. M. Waterman, K. Hertel, K. Adelman, T. Hall, T. Kunkel,
and P. Wade for critically reading of the manuscript; Drs. J. Ward and
D. Fargo for assistance with bioinformatics analysis; Dr. C. Limoli for
sharing equipment. This study was supported in part by the National
Institute of Environmental Health Sciences, National Institutes of
Health Intramural Research Program 1ZIAES102745-02 (to G. H., G. M. C.,
B. L., X. Z.), 1ZIAES102625-03 (to R. J., J. F.), NIH Grants GM090056
(to Y.S) and GM088342 (to Y.X.), American Cancer Society Grant
RSG-12-186 (to Y.S), National Science Foundation Grant DBI-084621 (to X.
X.), and a junior faculty grant from the Edward Mallinckrodt Jr.
Foundation (to Y.X.).
NR 37
TC 25
Z9 28
U1 3
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0261-4189
EI 1460-2075
J9 EMBO J
JI Embo J.
PD APR 16
PY 2014
VL 33
IS 8
BP 878
EP 889
DI 10.1002/embj.201386537
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AF2IR
UT WOS:000334536300008
PM 24596251
ER
PT J
AU Nayak, RK
Pearson, SD
Miller, FG
AF Nayak, Rahul K.
Pearson, Steven D.
Miller, Franklin G.
TI Cost-Related Motivations for Conducting Research Participants Should Be
Informed
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID MACULAR DEGENERATION; BEVACIZUMAB
C1 [Nayak, Rahul K.; Pearson, Steven D.; Miller, Franklin G.] NIH, Ctr Clin, Dept Bioeth, Bethesda, MD 20892 USA.
[Pearson, Steven D.] Inst Clin & Econ Review, Boston, MA USA.
RP Miller, FG (reprint author), NIH, Ctr Clin, Dept Bioeth, 10 Ctr Dr,Bldg 10,Rm 1C118, Bethesda, MD 20892 USA.
EM fmiller@nih.gov
OI Nayak, Rahul/0000-0001-6725-7634
NR 8
TC 3
Z9 3
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD APR 16
PY 2014
VL 311
IS 15
BP 1491
EP 1492
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA AE9DX
UT WOS:000334306000012
PM 24615527
ER
PT J
AU Cao, S
Xiao, L
Rao, JN
Zou, TT
Liu, L
Zhang, D
Turner, DJ
Gorospe, M
Wang, JY
AF Cao, Shan
Xiao, Lan
Rao, Jaladanki N.
Zou, Tongtong
Liu, Lan
Zhang, Dee
Turner, Douglas J.
Gorospe, Myriam
Wang, Jian-Ying
TI Inhibition of Smurf2 translation by miR-322/503 modulates TGF-beta/Smad2
signaling and intestinal epithelial homeostasis
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID MESSENGER-RNA STABILITY; BINDING PROTEIN HUR; UBIQUITIN LIGASE;
POLYAMINE DEPLETION; DEPENDENT DEGRADATION; MUCOSAL GROWTH; CELLS;
TARGETS; ACTIVATION; APOPTOSIS
AB Smad ubiquitin regulatory factor 2 (Smurf2) is an E3 ubiquitin ligase that regulates transforming growth factor beta (TGF-beta)/Smad signaling and is implicated in a wide variety of cellular responses, but the exact mechanisms that control Smurf2 abundance are largely unknown. Here we identify microRNA-322 (miR-322) and miR-503 as novel factors that regulate Smurf2 expression posttranscriptionally. Both miR-322 and miR-503 interact with Smurf2 mRNA via its 3'-untranslated region (UTR) and repress Smurf2 translation but do not affect total Smurf2 mRNA levels. Studies using heterologous reporter constructs reveal a greater repressive effect of miR-322/503 through a single binding site in the Smurf2 3'-UTR, whereas point mutation of this site prevents miR-322/503-induced repression of Smurf2 translation. Increased levels of endogenous Smurf2 via antagonism of miR-322/503 inhibits TGF-beta-induced Smad2 activation by increasing degradation of phosphorylated Smad2. Furthermore, the increase in Smurf2 in intestinal epithelial cells (IECs) expressing lower levels of miR-322/503 is associated with increased resistance to apoptosis, which is abolished by Smurf2 silencing. These findings indicate that miR-322/503 represses Smurf2 translation, in turn affecting intestinal epithelial homeostasis by altering TGF-beta/Smad2 signaling and IEC apoptosis.
C1 [Cao, Shan; Xiao, Lan; Rao, Jaladanki N.; Zou, Tongtong; Liu, Lan; Zhang, Dee; Turner, Douglas J.; Wang, Jian-Ying] Univ Maryland, Sch Med, Dept Surg, Cell Biol Grp, Baltimore, MD 21201 USA.
[Wang, Jian-Ying] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA.
[Cao, Shan; Xiao, Lan; Rao, Jaladanki N.; Zou, Tongtong; Liu, Lan; Zhang, Dee; Turner, Douglas J.; Wang, Jian-Ying] Baltimore Vet Affairs Med Ctr, Baltimore, MD 21201 USA.
[Gorospe, Myriam] NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Wang, JY (reprint author), Univ Maryland, Sch Med, Dept Surg, Cell Biol Grp, Baltimore, MD 21201 USA.
EM jwang@smail.umaryland.edu
FU Department of Veterans Affairs; National Institutes of Health [DK-57819,
DK-61972, DK-68491]; National Institute on Aging-Intramural Research
Program, National Institutes of Health
FX We thank Jennifer L. Martindale for technical support in studies of
polysome analysis. This work was supported by Merit Review Awards (to
J.Y.W., D.J.T., and J.N.R.) from the Department of Veterans Affairs and
by National Institutes of Health Grants DK-57819, DK-61972, and DK-68491
(to J.Y.W.). J.Y.W. is a Senior Research Career Scientist, Medical
Research Service, U.S. Department of Veterans Affairs. M. G. is
supported by the National Institute on Aging-Intramural Research
Program, National Institutes of Health.
NR 57
TC 22
Z9 22
U1 0
U2 5
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD APR 15
PY 2014
VL 25
IS 8
BP 1234
EP 1243
DI 10.1091/mbc.E13-09-0560
PG 10
WC Cell Biology
SC Cell Biology
GA AM2AC
UT WOS:000339649400004
PM 24554769
ER
PT J
AU Lin, FR
Ferrucci, L
An, Y
Goh, JO
Doshi, J
Metter, EJ
Davatzikos, C
Kraut, MA
Resnick, SM
AF Lin, F. R.
Ferrucci, L.
An, Y.
Goh, J. O.
Doshi, Jimit
Metter, E. J.
Davatzikos, C.
Kraut, M. A.
Resnick, S. M.
TI Association of hearing impairment with brain volume changes in older
adults
SO NEUROIMAGE
LA English
DT Article
DE Hearing loss; Hearing impairment; MRI Brain volume; Aging
ID VOXEL-BASED MORPHOMETRY; AUDITORY-CORTEX; SPEECH COMPREHENSION; INCIDENT
DEMENTIA; COGNITIVE DECLINE; UNITED-STATES; PATHWAY; STRESS; AGE;
POPULATION
AB Hearing impairment in older adults is independently associated in longitudinal studies with accelerated cognitive decline and incident dementia, and in cross-sectional studies, with reduced volumes in the auditory cortex. Whether peripheral hearing impairment is associated with accelerated rates of brain atrophy is unclear. We analyzed brain volume measurements from magnetic resonance brain scans of individuals with normal hearing versus hearing impairment (speech-frequency pure tone average > 25 dB) followed in the neuroimaging substudy of the Baltimore Longitudinal Study of Aging for a mean of 6.4 years after the baseline scan (n = 126, age 56-86 years). Brain volume measurements were performed with semi-automated region-ofinterest (ROI) algorithms, and brain volume trajectories were analyzed with mixed-effect regression models adjusted for demographic and cardiovascular factors. We found that individuals with hearing impairment (n = 51) compared to those with normal hearing (n = 75) had accelerated volume declines in whole brain and regional volumes in the right temporal lobe (superior, middle, and inferior temporal gyri, parahippocampus, p <.05). These results were robust to adjustment for multiple confounders and were consistent with voxel-based analyses, which also implicated right greater than left temporal regions. These findings demonstrate that peripheral hearing impairment is independently associated with accelerated brain atrophy in whole brain and regional volumes concentrated in the right temporal lobe. Further studies investigating the mechanistic basis of the observed associations are needed. 0 2014 Elsevier Inc. All rights reserved.
C1 [Lin, F. R.] Johns Hopkins Univ, Dept Otolaryngol Head & Neck Surg, Baltimore, MD USA.
[Lin, F. R.] Johns Hopkins Univ, Dept Geriatr Med, Baltimore, MD USA.
[Lin, F. R.] Johns Hopkins Univ, Dept Mental Hlth, Baltimore, MD USA.
[Lin, F. R.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Lin, F. R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
[Ferrucci, L.; Metter, E. J.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[An, Y.; Goh, J. O.; Resnick, S. M.] NIA, Lab Behav Neurosci, Intramural Res Program, Baltimore, MD 21224 USA.
[Goh, J. O.] Natl Taiwan Univ, Coll Med, Grad Inst Brain & Mind Sci, Taipei, Taiwan.
[Doshi, Jimit; Davatzikos, C.] Univ Penn, Dept Radiol, Sect Biomed Image Anal, Philadelphia, PA 19104 USA.
[Kraut, M. A.] Johns Hopkins Med Inst, Dept Radiol, Baltimore, MD 21205 USA.
RP Lin, FR (reprint author), Johns Hopkins Ctr Aging & Hlth, 2024 E Monument St,Suite 2-700, Baltimore, MD 21205 USA.
EM flin1@jhmi.edu
RI GOH, JOSHUA/C-8063-2016
OI GOH, JOSHUA/0000-0001-7808-5452
FU intramural research program of the National Institute on Aging; NIH
[K23DC011279]; Triological Society/American College of Surgeons
Clinician Scientist Award; Eleanor Schwartz Charitable Foundation
FX This study was supported by the intramural research program of the
National Institute on Aging. Dr. Lin was supported by NIH K23DC011279, a
Triological Society/American College of Surgeons Clinician Scientist
Award, and the Eleanor Schwartz Charitable Foundation.
NR 48
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PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD APR 15
PY 2014
VL 90
BP 84
EP 92
DI 10.1016/j.neuroimage.2013.12.059
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AL1TP
UT WOS:000338909500009
PM 24412398
ER
PT J
AU Banerjee, A
Pillai, AS
Sperling, JR
Smith, JF
Horwitz, B
AF Banerjee, Arpan
Pillai, Ajay S.
Sperling, Justin R.
Smith, Jason F.
Horwitz, Barry
TI Temporal microstructure of cortical networks (TMCN) underlying
task-related differences (vol 62, pg 1643, 2012)
SO NEUROIMAGE
LA English
DT Correction
C1 [Banerjee, Arpan; Pillai, Ajay S.; Sperling, Justin R.; Smith, Jason F.; Horwitz, Barry] NIDCD, Brain Imaging & Modeling Sect, NIH, Bethesda, MD 20892 USA.
RP Banerjee, A (reprint author), NIDCD, Brain Imaging & Modeling Sect, NIH, 10 Ctr Dr,Room 5D39, Bethesda, MD 20892 USA.
EM Arpan.Banerjee@nih.gov
NR 1
TC 0
Z9 0
U1 1
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD APR 15
PY 2014
VL 90
BP 469
EP 469
DI 10.1016/j.neuroimage.2013.12.034
PG 1
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AL1TP
UT WOS:000338909500045
ER
PT J
AU Malee, KM
Mellins, CA
Huo, Y
Tassiopoulos, K
Smith, R
Sirois, PA
Allison, SM
Kacanek, D
Kapetanovic, S
Williams, PL
Grant, ML
Marullo, D
Aidala, AA
AF Malee, Kathleen M.
Mellins, Claude A.
Huo, Yanling
Tassiopoulos, Katherine
Smith, Renee
Sirois, Patricia A.
Allison, Susannah M.
Kacanek, Deborah
Kapetanovic, Suad
Williams, Paige L.
Grant, Mitzie L.
Marullo, Daniel
Aidala, Angela A.
CA Pediat HIV AIDS Cohort Study PHACS
TI Prevalence, Incidence, and Persistence of Psychiatric and Substance Use
Disorders Among Mothers Living With HIV
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV; women; psychiatric disorder; substance use disorders; prevalence
ID MENTAL-HEALTH; ANTIRETROVIRAL THERAPY; DEPRESSIVE SYMPTOMS; SEROPOSITIVE
WOMEN; ANXIETY DISORDERS; POSITIVE WOMEN; INFECTED WOMEN; SELF-REPORT;
MORTALITY; TRAUMA
AB Objective: To evaluate prevalence, incidence, remission, and persistence of psychiatric and substance use disorders among HIV-infected mothers and identify biopsychosocial correlates.
Methods: HIV-infected mothers (n = 1223) of HIV-exposed uninfected children enrolled in a prospective cohort study; HIV-uninfected mothers (n = 128) served as a comparison group. Mothers provided sociodemographic and health information and completed the Client Diagnostic Questionnaire (CDQ). Prevalence of any psy-chiatric or substance use disorder at initial evaluation was compared between the 2 groups. Incident, remitting, and persisting disorders were identified for 689 mothers with HIV who completed follow-up CDQs. We used logistic regression to evaluate adjusted associations of biopsychosocial characteristics with presence, incidence, remission, and persistence of disorders.
Results: Thirty-five percent of mothers screened positive for any psychiatric or substance use disorder at initial evaluation, with no difference by maternal HIV status (P = 1.00). Among HIV-infected mothers, presence of any disorder was associated with younger age [adjusted odds ratio (aOR): 1.39; 95% CI: 1.09 to 1.75], single parenthood (aOR: 1.35; 95% CI: 1.08 to 1.68), and functional limitations (aOR: 2.29; 95% CI: 1.81 to 2.90). Incident disorders were associated with functional limitations (aOR: 1.92; 95% CI: 1.10 to 3.30). Among HIV-infected mothers with a disorder at initial evaluation (n = 238), 61% had persistent disorders. Persistent disorders were associated with lower income (aOR: 2.44; 95% CI: 1.33 to 4.76) and functional limitations (aOR: 3.19; 95% CI: 1.87 to 5.48). Receipt of treatment for any disorder was limited: 4.5% at study entry, 7% at follow-up, 5.5% at both entry and follow-up.
Conclusions: Psychiatric and substance use disorders remain significant comorbid conditions among HIV-infected mothers and require accessible evidence-informed treatment.
C1 [Malee, Kathleen M.] Northwestern Univ, Dept Psychiat & Behav Sci, Feinberg Sch Med, Chicago, IL 60611 USA.
[Mellins, Claude A.] New York State Psychiat Inst & Hosp, HIV Ctr Clin & Behav Studies, Div Gender Sexual & Hlth, New York, NY 10032 USA.
[Mellins, Claude A.] Columbia Univ, New York, NY USA.
[Huo, Yanling; Kacanek, Deborah; Williams, Paige L.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Tassiopoulos, Katherine] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Smith, Renee] Univ Illinois, Dept Pediat, Chicago, IL USA.
[Sirois, Patricia A.] Tulane Univ, Sch Med, Dept Pediat, New Orleans, LA 70112 USA.
[Allison, Susannah M.; Kapetanovic, Suad] NIMH, NIH, Bethesda, MD 20892 USA.
[Grant, Mitzie L.] Drexel Univ, Coll Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Marullo, Daniel] Childrens Alabama, Dept Childrens Behav Hlth, Birmingham, AL USA.
[Aidala, Angela A.] Columbia Univ, Dept Sociomed Sci, Mailman Sch Publ Hlth, New York, NY USA.
RP Malee, KM (reprint author), Ann & Robert H Lurie Childrens Hosp, 215 East Chicago Ave,Box 155, Chicago, IL 60614 USA.
EM kmalee@luriechildrens.org
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institute on Drug Abuse; National Institute of
Allergy and Infectious Diseases; Office of AIDS Research; National
Institute of Mental Health; National Institute of Neurological Disorders
and Stroke; National Institute on Deafness and Other Communication
Disorders; National Heart Lung and Blood Institute; National Institute
of Dental and Craniofacial Research; National Institute on Alcohol Abuse
and Alcoholism; Harvard University School of Public Health [HD052102, 3
U01 HD052102-05S1, 3 U01 HD052102-06S3]; Tulane University School of
Medicine [HD052104, 3U01HD052104-06S1]; Intramural Research Program of
the National Institute of Mental Health
FX The Pediatric HIV/AIDS Cohort Study (PHACS) was supported by the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
with cofunding from the National Institute on Drug Abuse, the National
Institute of Allergy and Infectious Diseases, the Office of AIDS
Research, the National Institute of Mental Health, the National
Institute of Neurological Disorders and Stroke, the National Institute
on Deafness and Other Communication Disorders, the National Heart Lung
and Blood Institute, the National Institute of Dental and Craniofacial
Research, and the National Institute on Alcohol Abuse and Alcoholism,
through cooperative agreements with the Harvard University School of
Public Health (HD052102, 3 U01 HD052102-05S1, 3 U01 HD052102-06S3) and
the Tulane University School of Medicine (HD052104, 3U01HD052104-06S1).
This project was also supported in part by the Intramural Research
Program of the National Institute of Mental Health.
NR 43
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U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD APR 15
PY 2014
VL 65
IS 5
BP 526
EP 534
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AJ4XX
UT WOS:000337684400007
PM 24759063
ER
PT J
AU Vogler, MA
Smeaton, LM
Wright, RL
Cardoso, SW
Sanchez, J
Infante, R
Moran, LE
Godfrey, C
Demeter, LM
Johnson, VA
AF Vogler, Mary A.
Smeaton, Laura M.
Wright, Rodney L.
Cardoso, Sandra W.
Sanchez, Jorge
Infante, Rosa
Moran, Laura E.
Godfrey, Catherine
Demeter, Lisa M.
Johnson, Victoria A.
TI Combination Antiretroviral Treatment for Women Previously Treated Only
in Pregnancy: Week 24 Results of AIDS Clinical Trials Group Protocol
A5227
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE antiretroviral therapy; postpartum women; efavirenz; adherence; pMTCT
ID STRUCTURED TREATMENT INTERRUPTIONS; SINGLE-DOSE NEVIRAPINE;
DRUG-RESISTANT HIV-1; VERTICAL TRANSMISSION; RECEIVING NEVIRAPINE;
HIV-1-INFECTED WOMEN; THERAPY; ZIDOVUDINE; MUTATIONS; ADHERENCE
AB Background: Women with HIV and prior exposure to combination antiretroviral therapy (cART) solely for prevention of mother-to-child transmission (pMTCT) need to know whether they can later be treated successfully with a commonly used regimen of efavirenz (EFV) and coformulated emtricitabine (FTC) and tenofovir disoproxil fumarate (TDF).
Methods: Nonpregnant women with plasma HIV-1 RNA of >= 500 copies per milliliter, previously cART exposed for pMTCT only, were eligible if they were off ART for >= 24 weeks before entry, were without evidence of drug resistance on standard genotyping, and were ready to start EFV plus FTC/TDF. The primary endpoint was virologic response (defined as plasma HIV RNA < 400 copies/mL) at 24 weeks.
Results: Fifty-four women were enrolled between October 2007 and December 2009; 52 of 54 completed 24 weeks of follow-up. Median baseline CD4+ T-cell count was 265/mm(3) and baseline plasma HIV-1 RNA was 4.6 log(10) copies per milliliter. Median prior cART duration was 14 weeks, and median time elapsed from the last pMTCT dose to entry was 22 months. Virologic response at 24 weeks was observed in 42 of 52 women or 81% (exact 95% confidence interval: 68% to 90%). There were no differences in response by country, by number, or class of prior pMTCT exposures. Although confirmed virologic failure occurred in 8 women, no virologic failures were observed in women reporting perfect early adherence.
Conclusions: In this first prospective clinical trial studying combination antiretroviral retreatment in women with a history of pregnancy-limited cART, the observed virologic response to TDF/FTC and EFV at 24 weeks was 81%. Virologic failures occurred and correlated with self-reported nonadherence.
C1 [Vogler, Mary A.] Cornell Univ, Weill Cornell Med Coll, New York Presbyterian Hosp, New York, NY 10021 USA.
[Smeaton, Laura M.] Harvard Univ, Sch Publ Hlth, Ctr Biostat & AIDS Res, Boston, MA 02115 USA.
[Wright, Rodney L.] Albert Einstein Coll Med, Dept Obstet & Gynecol, Bronx, NY 10467 USA.
[Cardoso, Sandra W.] Fundacao Oswaldo Cruz, Inst Pesquisa Clin Evandro Chagas, STD AIDS Clin Res Lab, Rio De Janeiro, Brazil.
[Sanchez, Jorge; Infante, Rosa] Asociac Civil IMPACTA Salud & Educ, Lima, Peru.
[Moran, Laura E.] Social & Sci Syst Inc, Silver Spring, MD USA.
[Godfrey, Catherine] NIAID, HIV Res Branch, Div Aids, NIH, Bethesda, MD 20892 USA.
[Demeter, Lisa M.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Johnson, Victoria A.] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
[Johnson, Victoria A.] Univ Alabama Birmingham, Sch Med, Birmingham, AL USA.
RP Vogler, MA (reprint author), Cornell Univ, Weill Cornell Med Coll, New York Presbyterian Hosp, New York, NY 10021 USA.
EM mav9046@med.cornell.edu
FU National Institute of Allergy and Infectious Diseases [U01AI068636];
National Institute of Mental Health, National Institute of Dental and
Craniofacial Research; Statistical and Data Management Center of the
AIDS Clinical Trials Group under the National Institute of Allergy and
Infectious Diseases [1 U01AI068634]; University of Alabama at Birmingham
ACTG CTU grant [U01 AI069918]; Instituto de Pesquisa Clinica Evandro
Chagas CRS Fiocruz Therapeutic and Prevention HIV AIDS CTU grant [12101,
1 U01 AI069476-01]; IMPACTA Peru CTU grant [1U01AI069438-01]; Weill
Cornell Medical College ACTG CTU grant [5U01AI069419]; University of
Rochester CTU grant [1U01 AI069511]
FX Supported by Award no. U01AI068636 from the National Institute of
Allergy and Infectious Diseases and supported by National Institute of
Mental Health, National Institute of Dental and Craniofacial Research.
The content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institute of
Allergy and Infectious Diseases or the National Institutes of Health.
Supported by the Statistical and Data Management Center of the AIDS
Clinical Trials Group under the National Institute of Allergy and
Infectious Diseases grant no. 1 U01AI068634. UAB Virology Specialty
Laboratory 54 support VSL UM1 AI068636 and UAB CFAR P30; AI27767 for
laboratory support and core research facilities within UAB Center for
AIDS Research/University of Alabama at Birmingham School of Medicine and
Birmingham Veterans Affairs Medical Center, Birmingham Alabama;
University of Alabama at Birmingham ACTG CTU grant no. U01 AI069918;
Instituto de Pesquisa Clinica Evandro Chagas CRS (12101) Fiocruz
Therapeutic and Prevention HIV AIDS CTU grant no. 1 U01 AI069476-01;
IMPACTA Peru CTU grant no. 1U01AI069438-01; Weill Cornell Medical
College ACTG CTU grant no. 5U01AI069419; University of Rochester CTU
grant no. 1U01 AI069511; Bristol Myers Squibb Company, Gilead Sciences,
Inc, and Merck & Co, Inc, provided study drugs.
NR 31
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD APR 15
PY 2014
VL 65
IS 5
BP 542
EP 550
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AJ4XX
UT WOS:000337684400009
PM 24759064
ER
PT J
AU Zhu, N
Jacobs, DR
Schreiner, PJ
Yaffe, K
Bryan, N
Launer, LJ
Whitmer, RA
Sidney, S
Demerath, E
Thomas, W
Bouchard, C
He, K
Reis, J
Sternfeld, B
AF Zhu, Na
Jacobs, David R., Jr.
Schreiner, Pamela J.
Yaffe, Kristine
Bryan, Nick
Launer, Lenore J.
Whitmer, Rachel A.
Sidney, Stephen
Demerath, Ellen
Thomas, William
Bouchard, Claude
He, Ka
Reis, Jared
Sternfeld, Barbara
TI Cardiorespiratory fitness and cognitive function in middle age The
CARDIA Study
SO NEUROLOGY
LA English
DT Article
ID YOUNG-ADULTS CARDIA; ARTERY RISK DEVELOPMENT; ALZHEIMER-DISEASE;
OLDER-ADULTS; MRI FINDINGS; IMPAIRMENT; EXERCISE; ASSOCIATION;
RECRUITMENT; PREDICTION
AB Objective:To investigate whether greater cardiorespiratory fitness (CRF) is associated with better cognitive function 25 years later.Methods:We studied 2,747 participants in the community-based Coronary Artery Risk Development in Young Adults Study of black and white men and women aged 18 to 30 years at recruitment in 1985-1986 (baseline year 0). Symptom-limited maximal treadmill test durations at years 0 and 20 provided measures of CRF. Cognitive tests at year 25 measured verbal memory (Rey Auditory Verbal Learning Test [RAVLT]), psychomotor speed (Digit Symbol Substitution Test [DSST]), and executive function (Stroop Test).Results:Per minute of baseline CRF, the RAVLT was 0.12 words recalled higher (standard error [SE] = 0.03, p < 0.0001), the DSST was 0.92 digits higher (SE = 0.13, p < 0.0001), and the Stroop Test score was 0.52 lower (better performance, SE = 0.11, p < 0.0001), after accounting for race, sex, age, education, and clinical center. Compared with the lowest quartile of CRF, each cognitive test was 21% to 34% of an SD better in the highest CRF quartile. Further adjustment for lifestyle and clinical measures attenuated coefficients for RAVLT and DSST slightly, while the coefficient predicting the Stroop Test lost more than half its value (p = 0.07). Analysis in the subset of 1,957 participants who also completed the year-20 treadmill test showed that 20-year change in CRF was positively associated only with DSST (p < 0.001).Conclusions:Better verbal memory and faster psychomotor speed at ages 43 to 55 years were clearly associated with better CRF 25 years earlier.
C1 [Zhu, Na; Jacobs, David R., Jr.; Schreiner, Pamela J.; Demerath, Ellen] Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA.
[Thomas, William] Univ Minnesota, Sch Publ Hlth, Div Biostat, Minneapolis, MN 55455 USA.
[Jacobs, David R., Jr.] Univ Oslo, Dept Nutr, N-0316 Oslo, Norway.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Bryan, Nick] Univ Penn Hlth Syst, Dept Radiol, Philadelphia, PA USA.
[Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Whitmer, Rachel A.; Sidney, Stephen; Sternfeld, Barbara] Kaiser Permanente Med Care Program, Div Res, Oakland, CA 94611 USA.
[Bouchard, Claude] Pennington Biomed Res Ctr, Human Genom Lab, Baton Rouge, LA 70808 USA.
[He, Ka] Indiana Univ, Dept Epidemiol & Biostat, Bloomington, IN USA.
[Reis, Jared] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Jacobs, DR (reprint author), Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA.
EM Jacob004@umn.edu
RI He, Ka/I-9906-2014; Bouchard, Claude/A-7637-2009
FU National Heart, Lung, and Blood Institute [HHSN268201300025C,
HHSN268201300026C, HHSN268201300027C, HHSN268201300028C,
HHSN268201300029C, HHSN268200900041C]; Intramural Research Program of
the National Institute on Aging; [R01 HL 078972]
FX The Coronary Artery Risk Development in Young Adults (CARDIA) Study is
supported by contracts HHSN268201300025C, HHSN268201300026C,
HHSN268201300027C, HHSN268201300028C, HHSN268201300029C, and
HHSN268200900041C from the National Heart, Lung, and Blood Institute and
the Intramural Research Program of the National Institute on Aging, plus
a grant for the CARDIA Fitness Study R01 HL 078972.
NR 40
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U1 1
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD APR 15
PY 2014
VL 82
IS 15
BP 1339
EP 1346
DI 10.1212/WNL.0000000000000310
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA AH9XG
UT WOS:000336498000013
PM 24696506
ER
PT J
AU Dominic, EA
Ramezani, A
Anker, SD
Verma, M
Mehta, N
Rao, M
AF Dominic, Elizabeth A.
Ramezani, Ali
Anker, Stefan D.
Verma, Mukesh
Mehta, Nehal
Rao, Madhumathi
TI Mitochondrial cytopathies and cardiovascular disease
SO HEART
LA English
DT Review
DE Heart Failure; Coronary Artery Disease
ID DILATED CARDIOMYOPATHY; RESPIRATORY-CHAIN; HEART-FAILURE;
CARDIAC-HYPERTROPHY; DNA MUTATIONS; MYOCARDIUM; MTDNA; AMPLIFICATION;
MECHANISMS; MUSCLE
AB The global epidemic of cardiovascular disease remains the leading cause of death in the USA and across the world. Functional and structural integrity of mitochondria are essential for the physiological function of the cardiovascular system. The metabolic adaptation observed in normal heart is lost in the failing myocardium, which becomes progressively energy depleted leading to impaired myocardial contraction and relaxation. Uncoupling of electron transfer from ATP synthesis leads to excess generation of reactive species, leading to widespread cellular injury and cardiovascular disease. Accumulation of mitochondrial DNA mutation has been linked to ischaemic heart disease, cardiomyopathy and atherosclerotic vascular disease. Mitochondria are known to regulate apoptotic and autophagic pathways that have been shown to play an important role in the development of cardiomyopathy and atherosclerosis. A number of pharmacological and non-pharmacological treatment options have been explored in the management of mitochondrial diseases with variable success.
C1 [Dominic, Elizabeth A.; Ramezani, Ali] George Washington Sch Med, Washington, DC USA.
[Anker, Stefan D.] Campus Virchow Klinikum, CharitA, Dept Cardiol, Berlin, Germany.
[Verma, Mukesh] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Mehta, Nehal] NHLBI, Sect Inflammat & Cardiometabol Dis, Bethesda, MD 20892 USA.
[Rao, Madhumathi] Tufts Univ, Sch Med, Dept Med, Boston, MA 02111 USA.
RP Ramezani, A (reprint author), George Washington Univ, Dept Med, 2300 1 St NW, Washington, DC 20037 USA.
EM Ramezani@gwu.edu
NR 30
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U1 1
U2 9
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1355-6037
EI 1468-201X
J9 HEART
JI Heart
PD APR 15
PY 2014
VL 100
IS 8
BP 611
EP 618
DI 10.1136/heartjnl-2013-304657
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AE0RA
UT WOS:000333672600006
PM 24449718
ER
PT J
AU Shahbazi, S
Peer, CJ
Polizzotto, MN
Uldrick, TS
Roth, J
Wyvill, KM
Aleman, K
Zeldis, JB
Yarchoan, R
Figg, WD
AF Shahbazi, Shandiz
Peer, Cody J.
Polizzotto, Mark N.
Uldrick, Thomas S.
Roth, Jeffrey
Wyvill, Kathleen M.
Aleman, Karen
Zeldis, Jerome B.
Yarchoan, Robert
Figg, William D.
TI A sensitive and robust HPLC assay with fluorescence detection for the
quantification of pomalidomide in human plasma for pharmacokinetic
analyses
SO JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS
LA English
DT Article
DE Pomalidomide; HPLC; Fluorescence; Pharmacokinetics; Liquid extraction
ID REFRACTORY MULTIPLE-MYELOMA; LOW-DOSE DEXAMETHASONE; PHASE-I;
THALIDOMIDE ANALOG; CELL-ACTIVATION; LENALIDOMIDE; CC-4047;
MYELOFIBROSIS; COMBINATION; MECHANISM
AB Pomalidomide is a second generation IMiD (immunomodulatory agent) that has recently been granted approval by the Food and Drug Administration for treatment of relapsed multiple myeloma after prior treatment with two antimyeloma agents, including lenalidomide and bortezomib. A simple and robust HPLC assay with fluorescence detection for pomalidomide over the range of 1-500 ng/mL has been developed for application to pharmacokinetic studies in ongoing clinical trials in various other malignancies. A liquid-liquid extraction from human plasma alone or pre-stabilized with 0.1% HCl was performed, using propyl paraben as the internal standard. From plasma either pre-stabilized with 0.1% HCl or not, the assay was shown to be selective, sensitive, accurate, precise, and have minimal matrix effects (<20%). Pomalidomide was stable in plasma through 4 freeze-thaw cycles (<12% change), in plasma at room temperature for up to 2 h for samples not pre-stabilized with 0.1% HCl and up to 8 h in samples pre-stabilized with 0.1% HCl, 24h post-preparation at 4 degrees C (<2% change), and showed excellent extraction recovery (similar to 90%). This is the first reported description of the freeze/thaw and plasma stability of pomalidomide in plasma either pre-stabilized with 0.1% HCl or not. The information presented in this manuscript is important when performing pharmacokinetic analyses. The method was used to analyze clinical pharmacokinetics samples obtained after a 5 mg oral dose of pomalidomide. This relatively simple HPLC-FL assay allows a broader range of laboratories to measure pomalidomide for application to clinical pharmacokinetics. Published by Elsevier B.V.
C1 [Shahbazi, Shandiz; Peer, Cody J.; Roth, Jeffrey; Figg, William D.] NCI, Clin Pharmacol Program, Bethesda, MD 20892 USA.
[Polizzotto, Mark N.; Uldrick, Thomas S.; Wyvill, Kathleen M.; Aleman, Karen; Yarchoan, Robert] NCI, HIV AIDS Malignancy Branch, Bethesda, MD 20892 USA.
[Zeldis, Jerome B.] Celgene Corp & Celgene Global Hlth, Summit, NJ USA.
RP Figg, WD (reprint author), Clin Pharmacol Program, 9000 Rockville Pike,Bldg 10,Room 5A01, Bethesda, MD 20892 USA.
EM figgw@helix.nih.gov
RI Figg Sr, William/M-2411-2016
FU NIH, National Cancer Institute; National Cancer Institute; Celgene
Corporation
FX This study was funded in part by the Intramural Research Program of the
NIH, National Cancer Institute, and a CRADA between the National Cancer
Institute and Celgene Corporation. This is a US Government work and
there are no restrictions on its use. The views expressed within this
paper do not necessarily reflect those of the US Government. We thank
the medical research staff of the HIV and AIDS Malignancy Branch, the
Center for Cancer Research, and the NIH Clinical Center who helped with
the study. We also thank the nursing staff of the National Cancer
Institute and the fellows of the Medical Oncology Branch at the National
Cancer Institute for their care of our patients; Cynthia Graves for data
management assistance; and Cancer Therapy and Evaluation Program for
sponsoring the trial. Most importantly, we appreciate the patients with
cancer who enroll in investigational trials to advance the knowledge of
this disease.
NR 29
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U2 14
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0731-7085
EI 1873-264X
J9 J PHARMACEUT BIOMED
JI J. Pharm. Biomed. Anal.
PD APR 15
PY 2014
VL 92
BP 63
EP 68
DI 10.1016/j.jpba.2014.01.001
PG 6
WC Chemistry, Analytical; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA AG5VR
UT WOS:000335487300009
PM 24486861
ER
PT J
AU Petersen, EJ
Henry, TB
Zhao, J
MacCuspie, RI
Kirschling, TL
Dobrovolskaia, MA
Hackley, V
Xing, BS
White, JC
AF Petersen, Elijah J.
Henry, Theodore B.
Zhao, Jian
MacCuspie, Robert I.
Kirschling, Teresa L.
Dobrovolskaia, Marina A.
Hackley, Vincent
Xing, Baoshan
White, Jason C.
TI Identification and Avoidance of Potential Artifacts and
Misinterpretations in Nanomaterial Ecotoxicity Measurements
SO ENVIRONMENTAL SCIENCE & TECHNOLOGY
LA English
DT Review
ID WALLED CARBON NANOTUBES; TITANIUM-DIOXIDE NANOPARTICLES; AQUEOUS C-60
CLUSTERS; TROUT ONCORHYNCHUS-MYKISS; DISSOLVED ORGANIC-MATTER;
CELL-CULTURE MEDIA; SILVER NANOPARTICLES; ENGINEERED NANOMATERIALS;
IN-VITRO; RAINBOW-TROUT
AB Novel physicochemistries of engineered nanomaterials (ENMs) offer considerable commercial potential for new products and processes, but also the possibility of unforeseen and negative consequences upon ENM release into the environment. Investigations of ENM ecotoxicity have revealed that the unique properties of ENMs and a lack of appropriate test methods can lead to results that are inaccurate or not reproducible. The occurrence of spurious results or misinterpretations of results from ENM toxicity tests that are unique to investigations of ENMs (as opposed to traditional toxicants) have been reported, but have not yet been systemically reviewed. Our objective in this manuscript is to highlight artifacts and misinterpretations that can occur at each step of ecotoxicity testing: procurement or synthesis of the ENMs and assessment of potential toxic impurities such as metals or endotoxins, ENM storage, dispersion of the ENMs in the test medium, direct interference with assay reagents and unacknowledged indirect effects such as nutrient depletion during the assay, and assessment of the ENM biodistribution in organisms. We recommend thorough characterization of initial ENMs including measurement of impurities, implementation of steps to minimize changes to the ENMs during storage, inclusion of a set of experimental controls (e.g., to assess impacts of nutrient depletion, ENM specific effects, impurities in ENM formulation, desorbed surface coatings, the dispersion process, and direct interference of ENM with toxicity assays), and use of orthogonal measurement methods when available to assess ENMs fate and distribution in organisms.
C1 [Petersen, Elijah J.] NIST, Biosyst & Biomat Div, Gaithersburg, MD 20899 USA.
[Henry, Theodore B.] Heriot Watt Univ, Sch Life Sci, Edinburgh, Midlothian, Scotland.
[Henry, Theodore B.] Univ Tennessee, Ctr Environm Biotechnol, Knoxville, TN 37932 USA.
[Henry, Theodore B.] Univ Tennessee, Dept Forestry Wildlife & Fisheries, Knoxville, TN USA.
[Zhao, Jian; Xing, Baoshan] Univ Massachusetts, Stockbridge Sch Agr, Amherst, MA 01003 USA.
[MacCuspie, Robert I.; Hackley, Vincent] NIST, Mat Measurement Sci Div, Gaithersburg, MD 20899 USA.
[MacCuspie, Robert I.] Florida Polytech Univ, Nanotechnol Program, Lakeland, FL 33801 USA.
[Kirschling, Teresa L.] NIST, Appl Chem & Mat Div, Boulder, CO 80305 USA.
[Dobrovolskaia, Marina A.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Nanotechnol Characterizat Lab, Canc Res Technol Program, Frederick, MD 21702 USA.
[White, Jason C.] Connecticut Agr Expt Stn, Dept Analyt Chem, New Haven, CT 06504 USA.
RP Petersen, EJ (reprint author), NIST, Biosyst & Biomat Div, Gaithersburg, MD 20899 USA.
EM elijah.petersen@nist.gov
RI Petersen, Elijah/E-3034-2013; Zhao, Jian/D-2798-2012; Nanotechnology
Characterization Lab, NCL/K-8454-2012;
OI Henry, Theodore/0000-0002-9675-9454; MacCuspie,
Robert/0000-0002-6618-6499; Kirschling, Teresa/0000-0003-1695-0521
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; EU [604602]
FX Certain commercial equipment or materials are identified in this paper
in order to specify adequately the experimental procedure. Such
identification does not imply recommendation or endorsement by the
National Institute of Standards and Technology, nor does it imply that
the materials or equipment identified are necessarily the best available
for the purpose. The study was supported in part by 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 U.S. Government.
T.B. Henry acknowledges EU FP7-NMP-2013-LARGE-7 Project Number 604602.
J.C. White also acknowledges USDA AFRI 2011-67006-30181.
NR 233
TC 79
Z9 79
U1 13
U2 167
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0013-936X
EI 1520-5851
J9 ENVIRON SCI TECHNOL
JI Environ. Sci. Technol.
PD APR 15
PY 2014
VL 48
IS 8
BP 4226
EP 4246
DI 10.1021/es4052999
PG 21
WC Engineering, Environmental; Environmental Sciences
SC Engineering; Environmental Sciences & Ecology
GA AF4CG
UT WOS:000334658400002
PM 24617739
ER
PT J
AU Liu, SL
Zhang, LJ
Wang, ZG
Zhang, ZL
Wu, QM
Sun, EZ
Shi, YB
Pang, DW
AF Liu, Shu-Lin
Zhang, Li-Juan
Wang, Zhi-Gang
Zhang, Zhi-Ling
Wu, Qiu-Mei
Sun, En-Ze
Shi, Yun-Bo
Pang, Dai-Wen
TI Globally Visualizing the Microtubule-Dependent Transport Behaviors of
Influenza Virus in Live Cells
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID A H7N9 VIRUS; AVIAN INFLUENZA; CARGO TRANSPORT; DYNEIN; INFECTION;
DYNAMICS; PATHWAY; MOTOR; MOTILITY; REVEALS
AB Understanding the microtubule-dependent behaviors of viruses in live cells is very meaningful for revealing the mechanisms of virus infection and endocytosis. Herein, we used a quantum dots-based single-particle tracking technique to dynamically and globally visualize the microtubule-dependent transport behaviors of influenza virus in live cells. We found that the intersection configuration of microtubules can interfere with the transport behaviors of the virus in live cells, which lead to the changing and long-time pausing of the transport behavior of viruses. Our results revealed that most of the viruses moved along straight microtubules rapidly and unidirectionally from the cell periphery to the microtubule organizing center (MTOC) near the bottom of the cell, and the viruses were confined in the grid of microtubules near the top of the cell and at the MTOC near the bottom of the cell. These results provided deep insights into the influence of entire microtubule geometry on the virus infection.
C1 [Liu, Shu-Lin; Zhang, Li-Juan; Wang, Zhi-Gang; Zhang, Zhi-Ling; Wu, Qiu-Mei; Sun, En-Ze; Pang, Dai-Wen] Wuhan Univ, Key Lab Analyt Chem Biol & Med, State Key Lab Virol, Coll Chem & Mol Sci,Minist Educ, Wuhan 430072, Hubei, Peoples R China.
[Liu, Shu-Lin; Zhang, Li-Juan; Wang, Zhi-Gang; Zhang, Zhi-Ling; Wu, Qiu-Mei; Sun, En-Ze; Pang, Dai-Wen] Wuhan Univ, Wuhan Inst Biotechnol, Wuhan 430072, Hubei, Peoples R China.
[Shi, Yun-Bo] NICHD, Sect Mol Morphogenesis, PCRM, NIH, Bethesda, MD 20892 USA.
RP Pang, DW (reprint author), Wuhan Univ, Key Lab Analyt Chem Biol & Med, State Key Lab Virol, Coll Chem & Mol Sci,Minist Educ, Wuhan 430072, Hubei, Peoples R China.
EM dwpang@whu.edu.cn
RI Zhang, Zhi-Ling/B-3135-2010;
OI Zhang, Zhi-Ling/0000-0001-7807-2264; Liu, Shu-Lin/0000-0002-1043-4238
FU National Basic Research Program of China (973 Program) [2011CB933600];
Science Fund for Creative Research Groups of NSFC [20921062]; 111
Project; 3551 Talent Program of the Administrative Committee of East
Lake Hi-Tech Development Zone [[2011]137]; Intramural Research Program
of NICHD, National Institutes of Health
FX This work was supported by the National Basic Research Program of China
(973 Program, No. 2011CB933600), the Science Fund for Creative Research
Groups of NSFC (No. 20921062), the 111 Project, and the 3551 Talent
Program of the Administrative Committee of East Lake Hi-Tech Development
Zone ([2011]137). Y.-B.S. was supported by the Intramural Research
Program of NICHD, National Institutes of Health.
NR 31
TC 13
Z9 14
U1 5
U2 48
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
EI 1520-6882
J9 ANAL CHEM
JI Anal. Chem.
PD APR 15
PY 2014
VL 86
IS 8
BP 3902
EP 3908
DI 10.1021/ac500640u
PG 7
WC Chemistry, Analytical
SC Chemistry
GA AF4CC
UT WOS:000334658000034
PM 24678700
ER
PT J
AU Zhang, M
Khripin, CY
Fagan, JA
McPhie, P
Ito, Y
Zheng, M
AF Zhang, Min
Khripin, Constantine Y.
Fagan, Jeffrey A.
McPhie, Peter
Ito, Yoichiro
Zheng, Ming
TI Single-Step Total Fractionation of Single-Wall Carbon Nanotubes by
Countercurrent Chromatography
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID PARTITION CHROMATOGRAPHY; CHIRALITY SEPARATION; GEL CHROMATOGRAPHY;
RECOGNITION; EVOLUTION
AB Development of simple processes to fractionate synthetic mixtures of single-wall carbon nanotubes (SWCNTs) into individual species is crucial to many applications. Existing methods for single-chirality SWCNT purification are cumbersome, often requiring multiple steps and different conditions for different species. Here, we report a method to achieve total fractionation of a synthetic SWCNT mixture by countercurrent chromatography, resulting in purification of many single-chirality SWCNT species in a single run. This method is based on a tunable partition of sodium deoxycholate dispersed SWCNTs in a polyethylene glycol/dextran aqueous two-phase system. By running the mobile phase with 0.02% of sodium deoxycholate and a gradient of sodium dodecyl sulfate from 0.1% to 0.7% (w/w), we observe clear diameter-dependent elution, with similar to 90% total recovery. Among all the fractions collected, a number of them are enriched in single-chirality (9,4), (7,5), (7,6), (8,3), (6,5) species, while most of the remaining ones contain no more than 2-3 major species. We also observe strong (n,m)-dependent elution peak width due to the enantiomer-resolved partition. These results demonstrate countercurrent chromatography (CCC) as an effective way to obtain high purity (n, m) species, and suggest the potential of CCC as an analytical tool for chirality distribution mapping of synthetic SWCNT mixtures.
C1 [Zhang, Min] E China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, Shanghai 200237, Peoples R China.
[Zhang, Min; Ito, Yoichiro] NHLBI, Lab Bioseparat Technol, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
[Khripin, Constantine Y.; Fagan, Jeffrey A.; Zheng, Ming] NIST, Mat Sci & Engn Div, Gaithersburg, MD 20899 USA.
[McPhie, Peter] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Ito, Y (reprint author), NHLBI, Lab Bioseparat Technol, Biochem & Biophys Ctr, NIH, 31 Ctr Dr, Bethesda, MD 20892 USA.
EM itoy@nhlbi.nih.gov; ming.zheng@nist.gov
OI Fagan, Jeffrey/0000-0003-1483-5554
FU Intramural NIH HHS [ZIA HL005107-06, Z01 HL001054-05]
NR 21
TC 18
Z9 19
U1 5
U2 60
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
EI 1520-6882
J9 ANAL CHEM
JI Anal. Chem.
PD APR 15
PY 2014
VL 86
IS 8
BP 3980
EP 3984
DI 10.1021/ac5003189
PG 5
WC Chemistry, Analytical
SC Chemistry
GA AF4CC
UT WOS:000334658000044
PM 24673411
ER
PT J
AU Selvin, E
Parrinello, CM
Sacks, DB
Coresh, J
AF Selvin, Elizabeth
Parrinello, Christina M.
Sacks, David B.
Coresh, Josef
TI Trends in Prevalence and Control of Diabetes in the United States,
1988-1994 and 1999-2010
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID FASTING PLASMA-GLUCOSE; NATIONAL-HEALTH; PREDIABETES PREVALENCE;
ATHEROSCLEROSIS RISK; GLYCATED HEMOGLOBIN; ADULTS; MELLITUS; US; A1C;
CLASSIFICATION
AB Background: Trends in the prevalence and control of diabetes defined by hemoglobin A(1c) (HbA(1c)) levels are important for health care policy and planning.
Objective: To update trends in the prevalence of diabetes, prediabetes, and glycemic control.
Design: Cross-sectional.
Setting: NHANES (National Health and Nutrition Examination Survey) in 1988-1994 and 1999-2010.
Participants: Adults aged 20 years or older.
Measurements: We used calibrated HbA(1c) levels to define undiagnosed diabetes (>= 6.5%); prediabetes (5.7% to 6.4%); and, among persons with diagnosed diabetes, glycemic control (<7.0% or <8.0%). Trends in HbA(1c) categories were compared with fasting glucose levels (>= 7.0 mmol/L [>= 126 mg/dL] and 5.6 to 6.9 mmol/L [100 to 125 mg/dL]).
Results: In 2010, approximately 21 million U. S. adults aged 20 years or older had total confirmed diabetes (self-reported diabetes or diagnostic levels for both fasting glucose and calibrated HbA(1c)). During 2 decades, the prevalence of total confirmed diabetes in-creased, but the prevalence of undiagnosed diabetes remained fairly stable, reducing the proportion of total diabetes cases that are undiagnosed to 11% in 2005-2010. The prevalence of prediabetes was lower when defined by calibrated HbA(1c) levels than when defined by fasting glucose levels but has increased from 5.8% in 1988-1994 to 12.4% in 2005-2010 when defined by HbA(1c) levels. Glycemic control improved overall, but total diabetes prevalence was greater and diabetes was less controlled among non-Hispanic blacks and Mexican Americans compared with non-Hispanic whites.
Limitation: Cross-sectional design.
Conclusion: Over the past 2 decades, the prevalence of total diabetes has increased substantially. However, the proportion of undiagnosed diabetes cases decreased, suggesting improvements in screening and diagnosis. Among the growing number of persons with diagnosed diabetes, glycemic control improved but remains a challenge, particularly among non-Hispanic blacks and Mexican Americans.
C1 [Selvin, Elizabeth] Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21287 USA.
Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD 21287 USA.
Johns Hopkins Univ, Baltimore, MD USA.
NIH, Bethesda, MD 20892 USA.
RP Selvin, E (reprint author), Welch Ctr Prevent Epidemiol & Clin Res, 2024 East Monument St,Suite 2-600, Baltimore, MD 21287 USA.
EM lselvin@jhsph.edu
OI Sacks, David/0000-0003-3100-0735
FU National Institute of Diabetes and Digestive and Kidney Diseases [R01
DK089174]; National Heart, Lung, and Blood Institute [T32 HL007024];
Intramural Program of the National Institutes of Health
FX By the National Institute of Diabetes and Digestive and Kidney Diseases
(grant R01 DK089174) to Dr. Selvin. Ms. Parrinello was supported by the
National Heart, Lung, and Blood Institute (grant T32 HL007024). Dr.
Sacks was supported by the Intramural Program of the National Institutes
of Health.
NR 43
TC 150
Z9 152
U1 6
U2 28
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
EI 1539-3704
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD APR 15
PY 2014
VL 160
IS 8
BP 517
EP +
DI 10.7326/M13-2411
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA AG0ZE
UT WOS:000335143700001
PM 24733192
ER
PT J
AU Palmore, TN
Henderson, DK
AF Palmore, Tara N.
Henderson, David K.
TI Carbapenem-Resistant Enterobacteriaceae: A Call for Cultural Change
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Editorial Material
C1 [Palmore, Tara N.; Henderson, David K.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Henderson, DK (reprint author), NIH, Ctr Clin, Bldg 10,Room 6-1480,10 Ctr Dr, Bethesda, MD 20892 USA.
EM dkh@nih.gov
NR 11
TC 4
Z9 4
U1 0
U2 1
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
EI 1539-3704
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD APR 15
PY 2014
VL 160
IS 8
BP 567
EP +
DI 10.7326/M13-1910
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA AG0ZE
UT WOS:000335143700008
PM 24733200
ER
PT J
AU Kirby, TW
DeRose, EF
Beard, WA
Shock, DD
Wilson, SH
London, RE
AF Kirby, Thomas W.
DeRose, Eugene F.
Beard, William A.
Shock, David D.
Wilson, Samuel H.
London, Robert E.
TI Substrate Rescue of DNA Polymerase beta Containing a Catastrophic L22P
Mutation
SO BIOCHEMISTRY
LA English
DT Article
ID BASE EXCISION-REPAIR; ENZYME SPECIFICITY; GASTRIC-CANCER; ACTIVE-SITE;
AMINO-ACIDS; INDUCED FIT; BINDING; MUTANT; DOMAIN; MECHANISM
AB DNA polymerase (pol) beta is a multidomain enzyme with two enzymatic activities that plays a central role in the overlapping base excision repair and single-strand break repair pathways. The high frequency of pol beta variants identified in tumor-derived tissues suggests a possible role in the progression of cancer, making the determination of the functional consequences of these variants of interest. Pol beta containing a proline substitution for leucine 22 in the lyase domain (LD), identified in gastric tumors, has been reported to exhibit severe impairment of both lyase and polymerase activities. Nuclear magnetic resonance (NMR) spectroscopic evaluations of both pol beta and the isolated LD containing the L22P mutation demonstrate destabilization sufficient to result in LD-selective unfolding with minimal structural perturbations to the polymerase domain. Unexpectedly, addition of single-stranded or hairpin DNA resulted in partial refolding of the mutated lyase domain, both in isolation and for the full-length enzyme. Further, formation of an abortive ternary complex using Ca2+ and a complementary dNTP indicates that the fraction of pol beta(L22P) containing the folded LD undergoes conformational activation similar to that of the wild-type enzyme. Kinetic characterization of the polymerase activity of L22P pol beta indicates that the L22P mutation compromises DNA binding, but nearly wild-type catalytic rates can be observed at elevated substrate concentrations. The organic osmolyte trimethylamine N-oxide (TMAO) is similarly able to induce folding and kinetic activation of both polymerase and lyase activities of the mutant. Kinetic data indicate synergy between the TMAO cosolvent and substrate binding. NMR data indicate that the effect of the DNA results primarily from interaction with the folded LD(L22P), while the effect of the TMAO results primarily from destabilization of the unfolded LD(L22P). These studies illustrate that substrate-induced catalytic activation of pol beta provides an optimal enzyme conformation even in the presence of a strongly destabilizing point mutation. Accordingly, it remains to be determined whether this mutation alters the threshold of cellular repair activity needed for routine genome maintenance or whether the "inactive" variant interferes with DNA repair.
C1 [Kirby, Thomas W.; DeRose, Eugene F.; Beard, William A.; Shock, David D.; Wilson, Samuel H.; London, Robert E.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
RP London, RE (reprint author), 111 TW Alexander Dr,POB 12233,MD MR 01, Res Triangle Pk, NC 27709 USA.
EM london@niehs.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences (NIEHS)
[Z01-ES050147, ZO1-ES050158, ZO1-ES050159]; National Institutes of
Health, NIEHS [HHSN273200700046U]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences (NIEHS), under Research Project Z01-ES050147 to R.E.L.
and Research Projects ZO1-ES050158 and ZO1-ES050159 to S.H.W. E.F.D. is
supported by the National Institutes of Health, NIEHS, under Delivery
Order HHSN273200700046U.
NR 43
TC 4
Z9 4
U1 0
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 15
PY 2014
VL 53
IS 14
BP 2413
EP 2422
DI 10.1021/bi5001855
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AF4CB
UT WOS:000334657900022
PM 24655288
ER
PT J
AU Kodet, JG
Beutler, JA
Wiemer, DF
AF Kodet, John G.
Beutler, John A.
Wiemer, David F.
TI Synthesis and structure activity relationships of schweinfurthin indoles
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Schweinfurthin; Indole; Stilbene analogues; SAR
ID MACARANGA-SCHWEINFURTHII; STILBENE; ANALOGS
AB As part of a program to explore the biological activity of analogues of the natural schweinfurthins, a set of compounds has been prepared where an indole system can be viewed as a substitution for the resorcinol substructure of the schweinfurthin's D-ring. Twelve of these schweinfurthin indoles have been prepared and evaluated in the 60 cell line screen of the National Cancer Institute. While a range of activity has been observed, it is now clear that schweinfurthin indoles can demonstrate the intriguing pattern of activity associated with the natural stilbenes. In the best cases, these indole analogues display both potency and differential activity across the various cell lines comparable to the best resorcinol analogues. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Kodet, John G.; Wiemer, David F.] Univ Iowa, Dept Chem, Iowa City, IA 52242 USA.
[Beutler, John A.] NCI Frederick, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Wiemer, DF (reprint author), Univ Iowa, Dept Chem, Iowa City, IA 52242 USA.
EM david-wiemer@uiowa.edu
FU UI Graduate College for a Presidential Fellowship; Intramural Research
Program of NIH, National Cancer Institute, Center for Cancer Research;
Roy J. Carver Charitable Trust as a Research Program of Excellence
FX We thank the UI Graduate College for a Presidential Fellowship (to
J.G.K.). This research was supported in part by the Intramural Research
Program of NIH, National Cancer Institute, Center for Cancer Research.
Financial support from the Roy J. Carver Charitable Trust as a Research
Program of Excellence is gratefully acknowledged. We thank the
Developmental Therapeutics Program, NCI, for the 60-cell testing.
NR 25
TC 3
Z9 3
U1 1
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
EI 1464-3391
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD APR 15
PY 2014
VL 22
IS 8
BP 2542
EP 2552
DI 10.1016/j.bmc.2014.02.043
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA AE9OT
UT WOS:000334338000019
PM 24656801
ER
PT J
AU Tajuddin, SM
Amaral, AFS
Fernandez, AF
Chanock, S
Silverman, DT
Tardon, A
Carrato, A
Garcia-Closas, M
Jackson, BP
Torano, EG
Marquez, M
Urdinguio, RG
Garcia-Closas, R
Rothman, N
Kogevinas, M
Real, FX
Fraga, MF
Malats, N
AF Tajuddin, S. M.
Amaral, A. F. S.
Fernandez, A. F.
Chanock, S.
Silverman, D. T.
Tardon, A.
Carrato, A.
Garcia-Closas, M.
Jackson, B. P.
Torano, E. G.
Marquez, M.
Urdinguio, R. G.
Garcia-Closas, R.
Rothman, N.
Kogevinas, M.
Real, F. X.
Fraga, M. F.
Malats, N.
CA Spanish Bladder Canc EPICURO Study
TI LINE-1 methylation in leukocyte DNA, interaction with
phosphatidylethanolamine N-methyltransferase variants and bladder cancer
risk
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE bladder cancer; LINE-1 repetitive sequences; DNA methylation; one-carbon
metabolism; epigenetic-gene interaction
ID GENOME-WIDE ASSOCIATION; ONE-CARBON METABOLISM; PANCREATIC-CANCER;
CHOLINE METABOLISM; PROSTATE-CANCER; SUSCEPTIBILITY; HYPOMETHYLATION;
GENE; EPIGENETICS; INSTABILITY
AB Background: Aberrant global DNA methylation is shown to increase cancer risk. LINE-1 has been proven a measure of global DNA methylation. The objectives of this study were to assess the association between LINE-1 methylation level and bladder cancer risk and to evaluate effect modification by environmental and genetic factors.
Methods: Bisulphite-treated leukocyte DNA from 952 cases and 892 hospital controls was used to measure LINE-1 methylation level at four CpG sites by pyrosequencing. Logistic regression model was fitted to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). Interactions between LINE-1 methylation levels and environmental and genetic factors were assessed.
Results: The risk of bladder cancer followed a nonlinear association with LINE-1 methylation. Compared with subjects in the middle tertile, the adjusted OR for subjects in the lower and the higher tertiles were 1.26 (95% CI 0.99-1.60, P = 0.06) and 1.33 (95% CI 1.05-1.69, P = 0.02), respectively. This association significantly increased among individuals homozygous for the major allele of five single-nucleotide polymorphisms located in the phosphatidylethanolamine N-methyltransferase gene (corrected P-interactiono<0.05).
Conclusions: The findings from this large-scale study suggest that both low and high levels of global DNA methylation are associated with the risk of bladder cancer.
C1 [Tajuddin, S. M.; Amaral, A. F. S.; Marquez, M.; Malats, N.] Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid 28029, Spain.
[Fernandez, A. F.; Torano, E. G.; Urdinguio, R. G.; Fraga, M. F.] Univ Oviedo, HUCA, Inst Univ Oncol Principado Asturias, Canc Epigenet Lab, E-33006 Oviedo, Asturias, Spain.
[Chanock, S.; Silverman, D. T.; Rothman, N.] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Tardon, A.] Univ Oviedo, Inst Univ Oncol, Mol Epidemiol Grp, E-33006 Oviedo, Asturias, Spain.
[Tardon, A.] CIBERESP, Barcelona, Spain.
[Carrato, A.] Hosp Gen Univ Elche, Mol Oncol Grp, Alicante 03203, Spain.
[Carrato, A.] Hosp Ramon & Cajal, Dept Med Oncol, E-28034 Madrid, Spain.
[Garcia-Closas, M.] Inst Canc Res, Div Genet & Epidemiol, Sutton SM2 5NG, Surrey, England.
[Jackson, B. P.] Dartmouth Coll, Dept Earth Sci, Trace Element Anal Core, Hanover, NH 03755 USA.
[Garcia-Closas, R.] Hosp Univ Canarias, Unidad Invest, San Cristobal la Laguna 38320, Spain.
[Kogevinas, M.] Ctr Res Environm Epidemiol CREAL, Barcelona 08003, Spain.
[Real, F. X.] Spanish Natl Canc Res Ctr CNIO, Epithelial Carcinogenesis Grp, Madrid 28029, Spain.
[Real, F. X.] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona 08002, Spain.
[Fraga, M. F.] Ctr Nacl Biotecnol CNB CSIC, Dept Immunol & Oncol, Madrid 28049, Spain.
RP Malats, N (reprint author), Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid 28029, Spain.
EM mffraga@cnb.csic.es; nmalats@cnio.es
RI Hernandez-Llodra, S/H-6863-2014; Murta-Nascimento,
Cristiane/G-3738-2012; Garcia-Closas, Montserrat /F-3871-2015; Malats,
Nuria/H-7041-2015; Real Arribas, Francisco/H-5275-2015; Fernandez ,
Irene/E-5705-2016; Fernandez, Agustin/N-7302-2014; Martinez,
Esther/H-2562-2013; Kogevinas, Manolis/C-3918-2017; Amaral,
Andre/A-7662-2008
OI Tajuddin, Salman M./0000-0002-7919-8528; Hernandez-Llodra,
S/0000-0003-3963-3756; Soto, Jose Luis/0000-0003-0234-9188; Puente,
Diana/0000-0003-4725-537X; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Malats, Nuria/0000-0003-2538-3784; Real Arribas,
Francisco/0000-0001-9501-498X; Fernandez, Agustin/0000-0002-3792-4085;
Amaral, Andre/0000-0002-0369-9449
FU Association for International Cancer Research [09-0780]; Fondo de
Investigacion Sanitaria, Spain [00/0745, PI051436, PI061614, G03/174];
Red Tematica de Investigacion Cooperativa en Cancer, Spain
[RD12/0036/0050-RTICC]; European Commission
[EU-FP7-HEALTH-F2-2008-201663-UROMOL,
EU-FP7-HEALTH-F2-2008-201333-DECanBio]; Fundacion Cientifica de la AECC,
Spain; US National Institutes of Health [USA-NIH-RO1-CA089715];
Intramural Research Program of the Division of Cancer Epidemiology and
Genetics, National Cancer Institute at the National Institutes of
Health, USA
FX We acknowledge the coordinators, field and administrative workers,
technicians and patients of the Spanish Bladder Cancer/EPICURO Study.
This work was supported by the Association for International Cancer
Research (grant number 09-0780); Fondo de Investigacion Sanitaria, Spain
(grant numbers 00/0745, PI051436, PI061614, G03/174); Red Tematica de
Investigacion Cooperativa en Cancer (grant number RD12/0036/0050-RTICC),
Spain; European Commission (grant numbers
EU-FP7-HEALTH-F2-2008-201663-UROMOL;
EU-FP7-HEALTH-F2-2008-201333-DECanBio); Fundacion Cientifica de la AECC,
Spain; US National Institutes of Health (grant number
USA-NIH-RO1-CA089715); and the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute
at the National Institutes of Health, USA.
NR 46
TC 7
Z9 7
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 15
PY 2014
VL 110
IS 8
BP 2123
EP 2130
DI 10.1038/bjc.2014.67
PG 8
WC Oncology
SC Oncology
GA AF3CA
UT WOS:000334587900026
PM 24595004
ER
PT J
AU Wongtrakoongate, P
Li, J
Andrews, PW
AF Wongtrakoongate, P.
Li, J.
Andrews, P. W.
TI Aza-deoxycytidine induces apoptosis or differentiation via DNMT3B and
targets embryonal carcinoma cells but not their differentiated
derivatives
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE Human teratocarcinoma stem cells; embryonic stem cells; nullipotent;
pluripotent; DNMT3B
ID STEM-CELLS; IN-SITU; DNA METHYLTRANSFERASE; EXPRESSION PROFILES; RNA
INTERFERENCE; GERM-CELLS; TERATOCARCINOMA; METHYLATION; TUMORS;
5-AZA-2-DEOXYCYTIDINE
AB Background: Teratocarcinoma is a malignant male germ cell tumour, which contains stem cells and differentiated cancer tissues. DNMT3B has been shown to be highly expressed in human teratocarcinoma stem cells, and to mediate cytotoxicity of Azadeoxycytidine (Aza-dC) in a pluripotent stem cell line NTERA2.
Methods: We have established DNMT3B or POU5F1 (hereafter referred to as OCT4) knockdown in teratocarcinoma stem cells N2102Ep and TERA1 and in the pluripotent NTERA2 by a doxycycline-inducible system, and tested the cytotoxicity induced by Aza-dC.
Results: Silencing of DNMT3B led to apoptosis of human teratocarcinoma stem cells N2102Ep and TERA1. Further, we found that induction of apoptosis or differentiation in NTERA2 and human embryonic stem cells by Aza-dC requires DNMT3B. To test whether Aza-dC inhibits proliferation of differentiated teratocarcinoma cells, we depleted OCT4 expression in N2102Ep and TERA1 cells treated with Aza-dC. Treatment with Aza-dC reduced cell number of differentiated cells to a lesser extent than their undifferentiated parental stem cells. Moreover, in contrast to the stem cells, Aza-dC failed to induce apoptosis of differentiated cells.
Conclusions: Our finding suggests that DNMT3B acts as an antiapoptotic gene in teratocarcinoma stem cells, and mediates apoptosis and differentiation of human pluripotent stem cells induced by Aza-dC, and that Aza-dC specifically induces apoptosis of teratocarcinoma stem cells.
C1 [Wongtrakoongate, P.; Li, J.; Andrews, P. W.] Univ Sheffield, Ctr Stem Cell Biol, Sheffield S10 2TN, S Yorkshire, England.
RP Wongtrakoongate, P (reprint author), Natl Inst Diabet & Digest & Kidney Dis, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM p.wongtrakoongate@gmail.com
FU Thai Commission on Higher Education
FX This research was supported by the Thai Commission on Higher Education
to PW.
NR 38
TC 3
Z9 3
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 15
PY 2014
VL 110
IS 8
BP 2131
EP 2138
DI 10.1038/bjc.2014.128
PG 8
WC Oncology
SC Oncology
GA AF3CA
UT WOS:000334587900027
PM 24603304
ER
PT J
AU Lowe, JM
Menendez, D
Bushel, PR
Shatz, M
Kirk, EL
Troester, MA
Garantziotis, S
Fessler, MB
Resnick, MA
AF Lowe, Julie M.
Menendez, Daniel
Bushel, Pierre R.
Shatz, Maria
Kirk, Erin L.
Troester, Melissa A.
Garantziotis, Stavros
Fessler, Michael B.
Resnick, Michael A.
TI p53 and NF-kappa B Coregulate Proinflammatory Gene Responses in Human
Macrophages
SO CANCER RESEARCH
LA English
DT Article
ID CANCER-CELLS; RADIATION PNEUMONITIS; TRANSCRIPTION FACTOR; SIGNALING
PATHWAY; DNA-DAMAGE; IN-VIVO; ACTIVATION; EXPRESSION; GROWTH;
INTERLEUKIN-6
AB Macrophages are sentinel immune cells that survey the tissue microenvironment, releasing cytokines in response to both exogenous insults and endogenous events such as tumorigenesis. Macrophages mediate tumor surveillance and therapy-induced tumor regression; however, tumor-associated macrophages (TAM) and their products may also promote tumor progression. Whereas NF-kappa B is prominent in macrophage-initiated inflammatory responses, little is known about the role of p53 in macrophage responses to environmental challenge, including chemotherapy or in TAMs. Here, we report that NF-kappa B and p53, which generally have opposing effects in cancer cells, coregulate induction of proinflammatory genes in primary human monocytes and macrophages. Using Nutlin-3 as a tool, we demonstrate that p53 and NF-kappa B rapidly and highly induce interleukin (IL)-6 by binding to its promoter. Transcriptome analysis revealed global p53/NF-kappa B co-regulation of immune response genes, including several chemokines, which effectively induced human neutrophil migration. In addition, we show that p53, activated by tumor cell paracrine factors, induces high basal levels of macrophage IL-6 in a TAM model system [tumor-conditioned macrophages (TCM)]. Compared with normal macrophages, TCMs exhibited higher p53 levels, enhanced p53 binding to the IL-6 promoter, and reduced IL-6 levels upon p53 inhibition. Taken together, we describe a mechanism by which human macrophages integrate signals through p53 and NF-kappa B to drive proinflammatory cytokine induction. Our results implicate a novel role for macrophage p53 in conditioning the tumor microenvironment and suggest a potential mechanism by which p53-activating chemotherapeutics, acting upon p53-sufficient macrophages and precursor monocytes, may indirectly impact tumors lacking functional p53. (C) 2014 AACR.
C1 [Lowe, Julie M.; Menendez, Daniel; Shatz, Maria; Resnick, Michael A.] NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Bushel, Pierre R.] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Garantziotis, Stavros; Fessler, Michael B.] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
[Kirk, Erin L.; Troester, Melissa A.] Univ N Carolina, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
RP Resnick, MA (reprint author), NIEHS, MD D3-01,POB 12233, Res Triangle Pk, NC 27709 USA.
EM julie.lowe@nih.gov; resnick@niehs.nih.gov
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
FU NIH, NIEHS, Breast Cancer; Environment Research Program grant
[U01-ES109472]; NIEHS Intramural Research Program
FX This study was supported by funding from NIH, NIEHS, Breast Cancer and
the Environment Research Program grant, U01-ES109472 (M.A. Troester and
E.L. Kirk) and the NIEHS Intramural Research Program.
NR 50
TC 30
Z9 30
U1 1
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2014
VL 74
IS 8
BP 2182
EP 2192
DI 10.1158/0008-5472.CAN-13-1070
PG 11
WC Oncology
SC Oncology
GA AF3AQ
UT WOS:000334584200007
PM 24737129
ER
PT J
AU Yaffe, K
Vittinghoff, E
Pletcher, MJ
Hoang, TD
Launer, LJ
Whitmer, R
Coker, LH
Sidney, S
AF Yaffe, Kristine
Vittinghoff, Eric
Pletcher, Mark J.
Hoang, Tina D.
Launer, Lenore J.
Whitmer, Rachel
Coker, Laura H.
Sidney, Stephen
TI Early Adult to Midlife Cardiovascular Risk Factors and Cognitive
Function
SO CIRCULATION
LA English
DT Article
DE blood pressure; cholesterol; cognition; glucose; risk factors
ID CORONARY CALCIUM LATER; LATE-LIFE; ALZHEIMERS-DISEASE; BLOOD-PRESSURE;
YOUNG-ADULTS; TEST-PERFORMANCE; DEMENTIA; CHOLESTEROL; HEALTH; AGE
AB Background Studies have linked midlife and late-life cardiovascular risk factors (CVRFs) to cognitive function, yet little is known about CVRF exposure in early adulthood and subsequent cognitive function. In addition, most studies rely on single assessments of CVRFs, which may not accurately reflect long-term exposure. We sought to determine the association between cumulative exposure to CVRFs from early to middle adulthood and cognitive function at midlife.
Methods and Results In a prospective study of 3381 adults (age, 18-30 years at baseline) with 25 years of follow-up, we assessed cognitive function at year 25 (2010-2011) with the Digit Symbol Substitution Test, Stroop Test, and Rey Auditory Verbal Learning Test analyzed with standardized z scores. The primary predictor was 25-year cumulative exposure estimated by areas under the curve for resting systolic and diastolic blood pressures, fasting blood glucose, and total cholesterol. Higher cumulative systolic and diastolic blood pressures and fasting blood glucose were consistently associated with worse cognition on all 3 tests. These associations were significant primarily for exposures above recommended guidelines; cognitive test z scores were between 0.06 and 0.30 points less, on average, for each 1-SD increase in risk factor area under the curve after adjustment for age, race, sex, and education (P<0.05 for all). Fewer significant associations were observed for cholesterol.
Conclusions Cumulative exposure to CVRFs from early to middle adulthood, especially above recommended guidelines, was associated with worse cognition in midlife. The meaning of this association and whether it warrants more aggressive treatment of CVRFs earlier in life require further investigation.
C1 [Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94121 USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94121 USA.
[Yaffe, Kristine; Vittinghoff, Eric; Pletcher, Mark J.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94121 USA.
[Pletcher, Mark J.] Univ Calif San Francisco, Dept Med, Div Gen Internal Med, San Francisco, CA 94121 USA.
[Yaffe, Kristine] San Francisco VA Med Ctr, San Francisco, CA USA.
[Hoang, Tina D.] Northern Calif Inst Res & Educ, San Francisco, CA USA.
[Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Whitmer, Rachel; Sidney, Stephen] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
[Coker, Laura H.] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
RP Yaffe, K (reprint author), Univ Calif San Francisco, Box 181,4150 Clement St, San Francisco, CA 94121 USA.
EM kristine.yaffe@ucsf.edu
FU National Heart, Lung, and Blood Institute (NHLBI) in collaboration with
the University of Alabama at Birmingham [HHSN268201300025C,
HHSN268201300026C]; Northwestern University [HHSN268201300027C];
University of Minnesota [HHSN268201300028C]; Kaiser Foundation Research
Institute [HHSN268201300029C]; Johns Hopkins University School of
Medicine [HHSN268200900041C]; Intramural Research Program of the
National Institute on Aging (NIA); NIA; NHLBI [AG0005]
FX The Coronary Artery Risk Development in Young Adults Study (CARDIA) is
conducted and supported by the National Heart, Lung, and Blood Institute
(NHLBI) in collaboration with the University of Alabama at Birmingham
(HHSN268201300025C & HHSN268201300026C), Northwestern University
(HHSN268201300027C), University of Minnesota (HHSN268201300028C), Kaiser
Foundation Research Institute (HHSN268201300029C), and Johns Hopkins
University School of Medicine (HHSN268200900041C). CARDIA is also
partially supported by the Intramural Research Program of the National
Institute on Aging (NIA) and an intra-agency agreement between NIA and
NHLBI (AG0005). This manuscript has been reviewed by CARDIA for
scientific content.
NR 50
TC 37
Z9 39
U1 0
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD APR 15
PY 2014
VL 129
IS 15
BP 1560
EP 1567
DI 10.1161/CIRCULATIONAHA.113.004798
PG 8
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AE9II
UT WOS:000334321100009
PM 24687777
ER
PT J
AU Malik, SM
Maher, VE
Bijwaard, KE
Becker, RL
Zhang, LJ
Tang, SHW
Song, PF
Liu, Q
Marathe, A
Gehrke, B
Helms, W
Hanner, D
Justice, R
Pazdur, R
AF Malik, Shakun M.
Maher, Virginia Ellen
Bijwaard, Karen E.
Becker, Robert L.
Zhang, Lijun
Tang, Shenghui W.
Song, Pengfei
Liu, Qi
Marathe, Anshu
Gehrke, Brenda
Helms, Whitney
Hanner, Diane
Justice, Robert
Pazdur, Richard
TI US Food and Drug Administration Approval: Crizotinib for Treatment of
Advanced or Metastatic Non-Small Cell Lung Cancer That Is Anaplastic
Lymphoma Kinase Positive
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID EML4-ALK FUSION GENE; ALK; CHEMOTHERAPY; TRANSCRIPTS; CARCINOMAS; EGFR
AB On August 26, 2011, the U. S. Food and Drug Administration (FDA) approved crizotinib (XALKORI Capsules, Pfizer Inc.) for treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) that is anaplastic lymphoma kinase (ALK) positive as detected by an FDA-approved test. The Vysis ALK Break-Apart FISH Probe Kit (Abbott Molecular, Inc.) was approved concurrently. In two multicenter, single-arm trials, patients with locally advanced or metastatic ALK-positive NSCLC previously treated with one or more systemic therapies received crizotinib orally at a dose of 250 mg twice daily. In 119 patients with ALK-positive NSCLC by local trial assay, the objective response rate (ORR) was 61% [95% confidence intervals (CI), 52%-70%] with a median response duration of 48 weeks. In 136 patients with ALK-positive NSCLC by the to-be-marketed test, the ORR was 50% (95% CI, 42%-59%) with a median response duration of 42 weeks. The most common adverse reactions (>= 25%) were vision disorder, nausea, diarrhea, vomiting, edema, and constipation. Accelerated approval was granted on the basis of the high ORRs and durable responses. On November 20, 2013, crizotinib received full approval based on an improvement in progression-free survival in patients with metastatic ALK-positive NSCLC previously treated with one platinum-based chemotherapy regimen. Clin Cancer Res; 20(8); 2029-34. (C) 2014 AACR.
C1 [Malik, Shakun M.] NCI, Clin Investigat Branch, Canc Therapy Evaluat Program, NIH, Bethesda, MD 20892 USA.
[Maher, Virginia Ellen; Gehrke, Brenda; Helms, Whitney; Hanner, Diane; Justice, Robert; Pazdur, Richard] US FDA, Off Hematol & Oncol Prod, Silver Spring, MD 20993 USA.
[Zhang, Lijun; Tang, Shenghui W.] US FDA, Off Biostat, Silver Spring, MD 20993 USA.
[Song, Pengfei; Liu, Qi; Marathe, Anshu] US FDA, Off Clin Pharmacol, Ctr Drug Evaluat & Res, Silver Spring, MD 20993 USA.
[Bijwaard, Karen E.; Becker, Robert L.] US FDA, Off In Vitro Diagnost & Radiol Hlth, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
RP Justice, R (reprint author), US FDA, 10903 New Hampshire Ave,Bldg 22,Room 2125, Silver Spring, MD 20993 USA.
EM robert.justice@fda.hhs.gov
NR 17
TC 41
Z9 41
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2014
VL 20
IS 8
BP 2029
EP 2034
DI 10.1158/1078-0432.CCR-13-3077
PG 6
WC Oncology
SC Oncology
GA AF3AJ
UT WOS:000334583500004
PM 24573551
ER
PT J
AU Kennedy-Nasser, AA
Ku, S
Castillo-Caro, P
Hazrat, Y
Wu, MF
Liu, H
Melenhorst, J
Barrett, AJ
Ito, S
Foster, A
Savoldo, B
Yvon, E
Carrum, G
Ramos, CA
Krance, RA
Leung, K
Heslop, HE
Brenner, MK
Bollard, CM
AF Kennedy-Nasser, Alana A.
Ku, Stephanie
Castillo-Caro, Paul
Hazrat, Yasmin
Wu, Meng-Fen
Liu, Hao
Melenhorst, Jos
Barrett, A. John
Ito, Sawa
Foster, Aaron
Savoldo, Barbara
Yvon, Eric
Carrum, George
Ramos, Carlos A.
Krance, Robert A.
Leung, Kathryn
Heslop, Helen E.
Brenner, Malcolm K.
Bollard, Catherine M.
TI Ultra Low-Dose IL-2 for GVHD Prophylaxis after Allogeneic Hematopoietic
Stem Cell Transplantation Mediates Expansion of Regulatory T Cells
without Diminishing Antiviral and Antileukemic Activity
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CHRONIC MYELOGENOUS LEUKEMIA; BONE-MARROW-TRANSPLANTATION; ACUTE
LYMPHOBLASTIC-LEUKEMIA; RECOMBINANT INTERLEUKIN-2; HEMATOLOGICAL
MALIGNANCY; CHEMO-RADIOTHERAPY; PEDIATRIC-PATIENTS; IMMUNE-RESPONSES;
HEALTHY DONORS; HOST-DISEASE
AB Purpose: GVHD after allogeneic hematopoietic stem cell transplantation (alloSCT) has been associated with low numbers of circulating CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tregs). Because Tregs express high levels of the interleukin (IL)-2 receptor, they may selectively expand in vivo in response to doses of IL-2 insufficient to stimulate T effector T-cell populations, thereby preventing GVHD.
Experimental Design: We prospectively evaluated the effects of ultra low-dose (ULD) IL-2 injections on Treg recovery in pediatric patients after alloSCT and compared this recovery with Treg reconstitution post alloSCT in patients without IL-2. Sixteen recipients of related (n = 12) or unrelated (n = 4) donor grafts received ULD IL-2 post hematopoietic stem cell transplantation (HSCT; 100,000-200,000 IU/m(2) x 3 per week), starting