FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Normand, J
Li, JH
Thomson, N
Jarlais, DD
AF Normand, Jacques
Li, Jih-Heng
Thomson, Nicholas
Jarlais, Don Des
TI Harm reduction
SO JOURNAL OF FOOD AND DRUG ANALYSIS
LA English
DT Article; Proceedings Paper
CT International Conference on Global Health (ICGH)
CY APR 17-19, 2013
CL Taipei, TAIWAN
DE Harm reduction; Methadone; Needle/syringe programs
AB The "Harm Reduction" session was chaired by Dr Jacques Normand, Director of the AIDS Research Program of the United States National Institute on Drug Abuse. The three presenters (and their presentation topics) were: Dr Don Des Jarlais (High coverage needle/syringe programs for people who inject drugs in low and middle income countries: a systematic review), Dr Nicholas Thomson (Harm reduction history, response, and current trends in Asia), and Dr Jih-Heng Li (Harm reduction strategies in Taiwan). Copyright (C) 2013, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC. All rights reserved.
C1 [Normand, Jacques] Natl Inst Drug Abuse, AIDS Res Program, Bethesda, MD 20892 USA.
[Li, Jih-Heng] Kaohsiung Med Univ, Coll Pharm, Sch Pharm, Kaohsiung, Taiwan.
[Li, Jih-Heng] Kaohsiung Med Univ, Coll Pharm, PhD Program Toxicol, Kaohsiung, Taiwan.
[Thomson, Nicholas] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Thomson, Nicholas] Univ Melbourne, Nossal Inst Global Hlth, Melbourne, Vic, Australia.
[Jarlais, Don Des] Beth Israel Deaconess Med Ctr, Baron Edmond De Rothschild Chem Dependency Inst, New York, NY 10003 USA.
RP Normand, J (reprint author), Natl Inst Drug Abuse, 6001 Execut Blvd,MSC 9581, Bethesda, MD 20892 USA.
EM jnormand@nida.nih.gov
FU NIDA NIH HHS [P30 DA016383, R13 DA035084]
NR 3
TC 0
Z9 0
U1 1
U2 5
PU FOOD & DRUG ADMINSTRATION
PI TAIPEI
PA 161-2 KUNYANG STREET, NANGANG, TAIPEI, 00000, TAIWAN
SN 1021-9498
J9 J FOOD DRUG ANAL
JI J. Food Drug Anal.
PD DEC
PY 2013
VL 21
SU 4
BP S10
EP S12
DI 10.1016/j.jfda.2013.09.022
PG 3
WC Food Science & Technology; Pharmacology & Pharmacy
SC Food Science & Technology; Pharmacology & Pharmacy
GA 285VJ
UT WOS:000329422800006
PM 25278732
ER
PT J
AU Normand, J
Montaner, J
Fang, CT
Wu, ZY
Chen, YM
AF Normand, Jacques
Montaner, Julio
Fang, Chi-Tai
Wu, Zunyou
Chen, Yi-Ming
TI HIV: Seek, test, treat, and retain
SO JOURNAL OF FOOD AND DRUG ANALYSIS
LA English
DT Article; Proceedings Paper
CT International Conference on Global Health (ICGH)
CY APR 17-19, 2013
CL Taipei, TAIWAN
DE HIV; Retain; Seek; Test; Treat
AB The "HIV: Seek, Test, Treat, and Retain" session was chaired by Dr Jacques Normand, the director of AIDS Research at the US National Institute on Drug Abuse. Dr Yi-Ming Chen served as the discussant. The three presenters (and their presentation topics) were: Dr Julio Montaner (Treatment as Prevention The Key to an AIDS-free Generation), Dr Chi-Tai Fang (Population-level Effect of Free Access to HAART on Reducing HIV Transmission in Taiwan), and Dr Zunyou Wu (Challenges in Promoting HIV Test and Treat Strategy in China). Copyright (C) 2013, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC. All rights reserved.
C1 [Normand, Jacques] Natl Inst Drug Abuse, Bethesda, MD 20892 USA.
[Montaner, Julio] Univ British Columbia, British Columbia Ctr Excellence HIV AIDS, Vancouver, BC V5Z 1M9, Canada.
[Fang, Chi-Tai] Natl Taiwan Univ, Coll Publ Hlth, Taipei 10764, Taiwan.
[Wu, Zunyou] China CDC, Natl Ctr AIDS STD Control & Prevent, Beijing, Peoples R China.
[Chen, Yi-Ming] Kaohsiung Med Univ, Ctr Infect Dis & Canc Res, Kaohsiung, Taiwan.
RP Normand, J (reprint author), Natl Inst Drug Abuse, AIDS Res Program, 6001 Execut Blvd,MSC 9581, Bethesda, MD 20892 USA.
EM jnormand@nida.nih.gov
RI Fang, Chi-Tai/P-2908-2016
OI Fang, Chi-Tai/0000-0002-7380-1699
FU NIDA NIH HHS [R13 DA035084, P30 DA016383]
NR 3
TC 2
Z9 3
U1 0
U2 1
PU FOOD & DRUG ADMINSTRATION
PI TAIPEI
PA 161-2 KUNYANG STREET, NANGANG, TAIPEI, 00000, TAIWAN
SN 1021-9498
J9 J FOOD DRUG ANAL
JI J. Food Drug Anal.
PD DEC
PY 2013
VL 21
SU 4
BP S4
EP S6
DI 10.1016/j.jfda.2013.09.020
PG 3
WC Food Science & Technology; Pharmacology & Pharmacy
SC Food Science & Technology; Pharmacology & Pharmacy
GA 285VJ
UT WOS:000329422800004
PM 25278735
ER
PT J
AU Tai, B
Saxon, AJ
Ling, W
AF Tai, Betty
Saxon, Andrew J.
Ling, Walter
TI Medication-assisted therapy for opioid addiction
SO JOURNAL OF FOOD AND DRUG ANALYSIS
LA English
DT Article; Proceedings Paper
CT International Conference on Global Health (ICGH)
CY APR 17-19, 2013
CL Taipei, TAIWAN
DE Buprenorphine; Chronic care model; Methadone; Opioid addiction
ID BUPRENORPHINE-NALOXONE; CARE
AB The "Medication-Assisted Therapy for Opioid Addiction" session was chaired by Dr Betty Tai and had three presenters. The presenters (and their topics) were: Dr Andrew J. Saxon (methadone and buprenorphine for treatment of opioid addiction and human immunodeficiency virus risk reduction); Dr Walter Ling (opioid antagonist treatment for opioid addiction); and Dr Betty Tai (chronic care model for substance use disorder). Copyright (C) 2013, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC. All rights reserved.
C1 [Tai, Betty] Natl Inst Drug Abuse, Ctr Clin Trials Network, Bethesda, MD 20892 USA.
[Saxon, Andrew J.] VA Puget Sound Hlth Care Syst, Ctr Excellence Subst Abuse Treatment & Educ, Seattle, WA USA.
[Saxon, Andrew J.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Ling, Walter] Univ Calif Los Angeles, David Geffen Sch Med, Integrated Subst Abuse Programs, Los Angeles, CA 90095 USA.
RP Tai, B (reprint author), Natl Inst Drug Abuse, Ctr Clin Trials Network, 6001 Execut Blvd, Bethesda, MD 20892 USA.
EM btai@nida.nih.gov
FU NIDA NIH HHS [R13 DA035084, P30 DA016383]
NR 11
TC 4
Z9 4
U1 0
U2 4
PU FOOD & DRUG ADMINSTRATION
PI TAIPEI
PA 161-2 KUNYANG STREET, NANGANG, TAIPEI, 00000, TAIWAN
SN 1021-9498
J9 J FOOD DRUG ANAL
JI J. Food Drug Anal.
PD DEC
PY 2013
VL 21
SU 4
BP S13
EP S15
DI 10.1016/j.jfda.2013.09.023
PG 3
WC Food Science & Technology; Pharmacology & Pharmacy
SC Food Science & Technology; Pharmacology & Pharmacy
GA 285VJ
UT WOS:000329422800007
PM 25264415
ER
PT J
AU Volkow, ND
AF Volkow, Nora D.
TI Special Issue on Promoting Global Health-Treatment and Prevention of
Substance Abuse and HIV in Asia Foreword
SO JOURNAL OF FOOD AND DRUG ANALYSIS
LA English
DT Editorial Material
C1 Natl Inst Drug Abuse, NIH, Bethesda, MD 20892 USA.
RP Volkow, ND (reprint author), Natl Inst Drug Abuse, NIH, Bethesda, MD 20892 USA.
FU NIDA NIH HHS [R13 DA035084, P30 DA016383]
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FOOD & DRUG ADMINSTRATION
PI TAIPEI
PA 161-2 KUNYANG STREET, NANGANG, TAIPEI, 00000, TAIWAN
SN 1021-9498
J9 J FOOD DRUG ANAL
JI J. Food Drug Anal.
PD DEC
PY 2013
VL 21
SU 4
BP S2
EP S2
DI 10.1016/j.jfda.2013.09.018
PG 1
WC Food Science & Technology; Pharmacology & Pharmacy
SC Food Science & Technology; Pharmacology & Pharmacy
GA 285VJ
UT WOS:000329422800002
PM 25530687
ER
PT J
AU Joo, JS
Song, JY
Baik, SC
Lee, WK
Cho, MJ
Lee, KH
Cho, Y
Youn, HS
Seo, JH
Rhee, KH
Kang, HL
AF Joo, Jung-Soo
Song, Jae-Young
Baik, Seung-Chul
Lee, Woo-Kon
Cho, Myung-Je
Lee, Kon-Ho
Cho, YoungAh
Youn, Hee-Shang
Seo, Ji-Hyun
Rhee, Kwang-Ho
Kang, Hyung-Lyun
TI Genetic organization and conjugal plasmid DNA transfer of pHP69, a
plasmid from a Korean isolate of Helicobacter pylori (vol 50, pg 955,
2012)
SO JOURNAL OF MICROBIOLOGY
LA English
DT Correction
C1 [Song, Jae-Young; Baik, Seung-Chul; Lee, Woo-Kon; Cho, Myung-Je; Lee, Kon-Ho; Cho, YoungAh; Rhee, Kwang-Ho; Kang, Hyung-Lyun] Gyeongsang Natl Univ, Sch Med, Dept Microbiol, Jinju 660751, South Korea.
[Youn, Hee-Shang; Seo, Ji-Hyun] Gyeongsang Natl Univ, Sch Med, Dept Pediat, Jinju 660751, South Korea.
[Song, Jae-Young; Baik, Seung-Chul; Lee, Woo-Kon; Cho, Myung-Je; Lee, Kon-Ho; Rhee, Kwang-Ho; Kang, Hyung-Lyun] Gyeongsang Natl Univ, Life Sci Res Inst, Jinju 660701, South Korea.
[Joo, Jung-Soo] Natl Inst Diabet Digest & Kidney Dis, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Joo, JS (reprint author), Natl Inst Diabet Digest & Kidney Dis, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 2
PU MICROBIOLOGICAL SOCIETY KOREA
PI SEOUL
PA KOREA SCIENCE & TECHNOLOGY CENTER 803, 635-4 YEOGSAM-DONG, KANGNAM-KU,
SEOUL 135-703, SOUTH KOREA
SN 1225-8873
EI 1976-3794
J9 J MICROBIOL
JI J. Microbiol.
PD DEC
PY 2013
VL 51
IS 6
BP 889
EP 889
DI 10.1007/s12275-013-0727-y
PG 1
WC Microbiology
SC Microbiology
GA 283IE
UT WOS:000329238900029
ER
PT J
AU Yoon, JH
Abdelmohsen, K
Kim, J
Yang, XL
Martindale, JL
Tominaga-Yamanaka, K
White, EJ
Orjalo, AV
Rinn, JL
Kreft, SG
Wilson, GM
Gorospe, M
AF Yoon, Je-Hyun
Abdelmohsen, Kotb
Kim, Jiyoung
Yang, Xiaoling
Martindale, Jennifer L.
Tominaga-Yamanaka, Kumiko
White, Elizabeth J.
Orjalo, Arturo V.
Rinn, John L.
Kreft, Stefan G.
Wilson, Gerald M.
Gorospe, Myriam
TI Scaffold function of long non-coding RNA HOTAIR in protein
ubiquitination
SO NATURE COMMUNICATIONS
LA English
DT Article
ID BINDING PROTEIN; REPLICATIVE SENESCENCE; INTERACTION NETWORK; HUR;
PHOSPHORYLATION; EXPRESSION; ATAXIN-1; DECAY; DIFFERENTIATION;
IDENTIFICATION
AB Although mammalian long non-coding (lnc) RNAs are best known for modulating transcription, their post-transcriptional influence on mRNA splicing, stability and translation is emerging. Here we report a post-translational function for the lncRNA HOTAIR as an inducer of ubiquitin-mediated proteolysis. HOTAIR associates with E3 ubiquitin ligases bearing RNA-binding domains, Dzip3 and Mex3b, as well as with their respective ubiquitination substrates, Ataxin-1 and Snurportin-1. In this manner, HOTAIR facilitates the ubiquitination of Ataxin-1 by Dzip3 and Snurportin-1 by Mex3b in cells and in vitro, and accelerates their degradation. HOTAIR levels are highly upregulated in senescent cells, causing rapid decay of targets Ataxin-1 and Snurportin-1, and preventing premature senescence. These results uncover a role for a lncRNA, HOTAIR, as a platform for protein ubiquitination.
C1 [Yoon, Je-Hyun; Abdelmohsen, Kotb; Kim, Jiyoung; Yang, Xiaoling; Martindale, Jennifer L.; Tominaga-Yamanaka, Kumiko; Gorospe, Myriam] NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[White, Elizabeth J.; Wilson, Gerald M.] Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA.
[White, Elizabeth J.; Wilson, Gerald M.] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Orjalo, Arturo V.] Biosearch Technol Inc, Novato, CA 94949 USA.
[Rinn, John L.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Kreft, Stefan G.] Univ Constance, Dept Biol, D-78457 Constance, Germany.
RP Yoon, JH (reprint author), NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM yoonjehyun@gmail.com
FU NIH [R01 CA102428]; NIA-IRP, NIH; [R01 ES020260-02]
FX We thank G.J. Hannon, H.Y. Chang, L.E. Maquat, H.T. Orr, R.P. Wersto, S.
Kang and J. Campisi for providing reagents and assistance. J.L.R. was
supported by R01 ES020260-02. E.J.W. and G.M.W. were supported by NIH
R01 CA102428. J.-H.Y., K.A., J.K., X.Y., J.L.M., K.T.-Y. and M.G. were
supported by NIA-IRP, NIH.
NR 39
TC 31
Z9 31
U1 2
U2 32
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2013
VL 4
DI 10.1038/ncomms3939
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 285LY
UT WOS:000329396700003
ER
PT J
AU Borotikar, BS
Sheehan, FT
AF Borotikar, B. S.
Sheehan, F. T.
TI In vivo patellofemoral contact mechanics during active extension using a
novel dynamic MRI-based methodology
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Article
DE Patella; Femur; Knee; Magnetic resonance imaging; Sensitivity; Accuracy;
Cartilage; Osteoarthritis; Patellofemoral pain syndrome
ID IMPACTED ARTICULAR-CARTILAGE; CINE-PC MRI; WEIGHT-BEARING; CHONDROCYTE
VIABILITY; PATELLAR TRACKING; JOINT MECHANICS; KNEE EXTENSION;
WATER-LOSS; KINEMATICS; OSTEOARTHRITIS
AB Objectives: To establish an in vivo, normative patellofemoral (PF) cartilage contact mechanics database acquired during voluntary muscle control using a novel, dynamic, magnetic resonance (MR) imagingbased, computational methodology and validate the contact mechanics sensitivity to the known submillimeter methodological accuracies.
Design: Dynamic cine phase-contrast and multi-plane cine (MPC) images were acquired while female subjects (n = 20, sample of convenience) performed an open kinetic chain (knee flexion-extension) exercise inside a 3-T MR scanner. Static cartilage models were created from high resolution threedimensional static MR data and accurately placed in their dynamic pose at each time frame based on the cine-PC (CPC) data. Cartilage contact parameters were calculated based on the surface overlap. Statistical analysis was performed using paired t-test and a one-sample repeated measures ANOVA. The sensitivity of the contact parameters to the known errors in the PF kinematics was determined.
Results: Peak mean PF contact area was 228.7 +/- 173.6 mm(2) at 40 degrees knee angle. During extension, contact centroid and peak strain locations tracked medially on the femoral and patellar cartilage and were not significantly different from each other. At 25 degrees, 30 degrees, 35 degrees, and 40 degrees of knee extension, contact area was significantly different. Contact area and centroid locations were insensitive to rotational and translational perturbations.
Conclusion: This study is a first step towards unfolding the biomechanical pathways to anterior PF pain and osteoarthritis (OA) using dynamic, in vivo, and accurate methodologies. The database provides crucial data for future studies and for validation of, or as an input to, computational models. Published by Elsevier Ltd on behalf of Osteoarthritis Research Society International.
C1 [Borotikar, B. S.; Sheehan, F. T.] NIH, Dept Rehabil Med, Funct & Appl Biomech Sect, Bethesda, MD 20892 USA.
RP Sheehan, FT (reprint author), NIH, Bldg 10 CRC RM 1-1469,10 Ctr Dr MSC 1604, Bethesda, MD 20892 USA.
EM fsheehan@cc.nih.gov
RI sheehan, frances/B-6962-2009
FU Intramural Research Program of the NIH Clinical Center
FX This research was supported by the Intramural Research Program of the
NIH Clinical Center.
NR 49
TC 10
Z9 11
U1 2
U2 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1063-4584
EI 1522-9653
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD DEC
PY 2013
VL 21
IS 12
BP 1886
EP 1894
DI 10.1016/j.joca.2013.08.023
PG 9
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA 283SG
UT WOS:000329266700009
PM 24012620
ER
PT J
AU Inge, TH
King, WC
Jenkins, TM
Courcoulas, AP
Mitsnefes, M
Flum, DR
Wolfe, BM
Pomp, A
Dakin, GF
Khandelwal, S
Zeller, MH
Horlick, M
Pender, JR
Chen, JY
Daniels, SR
AF Inge, Thomas H.
King, Wendy C.
Jenkins, Todd M.
Courcoulas, Anita P.
Mitsnefes, Mark
Flum, David R.
Wolfe, Bruce M.
Pomp, Alfons
Dakin, Greg F.
Khandelwal, Saurabh
Zeller, Meg H.
Horlick, Mary
Pender, John R.
Chen, Jia-Yuh
Daniels, Stephen R.
TI The Effect of Obesity in Adolescence on Adult Health Status
SO PEDIATRICS
LA English
DT Article
DE obesity; bariatric; weight history
ID BODY-MASS INDEX; CARDIOVASCULAR RISK-FACTORS; BARIATRIC SURGERY;
FOLLOW-UP; DURATION; WEIGHT; OVERWEIGHT; BMI; ADIPOSITY; HISTORY
AB OBJECTIVE: To test the hypothesis that adolescent obesity would be associated with greater risks of adverse health in severely obese adults.
METHODS: Before weight loss surgery, adult participants in the Longitudinal Assessment of Bariatric Surgery-2 underwent detailed anthropometric and comorbidity assessment. Weight status at age 18 was retrospectively determined. Participants who were >= 80% certain of recalled height and weight at age 18 (1502 of 2308) were included. Log binomial regression was used to evaluate whether weight status at age 18 was independently associated with risk of comorbid conditions at time of surgery controlling for potential confounders.
RESULTS: Median age and adult body mass index (BMI) were 47 years and 46, respectively. At age 18, 42% of subjects were healthy weight, 29% overweight, 16% class 1 obese, and 13% class >= 2 obese. Compared with healthy weight at age 18, class >= 2 obesity at age 18 independently increased the risk of lower-extremity venous edema with skin manifestations by 435% (P < .0001), severe walking limitation by 321% (P < .0001), abnormal kidney function by 302% (P < .0001), polycystic ovary syndrome by 74% (P = .03), asthma by 48% (P = .01), diabetes by 42% (P < .01), obstructive sleep apnea by 25% (P < .01), and hypertension (by varying degrees based on age and gender). Conversely, the associated risk of hyperlipidemia was reduced by 61% (P < .01).
CONCLUSIONS: Severe obesity at age 18 was independently associated with increased risk of several comorbid conditions in adults undergoing bariatric surgery.
C1 [Inge, Thomas H.; Jenkins, Todd M.; Mitsnefes, Mark; Zeller, Meg H.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat & Pediat Surg, Cincinnati, OH 45229 USA.
[Inge, Thomas H.; Jenkins, Todd M.; Mitsnefes, Mark; Zeller, Meg H.] Univ Cincinnati, Cincinnati, OH USA.
[King, Wendy C.; Chen, Jia-Yuh] Univ Pittsburgh, Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Courcoulas, Anita P.] Univ Pittsburgh, Med Ctr, Dept Surg, Pittsburgh, PA USA.
[Flum, David R.; Khandelwal, Saurabh] Univ Washington, Dept Surg, Seattle, WA 98195 USA.
[Wolfe, Bruce M.] Oregon Hlth & Sci Univ, Dept Surg, Portland, OR 97201 USA.
[Pomp, Alfons; Dakin, Greg F.] Weill Cornell Med Coll, Dept Surg, New York, NY USA.
[Horlick, Mary] Natl Inst Diabet & Digest & Kidney Dis, Div Digest Dis & Nutr, Bethesda, MD 20892 USA.
[Pender, John R.] E Carolina Univ, Dept Surg, Greenville, NC USA.
[Daniels, Stephen R.] Univ Colorado, Dept Pediat, Denver, CO 80202 USA.
RP Inge, TH (reprint author), Cincinnati Childrens Hosp Med Ctr, 3333 Burnet Ave,MLC 2023, Cincinnati, OH 45229 USA.
EM thomas.inge@cchmc.org
OI King, Wendy/0000-0002-0740-0029
FU National Institute of Diabetes and Digestive and Kidney Diseases: LABS-2
[DCC-U01DK066557]; National Institute of Diabetes and Digestive and
Kidney Diseases: Cincinnati Childrens Hospital Medical Center
[U01DK072493, UM1DK072493, UM1DK095710]; National Institute of Diabetes
and Digestive and Kidney Diseases: Columbia [U01DK66667]; National
Institute of Diabetes and Digestive and Kidney Diseases: Cornell
University Medical Center CTRC [UL1RR024996]; National Institute of
Diabetes and Digestive and Kidney Diseases: University of Washington
[U01DK66568]; National Institute of Diabetes and Digestive and Kidney
Diseases: CTRC [M01RR-00037, UL1RR024153]; National Institute of
Diabetes and Digestive and Kidney Diseases: Neuropsychiatric Research
Institute [U01DK66471]; National Institute of Diabetes and Digestive and
Kidney Diseases: East Carolina University [U01DK66526]; National
Institute of Diabetes and Digestive and Kidney Diseases: University of
Pittsburgh Medical Center [U01DK66585]; National Institute of Diabetes
and Digestive and Kidney Diseases: Oregon Health & Science University
[U01DK66555]; National Institute of Diabetes and Digestive and Kidney
Diseases: Teen LABS-2 consortium [1U01DK072493-01]
FX This analysis was conducted as a joint collaboration between members of
the LABS-2 and Teen-LABS consortia. These consortia were funded by
cooperative agreements with the National Institute of Diabetes and
Digestive and Kidney Diseases: LABS-2, grant DCC-U01DK066557; Cincinnati
Childrens Hospital Medical Center, grants U01DK072493, UM1DK072493, and
UM1DK095710; Columbia, grant U01DK66667 (in collaboration with Cornell
University Medical Center CTRC, grant UL1RR024996); University of
Washington, U01DK66568 (in collaboration with CTRC, grant M01RR-00037);
Neuropsychiatric Research Institute, grant U01DK66471; East Carolina
University, grant U01DK66526; University of Pittsburgh Medical Center,
grant U01DK66585 (in collaboration with CTRC, grant UL1RR024153); Oregon
Health & Science University, grant U01DK66555.; The LABS-2 consortium
acknowledges the Teen LABS-2 consortium (grant 1U01DK072493-01) for
development and use of the Weight History Questionnaire.
NR 24
TC 26
Z9 26
U1 4
U2 15
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD DEC
PY 2013
VL 132
IS 6
BP 1098
EP 1104
DI 10.1542/peds.2013-2185
PG 7
WC Pediatrics
SC Pediatrics
GA 282IG
UT WOS:000329163900051
PM 24249816
ER
PT J
AU Bell, EF
Hansen, NI
Brion, LP
Ehrenkranz, RA
Kennedy, KA
Walsh, MC
Shankaran, S
Acarregui, MJ
Johnson, KJ
Hale, EC
Messina, LA
Crawford, MM
Laptook, AR
Goldberg, RN
Van Meurs, KP
Carlo, WA
Poindexter, BB
Faix, RG
Carlton, DP
Watterberg, KL
Ellsbury, DL
Das, A
Higgins, RD
AF Bell, Edward F.
Hansen, Nellie I.
Brion, Luc P.
Ehrenkranz, Richard A.
Kennedy, Kathleen A.
Walsh, Michele C.
Shankaran, Seetha
Acarregui, Michael J.
Johnson, Karen J.
Hale, Ellen C.
Messina, Lynn A.
Crawford, Margaret M.
Laptook, Abbot R.
Goldberg, Ronald N.
Van Meurs, Krisa P.
Carlo, Waldemar A.
Poindexter, Brenda B.
Faix, Roger G.
Carlton, David P.
Watterberg, Kristi L.
Ellsbury, Dan L.
Das, Abhik
Higgins, Rosemary D.
CA Eunice Kennedy Shriver Natl Inst C
Neonatal Res Network
TI Serum Tocopherol Levels in Very Preterm Infants After a Single Dose of
Vitamin E at Birth
SO PEDIATRICS
LA English
DT Article
DE vitamin E; preterm infants
ID PREMATURE-INFANTS; INTRAVENTRICULAR HEMORRHAGE; NECROTIZING
ENTEROCOLITIS; E SUPPLEMENTATION; WEIGHT INFANTS; BREAST-MILK; CHILDREN;
LESS; ABSORPTION; NUTRITION
AB OBJECTIVE: Our aim was to examine the impact of a single enteral dose of vitamin E on serum tocopherol levels. The study was undertaken to see whether a single dose of vitamin E soon after birth can rapidly increase the low alpha-tocopherol levels seen in very preterm infants. If so, this intervention could be tested as a means of reducing the risk of intracranial hemorrhage.
METHODS: Ninety-three infants <27 weeks' gestation and <1000 g were randomly assigned to receive a single dose of vitamin E or placebo by gastric tube within 4 hours of birth. The vitamin E group received 50 IU/kg of vitamin E as dl-alpha-tocopheryl acetate (Aquasol E). The placebo group received sterile water. Blood samples were taken for measurement of serum tocopherol levels by high-performance liquid chromatography before dosing and 24 hours and 7 days after dosing.
RESULTS: Eighty-eight infants received the study drug and were included in the analyses. The alpha-tocopherol levels were similar between the groups at baseline but higher in the vitamin E group at 24 hours (median 0.63 mg/dL vs 0.42 mg/dL, P = .003) and 7 days (2.21 mg/dL vs 1.86 mg/dL, P = .04). There were no differences between groups in gamma-tocopherol levels. At 24 hours, 30% of vitamin E infants and 62% of placebo infants had a-tocopherol levels <0.5 mg/dL.
CONCLUSIONS: A 50-IU/kg dose of vitamin E raised serum alpha-tocopherol levels, but to consistently achieve a-tocopherol levels >0.5 mg/dL, a higher dose or several doses of vitamin E may be needed.
C1 [Bell, Edward F.; Acarregui, Michael J.; Johnson, Karen J.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Hansen, Nellie I.] RTI Int, Social Stat & Environm Sci Unit, Res Triangle Pk, NC USA.
[Brion, Luc P.] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
[Ehrenkranz, Richard A.] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06510 USA.
[Kennedy, Kathleen A.] Univ Texas Houston, Sch Med, Dept Pediat, Houston, TX USA.
[Walsh, Michele C.] Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA.
[Walsh, Michele C.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Shankaran, Seetha] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Hale, Ellen C.; Carlton, David P.] Emory Univ, Sch Med & Childrens Healthcare Atlanta, Dept Pediat, Atlanta, GA 30322 USA.
[Messina, Lynn A.] St Johns Mercy Med Ctr, Des Moines, IA USA.
[Crawford, Margaret M.; Das, Abhik] RTI Int, Social Stat & Environm Sci Unit, Rockville, MD USA.
[Laptook, Abbot R.] Women & Infants Hosp Rhode Isl, Dept Pediat, Providence, RI 02908 USA.
[Laptook, Abbot R.] Brown Univ, Providence, RI 02912 USA.
[Goldberg, Ronald N.] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
[Van Meurs, Krisa P.] Stanford Univ, Sch Med, Dept Pediat, Palo Alto, CA 94304 USA.
[Van Meurs, Krisa P.] Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA.
[Carlo, Waldemar A.] Univ Alabama Birmingham, Dept Pediat, Birmingham, AL USA.
[Poindexter, Brenda B.] Indiana Univ Sch Med, Dept Pediat, Indianapolis, IN 46202 USA.
[Faix, Roger G.] Univ Utah, Sch Med, Dept Pediat, Salt Lake City, UT USA.
[Watterberg, Kristi L.] Univ New Mexico, Hlth Sci Ctr, Dept Pediat, Albuquerque, NM 87131 USA.
[Ellsbury, Dan L.] Ctr Res Educ & Qual, Pediat Med Grp, Sunrise, FL USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Bell, EF (reprint author), Univ Iowa, Dept Pediat, 200 Hawkins Dr, Iowa City, IA 52242 USA.
EM edward-bell@uiowa.edu
FU The National Institutes of Health; Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD); NICHD; National
Institutes of Health (NIH)
FX The National Institutes of Health and the Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD)
provided grant support for the Neonatal Research Network's Generic
Database Study. Dr Higgins is employed by the NICHD. The institutions of
most of the other authors received grant funding from NICHD in support
of this study. Funded by the National Institutes of Health (NIH).
NR 39
TC 5
Z9 5
U1 1
U2 2
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD DEC
PY 2013
VL 132
IS 6
BP E1626
EP E1633
DI 10.1542/peds.2013-1684
PG 8
WC Pediatrics
SC Pediatrics
GA 282IG
UT WOS:000329163900021
PM 24218460
ER
PT J
AU Mire, CE
Geisbert, JB
Marzi, A
Agans, KN
Feldmann, H
Geisbert, TW
AF Mire, Chad E.
Geisbert, Joan B.
Marzi, Andrea
Agans, Krystle N.
Feldmann, Heinz
Geisbert, Thomas W.
TI Vesicular Stomatitis Virus-Based Vaccines Protect Nonhuman Primates
against Bundibugyo ebolavirus
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID ATTENUATED RECOMBINANT VACCINE; MARBURG HEMORRHAGIC-FEVER;
RESTON-EBOLAVIRUS; POSTEXPOSURE PROTECTION; AEROSOL CHALLENGE;
GUINEA-PIGS; INFECTION; IMMUNIZATION; ADENOVIRUS; VECTOR
AB Ebola virus (EBOV) causes severe and often fatal hemorrhagic fever in humans and nonhuman primates (NHPs). Currently, there are no licensed vaccines or therapeutics for human use. Recombinant vesicular stomatitis virus (rVSV)-based vaccine vectors, which encode an EBOV glycoprotein in place of the VSV glycoprotein, have shown 100% efficacy against homologous Sudan ebolavirus (SEBOV) or Zaire ebolavirus (ZEBOV) challenge in NHPs. In addition, a single injection of a blend of three rVSV vectors completely protected NHPs against challenge with SEBOV, ZEBOV, the former Cote d'Ivoire ebolavirus, and Marburg virus. However, recent studies suggest that complete protection against the newly discovered Bundibugyo ebolavirus (BEBOV) using several different heterologous filovirus vaccines is more difficult and presents a new challenge. As BEBOV caused nearly 50% mortality in a recent outbreak any filovirus vaccine advanced for human use must be able to protect against this new species. Here, we evaluated several different strategies against BEBOV using rVSV-based vaccines. Groups of cynomolgus macaques were vaccinated with a single injection of a homologous BEBOV vaccine, a single injection of a blended heterologous vaccine (SEBOV/ZEBOV), or a prime-boost using heterologous SEBOV and ZEBOV vectors. Animals were challenged with BEBOV 29-36 days after initial vaccination. Macaques vaccinated with the homologous BEBOV vaccine or the prime-boost showed no overt signs of illness and survived challenge. In contrast, animals vaccinated with the heterologous blended vaccine and unvaccinated control animals developed severe clinical symptoms consistent with BEBOV infection with 2 of 3 animals in each group succumbing. These data show that complete protection against BEBOV will likely require incorporation of BEBOV glycoprotein into the vaccine or employment of a prime-boost regimen. Fortunately, our results demonstrate that heterologous rVSV-based filovirus vaccine vectors employed in the prime-boost approach can provide protection against BEBOV using an abbreviated regimen, which may have utility in outbreak settings.
Author Summary Ebola viruses (EBOV), of which there are five species, are categorized as Category A Priority Pathogens and Tier 1 Select Agents by several US Government agencies as a result of their high mortality rates and potential for use as agents of bioterrorism. Currently, there are no vaccines or therapeutics approved for human use. Replication-competent, recombinant vesicular stomatitis virus (rVSV) vectors expressing filovirus glycoproteins (GP), in place of the VSV glycoprotein have shown promise in lethal nonhuman primate (NHP) models of filovirus infection as both single injection preventive vaccines and as post-exposure treatments. The recent outbreak of the fifth recognized EBOV species, Bundibugyo ebolavirus (BEBOV), demonstrates the need for vaccines that can be rapidly deployed to combat an outbreak of a new filovirus species. To date, rVSV-filovirus GP-based vaccines have only been able to protect against challenge with a homologous species of EBOV. Here, we show that the two heterologous rVSV-based filovirus vaccines available at the time of the original BEBOV outbreak can protect NHPs against BEBOV challenge using a short prime-boost vaccination strategy. While the prime-boost strategy was successful, a single injection blended vaccination strategy with the same vaccine vectors failed to provide protection. These data suggest that an abbreviated prime-boost regimen of 36 days may have utility for quickly responding to outbreaks caused by new species of EBOV.
C1 [Mire, Chad E.; Geisbert, Joan B.; Agans, Krystle N.; Geisbert, Thomas W.] Univ Texas Med Branch, Galveston Natl Lab, Galveston, TX 77555 USA.
[Mire, Chad E.; Geisbert, Joan B.; Agans, Krystle N.; Geisbert, Thomas W.] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA.
[Marzi, Andrea; Feldmann, Heinz] NIAID, Virol Lab, Div Intramural Res, NIH, Hamilton, MT USA.
RP Mire, CE (reprint author), Univ Texas Med Branch, Galveston Natl Lab, Galveston, TX 77555 USA.
EM twgeisbe@utmb.edu
FU University of Texas Medical Branch at Galveston; Intramural Research
Program of the NIH, NIAID; Department of Health and Human Services, NIH
[AI098817]
FX The animal portion of this research was supported by the University of
Texas Medical Branch at Galveston. Non-animal portions of the work were
supported by the Intramural Research Program of the NIH, NIAID and 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 44
TC 26
Z9 28
U1 1
U2 22
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2013
VL 7
IS 12
AR e2600
DI 10.1371/journal.pntd.0002600
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 282JU
UT WOS:000329168100022
PM 24367715
ER
PT J
AU Rabaa, MA
Simmons, CP
Fox, A
Le, MQ
Nguyen, TTT
Le, HY
Gibbons, RV
Nguyen, XT
Holmes, EC
Aaskov, JG
AF Rabaa, Maia A.
Simmons, Cameron P.
Fox, Annette
Mai Quynh Le
Thuy Thi Thu Nguyen
Hai Yen Le
Gibbons, Robert V.
Xuyen Thanh Nguyen
Holmes, Edward C.
Aaskov, John G.
TI Dengue Virus in Sub-tropical Northern and Central Viet Nam: Population
Immunity and Climate Shape Patterns of Viral Invasion and Maintenance
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID AEDES-AEGYPTI; MOLECULAR CHARACTERIZATION; PHYLOGENETIC UNCERTAINTY;
GUANGDONG PROVINCE; SOUTHERN VIETNAM; KAMPHAENG-PHET; CHINA; OUTBREAK;
THAILAND; FEVER
AB Dengue virus transmission occurs in both epidemic and endemic cycles across tropical and sub-tropical regions of the world. Incidence is particularly high in much of Southeast Asia, where hyperendemic transmission plagues both urban and rural populations. However, endemicity has not been established in some areas with climates that may not support year-round viral transmission. An understanding of how dengue viruses (DENV) enter these environments and whether the viruses persist in inapparent local transmission cycles is central to understanding how dengue emerges in areas at the margins of endemic transmission. Dengue is highly endemic in tropical southern Vietnam, while increasingly large seasonal epidemics have occurred in northern Viet Nam over the last decade. We have investigated the spread of DENV-1 throughout Vietnam to determine the routes by which the virus enters northern and central regions of the country. Phylogeographic analysis of 1,765 envelope (E) gene sequences from Southeast Asia revealed frequent movement of DENV between neighboring human populations and strong local clustering of viral lineages. Long-distance migration of DENV between human population centers also occurred regularly and on short time-scales, indicating human-mediated viral invasion into northern Vietnam. Human populations in southern Vietnam were found to be the primary source of DENV circulating throughout the country, while central and northern Vietnam acted as sink populations, likely due to reduced connectedness to other populations in the case of the central regions and to the influence of temperature variability on DENV replication and vector survival and competence in the north. Finally, phylogeographic analyses suggested that viral movement follows a gravity model and indicates that population immunity and physical and economic connections between populations may play important roles in shaping patterns of DENV transmission.
Author Summary Reports from sub-tropical regions of the world suggest a growing risk of introduction and establishment of dengue viruses (DENV) in new locales. Recent dengue epidemics in northern Viet Nam present an opportunity to study how DENV invades and spreads in these environments. The proximity of this region to tropical areas experiencing year-round endemic DENV transmission makes it an ideal site for studying the effects of human population movement and climate on DENV emergence. We performed a phylogenetic analysis using DENV-1 envelope gene sequences from Southeast Asia. We show that DENV are regularly imported into northern and central Viet Nam from southern Vietnam, and that increasingly large seasonal epidemics in the north are caused by newly introduced viruses each year. While tropical Vietnam maintains localized virus populations for multiple years, cool winter temperatures in sub-tropical northern Viet Nam may reduce mosquito populations and virus replication to levels that are not conducive to year-round DENV transmission. Finally, we found that the dispersal of DENV across the region is well-described using human movement and immunity data, and believe that increased epidemiological, entomological, and virological surveillance are needed to understand the processes by which endemic DENV transmission becomes established in new populations.
C1 [Rabaa, Maia A.] Univ Edinburgh, Ctr Immun Infect & Evolut, Edinburgh, Midlothian, Scotland.
[Rabaa, Maia A.; Simmons, Cameron P.] Univ Oxford, Clin Res Unit, Hosp Trop Dis, Ho Chi Minh City, Vietnam.
[Simmons, Cameron P.; Fox, Annette] Univ Oxford, Nuffield Dept Clin Med, Ctr Trop Med, Oxford, England.
[Fox, Annette] Univ Oxford, Clin Res Unit, Wellcome Trust Major Overseas Programme, Hanoi, Vietnam.
[Mai Quynh Le; Thuy Thi Thu Nguyen] Natl Inst Hyg & Epidemiol, Hanoi, Vietnam.
[Hai Yen Le; Xuyen Thanh Nguyen] Mil Inst Hyg & Epidemiol, Hanoi, Vietnam.
[Gibbons, Robert V.] Armed Forces Res Inst Med Sci, Bangkok 10400, Thailand.
[Holmes, Edward C.] Univ Sydney, Sch Biol Sci, Marie Bashir Inst Emerging Dis & Biosecur, Sydney, NSW 2006, Australia.
[Holmes, Edward C.] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Aaskov, John G.] Queensland Univ Technol, Brisbane, Qld 4001, Australia.
[Aaskov, John G.] Australian Army Malaria Inst, Brisbane, Qld, Australia.
RP Rabaa, MA (reprint author), Univ Edinburgh, Ctr Immun Infect & Evolut, Edinburgh, Midlothian, Scotland.
EM j.aaskov@qut.edu.au
OI Rabaa, Maia/0000-0003-0529-2228; Simmons, Cameron
P./0000-0002-9039-7392; Holmes, Edward/0000-0001-9596-3552
FU National Science Foundation Graduate Research Fellowship; Wellcome Trust
of the United Kingdom through the Vietnamese Initiative on Zoonotic
InfectiONS (WT-VIZIONS); National Health and Medical Research Council of
Australia; U.S. Global Emerging Infections Surveillance and Response
System; National Institutes of Health [R01 GM087405]
FX Funding to MAR was provided by a National Science Foundation Graduate
Research Fellowship and by the Wellcome Trust of the United Kingdom
through the Vietnamese Initiative on Zoonotic InfectiONS (WT-VIZIONS).
This study was supported by grants from the National Health and Medical
Research Council of Australia (including an Australia Fellowship to
ECH), the U.S. Global Emerging Infections Surveillance and Response
System, and the National Institutes of Health (grant R01 GM087405 to
ECH). The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 60
TC 10
Z9 10
U1 0
U2 18
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2013
VL 7
IS 12
AR e2581
DI 10.1371/journal.pntd.0002581
PG 12
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 282JU
UT WOS:000329168100016
PM 24340118
ER
PT J
AU Safronetz, D
Sogoba, N
Lopez, JE
Maiga, O
Dahlstrom, E
Zivcec, M
Feldmann, F
Haddock, E
Fischer, RJ
Anderson, JM
Munster, VJ
Branco, L
Garry, R
Porcella, SF
Schwan, TG
Feldmann, H
AF Safronetz, David
Sogoba, Nafomon
Lopez, Job E.
Maiga, Ousmane
Dahlstrom, Eric
Zivcec, Marko
Feldmann, Friederike
Haddock, Elaine
Fischer, Robert J.
Anderson, Jennifer M.
Munster, Vincent J.
Branco, Luis
Garry, Robert
Porcella, Stephen F.
Schwan, Tom G.
Feldmann, Heinz
TI Geographic Distribution and Genetic Characterization of Lassa Virus in
Sub-Saharan Mali
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID WEST-AFRICA; MASTOMYS-NATALENSIS; FEVER; INFECTION; ARENAVIRUSES;
DISEASE; RODENTS; REGION
AB Background Lassa fever is an acute viral illness characterized by multi-organ failure and hemorrhagic manifestations. Lassa fever is most frequently diagnosed in Nigeria, Sierra Leone, Liberia, and Guinea, although sporadic cases have been recorded in other West African countries, including Mali. The etiological agent of Lassa fever is Lassa virus (LASV), an Arenavirus which is maintained in nature and frequently transmitted to humans by Mastomys natalensis. The purpose of this study was to better define the geographic distribution of LASV-infected rodents in sub-Saharan Mali.
Methodologies/Principal Findings Small mammals were live-trapped at various locations across Mali for the purpose of identifying potential zoonotic pathogens. Serological and molecular assays were employed and determined LASV infected rodents were exclusively found in the southern Mali near the border of Cote d'Ivoire. Overall, 19.4% of Mastomys natalensis sampled in this region had evidence of LASV infection, with prevalence rates for individual villages ranging from 0 to 52%. Full-length genomic sequences were determined using high throughput sequencing methodologies for LASV isolates generated from tissue samples of rodents collected in four villages and confirmed the phylogenetic clustering of Malian LASV with strain AV.
Conclusions/Significance The risk of human infections with LASV is greatest in villages in southern Mali. Lassa fever should be considered in the differential diagnosis for febrile individuals and appropriate diagnostic techniques need to be established to determine the incidence of infection and disease in these regions.
Author Summary Lassa fever is an acute infection associated with hemorrhagic manifestations and multi-organ failure in West Africa. The etiological agent of Lassa fever is Lassa virus (LASV), a rodent-borne arenavirus, which is maintained in nature and transmitted to humans by the multimammate rat, Mastomys natalensis. Despite the ubiquitous nature of the rodent reservoir, LASV-infected animals are most commonly documented in Nigeria, Sierra Leone, Guinea and Liberia. These four countries represent the historic endemic region for Lassa fever, although there is increasing evidence of sporadic cases occurring in other West African nations including Mali. To better define the geographic distribution of LASV-infected rodents in Mali, we tested samples from small animals collected at 27 sites across the country. Although M. natalensis was the predominant rodent species in the majority of villages, evidence of LASV infection was exclusively found in southern Mali, where overall nearly 20% of rodents were positive. The full genomic sequence was determined for five isolates and confirmed LASV in Mali is closely related to strain AV. We conclude that there is a risk of human exposure to LASV in villages in southern Mali and Lassa fever should be considered in the differential diagnosis for acutely ill, febrile patients.
C1 [Safronetz, David; Zivcec, Marko; Haddock, Elaine; Munster, Vincent J.; Feldmann, Heinz] NIAID, Virol Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Sogoba, Nafomon; Maiga, Ousmane] Univ Sci Tech & Technol Bamako, Malaria Res & Training Ctr, Bamako, Mali.
[Lopez, Job E.; Fischer, Robert J.; Schwan, Tom G.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Dahlstrom, Eric; Porcella, Stephen F.] NIAID, Rocky Mt Lab, Res Technol Sect, Genom Unit,Rocky Mt Labs,NIH, Hamilton, MT 59840 USA.
[Zivcec, Marko; Feldmann, Heinz] Univ Manitoba, Dept Med Microbiol, Winnipeg, MB, Canada.
[Feldmann, Friederike] NIAID, Rocky Mt Vet Branch, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Anderson, Jennifer M.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Branco, Luis; Garry, Robert] Tulane Sch Med, Dept Microbiol & Immunol, New Orleans, LA USA.
[Branco, Luis] Autoimmune Technol LLC, New Orleans, LA USA.
RP Safronetz, D (reprint author), NIAID, Virol Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
EM safronetzd@naidi.nih.gov; feldmannh@niaid.nih.gov
OI Fischer, Robert/0000-0002-1816-472X; Zivcec, Marko/0000-0003-4337-8487;
Munster, Vincent/0000-0002-2288-3196; Branco, Luis/0000-0001-8161-0182
FU International Centers for Excellence in Research program of the Division
of Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health
FX This work was funded by the International Centers for Excellence in
Research program of the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. The funders had no role in the study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 28
TC 12
Z9 12
U1 3
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2013
VL 7
IS 12
AR e2582
DI 10.1371/journal.pntd.0002582
PG 9
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 282JU
UT WOS:000329168100013
PM 24340119
ER
PT J
AU Nguyen, THT
Nguyen, THQ
Vu, TT
Farrar, J
Hoang, TL
Dong, THT
Tran, VN
Phung, KL
Wolbers, M
Whitehead, SS
Hibberd, ML
Wills, B
Simmons, CP
AF Thi Hanh Tien Nguyen
Than Ha Quyen Nguyen
Tuan Trung Vu
Farrar, Jeremy
Truong Long Hoang
Thi Hoai Tam Dong
Van Ngoc Tran
Khanh Lam Phung
Wolbers, Marcel
Whitehead, Stephen S.
Hibberd, Martin L.
Wills, Bridget
Simmons, Cameron P.
TI Corticosteroids for Dengue - Why Don't They Work?
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID IMMUNE ACTIVATION; VIRUS-INFECTIONS; DISEASE SEVERITY; RECEPTOR;
LEAKAGE; BURDEN
AB Background Dysregulated immune responses may contribute to the clinical complications that occur in some patients with dengue.
Findings In Vietnamese pediatric dengue cases randomized to early prednisolone therapy, 81 gene-transcripts (0.2% of the 47,231 evaluated) were differentially abundant in whole-blood between high-dose (2 mg/kg) prednisolone and placebo-treated patients two days after commencing therapy. Prominent among the 81 transcripts were those associated with T and NK cell cytolytic functions. Additionally, prednisolone therapy was not associated with changes in plasma cytokine levels.
Conclusion The inability of prednisolone treatment to markedly attenuate the host immune response is instructive for planning future therapeutic strategies for dengue.
Author Summary Dengue is an acute, mosquito-borne febrile illness and around 390 million cases occur annually in more than 100 countries. A host pro-inflammatory immune response is widely believed to contribute to the clinical complications that occur in some patients with dengue. Synthetic glucocorticoids, which are immunomodulatory agents commonly used in medicine, have been suggested as a therapy for dengue. We recently performed a randomized, controlled trial of early oral glucocorticoid therapy in 225 dengue cases in Vietnam, comparing a three day regimen of high (2 mg/kg) or low (0.5 mg/kg) dose prednisolone with placebo. Here, we report on immunological changes occurring during prednisolone therapy with a view to understanding the lack of clinical benefit by glucocorticoid therapy and to guide future intervention strategies for dengue. In whole-blood gene expression arrays we found 81 transcripts from 64 genes differentially abundant between high-dose prednisolone and placebo treated patients. Prominent were the genes associated with T and NK cell cytolytic functions. These results are a reminder that the mechanisms causally behind some of the complications of dengue (e.g. altered capillary permeability) are very poorly understood and represent a major knowledge gap in our understanding of disease pathogenesis that also undermines attempts to improve clinical management.
C1 [Thi Hanh Tien Nguyen; Than Ha Quyen Nguyen; Tuan Trung Vu; Farrar, Jeremy; Khanh Lam Phung; Wolbers, Marcel; Wills, Bridget; Simmons, Cameron P.] Univ Oxford, Clin Res Unit, Hosp Trop Dis, Ho Chi Minh City, Vietnam.
[Farrar, Jeremy; Wolbers, Marcel; Wills, Bridget; Simmons, Cameron P.] Univ Oxford, Ctr Trop Med, Nuffield Dept Med, Oxford, England.
[Truong Long Hoang; Hibberd, Martin L.] Genome Inst Singapore, Singapore, Singapore.
[Thi Hoai Tam Dong; Van Ngoc Tran] Hosp Trop Dis, Ho Chi Minh City, Vietnam.
[Whitehead, Stephen S.] NIAID, LID, Bethesda, MD 20892 USA.
[Simmons, Cameron P.] Univ Melbourne, Nossal Inst Global Hlth, Sch Populat & Global Hlth, Parkville, Vic 3052, Australia.
RP Nguyen, THT (reprint author), Univ Oxford, Clin Res Unit, Hosp Trop Dis, Ho Chi Minh City, Vietnam.
EM tiennth@oucru.org
OI Simmons, Cameron P./0000-0002-9039-7392; Hibberd,
Martin/0000-0001-8587-1849; Farrar, Jeremy/0000-0002-2700-623X
FU Wellcome Trust [084368/Z/07/Z]
FX This work was supported by Wellcome Trust [084368/Z/07/Z]. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript
NR 17
TC 10
Z9 10
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2013
VL 7
IS 12
AR e2592
DI 10.1371/journal.pntd.0002592
PG 6
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 282JU
UT WOS:000329168100030
PM 24349598
ER
PT J
AU Dere, E
Anderson, LM
Coulson, M
McIntyre, BS
Boekelheide, K
Chapin, RE
AF Dere, Edward
Anderson, Linnea M.
Coulson, Michelle
McIntyre, Barry S.
Boekelheide, Kim
Chapin, Robert E.
TI SOT Symposium Highlight: Translatable Indicators of Testicular Toxicity:
Inhibin B, MicroRNAs, and Sperm Signatures
SO TOXICOLOGICAL SCIENCES
LA English
DT Editorial Material
DE biomarkers; testicular toxicity; inhibin B; microRNA; sperm
ID GLYCOL MONOMETHYL ETHER; MALE-RATS; LACTATE-DEHYDROGENASE; HUMAN
SPERMATOZOA; URINARY CREATINE; POTENTIAL BIOMARKER; GENE-EXPRESSION;
DIMERIC INHIBIN; INFERTILE MEN; C-ELEGANS
AB Testicular toxicity is an important safety endpoint in drug development and risk assessment, but reliable and translatable biomarkers for predicting injury have eluded researchers. However, this area shows great potential for improvement, with several avenues currently being pursued. This was the topic of a symposium session during the 2013 Society of Toxicology Annual Meeting in San Antonio, TX, entitled Translatable Indicators of Testicular Toxicity: Inhibin B, MicroRNAs, and Sperm Signatures. This symposium brought together stakeholders from academia, government, and industry to present the limitations and drawbacks of currently used indicators of injury and discussed the ongoing efforts in developing more predictive biomarkers of injury. The presentations highlighted the early challenges of using circulating inhibin B and microRNA levels, and sperm messenger RNA transcript abundance and DNA methylation profiles, as novel biomarkers of testicular toxicity.
C1 [Dere, Edward] Rhode Isl Hosp, Div Urol, Providence, RI 02903 USA.
[Dere, Edward; Anderson, Linnea M.; Boekelheide, Kim] Brown Univ, Dept Pathol & Lab Med, Providence, RI 02912 USA.
[Coulson, Michelle] AstraZeneca Res & Dev, Global Safety Assessment, Macclesfield SK10 4TG, Cheshire, England.
[McIntyre, Barry S.] NIEHS, NIH, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Chapin, Robert E.] Pfizer Drug Safety Res & Dev, Groton, CT 06340 USA.
RP Dere, E (reprint author), Brown Univ, Dept Pathol & Lab Med, Box G-E, Providence, RI 02912 USA.
EM edward_dere@brown.edu
OI Dere, Edward/0000-0002-8233-9774
FU NIEHS NIH HHS [P42 ES013660, T32ES007272-17, P42ES013660]
NR 87
TC 4
Z9 4
U1 0
U2 3
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 DEC
PY 2013
VL 136
IS 2
BP 265
EP 273
DI 10.1093/toxsci/kft207
PG 9
WC Toxicology
SC Toxicology
GA 275RQ
UT WOS:000328695500001
PM 24052563
ER
PT J
AU Burns, KA
Zorrilla, LM
Hamilton, KJ
Reed, CE
Birnbaum, LS
Korach, KS
AF Burns, Katherine A.
Zorrilla, Leah M.
Hamilton, Katherine J.
Reed, Casey E.
Birnbaum, Linda S.
Korach, Kenneth S.
TI A Single Gestational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin
Disrupts the Adult Uterine Response to Estradiol in Mice
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE TCDD; uterus; developmental exposure
ID LACTOFERRIN GENE-EXPRESSION; ARYL-HYDROCARBON RECEPTOR; TRANSCRIPTION
IN-VIVO; DIOXIN-LIKE CHEMICALS; ESTROGEN-RECEPTOR; MOUSE UTERUS;
POLYCHLORINATED-BIPHENYLS; LACTATIONAL EXPOSURE; OVARIAN-STEROIDS;
AH-RECEPTOR
AB 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) given as a cotreatment with estrogen exhibits antiestrogenic properties on the rodent adult uterus, but less is understood regarding hormonal responsiveness of the adult uterus from animals having been exposed to TCDD during critical periods of development. We characterized the inhibitory effects of TCDD (T) exposure at gestational day 15 (GD15), 4 weeks, and 9 weeks of age (TTT) on the adult uterus following hormone treatment. TTT-exposed mice in response to hormone treatment exhibited a blunted weight increase, had fewer uterine glands, displayed morphological anomalies, and had marked decreases in the hormonal regulation of genes involved in fluid transport (Aqp3 and Aqp5), cytoarchitectural (Dsc2 and Sprr2A), and immune (Lcn2 and Ltf) regulation. To determine if the 9-week exposure was responsible for the blunted uterine response, due to the 7- to 11-day half-life of TCDD in mice, a second set of experiments was performed to examine exposure to TCDD given at GD15, GD15 only (cross-fostered at birth), only during lactation (cross-fostered at birth), or at GD15 and 4 weeks of age. Our studies demonstrate that a single developmental TCDD exposure at GD15 is sufficient to elicit a blunted adult uterine response to estradiol and is due in part to fewer gland numbers and the reduced expression of forkhead box A2 (FoxA2), a gene involved in gland development. Together, these results provide insight regarding the critical nature of in utero exposure and the potential impact on ensuing uterine biology and reproductive health later in life.
C1 [Burns, Katherine A.; Hamilton, Katherine J.; Korach, Kenneth S.] NIEHS, Receptor Biol Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
[Zorrilla, Leah M.] Integrated Lab Syst Inc, Invest Toxicol Div, Res Triangle Pk, NC 27709 USA.
[Reed, Casey E.] NIEHS, Reprod Endocrinol Grp, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
[Birnbaum, Linda S.] NIEHS, NCI, Res Triangle Pk, NC 27709 USA.
RP Korach, KS (reprint author), NIEHS, LRDT, NIH, 111 Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
EM korach@niehs.nih.gov
OI Korach, Kenneth/0000-0002-7765-418X
FU Division of Intramural Research of the National Institute of
Environmental Health Sciences [Z01 ES70065]; National Institute of
Environmental Health Sciences contract [N01 ES00005]; Division of
Intramural Research of the National Cancer Institute at National
Institute of Environmental Health Science [ZIA BC011476]
FX Division of Intramural Research of the National Institute of
Environmental Health Sciences (Z01 ES70065 to K. S. K. and K. A. B.);
National Institute of Environmental Health Sciences contract (N01
ES00005 to L.M.Z.); Division of Intramural Research of the National
Cancer Institute at National Institute of Environmental Health Sciences
(ZIA BC011476 to L.S.B.).
NR 62
TC 4
Z9 4
U1 0
U2 2
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 DEC
PY 2013
VL 136
IS 2
BP 514
EP 526
DI 10.1093/toxsci/kft208
PG 13
WC Toxicology
SC Toxicology
GA 275RQ
UT WOS:000328695500021
PM 24052564
ER
PT J
AU Cunnington, AJ
Riley, EM
Walther, M
AF Cunnington, Aubrey J.
Riley, Eleanor M.
Walther, Michael
TI Stuck in a rut? Reconsidering the role of parasite sequestration in
severe malaria syndromes
SO TRENDS IN PARASITOLOGY
LA English
DT Review
DE severe malaria; sequestration; inflammation; endothelial activation;
biomass
ID PLASMODIUM-FALCIPARUM MALARIA; LIFE-THREATENING MALARIA;
TUMOR-NECROSIS-FACTOR; RED-BLOOD-CELLS; CEREBRAL MALARIA; INFECTED
ERYTHROCYTES; AFRICAN CHILDREN; ENDOTHELIAL-CELLS; MICROVASCULAR
DYSFUNCTION; MALAWIAN CHILDREN
AB Severe malaria defines individuals at increased risk of death from their infection. Proposed pathogenic mechanisms include parasite sequestration, inflammation, and endothelial dysfunction. Severe malaria is not a single entity, manifesting with distinct syndromes such as severe anemia, severe respiratory distress or coma, each characterized by differences in epidemiology, underlying biology, and risk of death. The relative contribution of the various pathogenic mechanisms may differ between syndromes, and this is supported by accumulating evidence, which challenges sequestration as the initiating event. Here we propose that high parasite biomass is the common initiating feature, but subtle variations in the interaction between the host and parasite exist, and understanding these differences may be crucial to improve outcomes in patients with severe malaria.
C1 [Cunnington, Aubrey J.] Univ London Imperial Coll Sci Technol & Med, Paediat Sect, London W2 1PG, England.
[Riley, Eleanor M.] Univ London London Sch Hyg & Trop Med, Dept Immunol & Infect, London WC1E 7HT, England.
[Walther, Michael] NIAID, Immune Regulat Sect, Lab Malaria Immunol & Vaccinol, Div Intramural Res,NIH, Rockville, MD 20852 USA.
RP Cunnington, AJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Paediat Sect, Norfolk Pl, London W2 1PG, England.
EM a.cunnington@imperial.ac.uk
RI Riley, Eleanor/C-8960-2013;
OI Riley, Eleanor/0000-0003-3447-3570; Cunnington,
Aubrey/0000-0002-1305-3529
FU Intramural NIH HHS [Z99 AI999999]; Medical Research Council [G0701427,
MC_U190081986]
NR 75
TC 19
Z9 19
U1 0
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4922
EI 1471-5007
J9 TRENDS PARASITOL
JI Trends Parasitol.
PD DEC
PY 2013
VL 29
IS 12
BP 585
EP 592
DI 10.1016/j.pt.2013.10.004
PG 8
WC Parasitology
SC Parasitology
GA 270IR
UT WOS:000328312600003
PM 24210256
ER
PT J
AU Li, J
Yuan, J
Cheng, KCC
Inglese, J
Su, XZ
AF Li, Jian
Yuan, Jing
Cheng, Ken Chih-Chien
Inglese, James
Su, Xin-zhuan
TI Chemical genomics for studying parasite gene function and interaction
SO TRENDS IN PARASITOLOGY
LA English
DT Review
DE high-throughput screening; genetics; genomics; gene function
ID PROTEIN IDENTIFICATION TECHNOLOGY; PLASMODIUM-FALCIPARUM GENOME;
HIGH-THROUGHPUT SCREEN; CANCER-CELL-LINES; SMALL MOLECULES; DRUG
DISCOVERY; DETERMINING CHEMOSENSITIVITY; ASSOCIATION ANALYSES; SHOTGUN
PROTEOMICS; TRYPANOSOMA-BRUCEI
AB With the development of new technologies in genome sequencing, gene expression profiling, genotyping, and high-throughput screening of chemical compound libraries, small molecules are playing increasingly important roles in studying gene expression regulation, gene-gene interaction, and gene function. Here we briefly review and discuss some recent advancements in drug target identification and phenotype characterization using combinations of high-throughput screening of small-molecule libraries and various genome-wide methods such as whole-genome sequencing, genome-wide association studies (GWAS), and genome-wide expression analysis. These approaches can be used to search for new drugs against parasite infections, to identify drug targets or drug resistance genes, and to infer gene function.
C1 [Li, Jian; Yuan, Jing] Xiamen Univ, Sch Life Sci, State Key Lab Cellular Stress Biol, Xiamen 361005, Fujian, Peoples R China.
[Cheng, Ken Chih-Chien; Inglese, James] Natl Ctr Adv Translat Sci, NIH, Bethesda, MD 20982 USA.
[Inglese, James] NHGRI, NIH, Bethesda, MD 20892 USA.
[Su, Xin-zhuan] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
RP Su, XZ (reprint author), NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
EM xsu@niaid.nih.gov
OI Su, Xinzhuan/0000-0003-3246-3248
FU National Natural Science Foundation of China [81220108019, 81271858,
81201324]; Project 111 of the State Bureau of Foreign Experts and
Ministry of Education of China [B06016]; Division of Intramural
Research, National Institute of Allergy and Infectious Diseases (NIAID),
National Center for Advancing Translational Sciences, National
Institutes of Health
FX This work was supported by the National Natural Science Foundation of
China (grants 81220108019, 81271858, and 81201324), by Project 111 of
the State Bureau of Foreign Experts and Ministry of Education of China
(B06016), and by the Division of Intramural Research, National Institute
of Allergy and Infectious Diseases (NIAID), National Center for
Advancing Translational Sciences, National Institutes of Health. We
thank Dr Ronald Johnson for comments, and intramural editor Brenda Rae
Marshall [Division of Intramural Research (DIR) Program Support Staff
(DPSS)], NIAID, for assistance. We apologize to those whose work on
screening for antiparasite drugs cannot be cited here owing to space
constraints.
NR 101
TC 2
Z9 3
U1 0
U2 15
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4922
EI 1471-5007
J9 TRENDS PARASITOL
JI Trends Parasitol.
PD DEC
PY 2013
VL 29
IS 12
BP 603
EP 611
PG 9
WC Parasitology
SC Parasitology
GA 270IR
UT WOS:000328312600005
PM 24215777
ER
PT J
AU Meier, JL
AF Meier, Jordan L.
TI Metabolic Mechanisms of Epigenetic Regulation
SO ACS CHEMICAL BIOLOGY
LA English
DT Article
ID ATP-CITRATE LYASE; HISTONE ACETYLTRANSFERASE ACTIVITY; NICOTINAMIDE
N-METHYLTRANSFERASE; NAD(+) SALVAGE PATHWAY; ADENOSYL-L-METHIONINE;
CHEMICAL PROBE; BREAST-CANCER; TRANSCRIPTIONAL COACTIVATOR;
ALPHA-KETOGLUTARATE; DNA METHYLATION
AB Chromatin modifications have been well-established to play a critical role in the regulation of genome function. Many of these modifications are introduced and removed by enzymes that utilize cofactors derived from primary metabolism. Recently, it has been shown that endogenous cofactors and metabolites can regulate the activity of chromatin-modifying enzymes, providing a direct link between the metabolic state of the cell and epigenetics. Here we review metabolic mechanisms of epigenetic regulation with an emphasis on their role in cancer. Focusing on three core mechanisms, we detail and draw parallels between metabolic and chemical strategies to modulate epigenetic signaling, and highlight opportunities for chemical biologists to help shape our knowledge of this emerging phenomenon. Continuing to integrate our understanding of metabolic and genomic regulatory mechanisms may help elucidate the role of nutrition in diseases such as cancer, while also providing a basis for new approaches to modulate epigenetic signaling for therapeutic benefit.
C1 NCI, Chem Genom Sect, Biol Chem Lab, Frederick, MD 21702 USA.
RP Meier, JL (reprint author), NCI, Chem Genom Sect, Biol Chem Lab, Frederick, MD 21702 USA.
RI Meier, Jordan/N-2608-2014
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research
FX We apologize to colleagues whose work could not be cited here due to
space limitations. We thank members of the Meier laboratory (D.
Montgomery, A. Sorum) and colleagues in the Chemical Biology Laboratory
for careful reading of this manuscript and many helpful comments. J.L.M.
is supported by the Intramural Research Program of the National
Institutes of Health, National Cancer Institute, Center for Cancer
Research.
NR 155
TC 17
Z9 17
U1 2
U2 43
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1554-8929
EI 1554-8937
J9 ACS CHEM BIOL
JI ACS Chem. Biol.
PD DEC
PY 2013
VL 8
IS 12
BP 2607
EP 2621
DI 10.1021/cb400689r
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 281CW
UT WOS:000329078100002
PM 24228614
ER
PT J
AU Xu, W
Liu, CY
Kaartinen, V
Chen, H
Lu, CH
Zhang, WM
Luo, YF
Shi, W
AF Xu, Wei
Liu, Chengyu
Kaartinen, Vesa
Chen, Hui
Lu, Chi-Han
Zhang, Wenming
Luo, Yongfeng
Shi, Wei
TI TACE in perinatal mouse lung epithelial cells promotes lung saccular
formation
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE tumor necrosis factor-alpha converting enzyme; lung development
ID NECROSIS-FACTOR-ALPHA; CONVERTING-ENZYME; ADAM METALLOPROTEINASES;
DIFFERENTIATION; ERBB4; GENE
AB Tumor necrosis factor-alpha converting enzyme (TACE) is a cell membrane sheddase, expressed in both developmental lung epithelia and mesenchyme. Global abrogation of TACE results in neonatal lethality and multiple organ developmental abnormalities, including dysplastic lung. To further define the roles of TACE in regulating lung development, lung epithelial and/or mesenchymal specific TACE conditional knockout mice were generated. Blockade of TACE function in developing lung epithelial cells caused reduced saccular formation, decreased cell proliferation, and reduced mid-distal lung epithelial cell differentiation. In contrast, mesenchymal TACE knockout did not have any phenotypic change in developing lung. Simultaneous abrogation of TACE in both lung epithelial and mesenchymal cells did not result in a more severe lung abnormality. Interestingly, these lung-specific TACE conditional knockout mice were not neonatal lethal, and their lung structures were essentially normal after alveolarization. In addition, TACE conditional knockout in developing cardiomyocytes resulted in noncompaction of ventricular myocardium, as seen in TACE conventional knockout mice. However, these mice were also not neonatal lethal. In conclusion, lung epithelial TACE is essential for promoting fetal lung saccular formation, but not postnatal lung alveolarization in mice. Because the developmental abnormality of either lung or heart induced by TACE deficiency does not directly lead to neonatal lethality, the neonatal death of TACE conventional knockout mice is likely a result of synergistic effects of multiple organ abnormalities.
C1 [Xu, Wei; Chen, Hui; Lu, Chi-Han; Zhang, Wenming; Luo, Yongfeng; Shi, Wei] Childrens Hosp Los Angeles, Dev Biol & Regenerat Med Program, Saban Res Inst, Los Angeles, CA 90027 USA.
[Xu, Wei] Nanchang Univ, Affiliated Hosp 2, Dept Resp Med, Nanchang, Peoples R China.
[Liu, Chengyu] NHLBI, IPSC & Genome Engn Core, NIH, Bethesda, MD 20892 USA.
[Kaartinen, Vesa] Univ Michigan, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA.
RP Shi, W (reprint author), Childrens Hosp Los Angeles, Dev Biol & Regenerat Med Program, 4650 Sunset Blvd,Mailstop 35, Los Angeles, CA 90027 USA.
EM wshi@chla.usc.edu
OI Kaartinen, Vesa/0000-0002-9432-510X
FU National Heart, Lung, and Blood Institute [HL-109932, HL-068597];
American Heart Association; California Institute of Regenerative
Medicine Training
FX This work was supported by National Heart, Lung, and Blood Institute
Grants HL-109932 and HL-068597 (W. Shi), an American Heart Association
Grant in Aid (W. Shi), and a California Institute of Regenerative
Medicine Training Grant (W. Xu and Y. Luo).
NR 27
TC 4
Z9 4
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1040-0605
EI 1522-1504
J9 AM J PHYSIOL-LUNG C
JI Am. J. Physiol.-Lung Cell. Mol. Physiol.
PD DEC
PY 2013
VL 305
IS 12
BP L953
EP L963
DI 10.1152/ajplung.00189.2013
PG 11
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA 276LD
UT WOS:000328750900006
PM 24142516
ER
PT J
AU Lee, IH
Finkel, T
AF Lee, In Hye
Finkel, Toren
TI Metabolic regulation of the cell cycle
SO CURRENT OPINION IN CELL BIOLOGY
LA English
DT Article
ID HEMATOPOIETIC STEM-CELLS; GENOME-WIDE ASSOCIATION; PROTEIN-KINASE; RAG
GTPASES; SACCHAROMYCES-CEREVISIAE; SIGNALS CONTROL; AMINO-ACIDS;
MITOCHONDRIAL; CHECKPOINT; PATHWAY
AB There is a growing appreciation that metabolic signals are integrated and coupled to cell cycle progression. However, the molecular wiring that connects nutrient availability, biosynthetic intermediates and energetic balance to the core cell cycle machinery remains incompletely understood. In this review, we explore the recent progress in this area with particular emphasis on how nutrient and energetic status is sensed within the cell to ultimately regulate cell growth and division. The role these pathways play in normal cell function including stem cell biology is also discussed. Furthermore, we describe the growing appreciation that dysregulation of these pathways might contribute to a variety of pathological conditions including metabolic diseases and tumor formation.
C1 [Lee, In Hye; Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Lee, In Hye] Ewha Womans Univ, Dept Life Sci, Div Life & Pharmaceut Sci, Seoul, South Korea.
RP Finkel, T (reprint author), NHLBI, Ctr Mol Med, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM finkelt@nih.gov
FU NIH
FX We are grateful to Ilsa Rovira for help with the figures. This work was
supported by NIH Intramural funds.
NR 55
TC 10
Z9 10
U1 2
U2 16
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0955-0674
EI 1879-0410
J9 CURR OPIN CELL BIOL
JI Curr. Opin. Cell Biol.
PD DEC
PY 2013
VL 25
IS 6
BP 724
EP 729
DI 10.1016/j.ceb.2013.07.002
PG 6
WC Cell Biology
SC Cell Biology
GA 277CO
UT WOS:000328796200008
PM 23890700
ER
PT J
AU Dunn, BM
Wlodawer, A
AF Dunn, Ben M.
Wlodawer, Alexander
TI The regulation of proteolysis around the World
SO CURRENT OPINION IN STRUCTURAL BIOLOGY
LA English
DT Editorial Material
C1 [Dunn, Ben M.] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.
[Wlodawer, Alexander] NCI, Macromol Crystallog Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Dunn, BM (reprint author), Univ Florida, Dept Biochem & Mol Biol, 1600 SW Archer Rd, Gainesville, FL 32610 USA.
EM bdunn@ufl.edu; wlodawer@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 3
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-440X
EI 1879-033X
J9 CURR OPIN STRUC BIOL
JI Curr. Opin. Struct. Biol.
PD DEC
PY 2013
VL 23
IS 6
BP 795
EP 796
DI 10.1016/j.sbi.2013.10.004
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 282CU
UT WOS:000329148700001
PM 24210951
ER
PT J
AU Aiello, FB
Graciotti, L
Procopio, AD
Keller, JR
Durum, SK
AF Aiello, Francesca B.
Graciotti, Laura
Procopio, Antonio D.
Keller, Jonathan R.
Durum, Scott K.
TI Stemness of T cells and the hematopoietic stem cells: Fate, memory,
niche, cytokines
SO CYTOKINE & GROWTH FACTOR REVIEWS
LA English
DT Review
DE Hematopoietic stem cells; T memory stem cells; T memory cells; Stem cell
markers; Self renewal
ID LONG-TERM MAINTENANCE; SLAM FAMILY RECEPTORS; HELPER TYPE-2 CELLS;
DNA-DAMAGE RESPONSE; RENEWAL IN-VIVO; C-KIT LIGAND; SELF-RENEWAL;
PROGENITOR CELLS; CD8(+) MEMORY; BETA-CATENIN
AB Stem cells are able to generate both cells that differentiate and cells that remain undifferentiated but potentially have the same developmental program. The prolonged duration of the protective immune memory for infectious diseases such as polio, small pox, and measles, suggested that memory T cells may have stem cell properties. Understanding the molecular basis for the life-long persistence of memory T cells may be useful to project targeted therapies for immune deficiencies and infectious diseases and to formulate vaccines. In the last decade evidence from different laboratories shows that memory T cells may share self-renewal pathways with bone marrow hematopoietic stem cells. In stem cells the intrinsic self-renewal activity, which depends on gene expression, is known to be modulated by extrinsic signals from the environment that may be tissue specific. These extrinsic signals for sternness of memory T cells include cytokines such as IL-7 and IL-15 and there are other cytokine signals for maintaining the cytokine signature (TH1, TH2, etc.) of memory T cells. Intrinsic and extrinsic pathways that might be common to bone marrow hematopoietic stem cells and memory T lymphocytes are discussed and related to self-renewal functions. Published by Elsevier Ltd.
C1 [Aiello, Francesca B.; Durum, Scott K.] Mol Immunoregulat Lab, Frederick, MD 21702 USA.
[Aiello, Francesca B.] Univ G dAnnunzio, Dept Med & Aging Sci, I-66013 Chieti, Italy.
[Graciotti, Laura; Procopio, Antonio D.] Marche Polytech Univ, Dept Clin & Med Sci, I-60100 Ancona, Italy.
[Keller, Jonathan R.] Lab Canc Prevent, Frederick, MD 21702 USA.
RP Durum, SK (reprint author), NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Bldg 560, Frederick, MD 21702 USA.
EM aiellofb@nih.mail.gov; 1.graciotti@univpm.it; a.d.procopio@univpm.it;
kellerjo@nih.mail.gov; durums@nih.mail.gov
NR 218
TC 4
Z9 4
U1 1
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6101
EI 1879-0305
J9 CYTOKINE GROWTH F R
JI Cytokine Growth Factor Rev.
PD DEC
PY 2013
VL 24
IS 6
BP 485
EP 501
DI 10.1016/j.cytogfr.2013.10.002
PG 17
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 278XT
UT WOS:000328923900001
PM 24231048
ER
PT J
AU Swaminathan, S
Dai, L
Lane, HC
Imamichi, T
AF Swaminathan, Sanjay
Dai, Luc
Lane, H. Clifford
Imamichi, Tomozumi
TI Evaluating the potential of IL-27 as a novel therapeutic agent in HIV-1
infection
SO CYTOKINE & GROWTH FACTOR REVIEWS
LA English
DT Review
DE Interleukin-27; HIV; Cytokines; SPTBN1; Therapy
ID VIRUS-LIKE PARTICLES; REGULATORY T-CELLS; HUMAN MACROPHAGES; DENDRITIC
CELLS; IMMUNE-RESPONSES; GENE-EXPRESSION; HUMAN MONOCYTES; CUTTING EDGE;
DC-SIGN; C-MAF
AB Interleukin 27 (IL-27) is an immunomodulatory cytokine with important roles in both the innate and adaptive immune systems. In the last five years, the addition of exogenous IL-27 to primary cell cultures has been demonstrated to decrease HIV-1 replication in a number of cell types including peripheral blood mononuclear cells (PBMCs), CD4+ T cells, macrophages and dendritic cells. These in vitro findings suggest that IL-27 may have therapeutic value in the setting of HIV-1 infection. In this review, we describe the current knowledge of the biology of IL-27, its effects primarily on HIV-1 replication but also in other viral infections and explore its potential role as a therapeutic cytokine for the treatment of patients with HIV-1 infection. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Swaminathan, Sanjay; Dai, Luc; Imamichi, Tomozumi] Sci Applicat Int Corp SAIC Frederick Inc, Frederick Natl Lab Canc Res, Lab Human Retrovirol, Appl & Dev Res Directorate, Frederick, MD 21702 USA.
[Lane, H. Clifford] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Imamichi, T (reprint author), Sci Applicat Int Corp SAIC Frederick Inc, Frederick Natl Lab Canc Res, Lab Human Retrovirol, Bldg 550,Room 126,1050 Boyles St, Frederick, MD 21702 USA.
EM sanjay.swaminathan@nih.gov; lue.dai@nih.gov; CLANE@niaid.nih.gov;
timamichi@mail.nih.gov
OI Swaminathan, Sanjay/0000-0001-5315-6445
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; National Institute of Allergy and Infectious
Disease
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract No. 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.
This research was supported [in part] by the National Institute of
Allergy and Infectious Disease.
NR 56
TC 2
Z9 2
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6101
EI 1879-0305
J9 CYTOKINE GROWTH F R
JI Cytokine Growth Factor Rev.
PD DEC
PY 2013
VL 24
IS 6
BP 571
EP 577
DI 10.1016/j.cytogfr.2013.07.001
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 278XT
UT WOS:000328923900008
PM 23962745
ER
PT J
AU Antony, S
Wu, YZ
Hewitt, SM
Anver, MR
Butcher, D
Jiang, GJ
Meitzler, JL
Liu, H
Juhasz, A
Lu, JM
Roy, KK
Doroshow, JH
AF Antony, Smitha
Wu, Yongzhong
Hewitt, Stephen M.
Anver, Miriam R.
Butcher, Donna
Jiang, Guojian
Meitzler, Jennifer L.
Liu, Han
Juhasz, Agnes
Lu, Jiamo
Roy, Krishnendu K.
Doroshow, James H.
TI Characterization of NADPH oxidase 5 expression in human tumors and tumor
cell lines with a novel mouse monoclonal antibody
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE NADPH oxidase 5; Tissue microarray; Mouse monoclonal Nox5 antibody;
Melanoma; UACC-257 cells; Reactive oxygen species; Superoxide; Free
radicals
ID PROSTATE-CANCER CELLS; ESOPHAGEAL ADENOCARCINOMA CELLS;
SMOOTH-MUSCLE-CELLS; REACTIVE OXYGEN; HYDROGEN-PEROXIDE; OXIDATIVE
STRESS; NAD(P)H OXIDASE; ENDOTHELIAL-CELLS; MELANOMA-CELLS; NOX ENZYMES
AB Reactive oxygen species generated by NADPH oxidase 5 (Nox5) have been implicated in physiological and pathophysiological signaling pathways, including cancer development and progression. However, because immunological tools are lacking, knowledge of the role of Nox5 in tumor biology has been limited; the expression of Nox5 protein across tumors and normal tissues is essentially unknown. Here, we report the characterization and use of a mouse monoclonal antibody against a recombinant Nox5 protein (bp 600-746) for expression profiling of Nox5 in human tumors by tissue microarray analysis. Using our novel antibody, we also report the detection of endogenous Nox5 protein in human UACC-257 melanoma cells. Immunofluorescence, confocal microscopy, and immunohistochemical techniques were employed to demonstrate Nox5 localization throughout UACC-257 cells, with perinuclear enhancement. Tissue microarray analysis revealed, for the first time, substantial Nox5 overexpression in several human cancers, including those of prostate, breast, colon, lung, brain, and ovary, as well as in malignant melanoma and non-Hodgkin lymphoma; expression in most nonmalignant tissues was negative to weak. This validated mouse monoclonal antibody will promote further exploration of the functional significance of Nox5 in human pathophysiology, including tumor cell growth and proliferation. (C) 2013 Published by Elsevier Inc.
C1 [Antony, Smitha; Wu, Yongzhong; Jiang, Guojian; Meitzler, Jennifer L.; Juhasz, Agnes; Lu, Jiamo; Doroshow, James H.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Hewitt, Stephen M.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Liu, Han; Roy, Krishnendu K.; Doroshow, James H.] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
[Anver, Miriam R.; Butcher, Donna] NIH, Pathol Histotechnol Lab, SAIC Frederick Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
RP Doroshow, JH (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM doroshoj@mail.NIH.gov
OI Hewitt, Stephen/0000-0001-8283-1788
FU Center for Cancer Research; Division of Cancer Treatment and Diagnosis;
NCI [HHSN261200800001E]; National Cancer Institute; National Institutes
of Health
FX This work was supported with federal funds from the Center for Cancer
Research, the Division of Cancer Treatment and Diagnosis, and NCI
Contract No. HHSN261200800001E, National Cancer Institute, National
Institutes of Health. The content of this publication does not
necessarily reflect the views or policies of the U.S. Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. government.
NR 79
TC 18
Z9 18
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 497
EP 508
DI 10.1016/j.freeradbiomed.2013.07.005
PG 12
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900049
PM 23851018
ER
PT J
AU Towner, RA
Garteiser, P
Bozza, F
Smith, N
Saunders, D
d'Avila, JCP
Magno, F
Oliveira, MF
Ehrenshaft, M
Lupu, F
Silasi-Mansat, R
Ramirez, DC
Gomez-Mejiba, SE
Mason, RP
Faria-Neto, HCC
AF Towner, Rheal A.
Garteiser, Philippe
Bozza, Fernando
Smith, Nataliya
Saunders, Debra
d'Avila, Joana C. P.
Magno, Flora
Oliveira, Marcus F.
Ehrenshaft, Marilyn
Lupu, Florea
Silasi-Mansat, Robert
Ramirez, Dario C.
Gomez-Mejiba, Sandra E.
Mason, Ronald P.
Castro Faria-Neto, Hugo C.
TI In vivo detection of free radicals in mouse septic encephalopathy using
molecular MRI and immuno-spin trapping
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Immuno-spin trapping; Free radicals; Molecular MRI; Sepsis; Cecal
ligation and puncture; Mice; in vivo; DMPO; Fluorescence microscopy;
4-Hydroxynonenal; 3-Nitrotyrosine
ID NECROSIS-FACTOR-ALPHA; OXIDATIVE STRESS; GROWTH-FACTOR; SEPSIS; BRAIN;
INFLAMMATION; DYSFUNCTION; MODEL; LIPOPOLYSACCHARIDE; ENDOTOXEMIA
AB Free radicals are known to play a major role in sepsis. Combined immuno-spin trapping and molecular magnetic resonance imaging (MRI) was used to detect in vivo and in situ levels of free radicals in murine septic encephalopathy after cecal ligation and puncture (CLP). DMPO (5,5-dimethyl pyrroline N-oxide) was injected over 6 h after CLP, before administration of an anti-DMPO probe (anti-DMPO antibody bound to albumin-gadolinium-diethylene triamine pentaacetic acid-biotin MRI targeting contrast agent). In vitro assessment of the anti-DMPO probe in oxidatively stressed mouse astrocytes significantly decreased T-1 relaxation (P < 0.0001) compared to controls. MRI detected the presence of anti-DMPO adducts via a substantial decrease in % T1 change within the hippocampus, striatum, occipital, and medial cortex brain regions (p < 0.01 for all) in septic animals compared to shams, which was sustained for over 60 mm (p < 0.05 for all). Fluorescently labeled streptavidin was used to target the anti-DMPO probe biotin, which was elevated in septic brain, liver, and lungs compared to sham. Ex vivo DMPO adducts (qualitative) and oxidative products, including 4-hydroxynonenal and 3-nitrotyrosine (quantitative, p < 0.05 for both), were elevated in septic brains compared to shams. This is the first study that has reported on the detection of in vivo and in situ levels of free radicals in murine septic encephalopathy. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Towner, Rheal A.; Garteiser, Philippe; Smith, Nataliya; Saunders, Debra] Oklahoma Med Res Fdn, Adv Magnet Resonance Ctr, Oklahoma City, OK 73104 USA.
[Bozza, Fernando; d'Avila, Joana C. P.; Magno, Flora] Inst Oswaldo Cruz, Inst Pesquisa Clin Evandro Chagas, BR-20001 Rio De Janeiro, Brazil.
[Oliveira, Marcus F.] Univ Fed Rio de Janeiro, Inst Bioquim Med, Programa Biol Mol & Biotecnol, Lab Bioquim Resposta Estresse, Rio De Janeiro, RJ, Brazil.
[Ehrenshaft, Marilyn; Mason, Ronald P.] NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA.
[Lupu, Florea; Silasi-Mansat, Robert] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
[Ramirez, Dario C.; Gomez-Mejiba, Sandra E.] Natl Univ San Luis, CONICET, Inst Multidisciplinario Invest Biol San Luis, Lab Expt Med & Therapeut, RA-5700 San Luis, Argentina.
[Castro Faria-Neto, Hugo C.] Inst Oswaldo Cruz, Lab Imunofarmacol, BR-20001 Rio De Janeiro, RJ, Brazil.
RP Towner, RA (reprint author), Oklahoma Med Res Fdn, Adv Magnet Resonance Ctr, 825 NE 13th St, Oklahoma City, OK 73104 USA.
EM Rheal-Towner@omrf.org
RI RAMIREZ, DARIO/K-3312-2013;
OI Silasi, Robert/0000-0001-9590-6160; RAMIREZ, DARIO/0000-0001-6725-3326;
Garteiser, Philippe/0000-0003-0157-8851
FU Oklahoma Medical Research Foundation; National Institute of
Environmental Health Sciences; CNPq; PAPES; FAPERJ
FX Funding was obtained by the Oklahoma Medical Research Foundation
(R.A.T.) and the National Institute of Environmental Health Sciences
(R.P.M.). H.C.C.F.-N. and F.A.B. were supported by CNPq, PAPES, and
FAPERJ. F.A.B., M.F.O., and H.C.C.F.-N. are research scholars from CNPq
and FAPERJ.
NR 43
TC 5
Z9 5
U1 1
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 828
EP 837
DI 10.1016/j.freeradbiomed.2013.08.172
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900078
PM 23978375
ER
PT J
AU Abdelmegeed, MA
Banerjee, A
Jang, S
Yoo, SH
Yun, JW
Gonzalez, FJ
Keshavarzian, A
Song, BJ
AF Abdelmegeed, Mohamed A.
Banerjee, Atrayee
Jang, Sehwan
Yoo, Seong-Ho
Yun, Jun-Won
Gonzalez, Frank J.
Keshavarzian, Ali
Song, Byoung-Joon
TI CYP2E1 potentiates binge alcohol-induced gut leakiness, steatohepatitis,
and apoptosis
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Liver; Binge ethanol; CYP2E1; Oxidative stress; Gut leakiness;
Steatohepatitis; Apoptosis; Free radicals
ID INDUCED LIVER-INJURY; INDUCED FATTY LIVER; MITOCHONDRIAL DYSFUNCTION;
CYTOCHROME P4502E1; PROTEIN-KINASE; ETHANOL; MICE; ACTIVATION;
STEATOSIS; STRESS
AB Ethanol-inducible cytochrome P450 2E1 (CYP2E1) contributes to increased oxidative stress and steatosis in chronic alcohol-exposure models. However, its role in binge ethanol-induced gut leakiness and hepatic injury is unclear. This study was aimed at investigating the role of CYP2E1 in binge alcohol-induced gut leakiness and the mechanisms of steatohepatitis. Female wild-type (WT) and Cyp2el-null mice were treated with three doses of binge ethanol (WT-EtOH or Cyp2e1-null-EtOH) (6 g/kg oral gavage at 12-h intervals) or dextrose (negative control). Intestinal histology of only WT-EtOH exhibited epithelial alteration and blebbing of lamina propria, and liver histology obtained at 6 h after the last ethanol dose showed elevated steatosis with scattered inflammatory foci. These were accompanied by increased levels of serum endotoxin, hepatic enterobacteria, and triglycerides. All these changes, including the intestinal histology and hepatic apoptosis, determined by TUNEL assay, were significantly reversed when WT-EtOH mice were treated with the specific inhibitor of CYP2E1 chlormethiazole and the antioxidant N-acetylcysteine, both of which suppressed oxidative markers including intestinal CYP2E1. WT-EtOH also exhibited elevated amounts of serum TNF-alpha, hepatic cytokines, CYP2E1, and lipid peroxidation, with decreased levels of mitochondrial superoxide dismutase and suppressed aldehyde dehydrogenase 2 activity. Increased hepatocyte apoptosis with elevated levels of proapoptotic proteins and decreased levels of active (phosphorylated) p-ART, p-AMPK, and peroxisome proliferator-activated receptor-a, all of which are involved in fat metabolism and inflammation, were observed in WT-EtOH. These changes were significantly attenuated in the corresponding Cyp2el-null-EtOH mice. These data indicate that both intestinal and hepatic CYP2E1 induced by binge alcohol seems critical in binge alcohol-mediated increased nitroxidative stress, gut leakage, and endotoxemia; altered fat metabolism; and inflammation contributing to hepatic apoptosis and steatohepatitis. Published by Elsevier Inc.
C1 [Abdelmegeed, Mohamed A.; Banerjee, Atrayee; Jang, Sehwan; Yun, Jun-Won; Song, Byoung-Joon] Natl Inst Alcohol Abuse & Alcoholism, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
[Yoo, Seong-Ho] Seoul Natl Univ, Coll Med, Dept Forens Med, Seoul, South Korea.
[Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Keshavarzian, Ali] Rush Univ, Med Ctr, Div Gastroenterol, Chicago, IL 60612 USA.
RP Song, BJ (reprint author), Natl Inst Alcohol Abuse & Alcoholism, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
EM bj.song@nih.gov
FU Intramural Program of the National Institute on Alcohol Abuse and
Alcoholism
FX This research was supported by the Intramural Program of the National
Institute on Alcohol Abuse and Alcoholism. We thank Dr. Klaus Gawrisch
for supporting this study.
NR 44
TC 36
Z9 37
U1 1
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 1238
EP 1245
DI 10.1016/j.freeradbiomed.2013.09.009
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900117
PM 24064383
ER
PT J
AU Esworthy, RS
Kim, BW
Wang, YF
Gao, Q
Doroshow, JH
Leto, TL
Chu, FF
AF Esworthy, R. Steven
Kim, Byung-Wook
Wang, Yufeng
Gao, Qiang
Doroshow, James H.
Leto, Thomas L.
Chu, Fong-Fong
TI The Gdac1 locus modifies spontaneous and Salmonella-induced colitis in
mice deficient in either Gpx2 or Gpx1 gene
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE DUOX2; GPX1; GPX2; GPX-deficiency-associated-colitis locus-1; Gdac1; Gut
dysbiosis; Metronidazole; Mouse genetics; Salmonella enterica serotype
typhimurium; Selenium; Free radicals
ID INFLAMMATORY-BOWEL-DISEASE; GLUTATHIONE-PEROXIDASE; NADPH-OXIDASE;
SELENIUM DEFICIENCY; EPITHELIAL-CELLS; TYPHIMURIUM INFECTION; INTESTINAL
EPITHELIUM; ENDOTHELIAL-CELLS; HOST-DEFENSE; DUAL OXIDASE
AB We previously identified the Gdac1 (Gpx-deficiency-associated colitis 1) locus, which influences the severity of spontaneous colitis in Gpxl- and Gpx2-double-knockout (Gpx1/2-DKO) mice. Congenic Gpx1/2-DKO mice in the 129S1/SvImJ (129) background but carrying the Gdac1(B6) allele have milder spontaneous colitis than 129 Gpx1/2-DKO mice carrying the Gdac/(129) allele. Here, we evaluated the effect of the Gdac1(B6) allele on 129 strain non-DKO mice that had a wild-type (WT) Gpx1 or Gpx2 allele and WT mice. We found that the congenic Gdac1(B6) Gpx2-KO, Gpx1-KO, and WT mice also had better health than the corresponding 129 mice measured by at least one of the parameters including disease signs, colon length, or weight gain. The Gdac1(B6) allele prevented loss of goblet cells and crypt epithelium exfoliation in the Gpx1/2-DKO mice, but did not affect epithelial cell apoptosis or proliferation. Because Gdac1(B6) affects gut dysbiosis in the DKO mice, we then tested its impact on bacteria-induced colitis in non-DKO mice. First, we found both Gpx1-KO and Gpx2-KO mice were susceptible to Salmonella enterica serotype typhimurium (S. Tm)-induced colitis under conditions where WT B6 and 129 mice were resistant. Second, the S. Tm-infected Gdac1(B6) Gpx1-KO mice had stronger inflammatory responses than 129 Gpx1-KO or 129 Gpx2-KO with both Gdac1 alleles and WT mice by having higher mRNA levels of Nod2, Nox2, Tnf and Cox2. We conclude that the Gdoc1 locus affects both spontaneous and S. Tm-induced colitis in 129 non-DKO mice, although in opposite directions. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Esworthy, R. Steven; Kim, Byung-Wook; Chu, Fong-Fong] City Hope Natl Med Ctr, Beckman Res Inst, Dept Radiat Biol, Duarte, CA 91010 USA.
[Wang, Yufeng; Gao, Qiang] Henan Univ Sci & Technol, Affiliated Hosp 1, Dept Gastroenterol & Hepatol, Luoyang 471000, Henan, Peoples R China.
[Doroshow, James H.] Natl Canc Inst, Bethesda, MD 20816 USA.
[Leto, Thomas L.] NIAID, Natl Inst Hlth, Host Def Lab, Rockville, MD 20852 USA.
RP Chu, FF (reprint author), City Hope Natl Med Ctr, Beckman Res Inst, Dept Radiat Biol, Duarte, CA 91010 USA.
EM fchu@coh.org
FU National Cancer Institute of the National Institutes of Health
[P30CA033572]
FX We thank Sofia Loera and Tina Montgomery at the Anatomic Pathology Core
of City of Hope for tissue processing. Research reported in this
publication was supported by the National Cancer Institute of the
National Institutes of Health under Grant P30CA033572. The content is
solely the responsibility of the authors and does not necessarily
represent the official views of the National Institutes of Health.
NR 56
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 1273
EP 1283
DI 10.1016/j.freeradbiomed.2013.09.013
PG 11
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900121
PM 24090658
ER
PT J
AU Uddin, MJ
Joe, Y
Zheng, M
Blackshear, PJ
Ryter, SW
Park, JW
Chung, HT
AF Uddin, Md Jamal
Joe, Yeonsoo
Zheng, Min
Blackshear, Perry J.
Ryter, Stefan W.
Park, Jeong Woo
Chung, Hun Taeg
TI A functional link between heme oxygenase-1 and tristetraprolin in the
anti-inflammatory effects of nicotine
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Nicotine; Anti-inflammatory effects; HO-1; STAT3; TTP; Free radicals
ID NECROSIS-FACTOR-ALPHA; INFLAMMATORY RESPONSE; GENE-EXPRESSION; VAGUS
NERVE; POSTTRANSCRIPTIONAL REGULATION; CYTOKINE PRODUCTION;
ENDOTHELIAL-CELLS; INDUCTION; MACROPHAGES; ACTIVATION
AB Nicotine stimulates the cholinergic anti-inflammatory pathway and prevents excessive inflammation by inhibiting the release of inflammatory cytokines from macrophages. We have previously reported that heme oxygenase-1 (HO-1) and tristetraprolin (UP) are induced by nicotine and mediate the anti-inflammatory function of nicotine in macrophages. However, it was not clear whether the two molecules are functionally linked. In this study, we sought to determine whether HO-1 associates with UP to mediate the anti-inflammatory effects of nicotine. Inhibition of HO-1 activity or HO-1 expression attenuated the effects of nicotine on STAT3 activation, UP induction, and TNF-alpha production in LPS-treated macrophages. Induction of HO-1 expression increased the level of UP in the absence of nicotine. In an LPS-induced endotoxemia model, HO-1 deficiency blocked the effects of nicotine on the STAT3 phosphorylation, UP induction, and LPS-induced TNF-alpha production in the liver. Downregulation of STAT3 by siRNA attenuated the effect of nicotine on UP expression and TNF-alpha production but did not affect the nicotine-mediated induction of HO-1. In UP knockout mice, nicotine treatment enhanced HO-1 expression and STAT3 activation but failed to inhibit LPS-induced TNF-alpha production. Our results suggest that HO-1 and UP are functionally linked in mediating the anti-inflammatory effects of nicotine; HO-1 is necessary for the induction of UP by nicotine. This novel nicotine-HO-1-UP signaling pathway provides new possibilities for the treatment of inflammatory diseases.(C) 2013 Elsevier Inc. All rights reserved.
C1 [Uddin, Md Jamal; Joe, Yeonsoo; Zheng, Min; Park, Jeong Woo; Chung, Hun Taeg] Univ Ulsan, Sch Biol Sci, Ulsan 680749, South Korea.
[Zheng, Min] YanBian Univ, Affiliated Hosp, Dept Thorac & Cardiovasc Surg, Yanji, Jilin, Peoples R China.
[Blackshear, Perry J.] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
[Ryter, Stefan W.] Harvard Univ, Brigham & Womens Hosp, Dept Pulm & Crit Care Med, Boston, MA 02115 USA.
RP Chung, HT (reprint author), Univ Ulsan, Sch Biol Sci, Ulsan 680749, South Korea.
EM chung@ulsan.ac.kr
OI Uddin, Md. Jamal/0000-0003-2911-3255
FU Korea Research Foundation; Korean government (MOEHRD)
[BRL-2009-0087350]; Bio & Medical Technology Development Program of the
National Research Foundation; Korean government (MEST)
[2012M3A9C3048687]
FX This study was supported by a Korea Research Foundation grant funded by
the Korean government (MOEHRD, BRL-2009-0087350) and the Bio & Medical
Technology Development Program of the National Research Foundation
funded by the Korean government (MEST) (2012M3A9C3048687).
NR 44
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Z9 6
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 1331
EP 1339
DI 10.1016/j.freeradbiomed.2013.09.027
PG 9
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900128
ER
PT J
AU Leinisch, F
Jiang, JJ
DeRose, EF
Khramtsov, VV
Mason, RP
AF Leinisch, Fabian
Jiang, Jinjie
DeRose, Eugene F.
Khramtsov, Valery V.
Mason, Ronald P.
TI Investigation of spin-trapping artifacts formed by the Forrester-Hepburn
mechanism
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Forrester-Hepburn mechanism; Spin trapping; False-positive; Artifact;
Nucleophile
ID PEROXIDASE-CATALYZED OXIDATION; FREE-RADICAL FORMATION;
NUCLEOPHILIC-ADDITION; NONRADICAL ADDITION; NITROSO-COMPOUNDS;
CAUTIONARY NOTE; SULFUR-DIOXIDE; RESONANCE; ADDUCTS; EPR
AB Free radical detection with ESR spin trapping relies on the specific addition of the radical to nitrone/nitroso compounds. It also has been proposed that spin traps can react in biological systems to give false-positive results. For nitrone spin traps, the reaction with nucleophiles, first described by Forrester and Hepburn, has been discussed as the most critical source of artifacts. For artifact identification, the ESR preincubation method may be used, which employs isotopically marked spin traps. Here we investigated the influence of fast sulfite-hydroxylamine equilibrium chemistry on the validity of this assay. Using the (faster) aspiration technique, we found that the Forrester-Hepburn mechanism also contributes to DMPO/(SO3-)-S-center dot adduct formation during ferricyanide-mediated sulfite oxidation, but no evidence for artifactual DMPO/(SO3-)-S-center dot formation was found if the more potent horseradish peroxidase was used. This is ESR evidence that the Forrester-Hepburn mechanism can occur under mild conditions, depending on the experimental details. This technique can also be used to test for other artifact mechanisms. We investigated the known ene reaction of DBNBS and tryptophan in more detail. We found that a strong artifact signal is induced by light; however, with atypically long incubations, we found that the artifact is also formed thermally. Published by Elsevier Inc.
C1 [Leinisch, Fabian; Jiang, Jinjie; Mason, Ronald P.] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
[DeRose, Eugene F.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Khramtsov, Valery V.] Ohio State Univ, Dept Internal Med, Div Pulm Allergy Crit Care & Sleep Med, Columbus, OH 43210 USA.
RP Leinisch, F (reprint author), NIEHS, Lab Toxicol & Pharmacol, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM leinischf@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences
FX We thank Dr. Ann G. Motten, Ms. Mary J. Mason, and Ms. Jean Corbett for
their help with the manuscript. This research was supported by the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences.
NR 39
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U1 1
U2 24
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 1497
EP 1505
DI 10.1016/j.freeradbiomed.2013.07.006
PG 9
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900144
PM 23851031
ER
PT J
AU Mason, RP
AF Mason, Ronald P.
TI Two hypotheses for the peroxidase activity of Mn-superoxide dismutase
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Letter
C1 NIEHS, NIH, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
RP Mason, RP (reprint author), NIEHS, NIH, Lab Toxicol & Pharmacol, POB 12233, Res Triangle Pk, NC 27709 USA.
EM mason4@niehs.nih.gov
NR 3
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2013
VL 65
BP 1533
EP 1533
DI 10.1016/j.freeradbiomed.2013.02.013
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 278DI
UT WOS:000328868900149
PM 23429047
ER
PT J
AU Chew, EY
AF Chew, Emily Y.
TI Nutrition Effects on Ocular Diseases in the Aging Eye
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE age-related macular degeneration; cataract type; antioxidants
ID AGE-RELATED MACULOPATHY; BLUE MOUNTAINS EYE; HIGH-DOSE SUPPLEMENTATION;
FATTY-ACID INTAKE; MACULAR DEGENERATION; BETA-CAROTENE; VITAMIN-E;
RANDOMIZED-TRIAL; CLINICAL-TRIAL; LENS OPACITIES
AB PURPOSE. We reviewed the data from the clinical trials of nutritional supplements for the treatment of age-related cataract and age-related macular degeneration (AMD) to determine future directions of research and treatment.
METHODS. Data from the controlled clinical trials are presented and reviewed for potential opportunities for further research into the treatment of cataracts and AMD.
RESULTS. Two trials using daily multivitamins/minerals demonstrated a reduction in the progression of nuclear cataract, but increased the risk of posterior subcapsular cataract. For AMD, the Age-Related Eye Disease Study (AREDS) formulation (vitamins C, E, beta-carotene, zinc, and copper) reduced the risk of progression to advanced AMD by 25% at 5 years. Because beta-carotene is associated with increased lung cancer in former smokers, lutein/zeaxanthin could replace beta-carotene and provide an incremental increase in the beneficial effects beyond the effects of the AREDS formulation. In addition, a randomized clinical trial of B vitamins demonstrated a beneficial effect for AMD with the vitamin B complex.
CONCLUSIONS. Future evaluation may include additional assessments of nutrients for the treatment of progression of cataract and AMD. A modest reduction would have significant impact as the numbers of persons affected with these two leading causes of blindness are projected to double in the next decade. An important step would be to develop surrogate outcomes to increase efficiency in clinical trials. More detailed phenotyping, especially of AMD, is required as it appears to be not one disease, but a group of diseases. Genotype-phenotype analyses may help to target pathways that are important in AMD.
C1 NEI, NIH, Bethesda, MD 20892 USA.
RP Chew, EY (reprint author), NEI, NIH, Bldg 10,CRC Room 3-2531,10 Ctr Dr,MSC 1204, Bethesda, MD 20892 USA.
EM echew@nei.nih.gov
NR 51
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Z9 2
U1 3
U2 15
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD DEC
PY 2013
VL 54
IS 14
SI SI
DI 10.1167/iovs.13-12914
PG 6
WC Ophthalmology
SC Ophthalmology
GA 278IX
UT WOS:000328884600009
ER
PT J
AU Shiels, MS
Pfeiffer, RM
Hildesheim, A
Engels, EA
Kemp, TJ
Park, JH
Katki, HA
Koshiol, J
Shelton, G
Caporaso, NE
Pinto, LA
Chaturvedi, AK
AF Shiels, Meredith S.
Pfeiffer, Ruth M.
Hildesheim, Allan
Engels, Eric A.
Kemp, Troy J.
Park, Ju-Hyun
Katki, Hormuzd A.
Koshiol, Jill
Shelton, Gloriana
Caporaso, Neil E.
Pinto, Ligia A.
Chaturvedi, Anil K.
TI Circulating Inflammation Markers and Prospective Risk for Lung Cancer
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID C-REACTIVE PROTEIN; SCREENING TRIAL; TUMOR MICROENVIRONMENT; PNEUMONIAE
INFECTION; SUBSEQUENT RISK; PREDICTION; PROSTATE; DISEASE; SMOKERS;
COHORT
AB Despite growing recognition of an etiologic role for inflammation in lung carcinogenesis, few prospective epidemiologic studies have comprehensively investigated the association of circulating inflammation markers with lung cancer.
We conducted a nested casecontrol study (n 526 lung cancer patients and n 592 control subjects) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Control subjects were matched to lung cancer case patients on age, sex, follow-up time (median 2.9 years), randomization year, and smoking (pack-years and time since quitting). Serum levels of 77 inflammation markers were measured using a Luminex bead-based assay. Conditional logistic regression and weighted Cox models were used to estimate odds ratios (ORs) and cumulative risks, respectively.
Of 68 evaluable markers, 11 were statistically significantly associated with lung cancer risk (P-trend across marker categories < .05), including acute-phase proteins (C-reactive protein [CRP], serum amyloid A [SAA]), proinflammatory cytokines (soluble tumor necrosis factor receptor 2 [sTNFRII]), anti-inflammatory cytokines (interleukin 1 receptor antagonist [IL-1RA]), lymphoid differentiation cytokines (interleukin 7 [IL-7]), growth factors (transforming growth factor alpha [TGF-A]), and chemokines (epithelial neutrophil-activating peptide 78 [ENA 78/CXCL5], monokine induced by gamma interferon [MIG/CXCL9], B cellattracting chemokine 1 [BCA-1/CXCL13], thymus activation regulated chemokine [TARC/CCL17], macrophage-derived chemokine [MDC/CCL22]). Elevated marker levels were associated with increased lung cancer risk, with odds ratios comparing the highest vs the lowest group ranging from 1.47 (IL-7) to 2.27 (CRP). For IL-1RA, elevated levels were associated with decreased lung cancer risk (OR 0.71; 95% confidence interval 0.51 to 1.00). Associations did not differ by smoking, lung cancer histology, or latency. A cross-validated inflammation score using four independent markers (CRP, BCA-1/CXCL13, MDC/CCL22, and IL-1RA) provided good separation in 10-year lung cancer cumulative risks among former smokers (quartile [Q] 1 1.1% vs Q4 3.1%) and current smokers (Q1 2.3% vs Q4 7.9%) even after adjustment for smoking.
Some circulating inflammation marker levels are associated with prospective lung cancer risk.
C1 [Shiels, Meredith S.; Hildesheim, Allan; Engels, Eric A.; Koshiol, Jill; Chaturvedi, Anil K.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Pfeiffer, Ruth M.; Katki, Hormuzd A.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Caporaso, Neil E.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Kemp, Troy J.; Shelton, Gloriana; Pinto, Ligia A.] SAIC Frederick Inc, HPV Immunol Lab, Frederick, MD USA.
[Park, Ju-Hyun] Dongguk Univ, Dept Stat, Seoul, South Korea.
RP Shiels, MS (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 7059, Rockville, MD USA.
EM shielsms@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Hildesheim, Allan/B-9760-2015; Chaturvedi,
Anil/J-2024-2015
OI Hildesheim, Allan/0000-0003-0257-2363; Chaturvedi,
Anil/0000-0003-2696-8899
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics; Division of Cancer Prevention, National Cancer Institute,
National Institutes of Health, Department of Health and Human Services
FX This research was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics and by contracts from the
Division of Cancer Prevention, National Cancer Institute, National
Institutes of Health, Department of Health and Human Services.
NR 44
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U1 1
U2 18
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD DEC
PY 2013
VL 105
IS 24
BP 1871
EP 1880
DI 10.1093/jnci/djt309
PG 10
WC Oncology
SC Oncology
GA 280UU
UT WOS:000329057100008
PM 24249745
ER
PT J
AU Polley, MYC
Leung, SCY
McShane, LM
Gao, DX
Hugh, JC
Mastropasqua, MG
Viale, G
Zabaglo, LA
Penault-Llorca, F
Bartlett, JMS
Gown, AM
Symmans, WF
Piper, T
Mehl, E
Enos, RA
Hayes, DF
Dowsett, M
Nielsen, TO
AF Polley, Mei-Yin C.
Leung, Samuel C. Y.
McShane, Lisa M.
Gao, Dongxia
Hugh, Judith C.
Mastropasqua, Mauro G.
Viale, Giuseppe
Zabaglo, Lila A.
Penault-Llorca, Frdrique
Bartlett, John M. S.
Gown, Allen M.
Symmans, W. Fraser
Piper, Tammy
Mehl, Erika
Enos, Rebecca A.
Hayes, Daniel F.
Dowsett, Mitch
Nielsen, Torsten O.
CA Breast Int Grp
North Amer Breast Cancer Grp
TI An International Ki67 Reproducibility Study
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID EARLY BREAST-CANCER; DIGITAL-IMAGE-ANALYSIS; NEUROENDOCRINE TUMORS;
POSTMENOPAUSAL WOMEN; NEOADJUVANT ANASTROZOLE; PREDICTIVE-VALUE;
LABELING INDEX; WORKING GROUP; KI-67; PROLIFERATION
AB In breast cancer, immunohistochemical assessment of proliferation using the marker Ki67 has potential use in both research and clinical management. However, lack of consistency across laboratories has limited Ki67s value. A working group was assembled to devise a strategy to harmonize Ki67 analysis and increase scoring concordance. Toward that goal, we conducted a Ki67 reproducibility study.
Eight laboratories received 100 breast cancer cases arranged into 1-mm core tissue microarraysuone set stained by the participating laboratory and one set stained by the central laboratory, both using antibody MIB-1. Each laboratory scored Ki67 as percentage of positively stained invasive tumor cells using its own method. Six laboratories repeated scoring of 50 locally stained cases on 3 different days. Sources of variation were analyzed using random effects models with log2-transformed measurements. Reproducibility was quantified by intraclass correlation coefficient (ICC), and the approximate two-sided 95% confidence intervals (CIs) for the true intraclass correlation coefficients in these experiments were provided.
Intralaboratory reproducibility was high (ICC 0.94; 95% CI 0.93 to 0.97). Interlaboratory reproducibility was only moderate (central staining: ICC 0.71, 95% CI 0.47 to 0.78; local staining: ICC 0.59, 95% CI 0.37 to 0.68). Geometric mean of Ki67 values for each laboratory across the 100 cases ranged 7.1% to 23.9% with central staining and 6.1% to 30.1% with local staining. Factors contributing to interlaboratory discordance included tumor region selection, counting method, and subjective assessment of staining positivity. Formal counting methods gave more consistent results than visual estimation.
Substantial variability in Ki67 scoring was observed among some of the worlds most experienced laboratories. Ki67 values and cutoffs for clinical decision-making cannot be transferred between laboratories without standardizing scoring methodology because analytical validity is limited.
C1 [Polley, Mei-Yin C.; McShane, Lisa M.] NCI, Biometr Res Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Leung, Samuel C. Y.; Gao, Dongxia; Mehl, Erika; Nielsen, Torsten O.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Hugh, Judith C.] Univ Alberta, Dept Lab Med & Pathol, Edmonton, AB T6G 2M7, Canada.
[Mastropasqua, Mauro G.; Viale, Giuseppe] European Inst Oncol, Div Pathol & Lab Med, Milan, Italy.
[Viale, Giuseppe] Univ Milan, Milan, Italy.
[Zabaglo, Lila A.] Inst Canc Res, Breakthrough Breast Canc Res Ctr, London SW3 6JB, England.
[Penault-Llorca, Frdrique] Ctr Jean Perrin, Dept Pathol, Clermont Ferrand, France.
[Penault-Llorca, Frdrique] Univ Auvergne, Clermont Ferrand, France.
[Bartlett, John M. S.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Gown, Allen M.] PhenoPath Labs, Seattle, WA USA.
[Symmans, W. Fraser] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
[Piper, Tammy] Western Gen Hosp, Edinburgh Canc Res Ctr, Edinburgh EH4 2XU, Midlothian, Scotland.
[Enos, Rebecca A.] EMMES Corp, Rockville, MD USA.
[Hayes, Daniel F.] Univ Michigan, Ctr Comprehens Canc, Breast Oncol Program, Ann Arbor, MI 48109 USA.
[Dowsett, Mitch] Royal Marsden Hosp, Acad Dept Biochem, London SW3 6JJ, England.
RP Nielsen, TO (reprint author), Univ British Columbia, JP 1401,855 W 12th Ave, Vancouver, BC V5Z 1M9, Canada.
EM torsten@mail.ubc.ca
FU Breast Cancer Research Foundation; Breakthrough Breast Cancer; National
Institute for Health Research Biomedical Research Centre at the Royal
Marsden Hospital; Government of Ontario
FX This work was supported by the Breast Cancer Research Foundation.
Additional funding for the UK labs was received from Breakthrough Breast
Cancer and the National Institute for Health Research Biomedical
Research Centre at the Royal Marsden Hospital. Funding for the Ontario
Institute for Cancer Research is provided by the Government of Ontario.
NR 31
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U1 1
U2 19
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD DEC
PY 2013
VL 105
IS 24
BP 1897
EP 1906
DI 10.1093/jnci/djt306
PG 10
WC Oncology
SC Oncology
GA 280UU
UT WOS:000329057100011
PM 24203987
ER
PT J
AU Ahn, J
Sinha, R
Pei, ZH
Dominianni, C
Wu, J
Shi, JX
Goedert, JJ
Hayes, RB
Yang, LY
AF Ahn, Jiyoung
Sinha, Rashmi
Pei, Zhiheng
Dominianni, Christine
Wu, Jing
Shi, Jianxin
Goedert, James J.
Hayes, Richard B.
Yang, Liying
TI Human Gut Microbiome and Risk for Colorectal Cancer
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID COLON-CANCER; BACTERIA; DIVERSITY; DISEASE; INDUCTION; COLITIS; PRIMERS;
HEALTH
AB We tested the hypothesis that an altered community of gut microbes is associated with risk of colorectal cancer (CRC) in a study of 47 CRC case subjects and 94 control subjects. 16S rRNA genes in fecal bacterial DNA were amplified by universal primers, sequenced by 454 FLX technology, and aligned for taxonomic classification to microbial genomes using the QIIME pipeline. Taxonomic differences were confirmed with quantitative polymerase chain reaction and adjusted for false discovery rate. All statistical tests were two-sided. From 794 217 16S rRNA gene sequences, we found that CRC case subjects had decreased overall microbial community diversity (P=.02). In taxonomy-based analyses, lower relative abundance of Clostridia (68.6% vs 77.8%) and increased carriage of Fusobacterium (multivariable odds ratio [OR] = 4.11; 95% confidence interval [CI] = 1.62 to 10.47) and Porphyromonas (OR = 5.17; 95% CI = 1.75 to 15.25) were found in case subjects compared with control subjects. Because of the potentially modifiable nature of the gut bacteria, our findings may have implications for CRC prevention.
C1 [Ahn, Jiyoung; Dominianni, Christine; Wu, Jing; Hayes, Richard B.] NYU, Div Epidemiol, Sch Med, Dept Populat Hlth, New York, NY 10016 USA.
[Pei, Zhiheng] NYU, Dept Pathol, Sch Med, New York, NY 10016 USA.
[Pei, Zhiheng; Yang, Liying] NYU, Sch Med, Dept Med, New York, NY 10010 USA.
[Ahn, Jiyoung; Pei, Zhiheng; Dominianni, Christine; Wu, Jing; Hayes, Richard B.] NYU, Inst Canc, New York, NY 10016 USA.
[Sinha, Rashmi; Shi, Jianxin; Goedert, James J.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Pei, Zhiheng] New York Vet Affairs Med Ctr, Dept Pathol & Lab Med, New York, NY USA.
RP Ahn, J (reprint author), NYU, Div Epidemiol, Sch Med, Dept Populat Hlth, 650 1st Ave, New York, NY 10016 USA.
EM jiyoung.ahn@nyumc.org; liying.yang@nyumc.org
RI Sinha, Rashmi/G-7446-2015;
OI Sinha, Rashmi/0000-0002-2466-7462; Yang, Liying/0000-0003-1442-4915;
Pei, Zhiheng/0000-0001-8570-6747; Hayes, Richard/0000-0002-0918-661X
FU National Cancer Institute [R03CA159414, R01CA159036]; Pancreatic Cancer
Action Network-AACR Career Development Award; Daniel and Janet Mordecai
Foundation [12-20-25-AHN]; Intramural Research Program of the National
Institutes of Health/National Cancer Institute, Division of Cancer
Epidemiology and Genetics
FX This work was supported by the National Cancer Institute (R03CA159414
and R01CA159036); a 2012 Pancreatic Cancer Action Network-AACR Career
Development Award, supported by the Daniel and Janet Mordecai Foundation
(grant 12-20-25-AHN); and the Intramural Research Program of the
National Institutes of Health/National Cancer Institute, Division of
Cancer Epidemiology and Genetics.
NR 29
TC 110
Z9 113
U1 10
U2 71
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD DEC
PY 2013
VL 105
IS 24
BP 1907
EP 1911
DI 10.1093/jnci/djt300
PG 5
WC Oncology
SC Oncology
GA 280UU
UT WOS:000329057100012
PM 24316595
ER
PT J
AU Clay, JR
AF Clay, John R.
TI A novel analysis of excitatory currents during an action potential from
suprachiasmatic nucleus neurons (Retracted article. See vol. 112, pg.
2668, 2014)
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE action potential clamp; suprachiasmatic nucleus neurons; mathematical
models
ID EFFICIENT ACTION-POTENTIALS; POTASSIUM CURRENT; CALCIUM CURRENTS;
DYNAMIC CLAMP; CHANNEL; SODIUM; INACTIVATION; MODEL; ELECTROPHYSIOLOGY;
MECHANISM
AB A new application of the action potential (AP) voltage-clamp technique is described based on computational analysis. An experimentally recorded AP is digitized. The resulting V-i vs. t(i) data set is applied to mathematical models of the ionic conductances underlying excitability for the cell from which the AP was recorded to test model validity. The method is illustrated for APs from suprachiasmatic nucleus (SCN) neurons and the underlying tetrodotoxin-sensitive Na+ current, I-Na, and the Ca2+ current, I-Ca. Voltage-step recordings have been made for both components from SCN neurons (Jackson et al. 2004). The combination of voltage-step and AP clamp results provides richer constraints for mathematical models of voltage-gated ionic conductances than either set of results alone, in particular the voltage-step results. For SCN neurons the long-term goal of this work is a realistic mathematical model of the SCN AP in which the equations for I-Na and I-Ca obtained from this analysis will be a part. Moreover, the method described in this report is general. It can be applied to any excitable cell.
C1 [Clay, John R.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Clay, JR (reprint author), Twinbrook TN-41,5625 Fishers Lane, Rockville, MD 20852 USA.
EM jrclay@ninds.nih.gov
FU National Institute of Neurological Disorders and Stroke, National
Institutes of Health, Bethesda, Maryland
FX This research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, National
Institutes of Health, Bethesda, Maryland.
NR 33
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U1 3
U2 9
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
EI 1522-1598
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD DEC
PY 2013
VL 110
IS 11
BP 2574
EP 2579
DI 10.1152/jn.00462.2013
PG 6
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 278JJ
UT WOS:000328886300008
PM 24047903
ER
PT J
AU Zhu, B
Dunson, DB
AF Zhu, Bin
Dunson, David B.
TI Locally Adaptive Bayes Nonparametric Regression via Nested Gaussian
Processes
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Article
DE Bayesian nonparametric regression; Nested smoothing spline; Penalized
sum-of-square; Reproducing kernel Hilbert space; Stochastic differential
equations
ID MASS-SPECTROMETRY DATA; VARIABLE SELECTION; POSTERIOR CONSISTENCY;
SPATIAL ADAPTATION; PENALIZED SPLINES; BINARY REGRESSION; WAVELET
SHRINKAGE; PROCESS PRIORS; QUANTIFICATION; PENALTIES
AB We propose a nested Gaussian process (nGP) as a locally adaptive prior for Bayesian nonparametric regression. Specified through a set of stochastic differential equations (SDEs), the nGP imposes a Gaussian process prior for the function's mth-order derivative. The nesting comes in through including a local instantaneous mean function, which is drawn from another Gaussian process inducing adaptivity to locally varying smoothness. We discuss the support of the nGP prior in terms of the closure of a reproducing kernel Hilbert space, and consider theoretical properties of the posterior. The posterior mean under the nGP prior is shown to be equivalent to the minimizer of a nested penalized sum-of-squares involving penalties for both the global and local roughness of the function. Using highly efficient Markov chain Monte Carlo for posterior inference, the proposed method performs well in simulation studies compared to several alternatives, and is scalable to massive data, illustrated through a proteomics application.
C1 [Zhu, Bin] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Dunson, David B.] Duke Univ, Dept Stat Sci, Durham, NC 27708 USA.
RP Zhu, B (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
EM bin.zhu@nih.gov; dunson@stat.duke.edu
FU National Institute of Environmental Health Sciences [R01ES017436,
R01ES17240]; National Institutes of Health [5P2O-RR020782-O3]; U.S.
Environmental Protection Agency [RD-83329301-0]; Intramural Research
Program of the National Cancer Institute, National Institutes of Health,
Maryland, USA
FX This work was supported by Award Numbers R01ES017436 and R01ES17240 from
the National Institute of Environmental Health Sciences, by funding from
the National Institutes of Health (5P2O-RR020782-O3) and the U.S.
Environmental Protection Agency (RD-83329301-0) and by the Intramural
Research Program of the National Cancer Institute, National Institutes
of Health, Maryland, USA. The content is solely the responsibility of
the authors and does not necessarily represent the official views of the
National Institute of Environmental Health Sciences, the National
Institutes of Health or the U. S. Environmental Protection Agency.
NR 57
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U1 0
U2 3
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 732 N WASHINGTON ST, ALEXANDRIA, VA 22314-1943 USA
SN 0162-1459
EI 1537-274X
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD DEC
PY 2013
VL 108
IS 504
BP 1445
EP 1456
DI 10.1080/01621459.2013.838568
PG 12
WC Statistics & Probability
SC Mathematics
GA 278RZ
UT WOS:000328908700029
ER
PT J
AU Minakawa, EN
Yamakado, H
Tanaka, A
Uemura, K
Takeda, S
Takahashi, R
AF Minakawa, Eiko N.
Yamakado, Hodaka
Tanaka, Atsushi
Uemura, Kengo
Takeda, Shunichi
Takahashi, Ryosuke
TI Chicken DT40 cell line lacking DJ-1, the gene responsible for familial
Parkinson's disease, displays mitochondrial dysfunction
SO NEUROSCIENCE RESEARCH
LA English
DT Article
DE Parkinson's disease; DJ-1; DT40; Mitochondria; Oxidative stress
ID PINK1; MUTATIONS; AUTOPHAGY; DYNAMICS; DROSOPHILA-PINK1; DEGENERATION;
PATHOLOGY
AB Parkinson's disease (PD) is the most common neurodegenerative movement disorder mainly due to gradual loss of dopaminergic neurons in the substantia nigra. Although the causative genes for autosomai recessive PD, Parkin, PINK1 and DJ-1, share a common pathway, at least in part, in mitochondrial quality control and protein quality control, their precise relationship remains elusive. Previous studies suggested the limitation of gene-modified mice model to solve this problem. DT40 is an avian leukosis virus-induced chicken B cell line with an exceptionally high ratio of targeted to random DNA integration, which enables efficient targeted disruption of multiple genes of interest. We generated DJ-1-deficient DT40 cells and analyzed PD-related phenotypes. These cells exhibited vulnerability to oxidative stress, mitochondrial dysfunction and fragmentation. Importantly, we showed that mitochondrial membrane potential and morphology are available for the phenotype analysis in DT40. These results suggest that genetically engineered DT40 cells would serve as a relevant model of PD, and help understand the genetic and functional relationship among multiple causative genes. Furthermore, in line with the recent concept of PD as a systemic disorder, elucidating the pathomechanism of PD using DT40 would lead to the development of noninvasive diagnostic tools and drug screening assays using patient-derived lymphocytes. (c) 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
C1 [Minakawa, Eiko N.; Yamakado, Hodaka; Uemura, Kengo; Takahashi, Ryosuke] Kyoto Univ, Grad Sch Med, Dept Neurol, Sakyo Ku, Kyoto 6068507, Japan.
[Tanaka, Atsushi] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
Kyoto Univ, Grad Sch Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan.
RP Takahashi, R (reprint author), Kyoto Univ, Grad Sch Med, Dept Neurol, Sakyo Ku, 54 Kawahara Cho, Kyoto 6068507, Japan.
EM minakawa@kuhp.kyoto-u.ac.jp; yamakado@kuhp.kyoto-u.ac.jp;
atsushi.tanaka@med.id.yamagata-u.ac.jp; ueken@kuhp.kyoto-u.ac.jp;
stakeda@rg.med.kyoto-u.ac.jp; ryosuket@kuhp.kyoto-u.ac.jp
FU CREST program of JST (Japan Science and Technology Agency); NINDS
FX This study was supported by CREST program of JST (Japan Science and
Technology Agency) and the intramural research program of NINDS. We
thank Dr. Richard J. Youle (NINDS, National Institutes of Health, USA)
for helpful discussion and advice. We also thank Mr. Satoshi Horimoto
(Department of Biophysics, Division of Biological Sciences, Kyoto
University Graduate School of Science), Dr. Koji Hirota (Department of
Radiation Genetics, Kyoto University Graduate School of Medicine), Dr.
Takaaki Hirai (NINDS, National Institutes of Health, USA) and Dr. Keizo
Tano (Research Reactor Institute, Kyoto University) for their technical
advice.
NR 33
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U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0168-0102
EI 1872-8111
J9 NEUROSCI RES
JI Neurosci. Res.
PD DEC
PY 2013
VL 77
IS 4
BP 228
EP 233
DI 10.1016/j.neures.2013.09.006
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 278XJ
UT WOS:000328922900006
PM 24064392
ER
PT J
AU Sciamanna, I
Gualtieri, A
Cossetti, C
Osimo, EF
Ferracin, M
Macchia, G
Arico, E
Prosseda, G
Vitullo, P
Misteli, T
Spadafora, C
AF Sciamanna, Ilaria
Gualtieri, Alberto
Cossetti, Cristina
Osimo, Emanuele Felice
Ferracin, Manuela
Macchia, Gianfranco
Arico, Eleonora
Prosseda, Gianni
Vitullo, Patrizia
Misteli, Tom
Spadafora, Corrado
TI A tumor-promoting mechanism mediated by retrotransposon-encoded reverse
transcriptase is active in human transformed cell lines
SO ONCOTARGET
LA English
DT Article
DE LINE-1 retrotransposons; reverse transcriptase; transcriptome; miRNAs;
DNA:RNA hybrids; cancer genome; reverse transcriptase inhibitor
ID NONCODING RNAS; L1 RETROTRANSPOSITION; ULTRACONSERVED REGIONS;
TRANSPOSABLE ELEMENTS; DNA METHYLATION; HUMAN MICRORNAS; BREAST-CANCER;
HUMAN GENOME; STEM-CELLS; EXPRESSION
AB LINE-1 elements make up the most abundant retrotransposon family in the human genome. Full-length LINE-1 elements encode a reverse transcriptase (RT) activity required for their own retrotranpsosition as well as that of non-autonomous Alu elements. LINE-1 are poorly expressed in normal cells and abundantly in cancer cells. Decreasing RT activity in cancer cells, by either LINE-1-specific RNA interference, or by RT inhibitory drugs, was previously found to reduce proliferation and promote differentiation and to antagonize tumor growth in animal models. Here we have investigated how RT exerts these global regulatory functions.
We report that the RT inhibitor efavirenz (EFV) selectively downregulates proliferation of transformed cell lines, while exerting only mild effects on non-transformed cells; this differential sensitivity matches a differential RT abundance, which is high in the former and undetectable in the latter. Using CsCl density gradients, we selectively identify Alu and LINE-1 containing DNA: RNA hybrid molecules in cancer but not in normal cells. Remarkably, hybrid molecules fail to form in tumor cells treated with EFV under the same conditions that repress proliferation and induce the reprogramming of expression profiles of coding genes, microRNAs (miRNAs) and ultraconserved regions (UCRs). The RT-sensitive miRNAs and UCRs are significantly associated with Alu sequences.
The results suggest that LINE-1-encoded RT governs the balance between single-stranded and double-stranded RNA production. In cancer cells the abundant RT reverse-transcribes retroelement-derived mRNAs forming RNA: DNA hybrids. We propose that this impairs the formation of double-stranded RNAs and the ensuing production of small regulatory RNAs, with a direct impact on gene expression. RT inhibition restores the 'normal' small RNA profile and the regulatory networks that depend on them. Thus, the retrotransposon-encoded RT drives a previously unrecognized mechanism crucial to the transformed state in tumor cells.
C1 [Sciamanna, Ilaria; Gualtieri, Alberto; Cossetti, Cristina; Osimo, Emanuele Felice; Macchia, Gianfranco; Arico, Eleonora; Vitullo, Patrizia; Spadafora, Corrado] Ist Superiore Sanit, Rome, Italy.
[Ferracin, Manuela] Univ Ferrara, LTTA, I-44100 Ferrara, Italy.
[Ferracin, Manuela] Univ Ferrara, Dept Morphol Surg & Expt Med, I-44100 Ferrara, Italy.
[Prosseda, Gianni] Univ Roma La Sapienza, Dept Biol & Biotechnol Charles Darwin, I-00185 Rome, Italy.
[Misteli, Tom] NIH, Bethesda, MD 20892 USA.
[Gualtieri, Alberto; Cossetti, Cristina] Univ Roma Tor Vergata, Dept Expt Med & Surg, Rome, Italy.
RP Spadafora, C (reprint author), Ist Superiore Sanit, Viale Regina Elena 299, Rome, Italy.
EM cspadaf@tin.it
RI Ferracin, Manuela/K-2097-2016; Cossetti, Cristina/K-5034-2016
OI Ferracin, Manuela/0000-0002-1595-6887; Cossetti,
Cristina/0000-0002-8809-4149
FU ISS-NIH; Italian Ministry of Health; Intramural Research Program of the
National Institutes of Health (NIH), NCI, Center for Cancer Research
FX We are indebted with Massimo Negrini (University of Ferrara, Ferrara,
Italy) for microarray analysis. We thank Giuseppe La Regina (Sapienza
University, Rome, Italy) for purification of EFV, and Patrizia Lavia and
Valeria de Turris (CNR, Rome, Italy) and Alessandro Rosa (Sapienza
University, Rome, Italy), for suggestions and critical reading of the
manuscript. We acknowledge the skillful assistance of Cosimo Curiano
with drawing preparation. This work was supported by ISS-NIH cooperation
grants ("Endogenous Reverse Transcriptase activity and chromatin
remodeling in normal and transformed cells and early embryos"), Italian
Ministry of Health grants "New therapeutic strategies based on studies
of tumor microenvironment and new targets identified through genomic
profile analysis", "Endogenous Reverse Transcriptase as tumour marker
and causative agent of tumour onset and progression", "Endogenous
Reverse Transcriptase in tumour onset and progression and in tumour
therapy" to CS, and by the Intramural Research Program of the National
Institutes of Health (NIH), NCI, Center for Cancer Research to TM.
NR 68
TC 18
Z9 19
U1 1
U2 4
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC
PY 2013
VL 4
IS 12
BP 2271
EP 2287
PG 17
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 279CK
UT WOS:000328936800012
PM 24345856
ER
PT J
AU Lee, P
Linderman, J
Smith, S
Brychta, RJ
Perron, R
Idelson, C
Werner, CD
Chen, KY
Celi, FS
AF Lee, P.
Linderman, J.
Smith, S.
Brychta, R. J.
Perron, R.
Idelson, C.
Werner, C. D.
Chen, K. Y.
Celi, F. S.
TI Fibroblast growth factor 21 (FGF21) and bone: is there a relationship in
humans?
SO OSTEOPOROSIS INTERNATIONAL
LA English
DT Article
DE Beige adipose tissue; Bone mineral density; Brown adipose tissue; FGF21;
Fibroblast growth factor-21
ID BROWN ADIPOSE-TISSUE; ADAPTIVE THERMOGENESIS; ADULT HUMANS; ADIPOCYTES
AB In animals, high fibroblast growth factor 21 (FGF21) states improve insulin resistance but induce bone loss. Whether FGF21 relates to bone mineral density (BMD) is unknown in humans. Contrary to prediction from animal findings, we found higher FGF21 levels associating with greater BMD in women, independent of age and body composition.
Introduction Recent laboratory studies suggest that FGF21 is involved in reciprocal regulation of bone and energy homeostasis. Systemic administration of FGF21 protects animals from obesity and diabetes but causes severe bone loss, smothering the enthusiasm over FGF21 as a potential antiobesity therapeutic. To date, there is no information on whether FGF21 relates to BMD in humans. We thus studied the relationship between plasma FGF21 levels and BMD in healthy adults.
Methods Fasting plasma FGF21 levels were measured by enzyme-linked immunosorbent assay and body composition by dual-energy X-ray absorptiometry.
Results Among 40 healthy volunteers (age 32 +/- 10 year, 16 women), men had significantly higher lean body mass (p<0.01) and total BMD (p<0.05), and lower percent body fat than women (p<0.01). Median plasma FGF21 levels were not different between the sexes. While therewas no association between FGF21 concentrations and body composition in men, FGF21 levels correlated positively with fat mass (p<0.01) in women. In men, no significant correlation between FGF21 with BMD was observed. However, in women, FGF21 correlated positively with total BMD(R-2=0.69, p=0.003) and spine BMD (R-2=0.76, p=0.001); the correlation remained significant after adjusting for age, ethnicity, and body composition.
Conclusions This study reveals for the first time a strong positive association between plasma FGF21 levels and BMD in healthy women, suggesting the association between bone loss and high FGF21 states in animals may not be directly translated to humans in physiologic states. We hypothesize that FGF21 may increase bonemass particularly in women through paracrine mechanisms in the bone-adipose interface.
C1 [Lee, P.; Linderman, J.; Smith, S.; Brychta, R. J.; Perron, R.; Idelson, C.; Werner, C. D.; Chen, K. Y.; Celi, F. S.] NIDDK, Obes Branch, NIH, CRC, Bethesda, MD 20892 USA.
RP Lee, P (reprint author), NIDDK, Obes Branch, NIH, CRC, Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM pcylee@gmail.com
OI Chen, Kong/0000-0002-0306-1904
FU Australian National Health Medical Research Council (NHMRC); Royal
Australasian College of Physicians (RACP) Foundations Diabetes Australia
Fellowship; Bushell Travelling Fellowship; Intramural Research Program
of NIDDK [Z01-DK047057-02, Z01-DK071044]
FX Paul Lee was supported by an Australian National Health Medical Research
Council (NHMRC) Early Career Fellowship, the Royal Australasian College
of Physicians (RACP) Foundations Diabetes Australia Fellowship, and
Bushell Travelling Fellowship. This study was supported by the
Intramural Research Program of NIDDK: programs Z01-DK047057-02 and
Z01-DK071044.
NR 19
TC 15
Z9 15
U1 1
U2 18
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0937-941X
EI 1433-2965
J9 OSTEOPOROSIS INT
JI Osteoporosis Int.
PD DEC
PY 2013
VL 24
IS 12
BP 3053
EP 3057
DI 10.1007/s00198-013-2464-9
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 281MK
UT WOS:000329105500015
PM 23912560
ER
PT J
AU Pedone, C
Napoli, N
Pozzilli, P
Lauretani, F
Bandinelli, S
Ferrucci, L
Rossi, FF
Antonelli-Incalzi, R
AF Pedone, Claudio
Napoli, Nicola
Pozzilli, Paolo
Lauretani, Fulvio
Bandinelli, Stefania
Ferrucci, Luigi
Rossi, Francesca Flavia
Antonelli-Incalzi, Raffaele
TI Bone Health As a Function of Adipokines and Vitamin D Pattern in Elderly
Patients
SO REJUVENATION RESEARCH
LA English
DT Article
ID MINERAL DENSITY; POSTMENOPAUSAL WOMEN; BIOCHEMICAL MARKERS; SERUM
ADIPONECTIN; OLDER-ADULTS; BODY-COMPOSITION; VISFATIN LEVELS; D
DEFICIENCY; FAT MASS; LEPTIN
AB Background: Adiponectin, leptin, and resistin are involved in bone metabolism, but the evidence regarding their effects is not conclusive. We analyzed the relationship between these adipokines, vitamin D, and bone health using a cluster analysis approach. Methods: We used cross-sectional data coming from the InCHIANTI study, in which bone density and area were estimated using computed tomography. The sample size was 690 (women, 57.5%; mean age, 75.2 years; range, 65-102). Five clusters were generated on the basis of gender, age, adipokines, and vitamin D concentrations. The clusters were characterized, respectively, by higher resistin and older age (hR-O, n=134), higher vitamin D and younger age (hD-Y, n=152), higher adiponectin (hA, n=65), and higher leptin (hL, n=52). The last cluster had intermediate values of all the constituting variables (I, n=287). The clusters were compared with respect to bone parameters and clinical characteristics. Results: Cluster hR-O had the lowest total and cortical bone density. Cluster hD-Y had the lowest adiponectin (9.29g/mL) and leptin (7.9ng/mL) serum concentrations, the highest prevalence of men (71.1%), and total/cortical bone density and area. No statistically significant difference across clusters was observed for age- and sex-standardized measures of bone mineral density and bone area, but leptin was associated with these parameters in a linear model adjusted for age, gender, vitamin D, resistin, and leptin. Conclusions: In an elderly population, age and sex almost completely explain the variability in bone status across cluster characterized by different levels of circulating adipokines and vitamin D. The role of leptin, however, seems worthy of consideration.
C1 [Pedone, Claudio; Rossi, Francesca Flavia; Antonelli-Incalzi, Raffaele] Univ Campus Biomed, Geriatr Unit, I-00128 Rome, Italy.
[Pedone, Claudio] Alberto Sordi Fdn, Rome, Italy.
[Napoli, Nicola; Pozzilli, Paolo] Univ Campus Biomed, Endocrinol Unit, I-00128 Rome, Italy.
[Lauretani, Fulvio] Univ Hosp Parma, Geriatr Unit, Parma, Italy.
[Lauretani, Fulvio] Univ Hosp Parma, Lab Movement Anal, Geriatr & Rehabil Dept, Parma, Italy.
[Bandinelli, Stefania] Florence Hlth Agcy, Geriatr Rehabil Unit, Florence, Italy.
[Ferrucci, Luigi] NIH, Longitudinal Studies Sect, Baltimore, MD USA.
[Antonelli-Incalzi, Raffaele] San Raffaele Cittadella Carita Fdn, Taranto, Italy.
RP Pedone, C (reprint author), Univ Campus Biomed, Via Alvaro del Portillo 5, I-00128 Rome, Italy.
EM c.pedone@unicampus.it
RI Lauretani, Fulvio/K-5115-2016;
OI Napoli, Nicola/0000-0002-3091-8205; Pedone, Claudio/0000-0003-1847-9032;
Antonelli Incalzi, Raffaele/0000-0003-2100-2075; Lauretani,
Fulvio/0000-0002-5287-9972; Pozzilli, Paolo/0000-0001-5090-636X
NR 42
TC 2
Z9 2
U1 0
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1549-1684
EI 1557-8577
J9 REJUV RES
JI Rejuv. Res.
PD DEC 1
PY 2013
VL 16
IS 6
BP 467
EP 474
DI 10.1089/rej.2013.1436
PG 8
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 273TD
UT WOS:000328558300005
PM 23829612
ER
PT J
AU Niemann, CU
Wiestner, A
AF Niemann, Carsten U.
Wiestner, Adrian
TI B-cell receptor signaling as a driver of lymphoma development and
evolution
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Ibrutinib; Idelalisib; Lymphoma; B-cell receptor; Antigen
ID CHRONIC-LYMPHOCYTIC-LEUKEMIA; NF-KAPPA-B; BRUTONS TYROSINE KINASE;
NON-HODGKIN-LYMPHOMA; HELICOBACTER-PYLORI ERADICATION; LYN-DEFICIENT
MICE; PHASE-II TRIAL; THERAPEUTIC TARGET; FOLLICULAR LYMPHOMA;
AUTOIMMUNE-DISEASE
AB The B-cell receptor (BCR) is essential for normal B-cell development and maturation. In an increasing number of B-cell malignancies, BCR signaling is implicated as a pivotal pathway in tumorigenesis. Mechanisms of BCR activation are quite diverse and range from chronic antigenic drive by microbial or viral antigens to autostimulation of B-cells by self-antigens to activating mutations in intracellular components of the BCR pathway. Hepatitis C virus infection can lead to the development of splenic marginal zone lymphoma, while Helicobacter pylori infection is associated with the development of mucosa-associated lymphoid tissue lymphomas. In some of these cases, successful treatment of the infection removes the inciting antigen and results in resolution of the lymphoma. Chronic lymphocytic leukemia has been recognized for decades as a malignancy of auto-reactive B-cells and its clinical course is in part determined by the differential response of the malignant cells to BCR activation. In a number of B-cell malignancies, activating mutations in signal transduction components of the BCR pathway have been identified; prominent examples are activated B-cell-like (ABC) diffuse large B-cell lymphomas (DLBCL) that carry mutations in CD79B and CARD11 and display chronic active BCR signaling resulting in constitutive activation of the NF-kappa B pathway. Despite considerable heterogeneity in biology and clinical course, many mature B-cell malignancies are highly sensitive to kinase inhibitors that disrupt BCR signaling. Thus, targeted therapy through inhibition of BCR signaling is emerging as a new treatment paradigm for many B-cell malignancies. Here, we review the role of the BCR in the pathogenesis of B-cell malignancies and summarize clinical results of the emerging class of kinase inhibitors that target this pathway. (C) 2013 Published by Elsevier Ltd.
C1 [Niemann, Carsten U.; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Wiestner, A (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,CRC 3E-5140, Bethesda, MD 20892 USA.
EM wiestnea@nhlbi.nih.gov
RI Niemann, Carsten/P-3497-2015
OI Niemann, Carsten/0000-0001-9880-5242
FU Danish Cancer Society; Heart, Lung, Blood Institute, National Institutes
of Health
FX CUN is supported by the Danish Cancer Society and AW is supported by the
intramural research program of the Heart, Lung, Blood Institute,
National Institutes of Health.
NR 170
TC 50
Z9 53
U1 2
U2 38
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD DEC
PY 2013
VL 23
IS 6
BP 410
EP 421
DI 10.1016/j.semcancer.2013.09.001
PG 12
WC Oncology
SC Oncology
GA 280EH
UT WOS:000329011000003
PM 24060900
ER
PT J
AU Aufderheide, TP
Nolan, JP
Jacobs, IG
van Belle, G
Bobrow, BJ
Marshall, J
Finn, J
Becker, LB
Bottiger, B
Cameron, P
Drajer, S
Jung, JJ
Kloeck, W
Koster, RW
Ma, MHM
Shin, SD
Sopko, G
Taira, BR
Timerman, S
Ong, MEH
AF Aufderheide, Tom P.
Nolan, Jerry P.
Jacobs, Ian G.
van Belle, Gerald
Bobrow, Bentley J.
Marshall, John
Finn, Judith
Becker, Lance B.
Bottiger, Bernd
Cameron, Peter
Drajer, Saul
Jung, Julianna J.
Kloeck, Walter
Koster, Rudolph W.
Ma, Matthew Huei-Ming
Shin, Sang Do
Sopko, George
Taira, Breena R.
Timerman, Sergio
Ong, Marcus Eng Hock
TI Global Health and Emergency Care: A Resuscitation Research Agenda-Part 1
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
ID HOSPITAL CARDIAC-ARREST; CARDIOPULMONARY-RESUSCITATION; LIFE-SUPPORT;
TRAUMA CARE; SYSTEMATIC ANALYSIS; DEVELOPING-COUNTRY; SURGICAL CAPACITY;
MORTALITY; DISEASE; BURDEN
AB At the 2013 Academic Emergency Medicine global health consensus conference, a breakout session on a resuscitation research agenda was held. Two articles focusing on cardiac arrest and trauma resuscitation are the result of that discussion. This article describes the burden of disease and outcomes, issues in resuscitation research, and global trends in resuscitation research funding priorities. Globally, cardiovascular disease and trauma cause a high burden of disease that receives a disproportionately smaller research investment. International resuscitation research faces unique ethical challenges. It needs reliable baseline statistics regarding quality of care and outcomes; data linkages between providers; reliable and comparable national databases; and an effective, efficient, and sustainable resuscitation research infrastructure to advance the field. Research in resuscitation in low- and middle-income countries is needed to understand the epidemiology, infrastructure and systems context, level of training needed, and potential for cost-effective care to improve outcomes. Research is needed on low-cost models of population-based research, ways to disseminate information to the developing world, and finding the most cost-effective strategies to improve outcomes. (C) 2013 by the Society for Academic Emergency Medicine
C1 [Aufderheide, Tom P.] Med Coll Wisconsin, Dept Emergency Med, Milwaukee, WI 53226 USA.
[Nolan, Jerry P.] Royal United Hosp, Bath BA1 3NG, Avon, England.
[Jacobs, Ian G.; Finn, Judith] Curtin Univ, Fac Hlth Sci, Prehosp Resuscitat & Emergency Care Res Unit, Perth, WA 6845, Australia.
[van Belle, Gerald] Univ Washington, Dept Biostat, Clin Trial Ctr, Seattle, WA 98195 USA.
[van Belle, Gerald] Univ Washington, Dept Environm & Occupat Hlth Sci, Clin Trial Ctr, Seattle, WA 98195 USA.
[Bobrow, Bentley J.] Univ Arizona, Coll Med, Dept Emergency Med, Maricopa Med Ctr, Phoenix, AZ USA.
[Bobrow, Bentley J.] Arizona Dept Hlth Serv, Bur EMS & Trauma Syst, Phoenix, AZ 85007 USA.
[Marshall, John] St Michaels Hosp, Div Gen Surg, Toronto, ON M5B 1W8, Canada.
[Finn, Judith] Monash Univ, Sch Publ Hlth & Prevent Med, Melbourne, Vic 3004, Australia.
[Becker, Lance B.] Univ Penn, Dept Emergency Med, Philadelphia, PA 19104 USA.
[Bottiger, Bernd] Univ Cologne, Univ Hosp, Dept Anaesthesiol & Intens Care Med, D-50931 Cologne, Germany.
[Cameron, Peter] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[Drajer, Saul] Univ Maimonides, Clin Esperanza, Buenos Aires, DF, Argentina.
[Jung, Julianna J.] Johns Hopkins Univ, Sch Med Emergency Med Clin Programs, Baltimore, MD USA.
[Kloeck, Walter] Univ Witwatersrand, Div Emergency Med, Johannesburg, South Africa.
[Koster, Rudolph W.] Univ Amsterdam, Acad Med Ctr, Dept Cardiol, NL-1105 AZ Amsterdam, Netherlands.
[Ma, Matthew Huei-Ming] Natl Taiwan Univ, Dept Emergency Med, Taipei 10764, Taiwan.
[Shin, Sang Do] Seoul Natl Univ, Coll Med, Dept Emergency Med, Seoul, South Korea.
[Sopko, George] NHLBI, NIH, Bethesda, MD 20892 USA.
[Taira, Breena R.] Olive View Univ Calif, Los Angeles Med Ctr, Dept Emergency Med, Sylmar, CA USA.
[Timerman, Sergio] Univ Sao Paulo, Sch Med, Inst Heart, Sao Paulo, Brazil.
[Ong, Marcus Eng Hock] Singapore Gen Hosp, Dept Emergency Med, Singapore, Singapore.
[Ong, Marcus Eng Hock] Duke NUS Grad Med Sch, Off Clin Sci, Singapore, Singapore.
RP Aufderheide, TP (reprint author), Med Coll Wisconsin, Dept Emergency Med, Milwaukee, WI 53226 USA.
EM taufderh@mcw.edu
RI Finn, Judith/B-2678-2010;
OI Finn, Judith/0000-0002-7307-7944; MA, MATTHEW
HUEI-MING/0000-0002-4388-9984; Nolan, Jerry/0000-0003-3141-3812
NR 58
TC 7
Z9 7
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
EI 1553-2712
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD DEC
PY 2013
VL 20
IS 12
BP 1289
EP 1296
DI 10.1111/acem.12270
PG 8
WC Emergency Medicine
SC Emergency Medicine
GA 273WK
UT WOS:000328566800012
PM 24341584
ER
PT J
AU Ong, MEH
Aufderheide, TP
Nichol, G
Bobrow, BJ
Bossaert, L
Cameron, P
Finn, J
Jacobs, I
Koster, RW
McNally, B
Ng, YY
Shin, SD
Sopko, G
Tanaka, H
Iwami, T
Hauswald, M
AF Ong, Marcus Eng Hock
Aufderheide, Tom P.
Nichol, Graham
Bobrow, Bentley J.
Bossaert, Leo
Cameron, Peter
Finn, Judith
Jacobs, Ian
Koster, Rudolph W.
McNally, Bryan
Ng, Yih Yng
Shin, Sang Do
Sopko, George
Tanaka, Hideharu
Iwami, Taku
Hauswald, Mark
TI Global Health and Emergency Care: A Resuscitation Research Agenda-Part 2
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
ID HOSPITAL CARDIAC-ARREST; AMERICAN-HEART-ASSOCIATION; TRAUMA SYSTEM;
POSTRESUSCITATION CARE; UNITED-STATES; MAJOR TRAUMA;
CARDIOPULMONARY-RESUSCITATION; CLINICAL CARDIOLOGY; TRANSPORT INTERVAL;
CONTROLLED-TRIALS
AB At the 2013 Academic Emergency Medicine global health consensus conference, a breakout session to develop a research agenda for resuscitation was held. Two articles are the result of that discussion. This second article addresses data collection, management, and analysis and regionalization of postresuscitation care, resuscitation programs, and research examples around the world and proposes a strategy to strengthen resuscitation research globally. There is a need for reliable global statistics on resuscitation, international standardization of data, and development of an electronic standard for reporting data. Regionalization of postresuscitation care is a priority area for future research. Large resuscitation clinical research networks are feasible and can give valuable data for improvement of service and outcomes. Low-cost models of population-based research, and emphasis on interventional and implementation studies that assess the clinical effects of programs and interventions, are needed to determine the most cost-effective strategies to improve outcomes. The global challenge is how to adapt research findings to a developing world situation to have an effect internationally. (C) 2013 by the Society for Academic Emergency Medicine
C1 [Ong, Marcus Eng Hock; Ng, Yih Yng] Singapore Gen Hosp, Dept Emergency Med, Singapore, Singapore.
[Ong, Marcus Eng Hock] Duke NUS Grad Med Sch, Off Clin Sci, Singapore, Singapore.
[Aufderheide, Tom P.] Med Coll Wisconsin, Dept Emergency Med, Milwaukee, WI 53226 USA.
[Nichol, Graham] Univ Washington, Harborview Ctr Prehosp Emergency Care, Seattle, WA 98195 USA.
[Bobrow, Bentley J.] Univ Arizona, Coll Med, Dept Emergency Med, Phoenix, AZ USA.
[Bobrow, Bentley J.] Maricopa Cty Gen Hosp, Phoenix, AZ USA.
[Bobrow, Bentley J.] Arizona Dept Hlth Serv, Bur EMS & Trauma Syst, Phoenix, AZ 85007 USA.
[Bossaert, Leo] Univ Antwerp, Dept Intens Care, B-2020 Antwerp, Belgium.
[Cameron, Peter] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[Finn, Judith; Jacobs, Ian] Curtin Univ, Prehosp Resuscitat & Emergency Care Res Unit, Fac Hlth Sci, Perth, WA 6845, Australia.
[Finn, Judith] Monash Univ, Sch Publ Hlth & Prevent Med, Melbourne, Vic 3004, Australia.
[Koster, Rudolph W.] Univ Amsterdam, Acad Med Ctr, Dept Cardiol, NL-1105 AZ Amsterdam, Netherlands.
[McNally, Bryan] Emory Univ, Dept Emergency Med, Atlanta, GA 30322 USA.
[Shin, Sang Do] Seoul Natl Univ, Coll Med, Dept Emergency Med, Seoul, South Korea.
[Sopko, George] NHLBI, NIH, Bethesda, MD 20892 USA.
[Tanaka, Hideharu] Kokushikan Univ, Dept Sport & Med Sci, Tokyo, Japan.
[Iwami, Taku] Kyoto Univ Hlth Serv, Dept Prevent Serv, Kyoto, Japan.
RP Ong, MEH (reprint author), Singapore Gen Hosp, Dept Emergency Med, Singapore, Singapore.
EM marcus.ong.e.h@sgh.com.sg
RI Finn, Judith/B-2678-2010
OI Finn, Judith/0000-0002-7307-7944
NR 61
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
EI 1553-2712
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD DEC
PY 2013
VL 20
IS 12
BP 1297
EP 1303
DI 10.1111/acem.12272
PG 7
WC Emergency Medicine
SC Emergency Medicine
GA 273WK
UT WOS:000328566800013
ER
PT J
AU Dawson, DA
AF Dawson, Deborah A.
TI Commentary on Tuithof et al. (2013): Implications of the DSM-5 revision
for the analysis of persistence/remission of alcohol use disorder
SO ADDICTION
LA English
DT Editorial Material
ID 3-YEAR FOLLOW-UP; GENERAL-POPULATION; DEPENDENCE; REMISSION; IV;
INDIVIDUALS; PREDICTORS; RECOVERY
C1 NIAAA, NIH, Bethesda, MD 20816 USA.
RP Dawson, DA (reprint author), NIAAA, NIH, Bethesda, MD 20816 USA.
EM deborah.anne.dawson@gmail.com
FU Intramural NIH HHS [Z99 AA999999]
NR 15
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0965-2140
EI 1360-0443
J9 ADDICTION
JI Addiction
PD DEC
PY 2013
VL 108
IS 12
BP 2100
EP 2101
DI 10.1111/add.12351
PG 2
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 265LT
UT WOS:000327954000012
PM 24237899
ER
PT J
AU Welzel, TM
Graubard, BI
Quraishi, S
Zeuzem, S
Davila, JA
El-Serag, HB
McGlynn, KA
AF Welzel, Tania M.
Graubard, Barry I.
Quraishi, Sabah
Zeuzem, Stefan
Davila, Jessica A.
El-Serag, Hashem B.
McGlynn, Katherine A.
TI Hepatocellular Carcinoma and Smoking: Oblivion or Contempt? Response
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Letter
C1 [Welzel, Tania M.; Zeuzem, Stefan] Johann Wolfgang Goethe Univ Hosp, Frankfurt, Germany.
[Graubard, Barry I.; Quraishi, Sabah; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Davila, Jessica A.; El-Serag, Hashem B.] Houston Vet Affairs Med Ctr, Houston, TX USA.
[Davila, Jessica A.; El-Serag, Hashem B.] Baylor Coll Med, Houston, TX 77030 USA.
RP McGlynn, KA (reprint author), NCI, DCEG, EPS 5022 6120 Execut Blvd, Rockville, MD 20852 USA.
EM mcglynnk@mail.nih.gov
NR 5
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 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD DEC
PY 2013
VL 108
IS 12
BP 1931
EP 1931
DI 10.1038/ajg.2013.342
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 272KM
UT WOS:000328459300020
PM 24300871
ER
PT J
AU Das, S
Seth, RK
Kumar, A
Kadiiska, MB
Michelotti, G
Diehl, AM
Chatterjee, S
AF Das, Suvarthi
Seth, Ratanesh Kumar
Kumar, Ashutosh
Kadiiska, Maria B.
Michelotti, Gregory
Diehl, Anna Mae
Chatterjee, Saurabh
TI Purinergic receptor X7 is a key modulator of metabolic oxidative
stress-mediated autophagy and inflammation in experimental nonalcoholic
steatohepatitis
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE 5,5-dimethyl-1-pyrroline N-oxide-nitrone adducts; lipid peroxidation;
tyrosine nitration; cytokines; CYP2E1; light chain 3 isoform B; GABA-A
receptor-associated protein
ID FATTY LIVER-DISEASE; OBESE MICE; ACTIVATION; PROTEIN; STEATOSIS;
FIBROSIS; CYP2E1; INJURY; DAMAGE
AB Recent studies indicate that metabolic oxidative stress, autophagy, and inflammation are hallmarks of nonalcoholic steatohepatitis (NASH) progression. However, the molecular mechanisms that link these important events in NASH remain unclear. In this study, we investigated the mechanistic role of purinergic receptor X7 (P2X7) in modulating autophagy and resultant inflammation in NASH in response to metabolic oxidative stress. The study uses two rodent models of NASH. In one of them, a CYP2E1 substrate bromodichloromethane is used to induce metabolic oxidative stress and NASH. Methyl choline-deficient diet feeding is used for the other NASH model. CYP2E1 and P2X7 receptor gene-deleted mice are used to establish their roles in regulating metabolic oxidative stress and autophagy. Autophagy gene expression, protein levels, confocal microscopy based-immunolocalization of lysosome-associated membrane protein (LAMP)2A and histopathological analysis were performed. CYP2E1-dependent metabolic oxidative stress induced increases in P2X7 receptor expression and chaperone-mediated autophagy markers LAMP2A and heat shock cognate 70 but caused depletion of light chain 3 isoform B (LC3B) protein levels. P2X7 receptor gene deletion significantly decreased LAMP2A and inflammatory indicators while significantly increasing LC3B protein levels compared with wild-type mice treated with bromodichloromethane. P2X7 receptor-deleted mice were also protected from NASH pathology as evidenced by decreased inflammation and fibrosis. Our studies establish that P2X7 receptor is a key regulator of autophagy induced by metabolic oxidative stress in NASH, thereby modulating hepatic inflammation. Furthermore, our findings presented here form a basis for P2X7 receptor as a potential therapeutic target in the treatment for NASH.
C1 [Das, Suvarthi; Seth, Ratanesh Kumar; Chatterjee, Saurabh] Univ S Carolina, Dept Environm Hlth Sci, Environm Hlth & Dis Lab, Arnold Sch Publ Hlth, Columbia, SC 29208 USA.
[Kumar, Ashutosh; Kadiiska, Maria B.] NIEHS, Free Radical Metab Grp, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
[Michelotti, Gregory; Diehl, Anna Mae] Duke Univ, Div Gastroenterol, Durham, NC USA.
RP Chatterjee, S (reprint author), Univ S Carolina, Dept Environm Hlth Sci, Environm Hlth & Dis Lab, Columbia, SC 29208 USA.
EM schatt@mailbox.sc.edu
RI Seth, Ratanesh/M-3700-2016;
OI Seth, Ratanesh/0000-0002-7078-0052
FU NIH [4R00ES019875-02, R01DK053792]; National Institutes of Health;
National Institute of Environmental Health Sciences
FX This work has been supported by NIH pathway to Independence Award
(4R00ES019875-02 to S. Chatterjee), NIH R01 (R01DK053792 to A. M.
Diehl), and the Intramural Research Program of the National Institutes
of Health and the National Institute of Environmental Health Sciences.
NR 36
TC 11
Z9 11
U1 0
U2 5
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD DEC
PY 2013
VL 305
IS 12
BP G950
EP G963
DI 10.1152/ajpgi.00235.2013
PG 14
WC Gastroenterology & Hepatology; Physiology
SC Gastroenterology & Hepatology; Physiology
GA 276OD
UT WOS:000328758700008
PM 24157968
ER
PT J
AU Campbell, KM
Lin, CD
Iamsirithawom, S
Scott, TW
AF Campbell, Karen M.
Lin, C. D.
Iamsirithawom, Sopon
Scott, Thomas W.
TI The Complex Relationship between Weather and Dengue Virus Transmission
in Thailand
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID AEDES-AEGYPTI DIPTERA; LIFE TABLE MODEL; TEMPERATURE-FLUCTUATIONS;
PUERTO-RICO; HUMAN MOVEMENT; CULICIDAE; BANGKOK; DYNAMICS; DISEASE;
VALIDATION
AB Using a novel analytical approach, weather dynamics and seasonal dengue virus transmission cycles were profiled for each Thailand province, 1983-2001, using monthly assessments of cases, temperature, humidity, and rainfall. We observed systematic differences in the structure of seasonal transmission cycles of different magnitude, the role of weather in regulating seasonal cycles, necessary versus optimal transmission "weather-space," basis of large epidemics, and predictive indicators that estimate risk. Larger epidemics begin earlier, develop faster, and are predicted at Onset change-point when case counts are low. Temperature defines a viable range for transmission; humidity amplifies the potential within that range. This duality is central to transmission. Eighty percent of 1.2 million severe dengue cases occurred when mean temperature was 27-29.5 degrees C and mean humidity was > 75%. Interventions are most effective when applied early. Most cases occur near Peak, yet small reductions at Onset can substantially reduce epidemic magnitude. Monitoring the Quiet-Phase is fundamental in effectively targeting interventions pre-emptively.
C1 [Campbell, Karen M.] San Diego State Univ, Computat Sci Res Ctr, San Diego, CA 92182 USA.
San Diego State Univ, Dept Math & Stat, San Diego, CA 92182 USA.
Off Dis Prevent & Control 1, Bangkok, Thailand.
Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Campbell, KM (reprint author), San Diego State Univ, Computat Sci Res Ctr, 5500 Campanile Dr, San Diego, CA 92182 USA.
EM kmca@roadrunner.com
FU Bill & Melinda Gates Foundation [OPP52250]; Research and Policy for
Infectious Disease Dynamics (RAPIDD) program of the Science and
Technology Directory, Department of Homeland Security; Fogarty
International Center, National Institutes of Health
FX This work was supported by the Bill & Melinda Gates Foundation
(OPP52250). TWS acknowledges funding from Research and Policy for
Infectious Disease Dynamics (RAPIDD) program of the Science and
Technology Directory, Department of Homeland Security, and Fogarty
International Center, National Institutes of Health.
NR 43
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U1 1
U2 11
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
EI 1476-1645
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD DEC
PY 2013
VL 89
IS 6
BP 1066
EP 1080
DI 10.4269/ajtmh.13-0321
PG 15
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 276CQ
UT WOS:000328726100006
PM 23958906
ER
PT J
AU Yoon, IK
Srikiatkhachorn, A
Hermann, L
Buddhari, D
Scott, TW
Jarman, RG
Aldstadt, J
Nisalak, A
Thammapalo, S
Bhoomiboonchoo, P
Mammen, MP
Green, S
Gibbons, RV
Endy, TP
Rothman, AL
AF Yoon, In-Kyu
Srikiatkhachorn, Anon
Hermann, Laura
Buddhari, Darunee
Scott, Thomas W.
Jarman, Richard G.
Aldstadt, Jared
Nisalak, Ananda
Thammapalo, Suwich
Bhoomiboonchoo, Piraya
Mammen, P. Mammen
Green, Sharone
Gibbons, Robert V.
Endy, Timothy P.
Rothman, Alan L.
TI Characteristics of Mild Dengue Virus Infection in Thai Children
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID PRIMARY-SCHOOL CHILDREN; DISEASE SEVERITY; LABORATORY INDICATORS;
HEMORRHAGIC-FEVER; KAMPHAENG PHET; FEATURES; EPIDEMIOLOGY; VILLAGES;
SAMPLES; BURDEN
AB A four-year longitudinal cohort and geographic cluster study in rural Thailand was conducted to characterize the clinical spectrum of dengue virus (DENY) infection. Symptomatic DENV infections in the cohort were detected by active school absence-based surveillance that triggered cluster investigations around ill cohort children. Data from 189 cohort children with symptomatic DENV infection and 126 contact children in the clusters with DENY infection were analyzed. Of injected contacts, only 19% were asymptomatic; 81% were symptomatic, but only 65.9% reported fever. Symptom-based case definitions were unreliable for diagnosis. Symptomatic infections in contacts were milder with lower DENV RNA levels than the cohort. Infections in contacts with fever history were more likely to have detectable DENV RNA than infections without fever history. Mild infections identified by cluster investigations account for a major proportion of all DENY infections. These findings are relevant for disease burden assessments, transmission modeling, and determination of vaccine impact.
C1 [Yoon, In-Kyu] Armed Forces Res Inst Med Sci, Dept Virol, Bangkok 10400, Thailand.
Univ Massachusetts, Sch Med, Worcester, MA USA.
Univ Toronto, Dept Med, Toronto, ON, Canada.
Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
SUNY Buffalo, Dept Geog, Buffalo, NY 14260 USA.
Minist Publ Hlth, Dept Med Sci, Bur Epidemiol, Nonthaburi, Thailand.
SUNY Syracuse, Dept Infect Dis, Syracuse, NY USA.
Univ Rhode Isl, Inst Immunol & Informat, Providence, RI 02908 USA.
NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Yoon, IK (reprint author), Armed Forces Res Inst Med Sci, Dept Virol, Bangkok 10400, Thailand.
EM yooni@afrims.org
RI Aldstadt, Jared/A-8508-2009
OI Aldstadt, Jared/0000-0001-9162-7439
FU National Institutes of Health [P01 AI34533, R01 GM083224]; U.S. Military
Infectious Diseases Research Program [S0016-04-AF]; Bill and Melinda
Gates Foundation Global Health Program [OPP52250]; Canadian Institutes
of Health Research Fellowship
FX This research was supported, in part, by the National Institutes of
Health (grants P01 AI34533 and R01 GM083224), the U.S. Military
Infectious Diseases Research Program (grant S0016-04-AF), the Bill and
Melinda Gates Foundation Global Health Program (grant OPP52250), and the
Canadian Institutes of Health Research Fellowship (Laura Hermann). The
funding source had no role in the study design, data collection,
analysis and interpretation, manuscript writing, or manuscript
submission for publication.
NR 28
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Z9 6
U1 0
U2 9
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
EI 1476-1645
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD DEC
PY 2013
VL 89
IS 6
BP 1081
EP 1087
DI 10.4269/ajtmh.13-0424
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 276CQ
UT WOS:000328726100007
PM 24127167
ER
PT J
AU Joseph, L
Thurm, A
Farmer, C
Shumway, S
AF Joseph, Lisa
Thurm, Audrey
Farmer, Cristan
Shumway, Stacy
TI Repetitive Behavior and Restricted Interests in Young Children with
Autism: Comparisons with Controls and Stability Over 2 Years
SO AUTISM RESEARCH
LA English
DT Article
DE autism spectrum disorders; repetitive behaviors; young children;
trajectory
ID SPECTRUM DISORDERS; ADOS SCORES; FOLLOW-UP; AGE; TRAJECTORIES;
ASSOCIATION; SEVERITY; SYMPTOMS; TODDLERS; INFANTS
AB Restricted, repetitive and stereotyped patterns of behavior, interests and activities [RRBs] are among the core symptoms of autism spectrum disorders (ASD). Previous studies have indicated that RRBs differentiate ASD from other developmental disorders and from typical development. This study examined the presentation of RRBs as reported on the Repetitive Behavior Scale-Revised, a caregiver report, in children with ASD [separated into autism and Pervasive Developmental Disorder-Not Otherwise Specified groups] compared with children with nonspectrum developmental delays or typical development. We examined the role of age, cognitive functioning, sex and social communication impairment as they relate to RRBs. The stability of RRBs in children with autism was also examined over the course of 2 years. Results of the study confirmed that the amount and type of RRBs differs by diagnosis. Age, cognitive functioning, sex and social-communication impairment were not significant correlates. Among children with autism, RRBs remained stable over time. Autism Res 2013, 6: 584-595. (c) 2013 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Joseph, Lisa; Thurm, Audrey; Farmer, Cristan; Shumway, Stacy] NIH, Pediat & Dev Neurosci Branch, Bethesda, MD 20892 USA.
RP Joseph, L (reprint author), NIMH, Pediat & Dev Neurosci Branch, 10 Ctr Dr,MSC 1255,Bldg 10,Room 1C250, Bethesda, MD 20892 USA.
EM jlisa@mail.nih.gov
OI Manwaring, Stacy/0000-0002-0835-9398
FU National Institute of Mental Health [NIMH] [NCT 00271622, 06-M-0065, NCT
NCT00298246, 06-M-0102]
FX This research was supported by the Intramural Program of the National
Institute of Mental Health [NIMH], studies NCT 00271622, 06-M-0065 and
NCT NCT00298246, 06-M-0102. The views expressed in this article do not
necessarily represent the views of the NIMH, NIH, HHS, or the United
Stated Government. The authors extend our gratitude for the children and
their families who volunteered their time and efforts during this
research.
NR 40
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U1 4
U2 24
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
EI 1939-3806
J9 AUTISM RES
JI Autism Res.
PD DEC
PY 2013
VL 6
IS 6
BP 584
EP 595
DI 10.1002/aur.1316
PG 12
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 274PG
UT WOS:000328617900012
PM 23868881
ER
PT J
AU Fu, D
Lippincott-Schwartz, J
Arias, IM
AF Fu, Dong
Lippincott-Schwartz, Jennifer
Arias, Irwin M.
TI Increased mitochondrial fusion and autophagy help isolated hepatocytes
repolarize in collagen sandwich cultures
SO AUTOPHAGY
LA English
DT Editorial Material
DE polarization; mitochondrial fusion; autophagy; oxidative
phosphorylation; lipid droplets
AB Freshly isolated, depolarized rat hepatocytes can repolarize into bile canalicular networks when plated in collagen sandwich cultures. We studied the events underlying this repolarization process, focusing on how hepatocytes restore ATP synthesis and resupply biosynthetic precursors after the stress of being isolated from liver. We found that soon after being plated in collagen sandwich cultures, hepatocytes converted their mitochondria into highly fused networks. This occurred through a combination of upregulation of mitochondrial fusion proteins and downregulation of a mitochondrial fission protein. Mitochondria also became more active for oxidative phosphorylation, leading to overall increased ATP levels within cells. We further observed that autophagy was upregulated in the repolarizing hepatocytes. Boosted autophagy levels likely served to recycle cellular precursors, supplying building blocks for repolarization. Repolarizing hepatocytes also extensively degraded lipid droplets, whose fatty acids provide precursors for -oxidation to fuel oxidative phosphorylation in mitochondria. Thus, through coordination of mitochondrial fusion, autophagy, and lipid droplet consumption, depolarized hepatocytes are able to boost ATP synthesis and biosynthetic precursors to efficiently repolarize in collagen sandwich cultures.
C1 [Fu, Dong] Univ Sydney, Fac Pharm, Sydney, NSW 2006, Australia.
[Lippincott-Schwartz, Jennifer; Arias, Irwin M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Lippincott-Schwartz, J (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
EM lippincj@mail.nih.gov; ariasi@cc.nih.gov
NR 0
TC 2
Z9 2
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD DEC 1
PY 2013
VL 9
IS 12
BP 2154
EP 2155
DI 10.4161/auto.26167
PG 2
WC Cell Biology
SC Cell Biology
GA 270DT
UT WOS:000328299800018
PM 24212064
ER
PT J
AU Towner, RA
Smith, N
Saunders, D
De Souza, PC
Henry, L
Lupu, F
Silasi-Mansat, R
Ehrenshaft, M
Mason, RP
Gomez-Mejiba, SE
Ramirez, DC
AF Towner, Rheal A.
Smith, Nataliya
Saunders, Debra
De Souza, Patricia Coutinho
Henry, Leah
Lupu, Florea
Silasi-Mansat, Robert
Ehrenshaft, Marilyn
Mason, Ronald P.
Gomez-Mejiba, Sandra E.
Ramirez, Dario C.
TI Combined molecular MRI and immuno-spin-trapping for in vivo detection of
free radicals in orthotopic mouse GL261 gliomas
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Article
DE Molecular magnetic resonance imaging; Glioma; Free radical;
Immuno-spin-trapping; In vivo; Mouse
ID HYDROGEN-PEROXIDE; LIPID-PEROXIDATION; NITRIC-OXIDE; DETAILED
CHARACTERIZATION; OXIDATIVE STRESS; GROWTH-FACTOR; MODEL; BRAIN; MICE;
ASTROCYTOMAS
AB Free radicals play a major role in gliomas. By combining immuno-spin-trapping (IST) arid molecular magnetic resonance imaging (mMRI), in vivo levels of free radicals were detected within mice bearing orthotopic GL261 gliomas. The nitrone spin trap DMPO (5,5-dimethyl pyrroline N-oxide) was administered prior to injection of an anti-DMPO probe (anti-DMPO antibody covalently bound to a bovine serum albumin (BSA)-Gd (gadolinium)-DTPA (diethylene triamine penta acetic acid)-biotin MRI contrast agent) to trap tumor-associated free radicals. mMRI detected the presence of anti-DMPO adducts by either a significant sustained increase (p < 0.001) in MR signal intensity or a significant decrease (p < 0.001) in T-1 relaxation, measured as %T-1 change. In vitro assessment of the anti-DMPO probe indicated a significant decrease (p < 0.0001) in T-1 relaxation in GL261 cells that were oxidatively stressed with hydrogen peroxide, compared to controls. The biotin moiety of the anti-DMPO probe was targeted with fluorescently-labeled streptavidin to locate the anti-DMPO probe in excised brain tissues. As a negative control a non-specific IgG antibody covalently bound to the albumin-Gd-DTPA-biotin construct was used. DMPO adducts were also confirmed in tumor tissue from animals administered DMPO, compared to non-tumor brain tissue. GL261 gliomas were found to have significantly increased malondialdehyde (MDA) protein adducts (p < 0.001) and 3-nitrotyrosine (3-NT) (p < 0.05) compared to normal mouse brain tissue, indicating increased oxidized lipids and proteins, respectively. Co-localization of the anti-DMPO probe with either 3-NT or 4-hydroxynonenal was also observed. This is the first report regarding the detection of in vivo levels of free radicals from a glioma model. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Towner, Rheal A.; Smith, Nataliya; Saunders, Debra; De Souza, Patricia Coutinho; Henry, Leah] Oklahoma Hlth Sci Ctr, Adv Magnet Resonance Ctr, Oklahoma City, OK 73104 USA.
[Lupu, Florea; Silasi-Mansat, Robert] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
[Ehrenshaft, Marilyn; Mason, Ronald P.] NIEHS, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
[Gomez-Mejiba, Sandra E.; Ramirez, Dario C.] Natl Univ San Luis, Lab Expt Med & Therapeut, Inst Multidisciplinario Invest Biol San Luis, CONICET, RA-5700 San Luis, Argentina.
RP Towner, RA (reprint author), Oklahoma Hlth Sci Ctr, Adv Magnet Resonance Ctr, Oklahoma City, OK 73104 USA.
EM Rheal-Towner@omrf.org; leah-henry@ouhsc.edu
RI RAMIREZ, DARIO/K-3312-2013;
OI RAMIREZ, DARIO/0000-0001-6725-3326; Silasi, Robert/0000-0001-9590-6160
FU Oklahoma Medical Research Foundation; National Institute of
Environmental Health Sciences (NIEHS)
FX Funding was obtained by the Oklahoma Medical Research Foundation (RAT)
and the National Institute of Environmental Health Sciences (NIEHS)
(RPM). We would like to thank Dr. Ting He for assisting with the GL261
mouse glioma model.
NR 37
TC 7
Z9 7
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0925-4439
EI 0006-3002
J9 BBA-MOL BASIS DIS
JI Biochim. Biophys. Acta-Mol. Basis Dis.
PD DEC
PY 2013
VL 1832
IS 12
BP 2153
EP 2161
DI 10.1016/j.bbadis.2013.08.004
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 260AO
UT WOS:000327567600026
PM 23959048
ER
PT J
AU Diao, GQ
Zeng, DL
Yang, S
AF Diao, Guoqing
Zeng, Donglin
Yang, Song
TI Efficient Semiparametric Estimation of Short-Term and Long-Term Hazard
Ratios with Right-Censored Data
SO BIOMETRICS
LA English
DT Article
DE Non-parametric likelihood; Proportional hazards model; Proportional odds
model; Semiparametric efficiency; Semiparametric hazards rate model
ID MAXIMUM-LIKELIHOOD-ESTIMATION; TIME-DEPENDENT COEFFICIENTS;
REGRESSION-MODELS; VARIANCE-COMPONENTS; SURVIVAL ANALYSIS; LINKAGE
ANALYSIS; COX REGRESSION; MIXTURE-MODELS; ORDINAL TRAITS; ASSOCIATION
AB The proportional hazards assumption in the commonly used Cox model for censored failure time data is often violated in scientific studies. Yang and Prentice (2005) proposed a novel semiparametric two-sample model that includes the proportional hazards model and the proportional odds model as sub-models, and accommodates crossing survival curves. The model leaves the baseline hazard unspecified and the two model parameters can be interpreted as the short-term and long-term hazard ratios. Inference procedures were developed based on a pseudo score approach. Although extension to accommodate covariates was mentioned, no formal procedures have been provided or proved. Furthermore, the pseudo score approach may not be asymptotically efficient. We study the extension of the short-term and long-term hazard ratio model of Yang and Prentice (2005) to accommodate potentially time-dependent covariates. We develop efficient likelihood-based estimation and inference procedures. The nonparametric maximum likelihood estimators are shown to be consistent, asymptotically normal, and asymptotically efficient. Extensive simulation studies demonstrate that the proposed methods perform well in practical settings. The proposed method successfully captured the phenomenon of crossing hazards in a cancer clinical trial and identified a genetic marker with significant long-term effect missed by using the proportional hazards model on age-at-onset of alcoholism in a genetic study.
C1 [Diao, Guoqing] George Mason Univ, Dept Stat, Fairfax, VA 22030 USA.
[Zeng, Donglin] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Yang, Song] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP Diao, GQ (reprint author), George Mason Univ, Dept Stat, Fairfax, VA 22030 USA.
EM gdiao@gmu.edu
FU NIH [GM31575, R15CA150698]
FX The authors thank the editor, an associate editor and a referee for
helpful comments. The authors are grateful to the COGA investigators and
Jean W. MacCluer for providing the COGA data from GAW14, which was
supported in part by the NIH Grant GM31575. The authors thank Dr.
William Rosenberger for making valuable comments and suggestions, which
lead to a considerable improvement in the presentation of this
manuscript. The work of the first author was supported by the NIH Grant
R15CA150698.
NR 42
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Z9 2
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-341X
EI 1541-0420
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 2013
VL 69
IS 4
BP 840
EP 849
DI 10.1111/biom.12097
PG 10
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA 271WT
UT WOS:000328423000005
PM 24328712
ER
PT J
AU Davidov, O
Peddada, S
AF Davidov, Ori
Peddada, Shyamal
TI Testing for the Multivariate Stochastic Order among Ordered Experimental
Groups with Application to Dose-Response Studies
SO BIOMETRICS
LA English
DT Article
DE Dose-response studies; Nonparametric tests; Ordered experimental
conditions; Order restricted statistical inference; Stochastic order
relations
ID INFERENCE; DISTRIBUTIONS
AB The comparison of two or more ordered experimental groups based on multivariate data is common in a variety of applications such as toxicology, clinical trials and drug development, to name just a few. In this article, we develop a nonparametric methodology for analyzing such data. In particular we propose a global K sample nonparametric test for order among vector valued outcomes. The testing procedure can also be used in a post-hoc fashion to answer questions about the ordering of subgroups and/or single outcomes within any subset of experimental groups. Such a methodology does not currently exist. In contrast with standard methodology such as multivariate analysis of variance (MANOVA), and its nonparametric analogues, we do not assume that the groups differ only by a location parameter or that the components of the response vector have the same marginal distributions between and across groups, that is, we allow for the shape of the distribution to change across groups. We emphasize that our test compares the outcome distributions, not just their mean tendencies, and explicitly incorporates and exploits the order constraints. Consequently it is more powerful than the existing unordered tests. The methodology is illustrated using genotoxicity data where the effect of hydrogen peroxide exposure on damage to DNA is evaluated using a comet assay.
C1 [Davidov, Ori] Univ Haifa, Dept Stat, IL-31905 Haifa, Israel.
[Peddada, Shyamal] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Davidov, O (reprint author), Univ Haifa, Dept Stat, IL-31905 Haifa, Israel.
EM davidov@stat.haifa.ac.il
FU Israeli Science Foundation [875/09]; Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences [Z01
ES101744-04]
FX The research of O.D. was partially supported by the Israeli Science
Foundation Grant No. 875/09. This research [in part] was supported by
the Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences (Z01 ES101744-04). We also thank Jack
Taylor, Epidemiology Branch, NIEHS, NIH, and David Dunson, Duke
University, for providing the data that were analyzed in this paper. We
also thank the Editor, the AE and referee for their comment which
improved the paper.
NR 27
TC 2
Z9 2
U1 1
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-341X
EI 1541-0420
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 2013
VL 69
IS 4
BP 982
EP 990
DI 10.1111/biom.12070
PG 9
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA 271WT
UT WOS:000328423000018
PM 24125397
ER
PT J
AU Baker, SG
AF Baker, Stuart G.
TI Comment on Hubbard and Miglioretti (2013), Consider Also a Selection
Model for the Cumulative Risk of False Positive Screening Tests
SO BIOMETRICS
LA English
DT Letter
C1 NCI, Biometry Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Baker, SG (reprint author), NCI, Biometry Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
NR 9
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-341X
EI 1541-0420
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 2013
VL 69
IS 4
BP 1084
EP 1084
DI 10.1111/biom.12116
PG 1
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA 271WT
UT WOS:000328423000028
PM 24328716
ER
PT J
AU Cunningham, BK
Hadley, DW
Hannoush, H
Meltzer, AC
Niforatos, N
Pineda-Alvarez, D
Sachdev, V
Warren-Mora, N
Solomon, BD
AF Cunningham, Bridget K.
Hadley, Donald W.
Hannoush, Hwaida
Meltzer, Andrew C.
Niforatos, Nickie
Pineda-Alvarez, Daniel
Sachdev, Vandana
Warren-Mora, Nicole
Solomon, Benjamin D.
TI Analysis of Cardiac Anomalies in VACTERL Association
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Article
DE VACTERL; VACTERL association; VATER; VATER association; congenital heart
defects
ID CONGENITAL HEART-DEFECTS; SUPERIOR VENA-CAVA; VATER ASSOCIATION;
MALFORMATIONS; SPECTRUM; DISEASE; BIRTH
AB BACKGROUNDCongenital heart disease (CHD) is estimated to affect between 3 and 5% of all newborns. Extra-cardiac malformations are observed in 7 to 50% of patients with CHD. One relatively well-known association that can occur in the context of CHD is VACTERL. Controversy still remains regarding the definition of VATER association and its expansion to VACTERL, the appropriate diagnostic criteria and the overall incidence.
METHODSWe conducted a description of a case series to characterize the cardiac findings present in a cohort of patients meeting the criteria for VACTERL association.
RESULTSForty-six of 220 were eligible for inclusion into the study, 67% (31 of 46) had CHD. The most common CHD was ventricular septal defect, present in 18 of 31 patients (58%). There was no statistically significant association between CHD severity and the presence or absence of other VACTERL component features, specifically anorectal malformation (p=0.18) or tracheo-esophageal fistula (p=0.72). CHD presence also did not correlate with the presence of tracheo-esophageal fistula or anorectal malformation.
CONCLUSIONAlthough this study does not, by design, provide further evidence toward the questions of whether CHD is a defining feature of VACTERL association, the frequency of CHD in our cohort does lend support to it being an important medical consideration in patients with VACTERL association. Based on our experience, we strongly recommend a screening echocardiogram to evaluate for CHD in individuals with a potential diagnosis of VACTERL association. Birth Defects Research (Part A) 97:792-797, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Cunningham, Bridget K.] Walter Reed Natl Mil Med Ctr Bethesda, Dept Pediat, Bethesda, MD USA.
[Cunningham, Bridget K.; Hadley, Donald W.; Pineda-Alvarez, Daniel; Warren-Mora, Nicole; Solomon, Benjamin D.] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Hannoush, Hwaida; Sachdev, Vandana] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Meltzer, Andrew C.] George Washington Univ, Dept Emergency Med, Washington, DC USA.
[Niforatos, Nickie] Childrens Natl Med Ctr, Dept Neonatol, Washington, DC 20010 USA.
[Solomon, Benjamin D.] Inova Hlth Syst, Inova Translat Med Inst, Div Med Genom, Falls Church, VA USA.
[Solomon, Benjamin D.] Inova Hlth Syst, Inova Childrens Hosp, Dept Pediat, Falls Church, VA USA.
RP Solomon, BD (reprint author), Inova Translat Med Inst, Claude Moore Bldg,3300 Gallows Rd, Falls Church, VA 22042 USA.
EM benjamin.solomon@inova.org
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX This research was supported (in part) by the Intramural Research Program
of the National Human Genome Research Institute, National Institutes of
Health. Pertaining to Dr. Cunningham, the views expressed in this
article are those of the authors and do not necessarily reflect the
official policy or position of the Department of the Navy, nor the U.S.
Government. Dr. Solomon thanks Dr. Max Muenke for his support and
mentorship. All of the authors express their deepest gratitude to the
patients and families who participate in their research on VACTERL
association and related disorders.
NR 24
TC 4
Z9 4
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD DEC
PY 2013
VL 97
IS 12
BP 792
EP 797
DI 10.1002/bdra.23211
PG 6
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 272RK
UT WOS:000328477700007
PM 24343877
ER
PT J
AU Foley, AR
Quijano-Roy, S
Collins, J
Straub, V
McCallum, M
Deconinck, N
Mercuri, E
Pane, M
D'Amico, A
Bertini, E
North, K
Ryan, MM
Richard, P
Allamand, V
Hicks, D
Lamande, S
Hu, Y
Gualandi, F
Auh, S
Muntoni, F
Bonnemann, CG
AF Foley, A. Reghan
Quijano-Roy, Susana
Collins, James
Straub, Volker
McCallum, Michelle
Deconinck, Nicolas
Mercuri, Eugenio
Pane, Marika
D'Amico, Adele
Bertini, Enrico
North, Kathryn
Ryan, Monique M.
Richard, Pascale
Allamand, Valerie
Hicks, Debbie
Lamande, Shireen
Hu, Ying
Gualandi, Francesca
Auh, Sungyoung
Muntoni, Francesco
Boennemann, Carsten G.
TI Natural history of pulmonary function in collagen VI-related myopathies
SO BRAIN
LA English
DT Article
DE collagen VI-related myopathies; natural history; forced vital capacity;
optimization of care; outcome measure
ID CONGENITAL MUSCULAR-DYSTROPHY; CONSENSUS STATEMENT; RESPIRATORY CARE;
BETHLEM MYOPATHY; MUSCLE; MYOSCLEROSIS; DISORDERS; MUTATIONS; PHENOTYPE;
MECHANISM
AB The spectrum of clinical phenotypes associated with a deficiency or dysfunction of collagen VI in the extracellular matrix of muscle are collectively termed 'collagen VI-related myopathies' and include Ullrich congenital muscular dystrophy, Bethlem myopathy and intermediate phenotypes. To further define the clinical course of these variants, we studied the natural history of pulmonary function in correlation to motor abilities in the collagen VI-related myopathies by analysing longitudinal forced vital capacity data in a large international cohort. Retrospective chart reviews of genetically and/or pathologically confirmed collagen VI-related myopathy patients were performed at 10 neuromuscular centres: USA (n = 2), UK (n = 2), Australia (n = 2), Italy (n = 2), France (n = 1) and Belgium (n = 1). A total of 486 forced vital capacity measurements obtained in 145 patients were available for analysis. Patients at the severe end of the clinical spectrum, conforming to the original description of Ullrich congenital muscular dystrophy were easily identified by severe muscle weakness either preventing ambulation or resulting in an early loss of ambulation, and demonstrated a cumulative decline in forced vital capacity of 2.6% per year (P < 0.0001). Patients with better functional abilities, in whom walking with/without assistance was achieved, were initially combined, containing both intermediate and Bethlem myopathy phenotypes in one group. However, one subset of patients demonstrated a continuous decline in pulmonary function whereas the other had stable pulmonary function. None of the patients with declining pulmonary function attained the ability to hop or run; these patients were categorized as intermediate collagen VI-related myopathy and the remaining patients as Bethlem myopathy. Intermediate patients had a cumulative decline in forced vital capacity of 2.3% per year (P < 0.0001) whereas the relationship between age and forced vital capacity in patients with Bethlem myopathy was not significant (P = 0.1432). Nocturnal non-invasive ventilation was initiated in patients with Ullrich congenital muscular dystrophy by 11.3 years (+/- 4.0) and in patients with intermediate collagen VI-related myopathy by 20.7 years (+/- 1.5). The relationship between maximal motor ability and forced vital capacity was highly significant (P < 0.0001). This study demonstrates that pulmonary function profiles can be used in combination with motor function profiles to stratify collagen VI-related myopathy patients phenotypically. These findings improve our knowledge of the natural history of the collagen VI-related myopathies, enabling proactive optimization of care and preparing this patient population for clinical trials.
C1 [Foley, A. Reghan; Muntoni, Francesco] UCL, Inst Child Hlth, Dubowitz Neuromuscular Ctr, London WC1N 1EH, England.
[Foley, A. Reghan; Muntoni, Francesco] Great Ormond St Hosp Sick Children, London WC1N 1EH, England.
[Quijano-Roy, Susana] Raymond Poincare Univ Hosp UVSQ, Garches Neuromuscular Ctr GNMH, F-92380 Garches, France.
[Collins, James] Cincinnati Childrens Hosp Med Ctr, Div Neurol, Cincinnati, OH 45229 USA.
[Straub, Volker; McCallum, Michelle; Hicks, Debbie] Univ Newcastle, Int Ctr Life, Inst Med Genet, Newcastle NE1 3BZ, England.
[Deconinck, Nicolas] Univ Libre Brussels, Queen Fabiola Univ Childrens Hosp, Dept Neurol, ULB, B-1000 Brussels, Belgium.
[Deconinck, Nicolas] Ghent Univ Hosp, Neuromuscular Reference Ctr, B-9000 Ghent, Belgium.
[Mercuri, Eugenio; Pane, Marika] Univ Cattolica Sacro Cuore, Dept Paediat Neurol, I-00168 Rome, Italy.
[D'Amico, Adele; Bertini, Enrico] Bambino Gesu Pediat Hosp, Mol Med Lab, I-00165 Rome, Italy.
[North, Kathryn] Univ Sydney, Childrens Hosp Westmead, Inst Neurosci & Muscle Res, Westmead, NSW 2145, Australia.
[Ryan, Monique M.] Univ Melbourne, Murdoch Childrens Res Inst, Royal Childrens Hosp, Dept Neurol, Parkville, Vic 3052, Australia.
[Richard, Pascale] Pitie Salpetriere Hosp Grp, AP HP, Cardiogenet & Myogenet Funct Unit, Metab Biochem Div, F-75013 Paris, France.
[Richard, Pascale; Allamand, Valerie] Univ Paris 06, IFR14, Inst Myol, F-75013 Paris, France.
[Allamand, Valerie] CNRS, UMR7215, F-75013 Paris, France.
[Allamand, Valerie] Univ Paris 06, INSERM, U974, F-75013 Paris, France.
[Lamande, Shireen] Univ Melbourne, Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia.
[Hu, Ying; Boennemann, Carsten G.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
[Gualandi, Francesca] Univ Ferrara, Dept Med Sci, Med Genet Sect, I-44100 Ferrara, Italy.
[Auh, Sungyoung] NINDS, Biostat Unit, NIH, Bethesda, MD 20892 USA.
RP Bonnemann, CG (reprint author), NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
EM carsten.bonnemann@nih.gov
RI d'amico, adele/J-9203-2016; Gualandi, Francesca/K-7513-2016;
OI d'amico, adele/0000-0003-2438-2624; Gualandi,
Francesca/0000-0001-9551-057X; Bertini, Enrico/0000-0001-9276-4590;
Ryan, Monique/0000-0001-6397-1910
FU National Institutes of Health/National Institute of Arthritis and
Musculoskeletal and Skin Diseases [R01AR051999]; Muscular Dystrophy
Association USA [MDA3896]; National Institute of Neurological Disorders
and Stroke/National Institutes of Health; Muscular Dystrophy Campaign
Centre; Great Ormond Street Children's Charity; NHS National Specialist
Commissioning Team; NMD-CHIP Consortium; European Commission
[HEALTH-F5-2008-223026]
FX This work was supported, in part, by grants from the National Institutes
of Health/National Institute of Arthritis and Musculoskeletal and Skin
Diseases [R01AR051999 to C.G.B.]; the Muscular Dystrophy Association USA
[MDA3896 to C.G.B]; intramural funds of the National Institute of
Neurological Disorders and Stroke/National Institutes of Health
(C.G.B.); the Muscular Dystrophy Campaign Centre Grant (F.M.). F.M. is
supported by the Great Ormond Street Children's Charity. A.R.F. is a
Muscular Dystrophy Campaign Fellow. The support of the NHS National
Specialist Commissioning Team to the Dubowitz Neuromuscular is also
gratefully acknowledged. This work was partly funded by the NMD-CHIP
Consortium, a FP7 HEALTH project of the European Commission (Development
of Targeted DNA Chips for High Throughput Diagnosis of Neuromuscular
Disorders - Collaborative Project - FP7 Grant Agreement Number:
HEALTH-F5-2008-223026; to V.A.).
NR 35
TC 16
Z9 16
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
EI 1460-2156
J9 BRAIN
JI Brain
PD DEC
PY 2013
VL 136
BP 3625
EP 3633
DI 10.1093/brain/awt284
PN 12
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 271BR
UT WOS:000328366000014
PM 24271325
ER
PT J
AU Berman, BD
Hallett, M
Herscovitch, P
Simonyan, K
AF Berman, Brian D.
Hallett, Mark
Herscovitch, Peter
Simonyan, Kristina
TI Striatal dopaminergic dysfunction at rest and during task performance in
writer's cramp
SO BRAIN
LA English
DT Article
DE dystonia; dopamine; PET; raclopride; striatum
ID FOCAL HAND DYSTONIA; POSITRON EMISSION TOMOGRAPHY; IDIOPATHIC CERVICAL
DYSTONIA; VOLUNTARY MUSCLE-RELAXATION; DOPA-RESPONSIVE DYSTONIA;
TRANSGENIC MOUSE MODEL; PRIMARY MOTOR CORTEX; GRAY-MATTER CHANGES;
DELTA-E-TORSINA; KNOCK-IN MOUSE
AB Writer's cramp is a task-specific focal hand dystonia characterized by involuntary excessive muscle contractions during writing. Although abnormal striatal dopamine receptor binding has been implicated in the pathophysiology of writer's cramp and other primary dystonias, endogenous dopamine release during task performance has not been previously investigated in writer's cramp. Using positron emission tomography imaging with the D-2/D-3 antagonist C-11-raclopride, we analysed striatal D-2/D-3 availability at rest and endogenous dopamine release during sequential finger tapping and speech production tasks in 15 patients with writer's cramp and 15 matched healthy control subjects. Compared with control subjects, patients had reduced C-11-raclopride binding to D-2/D-3 receptors at rest in the bilateral striatum, consistent with findings in previous studies. During the tapping task, patients had decreased dopamine release in the left striatum as assessed by reduced change in C-11-raclopride binding compared with control subjects. One cluster of reduced dopamine release in the left putamen during tapping overlapped with a region of reduced C-11-raclopride binding to D-2/D-3 receptors at rest. During the sentence production task, patients showed increased dopamine release in the left striatum. No overlap between altered dopamine release during speech production and reduced C-11-raclopride binding to D-2/D-3 receptors at rest was seen. Striatal regions where D-2/D-3 availability at rest positively correlated with disease duration were lateral and non-overlapping with striatal regions showing reduced D-2/D-3 receptor availability, except for a cluster in the left nucleus accumbens, which showed a negative correlation with disease duration and overlapped with striatal regions showing reduced D-2/D-3 availability. Our findings suggest that patients with writer's cramp may have divergent responses in striatal dopamine release during an asymptomatic motor task involving the dystonic hand and an unrelated asymptomatic task, sentence production. Our voxel-based results also suggest that writer's cramp may be associated with reduced striatal dopamine release occuring in the setting of reduced D-2/D-3 receptor availability and raise the possibility that basal ganglia circuits associated with premotor cortices and those associated with primary motor cortex are differentially affected in primary focal dystonias.
C1 [Berman, Brian D.] Univ Colorado, Dept Neurol, Denver, CO 80202 USA.
[Berman, Brian D.; Hallett, Mark] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
[Herscovitch, Peter] NIH, Positron Emiss Tomog Dept, Bethesda, MD 20892 USA.
[Simonyan, Kristina] Icahn Sch Med Mt Sinai, Dept Neurol, New York, NY USA.
[Simonyan, Kristina] Icahn Sch Med Mt Sinai, Dept Otolaryngol, New York, NY USA.
RP Berman, BD (reprint author), Univ Colorado Denver, Dept Neurol, 12631 E 17th Ave,Mail Stop B-185, Aurora, CO 80045 USA.
EM brian.berman@ucdenver.edu
OI Simonyan, Kristina/0000-0001-7444-0437
FU National Institute on Deafness and Other Communication Disorders, NIH
[DC009629]; National Institute of Neurological Disorders and Stroke, NIH
FX This work was supported by the National Institute on Deafness and Other
Communication Disorders, NIH [DC009629 to K.S.]; and the Intramural
Research Program of the National Institute of Neurological Disorders and
Stroke, NIH.
NR 93
TC 11
Z9 11
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
EI 1460-2156
J9 BRAIN
JI Brain
PD DEC
PY 2013
VL 136
BP 3645
EP 3658
DI 10.1093/brain/awt282
PN 12
PG 14
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 271BR
UT WOS:000328366000016
PM 24148273
ER
PT J
AU Kraemer, KH
Tamura, D
Khan, SG
DiGiovanna, JJ
AF Kraemer, K. H.
Tamura, D.
Khan, S. G.
DiGiovanna, J. J.
TI Burning issues in the diagnosis of xeroderma pigmentosum
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Editorial Material
C1 [Kraemer, K. H.; Tamura, D.; Khan, S. G.; DiGiovanna, J. J.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Kraemer, KH (reprint author), NCI, Dermatol Branch, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM kraemerk@nih.gov
NR 5
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-0963
EI 1365-2133
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD DEC
PY 2013
VL 169
IS 6
BP 1176
EP 1176
DI 10.1111/bjd.12707
PG 1
WC Dermatology
SC Dermatology
GA 259ZG
UT WOS:000327564200003
PM 24299525
ER
PT J
AU Kim, SYH
AF Kim, Scott Y. H.
TI Varieties of decisional incapacity: theory and practice
SO BRITISH JOURNAL OF PSYCHIATRY
LA English
DT Editorial Material
ID CAPACITY; CONSENT; COMPETENCE
AB Evaluation of decision-making capacity (DMC) for treatment is challenging. Owen et al, in this issue of the Journal, compare the abilities (understanding, appreciation and reasoning) relevant to DMC in medical and psychiatric patients. Here I discuss three key issues their article raises and that are relevant to the direction of future research.
C1 NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Kim, SYH (reprint author), NIH, Dept Bioeth, Ctr Clin, 10 Ctr Dr,1C118, Bethesda, MD 20892 USA.
EM scott.kim@nih.gov
NR 10
TC 2
Z9 2
U1 0
U2 0
PU ROYAL COLLEGE OF PSYCHIATRISTS
PI LONDON
PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON SW1X 8PG,
ENGLAND
SN 0007-1250
EI 1472-1465
J9 BRIT J PSYCHIAT
JI Br. J. Psychiatry
PD DEC
PY 2013
VL 203
IS 6
BP 403
EP 405
DI 10.1192/bjp.bp.113.128256
PG 3
WC Psychiatry
SC Psychiatry
GA 274HK
UT WOS:000328597200004
PM 24297786
ER
PT J
AU Truong, H
Logan, J
Turkbey, B
Siddiqui, MM
Rais-Bahrami, S
Hoang, AN
Pusateri, C
Shuch, B
Walton-Diaz, A
Vourganti, S
Nix, J
Stamatakis, L
Harris, C
Chua, C
Choyke, PL
Wood, BJ
Pinto, PA
AF Hong Truong
Logan, Jennifer
Turkbey, Baris
Siddiqui, M. Minhaj
Rais-Bahrami, Soroush
Hoang, Anthony N.
Pusateri, Chad
Shuch, Brian
Walton-Diaz, Annerleim
Vourganti, Srinivas
Nix, Jeffrey
Stamatakis, Lambros
Harris, Colette
Chua, Celene
Choyke, Peter L.
Wood, Bradford J.
Pinto, Peter A.
TI MRI characterization of the dynamic effects of 5 alpha-reductase
inhibitors on prostate zonal volumes
SO CANADIAN JOURNAL OF UROLOGY
LA English
DT Article
DE prostate volume; MRI; BPH; 5 alpha-reductase; inhibitors
ID TRANSRECTAL ULTRASOUND; CLINICAL PROGRESSION; TISSUE COMPOSITION;
ENLARGED PROSTATE; CANCER-DETECTION; FINASTERIDE; HYPERPLASIA;
DUTASTERIDE; MEN; THERAPY
AB Introduction: Prior studies of volumetric effects of 5 alpha-reductase inhibitors (5ARIs) on the prostate have used transrectal ultrasound which provides poor differentiation of prostatic zones. We utilized high-resolution prostate MRI to evaluate the true dynamic effects of 5ARI in men who underwent multiple MRIs.
Materials and methods: A retrospective study of patients who underwent serial 3.0 Tesla prostate MRI from 2007 to 2012 and were treated with 5ARI were studied. Nineteen patients who had a baseline MRI prior to 5ARI initiation and subsequent MRI follow up were selected. A randomly selected group of 40 patients who had not received any form of therapy was selected as the control cohort. Total prostate volume (TPV), transition zone volume (TZV), and peripheral zone volume (PZV) were calculated using 3D reconstructions and prostate segmentation from T2-weighted MRI. Changes in volumes were correlated with the duration of treatment using linear regression analysis.
Results: Following over 2 years of treatment, 5ARI decreased TPV significantly (16.7%, p < 0.0001). There were similar decreases in TZV (7.5%, p < 0.001) and PZV (27.4%, p = 0.0002) from baseline. In the control group, TPV and TZV increased (p < 0.0001) while PZV remained stable. When adjusted for the natural growth of prostate zonal volume dynamics seen in the control cohort, approximately 60% of the reduction of the TPV from 5ARI resulted from changes in the TZV and 40% of the reduction from changes in the PZV.
Conclusions: 3.0 Tesla MRI characterizations of the dynamic effects of 5ARI on prostate zonal volumes demonstrate significant decreases in TPV, TZV, and PZV. SARI blocks the natural growth of TZV as men age and decreases both TZV and PZV below their baselines. As imaging technology improves, prostate MRI allows for more accurate assessment of drug effects on dynamic prostate volumes.
C1 [Hong Truong; Logan, Jennifer; Siddiqui, M. Minhaj; Rais-Bahrami, Soroush; Hoang, Anthony N.; Pusateri, Chad; Shuch, Brian; Walton-Diaz, Annerleim; Vourganti, Srinivas; Nix, Jeffrey; Stamatakis, Lambros; Harris, Colette; Chua, Celene] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Turkbey, Baris; Choyke, Peter L.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Wood, Bradford J.; Pinto, Peter A.] NCI, Ctr Intervent Oncol, NIH, Bethesda, MD 20892 USA.
RP Pinto, PA (reprint author), NCI, Urol Oncol Branch, NIH, 10 Ctr Dr,MSC 1210,Bldg 10,CRC Room 2W-5940, Bethesda, MD 20892 USA.
OI Siddiqui, Mohummad/0000-0002-4484-6820
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. This
research was also 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
hap://www.fnih.org/work/programs-development/medical-research-scholars-
program. We also thank the administrative support staff of the Urologic
Oncology Branch, Center for Cancer Research for assisting with the
manuscript review and submission processes.
NR 21
TC 2
Z9 2
U1 0
U2 0
PU CANADIAN J UROLOGY
PI ST LAURENT
PA 2330 WARD ST, STE 604, ST LAURENT, QUEBEC H4M 2V6, CANADA
SN 1195-9479
J9 CAN J UROL
JI Can. J. Urol.
PD DEC
PY 2013
VL 20
IS 6
BP 7002
EP 7007
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 275ZG
UT WOS:000328717300002
PM 24331340
ER
PT J
AU Sasaki, T
Miller, CF
Hansford, R
Zipunnikov, V
Zviman, MM
Marine, JE
Spragg, D
Cheng, A
Tandri, H
Sinha, S
Kolandaivelu, A
Zimmerman, SL
Bluemke, DA
Tomaselli, GF
Berger, RD
Halperin, HR
Calkins, H
Nazarian, S
AF Sasaki, Takeshi
Miller, Christopher F.
Hansford, Rozann
Zipunnikov, Vadim
Zviman, Menekhem M.
Marine, Joseph E.
Spragg, David
Cheng, Alan
Tandri, Harikrishna
Sinha, Sunil
Kolandaivelu, Aravindan
Zimmerman, Stefan L.
Bluemke, David A.
Tomaselli, Gordon F.
Berger, Ronald D.
Halperin, Henry R.
Calkins, Hugh
Nazarian, Saman
TI Impact of Nonischemic Scar Features on Local Ventricular Electrograms
and Scar-Related Ventricular Tachycardia Circuits in Patients With
Nonischemic Cardiomyopathy
SO CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
LA English
DT Article
DE tachycardia; ventricular
ID CATHETER ABLATION; INFARCT SCARS; SUBSTRATE; IDENTIFICATION;
ENHANCEMENT; ARRHYTHMIA; DISEASE
AB Background The association of local electrogram features with scar morphology and distribution in nonischemic cardiomyopathy has not been investigated. We aimed to quantify the association of scar on late gadolinium-enhanced cardiac magnetic resonance with local electrograms and ventricular tachycardia circuit sites in patients with nonischemic cardiomyopathy.
Methods and Results Fifteen patients with nonischemic cardiomyopathy underwent late gadolinium-enhanced cardiac magnetic resonance before ventricular tachycardia ablation. The transmural extent and intramural types (endocardial, midwall, epicardial, patchy, transmural) of scar were measured in late gadolinium-enhanced cardiac magnetic resonance short-axis planes. Electroanatomic map points were registered to late gadolinium-enhanced cardiac magnetic resonance images. Myocardial wall thickness, scar transmurality, and intramural scar types were independently associated with electrogram amplitude, duration, and deflections in linear mixed-effects multivariable models, clustered by patient. Fractionated and isolated potentials were more likely to be observed in regions with higher scar transmurality (P<0.0001 by ANOVA) and in regions with patchy scar (versus endocardial, midwall, epicardial scar; P<0.05 by ANOVA). Most ventricular tachycardia circuit sites were located in scar with >25% scar transmurality.
Conclusions Electrogram features are associated with scar morphology and distribution in patients with nonischemic cardiomyopathy. Previous knowledge of electrogram image associations may optimize procedural strategies including the decision to obtain epicardial access.
C1 [Sasaki, Takeshi; Miller, Christopher F.; Hansford, Rozann; Zviman, Menekhem M.; Marine, Joseph E.; Spragg, David; Cheng, Alan; Tandri, Harikrishna; Sinha, Sunil; Kolandaivelu, Aravindan; Tomaselli, Gordon F.; Berger, Ronald D.; Halperin, Henry R.; Calkins, Hugh; Nazarian, Saman] Johns Hopkins Univ, Dept Cardiol, Baltimore, MD 21287 USA.
[Zipunnikov, Vadim] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21287 USA.
[Zimmerman, Stefan L.] Johns Hopkins Univ, Dept Radiol, Baltimore, MD 21287 USA.
[Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, Div Radiol & Imaging Sci, NIH Clin Ctr, Bethesda, MD USA.
RP Sasaki, T (reprint author), Johns Hopkins Univ, Div Cardiol, Carnegie 592A,600 N Wolfe St, Baltimore, MD 21287 USA.
EM tsasaki.cvm@tmd.ac.jp
OI Bluemke, David/0000-0002-8323-8086
FU Francis Chiaramonte MD Private Foundation; National Institutes of Health
[K23HL089333, R01HL116280, R01-HL094610]
FX The study was supported by grants from the Francis Chiaramonte MD
Private Foundation to T. S. and from the National Institutes of Health
(K23HL089333 and R01HL116280 to S.N. and R01-HL094610 to H.R.H.).
NR 26
TC 6
Z9 6
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-3149
EI 1941-3084
J9 CIRC-ARRHYTHMIA ELEC
JI Circ.-Arrhythmia Electrophysiol.
PD DEC
PY 2013
VL 6
IS 6
BP 1139
EP 1147
DI 10.1161/CIRCEP.113.000159
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 273HN
UT WOS:000328526000024
PM 24235267
ER
PT J
AU He, J
Kelly, TN
Zhao, Q
Li, HF
Huang, JF
Wang, LY
Jaquish, CE
Sung, YJ
Shimmin, LC
Lu, FH
Mu, JJ
Hu, DS
Ji, X
Shen, C
Guo, DS
Ma, JX
Wang, RP
Shen, JJ
Li, SX
Chen, J
Mei, H
Chen, CS
Chen, SF
Chen, JC
Li, JX
Cao, J
Lu, XF
Wu, XG
Rice, TK
Gu, CC
Schwander, K
Hamm, LL
Liu, DP
Rao, DC
Hixson, JE
Gu, DF
AF He, Jiang
Kelly, Tanika N.
Zhao, Qi
Li, Hongfan
Huang, Jianfeng
Wang, Laiyuan
Jaquish, Cashell E.
Sung, Yun Ju
Shimmin, Lawrence C.
Lu, Fanghong
Mu, Jianjun
Hu, Dongsheng
Ji, Xu
Shen, Chong
Guo, Dongshuang
Ma, Jixiang
Wang, Renping
Shen, Jinjin
Li, Shengxu
Chen, Jing
Mei, Hao
Chen, Chung-Shiuan
Chen, Shufeng
Chen, Jichun
Li, Jianxin
Cao, Jie
Lu, Xiangfeng
Wu, Xigui
Rice, Treva K.
Gu, C. Charles
Schwander, Karen
Hamm, L. Lee
Liu, Depei
Rao, Dabeeru C.
Hixson, James E.
Gu, Dongfeng
TI Genome-Wide Association Study Identifies 8 Novel Loci Associated With
Blood Pressure Responses to Interventions in Han Chinese
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE blood pressure; genomics; potassium; sodium
ID DIETARY-SODIUM INTERVENTION; QT INTERVAL DURATION; SALT-SENSITIVITY;
COMMON VARIANTS; SUSCEPTIBILITY LOCI; PULSE PRESSURE; FOLLOW-UP;
HYPERTENSION; POPULATION; DISEASE
AB Background Blood pressure (BP) responses to dietary sodium and potassium intervention and cold pressor test vary considerably among individuals. We aimed to identify novel genetic variants influencing individuals' BP responses to dietary intervention and cold pressor test.
Methods and Results We conducted a genome-wide association study of BP responses in 1881 Han Chinese and de novo genotyped top findings in 698 Han Chinese. Diet-feeding study included a 7-day low-sodium (51.3 mmol/d), a 7-day high-sodium (307.8 mmol/d), and a 7-day high-sodium plus potassium supplementation (60 mmol/d). Nine BP measurements were obtained during baseline observation and each intervention period. The meta-analyses identified 8 novel loci for BP phenotypes, which physically mapped in or near PRMT6 (P=7.29x10(-9)), CDCA7 (P=3.57x10(-8)), PIBF1 (P=1.78x10(-9)), ARL4C (P=1.86x10(-8)), IRAK1BP1 (P=1.44x10(-10)), SALL1 (P=7.01x10(-13)), TRPM8 (P=2.68x10(-8)), and FBXL13 (P=3.74x10(-9)). There was a strong dose-response relationship between the number of risk alleles of these independent single-nucleotide polymorphisms and the risk of developing hypertension during the 7.5-year follow-up in the study participants. Compared with those in the lowest quartile of risk alleles, odds ratios (95% confidence intervals) for those in the second, third, and fourth quartiles were 1.39 (0.97, 1.99), 1.72 (1.19, 2.47), and 1.84 (1.29, 2.62), respectively (P=0.0003 for trend).
Conclusions Our study identified 8 novel loci for BP responses to dietary sodium and potassium intervention and cold pressor test. The effect size of these novel loci on BP phenotypes is much larger than those reported by the previously published studies. Furthermore, these variants predict the risk of developing hypertension among individuals with normal BP at baseline.
C1 [He, Jiang; Kelly, Tanika N.; Zhao, Qi; Li, Shengxu; Chen, Jing; Mei, Hao; Chen, Chung-Shiuan; Hamm, L. Lee] Tulane Univ, Dept Epidemiol, Sch Publ Hlth & Trop Med, New Orleans, LA 70118 USA.
[He, Jiang; Chen, Jing; Hamm, L. Lee] Tulane Univ, Sch Med, Dept Med, New Orleans, LA 70112 USA.
[Li, Hongfan; Huang, Jianfeng; Chen, Shufeng; Chen, Jichun; Li, Jianxin; Cao, Jie; Lu, Xiangfeng; Wu, Xigui; Gu, Dongfeng] Fuwai Hosp, State Key Lab Cardiovasc Dis, Dept Epidemiol & Populat Genet, Natl Ctr Cardiovasc Dis, Beijing, Peoples R China.
[Liu, Depei] Chinese Acad Med Sci, Inst Basic Med Sci, Natl Lab Med Mol Biol, Peking Union Med Coll, Beijing 100730, Peoples R China.
[Li, Hongfan; Wang, Laiyuan] Natl Human Genome Ctr Beijing, Beijing, Peoples R China.
[Jaquish, Cashell E.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Sung, Yun Ju; Rice, Treva K.; Gu, C. Charles; Schwander, Karen; Rao, Dabeeru C.] Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA.
[Shimmin, Lawrence C.; Hixson, James E.] Univ Texas Sch Publ Hlth, Ctr Human Genet, Houston, TX USA.
[Lu, Fanghong] Shandong Acad Med Sci, Inst Basic Med, Shandong, Peoples R China.
[Ma, Jixiang] Ctr Dis Control & Prevent Shandong, Jinan, Shandong, Peoples R China.
[Mu, Jianjun] Xi An Jiao Tong Univ, Coll Med, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China.
[Hu, Dongsheng] Shenzhen Univ Med Ctr, Shenzhen, Guangdong, Peoples R China.
[Ji, Xu] Xinle Tradit Med Hosp, Xinle, Hebei, Peoples R China.
[Shen, Chong] Nanjing Med Univ Sch Publ Hlth, Dept Epidemiol & Biostat, Nanjing, Peoples R China.
[Guo, Dongshuang] Yuxian Peoples Hosp, Yangquan, Shanxi, Peoples R China.
[Wang, Renping] Hebei Changcheng Hosp, Shijiazhuang, Hebei, Peoples R China.
[Shen, Jinjin] Ctr Dis Control & Prevent Yancheng, Yancheng, Jiangsu, Peoples R China.
RP He, J (reprint author), Tulane Univ, Dept Epidemiol, Sch Publ Hlth & Trop Med, 1440 Canal St,Suite 2000, New Orleans, LA 70118 USA.
EM jhe@tulane.edu; gudf@yahoo.com
FU National Heart, Lung, and Blood Institute, National Institutes of Health
[U01HL072507, R01HL087263, R01HL090682]; Collins C. Diboll Private
Foundation, New Orleans, LA; High-Tech Research and Development Program
of China (863 Plan) from the Ministry of Science and Technology of China
[2012AA02A516]
FX GenSalt is supported by research grants (U01HL072507, R01HL087263, and
R01HL090682) from the National Heart, Lung, and Blood Institute,
National Institutes of Health, and partially supported by the Collins C.
Diboll Private Foundation, New Orleans, LA. This study is also partially
funded by research grant (2012AA02A516) of the High-Tech Research and
Development Program of China (863 Plan) from the Ministry of Science and
Technology of China.
NR 48
TC 16
Z9 16
U1 2
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-3268
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD DEC
PY 2013
VL 6
IS 6
BP 598
EP 607
DI 10.1161/CIRCGENETICS.113.000307
PG 10
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 274TR
UT WOS:000328629600011
PM 24165912
ER
PT J
AU Puggal, MA
Schully, SD
Srinivas, PR
Papanicolaou, GJ
Jaquish, CE
Fabsitz, RR
AF Puggal, Mona A.
Schully, Sheri D.
Srinivas, Pothur R.
Papanicolaou, George J.
Jaquish, Cashell E.
Fabsitz, Richard R.
TI Translation of Genetics Research to Clinical Medicine The National
Heart, Lung, and Blood Institute Perspective
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE genetics; humans; National Heart; Lung; and Blood Institute (U; S; );
National Institutes of Health (U; S; ); translational medical research
ID PERSONALIZED MEDICINE; INTEGRATION; GENOMICS; CARE; NIH
C1 [Puggal, Mona A.; Srinivas, Pothur R.; Papanicolaou, George J.; Jaquish, Cashell E.; Fabsitz, Richard R.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Schully, Sheri D.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Puggal, MA (reprint author), NHLBI DCVS PPSP EB, Rockledge 2,6701 Rockledge Dr,Room 10199,MSC 7936, Bethesda, MD 20892 USA.
EM mona.puggal@nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 35
TC 4
Z9 4
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-3268
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD DEC
PY 2013
VL 6
IS 6
BP 634
EP 639
DI 10.1161/CIRCGENETICS.113.000227
PG 6
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 274TR
UT WOS:000328629600015
PM 24347619
ER
PT J
AU Wilson, JLL
Miranda, CA
Knepper, MA
AF Wilson, Justin L. L.
Miranda, Carlos A.
Knepper, Mark A.
TI Vasopressin and the regulation of aquaporin-2
SO CLINICAL AND EXPERIMENTAL NEPHROLOGY
LA English
DT Review
DE Vasopressin; Trafficking; Transcription; Polyuria; Hyponatremia; SIADH
ID MEDULLARY COLLECTING DUCT; NEPHROGENIC DIABETES-INSIPIDUS; WATER CHANNEL
EXPRESSION; LONG-TERM REGULATION; PROTEIN-KINASE-A; URINARY
CONCENTRATING DEFECT; ADENYLATE-CYCLASE ACTIVITY; ENHANCER-BINDING
PROTEIN; INDUCED DOWN-REGULATION; RENAL EPITHELIAL-CELLS
AB Water excretion is regulated in large part through the regulation of osmotic water permeability of the renal collecting duct epithelium. Water permeability is controlled by vasopressin through regulation of the water channel, aquaporin-2 (AQP2). Two processes contribute: (1) regulation of AQP2 trafficking to the apical plasma membrane; and (2) regulation of the total amount of the AQP2 protein in the cells. Regulation of AQP2 abundance is defective in several water-balance disorders, including many polyuric disorders and the syndrome of inappropriate antidiuresis. Here we review vasopressin signaling in the renal collecting duct that is relevant to the two modes of water permeability regulation.
C1 [Wilson, Justin L. L.; Miranda, Carlos A.; Knepper, Mark A.] NHLBI, Epithelial Syst Biol Lab, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
RP Knepper, MA (reprint author), NHLBI, Epithelial Syst Biol Lab, Syst Biol Ctr, NIH, 10 Ctr Dr,Bldg 10,Room 6N260, Bethesda, MD 20892 USA.
EM knep@helix.nih.gov
FU Intramural NIH HHS [ZIA HL001285-26, Z01 HL001285-21, Z01 HL001285-22,
Z99 HL999999, ZIA HL001285-23, ZIA HL001285-24, ZIA HL006128-02, ZIA
HL006129-02]
NR 157
TC 28
Z9 31
U1 3
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1342-1751
EI 1437-7799
J9 CLIN EXP NEPHROL
JI Clin. Exp. Nephrol.
PD DEC
PY 2013
VL 17
IS 6
BP 751
EP 764
DI 10.1007/s10157-013-0789-5
PG 14
WC Urology & Nephrology
SC Urology & Nephrology
GA 272VR
UT WOS:000328490900001
PM 23584881
ER
PT J
AU Follmann, D
Brittain, E
Powers, JH
AF Follmann, Dean
Brittain, Erica
Powers, John H.
TI Discordant minimum inhibitory concentration analysis: A new path to
licensure for anti-infective drugs
SO CLINICAL TRIALS
LA English
DT Article
ID STAPHYLOCOCCUS-AUREUS BACTEREMIA; PNEUMONIA; TRIALS; RISK
AB Background Evaluation of anti-infective drugs for licensure often relies on a noninferiority (NI) design where new drug B is noninferior to comparator drug A if the difference in success rates is reliably not worse than some fixed margin. The margin must be based on historical studies that estimate the magnitude of the benefit of drug A over placebo. This approach hampers drug development because the obligatory evidence for margin determination is often nonexistent.
Purpose To develop a new method for licensure of anti-infective drugs when there is no historical evidence for reliable construction of the NI margin.
Methods The minimum inhibitory concentration (MIC) measures the minimum amount of drug that it takes to inhibit growth of bacteria in vitro. Patients who are infected with bacteria that have a low MIC to a given drug are expected to have good outcomes when treated with that drug. Thus, a differential effect of drug B versus drug A, if it exists, is likely to occur in patients whose pathogens have discordant MICs (e.g., low MIC for drug B, high MIC for drug A, or vice versa). A new paradigm for licensure of anti-infective drugs is proposed where a clinically acceptable NI margin is selected and licensure supported if the NI margin is met and B is reliably demonstrated superior to A in a subset of patients whose paired MICs favor B. The requirement for some evidence of superiority encourages a study that is carefully designed and executed.
Results Simulations indicate that the approach shows promise in realistic settings, provided adequate data are available. A simulated example illustrates use of the methods.
Limitations If the data have small sample size, weak MIC/success relationship, or high correlation between MIC-A, MIC-B, this procedure will have poor power.
Conclusion Discordant MIC analysis may offer a novel path to licensure for certain anti-infective drugs.
C1 [Follmann, Dean; Brittain, Erica] NIAID, Biostat Res Branch, Bethesda, MD 20892 USA.
[Powers, John H.] NIAID, SAIC Support, Div Clin Res, Bethesda, MD 20892 USA.
RP Follmann, D (reprint author), NIAID, Biostat Res Branch, 6700A Rockledge Dr Room 5138, Bethesda, MD 20892 USA.
EM dean.follmann@nih.gov
FU National Institutes of Health (NIH)
FX This work was supported by the National Institutes of Health (NIH). The
authors are either employees or contractors of the National Institute of
Allergy and Infectious Diseases (NIAID).
NR 14
TC 2
Z9 2
U1 0
U2 7
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD DEC
PY 2013
VL 10
IS 6
BP 876
EP 885
DI 10.1177/1740774513507503
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 275LB
UT WOS:000328676700006
PM 24287133
ER
PT J
AU Shmueli-Blumberg, D
Hu, L
Allen, C
Frasketi, M
Wu, LT
VanVeldhuisen, P
AF Shmueli-Blumberg, Dikla
Hu, Lian
Allen, Colleen
Frasketi, Michael
Wu, Li-Tzy
VanVeldhuisen, Paul
TI The National Drug Abuse Treatment Clinical Trials Network Data Share
project: Website design, usage, challenges, and future directions
SO CLINICAL TRIALS
LA English
DT Article
ID SUBSTANCE USE DISORDERS; ITEM RESPONSE THEORY; BRIEF SCREENERS; HIV
RISK; DEPENDENCE; ALCOHOL; GENDER; RATES
AB Background There are many benefits of data sharing, including the promotion of new research from effective use of existing data, replication of findings through re-analysis of pooled data files, meta-analysis using individual patient data, and reinforcement of open scientific inquiry. A randomized controlled trial is considered as the gold standard' for establishing treatment effectiveness, but clinical trial research is very costly, and sharing data is an opportunity to expand the investment of the clinical trial beyond its original goals at minimal costs.
Purpose We describe the goals, developments, and usage of the Data Share website (http://www.ctndatashare.org) for the National Drug Abuse Treatment Clinical Trials Network (CTN) in the United States, including lessons learned, limitations, and major revisions, and considerations for future directions to improve data sharing.
Methods Data management and programming procedures were conducted to produce uniform and Health Insurance Portability and Accountability Act (HIPAA)-compliant de-identified research data files from the completed trials of the CTN for archiving, managing, and sharing on the Data Share website.
Results Since its inception in 2006 and through October 2012, nearly 1700 downloads from 27 clinical trials have been accessed from the Data Share website, with the use increasing over the years. Individuals from 31 countries have downloaded data from the website, and there have been at least 13 publications derived from analyzing data through the public Data Share website.
Limitations Minimal control over data requests and usage has resulted in little information and lack of control regarding how the data from the website are used. Lack of uniformity in data elements collected across CTN trials has limited cross-study analyses.
Conclusions The Data Share website offers researchers easy access to de-identified data files with the goal to promote additional research and identify new findings from completed CTN studies. To maximize the utility of the website, ongoing collaborative efforts are needed to standardize the core measures used for data collection in the CTN studies with the goal to increase their comparability and to facilitate the ability to pool data files for cross-study analyses.
C1 [Shmueli-Blumberg, Dikla; Hu, Lian; Allen, Colleen; Frasketi, Michael; VanVeldhuisen, Paul] EMMES Corp, NIDA CTN Clin Coordinating Ctr, Rockville, MD 20850 USA.
[Wu, Li-Tzy] Duke Univ, Dept Psychiat & Behav Sci, Durham, NC USA.
RP Shmueli-Blumberg, D (reprint author), EMMES Corp, NIDA CTN Clin Coordinating Ctr, 401 N Washington St,Suite 700, Rockville, MD 20850 USA.
EM dblumberg@emmes.com
FU US National Institute on Drug Abuse (NIDA) of the National Institutes of
Health [HHSN271200900034C, HSN271200522071C]; NIDA [R33DA027503,
R01DA019623]
FX The work for the National Drug Abuse Treatment Clinical Trials Network
(CTN) Data Share website is made possible by the US National Institute
on Drug Abuse (NIDA) of the National Institutes of Health (grant number
HHSN271200900034C to The EMMES Corporation, and grant number
HSN271200522071C to Duke University). Li-Tzy Wu has received research
funding from NIDA (R33DA027503, R01DA019623).
NR 31
TC 2
Z9 2
U1 1
U2 8
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD DEC
PY 2013
VL 10
IS 6
BP 977
EP 986
DI 10.1177/1740774513503522
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 275LB
UT WOS:000328676700016
PM 24085772
ER
PT J
AU Fay, MP
AF Fay, Michael P.
TI An alternative property for evaluating sample size for normal data using
preliminary data
SO CLINICAL TRIALS
LA English
DT Letter
C1 NIAID, Bethesda, MD 20892 USA.
RP Fay, MP (reprint author), NIAID, 6700-B Rockledge Dr MSC 7630, Bethesda, MD 20892 USA.
EM mfay@niaid.nih.gov
OI Fay, Michael P./0000-0002-8643-9625
NR 2
TC 1
Z9 1
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD DEC
PY 2013
VL 10
IS 6
BP 990
EP 991
DI 10.1177/1740774513506965
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 275LB
UT WOS:000328676700018
PM 24287134
ER
PT J
AU Crampton, SP
Bolland, S
AF Crampton, Steve P.
Bolland, Silvia
TI Spontaneous activation of RNA-sensing pathways in autoimmune disease
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; TOLL-LIKE RECEPTORS;
AICARDI-GOUTIERES-SYNDROME; B-CELL RESPONSES; I INTERFERON; MURINE
LUPUS; NUCLEIC-ACID; IMMUNE-RESPONSES; DENDRITIC CELLS; SELF-RNA
AB Multiple intracellular RNA sensing innate immune pathways have been linked to autoimmune disease. RNA-related ligands taken up by the endocytic pathway activate TLRs, and affect primarily immune cells. This type of activation is enhanced by nucleic acid-specific antibodies and induces an inflammatory program. In contrast, spontaneous activation of cytoplasmic RNA sensing pathways targets mostly non-hematopoietic tissues and their effect on autoimmune disease is secondary to the release of interferon in the circulation. The fact that pathologies result from spontaneous activation of innate pathways implies that endogenous RNA ligands that might be sensed as pathogenic are commonly found in both immune and non-immune cells.
C1 [Crampton, Steve P.; Bolland, Silvia] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
RP Bolland, S (reprint author), NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
EM sbolland@niaid.nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health [Z108015]
FX The authors' work was supported by the Intramural Research Program of
the National Institute of Allergy and Infectious Diseases, National
Institutes of Health (Z108015).
NR 67
TC 4
Z9 4
U1 2
U2 8
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0952-7915
EI 1879-0372
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD DEC
PY 2013
VL 25
IS 6
BP 712
EP 719
DI 10.1016/j.coi.2013.09.011
PG 8
WC Immunology
SC Immunology
GA 276AG
UT WOS:000328719900008
PM 24455767
ER
PT J
AU Wu, Y
Christensen, R
Colon-Ramos, D
Shroff, H
AF Wu, Yicong
Christensen, Ryan
Colon-Ramos, Daniel
Shroff, Hari
TI Advanced optical imaging techniques for neurodevelopment
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID LIGHT-SHEET MICROSCOPY; STRUCTURED-ILLUMINATION MICROSCOPY; MOUSE-BRAIN;
FLUORESCENCE MICROSCOPY; GENERATION MICROSCOPY; PLANE ILLUMINATION;
LIVE; ZEBRAFISH; TOMOGRAPHY; RESOLUTION
AB Over the past decade, developmental neuroscience has been transformed by the widespread application of confocal and two-photon fluorescence microscopy. Even greater progress is imminent, as recent innovations in microscopy now enable imaging with increased depth, speed, and spatial resolution; reduced phototoxicity; and in some cases without external fluorescent probes. We discuss these new techniques and emphasize their dramatic impact on neurobiology, including the ability to image neurons at depths exceeding 1 mm, to observe neurodevelopment noninvasively throughout embryogenesis, and to visualize neuronal processes or structures that were previously too small or too difficult to target with conventional microscopy.
C1 [Wu, Yicong; Shroff, Hari] Natl Inst Biomed Imaging & Bioengn, Sect High Resolut Opt Imaging, NIH, Bethesda, MD 20892 USA.
[Christensen, Ryan; Colon-Ramos, Daniel] Yale Univ, Sch Med, Dept Cell Biol, Program Cellular Neurosci Neurodegenerat & Repair, New Haven, CT 06536 USA.
RP Wu, Y (reprint author), Natl Inst Biomed Imaging & Bioengn, Sect High Resolut Opt Imaging, NIH, 13 South Dr, Bethesda, MD 20892 USA.
EM yicong.wu@nih.gov; hari.shroff@nih.gov
RI Shroff, Hari/E-7247-2016
OI Shroff, Hari/0000-0003-3613-8215
FU Intramural NIH HHS [ZIA EB000074-01]; NINDS NIH HHS [R01 NS076558]
NR 52
TC 9
Z9 9
U1 0
U2 21
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
EI 1873-6882
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD DEC
PY 2013
VL 23
IS 6
BP 1090
EP 1097
DI 10.1016/j.conb.2013.06.008
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 273EN
UT WOS:000328517800026
PM 23831260
ER
PT J
AU Kozak, CA
AF Kozak, Christine A.
TI Evolution of different antiviral strategies in wild mouse populations
exposed to different gammaretroviruses
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID MURINE LEUKEMIA VIRUSES; CELL-SURFACE RECEPTOR; FOCUS-INDUCING VIRUSES;
HOST-RANGE VARIANTS; XENOTROPIC GAMMARETROVIRUSES; CYTIDINE DEAMINASE;
LABORATORY MOUSE; RETROVIRUS XMRV; ENVELOPE GENES; XPR1 RECEPTOR
AB Laboratory mice carry three host range groups of gammaretroviruses all of which are linked to leukemia induction. Although polytropic mouse leukemia viruses (PMLVs) are generally recognized as the proximate cause of MLV-induced leukemias in laboratory mice, wild mice that carry only endogenous P-MLVs do not produce infectious virus and are not prone to disease; these mice carry the permissive XPR1 retroviral receptor and an attenuated variant of the retroviral restriction factor, APOBEC3. In contrast, Eurasian mice carrying ecotropic and xenotropic MLVs have evolved multiple restrictive XPR1 variants, other factors that interfere with MLV entry, and more effectively antiviral variants of APOBEC3. These different antiviral restrictions in Mus muscu/us subspecies suggest that the different virus types found in these natural populations may pose different but largely uncharacterized survival risks in their host subspecies.
C1 NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
RP Kozak, CA (reprint author), NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
EM ckozak@niaid.nih.gov
FU Intramural Program of the NIAID, NIH, Bethesda, MD
FX This work was supported by the Intramural Program of the NIAID, NIH,
Bethesda, MD.
NR 59
TC 8
Z9 8
U1 0
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD DEC
PY 2013
VL 3
IS 6
BP 657
EP 663
DI 10.1016/j.coviro.2013.08.001
PG 7
WC Virology
SC Virology
GA 275YR
UT WOS:000328715800008
PM 23992668
ER
PT J
AU Strebel, K
AF Strebel, Klaus
TI HIV accessory proteins versus host restriction factors
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; AICARDI-GOUTIERES SYNDROME;
CYCLIN-DEPENDENT KINASES; E3 UBIQUITIN LIGASE; CD4(+) T-CELLS; SAMHD1
RESTRICTS; CBF-BETA; PARTICLE RELEASE; DOWN-MODULATION; DENDRITIC CELLS
AB Primate immunodeficiency viruses, including HIV-1, are characterized by the presence of accessory genes such as vif, vpr, vpx, vpu, and nef. Current knowledge indicates that none of the primate lentiviral accessory proteins has enzymatic activity. Instead, these proteins interact with cellular ligands to either act as adapter molecules to redirect the normal function of host factors for virus-specific purposes or to inhibit a normal host function by mediating degradation or causing intracellular mislocalization/sequestration of the factors involved. This review aims at providing an update of our current understanding of how Vif, Vpu, and Vpx control the cellular restriction factors APOBEC3G, BST-2, and SAMHD1 respectively.
C1 NIAID, Mol Microbiol Lab, Viral Biochem Sect, NIH, Bethesda, MD 20892 USA.
RP Strebel, K (reprint author), NIAID, Mol Microbiol Lab, Viral Biochem Sect, NIH, Bethesda, MD 20892 USA.
EM kstrebel@nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health [1 Z01 AI000669]
FX K Strebel is supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health (1 Z01 AI000669).
NR 82
TC 42
Z9 42
U1 1
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD DEC
PY 2013
VL 3
IS 6
BP 692
EP 699
DI 10.1016/j.coviro.2013.08.004
PG 8
WC Virology
SC Virology
GA 275YR
UT WOS:000328715800013
PM 24246762
ER
PT J
AU Gabel, SA
DeRose, EF
London, RE
AF Gabel, Scott A.
DeRose, Eugene F.
London, Robert E.
TI XRCC1 interaction with the REV1 C-terminal domain suggests a role in
post replication repair
SO DNA REPAIR
LA English
DT Article
DE XRCC1; REV1 C-terminal domain; Post replication repair; REV1 interacting
region; NMR spectroscopy
ID BASE EXCISION-REPAIR; DNA-LIGASE-III; NUCLEAR OVERHAUSER ENHANCEMENT;
SINGLE-STRAND BREAKS; TRANSLESION POLYMERASES; DAMAGE TOLERANCE;
STRUCTURAL BASIS; CANCER RISK; HUMAN-CELLS; PROTEIN
AB The function of X-ray cross complementing group 1 protein (XRCC1), a scaffold that binds to DNA repair enzymes involved in single-strand break and base excision repair, requires that it be recruited to sites of damaged DNA. However, structural insights into this recruitment are currently limited. Sequence analysis of the first unstructured linker domain of XRCC1 identifies a segment consistent with a possible REV1 interacting region (X1RIR) motif. The X1RIR motif is present in translesion polymerases that can be recruited to the pol zeta/REV1 DNA repair complex via a specific interaction with the REV1 C-terminal domain. NMR and fluorescence titration studies were performed on XRCC1-derived peptides containing this putative RIR motif in order to evaluate the binding affinity for the REV1 C-terminal domain. These studies demonstrate an interaction of the XRCC1-derived peptide with the human REV1 C-terminal domain characterized by dissociation constants in the low micromolar range. Ligand competition studies comparing the XRCC1 RIR peptide with previously studied RIR peptides were found to be inconsistent with the NMR based K-d values. These discrepancies were resolved using a fluorescence assay for which the RIR-REV1 system is particularly well suited. The structure of a REV1-XRCC1 peptide complex was determined by using NOE restraints to dock the unlabeled XRCC1 peptide with a labeled REV1 C-terminal domain. The structure is generally homologous with previously determined complexes with the pol kappa and pol eta RIR peptides, although the helical segment in XRCC1 is shorter than was observed in these cases. These studies suggest the possible involvement of XRCC1 and its associated repair factors in post replication repair. Published by Elsevier B.V.
C1 [Gabel, Scott A.; DeRose, Eugene F.; London, Robert E.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP London, RE (reprint author), NIEHS, Struct Biol Lab, MR-01,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM london@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences [Z01 ES050111];
National Institutes of Health, NIEHS [HHSN273200700046U]
FX This work was supported by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences, project numbers Z01
ES050111. E.F.D. is supported by National Institutes of Health, NIEHS,
under Delivery Order HHSN273200700046U.
NR 53
TC 7
Z9 7
U1 1
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD DEC
PY 2013
VL 12
IS 12
BP 1105
EP 1113
DI 10.1016/j.dnarep.2013.08.015
PG 9
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 274GO
UT WOS:000328595000012
PM 24409475
ER
PT J
AU Wolf, L
Gao, CS
Gueta, K
Xie, Q
Chevallier, T
Podduturi, NR
Sun, J
Conte, I
Zelenka, PS
Ashery-Padan, R
Zavadil, J
Cvekl, A
AF Wolf, Louise
Gao, Chun S.
Gueta, Karen
Xie, Qing
Chevallier, Tiphaine
Podduturi, Nikhil R.
Sun, Jian
Conte, Ivan
Zelenka, Peggy S.
Ashery-Padan, Ruth
Zavadil, Jiri
Cvekl, Ales
TI Identification and Characterization of FGF2-Dependent mRNA: microRNA
Networks During Lens Fiber Cell Differentiation
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE c-Maf; Dicer1; differentiation; FGF2; lens; microRNAs; signaling
ID FIBROBLAST-GROWTH-FACTOR; BONE MORPHOGENETIC PROTEIN;
ALPHA-A-CRYSTALLIN; EMBRYONIC STEM-CELLS; TRANSCRIPTION FACTORS; OCULAR
LENS; TERMINAL DIFFERENTIATION; ORGANELLE DEGRADATION; EPITHELIAL-CELLS;
PROGENITOR CELLS
AB MicroRNAs (miRNAs) and fibroblast growth factor (FGF) signaling regulate a wide range of cellular functions, including cell specification, proliferation, migration, differentiation, and survival. In lens, both these systems control lens fiber cell differentiation; however, a possible link between these processes remains to be examined. Herein, the functional requirement for miRNAs in differentiating lens fiber cells was demonstrated via conditional inactivation of Dicer1 in mouse (Mus musculus) lens. To dissect the miRNA-dependent pathways during lens differentiation, we used a rat (Rattus norvegicus) lens epithelial explant system, induced by FGF2 to differentiate, followed by mRNA and miRNA expression profiling. Transcriptome and miRNome analysis identified extensive FGF2-regulated cellular responses that were both independent and dependent on miRNAs. We identified 131 FGF2-regulated miRNAs. Seventy-six of these miRNAs had at least two in silico predicted and inversely regulated target mRNAs. Genes modulated by the greatest number of FGF-regulated miRNAs include DNA-binding transcription factors Nfib, Nfat5/OREBP, c-Maf, Ets1, and N-Myc. Activated FGF signaling influenced bone morphogenetic factor/transforming growth factor-, Notch, and Wnt signaling cascades implicated earlier in lens differentiation. Specific miRNA:mRNA interaction networks were predicted for c-Maf, N-Myc, and Nfib (DNA-binding transcription factors); Cnot6, Cpsf6, Dicer1, and Tnrc6b (RNA to miRNA processing); and Ash1l, Med1/PBP, and Kdm5b/Jarid1b/Plu1 (chromatin remodeling). Three miRNAs, including miR-143, miR-155, and miR-301a, down-regulated expression of c-Maf in the 3-UTR luciferase reporter assays. These present studies demonstrate for the first time global impact of activated FGF signaling in lens cell culture system and predicted novel gene regulatory networks connected by multiple miRNAs that regulate lens differentiation.
C1 [Wolf, Louise; Xie, Qing; Cvekl, Ales] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10461 USA.
[Wolf, Louise; Xie, Qing; Chevallier, Tiphaine; Sun, Jian; Cvekl, Ales] Albert Einstein Coll Med, Dept Ophthalmol & Visual Sci, Bronx, NY 10461 USA.
[Gao, Chun S.; Zelenka, Peggy S.] NEI, Lab Mol & Dev Biol, Bethesda, MD 20892 USA.
[Gueta, Karen; Ashery-Padan, Ruth] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel.
[Gueta, Karen; Ashery-Padan, Ruth] Tel Aviv Univ, Sagol Sch Neurosci, IL-69978 Tel Aviv, Israel.
[Podduturi, Nikhil R.; Zavadil, Jiri] NYU, Dept Pathol, Langone Med Ctr, New York, NY 10000 USA.
[Podduturi, Nikhil R.; Zavadil, Jiri] NYU, Langone Med Ctr, Ctr Hlth Informat & Bioinformat, New York, NY 10000 USA.
[Conte, Ivan] Telethon Inst Genet & Med, I-80131 Naples, Italy.
RP Cvekl, A (reprint author), Albert Einstein Coll Med, Ullmann 123,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM ZavadilJ@iarc.fr; ales.cvekl@einstein.yu.edu
OI Podduturi, Nikhil Reddy/0000-0002-2592-2090; Zavadil,
Jiri/0000-0003-0640-5562
FU National Institutes of Health/National Cancer Institute [P30
CA016087-30]; NEI [Z01-EY000238]; Research to Prevent Blindness, Inc.;
Israel Science Foundation [610/10]; Israel Ministry of Science [36494];
Ziegler Foundation; Binational Science Foundation; [R01 EY014237];
[EY014237-7S1]
FX We thank M. T. Pizzo at the TIGEM institute for excellent technical
help. We are grateful to Drs. Eran Hornstein (Weizman Institute of
Science, Haifa, Israel) and Michael L. Robinson (Miami University,
Miami, OH) for providing us the Dicer1flox/flox and the
MLR10-cre mouse, respectively. We also thank Drs. Antony Rodriguez
(Baylor College of Medicine) for the reference c-Maf 3'-UTR-luc
plasmids, and Robert Farris and Slava Tomarev (National Eye Institute)
for support. T. C. is a student in the Magistere de Genetique Graduate
Program at Universite Paris Diderot, Sorbonne Paris Cite. Core
facilities: AECOM Genomics and NYU Genome Technology Center supported in
part by the National Institutes of Health/National Cancer Institute P30
CA016087-30 grant. Grant support: R01 EY014237 and EY014237-7S1 (A. C.),
NEI intramural support Z01-EY000238 (P.S.Z.), and Research to Prevent
Blindness, Inc. unrestricted grant to the Department of Ophthalmology
and Visual Sciences. R.A.-P.'s research is supported by the Israel
Science Foundation 610/10, the Israel Ministry of Science 36494, the
Ziegler Foundation, and the Binational Science Foundation.
NR 124
TC 10
Z9 12
U1 1
U2 12
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD DEC
PY 2013
VL 3
IS 12
BP 2239
EP 2255
DI 10.1534/g3.113.008698
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 270QV
UT WOS:000328334500014
PM 24142921
ER
PT J
AU Koroshetz, WJ
Brown, J
AF Koroshetz, Walter J.
Brown, Jeremy
TI NIH: Developing And Funding Research In Emergency Care And Training The
Next Generation Of Emergency Care Researchers
SO HEALTH AFFAIRS
LA English
DT Article
ID ROUND-TABLE; INFORMED-CONSENT; TRIAL; CHALLENGES; HEMORRHAGE; EXCEPTION;
OUTCOMES
AB For the best health care to be provided in emergency settings, it must be based on the best available science. There are about 136 million visits to emergency departments (EDs) in the United States annually. Many of the nation's most critically ill patients are first stabilized and treated in EDs-the point of origin for nearly half of all medical intensive care unit admissions and a fourth of all surgical intensive care unit admissions. This article explores the role of the National Institutes of Health (NIH) in developing and funding research in emergency care and in training the next generation of emergency care researchers. Recognizing that effective emergency care research spans multiple organ systems and disciplines, the NIH established the Office of Emergency Care Research in December 2011 to facilitate and coordinate funding opportunities relevant to research and research training in emergency settings. Because the NIH funds education, basic research, and large clinical trials, it plays a key role in improving emergency care.
C1 [Koroshetz, Walter J.] NINDS, NIH, Bethesda, MD 20892 USA.
[Brown, Jeremy] NIGMS, Off Emergency Care Res, NIH, Bethesda, MD USA.
RP Koroshetz, WJ (reprint author), NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM koroshetzw@ninds.nih.gov
NR 30
TC 3
Z9 3
U1 0
U2 1
PU PROJECT HOPE
PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD DEC
PY 2013
VL 32
IS 12
BP 2186
EP 2192
DI 10.1377/hlthaff.2013.0833
PG 7
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 275QC
UT WOS:000328690900019
PM 24301404
ER
PT J
AU Ganmaa, D
Rich-Edwards, JW
Frazier, LA
Davaalkham, D
Oyunbileg, G
Janes, C
Potischman, N
Hoover, R
Troisi, R
AF Ganmaa, Davaasambuu
Rich-Edwards, Janet W.
Frazier, Lindsay A.
Davaalkham, Dambadarjaa
Oyunbileg, Gankhuyag
Janes, Craig
Potischman, Nancy
Hoover, Robert
Troisi, Rebecca
TI A comparison of migrants to, and women born in, urban Mongolia:
demographic, reproductive, anthropometric and lifestyle characteristics
SO INTERNATIONAL HEALTH
LA English
DT Article
DE Lifestyle; Reproductive factors; Diet; Non-communicable diseases;
Mongolia; Asia
ID CONSUMPTION; POPULATION; DISEASES; CHINA; RISK; DIET
AB Mongolia has experienced vast migration from rural to urban areas since the 1950s. We hypothesized that women migrating to Ulaanbaatar, the capital, would differ in factors related to future chronic disease risk compared with women who were born in Ulaanbaatar.
Premenopausal mothers (aged 44 years) of children attending two schools (one in the city centre and one in the outskirts) in Ulaanbaatar were recruited for the study. During April and May 2009, 420 women were interviewed about migration, reproductive history and lifestyle factors and anthropometric measurements were taken.
Women born in (n178) and outside (n242) Ulaanbaatar were similar in education and marital status, but the latter appeared to have a more traditional lifestyle including being more likely to have lived as a nomadic herder (22.3 vs 5.6; p0.001) and to currently live in a traditional yurt or ger (40.1 vs 29.2). Ever-use of hormonal contraception was more common in women born outside Ulaanbaatar (52.1 vs 38.2; p0.005) and their age at first live birth was older (26.0 vs 20.8 for 25 vs 25 years). Although the number of pregnancies was similar, the number of live births was greater for those born outside Ulaanbaatar (p0.002). Women born in Ulaanbaatar were more likely to have smoked cigarettes (24.7 vs 11.2; p0.001). Women born outside Ulaanbaatar were more likely to consume the traditional meat and dairy diet.
Rural migrants to Mongolias capital have retained a traditional lifestyle in some, but not all, respects. Internal migrant populations may provide the opportunity to assess the effect of changes in isolated risk factors for subsequent chronic disease.
C1 [Ganmaa, Davaasambuu] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Ganmaa, Davaasambuu; Rich-Edwards, Janet W.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Connors Ctr Womens Hlth & Gender Biol, Boston, MA 02115 USA.
[Ganmaa, Davaasambuu; Rich-Edwards, Janet W.; Frazier, Lindsay A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Frazier, Lindsay A.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Frazier, Lindsay A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, Boston, MA 02115 USA.
[Davaalkham, Dambadarjaa; Oyunbileg, Gankhuyag] Univ Mongolia, Ulaanbaatar, Mongol Peo Rep.
[Janes, Craig] Simon Fraser Univ, Fac Hlth Sci, Burnaby, BC V5A 1S6, Canada.
[Potischman, Nancy] NCI, Div Canc Control & Populat Sci, US Dept HHS, Bethesda, MD 20892 USA.
[Hoover, Robert; Troisi, Rebecca] NCI, Div Canc Epidemiol & Genet, US Dept HHS, Bethesda, MD 20892 USA.
RP Ganmaa, D (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave,Bldg 2,Room 341B, Boston, MA 02115 USA.
EM gdavaasa@hsph.harvard.edu
FU National Cancer Institute, National Institutes of Health, Bethesda, MD,
USA
FX This work was supported by a contract from the National Cancer
Institute, National Institutes of Health, Bethesda, MD, USA.
NR 17
TC 3
Z9 3
U1 2
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1876-3413
EI 1876-3405
J9 INT HEALTH
JI Int. Health
PD DEC
PY 2013
VL 5
IS 4
BP 244
EP 250
DI 10.1093/inthealth/iht020
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 271BH
UT WOS:000328364800002
PM 24021762
ER
PT J
AU McCaffery, JM
Papandonatos, GD
Huggins, GS
Peter, I
Kahn, SE
Knowler, WC
Hudnall, GE
Lipkin, EW
Kitabchi, AE
Wagenknecht, LE
Wing, RR
AF McCaffery, J. M.
Papandonatos, G. D.
Huggins, G. S.
Peter, I.
Kahn, S. E.
Knowler, W. C.
Hudnall, G. E.
Lipkin, E. W.
Kitabchi, A. E.
Wagenknecht, L. E.
Wing, R. R.
CA Genetic Subgrp Look AHEAD
Look AHEAD Res Grp
TI FTO predicts weight regain in the Look AHEAD clinical trial
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE type 2 diabetes; weight loss; diet; genetics
ID GENOME-WIDE ASSOCIATION; DIABETES PREVENTION PROGRAM; LIFE-STYLE
INTERVENTION; OBESITY-RELATED TRAITS; REDUCES ENERGY-INTAKE; BODY-MASS
INDEX; NEUROTROPHIC FACTOR; ADULT OBESITY; CHILDHOOD OBESITY;
RISK-FACTORS
AB BACKGROUND: Genome-wide association studies have provided new insights into the genetic factors that contribute to the development of obesity. We hypothesized that these genetic markers would also predict magnitude of weight loss and weight regain after initial weight loss.
METHODS: Established obesity risk alleles available on the Illumina CARe iSelect (IBC) chip were characterized in 3899 overweight or obese participants with type 2 diabetes from the Look AHEAD (Action for Health in Diabetes), a randomized trial to determine the effects of intensive lifestyle intervention (ILI) and diabetes support and education (DSE) on cardiovascular morbidity and mortality. Primary analyses examined the interaction between 13 obesity risk polymorphisms in eight genes and randomized treatment arm in predicting weight change at year 1, and weight regain at year 4 among individuals who lost 3% or more of their baseline weight by year 1.
RESULTS: No single-nucleotide polymorphisms (SNPs) were significantly associated with magnitude of weight loss or interacted with treatment arm at year 1. However, fat mass and obesity associated gene (FTO) rs3751812 predicted weight regain within DSE (1.56 kg per risk allele, P = 0.005), but not ILI (P = 0.761), resulting in SNP x treatment arm interaction (P = 0.009). In a partial replication of prior research, the obesity risk (G) allele at BDNF rs6265 was associated with greater weight regain across treatment arms (0.773 kg per risk allele), although results were of borderline statistical significance (P = 0.051).
CONCLUSIONS: Variations in the FTO and BDNF loci may contribute risk of weight regain after weight loss.
C1 [McCaffery, J. M.; Wing, R. R.] Miriam Hosp, Dept Psychiat & Human Behav, Weight Control & Diabet Res Ctr, Providence, RI 02903 USA.
[McCaffery, J. M.; Wing, R. R.] Brown Med Sch, Providence, RI USA.
[Papandonatos, G. D.] Brown Univ, Ctr Stat Sci, Providence, RI 02912 USA.
[Huggins, G. S.] Tufts Med Ctr, Mol Cardiol Res Inst, MCRI Ctr Translat Genom, Boston, MA USA.
[Peter, I.] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
[Kahn, S. E.; Kitabchi, A. E.] Univ Washington, Dept Med, Div Metab Endocrinol & Nutr, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Knowler, W. C.] Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ USA.
[Hudnall, G. E.] Baylor Coll Med, Houston, TX 77030 USA.
[Hudnall, G. E.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Lipkin, E. W.] Univ Tennessee, Ctr Hlth Sci, Div Endocrinol Diabet & Metab, Memphis, TN 38163 USA.
[Wagenknecht, L. E.] Wake Forest Univ, Bowman Gray Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27103 USA.
RP McCaffery, JM (reprint author), Miriam Hosp, Dept Psychiat & Human Behav, Weight Control & Diabet Res Ctr, 196 Richmond St, Providence, RI 02903 USA.
EM jeanne_mccaffery@brown.edu
RI Papandonatos, George/J-2328-2014;
OI Papandonatos, George/0000-0001-6770-932X; Kahn,
Steven/0000-0001-7307-9002
FU Department of Health and Human Services through National Institutes of
Health [DK57136, DK57149, DK56990, DK57177, DK57171, DK57151, DK57182,
DK57131, DK57002, DK57078, DK57154, DK57178, DK57219, DK57008, DK57135,
DK56992]; National Institute of Diabetes and Digestive and Kidney
Diseases; National Heart, Lung and Blood Institute; National Institute
of Nursing Research; National Center on Minority Health and Health
Disparities; Office of Research on Women's Health; Centers for Disease
Control and Prevention; Johns Hopkins Medical Institutions Bayview
General Clinical Research Center [M01RR02719]; Massachusetts General
Hospital Mallinckrodt General Clinical Research Center [M01RR01066];
University of Colorado Health Sciences Center General Clinical Research
Center [M01RR00051]; Clinical and Nutrition Research Unit [P30 DK48520];
University of Tennessee at Memphis General Clinical Research Center
[M01RR0021140]; University of Pittsburgh General Clinical Research
Center [M01RR000056 44]; NIH [DK 046204, DK072497]; VA Puget Sound
Health Care System and Department of Veterans Affairs; Frederic C
Bartter General Clinical Research Center [M01RR01346]; Training Program
in Cardiovascular Research (NIH) [5T32HL069770]
FX We acknowledge the Look AHEAD sites that participated in this ancillary
study. This study is supported by the Department of Health and Human
Services through the following cooperative agreements from the National
Institutes of Health: DK57136, DK57149, DK56990, DK57177, DK57171,
DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178, DK57219,
DK57008, DK57135 and DK56992. The following federal agencies have
contributed support: National Institute of Diabetes and Digestive and
Kidney Diseases; National Heart, Lung and Blood Institute; National
Institute of Nursing Research; National Center on Minority Health and
Health Disparities; Office of Research on Women's Health; and the
Centers for Disease Control and Prevention. Additional support was
received from The Johns Hopkins Medical Institutions Bayview General
Clinical Research Center (M01RR02719); the Massachusetts General
Hospital Mallinckrodt General Clinical Research Center (M01RR01066); the
University of Colorado Health Sciences Center General Clinical Research
Center (M01RR00051) Clinical and Nutrition Research Unit (P30 DK48520);
the University of Tennessee at Memphis General Clinical Research Center
(M01RR0021140); the University of Pittsburgh General Clinical Research
Center (M01RR000056 44) and NIH grants (DK 046204 and DK072497); and VA
Puget Sound Health Care System and Department of Veterans Affairs;
Frederic C Bartter General Clinical Research Center (M01RR01346). AKH
was supported by the Training Program in Cardiovascular Research (NIH,
5T32HL069770). The following organizations have committed to make major
contributions to Look AHEAD: Federal Express; Health Management
Resources; Johnson & Johnson, LifeScan Inc.; Optifast-Novartis
Nutrition; Roche Pharmaceuticals; Ross Product Division of Abbott
Laboratories; Slim-Fast Foods Company; and Unilever.
NR 38
TC 12
Z9 12
U1 0
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
EI 1476-5497
J9 INT J OBESITY
JI Int. J. Obes.
PD DEC
PY 2013
VL 37
IS 12
BP 1545
EP 1552
DI 10.1038/ijo.2013.54
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 272JJ
UT WOS:000328456200005
PM 23628854
ER
PT J
AU Leon, B
Jenkins, S
Pepin, K
Chaudhry, H
Smith, K
Zalos, G
Miller, BV
Chen, KY
Remaley, AT
Waclawiw, MA
Sumner, AE
Cannon, RO
AF Leon, B.
Jenkins, S.
Pepin, K.
Chaudhry, H.
Smith, K.
Zalos, G.
Miller, B. V., III
Chen, K. Y.
Remaley, A. T.
Waclawiw, M. A.
Sumner, A. E.
Cannon, R. O., III
TI Insulin and extremity muscle mass in overweight and obese women
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE insulin; skeletal muscle; weight loss; women's health
ID INTERMUSCULAR ADIPOSE-TISSUE; SKELETAL-MUSCLE; WEIGHT-LOSS; INDUCED
HYPERTROPHY; PROTEIN-SYNTHESIS; BODY-COMPOSITION; OLDER-ADULTS;
AMINO-ACIDS; HYPERINSULINEMIA; RESISTANCE
AB BACKGROUND: Obesity disproportionately affects women, especially those of African descent, and is associated with increases in both fat and muscle masses.
OBJECTIVE: Although increased extremity muscle mass may be compensatory to fat mass load, we propose that elevated insulin levels resulting from diminished insulin sensitivity may additionally contribute to extremity muscle mass in overweight or obese women.
METHODS: The following measurements were performed in 197 non-diabetic women (57% black, 35% white; age 46 +/- 11 years (mean +/- s.d.), body mass index (BMI) range 25.0-57.7 kg m(-2)): dual-energy X-ray absorptiometry for fat and extremity muscle masses; exercise performance by duration and peak oxygen consumption (VO2 peak) during graded treadmill exercise; fasting insulin and, in 183 subjects, insulin sensitivity index (SI) calculated from the minimal model.
RESULTS: SI (range 0.5-14.1 lmU(-1) min(-1)) was negatively, and fasting insulin (range 1.9-35.6 mu Uml(-1)) positively associated with extremity muscle mass (both P<0.001), independent of age and height. Sixty-seven percent of women completed 6 months of participation in a weight loss and exercise program: we found a significant association between reduction in fasting insulin and a decrease in extremity muscle mass (P = 0.038), independent of reduction in fat mass or improvement in exercise performance by VO2 peak and exercise duration, and without association with change in SI or interaction by race.
CONCLUSIONS: Hyperinsulinemia in overweight or obese women is associated with increased extremity muscle mass, which is partially reversible with reduction in fasting insulin concentration, consistent with the stimulatory effects of insulin on skeletal muscle.
C1 [Leon, B.; Jenkins, S.; Pepin, K.; Chaudhry, H.; Smith, K.; Zalos, G.; Remaley, A. T.; Cannon, R. O., III] Natl Inst Diabet Digest Dis & Kidney Dis, Cardiovasc & Pulm Branch, Bethesda, MD USA.
[Leon, B.; Jenkins, S.; Pepin, K.; Chaudhry, H.; Smith, K.; Zalos, G.; Miller, B. V., III; Chen, K. Y.; Remaley, A. T.; Waclawiw, M. A.; Sumner, A. E.; Cannon, R. O., III] NIH, Bethesda, MD 20892 USA.
[Miller, B. V., III; Chen, K. Y.; Sumner, A. E.] NHLBI, Bethesda, MD 20892 USA.
[Miller, B. V., III; Chen, K. Y.; Sumner, A. E.] Natl Inst Diabet Digest Dis & Kidney Dis, Diabet Endocrinol & Obes Branch, Bethesda, MD USA.
[Waclawiw, M. A.] Natl Inst Diabet Digest Dis & Kidney Dis, Off Biostat Res, Bethesda, MD USA.
RP Cannon, RO (reprint author), NHLBI, NIH, Bldg 10 CRC Room 5-3330,10 Ctr Dr, Bethesda, MD 20892 USA.
EM cannonr@nih.gov
OI Chen, Kong/0000-0002-0306-1904
FU National Heart, Lung, and Blood Institute; National Institute of
Diabetes, and Digestive and Kidney Diseases, National Institutes of
Health
FX We gratefully acknowledge the contributions of Janet Dejesus, Rachel
Permuth-Levine, Nancy Sebring, Amber Courville, Rita Lapointe, Diane
Dellavalle, Greg McMahon, Catherine Marinac, Rachel Perron, Chris
Idelson and Megan Sabo to this study. This research was supported by the
intramural research programs of the National Heart, Lung, and Blood
Institute and the National Institute of Diabetes, and Digestive and
Kidney Diseases, National Institutes of Health.
NR 32
TC 2
Z9 2
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
EI 1476-5497
J9 INT J OBESITY
JI Int. J. Obes.
PD DEC
PY 2013
VL 37
IS 12
BP 1560
EP 1564
DI 10.1038/ijo.2013.45
PG 5
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 272JJ
UT WOS:000328456200007
PM 23609936
ER
PT J
AU Hall, KD
Chow, CC
AF Hall, K. D.
Chow, C. C.
TI Why is the 3500 kcal per pound weight loss rule wrong?
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Letter
C1 [Hall, K. D.; Chow, C. C.] Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA.
RP Hall, KD (reprint author), Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA.
EM kevinh@niddk.nih.gov
FU Intramural NIH HHS [ZIA DK013022-09]
NR 6
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 0307-0565
EI 1476-5497
J9 INT J OBESITY
JI Int. J. Obes.
PD DEC
PY 2013
VL 37
IS 12
BP 1614
EP 1614
DI 10.1038/ijo.2013.112
PG 1
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 272JJ
UT WOS:000328456200017
PM 23774459
ER
PT J
AU Agarwal, N
AF Agarwal, Neeraj
TI RGC-5 Cells
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Letter
ID RETINAL GANGLION-CELLS; LINE; DEATH; DIFFERENTIATION; EXPRESSION; MICE
C1 NEI, NIH, Div Extramural Res, Rockville, MD USA.
RP Agarwal, N (reprint author), NEI, NIH, Div Extramural Res, Rockville, MD USA.
EM agarwalnee@nei.nih.gov
NR 21
TC 5
Z9 5
U1 0
U2 3
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD DEC
PY 2013
VL 54
IS 13
BP 7884
EP 7884
DI 10.1167/iovs.13-13292
PG 1
WC Ophthalmology
SC Ophthalmology
GA 267YH
UT WOS:000328133800007
ER
PT J
AU Pogue-Geile, KL
Kim, C
Jeong, JH
Tanaka, N
Bandos, H
Gavin, PG
Fumagalli, D
Goldstein, LC
Sneige, N
Burandt, E
Taniyama, Y
Bohn, OL
Lee, A
Kim, SI
Reilly, ML
Remillard, MY
Blackmon, NL
Kim, SR
Horne, ZD
Rastogi, P
Fehrenbacher, L
Romond, EH
Swain, SM
Mamounas, EP
Wickerham, DL
Geyer, CE
Costantino, JP
Wolmark, N
Paik, S
AF Pogue-Geile, Katherine L.
Kim, Chungyeul
Jeong, Jong-Hyeon
Tanaka, Noriko
Bandos, Hanna
Gavin, Patrick G.
Fumagalli, Debora
Goldstein, Lynn C.
Sneige, Nour
Burandt, Eike
Taniyama, Yusuke
Bohn, Olga L.
Lee, Ahwon
Kim, Seung-Il
Reilly, Megan L.
Remillard, Matthew Y.
Blackmon, Nicole L.
Kim, Seong-Rim
Horne, Zachary D.
Rastogi, Priya
Fehrenbacher, Louis
Romond, Edward H.
Swain, Sandra M.
Mamounas, Eleftherios P.
Wickerham, D. Lawrence
Geyer, Charles E., Jr.
Costantino, Joseph P.
Wolmark, Norman
Paik, Soonmyung
TI Predicting Degree of Benefit From Adjuvant Trastuzumab in NSABP Trial
B-31
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID HER2-POSITIVE BREAST-CANCER; FACTOR-I RECEPTOR; CHEMOTHERAPY;
EXPRESSION; RESISTANCE; PLUS; HER2; HERCEPTIN; TAMOXIFEN; ANTIBODY
AB National Surgical Adjuvant Breast and Bowel Project (NSABP) trial B-31 suggested the efficacy of adjuvant trastuzumab, even in HER2-negative breast cancer. This finding prompted us to develop a predictive model for degree of benefit from trastuzumab using archived tumor blocks from B-31.
Case subjects with tumor blocks were randomly divided into discovery (n 588) and confirmation cohorts (n 991). A predictive model was built from the discovery cohort through gene expression profiling of 462 genes with nCounter assay. A predefined cut point for the predictive model was tested in the confirmation cohort. Gene-by-treatment interaction was tested with Cox models, and correlations between variables were assessed with Spearman correlation. Principal component analysis was performed on the final set of selected genes. All statistical tests were two-sided.
Eight predictive genes associated with HER2 (ERBB2, c17orf37, GRB7) or ER (ESR1, NAT1, GATA3, CA12, IGF1R) were selected for model building. Three-dimensional subset treatment effect pattern plot using two principal components of these genes was used to identify a subset with no benefit from trastuzumab, characterized by intermediate-level ERBB2 and high-level ESR1 mRNA expression. In the confirmation set, the predefined cut points for this model classified patients into three subsets with differential benefit from trastuzumab with hazard ratios of 1.58 (95% confidence interval [CI] 0.67 to 3.69; P .29; n 100), 0.60 (95% CI 0.41 to 0.89; P .01; n 449), and 0.28 (95% CI 0.20 to 0.41; P < .001; n 442; P-interaction between the model and trastuzumab < .001).
We developed a gene expressionbased predictive model for degree of benefit from trastuzumab and demonstrated that HER2-negative tumors belong to the moderate benefit group, thus providing justification for testing trastuzumab in HER2-negative patients (NSABP B-47).
C1 [Jeong, Jong-Hyeon; Bandos, Hanna; Rastogi, Priya; Fehrenbacher, Louis; Romond, Edward H.; Swain, Sandra M.; Mamounas, Eleftherios P.; Wickerham, D. Lawrence; Geyer, Charles E., Jr.; Costantino, Joseph P.; Wolmark, Norman; Paik, Soonmyung] Natl Surg Adjuvant Breast & Bowel Project Operat, Pittsburgh, PA USA.
[Jeong, Jong-Hyeon; Bandos, Hanna; Rastogi, Priya; Fehrenbacher, Louis; Romond, Edward H.; Swain, Sandra M.; Mamounas, Eleftherios P.; Wickerham, D. Lawrence; Geyer, Charles E., Jr.; Costantino, Joseph P.; Wolmark, Norman; Paik, Soonmyung] Natl Surg Adjuvant Breast & Bowel Project Biostat, Pittsburgh, PA USA.
[Pogue-Geile, Katherine L.; Kim, Chungyeul; Tanaka, Noriko; Gavin, Patrick G.; Fumagalli, Debora; Taniyama, Yusuke; Bohn, Olga L.; Lee, Ahwon; Kim, Seung-Il; Reilly, Megan L.; Remillard, Matthew Y.; Blackmon, Nicole L.; Kim, Seong-Rim; Horne, Zachary D.] NSABP, Div Pathol, Pittsburgh, PA 15212 USA.
[Jeong, Jong-Hyeon; Bandos, Hanna; Costantino, Joseph P.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
[Goldstein, Lynn C.] PLLC, PhenoPath Labs, Seattle, WA USA.
[Sneige, Nour] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
[Burandt, Eike] Univ Canc Ctr, Univ Med Ctr Hamburg Eppendorf, Dept Pathol, Hamburg, Germany.
[Lee, Ahwon] Catholic Univ Korea, Dept Pathol, Seoul, South Korea.
[Rastogi, Priya] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[Fehrenbacher, Louis] Kaiser Permanente No Calif, Dept Oncol, Vallejo, CA USA.
[Romond, Edward H.] Univ Kentucky, Markey Canc Ctr, Dept Internal Med, Lexington, KY USA.
[Swain, Sandra M.] MedStar Washington Hosp Ctr, Washington Canc Inst, Dept Med, Washington, DC USA.
[Mamounas, Eleftherios P.] MD Anderson Canc Ctr, Dept Surg, Orlando, FL USA.
[Geyer, Charles E., Jr.] Virginia Commonwealth Univ, Dept Med, Richmond, VA 23298 USA.
[Wickerham, D. Lawrence; Wolmark, Norman] Allegheny Gen Hosp, Dept Surg, Allegheny Canc Ctr, Pittsburgh, PA 15212 USA.
[Paik, Soonmyung] Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Dept Biomed Sci, Seoul, South Korea.
[Paik, Soonmyung] Yonsei Univ, Coll Med, Yonsei Canc Ctr, Dept Oncol, Seoul, South Korea.
RP Paik, S (reprint author), NSABP, Div Pathol, 1307 Fed St,Ste 303, Pittsburgh, PA 15212 USA.
EM soon.paik@nsabp.org
OI kim, chungyeul/0000-0002-9636-5228; Jeong, Jong/0000-0003-0596-2201
FU National Cancer Institute, Department of Health and Human Services,
Public Health Service [U10-CA-12027, U10-CA-69651, U10-CA-37377,
U10-CA-69974]; Pennsylvania Department of Health
FX This work was supported by the National Cancer Institute, Department of
Health and Human Services, Public Health Service (grants U10-CA-12027,
U10-CA-69651, U10-CA-37377, and U10-CA-69974) and by a grant from the
Pennsylvania Department of Health. The latter Department specifically
disclaims responsibility for any analysis, interpretations, or
conclusions.
NR 22
TC 37
Z9 39
U1 1
U2 14
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD DEC
PY 2013
VL 105
IS 23
BP 1782
EP 1788
DI 10.1093/jnci/djt321
PG 7
WC Oncology
SC Oncology
GA 271DE
UT WOS:000328370000007
PM 24262440
ER
PT J
AU Rutter, CM
Johnson, EA
Feuer, EJ
Knudsen, AB
Kuntz, KM
Schrag, D
AF Rutter, Carolyn M.
Johnson, Eric A.
Feuer, Eric J.
Knudsen, Amy B.
Kuntz, Karen M.
Schrag, Deborah
TI Secular Trends in Colon and Rectal Cancer Relative Survival
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; FECAL-OCCULT-BLOOD; RANDOMIZED
CONTROLLED-TRIAL; ADJUVANT THERAPY; UNITED-STATES; MORTALITY;
METAANALYSIS; FLUOROURACIL; CHEMOTHERAPY; POPULATIONS
AB Treatment options for colorectal cancer (CRC) have improved substantially over the past 25 years. Measuring the impact of these improvements on survival outcomes is challenging, however, against the background of overall survival gains from advancements in the prevention, screening, and treatment of other conditions. Relative survival is a metric that accounts for these concurrent changes, allowing assessment of changes in CRC survival. We describe stage- and location-specific trends in relative survival after CRC diagnosis.
We analyzed survival outcomes for 233965 people in the Surveillance Epidemiology and End Results (SEER) program who were diagnosed with CRC between January 1, 1975, and December 31, 2003. All models were adjusted for sex, race (black vs white), age at diagnosis, time since diagnosis, and diagnosis year. We estimated the proportional difference in survival for CRC patients compared with overall survival for age-, sex-, race-, and period-matched controls to account for concurrent changes in overall survival using two-sided Wald tests.
We found statistically significant reductions in excess hazard of mortality from CRC in 2003 relative to 1975, with excess hazard ratios ranging from 0.75 (stage IV colon cancer; P < .001) to 0.32 (stage I rectal cancer; P < .001), indicating improvements in relative survival for all stages and cancer locations. These improvements occurred in earlier years for patients diagnosed with stage I cancers, with smaller but continuing improvements for later-stage cancers.
Our results demonstrate a steady trend toward improved relative survival for CRC, indicating that treatment and surveillance improvements have had an impact at the population level.
C1 [Rutter, Carolyn M.; Johnson, Eric A.] Grp Hlth Res Inst, Seattle, WA 98101 USA.
[Feuer, Eric J.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Knudsen, Amy B.] Massachusetts Gen Hosp, Inst Technol Assessment, Dept Radiol, Boston, MA 02114 USA.
[Kuntz, Karen M.] Univ Minnesota, Sch Publ Hlth, Div Hlth Policy & Management, Minneapolis, MN USA.
[Schrag, Deborah] Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA.
RP Rutter, CM (reprint author), Grp Hlth Res Inst, 1730 Minor Ave,Ste 1600, Seattle, WA 98101 USA.
EM rutter.c@ghc.org
FU National Cancer Institute of the National Institutes of Health
[U01CA52959]
FX Research reported in this publication was supported by the National
Cancer Institute of the National Institutes of Health under award No.
U01CA52959.
NR 44
TC 17
Z9 17
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD DEC
PY 2013
VL 105
IS 23
BP 1806
EP 1813
DI 10.1093/jnci/djt299
PG 8
WC Oncology
SC Oncology
GA 271DE
UT WOS:000328370000010
PM 24174654
ER
PT J
AU Brown, DA
Lamb, ME
Lewis, C
Pipe, ME
Orbach, Y
Wolfman, M
AF Brown, Deirdre A.
Lamb, Michael E.
Lewis, Charlie
Pipe, Margaret-Ellen
Orbach, Yael
Wolfman, Missy
TI The NICHD Investigative Interview Protocol: An Analogue Study
SO JOURNAL OF EXPERIMENTAL PSYCHOLOGY-APPLIED
LA English
DT Article
DE children's memory; eyewitness testimony; forensic interviews;
interviewing protocols; suggestibility
ID CHILD SEXUAL-ABUSE; NARRATIVE ELABORATION; FORENSIC INTERVIEWS;
COGNITIVE INTERVIEW; ALLEGED VICTIMS; QUESTION FORMAT; EVENT MEMORY;
RECALL; PRESCHOOLERS; WITNESSES
AB One hundred twenty-eight 5-to 7-year-old children were interviewed using the National Institute of Child Health and Human Development (NICHD) Investigative Interview Protocol about an event staged 4 to 6 weeks earlier. Children were prepared for talking about the investigated event using either an invitational or directive style of prompting, with or without additional practice describing experienced events. The open invitation prompts (including those using children's words to encourage further reporting) elicited more detailed responses than the more focused directive prompts without reducing accuracy. Children were most responsive when they had received preparation that included practice describing experienced events in response to invitation prompts. Overall, children were highly accurate regardless of prompt type. Errors mostly related to peripheral rather than central information and were more likely to be elicited by directive or yes/no questions than by invitations. Children who provided accounts when asked about a false event were less accurate when describing the true event. Children who received preparation that included practice recalling a recent event in response to directive and yes/no questions were least accurate when questioned about the false event first. The data provide the first direct evaluation of the accuracy of information elicited using different prompt types in the course of NICHD Protocol interviews, and underscore the importance of how children are prepared for subsequent reporting.
C1 [Brown, Deirdre A.; Lewis, Charlie] Univ Lancaster, Dept Psychol, Lancaster LA1 4YF, Lancs, England.
[Lamb, Michael E.] Univ Cambridge, Dept Psychol, Cambridge, England.
[Pipe, Margaret-Ellen] CUNY Brooklyn Coll, Dept Psychol, Brooklyn, NY 11210 USA.
[Orbach, Yael] NICHHD, Bethesda, MD 20892 USA.
[Brown, Deirdre A.; Wolfman, Missy] Victoria Univ Wellington, Sch Psychol, Wellington 6012, New Zealand.
RP Brown, DA (reprint author), Victoria Univ Wellington, Sch Psychol, POB 600, Wellington 6012, New Zealand.
EM Deirdre.Brown@vuw.ac.nz
NR 78
TC 16
Z9 16
U1 2
U2 17
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1076-898X
EI 1939-2192
J9 J EXP PSYCHOL-APPL
JI J. Exp. Psychol.-Appl.
PD DEC
PY 2013
VL 19
IS 4
BP 367
EP 382
DI 10.1037/a0035143
PG 16
WC Psychology, Applied
SC Psychology
GA 277KH
UT WOS:000328817200008
PM 24341318
ER
PT J
AU Ghedin, E
Rogers, MB
Widen, SG
Guzman, H
da Rosa, APAT
Wood, TG
Fitch, A
Popov, V
Holmes, EC
Walker, PJ
Vasilakis, N
Tesh, RB
AF Ghedin, Elodie
Rogers, Matthew B.
Widen, Steven G.
Guzman, Hilda
da Rosa, Amelia P. A. Travassos
Wood, Thomas G.
Fitch, Adam
Popov, Vsevolod
Holmes, Edward C.
Walker, Peter J.
Vasilakis, Nikos
Tesh, Robert B.
TI Kolente virus, a rhabdovirus species isolated from Communication ticks
and bats in the Republic of Guinea
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID VESICULAR STOMATITIS-VIRUS; PHYLOGENETIC-RELATIONSHIPS; GENOMIC
CHARACTERIZATION; PHLEBOTOMINE SANDFLIES; BORNE VIRUSES; SEQUENCE; GENE;
PROTEIN; VERTEBRATES; LYSSAVIRUS
AB Kolente virus (KOLEV) is a rhabdovirus originally isolated from ticks and a bat in Guinea, West Africa, in 1985. Although tests at the time of isolation suggested that KOLEV is a novel rhabdovirus, it has remained largely uncharacterized. We assembled the complete genome sequence of the prototype strain DakAr K7292, which was found to encode the five canonical rhabdovirus structural proteins (N, P, M, G and L) with alternative ORFs (>180 nt) in the P and L genes. Serologically, KOLEV exhibited a weak antigenic relationship with Barur and Fukuoka viruses in the Kern Canyon group. Phylogenetic analysis revealed that KOLEV represents a distinct and divergent lineage that shows no clear relationship to any rhabdovirus except Oita virus, although with limited phylogenetic resolution. In summary, KOLEV represents a novel species in the family Rhabdoyiridae.
C1 [Ghedin, Elodie; Rogers, Matthew B.; Fitch, Adam] Univ Pittsburgh, Sch Med, Dept Computat & Syst Biol, Ctr Vaccine Res, Pittsburgh, PA USA.
[Widen, Steven G.; Wood, Thomas G.] Univ Texas Med Branch, Dept Biochem, Galveston, TX 77555 USA.
[Guzman, Hilda; da Rosa, Amelia P. A. Travassos; Popov, Vsevolod; Vasilakis, Nikos; Tesh, Robert B.] Univ Texas Med Branch, Ctr Biodef & Emerging Infect Dis, Galveston, TX 77555 USA.
[Guzman, Hilda; da Rosa, Amelia P. A. Travassos; Popov, Vsevolod; Vasilakis, Nikos; Tesh, Robert B.] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
[Popov, Vsevolod; Vasilakis, Nikos; Tesh, Robert B.] Univ Texas Med Branch, Ctr Trop Dis, Galveston, TX 77555 USA.
[Popov, Vsevolod; Vasilakis, Nikos; Tesh, Robert B.] Univ Texas Med Branch, Inst Human Infect & Immun, Galveston, TX 77555 USA.
[Holmes, Edward C.] Univ Sydney, Sch Biol Sci, Sydney Emerging Infect & Biosecur Inst, Sydney, NSW 2006, Australia.
[Holmes, Edward C.] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Walker, Peter J.] CSIRO Anim Food & Hlth Sci, Australian Anim Hlth Lab, Geelong, Vic 3220, Australia.
RP Vasilakis, N (reprint author), Univ Texas Med Branch, Ctr Biodef & Emerging Infect Dis, Galveston, TX 77555 USA.
EM nivasila@utmb.edu
RI Walker, Peter/H-6059-2013
OI Walker, Peter/0000-0003-1851-642X
FU Department of Pathology; Institute for Human Infections and Immunity,
University of Texas Medical Branch, NIH
[HHSN272201000040I/HHSN27200004/D04]; NHMRC Australia Fellowship
FX This work was supported in part by the Department of Pathology start-up
funds and a grant from the Institute for Human Infections and Immunity,
University of Texas Medical Branch (NV), NIH contract
HHSN272201000040I/HHSN27200004/D04 (R. B. T.). E. C. H. is supported by
an NHMRC Australia Fellowship.
NR 40
TC 10
Z9 10
U1 0
U2 5
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
EI 1465-2099
J9 J GEN VIROL
JI J. Gen. Virol.
PD DEC
PY 2013
VL 94
BP 2609
EP 2615
DI 10.1099/vir.0.055939-0
PN 12
PG 7
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 277GW
UT WOS:000328808000003
PM 24062532
ER
PT J
AU Koscso, B
Csoka, B
Kokai, E
Nemeth, ZH
Pacher, P
Virag, L
Leibovich, SJ
Hasko, G
AF Koscso, Balazs
Csoka, Balazs
Kokai, Endre
Nemeth, Zoltan H.
Pacher, Pal
Virag, Laszlo
Leibovich, S. Joseph
Hasko, Gyoergy
TI Adenosine augments IL-10-induced STAT3 signaling in M2c macrophages
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE arginase; TIMP-1; alternative activation
ID NECROSIS-FACTOR-ALPHA; IL-10 PRODUCTION; RECEPTOR AGONISTS; TIMP-1
PRODUCTION; TNF-ALPHA; A(2B); INFLAMMATION; ACTIVATION; CELLS;
EXPRESSION
AB Adenosine signaling augments IL-10-induced STAT-3 dependent gene expression in macrophages, suggesting its role in M2c polarization. The alternatively activated macrophage phenotype induced by IL-10 is called M2c. Adenosine is an endogenous purine nucleoside that accumulates in the extracellular space in response to metabolic disturbances, hypoxia, inflammation, physical damage, or apoptosis. As adenosine is known to regulate classically activated M1 and IL4- and IL-13-activated M2a macrophages, the goal of the present study was to explore its effects on M2c macrophages. We found that adenosine augmented the IL-10-induced expression of TIMP-1 and arginase-1 by the mouse macrophage cell line RAW 264.7 and by mouse BMDMs. The effects of AR stimulation on IL-10-induced TIMP-1 or arginase-1 expression were lacking in A(2B)AR KO macrophages. The role of A(2B)AR on TIMP-1 production of RAW 264.7 cells was confirmed with specific agonist BAY606583 and antagonist PSB0788. AR stimulation augmented IL-10-induced STAT3 phosphorylation in macrophages, and pharmacological inhibition or silencing of STAT3 using siRNA reduced the stimulatory effect of AR stimulation on TIMP-1 production. In contrast to its stimulatory effect on IL-10-induced STAT3 activation, adenosine inhibited IL-6-induced STAT3 phosphorylation and SAA3 expression. In conclusion, adenosine enhances IL-10-induced STAT3 signaling and M2c macrophage activation.
C1 [Koscso, Balazs; Csoka, Balazs; Kokai, Endre; Hasko, Gyoergy] Rutgers New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA.
[Leibovich, S. Joseph] Rutgers New Jersey Med Sch, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA.
[Hasko, Gyoergy] Rutgers New Jersey Med Sch, Ctr Immun & Inflammat, Newark, NJ 07103 USA.
[Nemeth, Zoltan H.] Morristown Med Ctr, Dept Surg, Morristown, NJ USA.
[Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, Bethesda, MD USA.
[Kokai, Endre; Virag, Laszlo; Hasko, Gyoergy] Univ Debrecen, Dept Med Chem, Debrecen, Hungary.
[Kokai, Endre; Virag, Laszlo; Hasko, Gyoergy] Univ Debrecen, Med & Hlth Sci Ctr, Debrecen, Hungary.
RP Hasko, G (reprint author), Rutgers New Jersey Med Sch, Dept Surg, 185 S Orange Ave, Newark, NJ 07103 USA.
EM haskoge@njms.rutgers.edu
RI Pacher, Pal/B-6378-2008;
OI Pacher, Pal/0000-0001-7036-8108; Csoka, Balazs/0000-0002-7562-1130
FU U.S. National Institutes of Health [R01GM66189, R01GM068636]; U.S. Army
Medical Research and Materiel Command [09065004]; Hungarian Scientific
Research Fund (OTKA) [K 109178]; Hungarian Scientific Research Fund
grant [Human MB08-1-2011-0015, OTKA 84685]
FX This work was supported by the U.S. National Institutes of Health grants
R01GM66189 and R01GM068636, U.S. Army Medical Research and Materiel
Command Grant 09065004, and Hungarian Scientific Research Fund (OTKA)
grant K 109178 to G. H. and by a Hungarian Scientific Research Fund
grant (Human MB08-1-2011-0015; OTKA 84685) to E.K.
NR 53
TC 22
Z9 25
U1 1
U2 13
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
EI 1938-3673
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD DEC
PY 2013
VL 94
IS 6
BP 1309
EP 1315
DI 10.1189/jlb.0113043
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 275NH
UT WOS:000328683600022
PM 23922379
ER
PT J
AU Tae, HJ
Kim, JM
Park, S
Tomiya, N
Li, G
Wei, W
Petrashevskaya, N
Ahmet, I
Pang, J
Cruschwitz, S
Riebe, RA
Zhang, YH
Morrell, CH
Browe, D
Lee, YC
Xiao, RP
Talan, MI
Lakatta, EG
Lin, L
AF Tae, Hyun-Jin
Kim, Ji Min
Park, Sungha
Tomiya, Noboru
Li, Geng
Wei, Wen
Petrashevskaya, Natalia
Ahmet, Ismayil
Pang, John
Cruschwitz, Stefanie
Riebe, Rebecca A.
Zhang, Yinghua
Morrell, Christopher H.
Browe, David
Lee, Yuan Chuan
Xiao, Rui-ping
Talan, Mark I.
Lakatta, Edward G.
Lin, Li
TI The N-glycoform of sRAGE is the key determinant for its therapeutic
efficacy to attenuate injury-elicited arterial inflammation and
neointimal growth
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Article
DE sRAGE; N-glycoform; Arterial injury; Arterial inflammation; Neointimal
hyperplasia; Therapeutic window
ID GLYCATION END-PRODUCTS; VASCULAR ENDOTHELIAL-CELLS; SMOOTH-MUSCLE-CELLS;
MYOCARDIAL-INFARCTION; RECEPTOR; RAGE; PROTEINS; BINDING; GLYCOSYLATION;
EXPRESSION
AB Signaling of the receptor for advanced glycation end products (RAGE) has been implicated in the development of injury-elicited vascular complications. Soluble RAGE (sRAGE) acts as a decoy of RAGE and has been used to treat pathological vascular conditions in animal models. However, previous studies used a high dose of sRAGE produced in insect Sf9 cells (sRAGE(Sf9))and multiple injections to achieve the therapeutic outcome. Here, we explore whether modulation of sRAGE N-glycoform impacts its bioactivity and augments its therapeutic efficacy. We first profiled carbohydrate components of sRAGE produced in Chinese hamster Ovary cells (sRAGE(CHO)) to show that a majority of its N-glycans belong to sialylated complex types that are not shared by sRAGE(Sf9). In cell-based NF-kappa B activation and vascular smooth muscle cell (VSMC) migration assays, sRAGE(CHO) exhibited a significantly higher bioactivity relative to sRAGE(Sf9) to inhibit RAGE alarmin ligand-induced NF-kappa B activation and VSMC migration. We next studied whether this N-glycoform-associated bioactivity of sRAGE(CHO) is translated to higher in vivo therapeutic efficacy in a rat carotid artery balloon injury model. Consistent with the observed higher bioactivity in cell assays, sRAGE(CHO) significantly reduced injury-induced neointimal growth and the expression of inflammatory markers in injured vasculature. Specifically, a single dose of 3 ng/g of sRAGE(CHO) reduced neointimal hyperplasia by over 70 %, whereas the same dose of sRAGE(Sf9) showed no effect. The administered sRAGE(CHO) is rapidly and specifically recruited to the injured arterial locus, suggesting that early intervention of arterial injury with sRAGE(CHO) may offset an inflammatory circuit and reduce the ensuing tissue remodeling. Our findings showed that the N-glycoform of sRAGE is the key determinant underlying its bioactivity and thus is an important glycobioengineering target to develop a highly potent therapeutic sRAGE for future clinical applications.
Key message
The specific N-glycoform modification is the key underlying sRAGE bioactivity
Markedly reduced sRAGE dose to attenuate neointimal hyperplasia and inflammation
Provide a molecular target for glycobioengineering of sRAGE as a therapeutic protein
Blocking RAGE alarmin ligands during acute injury phase offsets neointimal growth.
C1 [Tae, Hyun-Jin; Kim, Ji Min; Park, Sungha; Wei, Wen; Petrashevskaya, Natalia; Ahmet, Ismayil; Pang, John; Cruschwitz, Stefanie; Riebe, Rebecca A.; Morrell, Christopher H.; Browe, David; Xiao, Rui-ping; Talan, Mark I.; Lakatta, Edward G.; Lin, Li] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
[Tae, Hyun-Jin] Hallym Univ, Dept Biomed Sci, Chunchon, South Korea.
[Tae, Hyun-Jin] Hallym Univ, Res Inst Biosci & Biotechnol, Chunchon, South Korea.
[Park, Sungha] Yonsei Univ, Coll Med, Ctr Cardiovasc, Div Cardiol, Seoul 120749, South Korea.
[Tomiya, Noboru; Lee, Yuan Chuan] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
[Li, Geng; Xiao, Rui-ping] Peking Univ, Inst Mol Med, Beijing 100871, Peoples R China.
[Zhang, Yinghua] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
[Morrell, Christopher H.] Loyola Univ, Dept Math & Stat, Baltimore, MD USA.
RP Lin, L (reprint author), NIA, Cardiovasc Sci Lab, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM linli@mail.nih.gov
FU NIH, National Institute on Aging; Korea Research Foundation
[KRF-2009-013-E00008]; Oak Ridge Institute for Science and Education's
Research Associates Program at NIH; Johns Hopkins "Excellent in Medical
Student Research Award"; NIH
FX We thank Robert Monticone for rat VSMCs and advice on cell migration
assays. We also thank reviewers of this manuscript for their inputs that
improve our work. The work was supported by the intramural research
program of the NIH, National Institute on Aging (LL, MIT, RPX, and EGL),
and the Korea Research Foundation grant KRF-2009-013-E00008 (SP). WW was
supported in part by the Oak Ridge Institute for Science and Education's
Research Associates Program at NIH; JP was a recipient of the 2011 Johns
Hopkins "Excellent in Medical Student Research Award"; and RAR and DB
were supported by intramural research training awards from NIH.
NR 42
TC 7
Z9 8
U1 0
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD DEC
PY 2013
VL 91
IS 12
BP 1369
EP 1381
DI 10.1007/s00109-013-1091-4
PG 13
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA 255NL
UT WOS:000327246700005
PM 24132651
ER
PT J
AU Liang, JR
Ito, Y
Zhang, XX
He, J
Sun, WJ
AF Liang, Jinru
Ito, Yoichiro
Zhang, Xinxin
He, Jiao
Sun, Wenji
TI Rapid preparative separation of six bioactive compounds from Gentiana
crassicaulis Duthie ex Burk. using microwave-assisted extraction coupled
with high-speed counter-current chromatography
SO JOURNAL OF SEPARATION SCIENCE
LA English
DT Article
DE Gentiana crassicaulis Duthie ex Burk; High-speed counter-current
chromatography; Microwave-assisted extraction; Quadrupole TOF MS;
Response surface methodology
ID RESPONSE-SURFACE METHODOLOGY; OPTIMIZATION; GLYCOSIDES; PURIFICATION
AB A rapid method combining microwave-assisted extraction (MAE) and high-speed counter-current chromatography (HSCCC) was applied for preparative separation of six bioactive compounds including loganic acid (I), isoorientin-4-O-glucoside (II), 6-O--d-glucopyranosyl gentiopicroside (III), swertiamarin (IV), gentiopicroside (V), sweroside (VI) from traditional Tibetan medicine Gentiana crassicaulisDuthie ex Burk. MAE parameters were predicted by central composite design response surface methodology. That is, 5.0 g dried roots of G. crassicaulis were extracted with 50 mL 57.5% aqueous ethanol under 630 W for 3.39 min. The extract (gentian total glycosides) was separated by HSCCC with n-butanol/ethyl acetate/methanol/1% acetic acid water (7.5:0.5:0.5:3.5, v/v/v/v) using upper phase mobile in tail-to-head elution mode. 16.3, 8.8, 12., 25.1, 40.7, and 21.8 mg of compounds I-VI were obtained with high purities in one run from 500 mg of original sample. The purities and identities of separated components were confirmed using HPLC with photo diode array detection and quadrupole TOF-MS and NMR spectroscopy. The study reveals that response surface methodology is convenient and highly predictive for optimizing extraction process, MAE coupled with HSCCC could be an expeditious method for extraction and separation of phytochemicals from ethnomedicine.
C1 [Liang, Jinru; Zhang, Xinxin; He, Jiao; Sun, Wenji] NW Univ Xian, Biomed Key Lab Shaanxi Prov, Xian 710069, Peoples R China.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Sun, WJ (reprint author), NW Univ Xian, Biomed Key Lab Shaanxi Prov, 229 Taibai North Rd, Xian 710069, Peoples R China.
EM cxbml@nwu.edu.cn
FU Northwest University [PR12079]
FX Financial support from Funds of scientific research launched project of
Northwest University (PR12079) is gratefully acknowledged.
NR 28
TC 10
Z9 10
U1 4
U2 58
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA BOSCHSTRASSE 12, D-69469 WEINHEIM, GERMANY
SN 1615-9306
EI 1615-9314
J9 J SEP SCI
JI J. Sep. Sci.
PD DEC
PY 2013
VL 36
IS 24
BP 3934
EP 3940
DI 10.1002/jssc.201300897
PG 7
WC Chemistry, Analytical
SC Chemistry
GA 267ZW
UT WOS:000328138200017
PM 24151213
ER
PT J
AU Dy, SM
Pfoh, ER
Salive, ME
Boyd, CM
AF Dy, Sydney M.
Pfoh, Elizabeth R.
Salive, Marcel E.
Boyd, Cynthia M.
TI Health-Related Quality of Life and Functional Status Quality Indicators
for Older Persons with Multiple Chronic Conditions
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE multiple chronic conditions; quality indicators; quality measurement;
functional status; health-related quality of life
ID PRIMARY-CARE; MULTIMORBIDITY
AB ObjectivesTo explore central challenges with translating self-reported measurement tools for functional status and health-related quality of life (HRQOL) into ambulatory quality indicators for older people with multiple chronic conditions (MCCs).
DesignReview.
SettingSources including the National Quality Measures Clearinghouse and National Quality Forum were reviewed for existing ambulatory quality indicators relevant to functional status, HRQOL, and people with MCCs.
ParticipantsSeven informants with expertise in indicators using functional status and HRQOL.
MeasurementsInformant interviews were conducted to explore knowledge about these types of indicators, particularly usability and feasibility.
ResultsNine important existing indicators were identified in the review. For process, identified indicators addressed whether providers assessed functional status; outcome indicators addressed quality of life. In interviews, informants agreed that indicators using self-reported data were important in this population. Challenges identified included concerns about usability due to inability to discriminate quality of care adequately between organizations and feasibility concerns regarding high data collection burden, with a correspondingly low response rate. Validity was also a concern because evidence is mixed that healthcare interventions can improve HRQOL or functional status for this population. As a possible first step, a structural standard could be systematic collection of these measures in a specific setting.
ConclusionAlthough functional status and HRQOL are important outcomes for older people with MCCs, few relevant ambulatory quality indicators exist, and there are concerns with usability, feasibility, and validity. Further research is needed on how best to incorporate these outcomes into quality indicators for people with MCCs.
C1 [Dy, Sydney M.; Pfoh, Elizabeth R.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD 21205 USA.
[Salive, Marcel E.] NIA, Div Geriatr & Clin Gerontol, Bethesda, MD 20892 USA.
[Boyd, Cynthia M.] Johns Hopkins Univ, Dept Med, Sch Med, Baltimore, MD 21205 USA.
RP Dy, SM (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Hlth Policy & Management, Room 609,624 N Broadway, Baltimore, MD 21205 USA.
EM sdy@jhsph.edu
FU National Institute on Aging (NIA); Paul Beeson K23 Program; NIA; AFAR;
Atlantic Philanthropies; Hartford Foundation; Starr Foundation
FX This work was funded by the National Institute on Aging (NIA). Dr. Boyd
was supported by the Paul Beeson K23 Program (NIA/AFAR/Atlantic
Philanthropies/Hartford Foundation/Starr Foundation/Anonymous Donor).
Dr. Dy and Ms Pfoh received contract funding from the NIA, Dr. Boyd
received an honorarium and has grant funding from NIA, and Dr. Salive is
an employee of NIA.
NR 19
TC 5
Z9 7
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
EI 1532-5415
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD DEC
PY 2013
VL 61
IS 12
BP 2120
EP 2127
DI 10.1111/jgs.12555
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 271UB
UT WOS:000328416000008
PM 24320819
ER
PT J
AU Parsa, A
Fuchsberger, C
Kottgen, A
O'Seaghdha, CM
Pattaro, C
de Andrade, M
Chasman, DI
Teumer, A
Endlich, K
Olden, M
Chen, MH
Tin, A
Kim, YJ
Taliun, D
Li, M
Feitosa, M
Gorski, M
Yang, Q
Hundertmark, C
Foster, MC
Glazer, N
Isaacs, A
Rao, M
Smith, AV
O'Connell, JR
Struchalin, M
Tanaka, T
Li, G
Hwang, SJ
Atkinson, EJ
Lohman, K
Cornelis, MC
Johansson, A
Toenjes, A
Dehghan, A
Couraki, V
Holliday, EG
Sorice, R
Kutalik, Z
Lehtimaeki, T
Esko, T
Deshmukh, H
Ulivi, S
Chu, AY
Murgia, F
Trompet, S
Imboden, M
Kollerits, B
Pistis, G
Harris, TB
Launer, LJ
Aspelund, T
Eiriksdottir, G
Mitchell, BD
Boerwinkle, E
Schmidt, H
Hofer, E
Hu, F
Demirkan, A
Oostra, BA
Turner, ST
Ding, J
Andrews, JS
Freedman, BI
Giulianini, F
Koenig, W
Illig, T
Doering, A
Wichmann, HE
Zgaga, L
Zemunik, T
Boban, M
Minelli, C
Wheeler, HE
Igl, W
Zaboli, G
Wild, SH
Wright, AF
Campbell, H
Ellinghaus, D
Noethlings, U
Jacobs, G
Biffar, R
Ernst, F
Homuth, G
Kroemer, HK
Nauck, M
Stracke, S
Voelker, U
Voelzke, H
Kovacs, P
Stumvoll, M
Maegi, R
Hofman, A
Uitterlinden, AG
Rivadeneira, F
Aulchenko, YS
Polasek, O
Hastie, N
Vitart, V
Helmer, C
Wang, JJ
Stengel, B
Ruggiero, D
Bergmann, S
Kaehoenen, M
Viikari, J
Nikopensius, T
Province, M
Colhoun, H
Doney, A
Robino, A
Kraemer, BK
Portas, L
Ford, I
Buckley, BM
Adam, M
Thun, GA
Paulweber, B
Haun, M
Sala, C
Mitchell, P
Ciullo, M
Vollenweider, P
Raitakari, O
Metspalu, A
Palmer, C
Gasparini, P
Pirastu, M
Jukema, JW
Probst-Hensch, NM
Kronenberg, F
Toniolo, D
Gudnason, V
Shuldiner, AR
Coresh, J
Schmidt, R
Ferrucci, L
Van Duijn, CM
Borecki, I
Kardia, SLR
Liu, Y
Curhan, GC
Rudan, I
Gyllensten, U
Wilson, JF
Franke, A
Pramstaller, PP
Rettig, R
Prokopenko, I
Witteman, J
Hayward, C
Ridker, PM
Bochud, M
Heid, IM
Siscovick, DS
Fox, CS
Kao, WL
Boeger, CA
AF Parsa, Afshin
Fuchsberger, Christian
Koettgen, Anna
O'Seaghdha, Conall M.
Pattaro, Cristian
de Andrade, Mariza
Chasman, Daniel I.
Teumer, Alexander
Endlich, Karlhans
Olden, Matthias
Chen, Ming-Huei
Tin, Adrienne
Kim, Young J.
Taliun, Daniel
Li, Man
Feitosa, Mary
Gorski, Mathias
Yang, Qiong
Hundertmark, Claudia
Foster, Meredith C.
Glazer, Nicole
Isaacs, Aaron
Rao, Madhumathi
Smith, Albert V.
O'Connell, Jeffrey R.
Struchalin, Maksim
Tanaka, Toshiko
Li, Guo
Hwang, Shih-Jen
Atkinson, Elizabeth J.
Lohman, Kurt
Cornelis, Marilyn C.
Johansson, Asa
Toenjes, Anke
Dehghan, Abbas
Couraki, Vincent
Holliday, Elizabeth G.
Sorice, Rossella
Kutalik, Zoltan
Lehtimaeki, Terho
Esko, Tonu
Deshmukh, Harshal
Ulivi, Sheila
Chu, Audrey Y.
Murgia, Federico
Trompet, Stella
Imboden, Medea
Kollerits, Barbara
Pistis, Giorgio
Harris, Tamara B.
Launer, Lenore J.
Aspelund, Thor
Eiriksdottir, Gudny
Mitchell, Braxton D.
Boerwinkle, Eric
Schmidt, Helena
Hofer, Edith
Hu, Frank
Demirkan, Ayse
Oostra, Ben A.
Turner, Stephen T.
Ding, Jingzhong
Andrews, Jeanette S.
Freedman, Barry I.
Giulianini, Franco
Koenig, Wolfgang
Illig, Thomas
Doering, Angela
Wichmann, H. -Erich
Zgaga, Lina
Zemunik, Tatijana
Boban, Mladen
Minelli, Cosetta
Wheeler, Heather E.
Igl, Wilmar
Zaboli, Ghazal
Wild, Sarah H.
Wright, Alan F.
Campbell, Harry
Ellinghaus, David
Noethlings, Ute
Jacobs, Gunnar
Biffar, Reiner
Ernst, Florian
Homuth, Georg
Kroemer, Heyo K.
Nauck, Matthias
Stracke, Sylvia
Voelker, Uwe
Voelzke, Henry
Kovacs, Peter
Stumvoll, Michael
Maegi, Reedik
Hofman, Albert
Uitterlinden, Andre G.
Rivadeneira, Fernando
Aulchenko, Yurii S.
Polasek, Ozren
Hastie, Nick
Vitart, Veronique
Helmer, Catherine
Wang, Jie Jin
Stengel, Benedicte
Ruggiero, Daniela
Bergmann, Sven
Kaehoenen, Mika
Viikari, Jorma
Nikopensius, Tiit
Province, Michael
Colhoun, Helen
Doney, Alex
Robino, Antonietta
Kraemer, Bernhard K.
Portas, Laura
Ford, Ian
Buckley, Brendan M.
Adam, Martin
Thun, Gian-Andri
Paulweber, Bernhard
Haun, Margot
Sala, Cinzia
Mitchell, Paul
Ciullo, Marina
Vollenweider, Peter
Raitakari, Olli
Metspalu, Andres
Palmer, Colin
Gasparini, Paolo
Pirastu, Mario
Jukema, J. Wouter
Probst-Hensch, Nicole M.
Kronenberg, Florian
Toniolo, Daniela
Gudnason, Vilmundur
Shuldiner, Alan R.
Coresh, Josef
Schmidt, Reinhold
Ferrucci, Luigi
Van Duijn, Cornelia M.
Borecki, Ingrid
Kardia, Sharon L. R.
Liu, Yongmei
Curhan, Gary C.
Rudan, Igor
Gyllensten, Ulf
Wilson, James F.
Franke, Andre
Pramstaller, Peter P.
Rettig, Rainer
Prokopenko, Inga
Witteman, Jacqueline
Hayward, Caroline
Ridker, Paul M.
Bochud, Murielle
Heid, Iris M.
Siscovick, David S.
Fox, Caroline S.
Kao, W. Linda
Boeger, Carsten A.
TI Common Variants in Mendelian Kidney Disease Genes and Their Association
with Renal Function
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID COMMUNITY-BASED POPULATION; BLOOD-PRESSURE; METAANALYSIS; LOCI;
HYPERTENSION; NEPHROPATHY; PROTEINURIA; PROGRESSION; PREDICTORS;
ADJUSTMENT
AB Many common genetic variants identified by genome-wide association studies for complex traits map to genes previously linked to rare inherited Mendelian disorders. A systematic analysis of common single-nucleotide polymorphisms (SNPs) in genes responsible for Mendelian diseases with kidney phenotypes has not been performed. We thus developed a comprehensive database of genes for Mendelian kidney conditions and evaluated the association between common genetic variants within these genes and kidney function in the general population. Using the Online Mendelian Inheritance in Man database, we identified 731 unique disease entries related to specific renal search terms and confirmed a kidney phenotype in 218 of these entries, corresponding to mutations in 258 genes. We interrogated common SNPs (minor allele frequency >5%) within these genes for association with the estimated GFR in 74,354 European-ancestry participants from the CKDGen Consortium. However, the top four candidate SNPs (rs6433115 at LRP2, rs1050700 at TSC1, rs249942 at PALB2, and rs9827843 at ROBO2) did not achieve significance in a stage 2 meta-analysis performed in 56,246 additional independent individuals, indicating that these common SNPs are not associated with estimated GFR. The effect of less common or rare variants in these genes on kidney function in the general population and disease-specific cohorts requires further research.
C1 [Parsa, Afshin] Univ Maryland, Sch Med, Div Nephrol, Baltimore, MD 21201 USA.
[Fuchsberger, Christian] Univ Michigan, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Koettgen, Anna; Hundertmark, Claudia] Freiburg Univ Clin, Div Renal, Freiburg, Germany.
[Koettgen, Anna; Tin, Adrienne; Li, Man; Coresh, Josef; Kao, W. Linda] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[O'Seaghdha, Conall M.; Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[O'Seaghdha, Conall M.; Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] Ctr Populat Studies, Framingham, MA USA.
[O'Seaghdha, Conall M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Nephrol, Boston, MA 02115 USA.
[Pattaro, Cristian; Taliun, Daniel; Minelli, Cosetta; Pramstaller, Peter P.] European Acad Bozen Bolzano, Biomed Ctr, Bolzano, Italy.
[de Andrade, Mariza; Atkinson, Elizabeth J.] Mayo Clin, Div Biomed Stat & Informat, Rochester, MN USA.
[Chasman, Daniel I.; Chu, Audrey Y.; Giulianini, Franco; Ridker, Paul M.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Chasman, Daniel I.; Ridker, Paul M.] Harvard Univ, Sch Med, Boston, MA USA.
[Teumer, Alexander; Campbell, Harry; Ellinghaus, David; Ernst, Florian; Homuth, Georg; Voelker, Uwe] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[Endlich, Karlhans] Ernst Moritz Arndt Univ Greifswald, Inst Anat & Cell Biol, Greifswald, Germany.
[Olden, Matthias; Gorski, Mathias; Boeger, Carsten A.] Univ Hosp Regensburg, Div Nephrol, Dept Internal Med 2, Regensburg, Germany.
[Olden, Matthias; Heid, Iris M.] Univ Regensburg, Inst Epidemlol & Prevent Med, Dept Genet Epidemlol, D-93053 Regensburg, Germany.
[Chen, Ming-Huei] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
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[Smith, Albert V.; Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
[Struchalin, Maksim] Erasmus MC, Dept Epidemiol & Biostat, Rotterdam, Netherlands.
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[Toenjes, Anke; Kovacs, Peter; Stumvoll, Michael] Univ Leipzig, Dept Med, D-04109 Leipzig, Germany.
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[Couraki, Vincent] Inst Pasteur, INSERM, UMR744, F-59019 Lille, France.
[Holliday, Elizabeth G.] Univ Newcastle, Sch Med & Publ Hlth, Ctr Clin Epidemiol & Biostat, Newcastle, NSW 2300, Australia.
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[Sorice, Rossella; Ruggiero, Daniela; Ciullo, Marina] Adriano Buzzati Traverso CNR Inst Genet & Biophys, Naples, Italy.
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[Kutalik, Zoltan; Bergmann, Sven] Swiss Inst Bioinformat, Lausanne, Switzerland.
[Lehtimaeki, Terho] Univ Tampere, Sch Med, Dept Clin Chem, Fimlab Labs, FIN-33101 Tampere, Finland.
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[Murgia, Federico; Portas, Laura; Pirastu, Mario] CNR Inst Populat Genet, Sassari, Italy.
[Trompet, Stella; Jukema, J. Wouter] Leiden Univ Med Ctr, Dept Cardiol, Leiden, Netherlands.
[Imboden, Medea; Adam, Martin; Thun, Gian-Andri; Probst-Hensch, Nicole M.] Swiss Trop & Publ Hlth Inst, Basel, Switzerland.
[Imboden, Medea; Adam, Martin; Thun, Gian-Andri; Probst-Hensch, Nicole M.] Univ Basel, Basel, Switzerland.
[Kollerits, Barbara; Haun, Margot; Kronenberg, Florian] Med Univ Innsbruck, Div Genet Epidemiol, A-6020 Innsbruck, Austria.
[Pistis, Giorgio; Sala, Cinzia; Toniolo, Daniela] Ist Sci San Raffaele, Div Genet & Cell Biol, I-20132 Milan, Italy.
[Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
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[Oostra, Ben A.] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Turner, Stephen T.] Mayo Clin, Dept Internal Med, Div Nephrol & Hypertens, Rochester, MN USA.
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[Koenig, Wolfgang] Univ Ulm, Ulm Univ Clin, Dept Internal Med 2, D-89069 Ulm, Germany.
[Illig, Thomas] Hanover Med Sch, Hanover Unified Biobank, Hanover, NH USA.
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[Wichmann, H. -Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Wichmann, H. -Erich] Grosshadern Clin, Neuherberg, Germany.
[Zgaga, Lina; Rudan, Igor; Wilson, James F.] Univ Edinburgh Med Sch, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
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[Wheeler, Heather E.] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
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[Franke, Andre] Univ Kiel, Inst Clin Mol Biol, Kiel, Germany.
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[Zaboli, Ghazal; Wild, Sarah H.] Univ Kiel, Inst Epidemiol, Kiel, Germany.
[Zaboli, Ghazal] Univ Bonn, Dept Nutr & Food Sci, Bonn, Germany.
[Wright, Alan F.] Ernst Moritz Arndt Univ Greifswald, Clin Prosthodont Dent Gerostomatol & Mat Sci, Greifswald, Germany.
[Noethlings, Ute; Kroemer, Heyo K.] Ernst Moritz Arndt Univ Greifswald, Dept Pharmacol, Greifswald, Germany.
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[Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Greifswald, Germany.
[Maegi, Reedik; Prokopenko, Inga] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Uitterlinden, Andre G.; Rivadeneira, Fernando] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Helmer, Catherine] Univ Bordeaux 2, Inst Publ Hlth, INSERM, U897, F-33076 Bordeaux, France.
[Helmer, Catherine] Univ Bordeaux 2, F-33076 Bordeaux, France.
[Wang, Jie Jin; Mitchell, Paul] Univ Sydney, Westmead Hosp, Westmead Millennium Inst, Ctr Vis Res, Sydney, NSW 2006, Australia.
[Wang, Jie Jin] Univ Melbourne, Ctr Eye Res Australia, East Melbourne, Australia.
[Stengel, Benedicte] INSERM, UMRS 1018, Villejuif, France.
[Stengel, Benedicte] Univ Paris Sud, UMRS 1018, Paris, France.
[Kaehoenen, Mika] Univ Tampere, Sch Med, Tampere Univ Hosp, Dept Clin Physiol, FIN-33101 Tampere, Finland.
[Viikari, Jorma] Univ Turku, Turku Univ Hosp, Dept Med, Turku, Finland.
[Doney, Alex] Ninewells Hosp, Clin Res Ctr, Wellcome Trust Ctr Mol Med, Natl Hlth Serv Tayside, Dundee DD1 9SY, Scotland.
[Kraemer, Bernhard K.] Mannheim Univ Med Ctr, Dept Med 5, Mannheim, Germany.
[Ford, Ian] Univ Glasgow, Robertson Ctr Biostat, Glasgow, Lanark, Scotland.
[Buckley, Brendan M.] Natl Univ Ireland Univ Coll Cork, Dept Pharmacol & Therapeut, Cork, Ireland.
[Paulweber, Bernhard] Paracelsus Med Univ, Dept Internal Med 1, Salzburg, Austria.
[Vollenweider, Peter] Univ Lausanne, Vaudois Univ Hosp Ctr, Dept Internal Med, Lausanne, Switzerland.
[Raitakari, Olli] Turku Univ Hosp, Dept Clin Physiol & Nucl Med, Res Ctr Appl & Prevent Cardiovasc Med, FIN-20520 Turku, Finland.
[Palmer, Colin] Univ Dundee, Ninewells Hosp & Med Sch, Biomed Res Inst, Dundee DD1 9SY, Scotland.
[Jukema, J. Wouter] Interuniv Cardiol Inst Netherlands, Utrecht, Netherlands.
[Jukema, J. Wouter] Einthoven Lab Expt Vasc Med, Leiden, Netherlands.
[Jukema, J. Wouter] Durrer Ctr Cardiogenet Res, Amsterdam, Netherlands.
[Toniolo, Daniela] CNR Inst Mol Genet, Pavia, Italy.
[Shuldiner, Alan R.] Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Baltimore, MD USA.
[Coresh, Josef; Kao, W. Linda] Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Van Duijn, Cornelia M.] Netherlands Genom Initiat, Netherlands Consortium Healthy Aging, Leiden, Netherlands.
[Kardia, Sharon L. R.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Curhan, Gary C.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab, Boston, MA 02115 USA.
[Rettig, Rainer] Ernst Moritz Arndt Univ Greifswald, Inst Physiol, Karlsburg, Germany.
[Prokopenko, Inga] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[Bochud, Murielle] Univ Lausanne, Vaudois Univ Hosp Ctr, Univ Inst Social & Prevent Med, Lausanne, Switzerland.
[Heid, Iris M.] Helmholtz Zentrum Munchen, Inst Genet Epidemiol, Neuherberg, Germany.
[Fox, Caroline S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol, Boston, MA 02115 USA.
RP Parsa, A (reprint author), Univ Maryland, Sch Med, Div Nephrol, 685 W Baltimore St,MSTF 314, Baltimore, MD 21201 USA.
EM aparsa@medicine.umaryland.edu
RI Kronenberg, Florian/B-1736-2008; Aulchenko, Yurii/M-8270-2013; Stengel,
Benedicte/G-5730-2015; Rudan, Igor/I-1467-2012; Smith,
Albert/K-5150-2015; ruggiero, daniela/K-5638-2016; Bochud,
Murielle/A-3981-2010; Hayward, Caroline/M-8818-2016; Ellinghaus,
David/G-4467-2012; Franke, Andre/B-2151-2010; Boban, Mladen/E-2777-2017;
Feitosa, Mary/K-8044-2012; Rivadeneira, Fernando/O-5385-2015;
Prokopenko, Inga/H-3241-2014; Colaus, PsyColaus/K-6607-2013; Nothlings,
Ute/B-2713-2010; Yang, Qiong/G-5438-2014; Aspelund, Thor/C-5983-2008;
Pramstaller, Peter/C-2357-2008; Wang, Jie Jin/P-1499-2014; Mitchell,
Paul/P-1498-2014; HELMER, Catherine/I-6581-2015; Gudnason,
Vilmundur/K-6885-2015; Wilson, James F/A-5704-2009; Polasek,
Ozren/B-6002-2011
OI Mitchell, Braxton/0000-0003-4920-4744; Johansson,
Asa/0000-0002-2915-4498; Bergmann, Sven/0000-0002-6785-9034; Dehghan,
Abbas/0000-0001-6403-016X; Magi, Reedik/0000-0002-2964-6011;
Fuchsberger, Christian/0000-0002-5918-8947; Zgaga,
Lina/0000-0003-4089-9703; Wheeler, Heather/0000-0003-1365-9667; Palmer,
Colin/0000-0002-6415-6560; Colhoun, Helen/0000-0002-8345-3288;
Kronenberg, Florian/0000-0003-2229-1120; Aulchenko,
Yurii/0000-0002-7899-1575; Rudan, Igor/0000-0001-6993-6884; Smith,
Albert/0000-0003-1942-5845; ruggiero, daniela/0000-0003-3898-7827;
Bochud, Murielle/0000-0002-5727-0218; Hayward,
Caroline/0000-0002-9405-9550; Franke, Andre/0000-0003-1530-5811;
Feitosa, Mary/0000-0002-0933-2410; Thun, Gian Andri/0000-0003-4436-3455;
Rivadeneira, Fernando/0000-0001-9435-9441; Prokopenko,
Inga/0000-0003-1624-7457; Aspelund, Thor/0000-0002-7998-5433; Wang, Jie
Jin/0000-0001-9491-4898; HELMER, Catherine/0000-0002-5169-7421;
Gudnason, Vilmundur/0000-0001-5696-0084; Wilson, James
F/0000-0001-5751-9178; Polasek, Ozren/0000-0002-5765-1862
FU National Institutes of Health (NIH) [N01AG12100]; National Institute on
Aging (NIA) Intramural Research Program; Hjartavernd (the Icelandic
Heart Association); Althingi (the Icelandic Parliament); NIH
[R01AG18728, R01HL088119, U01GM07451804, U01HL072515-06, U01-HL084756,
K12RR023250, HHSN268200625226C, HHSN268200782096C]; University of
Maryland (MCRDP); University of Maryland General Clinical Research
Center [M01RR16500]; Baltimore Veterans Affairs Medical Center
Geriatrics Research and Education Clinical Center; Paul Beeson Physician
Faculty Scholars in Aging Program; Austrian Science Fund [P20545P05,
P13180]; National Heart, Lung, and Blood Institute (NHLBI)
[HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
HHSN268201100011C, HHSN268201100012C, R01HL087641, R01HL59367,
R01HL086694]; National Human Genome Research Institute (NHGRI)
[U01HG004402]; NIH Roadmap for Medical Research [UL1RR025005]; NIH; Emmy
Noether programme of the German Research Foundation [K03598/2-1]; NIH
NIA; NHLBI [N01HC85079, N01HC85086, N01HC35129, N01HC15103, N01HC55222,
N01HC75150, N01HC45133, U01HL080295, R01HL087652, 5R01HL08770003,
5R01HL08821502, N01HC25195, R01HL87660, HL043851, HL69757]; National
Center for Research Resources grant [M01RR00425]; National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK) [DK063491];
Netherlands Organization for Scientific Research; Erasmus Medical
Center; Centre for Medical Systems Biology; Netherlands Kidney
Foundation; NIDDK [5R01DK07568102, 5R01DK06833603, R01DK058845,
DK66574]; Affymetrix contract for genotyping services [N02HL64278];
Robert Dawson Evans Endowment of the Department of Medicine at Boston
University School of Medicine and Boston Medical Center; NIA; NIA
[N01AG62101, N01AG62103, N01AG62106, 1R01AG032098-01A1]; NIH from
Children's Hospital Boston [1 R01DK07578701A1]; German National Genome
Research Net NGFN2 and NGFNplus [01GS0823, A3, 01GS0834]; Munich Center
of Health Sciences as part of LMUinnovativ; Else
Kroner-Fresenius-Stiftung [P48/08//All/08, 2012_A147]; Else
Krdner-Fresenius-Stiftung; Regensburg University Medical Center,
Germany; University of Ulm, Germany; Else Kroner-Fresenius-Stiftung; KfH
Stiftung Praventivmedizin; Doktor Robert Pfleger-Stiftung; German
Research Center for Enviromnental Health; German Research Center for
Environmental Health; German Federal Ministry of Education and Research;
State of Bavaria; University of Regensburg for the Department of
Epidemiology and Preventive Medicine at the Regensburg University
Medical Center; NHGRI [U01HG004402, U01HG004738, U01HG004422,
U01HG004729, U01HG004726, U01HG004735, U01HG004415, U01HG004436,
U01HG004423, U01HG004728, RFAHG006033]; National Institute of Dental and
Craniofacial Research [U01DE018993]; Gene Environment-Association
Studies (GENEVA) under the NTH Genes, Environment, and Health Initiative
(GEI); NIH GET [U01HG04424]; Johns Hopkins University Center for
Inherited Disease Research; NIH GEI [U01HG004438]; National Cancer
Institute (NCI) [P01CA087969, P01CA055075]; Medical Research Council UK;
Ministry of Science, Education, and Sport of the Republic of Croatia
[108-1080315-0302]; Ministry of Health and Department of Educational
Assistance; Universities and Research of the Autonomous Province of
Bolzano; South Tyrolean Sparkasse Foundation; European Union framework
program 6 EUROSPAN project [LSHG-CT-2006018947, LSHG-CT-2006-018947];
Swedish Natural Sciences Research Council; European Union through the
EUROSPAN project [LSHG-CT-2006018947]; Foundation for Strategic Research
(SSF); Linneaus Centre for Bioinformatics; NCI [P01CA087969,
P01CA055075, CA047988]; Chief Scientist Office of the Scottish
Government; Royal Society; German Ministry of Education and Research
through the National Genome Research Network; Ministry of Science,
Commerce, and Transportation of the State of Schleswig-Holstein; DFG
"Inflammation at Interfaces" excellence cluster; German Research Council
[KFO152]; Adiposity Diseases Integrated Research and Treatment Center
[K7-37]; European Community's Seventh Framework Programme, ENGAGE
project [HEALTH-F4-2007-201413]; European Commission under Marie Curie
Intra-European Fellowship; Netherlands Organization of Scientific
Research (NWO) [175-010-2005-011, 911-03-012]; Research Institute for
Diseases in the Elderly (RIDE2) [014-93-015]; Netherlands Genomics
Initiative (NGI)/Netherlands Consortium for Healthy Aging (NCHA) project
[050-060-810]; Erasmus Medical Center, Erasmus University; Netherlands
Organization for Health Research and Development; Research Institute for
Diseases in the Elderly (RIDE); Ministry of Education, Culture, and
Science; Ministry for Health, Welfare, and Sports; European Commission
(DG XI); Municipality of Rotterdam; German Bundesministerium fuer
Forschung und Technology [01-AK803A-H, 01-IG07015G]; NWO (vici)
[918-76-619]; Federal Ministry of Education and Research [01ZZ9603,
01ZZ0103, 01ZZ0403, 03ZIK012]; Ministry of Cultural Affairs; Social
Ministry of the Federal State of Mecklenburg-West Pomerania; Siemens
Healthcare (Erlangen, Germany); Federal State of Mecklenburg-West
Pomerania; Donald W. Reynolds Foundation; Fondation Leducq; Amgen;
National Foundation for Alzheimer's Disease and Related Disorders;
Institut Pasteur de Lille; Centre National de Genotypage; Fondation pour
la Recherche Medicale; Caisse Nationale Maladie des Travailleurs
Salaries; Direction Generale de la Sante; MGEN; Institut de la
Longevite; Agence Francaise de Securite Sanitaire des Produits de Sante;
Aquitaine and Bourgogne Regional Councils; Fondation de France; French
Ministry of Research/INSERM "Cohortes et collections de donnees
biologiques" programme; Eisai; Australian Research and Development
Grants Advisory Committee [1992-94]; Australian National Health and
Medical Research Council, Canberra Australia [974159, 211069, 991407,
457349]; Australian National Health and Medical Research Council
[512423, 475604, 529912]; Wellcome Trust UK; Wellcome Trust Case Control
Consortium 2 [085475/B/08/Z, 085475/08/Z]; Australian National Health
and Medical Research Council; GlaxoSmithKline; Faculty of Biology and
Medicine of Lausanne; Swiss National Science Foundation [33CSCO-122661,
33CSCO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896,
3100-059302, 3200-052720, 3200-042532, 4026-028099]; Swiss School of
Public Health Plus; Academy of Finland [117797, 121584, 126925]; Social
Insurance Institution of Finland; University Hospital Medical funds;
Finnish Foundation of Cardiovascular Research; Emil Aaaltonen
Foundation; FP7 grants [201413 ENGAGE, 212111 BBMRI, 205419 ECOGENE,
245536 OPENGENE]; Estonian Government [SF0180142s08]; European Union
through the European Regional Development Fund, Centre of Excellence in
Genomics; NHLBI Family Heart Study; NIH grant [5R01HL08770002]; Wellcome
Trust; Telethon; FVG region; Fondo Trieste; European Union
[Vasoplus-037254]; Italian Ministry of Universities [FIRB -RBIN064YAT];
Assessorato Ricerca Regione Campania; Ente Parco Nazionale del Cilento e
Vallo di Diano; Fondazione Banco di Napoli to M Ciullo; Compagnia di San
Paolo (Torino, Italy); Cariplo Fundation (Milano, Italy); Italian
Ministry of Health Progetto Finalizzato; AstraZeneca; Italian Ministry
of Education, University, and Research [5571/DSPAR/2002, 718/Ric/2005];
Bristol-Myers Squibb; European Union's Seventh Framework Programme
[HEALTH-F2-2009-223004]; Netherlands Consortium of Healthy Aging [NGI
05060810]; Federal Office for Forest, Environment, and Landscape;
Federal Office of Public Health; Federal Office of Roads and Transport;
canton government of Aargau; canton government of Basel-Stadt; canton
government of Basel-Land; canton government of Geneva; canton government
of Luzern; canton government of Ticino; canton government of Zurich;
Swiss Lung League; canton Lung League government of Basel Stadt/Basel
Landschaft; canton Lung League government of Geneva; canton Lung League
government of Ticino; canton Lung League government of Zurich; Kamillo
Eisner Stiftung; Genomics of Lipid-Associated Disorders of the Austrian
Genome Research Programme GEN-AU; Ellison Medical Foundation/American
Federation for Aging Research postdoctoral fellowship; Stanford Dean's
postdoctoral fellowship; NHGRI; NIGMS
FX AGES. The Age, Gene/Environment Susceptibility (AGES) study was funded
by the National Institutes of Health (NIH) (contract N01AG12100), the
National Institute on Aging (NIA) Intramural Research Program,
Hjartavernd (the Icelandic Heart Association), and the Althingi (the
Icelandic Parliament).; Amish Study. The Amish study was supported by
NIH grants and contracts (R01AG18728, Amish Longevity Study;
R01HL088119, Amish Calcification Study; U01GM07451804, Pharmacogenomics
of Anti-Platelet Intervention [PAPI] Study; U01HL072515-06, Heredity and
Phenotype Interaction [HAPI] Study; and U01-HL084756 and K12RR023250),
as well as grants from the University of Maryland (MCRDP grant),
University of Maryland General Clinical Research Center (M01RR16500),
Baltimore Veterans Affairs Medical Center Geriatrics Research and
Education Clinical Center, and the Paul Beeson Physician Faculty
Scholars in Aging Program.; ASPS. The Austrian Stroke Prevention Study
(ASPS) research reported in this article was funded by grants from the
Austrian Science Fund (P20545P05 and P13180). The Medical University of
Graz supported the databank of the ASPS.; ARIC. The Atherosclerosis Risk
in Communities (ARIC) study is carried out as a collaborative study
supported by the National Heart, Lung, and Blood Institute (NHLBI)
(contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
HHSN268201100011C, HHSN268201100012C, R01HL087641, R01HL59367, and
R01HL086694), the National Human Genome Research Institute (NHGRI)
(U01HG004402), and the NIH (HHSN268200625226C). Infrastructure was
partly supported by a component of the NIH and NIH Roadmap for Medical
Research (Grant UL1RR025005). A. K. and C. H. were supported by the Emmy
Noether programme of the German Research Foundation (K03598/2-1). The
authors thank the staff and participants of the ARIC study for their
important contributions.; BLSA. The Baltimore Longitudinal Study of
Aging (BLSA) was supported in part by the Intramural Research Program of
the NIH NIA.; CHS. The Cardiovascular Health Study (CHS) research
reported in this article was supported by the NHLBI (contracts
N01HC85079 through N01HC85086, N01HC35129, N01HC15103, N01HC55222,
N01HC75150, and N01HC45133; grants U01HL080295 and R01HL087652), with
additional contributions from the National Institute of Neurological
Disorders and Stroke. A full list of principal CHS investigators and
institutions is available at http://www.chs-nhlbi.org/pi.htm. DNA
handling and genotyping was supported in part by a National Center for
Research Resources grant (M01RR00425) to the Cedars-Sinai General
Clinical Research Center genotyping core and a National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK) grant (DK063491) to
the Southern California Diabetes Endocrinology Research Center.; ERE The
Erasmus Rucphen Family (ERF) study was supported by grants from the
Netherlands Organization for Scientific Research (Pioneer grant),
Erasmus Medical Center, Centre for Medical Systems Biology, and
Netherlands Kidney Foundation.; FHS. The Family Heart Study (FHS) work
was supported in part by the NHLBI (grants 5R01HL08770003 and
5R01HL08821502 to M. P.) and the NIDDK (5R01DK07568102 and
5R01DK06833603 to I.B.).; Framingham Heart Study. The Framingham Heart
Study research reported in this paper was conducted in part using data
and resources from the Framingham Heart Study of the NIH NHLBI and the
Boston University School of Medicine. The analyses reflect intellectual
input and resource development from the Framingham Heart Study
investigators participating in the SNP Health Association Resource
(SHARe) project. This work was partially supported by NHLBI Framingham
Heart Study contracts (N01HC25195) as well as an Affymetrix contract for
genotyping services (N02HL64278). A portion of this research utilized
the Linux Cluster for Genetic Analysis funded by the Robert Dawson Evans
Endowment of the Department of Medicine at Boston University School of
Medicine and Boston Medical Center.; GENOA. The Genetic Epidemiology
Network of Arteriopathy (GENOA) research was partially supported by the
NHLBI (R01HL87660).; Health ABC. The Health Aging and Body Composition
Study (Health ABC) was funded by the NIA. This research was supported by
the NIA (contracts N01AG62101, N01AG62103, and N01AG62106). The GWAS was
funded by a NIA grant (1R01AG032098-01A1) to Wake Forest University
Health Sciences. Genotyping services were provided by the Center for
Inherited Disease Research (CIDR). CIDR is fully funded through a
federal contract from the NIH to Johns Hopkins University
(HHSN268200782096C). This research was supported in part by the
Intramural Research Program of the NIH NIA.; KORA. For the Kooperative
Gesundheitsforschung in der Region Augsburg (KORA) F3 and F4 studies,
the genetic epidemiological work was funded by an NIH subcontract from
the Children's Hospital Boston (prime grant 1 R01DK07578701A1 to H. E.
W. and I. M. H.), the German National Genome Research Net NGFN2 and
NGFNplus (01GS0823 to H. E. W.; WK project A3, 01GS0834), the Munich
Center of Health Sciences as part of LMUinnovativ, and by Else
Kroner-Fresenius-Stiftung (P48/08//All/08 to C. A. B. and B. K. K. and
2012_A147 to C. A. B. and I. M. H.). The F3 kidney parameter
measurements were funded by Else Krdner-Fresenius-Stiftung (to C. A. B.
and B. K. K.) and the Regensburg University Medical Center, Germany, and
the F4 measurements were funded by the University of Ulm, Germany (to W.
K.). Genome-wide genotyping costs in F3 and F4 were funded in part by
Else Kroner-Fresenius-Stiftung (to C. A. B. and B. K. K.). De novo
genotyping in F3 and F4 was funded by the Else Kroner-Fresenius-Stiftung
(C. A. B. and B. K. K.). C. A. B. has received research funding from
Else Kroner-Fresenius-Stiftung, KfH Stiftung Praventivmedizin, and
Doktor Robert Pfleger-Stiftung. The KORA research platform and the
Multinational Monitoring of Trends and Determinants in Cardiovascular
Disease (MONICA) Augsburg studies were initiated and financed by the
German Research Center for Enviromnental Health, the German Research
Center for Environmental Health, the German Federal Ministry of
Education and Research, and the State of Bavaria. Genotyping was
performed in the Genome Analysis Center of the German Research Center
for Environmental Health. The LINUX platform for computation was funded
by the University of Regensburg for the Department of Epidemiology and
Preventive Medicine at the Regensburg University Medical Center.;
NHS/HPFS. The Nurses' Health Study (NHS)/Health Professionals' Follow-Up
Study (HPFS) type 2 diabetes GWAS (U01HG004399) is a component of a
collaborative project that includes 13 other GWAS (U01HG004738,
U01HG004422, U01HG004402, U01HG004729, U01HG004726, U01HG004735,
U01HG004415, U01HG004436, U01HG004423, U01HG004728, RFAHG006033;
U01DE018993, all funded by the NHGRI; U01DE018903 from the National
Institute of Dental and Craniofacial Research). The study is also funded
as part of the Gene Environment-Association Studies (GENEVA) under the
NTH Genes, Environment, and Health Initiative (GEI). Assistance with
phenotype harmonization and genotype cleaning, as well as with general
study coordination, was provided by the GENEVA Coordinating Center
(U01HG004446). Assistance with data cleaning was provided by the
National Center for Biotechnology Information. Genotyping was performed
at the Broad Institute of the Massachusetts Institute of Technology and
Harvard University, with funding support from the NIH GET (U01HG04424),
as well as the Johns Hopkins University Center for Inherited Disease
Research, with support from the NIH GEI (U01HG004438) and the NIH
(contract HHSN268200782096C). Additional funding for the current
research was provided by the National Cancer Institute (NCI)
(P01CA087969 and P01CA055075) and the NIDDK (R01DK058845). The authors
thank the staff and participants of the NHS and HPFS for their
dedication and commitment.; Korcula. The Korcula study was supported
through grants from the Medical Research Council UK (to H. C., A.F.W.,
and I. R.) and by the Ministry of Science, Education, and Sport of the
Republic of Croatia (108-1080315-0302 to I.R.).; MICROS. The MICROS
study was supported by the Ministry of Health and Department of
Educational Assistance, the Universities and Research of the Autonomous
Province of Bolzano, the South Tyrolean Sparkasse Foundation, and the
European Union framework program 6 EUROSPAN project (contract
LSHG-CT-2006018947).; Northern Swedish Population Health Study. The
Northern Swedish Population Health Study was supported by grants from
the Swedish Natural Sciences Research Council, the European Union
through the EUROSPAN project (contract LSHG-CT-2006018947), the
Foundation for Strategic Research (SSF), and the Linneaus Centre for
Bioinformatics.; NHS. The Nurses' Health Study (NHS) renal function and
albuminuria work was supported by a NIDDK grant (DK66574). Additional
funding for the current research was provided by the NCI (P01CA087969
and P01CA055075) and the NIDDK (R01DK058845).; ORCADES. The Orkney
Complex Disease Study (ORCADES) was supported by the Chief Scientist
Office of the Scottish Government, the Royal Society, and the European
Union framework program 6 EUROSPAN project (contract
LSHG-CT-2006018947). DNA extractions were performed at the Wellcome
Trust Clinical Research Facility in Edinburgh.; PopGen. The PopGen study
was supported by the German Ministry of Education and Research through
the National Genome Research Network, and the Ministry of Science,
Commerce, and Transportation of the State of Schleswig-Holstein. The
project has also received infrastructure support through the DFG
"Inflammation at Interfaces" excellence cluster.; SORBS. The SORBS study
was funded by grants from the German Research Council (KFO152 to M. S.)
and the Adiposity Diseases Integrated Research and Treatment Center
(K7-37 to M. S. and A. T.). The authors also thank Dr. Knut Krohn
(Microarray Core Facility of the Interdisciplinary Centre for Clinical
Research, University of Leipzig, Germany) for providing the genotyping
platform. I. P. is funded in part through the European Community's
Seventh Framework Programme (FP7/2007-2013), ENGAGE project (grant
agreement HEALTH-F4-2007-201413). R. M. acknowledges financial support
from the European Commission under a Marie Curie Intra-European
Fellowship.; Rotterdam Study-I and Rotterdam Study-II. For the Rotterdam
Study-I and Rotterdam Study-II, the GWAS was funded by the Netherlands
Organization of Scientific Research (NWO) (175-010-2005-011 and
911-03-012), the Research Institute for Diseases in the Elderly (RIDE2;
014-93-015,), and the Netherlands Genomics Initiative (NGI)/Netherlands
Consortium for Healthy Aging (NCHA) project (050-060-810). The Rotterdam
Study is funded by Erasmus Medical Center, Erasmus University,
Netherlands Organization for Health Research and Development, Research
Institute for Diseases in the Elderly (RIDE), the Ministry of Education,
Culture, and Science, the Ministry for Health, Welfare, and Sports, the
European Commission (DG XI), and the Municipality of Rotterdam. The
Erasmus Computing Grid (Rotterdam, The Netherlands) and the national
German MediGRID and Services@MediGRID part of the German D-Grid were
both funded by grants from the German Bundesministerium fuer Forschung
und Technology (01-AK803A-H and 01-IG07015G) for access to their grid
resources. A. D. is supported by an NWO grant (vici, 918-76-619).; SHIP.
The Study of Health in Pomerania (SHIP) is part of the Community
Medicine Research net of the University of Greifswald, Germany, funded
by grants from the Federal Ministry of Education and Research (01ZZ9603,
01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs, as well as
the Social Ministry of the Federal State of Mecklenburg-West Pomerania.
Genome-wide data have been supported by a grant from the Federal
Ministry of Education and Research (03ZIK012) as well as a joint grant
from Siemens Healthcare (Erlangen, Germany) and the Federal State of
Mecklenburg-West Pomerania. The University of Greifswald is a member of
the Center of Knowledge Interchange program of Siemens AG.; Vis. The Vis
study was supported through grants from the Medical Research Council UK
(to H. C., A. F. W., and I. R.), the Ministry of Science, Education, and
Sport of the Republic of Croatia (108-1080315-0302 to I. R.), and the
European Union framework program 6 EUROSPAN project (contract
LSHG-CT-2006-018947).; WGHS. The Women's Genome Health Study (WGHS) is
supported by the NHLBI (HL043851 and HL69757) and the NCI (CA047988),
the Donald W. Reynolds Foundation, and the Fondation Leducq, with
collaborative scientific support and funding for genotyping provided by
Amgen.; 3 City Study. The 3 City Study was supported by the National
Foundation for Alzheimer's Disease and Related Disorders, the Institut
Pasteur de Lille, and the Centre National de Genotypage. The 3 City
Study was performed as part of a collaboration between the Institut
National de la Sante et de la Recherche Medicale (INSERM), the Victor
Segalen Bordeaux II University, and Sanofi-Synthelabo. The Fondation
pour la Recherche Medicale funded the preparation and initiation of the
study. The 3 City Study was also funded by the Caisse Nationale Maladie
des Travailleurs Salaries, Direction Generale de la Sante, MGEN,
Institut de la Longevite, Agence Francaise de Securite Sanitaire des
Produits de Sante, the Aquitaine and Bourgogne Regional Councils,
Fondation de France and the joint French Ministry of Research/INSERM
"Cohortes et collections de donnees biologiques" programme. L. G.
received an unconditional grant from Eisai.; BMES. The Blue Mountains
Eye Study (BMES) has been supported by grants from the Australian
Research and Development Grants Advisory Committee (1992-94) and the
Australian National Health and Medical Research Council, Canberra
Australia (974159, 211069, 991407, and 457349). The GWAS studies of he
BMES population are supported by grants from the Australian National
Health and Medical Research Council (512423, 475604, 529912) and the
Wellcome Trust UK (2008), as part of Wellcome Trust Case Control
Consortium 2 (085475/B/08/Z and 085475/08/Z to A. V., P.Mc., P.Mi., ET.,
P. RE). E. G. H. and J.J.W. are funded by the Australian National Health
and Medical Research Council Fellowship Schemes.; CoLaus. The CoLaus
study received financial contributions from GlaxoSmithKline, the Faculty
of Biology and Medicine of Lausanne, and the Swiss National Science
Foundation (33CSCO-122661). M.Bo. is supported by the Swiss School of
Public Health Plus.; YFS. The Cardiovascular Risk in Young Finns study
(YFS) is supported by grants from the Academy of Finland (117797,
121584, and 126925), the Social Insurance Institution of Finland,
University Hospital Medical funds to Tampere and Turku University
Hospitals, the Finnish Foundation of Cardiovascular Research, and the
Emil Aaaltonen Foundation (to T.L.).; University of Tartu Estonian Gene
Project. The Estonian Genome Center of the University of Tartu (EGCUT)
received support from FP7 grants (201413 ENGAGE, 212111 BBMRI, 205419
ECOGENE, 245536 OPENGENE) and also received targeted financing from
Estonian Government (SF0180142s08) and from the European Union through
the European Regional Development Fund, in the frame of the Centre of
Excellence in Genomics.; FPanHS-II. The research of the FamHS-II was
conducted in part using data and resources from the NHLBI Family Heart
Study supported in part by an NIH grant (5R01HL08770002).; GoDARTS. For
the Genetics of Diabetes Audit and Research Tayside (GoDARTS) study, the
Wellcome Trust provides support for the Wellcome Trust United Kingdom
Type 2 Diabetes Case Control Collection and the informatics support is
provided by the Chief Scientist Office, and the Wellcome Trust funded
Scottish Health Informatics Programme.; INGI-Carlantino and INGI-FVG.
The INGI-Carlantino and INGI-FVG studies were supported by grants from
Telethon, FVG region, and Fondo Trieste. The INGI-Cilento study was
supported by grants from the European Union (Vasoplus-037254), the
Italian Ministry of Universities (FIRB -RBIN064YAT), the Assessorato
Ricerca Regione Campania, the Ente Parco Nazionale del Cilento e Vallo
di Diano, and the Fondazione Banco di Napoli to M Ciullo. The INGI-Val
Borbera Study was supported from Compagnia di San Paolo (Torino, Italy),
Cariplo Fundation (Milano, Italy), and Italian Ministry of Health
Progetto Finalizzato 2007 and 2009.; JUPITER. The Justification for the
Use of Statins in Primary Prevention: An Intervention Trial Evaluating
Rosuvastatin (JUPITER) trial and the genotyping were supported by
AstraZeneca. The Ogliastra Genetic Park (OGP) Replication Study and the
OGP Talana study were supported by grants from the Italian Ministry of
Education, University (5571/DSPAR/2002), and Research (718/Ric/2005).;
PROSPER. The Prospective Study of Pravastatin in the Elderly at Risk
(PROSPER) trial was supported by an investigator-initiated grant from
Bristol-Myers Squibb. The study was conducted, analyzed, and reported
independently of the company. The research leading to these results has
received funding from the European Union's Seventh Framework Programme
(FP7/2007-2013, under Grant Agreement HEALTH-F2-2009-223004). For a part
of the genotyping, we received funding from the Netherlands Consortium
of Healthy Aging (NGI 05060810).; SAPALDIA. The Swiss Study on Air
Pollution and Lung Disease in Adults (SAPALDIA) was supported by grants
from the Swiss National Science Foundation (33CSCO-108796,
3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302,
3200-052720, 3200-042532, and 4026-028099), the Federal Office for
Forest, Environment, and Landscape, the Federal Office of Public Health,
the Federal Office of Roads and Transport, the canton's government of
Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Zurich, the
Swiss Lung League and the canton's Lung League government of Basel
Stadt/Basel Landschaft, Geneva, Ticino, and Zurich.; SAPHIR. The
Salzburg Atherosclerosis Prevention program in subjects at High
Individual Risk (SAPHIR) study was partially supported by a grant from
the Kamillo Eisner Stiftung (to B. P.) and by grants from the Genomics
of Lipid-Associated Disorders of the Austrian Genome Research Programme
GEN-AU (to EK.). For eQTL analysis, H.J.G received support from a
Ellison Medical Foundation/American Federation for Aging Research
postdoctoral fellowship and a Stanford Dean's postdoctoral fellowship.
H. E. W. and S. K. K. were supported by grants from the NIA, NHGRI, and
NIGMS.
NR 32
TC 9
Z9 9
U1 1
U2 23
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD DEC
PY 2013
VL 24
IS 12
BP 2105
EP 2117
DI 10.1681/ASN.2012100983
PG 13
WC Urology & Nephrology
SC Urology & Nephrology
GA 277KI
UT WOS:000328817300021
PM 24029420
ER
PT J
AU Mizurini, D
Calvo, E
Francischetti, I
Monteiro, R
AF Mizurini, D.
Calvo, E.
Francischetti, I
Monteiro, R.
TI Molecular mechanisms involved in the antithrobotic activity of aegyptin,
a novel mosquito-derived collagen-binding protein
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Meeting Abstract
C1 [Mizurini, D.; Monteiro, R.] Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
[Calvo, E.; Francischetti, I] NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
EI 1538-7836
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD DEC
PY 2013
VL 11
SU 3
SI SI
BP 67
EP 68
PG 2
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 265BL
UT WOS:000327924600175
ER
PT J
AU Herman, SEM
Sun, X
McAuley, EM
Hsieh, MM
Pittaluga, S
Raffeld, M
Liu, D
Keyvanfar, K
Chapman, CM
Chen, J
Buggy, JJ
Aue, G
Tisdale, JF
Perez-Galan, P
Wiestner, A
AF Herman, S. E. M.
Sun, X.
McAuley, E. M.
Hsieh, M. M.
Pittaluga, S.
Raffeld, M.
Liu, D.
Keyvanfar, K.
Chapman, C. M.
Chen, J.
Buggy, J. J.
Aue, G.
Tisdale, J. F.
Perez-Galan, P.
Wiestner, A.
TI Modeling tumor-host interactions of chronic lymphocytic leukemia in
xenografted mice to study tumor biology and evaluate targeted therapy
SO LEUKEMIA
LA English
DT Article
DE ibrutinib; BCR; CLL; xenograft; NF-kappaB; kinase inhibitor
ID B-CELL RECEPTOR; FOSTAMATINIB DISODIUM; ANTIGEN RECEPTORS; IN-VIVO;
PROLIFERATION; PCI-32765; CLL; ACTIVATION; SURVIVAL; MICROENVIRONMENT
AB Chronic lymphocytic leukemia (CLL) cells depend on microenvironmental factors for proliferation and survival. In particular, the B-cell receptor (BCR) and nuclear factor-kappa B (NF-kappa B) pathways are activated in the lymph node (LN) microenvironment. Thus, model systems mimicking tumor-host interactions are important tools to study CLL biology and pathogenesis. We investigated whether the recently established NOD/scid/gamma c(null) (NSG) mouse xenograft model can recapitulate the effects of the human microenvironment. We assessed, therefore, tumor characteristics previously defined in LN-resident CLL cells, including proliferation, and activation of the BCR and NF-kappa B pathways. We found that the murine spleen (SP) microenvironment supported CLL cell proliferation and activation to a similar degree than the human LN, including induction of BCR and NF-kappa B signaling in the xenografted cells. Next, we used this model to study ibrutinib, a Bruton's tyrosine kinase inhibitor in clinical development. Ibrutinib inhibited BCR and NF-kappa B signaling induced by the microenvironment, decreased proliferation, induced apoptosis and reduced the tumor burden in vivo. Thus, our data demonstrate that the SP of xenografted NSG mice can, in part, recapitulate the role of the human LN for CLL cells. In addition, we show that ibrutinib effectively disrupts tumor-host interactions essential for CLL cell proliferation and survival in vivo.
C1 [Herman, S. E. M.; Sun, X.; McAuley, E. M.; Hsieh, M. M.; Liu, D.; Keyvanfar, K.; Chapman, C. M.; Chen, J.; Aue, G.; Tisdale, J. F.; Wiestner, A.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Pittaluga, S.; Raffeld, M.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Buggy, J. J.] Pharmacyclics Inc, Sunnyvale, CA USA.
[Perez-Galan, P.] Inst Invest Biomed August Pi & Sunyer IDIBAPS, Dept Hematooncol, Barcelona, Spain.
RP Wiestner, A (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,CRC 3-5140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Adrian.Wiestner@nih.gov
FU National, Heart, Lung and Blood Institute
FX We thank Dr Nalini Raghavachari for her assistance setting up the Taqman
microfluidics cards, Dr Zu Xi Yu and the NHLBI pathology core for help
with slide preparation, and Christina Corsino and the NIAID building 50
animal technicians for their assistance with animal experiments. This
research was funded through the Intramural Research Program of the
National, Heart, Lung and Blood Institute.
NR 48
TC 28
Z9 30
U1 3
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
EI 1476-5551
J9 LEUKEMIA
JI Leukemia
PD DEC
PY 2013
VL 27
IS 12
BP 2311
EP 2321
DI 10.1038/leu.2013.131
PG 11
WC Oncology; Hematology
SC Oncology; Hematology
GA 272KX
UT WOS:000328460600006
PM 23619564
ER
PT J
AU Zhao, X
Lwin, T
Zhang, X
Huang, A
Wang, J
Marquez, VE
Chen-Kiang, S
Dalton, WS
Sotomayor, E
Tao, J
AF Zhao, X.
Lwin, T.
Zhang, X.
Huang, A.
Wang, J.
Marquez, V. E.
Chen-Kiang, S.
Dalton, W. S.
Sotomayor, E.
Tao, J.
TI Disruption of the MYC-miRNA-EZH2 loop to suppress aggressive B-cell
lymphoma survival and clonogenicity
SO LEUKEMIA
LA English
DT Article
DE B-cell lymphoma; MYC; EZH2; miRNA-26a; survival; clonogenicity
ID NON-HODGKIN-LYMPHOMA; MANTLE CELL; C-MYC; SELECTIVE-INHIBITION;
THERAPEUTIC STRATEGY; SOMATIC MUTATIONS; BET BROMODOMAINS; TRANSGENIC
MICE; DOWN-REGULATION; EZH2
AB c-MYC (hereafter MYC) overexpression has been recognized in aggressive B-cell lymphomas and linked to adverse prognosis. MYC activation results in widespread repression of micro-RNA (miRNA) expression and associated with lymphoma aggressive progression. Our recent study identified a MYC-miRNA-EZH2 feed-forward loop linking overexpression of MYC, EZH2 and miRNA repression. Here, using a novel small-molecule BET bromodomain inhibitor, JQ1, and the EZH2 inhibitor, DZNep, we demonstrated that combined treatment of JQ1 and DZNep cooperatively disrupted MYC activation, resulting in a greater restoration of miR-26a expression and synergistically suppressed lymphoma growth and clonogenicity in aggressive lymphoma cells. Furthermore, CHIP assay demonstrated that MYC recruited EZH2 to miR-26a promoter and cooperatively repressed miR-26a expression in aggressive lymphoma cell lines, as well as primary lymphoma cells. Loss-or gain-of-function approaches revealed that miR-26a functioned as a tumor suppressor miRNA and mediated the combinatorial effects of JQ1 and DZNep. These findings represent a novel promising approach for silencing MYC-miRNA-EZH2 amplification loop for combinatorial therapy of aggressive B-cell lymphomas.
C1 [Zhao, X.; Lwin, T.; Zhang, X.; Huang, A.; Wang, J.; Dalton, W. S.; Sotomayor, E.; Tao, J.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Malignant Hematol, Tampa, FL 33612 USA.
[Zhao, X.; Lwin, T.; Zhang, X.; Huang, A.; Wang, J.; Dalton, W. S.; Sotomayor, E.; Tao, J.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Expt Therapeut Program, Tampa, FL 33612 USA.
[Zhang, X.; Wang, J.] Tianjin Canc Hosp, Dept Immunol & Surg, Tianjin, Peoples R China.
[Marquez, V. E.] NCI, Chem Biol Lab, Frederick Natl Lab Canc Res, CCR,NIH, Frederick, MD 21701 USA.
[Chen-Kiang, S.] Weill Cornell Med Coll, Dept Pathol, New York, NY USA.
RP Tao, J (reprint author), Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Malignant Hematol, MCC LAB 2071,12902 Magnolia Dr, Tampa, FL 33612 USA.
EM Jianguo.Tao@moffitt.org
FU National Cancer Institutes [R01 CA137123]; Maher Fund; Lymphoma Research
Foundation; NIH, National Cancer Institute, Center for Cancer Research
FX This work was supported by grants from the National Cancer Institutes
(R01 CA137123, to JT), Maher Fund (to JT) and Lymphoma Research
Foundation (to JT), and supported in part by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research (to VM). JQ1 was kindly provided by James E Bradner (Boston,
MA, USA), and DZNep was kindly provided by Victor E Marquez (Frederick,
MD, USA).
NR 37
TC 49
Z9 54
U1 2
U2 17
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
EI 1476-5551
J9 LEUKEMIA
JI Leukemia
PD DEC
PY 2013
VL 27
IS 12
BP 2341
EP 2350
DI 10.1038/leu.2013.94
PG 10
WC Oncology; Hematology
SC Oncology; Hematology
GA 272KX
UT WOS:000328460600009
PM 23538750
ER
PT J
AU Denny, JC
Bastarache, L
Ritchie, MD
Carroll, RJ
Zink, R
Mosley, JD
Field, JR
Pulley, JM
Ramirez, AH
Bowton, E
Basford, MA
Carrell, DS
Peissig, PL
Kho, AN
Pacheco, JA
Rasmussen, LV
Crosslin, DR
Crane, PK
Pathak, J
Bielinski, SJ
Pendergrass, SA
Xu, H
Hindorff, LA
Li, RL
Manolio, TA
Chute, CG
Chisholm, RL
Larson, EB
Jarvik, GP
Brilliant, MH
McCarty, CA
Kullo, IJ
Haines, JL
Crawford, DC
Masys, DR
Roden, DM
AF Denny, Joshua C.
Bastarache, Lisa
Ritchie, Marylyn D.
Carroll, Robert J.
Zink, Raquel
Mosley, Jonathan D.
Field, Julie R.
Pulley, Jill M.
Ramirez, Andrea H.
Bowton, Erica
Basford, Melissa A.
Carrell, David S.
Peissig, Peggy L.
Kho, Abel N.
Pacheco, Jennifer A.
Rasmussen, Luke V.
Crosslin, David R.
Crane, Paul K.
Pathak, Jyotishman
Bielinski, Suzette J.
Pendergrass, Sarah A.
Xu, Hua
Hindorff, Lucia A.
Li, Rongling
Manolio, Teri A.
Chute, Christopher G.
Chisholm, Rex L.
Larson, Eric B.
Jarvik, Gail P.
Brilliant, Murray H.
McCarty, Catherine A.
Kullo, Iftikhar J.
Haines, Jonathan L.
Crawford, Dana C.
Masys, Daniel R.
Roden, Dan M.
TI Systematic comparison of phenome-wide association study of electronic
medical record data and genome-wide association study data
SO NATURE BIOTECHNOLOGY
LA English
DT Article
ID RISK; VARIANTS; DISEASES; BIOBANK; TRAITS; TOOL; METAANALYSIS;
PHENOTYPES; MELANOMA
AB Candidate gene and genome-wide association studies (GWAS) have identified genetic variants that modulate risk for a human disease; many of these associations require further study to replicate the results. Here we report the first c large-scale application of the phenome-wide association "study (PheWAS) paradigm within electronic medical records E (EMRs), an unbiased approach to replication and discovery. v that interrogates relationships between targeted genotypes 1s and multiple phenotypes. We scanned for associations z between 3,144 single-nucleotide polymorphisms (previously N implicated by GWAS as mediators of human traits) and 1,358 EMR-derived phenotypes in 13,835 individuals of European ancestry. This PheWAS replicated 66% (51/77) of sufficiently powered prior GWAS associations and revealed 63 potentially pleiotropic associations with P < 4.6 x 10(-6) (false discovery rate < 0.1); the strongest of these novel associations were replicated in an independent cohort (n = 7,406). These findings validate PheWAS as a tool to allow unbiased interrogation across multiple phenotypes in EMR-based cohorts and to enhance analysis of the genomic basis of human disease.
C1 [Denny, Joshua C.; Mosley, Jonathan D.; Ramirez, Andrea H.; Roden, Dan M.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
[Denny, Joshua C.; Bastarache, Lisa; Carroll, Robert J.; Zink, Raquel] Vanderbilt Univ, Sch Med, Dept Biomed Informat, Nashville, TN 37212 USA.
[Ritchie, Marylyn D.; Pendergrass, Sarah A.] Penn State Univ, Dept Biochem & Mol Biol, Ctr Syst Genom, University Pk, PA 16802 USA.
[Field, Julie R.; Pulley, Jill M.; Bowton, Erica; Basford, Melissa A.] Vanderbilt Univ, Sch Med, Res Off, Nashville, TN 37212 USA.
[Pulley, Jill M.] Vanderbilt Univ, Sch Med, Dept Med Adm, Nashville, TN 37212 USA.
[Carrell, David S.; Larson, Eric B.] Grp Hlth Res Inst, Seattle, WA USA.
[Peissig, Peggy L.] Marshfield Clin Res Fdn, Biomed Informat Res Ctr, Marshfield, WI USA.
[Kho, Abel N.] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Pacheco, Jennifer A.] Northwestern Univ, Ctr Genet Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Rasmussen, Luke V.] Northwestern Univ, Dept Preventat Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Crosslin, David R.; Jarvik, Gail P.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Crane, Paul K.; Jarvik, Gail P.] Univ Washington, Dept Med, Seattle, WA USA.
[Pathak, Jyotishman; Chute, Christopher G.] Mayo Clin, Div Biomed Informat, Rochester, MN USA.
[Pathak, Jyotishman; Jarvik, Gail P.] Mayo Clin, Div Stat, Rochester, MN USA.
[Bielinski, Suzette J.] Mayo Clin, Div Epidemiol, Rochester, MN USA.
[Xu, Hua] Univ Texas Hlth Sci Ctr Houston, Sch Biomed Informat, Houston, TX 77030 USA.
[Li, Rongling; Manolio, Teri A.] NHGRI, Div Genom Med, Bethesda, MD 20892 USA.
[Chisholm, Rex L.] Northwestern Univ, Dept Cell & Mol Biol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Brilliant, Murray H.] Marshfield Clin Res Fdn, Ctr Human Genet, Marshfield, WI USA.
[McCarty, Catherine A.] Essentia Inst Rural Hlth, Duluth, MN USA.
[Kullo, Iftikhar J.] Mayo Clin, Div Cardiovasc Dis, Rochester, MN USA.
[Haines, Jonathan L.; Crawford, Dana C.] Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, Ctr Human Genet Res, Nashville, TN 37212 USA.
[Masys, Daniel R.] Univ Washington, Dept Biomed Informat & Med Educ, Seattle, WA 98195 USA.
[Roden, Dan M.] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37212 USA.
RP Denny, JC (reprint author), Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
EM josh.denny@vanderbilt.edu
RI Crane, Paul/C-8623-2014; Jarvik, Gail/N-6476-2014; Bielinski,
Suzette/A-2238-2009;
OI Jarvik, Gail/0000-0002-6710-8708; Bielinski,
Suzette/0000-0002-2905-5430; Rasmussen, Luke/0000-0002-4497-8049; Crane,
Paul/0000-0003-4278-7465
FU eMERGE Network; National Human Genome Research Institute (NHGRI);
National Institute of General Medical Sciences (NIGMS) (Group Health
Cooperative/University of Washington) [U01-HG004610, U01-HG006375];
Marshfield Clinic [U01-HG004608]; Mayo Clinic [U01-HG004599,
U01-HG006379]; Northwestern University [U01-HG004609, U01-HG006388];
Essentia Institute of Rural Health/Marshfield Clinic [U01-HG006389];
Vanderbilt University [U01-HG004603, U01-HG006378]; Vanderbilt
University serving as the Coordinating Center [U01-HG006385]; NHGRI
[U01-HG004424]; Johns Hopkins University, Center for Inherited Disease
Research [U01-HG004438]; NIGMS [RC2-GM092318]; National Library of
Medicine [R01-LM010685]; National Center for Advancing Translational
Sciences [UL1TR000427, UL1 RR024975, 2 UL1 TR000445]
FX This work was supported by the eMERGE Network, initiated and funded by
the National Human Genome Research Institute (NHGRI), with additional
funding from the National Institute of General Medical Sciences (NIGMS),
through the following grants: U01-HG004610 and U01-HG006375 (Group
Health Cooperative/University of Washington); U01-HG004608 (Marshfield
Clinic); U01-HG004599 and U01-HG006379 (Mayo Clinic); U01-HG004609 and
U01-HG006388 (Northwestern University); U01-HG006389 (Essentia Institute
of Rural Health/Marshfield Clinic); U01-HG004603 and U01-HG006378
(Vanderbilt University); and U01-HG006385 (Vanderbilt University serving
as the Coordinating Center). Funding support for eMERGE genotyping was
provided by NHGRI through the grants: U01-HG004424 (The Broad Institute)
and U01-HG004438 (Johns Hopkins University, Center for Inherited Disease
Research). Replication genotypes were derived from a pharmacogenomics
resource supported by NIGMS RC2-GM092318. Development of the PheWAS
method is also supported by R01-LM010685 from the National Library of
Medicine. BioVU received and continues to receive support through the
National Center for Research Resources UL1 RR024975, which is now the
National Center for Advancing Translational Sciences, 2 UL1 TR000445.
Additional support for this work at the University of Washington was
partially provided by the National Center for Advancing Translational
Sciences grant UL1TR000427.
NR 48
TC 130
Z9 131
U1 2
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1087-0156
EI 1546-1696
J9 NAT BIOTECHNOL
JI Nat. Biotechnol.
PD DEC
PY 2013
VL 31
IS 12
BP 1102
EP +
DI 10.1038/nbt.2749
PG 12
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 269OW
UT WOS:000328251900023
PM 24270849
ER
PT J
AU Chuang, PY
Hsieh, CH
Addullah, B
AF Chuang, Pei-Ying
Hsieh, Ching Hsiu
Addullah, Bashira
TI Nursing Genomics Its Role in Health Trajectory
SO NURSING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Human genomics; Nursing science; Essential competencies; Clinical
practice; Bioscience skills
ID DNA METHYLATION; PROSTATE-CANCER; GENETICS; EDUCATION; COMPETENCES;
CURRICULA; DISEASE; PROJECT; RECOMMENDATIONS; HYBRIDIZATION
AB The human genome, which is the complete set of human genetic information, significantly contributes to the health of an individual; it can lead to single or complex medical conditions (including cancer and heart disease) also affected by environmental and behavioral risk factors. To date, the challenges related to human genomics and nursing science focus on the following areas: (1) curriculum application, (2) advanced clinical practice in specific fields, and (3) hands-on bioscience laboratory skills. This review article summarizes current efforts and addresses critical components in nursing genomics.
C1 [Chuang, Pei-Ying] Univ Texas Hlth Sci Ctr Houston, Sch Nursing, Houston, TX 77030 USA.
[Hsieh, Ching Hsiu] Chang Gung Univ Sci & Technol, Dept Nursing, Putzu City 61363, Chiayi County, Taiwan.
[Addullah, Bashira] NHGRI, Ctr Res Genom & Global Hlth, NIH, Bethesda, MD 20814 USA.
RP Chuang, PY (reprint author), Univ Texas Hlth Sci Ctr Houston, Sch Nursing, 6901 Bertner Ave,Room 613, Houston, TX 77030 USA.
EM peiyingc@yahoo.com
NR 112
TC 0
Z9 0
U1 0
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0029-6465
EI 1558-1357
J9 NURS CLIN N AM
JI Nurs. Clin. North Am.
PD DEC
PY 2013
VL 48
IS 4
BP 523
EP +
DI 10.1016/j.cnur.2013.08.003
PG 35
WC Nursing
SC Nursing
GA 278VD
UT WOS:000328917100003
PM 24295186
ER
PT J
AU Tronnes, H
Wilcox, AJ
Lie, RT
Markestad, T
Moster, D
AF Tronnes, Havard
Wilcox, Allen J.
Lie, Rolv Terje
Markestad, Trond
Moster, Dag
TI The association of preterm birth with severe asthma and atopic
dermatitis: a national cohort study
SO PEDIATRIC ALLERGY AND IMMUNOLOGY
LA English
DT Article
DE premature birth; atopic dermatitis; asthma; pregnancy complications;
gestational age
ID CHILDHOOD ASTHMA; GESTATIONAL-AGE; RISK-FACTORS; CHILDREN; PREGNANCY;
ECZEMA; SCHOOLCHILDREN; PREVALENCE; PREMATURE; DISEASE
AB BackgroundAsthma and atopic dermatitis are both regarded as atopic diseases. Being born too early is associated with increased risk of asthma, but some studies have indicated that the opposite might be true for atopic dermatitis. We explored in more detail the associations between preterm birth, asthma, and atopic dermatitis.
MethodsWe analyzed data from Norwegian registries with prospectively collected data. All live births in Norway from 1967 through 2001 were followed through 2005 by linking the Medical Birth Registry of Norway to the National Insurance Scheme and to Statistics Norway. Only severe asthma and atopic dermatitis were registered in the National Insurance Scheme.
ResultsOf a total of 1,760,821 children, we identified 9,349 cases (0.5%) with severe asthma and 6,930 cases (0.4%) with severe atopic dermatitis. Compared with children born at term (37-41wk gestation), preterm birth was associated with increased odds for severe asthma (odds ratio (OR) 1.7 (95% confidence interval (CI): 1.6-1.8) for 32-36wk gestation and OR 3.6 (95% CI: 3.1-4.2) for 23-31wk) and decreased odds for severe atopic dermatitis (OR 0.9 (95% CI: 0.8-1.0) for 32-36wk gestation and OR 0.7 (95% CI: 0.5-1.0) for 23-31wk). Adjustment for perinatal and socio-demographic factors weakened the association between gestational age and severe asthma, while slightly strengthening the association between gestational age and severe atopic dermatitis.
ConclusionsPreterm birth was associated with increased risk of severe asthma and decreased risk of severe atopic dermatitis.
image= 12 years was assessed by computer-assisted self-interviewing methods. Respondents' self-reported race/ethnicity, age, gender, household income, government assistance, county type, residential stability, major depressive episode, history of being arrested, tobacco use, and alcohol use were examined as correlates. We stratified the analysis by race/ethnicity and used logistic regression to estimate odds of drug use.
Results: Prevalence of past-year marijuana use among Whites increased from 10.7% in 2005 to 11.6-11.8% in 2009-2011 (P < 0.05). There were no significant yearly changes in drug use prevalences among Asian-Americans, NHs/PIs, and mixed-race people; but use of any drug, especially marijuana, was prevalent among NHs/PIs and mixed-race people (21.2% and 23.3%, respectively, in 2011). Compared with Asian-Americans, NHs/PIs had higher odds of marijuana use, and mixed-race individuals had higher odds of using marijuana, cocaine, hallucinogens, stimulants, sedatives, and tranquilizers. Compared with Whites, mixed-race individuals had greater odds of any drug use, mainly marijuana, and NHs/PIs resembled Whites in odds of any drug use.
Conclusions: Findings reveal alarmingly prevalent drug use among NHs/PIs and mixed-race people. Research on drug use is needed in these rising populations to inform prevention and treatment efforts. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Wu, Li-Tzy; Blazer, Dan G.; Swartz, Marvin S.; Burchett, Bruce] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27710 USA.
[Brady, Kathleen T.] Med Univ S Carolina, Clin Neurosci Div, Charleston, SC 29425 USA.
[NIDA AAPI Workgrp] NIDA, Asian Amer & Pacific Islander Researchers & Schol, Bethesda, MD 20892 USA.
RP Wu, LT (reprint author), Duke Univ, Sch Med, Dept Psychiat & Behav Sci, Med Ctr, Box 3903, Durham, NC 27710 USA.
EM litzy.wu@duke.edu
FU U.S. National Institute on Drug Abuse of the National Institutes of
Health [HHSN271200900499P, R01DA019623, R01DA019901, R33DA027503]; Duke
University Department of Psychiatry and Behavioral Sciences
FX This work was made possible by research support from the U.S. National
Institute on Drug Abuse of the National Institutes of Health
(HHSN271200900499P, R01DA019623, R01DA019901, and R33DA027503 to Li-Tzy
Wu) and by Duke University Department of Psychiatry and Behavioral
Sciences. The sponsoring agency had no further role in the study design
and analysis, the writing of the report, or the decision to submit the
paper for publication. The opinions expressed in this paper are solely
those of the authors.
NR 44
TC 7
Z9 7
U1 1
U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
EI 1879-0046
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD DEC 1
PY 2013
VL 133
IS 2
BP 360
EP 367
DI 10.1016/j.drugalcdep.2013.06.008
PG 8
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 269KT
UT WOS:000328240900009
PM 23890491
ER
PT J
AU Belkaid, Y
Artis, D
AF Belkaid, Yasmine
Artis, David
TI Immunity at the Barriers Preface
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Editorial Material
DE Gastrointestinal tract; Lung; Mucosal immunity; Skin
ID DENDRITIC CELLS; INNATE
C1 [Belkaid, Yasmine] NIAID, Program Barrier Immun & Repair, Bethesda, MD 20892 USA.
[Belkaid, Yasmine] NIAID, Mucosal Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Artis, David] Univ Penn, Dept Microbiol, Philadelphia, PA 19104 USA.
[Artis, David] Perelman Sch Med, Inst Immunol, Philadelphia, PA USA.
[Artis, David] Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 USA.
RP Belkaid, Y (reprint author), NIAID, Mucosal Immunol Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ybelkaid@niaid.nih.gov; dartis@mail.med.upenn.edu
FU Intramural NIH HHS [Z01 AI001061-01]; NIAID NIH HHS [AI061570, AI087990,
AI097333, R01 AI074878, R01 AI102942, R01 AI097333, AI074878, AI095466,
AI095608, AI095776, AI102942, R01 AI061570, R21 AI087990, U01 AI095608,
U01 AI095776, R01 AI095466]
NR 13
TC 4
Z9 4
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD DEC
PY 2013
VL 43
IS 12
BP 3096
EP 3097
DI 10.1002/eji.201344133
PG 2
WC Immunology
SC Immunology
GA 266YX
UT WOS:000328061600005
PM 24166766
ER
PT J
AU Hillyer, P
Raviv, N
Gold, DM
Dougherty, D
Liu, J
Johnson, TR
Graham, BS
Rabin, RL
AF Hillyer, Philippa
Raviv, Nataly
Gold, Doria M.
Dougherty, Danielle
Liu, Jie
Johnson, Teresa R.
Graham, Barney S.
Rabin, Ronald L.
TI Subtypes of type I IFN differentially enhance cytokine expression by
suboptimally stimulated CD4(+) T cells
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE CD4(+) Tcells; Cytokine expression; IFNs; Memory cells; Th cells
ID RESPIRATORY SYNCYTIAL VIRUS; HUMAN INTERFERON-ALPHA; DENDRITIC CELLS;
EFFECTOR FUNCTIONS; CD154 EXPRESSION; C-MAF; RESPONSES; INFECTION;
MEMORY; INTERLEUKIN-10
AB Human type I interferons (IFNs) include IFN- and 12 subtypes of IFN-. During viral infection, infiltrating memory CD4(+) T cells are exposed to IFNs, but their impact on memory T-cell function is poorly understood. To address this, we pretreated PBMCs with different IFNs for 16 h before stimulation with Staphylococcus aureus enterotoxin B and measured cytokine expression by flow cytometry. IFN-8 and -10 most potently enhanced expression of IFN-, IL-2, and IL-4. Potency among the subtypes differed most at doses between 10 and 100 U/mL. While enhancement of IL-2 and IL-4 correlated with the time of preincubation with type I IFN, IFN- production was enhanced best when IFN- was added immediately preceding or simultaneously with T-cell stimulation. Comparison of T-cell responses to multiple doses of Staphylococcus aureus enterotoxin B and to peptide libraries from RSV or CMV demonstrated that IFN- best enhanced cytokine expression when CD4(+) T cells were suboptimally stimulated. We conclude that type I IFNs enhance Th1 and Th2 function with dose dependency and subtype specificity, and best when T-cell stimulation is suboptimal. While type I IFNs may beneficially enhance CD4(+) T-cell memory responses to vaccines or viral pathogens, they may also enhance the function of resident Th2 cells and exacerbate allergic inflammation.
C1 [Hillyer, Philippa; Raviv, Nataly; Gold, Doria M.; Dougherty, Danielle; Rabin, Ronald L.] US FDA, Lab Immunobiochem, Div Bacterial Parasit & Allergen Prod, Off Vaccines Res & Review,Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
[Liu, Jie; Johnson, Teresa R.; Graham, Barney S.] NIAID, Viral Pathogenesis Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Rabin, RL (reprint author), US FDA, Div Bacterial Parasit & Allergen Prod, Off Vaccines Res & Review, Ctr Biol Evaluat & Res, Bldg 29,Room 203A,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM ronald.rabin@fda.hhs.gov
FU CBER
FX The authors thank Howard Mostowski for performing flow-activated cell
sorting, Joanne Yu for antibody conjugation, Rachel Shepard for help
with preparing the figures, Joe Casazza for the CMV pp65 peptide
library, and Dragana Jankovic, Jack Ragheb, and Calman Prussin for
helpful discussion in preparing the manuscript. This project was
supported by CBER intramural funds.
NR 62
TC 5
Z9 5
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD DEC
PY 2013
VL 43
IS 12
BP 3197
EP 3208
DI 10.1002/eji.201243288
PG 12
WC Immunology
SC Immunology
GA 266YX
UT WOS:000328061600018
PM 24030809
ER
PT J
AU Nakaya, N
Sultana, A
Munasinghe, J
Cheng, AW
Mattson, MP
Tomarev, SI
AF Nakaya, Naoki
Sultana, Afia
Munasinghe, Jeeva
Cheng, Aiwu
Mattson, Mark P.
Tomarev, Stanislav I.
TI Deletion in the N-terminal half of olfactomedin 1 modifies its
interaction with synaptic proteins and causes brain dystrophy and
abnormal behavior in mice
SO EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Olfactomedin 1; AMPA receptor; Neurobiology; Proteomics; Cell signaling;
Mouse; Anxiety behavior; Olfactory defects
ID OPEN-ANGLE GLAUCOMA; PAIR-RULE GENE; IN-VIVO; RECEPTOR; CALCIUM;
IDENTIFICATION; EXPRESSION; DISTINCT; DOMAIN; AMPA
AB Olfactomedin 1 (Olfm1) is a secreted glycoprotein that is preferentially expressed in neuronal tissues. Here we show that deletion of exons 4 and 5 from the Olfm1 gene, which encodes a 52 amino acid long region in the N-terminal part of the protein, increased neonatal death and reduced body weight of surviving homozygous mice. Magnetic resonance imaging analyses revealed reduced brain volume and attenuated size of white matter tracts such as the anterior commissure, corpus callosum, and optic nerve. Adult Olfm1 mutant mice demonstrated abnormal behavior in several tests including reduced marble digging, elevated plus maze test, nesting activity and latency on balance beam tests as compared with their wild-type littermates. The olfactory system was both structurally and functionally disturbed by the mutation in the Olfml gene as shown by functional magnetic resonance imaging analysis and a smell test. Deficiencies of the olfactory system may contribute to the neonatal death and loss of body weight of Olfm1 mutant. Shotgun proteomics revealed 59 candidate proteins that coprecipitated with wild-type or mutant Olfml proteins in postnatal day 1 brain. Olfm1-binding targets included GluR2, Cav2.1, teneurin-4 and Kidins220. Modified interaction of Olfml with binding targets led to an increase in intracellular Ca2+ concentration and activation of ERK1/2, MEK1 and CaMKII in the hippocampus and olfactory bulb of If-TO mutant mice compared with their wild-type littermates. Excessive activation of the CaMKII and Ras-ERK pathways in the Olfm1 mutant olfactory bulb and hippocampus by elevated intracellular calcium may contribute to the abnormal behavior and olfactory activity of Olfm1 mutant mice. Published by Elsevier Inc.
C1 [Nakaya, Naoki; Sultana, Afia; Tomarev, Stanislav I.] NEI, Gangl Cell Biol Sect, Lab Retinal Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
[Munasinghe, Jeeva] NINDS, In Vivo NMR Ctr, NIH, Bethesda, MD 20892 USA.
[Cheng, Aiwu; Mattson, Mark P.] NIA, Neurosci Lab, NIH, Baltimore, MD 21224 USA.
RP Tomarev, SI (reprint author), NEI, Gangl Cell Biol Sect, Lab Retinal Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
EM nakayan@nei.nih.gov; sultana@nei.nih.gov; munasinj@ninds.nih.gov;
chengai@grc.nia.nih.gov; mattsonm@grc.nia.nih.gov; tomarevs@nei.nih.gov
FU Intramural Research Programs of the National Eye Institute, National
Institute of Neurological Disorders; National Aging Institute National
Institutes of Health
FX This work was supported by the Intramural Research Programs of the
National Eye Institute, National Institute of Neurological Disorders,
and National Aging Institute - National Institutes of Health.
NR 56
TC 6
Z9 6
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
EI 1090-2430
J9 EXP NEUROL
JI Exp. Neurol.
PD DEC
PY 2013
VL 250
BP 205
EP 218
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 270FZ
UT WOS:000328305600022
PM 24095980
ER
PT J
AU Wellman, CL
Camp, M
Jones, VM
MacPherson, KP
Ihne, J
Fitzgerald, P
Maroun, M
Drabant, E
Bogdan, R
Hariri, AR
Holmes, A
AF Wellman, Cara L.
Camp, Marguerite
Jones, V. Morgan
MacPherson, Kathryn P.
Ihne, Jessica
Fitzgerald, Paul
Maroun, Mouna
Drabant, Emily
Bogdan, Ryan
Hariri, Ahmad R.
Holmes, Andrew
TI Convergent effects of mouse Pet-1 deletion and human PET-1 variation on
amygdala fear and threat processing
SO EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Basolateral amygdala; Medial prefrontal cortex; Fear conditioning;
Serotonin; FEV
ID TRANSPORTER KNOCKOUT MICE; SEROTONIN TRANSPORTER; STRAIN DIFFERENCES;
BASOLATERAL AMYGDALA; MOLECULAR-GENETICS; CONDITIONED FEAR;
BRAIN-SEROTONIN; CANDIDATE GENE; STRESS; EXTINCTION
AB Serotonin is critical for shaping the development of neural circuits regulating emotion. Pet-1 (FEV-1) is an ETS-domain transcription factor essential for differentiation and forebrain targeting of serotonin neurons. Constitutive P knockout (KO) causes major loss of serotonin neurons and forebrain serotonin availability, and behavioral abnormalities. We phenotyped Pet-1 KO mice for fear conditioning and extinction, and on a battery of assays for anxiety- and depression-related behaviors. Morphology of Golgi-stained neurons in basolateral amygdala (BLA) and prelimbic cortex was examined. Using human imaging genetics, a common variant (rs860573) in the PET-1 (FEY) gene was tested for effects on threat-related amygdala reactivity and psychopathology in 88 Asian-ancestry subjects. Pet-1 KO mice exhibited increased acquisition and expression of fear, and elevated fear recovery following extinction, relative to wild-type (WT). BLA dendrites of Pet-1 KO mice were significantly longer than in WT. Human PET-1 variation associated with differences in amygdala threat processing and psychopathology. This novel evidence for the role of Pet-1 in fear processing and dendritic organization of amygdala neurons and in human amygdala threat processing extends a growing literature demonstrating the influence of genetic variation in the serotonin system on emotional regulation via effects on structure and function of underlying corticolimbic circuitry. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Wellman, Cara L.; Jones, V. Morgan] Indiana Univ, Ctr Integrat Study Anim Behav, Dept Psychol & Brain Sci, Bloomington, IN 47405 USA.
[Camp, Marguerite; MacPherson, Kathryn P.; Ihne, Jessica; Fitzgerald, Paul; Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, NIH, Bethesda, MD USA.
[Maroun, Mouna] Univ Haifa, Fac Nat Sci, Dept Neurobiol, IL-31999 Haifa, Israel.
[Drabant, Emily] 23&Me, Mountain View, CA USA.
[Bogdan, Ryan; Hariri, Ahmad R.] Duke Univ, Lab NeuroGenet, Dept Psychol & Neurosci, Inst Genome Sci & Policy, Durham, NC USA.
RP Wellman, CL (reprint author), Indiana Univ, 1101 E 10th St, Bloomington, IN 47405 USA.
EM wellmanc@indiana.edu
OI Bogdan, Ryan/0000-0002-1430-1045; Reed, Jessica/0000-0003-0550-7284
FU US-Israel Binational Science Foundation [2007096]; Intramural Research
Program of the National Institute on Alcoholism and Alcohol Abuse
[Z01-AA000411]; Duke University
FX This work was supported by the US-Israel Binational Science Foundation
(grant number 2007096 to AH, CLW, MM); the Intramural Research Program
of the National Institute on Alcoholism and Alcohol Abuse (Z01-AA000411
to AH), and Duke University.
NR 74
TC 9
Z9 9
U1 1
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
EI 1090-2430
J9 EXP NEUROL
JI Exp. Neurol.
PD DEC
PY 2013
VL 250
BP 260
EP 269
DI 10.1016/j.expneurol.2013.09.025
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 270FZ
UT WOS:000328305600028
PM 24100022
ER
PT J
AU Dalal, M
Jacobs-El, N
Nicholson, B
Tuo, J
Chew, E
Chan, CC
Nussenblatt, R
Ferris, F
Meyerle, C
AF Dalal, Monica
Jacobs-El, Naima
Nicholson, Benjamin
Tuo, Jingsheng
Chew, Emily
Chan, Chi-Chao
Nussenblatt, Robert
Ferris, Frederick
Meyerle, Catherine
TI Subconjunctival Palomid 529 in the treatment of neovascular age-related
macular degeneration
SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
LA English
DT Article
DE Akt/mTOR; Choroidal neovascularization; Neovascular age-related macular
degeneration; Palomid 529
ID ANGIOGENESIS; RAPAMYCIN; INHIBITOR; NLRP3; CELLS
AB Recent evidence suggests that neovascular age-related macular degeneration (AMD) may have an immune mediated component. Palomid 529, an investigational medication involving the immune Akt/mTOR pathway, is unique in dissociating both targets of rapamycin complexes TORC1 and TORC2. This small short-term pilot study assesses the safety of subconjunctival Palomid 529 in the treatment of neovascular AMD, with some limited efficacy information.
In this 12-week phase I open-label prospective pilot study, five participants with neovascular age-related macular degeneration that were refractory to intravitreal anti-vascular endothelial growth factor (VEGF) received three serial monthly subconjunctival doses of 1.9 mg Palomid 529. All participants were also offered concomitant monthly intravitreal anti-VEGF injections. Safety was monitored via adverse events recording. Additional outcome measures included visual acuity, optical coherence tomography, fluorescein angiography, indocyanine green angiography and fundus photography.
The study drug was well-tolerated by all participants. There were no drug-related adverse events and no serious adverse events. A depot formed at the injection site, which persisted at the end of the study. In these anti-VEGF refractory patients, no clinically important changes in best-corrected visual acuity, fluorescein leakage pattern, choroidal neovascularization size on indocyanine green angiography, or autofluorescence pattern on fundus autofluorescence were observed compared to baseline. The fluid status, assessed with optical coherence tomography showed that central retinal thickness and macular volume remained stable in three participants, while the other two participants clinically progressed.
Serial subconjunctival injections of Palomid 529 were well-tolerated and resulted in depot formation. There were no concerns for any ocular or systemic toxicity during this small short-term study. Larger randomized studies are required to determine efficacy.
C1 [Dalal, Monica; Tuo, Jingsheng; Chan, Chi-Chao; Nussenblatt, Robert] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Jacobs-El, Naima; Nicholson, Benjamin; Chew, Emily; Ferris, Frederick; Meyerle, Catherine] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
RP Meyerle, C (reprint author), NEI, Div Epidemiol & Clin Applicat, NIH, Bldg 10 Magnuson Room 10D40,10 Ctr Dr, Bethesda, MD 20892 USA.
EM meyerlec@nei.nih.gov
FU Intramural NIH HHS [ZIA EY000418-10]
NR 18
TC 8
Z9 8
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0721-832X
EI 1435-702X
J9 GRAEF ARCH CLIN EXP
JI Graefes Arch. Clin. Exp. Ophthalmol.
PD DEC
PY 2013
VL 251
IS 12
BP 2705
EP 2709
DI 10.1007/s00417-013-2375-7
PG 5
WC Ophthalmology
SC Ophthalmology
GA 270US
UT WOS:000328345000006
PM 23689994
ER
PT J
AU Kessler, RC
Colpe, LJ
Fullerton, CS
Gebler, N
Naifeh, JA
Nock, MK
Sampson, NA
Schoenbaum, M
Zaslavsky, AM
Stein, MB
Ursano, RJ
Heeringa, SG
AF Kessler, Ronald C.
Colpe, Lisa J.
Fullerton, Carol S.
Gebler, Nancy
Naifeh, James A.
Nock, Matthew K.
Sampson, Nancy A.
Schoenbaum, Michael
Zaslavsky, Alan M.
Stein, Murray B.
Ursano, Robert J.
Heeringa, Steven G.
TI Design of the Army Study to Assess Risk and Resilience in Servicemembers
(Army STARRS)
SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH
LA English
DT Article
DE Suicide; mental disorders; US Army; epidemiologic research design;
design effects; sample bias; sample weights; survey design efficiency;
survey sampling
ID ADOLESCENT SUICIDE; PROPENSITY SCORE; VETERANS; BEHAVIORS; DISORDER; MEN
AB The Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS) is a multi-component epidemiological and neurobiological study designed to generate actionable evidence-based recommendations to reduce US Army suicides and increase basic knowledge about the determinants of suicidality. This report presents an overview of the designs of the six components of the Army STARRS. These include: an integrated analysis of the Historical Administrative Data Study (HADS) designed to provide data on significant administrative predictors of suicides among the more than 1.6 million soldiers on active duty in 2004-2009; retrospective case-control studies of suicide attempts and fatalities; separate large-scale cross-sectional studies of new soldiers (i.e. those just beginning Basic Combat Training [BCT], who completed self-administered questionnaires [SAQs] and neurocognitive tests and provided blood samples) and soldiers exclusive of those in BCT (who completed SAQs); a pre-post deployment study of soldiers in three Brigade Combat Teams about to deploy to Afghanistan (who completed SAQs and provided blood samples) followed multiple times after returning from deployment; and a platform for following up Army STARRS participants who have returned to civilian life. Department of Defense/Army administrative data records are linked with SAQ data to examine prospective associations between self-reports and subsequent suicidality. The presentation closes with a discussion of the methodological advantages of cross-component coordination. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Kessler, Ronald C.; Sampson, Nancy A.; Zaslavsky, Alan M.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Colpe, Lisa J.; Schoenbaum, Michael] NIMH, Bethesda, MD 20892 USA.
[Fullerton, Carol S.; Naifeh, James A.; Ursano, Robert J.] Univ Sch Med, Ctr Study Traumat Stress, Dept Psychiat, Uniformed Serv, Bethesda, MD USA.
[Gebler, Nancy; Heeringa, Steven G.] Univ Michigan, Inst Social Res, Ann Arbor, MI USA.
[Nock, Matthew K.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Stein, Murray B.] VA San Diego Healthcare Syst, San Diego, CA USA.
RP Kessler, RC (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
EM NCS@hcp.med.harvard.edu
FU US Department of Health and Human Services, National Institutes of
Health, National Institute of Mental Health (NIH/NIMH); Department of
the Army [U01MH087981]
FX Army STARRS was sponsored by the Department of the Army and funded under
cooperative agreement number U01MH087981 with the US Department of
Health and Human Services, National Institutes of Health, National
Institute of Mental Health (NIH/NIMH). The contents are solely the
responsibility of the authors and do not necessarily represent the views
of the Department of Health and Human Services, NIMH, the Department of
the Army, or the Department of Defense.
NR 25
TC 30
Z9 30
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1049-8931
EI 1557-0657
J9 INT J METH PSYCH RES
JI Int. J. Methods Psychiatr. Res.
PD DEC
PY 2013
VL 22
IS 4
SI SI
BP 267
EP 275
DI 10.1002/mpr.1401
PG 9
WC Psychiatry
SC Psychiatry
GA 266BP
UT WOS:000327997600001
PM 24318217
ER
PT J
AU Heeringa, SG
Gebler, N
Colpe, LJ
Fullerton, CS
Hwang, I
Kessler, RC
Naifeh, JA
Nock, MK
Sampson, NA
Schoenbaum, M
Zaslavsky, AM
Stein, MB
Ursano, RJ
AF Heeringa, Steven G.
Gebler, Nancy
Colpe, Lisa J.
Fullerton, Carol S.
Hwang, Irving
Kessler, Ronald C.
Naifeh, James A.
Nock, Matthew K.
Sampson, Nancy A.
Schoenbaum, Michael
Zaslavsky, Alan M.
Stein, Murray B.
Ursano, Robert J.
TI Field procedures in the Army Study to Assess Risk and Resilience in
Servicemembers (Army STARRS)
SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH
LA English
DT Article
DE suicide; mental disorders; US Army; epidemiologic research design;
design effects; sample bias; sample weights; survey design efficiency;
survey sampling
ID SEROTONIN TRANSPORTER BINDING; DEPRESSED SUICIDE ATTEMPTERS;
ADRENERGIC-RECEPTOR BINDING; OXIDASE-A GENE; IMPULSIVE BEHAVIOR; MAJOR
DEPRESSION; MENTAL-HEALTH; VICTIMS; POLYMORPHISM; BRAIN
AB The Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS) is a multi-component epidemiological and neurobiological study of unprecedented size and complexity designed to generate actionable evidence-based recommendations to reduce US Army suicides and increase basic knowledge about determinants of suicidality by carrying out coordinated component studies. A number of major logistical challenges were faced in implementing these studies. The current report presents an overview of the approaches taken to meet these challenges, with a special focus on the field procedures used to implement the component studies. As detailed in the paper, these challenges were addressed at the onset of the initiative by establishing an Executive Committee, a Data Coordination Center (the Survey Research Center [SRC] at the University of Michigan), and study-specific design and analysis teams that worked with staff on instrumentation and field procedures. SRC staff, in turn, worked with the Office of the Deputy Under Secretary of the Army (ODUSA) and local Army Points of Contact (POCs) to address logistical issues and facilitate data collection. These structures, coupled with careful fieldworker training, supervision, and piloting, contributed to the major Army STARRS data collection efforts having higher response rates than previous large-scale studies of comparable military samples. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Heeringa, Steven G.; Gebler, Nancy] Univ Michigan, Inst Social Res, Ann Arbor, MI USA.
[Colpe, Lisa J.; Schoenbaum, Michael] NIMH, Bethesda, MD 20892 USA.
[Fullerton, Carol S.; Naifeh, James A.; Ursano, Robert J.] Uniformed Serv Univ Hlth Sci, Sch Med, Ctr Study Traumat Stress, Dept Psychiat, Bethesda, MD 20814 USA.
[Hwang, Irving; Kessler, Ronald C.; Sampson, Nancy A.; Zaslavsky, Alan M.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Nock, Matthew K.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Stein, Murray B.] VA San Diego Healthcare Syst, San Diego, CA USA.
RP Kessler, RC (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
EM NCS@hcp.med.harvard.edu
FU Department of the Army [U01MH087981]; US Department of Health and Human
Services, National Institutes of Health, National Institute of Mental
Health (NIH/NIMH)
FX Army STARRS was sponsored by the Department of the Army and funded under
cooperative agreement number U01MH087981 with the US Department of
Health and Human Services, National Institutes of Health, National
Institute of Mental Health (NIH/NIMH). The contents are solely the
responsibility of the authors and do not necessarily represent the views
of the Department of Health and Human Services, NIMH, the Department of
the Army, or the Department of Defense.
NR 51
TC 7
Z9 7
U1 2
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1049-8931
EI 1557-0657
J9 INT J METH PSYCH RES
JI Int. J. Methods Psychiatr. Res.
PD DEC
PY 2013
VL 22
IS 4
SI SI
BP 276
EP 287
DI 10.1002/mpr.1400
PG 12
WC Psychiatry
SC Psychiatry
GA 266BP
UT WOS:000327997600002
PM 24038395
ER
PT J
AU Kessler, RC
Heeringa, SG
Colpe, LJ
Fullerton, CS
Gebler, N
Hwang, I
Naifeh, JA
Nock, MK
Sampson, NA
Schoenbaum, M
Zaslavsky, AM
Stein, MB
Ursano, RJ
AF Kessler, Ronald C.
Heeringa, Steven G.
Colpe, Lisa J.
Fullerton, Carol S.
Gebler, Nancy
Hwang, Irving
Naifeh, James A.
Nock, Matthew K.
Sampson, Nancy A.
Schoenbaum, Michael
Zaslavsky, Alan M.
Stein, Murray B.
Ursano, Robert J.
TI Response bias, weighting adjustments, and design effects in the Army
Study to Assess Risk and Resilience in Servicemembers (Army STARRS)
SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH
LA English
DT Article
DE suicide; mental disorders; US Army; epidemiologic research design;
design effects; sample bias; sample weights; survey design efficiency;
survey sampling
ID MENTAL-HEALTH; SURVEY PARTICIPATION; SEXUAL-BEHAVIOR; DATA-COLLECTION;
DRUG-USE; COMBAT; ANONYMITY; DISCLOSURE; IMPACT
AB The Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS) is a multi-component epidemiological and neurobiological study designed to generate actionable recommendations to reduce US Army suicides and increase knowledge about determinants of suicidality. Three Army STARRS component studies are large-scale surveys: one of new soldiers prior to beginning Basic Combat Training (BCT; n=50,765 completed self-administered questionnaires); another of other soldiers exclusive of those in BCT (n=35,372); and a third of three Brigade Combat Teams about to deploy to Afghanistan who are being followed multiple times after returning from deployment (n=9421). Although the response rates in these surveys are quite good (72.0-90.8%), questions can be raised about sample biases in estimating prevalence of mental disorders and suicidality, the main outcomes of the surveys based on evidence that people in the general population with mental disorders are under-represented in community surveys. This paper presents the results of analyses designed to determine whether such bias exists in the Army STARRS surveys and, if so, to develop weights to correct for these biases. Data are also presented on sample inefficiencies introduced by weighting and sample clustering and on analyses of the trade-off between bias and efficiency in weight trimming. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Kessler, Ronald C.; Hwang, Irving; Sampson, Nancy A.; Zaslavsky, Alan M.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Heeringa, Steven G.; Gebler, Nancy] Univ Michigan, Inst Social Res, Ann Arbor, MI USA.
[Colpe, Lisa J.; Schoenbaum, Michael] NIMH, Bethesda, MD 20892 USA.
[Fullerton, Carol S.; Naifeh, James A.; Ursano, Robert J.] Uniformed Serv Univ Hlth Sci, Sch Med, Ctr Study Traumat Stress, Dept Psychiat, Bethesda, MD 20814 USA.
[Nock, Matthew K.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Stein, Murray B.] VA San Diego Healthcare Syst, San Diego, CA USA.
RP Kessler, RC (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
EM NCS@hcp.med.harvard.edu
FU Department of the Army [U01MH087981]; US Department of Health and Human
Services, National Institutes of Health, National Institute of Mental
Health (NIH/NIMH)
FX Army STARRS was sponsored by the Department of the Army and funded under
cooperative agreement number U01MH087981 with the US Department of
Health and Human Services, National Institutes of Health, National
Institute of Mental Health (NIH/NIMH). The contents are solely the
responsibility of the authors and do not necessarily represent the views
of the Department of Health and Human Services, NIMH, the Department of
the Army, or the Department of Defense.
NR 29
TC 14
Z9 14
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1049-8931
EI 1557-0657
J9 INT J METH PSYCH RES
JI Int. J. Methods Psychiatr. Res.
PD DEC
PY 2013
VL 22
IS 4
SI SI
BP 288
EP 302
DI 10.1002/mpr.1399
PG 15
WC Psychiatry
SC Psychiatry
GA 266BP
UT WOS:000327997600003
PM 24318218
ER
PT J
AU Kessler, RC
Santiago, PN
Colpe, LJ
Dempsey, CL
First, MB
Heeringa, SG
Stein, MB
Fullerton, CS
Gruber, MJ
Naifeh, JA
Nock, MK
Sampson, NA
Schoenbaum, M
Zaslavsky, AM
Ursano, RJ
AF Kessler, Ronald C.
Santiago, Patcho N.
Colpe, Lisa J.
Dempsey, Catherine L.
First, Michael B.
Heeringa, Steven G.
Stein, Murray B.
Fullerton, Carol S.
Gruber, Michael J.
Naifeh, James A.
Nock, Matthew K.
Sampson, Nancy A.
Schoenbaum, Michael
Zaslavsky, Alan M.
Ursano, Robert J.
TI Clinical reappraisal of the Composite International Diagnostic Interview
Screening Scales (CIDI-SC) in the Army Study to Assess Risk and
Resilience in Servicemembers (Army STARRS)
SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH
LA English
DT Article
DE Composite International Diagnostic Interview (CIDI); CIDI Screening
Scales (CIDI-SC); diagnostic concordance; PTSD checklist (PCL);
screening scales; validity
ID COMORBIDITY SURVEY REPLICATION; WORLD-HEALTH-ORGANIZATION; DEFICIT
HYPERACTIVITY DISORDER; POSTTRAUMATIC-STRESS-DISORDER; BIPOLAR SPECTRUM
DISORDER; PSYCHOMETRIC PROPERTIES; PSYCHIATRIC-DISORDERS; MULTIPLE
IMPUTATION; GENERAL-POPULATION; MAJOR DEPRESSION
AB A clinical reappraisal study was carried out in conjunction with the Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS) All-Army Study (AAS) to evaluate concordance of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) diagnoses based on the Composite International Diagnostic Interview Screening Scales (CIDI-SC) and post-traumatic stress disorder (PTSD) checklist (PCL) with diagnoses based on independent clinical reappraisal interviews (Structured Clinical Interview for DSM-IV [SCID]). Diagnoses included: lifetime mania/hypomania, panic disorder, and intermittent explosive disorder; six-month adult attention-deficit/hyperactivity disorder; and 30-day major depressive episode, generalized anxiety disorder, PTSD, and substance (alcohol or drug) use disorder (abuse or dependence). The sample (n=460) was weighted for over-sampling CIDI-SC/PCL screened positives. Diagnostic thresholds were set to equalize false positives and false negatives. Good individual-level concordance was found between CIDI-SC/PCL and SCID diagnoses at these thresholds (area under curve [AUC]=0.69-0.79). AUC was considerably higher for continuous than dichotomous screening scale scores (AUC=0.80-0.90), arguing for substantive analyses using not only dichotomous case designations but also continuous measures of predicted probabilities of clinical diagnoses. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Kessler, Ronald C.; Gruber, Michael J.; Sampson, Nancy A.; Zaslavsky, Alan M.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Santiago, Patcho N.; Dempsey, Catherine L.; Fullerton, Carol S.; Naifeh, James A.; Ursano, Robert J.] Uniformed Serv Univ Hlth Sci, Ctr Study Traumat Stress, Dept Psychiat, Bethesda, MD 20814 USA.
[Colpe, Lisa J.; Schoenbaum, Michael] NIMH, Bethesda, MD 20892 USA.
[First, Michael B.] Columbia Univ, Dept Psychiat, New York, NY USA.
[First, Michael B.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Heeringa, Steven G.] Univ Michigan, Inst Social Res, Ann Arbor, MI USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Stein, Murray B.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Stein, Murray B.] VA San Diego Healthcare Syst, San Diego, CA USA.
[Nock, Matthew K.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
RP Kessler, RC (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM NCS@hcp.med.harvard.edu
FU Department of the Army [U01MH087981]; US Department of Health and Human
Services, National Institutes of Health, National Institute of Mental
Health (NIH/NIMH)
FX Army STARRS was sponsored by the Department of the Army and funded under
cooperative agreement number U01MH087981 with the US Department of
Health and Human Services, National Institutes of Health, National
Institute of Mental Health (NIH/NIMH). The contents are solely the
responsibility of the authors and do not necessarily represent the views
of the Department of Health and Human Services, NIMH, the Department of
the Army, or the Department of Defense.
NR 59
TC 15
Z9 15
U1 2
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1049-8931
EI 1557-0657
J9 INT J METH PSYCH RES
JI Int. J. Methods Psychiatr. Res.
PD DEC
PY 2013
VL 22
IS 4
SI SI
BP 303
EP 321
DI 10.1002/mpr.1398
PG 19
WC Psychiatry
SC Psychiatry
GA 266BP
UT WOS:000327997600004
PM 24318219
ER
PT J
AU Bottaro, S
Lindorff-Larsen, K
Best, RB
AF Bottaro, Sandro
Lindorff-Larsen, Kresten
Best, Robert B.
TI Variational Optimization of an All-Atom Implicit Solvent Force Field To
Match Explicit Solvent Simulation Data
SO JOURNAL OF CHEMICAL THEORY AND COMPUTATION
LA English
DT Article
ID MOLECULAR-DYNAMICS SIMULATIONS; PROTEIN-FOLDING THERMODYNAMICS;
INHOMOGENEOUS FLUID APPROACH; BETA-HAIRPIN FORMATION; CONTINUUM
ELECTROSTATICS; SOLVATION THERMODYNAMICS; NMR-SPECTROSCOPY; ALANINE
PEPTIDES; AQUEOUS-SOLUTION; CHEMICAL-SHIFTS
AB The development of accurate implicit solvation models with low computational cost is essential for addressing many large-scale biophysical problems. Here, we present an efficient solvation term based on a Gaussian solvent-exclusion model (EEF1) for simulations of proteins in aqueous environment, with the primary aim of having a good overlap with explicit solvent simulations, particularly for unfolded and disordered states as would be needed for multiscale applications. In order to achieve this, we have used a recently proposed coarse-graining procedure based on minimization of an entropy-related objective function to train the model to reproduce the equilibrium distribution obtained from explicit water simulations. Via this methodology, we have optimized both a charge screening parameter and a backbone torsion term against explicit solvent simulations of an alpha-helical and a beta-stranded peptide. The performance of the resulting effective energy function, termed EEF1-SB, is tested with respect to the properties of folded proteins, the folding of small peptides or fast-folding proteins, and NMR data for intrinsically disordered proteins. The results show that EEF-SB provides a reasonable description of a wide range of systems, but its key advantage over other methods tested is that it captures very well the structure and dimensions of disordered or weakly structured peptides. EEF1-SB is thus a computationally inexpensive (similar to 10 times faster than Generalized-Born methods) and transferable approximation for treating solvent effects.
C1 [Bottaro, Sandro; Lindorff-Larsen, Kresten] Univ Copenhagen, Dept Biol, Copenhagen, Denmark.
[Best, Robert B.] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
[Best, Robert B.] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Bottaro, Sandro] SISSA, I-34014 Trieste, Italy.
RP Lindorff-Larsen, K (reprint author), Univ Copenhagen, Dept Biol, Copenhagen, Denmark.
EM lindorff@bio.ku.dk; robertbe@helix.nih.gov
RI Lindorff-Larsen, Kresten/K-6469-2014; Bottaro, Sandro/A-4141-2015; Best,
Robert/H-7588-2016
OI Lindorff-Larsen, Kresten/0000-0002-4750-6039; Bottaro,
Sandro/0000-0003-1606-890X; Best, Robert/0000-0002-7893-3543
FU Royal Society University Research Fellowship at Cambridge; National
Institute for Diabetes and Digestive and Kidney Diseases of the National
Institutes of Health; Novo-Nordisk Foundation
FX R.B.B. was supported by a Royal Society University Research Fellowship
while at Cambridge and by the Intramural Research Program of the
National Institute for Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health. S.B. and K.L.-L. were supported by a
Hallas-Moller stipend from the Novo-Nordisk Foundation. 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).
NR 90
TC 14
Z9 14
U1 0
U2 30
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9618
EI 1549-9626
J9 J CHEM THEORY COMPUT
JI J. Chem. Theory Comput.
PD DEC
PY 2013
VL 9
IS 12
BP 5641
EP 5652
DI 10.1021/ct400730n
PG 12
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 272CI
UT WOS:000328437500044
PM 24748852
ER
PT J
AU Lionakis, MS
Swamydas, M
Fischer, BG
Plantinga, TS
Johnson, MD
Jaeger, M
Green, NM
Masedunskas, A
Weigert, R
Mikelis, C
Wan, WZ
Lee, CCR
Lim, JK
Rivollier, A
Yang, JC
Laird, GM
Wheeler, RT
Alexander, BD
Perfect, JR
Gao, JL
Kullberg, BJ
Netea, MG
Murphy, PM
AF Lionakis, Michail S.
Swamydas, Muthulekha
Fischer, Brett G.
Plantinga, Theo S.
Johnson, Melissa D.
Jaeger, Martin
Green, Nathaniel M.
Masedunskas, Andrius
Weigert, Roberto
Mikelis, Constantinos
Wan, Wuzhou
Lee, Chyi-Chia Richard
Lim, Jean K.
Rivollier, Aymeric
Yang, John C.
Laird, Greg M.
Wheeler, Robert T.
Alexander, Barbara D.
Perfect, John R.
Gao, Ji-Liang
Kullberg, Bart-Jan
Netea, Mihai G.
Murphy, Philip M.
TI CX(3)CR1-dependent renal macrophage survival promotes Candida control
and host survival
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CHEMOKINE FRACTALKINE; CELL PROLIFERATION; UNITED-STATES; CX(3)CR1;
CX3CR1; MICE; INFLAMMATION; MONOCYTES; DIFFERENTIATION; SUSCEPTIBILITY
AB Systemic Candida albicans infection causes high morbidity and mortality and is associated with neutropenia; however, the roles of other innate immune cells in pathogenesis are poorly defined. Here, using a mouse model of systemic candidiasis, we found that resident macrophages accumulated in the kidney, the main target organ of infection, and formed direct contacts with the fungus in vivo mainly within the first few hours after infection. Macrophage accumulation and contact with Candida were both markedly reduced in mice lacking chemokine receptor CX(3)CR1, which was found almost exclusively on resident macrophages in uninfected kidneys. Infected Cx3cr1(-/-) mice uniformly succumbed to Candida-induced renal failure, but exhibited clearance of the fungus in all other organs tested. Renal macrophage deficiency in infected Cx3cr1(-/-) mice was clue to reduced macrophage survival, not impaired proliferation, trafficking, or differentiation. In humans, the dysfunctional CX(3)CR1 allele CX(3)CR1-M280 was associated with increased risk of systemic candidiasis. Together, these data indicate that CX(3)CR1-mediated renal resident macrophage survival is a critical innate mechanism of early fungal control that influences host survival in systemic candidiasis.
C1 [Lionakis, Michail S.; Swamydas, Muthulekha; Fischer, Brett G.] NIAID, Clin Mycol Unit, NIH, Bethesda, MD 20892 USA.
[Lionakis, Michail S.; Fischer, Brett G.; Wan, Wuzhou; Lim, Jean K.; Gao, Ji-Liang; Murphy, Philip M.] NIAID, Mol Signaling Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Lionakis, Michail S.; Swamydas, Muthulekha; Green, Nathaniel M.] NIAID, Fungal Pathogenesis Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Plantinga, Theo S.; Jaeger, Martin; Kullberg, Bart-Jan; Netea, Mihai G.] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Johnson, Melissa D.; Yang, John C.; Laird, Greg M.; Alexander, Barbara D.; Perfect, John R.] Duke Univ, Sch Med, Div Infect Dis, Durham, NC USA.
[Masedunskas, Andrius; Weigert, Roberto] Natl Inst Dent & Craniofacial Res, Intracellular Membrane Trafficking Unit, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
[Mikelis, Constantinos] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
[Lee, Chyi-Chia Richard] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Rivollier, Aymeric] NIAID, Mucosal Immunobiol Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Wheeler, Robert T.] Univ Maine, Dept Mol & Biomed Sci, Orono, ME USA.
RP Lionakis, MS (reprint author), NIH, Bldg 10,Room 11C102,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM lionakism@mail.nih.gov; pmm@nih.gov
RI Kullberg, Bart Jan/C-8520-2013; Plantinga, Theo/A-6895-2015; Netea,
Mihai/N-5155-2014; Jaeger, Martin/H-3359-2015;
OI Masedunskas, Andrius/0000-0002-4533-5467; Johnson,
Melissa/0000-0002-6606-9460; Wheeler, Robert/0000-0003-3223-7021
FU Division of Intramural Research (DIR), NIAID, NIH; Transition Program in
Clinical Research (TPCR) of the DIR, NIAID, NIH; ERC [310372]
FX This work was supported by the Division of Intramural Research (DIR),
NIAID, NIH, and in part by the Transition Program in Clinical Research
(TPCR) of the DIR, NIAID, NIH. M.G. Netea was supported by an ERC
Consolidator Grant (no. 310372). The funding source had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript. The authors thank Elizabeth Fischer of
the Research Technologies Branch, NIAID, for performing the TEM, and the
NIAID FACS sorting facility and the Comparative Medicine Branch animal
facilities for technical assistance and animal handling. This work was
presented in part at the 52nd Interscience Conference on Antimicrobial
Agents and Chemotherapy, San Francisco, California, September 9-12,
2012, and at the 2nd Gordon Research Conference on Immunology of Fungal
Infections, Galveston, Texas, January 13-18,2013.
NR 46
TC 62
Z9 63
U1 0
U2 6
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2013
VL 123
IS 12
BP 5035
EP 5051
DI 10.1172/JCI71307
PG 17
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 263RQ
UT WOS:000327826100012
PM 24177428
ER
PT J
AU Price, JV
Haddon, DJ
Kemmer, D
Delepine, G
Mandelbaum, G
Jarrell, JA
Gupta, R
Balboni, I
Chakravarty, EF
Sokolove, J
Shum, AK
Anderson, MS
Cheng, MH
Robinson, WH
Browne, SK
Holland, SM
Baechler, EC
Utz, PJ
AF Price, Jordan V.
Haddon, David J.
Kemmer, Dodge
Delepine, Guillaume
Mandelbaum, Gil
Jarrell, Justin A.
Gupta, Rohit
Balboni, Imelda
Chakravarty, Eliza F.
Sokolove, Jeremy
Shum, Anthony K.
Anderson, Mark S.
Cheng, Mickie H.
Robinson, William H.
Browne, Sarah K.
Holland, Steven M.
Baechler, Emily C.
Utz, Paul J.
TI Protein microarray analysis reveals BAFF-binding autoantibodies in
systemic lupus erythematosus
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID ANTI-CYTOKINE AUTOANTIBODIES; CELL-ACTIVATING FACTOR; CHRONIC
MUCOCUTANEOUS CANDIDIASIS; INTERFERON-REGULATED CHEMOKINES; B-CELLS;
ANTICYTOKINE AUTOANTIBODIES; AUTOIMMUNE-DISEASES; SIGNATURE; GAMMA;
IMMUNODEFICIENCY
AB Autoantibodies against cytokines, chemokines, and growth factors inhibit normal immunity and are implicated in inflammatory autoimmune disease and diseases of immune deficiency. In an effort to evaluate serum from autoimmune and immunodeficient patients for Abs against cytokines, chemokines, and growth factors in a high-throughput and unbiased manner, we constructed a multiplex protein microarray for detection of serum factor-binding Abs and used the microarray to detect autoantibody targets in SLE. We designed a nitrocellulose-surface microarray containing human cytoldnes, chemokines, and other circulating proteins and demonstrated that the array permitted specific detection of serum factor-binding probes. We used the arrays to detect previously described autoantibodies against cytokines in samples from individuals with autoimmune polyenclocrine syndrome type 1 and chronic mycobacterial infection. Serum profiling from individuals with SLE revealed that among several targets, elevated IgG autoantibody reactivity to B cell-activating factor (BAFF) was associated with SLE compared with control samples. BAFF reactivity correlated with the severity of disease-associated features, including IFN-alpha-driven SLE pathology. Our results showed that serum factor protein microarrays facilitate detection of autoantibod.y reactivity to serum factors in human samples and that BAFF-reactive autoantibodies may be associated with an elevated inflammatory disease state within the spectrum of SLE.
C1 [Price, Jordan V.; Haddon, David J.; Kemmer, Dodge; Delepine, Guillaume; Mandelbaum, Gil; Jarrell, Justin A.; Gupta, Rohit; Sokolove, Jeremy; Robinson, William H.; Utz, Paul J.] Stanford Univ, Sch Med, Div Rheumatol & Immunol, Dept Med, Stanford, CA 94305 USA.
[Price, Jordan V.; Haddon, David J.; Kemmer, Dodge; Delepine, Guillaume; Mandelbaum, Gil; Jarrell, Justin A.; Gupta, Rohit; Utz, Paul J.] Stanford Univ, Sch Med, Inst Immun Transplantat & Infect ITI, Stanford, CA 94305 USA.
[Balboni, Imelda] Stanford Univ, Sch Med, Dept Pediat, Div Allergy Immunol & Rheumatol, Stanford, CA 94305 USA.
[Chakravarty, Eliza F.] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
[Sokolove, Jeremy; Robinson, William H.] VA Palo Alto Hlth Care Syst, Palo Alto, CA USA.
[Shum, Anthony K.] UCSF, Dept Med, Div Pulm & Crit Care, San Francisco, CA USA.
[Anderson, Mark S.; Cheng, Mickie H.] UCSF, Dept Med, Diabet Ctr, Div Endocrinol & Metab, San Francisco, CA USA.
[Browne, Sarah K.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Baechler, Emily C.] Univ Minnesota, Sch Med, Ctr Immunol, Minneapolis, MN 55455 USA.
RP Price, JV (reprint author), Stanford Univ, Sch Med, Div Rheumatol & Immunol, CCSR Bldg,Room 2215, Stanford, CA 94305 USA.
EM jvp2099@gmail.com; pjutz@stanford.edu
FU US National Science Foundation Graduate Research Fellowship (NSF GRFP);
Stanford Genome Training Program (SGTP); Canadian Institutes of Health
Research (CIHR); NIH [K08 AI080945, 5 U19AI082719, 1 U19-AI090019];
NHLBI Proteomics [HHSN288201000034C]; Alliance for Lupus Research
[21858]; Canadian Institutes of Health Research [OR-92141]; Stanford
Institute for Immunity, Transplantation, and Infection (ITI) Pilot
Grant; FP [261]; European Union Seventh Framework Programme [261382];
NIH, US National Human Genome Research Institute; National Organization
for Rare Disorders; Donald E. and Delia B. Baxter Foundation Career
Development Award
FX We thank E. Munoz and L. Tarter for coordination with the Stanford
Chronic Immunologic Disease Registry and Repository and A. Meager for
providing the FL-17 BAFF reporter cell line. J.V. Price was funded by a
US National Science Foundation Graduate Research Fellowship (NSF GRFP)
and was supported by the Stanford Genome Training Program (SGTP; NIH, US
National Human Genome Research Institute). DJ. Haddon was funded by a
Canadian Institutes of Health Research (CIHR) postdoctoral fellowship.
A.K. Shum, M.H. Cheng, and M.S. Anderson were funded by the National
Organization for Rare Disorders. I. Balboni is supported by NIH grant
K08 AI080945. P.J. Utz is the recipient of a Donald E. and Delia B.
Baxter Foundation Career Development Award, a gift from the Floren
Family Trust, and a gift from the Ben May Charitable Trust of Mobile,
Alabama, and is supported by NHLBI Proteomics Contract
HHSN288201000034C, Proteomics of Inflammatory Immunity and Pulmonary
Arterial Hypertension, NIH (grant nos. 5 U19AI082719 and 1
U19-AI090019), Alliance for Lupus Research (grant no. 21858), Canadian
Institutes of Health Research (grant no. OR-92141), Stanford Institute
for Immunity, Transplantation, and Infection (ITI) Pilot Grant, and FP
grant no. 261. The research leading to these results has received
funding from the European Union Seventh Framework Programme
(FP7/2007-2013) under grant agreement no. 261382.
NR 51
TC 35
Z9 37
U1 1
U2 10
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2013
VL 123
IS 12
BP 5135
EP 5145
DI 10.1172/JCI70231
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 263RQ
UT WOS:000327826100020
PM 24270423
ER
PT J
AU Mondal, AM
Horikawa, I
Pine, SR
Fujita, K
Morgan, KM
Vera, E
Mazur, SJ
Appella, E
Vojtesek, B
Blasco, MA
Lane, DP
Harris, CC
AF Mondal, Abdul M.
Horikawa, Izumi
Pine, Sharon R.
Fujita, Kaori
Morgan, Katherine M.
Vera, Elsa
Mazur, Sharlyn J.
Appella, Ettore
Vojtesek, Borivoj
Blasco, Maria A.
Lane, David P.
Harris, Curtis C.
TI p53 isoforms regulate aging- and tumor-associated replicative senescence
in T lymphocytes
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CELLULAR SENESCENCE; HUMAN-CELLS; THERAPEUTIC OPPORTUNITIES; SHORTENED
TELOMERES; SECRETORY PHENOTYPE; HIV-INFECTION; LIFE-SPAN; EXPRESSION;
CANCER; MEMORY
AB Cellular senescence contributes to aging and decline in tissue function. p53 isoform switching regulates replicative senescence in cultured fibroblasts and is associated with tumor progression. Here, we found that the endogenous p53 isoforms Delta 133p53 and p53 beta are physiological regulators of proliferation and senescence in human T lymphocytes in vivo. Peripheral blood CD8(+) T lymphocytes collected from healthy donors displayed an age-dependent accumulation of senescent cells (CD28(-)CD57(+)) with decreased Delta 133p53 and increased p53 beta expression. Human lung tumor-associated CD8+ T lymphocytes also harbored senescent cells. Cultured CD8(+) blood T lymphocytes underwent replicative senescence that was associated with loss of CD28 and Delta 133p53 protein. In poorly proliferative, Delta 133p53-low CD8(+)CD28(-) cells, reconstituted expression of either Delta 133p53 or CD28 upregulated endogenous expression of each other, which restored cell proliferation, extended replicative lifespan and rescued senescence phenotypes. Conversely, Delta 133p53 knockdown or p53 beta overexpression in CD8(+)CD28(+) cells inhibited cell proliferation and induced senescence. This study establishes a role for Delta 133p53 and p53 beta in regulation of cellular proliferation and senescence in vivo. Furthermore, Delta 133p53-induced restoration of cellular replicative potential may lead to a new therapeutic paradigm for treating immunosenescence disorders, including those associated with aging, cancer, autoimmune diseases, and HIV infection.
C1 [Mondal, Abdul M.; Horikawa, Izumi; Pine, Sharon R.; Fujita, Kaori; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Pine, Sharon R.; Morgan, Katherine M.] UMDNJ Robert Wood Johnson Med Sch, Dept Med, Canc Inst New Jersey, New Brunswick, NJ USA.
[Vera, Elsa; Blasco, Maria A.] Ctr Nacl Invest Oncol, Mol Oncol Programme, Telomeres & Telomerase Grp, Madrid, Spain.
[Mazur, Sharlyn J.; Appella, Ettore] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Vojtesek, Borivoj] Masaryk Mem Canc Inst, Reg Ctr Appl Mol Oncol, Brno, Czech Republic.
[Lane, David P.] ASTAR, Inst Mol & Cell Biol, Agcy Sci, Singapore, Singapore.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr, Bethesda, MD 20892 USA.
EM Curtis_Harris@nih.gov
RI ASTAR, IMCB/E-2320-2012;
OI Blasco, Maria A./0000-0002-4211-233X
FU Intramural Research Program of the NIH, NCI; Grant Agency of the Czech
Republic [P301/11/1678, P206/12/G151]; RECAMO [CZ.1.05/2.1.00/03.0101];
Biospecimen Repository Service; FACS Sorting; CINJ [P30CA072720]; NIH,
NCI [5K22CA140719]; ERC Project TEL STEM CELL; FP7 Project MARK-AGE; FP7
Project EuroBATS; [SAF2008-05384]; [CSD2007-00017]; [S2010/BMD-2303]
FX We thank Rita Effros and Mark E. Dudley for reagents, Aaron Schetter and
Ana Robles for statistical analysis, Barbara J. Taylor and Subhadra
Banerjee for cell sorting, and Elisa Spillare for technical assistance.
This research was supported in part by the Intramural Research Program
of the NIH, NCI. B. Vojtesek was funded by grants from the Grant Agency
of the Czech Republic (P301/11/1678 and P206/12/G151) and the RECAMO
(CZ.1.05/2.1.00/03.0101). S.R. Pine was supported by the Biospecimen
Repository Service (Julia Friedman), FACS Sorting (Arthur Roberts)
Shared Resources of the CINJ (P30CA072720) and by a grant from the NIH,
NCI (5K22CA140719). M.A. Blasco was funded by ERC Project TEL STEM CELL,
FP7 Projects MARK-AGE and EuroBATS, and other projects SAF2008-05384,
CSD2007-00017 and S2010/BMD-2303 (Spain).
NR 59
TC 18
Z9 18
U1 2
U2 13
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2013
VL 123
IS 12
BP 5247
EP 5257
DI 10.1172/JCI70355
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 263RQ
UT WOS:000327826100029
PM 24231352
ER
PT J
AU Anderson, SAR
Michaelides, M
Zarnegar, P
Ren, YH
Fagergren, P
Thanos, PK
Wang, GJ
Bannon, M
Neumaier, JF
Keller, E
Volkow, ND
Hurd, YL
AF Anderson, Sarah Ann R.
Michaelides, Michael
Zarnegar, Parisa
Ren, Yanhua
Fagergren, Pernilla
Thanos, Panayotis K.
Wang, Gene-Jack
Bannon, Michael
Neumaier, John F.
Keller, Eva
Volkow, Nora D.
Hurd, Yasmin L.
TI Impaired periamygdaloid-cortex prodynorphin is characteristic of opiate
addiction and depression
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID MESSENGER-RNA EXPRESSION; GLUCOSE-METABOLISM; GENE-EXPRESSION;
PARKINSONS-DISEASE; EXTENDED AMYGDALA; ANXIETY DISORDERS;
DRUG-ADDICTION; HEROIN ABUSERS; OPIOID-SYSTEM; HUMAN BRAIN
AB Negative affect is critical for conferring vulnerability to opiate addiction as reflected by the high comorbidity of opiate abuse with major depressive disorder (MDD). Rodent models implicate amygdala prodynorphin (Pdyn) as a mediator of negative affect; however, evidence of PDYN involvement in human negative affect is limited. Here, we found reduced PDYN mRNA expression in the postmortem human amygdala nucleus of the periamygdaloid. cortex (PAC) in both heroin abusers and MDD subjects. Similar to humans, rats that chronically self-administered heroin had reduced Pdyn mRNA expression in the PAC at a time point associated with a negative affective state. Using the in vivo functional imaging technology DREAMM (DREADD-assisted. metabolic mapping, where DREADD indicates designer receptors exclusively activated. by designer drugs), we found that selective inhibition of Pdyn-expressing neurons in the rat PAC increased metabolic activity in the extended amygdala, which is a key substrate of the extrahypothalamic brain stress system. In parallel, PAC-specific Pdyn inhibition provoked negative affect-related physiological and behavioral changes. Altogether, our translational study supports a functional role for impaired Pdyn in the PAC in opiate abuse through activation of the stress and negative affect neurocircuitry implicated in addiction vulnerability.
C1 [Anderson, Sarah Ann R.; Michaelides, Michael; Ren, Yanhua; Hurd, Yasmin L.] Icahn Sch Med Mt Sinai, Dept Psychiat, New York, NY USA.
[Anderson, Sarah Ann R.; Michaelides, Michael; Ren, Yanhua; Hurd, Yasmin L.] Icahn Sch Med Mt Sinai, Dept Neurosci, New York, NY USA.
[Anderson, Sarah Ann R.; Michaelides, Michael; Ren, Yanhua; Hurd, Yasmin L.] Icahn Sch Med Mt Sinai, Friedman Brain Inst, New York, NY USA.
[Zarnegar, Parisa; Fagergren, Pernilla] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Thanos, Panayotis K.; Volkow, Nora D.] NIAAA, Bethesda, MD USA.
[Wang, Gene-Jack] SUNY Stony Brook, Dept Radiol, Upton, NY USA.
[Bannon, Michael] Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.
[Neumaier, John F.] Univ Washington, Dept Psychiat, Seattle, WA 98195 USA.
[Neumaier, John F.] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA.
[Keller, Eva] Semmelweis Univ, Dept Forens & Insurance Med, H-1085 Budapest, Hungary.
[Hurd, Yasmin L.] James J Peters VA Med Ctr, New York, NY USA.
RP Hurd, YL (reprint author), Hess Ctr Sci & Med, 1 Gustave L Levy Pl,Box 1065,1470 Madison Ave,Flo, New York, NY 10029 USA.
EM Yasmin.hurd@mssm.edu
FU UNCF-Merck Graduate Fellowship [DA015546,
T32-GM007280-34S1-NHLBI/NIGMS]; NIDA Postdoctoral Training Program
[DA007135]; [DA023214]; [DA030359]; [DA006470]
FX This work was supported by DA015546, DA023214, DA030359, DA006470.
S.A.R. Anderson was supported by the UNCF-Merck Graduate Fellowship,
Diversity Supplement to DA015546 and T32-GM007280-34S1-NHLBI/NIGMS
supplement to the Mount Sinai Medical Scientist Training Program. M.
Michaelides was supported by NIDA Postdoctoral Training Program
DA007135.
NR 56
TC 12
Z9 12
U1 2
U2 9
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2013
VL 123
IS 12
BP 5334
EP 5341
DI 10.1172/JCI70395
PG 8
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 263RQ
UT WOS:000327826100036
PM 24231353
ER
PT J
AU Michaelides, M
Anderson, SAR
Ananth, M
Smirnov, D
Thanos, PK
Neumaier, JF
Wang, GJ
Volkow, ND
Hurd, YL
AF Michaelides, Michael
Anderson, Sarah Ann R.
Ananth, Mala
Smirnov, Denis
Thanos, Panayotis K.
Neumaier, John F.
Wang, Gene-Jack
Volkow, Nora D.
Hurd, Yasmin L.
TI Whole-brain circuit dissection in free-moving animals reveals
cell-specific mesocorticolimbic networks
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID STRIATOPALLIDAL NEURONS; RAT-BRAIN; PET; NORMALIZATION; ORGANIZATION;
INHIBITION; MODULATION; TEMPLATE; PATHWAYS; F-18-FDG
AB The ability to map the functional connectivity of discrete cell types in the intact mammalian brain during behavior is crucial for advancing our understanding of brain function in normal and disease states. We combined designer receptor exclusively activated by designer drug (DREADD) technology and behavioral imaging with mu PET and [F-18]fluorodeoxyglucose (FDG) to generate whole-brain metabolic maps of cell-specific functional circuits during the awake, freely moving state. We have termed this approach DREADD-assisted metabolic mapping (DREAMM) and documented its ability in rats to map whole-brain functional anatomy. We applied this strategy to evaluating changes in the brain associated with inhibition of prodynorphin-expressing (Pdyn-expressing) and of proenkephalin-expressing (Penk-expressing) medium spiny neurons (MSNs) of the nucleus accumbens shell (NAcSh), which have been implicated in neuropsychiatric disorders. DREAMM revealed discrete behavioral manifestations and concurrent engagement of distinct corticolimbic networks associated with dysregulation of Pdyn and Penk in MSNs of the NAcSh. Furthermore, distinct neuronal networks were recruited in awake versus anesthetized conditions. These data demonstrate that DREAMM is a highly sensitive, molecular, high-resolution quantitative imaging approach.
C1 [Michaelides, Michael; Anderson, Sarah Ann R.; Wang, Gene-Jack; Hurd, Yasmin L.] Icahn Sch Med Mt Sinai, Dept Psychiat, Friedman Brain Inst, New York, NY 10029 USA.
[Michaelides, Michael; Anderson, Sarah Ann R.; Hurd, Yasmin L.] Icahn Sch Med Mt Sinai, Dept Neurosci, Friedman Brain Inst, New York, NY 10029 USA.
[Ananth, Mala; Thanos, Panayotis K.; Wang, Gene-Jack] Brookhaven Natl Lab, Dept Biosci, Upton, NY 11973 USA.
[Smirnov, Denis; Neumaier, John F.] Univ Washington, Seattle, WA 98195 USA.
[Thanos, Panayotis K.; Volkow, Nora D.] NIAAA, Lab Neuroimaging, Bethesda, MD USA.
[Hurd, Yasmin L.] James J Peters VA Med Ctr, New York, NY USA.
RP Hurd, YL (reprint author), Icahn Sch Med Mt Sinai, Hess Ctr Sci & Med, 10th Floor Room 105,1470 Madison Ave, New York, NY 10029 USA.
EM yasmin.hurd@mssm.edu
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA) [AA11034,
AA07574, AA07611]; National Institute on Drug Abuse (NIDA) [DA015446,
DA023214, DA030359]; NIDA Postdoctoral Training Program at MSSM
[DA007135]
FX This work was supported by the National Institute on Alcohol Abuse and
Alcoholism (NIAAA) (AA11034, AA07574, and AA07611) and the National
Institute on Drug Abuse (NIDA) (DA015446, DA023214, and DA030359). M.
Michaelides was supported by the NIDA Postdoctoral Training Program at
MSSM (DA007135). The authors thank the Mount Sinai Microscopy Shared
Resource Facility and the microPET Facility (Wade Koba, Linda Jelicks)
at the Albert Einstein College of Medicine of Yeshiva University.
NR 30
TC 19
Z9 19
U1 2
U2 8
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2013
VL 123
IS 12
BP 5342
EP 5350
DI 10.1172/JCI72117
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 263RQ
UT WOS:000327826100037
PM 24231358
ER
PT J
AU Uzasci, L
Nath, A
AF Uzasci, Lerna
Nath, Avindra
TI Robert J. Cotter (1943-2012): From Mass Spectrometer Development to the
Exploration of Life
SO JOURNAL OF NEUROIMMUNE PHARMACOLOGY
LA English
DT Editorial Material
DE Mass spectrometry; Time-of flightmass spectrometers; MALDI-ToFmass
spectrometry; Biomarkers
C1 [Uzasci, Lerna] Johns Hopkins Univ, Dept Pharmacol, Baltimore, MD USA.
[Nath, Avindra] NINDS, NIH, Bethesda, MD 20892 USA.
RP Nath, A (reprint author), NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM avindra.nath@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1890
EI 1557-1904
J9 J NEUROIMMUNE PHARM
JI J. Neuroimmune Pharm.
PD DEC
PY 2013
VL 8
IS 5
BP 1049
EP 1050
DI 10.1007/s11481-013-9482-4
PG 2
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 272XI
UT WOS:000328496000001
PM 23771593
ER
PT J
AU Uzasci, L
Nath, A
Cotter, R
AF Uzasci, Lerna
Nath, Avindra
Cotter, Robert
TI Oxidative Stress and the HIV-Infected Brain Proteome
SO JOURNAL OF NEUROIMMUNE PHARMACOLOGY
LA English
DT Review
DE HIV; Dementia; Oxidation; Nitration; Biomarker; Mass spectrometry
ID HUMAN-IMMUNODEFICIENCY-VIRUS; NITRIC-OXIDE SYNTHASE;
CENTRAL-NERVOUS-SYSTEM; NF-KAPPA-B; CEREBROSPINAL-FLUID; TAT PROTEIN;
MASS-SPECTROMETRY; NEUROCOGNITIVE DISORDERS; NITROSATIVE STRESS; NADPH
OXIDASE
AB Human immunodeficiency virus (HIV) is capable of infiltrating the brain and infecting brain cells. In the years following HIV infection, patients show signs of various levels of neurocognitive problems termed HIV-associated neurocognitive disorders (HAND). Although the introduction of highly active antiretroviral therapy (HAART) has reduced the incidence of HIV-dementia, which is the most severe form of HAND, the milder forms have become more prevalent today due to the increased life expectancy of infected individuals. Pre-HAART era markers such as HIV RNA level, CD4+ count, TNF-alpha, MCP-1 and M-CSF are not able to clearly distinguish mild from advanced HAND. One promising approach for new biomarker discovery is the identification and quantitation of proteins that are post-translationally modified by oxidative and nitrosative species. The occurrence of oxidative and nitrosative stress in HIV-infected brain, both through the early direct and indirect effects of viral proteins and through the later effect on mitochondrial integrity during apoptosis, is well-established. This review will focus on how the reactive species are produced in the brain after HIV infection, the specific oxidative and nitrosative species that are involved in the post-translational modification of the brain proteome, and the methods that are currently used for the detection of such modified proteins. This review also provides an overview of related research pertaining to oxidative stress-related HAND using cerebrospinal fluid and human brain tissue.
C1 [Uzasci, Lerna; Cotter, Robert] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA.
[Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
RP Uzasci, L (reprint author), Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA.
EM luzasci1@jhu.edu
FU National Institute of Neurological Disorders and Stroke [R01NS039253];
National Institute of Mental Health [P30MH075673]; NIH
FX RJC and LU were supported by grants R01NS039253 (Cotter R, PI) from the
National Institute of Neurological Disorders and Stroke and P30MH075673
(McArthur J, PI) from the National Institute of Mental Health. AN is
supported by intramural NIH funds.
NR 124
TC 10
Z9 10
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1890
EI 1557-1904
J9 J NEUROIMMUNE PHARM
JI J. Neuroimmune Pharm.
PD DEC
PY 2013
VL 8
IS 5
BP 1167
EP 1180
DI 10.1007/s11481-013-9444-x
PG 14
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 272XI
UT WOS:000328496000015
PM 23475542
ER
PT J
AU Ferenczy, MW
Johnson, KR
Steinberg, SM
Marshall, LJ
Monaco, MC
Beschloss, AM
Jensen, PN
Major, EO
AF Ferenczy, Michael W.
Johnson, Kory R.
Steinberg, Shannon M.
Marshall, Leslie J.
Monaco, Maria Chiara
Beschloss, Alexander M.
Jensen, Peter N.
Major, Eugene O.
TI Clonal Immortalized Human Glial Cell Lines Support Varying Levels of JC
Virus Infection due to Differences in Cellular Gene Expression
SO JOURNAL OF NEUROIMMUNE PHARMACOLOGY
LA English
DT Article
DE SVG; JC Virus; SVG-10B1; SVG-5F4; Progressive multifocal
leukoenephalopathy; Persistent infection
ID NERVE GROWTH-FACTOR; PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HUMAN
B-LYMPHOCYTES; LARGE T-ANTIGEN; NF-KAPPA-B; PROGENITOR CELLS; C-JUN;
HUMAN-BRAIN; HUMAN POLYOMAVIRUS; TUMOR-SUPPRESSOR
AB JC virus (JCV) is a ubiquitous human polyomavirus that causes the demyelinating disease Progressive Multifocal Leukoencephalopathy (PML). JCV replicates in limited cell types in culture, predominantly in human glial cells. Following introduction of a replication defective SV40 mutant that expressed large T protein into a heterogeneous culture of human fetal brain cells, multiple phenotypes became immortalized (SVG cells). A subset of SVG cells could support JCV replication. In the current study, clonal cell lines were selected from the original SVG cell culture. The 5F4 clone showed low levels of viral growth. The 10B1 clone was highly permissive for JCV DNA replication and gene expression and supported persistent and stable JCV infection over months in culture. Microarray analysis revealed that viral infection did not significantly change gene expression in these cells. More resistant 5F4 cells expressed high levels of transcription factors known to inhibit JCV transcription. Interestingly, 5F4 cells expressed high levels of RNA of markers of radial glia and 10B1 cells had high expression of markers of immature glial cells and activation of transcription regulators important for stem/progenitor cell self-renewal. These SVG-derived clonal cell lines provide a biologically relevant model to investigate cell type differences in JCV host range and pathogenesis, as well as neural development. Several transcription regulators were identified which may be targets for therapeutic modulation of expression to abrogate JCV replication in PML patients. Additionally, these clonal cell lines can provide a consistent culture platform for testing therapies against JCV infection of the central nervous system.
C1 [Ferenczy, Michael W.; Steinberg, Shannon M.; Marshall, Leslie J.; Monaco, Maria Chiara; Beschloss, Alexander M.; Jensen, Peter N.; Major, Eugene O.] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
[Johnson, Kory R.] NINDS, Bioinformat Sect, NIH, Bethesda, MD 20892 USA.
[Ferenczy, Michael W.; Major, Eugene O.] Lab Mol Med & Neurosci, Bethesda, MD 20892 USA.
RP Ferenczy, MW (reprint author), Lab Mol Med & Neurosci, NINDS Bldg 10,Room 3B13 10 Ctr Dr,MSC 1296, Bethesda, MD 20892 USA.
EM michael.ferenczy@nih.gov; majorg@ninds.nih.gov
OI Steinberg, Shannon/0000-0003-1711-2423
FU Intramural AIDS Research Fellowship from the NIH Office of AIDS
Research; Division of Intramural Research of the NINDS
FX The authors would like to thank members of the Laboratory of Molecular
Medicine and Neuroscience for helpful comments and insight and Rick V.
Dreyfuss from the NIH Medical Imaging Branch for help preparing in situ
hybridization images. RNA sample processing and initial analysis of DNA
microarrays were performed by Dr. Abdel Elkahloun and Weiwei Wu of the
Microarray Core Facility of the National Human Genome Institute. M.W.F.
is supported in part by the Intramural AIDS Research Fellowship from the
NIH Office of AIDS Research. The Laboratory of Molecular Medicine and
Neuroscience and the Bioinformatics Section are supported by the
Division of Intramural Research of the NINDS.
NR 60
TC 3
Z9 3
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1890
EI 1557-1904
J9 J NEUROIMMUNE PHARM
JI J. Neuroimmune Pharm.
PD DEC
PY 2013
VL 8
IS 5
BP 1303
EP 1319
DI 10.1007/s11481-013-9499-8
PG 17
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 272XI
UT WOS:000328496000025
PM 24052414
ER
PT J
AU Skates, SJ
Gillette, MA
LaBaer, J
Carr, SA
Anderson, L
Liebler, DC
Ransohoff, D
Rifai, N
Kondratovich, M
Tezak, Z
Mansfield, E
Oberg, AL
Wright, I
Barnes, G
Gail, M
Mesri, M
Kinsinger, CR
Rodriguez, H
Boja, ES
AF Skates, Steven J.
Gillette, Michael A.
LaBaer, Joshua
Carr, Steven A.
Anderson, Leigh
Liebler, Daniel C.
Ransohoff, David
Rifai, Nader
Kondratovich, Marina
Tezak, Zivana
Mansfield, Elizabeth
Oberg, Ann L.
Wright, Ian
Barnes, Grady
Gail, Mitchell
Mesri, Mehdi
Kinsinger, Christopher R.
Rodriguez, Henry
Boja, Emily S.
TI Statistical Design for Biospecimen Cohort Size in Proteomics-based
Biomarker Discovery and Verification Studies
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE statistical experiment design; biomarker; proteomics; unbiasedness;
power calculation
ID MONITORING MASS-SPECTROMETRY; CARDIOVASCULAR-DISEASE; PROTEIN
BIOMARKERS; MULTIPLEX ASSAYS; PIPELINE; PLASMA; ASSOCIATION;
DIAGNOSTICS; VALIDATION; MARKERS
AB Protein biomarkers are needed to deepen our understanding of cancer biology and to improve our ability to diagnose, monitor, and treat cancers. Important analytical and clinical hurdles must be overcome to allow the most promising protein biomarker candidates to advance into clinical validation studies. Although contemporary proteomics technologies support the measurement of large numbers of proteins in individual clinical specimens, sample throughput remains comparatively low. This problem is amplified in typical clinical proteomics research studies, which routinely suffer from a lack of proper experimental design, resulting in analysis of too few biospecimens to achieve adequate statistical power at each stage of a biomarker pipeline. To address this critical shortcoming, a joint workshop was held by the National Cancer Institute (NCI), National Heart, Lung, and Blood Institute (NHLBI), and American Association for Clinical Chemistry (AACC) with participation from the U.S. Food and Drug Administration (FDA). An important output from the workshop was a statistical framework for the design of biomarker discovery and verification studies. Herein, we describe the use of quantitative clinical judgments to set statistical criteria for clinical relevance and the development of an approach to calculate biospecimen sample size for proteomic studies in discovery and verification stages prior to clinical validation stage. This represents a first step toward building a consensus on quantitative criteria for statistical design of proteomics biomarker discovery and verification research.
C1 [Skates, Steven J.] Massachusetts Gen Hosp, Ctr Canc, Ctr Biostat, Boston, MA 02114 USA.
[Gillette, Michael A.; Carr, Steven A.] Broad Inst Massachusetts Inst Technol & Harvard, Prote Platform, Cambridge, MA 02142 USA.
[LaBaer, Joshua] Arizona State Univ, Biodesign Inst, Tempe, AZ 85287 USA.
[Anderson, Leigh] Plasma Proteome Inst, Washington, DC 20009 USA.
[Anderson, Leigh; Wright, Ian] SISCAPA Technol Inc, Washington, DC 20009 USA.
[Liebler, Daniel C.] Vanderbilt Univ, Sch Med, Jim Ayers Inst Precanc Detect & Diag, Nashville, TN 37232 USA.
[Liebler, Daniel C.] Vanderbilt Univ, Sch Med, Dept Biochem, Nashville, TN 37232 USA.
[Ransohoff, David] Univ N Carolina, Dept Med, Div Gastroenterol & Hepatol, Chapel Hill, NC 27514 USA.
[Rifai, Nader] Childrens Hosp, Dept Lab Med, Boston, MA 02115 USA.
[Rifai, Nader] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Rifai, Nader] King Abdulaziz Univ, Jeddah 22254, Saudi Arabia.
[Kondratovich, Marina; Tezak, Zivana; Mansfield, Elizabeth] US FDA, Off In Vitro Diagnost & Radiol Hlth, Ctr Devices & Radiol Hlth, Dept Hlth & Human Serv, Silver Spring, MD 20993 USA.
[Oberg, Ann L.] Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN 55905 USA.
[Barnes, Grady] Fujirebio Diagnost Inc, Malvern, PA 19355 USA.
[Gail, Mitchell] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Mesri, Mehdi; Kinsinger, Christopher R.; Rodriguez, Henry; Boja, Emily S.] NCI, Off Canc Clin Prote Res, Ctr Strateg Sci Initiat, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Skates, SJ (reprint author), Massachusetts Gen Hosp, 50 Staniford St,Suite 560, Boston, MA 02114 USA.
EM sskates@partners.org; bojae@mail.nih.gov
OI Liebler, Daniel/0000-0002-7873-3031
FU National Cancer Institute of the National Institutes of Health through
the Clinical Proteomic Tumor Analysis Consortium (CPTAC) [10XS136,
U24CA160034]; Early Detection Research Network [U01CAI52990]; Mayo
Clinic Specialized Program in Research Excellence [P50CA136393]
FX Research reported in this publication was supported by the National
Cancer Institute of the National Institutes of Health under grants and
contracts through the Clinical Proteomic Tumor Analysis Consortium
(CPTAC) program (10XS136 SJS, U24CA160034 SAC, MAG), the Early Detection
Research Network (U01CAI52990 SJS), and Mayo Clinic Specialized Program
in Research Excellence grant (P50CA136393 AO).
NR 29
TC 32
Z9 32
U1 2
U2 18
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD DEC
PY 2013
VL 12
IS 12
BP 5383
EP 5394
DI 10.1021/pr400132j
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 269HD
UT WOS:000328231300004
PM 24063748
ER
PT J
AU Cossio, P
Hummer, G
AF Cossio, Pilar
Hummer, Gerhard
TI Bayesian analysis of individual electron microscopy images: Towards
structures of dynamic and heterogeneous biomolecular assemblies
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE Electron microscopy; Cryo-EM; Bayesian inference; Ensemble refinement;
Validation; Disorder; GroEL; ESCRT
ID EM STRUCTURE DETERMINATION; AB-INITIO RECONSTRUCTION; MACROMOLECULAR
STRUCTURE DETERMINATION; CRYOELECTRON MICROSCOPY; CRYO-EM;
CRYSTAL-STRUCTURE; CHAPERONIN GROEL; PARTICLE ORIENTATION; ANGSTROM
RESOLUTION; MOLECULAR-DYNAMICS
AB We develop a method to extract structural information from electron microscopy (EM) images of dynamic and heterogeneous molecular assemblies. To overcome the challenge of disorder in the imaged structures, we analyze each image individually, avoiding information loss through clustering or averaging. The Bayesian inference of EM (BioEM) method uses a likelihood-based probabilistic measure to quantify the consistency between each EM image and given structural models. The likelihood function accounts for uncertainties in the molecular position and orientation, variations in the relative intensities and noise in the experimental images. The BioEM formalism is physically intuitive and mathematically simple. We show that for experimental GroEL images, BioEM correctly identifies structures according to the functional state. The top-ranked structure is the corresponding X-ray crystal structure, followed by an EM structure generated previously from a superset of the EM images used here. To analyze EM images of highly flexible molecules, we propose an ensemble refinement procedure, and validate it with synthetic EM maps of the ESCRT-I-II supercomplex. Both the size of the ensemble and its structural members are identified correctly. BioEM offers an alternative to 3D-reconstruction methods, extracting accurate population distributions for highly flexible structures and their assemblies. We discuss limitations of the method, and possible applications beyond ensemble refinement, including the cross-validation and unbiased post-assessment of model structures, and the structural characterization of systems where traditional approaches fail. Overall, our results suggest that the BioEM framework can be used to analyze EM images of both ordered and disordered molecular systems. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Hummer, Gerhard] Max Planck Inst Biophys, Dept Theoret Biophys, D-60438 Frankfurt, Germany.
Natl Inst Diabet & Digest & Kidney Dis, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Hummer, G (reprint author), Max Planck Inst Biophys, Dept Theoret Biophys, Max von Laue Strage 3, D-60438 Frankfurt, Germany.
EM gerhard.hummer@biophys.mpg.de
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases, National Institutes of Health; Max Planck
Society
FX To obtain the source code please contact the corresponding author. The
authors thank Dr. J. Bernard Heymann for help with the Bsoft program,
and Drs. James Hurley and Alasdair Steven for stimulating discussions.
We also thank Dr. Jurgen Kofinger for useful discussions concerning the
Bayesian methodology. This work was supported by the Intramural Research
Program of the National Institute of Diabetes and Digestive and Kidney
Diseases, National Institutes of Health, and by the Max Planck Society,
and used the biowulf computing resource at the National Institutes of
Health, and the high-performance computers at the Rechenzentrum Garching
of the Max Planck Society.
NR 72
TC 9
Z9 9
U1 1
U2 24
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
EI 1095-8657
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD DEC
PY 2013
VL 184
IS 3
BP 427
EP 437
DI 10.1016/j.jsb.2013.10.006
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 274FA
UT WOS:000328591000006
PM 24161733
ER
PT J
AU Kuczmarski, MF
Mason, MA
Allegro, D
Zonderman, AB
Evans, MK
AF Kuczmarski, Marie Fanelli
Mason, Marc A.
Allegro, Deanne
Zonderman, Alan B.
Evans, Michele K.
TI Diet Quality Is Inversely Associated with C-Reactive Protein Levels in
Urban, Low-Income African-American and White Adults
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Article
DE C-reactive protein; Dietary quality; Micronutrients
ID SOCIOECONOMIC-STATUS; UNITED-STATES; CARDIOVASCULAR-DISEASE; US ADULTS;
INFLAMMATION; POPULATION; MARKERS; PATTERNS; OBESITY; CONSEQUENCES
AB Background C-reactive protein (CRP), an inflammatory biomarker, is influenced by many factors, including socioeconomic position, genetics, and diet. The inverse association between diet and CRP is biologically feasible because micronutrients with antioxidative properties may enable the body to manage the balance between production and accumulation of reactive species that cause oxidative stress.
Objective To determine the quality of the diet consumed by urban, low-income African-American and white adults aged 30 to 64 years, and association of diet quality with CRP.
Design Data from a cross-sectional study were used to evaluate diet quality assessed by mean adequacy ratio (MAR). Two 24-hour recalls were collected by trained interviewers using the US Department of Agriculture automated multiple pass method.
Participants The sample consisted of Healthy Aging in Neighborhoods of Diversity across the Life Span baseline study participants, 2004-2009, who completed both recalls (n=2,017).
Main outcome measures MAR equaled the average of the ratio of intakes to Recommended Dietary Allowance for 15 vitamins and minerals. CRP levels were assessed by the nephelometric method utilizing latex particles coated with CRP monoclonal antibodies.
Statistical analysis Linear ordinary least square regression and generalized linear models were performed to determine the association of MAR (independent variable) with CRP (dependent variable) while adjusting for potential confounders.
Results MAR scores ranged from 74.3 to 82.2. Intakes of magnesium and vitamins A, C, and E were the most inadequate compared with Estimated Average Requirements. CRP levels were significantly associated with MAR, dual-energy x-ray absorptiometry-measured body fat, and hypertension. A 10% increase in MAR was associated with a 4% decrease in CRP.
Conclusions The MAR was independently and significantly inversely associated with CRP, suggesting diet is associated with the regulation of inflammation. Interventions to assist people make better food choices may not only improve diet quality but also their health, thereby possibly reducing risk for cardiovascular disease.
C1 [Kuczmarski, Marie Fanelli] Univ Delaware, Dept Behav Hlth & Nutr, Newark, DE 19716 USA.
[Kuczmarski, Marie Fanelli] Univ Delaware, Dept Behav Hlth & Nutr, HANDLS Study, Newark, DE 19716 USA.
[Allegro, Deanne] Univ Delaware, Dept Behav Hlth & Nutr, HANDLS Hlth Aging Neighborhoods Divers Life Span, Newark, DE 19716 USA.
[Mason, Marc A.] NIA, NIH, Baltimore, MD 21224 USA.
[Mason, Marc A.] NIA, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
[Zonderman, Alan B.] NIA, Lifespan Cognit & Hlth Sect, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
[Evans, Michele K.] NIA, Baltimore, MD 21224 USA.
[Evans, Michele K.] NIA, HANDLS Study, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
RP Kuczmarski, MF (reprint author), Univ Delaware, Dept Behav Hlth & Nutr, 010 Carpenter Sports Bldg, Newark, DE 19716 USA.
EM mfk@udel.edu
OI Zonderman, Alan B/0000-0002-6523-4778
FU Intramural Research Program, National Institute on Aging, National
Institutes of Health
FX This work is supported by the Intramural Research Program, National
Institute on Aging, National Institutes of Health.
NR 54
TC 12
Z9 12
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD DEC
PY 2013
VL 113
IS 12
BP 1620
EP 1631
DI 10.1016/j.jand.2013.07.004
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 269JU
UT WOS:000328238400006
PM 24035460
ER
PT J
AU Pan, X
Liu, J
Nguyen, T
Liu, CY
Sun, JH
Teng, YJ
Fergusson, MM
Rovira, II
Allen, M
Springer, DA
Aponte, AM
Gucek, M
Balaban, RS
Murphy, E
Finkel, T
AF Pan, Xin
Liu, Jie
Nguyen, Tiffany
Liu, Chengyu
Sun, Junhui
Teng, Yanjie
Fergusson, Maria M.
Rovira, Ilsa I.
Allen, Michele
Springer, Danielle A.
Aponte, Angel M.
Gucek, Marjan
Balaban, Robert S.
Murphy, Elizabeth
Finkel, Toren
TI The physiological role of mitochondrial calcium revealed by mice lacking
the mitochondrial calcium uniporter
SO NATURE CELL BIOLOGY
LA English
DT Article
ID PERMEABILITY TRANSITION PORE; RAT KIDNEY MITOCHONDRIA; ESSENTIAL
COMPONENT; S-NITROSYLATION; CYCLOSPORINE-A; CA2+ UPTAKE; CELL-DEATH;
TRANSPORT; PHOSPHORYLATION; ENERGETICS
AB Mitochondrial calcium has been postulated to regulate a wide range of processes from bioenergetics to cell death. Here, we characterize a mouse model that lacks expression of the recently discovered mitochondrial calcium uniporter (MCU). Mitochondria derived from MCU-/- mice have no apparent capacity to rapidly uptake calcium. Whereas basal metabolism seems unaffected, the skeletal muscle of MCU-/- mice exhibited alterations in the phosphorylation and activity of pyruvate dehydrogenase. In addition, MCU-/- mice exhibited marked impairment in their ability to perform strenuous work. We further show that mitochondria from MCU-/- mice lacked evidence for calcium-induced permeability transition pore (PIP) opening. The lack of PIP opening does not seem to protect MCU-/- cells and tissues from cell death, although MCU-/- hearts fail to respond to the PIP inhibitor cyclosporin A. Taken together, these results clarify how acute alterations in mitochondrial matrix calcium can regulate mammalian physiology.
C1 [Pan, Xin; Liu, Jie; Teng, Yanjie; Fergusson, Maria M.; Rovira, Ilsa I.; Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Pan, Xin] Natl Ctr Biomed Anal, Beijing 100850, Peoples R China.
[Nguyen, Tiffany; Sun, Junhui; Balaban, Robert S.; Murphy, Elizabeth] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Liu, Chengyu] NHLBI, IPSC, NIH, Bethesda, MD 20892 USA.
[Liu, Chengyu] NHLBI, Genome Engn Core, NIH, Bethesda, MD 20892 USA.
[Allen, Michele; Springer, Danielle A.] NHLBI, Murine Phenotyping Core, NIH, Bethesda, MD 20892 USA.
[Aponte, Angel M.; Gucek, Marjan] NHLBI, Prote Core, NIH, Bethesda, MD 20892 USA.
RP Murphy, E (reprint author), NHLBI, Syst Biol Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM murphy1@nih.gov; finkelt@nih.gov
FU NIH
FX We are grateful to C. Brantner, P. S. Connelly and M. P. Daniels of the
NHLBI Electron Microscopy Core Facility for assistance with electron
microscopy, C. Petucci of the Metabolomics Core Facility Sanford-Burnham
Medical Research Institute for aiding in the metabolomic profiling, C.
Combs and the NHLBI Microscopy Core for help with the Rhod-2 fluorescent
measurements and A. Wiederkehr for the original mito-aequorin
adenovirus. This work was supported by NIH Intramural funds.
NR 48
TC 152
Z9 156
U1 5
U2 34
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
EI 1476-4679
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD DEC
PY 2013
VL 15
IS 12
BP 1464
EP +
DI 10.1038/ncb2868
PG 20
WC Cell Biology
SC Cell Biology
GA 265IL
UT WOS:000327944200011
PM 24212091
ER
PT J
AU Solomon, DA
Kim, JS
Bondaruk, J
Shariat, SF
Wang, ZF
Elkahloun, AG
Ozawa, T
Gerard, J
Zhuang, DZ
Zhang, SZ
Navai, N
Siefker-Radtke, A
Phillips, JJ
Robinson, BD
Rubin, MA
Volkmer, B
Hautmann, R
Kufer, R
Hogendoorn, PCW
Netto, G
Theodorescu, D
James, CD
Czerniak, B
Miettinen, M
Waldman, T
AF Solomon, David A.
Kim, Jung-Sik
Bondaruk, Jolanta
Shariat, Shahrokh F.
Wang, Zeng-Feng
Elkahloun, Abdel G.
Ozawa, Tomoko
Gerard, Julia
Zhuang, DaZhong
Zhang, Shizhen
Navai, Neema
Siefker-Radtke, Arlene
Phillips, Joanna J.
Robinson, Brian D.
Rubin, Mark A.
Volkmer, Bjoern
Hautmann, Richard
Kuefer, Rainer
Hogendoorn, Pancras C. W.
Netto, George
Theodorescu, Dan
James, C. David
Czerniak, Bogdan
Miettinen, Markku
Waldman, Todd
TI Frequent truncating mutations of STAG2 in bladder cancer
SO NATURE GENETICS
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; INACTIVATION; ANEUPLOIDY
AB Here we report the discovery of truncating mutations of the gene encoding the cohesin subunit STAG2, which regulates sister chromatid cohesion and segregation, in 36% of papillary non-invasive urothelial carcinomas and 16% of invasive urothelial carcinomas of the bladder. Our studies suggest that STAG2 has a role in controlling chromosome number but not the proliferation of bladder cancer cells. These findings identify STAG2 as one of the most commonly mutated genes in bladder cancer.
C1 [Solomon, David A.; Kim, Jung-Sik; Gerard, Julia; Waldman, Todd] Georgetown Univ, Sch Med, Dept Oncol, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Solomon, David A.; Phillips, Joanna J.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94140 USA.
[Bondaruk, Jolanta; Zhang, Shizhen; Czerniak, Bogdan] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
[Shariat, Shahrokh F.; Zhuang, DaZhong; Robinson, Brian D.; Rubin, Mark A.] Weill Cornell Coll Med, Dept Urol, New York, NY USA.
[Shariat, Shahrokh F.] Weill Cornell Coll Med, Div Med Oncol, New York, NY USA.
[Wang, Zeng-Feng; Miettinen, Markku] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Elkahloun, Abdel G.] NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA.
[Ozawa, Tomoko; James, C. David] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA USA.
[Navai, Neema] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA.
[Siefker-Radtke, Arlene] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Robinson, Brian D.; Rubin, Mark A.] Weill Cornell Coll Med, Dept Pathol, New York, NY USA.
[Volkmer, Bjoern] Hosp Kassel, Dept Urol, Kassel, Germany.
[Hautmann, Richard] Univ Hosp Ulm, Dept Urol, Ulm, Germany.
[Kuefer, Rainer] Hosp Eichert, Dept Urol, Goppingen, Germany.
[Hogendoorn, Pancras C. W.] Leiden Univ, Dept Pathol, Med Ctr, Leiden, Netherlands.
[Netto, George] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Theodorescu, Dan] Univ Colorado, Sch Med, Ctr Canc, Dept Surg, Aurora, CO USA.
RP Waldman, T (reprint author), Georgetown Univ, Sch Med, Dept Oncol, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
EM waldmant@georgetown.edu
RI Hogendoorn, Pancras/H-5859-2015;
OI Hogendoorn, Pancras/0000-0002-1513-8104; Rubin, Mark/0000-0002-8321-9950
FU US National Institutes of Health [R01CA169345, R01CA159467,
R21CA143282]; MD Anderson Cancer Center Bladder Cancer SPORE grant
[P50CA091846]; National Human Genome Research Institute, US National
Institutes of Health
FX We thank B. Vogelstein for assistance in acquiring samples and preparing
genomic DNA. This work was supported by US National Institutes of Health
grants R01CA169345, R01CA159467 and R21CA143282 to T. W., by the MD
Anderson Cancer Center Bladder Cancer SPORE grant P50CA091846 and by the
Intramural Research Program of the National Human Genome Research
Institute, US National Institutes of Health.
NR 13
TC 56
Z9 57
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2013
VL 45
IS 12
BP 1428
EP U171
DI 10.1038/ng.2800
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 262EA
UT WOS:000327715800006
PM 24121789
ER
PT J
AU Lambert, JC
Ibrahim-Verbaas, CA
Harold, D
Naj, AC
Sims, R
Bellenguez, C
Jun, G
DeStefano, AL
Bis, JC
Beecham, GW
Grenier-Boley, B
Russo, G
Thornton-Wells, TA
Jones, N
Smith, AV
Chouraki, V
Thomas, C
Ikram, MA
Zelenika, D
Vardarajan, BN
Kamatani, Y
Lin, CF
Gerrish, A
Schmidt, H
Kunkle, B
Dunstan, ML
Ruiz, A
Bihoreau, MT
Choi, SH
Reitz, C
Pasquier, F
Hollingworth, P
Ramirez, A
Hanon, O
Fitzpatrick, AL
Buxbaum, JD
Campion, D
Crane, PK
Baldwin, C
Becker, T
Gudnason, V
Cruchaga, C
Craig, D
Amin, N
Berr, C
Lopez, OL
De Jager, PL
Deramecourt, V
Johnston, JA
Evans, D
Lovestone, S
Letenneur, L
Moron, FJ
Rubinsztein, DC
Eiriksdottir, G
Sleegers, K
Goate, AM
Fievet, N
Huentelman, MJ
Gill, M
Brown, K
Kamboh, MI
Keller, L
Barberger-Gateau, P
McGuinness, B
Larson, EB
Green, R
Myers, AJ
Dufouil, C
Todd, S
Wallon, D
Love, S
Rogaeva, E
Gallacher, J
St George-Hyslop, P
Clarimon, J
Lleo, A
Bayer, A
Tsuang, DW
Yu, L
Tsolaki, M
Bossu, P
Spalletta, G
Proitsi, P
Collinge, J
Sorbi, S
Sanchez-Garcia, F
Fox, NC
Hardy, J
Naranjo, MCD
Bosco, P
Clarke, R
Brayne, C
Galimberti, D
Mancuso, M
Matthews, F
Moebus, S
Mecocci, P
Del Zompo, M
Maier, W
Hampel, H
Pilotto, A
Bullido, M
Panza, F
Caffarra, P
Nacmias, B
Gilbert, JR
Mayhaus, M
Lannfelt, L
Hakonarson, H
Pichler, S
Carrasquillo, MM
Ingelsson, M
Beekly, D
Alvarez, V
Zou, FG
Valladares, O
Younkin, SG
Coto, E
Hamilton-Nelson, KL
Gu, W
Razquin, C
Pastor, P
Mateo, I
Owen, MJ
Faber, KM
Jonsson, PV
Combarros, O
O'Donovan, MC
Cantwell, LB
Soininen, H
Blacker, D
Mead, S
Mosley, TH
Bennett, DA
Harris, TB
Fratiglioni, L
Holmes, C
de Bruijn, RFAG
Passmore, P
Montine, TJ
Bettens, K
Rotter, JI
Brice, A
Morgan, K
Foroud, TM
Kukull, WA
Hannequin, D
Powell, JF
Nalls, MA
Ritchie, K
Lunetta, KL
Kauwe, JSK
Boerwinkle, E
Riemenschneider, M
Boada, M
Hiltunen, M
Martin, ER
Schmidt, R
Rujescu, D
Wang, LS
Dartigues, JF
Mayeux, R
Tzourio, C
Hofman, A
Nothen, MM
Graff, C
Psaty, BM
Jones, L
Haines, JL
Holmans, PA
Lathrop, M
Pericak-Vance, MA
Launer, LJ
Farrer, LA
van Duijn, CM
Van Broeckhoven, C
Moskvina, V
Seshadri, S
Williams, J
Schellenberg, GD
Amouyel, P
AF Lambert, Jean-Charles
Ibrahim-Verbaas, Carla A.
Harold, Denise
Naj, Adam C.
Sims, Rebecca
Bellenguez, Celine
Jun, Gyungah
DeStefano, Anita L.
Bis, Joshua C.
Beecham, Gary W.
Grenier-Boley, Benjamin
Russo, Giancarlo
Thornton-Wells, Tricia A.
Jones, Nicola
Smith, Albert V.
Chouraki, Vincent
Thomas, Charlene
Ikram, M. Arfan
Zelenika, Diana
Vardarajan, Badri N.
Kamatani, Yoichiro
Lin, Chiao-Feng
Gerrish, Amy
Schmidt, Helena
Kunkle, Brian
Dunstan, Melanie L.
Ruiz, Agustin
Bihoreau, Marie-Therese
Choi, Seung-Hoan
Reitz, Christiane
Pasquier, Florence
Hollingworth, Paul
Ramirez, Alfredo
Hanon, Olivier
Fitzpatrick, Annette L.
Buxbaum, Joseph D.
Campion, Dominique
Crane, Paul K.
Baldwin, Clinton
Becker, Tim
Gudnason, Vilmundur
Cruchaga, Carlos
Craig, David
Amin, Najaf
Berr, Claudine
Lopez, Oscar L.
De Jager, Philip L.
Deramecourt, Vincent
Johnston, Janet A.
Evans, Denis
Lovestone, Simon
Letenneur, Luc
Moron, Francisco J.
Rubinsztein, David C.
Eiriksdottir, Gudny
Sleegers, Kristel
Goate, Alison M.
Fievet, Nathalie
Huentelman, Matthew J.
Gill, Michael
Brown, Kristelle
Kamboh, M. Ilyas
Keller, Lina
Barberger-Gateau, Pascale
McGuinness, Bernadette
Larson, Eric B.
Green, Robert
Myers, Amanda J.
Dufouil, Carole
Todd, Stephen
Wallon, David
Love, Seth
Rogaeva, Ekaterina
Gallacher, John
St George-Hyslop, Peter
Clarimon, Jordi
Lleo, Alberto
Bayer, Anthony
Tsuang, Debby W.
Yu, Lei
Tsolaki, Magda
Bossu, Paola
Spalletta, Gianfranco
Proitsi, Petroula
Collinge, John
Sorbi, Sandro
Sanchez-Garcia, Florentino
Fox, Nick C.
Hardy, John
Naranjo, Maria Candida Deniz
Bosco, Paolo
Clarke, Robert
Brayne, Carol
Galimberti, Daniela
Mancuso, Michelangelo
Matthews, Fiona
Moebus, Susanne
Mecocci, Patrizia
Del Zompo, Maria
Maier, Wolfgang
Hampel, Harald
Pilotto, Alberto
Bullido, Maria
Panza, Francesco
Caffarra, Paolo
Nacmias, Benedetta
Gilbert, John R.
Mayhaus, Manuel
Lannfelt, Lars
Hakonarson, Hakon
Pichler, Sabrina
Carrasquillo, Minerva M.
Ingelsson, Martin
Beekly, Duane
Alvarez, Victoria
Zou, Fanggeng
Valladares, Otto
Younkin, Steven G.
Coto, Eliecer
Hamilton-Nelson, Kara L.
Gu, Wei
Razquin, Cristina
Pastor, Pau
Mateo, Ignacio
Owen, Michael J.
Faber, Kelley M.
Jonsson, Palmi V.
Combarros, Onofre
O'Donovan, Michael C.
Cantwell, Laura B.
Soininen, Hilkka
Blacker, Deborah
Mead, Simon
Mosley, Thomas H., Jr.
Bennett, David A.
Harris, Tamara B.
Fratiglioni, Laura
Holmes, Clive
de Bruijn, Renee F. A. G.
Passmore, Peter
Montine, Thomas J.
Bettens, Karolien
Rotter, Jerome I.
Brice, Alexis
Morgan, Kevin
Foroud, Tatiana M.
Kukull, Walter A.
Hannequin, Didier
Powell, John F.
Nalls, Michael A.
Ritchie, Karen
Lunetta, Kathryn L.
Kauwe, John S. K.
Boerwinkle, Eric
Riemenschneider, Matthias
Boada, Merce
Hiltunen, Mikko
Martin, Eden R.
Schmidt, Reinhold
Rujescu, Dan
Wang, Li-San
Dartigues, Jean-Francois
Mayeux, Richard
Tzourio, Christophe
Hofman, Albert
Noethen, Markus M.
Graff, Caroline
Psaty, Bruce M.
Jones, Lesley
Haines, Jonathan L.
Holmans, Peter A.
Lathrop, Mark
Pericak-Vance, Margaret A.
Launer, Lenore J.
Farrer, Lindsay A.
van Duijn, Cornelia M.
Van Broeckhoven, Christine
Moskvina, Valentina
Seshadri, Sudha
Williams, Julie
Schellenberg, Gerard D.
Amouyel, Philippe
CA EADI
GERAD
ADGC
CHARGE
TI Meta-analysis of 74,046 individuals identifies 11 new susceptibility
loci for Alzheimer's disease
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COMMON VARIANTS; GENETIC RISK; RECEPTOR; CD33;
IMPUTATION; MUTATIONS; GENOTYPES; SEQUENCE; NEURONS
AB Eleven susceptibility loci for late-onset Alzheimer's disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large, two-stage meta-analysis of genome-wide association studies (GWAS) in individuals of European ancestry. In stage 1, we used genotyped and imputed data (7,055,881 SNPs) to perform meta-analysis on 4 previously published GWAS data sets consisting of 17,008 Alzheimer's disease cases and 37,154 controls. In stage 2, 11,632 SNPs were genotyped and tested for association in an independent set of 8,572 Alzheimer's disease cases and 11,312 controls. In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 x 10(-8)) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
C1 [Lambert, Jean-Charles; Bellenguez, Celine; Grenier-Boley, Benjamin; Chouraki, Vincent; Fievet, Nathalie; Amouyel, Philippe] INSERM, U744, F-59045 Lille, France.
[Lambert, Jean-Charles; Bellenguez, Celine; Grenier-Boley, Benjamin; Chouraki, Vincent; Pasquier, Florence; Deramecourt, Vincent; Amouyel, Philippe] Univ Lille 2, Lille, France.
[Lambert, Jean-Charles; Bellenguez, Celine; Grenier-Boley, Benjamin; Chouraki, Vincent; Fievet, Nathalie; Amouyel, Philippe] Inst Pasteur, F-59019 Lille, France.
[Ibrahim-Verbaas, Carla A.; Ikram, M. Arfan; de Bruijn, Renee F. A. G.] Erasmus MC Univ Med Ctr, Dept Neurol, Rotterdam, Netherlands.
[Ibrahim-Verbaas, Carla A.; Ikram, M. Arfan; Amin, Najaf; de Bruijn, Renee F. A. G.; Hofman, Albert; van Duijn, Cornelia M.] Erasmus MC Univ Med Ctr, Dept Epidemiol, Rotterdam, Netherlands.
[Harold, Denise; Sims, Rebecca; Jones, Nicola; Thomas, Charlene; Gerrish, Amy; Dunstan, Melanie L.; Hollingworth, Paul; Owen, Michael J.; O'Donovan, Michael C.; Jones, Lesley; Holmans, Peter A.; Moskvina, Valentina; Williams, Julie] Cardiff Univ, Inst Psychol Med & Clin Neurosci, MRC, Ctr Neuropsychiat Genet & Genom, Cardiff CF10 3AX, S Glam, Wales.
[Naj, Adam C.] Univ Penn, Dept Biostat & Epidemiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Naj, Adam C.] Univ Penn, Ctr Clin Epidemiol & Biostat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Jun, Gyungah; Vardarajan, Badri N.; Baldwin, Clinton; Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Med Biomed Genet, Boston, MA USA.
[Jun, Gyungah; Farrer, Lindsay A.] Boston Univ, Sch Med, Dept Ophthalmol, Boston, MA 02118 USA.
[Jun, Gyungah; DeStefano, Anita L.; Choi, Seung-Hoan; Lunetta, Kathryn L.; Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Bis, Joshua C.; Fitzpatrick, Annette L.; Harris, Tamara B.; Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Beecham, Gary W.; Kunkle, Brian; Gilbert, John R.; Hamilton-Nelson, Kara L.; Martin, Eden R.; Pericak-Vance, Margaret A.] Univ Miami, John P Hussman Inst Human Genom, Miami, FL USA.
[Beecham, Gary W.; Gilbert, John R.; Martin, Eden R.; Pericak-Vance, Margaret A.] Univ Miami, Dept Human Genet, Dr John T Macdonald Fdn, Miami, FL USA.
[Russo, Giancarlo] Univ Zurich, ETH, Funct Genom Ctr Zurich, Zurich, Switzerland.
[Thornton-Wells, Tricia A.; Haines, Jonathan L.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
[Smith, Albert V.; Gudnason, Vilmundur; Jonsson, Palmi V.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Smith, Albert V.; Gudnason, Vilmundur; Eiriksdottir, Gudny] Iceland Heart Assoc, Kopavogur, Iceland.
[Ikram, M. Arfan] Erasmus MC Univ Med Ctr, Dept Radiol, Rotterdam, Netherlands.
[Ikram, M. Arfan; de Bruijn, Renee F. A. G.; Hofman, Albert; van Duijn, Cornelia M.] Netherlands Consortium Hlth Aging, Leiden, Netherlands.
[Zelenika, Diana; Bihoreau, Marie-Therese; Lathrop, Mark] CEA, Inst Genom, Ctr Natl Genotypage, Evry, France.
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[Ramirez, Alfredo; Maier, Wolfgang] Univ Bonn, Dept Psychiat & Psychotherapy, Bonn, Germany.
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[Fitzpatrick, Annette L.; Kukull, Walter A.; Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
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[Berr, Claudine; Ritchie, Karen] Hop La Colombiere, Fac Med, U1061, INSERM, Montpellier, France.
[Lopez, Oscar L.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA.
[De Jager, Philip L.] Brigham & Womens Hosp, Dept Neurol & Psychiat, Inst Neurosci, Program Translat NeuroPsychiat Genom, Boston, MA 02115 USA.
[De Jager, Philip L.; Green, Robert] Harvard Univ, Sch Med, Boston, MA USA.
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[Lovestone, Simon; Proitsi, Petroula; Powell, John F.] Univ London, Kings Coll London, Inst Psychiat, London SW3 6LX, England.
[Letenneur, Luc; Barberger-Gateau, Pascale; Dufouil, Carole; Dartigues, Jean-Francois] Victor Segalen Univ, INSERM, U897, Bordeaux, France.
[Moron, Francisco J.] Neocodex, Dept Genom Estruct, Seville, Spain.
[Rubinsztein, David C.; St George-Hyslop, Peter] Univ Cambridge, Cambridge Inst Med Res, Cambridge, England.
[Sleegers, Kristel; Bettens, Karolien; Van Broeckhoven, Christine] Univ Antwerp VIB, Dept Mol Genet, Neurodegenerat Brain Dis Grp, B-2610 Antwerp, Belgium.
[Sleegers, Kristel; Bettens, Karolien; Van Broeckhoven, Christine] Univ Antwerp, Neurogenet Lab, Inst Born Bunge, B-2020 Antwerp, Belgium.
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[Gill, Michael] Univ Dublin Trinity Coll, Dublin 2, Ireland.
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[Larson, Eric B.; Psaty, Bruce M.] Grp Hlth, Grp Hlth Res Inst, Seattle, WA USA.
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[Clarimon, Jordi; Lleo, Alberto] Ctr Networker Biomed Res Neurodegenerat Dis, Barcelona, Spain.
[Tsuang, Debby W.] Vet Adm Puget Sound Hlth Care Syst, GRECC, Seattle, WA USA.
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[Tsolaki, Magda] Aristotle Univ Thessaloniki, Dept Neurol, GR-54006 Thessaloniki, Greece.
[Bossu, Paola; Spalletta, Gianfranco] Fdn Santa Lucia, Rome, Italy.
[Collinge, John; Mead, Simon] UCL, Inst Neurol, MRC, Pr Unit,Dept Neurodegenerat Dis, London, England.
[Sorbi, Sandro; Nacmias, Benedetta] Univ Florence, NEUROFARBA Dept Neurosci Psychol Drug Res & Child, Florence, Italy.
[Sorbi, Sandro; Nacmias, Benedetta] Univ Florence, Ctr Ric Trasferimento Alta Formaz DENOTH, Florence, Italy.
[Sanchez-Garcia, Florentino; Naranjo, Maria Candida Deniz] Hosp Univ Dr Negrin, Dept Immunol, Las Palmas Gran Canaria, Spain.
[Fox, Nick C.] UCL, Dementia Res Ctr, Dept Neurodegenerat Dis, Inst Neurol, London, England.
[Hardy, John] Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England.
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[Bosco, Paolo] Assoc Oasi Maria Santissima Srl, IRCCS, Troina, Italy.
[Clarke, Robert] Univ Oxford, Clin Trial Serv Unit, OHAP, Oxford, England.
[Brayne, Carol] Univ Cambridge, Inst Publ Hlth, Cambridge, England.
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[Matthews, Fiona] MRC, Biostat Unit, Cambridge CB2 2BW, England.
[Moebus, Susanne] Univ Duisburg Essen, Univ Hosp Essen, Inst Med Informat Biometry & Epidemiol, Essen, Germany.
[Mecocci, Patrizia] Univ Perugia, Sect Gerontol & Geriatr, Dept Clin & Expt Med, I-06100 Perugia, Italy.
[Del Zompo, Maria] Univ Cagliari, Sect Neurosci & Clin Pharmacol, Dept Biomed Sci, Cagliari, Italy.
[Hampel, Harald] Goethe Univ Frankfurt, Dept Psychiat, D-60054 Frankfurt, Germany.
[Hampel, Harald] Univ Munich, Dept Psychiat, D-80539 Munich, Germany.
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[Pastor, Pau] Inst Salud Carlos III, CIBERNED, Madrid, Spain.
[Mateo, Ignacio; Combarros, Onofre] Univ Cantabria, Neurol Serv, Marques de Valdecilla Univ Hosp, E-39005 Santander, Spain.
[Mateo, Ignacio; Combarros, Onofre] Inst Formac & Invest Marques Valdecilla IFIMAV, Santander, Spain.
[Mateo, Ignacio; Combarros, Onofre] Univ Cantabria, Marques de Valdecilla Univ Hosp, CIBERNED, E-39005 Santander, Spain.
[Mateo, Ignacio; Combarros, Onofre] IFIMAV, Santander, Spain.
[Faber, Kelley M.; Foroud, Tatiana M.] Indiana Univ, Dept Med & Mol Genet, Indianapolis, IN 46204 USA.
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[Bennett, David A.; Graff, Caroline] Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA.
[Fratiglioni, Laura] Karolinska Univ Hosp Huddinge, Dept Geriatr Med, Stockholm, Sweden.
[Holmes, Clive] Univ Southampton, Sch Med, Div Clin Neurosci, Southampton, Hants, England.
[Montine, Thomas J.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
[Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Brice, Alexis] Univ Paris 06, Inst Cerveau & Moelle Epiniere CRICM, INSERM, UMRS 975,CNRS,UMR 7225,Ctr Rech,Hosp La Salpetrie, Paris, France.
[Brice, Alexis] Hop La Pitie Salpetriere, AP HP, Paris, France.
[Nalls, Michael A.] NIA, Neurogenet Lab, Intramural Res Program, Bethesda, MD 20892 USA.
[Ritchie, Karen] Univ London Imperial Coll Sci Technol & Med, Fac Med, St Marys Hosp, London, England.
[Kauwe, John S. K.] Brigham Young Univ, Dept Biol, Provo, UT 84602 USA.
[Boerwinkle, Eric] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Ctr Human Genet, Houston, TX 77030 USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Div Epidemiol, Houston, TX 77030 USA.
[Boada, Merce] Univ Autonoma Barcelona VHIR UAB, Hosp Univ Vall dHebron, Inst Recerca, Barcelona, Spain.
[Schmidt, Reinhold] Med Univ Graz, Dept Neurol, Graz, Austria.
[Rujescu, Dan] Univ Halle, Dept Psychiat, Halle, Germany.
[Dartigues, Jean-Francois] CHU Bordeaux, Ctr Memoire Ressources & Rech Bordeaux, Bordeaux, France.
[Tzourio, Christophe] Victor Segalen Univ, INSERM, U708, Bordeaux, France.
[Noethen, Markus M.] Univ Bonn, Inst Human Genet, Dept Genom, Life & Brain Ctr, Bonn, Germany.
[Graff, Caroline] Karolinska Inst, Dept Neurobiol, Alzheimers Dis Res Ctr, Stockholm, Sweden.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Haines, Jonathan L.] Vanderbilt Univ, Vanderbilt Ctr Human Genet Res, Nashville, TN 37235 USA.
[Lathrop, Mark] McGill Univ, Montreal, PQ, Canada.
[Lathrop, Mark] Genome Quebec Innovat Ctr, Montreal, PQ, Canada.
[Launer, Lenore J.] NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, Bethesda, MD 20892 USA.
[Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Farrer, Lindsay A.; Seshadri, Sudha] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[van Duijn, Cornelia M.] Ctr Med Syst Biol, Leiden, Netherlands.
[Amouyel, Philippe] Ctr Hosp Reg Univ Lille, Lille, France.
RP Amouyel, P (reprint author), INSERM, U744, F-59045 Lille, France.
EM williamsj@cardiff.ac.uk; philippe.amouyel@pasteur-lille.fr
RI Kowall, Neil/G-6364-2012; Hardy, John/C-2451-2009; Reposo,
Ramirez-Lorca/D-7907-2014; Aspelund, Thor/C-5983-2008; Powell,
John/G-4412-2011; Lambert, jean-charles/A-9553-2014; Gu,
Wei/G-4003-2010; Crane, Paul/C-8623-2014; berr, Claudine/D-5238-2014;
Bosso, Paola/E-4832-2014; Schott, Jonathan/A-9065-2011; Singleton,
Andrew/C-3010-2009; Ciaramella, Antonio/F-1170-2011; Deloukas,
Panos/B-2922-2013; Pastor, Pau/C-9834-2009; Tzourio,
christophe/B-4015-2009; Fox, Nick/B-1319-2009; lambert,
jean-charles/F-8787-2013; Holmans, Peter/F-4518-2015; LICEND,
CEMND/F-1296-2015; Frank Garcia, Ana/I-5159-2015; Gudnason,
Vilmundur/K-6885-2015; Kamatani, Yoichiro/N-5513-2015; graff,
caroline/A-2545-2009; Bullido, Maria/C-8509-2014; IBIS, TERAPIA
CELULA/P-3297-2015; Smith, Albert/K-5150-2015; Ritchie,
Karen/G-3571-2013; Caffarra, Paolo/K-6567-2016; Tsuang,
Debby/L-7234-2016; Guerreiro, Rita/A-1327-2011; Vandenberghe,
Rik/K-2145-2014; Epelbaum, Jacques/B-2263-2013;
OI Kowall, Neil/0000-0002-6624-0213; Aspelund, Thor/0000-0002-7998-5433;
Powell, John/0000-0001-6124-439X; Lambert,
jean-charles/0000-0003-0829-7817; Gu, Wei/0000-0003-3951-6680; berr,
Claudine/0000-0001-5254-7655; Bosso, Paola/0000-0002-1432-0078; Schott,
Jonathan/0000-0003-2059-024X; Ciaramella, Antonio/0000-0001-9888-8156;
Deloukas, Panos/0000-0001-9251-070X; Pastor, Pau/0000-0002-7493-8777;
Tzourio, christophe/0000-0002-6517-2984; Fox, Nick/0000-0002-6660-657X;
Holmans, Peter/0000-0003-0870-9412; Frank Garcia,
Ana/0000-0003-3858-9116; Gudnason, Vilmundur/0000-0001-5696-0084;
Bullido, Maria/0000-0002-6477-1117; Smith, Albert/0000-0003-1942-5845;
Caffarra, Paolo/0000-0003-2246-5223; Tsuang, Debby/0000-0002-4716-1894;
Vandenberghe, Rik/0000-0001-6237-2502; Ibrahim-verbaas,
Carla/0000-0002-4325-0857; Ikram, Mohammad Arfan/0000-0003-0372-8585;
Seshadri, Sudha/0000-0001-6135-2622; Chouraki,
Vincent/0000-0002-4698-1794; Bayer, Antony/0000-0002-7514-248X; Kamboh,
M. Ilyas/0000-0002-3453-1438; Sanchez-Garcia,
Florentino/0000-0003-0304-6023; Escott-Price,
Valentina/0000-0003-1784-5483; Reisberg, Barry/0000-0002-9104-7423;
duron, emmanuelle/0000-0001-6680-3613; Harold,
Denise/0000-0001-5195-0143; Lacour, Andre/0000-0003-2692-2583; Ferris,
Steven/0000-0001-8641-6223; Buxbaum, Joseph/0000-0001-8898-8313; Panza,
Francesco/0000-0002-7220-0656; Nothen, Markus/0000-0002-8770-2464;
Pickering-Brown, Stuart/0000-0003-1561-6054; Squassina,
Alessio/0000-0001-7415-7607; Beiser, Alexa/0000-0001-8551-7778; Alcolea,
Daniel/0000-0002-3819-3245; Todd, Stephen/0000-0002-2312-9195; Matthews,
Fiona/0000-0002-1728-2388
FU French National Foundation on Alzheimer's Disease and Related Disorders;
Institut Pasteur de Lille; INSERM; FRC (Fondation pour la Recherche sur
le Cerveau); Rotary; LABEX (Laboratory of Excellence Program Investment
for the Future); DISTALZ grant (Development of Innovative Strategies for
a Transdisciplinary Approach to Alzheimer's Disease); Alzheimer's
Association (Chicago, Illinois); Wellcome Trust; MRC; Alzheimer's
Research UK (ARUK); Welsh government; US National Institutes of Health,
National Institute on Aging (NIH-NIA) [U01 AG032984, R01 AG033193]; US
National Institutes of Health; Erasmus Medical Center; Erasmus
University
FX This work was made possible by the generous participation of the control
subjects, the patients and their families. iSelect chips were funded by
the French National Foundation on Alzheimer's Disease and Related
Disorders. Data management involved the Centre National de Genotypage
and was supported by the Institut Pasteur de Lille, INSERM, FRC
(Fondation pour la Recherche sur le Cerveau) and Rotary. This work has
been developed and supported by the LABEX (Laboratory of Excellence
Program Investment for the Future) DISTALZ grant (Development of
Innovative Strategies for a Transdisciplinary Approach to Alzheimer's
Disease). The French National Foundation on Alzheimer's Disease and
Related Disorders and the Alzheimer's Association (Chicago, Illinois)
grant supported in-person meetings and communication for IGAP, and the
Alzheimer's Association (Chicago, Illinois) grant provided some funds to
each consortium for analyses.; GERAD was supported by the Wellcome
Trust, the MRC, Alzheimer's Research UK (ARUK) and the Welsh government.
ADGC and CHARGE were supported by the US National Institutes of Health,
National Institute on Aging (NIH-NIA), including grants U01 AG032984 and
R01 AG033193 (additional US National Institutes of Health grant numbers
are listed in the Supplementary Note).; CHARGE was also supported by
Erasmus Medical Center and Erasmus University.
NR 52
TC 620
Z9 631
U1 29
U2 215
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2013
VL 45
IS 12
BP 1452
EP U206
DI 10.1038/ng.2802
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 262EA
UT WOS:000327715800010
PM 24162737
ER
PT J
AU Guo, GW
Sun, XJ
Chen, C
Wu, S
Huang, PD
Li, ZS
Dean, M
Huang, Y
Jia, WL
Zhou, Q
Tang, AF
Yang, ZQ
Li, XX
Song, PF
Zhao, XK
Ye, R
Zhang, SQ
Lin, Z
Qi, MF
Wan, SQ
Xie, LF
Fan, F
Nickerson, ML
Zou, XJ
Hu, XD
Xing, L
Lv, ZJ
Mei, HB
Gao, SJ
Liang, CZ
Gao, ZB
Lu, JX
Yu, Y
Liu, CX
Li, L
Fang, XD
Jiang, ZM
Yang, J
Li, CL
Zhao, X
Chen, J
Zhang, F
Lai, YQ
Lin, ZG
Zhou, FJ
Chen, H
Chan, HC
Tsang, S
Theodorescu, D
Li, YR
Zhang, XQ
Wang, J
Yang, HM
Gui, YT
Wang, J
Cai, ZM
AF Guo, Guangwu
Sun, Xiaojuan
Chen, Chao
Wu, Song
Huang, Peide
Li, Zesong
Dean, Michael
Huang, Yi
Jia, Wenlong
Zhou, Quan
Tang, Aifa
Yang, Zuoquan
Li, Xianxin
Song, Pengfei
Zhao, Xiaokun
Ye, Rui
Zhang, Shiqiang
Lin, Zhao
Qi, Mingfu
Wan, Shengqing
Xie, Liangfu
Fan, Fan
Nickerson, Michael L.
Zou, Xiangjun
Hu, Xueda
Xing, Li
Lv, Zhaojie
Mei, Hongbin
Gao, Shengjie
Liang, Chaozhao
Gao, Zhibo
Lu, Jingxiao
Yu, Yuan
Liu, Chunxiao
Li, Lin
Fang, Xiaodong
Jiang, Zhimao
Yang, Jie
Li, Cailing
Zhao, Xin
Chen, Jing
Zhang, Fang
Lai, Yongqi
Lin, Zheguang
Zhou, Fangjian
Chen, Hao
Chan, Hsiao Chang
Tsang, Shirley
Theodorescu, Dan
Li, Yingrui
Zhang, Xiuqing
Wang, Jian
Yang, Huanming
Gui, Yaoting
Wang, Jun
Cai, Zhiming
TI Whole-genome and whole-exome sequencing of bladder cancer identifies
frequent alterations in genes involved in sister chromatid cohesion and
segregation
SO NATURE GENETICS
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; SHORT READ ALIGNMENT; COLORECTAL CANCERS;
CELL-CARCINOMA; RNA-SEQ; MUTATIONS; FGFR3; ANEUPLOIDY; FUSIONS; VARIANT
AB Bladder cancer is one of the most common cancers worldwide, with transitional cell carcinoma (TCC) being the predominant form. Here we report a genomic analysis of TCC by both whole-genome and whole-exome sequencing of 99 individuals with TCC. Beyond confirming recurrent mutations in genes previously identified as being mutated in TCC, we identified additional altered genes and pathways that were implicated in TCC. Notably, we discovered frequent alterations in STAG2 and ESPL1, two genes involved in the sister chromatid cohesion and segregation (SCCS) process. Furthermore, we also detected a recurrent fusion involving FGFR3 and TACC3, another component of SCCS, by transcriptome sequencing of 42 DNA-sequenced tumors. Overall, 32 of the 99 tumors (32%) harbored genetic alterations in the SCCS process. Our analysis provides evidence that genetic alterations affecting the SCCS process may be involved in bladder tumorigenesis and identifies a new therapeutic possibility for bladder cancer.
C1 [Guo, Guangwu; Sun, Xiaojuan; Wu, Song; Li, Zesong; Huang, Yi; Tang, Aifa; Zhang, Shiqiang; Qi, Mingfu; Xie, Liangfu; Zou, Xiangjun; Xing, Li; Lv, Zhaojie; Mei, Hongbin; Chen, Hao; Cai, Zhiming] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Dept Urol Surg, Shenzhen, Peoples R China.
[Guo, Guangwu; Chen, Chao; Huang, Peide; Jia, Wenlong; Zhou, Quan; Yang, Zuoquan; Song, Pengfei; Ye, Rui; Lin, Zhao; Wan, Shengqing; Fan, Fan; Hu, Xueda; Gao, Shengjie; Gao, Zhibo; Yu, Yuan; Li, Lin; Fang, Xiaodong; Yang, Jie; Zhao, Xin; Zhang, Fang; Li, Yingrui; Zhang, Xiuqing; Wang, Jian; Yang, Huanming; Wang, Jun] BGI Shenzhen, Shenzhen, Peoples R China.
[Sun, Xiaojuan; Wu, Song; Li, Zesong; Huang, Yi; Tang, Aifa; Zhang, Shiqiang; Qi, Mingfu; Xie, Liangfu; Zou, Xiangjun; Xing, Li; Lv, Zhaojie; Mei, Hongbin; Chen, Hao; Cai, Zhiming] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Natl Reg Key Technol Engn Lab Clin Applicat Canc, Shenzhen, Peoples R China.
[Sun, Xiaojuan; Wu, Song; Li, Zesong; Huang, Yi; Tang, Aifa; Zhang, Shiqiang; Qi, Mingfu; Xie, Liangfu; Zou, Xiangjun; Xing, Li; Lv, Zhaojie; Mei, Hongbin; Chen, Hao; Cai, Zhiming] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Shenzhen Engn Lab Tumor Clin Immune Gene Therapy, Shenzhen, Peoples R China.
[Sun, Xiaojuan; Wu, Song; Li, Zesong; Huang, Yi; Tang, Aifa; Zhang, Shiqiang; Qi, Mingfu; Xie, Liangfu; Zou, Xiangjun; Xing, Li; Lv, Zhaojie; Mei, Hongbin; Chen, Hao; Cai, Zhiming] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Shenzhen Key Lab Genitourinary Tumor, Shenzhen, Peoples R China.
[Wu, Song] Sun Yat Sen Univ, Zhongshan Sch Med, Inst Immunol, Guangzhou 510275, Guangdong, Peoples R China.
[Wu, Song; Zhou, Fangjian] Sun Yat Sen Univ, Ctr Canc, Dept Urol, Guangzhou 510275, Guangdong, Peoples R China.
[Dean, Michael; Nickerson, Michael L.] NCI, Canc & Inflammat Program, US Natl Inst Hlth NIH, Frederick, MD 21701 USA.
[Li, Xianxin; Lu, Jingxiao; Jiang, Zhimao; Li, Cailing; Chen, Jing; Lai, Yongqi; Lin, Zheguang; Gui, Yaoting] Peking Univ Shenzhen Hosp, Shenzhen PKU HKUST Med Ctr, Inst Urol, Guangdong & Shenzhen Key Lab Male Reprod Med & Ge, Shenzhen, Peoples R China.
[Zhao, Xiaokun] Cent Southern Univ, Xiangya Hosp 2, Dept Urol, Changsha, Hunan, Peoples R China.
[Liang, Chaozhao] Anhui Med Univ, Affiliated Hosp 1, Dept Urol, Hefei, Peoples R China.
[Liu, Chunxiao] Southern Med Univ, Zhujiang Hosp, Dept Urol, Guangzhou, Guangdong, Peoples R China.
[Chan, Hsiao Chang] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Epithelial Cell Biol Res Ctr, Shatin, Hong Kong, Peoples R China.
[Tsang, Shirley] BioMatrix, Rockville, MD USA.
[Theodorescu, Dan] Univ Colorado, Ctr Comprehens Canc, Dept Surg, Aurora, CO USA.
[Wang, Jun] Univ Copenhagen, Dept Biol, Copenhagen, Denmark.
[Wang, Jun] Univ Copenhagen, Novo Nordisk Fdn, Ctr Basic Metab Res, Copenhagen, Denmark.
RP Cai, ZM (reprint author), Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Dept Urol Surg, Shenzhen, Peoples R China.
EM guiyaoting@hotmail.com; wangj@genomics.org.cn; caizhiming2000@163.com
RI Chen, Hao/D-3425-2012; Li, Yingrui/K-1064-2015; Wang, Jun/C-8434-2016;
Chan, Hsiao Chang/E-1507-2016; Wang, Jun/B-9503-2016
OI Wang, Jun/0000-0002-8540-8931; Peide, Huang/0000-0001-6108-5069; Wang,
Jun/0000-0002-2113-5874
FU Chinese High-Tech (863) Program [2012AA02A201, 2012AA02A208]; Guangdong
Innovative Research Team Program [2009010016]; State Key Development
Program for Basic Research of China-973 Program [2011CB809203,
2014CB745200]; Shenzhen Municipal Government of China [JC201005260191A,
CXB201108250096A, ZDSY20120615154448514, BGI20100001]
FX This work was supported by grants from the Chinese High-Tech (863)
Program (2012AA02A201 and 2012AA02A208), the Guangdong Innovative
Research Team Program (2009010016), the State Key Development Program
for Basic Research of China-973 Program (2011CB809203 and 2014CB745200)
and the Shenzhen Municipal Government of China (JC201005260191A,
CXB201108250096A, ZDSY20120615154448514 and BGI20100001).
NR 39
TC 140
Z9 146
U1 13
U2 70
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2013
VL 45
IS 12
BP 1459
EP U213
DI 10.1038/ng.2798
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 262EA
UT WOS:000327715800011
PM 24121792
ER
PT J
AU Balbas-Martinez, C
Sagrera, A
Carrillo-de-Santa-Pau, E
Earl, J
Marquez, M
Vazquez, M
Lapi, E
Castro-Giner, F
Beltran, S
Bayes, M
Carrato, A
Cigudosa, JC
Dominguez, O
Gut, M
Herranz, J
Juanpere, N
Kogevinas, M
Langa, X
Lopez-Knowles, E
Lorente, JA
Lloreta, J
Pisano, DG
Richart, L
Rico, D
Salgado, RN
Tardon, A
Chanock, S
Heath, S
Valencia, A
Losada, A
Gut, I
Malats, N
Real, FX
AF Balbas-Martinez, Cristina
Sagrera, Ana
Carrillo-de-Santa-Pau, Enrique
Earl, Julie
Marquez, Mirari
Vazquez, Miguel
Lapi, Eleonora
Castro-Giner, Francesc
Beltran, Sergi
Bayes, Monica
Carrato, Alfredo
Cigudosa, Juan C.
Dominguez, Orlando
Gut, Marta
Herranz, Jesus
Juanpere, Nuria
Kogevinas, Manolis
Langa, Xavier
Lopez-Knowles, Elena
Lorente, Jose A.
Lloreta, Josep
Pisano, David G.
Richart, Laia
Rico, Daniel
Salgado, Rocio N.
Tardon, Adonina
Chanock, Stephen
Heath, Simon
Valencia, Alfonso
Losada, Ana
Gut, Ivo
Malats, Nuria
Real, Francisco X.
TI Recurrent inactivation of STAG2 in bladder cancer is not associated with
aneuploidy
SO NATURE GENETICS
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; COPY-NUMBER; FUNCTIONAL IMPACT; FGFR3 MUTATIONS;
CELL-CARCINOMA; GENOME; COHESIN-SA1; VARIANTS; TUMORS; GENES
AB Urothelial bladder cancer (UBC) is heterogeneous at the clinical, pathological and genetic levels. Tumor invasiveness (T) and grade (G) are the main factors associated with outcome and determine patient management(1). A discovery exome sequencing screen (n = 17), followed by a prevalence screen (n = 60), identified new genes mutated in this tumor coding for proteins involved in chromatin modification (MLL2, ASXL2 and BPTF), cell division (STAG2, SMC1A and SMC1B) and DNA repair (ATM, ERCC2 and FANCA). STAG2, a subunit of cohesin, was significantly and commonly mutated or lost in UBC, mainly in tumors of low stage or grade, and its loss was associated with improved outcome. Loss of expression was often observed in chromosomally stable tumors, and STAG2 knockdown in bladder cancer cells did not increase aneuploidy. STAG2 reintroduction in non-expressing cells led to reduced colony formation. Our findings indicate that STAG2 is a new UBC tumor suppressor acting through mechanisms that are different from its role in preventing aneuploidy.
C1 [Balbas-Martinez, Cristina; Sagrera, Ana; Carrillo-de-Santa-Pau, Enrique; Earl, Julie; Lapi, Eleonora; Langa, Xavier; Richart, Laia; Real, Francisco X.] CNIO Spanish Natl Canc Res Ctr, Mol Pathol Programme, Epithelial Carcinogenesis Grp, Madrid, Spain.
[Earl, Julie; Carrato, Alfredo] Hosp Ramon & Cajal, Serv Oncol Med, E-28034 Madrid, Spain.
[Marquez, Mirari; Herranz, Jesus; Malats, Nuria] CNIO Spanish Natl Canc Res Ctr, Human Canc Genet Programme, Genet & Mol Epidemiol Grp, Madrid, Spain.
[Vazquez, Miguel; Rico, Daniel; Valencia, Alfonso] CNIO Spanish Natl Canc Res Ctr, Struct Biol & Biocomp Programme, Struct Computat Biol Grp, Madrid, Spain.
[Castro-Giner, Francesc; Beltran, Sergi; Bayes, Monica; Gut, Marta; Heath, Simon; Gut, Ivo] CNAG, Barcelona, Spain.
[Cigudosa, Juan C.; Salgado, Rocio N.] CNIO Spanish Natl Canc Res Ctr, Human Canc Genet Programme, Mol Cytogenet Grp, Madrid, Spain.
[Dominguez, Orlando] CNIO Spanish Natl Canc Res Ctr, Biotechnol Programme, Madrid, Spain.
[Juanpere, Nuria; Lloreta, Josep] Hosp Mar Parc Salut Mar, Dept Pathol, Barcelona, Spain.
[Kogevinas, Manolis] Ctr Recerca Epidemiol Ambiental, Barcelona, Spain.
[Kogevinas, Manolis; Lopez-Knowles, Elena] Inst Recerca Hosp Mar, IMIM, Barcelona, Spain.
[Kogevinas, Manolis] CIBERESP, Barcelona, Spain.
[Kogevinas, Manolis] Natl Sch Publ Hlth, Athens, Greece.
[Lorente, Jose A.] Hosp Mar Parc Salut Mar, Urol Serv, Barcelona, Spain.
[Lloreta, Josep; Real, Francisco X.] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona, Spain.
[Pisano, David G.] CNIO Spanish Natl Canc Res Ctr, Struct Biol & Biocomp Programme, Bioinformat Unit, Madrid, Spain.
[Tardon, Adonina] Univ Oviedo, Dept Med, Oviedo, Spain.
[Chanock, Stephen] NCI, Translat Genom Lab, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Losada, Ana] CNIO Spanish Natl Canc Res Ctr, Mol Oncol Programme, Chromosome Dynam Grp, Madrid, Spain.
RP Real, FX (reprint author), CNIO Spanish Natl Canc Res Ctr, Mol Pathol Programme, Epithelial Carcinogenesis Grp, Madrid, Spain.
EM preal@cnio.es
RI Real Arribas, Francisco/H-5275-2015; Kogevinas, Manolis/C-3918-2017;
Castro-Giner, Francesc/D-7992-2014; Lloreta, J/I-2112-2014; Losada,
Ana/H-5917-2015; Valencia, Alfonso/I-3127-2015; Beltran,
Sergi/I-3408-2015; Pisano, David/N-5817-2014; Herranz Valera,
Jesus/M-8657-2014;
OI Real Arribas, Francisco/0000-0001-9501-498X; Castro-Giner,
Francesc/0000-0001-6111-0754; Lloreta, J/0000-0003-1644-9470; Losada,
Ana/0000-0001-5251-3383; Valencia, Alfonso/0000-0002-8937-6789; Beltran,
Sergi/0000-0002-2810-3445; Pisano, David/0000-0002-4895-4124; Herranz
Valera, Jesus/0000-0002-7385-1311; Rico, Daniel/0000-0002-6561-2310;
Malats, Nuria/0000-0003-2538-3784
FU Ministerio de Economia y Competitividad, Madrid [SAF-2010-21517,
SAF2011-15934-E]; Instituto de Salud Carlos III [G03/174, 00/0745,
PI051436, PI061614, PI080440, PI120425]; Asociacion Espanola Contra el
Cancer [EU-FP7-201663]; US National Institutes of Health [RO1 CA089715];
La Caixa International PhD Fellowship; Fundacion Banco Santander
Postdoctoral Programme
FX We thank F. Algaba, Y. Allory, A. Cuadrado, C. Gonzalez, E. Lopez, P.
Lapunzina, T. Lobato, M. Malumbres, S. Remeseiro, V.J. Sanchez-Arevalo,
F. Waldman and the CNIO core facilities for valuable contributions. We
also thank TCGA investigators for providing unpublished information for
analysis. This work was supported, in part, by grants from Ministerio de
Economia y Competitividad, Madrid (grants Consolider ONCOBIO, Consolider
INESGEN, SAF-2010-21517 and SAF2011-15934-E), Instituto de Salud Carlos
III (grants G03/174, 00/0745, PI051436, PI061614, G03/174, PI080440,
PI120425 and Red Tematica de Investigacion Cooperativa en Cancer
(RTICC)), Asociacion Espanola Contra el Cancer, EU-FP7-201663 and US
National Institutes of Health grant RO1 CA089715. C. B.-M. is the
recipient of a La Caixa International PhD Fellowship. E. L. is supported
by a grant from the Fundacion Banco Santander Postdoctoral Programme.
NR 34
TC 82
Z9 82
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2013
VL 45
IS 12
BP 1464
EP U221
DI 10.1038/ng.2799
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 262EA
UT WOS:000327715800012
PM 24121791
ER
PT J
AU Levine, DM
Ek, WE
Zhang, R
Liu, XX
Onstad, L
Sather, C
Lao-Sirieix, P
Gammon, MD
Corley, DA
Shaheen, NJ
Bird, NC
Hardie, LJ
Murray, LJ
Reid, BJ
Chow, WH
Risch, HA
Nyren, O
Ye, WM
Liu, G
Romero, Y
Bernstein, L
Wu, AH
Casson, AG
Chanock, SJ
Harrington, P
Caldas, I
Debiram-Beecham, I
Caldas, C
Hayward, NK
Pharoah, PD
Fitzgerald, RC
MacGregor, S
Whiteman, DC
Vaughan, TL
AF Levine, David M.
Ek, Weronica E.
Zhang, Rui
Liu, Xinxue
Onstad, Lynn
Sather, Cassandra
Lao-Sirieix, Pierre
Gammon, Marilie D.
Corley, Douglas A.
Shaheen, Nicholas J.
Bird, Nigel C.
Hardie, Laura J.
Murray, Liam J.
Reid, Brian J.
Chow, Wong-Ho
Risch, Harvey A.
Nyren, Olof
Ye, Weimin
Liu, Geoffrey
Romero, Yvonne
Bernstein, Leslie
Wu, Anna H.
Casson, Alan G.
Chanock, Stephen J.
Harrington, Patricia
Caldas, Isabel
Debiram-Beecham, Irene
Caldas, Carlos
Hayward, Nicholas K.
Pharoah, Paul D.
Fitzgerald, Rebecca C.
MacGregor, Stuart
Whiteman, David C.
Vaughan, Thomas L.
TI A genome-wide association study identifies new susceptibility loci for
esophageal adenocarcinoma and Barrett's esophagus
SO NATURE GENETICS
LA English
DT Article
ID EPIDERMAL-GROWTH-FACTOR; GASTROESOPHAGEAL-REFLUX; QUALITY-CONTROL;
CANCER; RISK; POLYMORPHISM; METAANALYSIS; POPULATION; CARCINOMA;
VARIANTS
AB Esophageal adenocarcinoma is a cancer with rising incidence and poor survival. Most such cancers arise in a specialized intestinal metaplastic epithelium, which is diagnostic of Barrett's esophagus. In a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individuals with precancerous Barrett's esophagus (n = 3,175) with 10,120 controls in 2 phases. For the combined case group, we identified three new associations. The first is at 19p13 (rs10419226: P = 3.6 x 10(-10)) in CRTC1 (encoding CREB-regulated transcription coactivator), whose aberrant activation has been associated with oncogenic activity. A second is at 9q22 (rs11789015: P = 1.0 x 10(-9)) in BARX1, which encodes a transcription factor important in esophageal specification. A third is at 3p14 (rs2687201: P = 5.5 x 10(-9)) near the transcription factor FOXP1, which regulates esophageal development. We also refine a previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 and extend our findings to now include esophageal adenocarcinoma.
C1 [Levine, David M.; Zhang, Rui] Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA.
[Ek, Weronica E.; MacGregor, Stuart; Whiteman, David C.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
[Liu, Xinxue; Lao-Sirieix, Pierre; Debiram-Beecham, Irene; Fitzgerald, Rebecca C.] Hutchison MRC Res Ctr, Med Res Council MRC Canc Cell Unit, Cambridge, England.
[Liu, Xinxue; Lao-Sirieix, Pierre; Debiram-Beecham, Irene; Fitzgerald, Rebecca C.] Univ Cambridge, Cambridge, England.
[Onstad, Lynn; Reid, Brian J.; Vaughan, Thomas L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Sather, Cassandra] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Gammon, Marilie D.] Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
[Corley, Douglas A.] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
[Corley, Douglas A.] Kaiser Permanente No Calif, San Francisco Med Ctr, San Francisco, CA USA.
[Shaheen, Nicholas J.] Univ N Carolina, Sch Med, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Bird, Nigel C.] Univ Sheffield, Sch Med, Dept Oncol, Sheffield, S Yorkshire, England.
[Hardie, Laura J.] Univ Leeds, Div Epidemiol, Leeds, W Yorkshire, England.
[Murray, Liam J.] Queens Univ Belfast, Ctr Publ Hlth, Belfast, Antrim, North Ireland.
[Reid, Brian J.] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98104 USA.
[Chow, Wong-Ho] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Risch, Harvey A.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Nyren, Olof; Ye, Weimin] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Liu, Geoffrey] Ontario Canc Inst, Toronto, ON M4X 1K9, Canada.
[Romero, Yvonne] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Romero, Yvonne] Mayo Clin, Romero Registry, Rochester, MN USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA 91010 USA.
[Bernstein, Leslie] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Wu, Anna H.] Univ So Calif, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA 90089 USA.
[Casson, Alan G.] Univ Saskatchewan, Dept Surg, Saskatoon, SK, Canada.
[Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Harrington, Patricia; Pharoah, Paul D.] Univ Cambridge, Dept Publ Hlth, Cambridge, England.
[Harrington, Patricia; Pharoah, Paul D.] Univ Cambridge, Dept Primary Care, Cambridge, England.
[Harrington, Patricia; Caldas, Isabel; Caldas, Carlos; Pharoah, Paul D.] Univ Cambridge, Dept Oncol, Cambridge, England.
[Caldas, Carlos] Univ Cambridge, Canc Res UK Cambridge Inst, Cambridge, England.
[Hayward, Nicholas K.] QIMR Berghofer Med Res Inst, Oncogen Lab, Brisbane, Qld, Australia.
RP Vaughan, TL (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
EM tvaughan@u.washington.edu
RI Macgregor, Stuart/C-6442-2009; hayward, nicholas/C-1367-2015; Whiteman,
David/P-2728-2014; Liu, Geoffrey/N-4421-2016
OI Macgregor, Stuart/0000-0001-6731-8142; hayward,
nicholas/0000-0003-4760-1033; Whiteman, David/0000-0003-2563-9559;
FU US National Institutes of Health (NIH) [R01CA136725]; Australian
Research Council [FT0990987]; Australian National Health and Medical
Research Council (NHMRC); NHMRC of Australia; US NIH [NIDDK 02956,
R01DK63616, R01CA59636, R01CA100264, P30CA016672, R01CA133996,
HHSN268200782096C, U01CA57949, U01CA57983, U01CA57923]; Robert Wood
Johnson Foundation; Fraternal Order of the Eagles; National Cancer
Institute [R01 CA57947-03]; Swedish Cancer Society [4559-B01-01XAA,
4758-B02-01XAB]; California Tobacco-Related Research Program [3RT-0122,
10RT-0251]; Medical Research Council; Cancer Research UK; Cambridge
National Institute for Health Research Biomedical Research Centre;
Cambridge Experimental Cancer Medicine Centre; Cancer Research UK
[C490/A10119, C490/A10124]; UTMDACC NIH SPORE in Melanoma
[2P50CA093459]; Marit Peterson Fund for Melanoma Research; Wellcome
Trust [076113]; American Digestive Health Foundation Endoscopic Research
Award; American College of Gastroenterology Junior Faculty Development
Award; Glaxo Wellcome, Inc.; Institute for Digestive Health Clinical
Research Award; Miles and Shirley Fiterman Center for Digestive Diseases
at the Mayo Clinic (Rochester, Minnesota); [K05CA124911]
FX This work was primarily funded by a US National Institutes of Health
(NIH) grant (R01CA136725) to T. L. V. and D. C. W. T. L. V. is also
supported by grant K05CA124911. D. C. W. is supported by a Future
Fellowship (FT0990987) from the Australian Research Council. S. M. is
supported by an Australian National Health and Medical Research Council
(NHMRC) Career Development Award. N.K.H. is supported by Research
Fellowships from the NHMRC of Australia. Y.R. is supported in part by a
grant from the US NIH (NIDDK 02956), the Robert Wood Johnson Foundation
Harold Amos Medical Faculty Development Program and the Fraternal Order
of the Eagles.; The Swedish Esophageal Cancer Study was funded by grants
(R01 CA57947-03) from the National Cancer Institute and the Swedish
Cancer Society (4559-B01-01XAA and 4758-B02-01XAB). The
Kaiser-Permanente Study was supported by grants from the US NIH
(R01DK63616 and R01CA59636) and from the California Tobacco-Related
Research Program (3RT-0122 and 10RT-0251). The UK Barrett's oesophagus
gene study was funded by a Medical Research Council Programme grant, and
the UK SOCS study was funded by Cancer Research UK as well as by the
Cambridge National Institute for Health Research Biomedical Research
Centre and the Cambridge Experimental Cancer Medicine Centre. The SEARCH
grant was funded by Cancer Research UK grants C490/A10119 and
C490/A10124.; Genotyping of MD Anderson controls (C. Amos, PI) was
performed through the University of Texas MD Anderson Cancer Center
(UTMDACC) and the Johns Hopkins University Center for Inherited Disease
Research (CIDR), supported in part by US NIH grants R01CA100264,
P30CA016672 and R01CA133996 and the UTMDACC NIH SPORE in Melanoma
2P50CA093459, as well as by the Marit Peterson Fund for Melanoma
Research. CIDR is supported by contract HHSN268200782096C from the US
NIH.; This study made use of data generated by the Wellcome Trust Case
Control Consortium. Funding for the project was provided by the Wellcome
Trust under award 076113. A full list of the investigators who
contributed to the generation of the data is available from the website
(see URLs).; The Romero Registry is supported in part by the American
Digestive Health Foundation Endoscopic Research Award, the American
College of Gastroenterology Junior Faculty Development Award, the Glaxo
Wellcome, Inc., Institute for Digestive Health Clinical Research Award
and the Miles and Shirley Fiterman Center for Digestive Diseases at the
Mayo Clinic (Rochester, Minnesota). The Romero Registry also receives
charitable gifts from five industry partners (Affymetrix, AstraZeneca,
Santarus, Takeda and Wyeth). The US Multicenter Study was funded by
grants U01CA57949, U01CA57983 and U01CA57923 from the US NIH.
NR 39
TC 68
Z9 69
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2013
VL 45
IS 12
BP 1487
EP U119
DI 10.1038/ng.2796
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 262EA
UT WOS:000327715800017
PM 24121790
ER
PT J
AU Perez-Andreu, V
Roberts, KG
Harvey, RC
Yang, WJ
Cheng, C
Pei, DQ
Xu, H
Gastier-Foster, J
E, SY
Lim, JYS
Chen, IM
Fan, YP
Devidas, M
Borowitz, MJ
Smith, C
Neale, G
Burchard, EG
Torgerson, DG
Klussmann, FA
Villagran, CRN
Winick, NJ
Camitta, BM
Raetz, E
Wood, B
Yue, F
Carroll, WL
Larsen, E
Bowman, WP
Loh, ML
Dean, M
Bhojwani, D
Pui, CH
Evans, WE
Relling, MV
Hunger, SP
Willman, CL
Mullighan, CG
Yang, JJ
AF Perez-Andreu, Virginia
Roberts, Kathryn G.
Harvey, Richard C.
Yang, Wenjian
Cheng, Cheng
Pei, Deqing
Xu, Heng
Gastier-Foster, Julie
E, Shuyu
Lim, Joshua Yew-Suang
Chen, I-Ming
Fan, Yiping
Devidas, Meenakshi
Borowitz, Michael J.
Smith, Colton
Neale, Geoffrey
Burchard, Esteban G.
Torgerson, Dara G.
Antillon Klussmann, Federico
Najera Villagran, Cesar Rolando
Winick, Naomi J.
Camitta, Bruce M.
Raetz, Elizabeth
Wood, Brent
Yue, Feng
Carroll, William L.
Larsen, Eric
Bowman, W. Paul
Loh, Mignon L.
Dean, Michael
Bhojwani, Deepa
Pui, Ching-Hon
Evans, William E.
Relling, Mary V.
Hunger, Stephen P.
Willman, Cheryl L.
Mullighan, Charles G.
Yang, Jun J.
TI Inherited GATA3 variants are associated with Ph-like childhood acute
lymphoblastic leukemia and risk of relapse
SO NATURE GENETICS
LA English
DT Article
ID CHILDRENS ONCOLOGY GROUP; MINIMAL RESIDUAL DISEASE; GENOME-WIDE
ASSOCIATION; ACUTE MYELOID-LEUKEMIA; MYELOPROLIFERATIVE NEOPLASMS;
GENE-EXPRESSION; JAK2 HAPLOTYPE; CELL-TYPES; SUSCEPTIBILITY; POPULATIONS
AB Recent genomic profiling of childhood acute lymphoblastic leukemia (ALL) identified a high-risk subtype with an expression signature resembling that of Philadelphia chromosome-positive ALL and poor prognosis (Ph-like ALL). However, the role of inherited genetic variation in Ph-like ALL pathogenesis remains unknown. In a genome-wide association study (GWAS) of 511 ALL cases and 6,661 non-ALL controls, we identified a susceptibility locus for Ph-like ALL (GATA3, rs3824662; P = 2.17 x 10(-14), odds ratio (OR) = 3.85 for Ph-like ALL versus non-ALL; P = 1.05 x 10(-8), OR = 3.25 for Ph-like ALL versus non-Ph-like ALL), with independent validation. The rs3824662 risk allele was associated with somatic lesions underlying Ph-like ALL (CRLF2 rearrangement, JAK gene mutation and IKZF1 deletion) and with variation in GATA3 expression. Finally, genotype at the GATA3 SNP was also associated with early treatment response and risk of ALL relapse. Our results provide insights into interactions between inherited and somatic variants and their role in ALL pathogenesis and prognosis.
C1 [Perez-Andreu, Virginia; Yang, Wenjian; Xu, Heng; E, Shuyu; Lim, Joshua Yew-Suang; Smith, Colton; Evans, William E.; Relling, Mary V.; Yang, Jun J.] St Jude Childrens Res Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA.
[Roberts, Kathryn G.; Mullighan, Charles G.] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Harvey, Richard C.; Chen, I-Ming; Willman, Cheryl L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Cheng, Cheng; Pei, Deqing] St Jude Childrens Res Hosp, Dept Biostat, Memphis, TN 38105 USA.
[Gastier-Foster, Julie] Nationwide Childrens Hosp, Dept Pathol & Lab Med, Columbus, OH USA.
[Gastier-Foster, Julie] Ohio State Univ, Sch Med, Dept Pediat, Columbus, OH 43210 USA.
[Lim, Joshua Yew-Suang] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Pediat, Singapore 117595, Singapore.
[Fan, Yiping] St Jude Childrens Res Hosp, Dept Computat Biol, Memphis, TN 38105 USA.
[Devidas, Meenakshi] Univ Florida, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
[Borowitz, Michael J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Neale, Geoffrey] St Jude Childrens Res Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA.
[Burchard, Esteban G.; Torgerson, Dara G.] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci & Med, San Francisco, CA 94143 USA.
[Antillon Klussmann, Federico; Najera Villagran, Cesar Rolando] Unidad Nacl Oncol Pediat, Guatemala City, Guatemala.
[Winick, Naomi J.] Univ Texas SW Med Ctr Dallas, Dept Pediat Hematol Oncol, Dallas, TX 75390 USA.
[Camitta, Bruce M.] Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA.
[Raetz, Elizabeth; Carroll, William L.] NYU, Inst Canc, New York, NY USA.
[Wood, Brent] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA.
[Yue, Feng] Penn State Univ, Coll Med, Dept Biochem & Mol Biol, Hershey, PA USA.
[Larsen, Eric] Maine Childrens Canc Program, Scarborough, ME USA.
[Bowman, W. Paul] Cook Childrens Med Ctr, Dept Hematol & Oncol, Ft Worth, TX USA.
[Loh, Mignon L.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA.
[Dean, Michael] NCI, Expt Immunol Lab, Frederick, MD 21701 USA.
[Bhojwani, Deepa; Pui, Ching-Hon] St Jude Childrens Res Hosp, Dept Oncol, Memphis, TN 38105 USA.
[Hunger, Stephen P.] Univ Colorado, Childrens Hosp Colorado, Dept Hematol & Oncol, Aurora, CO USA.
RP Yang, JJ (reprint author), St Jude Childrens Res Hosp, Dept Pharmaceut Sci, 332 N Lauderdale St, Memphis, TN 38105 USA.
EM jun.yang@stjude.org
OI Harvey, Richard/0000-0002-4904-9767; Mullighan,
Charles/0000-0002-1871-1850; Bhojwani, Deepa/0000-0002-7559-7927
FU Jeffrey Pride Foundation; National Childhood Cancer Foundation; Spanish
Ministry of Education; St. Jude Children's Research Hospital Academic
Programs Special Fellowship; American Society of Hematology Scholar
Award; Alex Lemonade Stand Foundation for Childhood Cancer Young
Investigator Grant; Order of St. Francis Foundation; National Health and
Medical Research Council (Australia); Haematology Society of Australia;
New Zealand Novartis New Investigator Scholarship; US National
Institutes of Health [CA156449, CA21765, CA36401, CA98543, CA114766,
CA98413, CA140729, GM92666]; National Cancer Institute; American
Lebanese Syrian Associated Charities (ALSAC)
FX We thank the patients and parents who participated in the COG protocols
included in this study, the clinicians and research staff at COG
institutions and J. Pullen (University of Mississippi at Jackson) for
assistance in the classification of patients with ALL. Genome-wide
genotyping of COG P9905 samples was performed by the Center for
Molecular Medicine with generous financial support from the Jeffrey
Pride Foundation and the National Childhood Cancer Foundation. V. P.-A.
is supported by a Spanish Ministry of Education Fellowship Grant and by
a St. Jude Children's Research Hospital Academic Programs Special
Fellowship. J.J.Y. is supported by an American Society of Hematology
Scholar Award, an Alex Lemonade Stand Foundation for Childhood Cancer
Young Investigator Grant and by the Order of St. Francis Foundation. K.
G. R. is supported by a National Health and Medical Research Council
(Australia) Overseas Training Fellowship and by a Haematology Society of
Australia and New Zealand Novartis New Investigator Scholarship. C. G.
M. is a Pew Scholar in the Biomedical Sciences and a St. Baldrick's
Scholar. We thank M. Shriver (Pennsylvania State University) for sharing
SNP genotype data for the Native American references, J. Pritchard and
J. Degner (University of Chicago) for sharing DNase I hypersensitivity
data for HapMap YRI cell lines, R. C. Ribeiro (St. Jude Children's
Research Hospital) and P. De Alarcon (University of Illinois College of
Medicine at Peoria) for coordinating collaborations in Guatemala and S.
Naron for her editorial assistance. This work was supported by the US
National Institutes of Health (grant numbers CA156449, CA21765, CA36401,
CA98543, CA114766, CA98413, CA140729 and GM92666), in part by the
intramural Program of the National Cancer Institute and by the American
Lebanese Syrian Associated Charities (ALSAC). Study sponsors were not
directly involved in the design of the study, the collection, analysis
and interpretation of data, the writing of the manuscript or the
decision to submit the manuscript. Detailed acknowledgments for the
dbGaP data sets are provided in the Supplementary Note.
NR 48
TC 58
Z9 60
U1 4
U2 20
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2013
VL 45
IS 12
BP 1494
EP U127
DI 10.1038/ng.2803
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 262EA
UT WOS:000327715800018
PM 24141364
ER
PT J
AU He, Y
Yu, SJ
Bae, E
Shen, H
Wang, Y
AF He, Yi
Yu, Seongjin
Bae, Eunkyung
Shen, Hui
Wang, Yun
TI Methamphetamine alters reference gene expression in nigra and striatum
of adult rat brain
SO NEUROTOXICOLOGY
LA English
DT Article
DE Methamphetamine; Housekeeping genes; Nigra; Real-time PCR; Reference
genes; Striatum
ID REAL-TIME PCR; HOUSEKEEPING GENES; RT-PCR; IN-VITRO; NORMALIZATION;
ISCHEMIA; CORTEX
AB The nigrostriatal dopaminergic system is a major lesion target for methamphetamine (MA), one of the most addictive and neurotoxic drugs of abuse. High doses of MA alter the expression of a large number of genes. Reference genes (RGs) are considered relatively stable and are often used as standards for quantitative real-time PCR (qRT-PCR) reactions. The purpose of this study was to determine whether MA altered the expression of RGs and to identify the appropriate RGs for gene expression studies in animals receiving MA. Adult male Sprague-Dawley rats were treated with high doses of MA or saline. Striatum and substantia nigra were harvested at 2 h or 24 h after MA administration. The expression and stability of 10 commonly used RGs were examined using qRT-PCR and then evaluated by geNorm and Normfinder. We found that MA altered the expression of selected RGs. These candidate RGs presented differential stability in the striatum and in substantia nigra at both 2 h and 24 h after MA injection. Selection of an unstable RG as a standard altered the significance of tyrosine hydroxylase (TH) mRNA expression after MA administration. In conclusion, our data show that MA site- and time-dependently altered the expression of RGs in nigrostriatal dopaminergic system. These temporal and spatial factors should be considered when selecting appropriate RGs for interpreting the expression of target genes in animals receiving MA. Published by Elsevier Inc.
C1 [He, Yi; Shen, Hui; Wang, Yun] NIDA, Neural Protect & Regenerat Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Yu, Seongjin; Bae, Eunkyung; Wang, Yun] Natl Hlth Res Inst, Ctr Neuropsychiat Res, Zhunan 35053, Miaoli County, Taiwan.
RP Wang, Y (reprint author), Natl Hlth Res Inst, Ctr Neuropsychiat Res, 35 Keyan Rd, Zhunan 35053, Miaoli County, Taiwan.
EM yi.he2@nih.gov; b7508@nhri.org.tw; baee@nhri.org.tw;
HShen@intra.nida.nih.gov; ywang@nhri.org.tw
FU National Health Research Institutes, Taiwan; National Institute on Drug
Abuse, IRP, USA
FX This study was supported by National Health Research Institutes, Taiwan
and National Institute on Drug Abuse, IRP, USA.
NR 26
TC 3
Z9 3
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0161-813X
EI 1872-9711
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PD DEC
PY 2013
VL 39
BP 138
EP 145
DI 10.1016/j.neuro.2013.08.009
PG 8
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA 270GK
UT WOS:000328306700018
PM 24042092
ER
PT J
AU Edderkaoui, B
Kesavan, C
Baylink, DJ
Wergedal, JE
Srivastava, AK
Mohan, S
AF Edderkaoui, Bouchra
Kesavan, Chandrasekhar
Baylink, David J.
Wergedal, Jon E.
Srivastava, Apurva K.
Mohan, Subburaman
TI ENU mutation mapped to a distal region of chromosome 11 is a major
determinant of bone size
SO PHYSIOLOGICAL GENOMICS
LA English
DT Article
DE mutation; growth hormone; bone formation
ID QUANTITATIVE TRAIT LOCI; NITROSOUREA-MUTAGENIZED MICE; CHEMICAL
MUTAGENESIS; GENETIC-LOCI; MECHANICAL-PROPERTIES; MOUSE STRAINS;
C57BL/6J MICE; SCREEN; GROWTH; IDENTIFICATION
AB Using a phenotype driven n-ethyl-nitrosourea (ENU) screen in growth hormone-deficient mice, we have identified a mutant (named 14104) that exhibited a smaller bone size. Phenotype measurements by microcomputed tomography revealed that mutant mice exhibited a 43 and 34% reduction in tissue area and bone area, respectively at the femur middiaphysis. Dynamic histomorphometry revealed a 30 and 15% lower bone formation rate at the periosteal and endosteal surface, respectively. Breaking strength of the femur was reduced by 30% in the mutant mice. To determine if the 14104 locus is involved in a mechanical loading signaling pathway, the skeletal anabolic response to tibia axial loading was evaluated. The increase in trabecular response in the loaded region was severely compromised by the 14014 mutation. To identify the location of mutation, we performed linkage analysis using 62 polymorphic markers in the B6-DBA/2J F2 mice. The genome-wide linkage analysis identified the location of the mutation to a 72 to 83 cM region on chromosome 11 with peak logarithm of the odds scores of 15 for periosteal circumference at marker D11mit338. Sequence analysis revealed no mutation in the coding region of 11 potential candidate genes. Based on these data and published data on the skeletal phenotype of genes in this region, we concluded that the 109-119 Mb region of chromosome 11 harbors a bone size gene that regulates periosteal bone formation. The mutant strain developed in this study provides an important tool to identify a novel mechanosensitive gene that determines bone size during postnatal development.
C1 [Edderkaoui, Bouchra; Kesavan, Chandrasekhar; Wergedal, Jon E.; Mohan, Subburaman] Loma Linda VA Hlth Care Syst, Musculoskeletal Dis Ctr, Loma Linda, CA 92357 USA.
[Edderkaoui, Bouchra; Kesavan, Chandrasekhar; Baylink, David J.; Wergedal, Jon E.; Mohan, Subburaman] Loma Linda Univ, Dept Med, Loma Linda, CA 92350 USA.
[Srivastava, Apurva K.] Frederick Natl Lab Canc Res, Lab Human Toxicol Pharmacol, Appl Dev Res Directorate, SAIC Frederick, Frederick, MD USA.
RP Mohan, S (reprint author), Loma Linda VA Hlth Care Syst, Musculoskeletal Dis Ctr, 11201 Benton St, Loma Linda, CA 92357 USA.
EM Subburaman.Mohan@va.gov
FU Army Assistance Award [DAMD17-99-1-9571]; National Institute of
Arthritis and Musculoskeletal and Skin Diseases [AR-048139]
FX This work was supported by the Army Assistance Award No.
DAMD17-99-1-9571 and National Institute of Arthritis and Musculoskeletal
and Skin Diseases Grant AR-048139.
NR 25
TC 0
Z9 0
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1094-8341
EI 1531-2267
J9 PHYSIOL GENOMICS
JI Physiol. Genomics
PD DEC
PY 2013
VL 45
IS 24
BP 1222
EP 1228
DI 10.1152/physiolgenomics.00142.2013
PG 7
WC Cell Biology; Genetics & Heredity; Physiology
SC Cell Biology; Genetics & Heredity; Physiology
GA 273CA
UT WOS:000328509600006
PM 24151243
ER
PT J
AU de las Heras, H
Minniti, R
Wilson, S
Mitchell, C
Skopec, M
Brunner, CC
Chakrabarti, K
AF de las Heras, Hugo
Minniti, Ronaldo
Wilson, Sean
Mitchell, Chad
Skopec, Marlene
Brunner, Claudia C.
Chakrabarti, Kish
TI Experimental estimates of peak skin dose and its relationship to the CT
dose index using the CTDI head phantom
SO RADIATION PROTECTION DOSIMETRY
LA English
DT Article
ID PERFUSION COMPUTED-TOMOGRAPHY; RADIOCHROMIC FILM; CORONARY-ANGIOGRAPHY;
ENERGY-DEPENDENCE; DOSIMETRY; SIMULATIONS; SCANNER; PATIENT
AB A straightforward method is presented to estimate peak skin doses (PSDs) delivered by computed tomography (CT) scanners. The measured PSD values are related to the well-known volume CT dose index (CTDIvol), displayed on the console of CT scanners. PSD measurement estimates were obtained, in four CT units, by placing radiochromic film on the surface of a CTDI head phantom. Six different X-ray tube currents including the maximum allowed value were used to irradiate the phantom. PSD and CTDIvol were independently measured and later related to the CTDIvol value displayed on the console. A scanner-specific relationship was found between the measured PSD and the associated CTDIvol displayed on the console. The measured PSD values varied between 27 and 136 mGy among all scanners when the routine head scan parameters were used. The results of this work allow relating the widely used CTDIvol to an actual radiation dose delivered to the skin of a patient.
C1 [de las Heras, Hugo; Brunner, Claudia C.; Chakrabarti, Kish] US FDA, Silver Spring, MD 20993 USA.
[Minniti, Ronaldo] NIST, Gaithersburg, MD 20899 USA.
[Wilson, Sean; Mitchell, Chad] Walter Reed Natl Mil Med Ctr, Bethesda, MD 20889 USA.
[Skopec, Marlene] NIH, Bethesda, MD 20892 USA.
RP de las Heras, H (reprint author), US FDA, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM hugo.heras@daad-alumni.de
OI de las Heras, Hugo/0000-0003-3227-0032
FU Critical Path Project of FDA
FX Kish Chakrabarti acknowledges funding from Critical Path Project of FDA,
which enabled him to fund H.H. and C.B. for this work.
NR 40
TC 0
Z9 0
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0144-8420
EI 1742-3406
J9 RADIAT PROT DOSIM
JI Radiat. Prot. Dosim.
PD DEC
PY 2013
VL 157
IS 4
BP 536
EP 542
DI 10.1093/rpd/nct171
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA 271FI
UT WOS:000328376600008
PM 23864642
ER
PT J
AU Lamart, S
Moroz, BE
Lee, C
AF Lamart, Stephanie
Moroz, Brian E.
Lee, Choonsik
TI Evaluation of the use of surrogate tissues for calculating radiation
dose to lymphatic nodes from external photon beams
SO RADIATION PROTECTION DOSIMETRY
LA English
DT Article
ID ADULT HUMAN PHANTOMS; COMPUTATIONAL PHANTOMS; RADIOLOGICAL PROTECTION;
HYBRID PHANTOMS; HUMAN ANATOMY; DOSIMETRY; MODELS; CONSTRUCTION;
DISTRIBUTIONS; EXPOSURES
AB Lymphatic node chains of the human body are particularly difficult to realistically model in computational human phantoms. In the absence of a lymphatic node model, researchers have used the following surrogate tissues to calculate the radiation dose to the lymphatic nodes: blood vessels, muscle and the combination of the muscle and adipose tissues. In the present work, the authors investigated whether and in which extent the use of different surrogate tissues is appropriate to assess the lymph node dose, using a realistic model of lymphatic nodes that the authors recently reported. Using a Monte Carlo radiation transport method coupled with the adult male hybrid phantom that included the lymph node model, the air kerma-to-absorbed dose conversion coefficients (Gy Gy(1)) to the lymph nodes and other tissues used as surrogates for external photon beams of 15 discrete energies (0.01510 MeV) were computed using the following six idealised geometries: anteriorposterior (AP), posterioranterior (PA), right lateral, left lateral, rotational and isotropic. To validate the results of this study, the lymph node dose calculated here was compared with the dose published by the International Commission on Radiological Protection for the adult male reference phantom. The lymph node dose conversion coefficients with the values calculated for the blood vessels, muscle, adipose tissue and the combination of muscle and adipose tissues were then compared. It was found that muscle was the best estimator for the lymph nodes, with a dose difference averaged across energies 0.08 MeV of 8 in all irradiation geometries excluding the AP and PA geometries for which the blood vessels were found to be the best estimator. In conclusion, muscle and blood vessels may preferably be used as surrogate tissues in the absence of lymphatic nodes in a given voxel phantom. For energies 0.08 MeV, for which the authors observed a difference of up to 30-fold, an explicit lymph node model may be required to prevent increasing differences with the lymph node dose as the photon energy decreases, though the absolute values of the dose conversion coefficients are smaller than at higher energy.
C1 [Lamart, Stephanie; Moroz, Brian E.; Lee, Choonsik] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
RP Lee, C (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
EM leechoonsik@mail.nih.gov
RI Lee, Choonsik/C-9023-2015
OI Lee, Choonsik/0000-0003-4289-9870
FU National Cancer Institute, National Institutes of Health, US Department
of Health and Human Services
FX This study was funded by the Intramural Research Program of the National
Cancer Institute, National Institutes of Health, US Department of Health
and Human Services.
NR 34
TC 0
Z9 0
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0144-8420
EI 1742-3406
J9 RADIAT PROT DOSIM
JI Radiat. Prot. Dosim.
PD DEC
PY 2013
VL 157
IS 4
BP 600
EP 609
DI 10.1093/rpd/nct164
PG 10
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA 271FI
UT WOS:000328376600017
PM 23847324
ER
PT J
AU Wang, D
Piknova, B
Solomon, SB
Cortes-Puch, I
Kern, SJ
Sun, JF
Kanias, T
Gladwin, MT
Helms, C
Kim-Shapiro, DB
Schechter, AN
Natanson, C
AF Wang, Dong
Piknova, Barbora
Solomon, Steven B.
Cortes-Puch, Irene
Kern, Steven J.
Sun, Junfeng
Kanias, Tamir
Gladwin, Mark T.
Helms, Christine
Kim-Shapiro, Daniel B.
Schechter, Alan N.
Natanson, Charles
TI In vivo reduction of cell-free methemoglobin to oxyhemoglobin results in
vasoconstriction in canines
SO TRANSFUSION
LA English
DT Article
ID INHALED NITRIC-OXIDE; HEME-GLOBIN LINKAGE; PLASMA HEMOGLOBIN; BLOOD
SUBSTITUTES; MYOCARDIAL-INFARCTION; HEMORRHAGIC-SHOCK; OXYGEN CARRIERS;
S-NITROSOTHIOLS; BYPASS-SURGERY; BLINDED TRIAL
AB BackgroundCell-free hemoglobin (Hb) in the vasculature leads to vasoconstriction and injury. Proposed mechanisms have been based on nitric oxide (NO) scavenging by oxyhemoglobin (oxyHb) or processes mediated by oxidative reactions of methemoglobin (metHb). To clarify this, we tested the vascular effect and fate of oxyHb or metHb infusions.
Study Design and MethodsTwenty beagles were challenged with 1-hour similar infusions of (200mol/L) metHb (n=5), oxyHb (n=5), albumin (n=5), or saline (n=5). Measurements were taken over 3 hours.
ResultsInfusions of the two pure Hb species resulted in increases in mean arterial blood pressure (MAP), systemic vascular resistance index, and NO consumption capacity of plasma (all p<0.05) with the effects of oxyHb being greater than that from metHb (MAP; increase 0 to 3hr; 276% vs. 7 +/- 2%, respectively; all p<0.05). The significant vasoconstrictive response of metHb (vs. albumin and saline controls) was related to in vivo autoreduction of metHb to oxyHb, and the vasoactive Hb species that significantly correlated with MAP was always oxyHb, either from direct infusion or after in vivo reduction from metHb. Clearance of total Hb from plasma was faster after metHb than oxyHb infusion (p<0.0001).
ConclusionThese findings indicate that greater NO consumption capacity makes oxyHb more vasoactive than metHb. Additionally, metHb is reduced to oxyHb after infusion and cleared faster or is less stable than oxyHb. Although we found no direct evidence that metHb itself is involved in acute vascular effects, in aggregate, these studies suggest that metHb is not inert and its mechanism of vasoconstriction is due to its delayed conversion to oxyHb by plasma-reducing agents.
C1 NIDDK, Dept Crit Care Med, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Piknova, Barbora] NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
Wake Forest Univ, Dept Phys, Winston Salem, NC 27109 USA.
Wake Forest Univ, Translat Sci Ctr, Winston Salem, NC 27109 USA.
Sichuan Univ, Anesthesia & Crit Care Med Dept, West China Hosp, Chengdu 610064, Peoples R China.
Hosp Univ Getafe, Dept Crit Care Med, Madrid, Spain.
RP Piknova, B (reprint author), NIDDK, Mol Med Branch, NIH, 10 Ctr Dr,9N318, Bethesda, MD 20892 USA.
EM piknovab@mail.nih.gov
RI Kanias, Tamir/K-2384-2016;
OI Kanias, Tamir/0000-0001-6558-0913; Schechter, Alan N/0000-0002-5235-9408
FU NIH [HL058091, HL098032, RO1HL096973, P01HL103455]; Institute for
Transfusion Medicine; Hemophilia Center of Western Pennsylvania; US
government
FX This study was conducted using intramural NIH funds and NIH grants
HL058091 (DK-S) and HL098032 (MTG and DKS). MTG also receives research
support from NIH grants RO1HL096973, and P01HL103455, the Institute for
Transfusion Medicine and the Hemophilia Center of Western Pennsylvania.
The work by the authors was done as part of US government-funded
research; however, the opinions expressed are not necessarily those of
the National Institutes of Health.
NR 66
TC 4
Z9 4
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0041-1132
EI 1537-2995
J9 TRANSFUSION
JI Transfusion
PD DEC
PY 2013
VL 53
IS 12
BP 3149
EP 3163
DI 10.1111/trf.12162
PG 15
WC Hematology
SC Hematology
GA 265CD
UT WOS:000327926400016
PM 23488474
ER
PT J
AU Cherry, JL
AF Cherry, Joshua L.
TI Inbreeding and asexuality: a response to Szulkin et al
SO TRENDS IN ECOLOGY & EVOLUTION
LA English
DT Letter
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Cherry, JL (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM jcherry@nebi.nlm.nih.gov
NR 2
TC 2
Z9 2
U1 2
U2 13
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0169-5347
J9 TRENDS ECOL EVOL
JI Trends Ecol. Evol.
PD DEC
PY 2013
VL 28
IS 12
BP 683
EP 683
DI 10.1016/j.tree.2013.08.001
PG 1
WC Ecology; Evolutionary Biology; Genetics & Heredity
SC Environmental Sciences & Ecology; Evolutionary Biology; Genetics &
Heredity
GA 270IU
UT WOS:000328312900003
PM 24189156
ER
PT J
AU Yamashita, S
Segawa, R
Satou, N
Hiratsuka, M
Leonard, WJ
Hirasawa, N
AF Yamashita, Saori
Segawa, Ryosuke
Satou, Nozomi
Hiratsuka, Masahiro
Leonard, Warren J.
Hirasawa, Noriyasu
TI Induction of Thymic Stromal Lymphopoietin Production by Nonanoic Acid
and Exacerbation of Allergic Inflammation in Mice
SO ALLERGOLOGY INTERNATIONAL
LA English
DT Article
DE fatty acid; nonanoic acid; ovalbumin; picryl chloride; thymic stromal
lymphopoietin
ID ARYL-HYDROCARBON RECEPTOR; IN-VIVO; EXPRESSION; TSLP; SKIN;
KERATINOCYTES; DERMATITIS; IRRITANTS; CYTOKINES; LIGANDS
AB Background: Thymic stromal lymphopoietin (TSLP) plays critical roles in the induction and exacerbation of allergic diseases. We tested various chemicals in the environment and found that xylene and 1,2,4-trimethylbenzene induced the production of TSLP in vivo. These findings prompted us to search for additional chemicals that induce TSLP production. In this study, we examined whether fatty acids could induce the production of TSLP in vivo and exacerbate allergic inflammation.
Methods: Various fatty acids and related compounds were painted on the ear lobes of mice and the amount of TSLP in the homogenate of ear lobe tissue was determined. The effects of nonanoic acid on allergic inflammation were also examined.
Results: Octanoic acid, nonanoic acid, and decanoic acid markedly induced TSLP production, while a medium-chain aldehyde and alcohol showed only weak activity. Nonanoic acid induced the production of TSLP with a maximum at 24 h. TSLP production was even observed in nonanoic acid-treated C3H/HeJ mice that lacked functional toll-like receptor 4. The aryl hydrocarbon receptor agonist beta-naphthoflavone did not induce TSLP production. Nonanoic acid promoted sensitization to ovalbumin, resulting in an enhancement in the cutaneous anaphylactic response. In addition, painting of nonanoic acid after the sensitization augmented picryl chloride-induced thickening of the ear, which was reversed in TSLP receptor-deficient mice.
Conclusions: Nonanoic acid and certain fatty acids induced TSLP production, resulting in the exacerbation of allergic inflammation. We propose that TSLP-inducing chemical compounds such as nonanoic acid be recognized as chemical allergo-accelerators.
C1 [Yamashita, Saori; Segawa, Ryosuke; Satou, Nozomi; Hiratsuka, Masahiro; Hirasawa, Noriyasu] Tohoku Univ, Grad Sch Pharmaceut Sci, Sendai, Miyagi 9808578, Japan.
[Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Hirasawa, N (reprint author), Tohoku Univ, Grad Sch Pharmaceut Sci, Lab Pharmacotherapy Life Style Related Dis, Aoba Ku, 6-3 Aoba Aramaki, Sendai, Miyagi 9808578, Japan.
EM hirasawa@m.tohoku.ac.jp
FU Long-range Research Initiative (LRI) by the Japan Chemical Industry
Association (JCIA); Japan Society for the Promotion of Science
[22659025]; Smoking Research Foundation; Division of Intramural
Research, National Heart, Lung, and Blood Institute, National Institute
of Health, USA
FX The study was supported in part by a grant from the Long-range Research
Initiative (LRI) by the Japan Chemical Industry Association (JCIA), a
Grant-in-aid for Challenging Exploratory Research (22659025) from the
Japan Society for the Promotion of Science, a grant from the Smoking
Research Foundation, and by the Division of Intramural Research,
National Heart, Lung, and Blood Institute, National Institute of Health,
USA.
NR 33
TC 4
Z9 4
U1 1
U2 5
PU JAPANESE SOCIETY ALLERGOLOGY
PI TOKYO
PA MY BLDG 4F, 1-13-3, UENO, TAITO-KU, TOKYO, 110-0005, JAPAN
SN 1323-8930
EI 1440-1592
J9 ALLERGOL INT
JI Allergol. Int.
PD DEC
PY 2013
VL 62
IS 4
BP 463
EP 471
DI 10.2332/allergolint.13-OA-0552
PG 9
WC Allergy; Immunology
SC Allergy; Immunology
GA 268OE
UT WOS:000328179600007
PM 24060765
ER
PT J
AU Mueller, GA
Maleki, SJ
Johnson, K
Hurlburt, BK
Cheng, H
Ruan, S
Nesbit, JB
Pomes, A
Edwards, LL
Schorzman, A
Deterding, LJ
Park, H
Tomer, KB
London, RE
Williams, JG
AF Mueller, G. A.
Maleki, S. J.
Johnson, K.
Hurlburt, B. K.
Cheng, H.
Ruan, S.
Nesbit, J. B.
Pomes, A.
Edwards, L. L.
Schorzman, A.
Deterding, L. J.
Park, H.
Tomer, K. B.
London, R. E.
Williams, J. G.
TI Identification of Maillard reaction products on peanut allergens that
influence binding to the receptor for advanced glycation end products
SO ALLERGY
LA English
DT Article
DE advanced glycation end product; allergens; epitopes; peanuts; receptor
for AGE
ID ARA H 1; PROCESSED PEANUTS; CRYSTAL-STRUCTURE; IGE BINDING; FOOD;
ENDPRODUCTS; PREVALENCE; PROTEINS; CACO-2; CELLS
AB BackgroundRecent immunological data demonstrated that dendritic cells preferentially recognize advanced glycation end product (AGE)-modified proteins, upregulate expression of the receptor for AGE (RAGE), and consequently bias the immune response toward allergy.
MethodsPeanut extract was characterized by mass spectrometry (MS) to elucidate the specific residues and specific AGE modifications found in raw and roasted peanuts and on rAra h 1 that was artificially glycated by incubation with glucose or xylose. The binding of the RAGE-V1C1 domain to peanut allergens was assessed by PAGE and Western analysis with anti-Ara h 1, 2, and 3 antibodies. IgE binding to rAra h 1 was also assessed using the same methods.
ResultsAGE modifications were found on Ara h 1 and Ara h 3 in both raw and roasted peanut extract. No AGE modifications were found on Ara h 2. Mass spectrometry and Western blot analysis demonstrated that RAGE binds selectively to Ara h 1 and Ara h 3 derived from peanut extract, whereas the analysis failed to demonstrate Ara h 2 binding to RAGE. rAra h 1 with no AGE modifications did not bind RAGE; however, after AGE modification with xylose, rAra h 1 bound to RAGE.
ConclusionsAGE modifications to Ara h 1 and Ara h 3 can be found in both raw and roasted peanuts. Receptor for AGE was demonstrated to selectively interact with AGE-modified rAra h 1. If sensitization to peanut allergens occurs in dendritic cells via RAGE interactions, these cells are likely interacting with modified Ara h 1 and Ara h 3, but not Ara h 2.
C1 [Mueller, G. A.; Johnson, K.; Edwards, L. L.; Schorzman, A.; Deterding, L. J.; Tomer, K. B.; London, R. E.; Williams, J. G.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Maleki, S. J.; Hurlburt, B. K.; Cheng, H.; Ruan, S.; Nesbit, J. B.] ARS, USDA, So Reg Res Ctr, New Orleans, LA USA.
[Pomes, A.] Indoor Biotechnol Inc, Charlottesville, VA USA.
[Park, H.] Scripps Res Inst, Jupiter, FL USA.
RP Mueller, GA (reprint author), NIEHS, 111 TW Alexander Dr,MD MR 01, Res Triangle Pk, NC 27709 USA.
EM Mueller3@niehs.nih.gov
OI Pomes, Anna/0000-0002-8729-1829
FU National Institute of Environmental Health Sciences, National Institutes
of Health [Z01-ES102885-01, Z01-ES50161, Z01-ES102488-05]; Agricultural
Research Service, U.S. Department of Agriculture
FX This research was supported in part by Research Project Number
Z01-ES102885-01 to REL, Z01-ES50161 to KBT, and Z01-ES102488-05 to JGW
in the Intramural Research Program of the National Institute of
Environmental Health Sciences, National Institutes of Health. This work
was supported in part by the Agricultural Research Service, U.S.
Department of Agriculture.
NR 23
TC 17
Z9 17
U1 8
U2 37
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-4538
EI 1398-9995
J9 ALLERGY
JI Allergy
PD DEC
PY 2013
VL 68
IS 12
BP 1546
EP 1554
DI 10.1111/all.12261
PG 9
WC Allergy; Immunology
SC Allergy; Immunology
GA 263IK
UT WOS:000327801600006
PM 24266677
ER
PT J
AU Freedman, DS
Horlick, M
Berenson, GS
AF Freedman, David S.
Horlick, Mary
Berenson, Gerald S.
TI A comparison of the Slaughter skinfold-thickness equations and BMI in
predicting body fatness and cardiovascular disease risk factor levels in
children
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID X-RAY ABSORPTIOMETRY; INDEX-FOR-AGE; MASS INDEX; METABOLIC RISK;
BLOOD-PRESSURE; FAT MASS; ADOLESCENTS; ADIPOSITY; OBESITY; YOUTH
AB Background: Although estimation of percentage body fat with the Slaughter skinfold-thickness equations (PBFSlaughter) is widely used, the accuracy of this method has not been well studied.
Objective: The objective was to determine the accuracy of the Slaughter skinfold-thickness equations.
Design: We compared agreement between PBFSlaughter and estimations derived from dual-energy X-ray absorptiometry (PBFDXA) in 1169 children in the Pediatric Rosetta Body Composition Project and the relation to cardiovascular disease risk factors, as compared with body mass index (BMI), in 6725 children in the Bogalusa Heart Study.
Results: PBFSlaughter was highly correlated (r = 0.90) with PBFDXA, but it markedly overestimated levels of PBFDXA in children with large skinfold thicknesses. In the 65 boys with a sum of skinfold thicknesses (subscapular- plus triceps-skinfold thicknesses) >= 50 mm, PBFSlaughter overestimated PBFDXA by 12 percentage points. The comparable overestimation in girls with a high skinfold sum was 6 percentage points. We also found that, after adjustment for sex and age, BMI showed slightly stronger associations with lipid, lipoprotein, insulin, and blood pressure values than did PBFSlaughter.
Conclusions: These results indicate that PBFSlaughter which was developed among a group of much thinner children and adolescents, is fairly accurate among nonobese children, but markedly overestimates the body fatness of children who have thick skinfold thicknesses. Furthermore, PBFSlaughter has no advantage over sex- and age-adjusted BMIs at identifying children who are at increased risk of cardiovascular disease based on lipid, lipoprotein, insulin, and blood pressure values.
C1 [Freedman, David S.] CDC, Div Nutr Phys Act & Obes, Atlanta, GA 30333 USA.
[Horlick, Mary] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
[Berenson, Gerald S.] Tulane Univ, Sch Publ Hlth & Trop Med, Tulane Ctr Cardiovasc Hlth, New Orleans, LA USA.
RP Freedman, DS (reprint author), CDC F77,4770 Buford Highway, Atlanta, GA 30341 USA.
EM dxf1@cdc.gov
FU NIH [DK37352, AG16592]
FX Supported by grants DK37352 and AG16592 from the NIH.
NR 49
TC 18
Z9 20
U1 3
U2 10
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 DEC
PY 2013
VL 98
IS 6
BP 1417
EP 1424
DI 10.3945/ajcn.113.065961
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 266DG
UT WOS:000328002000008
PM 24153344
ER
PT J
AU Cogswell, ME
Wang, CY
Chen, TC
Pfeiffer, CM
Elliott, P
Gillespie, CD
Carriquiry, AL
Sempos, CT
Liu, K
Perrine, CG
Swanson, CA
Caldwell, KL
Loria, CM
AF Cogswell, Mary E.
Wang, Chia-Yih
Chen, Te-Ching
Pfeiffer, Christine M.
Elliott, Paul
Gillespie, Cathleen D.
Carriquiry, Alicia L.
Sempos, Christopher T.
Liu, Kiang
Perrine, Cria G.
Swanson, Christine A.
Caldwell, Kathleen L.
Loria, Catherine M.
TI Validity of predictive equations for 24-h urinary sodium excretion in
adults aged 18-39 y
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID DAILY SALT INTAKE; POTASSIUM EXCRETION; BLOOD-PRESSURE; CREATININE;
COLLECTIONS; VARIABILITY; SPECIMEN; CALCIUM; OUTPUT; MEN
AB Background: Collecting a 24-h urine sample is recommended for monitoring the mean population sodium intake, but implementation can be difficult.
Objective: The objective was to assess the validity of published equations by using spot urinary sodium concentrations to predict 24-h sodium excretion.
Design: This was a cross-sectional study, conducted from June to August 2011 in metropolitan Washington, DC, of 407 adults aged 18-39 y, 48% black, who collected each urine void in a separate container for 24 h. Four timed voids (morning, afternoon, evening, and overnight) were selected from each 24-h collection. Published equations were used to predict 24-h sodium excretion with spot urine by specimen timing and race-sex subgroups. We examined mean differences with measured 24-h sodium excretion (bias) and individual differences with the use of Bland-Altman plots.
Results: Across equations and specimens, mean bias in predicting 24-h sodium excretion for all participants ranged from -267 to 1300 mg (Kawasaki equation). Bias was least with International Cooperative Study on Salt, Other Factors, and Blood Pressure (INTERSALT) equations with morning (-165 mg; 95% CI: -295, 36 mg), afternoon (-90 mg; -208, 28 mg), and evening (-120 mg; -230, -11 mg) specimens. With overnight specimens, mean bias was least when the Tanaka (-23 mg; 95% CI: -141, 95 mg) or Mage (-145 mg; -314, 25 mg) equations were used but was statistically significant when using the Tanaka equations among females (216 to 243 mg) and the Mage equations among races other than black (-554 to -372 mg). Significant over- and underprediction occurred across individual sodium excretion concentrations.
Conclusions: Using a single spot urine, INTERSALT equations may provide the least biased information about population mean sodium intakes among young US adults. None of the equations evaluated provided unbiased estimates of individual 24-h sodium excretion.
C1 [Cogswell, Mary E.; Gillespie, Cathleen D.] CDC, Div Heart Dis & Stroke Prevent, Atlanta, GA 30341 USA.
[Perrine, Cria G.] CDC, Div Nutr Phys Act & Obes, Atlanta, GA 30341 USA.
[Pfeiffer, Christine M.; Caldwell, Kathleen L.] CDC, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA 30341 USA.
[Pfeiffer, Christine M.; Caldwell, Kathleen L.] CDC, Div Sci Lab, Natl Ctr Environm Hlth, Atlanta, GA 30341 USA.
[Wang, Chia-Yih; Chen, Te-Ching] CDC, Div Hlth & Nutr Examinat Surveys, Natl Ctr Hlth Stat, Hyattsville, MD USA.
[Loria, Catherine M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Sempos, Christopher T.; Swanson, Christine A.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Carriquiry, Alicia L.] Iowa State Univ, Dept Stat, Ames, IA USA.
[Liu, Kiang] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Elliott, Paul] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London, England.
[Elliott, Paul] MRC, Hlth Protect Agcy, Ctr Environm & Hlth, London, England.
RP Cogswell, ME (reprint author), CDC, Mailstop F-72,4770 Buford Highway NE, Atlanta, GA 30341 USA.
EM mcogswell@cdc.gov
FU National Institute for Health Research Biomedical Research Centre;
Imperial College Healthcare National Health Service Trust; Imperial
College
FX The authors' responsibilities were as follows-MEC, C-YW, T-CC, CMP, PE,
CDG, ALC, CTS, KL, COP, CAS, KLC, and CML: designed the analysis; MEC,
C-YW, T-CC, and CDG: analyzed the data; MEC: wrote the initial draft,
which was modified based on critical review from all coauthors, and had
primary responsibility for all of the content. All authors read and
approved the final manuscript. PE acknowledges support from the National
Institute for Health Research Biomedical Research Centre, Imperial
College Healthcare National Health Service Trust and Imperial College.
PE is a Senior Investigator at the National Institute for Health
Research. None of the authors had any conflicts of interest.
NR 46
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U1 1
U2 2
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 DEC
PY 2013
VL 98
IS 6
BP 1502
EP 1513
DI 10.3945/ajcn.113.059436
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 266DG
UT WOS:000328002000018
PM 24047921
ER
PT J
AU Steer, CD
Lattka, E
Koletzko, B
Golding, J
Hibbeln, JR
AF Steer, Colin D.
Lattka, Eva
Koletzko, Berthold
Golding, Jean
Hibbeln, Joseph R.
TI Maternal fatty acids in pregnancy, FADS polymorphisms, and child
intelligence quotient at 8 y of age
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID LINOLEIC-ACID; WHITE-MATTER; FISH INTAKE; BRAIN; SUPPLEMENTATION;
ALSPAC; IQ; PHOSPHOLIPIDS; SERUM; DIET
AB Background: Brain tissue is selectively enriched with highly unsaturated fatty acids (FAs). Altering the maternal FA status in pregnancy may improve fetal neural development with lasting consequences for child development.
Objective: We explored whether maternal FAs in erythrocytes, either measured directly or indirectly by maternal FADS genetic variants, are associated with child intelligence quotient (IQ).
Design: Linear regression analyses, adjusted for 18 confounders, were used to investigate the associations in 2839 mother-child pairs from the population-based Avon Longitudinal Study of Parents and Children cohort.
Results: Low levels of arachidonic acid (20:4n-6) were associated with lower performance IQ (-2.0 points; 95% CI: -3.5, -0.6 points; P = 0.007, increased R-2 = 0.27%), high levels of osbond acid (22:5n-6) were associated with verbal IQ (-1.8 points; 95% CI: -3.2, -0.4 points; P = 0.014, R-2 = 0.20%), and high levels of adrenic acid (22:4n-6) were associated with verbal IQ (-1.7 points; 95% CI: -3.1, -0.3 points; P = 0.016, R-2 = 0.19%). There was some evidence to support a negative association of low docosahexaenoic acid (DHA; 22:6n-3) with full-scale IQ (R-2 = 0.15%). Novel weak associations were also observed for low levels of osbond acid (R-2 <= 0.29%) and FADS variants with opposite effects for intron variants and variants in the promoter region such as rs3834458 (R-2 <= 0.38%).
Conclusions: These results support the positive role of maternal arachidonic acid and DHA on fetal neural development, although the effects on child IQ by 8 y of age were small (0.1 SD), with other factors contributing more substantially. The endogenous synthesis of these FAs by FADS genes, especially FADS2, may also be important. The replication of these results is recommended.
C1 [Steer, Colin D.; Golding, Jean] Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
[Lattka, Eva] Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, German Res Ctr Environm Hlth, Neuherberg, Germany.
[Koletzko, Berthold] Univ Munich, Med Ctr, Dept Pediat, Dr von Hauner Childrens Hosp, Munich, Germany.
[Hibbeln, Joseph R.] NIAAA, NIH, Bethesda, MD USA.
RP Steer, CD (reprint author), Sch Social & Community Med, Ctr Child & Adolescent Hlth, Barley House, Bristol BS8 2BN, Avon, England.
EM colin.steer@bristol.ac.uk
RI Reischl, Eva/B-9311-2013;
OI Reischl, Eva/0000-0003-4055-8060; Golding, Jean/0000-0003-2826-3307
FU Wellcome Trust [092731]
FX We are extremely grateful to all families who took part in this study,
mid-wives for their help in recruiting them, and the whole ALSPAC team,
which includes interviewers, computer and laboratory technicians,
clerical workers, research scientists, volunteers, managers,
receptionists, and nurses. The UK Medical Research Council and the
Wellcome Trust (grant 092731) and the University of Bristol currently
provide core support for the ALSPAC.
NR 51
TC 19
Z9 19
U1 1
U2 11
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 DEC
PY 2013
VL 98
IS 6
BP 1575
EP 1582
DI 10.3945/ajcn.112.051524
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 266DG
UT WOS:000328002000025
PM 24067669
ER
PT J
AU Dwyer, JT
Peterson, J
AF Dwyer, Johanna T.
Peterson, Julia
TI Tea and flavonoids: where we are, where to go next
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article; Proceedings Paper
CT 5th International Scientific Symposium on Tea and Human Health
CY SEP 19-19, 2012
CL Washington, DC
ID CARDIOVASCULAR-DISEASE MORTALITY; GREEN TEA; DIETARY-SUPPLEMENTS;
PROSPECTIVE COHORT; BLOOD-PRESSURE; FOOD SOURCES; BLACK TEA; RISK;
METAANALYSIS; CONSUMPTION
AB There is a need to evaluate the evidence about the health effects of tea flavonoids and to provide valid, specific, and actionable tea consumption information to consumers. Emerging evidence suggests that the flavonoids in tea may be associated with beneficial health outcomes, whereas the benefits and risks of tea extracts and supplements are less well known. The next steps in developing tea science should include a focus on the most promising leads, such as reducing the risk of cardiovascular disease and stroke, rather than pursuing smaller, more diffuse studies of many different health outcomes. Future tea research should also include the use of common reference standards, better characterization of intervention products, and application of batteries of biomarkers of intakes and outcomes across studies, which will allow a common body of evidence to be developed. Mechanistic studies should determine which tea bioactive constituents have effects, whether they act alone or in combination, and how they influence health. Clinical studies should use well-characterized test products, better descriptions of baseline diets, and validated biomarkers of intake and disease risk reduction. There should be more attention to careful safety monitoring and adverse event reporting. Epidemiologic investigations should be of sufficient size and duration to detect small effects, involve populations most likely to benefit, use more complete tea exposure assessment, and include both intermediary markers of risk as well as morbidity and mortality outcomes. The construction of a strong foundation of scientific evidence on tea and health outcomes is essential for developing more specific and actionable messages on tea for consumers.
C1 [Dwyer, Johanna T.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Dwyer, Johanna T.] Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[Peterson, Julia] Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
RP Dwyer, JT (reprint author), NIH, Off Dietary Supplements, Room 3B01,MSC 7517, Bethesda, MD 20892 USA.
EM dwyerj1@od.nih.gov
OI Dwyer, Johanna/0000-0002-0783-1769
FU Tea Council of the USA
FX The authors' responsibilities were as follows-JTD: designed the review
and had primary responsibility for preparing the final manuscript and
for final content; and JTD and JP: collected and analyzed the data and
wrote the manuscript. Both authors read and approved the final
manuscript. JTD performed this work as a contractor at the Office of
Dietary Supplements, NIH. JP received a grant for travel and
accommodations to attend the symposium from the Tea Council of the USA.
The authors declared no competing financial interests.
NR 41
TC 4
Z9 4
U1 0
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 DEC
PY 2013
VL 98
IS 6
SU S
BP 1611S
EP 1618S
DI 10.3945/ajcn.113.059584
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 266DJ
UT WOS:000328002400002
PM 24172298
ER
PT J
AU Vichinsky, E
Torres, M
Minniti, CP
Barrette, S
Habr, D
Zhang, YY
Files, B
AF Vichinsky, Elliott
Torres, Marcela
Minniti, Caterina P.
Barrette, Stephane
Habr, Dany
Zhang, Yiyun
Files, Beatrice
CA CICL670A2201 Investigators
TI Efficacy and safety of deferasirox compared with deferoxamine in sickle
cell disease: Two-year results including pharmacokinetics and
concomitant hydroxyurea
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID TUMOR-ASSOCIATED MACROPHAGES; ABSOLUTE LYMPHOCYTE COUNT;
NON-HODGKINS-LYMPHOMA; B-CELL; R-CHOP; PROGNOSTIC-SIGNIFICANCE; MONOCYTE
COUNT; SURVIVAL; RITUXIMAB; CHEMOTHERAPY
AB We report a prospective, randomized, Phase II study of deferasirox and deferoxamine (DFO) in sickle cell disease patients with transfusional iron overload, with all patients continuing on deferasirox after 24 weeks, for up to 2 years. The primary objective was to evaluate deferasirox safety compared with DFO; long-term efficacy and safety of deferasirox was also assessed. We also report, for the first time, the safety and pharmacokinetics of deferasirox in patients concomitantly receiving hydroxyurea. Deferasirox (n=135) and DFO (n=68) had comparable safety profiles over 24 weeks. Adverse events (AEs) secondary to drug administration were reported in 26.7% of patients in the deferasirox cohort and 28.6% in the DFO cohort. Gastrointestinal disorders were more common with deferasirox, including diarrhea (10.4% versus 3.6%) and nausea (5.2% versus 3.6%). The most common AE in the DFO group was injection-site pain irritation, which occurred in 7% of patients. Acute renal failure occurred in one patient on deferasirox who was continued on medication despite progressive impairment of renal function parameters. Serum ferritin levels were reduced in both treatment groups. Patients continuing on deferasirox for up to 2 years demonstrated an absolute median serum ferritin decrease of 2614 ng/mL (n=96). Increasing deferasirox dose was associated with improved response and a continued manageable safety profile. Concomitant hydroxyurea administration (n=28) did not appear to influence the efficacy, safety (including liver and kidney function), and pharmacokinetic parameters of deferasirox. Am. J. Hematol. 88: 1068-1073, 2013. (C) 2013 Wiley Periodicals, Inc.
C1 [Vichinsky, Elliott] Childrens Hosp & Res Ctr Oakland, Oakland, CA 94609 USA.
[Torres, Marcela] Cook Childrens Hosp, Ft Worth, TX USA.
[Minniti, Caterina P.] NHLBI, Bethesda, MD 20892 USA.
[Barrette, Stephane] St Justine Hosp, Montreal, PQ, Canada.
[Habr, Dany; Zhang, Yiyun] Novartis Pharmaceut, E Hanover, NJ USA.
[Files, Beatrice] Emory Univ, Atlanta, GA 30322 USA.
RP Vichinsky, E (reprint author), Childrens Hosp & Res Ctr Oakland, Hematol Oncol Dept, 747 52nd St, Oakland, CA 94609 USA.
EM evichinsky@mail.cho.org
FU Novartis Pharma AG; Novartis Pharmaceuticals
FX Contract sponsors: Novartis Pharma AG and Novartis Pharmaceuticals.
NR 41
TC 7
Z9 7
U1 1
U2 2
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 DEC
PY 2013
VL 88
IS 12
BP 1068
EP 1073
DI 10.1002/ajh.23569
PG 6
WC Hematology
SC Hematology
GA 255FE
UT WOS:000327224000137
PM 23946212
ER
PT J
AU Stern, W
Mathews, D
McKew, J
Seiler, SR
Shen, XG
Kato, GJ
AF Stern, Warren
Mathews, David
McKew, John
Seiler, Stephen R.
Shen, Xiqgiang
Kato, Gregory J.
TI ASE 1, FIRST-IN-MAN, DOSE-RESPONSE STUDY OF AES-103 (5-HMF), AN
ANTI-SICKLING, ALLOSTERIC MODIFIER OF HEMOGLOBIN OXYGEN AFFINITY IN
HEALTHY NORMAL VOLUNTEERS
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Meeting Abstract
C1 [Stern, Warren; Seiler, Stephen R.] AesRx LLC, Newton, MA USA.
[Mathews, David] Quintiles Phase 1 Serv Inc, Durham, NC USA.
[McKew, John; Shen, Xiqgiang] NIH, Bethesda, MD USA.
[Kato, Gregory J.] NHLBI, Hematol Branch, MD Sickle Cell Vasc Dis Sect, Bethesda, MD USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 1
U2 1
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 DEC
PY 2013
VL 88
IS 12
BP E79
EP E79
PG 1
WC Hematology
SC Hematology
GA 255FE
UT WOS:000327224000114
ER
PT J
AU Rice, MB
Ljungman, PL
Wilker, EH
Gold, DR
Schwartz, JD
Koutrakis, P
Washko, GR
O'Connor, GT
Mittleman, MA
AF Rice, Mary B.
Ljungman, Petter L.
Wilker, Elissa H.
Gold, Diane R.
Schwartz, Joel D.
Koutrakis, Petros
Washko, George R.
O'Connor, George T.
Mittleman, Murray A.
TI Short-Term Exposure to Air Pollution and Lung Function in the Framingham
Heart Study
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE chronic obstructive pulmonary disease; asthma; air pollutants; US
Environmental Protection Agency
ID OBSTRUCTIVE PULMONARY-DISEASE; RESPIRATORY HEALTH; OZONE EXPOSURE;
DEFICIENT MICE; INFLAMMATION; ADULTS; POLLUTANTS; SMOKERS; ASTHMA; RISK
AB Rationale: Short-term exposure to ambient air pollution has been associated with lower lung function. Few studies have examined whether these associations are detectable at relatively low levels of pollution within current U. S. Environmental Protection Agency (EPA) standards.
Objectives: To examine exposure to ambient air pollutants within EPA standards and lung function in a large cohort study.
Methods: We included 3,262 participants of the Framingham Offspring and Third Generation cohorts living within 40 km of the Harvard Supersite monitor in Boston, Massachusetts (5,358 examinations, 1995-2011) who were not current smokers, with previous-day pollutant levels in compliance with EPA standards. We compared lung function (FEV1 and FVC) after previous-day exposure to particulate matter less than 2.5 mu m in diameter (PM2.5), nitrogen dioxide (NO2), and ozone (O-3) in the "moderate" range of the EPA Air Quality Index to exposure in the "good" range. We also examined linear relationships between moving averages of pollutant concentrations 1, 2, 3, 5, and 7 days before spirometry and lung function.
Measurements and Main Results: Exposure to pollutant concentrations in the "moderate" range of the EPA Air Quality Index was associated with a 20.1-ml lower FEV1 for PM2.5 (95% confidence interval [CI], -33.4, -6.9), a 30.6-ml lower FEV1 for NO2 (95% CI, -60.9, -0.2), and a 55.7-ml lower FEV1 for O-3 (95% CI, -100.7, -10.8) compared with the "good" range. The 1- and 2-day moving averages of PM2.5, NO2, and O-3 before testing were negatively associated with FEV1 and FVC.
Conclusions: Short-term exposure to PM2.5, NO2, and O-3 within current EPA standards was associated with lower lung function in this cohort of adults.
C1 [Rice, Mary B.; Ljungman, Petter L.; Wilker, Elissa H.; Mittleman, Murray A.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Cardiovasc Epidemiol Res Unit, Boston, MA 02215 USA.
[Rice, Mary B.] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Ljungman, Petter L.] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
[Gold, Diane R.; Schwartz, Joel D.; Koutrakis, Petros] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Washko, George R.] Brigham & Womens Hosp, Dept Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA.
[Washko, George R.; O'Connor, George T.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[O'Connor, George T.] Boston Univ, Sch Med, Dept Med, Ctr Pulm, Boston, MA 02118 USA.
RP Rice, MB (reprint author), Massachusetts Gen Hosp, Pulm & Crit Care Unit, Bulfinch 148,55 Fruit St, Boston, MA 02114 USA.
EM mrice2@partners.org
RI Ljungman, Petter/C-6371-2014;
OI Ljungman, Petter/0000-0002-7815-2632; O'Connor,
George/0000-0002-6476-3926
FU U.S. Environmental Protection Agency [R832416, RD834798]; National
Heart, Lung, and Blood Institute [N01-HC 25195, 1R01HL60040,
1R01HL70100, T32HL007374]; National Institute of Environmental Health
Sciences [1F32ES023352-01, P30ES000002]; Swedish Heart Lung Foundation;
Swedish Council for Working Life and Social Research Marie Curie
International Postdoc Fellowship Programme; Swedish Society of
Cardiology; Swedish Society for Medical Research
FX Supported by U.S. Environmental Protection Agency grants R832416 and
RD834798. Further supported by National Heart, Lung, and Blood Institute
grants N01-HC 25195, 1R01HL60040, 1R01HL70100, and T32HL007374, and
National Institute of Environmental Health Sciences grants
1F32ES023352-01 and P30ES000002. Support from the Swedish Heart Lung
Foundation, the Swedish Council for Working Life and Social Research
Marie Curie International Postdoc Fellowship Programme, the Swedish
Society of Cardiology, and the Swedish Society for Medical Research
(P.L.L.).
NR 48
TC 37
Z9 39
U1 7
U2 48
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC 1
PY 2013
VL 188
IS 11
BP 1351
EP 1357
DI 10.1164/rccm.201308-1414OC
PG 7
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 268UY
UT WOS:000328197300015
PM 24200465
ER
PT J
AU Leung, JM
Fowler, C
Smith, C
Adjemian, J
Frein, C
Claypool, RJ
Holland, SM
Prevots, RD
Olivier, K
AF Leung, Janice M.
Fowler, Cedar
Smith, Caroline
Adjemian, Jennifer
Frein, Cathleen
Claypool, Reginald J.
Holland, Steven M.
Prevots, Rebecca D.
Olivier, Kenneth
TI A Familial Syndrome of Pulmonary Nontuberculous Mycobacteria Infections
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Letter
ID MITRAL-VALVE-PROLAPSE; PECTUS EXCAVATUM; IDIOPATHIC SCOLIOSIS;
LUNG-DISEASE; PREVALENCE; CT
C1 [Leung, Janice M.; Fowler, Cedar; Smith, Caroline; Adjemian, Jennifer; Frein, Cathleen; Claypool, Reginald J.; Holland, Steven M.; Prevots, Rebecca D.; Olivier, Kenneth] NIH, Bethesda, MD 20892 USA.
RP Leung, JM (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 20
TC 6
Z9 6
U1 0
U2 2
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC 1
PY 2013
VL 188
IS 11
BP 1373
EP 1376
PG 5
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 268UY
UT WOS:000328197300026
PM 24289782
ER
PT J
AU Yao, XL
Gao, MX
Dai, CL
Meyer, KS
Chen, JC
Keeran, KJ
Nugent, GZ
Qu, X
Yu, ZX
Dagur, PK
Mccoy, JP
Levine, SJ
AF Yao, Xianglan
Gao, Meixia
Dai, Cuilian
Meyer, Katharine S.
Chen, Jichun
Keeran, Karen J.
Nugent, Gayle Z.
Qu, Xuan
Yu, Zu-Xi
Dagur, Pradeep K.
Mccoy, J. Philip
Levine, Stewart J.
TI Peptidoglycan Recognition Protein 1 Promotes House Dust Mite-Induced
Airway Inflammation in Mice
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE asthma; house dust mite; innate immunity; pattern recognition proteins;
peptidoglycan recognition protein 1
ID ALLERGIC-ASTHMA; T-CELLS; RESPONSES; CHEMOKINE; INNATE;
HYPERRESPONSIVENESS; LYMPHOCYTES; CHALLENGE; EOTAXIN-2; DISEASE
AB Peptidoglycan recognition protein (Pglyrp) 1 is a pattern-recognition protein that mediates antibacterial host defense. Because we had previously shown that Pglyrp1 expression is increased in the lungs of house dust mite (HDM)-challenged mice, we hypothesized that it might modulate the pathogenesis of asthma. Wild-type and Pglyrp1(-/-) mice on a BALB/c background received intranasal HDM or saline, 5 days/week for 3 weeks. HDM-challenged Pglyrp1(-/-) mice showed decreases in bronchoalveolar lavage fluid eosinophils and lymphocytes, serum IgE, and mucous cell metaplasia, whereas airway hyperresponsiveness was not changed when compared with wild-type mice. T helper type 2 (Th2) cytokines were reduced in the lungs of HDM-challenged Pglyrp1(-/-) mice, which reflected a decreased number of CD4(+) Th2 cells. There was also a reduction in C-C chemokines in bronchoalveolar lavage fluid and lung homogenates from HDM-challenged Pglyrp1(-/-) mice. Furthermore, secretion of CCL17, CCL22, and CCL24 by alveolar macrophages from HDM-challenged Pglyrp1(-/-) mice was markedly reduced. As both inflammatory cells and airway epithelial cells express Pglyrp1, bone marrow transplantation was performed to generate chimeric mice and assess which cell type promotes HDM-induced airway inflammation. Chimeric mice lacking Pglyrp1 on hematopoietic cells, not structural cells, showed a reduction in HDM-induced eosinophilic and lymphocytic airway inflammation. We conclude that Pglyrp1 expressed by hematopoietic cells, such as alveolar macrophages, mediates HDM-induced airway inflammation by up-regulating the production of C-C chemokines that recruit eosinophils and Th2 cells to the lung. This identifies a new family of innate immune response proteins that promotes HDM-induced airway inflammation in asthma.
C1 [Yao, Xianglan; Gao, Meixia; Dai, Cuilian; Meyer, Katharine S.; Levine, Stewart J.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Chen, Jichun] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Keeran, Karen J.; Nugent, Gayle Z.] NHLBI, Lab Anim Surg, NIH, Bethesda, MD 20892 USA.
[Keeran, Karen J.; Nugent, Gayle Z.] NHLBI, Resources Core Facil, NIH, Bethesda, MD 20892 USA.
[Qu, Xuan; Yu, Zu-Xi] NHLBI, Pathol Core Facil, NIH, Bethesda, MD 20892 USA.
[Dagur, Pradeep K.; Mccoy, J. Philip] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
RP Levine, SJ (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10,Room 6D03,MSC 1590, Bethesda, MD 20892 USA.
EM levines@nhlbi.nih.gov
FU Division of Intramural Research, National Heart, Lung, and Blood
Institute
FX This work was supported by the Division of Intramural Research, National
Heart, Lung, and Blood Institute.
NR 35
TC 4
Z9 5
U1 0
U2 8
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1044-1549
EI 1535-4989
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD DEC
PY 2013
VL 49
IS 6
BP 902
EP 911
DI 10.1165/rcmb.2013-0001OC
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA 269SI
UT WOS:000328261800004
PM 23808363
ER
PT J
AU Yin, HE
Cabrera-Perez, J
Lai, ZA
Michael, D
Weller, M
Swaim, WD
Liu, XB
Catalan, MA
Rocha, EM
Ismail, N
Afione, S
Rana, NA
Di Pasquale, G
Alevizos, I
Ambudkar, I
Illei, GG
Chiorini, JA
AF Yin, Hongen
Cabrera-Perez, Javier
Lai, Zhenan
Michael, Drew
Weller, Melodie
Swaim, William D.
Liu, Xibao
Catalan, Marcelo A.
Rocha, Eduardo M.
Ismail, Nevien
Afione, Sandra
Rana, Noreen A.
Di Pasquale, Giovanni
Alevizos, Ilias
Ambudkar, Indu
Illei, Gabor G.
Chiorini, John A.
TI Association of Bone Morphogenetic Protein 6 With Exocrine Gland
Dysfunction in Patients With Sjogren's Syndrome and in Mice
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID TRANSGENIC MICE; SALIVARY-GLANDS; MICROARRAY DATA; MOUSE MODEL;
EXPRESSION; CELLS; IRON; OVEREXPRESSION; SECRETION; INFECTION
AB ObjectivePrimary Sjogren's syndrome (SS) is characterized by autoimmune activation and loss of function in secretory epithelia. The present study was undertaken to investigate and characterize changes in the epithelia associated with the loss of gland function in primary SS.
MethodsTo identify changes in epithelial gene expression, custom microarrays were probed with complementary RNA (cRNA) isolated from minor salivary glands (MSGs) of female patients with primary SS who had low focus scores and low salivary flow rates, and the results were compared with those obtained using cRNA from the MSGs of sex-matched healthy volunteers. The effect of bone morphogenetic protein 6 (BMP-6) on salivary gland function was tested using adeno-associated virus-mediated gene transfer to the salivary glands of C57BL/6 mice.
ResultsA significant increase in expression of BMP-6 was observed in RNA isolated from SS patients compared with healthy volunteers. Overexpression of BMP-6 locally in the salivary or lacrimal glands of mice resulted in the loss of fluid secretion as well as changes in the connective tissue of the salivary gland. Assessment of the fluid movement in either isolated acinar cells from mice overexpressing BMP-6 or a human salivary gland cell line cultured with BMP-6 revealed a loss in volume regulation in these cells. Lymphocytic infiltration in the submandibular gland of BMP-6 vector-treated mice was increased. No significant changes in the production of proinflammatory cytokines or autoantibodies associated with SS (anti-Ro/SSA and anti-La/SSB) were found after BMP-6 overexpression.
ConclusionIn addition to identifying BMP-6 expression in association with xerostomia and xerophthalmia in primary SS, the present results suggest that BMP-6-induced salivary and lacrimal gland dysfunction in primary SS is independent of the autoantibodies and immune activation associated with the disease.
C1 [Yin, Hongen; Cabrera-Perez, Javier; Lai, Zhenan; Michael, Drew; Weller, Melodie; Swaim, William D.; Liu, Xibao; Catalan, Marcelo A.; Rocha, Eduardo M.; Ismail, Nevien; Afione, Sandra; Rana, Noreen A.; Di Pasquale, Giovanni; Alevizos, Ilias; Ambudkar, Indu; Illei, Gabor G.; Chiorini, John A.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA.
RP Chiorini, JA (reprint author), Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, 10-1A21,10 Ctr Dr,MSC1190, Bethesda, MD 20892 USA.
EM jchiorini@dir.nidcr.nih.gov
RI Rocha, Eduardo/D-6002-2011;
OI Rocha, Eduardo/0000-0001-9888-7313; Catalan, Marcelo/0000-0003-3544-2821
FU NIH (National Institute of Dental and Craniofacial Research)
FX Supported by the NIH (National Institute of Dental and Craniofacial
Research intramural grants to Dr. Chiorini).
NR 43
TC 6
Z9 6
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD DEC
PY 2013
VL 65
IS 12
BP 3228
EP 3238
DI 10.1002/art.38123
PG 11
WC Rheumatology
SC Rheumatology
GA 261VL
UT WOS:000327692600026
PM 23982860
ER
PT J
AU Miller, FW
Cooper, RG
Vencovsky, J
Rider, LG
Danko, K
Wedderburn, LR
Lundberg, IE
Pachman, LM
Reed, AM
Ytterberg, SR
Padyukov, L
Selva-O'Callaghan, A
Radstake, TRDJ
Isenberg, DA
Chinoy, H
Ollier, WER
O'Hanlon, TP
Peng, B
Lee, A
Lamb, JA
Chen, W
Amos, CI
Gregersen, PK
AF Miller, Frederick W.
Cooper, Robert G.
Vencovsky, Jiri
Rider, Lisa G.
Danko, Katalin
Wedderburn, Lucy R.
Lundberg, Ingrid E.
Pachman, Lauren M.
Reed, Ann M.
Ytterberg, Steven R.
Padyukov, Leonid
Selva-O'Callaghan, Albert
Radstake, Timothy R. D. J.
Isenberg, David A.
Chinoy, Hector
Ollier, William E. R.
O'Hanlon, Terrance P.
Peng, Bo
Lee, Annette
Lamb, Janine A.
Chen, Wei
Amos, Christopher I.
Gregersen, Peter K.
CA Myositis Genetics Consortium
TI Genome-Wide Association Study of Dermatomyositis Reveals Genetic Overlap
With Other Autoimmune Disorders
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID IDIOPATHIC INFLAMMATORY MYOPATHIES; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
RHEUMATOID-ARTHRITIS; JUVENILE DERMATOMYOSITIS; SUSCEPTIBILITY LOCI;
CROHNS-DISEASE; RISK LOCUS; METAANALYSIS; PATHOGENESIS; EXPRESSION
AB ObjectiveTo identify new genetic associations with juvenile and adult dermatomyositis (DM).
MethodsWe performed a genome-wide association study (GWAS) of adult and juvenile DM patients of European ancestry (n = 1,178) and controls (n = 4,724). To assess genetic overlap with other autoimmune disorders, we examined whether 141 single-nucleotide polymorphisms (SNPs) outside the major histocompatibility complex (MHC) locus, and previously associated with autoimmune diseases, predispose to DM.
ResultsCompared to controls, patients with DM had a strong signal in the MHC region consisting of GWAS-level significance (P < 5 x 10(-8)) at 80 genotyped SNPs. An analysis of 141 non-MHC SNPs previously associated with autoimmune diseases showed that 3 SNPs linked with 3 genes were associated with DM, with a false discovery rate (FDR) of <0.05. These genes were phospholipase C-like 1 (PLCL1; rs6738825, FDR = 0.00089), B lymphoid tyrosine kinase (BLK; rs2736340, FDR = 0.0031), and chemokine (C-C motif) ligand 21 (CCL21; rs951005, FDR = 0.0076). None of these genes was previously reported to be associated with DM.
ConclusionOur findings confirm the MHC as the major genetic region associated with DM and indicate that DM shares non-MHC genetic features with other autoimmune diseases, suggesting the presence of additional novel risk loci. This first identification of autoimmune disease genetic predispositions shared with DM may lead to enhanced understanding of pathogenesis and novel diagnostic and therapeutic approaches.
C1 [Miller, Frederick W.; Rider, Lisa G.; O'Hanlon, Terrance P.] NIEHS, NIH, Bethesda, MD 20892 USA.
[Cooper, Robert G.] Univ Manchester, Manchester, Lancs, England.
[Cooper, Robert G.] Salford Royal Natl Hlth Serv Fdn Trust, Salford, Lancs, England.
[Vencovsky, Jiri] Inst Rheumatol, Prague, Czech Republic.
[Danko, Katalin] Univ Debrecen, H-4012 Debrecen, Hungary.
[Wedderburn, Lucy R.; Isenberg, David A.] UCL, London, England.
[Lundberg, Ingrid E.; Padyukov, Leonid] Karolinska Univ Hosp, Solna, Sweden.
[Lundberg, Ingrid E.; Padyukov, Leonid] Karolinska Inst, Stockholm, Sweden.
[Pachman, Lauren M.] Childrens Hosp Chicago, Chicago, IL USA.
[Pachman, Lauren M.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Reed, Ann M.; Ytterberg, Steven R.] Mayo Clin, Rochester, MN USA.
[Selva-O'Callaghan, Albert] Hosp Gen Valle Hebron, Barcelona, Spain.
[Radstake, Timothy R. D. J.] Univ Utrecht, Med Ctr, Utrecht, Netherlands.
[Radstake, Timothy R. D. J.] Nijmegen Ctr Mol Life Sci, Nijmegen, Netherlands.
[Chinoy, Hector; Ollier, William E. R.; Lamb, Janine A.] Univ Manchester, Manchester, NH USA.
[Peng, Bo; Chen, Wei; Amos, Christopher I.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Lee, Annette; Gregersen, Peter K.] North Shore LIJ Hlth Syst, New York, NY USA.
[Lee, Annette; Gregersen, Peter K.] Feinstein Inst Med Res, New York, NY USA.
RP Miller, FW (reprint author), NIEHS, NIH Clin Res Ctr, NIH 10,Room 4-2352,10 Ctr Dr,MSC 1301, Bethesda, MD 20892 USA.
EM millerf@mail.nih.gov
OI Miller, Frederick/0000-0003-2831-9593; Chinoy,
Hector/0000-0001-6492-1288; Padyukov, Leonid/0000-0003-2950-5670;
Isenberg, David/0000-0001-9514-2455; Peng, Bo/0000-0001-8225-2284;
Lundberg, Ingrid/0000-0002-6068-9212; Rider, Lisa/0000-0002-6912-2458
FU NIH (Intramural Program, National Institute of Environmental Health
Sciences) [Z01-ES-101074]; European Union [LSHB CT-2006-018661]; UK
Myositis Support Group; Arthritis Research UK [18474]; Cure JM
Foundation; European Science Foundation; Wellcome Trust; Henry Smith
Charity (UK); Action Medical Research (UK); Swedish Research Council;
Ministry of Health, Czech Republic [00023728]
FX Supported in part by the NIH (Intramural Program, National Institute of
Environmental Health Sciences grant Z01-ES-101074), the European Union
Sixth Framework Programme (project AutoCure; LSHB CT-2006-018661), the
UK Myositis Support Group, Arthritis Research UK (grant 18474), the Cure
JM Foundation, the European Science Foundation, the Wellcome Trust, the
Henry Smith Charity (UK), Action Medical Research (UK), and the Swedish
Research Council. The Czech cohort was supported in part by the Ministry
of Health, Czech Republic (grant 00023728).
NR 39
TC 36
Z9 37
U1 0
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD DEC
PY 2013
VL 65
IS 12
BP 3239
EP 3247
DI 10.1002/art.38137
PG 9
WC Rheumatology
SC Rheumatology
GA 261VL
UT WOS:000327692600027
PM 23983088
ER
PT J
AU Nordstrom, R
Cherry, S
Azhdarinia, A
Sevick-Muraca, E
VanBrocklin, H
AF Nordstrom, Robert
Cherry, Simon
Azhdarinia, Ali
Sevick-Muraca, Eva
VanBrocklin, Henry
TI Photons across medicine: relating optical and nuclear imaging
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
ID TRANSLATIONAL RESEARCH; INDOCYANINE GREEN; CLINICAL-USE; SYSTEM;
TOMOGRAPHY; SURGERY; CANCER; PET; RECONSTRUCTION; LOCALIZATION
AB The Optics in the Life Sciences conference sponsored by the Optical Society of America was held in Waikoloa Beach, HI on April 14 18, 2013. Papers were presented in the areas of Bio-Optics: Design & Application, Novel Techniques in Microscopy, Optical Molecular Probes, Imaging & Drug Delivery, and Optical Trapping Applications. A focal point of the meeting was a special symposium entitled "Photons Across Medicine", organized by Adam Wax, Duke University, highlighting activities of joint interest between the Optical Society of America (OSA) and the Society for Nuclear Medicine and Molecular Imaging (SNMMI). This paper is a synopsis of the presentations made at this joint symposium. Central to the special symposium presentations was the fact that the optical and nuclear imaging communities share common interests and challenges. These are highlighted in this article. Also discussed was the fact that the nuclear technologies in imaging have found their way into general clinical utility, a feat that has yet to be achieved by optical methods. Because of the common ground shared by the two technologies, coordination between the two societies should be planned. (C) 2013 Optical Society of America
C1 [Nordstrom, Robert] NCI, NIH, Bethesda, MD 20892 USA.
[Cherry, Simon] Univ Calif Davis, Dept Biomed Engn, Davis, CA 95616 USA.
[Azhdarinia, Ali; Sevick-Muraca, Eva] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[VanBrocklin, Henry] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
RP Nordstrom, R (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM nordstrr@mail.nih.gov
RI Sevick-Muraca, Eva/A-4152-2017
OI Sevick-Muraca, Eva/0000-0002-8152-4847
NR 42
TC 1
Z9 1
U1 3
U2 15
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD DEC 1
PY 2013
VL 4
IS 12
BP 2751
EP 2762
DI 10.1364/BOE.4.002751
PG 12
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA 267EA
UT WOS:000328078300003
PM 24409377
ER
PT J
AU Hourigan, CS
Karp, JE
AF Hourigan, Christopher S.
Karp, Judith E.
TI Personalized Therapy for Acute Myeloid Leukemia
SO CANCER DISCOVERY
LA English
DT Editorial Material
ID EVOLUTION
AB Patient-specific ex vivo drug sensitivity and resistance screening can identify rational drug candidates for the testing of personalized targeted therapy. An iterative approach of genomic and drug susceptibility characterization at sequential time points during clinical trials of targeted therapy in acute myeloid leukemia may be useful both for characterizing mechanisms of resistance and clonal evolution and also for identification of novel therapeutic targets and drug combinations. (C) 2013 AACR.
C1 [Hourigan, Christopher S.] NHLBI, Myeloid Malignancies Sect, Hematol Branch, Bethesda, MD 20892 USA.
[Karp, Judith E.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
RP Hourigan, CS (reprint author), NHLBI, Myeloid Malignancies Sect, Room 6C-103C,10 Ctr Dr, Bethesda, MD 20892 USA.
EM hourigan@nih.gov
RI Hourigan, Christopher/S-2476-2016
OI Hourigan, Christopher/0000-0002-6189-8067
FU Intramural NIH HHS [ZIA HL006163-01]
NR 11
TC 3
Z9 3
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD DEC
PY 2013
VL 3
IS 12
BP 1336
EP 1338
DI 10.1158/2159-8290.CD-13-0832
PG 3
WC Oncology
SC Oncology
GA 269QR
UT WOS:000328257500019
PM 24327695
ER
PT J
AU O'Connell, MP
Marchbank, K
Webster, MR
Valiga, AA
Kaur, A
Vultur, A
Li, L
Herlyn, M
Villanueva, J
Liu, Q
Yin, XF
Widura, S
Nelson, J
Ruiz, N
Camilli, TC
Indig, FE
Flaherty, KT
Wargo, JA
Frederick, DT
Cooper, ZA
Nair, S
Amaravadi, RK
Schuchter, LM
Karakousis, GC
Xu, W
Xu, XW
Weeraratna, AT
AF O'Connell, Michael P.
Marchbank, Katie
Webster, Marie R.
Valiga, Alexander A.
Kaur, Amanpreet
Vultur, Adina
Li, Ling
Herlyn, Meenhard
Villanueva, Jessie
Liu, Qin
Yin, Xiangfan
Widura, Sandy
Nelson, Janelle
Ruiz, Nivia
Camilli, Tura C.
Indig, Fred E.
Flaherty, Keith T.
Wargo, Jennifer A.
Frederick, Dennie T.
Cooper, Zachary A.
Nair, Suresh
Amaravadi, Ravi K.
Schuchter, Lynn M.
Karakousis, Giorgos C.
Xu, Wei
Xu, Xiaowei
Weeraratna, Ashani T.
TI Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma
via the Tyrosine Kinase Receptors ROR1 and ROR2
SO CANCER DISCOVERY
LA English
DT Article
ID UBIQUITIN LIGASE SIAH2; BETA-CATENIN; MESENCHYMAL TRANSITION;
MALIGNANT-MELANOMA; EXPRESSION; METASTASIS; CELLS; INVASION; INHIBITION;
PATHWAY
AB An emerging concept in melanoma biology is that of dynamic, adaptive phenotype switching, where cells switch from a highly proliferative, poorly invasive phenotype to a highly invasive, less proliferative one. This switch may hold significant implications not just for metastasis, but also for therapy resistance. We demonstrate that phenotype switching and subsequent resistance can be guided by changes in expression of receptors involved in the noncanonical Wnt5A signaling pathway, ROR1 and ROR2. ROR1 and ROR2 are inversely expressed in melanomas and negatively regulate each other. Furthermore, hypoxia initiates a shift of ROR1-positive melanomas to a more invasive, ROR2-positive phenotype. Notably, this receptor switch induces a 10-fold decrease in sensitivity to BRAF inhibitors. In patients with melanoma treated with the BRAF inhibitor vemurafenib, Wnt5A expression correlates with clinical response and therapy resistance. These data highlight the fact that mechanisms that guide metastatic progression may be linked to those that mediate therapy resistance.
SIGNIFICANCE: These data show for the first time that a single signaling pathway, the Wnt signaling pathway, can effectively guide the phenotypic plasticity of tumor cells, when primed to do so by a hypoxic microenvironment. Importantly, this increased Wnt5A signaling can give rise to a subpopulation of highly invasive cells that are intrinsically less sensitive to novel therapies for melanoma, and targeting the Wnt5A/ROR2 axis could improve the efficacy and duration of response for patients with melanoma on vemurafenib. (C) 2013 AACR.
C1 [O'Connell, Michael P.; Marchbank, Katie; Webster, Marie R.; Valiga, Alexander A.; Kaur, Amanpreet; Vultur, Adina; Li, Ling; Herlyn, Meenhard; Widura, Sandy; Nelson, Janelle; Ruiz, Nivia; Weeraratna, Ashani T.] Wistar Inst Anat & Biol, Tumor Microenvironm & Metastasis Program, Philadelphia, PA 19104 USA.
[Villanueva, Jessie; Liu, Qin; Yin, Xiangfan] Wistar Inst Anat & Biol, Mol & Cellular Oncogenesis Program, Philadelphia, PA 19104 USA.
[Amaravadi, Ravi K.; Schuchter, Lynn M.; Karakousis, Giorgos C.; Xu, Wei; Xu, Xiaowei] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Nair, Suresh] Lehigh Valley Hlth Network, Allentown, PA USA.
[Camilli, Tura C.; Indig, Fred E.] NIA, NIH, Baltimore, MD 21224 USA.
[Flaherty, Keith T.; Wargo, Jennifer A.; Frederick, Dennie T.; Cooper, Zachary A.] Dana Farber Harvard Canc Ctr, Boston, MA USA.
RP Weeraratna, AT (reprint author), Wistar Inst Anat & Biol, Tumor Microenvironm & Metastasis Program, 3601 Spruce St, Philadelphia, PA 19104 USA.
EM aweeraratna@wistar.org
OI Cooper, Zachary/0000-0003-1059-0940
FU National Institute on Aging Intramural Research Program; PA Department
of Health (CURE) funding; Joanna M Nicolay Foundation; PHS [2 T32 CA
9171-36, 1K23CA120862, CA25874]
FX This work was supported in part by funds from the National Institute on
Aging Intramural Research Program (to F.E. Indig and T.C. Camilli), PA
Department of Health (CURE) funding (to A.T. Weeraratna, M.P. O'Connell,
K. Marchbank, A. Vultur, N. Ruiz, Q. Liu, X. Yin, and S. Widura), and
the Joanna M Nicolay Foundation (to A. Kaur). Additional support for
other authors comes from PHS 2 T32 CA 9171-36 (to M. R. Webster),
1K23CA120862 (to R.K. Amaravadi), and CA25874 (to M. Herlyn).
NR 51
TC 64
Z9 65
U1 0
U2 16
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD DEC
PY 2013
VL 3
IS 12
BP 1378
EP 1393
DI 10.1158/2159-8290.CD-13-0005
PG 16
WC Oncology
SC Oncology
GA 269QR
UT WOS:000328257500024
PM 24104062
ER
PT J
AU Walter, AO
Sjin, RTT
Haringsma, HJ
Ohashi, K
Sun, J
Lee, K
Dubrovskiy, A
Labenski, M
Zhu, ZD
Wang, ZG
Sheets, M
St Martin, T
Karp, R
van Kalken, D
Chaturvedi, P
Niu, DQ
Nacht, M
Petter, RC
Westlin, W
Lin, K
Jaw-Tsai, S
Raponi, M
Van Dyke, T
Etter, J
Weaver, Z
Pao, W
Singh, J
Simmons, AD
Harding, TC
Allen, A
AF Walter, Annette O.
Sjin, Robert Tjin Tham
Haringsma, Henry J.
Ohashi, Kadoaki
Sun, Jing
Lee, Kwangho
Dubrovskiy, Aleksandr
Labenski, Matthew
Zhu, Zhendong
Wang, Zhigang
Sheets, Michael
St Martin, Thia
Karp, Russell
van Kalken, Dan
Chaturvedi, Prasoon
Niu, Deqiang
Nacht, Mariana
Petter, Russell C.
Westlin, William
Lin, Kevin
Jaw-Tsai, Sarah
Raponi, Mitch
Van Dyke, Terry
Etter, Jeff
Weaver, Zoe
Pao, William
Singh, Juswinder
Simmons, Andrew D.
Harding, Thomas C.
Allen, Andrew
TI Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that
Overcomes T790M-Mediated Resistance in NSCLC
SO CANCER DISCOVERY
LA English
DT Article
ID CELL LUNG-CANCER; TYROSINE KINASE INHIBITOR; FACTOR RECEPTOR MUTATIONS;
ACQUIRED-RESISTANCE; T790M MUTATION; GEFITINIB RESISTANCE; MET
AMPLIFICATION; AKT INHIBITOR; AXL KINASE; OPEN-LABEL
AB Patients with non-small cell lung cancer (NSCLC) with activating EGF receptor (EGFR) mutations initially respond to first-generation reversible EGFR tyrosine kinase inhibitors. However, clinical efficacy is limited by acquired resistance, frequently driven by the EGFR(T790M) mutation. CO-1686 is a novel, irreversible, and orally delivered kinase inhibitor that specifically targets the mutant forms of EGFR, including T790M, while exhibiting minimal activity toward the wild-type (WT) receptor. Oral administration of CO-1686 as single agent induces tumor regression in EGFR-mutated NSCLC tumor xenograft and transgenic models. Minimal activity of CO-1686 against the WT EGFR receptor was observed. In NSCLC cells with acquired resistance to CO-1686 in vitro, there was no evidence of additional mutations or amplification of the EGFR gene, but resistant cells exhibited signs of epithelial-mesenchymal transition and demonstrated increased sensitivity to AKT inhibitors. These results suggest that CO-1686 may offer a novel therapeutic option for patients with mutant EGFR NSCLC.
SIGNIFICANCE: We report the preclinical development of a novel covalent inhibitor, CO-1686, that irreversibly and selectively inhibits mutant EGFR, in particular the T790M drug-resistance mutation, in NSCLC models. CO-1686 is the first drug of its class in clinical development for the treatment of T790M-positive NSCLC, potentially offering potent inhibition of mutant EGFR while avoiding the on-target toxicity observed with inhibition of the WT EGFR. (C) 2013 AACR.
C1 [Walter, Annette O.; Haringsma, Henry J.; Lin, Kevin; Jaw-Tsai, Sarah; Raponi, Mitch; Etter, Jeff; Simmons, Andrew D.; Harding, Thomas C.; Allen, Andrew] Clovis Oncol Inc, San Francisco, CA 94158 USA.
[Sjin, Robert Tjin Tham; Lee, Kwangho; Dubrovskiy, Aleksandr; Labenski, Matthew; Zhu, Zhendong; Wang, Zhigang; Sheets, Michael; St Martin, Thia; Karp, Russell; van Kalken, Dan; Chaturvedi, Prasoon; Niu, Deqiang; Nacht, Mariana; Petter, Russell C.; Westlin, William; Singh, Juswinder] Celgene Avil Res, Bedford, MA USA.
[Ohashi, Kadoaki; Sun, Jing; Pao, William] Vanderbilt Univ, Sch Med, Dept Med, Div Hematol Oncol, Nashville, TN 37212 USA.
[Van Dyke, Terry] NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
[Van Dyke, Terry; Weaver, Zoe] NCI, Ctr Adv Preclin Res, Sci Applicat Int Corp Frederick Inc, Frederick, MD 21701 USA.
RP Harding, TC (reprint author), Clovis Oncol Inc, 1700 Owens St,Suite 205, San Francisco, CA 94158 USA.
EM tharding@clovisoncology.com
FU National Cancer Institute, NIH [HHSN261200800001E]; NIH NCI
[R01CA121210, P01CA129243, U54CA143798, P30CA68485]
FX This project was funded in part with federal funds from the National
Cancer Institute, NIH, under Contract No. HHSN261200800001E. W. Pao
received additional funding from NIH NCI grants R01CA121210,
P01CA129243, U54CA143798, and P30CA68485.
NR 43
TC 203
Z9 210
U1 8
U2 51
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD DEC
PY 2013
VL 3
IS 12
BP 1404
EP 1415
DI 10.1158/2159-8290.CD-13-0314
PG 12
WC Oncology
SC Oncology
GA 269QR
UT WOS:000328257500026
PM 24065731
ER
PT J
AU Walcott, F
Rajaraman, P
Gadalla, SM
Inskip, PD
Purdue, MP
Albanes, D
Orr, E
De Vivo, I
Savage, SA
AF Walcott, Farzana
Rajaraman, Preetha
Gadalla, Shahinaz M.
Inskip, Peter D.
Purdue, Mark P.
Albanes, Demetrius
Orr, Esther
De Vivo, Immaculata
Savage, Sharon A.
TI Telomere length and risk of glioma
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Telomere length; Glioma; Epidemiology; Cancer risk
ID UNITED-STATES; CANCER-RISK; VARIANTS; TUMORS; METAANALYSIS; ASSOCIATION;
SURVIVAL; TISSUES; BRAIN; RATES
AB Background: Telomere length in blood or buccal cell DNA has been associated with risk of various cancers. Glioma can be a highly malignant brain tumor and has few known risk factors. Genetic variants in or near RTEL1 and TERT, key components of telomere biology, are associated with glioma risk. Therefore, we evaluated the association between relative telomere length (RTL) and glioma in a prospective study.
Materials and methods: We performed a nested case-control study within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. RTL was determined by quantitative PCR on blood or buccal cell DNA obtained at least 2 years prior to diagnosis from 101 individuals with glioma cases. Healthy controls (n = 198) were matched to cases (2:1) on age, gender, smoking status, calendar year, and DNA source. Conditional logistic regression was used to investigate the association between RTL and glioma.
Results: As expected, RTL declined with increasing age in both cases and controls. There was no statistically significant association between RTL and glioma overall. An analysis stratified by gender suggested that short RTL (1st tertile) in males was associated with glioma (odds ratio, [ OR] = 2.29, 95% confidence interval [CI] 1.02-5.11); this association was not observed for females (OR = 0.41, 95% CI 0.14-1.17).
Conclusions: This prospective study did not identify significant associations between RTL and glioma risk, but there may be gender-specific differences. Larger, prospective studies are needed to evaluate these findings. Published by Elsevier Ltd.
C1 [Walcott, Farzana] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Rajaraman, Preetha] NCI, Ctr Global Hlth, NIH, Bethesda, MD 20892 USA.
[Rajaraman, Preetha; Inskip, Peter D.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Gadalla, Shahinaz M.; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
[Purdue, Mark P.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Orr, Esther; De Vivo, Immaculata] Harvard Univ, Dept Med, Brigham & Womens Hosp, Channing Lab,Med Sch, Boston, MA 02115 USA.
[De Vivo, Immaculata] Harvard Univ, Sch Med, Dept Epidemiol, Boston, MA 02115 USA.
RP Savage, SA (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Rm 6E454,MSC 9772, Rockville, MD 20850 USA.
EM savagesh@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015; Purdue, Mark/C-9228-2016; Savage,
Sharon/B-9747-2015
OI Purdue, Mark/0000-0003-1177-3108; Savage, Sharon/0000-0001-6006-0740
FU intramural research program of the Division of Cancer Epidemiology and
Genetics, National Cancer Institute, National Institutes of Health
FX This study was supported by the intramural research program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health.
NR 27
TC 13
Z9 13
U1 0
U2 8
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
EI 1877-783X
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD DEC
PY 2013
VL 37
IS 6
BP 935
EP 938
DI 10.1016/j.canep.2013.10.002
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 269OO
UT WOS:000328251000027
PM 24231251
ER
PT J
AU Murthy, SRK
Dupart, E
Al-Sweel, N
Chen, A
Cawley, NX
Loh, YP
AF Murthy, Saravana R. K.
Dupart, Evan
Al-Sweel, Najla
Chen, Alexander
Cawley, Niamh X.
Loh, Y. Peng
TI Carboxypeptidase E promotes cancer cell survival, but inhibits migration
and invasion
SO CANCER LETTERS
LA English
DT Article
DE Pheochromocytoma; Hepatocellular carcinoma; Fibrosarcoma; Cell survival;
Cell invasion
ID NF-KAPPA-B; BETA-CATENIN; PATHWAY; PROTEIN; BCL-2; PHEOCHROMOCYTOMA;
PROLIFERATION; ACTIVATION; EXPRESSION; MUTATIONS
AB Carboxypeptidase E (CPE), a prohormone processing enzyme is highly expressed and secreted from (neuro)endocrine tumors and gliomas, and has been implicated in cancer progression by promoting tumor growth. Our study demonstrates that secreted or exogenously applied CPE promotes survival of pheochromocytoma (PC12) and hepatocellular carcinoma (MHCC97H) cells under nutrient starvation and hypoxic conditions, but had no effect on their proliferation. CPE also reduced migration and invasion of fibrosarcoma (HT1080) cells. We show that CPE treatment mediates survival of MHCC97H cells during metabolic stress by up-regulating the expression of anti-apoptotic protein BCL-2, and other pro-survival genes, via activation of the ERK1/2 pathway. Published by Elsevier Ireland Ltd.
C1 [Murthy, Saravana R. K.; Dupart, Evan; Al-Sweel, Najla; Chen, Alexander; Cawley, Niamh X.; Loh, Y. Peng] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cellular Neurobiol Sect, Program Dev Biol, Bethesda, MD 20892 USA.
RP Loh, YP (reprint author), 49,Convent Dr,Bldg 49,Rm 5A22, Bethesda, MD 20892 USA.
EM lohp@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, USA
FX This research was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, USA,
NR 43
TC 10
Z9 10
U1 0
U2 4
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 DEC 1
PY 2013
VL 341
IS 2
BP 204
EP 213
DI 10.1016/j.canlet.2013.08.011
PG 10
WC Oncology
SC Oncology
GA 267KK
UT WOS:000328096300011
PM 23941827
ER
PT J
AU Janakiram, NB
Mohammed, A
Zhang, YT
Brewer, M
Bryant, T
Lightfoot, S
Steele, VE
Rao, CV
AF Janakiram, Naveena B.
Mohammed, Altaf
Zhang, Yuting
Brewer, Misty
Bryant, Taylor
Lightfoot, Stan
Steele, Vernon E.
Rao, Chinthalapally V.
TI Chemopreventive Efficacy of Raloxifene, Bexarotene, and Their
Combination on the Progression of Chemically Induced Colon Adenomas to
Adenocarcinomas in Rats
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ESTROGEN-RECEPTOR-BETA; HORMONE REPLACEMENT THERAPY; COLORECTAL-CANCER
INCIDENCE; RANDOMIZED CONTROLLED-TRIAL; POSTMENOPAUSAL WOMEN;
BREAST-CANCER; MAMMARY-CARCINOMA; LGD1069 TARGRETIN; SELECTIVE LIGAND;
TRANSGENIC MICE
AB Estrogen receptor (ER)-beta signaling is associated positively in colon tumor progression, whereas down-regulation or loss of function of retinoid X receptor (RXR)-alpha occurs in colon tumors. The chemopreventive efficacies of the estrogen antagonist raloxifene and the selective RXR agonist bexarotene were tested individually and in combination, during promotion and progression stages of colon tumorigenesis. Colon tumors were induced in male F344 rats with azoxymethane and at early adenoma stage, groups of rats (36 or 45 per group) were fed diets containing raloxifene (1.5 or 3 ppm), bexarotene (50 or 100 ppm), or their low-dose combinations for 40 weeks. Raloxifene or bexarotene alone significantly suppressed colon adenocarcinoma formation in terms of multiplicities (mean +/- SE): control, 3.59 +/- 0.25; 1.5 ppm raloxifene, 2.51 +/- 0.29 (P < 0.004); 3 ppm raloxifene, 2.14 +/- 0.28 (P < 0.0001); 50 ppm bexarotene, 2.25 +/- 0.32 (P < 0.001); 100 ppm bexarotene, 2.1 +/- 0.27 (P < 0.0001); and 1.5 ppm raloxifene + 50 ppm bexarotene, 1.57 +/- 0.21 (P < 0.0001). The low-dose combination caused significant (56%) inhibition of adenocarcinomas as compared with control diet fed rats. Tumors exposed to raloxifene, bexarotene and/or the combination showed significant suppression of proliferating cell nuclear antigen, cyclin D1, and beta-catenin with an increased apoptotic cells (3-fold) and p21 expression (3.8-fold) as compared tumors of rats fed control diet. The combination of low doses of raloxifene and bexarotene significantly suppressed the progression of colonic adenomas to adenocarcinomas and may be useful for colon cancer prevention and/or treatment in high-risk individuals. (C) 2013 AACR.
C1 [Janakiram, Naveena B.; Mohammed, Altaf; Zhang, Yuting; Brewer, Misty; Bryant, Taylor; Rao, Chinthalapally V.] Univ Oklahoma, Hlth Sci Ctr, Ctr Canc Prevent & Drug Dev, Hematol Oncol Sect,Dept Med,PCS Canc Ctr, Oklahoma City, OK 73104 USA.
[Lightfoot, Stan] Univ Oklahoma, Hlth Sci Ctr, VA Med Ctr, Dept Pathol, Oklahoma City, OK 73104 USA.
[Steele, Vernon E.] NCI, Chemoprevent Agent Dev Res Grp, Div Canc Prevent, Bethesda, MD 20892 USA.
RP Rao, CV (reprint author), Univ Oklahoma, Hlth Sci Ctr, Ctr Canc Prevent & Drug Dev, 975 NE 10th St,BRC 1203, Oklahoma City, OK 73104 USA.
EM cv-rao@ouhsc.edu
FU National Cancer Institute [NCI-N01 CN-53300]
FX This investigation was supported by Grant NCI-N01 CN-53300 from the
National Cancer Institute to C.V. Rao.
NR 48
TC 5
Z9 5
U1 2
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2013
VL 6
IS 12
BP 1251
EP 1261
DI 10.1158/1940-6207.CAPR-13-0249
PG 11
WC Oncology
SC Oncology
GA 268SL
UT WOS:000328190700001
PM 24080207
ER
PT J
AU Disis, ML
Gad, E
Herendeen, DR
Vy, PL
Park, KH
Cecil, DL
O'Meara, MM
Treuting, PM
Lubet, RA
AF Disis, Mary L.
Gad, Ekram
Herendeen, Daniel R.
Vy Phan-Lai
Park, Kyong Hwa
Cecil, Denise L.
O'Meara, Megan M.
Treuting, Piper M.
Lubet, Ronald A.
TI A Multiantigen Vaccine Targeting Neu, IGFBP-2, and IGF-IR Prevents Tumor
Progression in Mice with Preinvasive Breast Disease
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID CARCINOMA IN-SITU; FACTOR-BINDING PROTEIN-2; GROWTH-FACTOR-I; TRANSGENIC
MICE; PREMALIGNANT LESIONS; MAMMARY-TUMORS; CANCER; EXPRESSION;
IMMUNITY; RECEPTOR
AB A multiantigen multipeptide vaccine, targeting proteins expressed in preinvasive breast lesions, can stimulate type I CD4(+) T cells which have been shown to be deficient in both patients with breast cancer and mice that develop mammary tumors. Transgenic mice (TgMMTV-neu) were immunized with a multiantigen peptide vaccine specific for neu, insulin-like growth factor-binding protein 2 and insulin-like growth factor receptor-I at a time when some of the animals already had preinvasive lesions (18 weeks of age). Although immunization with each individual antigen was partially effective in inhibiting tumor growth, immunization with the multiantigen vaccine was highly effective, blocking development of palpable lesions in 65% of mice and slowing tumor growth in the infrequent palpable tumors, which did arise. Protection was mediated by CD4(+) T cells, and the few slow-growing tumors that did develop demonstrated a significant increase in intratumoral CD8(+) T cells as compared with controls (P = 0.0007). We also combined the vaccine with agents that were, by themselves, partially effective inhibitors of tumor progression in this model; lapatinib and the RXR agonist bexarotene. Although the combination of lapatinib and vaccination performed similarly to vaccination alone (P = 0.735), bexarotene and vaccination significantly enhanced disease-free survival (P < 0.0001), and approximately 90% of the mice showed no pathologic evidence of carcinomas at one year. The vaccine also demonstrated significant clinical efficacy in an additional transgenic model of breast cancer (TgC3(I)-Tag). Chemoimmunoprevention combinations may be an effective approach to breast cancer prevention even when the vaccine is administered in the presence of subclinical disease. (C) 2013 AACR.
C1 [Disis, Mary L.; Gad, Ekram; Herendeen, Daniel R.; Vy Phan-Lai; Cecil, Denise L.; O'Meara, Megan M.] Univ Washington, Tumor Vaccine Grp, Ctr Translat Med Womens Hlth, Seattle, WA 98109 USA.
[Treuting, Piper M.] Univ Washington, Dept Comparat Med, Seattle, WA 98109 USA.
[Park, Kyong Hwa] Korea Univ, Dept Internal Med, Div Oncol Hematol, Seoul, South Korea.
[Lubet, Ronald A.] NCI, Canc Chemoprevent Branch, Bethesda, MD 20892 USA.
RP Disis, ML (reprint author), Univ Washington, Tumor Vaccine Grp, Ctr Translat Med Womens Hlth, 850 Republican St,Box 358050, Seattle, WA 98109 USA.
EM ndisis@uw.edu
FU National Cancer Institute [N01-CN-53300/WA10, U01 CA141539, P50
CA083636]; Ovarian Cancer Research Fund; Athena Distinguished
Professorship of Breast Cancer Research
FX M.L. Disis was supported by a National Cancer Institute grant
(N01-CN-53300/WA#10, U01 CA141539, P50 CA083636), the Ovarian Cancer
Research Fund, and by the Athena Distinguished Professorship of Breast
Cancer Research.
NR 39
TC 23
Z9 23
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2013
VL 6
IS 12
BP 1273
EP 1282
DI 10.1158/1940-6207.CAPR-13-0182
PG 10
WC Oncology
SC Oncology
GA 268SL
UT WOS:000328190700003
PM 24154719
ER
PT J
AU DeCicco-Skinner, KL
Jung, SA
Tabib, T
Gwilliam, JC
Alexander, H
Goodheart, SE
Merchant, AS
Shan, MG
Garber, C
Wiest, JS
AF DeCicco-Skinner, Kathleen L.
Jung, Sarah A.
Tabib, Tracy
Gwilliam, J. Curtis
Alexander, Hepzibha
Goodheart, Sarah E.
Merchant, Anand S.
Shan, Mengge
Garber, Caroline
Wiest, Jonathan S.
TI Tpl2 knockout keratinocytes have increased biomarkers for invasion and
metastasis
SO CARCINOGENESIS
LA English
DT Article
ID GELATINASE-ASSOCIATED LIPOCALIN; SQUAMOUS-CELL CARCINOMA; ACTIVATED
PROTEIN-KINASE; GENE-EXPRESSION ANALYSIS; MATRIX METALLOPROTEINASES;
TUMOR PROGRESSION; BREAST-CANCER; IN-VITRO; PANCREATIC ADENOCARCINOMAS;
MALIGNANT CONVERSION
AB Skin cancer is the most common form of cancer in the USA, with an estimated two million cases diagnosed annually. Tumor progression locus 2 (Tpl2), also known as MAP3K8, is a serine/threonine protein kinase in the mitogen-activated protein kinase signal transduction cascade. Tpl2 was identified by our laboratory as having a tumor suppressor function in skin carcinogenesis, with the absence of this gene contributing to heightened inflammation and increased skin carcinogenesis. In this study, we used gene expression profiling to compare expression levels between Tpl2+/+ and Tpl2-/- keratinocytes. We identified over 2000 genes as being differentially expressed between genotypes. Functional annotation analysis identified cancer, cell growth/proliferation, cell death, cell development, cell movement and cell signaling as the top biological processes to be differentially regulated between genotypes. Further microarray analysis identified several candidate genes, including Mmp1b, Mmp2, Mmp9 and Mmp13, involved in migration and invasion to be upregulated in Tpl2-/- keratinocytes. Moreover, Tpl2-/- keratinocytes had a significant downregulation in the matrix metalloproteinase (MMP) inhibitor Timp3. Real-time PCR validated the upregulation of the MMPs in Tpl2-/- keratinocytes and zymography confirmed that MMP2 and MMP9 activity was higher in conditioned media from Tpl2-/- keratinocytes. Immunohistochemistry confirmed higher MMP9 staining in 12-O-tetradecanoylphorbol-13-acetate-treated skin from Tpl2-/- mice and grafted tumors formed from v-ras(Ha) retrovirus-infected Tpl2-/- keratinocytes. Additionally, Tpl2-/- keratinocytes had significantly higher invasion, malignant conversion rates and increased endothelial cell tube formation when compared with Tpl2+/+ keratinocytes. In summary, our studies reveal that keratinocytes from Tpl2-/- mice demonstrate a higher potential to be invasive and metastatic.
C1 [DeCicco-Skinner, Kathleen L.; Jung, Sarah A.; Tabib, Tracy; Gwilliam, J. Curtis; Alexander, Hepzibha; Goodheart, Sarah E.] Amer Univ, Dept Biol, Washington, DC 20016 USA.
[Merchant, Anand S.] NCI, CCRIFX Bioinformat Core, NIH, Bethesda, MD 20892 USA.
[Shan, Mengge] NCI, Off Sci & Technol Partnerships, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Garber, Caroline; Wiest, Jonathan S.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP DeCicco-Skinner, KL (reprint author), Amer Univ, Dept Biol, Washington, DC 20016 USA.
EM decicco@american.edu
FU Intramural Research Program of the National Cancer Institute at the
National Institutes of Health; National Cancer Institute grant
[UA5CA152907]
FX Intramural Research Program of the National Cancer Institute at the
National Institutes of Health; National Cancer Institute grant
(UA5CA152907).
NR 66
TC 3
Z9 3
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 2013
VL 34
IS 12
BP 2789
EP 2798
DI 10.1093/carcin/bgt319
PG 10
WC Oncology
SC Oncology
GA 269XX
UT WOS:000328278900012
PM 24067898
ER
PT J
AU Bates, SE
AF Bates, Susan E.
TI On Masterpieces and Breast Cancer Research
SO CLINICAL CANCER RESEARCH
LA English
DT Editorial Material
C1 NCI, Bethesda, MD 20892 USA.
RP Bates, SE (reprint author), NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2013
VL 19
IS 23
BP 6352
EP 6352
DI 10.1158/1078-0432.CCR-13-2847
PG 1
WC Oncology
SC Oncology
GA 263PE
UT WOS:000327819700004
PM 24298064
ER
PT J
AU Lin, NU
Amiri-Kordestani, L
Palmieri, D
Liewehr, DJ
Steeg, PS
AF Lin, Nancy U.
Amiri-Kordestani, Laleh
Palmieri, Diane
Liewehr, David J.
Steeg, Patricia S.
TI CNS Metastases in Breast Cancer: Old Challenge, New Frontiers
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID NERVOUS-SYSTEM METASTASES; POSITRON-EMISSION-TOMOGRAPHY;
BLOOD-BRAIN-BARRIER; LAPATINIB PLUS CAPECITABINE; TYROSINE KINASE
INHIBITOR; ADVANCED SOLID TUMORS; PHASE-II; INTRATHECAL TRASTUZUMAB;
CLINICAL-OUTCOMES; MENINGEAL CARCINOMATOSIS
AB Despite major therapeutic advances in the management of patients with breast cancer, central nervous system (CNS) metastases remain an intractable problem, particularly in patients with metastatic HER2-positive and triple-negative breast cancer. As systemic therapies to treat extracranial disease improve, some patients are surviving longer, and the frequency of CNS involvement seems to be increasing. Furthermore, in the early-stage setting, the CNS remains a potential sanctuary site for relapse. This review highlights advances in the development of biologically relevant preclinical models, including the development of brain-tropic cell lines for testing of agents to prevent and treat brain metastases, and summarizes our current understanding of the biology of CNS relapse. From a clinical perspective, a variety of therapeutic approaches are discussed, including methods to improve drug delivery, novel cytotoxic agents, and targeted therapies. Challenges in current trial design and endpoints are reviewed. Finally, we discuss promising new directions, including novel trial designs, correlative imaging techniques, and enhanced translational opportunities. Clin Cancer Res; 19(23); 6404-18. (C) 2013 AACR.
C1 [Lin, Nancy U.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Amiri-Kordestani, Laleh] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Palmieri, Diane; Steeg, Patricia S.] NCI, Womens Canc Sect, Lab Mol Pharmacol, Bethesda, MD 20892 USA.
[Liewehr, David J.] NCI, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Lin, NU (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM nlin@partners.org
RI Palmieri, Diane/B-4258-2015
FU Intramural Program of the National Cancer Institute; DOD Breast Cancer
Research Program [W81XWH-062-0033]; Breast Cancer Research Foundation
FX The statistical assistance of S. Steinberg, Biostatistics and Data
Management Section, Center for Cancer Research, National Cancer
Institute, Bethesda, MD, is appreciated. The authors thank the following
individuals for providing figures: National Cancer Institute Molecular
Imaging Program Staff (M. Liza Lindenberg, MD, Esther Mena Gonzalex,
PhD, Peter L. Choyke, MD, Karen A. Kurdziel, MD), Kyrre E. Emblem, PhD
(Massachusetts General Hospital, Boston, MA), Elizabeth Gerstner, MD
(Massachusetts General Hospital, Boston, MA), and Professor E. G.
Elisabeth de Vries, MD, PhD (University Medical Centre, Groningen, the
Netherlands). This work was funded, in part, by the Intramural Program
of the National Cancer Institute, DOD Breast Cancer Research Program
grant W81XWH-062-0033 (P.S. Steeg, D. Palmieri), and the Breast Cancer
Research Foundation (N.U. Lin).
NR 108
TC 42
Z9 43
U1 1
U2 18
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 DEC 1
PY 2013
VL 19
IS 23
BP 6404
EP 6418
DI 10.1158/1078-0432.CCR-13-0790
PG 15
WC Oncology
SC Oncology
GA 263PE
UT WOS:000327819700011
PM 24298071
ER
PT J
AU Dynkevich, Y
Rother, KI
Whitford, I
Qureshi, S
Galiveeti, S
Szulc, AL
Danoff, A
Breen, TL
Kaviani, N
Shanik, MH
LeRoith, D
Vigneri, R
Koch, CA
Roth, J
AF Dynkevich, Yevgeniya
Rother, Kristina I.
Whitford, Ian
Qureshi, Sana
Galiveeti, Sneha
Szulc, Alessandra L.
Danoff, Ann
Breen, Tracy L.
Kaviani, Nargess
Shanik, Michael H.
LeRoith, Derek
Vigneri, Riccardo
Koch, Christian A.
Roth, Jesse
TI Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the
Laboratory, and the Historical Archive
SO ENDOCRINE REVIEWS
LA English
DT Review
ID GROWTH-FACTOR-II; ISLET-CELL TUMOR; SOLITARY FIBROUS TUMOR;
FACTOR-BINDING-PROTEINS; NONSUPPRESSIBLE INSULIN-LIKE; GASTROINTESTINAL
STROMAL TUMOR; II/MANNOSE 6-PHOSPHATE RECEPTOR; HYPERINSULINEMIC
HYPOGLYCEMIA; GASTRIC-BYPASS; NSILA-S
AB Tumors of mesenchymal and epithelial origin produce IGF-2, which activates pathways in the tumors. In a minority of patients, the tumors (hepatomas, fibromas, and fibrosarcomas are the most common among many) release into the circulation enough IGF-2-related peptides to mimic the fasting hypoglycemia characteristic of patients with insulin-producing islet-cell tumors. Rarely, markedly elevated IGF-2 levels produce somatic changes suggestive of acromegaly. Typically, the elevated IGF-2 levels are associated with suppressed plasma levels of insulin, IGF-1, and GH. Complicating the pathophysiology are the IGF binding proteins (IGFBPs) that can bind IGF-2 and IGF-1, modifying hormone metabolism and action. IGFBP concentrations are often altered in the presence of these tumors. At the cellular level, the 3 hormone-related ligands, IGF-2, IGF-1, and insulin, all bind to 4 (or more) types of IGF-1 receptor (IGF-1R) and insulin receptor (IR). Each receptor has its own characteristic affinity for each ligand, a tyrosine kinase, and overlapping profiles of action in the target cells. The IGF-2R, in addition to binding mannose-6-phosphate-containing proteins, provides an IGF-2 degradation pathway. Recent evidence suggests IGF-2R involvement also in signal transduction. Surgery, the treatment of choice, can produce a cure. For patients not cured by surgery, multiple therapies exist, for the tumor and for hypoglycemia. Potential future therapeutic approaches are sketched. From 1910 to 1930, hypoglycemia, insulin, insulinomas, and non-islet-cell tumors were recognized. The latter third of the century witnessed the emergence of the immunoassay for insulin; the IGFs, their binding proteins, and assays to measure them; and receptors for the insulin-related peptides as well as the intracellular pathways beyond the receptor. In closing, we replace non-islet-cell tumor hypoglycemia, an outdated and misleading label, with IGF-2-oma, self-explanatory and consistent with names of other hormone-secreting tumors.
C1 [Dynkevich, Yevgeniya] North Shore Long Isl Jewish NS LIJ Hlth Syst, Queens Long Isl Med Grp, Hicksville, NY 11801 USA.
[Rother, Kristina I.] NIDDK, Bethesda, MD 20892 USA.
[Whitford, Ian; Qureshi, Sana; Galiveeti, Sneha; Roth, Jesse] NS LIJ Hlth Syst, Lab Diabet & Diabet Related Res, Feinstein Inst Med Res, Manhasset, NY 11030 USA.
[Szulc, Alessandra L.; Roth, Jesse] Yeshiva Univ, Albert Einstein Coll Med, Bronx, NY 10461 USA.
[Danoff, Ann] NYU, Sch Med, Div Endocrinol Diabet & Metab, New York, NY 10016 USA.
[Danoff, Ann] Vet Adm New York Harbor Healthcare Syst, New York, NY 10010 USA.
[Breen, Tracy L.] NS LIJ Hlth Syst, Div Endocrinol, Great Neck, NY 11021 USA.
[Breen, Tracy L.; Roth, Jesse] NS LIJ Hlth Syst, Hofstra NS LIJ Sch Med, Manhasset, NY 11549 USA.
[Kaviani, Nargess] Geisinger Hlth Syst, Endocrinol & Metab, State Coll, PA 16801 USA.
[Shanik, Michael H.] Endocrine Associates Long Isl PC, Smithtown, NY 11787 USA.
[Shanik, Michael H.] Stony Brook Univ Hosp, Stony Brook, NY 11794 USA.
[LeRoith, Derek] Mt Sinai Sch Med, Div Endocrinol Diabet & Bone Dis, Samuel Bronfman Dept Med, New York, NY 10029 USA.
[LeRoith, Derek] Clin Res Inst Rambam, Diabet & Metab Clin Res Ctr Excellence, IL-31096 Haifa, Israel.
[Vigneri, Riccardo] Univ Catania, Endocrine Unit, Dept Clin & Mol Biomed, Garibaldi Nesima Hosp, Catania, Italy.
Consilgio Nazl Richerche Catania Sect, Ist Biostrutture & Bioimmagini, I-95131 Catania, Italy.
[Koch, Christian A.] Univ Mississippi, Sch Med, Div Endocrinol, Dept Med, Jackson, MS 39216 USA.
RP Roth, J (reprint author), Feinstein Inst Med Res, Lab Diabet & Diabet Related Res, 350 Community Dr, Manhasset, NY 11030 USA.
EM jesserothmd@hotmail.com
OI Koch, Christian/0000-0003-0678-1242
FU Feinstein Institute for Medical Research, Manhasset, New York
FX This work was funded by the Feinstein Institute for Medical Research,
Manhasset, New York.
NR 287
TC 20
Z9 20
U1 1
U2 6
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD DEC
PY 2013
VL 34
IS 6
BP 798
EP 826
DI 10.1210/er.2012-1033
PG 29
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 267FU
UT WOS:000328082900004
PM 23671155
ER
PT J
AU Kistemaker, LEM
Bos, IST
Hylkema, MN
Nawijn, MC
Hiemstra, PS
Wess, J
Meurs, H
Kerstjens, HAM
Gosens, R
AF Kistemaker, Loes E. M.
Bos, I. S. T.
Hylkema, Machteld N.
Nawijn, Martijn C.
Hiemstra, Pieter S.
Wess, Juergen
Meurs, Herman
Kerstjens, Huib A. M.
Gosens, Reinoud
TI Muscarinic receptor subtype-specific effects on cigarette smoke-induced
inflammation in mice
SO EUROPEAN RESPIRATORY JOURNAL
LA English
DT Article
ID OBSTRUCTIVE PULMONARY-DISEASE; NONNEURONAL CHOLINERGIC SYSTEM; BRONCHIAL
EPITHELIAL-CELLS; AIRWAY SMOOTH-MUSCLE; PHARMACOLOGICAL-PROPERTIES;
ACETYLCHOLINE-RECEPTOR; CHEMOTACTIC ACTIVITY; TIOTROPIUM BROMIDE; MURINE
AIRWAYS; IN-VITRO
AB Cholinergic tone contributes to airflow obstruction in chronic obstructive pulmonary disease. Accordingly, anticholinergics are effective bronchodilators by blocking the muscarinic M-3 receptor on airway smooth muscle. Recent evidence indicates that acetylcholine also contributes to airway inflammation. However, which muscarinic receptor subtype(s) regulates this process is unknown.
In this study, the contribution of the M-1, M-2 and M-3 receptor subtypes to cigarette smoke-induced airway inflammation was investigated by exposing muscarinic receptor subtype deficient mice to cigarette smoke for 4 days.
In wild-type mice, cigarette smoke induced an increase in macrophages, neutrophils and lymphocytes in bronchoalveolar lavage fluid. Neutrophilic inflammation was higher in M-1(-/-) and M-2(-/-) mice compared to wild-type mice, but lower in M-3(-/-) mice. Accordingly, the release of keratinocyte-derived chemokine (KC), monocyte chemotactic protein-1 and interleukin-6 was higher in M-1(-/-) and M-2(-/-) mice, and reduced in M-3(-/-) mice. Markers of remodelling were not increased after cigarette smoke exposure. However, M-3(-/-) mice had reduced expression of transforming growth factor-beta 1 and matrix proteins. Cigarette smoke-induced inflammatory cell recruitment and KC release were also prevented by the M-3-receptor selective antagonist 1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP) in wild-type mice.
Collectively, our data indicate a pro-inflammatory role for the M-3 receptor in cigarette smoke-induced neutrophilia and cytokine release, yet an anti-inflammatory role for M-1 and M-2 receptors.
C1 [Kistemaker, Loes E. M.; Bos, I. S. T.; Meurs, Herman; Gosens, Reinoud] Univ Groningen, Dept Mol Pharmacol, NL-9713 AV Groningen, Netherlands.
[Kistemaker, Loes E. M.; Bos, I. S. T.; Hylkema, Machteld N.; Nawijn, Martijn C.; Meurs, Herman; Kerstjens, Huib A. M.; Gosens, Reinoud] Univ Groningen, Univ Med Ctr Groningen, GRIAC Res Inst, NL-9713 AV Groningen, Netherlands.
[Hylkema, Machteld N.; Nawijn, Martijn C.] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol & Med Biol, NL-9713 AV Groningen, Netherlands.
[Hiemstra, Pieter S.] Leiden Univ, Med Ctr, Dept Pulmonol, Leiden, Netherlands.
[Kerstjens, Huib A. M.] Univ Groningen, Univ Med Ctr Groningen, Dept Resp Med, NL-9713 AV Groningen, Netherlands.
[Wess, Juergen] NIDDK, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Kistemaker, LEM (reprint author), Univ Groningen, Dept Mol Pharmacol, A Deusinglaan 1, NL-9713 AV Groningen, Netherlands.
EM l.e.m.kistemaker@rug.nl
FU Netherlands Asthma Foundation [3.2.08.014]
FX We would like to thank the Netherlands Asthma Foundation for financial
support (grant 3.2.08.014).
NR 41
TC 12
Z9 13
U1 1
U2 7
PU EUROPEAN RESPIRATORY SOC JOURNALS LTD
PI SHEFFIELD
PA 442 GLOSSOP RD, SHEFFIELD S10 2PX, ENGLAND
SN 0903-1936
EI 1399-3003
J9 EUR RESPIR J
JI Eur. Resp. J.
PD DEC
PY 2013
VL 42
IS 6
BP 1677
EP 1688
DI 10.1183/09031936.00112412
PG 12
WC Respiratory System
SC Respiratory System
GA 264ZQ
UT WOS:000327919900031
PM 23397297
ER
PT J
AU Gabitzsch, EK
Hashmi, SS
Koenig, MK
Raia, MH
Whittemore, VH
Northrup, H
Nader, S
Gambello, MJ
AF Gabitzsch, Emily K.
Hashmi, Syed S.
Koenig, Mary Kay
Raia, Marianna H.
Whittemore, Vicky H.
Northrup, Hope
Nader, Shahla
Gambello, Michael J.
TI Self- reported reproductive health in women with tuberous sclerosis
complex
SO GENETICS IN MEDICINE
LA English
DT Article
DE reproductive health; tuberous sclerosis complex
ID PREMATURE OVARIAN FAILURE; PRIMORDIAL FOLLICLES; TSC2; ACTIVATION; GENE;
LYMPHANGIOLEIOMYOMATOSIS; IDENTIFICATION; MISCARRIAGE; PREVALENCE;
PATHWAY
AB Purpose: Little is known about sex-specific manifestations of tuberous sclerosis complex. Inactivating mutations in the TSC1 and TSC2 genes cause tuberous sclerosis complex, and recent evidence points to a crucial role for these genes in maintaining appropriate ovarian function. The main objective of this study was to estimate reproductive dysfunction in a sample of women with tuberous sclerosis complex.
Methods: We designed a three-part questionnaire that included demographic information, reproductive history, and tuberous sclerosis complex history, and developed strict criteria to assess patterns in menstrual cyclicity; we analyzed 182 responses from female adult members of the Tuberous Sclerosis Alliance.
Results: More than one-third of women in our sample displayed some degree of menstrual irregularity, and their reported miscarriage rate was 41%. More than 4% of women had reproductive histories suggestive of premature ovarian insufficiency, higher than the general population estimate of 1%.
Conclusion: Our data reveal an underappreciated aspect of tuberous sclerosis complex in affected women, suggesting that a further exploration of the role the tuberous sclerosis complex genes play in reproductive function is warranted.
C1 [Gabitzsch, Emily K.; Gambello, Michael J.] Univ Texas Hlth Sci Ctr Houston, Grad Sch Biomed Sci, Genet Counseling Program, Houston, TX 77030 USA.
[Hashmi, Syed S.; Koenig, Mary Kay; Raia, Marianna H.; Northrup, Hope] Univ Texas Hlth Sci Ctr Houston, Dept Pediat, Houston, TX 77030 USA.
[Whittemore, Vicky H.] NINDS, NIH, Rockville, MD USA.
[Nader, Shahla] Univ Texas Hlth Sci Ctr Houston, Dept Obstet Gynecol & Reprod Sci, Houston, TX 77030 USA.
RP Gambello, MJ (reprint author), Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA 30322 USA.
EM Michael.j.gambello@emory.edu
OI Hashmi, S. Shahrukh/0000-0001-8758-8254
FU University of Texas-Memorial Hermann Hospital TSC Center of Excellence
FX We sincerely thank the respondents and members of the Tuberous Sclerosis
Alliance organization for their participation, and the Alliance staff
for assisting in the distribution of these surveys. The University of
Texas-Memorial Hermann Hospital TSC Center of Excellence generously
provided financial support for the development of this survey.
NR 24
TC 2
Z9 2
U1 2
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2013
VL 15
IS 12
BP 966
EP 971
DI 10.1038/gim.2013.60
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 266XI
UT WOS:000328056900009
PM 23660529
ER
PT J
AU Berry, SA
Kenney, MK
Harris, KB
Singh, RH
Cameron, CA
Kraszewski, JN
Levy-Fisch, J
Shuger, JF
Greene, CL
Lloyd-Puryear, MA
Boyle, CA
AF Berry, Susan A.
Kenney, Mary Kay
Harris, Katharine B.
Singh, Rani H.
Cameron, Cynthia A.
Kraszewski, Jennifer N.
Levy-Fisch, Jill
Shuger, Jill F.
Greene, Carol L.
Lloyd-Puryear, Michele A.
Boyle, Coleen A.
TI Insurance coverage of medical foods for treatment of inherited metabolic
disorders
SO GENETICS IN MEDICINE
LA English
DT Article
DE diet therapy; inborn errors of metabolism; insurance coverage; neonatal
screening
AB Purpose: Treatment of inherited metabolic disorders is accomplished by use of specialized diets employing medical foods and medically necessary supplements. Families seeking insurance coverage for these products express concern that coverage is often limited; the extent of this challenge is not well defined.
Methods: To learn about limitations in insurance coverage, parents of 305 children with inherited metabolic disorders completed a paper survey providing information about their use of medical foods, modified low-protein foods, prescribed dietary supplements, and medical feeding equipment and supplies for treatment of their child's disorder as well as details about payment sources for these products.
Results: Although nearly all children with inherited metabolic disorders had medical coverage of some type, families paid "out of pocket" for all types of products. Uncovered spending was reported for 11% of families purchasing medical foods, 26% purchasing supplements, 33% of those needing medical feeding supplies, and 59% of families requiring modified low-protein foods. Forty-two percent of families using modified low-protein foods and 21% of families using medical foods reported additional treatment-related expenses of $ 100 or more per month for these products.
Conclusion: Costs of medical foods used to treat inherited metabolic disorders are not completely covered by insurance or other resources.
C1 [Berry, Susan A.] Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA.
[Kenney, Mary Kay] US Hlth Resources & Serv Adm, Off Epidemiol Policy & Evaluat, Rockville, MD 20857 USA.
[Harris, Katharine B.] New York State Dept Hlth, Wadsworth Ctr, Albany, NY USA.
[Singh, Rani H.] Emory Univ, Dept Human Genet, Atlanta, GA 30322 USA.
[Cameron, Cynthia A.] Michigan Publ Hlth Inst, Okemos, MI USA.
[Kraszewski, Jennifer N.] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Levy-Fisch, Jill] Save Babies Screening Fdn Inc, Cincinnati, OH USA.
[Shuger, Jill F.] US Hlth Resources & Serv Adm, Maternal & Child Hlth Bur, Rockville, MD 20857 USA.
[Greene, Carol L.] Univ Maryland, Sch Med, Dept Pediat, Baltimore, MD 21201 USA.
[Lloyd-Puryear, Michele A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Boyle, Coleen A.] Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA USA.
RP Berry, SA (reprint author), Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA.
EM berry002@umn.edu
OI Berry, Susan/0000-0001-7970-688X
FU Cooperative Agreement between the Maternal and Child Health Bureau
(MCHB); Genetic Services Branch, and the University of Texas Health
Science Center at San Antonio; National Newborn Screening and Genetics
Resource Center; Health Resources and Services Administration (HRSA)
[U32MC00148]; HRSA-MCHB Regional Genetic and Newborn Screening Services
Collaboratives; Heritable Disorders Program: Region 2 New
York-Mid-Atlantic Consortium for Genetic and Newborn Screening Services
[U22MC03956]; Region 3 Southeast Newborn Screening and Genetics
Collaborative [U22MC10979]; Region 4 Midwest Genetics Collaborative
[U22MC03963]
FX The project was supported through a Cooperative Agreement between the
Maternal and Child Health Bureau (MCHB), Genetic Services Branch, and
the University of Texas Health Science Center at San Antonio, National
Newborn Screening and Genetics Resource Center, Health Resources and
Services Administration (HRSA) grant no. U32MC00148 and by HRSA-MCHB
Regional Genetic and Newborn Screening Services Collaboratives,
Heritable Disorders Program: Region 2 New York-Mid-AtlantiConsortium for
Genetic and Newborn Screening Services, Cooperative Agreement No.
U22MC03956; Region 3 Southeast Newborn Screening and Genetics
Collaborative, Cooperative Agreement No. U22MC10979; and Region 4
Midwest Genetics Collaborative, Cooperative Agreement No. U22MC03963.
The authors thank the investigators at the following institutions: -
University of - Minnesota Amplatz Children's Hospital (Kristi Bentler);
- Cincinnati Children's Hospital Medical Center (Nancy Leslie); Emory -
University (Mary Brauchla); Greenwood Genetics Center (Melinda Whetsell
and Neena Champaigne); University of Florida (Helen McCune and Robert
Zori); University of North - Carolina-Chapel Hill (Dianne - Frazier);
University of Tennessee (Darla Henderson Smith); Vanderbilt University
Medical Center (Gina Wey); Mount Sinai Medical Center (Roberta
Salveson); Children's Hospital at Albany Medical Center (Katherine
Marra); Children's Hospital of Pittsburgh (Judith Henry); Golisano
Children's Hospital at Strong (Eileen Blakely); Maria Fareri Children's
Hospital at Westchester Medical Center (Shideh Mofidi); University of
Maryland Hospital for Children (Megan Skinner).
NR 8
TC 5
Z9 5
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2013
VL 15
IS 12
BP 978
EP 982
DI 10.1038/gim.2013.46
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 266XI
UT WOS:000328056900011
PM 23598714
ER
PT J
AU Kruszka, PS
Manoli, I
Sloan, JL
Kopp, JB
Venditti, CP
AF Kruszka, Paul S.
Manoli, Irini
Sloan, Jennifer L.
Kopp, Jeffrey B.
Venditti, Charles P.
TI Renal growth in isolated methylmalonic acidemia
SO GENETICS IN MEDICINE
LA English
DT Article
DE chronic kidney disease; cystatin C; isolated methylmalonic acidemia;
methylmalonyl-CoA mutase; renal growth; renal ultrasound; vitamin B12
ID GLOMERULAR-FILTRATION-RATE; SERUM CREATININE; CYSTATIN-C; SONOGRAPHIC
ASSESSMENT; HEALTHY-CHILDREN; LENGTH; MANAGEMENT; ACIDURIAS;
TRANSPLANTATION; NOMOGRAM
AB Purpose: We sought to predict renal growth based on clinical and metabolic parameters in patients with isolated methylmalonic acidemia, a group of disorders associated with chronic kidney disease.
Methods: Fifty patients with methylmalonic acidemia, followed from 2004 to 2011, were classified by molecular genetics and studied using a combined cross-sectional and longitudinal design that included renal ultrasound examinations, anthropometric measurements, and metabolic phenotyping. Renal length was compared with that of healthy controls and modeled to other clinical parameters using multiple-regression analyses.
Results: Comparisons with age-matched controls showed that renal length in subjects with methylmalonic acidemia was significantly decreased (P < 0.05). Stepwise regression modeling found that combinations of height, serum cystatin C, and serum methymalonic acid concentrations best predicted kidney size. The regression equations used to generate methylmalonic acidemia kidney nomograms were renal length (cm) = 6.79 + 0.22 x age for the controls and 6.80 + 0.09 x age for the methylmalonic acidemia cohort (P < 0.001; constant and slope).
Conclusion: Renal length, reflective of kidney growth, significantly decreased in patients with methylmalonic acidemia over time as compared with controls and was predictable with select clinical parameters. Cystatin C and serum methylmalonic acid concentrations were highly correlated with smaller kidneys and decreased renal function in this patient population.
C1 [Kruszka, Paul S.; Manoli, Irini; Sloan, Jennifer L.; Venditti, Charles P.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Kopp, Jeffrey B.] Natl Inst Diabet & Digest & Kidney Dis, Kidney Dis Sect, NIH, Bethesda, MD USA.
RP Venditti, CP (reprint author), NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
EM venditti@mail.nih.gov
OI Manoli, Irini/0000-0003-1543-2941; Kopp, Jeffrey/0000-0001-9052-186X
FU National Human Genome Research Institute; National Institute of Diabetes
and Digestive and Kidney Diseases, National Institutes of Health
FX This work was supported by the intramural research programs of the
National Human Genome Research Institute and National Institute of
Diabetes and Digestive and Kidney Diseases, National Institutes of
Health.
NR 37
TC 7
Z9 7
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2013
VL 15
IS 12
BP 990
EP 996
DI 10.1038/gim.2013.42
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 266XI
UT WOS:000328056900013
PM 23639900
ER
PT J
AU Weil, CJ
Mechanic, LE
Green, T
Kinsinger, C
Lockhart, NC
Nelson, SA
Rodriguez, LL
Buccini, LD
AF Weil, Carol J.
Mechanic, Leah E.
Green, Tiffany
Kinsinger, Christopher
Lockhart, Nicole C.
Nelson, Stefanie A.
Rodriguez, Laura L.
Buccini, Laura D.
TI NCI think tank concerning the identifiability of biospecimens and "omic"
data
SO GENETICS IN MEDICINE
LA English
DT Article
DE biospecimens; data sharing; identifiability; research participant
engagement
ID GENOMIC RESEARCH; PRIVACY; PARTICIPANTS
AB Purpose: On 11 and 12 June 2012, the National Cancer Institute hosted a think tank concerning the identifiability of biospecimens and "omic" data in order to explore challenges surrounding this complex and multifaceted topic.
Methods: The think tank brought together 46 leaders from several fields, including cancer genomics, bioinformatics, human subject protection, patient advocacy, and commercial genetics.
Results: The first day involved presentations regarding the state of the science of reidentification; current and proposed regulatory frameworks for assessing identifiability; developments in law, industry, and biotechnology; and the expectations of patients and research participants. The second day was spent by think tank participants in small breakout groups designed to address specific subtopics under the umbrella issue of identifiability, including considerations for the development of best practices for data sharing and consent, and targeted opportunities for further empirical research.
Conclusion: We describe the outcomes of this 2-day meeting, including two complementary themes that emerged from moderated discussions following the presentations on day 1, and ideas presented for further empirical research to discern the preferences and concerns of research participants about data sharing and individual identifiability.
C1 [Weil, Carol J.] NCI, Diagnost Evaluat Branch, Canc Diag Program, Div Canc Treatment & Diag,NIH, Bethesda, MD 20892 USA.
[Mechanic, Leah E.; Green, Tiffany; Nelson, Stefanie A.; Buccini, Laura D.] NCI, Host Susceptibil Factors Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
[Kinsinger, Christopher] NCI, Off Canc Clin Prote Res, Ctr Strateg & Sci Initiat, NIH, Bethesda, MD 20892 USA.
[Lockhart, Nicole C.] NHGRI, Div Genom & Soc, NIH, Bethesda, MD 20892 USA.
[Rodriguez, Laura L.] NHGRI, Div Policy Commun & Educ, NIH, Bethesda, MD 20892 USA.
[Buccini, Laura D.] Cleveland Clin, Digest Dis Inst, Cleveland, OH 44106 USA.
RP Weil, CJ (reprint author), NCI, Diagnost Evaluat Branch, Canc Diag Program, Div Canc Treatment & Diag,NIH, Bethesda, MD 20892 USA.
EM carol.weil@nih.gov
FU Host Susceptibility Factors Branch (HSFB); Epidemiology and Genomics
Research Program (EGRP) in the Division of Cancer Control and Population
Sciences, NCI; Biorepositories and Biospecimen Research Branch (BBRB),
Division of Cancer Treatment and Diagnosis, NCI
FX Funds for the National Cancer Institute (NCI) think tank were provided
by the Host Susceptibility Factors Branch (HSFB) and the Epidemiology
and Genomics Research Program (EGRP) in the Division of Cancer Control
and Population Sciences, NCI and the Biorepositories and Biospecimen
Research Branch (BBRB), Division of Cancer Treatment and Diagnosis, NCI.
The authors acknowledge the assistance with meeting planning of
Elizabeth Gillanders (HSFB) and Jim Vaught (BBRB). The authors thank all
of the participants of the NCI Identifiability think tank listed in
Supplementary Appendix S2 online for their intellectual contributions
throughout the meeting.
NR 18
TC 5
Z9 5
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2013
VL 15
IS 12
BP 997
EP 1003
DI 10.1038/gim.2013.40
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 266XI
UT WOS:000328056900014
PM 23579437
ER
PT J
AU Sacks, DL
Ribeiro-Gomes, FL
Peters, NC
AF Sacks, D. L.
Ribeiro-Gomes, F. L.
Peters, N. C.
TI The influence of vector transmission and neutrophils on the immune
response to Leishmania major
SO IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Congress of the British-Society-for-Immunology
CY DEC 02-05, 2013
CL Liverpool, ENGLAND
SP British Soc Immunol
C1 [Sacks, D. L.; Peters, N. C.] NIH, Bethesda, MD 20892 USA.
[Ribeiro-Gomes, F. L.] NIAID, NIH, Bethesda, MD 20892 USA.
RI Ribeiro-Gomes, Flavia/F-7609-2015
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2013
VL 140
SU 1
SI SI
BP 12
EP 12
PG 1
WC Immunology
SC Immunology
GA 258VV
UT WOS:000327487700024
ER
PT J
AU Roychoudhuri, R
Hirahara, K
Mousavi, K
Clever, D
Bonelli, M
Sciume, G
Zare, H
Vahedi, G
Klebanoff, C
Sartorelli, V
Kanno, Y
Gattinoni, L
Nakamura, A
Muto, A
O'Shea, J
Restifo, N
AF Roychoudhuri, R.
Hirahara, K.
Mousavi, K.
Clever, D.
Bonelli, M.
Sciume, G.
Zare, H.
Vahedi, G.
Klebanoff, C.
Sartorelli, V.
Kanno, Y.
Gattinoni, L.
Nakamura, A.
Muto, A.
O'Shea, J.
Restifo, N.
TI BACH2 represses effector programmes to stabilize T-reg-mediated immune
homeostasis
SO IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Congress of the British-Society-for-Immunology
CY DEC 02-05, 2013
CL Liverpool, ENGLAND
SP British Soc Immunol
C1 [Roychoudhuri, R.; Clever, D.; Klebanoff, C.; Gattinoni, L.; Restifo, N.] NCI, NIH, Bethesda, MD 20892 USA.
[Hirahara, K.; Mousavi, K.; Bonelli, M.; Sciume, G.; Zare, H.; Vahedi, G.; Sartorelli, V.; Kanno, Y.; O'Shea, J.] NIAMSD, Bethesda, MD 20892 USA.
[Nakamura, A.; Muto, A.] Tohoku Univ, Sendai, Miyagi 980, Japan.
RI Roychoudhuri, Rahul/A-7442-2010; Hirahara, Kiyoshi/E-2460-2017
OI Roychoudhuri, Rahul/0000-0002-5392-1853; Hirahara,
Kiyoshi/0000-0002-9128-9449
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2013
VL 140
SU 1
SI SI
BP 43
EP 43
PG 1
WC Immunology
SC Immunology
GA 258VV
UT WOS:000327487700086
ER
PT J
AU Tregoning, JS
Wang, B
McDonald, JU
Yamaguchi, Y
Harker, JA
Goritzka, M
Johansson, C
Bukreyev, A
Collins, PL
Openshaw, PJ
AF Tregoning, J. S.
Wang, B.
McDonald, J. U.
Yamaguchi, Y.
Harker, J. A.
Goritzka, M.
Johansson, C.
Bukreyev, A.
Collins, P. L.
Openshaw, P. J.
TI Respiratory syncytial virus (RSV) infection during early life suppresses
antibody responses by the induction of interferon gamma
SO IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Congress of the British-Society-for-Immunology
CY DEC 02-05, 2013
CL Liverpool, ENGLAND
SP British Soc Immunol
C1 [Tregoning, J. S.; McDonald, J. U.] Univ London Imperial Coll Sci Technol & Med, Infect Dis Sect, London, England.
[Wang, B.; Yamaguchi, Y.; Harker, J. A.; Goritzka, M.; Johansson, C.; Openshaw, P. J.] Univ London Imperial Coll Sci Technol & Med, Dept Resp Med, London, England.
[Bukreyev, A.; Collins, P. L.] NIH, Infect Dis Lab, Bethesda, MD 20892 USA.
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2013
VL 140
SU 1
SI SI
BP 104
EP 104
PG 1
WC Immunology
SC Immunology
GA 258VV
UT WOS:000327487700260
ER
PT J
AU Dhanda, AD
Liu, B
Lait, P
Schewitz-Bowers, L
Collins, PL
Dick, AD
Nussenblatt, R
Lee, RW
AF Dhanda, A. D.
Liu, B.
Lait, P.
Schewitz-Bowers, L.
Collins, P. L.
Dick, A. D.
Nussenblatt, R.
Lee, R. W.
TI CD14(++)CD16(-) monocytes polarise memory T cells to a Th17 phenotype
which is refractory to glucocorticoid treatment
SO IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Congress of the British-Society-for-Immunology
CY DEC 02-05, 2013
CL Liverpool, ENGLAND
SP British Soc Immunol
C1 [Dhanda, A. D.; Lait, P.; Schewitz-Bowers, L.; Dick, A. D.; Lee, R. W.] Univ Bristol, Sch Clin Sci, Bristol, Avon, England.
[Dhanda, A. D.; Collins, P. L.] Univ Hosp Bristol NHS Fdn Trust, Dept Liver Med, Bristol, Avon, England.
[Liu, B.; Nussenblatt, R.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Dick, A. D.] Univ Hosp Bristol NHS Fdn Trust, Acad Unit Ophthalmol, Bristol, Avon, England.
[Dick, A. D.; Lee, R. W.] Moorfields Eye Hosp NHS Fdn Trust, Natl Inst Hlth Res Biomed Res Ctr, Bristol, Avon, England.
[Dick, A. D.; Lee, R. W.] Univ Hosp Bristol NHS Fdn Trust, UCL Inst Ophthalmol, Bristol, Avon, England.
[Dick, A. D.; Lee, R. W.] Univ Bristol, Bristol, Avon, England.
RI Lee, Richard/A-3116-2017
OI Lee, Richard/0000-0002-9480-6843
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2013
VL 140
SU 1
SI SI
BP 154
EP 154
PG 1
WC Immunology
SC Immunology
GA 258VV
UT WOS:000327487700400
ER
PT J
AU Gabay, O
Zaal, KJ
Sanchez, C
Dvir-Ginzberg, M
Gagarina, V
Song, YJ
He, XH
McBurney, MW
AF Gabay, Odile
Zaal, Kristien J.
Sanchez, Christelle
Dvir-Ginzberg, Mona
Gagarina, Viktoria
Song, Yingjie
He, Xiao Hong
McBurney, Michael W.
TI Sirt1-deficient mice exhibit an altered cartilage phenotype
SO JOINT BONE SPINE
LA English
DT Article
DE Sirtuin 1; Cartilage; Osteoarthritis; Animal models
ID HUMAN OSTEOARTHRITIC CHONDROCYTES; SIR2-ALPHA PROTEIN; STEM-CELLS;
SIRTUIN 1; APOPTOSIS; MAMMALS; PATHWAY; MOUSE
AB Objective: We previously demonstrated that Sirt1 regulates apoptosis in cartilage in vitro. Here we attempt to examine in vivo cartilage homeostasis, using Sirt1 total body knockout (KO) mice.
Method: Articular cartilage was harvested from hind paws of 1-week and 3-week-old mice carrying wild type (WT) or null Sirt1 gene. Knees of Sirt1 haploinsufficient mice also were examined, at 6 months. Joint cartilage was processed for histologic examination or biochemical analyses of chondrocyte cultures.
Results: We found that articular cartilage tissue sections from Sirt1 KO mice up to 3 weeks of age exhibited low levels of type 2 collagen, aggrecan, and glycosaminoglycan content. In contrast, protein levels of MMP-13 were elevated in the Sirt1 KO mice, leading to a potential increase of cartilage breakdown, already shown in the heterozygous mice. Additional results showed elevated chondrocyte apoptosis in Sirt1 KO mice, as compared to WT controls. In addition to these observations, PTP1b (protein tyrosine phosphatase b) was elevated in the Sirt1 KO mice, in line with previous reports.
Conclusion: The findings from this animal model demonstrated that Sirt1 KO mice presented an altered cartilage phenotype, with an elevated apoptotic process and a potential degradative cartilage process. Published by Elsevier Masson SAS.
C1 [Gabay, Odile; Gagarina, Viktoria] NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Bethesda, MD 20892 USA.
[Zaal, Kristien J.] NIAMSD, Light Imaging Sect, Off Sci & Technol, NIH, Bethesda, MD 20892 USA.
[Sanchez, Christelle] Univ Liege, Bone & Cartilage Res Unit, Inst Pathol B23, Liege, Belgium.
[Dvir-Ginzberg, Mona] Hebrew Univ Hadassah Ein Kerem, Fac Med Dent, Inst Dent Sci, Lab Cartilage Biol, Jerusalem, Israel.
[Song, Yingjie] Uniformed Serv Univ Hlth Sci, Dept Surg, Bethesda, MD 20814 USA.
[He, Xiao Hong; McBurney, Michael W.] Ottawa Hosp Res Inst, Ottawa, ON K1H 8L6, Canada.
RP Gabay, O (reprint author), NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM gabayo@mail.nih.gov
OI Dvir-Ginzberg, Mona/0000-0003-3089-6875
FU National Institutes of Arthritis and Musculoskeletal and Skin Diseases
of the National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institutes of Arthritis and Musculoskeletal and Skin Diseases
of the National Institutes of Health.
NR 26
TC 18
Z9 20
U1 2
U2 8
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 1297-319X
EI 1778-7254
J9 JOINT BONE SPINE
JI Joint Bone Spine
PD DEC
PY 2013
VL 80
IS 6
BP 613
EP 620
DI 10.1016/j.jbspin.2013.01.001
PG 8
WC Rheumatology
SC Rheumatology
GA 262XD
UT WOS:000327770300011
PM 23587642
ER
PT J
AU McCrae, RR
Chan, W
Jussim, L
De Fruyt, F
Lockenhoff, CE
De Bolle, M
Costa, PT
Hrebickova, M
Graf, S
Realo, A
Allik, J
Nakazato, K
Shimonaka, Y
Yik, M
Fickova, E
Brunner-Sciarra, M
Reatigui, N
de Figueora, NL
Schmidt, V
Ahn, CK
Ahn, HN
Aguilar-Vafaie, ME
Siuta, J
Szmigielska, B
Cain, TR
Crawford, JT
Mastor, KA
Rolland, JP
Nansubuga, F
Miramontez, DR
Benet-Martinez, V
Rossier, J
Bratko, D
Marusic, I
Halberstadt, J
Yamaguchi, M
Knezevic, G
Puric, D
Martin, TA
Gheorghiu, M
Smith, PB
Barbaranelli, C
Wang, L
Shakespeare-Finch, J
Lima, MP
Klinkosz, W
Sekowski, A
Alcalay, L
Simonetti, F
Avdeyeva, TV
Pramila, VS
Terracciano, A
AF McCrae, Robert R.
Chan, Wayne
Jussim, Lee
De Fruyt, Filip
Loeckenhoff, Corinna E.
De Bolle, Marleen
Costa, Paul T., Jr.
Hrebickova, Martina
Graf, Sylvie
Realo, Anu
Allik, Jueri
Nakazato, Katsuharu
Shimonaka, Yoshiko
Yik, Michelle
Fickova, Emilia
Brunner-Sciarra, Marina
Reatigui, Norma
Leibovich de Figueora, Nora
Schmidt, Vanina
Ahn, Chang-Kyu
Ahn, Hyun-Nie
Aguilar-Vafaie, Maria E.
Siuta, Jerzy
Szmigielska, Barbara
Cain, Thomas R.
Crawford, Jarret T.
Mastor, Khairul Anwar
Rolland, Jean-Pierre
Nansubuga, Florence
Miramontez, Daniel R.
Benet-Martinez, Veronica
Rossier, Jerome
Bratko, Denis
Marusic, Iris
Halberstadt, Jamin
Yamaguchi, Mami
Knezevic, Goran
Puric, Danka
Martin, Thomas A.
Gheorghiu, Mirona
Smith, Peter B.
Barbaranelli, Claudio
Wang, Lei
Shakespeare-Finch, Jane
Lima, Margarida P.
Klinkosz, Waldemar
Sekowski, Andrzej
Alcalay, Lidia
Simonetti, Franco
Avdeyeva, Tatyana V.
Pramila, V. S.
Terracciano, Antonio
TI The inaccuracy of national character stereotypes
SO JOURNAL OF RESEARCH IN PERSONALITY
LA English
DT Article
DE National character; Stereotypes; Five-Factor Model; Personality traits;
Cross-cultural
ID NEO-PI-R; SELF-REPORTED CONSCIENTIOUSNESS; CROSS-CULTURAL COMPARISONS;
PERSONALITY-TRAITS; 5-FACTOR MODEL; BIG 5; PROFILES; COUNTRIES;
PERCEPTIONS; UNIVERSAL
AB Consensual stereotypes of some groups are relatively accurate, whereas others are not. Previous work suggesting that national character stereotypes are inaccurate has been criticized on several grounds. In this article we (a) provide arguments for the validity of assessed national mean trait levels as criteria for evaluating stereotype accuracy and (b) report new data on national character in 26 cultures from descriptions (N= 3323) of the typical male or female adolescent, adult, or old person in each. The average ratings were internally consistent and converged with independent stereotypes of the typical culture member, but were weakly related to objective assessments of personality. We argue that this conclusion is consistent with the broader literature on the inaccuracy of national character stereotypes. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Chan, Wayne; Costa, Paul T., Jr.] Natl Inst Aging, Baltimore, MD USA.
[Jussim, Lee] Rutgers State Univ, Dept Psychol, New Brunswick, NJ 08903 USA.
[De Fruyt, Filip; De Bolle, Marleen] Univ Ghent, Dept Dev Personal & Social Psychol, B-9000 Ghent, Belgium.
[Loeckenhoff, Corinna E.] Cornell Univ, Dept Human Dev, Ithaca, NY USA.
[Hrebickova, Martina; Graf, Sylvie] Acad Sci Czech Republic, Inst Psychol, Brno, Czech Republic.
[Realo, Anu; Allik, Jueri] Univ Tartu, Dept Psychol, EE-50090 Tartu, Estonia.
[Allik, Jueri] Estonian Acad Sci, Tallinn, Estonia.
[Nakazato, Katsuharu] Iwate Prefectural Univ, Fac Social Welf, Takizawa, Iwate, Japan.
[Shimonaka, Yoshiko] Bunkyo Gakuin Univ, Dept Human Studies, Bunkyo, Japan.
[Yik, Michelle] Hong Kong Univ Sci & Technol, Div Social Sci, Kowloon, Hong Kong, Peoples R China.
[Fickova, Emilia] Slovak Acad Sci, Inst Expt Psychol, Bratislava, Slovakia.
[Brunner-Sciarra, Marina; Reatigui, Norma] Univ Peruana Cayetano Heredia, Fac Psychol, Lima, Peru.
[Leibovich de Figueora, Nora; Schmidt, Vanina] Univ Buenos Aires, Dept Psychol, Buenos Aires, DF, Argentina.
[Ahn, Chang-Kyu] Pusan Natl Univ, Dept Educ, Pusan, South Korea.
[Ahn, Hyun-Nie] Ewha Womans Univ, Dept Psychol, Seoul, South Korea.
[Aguilar-Vafaie, Maria E.] Tarbiat Modares Univ, Dept Psychol, Tehran, Iran.
[Siuta, Jerzy; Szmigielska, Barbara] Jagiellonian Univ, Inst Psychol, Krakow, Poland.
[Cain, Thomas R.] Hampshire Coll, Sch Cognit Sci, Amherst, MA 01002 USA.
[Crawford, Jarret T.] Coll New Jersey, Dept Psychol, Ewing, NJ USA.
[Mastor, Khairul Anwar] Univ Kebangsaan Malaysia, Personal Res Grp, Bangi, NJ, Malaysia.
[Rolland, Jean-Pierre] Univ Paris Ouest Nanterre Def, UFR STAPS, Nanterre, France.
[Nansubuga, Florence] Makerere Univ, Inst Psychol, Kampala, Uganda.
[Miramontez, Daniel R.] Off Inst Res & Planning, San Diego, CA USA.
[Benet-Martinez, Veronica] Univ Pompeu Fabra, ICREA, Barcelona, Spain.
[Benet-Martinez, Veronica] Univ Pompeu Fabra, Dept Polit & Social Sci, Barcelona, Spain.
[Rossier, Jerome] Univ Lausanne, Inst Psychol, Lausanne, Switzerland.
[Bratko, Denis] Univ Zagreb, Dept Psychol, Zagreb 41000, Croatia.
[Marusic, Iris] Inst Social Res Zagreb, Zagreb, Croatia.
[Halberstadt, Jamin; Yamaguchi, Mami] Univ Otago, Dept Psychol, Dunedin, New Zealand.
[Knezevic, Goran; Puric, Danka] Univ Belgrade, Dept Psychol, Belgrade, Serbia.
[Martin, Thomas A.] Susquehanna Univ, Dept Psychol, Selinsgrove, PA USA.
[Gheorghiu, Mirona] Queens Univ, Sch Psychol, Belfast, Antrim, North Ireland.
[Smith, Peter B.] Univ Sussex, Sch Psychol, Falmer, England.
[Barbaranelli, Claudio] Univ Roma La Sapienza, Dept Psychol, Rome, Italy.
[Wang, Lei] Peking Univ, Dept Psychol, Beijing 100871, Peoples R China.
[Shakespeare-Finch, Jane] Queensland Univ Technol, Sch Psychol & Counseling, Brisbane, Qld 4001, Australia.
[Lima, Margarida P.] Univ Coimbra, Fac Psychol & Educ Sci, Coimbra, Portugal.
[Klinkosz, Waldemar; Sekowski, Andrzej] John Paul II Cathol Univ Lublin, Dept Psychol, Lublin, Poland.
[Alcalay, Lidia; Simonetti, Franco] Pontificia Univ Catolica Chile, Escuela Psicol, Santiago, Chile.
[Avdeyeva, Tatyana V.] Univ St Thomas, Grad Sch Profess Psychol, Minneapolis, MN USA.
[Terracciano, Antonio] Florida State Univ, Coll Med, Dept Geriatr, Tallahassee, FL 32306 USA.
RP Terracciano, A (reprint author), Florida State Univ, Coll Med, 1115W Call St,Room 4425-B, Tallahassee, FL 32306 USA.
EM antonio.terracciano@med.fsu.edu
RI Rossier, Jerome/A-3494-2009; Benet-Martinez, Veronica/B-5398-2011;
Allik, Juri/D-5609-2009; Wang, Lei/D-2501-2016; Realo, Anu/M-9524-2016;
Sekowski, Andrzej/O-7807-2016; Graf, Sylvie/D-9732-2014; Hrebickova,
Martina/H-4410-2014;
OI Rossier, Jerome/0000-0002-9924-3672; Benet-Martinez,
Veronica/0000-0002-3352-9731; Allik, Juri/0000-0002-8358-4747; Wang,
Lei/0000-0002-6156-9028; Shakespeare-Finch, Jane/0000-0003-4237-1320;
Chan, Wayne/0000-0001-5061-1713; Graf, Sylvie/0000-0002-7810-5457;
Hrebickova, Martina/0000-0003-4356-567X; Loeckenhoff,
Corinna/0000-0003-1605-1323
NR 73
TC 10
Z9 10
U1 5
U2 47
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0092-6566
EI 1095-7251
J9 J RES PERS
JI J. Res. Pers.
PD DEC
PY 2013
VL 47
IS 6
BP 831
EP 842
DI 10.1016/j.jrp.2013.08.006
PG 12
WC Psychology, Social
SC Psychology
GA 267LI
UT WOS:000328098800017
ER
PT J
AU Pine, DS
AF Pine, Daniel S.
TI A 60-Year Climb on the Mountain of Nosology
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID CLASSIFICATION; PREVALENCE; DISORDERS
C1 NIMH, Intramural Res Program, Bethesda, MD 20892 USA.
RP Pine, DS (reprint author), NIMH, Intramural Res Program, 15K North Dr,MSC 2670, Bethesda, MD 20892 USA.
EM Daniel.pine@Nih.gov
FU Intramural NIH HHS
NR 9
TC 1
Z9 1
U1 1
U2 4
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 DEC
PY 2013
VL 52
IS 12
BP 1251
EP 1254
DI 10.1016/j.jaac.2013.08.023
PG 4
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 266HG
UT WOS:000328014100003
PM 24290456
ER
PT J
AU Dougherty, LR
Smith, VC
Bufferd, SJ
Stringaris, A
Leibenluft, E
Carlson, GA
Klein, DN
AF Dougherty, Lea R.
Smith, Victoria C.
Bufferd, Sara J.
Stringaris, Argyris
Leibenluft, Ellen
Carlson, Gabrielle A.
Klein, Daniel N.
TI Preschool Irritability: Longitudinal Associations With Psychiatric
Disorders at Age 6 and Parental Psychopathology
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE irritability; longitudinal; mood dysregulation; preschool
ID DIAGNOSTIC INTERVIEW; MOOD DYSREGULATION; MENTAL-DISORDERS; YOUTH;
CHILDHOOD; CHILDREN; OPPOSITIONALITY; PREVALENCE; DIMENSIONS; TELEPHONE
AB Objective: There is increasing scientific and clinical attention to chronic irritability in youth. However, little is known about the predictive validity and clinical significance of chronic irritability during early childhood. This prospective, longitudinal study examined associations of chronic irritability with psychiatric disorders and parental psychopathology in a large community sample of preschoolers. Method: Four hundred sixty-two preschool-age children were assessed at 3 and 6 years of age. Child psychopathology was assessed at baseline (3 years) and follow-up (6 years) using a diagnostic interview, the Preschool Age Psychiatric Assessment, with parents. Items from the Preschool Age Psychiatric Assessment were used to create a dimensional measurement of chronic irritability. Parental psychopathology was assessed with a diagnostic interview at baseline. Results: Chronic irritability was concurrently associated with a wide range of psychiatric disorders and functional impairment at 3 and 6 years of age. Irritability at 3 years predicted depression, oppositional defiant disorder, and functional impairment at 6 years after controlling for baseline disorders. Irritability also was associated with parental depression and anxiety. Conclusions: Findings underscore the central role of irritability in early-emerging mental health problems. They are consistent with longitudinal studies in older youth indicating that chronic irritability predicts later depression and anxiety and support the importance of early detection and interventions targeting preschool irritability.
C1 [Dougherty, Lea R.; Smith, Victoria C.] Univ Maryland, College Pk, MD 20742 USA.
[Bufferd, Sara J.] Calif State Univ, San Marcos, TX USA.
[Stringaris, Argyris] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
[Leibenluft, Ellen] NIMH, Bipolar Spectrum Disorders Emot & Dev Branch, Bethesda, MD USA.
[Carlson, Gabrielle A.; Klein, Daniel N.] Stony Brook Sch Med, Stony Brook, NY USA.
[Klein, Daniel N.] SUNY Stony Brook, Stony Brook, NY USA.
RP Dougherty, LR (reprint author), Univ Maryland, Dept Psychol, College Pk, MD 20742 USA.
EM ldougher@umd.edu
FU National Institute of Mental Health [R01 MH069942]; General Clinical
Research Center from Stony Brook University, National Center for
Research Resources [M01 RR10710]
FX This research was supported by National Institute of Mental Health grant
R01 MH069942 (D.K.N.) and General Clinical Research Center grant M01
RR10710 from Stony Brook University, National Center for Research
Resources.
NR 33
TC 22
Z9 22
U1 1
U2 20
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 DEC
PY 2013
VL 52
IS 12
BP 1304
EP 1313
DI 10.1016/j.jaac.2013.09.007
PG 10
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 266HG
UT WOS:000328014100010
PM 24290463
ER
PT J
AU Strazzula, L
Brown, KK
Brieva, JC
Camp, BJ
Frankel, HC
Kissin, E
Mahlberg, MJ
Mina, MA
Pomeranz, MK
Brownell, I
Kroshinsky, D
AF Strazzula, Lauren
Brown, Katherine K.
Brieva, Joaquin C.
Camp, Brendan J.
Frankel, Hillary C.
Kissin, Eugene
Mahlberg, Matthew J.
Mina, Mary Alice
Pomeranz, Miriam K.
Brownell, Isaac
Kroshinsky, Daniela
TI Levamisole toxicity mimicking autoimmune disease
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Article
DE antineutrophil cytoplasmic antibody; cocaine; granulomatosis with
polyangiitis (Wegener); levamisole; purpura; vasculitis; vasculopathy
ID INDUCED VASCULITIS; RETIFORM PURPURA; COCAINE; NEUTROPENIA; EARS
AB Background: Levamisole is present as a contaminant or additive in most cocaine sold in the United States. Cases of agranulocytosis attributed to levamisole-tainted cocaine have been widely described. A vasculopathic reaction to levamisole has also been reported; however, diagnostic features such as antineutrophil cytoplasmic antibody (ANCA) and additional autoimmune marker positivity are not well recognized. As such, many patients are given a misdiagnosis, prompting aggressive and often unnecessary treatment.
Objective: We hope to educate practitioners about the clinical and laboratory features of levamisole-induced vasculopathy to ensure accurate diagnosis and management.
Methods: This was a case series.
Results: Six patients were admitted with purpuric lesions and vasculitic changes on biopsy specimen; 5 of them were given the diagnosis of and treated for autoimmune conditions before their true diagnosis was revealed. All patients had ANCA positivity, and 4 had additional abnormalities in autoimmune markers. All patients reported recent cocaine abuse, and were ultimately given the diagnosis of levamisole-induced vasculopathy.
Limitations: This observational study is limited by sample size.
Conclusions: Patients presenting with purpuric lesions with ANCA positivity should be assessed for cocaine exposure. It is important to recognize that levamisole may not only induce ANCA positivity but also other autoimmune marker abnormalities. Patients can often be treated with less aggressive therapeutic strategies than what is used for primary ANCA-associated vasculitides.
C1 [Strazzula, Lauren; Frankel, Hillary C.; Mina, Mary Alice; Kroshinsky, Daniela] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Brown, Katherine K.; Brieva, Joaquin C.] Northwestern Univ, Feinberg Sch Med, Dept Dermatol, Chicago, IL 60611 USA.
[Camp, Brendan J.] New York Presbyterian Hosp, Dept Dermatol, New York, NY USA.
[Camp, Brendan J.] Weill Cornell Med Ctr, New York, NY USA.
[Frankel, Hillary C.; Mina, Mary Alice; Kroshinsky, Daniela] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Kissin, Eugene] Boston Univ, Dept Rheumatol, Boston, MA 02215 USA.
[Mahlberg, Matthew J.; Pomeranz, Miriam K.] NYU, Med Ctr, Ronald O Perelman Dept Dermatol, New York, NY 10003 USA.
[Brownell, Isaac] NCI, Dermatol Branch, Bethesda, MD 20892 USA.
RP Kroshinsky, D (reprint author), Dermatol Associates, 50 Staniford St,2nd Floor, Boston, MA 02114 USA.
EM dkroshinsky@partners.org
OI Pomeranz, Miriam Keltz/0000-0002-6959-9280
NR 15
TC 7
Z9 7
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD DEC
PY 2013
VL 69
IS 6
BP 954
EP 959
DI 10.1016/j.jaad.2013.07.037
PG 6
WC Dermatology
SC Dermatology
GA 262LN
UT WOS:000327736900029
PM 24075227
ER
PT J
AU Aung, PP
Ballester, LY
Abdullaev, Z
Pack, SD
Cummins, DL
Mahalingam, M
AF Aung, Phyu P.
Ballester, Leomar Y.
Abdullaev, Zied
Pack, Svetlana D.
Cummins, Deborah L.
Mahalingam, Meera
TI ER/PR positive epidermotropic primary cutaneous eccrine carcinoma as a
cutaneous manifestation of MEN 2B
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Letter
C1 [Aung, Phyu P.; Mahalingam, Meera] Boston Univ, Sch Med, Dept Dermatol, Dermatopathol Sect, Boston, MA 02118 USA.
[Cummins, Deborah L.] Boston Univ, Sch Med, Dept Dermatol, Boston, MA 02118 USA.
[Ballester, Leomar Y.; Abdullaev, Zied; Pack, Svetlana D.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Mahalingam, M (reprint author), Boston Univ, Sch Med, Dept Dermatol, Dermatopathol Sect, 609 Albany St,J-301, Boston, MA 02118 USA.
EM mmahalin@bu.edu
RI Pack, Svetlana/C-2020-2014
NR 5
TC 1
Z9 1
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD DEC
PY 2013
VL 69
IS 6
BP E310
EP E312
DI 10.1016/j.jaad.2013.08.001
PG 4
WC Dermatology
SC Dermatology
GA 262LN
UT WOS:000327736900014
PM 24238193
ER
PT J
AU Helms, CC
Marvel, M
Zhao, W
Stahle, M
Vest, R
Kato, GJ
Lee, JS
Christ, G
Gladwin, MT
Hantgan, RR
Kim-Shapiro, DB
AF Helms, C. C.
Marvel, M.
Zhao, W.
Stahle, M.
Vest, R.
Kato, G. J.
Lee, J. S.
Christ, G.
Gladwin, M. T.
Hantgan, R. R.
Kim-Shapiro, D. B.
TI Mechanisms of hemolysis-associated platelet activation
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE hemoglobin; hemolysis; nitric oxide; platelets; red blood cells
ID SICKLE-CELL-DISEASE; RED-BLOOD-CELLS; NITRIC-OXIDE BIOAVAILABILITY;
PULMONARY-HYPERTENSION; FREE HEMOGLOBIN; BLEEDING-TIME; AGGREGATION;
ERYTHROCYTES; RATS; HYPERCOAGULABILITY
AB BackgroundIntravascular hemolysis occurs after blood transfusion, in hemolytic anemias, and in other conditions, and is associated with hypercoagulable states. Hemolysis has been shown to potently activate platelets invitro and invivo, and several mechanisms have been suggested to account for this, including: (i) direct activation by hemoglobin (Hb); (ii) increase in reactive oxygen species (ROS); (iii) scavenging of nitric oxide (NO) by released Hb; and (iv) release of intraerythrocytic ADP.
ObjectiveTo elucidate the mechanism of hemolysis-mediated platelet activation.
MethodsWe used flow cytometry to detect PAC-1 binding to activated platelets for invitro experiments, and a Siemens' Advia120 hematology system to assess platelet aggregation by using platelet counts from invivo experiments in a rodent model.
ResultsWe found that Hb did not directly activate platelets. However, ADP bound to Hb could cause platelet activation. Furthermore, platelet activation caused by shearing of red blood cells (RBCs) was reduced in the presence of apyrase, which metabolizes ADP to AMP. The use of ROS scavengers did not affect platelet activation. We also found that cell-free Hb enhanced platelet activation by abrogating the inhibitory effect of NO on platelet activation. Invivo infusions of ADP and purified (ADP-free) Hb, as well as hemolysate, resulted in platelet aggregation, as shown by decreased platelet counts.
ConclusionTwo primary mechanisms account for RBC hemolysis-associated platelet activation: ADP release, which activates platelets; and cell-free Hb release, which enhances platelet activation by lowering NO bioavailability.
C1 [Helms, C. C.] Univ Richmond, Dept Phys, Richmond, VA 23173 USA.
[Marvel, M.; Vest, R.; Kim-Shapiro, D. B.] Wake Forest Univ, Dept Phys, Winston Salem, NC 27109 USA.
[Zhao, W.; Christ, G.] Wake Forest Inst Regenerat Med, Winston Salem, NC USA.
[Stahle, M.; Hantgan, R. R.] Wake Forest Univ, Sch Med, Dept Biochem, Winston Salem, NC 27109 USA.
[Kato, G. J.] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
[Lee, J. S.; Gladwin, M. T.] Univ Pittsburgh, Dept Med, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Lee, J. S.; Gladwin, M. T.] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
[Kim-Shapiro, D. B.] Wake Forest Univ, Translat Sci Ctr, Winston Salem, NC 27109 USA.
RP Kim-Shapiro, DB (reprint author), Wake Forest Univ, Dept Phys, Olin Phys Lab, 1834 Wake Forest Rd, Winston Salem, NC 27109 USA.
EM shapiro@wfu.edu
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU NIH [HL058091, HL098032, 1 ZIA HL006014]; Harbert Family Distinguished
Chair funds
FX This work was supported by NIH grants HL058091 and HL098032, and Harbert
Family Distinguished Chair funds. G. J. Kato was supported by the NIH
Intramural Program 1 ZIA HL006014.
NR 46
TC 25
Z9 26
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
EI 1538-7836
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD DEC
PY 2013
VL 11
IS 12
BP 2148
EP 2154
DI 10.1111/jth.12422
PG 7
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 266DQ
UT WOS:000328003900009
PM 24119131
ER
PT J
AU Kopp, JB
AF Kopp, Jeffrey B.
TI JC viruria and kidney disease in APOL1 risk genotype individuals: is
this a clue to a gene x environment interaction?
SO KIDNEY INTERNATIONAL
LA English
DT Editorial Material
ID AFRICAN-AMERICANS; MERKEL CELL; VARIANTS ASSOCIATE; HUMAN POLYOMAVIRUS;
NEPHROPATHY; BK; TRANSPLANTATION; IDENTIFICATION
AB APOL1 nephropathy occurs in a minority of genetically at-risk individuals, suggesting that other factors, such as other genes or environmental factors, contribute. Divers and colleagues report that among individuals with two APOL1 risk alleles, those with JC viruria are less likely to manifest kidney disease compared with those lacking JC viruria. These data might suggest that JC virus infection confers protection against glomerular injury, perhaps by altering cell function or generating immunity against a related polyomavirus.
C1 NIDDK, Kidney Dis Sect, Kidney Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Kopp, JB (reprint author), NIDDK, Kidney Dis Sect, Kidney Dis Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM jbkopp@nih.gov
OI Kopp, Jeffrey/0000-0001-9052-186X
FU Intramural NIH HHS
NR 30
TC 6
Z9 6
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD DEC
PY 2013
VL 84
IS 6
BP 1069
EP 1072
DI 10.1038/ki.2013.299
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 264ND
UT WOS:000327884000003
PM 24280748
ER
PT J
AU Thapa, M
Bommakanti, A
Shamsuzzaman, M
Gregory, B
Samsel, L
Zengel, JM
Lindahl, L
AF Thapa, Mamata
Bommakanti, Ananth
Shamsuzzaman, Md
Gregory, Brian
Samsel, Leigh
Zengel, Janice M.
Lindahl, Lasse
TI Repressed synthesis of ribosomal proteins generates protein-specific
cell cycle and morphological phenotypes
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID DIAMOND-BLACKFAN ANEMIA; SACCHAROMYCES-CEREVISIAE; ASSEMBLY FACTORS;
YEAST RRP14P; BIOGENESIS; RNA; SIZE; 40S; MATURATION; ACTIVATION
AB The biogenesis of ribosomes is coordinated with cell growth and proliferation. Distortion of the coordinated synthesis of ribosomal components affects not only ribosome formation, but also cell fate. However, the connection between ribosome biogenesis and cell fate is not well understood. To establish a model system for inquiries into these processes, we systematically analyzed cell cycle progression, cell morphology, and bud site selection after repression of 54 individual ribosomal protein (r-protein) genes in Saccharomyces cerevisiae. We found that repression of nine 60S r-protein genes results in arrest in the G2/M phase, whereas repression of nine other 60S and 22 40S r-protein genes causes arrest in the G1 phase. Furthermore, bud morphology changes after repression of some r-protein genes. For example, very elongated buds form after repression of seven 60S r-protein genes. These genes overlap with, but are not identical to, those causing the G2/M cell cycle phenotype. Finally, repression of most r-protein genes results in changed sites of bud formation. Strikingly, the r-proteins whose repression generates similar effects on cell cycle progression cluster in the ribosome physical structure, suggesting that different topological areas of the precursor and/or mature ribosome are mechanistically connected to separate aspects of the cell cycle.
C1 [Thapa, Mamata; Bommakanti, Ananth; Shamsuzzaman, Md; Gregory, Brian; Zengel, Janice M.; Lindahl, Lasse] Univ Maryland Baltimore Cty, Dept Biol Sci, Baltimore, MD 21250 USA.
[Samsel, Leigh] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
RP Lindahl, L (reprint author), Univ Maryland Baltimore Cty, Dept Biol Sci, Baltimore, MD 21250 USA.
EM lindahl@umbc.edu
FU National Science Foundation [MCB0349443, 0920578, DBI-0722569]; National
Institute of General Medical Sciences [P41-GM103311]
FX We thank Susan Fretz for help with strain construction and Philipp
Milkereit and John Woolford for strains. We also thank John Woolford for
helpful discussions. We gratefully acknowledge our departmental
colleagues (Suzanne Rosenberg, Stephen Miller, Michelle Starz-Gaiano,
Rachel Brewster, and Chere Petty) for use of and help with flow
cytometer and microscopes. We thank the National Heart, Lung and Blood
Institute at the National Institutes of Health for use of the Flow
Cytometry Core Facility. This work was supported by National Science
Foundation Grants MCB0349443 and 0920578 to J.M.Z. and L. L. and
National Science Foundation Major Research Instrumentation Grant
DBI-0722569 to D. B. and T. G. Finally, we acknowledge the use of the
UCSF Chimera Package supported by National Institute of General Medical
Sciences Grant P41-GM103311.
NR 63
TC 7
Z9 7
U1 1
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 DEC 1
PY 2013
VL 24
IS 23
BP 3620
EP 3633
DI 10.1091/mbc.E13-02-0097
PG 14
WC Cell Biology
SC Cell Biology
GA 267UZ
UT WOS:000328125100004
PM 24109599
ER
PT J
AU Jain, N
Miu, B
Jiang, JK
McKinstry, KK
Prince, A
Swain, SL
Greiner, DL
Thomas, CJ
Sanderson, MJ
Berg, LJ
Kang, J
AF Jain, Nitya
Miu, Bing
Jiang, Jian-kang
McKinstry, Kai K.
Prince, Amanda
Swain, Susan L.
Greiner, Dale L.
Thomas, Craig J.
Sanderson, Michael J.
Berg, Leslie J.
Kang, Joonsoo
TI CD28 and ITK signals regulate autoreactive T cell trafficking
SO NATURE MEDICINE
LA English
DT Article
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; COSTIMULATORY MOLECULES;
B7/CD28 COSTIMULATION; ACTIN CYTOSKELETON; DEFICIENT MICE; ACTIVATION;
CTLA-4; ANTIGEN; FAMILY; MOUSE
AB Activation of self-reactive T cells and their trafficking to target tissues leads to autoimmune organ destruction. Mice lacking the co-inhibitory receptor cytotoxic T lymphocyte antigen-4 (CTLA-4) develop fatal autoimmunity characterized by lymphocytic infiltration into nonlymphoid tissues. Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues. Concurrent ablation of the CD28-activated Tec family kinase Ilk does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs. Despite excessive spontaneous T cell activation and proliferation in lymphoid organs, Itk(-/-); Ctla4(-/-) mice are otherwise healthy, mount antiviral immune responses and exhibit a long lifespan. We propose that ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses. Notably, ITK inhibitors mimic the null mutant phenotype and also prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes, highlighting their potential utility for the treatment of human autoimmune disorders.
C1 [Jain, Nitya; Miu, Bing; McKinstry, Kai K.; Prince, Amanda; Swain, Susan L.; Berg, Leslie J.; Kang, Joonsoo] Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01605 USA.
[Jiang, Jian-kang; Thomas, Craig J.] NIH, Chem Genom Ctr, Rockville, MD USA.
[Greiner, Dale L.] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA.
[Sanderson, Michael J.] Univ Massachusetts, Sch Med, Dept Microbiol & Physiol Syst, Worcester, MA 01605 USA.
RP Kang, J (reprint author), Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01605 USA.
EM joonsoo.kang@umassmed.edu
FU US National Institutes of Health (NIH) [AI46629, AI050864, AI046530,
AI083505, RC1 DK086474]; Molecular Libraries Initiative; Intramural
Research Program of the NIH National Human Genome Research Institute
FX We thank E. Huseby, B. Seed and R. Friedline for discussion, S. Turley
for advice with stromal cells, T. Hunig (University of Wurzburg) for the
SACD28 antibody, M. Coles for assistance with microscopy, M. Krummel for
advice on imaging, D. Serreze for studies with diabetogenic
CD8+ T cells, E. Huseby (University of Massachusetts Medical
School) for MHC class II-deficient Rag1-/- mice and R. Welsh
for the LCMV infection protocol. Core resources supported by the
University of Massachusetts Medical School Diabetes Endocrinology
Research Center grant DK32520 were used. This work was supported by US
National Institutes of Health (NIH) grants to D.L.G. (AI46629,
AI050864), S.L.S. (AI046530), L.J.B. (AI083505) and J.K. (RC1 DK086474
and AI083505). US NIH Chemical Genomics Center was supported by the
Molecular Libraries Initiative and the Intramural Research Program of
the NIH National Human Genome Research Institute.
NR 58
TC 19
Z9 19
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2013
VL 19
IS 12
BP 1632
EP 1637
DI 10.1038/nm.3393
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 268OW
UT WOS:000328181400032
PM 24270545
ER
PT J
AU Park, SH
Veerapu, NS
Shin, EC
Biancotto, A
McCoy, JP
Capone, S
Folgori, A
Rehermann, B
AF Park, Su-Hyung
Veerapu, Naga Suresh
Shin, Eui-Cheol
Biancotto, Angelique
McCoy, J. Philip
Capone, Stefania
Folgori, Antonella
Rehermann, Barbara
TI Subinfectious hepatitis C virus exposures suppress T cell responses
against subsequent acute infection
SO NATURE MEDICINE
LA English
DT Article
ID INJECTION-DRUG USERS; IMMUNE-RESPONSES; REGULATORY CELLS; IN-VIVO;
RECOVERED CHIMPANZEES; MEMORY; HCV; PERSISTENCE; SEROCONVERSION;
RECHALLENGE
AB Hepatitis C virus (HCV) is endemic in many countries due to its high propensity for establishing persistence(1). The presence of HCV-specific T cells in subjects repeatedly exposed to HCV who test negative for HCV RNA and antibodies and who do not have any history of HCV infection has been interpreted as T cell-mediated protection(2-5). Here, we show in nonhuman primates that repeated exposure to human plasma with trace amounts of HCV induced HCV-specific T cells without seroconversion and systemic viremia but did not protect upon subsequent HCV challenge. Rather, HCV-specific recall and de novo T cell responses, as well as intrahepatic T cell recruitment and interferon-gamma (IFN-gamma) production, were suppressed upon HCV challenge, concomitant with quantitative and qualitative changes in regulatory T cells (T-reg cells) that occurred after subinfectious HCV exposure and increased after HCV challenge. In vitro T-reg cell depletion restored HCV-specific T cell responses. Thus, T cells primed by trace amounts of HCV do not generate effective recall responses upon subsequent HCV infection. Subinfectious HCV exposure predisposes to T-reg cell expansion, which suppresses effector T cells during subsequent infection. Strategies to reverse this exposure-induced immune suppression should be examined to aid in the development of T cell-based vaccines against HCV and other endemic pathogens.
C1 [Park, Su-Hyung; Veerapu, Naga Suresh; Shin, Eui-Cheol; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Biancotto, Angelique; McCoy, J. Philip] NHLBI, Flow Cytometry Core Facil, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Capone, Stefania; Folgori, Antonella] Okairos, Rome, Italy.
RP Rehermann, B (reprint author), NIDDK, Immunol Sect, Liver Dis Branch, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM rehermann@nih.gov
RI Park, Su-Hyung/N-3514-2014; Shin, Eui-Cheol/C-1690-2011;
OI Capone, Stefania/0000-0002-2272-120X
FU intramural research program of the NIDDK
FX We thank T.J. Rowell, J. Fontenot and the staff at New Iberia Research
Center for the care of the chimpanzees and technical support and L. Holz
(NIDDK) and W. Kastenmuller (NIAID) for discussion and reading of the
manuscript. This work was supported by the intramural research program
of the NIDDK.
NR 40
TC 22
Z9 26
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2013
VL 19
IS 12
BP 1638
EP 1642
DI 10.1038/nm.3408
PG 5
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 268OW
UT WOS:000328181400033
PM 24270546
ER
PT J
AU Madan, RA
Gulley, JL
AF Madan, Ravi A.
Gulley, James L.
TI PROSTATE CANCER Intermediate efficacy end points to assess modern
therapies
SO NATURE REVIEWS UROLOGY
LA English
DT Editorial Material
ID METASTASIS-FREE SURVIVAL; PHASE-3; DISEASE; TRIALS; MEN
AB A retrospective, single institution study of 450 men with biochemical recurrence after radical prostatectomy included 140 men with androgen deprivation therapy deferred until metastatic disease onset. Metastasis-free survival was an independent predictor of overall survival. This research highlights the need to develop appropriate intermediate end points to expedite prostate cancer treatment.
C1 [Madan, Ravi A.; Gulley, James L.] NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Gulley, JL (reprint author), NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, 10 Ctr Dr,Room 8B09, Bethesda, MD 20892 USA.
EM gulleyj@mail.nih.gov
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
NR 10
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 1759-4812
EI 1759-4820
J9 NAT REV UROL
JI Nat. Rev. Urol.
PD DEC
PY 2013
VL 10
IS 12
BP 686
EP 687
DI 10.1038/nrurol.2013.269
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 267VT
UT WOS:000328127100003
PM 24276080
ER
PT J
AU Lapkouski, M
Tian, L
Miller, JT
Le Grice, SFJ
Yang, W
AF Lapkouski, Mikalai
Tian, Lan
Miller, Jennifer T.
Le Grice, Stuart F. J.
Yang, Wei
TI Structural requirements for RNA degradation by HIV-1 reverse
transcriptase reply
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Letter
ID RNA/DNA HYBRID; COMPLEX; DNA
C1 [Lapkouski, Mikalai; Tian, Lan; Yang, Wei] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Miller, Jennifer T.; Le Grice, Stuart F. J.] NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA.
RP Lapkouski, M (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM wei.yang@nih.gov
FU Intramural NIH HHS [Z01 DK036144-02]
NR 6
TC 1
Z9 1
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
EI 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD DEC
PY 2013
VL 20
IS 12
BP 1342
EP 1343
PG 2
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 266FA
UT WOS:000328007600002
PM 24304911
ER
PT J
AU Bartesaghi, A
Merk, A
Borgnia, MJ
Milne, JLS
Subramaniam, S
AF Bartesaghi, Alberto
Merk, Alan
Borgnia, Mario J.
Milne, Jacqueline L. S.
Subramaniam, Sriram
TI Prefusion structure of trimeric HIV-1 envelope glycoprotein determined
by cryo-electron microscopy
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID VIRAL MEMBRANE-FUSION; INFLUENZA-VIRUS; MOLECULAR ARCHITECTURE; POTENT
NEUTRALIZATION; HUMAN-ANTIBODY; GP120 CORE; CRYO-EM; HEMAGGLUTININ;
TOMOGRAPHY; RESOLUTION
AB The activation of trimeric HIV-1 envelope glycoprotein (Env) by its binding to the cell-surface receptor CD4 and co-receptors (CCR5 or CXCR4) represents the first of a series of events that lead to fusion between viral and target-cell membranes. Here, we present the cryo-EM structure, at subnanometer resolution (similar to 6 angstrom at 0.143 FSC), of the 'closed', prefusion state of trimeric HIV-1 Env complexed to the broadly neutralizing antibody VRC03. We show that three gp41 helices at the core of the trimer serve as an anchor around which the rest of Env is reorganized upon activation to the 'open' quaternary conformation. The architecture of trimeric HIV-1 Env in the prefusion state and in the activated intermediate state resembles the corresponding states of influenza hemagglutinin trimers, thus providing direct evidence for the similarity in entry mechanisms used by HIV-1, influenza and related enveloped viruses.
C1 [Bartesaghi, Alberto; Merk, Alan; Borgnia, Mario J.; Milne, Jacqueline L. S.; Subramaniam, Sriram] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Subramaniam, S (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM ss1@nih.gov
FU Center for Cancer Research at the National Cancer Institute, US National
Institutes of Health (NIH); NIH Intramural AIDS Targeted Antiviral
Program
FX This work was supported by funds to S.S. and J.L.S.M. from the Center
for Cancer Research at the National Cancer Institute, US National
Institutes of Health (NIH), and to S.S. from the NIH Intramural AIDS
Targeted Antiviral Program. We thank J. Mascola (Vaccine Research
Center, NIH) for providing VRC03 antibodies; K. Kang and W. Olson
(Progenies) for providing soluble KNH1144 gp140 trimers; S. Fellini, S.
Chacko and their colleagues for continued support with use of the
Biowulf cluster for computing at NIH; D. Schauder and H. He for
assistance with data collection; P. Rao and the NIH-FEI Living Lab for
Structural Biology for assistance with collection of the tilt-pair
images; and L. Earl for helpful discussions and comments.
NR 39
TC 82
Z9 82
U1 6
U2 34
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
EI 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD DEC
PY 2013
VL 20
IS 12
BP 1352
EP 1357
DI 10.1038/nsmb.2711
PG 6
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 266FA
UT WOS:000328007600006
PM 24154805
ER
PT J
AU Low, LA
AF Low, Lucie A.
TI The impact of pain upon cognition: What have rodent studies told us?
SO PAIN
LA English
DT Review
ID DECISION-MAKING TASK; INFLAMMATORY PAIN; PREFRONTAL CORTEX; NEUROPATHIC
PAIN; CHRONIC MORPHINE; RISK-ASSESSMENT; RAT MODEL; BEHAVIOR; DEFICITS;
MEMORY
C1 NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
RP Low, LA (reprint author), NIH, Natl Ctr Complementary & Alternat Med, 35 Convent Dr,Room 1C-1012, Bethesda, MD 20892 USA.
EM lucie.low@nih.gov
OI Low, Lucie/0000-0001-6082-8625
FU Intramural Research Program of the NIH
FX This research was supported (in part) by the Intramural Research Program
of the NIH. Thanks are due to M. Catherine Bushnell, Mark Pitcher, David
Seminowicz, Wiebke Gandhi, and Susanne Becker for critical reading and
helpful suggestions.
NR 36
TC 6
Z9 6
U1 5
U2 21
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
EI 1872-6623
J9 PAIN
JI Pain
PD DEC
PY 2013
VL 154
IS 12
BP 2603
EP 2605
DI 10.1016/j.pain.2013.06.012
PG 3
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 260LK
UT WOS:000327596200007
PM 23774574
ER
PT J
AU Person, RJ
Tokar, EJ
Xu, YY
Orihuela, R
Ngalame, NNO
Waalkes, MP
AF Person, Rachel J.
Tokar, Erik J.
Xu, Yuanyuan
Orihuela, Ruben
Ngalame, Ntube N. Olive
Waalkes, Michael P.
TI Chronic cadmium exposure in vitro induces cancer cell characteristics in
human lung cells
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Cadmium; Human lung cells; Transformation; Adaptation; Lung cancer;
Epithelial-to-mesenchymal transition
ID INDUCED MALIGNANT-TRANSFORMATION; EPITHELIAL-MESENCHYMAL TRANSITION;
INDUCED OXIDATIVE STRESS; ZINC TRANSPORTERS; EXPRESSION;
METALLOTHIONEIN; PROGNOSIS; TESTIS; FAMILY; GENE
AB Cadmium is a known human lung carcinogen. Here, we attempt to develop an in vitro model of cadmium-induced human lung carcinogenesis by chronically exposing the peripheral lung epithelia cell line, HPL-1D, to a low level of cadmium. Cells were chronically exposed to 5 mu M cadmium, a noncytotoxic level, and monitored for acquired cancer characteristics. By 20 weeks of continuous cadmium exposure, these chronic cadmium treated lung (CCT-LC) cells showed marked increases in secreted MMP-2 activity (3.5-fold), invasion (3.4-fold), and colony formation in soft agar (2-fold). CCT-LC cells were hyperproliferative, grew well in serum-free media, and overexpressed cyclin D1. The CCT-LC cells also showed decreased expression of the tumor suppressor genes p16 and SLC38A3 at the protein levels. Also consistent with an acquired cancer cell phenotype, CCT-LC cells showed increased expression of the oncoproteins K-RAS and N-RAS as well as the epithelial-to-mesenchymal transition marker protein Vimentin. Metallothionein (MT) expression is increased by cadmium, and is typically overexpressed in human lung cancers. The major MT isoforms, MT-1A and MT-2A were elevated in CCT-LC cells. Oxidant adaptive response genes HO-1 and HIF-1A were also activated in CCT-LC cells. Expression of the metal transport genes ZNT-1, ZNT-5, and ZIP-8 increased in CCT-LC cells culminating in reduced cadmium accumulation, suggesting adaptation to the metal. Overall, these data suggest that exposure of human lung epithelial cells to cadmium causes acquisition of cancer cell characteristics. Furthermore, transformation occurs despite the cell's ability to adapt to chronic cadmium exposure. Published by Elsevier Inc.
C1 [Person, Rachel J.; Tokar, Erik J.; Xu, Yuanyuan; Orihuela, Ruben; Ngalame, Ntube N. Olive; Waalkes, Michael P.] NIEHS, Div Natl Toxicol Program, Natl Toxicol Program Lab, Inorgan Toxicol Grp, Res Triangle Pk, NC 27709 USA.
RP Waalkes, MP (reprint author), Div Natl Toxicol Program Lab, 111 TW Alexander Dr,MD E1-07, Res Triangle Pk, NC 27709 USA.
EM waalkes@niehs.nih.gov
OI ORIHUELA, RUBEN/0000-0001-6718-6194
FU Intramural NIH HHS [ZIA ES102925-03, ZIA ES102925-02]
NR 60
TC 22
Z9 25
U1 4
U2 19
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD DEC 1
PY 2013
VL 273
IS 2
BP 281
EP 288
DI 10.1016/j.taap.2013.06.013
PG 8
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 267LP
UT WOS:000328099500005
PM 23811327
ER
PT J
AU Emond, C
Sanders, JM
Wikoff, D
Birnbaum, LS
AF Emond, Claude
Sanders, J. Michael
Wikoff, Daniele
Birnbaum, Linda S.
TI Proposed mechanistic description of dose-dependent BDE-47 urinary
elimination in mice using a physiologically based pharmacokinetic model
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE PBPK; PBDE; BDE-47; m-MUP; P-gp; Mouse
ID POLYBROMINATED DIPHENYL ETHERS; P-GLYCOPROTEIN; HOUSE MOUSE;
METHYLSULFONYL METABOLITE; POLYCHLORINATED BIPHENYL; MOLECULAR
HETEROGENEITY; TISSUE DISTRIBUTION; GENETIC-VARIATION; RISK-ASSESSMENT;
PROTEINS
AB Polybrominated diphenyl ethers (PBDEs) have been used in a wide variety of consumer applications as additive flame retardants. In North America, scientists have noted continuing increases in the levels of PBDE congeners measured in human serum. Some recent studies have found that PBDEs are associated with adverse health effects in humans, in experimental animals, and wildlife. This laboratory previously demonstrated that urinary elimination of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) is saturable at high doses in mice; however, this dose-dependent urinary elimination has not been observed in adult rats or immature mice. Thus, the primary objective of this study was to examine the mechanism of urinary elimination of BDE-47 in adult mice using a physiologically based pharmacokinetic (PBPK) model. To support this objective, additional laboratory data were collected to evaluate the predictions of the PBPK model using novel information from adult multi-drug resistance 1a/b knockout mice. Using the PBPK model, the roles of mouse major urinary protein (a blood protein carrier) and P-glycoprotein (an apical membrane transporter in proximal tubule cells in the kidneys, brain, intestines, and liver) were investigated in BDE-47 elimination. The resulting model and new data supported the major role of m-MUP in excretion of BDE-47 in the urine of adult mice, and a lesser role of P-gp as a transporter of BDE-47 in mice. This work expands the knowledge of BDE-47 kinetics between species and provides information for determining the relevancy of these data for human risk assessment purposes. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Emond, Claude] BioSimulat Consulting Inc, Newark, DE USA.
[Emond, Claude] Univ Montreal, Fac Med, Dept Environm, Montreal, PQ H3T 1A8, Canada.
[Emond, Claude] Univ Montreal, Fac Med, Dept Occupat Hlth, Montreal, PQ H3T 1A8, Canada.
[Sanders, J. Michael; Birnbaum, Linda S.] NCI, Res Triangle Pk, NC USA.
[Wikoff, Daniele] ToxStrategies, Austin, TX USA.
RP Emond, C (reprint author), Univ Montreal, Fac Med, Dept Environm & Occupat Hlth, 2375 Chemin Cote Ste Catherine,Bur 7085, Montreal, PQ H3T 1A8, Canada.
EM claude.emond@umontreal.ca; sander10@mail.nih.gov;
dwikoff@toxstrategies.com; bimbaumls@niehs.nih.gov
FU Intramural Research Program of the NIH/National Cancer Institute [ZIA BC
011476]
FX This work was supported by the Intramural Research Program of the
NIH/National Cancer Institute [Project # ZIA BC 011476]. Any mention of
trade names or commercial products in this manuscript does not
constitute endorsement or recommendation for use.
NR 49
TC 5
Z9 5
U1 2
U2 20
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD DEC 1
PY 2013
VL 273
IS 2
BP 335
EP 344
DI 10.1016/j.taap.2013.09.007
PG 10
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 267LP
UT WOS:000328099500010
PM 24055880
ER
PT J
AU Titov, LP
Siniuk, KV
Wollenberg, KK
Unemo, M
Hedberg, ST
Glazkova, SE
Lebedzeu, FA
Nosava, AS
Yanovich, VO
Xirasagar, S
Hurt, D
Huyen, Y
AF Titov, Leonid P.
Siniuk, Kanstantsin V.
Wollenberg, Kurt K.
Unemo, Magnus
Hedberg, Sara Thulin
Glazkova, Slavyana E.
Lebedzeu, Fiodar A.
Nosava, Alena S.
Yanovich, Volcha O.
Xirasagar, Sadhia
Hurt, Darrell
Huyen, Yentram
TI EVOLUTIONARY EPIDEMIOLOGY OF NEISSERIA MENINGITIDIS STRAINS IN BELARUS
COMPARED TO OTHER EUROPEAN COUNTRIES
SO ACTA MICROBIOLOGICA ET IMMUNOLOGICA HUNGARICA
LA English
DT Article
DE Neisseria meningitidis; multilocus sequence typing (MLST); sequence type
(ST); clonal complex (CC); evolution; Belarus
ID RECOMBINATION; POPULATION; IDENTIFICATION; CARRIAGE; VACCINE; CLONES
AB Introduction. Meningococcal infections are major causes of death in children globally. In Belarus, the incidence of cases and fatality rate of meningococcal infections are low and comparable to the levels in other European countries. Aim. In the present study, the molecular and epidemiological traits of Neisseria meningitidis strains circulating in Belarus were characterized and compared to isolates from other European countries. Materials and Methods. Twenty N. meningitidis strains isolated from patients (n = 13) and healthy contacts (n = 7) during 2006-2012 in Belarus were selected for multilocus sequence typing (MLST), genosubtyping and FetA typing. The STs of the Belarusian strains were phylogenetically compared to the STs of 110 selected strains from 22 other European countries. Results. Overall, eleven different genosubtypes were observed, there were seven variants of variable region of the fetA gene detected. The majority of the STs (95%) found in Belarus were novel and all those were submitted to the Neisseria MLST database for assignment. Several newly discovered alleles of fumC (allele 451) and gdh (allele 560 and 621) appeared to be descendants of alleles which are widespread in Europe, and single aroE alleles (602 and 603) occurred as a result of separate evolution. Conclusions. N. meningitidis strains circulating in Belarus are heterogeneous and include sequence types, possibly, locally evolved in Belarus as well as representatives of widespread European hyperinvasive clonal complexes.
C1 [Titov, Leonid P.; Siniuk, Kanstantsin V.; Glazkova, Slavyana E.; Lebedzeu, Fiodar A.; Nosava, Alena S.; Yanovich, Volcha O.] Republ Res & Pract Ctr Epidemiol & Microbiol, Minsk, Byelarus.
[Wollenberg, Kurt K.; Xirasagar, Sadhia; Hurt, Darrell; Huyen, Yentram] NIAID, NIH, Bethesda, MD 20892 USA.
[Unemo, Magnus; Hedberg, Sara Thulin] Orebro Univ Hosp, Dept Lab Med, Natl Reference Lab Pathogen Neisseria, Orebro, Sweden.
RP Titov, LP (reprint author), Republ Res & Pract Ctr Epidemiol & Microbiol, 23 Filimonova St, Minsk, Byelarus.
EM leonidtitov@tut.by
NR 22
TC 0
Z9 0
U1 1
U2 4
PU AKADEMIAI KIADO RT
PI BUDAPEST
PA PRIELLE K U 19, PO BOX 245,, H-1117 BUDAPEST, HUNGARY
SN 1217-8950
EI 1588-2640
J9 ACTA MICROBIOL IMM H
JI Acta Microbiol. Immunol. Hung.
PD DEC
PY 2013
VL 60
IS 4
BP 397
EP 410
DI 10.1556/AMicr.60.2013.4.2
PG 14
WC Immunology; Microbiology
SC Immunology; Microbiology
GA 261WV
UT WOS:000327696200002
PM 24292084
ER
PT J
AU Litten, RZ
Castle, IJP
Falk, D
Ryan, M
Fertig, J
Chen, CM
Yi, HY
AF Litten, Raye Z.
Castle, I-Jen P.
Falk, Daniel
Ryan, Megan
Fertig, Joanne
Chen, Chiung M.
Yi, Hsiao-ye
TI The Placebo Effect in Clinical Trials for Alcohol Dependence: An
Exploratory Analysis of 51 Naltrexone and Acamprosate Studies
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Dependence; Placebo Effect; Naltrexone; Acamprosate;
Meta-Analysis
ID RANDOMIZED CONTROLLED-TRIAL; MAJOR DEPRESSIVE DISORDER;
COGNITIVE-BEHAVIORAL THERAPY; COPING SKILLS THERAPY; DOUBLE-BLIND;
RELAPSE PREVENTION; META-REGRESSION; PSYCHIATRIC-DISORDERS; OUTPATIENT
ALCOHOLICS; WEANED ALCOHOLICS
AB BackgroundThe placebo effect often undermines efforts to determine treatment effectiveness in clinical trials. A significant placebo response occurs in alcohol trials, but it is not well understood. The purpose of this study was to characterize the placebo response across multiple naltrexone and acamprosate studies.
MethodsFifty-one trials, 3 with a naltrexone and an acamprosate arm, 31 with at least 1 naltrexone arm, and 17 with at least 1 acamprosate arm, were identified from Cochrane reviews and PubMed search. To be included in this study, patients had to be at least 18years old, abstinent from alcohol before randomization, and meet a diagnosis of alcohol dependence. Pearson correlation coefficients (r(p)) and simple linear regression were used to describe the strength of linear relationships between placebo response and treatment effect size. Spearman's rank correlation coefficients (r(s)) were used to examine the strength of associations between study characteristics and placebo response.
ResultsFor the end point measures of percent days abstinent and total abstinence, a negative relationship was evident between placebo response and treatment effect size in the naltrexone trials (r(p)=-0.55, p<0.01 and r(p)=-0.20, p=0.35, respectively) as well as in the acamprosate trials (r(p)=-0.45, p=0.09 and r(p)=-0.56, p=0.01, respectively). The placebo response for percent days abstinent was negatively correlated with mean age of participants (r(s)=-0.42, p=0.05) across naltrexone trials and positively correlated with publication year (r(s)=0.57, p=0.03) across acamprosate trials. However, these 2 study characteristics were not significantly correlated with treatment effect size.
ConclusionsThe placebo response varied considerably across trials and was negatively correlated with the treatment effect size. Additional studies are required to fully understand the complex nature of the placebo response and to evaluate approaches to minimize its effects.
C1 [Litten, Raye Z.; Falk, Daniel; Ryan, Megan; Fertig, Joanne] NIAAA, Div Treatment & Recovery Res, Bethesda, MD 20892 USA.
[Castle, I-Jen P.; Chen, Chiung M.; Yi, Hsiao-ye] CSR Inc, Arlington, VA USA.
RP Litten, RZ (reprint author), NIAAA, Div Treatment & Recovery Res, 5635 Fishers Lane, Bethesda, MD 20892 USA.
EM rlitten@mail.nih.gov
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA); Medications
Development Program Analytic Contract; NIAAA [HHSN275201100002G];
National Institutes of Health, Department of Health and Human Services,
Bethesda, MD
FX This research was supported by the National Institute on Alcohol Abuse
and Alcoholism (NIAAA), National Institutes of Health, Department of
Health and Human Services, Bethesda, MD and by the Medications
Development Program Analytic Contract funded by NIAAA Contract No.
HHSN275201100002G to CSR, Incorporated, Arlington, VA. The authors thank
Barbara Vann (CSR, Incorporated) for her excellent editorial comments,
Robin A. LaVallee (CSR, Incorporated) for data entry, and Drs. Patrick
K. Randall and Raymond F. Anton (Medical University of South Carolina,
Charleston, SC), Drs. William D. Dundon and Helen M. Pettinati
(University of Pennsylvania School of Medicine, Philadelphia, PA), and
Dr. Wolfgang Wolwer (Heinrich Heine University, Dusseldorf, Germany) for
providing their unpublished results.
NR 98
TC 10
Z9 10
U1 7
U2 15
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 DEC
PY 2013
VL 37
IS 12
BP 2128
EP 2137
DI 10.1111/acer.12197
PG 10
WC Substance Abuse
SC Substance Abuse
GA 261VI
UT WOS:000327692300016
PM 23889231
ER
PT J
AU Xiao, Q
Arem, H
Moore, SC
Hollenbeck, AR
Matthews, CE
AF Xiao, Qian
Arem, Hannah
Moore, Steven C.
Hollenbeck, Albert R.
Matthews, Charles E.
TI A Large Prospective Investigation of Sleep Duration, Weight Change, and
Obesity in the NIH-AARP Diet and Health Study Cohort
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE body mass index; obesity; sleep
ID BODY-MASS INDEX; BROWN ADIPOSE-TISSUE; GHRELIN LEVELS; QUEBEC FAMILY;
LEPTIN LEVELS; ASSOCIATION; GAIN; ADULTS; MELATONIN; POPULATION
AB The relationship between sleep and obesity or weight gain in adults, particularly older populations, remains unclear. In a cohort of 83,377 US men and women aged 5172 years, we prospectively investigated the association between self-reported sleep duration and weight change over an average of 7.5 years of follow-up (19952004). Participants were free of cancer, heart disease, and stroke at baseline and throughout the follow-up. We observed an inverse association between sleep duration per night and weight gain in both men (P for trend 0.02) and women (P for trend 0.001). Compared with 78 hours of sleep, shorter sleep (5 hours or 56 hours) was associated with more weight gain (in kilograms; men: for 5 hours, 0.66, 95 confidence interval (CI): 0.19, 1.13, and for 56 hours, 0.12, 95 CI: 0.02, 0.26; women: for 5 hours, 0.43, 95 CI: 0.00, 0.86, and for 56 hours, 0.23, 95 CI: 0.08, 0.37). Among men and women who were not obese at baseline, participants who reported less than 5 hours of sleep per night had an approximately 40 higher risk of developing obesity than did those who reported 78 hours of sleep (for men, odds ratio 1.45, 95 CI: 1.06, 1.99; for women, odds ratio 1.37, 95 CI: 1.04, 1.79). The association between short sleep and excess weight gain was generally consistent across different categories of age, educational level, smoking status, baseline body mass index, and physical activity level.
C1 [Xiao, Qian; Arem, Hannah; Moore, Steven C.; Matthews, Charles E.] NCI, Nutrit Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Xiao, Q (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM qian.xiao@nih.gov
RI matthews, Charles/E-8073-2015; Moore, Steven/D-8760-2016
OI matthews, Charles/0000-0001-8037-3103; Moore, Steven/0000-0002-8169-1661
FU National Institutes of Health, National Cancer Institute, Department of
Health and Human Services
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Department of
Health and Human Services.
NR 43
TC 32
Z9 34
U1 0
U2 18
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 2013
VL 178
IS 11
BP 1600
EP 1610
DI 10.1093/aje/kwt180
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 262ER
UT WOS:000327717600002
PM 24049160
ER
PT J
AU Conde-Agudelo, A
Romero, R
AF Conde-Agudelo, Agustin
Romero, Roberto
TI Transdermal nitroglycerin for the treatment of preterm labor: a
systematic review and metaanalysis
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE beta(2)-adrenergic receptor agonist; magnesium sulfate; neonatal
morbidity; nifedipine; nitric-oxide donor; preterm birth; tocolytic
agent
ID PLACEBO-CONTROLLED TRIAL; RANDOMIZED CLINICAL-TRIAL; NITRIC-OXIDE
DONORS; DOUBLE-BLIND; GLYCERYL TRINITRATE; MAGNESIUM-SULFATE;
NEURODEVELOPMENTAL OUTCOMES; PARTURITION SYNDROME; ANTAGONIST ATOSIBAN;
COMPOSITE OUTCOMES
AB OBJECTIVE: The purpose of this study was to evaluate the efficacy and safety of transdermal nitroglycerin as a tocolytic agent in women with preterm labor.
STUDY DESIGN: We conducted a systematic review and metaanalysis of randomized controlled trials.
RESULTS: Thirteen studies were included (1302 women) comparing transdermal nitroglycerin vs placebo (2 studies; n = 186); beta(2)-adrenergic receptor agonists (9 studies; n = 1024); nifedipine (1 study; n = 50); and magnesium sulfate (1 study; n = 42). There were no significant differences between transdermal nitroglycerin and placebo for delivery within 48 hours of the initiation of treatment or at < 28, < 34, or < 37 weeks of gestation, adverse neonatal outcomes, and neurodevelopmental status at 24 months of life. Nevertheless, 1 study found a marginally significant reduction in the risk of a composite outcome of major neonatal morbidity and perinatal death (3/74 [4.1%] vs 11/79 [13.9%]; relative risk, 0.29; 95% confidence interval, 0.08-1.00). When compared with beta(2)-adrenergic receptor agonists, transdermal nitroglycerin was associated with a significant reduction in the risk of preterm birth at < 34 and < 37 weeks of gestation, admission to the neonatal intensive care unit, use of mechanical ventilation, and maternal side effects. There were no significant differences between transdermal nitroglycerin and nifedipine and magnesium sulfate in delivery within 48 hours of treatment and pregnancy prolongation, respectively. Overall, women who received transdermal nitroglycerin had a higher risk of headache.
CONCLUSION: Although transdermal nitroglycerin appears to be more effective than b2-adrenergic receptor agonists, the current evidence does not support its routine use as a tocolytic agent for the treatment of preterm labor. Further double-blind placebo-controlled trials are needed.
C1 [Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Bethesda, MD USA.
[Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Natl Inst Human Serv, Bethesda, MD USA.
[Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Detroit, MI USA.
[Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Natl Inst Human Serv, Detroit, MI USA.
Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
RP Conde-Agudelo, A (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Bethesda, MD USA.
FU 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
FX Supported by the 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.
NR 83
TC 0
Z9 1
U1 0
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 2013
VL 209
IS 6
AR 551.e1
DI 10.1016/j.ajog.2013.07.022
PG 18
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 259PN
UT WOS:000327538900013
PM 23891631
ER
PT J
AU Huynh, N
Blain, D
Glaser, T
Doss, EL
Zein, WM
Lang, DM
Baker, EH
Hill, S
Brewer, CC
Kopp, JB
Bardakjian, TM
Maumenee, IH
Bateman, BJ
Brooks, BP
AF Huynh, Nancy
Blain, Delphine
Glaser, Tanya
Doss, E. Lauren
Zein, Wadih M.
Lang, David M.
Baker, Eva H.
Hill, Suvimol
Brewer, Carmen C.
Kopp, Jeffrey B.
Bardakjian, Tanya M.
Maumenee, Irene H.
Bateman, Bronwyn J.
Brooks, Brian P.
TI Systemic Diagnostic Testing in Patients With Apparently Isolated Uveal
Coloboma
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID CONGENITAL EYE MALFORMATIONS; UNILATERAL RENAL AGENESIS; CHARGE
ASSOCIATION; CONSECUTIVE BIRTHS; CLINICAL-FEATURES; UNITED-KINGDOM;
VISUAL-ACUITY; ANOMALIES; CHILDREN; MICROPHTHALMOS
AB PURPOSE: To investigate the frequency and types of systemic findings in patients with apparently isolated uveal coloboma.
DESIGN: Cross-sectional observational study.
METHODS: SETTING: Single-center ophthalmic genetics clinic. STUDY POPULATION: Ninety-nine patients with uveal coloboma seen at the National Eye Institute. OBSERVATIONAL PROCEDURE: Results of audiology testing, echocardiogram, brain magnetic resonance imaging, renal ultrasound, and total spine radiographs. MAIN OUTCOME MEASURE: Prevalence of abnormal findings on systemic testing.
RESULTS: Uveal coloboma affected only the anterior segment in 8 patients, only the posterior segment in 23 patients, and both anterior and posterior segments in 68 patients. Best-corrected visual acuity (BCVA) of eyes with coloboma was >= 20/40 in 45% of eyes; 23% of eyes had BCVA of <= 20/400. The majority of patients (74%) had good vision (>20/60) in at least 1 eye. Ten of the 19 patients (53%) who underwent echocardiography had abnormalities, with ventral septal defects being the most prevalent. Abnormal findings were observed in 5 of 72 patients (7%) who had a renal ultrasound and in 5 of 29 patients (17%) who underwent a brain MRI. Audiology testing revealed abnormalities in 13 of 75 patients (17%), and spine radiographs showed anomalies in 10 of 77 patients (13%). Most findings required no acute intervention.
CONCLUSIONS: Although some patients with coloboma had evidence of extraocular abnormalities, the majority of findings on routine clinical examination did not require acute intervention, but some warranted follow-up. Results from the systemic evaluation of patients with coloboma should be interpreted with caution and in view of their clinical context. (Published by Elsevier Inc.)
C1 [Huynh, Nancy; Blain, Delphine; Glaser, Tanya; Doss, E. Lauren; Zein, Wadih M.; Brooks, Brian P.] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
[Lang, David M.] NEI, Pediat Consult Serv, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Baker, Eva H.; Hill, Suvimol] NEI, Dept Radiol & Imaging Sci, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Brewer, Carmen C.] Natl Inst Deafness & Other Commun Disorders, Otolaryngol Branch, Bethesda, MD USA.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, Bethesda, MD 20892 USA.
[Bardakjian, Tanya M.] Einstein Med Ctr Philadelphia, Div Genet, Philadelphia, PA USA.
[Maumenee, Irene H.] Univ Illinois, Coll Med, Dept Ophthalmol, Chicago, IL USA.
[Bateman, Bronwyn J.] Univ Colorado, Childrens Hosp, Sch Med, Rocky Mt Lions Eye Inst, Aurora, CO USA.
RP Brooks, BP (reprint author), NEI, NIH, 10 Ctr Dr,Bldg 10,Room 10N226,MSC 1860, Bethesda, MD 20892 USA.
EM brooksb@nei.nih.gov
OI Kopp, Jeffrey/0000-0001-9052-186X
FU National Eye Institute, National Institute of Diabetes and Digestive and
Kidney Diseases, National Institute on Deafness and Other Communication
Disorders; Clinical Center of the National Institutes of Health, U.S.
Department of Health and Human Services, Bethesda, Maryland, USA
FX ALL AUTHORS HAVE COMPLETED AND SUBMITTED THE ICMJE FORM FOR DISCLOSURE
OF POTENTIAL CONFLICTS OF INTEREST and none were reported. This work was
supported by the intramural research programs of the National Eye
Institute, National Institute of Diabetes and Digestive and Kidney
Diseases, National Institute on Deafness and Other Communication
Disorders, and the Clinical Center of the National Institutes of Health,
U.S. Department of Health and Human Services, Bethesda, Maryland, USA.
Contributions of authors: design of study (N.H., D.B., D.L.L., E.H.B.,
S.H., C.C.B., J.B.K., B.P.B.); acquisition of data (B.P.B., N.H., D.B.,
TO,, E.L.D., W.Z., D.L.L., E.H.B:, S.H., C.C.B., J.B.K., T.M.B., I.H.M.,
B.J.B., B.P.B.); interpretation of data (N.H., D.B., T.G., B.P.B.);
preparation of manuscript (N.H., B.P.B.); review and approval of
manuscript (N.H., W.Z., D.L.L., E.H.B., S.H., C.C.B., J.B.K., T.M.B.,
I.H.M., B.J.B., B.P.B.).
NR 22
TC 3
Z9 4
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
EI 1879-1891
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD DEC
PY 2013
VL 156
IS 6
BP 1159
EP 1168
DI 10.1016/j.ajo.2013.06.037
PG 10
WC Ophthalmology
SC Ophthalmology
GA 261OQ
UT WOS:000327674900013
PM 24012100
ER
PT J
AU Kohn, EC
Romano, S
Lee, JM
AF Kohn, E. C.
Romano, S.
Lee, J. -M.
TI Clinical implications of using molecular diagnostics for ovarian cancers
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE morphological; biomarker; high-grade serous ovarian cancer; molecular;
therapeutics
ID GRADE SEROUS CARCINOMA; BREAST-CANCER; 2-TIER SYSTEM; PERITONEAL
CARCINOMA; INHERITED OVARIAN; CELL CARCINOMA; BRAF MUTATION; OPEN-LABEL;
EXPRESSION; HER2
AB In the era of morphologic diagnostics, any epithelial tumor on or involving the ovaries was presumed to come from and be strictly of ovarian origin, apart from the rare but clearly metastatic tumors. Thus, many women who might have had small fallopian tube primary cancers that rapidly extended on to or into the ovary were deemed to have ovarian cancer. Now, as we begin to better understand that there are different types of cancers of nonuterine Muellerian origin, we expand upon the morphologic to add the molecular characteristics. Morphomolecular characteristics are being applied to drive clinical advances including development and optimization of predictive and prognostic biomarkers, redefinition of historical controls, and consideration of novel clinical trial designs. Ovarian cancer, not a common cancer to start with, is now subdivided into types, making ever smaller clinical cohorts. The first studies evaluating tubo-ovarian Muellerian cancers of morphomolecular types have begun. Deleterious mutations in BRCA1 or 2 have been validated as the first new predictive and prognostic biomarker of the high-grade serous ovarian cancer type and polyADPribose polymerase inhibitors, the first targeted agents for this morphomolecular entity. Similar progress is developing in other tubo-ovarian cancer types. This new knowledge is driving the building of a structure-function-type relationship that is generating novel clinically applicable hypotheses for testing.
C1 [Kohn, E. C.; Romano, S.; Lee, J. -M.] NCI, Mol Signaling Sect, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Romano, S.] Walter Reed Natl Mil Med Ctr, Gynecol Oncol Ctr Excellence, John P Murtha Canc Ctr, Bethesda, MD USA.
RP Kohn, EC (reprint author), 9609 Med Ctr Dr 5W426 MSC9737, Rockville, MD 20850 USA.
EM kohne@mail.nih.gov
FU Intramural Program of the Center for Cancer Research, National Cancer
Institute, National Institutes of Health, USA
FX This work was supported by the Intramural Program of the Center for
Cancer Research, National Cancer Institute, National Institutes of
Health, USA.
NR 49
TC 6
Z9 6
U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD DEC
PY 2013
VL 24
SU 10
BP 22
EP 26
DI 10.1093/annonc/mdt464
PG 5
WC Oncology
SC Oncology
GA 259EZ
UT WOS:000327511500003
ER
PT J
AU Sassi, A
Lazaroski, S
Wu, G
Haslam, SM
Mellouli, F
Patiroglu, T
Jouhadi, Z
Khadir, K
Pfeifer, D
Jakob, T
Khemiri, M
Ben-Mustapha, I
Asplund, C
Gustafsson, M
Lundin, K
Falk-Sorqvist, E
Moens, L
Unal, E
Ozdemir, MA
Gungor, HE
Engelhardt, K
Dziadzio, M
Stauss, H
Fleckenstein, B
Fliegauf, M
Meier, R
Ben-Khemis, L
Kraus, H
Nadifi, S
Eibel, H
Nilsson, M
Bejaoui, M
Schaffer, A
Smith, E
Dell, A
Barbouche, MR
Grimbacher, B
AF Sassi, Atfa
Lazaroski, Sandra
Wu, Gang
Haslam, Stuart M.
Mellouli, Fethi
Patiroglu, Turkan
Jouhadi, Zineb
Khadir, Khadija
Pfeifer, Dietmar
Jakob, Thilo
Khemiri, Monia
Ben-Mustapha, Imen
Asplund, Charlotta
Gustafsson, Manuela
Lundin, Karin
Falk-Sorqvist, Elin
Moens, Lotte
Unal, Ekrem
Ozdemir, Mehmet Akif
Gungor, Hatice Eke
Engelhardt, Karin
Dziadzio, Magdalena
Stauss, Hans
Fleckenstein, Bernhard
Fliegauf, Manfred
Meier, Rebecca
Ben-Khemis, Leila
Kraus, Helene
Nadifi, Sellama
Eibel, Hermann
Nilsson, Mats
Bejaoui, Mohamed
Schaeffer, Alejandro
Smith, Edvard
Dell, Anne
Barbouche, Mohamed-Ridha
Grimbacher, Bodo
TI Hypomorphic, Homozygous Mutations In Phosphoglucomutase-3 Impair
Immunity And Increase Serum IgE Levels
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT UK-Primary-Immunodeficiency-Network (UK PIN) Meeting
CY DEC 06-07, 2013
CL Liverpool, ENGLAND
SP UK Primary Immunodeficiency Network
C1 [Sassi, Atfa; Ben-Mustapha, Imen; Ben-Khemis, Leila; Barbouche, Mohamed-Ridha] Pasteur Inst Tunis, Lab Immunopathol Vaccinol & Mol Genet, Tunis, Tunisia.
[Sassi, Atfa; Ben-Mustapha, Imen; Ben-Khemis, Leila; Barbouche, Mohamed-Ridha] Univ Tunis, Tunis, Tunisia.
[Lazaroski, Sandra; Fliegauf, Manfred; Meier, Rebecca; Kraus, Helene; Eibel, Hermann; Grimbacher, Bodo] Univ Med Ctr Freiburg, Ctr Chron Immunodeficiency, Freiburg, Germany.
[Wu, Gang; Dell, Anne] Univ London Imperial Coll Sci Technol & Med, Dept Life Sci, London SW7 2AZ, England.
[Haslam, Stuart M.; Bejaoui, Mohamed] Bone Marrow Transplantat Ctr, Dept Pediat, Tunis, Tunisia.
[Mellouli, Fethi; Unal, Ekrem; Ozdemir, Mehmet Akif] Erciyes Univ, Fac Med, Div Pediat Hematol & Oncol, Dept Pediat, Kayseri, Turkey.
[Patiroglu, Turkan; Gungor, Hatice Eke] Erciyes Univ, Fac Med, Div Pediat Immunol, Dept Pediat, Kayseri, Turkey.
[Jouhadi, Zineb; Khadir, Khadija] Hassan II Univ, Dept Pediat Infect Dis, Casablanca, Morocco.
[Pfeifer, Dietmar] Univ Med Ctr Freiburg, Dept Hematol & Oncol, Freiburg, Germany.
[Jakob, Thilo] Univ Med Ctr Freiburg, Dept Dermatol, Allergy Res Grp, Freiburg, Germany.
[Khemiri, Monia] Childrens Hosp Tunis, Pediat Dept A, Tunis, Tunisia.
[Asplund, Charlotta; Gustafsson, Manuela; Lundin, Karin; Smith, Edvard] Karolinska Inst, Dept Lab Med, Clin Res Ctr, S-10401 Stockholm, Sweden.
[Falk-Sorqvist, Elin; Moens, Lotte; Nilsson, Mats] Uppsala Univ, Dept Immunol Genet & Pathol, Uppsala, Sweden.
[Engelhardt, Karin; Dziadzio, Magdalena; Stauss, Hans] UCL, Dept Immunol, Royal Free Hosp, London WC1E 6BT, England.
[Fleckenstein, Bernhard] Univ Erlangen Nurnberg, Inst Virol, D-91054 Erlangen, Germany.
[Nadifi, Sellama] Hassan II Univ, Dept Genet, Casablanca, Morocco.
[Schaeffer, Alejandro] NCBI, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
EI 1365-2249
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD DEC
PY 2013
VL 174
SU 1
SI SI
BP 2
EP 2
PG 1
WC Immunology
SC Immunology
GA 256IO
UT WOS:000327303400004
ER
PT J
AU Dhalla, F
Murray, S
Miller, J
Sadler, R
Soilleux, E
Bhole, M
Uzel, G
Ferry, B
Patel, YS
Chapel, H
AF Dhalla, Fatima
Murray, Sarah
Miller, Joanne
Sadler, Ross
Soilleux, Elizabeth
Bhole, Malini
Uzel, Gulbu
Ferry, Berne
Patel, Smita Y.
Chapel, Helen
TI X-MEN: The new mutants
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT UK-Primary-Immunodeficiency-Network (UK PIN) Meeting
CY DEC 06-07, 2013
CL Liverpool, ENGLAND
SP UK Primary Immunodeficiency Network
C1 [Dhalla, Fatima] John Radcliffe Hosp, Dept Immunol, Oxford Univ Hosp, Oxford OX3 9DU, England.
[Miller, Joanne; Patel, Smita Y.; Chapel, Helen] Oxford Univ Hosp, Dept Immunol, Oxford, England.
[Soilleux, Elizabeth] Oxford Univ Hosp, Dept Pathol, Oxford, England.
[Uzel, Gulbu] NIH, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
EI 1365-2249
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD DEC
PY 2013
VL 174
SU 1
SI SI
BP 6
EP 7
PG 2
WC Immunology
SC Immunology
GA 256IO
UT WOS:000327303400012
ER
PT J
AU Mechanic, L
Mendez, A
Merrill, L
Rogers, J
Layton, M
Todd, D
Varanasi, A
O'Brien, B
Meyer, WA
Zhang, M
Schleicher, RL
Moye, J
AF Mechanic, Leah
Mendez, Armando
Merrill, Lori
Rogers, John
Layton, Marnie
Todd, Deborah
Varanasi, Arti
O'Brien, Barbara
Meyer, William A., III
Zhang, Ming
Schleicher, Rosemary L.
Moye, Jack, Jr.
TI Planned variation in preanalytical conditions to evaluate biospecimen
stability in the National Children's Study (NCS)
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article
DE adrenocorticotropic hormone (ACTH); biospecimen stability;
carbohydrate-deficient transferrin (CDT); estradiol; free T-4; IGF-1;
IL-6; insulin; preanalytical variation; vitamin C
ID INSULIN-RESISTANCE; SAMPLE COLLECTION; ASCORBIC-ACID; WHOLE-BLOOD;
PLASMA; SERUM; STORAGE; GLUCOSE; ANTICOAGULANTS; INTERLEUKIN-6
AB Background: Preanalytical conditions encountered during collection, processing, and storage of biospecimens may influence laboratory results. The National Children's Study (NCS) is a planned prospective cohort study of 100,000 families to examine the influence of a wide variety of exposures on child health. In developing biospecimen collection, processing, and storage procedures for the NCS, we identified several analytes of different biochemical categories for which it was unclear to what extent deviations from NCS procedures could influence measurement results.
Methods: A pilot study was performed to examine effects of preanalytic sample handling conditions (delays in centrifugation, freezing delays, delays in separation from cells, additive delay, and tube type) on concentrations of eight different analytes. A total of 2825 measurements were made to assess 15 unique combinations of analyte and handling conditions in blood collected from 151 women of childbearing age (>= 20 individuals per handling condition).
Results: The majority of analytes were stable under the conditions evaluated. However, levels of plasma -interleukin-6 and serum insulin were decreased in response to sample centrifugation delays of up to 5.5 h post-collection (p<0.0001). In addition, delays in freezing centrifuged plasma samples (comparing 24, 48 and 72 h to immediate freezing) resulted in increased levels of adrenocorticotropic hormone (p=0.0014).
Conclusions: Determining stability of proposed analytes in response to preanalytical conditions and handling helps to ensure high-quality specimens for study now and in the future. The results inform development of procedures, plans for measurement of analytes, and interpretation of laboratory results.
C1 [Moye, Jack, Jr.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Childrens Study, NIH, Bethesda, MD 20892 USA.
[Mechanic, Leah] NCI, Host Susceptibil Factors Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
[Mendez, Armando] Univ Miami, Miller Sch Med, Diabet Res Inst, Miami, FL 33136 USA.
[Merrill, Lori; Rogers, John; Layton, Marnie; Todd, Deborah; O'Brien, Barbara] Westat Corp, Rockville, MD USA.
[Varanasi, Arti] Adv Synergy LLC, Baltimore, MD USA.
[Meyer, William A., III] Quest Diagnost, Baltimore, MD USA.
[Zhang, Ming; Schleicher, Rosemary L.] Ctr Dis Control & Prevent CDC, Nutr Biomarkers Branch, Atlanta, GA USA.
RP Moye, J (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Childrens Study, NIH, 6100 Execut Blvd,Room 5C01D,MSC 7510, Bethesda, MD 20892 USA.
EM moyej@mail.nih.gov
OI moye, john/0000-0001-9976-8586
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; Office of the Director of the National Institutes of
Health; NICHD [HHSN275200503395C, HHSN275201000107U, HHSN275200900010C,
HHSN275201000121U]
FX Research funding: This analysis was conducted as part of the National
Children's Study, supported by the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, and funded, through its
appropriation, by the Office of the Director of the National Institutes
of Health. Supported by NICHD Contracts HHSN275200503395C,
HHSN275201000107U, HHSN275200900010C, and HHSN275201000121U. The
manuscript was developed by a Writing Team identified by the National
Children's Study Publications Committee for the purpose of timely
sharing of NCS data.
NR 35
TC 4
Z9 4
U1 1
U2 9
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD DEC
PY 2013
VL 51
IS 12
BP 2287
EP 2294
DI 10.1515/cclm-2013-0454
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 262MH
UT WOS:000327739000024
PM 23924524
ER
PT J
AU Berngard, SC
Berngard, JB
Krebs, NF
Garces, A
Miller, LV
Westcott, J
Wright, LL
Kindem, M
Hambidge, KM
AF Berngard, Samuel Clark
Berngard, Jennifer Bishop
Krebs, Nancy F.
Garces, Ana
Miller, Leland V.
Westcott, Jamie
Wright, Linda L.
Kindem, Mark
Hambidge, K. Michael
TI Newborn length predicts early infant linear growth retardation and
disproportionately high weight gain in a low-income population
SO EARLY HUMAN DEVELOPMENT
LA English
DT Article
DE Infant growth; Linear growth; Birth weight; Predictors of infant growth
ID CHILD UNDERNUTRITION; BIRTH-WEIGHT; FETAL-GROWTH; GUATEMALAN INFANTS;
MATERNAL STATURE; RURAL MALAWI; RISK-FACTORS; SUPPLEMENTATION;
INTERVENTIONS; 1ST-TRIMESTER
AB Background: Stunting is prevalent by the age of 6 months in the indigenous population of the Western Highlands of Guatemala.
Aim: The objective of this study was to determine the time course and predictors of linear growth failure and weight-for-age in early infancy.
Study design and subjects: One hundred and forty eight term newborns had measurements of length and weight in their homes, repeated at 3 and 6 months. Maternal measurements were also obtained.
Results: Mean +/- SD length-for-age Z-score (LAZ) declined from newborn -1.0 +/- 1.01 to -2.20 +/- 1.05 and -2.26 +/- 1.01 at 3 and 6 months respectively. Stunting rates for newborn, 3 and 6 months were 47%, 53% and 56% respectively. A multiple regression model (R-2 = 0.64) demonstrated that the major predictor of LAZ at 3 months was newborn [AZ with the other predictors being newborn weight-for-age Z-score (WAZ), gender and maternal education * maternal age interaction. Because WAZ remained essentially constant and LAZ declined during the same period, weight-for-length Z-score (WLZ) increased from -0.44 to +1.28 from birth to 3 months. The more severe the linear growth failure, the greater WAZ was in proportion to the LAZ.
Conclusion: The primary conclusion is that impaired fetal linear growth is the major predictor of early infant linear growth failure indicating that prevention needs to start with maternal interventions. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Berngard, Samuel Clark; Berngard, Jennifer Bishop; Krebs, Nancy F.; Miller, Leland V.; Westcott, Jamie; Hambidge, K. Michael] Univ Colorado Denver, Aurora, CO 80045 USA.
[Garces, Ana] IMSALUD, Guatemala City, Guatemala.
[Wright, Linda L.] NICHHD, NIH, Rockville, MD 20852 USA.
[Kindem, Mark] RTI Int, Res Triangle Pk, NC 27709 USA.
RP Hambidge, KM (reprint author), Univ Colorado Denver, 12700 East 19th Ave,Box C225, Aurora, CO 80045 USA.
EM Michael.Hambidge@ucdenver.edu
OI Berngard, Samuel Clark/0000-0002-4335-105X
FU NIH Eunice Kennedy Shriver NICHD, NIH, Global Network for Women's and
Children's Health Research [U01 HD 40657]; Rotary Scholarship; Adler
Scholarship; Robinson-Durst Scholarship
FX Supported by NIH Eunice Kennedy Shriver NICHD, NIH, Global Network for
Women's and Children's Health Research U01 HD 40657; and Rotary, Adler,
and Robinson-Durst Scholarships.
NR 52
TC 13
Z9 13
U1 1
U2 12
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-3782
EI 1872-6232
J9 EARLY HUM DEV
JI Early Hum. Dev.
PD DEC
PY 2013
VL 89
IS 12
BP 967
EP 972
DI 10.1016/j.earlhumdev.2013.09.008
PG 6
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 262RO
UT WOS:000327755500009
PM 24083893
ER
PT J
AU Lowe, JR
Duncan, AF
Bann, CM
Fuller, J
Hintz, SR
Das, A
Higgins, RD
Watterberg, KL
AF Lowe, Jean R.
Duncan, Andrea Freeman
Bann, Carla M.
Fuller, Jane
Hintz, Susan R.
Das, Abhik
Higgins, Rosemary D.
Watterberg, Kristi L.
CA Eunice Kennedy Shriver Natl Inst
TI Early working memory as a racially and ethnically neutral measure of
outcome in extremely preterm children at 18-22 months
SO EARLY HUMAN DEVELOPMENT
LA English
DT Article
DE Working memory; Prematurity; Development
ID LOW-BIRTH-WEIGHT; PRESCHOOL-CHILDREN; EXECUTIVE FUNCTION; BRAIN-INJURY;
SCHOOL-AGE; INFANTS; BORN; DEFICITS
AB Background: Difficulties with executive function have been found in preterm children, resulting in difficulties with learning and school performance.
Aim: This study evaluated the relationship of early working memory as measured by object permanence items to the cognitive and language scores on the Bayley Scales-III in a cohort of children born extremely preterm.
Study design: Logistic regression models were conducted to compare object permanence scores derived from the Bayley Scales-III by race/ethnicity and maternal education, controlling for medical covariates.
Subjects: Extremely preterm toddlers (526), who were part of a Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network's multi-center study, were evaluated at 18-22 months corrected age.
Outcome measures: Object permanence scores derived from the Bayley Developmental Scales were compared by race/ethnicity and maternal education, controlling for medical covariates.
Results: There were no significant differences in object permanence mastery and scores among the treatment groups after controlling for medical and social variables, including maternal education and race/ethnicity. Males and children with intraventricular hemorrhage, retinopathy of prematurity, and bronchopulmonary dysplasia were less likely to demonstrate object permanence mastery and had lower object permanence scores. Children who attained object permanence mastery had significantly higher Bayley Scales-III cognitive and language scores after controlling for medical and socio-economic factors.
Conclusions: Our measure of object permanence is free of influence from race, ethnic and socio-economic factors. Adding this simple task to current clinical practice could help detect early executive function difficulties in young children. Published by Elsevier Ireland Ltd.
C1 [Lowe, Jean R.; Duncan, Andrea Freeman; Fuller, Jane; Watterberg, Kristi L.] Univ New Mexico, Hlth Sci Ctr, Albuquerque, NM 87131 USA.
[Bann, Carla M.] RTI Int, Stat & Epidemiol Unit, Res Triangle Pk, NC USA.
[Hintz, Susan R.] Stanford Univ, Palo Alto, CA 94304 USA.
[Das, Abhik] RTI Int, Stat & Epidemiol Unit, Rockville, MD USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Lowe, JR (reprint author), 1 Univ New Mexico, Dept Pediat MSC10 5590, Albuquerque, NM 87131 USA.
EM jrlowe@unm.edu
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD)
FX The National Institutes of Health and the Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD)
provided grant support for the Neonatal Research Network Follow-up
studies.
NR 29
TC 3
Z9 3
U1 3
U2 16
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-3782
EI 1872-6232
J9 EARLY HUM DEV
JI Early Hum. Dev.
PD DEC
PY 2013
VL 89
IS 12
BP 1055
EP 1061
DI 10.1016/j.earlhumdev.2013.08.009
PG 7
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 262RO
UT WOS:000327755500024
PM 23993309
ER
PT J
AU Rubin, C
Myers, T
Stokes, W
Dunham, B
Harris, S
Lautner, B
Annelli, J
AF Rubin, Carol
Myers, Tanya
Stokes, William
Dunham, Bernadette
Harris, Stic
Lautner, Beth
Annelli, Joseph
TI Review of Institute of Medicine and National Research Council
Recommendations for One Health Initiative
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
AB Human health is inextricably linked to the health of animals and the viability of ecosystems; this is a concept commonly known as One Health. Over the last 2 decades, the Institute of Medicine (IOM) and the National Research Council (NRC) have published consensus reports and workshop summaries addressing a variety of threats to animal, human, and ecosystem health. We reviewed a selection of these publications and identified recommendations from NRC and IOM/NRC consensus reports and from opinions expressed in workshop summaries that are relevant to implementation of the One Health paradigm shift. We grouped these recommendations and opinions into thematic categories to determine if sufficient attention has been given to various aspects of One Health. We conclude that although One Health themes have been included throughout numerous IOM and NRC publications, identified gaps remain that may warrant targeted studies related to the One Health approach.
C1 [Rubin, Carol; Myers, Tanya] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA.
[Stokes, William] NIEHS, Res Triangle Pk, NC 27709 USA.
[Dunham, Bernadette] US FDA, Rockville, MD 20857 USA.
[Harris, Stic] Dept Homeland Secur, Washington, DC USA.
[Lautner, Beth] USDA, Des Moines, IA USA.
[Annelli, Joseph] USDA, Riverdale, MD USA.
RP Rubin, C (reprint author), Ctr Dis Control & Prevent, 1600 Clifton Rd NE,Mailstop A30, Atlanta, GA 30333 USA.
EM crubin@cdc.gov
NR 29
TC 6
Z9 6
U1 1
U2 10
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD DEC
PY 2013
VL 19
IS 12
BP 1913
EP 1917
DI 10.3201/eid1912.121659
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 263RV
UT WOS:000327826600001
PM 24274461
ER
PT J
AU Patayova, H
Wimmerova, S
Lancz, K
Palkovicova, L
Drobna, B
Fabisikova, A
Kovac, J
Hertz-Picciotto, I
Jusko, TA
Trnovec, T
AF Patayova, Henrieta
Wimmerova, Sona
Lancz, Kinga
Palkovicova, L'ubica
Drobna, Beata
Fabisikova, Anna
Kovac, Jan
Hertz-Picciotto, Irva
Jusko, Todd A.
Trnovec, Tomas
TI Anthropometric, socioeconomic, and maternal health determinants of
placental transfer of organochlorine compounds
SO ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
LA English
DT Article; Proceedings Paper
CT Contaminated land, ecological assessment, and remediation conference
series (CLEAR)
CY NOV 04-08, 2012
CL Hangzhou, PEOPLES R CHINA
DE Placental transfer; Alcohol; PCB; Organochlorine pesticides
ID PERSISTENT ORGANIC POLLUTANTS; POLYCHLORINATED-BIPHENYLS;
PREGNANT-WOMEN; ADIPOSE-TISSUE; PRENATAL EXPOSURES; SOUTHERN SPAIN;
BLOOD-LEVELS; HUMAN SERUM; CORD BLOOD; PCBS
AB The aim of this study was to relate placental transfer, quantified by the cord to maternal serum concentration ratio (C/M), of five organochlorine pesticides (OCP) hexachlorobenzene (HCB), beta-hexachlorocyclohexane (beta-HCH), gamma-hexachlorocyclohexane (gamma-HCH) , p,p'-DDT, p,p'-DDE and 15 polychlorinated biphenyl (PCB) congeners (28, 52, 101, 105, 114, 118, 123(+149), 138(+163), 153, 156(+171), 157, 167, 170, 180, and 189) to anthropometric, socioeconomic, and maternal health characteristics. We included into the study 1,134 births during the period 2002-2004 from two districts in eastern Slovakia with high organochlorine concentrations relative to other areas of the world. Only concentrations > LOD were taken into account. Variables as age, weight and height of mothers, parity, ethnicity, alcohol consumption, illness during pregnancy, smoking during pregnancy, hypertension, respiratory diseases, rheumatoid arthritis and diabetes mellitus, and birth weight were related to C/M. Results of regression analyses showed that C/M was predicted by several factors studied. Positive associations were observed for gestational alcohol consumption, fewer illnesses during pregnancy, maternal age, and maternal weight. Caucasians had a greater C/M compared to Romani for wet weight data of congeners 170 and 180 and in contrast C/M for HCB was greater in Romani. Our results show that drinking mothers compared to abstaining expose their fetuses not only to alcohol but to an increased level of several PCB congeners. A straightforward explanation of associations between C/M shifts and factors studied is very difficult, however, with regard to the high lipophilicity of OCPs and PCBs, changes in their kinetics probably reflect lipid kinetics.
C1 [Patayova, Henrieta; Lancz, Kinga; Palkovicova, L'ubica; Trnovec, Tomas] Slovak Med Univ, Dept Environm Med, Bratislava 83303, Slovakia.
[Drobna, Beata; Fabisikova, Anna] Slovak Med Univ, Dept Tox Organ Pollutants, Bratislava 83303, Slovakia.
[Wimmerova, Sona] Slovak Med Univ, Inst Biophys Informat & Biostat, Bratislava 83303, Slovakia.
[Kovac, Jan] Comenius Univ, Fac Med Bratislava, Dept Stomatol & Maxillofacial Surg, Bratislava 81372, Slovakia.
[Hertz-Picciotto, Irva] Univ Calif Davis, Sch Med, Div Epidemiol, Dept Publ Hlth Sci, Davis, CA 95616 USA.
[Jusko, Todd A.] NIEHS, Epidemiol Branch, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA.
RP Trnovec, T (reprint author), Slovak Med Univ, Dept Environm Med, Limbova 12, Bratislava 83303, Slovakia.
EM tomas.trnovec@szu.sk
RI Tuomisto, Jouko/J-7450-2012
FU US National Institutes of Health, National Cancer Institute
[R01-CA96525]; European Commission [227391]
FX This project has been funded by the US National Institutes of Health,
National Cancer Institute, grant R01-CA96525 and by the European
Commission through the 7FP project OBELIX (No. 227391).
NR 50
TC 9
Z9 9
U1 2
U2 21
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0944-1344
EI 1614-7499
J9 ENVIRON SCI POLLUT R
JI Environ. Sci. Pollut. Res.
PD DEC
PY 2013
VL 20
IS 12
BP 8557
EP 8566
DI 10.1007/s11356-013-1786-7
PG 10
WC Environmental Sciences
SC Environmental Sciences & Ecology
GA 259AA
UT WOS:000327498600026
PM 23677752
ER
PT J
AU Brooks-Kayal, AR
Bath, KG
Berg, AT
Galanopoulou, AS
Holmes, GL
Jensen, FE
Kanner, AM
O'Brien, TJ
Whittemore, VH
Winawer, MR
Patel, M
Scharfman, HE
AF Brooks-Kayal, Amy R.
Bath, Kevin G.
Berg, Anne T.
Galanopoulou, Aristea S.
Holmes, Gregory L.
Jensen, Frances E.
Kanner, Andres M.
O'Brien, Terence J.
Whittemore, Vicky H.
Winawer, Melodie R.
Patel, Manisha
Scharfman, Helen E.
TI Behavioral and neuroendocrine assays for studying epilepsy-associated
depression Response
SO EPILEPSIA
LA English
DT Letter
C1 [Brooks-Kayal, Amy R.] Univ Colorado, Childrens Hosp Colorado, Sch Med, Dept Pediat, Aurora, CO 80045 USA.
[Brooks-Kayal, Amy R.] Univ Colorado, Childrens Hosp Colorado, Sch Med, Dept Neurol, Aurora, CO USA.
[Brooks-Kayal, Amy R.] Univ Colorado, Childrens Hosp Colorado, Sch Med, Dept Pharmaceut Sci, Aurora, CO USA.
[Brooks-Kayal, Amy R.] Univ Colorado, Childrens Hosp Colorado, Sch Pharm, Dept Pediat, Aurora, CO USA.
[Brooks-Kayal, Amy R.] Univ Colorado, Childrens Hosp Colorado, Sch Pharm, Dept Neurol, Aurora, CO USA.
[Brooks-Kayal, Amy R.] Univ Colorado, Childrens Hosp Colorado, Sch Pharm, Dept Pharmaceut Sci, Aurora, CO USA.
[Bath, Kevin G.] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
[Berg, Anne T.] Ann & Robert H Lurie Childrens Hosp Chicago, Chicago, IL USA.
[Galanopoulou, Aristea S.] Albert Einstein Coll Med, Lab Dev Epilepsy, Dominick P Purpura Dept Neurosci, Saul R Korey Dept Neurol, Bronx, NY 10467 USA.
[Holmes, Gregory L.] Univ Vermont, Dept Neurol Sci, Burlington, VT USA.
[Jensen, Frances E.] Univ Penn, Dept Neurol, Perlman Sch Med, Philadelphia, PA 19104 USA.
[Kanner, Andres M.] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
[O'Brien, Terence J.] Univ Melbourne, Dept Med, Royal Melbourne Hosp, Melbourne Brain Ctr, Parkville, Vic 3052, Australia.
[Whittemore, Vicky H.] NINDS, NIH, Bethesda, MD 20892 USA.
[Winawer, Melodie R.] Columbia Univ, Dept Neurol, GH Sergievsky Ctr, New York, NY USA.
[Patel, Manisha] Univ Colorado, Skaggs Sch Pharm & Pharmaceut Sci, Dept Pharmaceut Sci, Aurora, CO USA.
[Scharfman, Helen E.] NYU, Dept Psychiat, Nathan Kline Inst Psychiat Res, Langone Med Ctr, New York, NY 10016 USA.
[Scharfman, Helen E.] NYU, Dept Physiol, Nathan Kline Inst Psychiat Res, Langone Med Ctr, New York, NY USA.
[Scharfman, Helen E.] NYU, Dept Neurosci, Nathan Kline Inst Psychiat Res, Langone Med Ctr, New York, NY USA.
RP Brooks-Kayal, AR (reprint author), Univ Colorado, Childrens Hosp Colorado, Sch Med, Dept Pediat, Aurora, CO 80045 USA.
EM amy.brooks-kayal@childrens-colorado.org
RI O'Brien, Terence/L-8102-2013
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 0013-9580
EI 1528-1167
J9 EPILEPSIA
JI Epilepsia
PD DEC
PY 2013
VL 54
IS 12
BP 2229
EP 2230
DI 10.1111/epi.12414
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 262PR
UT WOS:000327750600027
PM 24304440
ER
PT J
AU Yamaguchi, T
Wang, HL
Morales, M
AF Yamaguchi, Tsuyoshi
Wang, Hui-Ling
Morales, Marisela
TI Glutamate neurons in the substantia nigra compacta and retrorubral field
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE A8; A9; dopamine; midbrain glutamatergic neurons; VGluT2; VTA
ID VENTRAL TEGMENTAL AREA; DOPAMINERGIC-NEURONS; RAT-BRAIN; INTERFASCICULAR
NUCLEUS; TERMINALS; ACCUMBENS; STRIATUM; MIDBRAIN; TSAI
AB Dopaminergic neurons of the substantia nigra compacta (SNC), ventral tegmental area (VTA) and retrorubral field (RRF) play a role in reward, motivation, learning, memory, and movement. These neurons are intermingled with GABAergic neurons. Recent evidence shows that the VTA contains glutamatergic neurons expressing vesicular glutamate transporter type 2 (VGluT2); some of them co-express tyrosine hydroxylase (TH). Here, we used a combination of radioactive in situ hybridisation and immunohistochemistry to explore whether any of the vesicular glutamate transporters [vesicular glutamate transporter type 1 (VGluT1), VGluT2, or vesicular glutamate transporter type 3 (VGluT3)] were encoded by neurons in the SNC or RRF. We found expression of VGluT2 mRNA, but not of VGluT1 or VGluT3, in the SNC and RRF. These VGluT2 neurons rarely showed TH immunoreactivity. Within the SNC, the VGluT2 neurons were infrequently found at the rostral level, but were often seen at the medial and caudal levels intercalated in the mediolateral portion of the dorsal tier, at a ratio of one VGluT2 neuron per 4.4 TH neurons. At this level, VGluT2 neurons were also found in the adjacent substantia nigra reticulata and substantia nigra pars lateralis. Within the RRF, the VGluT2 neurons showed an increasing rostrocaudal gradient of distribution. The RRF proportion of VGluT2 neurons in relation to TH neurons was constant throughout the rostrocaudal levels, showing an average ratio of one VGluT2 neuron per 1.7 TH neurons. In summary, we provide evidence indicating that the SNC and RRF, which are traditionally considered to be dopaminergic areas, have neurons with the ability to participate in glutamate signaling.
C1 [Yamaguchi, Tsuyoshi; Wang, Hui-Ling; Morales, Marisela] NIDA, Intramural Res Program, Neuronal Networks Sect, Baltimore, MD 21224 USA.
RP Morales, M (reprint author), NIDA, Intramural Res Program, Neuronal Networks Sect, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mmorales@intra.nida.nih.gov
OI YAMAGUCHI, TSUYOSHI/0000-0002-0058-9244
FU Intramural Research Program of the National Institute on Drug Abuse
FX This work was supported by the Intramural Research Program of the
National Institute on Drug Abuse.
NR 26
TC 23
Z9 23
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
EI 1460-9568
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD DEC
PY 2013
VL 38
IS 11
BP 3602
EP 3610
DI 10.1111/ejn.12359
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 259IC
UT WOS:000327519600008
PM 24102658
ER
PT J
AU Preuss, N
van der Veen, JW
Carlson, PJ
Shen, J
Hasler, G
AF Preuss, Nora
van der Veen, Jan Willem
Carlson, Paul J.
Shen, Jun
Hasler, Gregor
TI Low single dose gabapentin does not affect prefrontal and occipital
gamma-aminobutyric acid concentrations
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Gamma-aminobutyric acid; Gabapentin; Magnetic resonance spectroscopy;
Epilepsy; Anxiety; Mood disorders
ID MAGNETIC-RESONANCE SPECTROSCOPY; PANIC DISORDER; BRAIN GABA; ANXIETY
DISORDERS; MAJOR DEPRESSION; GLUTAMATE; EPILEPSY; RELEASE; MOOD; DRUG
AB The gamma-aminobutyric acid (GABA) system has been proposed as a target for novel antidepressant and anxiolytic treatments. Emerging evidence suggests that gabapentin (GBP), an anticonvulsant drug that significantly increases brain GABA levels, is effective in the treatment of anxiety disorders. The current study was designed to measure prefrontal and occipital GABA levels in medication-free healthy subjects after taking 0 mg, 150 mg and 300 mg GBP. Subjects were scanned on a 3T scanner using a transmit-receive head coil that provided a relatively homogenous radiofrequency field to obtain spectroscopy measurement in the medial prefrontal (MPFC) and occipital cortex (OCC). There was no dose-dependent effect of GBP on GABA levels in the OCC or MPFC. There was also no effect on Glx, choline or N-acetyl-aspartate concentrations. The previously reported finding of increased GABA levels after GBP treatment is not evident for healthy subjects at the dose of 150 and 300 mg. As a result, if subjects are scanned on a 3T scanner, low dose GPB is not useful as an experimental challenge agent on the GABA system. (C) 2013 Elsevier B.V. and ECNP. All rights reserved.
C1 [Preuss, Nora] Univ Bern, Dept Psychol, CH-3000 Bern, Switzerland.
[van der Veen, Jan Willem; Shen, Jun] NIMH, Magnet Resonance Spect Core, NIH, Bethesda, MD 20892 USA.
[Carlson, Paul J.] Univ Utah, Sch Med, Salt Lake City Vet Affairs Med Ctr, Salt Lake City, UT USA.
[Carlson, Paul J.] Univ Utah, Sch Med, Dept Psychiat, Salt Lake City, UT 84112 USA.
[Shen, Jun] NIMH, Sect Magnet Resonance Spect, NIH, Bethesda, MD 20892 USA.
[Hasler, Gregor] Univ Bern, Psychiat Univ Hosp, CH-3000 Bern 60, Switzerland.
RP Hasler, G (reprint author), Univ Bern, Psychiat Univ Hosp, Bolligenstr 111, CH-3000 Bern 60, Switzerland.
EM g.hasler@bluewin.ch
RI Hasler, Gregor/E-4845-2012
OI Hasler, Gregor/0000-0002-8311-0138
NR 48
TC 1
Z9 1
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD DEC
PY 2013
VL 23
IS 12
BP 1708
EP 1713
DI 10.1016/j.euroneuro.2013.08.006
PG 6
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 265AK
UT WOS:000327921900005
PM 24071367
ER
PT J
AU Xiao, M
Prabakaran, P
Chen, WZ
Kessing, B
Dimitrov, DS
AF Xiao, Madelyne
Prabakaran, Ponraj
Chen, Weizao
Kessing, Bailey
Dimitrov, Dimiter S.
TI Deep sequencing and Circos analyses of antibody libraries reveal
antigen-driven selection of Ig V-H genes during HIV-1 infection
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Article
DE 454 sequencing; Antibodyome; Antibody repertoire; HIV-1; Human
monoclonal antibody; VDJ analysis
ID NEUTRALIZING ANTIBODIES; IMMUNE-RESPONSE; REPERTOIRE; EVOLUTION; NAIVE
AB The vast diversity of antibody repertoires is largely attributed to heavy chain (V-H) recombination of variable (V), diversity (D) and joining (J) gene segments. We used 454 sequencing information of the variable domains of the antibody heavy chain repertoires from neonates, normal adults and an HIV-1-infected individual, to analyze, with Circos software, the VDJ pairing patterns at birth, adulthood and a time-dependent response to HIV-1 infection. Our comparative analyses of the Ig VDJ repertoires from these libraries indicated that, from birth to adulthood, VDJ recombination patterns remain the same with some slight changes, whereas some VH families are selected and preferentially expressed after long-term infection with HIV-1. We also demonstrated that the immune system responds to HIV-1 chronic infection by selectively expanding certain HV families in an attempt to combat infection. Our findings may have implications for understanding immune responses in pathology as well as for development of new therapeutics and vaccines. Published by Elsevier Inc.
C1 [Xiao, Madelyne] Urbana High Sch, Ijamsville, MD 21754 USA.
[Prabakaran, Ponraj; Chen, Weizao; Dimitrov, Dimiter S.] NCI, Prot Interact Grp, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
[Prabakaran, Ponraj] Leidos Biomed Res Inc, Basic Sci Program, Frederick Natl Lab, Frederick, MD 21702 USA.
[Xiao, Madelyne; Kessing, Bailey] Leidos Biomed Res Inc, BSP CCR Genet Core, Frederick Natl Lab, Frederick, MD 21702 USA.
[Xiao, Madelyne] NCI, Werner H Kirsten Student Intern Program, NIH, Frederick, MD 21702 USA.
RP Prabakaran, P (reprint author), NCI Frederick, 1050 Boyles St,Bldg 469,Rm 140, Frederick, MD 21702 USA.
EM prabakaran.ponraj@nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; NIH, National Cancer Institute
[NO1-CO-12400, HHSN261200800001E]
FX We thank Drs. B. Haynes, H. Liao, C. Broder, and T. Fouts for reagents.
We thank the Laboratory of Molecular Technology and Advanced Biomedical
Computing Center of SAIC-Frederick Inc. for sequencing service. We thank
Ms. Maria G. Singarayan for constructing the PostgreSQL database and
developing JAVA applications. This research was supported by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, and by the Federal Funds from the NIH,
National Cancer Institute, under Contract No. NO1-CO-12400 and
HHSN261200800001E. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does the mention of trade names, commercial products, or
organizations imply endorsement by the U.S. Government.
NR 24
TC 7
Z9 8
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD DEC
PY 2013
VL 95
IS 3
BP 357
EP 363
DI 10.1016/j.yexmp.2013.10.004
PG 7
WC Pathology
SC Pathology
GA 266EZ
UT WOS:000328007500016
PM 24158018
ER
PT J
AU Bogich, TL
Anthony, SJ
Nichols, JD
AF Bogich, Tiffany L.
Anthony, Simon J.
Nichols, James D.
TI Surveillance theory applied to virus detection: a case for targeted
discovery
SO FUTURE VIROLOGY
LA English
DT Review
DE adaptive management; detection; modeling; structured decision-making;
surveillance; virus discovery
ID BORNA-DISEASE AGENT; INFECTIOUS-DISEASES; VACCINATION STRATEGIES;
PATHOGEN DISCOVERY; OPTIMAL MANAGEMENT; HOST-SPECIFICITY; TRANSMISSION;
CORONAVIRUS; UNCERTAINTY; EMERGENCE
AB Virus detection and mathematical modeling have gone through rapid developments in the past decade. Both offer new insights into the epidemiology of infectious disease and characterization of future risk; however, modeling has not yet been applied to designing the best surveillance strategies for viral and pathogen discovery. We review recent developments and propose methods to integrate viral and pathogen discovery and mathematical modeling through optimal surveillance theory, arguing for a more targeted approach to novel virus detection guided by the principles of adaptive management and structured decision-making.
C1 [Bogich, Tiffany L.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Bogich, Tiffany L.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Anthony, Simon J.] Columbia Univ, Mailman Sch Publ Hlth, Ctr Infect & Immun, New York, NY USA.
[Anthony, Simon J.] EcoHealth Alliance, New York, NY USA.
[Nichols, James D.] US Geol Survey, Patuxent Wildlife Res Ctr, Laurel, MD USA.
RP Bogich, TL (reprint author), NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM tbogich@princeton.edu
OI Bogich, Tiffany/0000-0002-8143-5289
NR 42
TC 1
Z9 1
U1 1
U2 13
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1746-0794
EI 1746-0808
J9 FUTURE VIROL
JI Future Virol.
PD DEC
PY 2013
VL 8
IS 12
BP 1201
EP 1206
DI 10.2217/fvl.13.105
PG 6
WC Virology
SC Virology
GA 258PE
UT WOS:000327470400010
ER
PT J
AU Chandler, RJ
Tarasenko, TN
Cusmano-Ozog, K
Sun, Q
Sutton, VR
Venditti, CP
McGuire, PJ
AF Chandler, R. J.
Tarasenko, T. N.
Cusmano-Ozog, K.
Sun, Q.
Sutton, V. R.
Venditti, C. P.
McGuire, P. J.
TI Liver-directed adeno-associated virus serotype 8 gene transfer rescues a
lethal murine model of citrullinemia type 1
SO GENE THERAPY
LA English
DT Article
DE urea cycle disorders; citrullinemia; AAV8; hyperammonemia
ID UREA CYCLE DISORDERS; ESSENTIAL AMINO-ACID; ARGININOSUCCINATE
SYNTHETASE; OTC DEFICIENCY; AAV8 VECTOR; TRANSPLANTATION; ARGININE;
METABOLISM; THERAPY; ENZYME
AB Citrullinemia type 1 (CTLN1) is an autosomal recessive disorder of metabolism caused by a deficiency of argininosuccinate synthetase. Despite optimal management, CTLN1 patients still suffer from lethal metabolic instability and experience life-threatening episodes of acute hyperammonemia. A murine model of CTLN1 (fold/fold) that displays lethality within the first 21 days of life was used to determine the efficacy of adeno-associated viral (AAV) gene transfer as a potential therapy. An AAV serotype 8 (AAV8) vector was engineered to express the human ASS1 cDNA under the control of a liver-specific promoter (thyroxine-binding globulin, TBG), AAV8-TBG-hASS1, and delivered to 7-10 days old mice via intraperitoneal injection. Greater than 95% of the mice were rescued from lethality and survival was extended beyond 100 days after receiving a single dose of vector. AAV8-TBG-hASS7 treatment resulted in liver-specific expression of hASS1, increased ASS1 enzyme activity, reduction in plasma ammonia and citrulline concentrations and significant phenotypic improvement of the fold/fold growth and skin phenotypes. These experiments highlight a gene transfer approach using AAV8 vector for liver-targeted gene therapy that could serve as a treatment for CTLN1.
C1 [Chandler, R. J.; Venditti, C. P.] NHGRI, Organ Acid Res Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Tarasenko, T. N.; McGuire, P. J.] NHGRI, Phys Scientist Dev Program, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Cusmano-Ozog, K.] Childrens Natl Med Ctr, Dept Genet & Metab, Washington, DC 20010 USA.
[Sun, Q.; Sutton, V. R.] Baylor Coll Med, Biochem Genet Lab, Houston, TX 77030 USA.
RP McGuire, PJ (reprint author), NHGRI, NIH, 49 Convent Dr,Room 4A62, Bethesda, MD 20892 USA.
EM peter.mcguire@nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX For this work, RJC, TNT, CPV, and PJM were supported by the Intramural
Research Program of the National Human Genome Research Institute,
National Institutes of Health. Thanks to the National Human Genome
Research Institute mouse core for mouse care and technical assistance.
NR 23
TC 5
Z9 5
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0969-7128
EI 1476-5462
J9 GENE THER
JI Gene Ther.
PD DEC
PY 2013
VL 20
IS 12
BP 1188
EP 1191
DI 10.1038/gt.2013.53
PG 4
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity; Research & Experimental Medicine
GA 265CB
UT WOS:000327926200012
PM 24131980
ER
PT J
AU Rimbault, M
Beale, HC
Schoenebeck, JJ
Hoopes, BC
Allen, JJ
Kilroy-Glynn, P
Wayne, RK
Sutter, NB
Ostrander, EA
AF Rimbault, Maud
Beale, Holly C.
Schoenebeck, Jeffrey J.
Hoopes, Barbara C.
Allen, Jeremy J.
Kilroy-Glynn, Paul
Wayne, Robert K.
Sutter, Nathan B.
Ostrander, Elaine A.
TI Derived variants at six genes explain nearly half of size reduction in
dog breeds
SO GENOME RESEARCH
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GROWTH-HORMONE; POSTNATAL-GROWTH; DOMESTIC DOG;
HUMAN HEIGHT; TGF-BETA; BIOLOGICAL PATHWAYS; BODY HEIGHT; HMGI-C; ADULT
AB Selective breeding of dogs by humans has generated extraordinary diversity in body size. A number of multibreed analyses have been undertaken to identify the genetic basis of this diversity. We analyzed four loci discovered in a previous genome-wide association study that used 60,968 SNPs to identify size-associated genomic intervals, which were too large to assign causative roles to genes. First, we performed fine-mapping to define critical intervals that included the candidate genes GHR, HMGA2, SMAD2, and STC2, identifying five highly associated markers at the four loci. We hypothesize that three of the variants are likely to be causative. We then genotyped each marker, together with previously reported size-associated variants in the IGF1 and IGF1R genes, on a panel of 500 domestic dogs from 93 breeds, and identified the ancestral allele by genotyping the same markers on 30 wild canids. We observed that the derived alleles at all markers correlated with reduced body size, and smaller dogs are more likely to carry derived alleles at multiple markers. However, breeds are not generally fixed at all markers; multiple combinations of genotypes are found within most breeds. Finally, we show that 46%-52.5% of the variance in body size of dog breeds can be explained by seven markers in proximity to exceptional candidate genes. Among breeds with standard weights <41 kg (90 lb), the genotypes accounted for 64.3% of variance in weight. This work advances our understanding of mammalian growth by describing genetic contributions to canine size determination in non-giant dog breeds.
C1 [Rimbault, Maud; Beale, Holly C.; Schoenebeck, Jeffrey J.; Ostrander, Elaine A.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Hoopes, Barbara C.] Colgate Univ, Dept Biol, Hamilton, NY 13346 USA.
[Allen, Jeremy J.; Sutter, Nathan B.] Cornell Univ, Dept Clin Sci, Coll Vet Med, Ithaca, NY 14853 USA.
[Kilroy-Glynn, Paul] Dublin City Univ, Sch Biotechnol, Dublin 9, Ireland.
[Wayne, Robert K.] Univ Calif Los Angeles, Dept Ecol & Evolutionary Biol, Los Angeles, CA 90095 USA.
RP Ostrander, EA (reprint author), NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
EM eostrand@mail.nih.gov
OI Ostrander, Elaine/0000-0001-6075-9738
FU American Kennel Club-Canine Health Foundation; Intramural Program of the
National Human Genome Research Institute of the National Institutes of
Health; Cornell University; NIGMS PRAT postdoctoral fellowship; Research
Council of Colgate University; NSF-DEB [1021397, 0733033]; NIH
[5R21HG006051-02]
FX We thank the American Kennel Club-Canine Health Foundation, the
Intramural Program of the National Human Genome Research Institute of
the National Institutes of Health (E.A.O., M. R., H. C. B., and J.J.S.),
and Cornell University (N.B.S. and J.J.A.) for supporting this work.
J.J.S. was funded by an NIGMS PRAT postdoctoral fellowship. Sabbatical
support for B. C. H. was provided by a grant from the Research Council
of Colgate University. R. K. W. is supported by grants NSF-DEB 1021397
and 0733033, and N.B.S. by NIH grant 5R21HG006051-02. We thank Drs. John
Novembre, Heidi Parker, and Jonine Figueroa for their helpful insights
and feedback. We thank the NIH Intramural Sequencing Center staff for
valuable technical and computational assistance. We thank Dr. Shelley
Hoogstraten-Miller and Irene Ginty for assistance in blood draws.
Finally, we are grateful to the many dog owners and breeders who
generously provided DNA samples for this study.
NR 64
TC 23
Z9 23
U1 10
U2 51
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD DEC
PY 2013
VL 23
IS 12
BP 1985
EP 1995
DI 10.1101/gr.157339.113
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 265JJ
UT WOS:000327946900003
PM 24026177
ER
PT J
AU Lai, AY
Mav, D
Shah, R
Grimm, SA
Phadke, D
Hatzi, K
Melnick, A
Geigerman, C
Sobol, SE
Jaye, DL
Wade, PA
AF Lai, Anne Y.
Mav, Deepak
Shah, Ruchir
Grimm, Sara A.
Phadke, Dhiral
Hatzi, Katerina
Melnick, Ari
Geigerman, Cissy
Sobol, Steve E.
Jaye, David L.
Wade, Paul A.
TI DNA methylation profiling in human B cells reveals immune regulatory
elements and epigenetic plasticity at Alu elements during B-cell
activation
SO GENOME RESEARCH
LA English
DT Article
ID STEM-CELLS; METHYLTRANSFERASE GENE; HUMAN GENOME; TRANSCRIPTIONAL
REPRESSION; IMMUNODEFICIENCY SYNDROME; T-CELLS; MEMORY; DIFFERENTIATION;
PLURIPOTENT; EXPRESSION
AB Memory is a hallmark of adaptive immunity, wherein lymphocytes mount a superior response to a previously encountered antigen. It has been speculated that epigenetic alterations in memory lymphocytes contribute to their functional distinction from their naive counterparts. However, the nature and extent of epigenetic alterations in memory compartments remain poorly characterized. Here we profile the DNA methylome and the transcriptome of B-lymphocyte subsets representing stages of the humoral immune response before and after antigen exposure in vivo from multiple humans. A significant percentage of activation-induced losses of DNA methylation mapped to transcription factor binding sites. An additional class of demethylated loci mapped to Alu elements across the genome and accompanied repression of DNA methyltransferase 3A. The activation-dependent DNA methylation changes were largely retained in the progeny of activated B cells, generating a similar epigenetic signature in downstream memory B cells and plasma cells with distinct transcriptional programs. These findings provide insights into the methylation dynamics of the genome during cellular differentiation in an immune response.
C1 [Lai, Anne Y.; Wade, Paul A.] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
[Mav, Deepak; Shah, Ruchir; Phadke, Dhiral] SRA Int Inc, Durham, NC 27709 USA.
[Grimm, Sara A.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Hatzi, Katerina; Melnick, Ari] Weill Cornell Med Coll, New York, NY 10065 USA.
[Geigerman, Cissy; Jaye, David L.] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
[Sobol, Steve E.] Emory Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Atlanta, GA 30322 USA.
RP Wade, PA (reprint author), NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
EM wadep2@niehs.nih.gov
FU National Institute of Environmental Health Sciences, NIH [Z01ES101965];
National Institutes of Health [DK60647]; National Institute of
Environmental Health Sciences, National Institutes of Health, Department
of Health and Human Services [HHSN291200555547C]; GSA [GS-00F-003L]
FX We thank the members of the Wade laboratory, Drs. T. Archer, K. Adelman,
R. Jothi, J. Taylor, and M. Resnick for critical comments and
suggestions for this manuscript. We thank the NIEHS Microarray, Flow
Cytometry, and DNA Sequencing core facilities, as well as the NIH
Intramural Sequencing Center, for their assistance. We also thank Diane
Lawson for technical assistance with immunohistochemistry, Hrisavgi
Kondilis-Mangum for assistance with graphics, and Dr. M. Kondo for
assistance with cell sorting. This work was supported by the Intramural
Research Program of the National Institute of Environmental Health
Sciences, NIH (project number Z01ES101965 to P. A. W.), and by grants
from the National Institutes of Health (DK60647 to D. L. J.). D. M., D.
P., and R. S. were supported in whole or in part with federal funds from
the National Institute of Environmental Health Sciences, National
Institutes of Health, Department of Health and Human Services, under
delivery order number HHSN291200555547C and GSA contract number
GS-00F-003L.
NR 62
TC 20
Z9 20
U1 0
U2 6
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD DEC
PY 2013
VL 23
IS 12
BP 2030
EP 2041
DI 10.1101/gr.155473.113
PG 12
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 265JJ
UT WOS:000327946900007
PM 24013550
ER
PT J
AU Oh, J
Freeman, AF
Park, M
Sokolic, R
Candotti, F
Holland, SM
Segre, JA
Kong, HDH
AF Oh, Julia
Freeman, Alexandra F.
Park, Morgan
Sokolic, Robert
Candotti, Fabio
Holland, Steven M.
Segre, Julia A.
Kong, Heidi H.
CA NISC Comparative Sequencing Progra
TI The altered landscape of the human skin microbiome in patients with
primary immunodeficiencies
SO GENOME RESEARCH
LA English
DT Article
ID HYPER-IGE SYNDROME; STAPHYLOCOCCUS-AUREUS; ATOPIC-DERMATITIS;
DIAGNOSTIC-CRITERIA; BINDING PROTEIN; SCORAD INDEX; MUTATIONS;
BACTERIAL; DISEASE; EPIDERMIDIS
AB While landmark studies have shown that microbiota activate and educate host immunity, how immune systems shape microbiomes and contribute to disease is incompletely characterized. Primary immunodeficiency (PID) patients suffer recurrent microbial infections, providing a unique opportunity to address this issue. To investigate the potential influence of host immunity on the skin microbiome, we examined skin microbiomes in patients with rare monogenic PIDs: hyper-IgE (STAT3-deficient), Wiskott-Aldrich, and dedicator of cytokinesis 8 syndromes. While specific immunologic defects differ, a shared hallmark is atopic dermatitis (AD)-like eczema. We compared bacterial and fungal skin microbiomes (41 PID, 13 AD, 49 healthy controls) at four clinically relevant sites representing the major skin microenvironments. PID skin displayed increased ecological permissiveness with altered population structures, decreased site specificity and temporal stability, and colonization with microbial species not observed in controls, including Clostridium species and Serratia marcescens. Elevated fungal diversity and increased representation of opportunistic fungi (Candida, Aspergillus) supported increased PID skin permissiveness, suggesting that skin may serve as a reservoir for the recurrent fungal infections observed in these patients. The overarching theme of increased ecological permissiveness in PID skin was counterbalanced by the maintenance of a phylum barrier in which colonization remained restricted to typical human-associated phyla. Clinical parameters, including markers of disease severity, were positively correlated with prevalence of Staphylococcus, Corynebacterium, and other less abundant taxa. This study examines differences in microbial colonization and community stability in PID skin and informs our understanding of host-microbiome interactions, suggesting a bidirectional dialogue between skin commensals and the host organism.
C1 [Oh, Julia; Sokolic, Robert; Candotti, Fabio; Segre, Julia A.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Freeman, Alexandra F.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Park, Morgan; NISC Comparative Sequencing Progra] NHGRI, NIH, Intramural Sequencing Ctr, Bethesda, MD 20892 USA.
[Kong, Heidi H.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Segre, JA (reprint author), NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
EM jsegre@mail.nih.gov; konghe@mail.nih.gov
OI Kong, Heidi/0000-0003-4424-064X
FU NIH NHGRI; NCI; National Institutes of Health [1UH2AR057504-01,
4UH3AR057504-02]; [1K99AR059222]
FX We thank members of the Segre laboratory, Helen C. Su, and Mark C. Udey
for their helpful discussions and, in particular, Sean Conlan, Clayton
Deming, Jennifer Meyer, Effie Nomicos, Deborah Schoenfeld, and Elizabeth
Garabedian for their underlying efforts. This work was supported by NIH
NHGRI and NCI Intramural Research Programs and in part by 1K99AR059222
(H. H. K.). Sequencing was funded by grants from the National Institutes
of Health (1UH2AR057504-01 and 4UH3AR057504-02).
NR 51
TC 48
Z9 49
U1 4
U2 48
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD DEC
PY 2013
VL 23
IS 12
BP 2103
EP 2114
DI 10.1101/gr.159467.113
PG 12
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 265JJ
UT WOS:000327946900013
PM 24170601
ER
PT J
AU Kohli, A
Sims, Z
Marti, M
Nelson, AK
Osinusi, A
Bon, D
Herrmann, E
Kotb, C
Silk, R
Teferi, G
Symonds, WT
Pang, PS
McHutchison, JG
Subramanian, M
Polis, MA
Masur, H
Kottilil, S
AF Kohli, Anita
Sims, Zayani
Marti, Miriam
Nelson, Amy K.
Osinusi, Anu
Bon, Dimitra
Herrmann, Eva
Kotb, Colleen
Silk, Rachel
Teferi, Gebeyehu
Symonds, William T.
Pang, Phil S.
McHutchison, John G.
Subramanian, Mani
Polis, Michael A.
Masur, Henry
Kottilil, Shyam
TI Combination Oral, Ribavirin Free, Antiviral Therapy to Optimize
Treatment Outcomes for Hepatitis C GT-1 Treatment Naive Patients:
Interim Results from the NIAID SYNERGY Trial
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 [Kohli, Anita; Kotb, Colleen; Silk, Rachel] SAIC Frederick Inc, Clin Res Directorate Clin Monitoring Res Program, Frederick, MD USA.
[Kohli, Anita; Sims, Zayani; Osinusi, Anu; Masur, Henry] NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Marti, Miriam; Nelson, Amy K.; Polis, Michael A.; Kottilil, Shyam] NIAID, NIH, Immunoregulat Lab, Bethesda, MD 20892 USA.
[Osinusi, Anu] Univ Maryland, Dept Infect Dis, Baltimore, MD 21201 USA.
[Bon, Dimitra; Herrmann, Eva] Goethe Univ Frankfurt, Inst Biostst & Math Modeling, D-60054 Frankfurt, Germany.
[Teferi, Gebeyehu] Unity Hlth Care Inc, Washington, DC USA.
[Symonds, William T.; Pang, Phil S.; McHutchison, John G.; Subramanian, Mani] Gilead Sci, Foster City, CA USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2013
VL 58
IS 6
MA LB8
BP 1382A
EP 1382A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 257LH
UT WOS:000327385000009
ER
PT J
AU Koh, C
Zhao, XC
Samala, N
Sakiani, S
Liang, TJ
Talwalkar, JA
AF Koh, Christopher
Zhao, Xiongce
Samala, Niharika
Sakiani, Sasan
Liang, T. Jake
Talwalkar, Jayant A.
TI AASLD Clinical Practice Guidelines: A Critical Review of Scientific
Evidence and Evolving Recommendations
SO HEPATOLOGY
LA English
DT Article
ID INTRAHEPATIC PORTOSYSTEMIC SHUNT; PRIMARY BILIARY-CIRRHOSIS; ACUTE
LIVER-FAILURE; AMERICAN ASSOCIATION; AUTOIMMUNE HEPATITIS;
PORTAL-HYPERTENSION; POSITION PAPER; WILSON-DISEASE; ADULT PATIENTS;
UPDATE 2009
AB The American Association for the Study of Liver Diseases (AASLD) practice guidelines provide recommendations in diagnosing and managing patients with liver disease from available scientific evidence in combination with expert consensus opinions. The aim was to systematically review the evolution of recommendations from AASLD guidelines and identify gaps limiting the evidence-based foundations of these guidelines. Initial and current AASLD guidelines published from January 1998 to August 2012 were reviewed. The AGREE II instrument was used to evaluate rigor and transparency of guideline development. The number of recommendations, distribution of grades (strength or certainty), classes (benefit versus risk), and types of recommendations were evaluated. Whenever possible, multiple versions were evaluated for evolving scientific evidence. A total of 991 recommendations from 28 guidelines on 17 topics were evaluated. From initial to current guidelines, the total number of recommendations increased by 36% (512 to 699). The largest increases were from chronic hepatitis B virus (HBV) (+71), liver transplantation (+53), and autoimmune hepatitis (AIH) (+27). Most current recommendations are grade II (44%) and less than 20% are grade I. The AGREE II evaluation showed global improvement in guideline quality. Both HBV and chronic hepatitis C guidelines had greatest increases in grade I recommendations (+383% and +67%, respectively). The greatest increases in treatment recommendations were from HBV (grade I, +1,150%), liver transplantation (grade II, +112%), and AIH (grade III, +105%). Conclusion: Despite significant increases in the numbers of recommendations within AASLD practice guidelines over time, only a minority are supported by grade I evidence, highlighting the need for developing well-designed investigations to provide evidence for areas of uncertainty and improving the quality of future guidelines in hepatobiliary diseases. (Hepatology 2013; 58:2142-2152)
C1 [Koh, Christopher; Samala, Niharika; Sakiani, Sasan; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Zhao, Xiongce] NIDDK, Off Director, NIH, Bethesda, MD 20892 USA.
[Talwalkar, Jayant A.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
RP Koh, C (reprint author), NIDDK, Liver Dis Branch, NIH, Bldg 10,Rm 9B-16,10 Ctr Dr,MSC 1800, Bethesda, MD 20892 USA.
EM Christopher.koh@nih.gov
FU NIDDK, NIH
FX Supported by the Intramural Research Programs of the NIDDK, NIH.
NR 40
TC 17
Z9 22
U1 2
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD DEC
PY 2013
VL 58
IS 6
BP 2142
EP 2152
DI 10.1002/hep.26578
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 257LH
UT WOS:000327385000061
PM 23775835
ER
PT J
AU Ogawa, S
Watanabe, M
Sakurai, Y
Inutake, Y
Watanabe, S
Tai, XG
Abe, R
AF Ogawa, Shuhei
Watanabe, Masashi
Sakurai, Yuichi
Inutake, Yu
Watanabe, Shiho
Tai, Xuguang
Abe, Ryo
TI CD28 signaling in primary CD4(+) T cells: identification of both
tyrosine phosphorylation-dependent and phosphorylation-independent
pathways
SO INTERNATIONAL IMMUNOLOGY
LA English
DT Article
DE CD28; co-stimulation; phosphorylation; T-cell activation
ID PROTEIN-KINASE-C; NF-KAPPA-B; COSTIMULATORY MOLECULE CD28;
PHOSPHATIDYLINOSITOL 3-KINASE; CD28-MEDIATED COSTIMULATION;
IMMUNOLOGICAL SYNAPSE; CYTOPLASMIC DOMAIN; RECEPTOR CD28; ANTIGEN
RECEPTOR; CUTTING EDGE
AB In addition to TCR signaling, the activation and proliferation of naive T cells require CD28-mediated co-stimulation. Once engaged, CD28 is phosphorylated and can then activate signaling pathways by recruiting molecules to its YMNM motif and two PxxP motifs. In this study, we analyzed the relationship between tyrosine phosphorylation and the co-stimulatory function of CD28 in murine primary CD4(+) T cells. Tyrosine phosphorylation is decreased in CD28 where the N-terminal PxxP motif is mutated (nPA). In cells expressing nPA, activation of Akt and functional co-stimulation were decreased. In contrast, where the C-terminal PxxP motif is mutated, tyrosine phosphorylation and activation of the ERK, Akt and NF-kappa B were intact, but proliferation and IL-2 production were decreased. Using the Y-189 to F mutant, we also demonstrated that in naive CD4(+) T cells, tyrosine at position 189 in the YMNM motif is critical for both tyrosine phosphorylation and the functional co-stimulatory effects of CD28. This mutation did not affect unfractionated T-cell populations. Overall, our data suggest that CD28 signaling uses tyrosine phosphorylation-dependent and phosphorylation-independent pathways.
C1 [Ogawa, Shuhei; Watanabe, Shiho; Abe, Ryo] Tokyo Univ Sci, Res Inst Biomed Sci, Noda, Chiba 2780022, Japan.
[Ogawa, Shuhei; Abe, Ryo] Tokyo Univ Sci, Ctr Technol Canc, Noda, Chiba 2780022, Japan.
[Watanabe, Masashi; Tai, Xuguang] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Sakurai, Yuichi; Inutake, Yu; Abe, Ryo] Tokyo Univ Sci, Fac Pharmaceut Sci, Noda, Chiba 2780022, Japan.
RP Abe, R (reprint author), Tokyo Univ Sci, Res Inst Biomed Sci, 2669 Yamazaki, Noda, Chiba 2780022, Japan.
EM rabe@rs.noda.tus.ac.jp
FU Japan Society for the Promotion of Science [21590541]
FX Japan Society for the Promotion of Science (C; 21590541).
NR 58
TC 6
Z9 6
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0953-8178
EI 1460-2377
J9 INT IMMUNOL
JI Int. Immunol.
PD DEC
PY 2013
VL 25
IS 12
BP 671
EP 681
DI 10.1093/intimm/dxt028
PG 11
WC Immunology
SC Immunology
GA 263FM
UT WOS:000327792300002
PM 24048955
ER
PT J
AU Siegel, AM
Stone, KD
Cruse, G
Lawrence, MG
Olivera, A
Jung, MY
Barber, JS
Freeman, AF
Holland, SM
O'Brien, M
Jones, N
Wisch, LB
Kong, HH
Desai, A
Farber, O
Gilfillan, AM
Rivera, J
Milner, JD
AF Siegel, Andrea M.
Stone, Kelly D.
Cruse, Glenn
Lawrence, Monica G.
Olivera, Ana
Jung, Mi-yeon
Barber, John S.
Freeman, Alexandra F.
Holland, Steven M.
O'Brien, Michelle
Jones, Nina
Wisch, Laura B.
Kong, Heidi H.
Desai, Avanti
Farber, Orly
Gilfillan, Alasdair M.
Rivera, Juan
Milner, Joshua D.
TI Diminished allergic disease in patients with STAT3 mutations reveals a
role for STAT3 signaling in mast cell degranulation
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Autosomal dominant hyper-IgE syndrome; Job syndrome; signal transducer
and activator of transcription 3; mast cell; degranulation
ID HYPER-IGE SYNDROME; FOLLICULAR-HELPER-CELLS; TRANSCRIPTION FACTOR; FOOD
ALLERGY; B-CELLS; RECEPTOR; GENERATION; BASOPHILS; CHILDREN; BCL6
AB Background: Severe atopic conditions associated with elevated serum IgE are heterogeneous with few known causes. Nearly every patient with autosomal-dominant hyper-IgE syndrome (AD-HIES) due to signal transducer and activator of transcription 3 (STAT3) mutations has a history of eczematous dermatitis and elevated IgE; however, clinical atopy has never been systematically studied.
Objective: Understanding of genetic determinants of allergic disease may lead to novel therapies in controlling allergic disease.
Methods: We conducted clinical evaluation of the rates of food allergies and anaphylaxis in patients with AD-HIES, a cohort of patients with no STAT3 mutation but with similar histories of elevated IgE and atopic dermatitis, and healthy volunteers with no history of atopy. Morphine skin prick testing, ImmunoCAP assays for allergen-specific IgE, and basophil activation were measured. A model of systemic anaphylaxis was studied in transgenic mice carrying an AD-HIES mutation. STAT3 was silenced in LAD2 and primary human mast cells to study the role of STAT3 in signaling and degranulation after IgE cross-linking.
Results: Food allergies and anaphylaxis were markedly diminished in patients with AD-HIES compared with a cohort of patients with no STAT3 mutation but with similar histories of elevated IgE and atopic dermatitis. Morphine skin prick testing and basophil activation were diminished in patients with AD-HIES, whereas mice carrying an AD-HIES mutation were hyporesponsive to systemic anaphylaxis models. Rapid mast cell STAT3 serine727 phosphorylation was noted after IgE cross-linking, and inhibition of STAT3 signaling in mast cells lead to impaired FceRI-mediated proximal and distal signaling, as well as reduced degranulation.
Conclusion: This study serves as an example for how mutations in specific atopic pathways can lead to discrete allergic phenotypes, encompassing increased risk of some phenotypes but a relative protection from others.
C1 [Siegel, Andrea M.; Stone, Kelly D.; Cruse, Glenn; Lawrence, Monica G.; Jung, Mi-yeon; Barber, John S.; O'Brien, Michelle; Jones, Nina; Wisch, Laura B.; Desai, Avanti; Farber, Orly; Gilfillan, Alasdair M.; Milner, Joshua D.] NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA.
[Olivera, Ana; Rivera, Juan] NIAMSD, Immunogenet Mol Lab, Bethesda, MD 20892 USA.
[Freeman, Alexandra F.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Kong, Heidi H.] NIH, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Milner, JD (reprint author), NIAID, Lab Allerg Dis, Bldg 10,Room 12S236A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM jdmilner@niaid.nih.gov
OI Kong, Heidi/0000-0003-4424-064X
FU Division of Intramural Research of the National Institute of Allergy and
Infectious Diseases; National Institute of Arthritis and Musculoskeletal
and Skin Diseases within the National Institutes of Health
FX Supported by the Division of Intramural Research of the National
Institute of Allergy and Infectious Diseases and National Institute of
Arthritis and Musculoskeletal and Skin Diseases within the National
Institutes of Health.
NR 32
TC 30
Z9 30
U1 1
U2 12
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2013
VL 132
IS 6
BP 1388
EP +
DI 10.1016/j.jaci.2013.08.045
PG 12
WC Allergy; Immunology
SC Allergy; Immunology
GA 259PG
UT WOS:000327538200018
PM 24184145
ER
PT J
AU Mueller, GA
Pedersen, LC
Lih, FB
Glesner, J
Moon, AF
Chapman, MD
Tomer, KB
London, RE
Pomes, A
AF Mueller, Geoffrey A.
Pedersen, Lars C.
Lih, Fred B.
Glesner, Jill
Moon, Andrea F.
Chapman, Martin D.
Tomer, Kenneth B.
London, Robert E.
Pomes, Anna
TI The novel structure of the cockroach allergen Bla g 1 has implications
for allergenicity and exposure assessment
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Allergen; asthma; Bla g 1; cockroach; structure; ligand-binding
proteins; exposure assessment
ID INNER-CITY CHILDREN; GREEN FLUORESCENT PROTEIN; MAJOR HUMAN ALLERGEN;
AMERICAN COCKROACH; BLATTELLA-GERMANICA; INDOOR ALLERGENS;
MONOCLONAL-ANTIBODY; CRYSTAL-STRUCTURE; GENE-EXPRESSION; ASTHMA
AB Background: Sensitization to cockroach allergens is a major risk factor for asthma. The cockroach allergen Bla g 1 has multiple repeats of approximately 100 amino acids, but the fold of the protein and its biological function are unknown.
Objective: We sought to determine the structure of Bla g 1, investigate the implications for allergic disease, and standardize cockroach exposure assays.
Methods: nBla g 1 and recombinant constructs were compared by using ELISA with specific murine IgG and human IgE. The structure of Bla g 1 was determined by x-ray crystallography. Mass spectrometry and nuclear magnetic resonance spectroscopy were used to examine the ligand-binding properties of the allergen.
Results: The structure of an rBla g 1 construct with comparable IgE and IgG reactivity to the natural allergen was solved by x-ray crystallography. The Bla g 1 repeat forms a novel fold with 6 helices. Two repeats encapsulate a large and nearly spherical hydrophobic cavity, defining the basic structural unit. Lipids in the cavity varied depending on the allergen origin. Palmitic, oleic, and stearic acids were associated with nBla g 1 from cockroach frass. One unit of Bla g 1 was equivalent to 104 ng of allergen.
Conclusions: Bla g 1 has a novel fold with a capacity to bind various lipids, which suggests a digestive function associated with nonspecific transport of lipid molecules in cockroaches. Defining the basic structural unit of Bla g 1 facilitates the standardization of assays in absolute units for the assessment of environmental allergen exposure.
C1 [Mueller, Geoffrey A.; Pedersen, Lars C.; Lih, Fred B.; Moon, Andrea F.; Tomer, Kenneth B.; London, Robert E.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Glesner, Jill; Chapman, Martin D.; Pomes, Anna] Indoor Biotechnol, Charlottesville, VA USA.
RP Mueller, GA (reprint author), NIEHS, 111 TW Alexander Dr,MD MR 01, Res Triangle Pk, NC 27709 USA.
EM Mueller3@niehs.nih.gov
OI Pomes, Anna/0000-0002-8729-1829
FU Intramural Research Program of the National Institute of Environmental
Health Sciences, National Institutes of Health [Z01-ES102885-01,
Z01-ES50161, ZIA-ES102645]; National Institute of Allergy and Infectious
Diseases of the National Institutes of Health [R01AI077653]; US
department of Energy, Basic Energy Sciences, Office of Science
[W-31-109-Eng-38]
FX Supported in part by Research Project no. Z01-ES102885-01 to R.E.L.,
Z01-ES50161 to K.B.T., and ZIA-ES102645 to L.C.P. in the Intramural
Research Program of the National Institute of Environmental Health
Sciences, National Institutes of Health. Research reported in this
publication was supported in part by the National Institute of Allergy
and Infectious Diseases of the National Institutes of Health under award
no. R01AI077653 (to A.P. and M.D.C.). The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health. Use of the Advanced
Photon Source, Argonne National Laboratory, was supported by the US
department of Energy, Basic Energy Sciences, Office of Science, under
contract no. W-31-109-Eng-38.
NR 60
TC 15
Z9 15
U1 1
U2 12
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2013
VL 132
IS 6
BP 1420
EP +
DI 10.1016/j.jaci.2013.06.014
PG 16
WC Allergy; Immunology
SC Allergy; Immunology
GA 259PG
UT WOS:000327538200021
PM 23915714
ER
PT J
AU Lawrence, MG
Barber, JS
Sokolic, RA
Garabedian, EK
Desai, AN
O'Brien, M
Jones, N
Bali, P
Hershfield, MS
Stone, KD
Candotti, F
Milner, JD
AF Lawrence, Monica G.
Barber, John S.
Sokolic, Robert A.
Garabedian, Elizabeth K.
Desai, Avanti N.
O'Brien, Michelle
Jones, Nina
Bali, Pawan
Hershfield, Michael S.
Stone, Kelly D.
Candotti, Fabio
Milner, Joshua D.
TI Elevated IgE and atopy in patients treated for early-onset ADA-SCID
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Letter
ID ALLERGIC DISEASE; DEFICIENCY; CELLS
C1 [Lawrence, Monica G.; Barber, John S.; Desai, Avanti N.; O'Brien, Michelle; Stone, Kelly D.; Milner, Joshua D.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Sokolic, Robert A.; Garabedian, Elizabeth K.; Candotti, Fabio] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Jones, Nina] SAIC Frederick Inc, Clin Res Directorate CMRP, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Bali, Pawan; Hershfield, Michael S.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Bali, Pawan; Hershfield, Michael S.] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA.
RP Lawrence, MG (reprint author), NIAID, Lab Allerg Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jdmilner@niaid.nih.gov
FU CCR NIH HHS [HHSN261200800001C]; Intramural NIH HHS [ZIA AI001099-04];
NCI NIH HHS [HHSN261200800001E]; PHS HHS [HHSN261200800001E]
NR 9
TC 5
Z9 5
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2013
VL 132
IS 6
BP 1444
EP 1446
DI 10.1016/j.jaci.2013.05.040
PG 6
WC Allergy; Immunology
SC Allergy; Immunology
GA 259PG
UT WOS:000327538200029
PM 23895897
ER
PT J
AU Rosemblat, G
Shin, D
Kilicoglu, H
Sneiderman, C
Rindflesch, TC
AF Rosemblat, Graciela
Shin, Dongwook
Kilicoglu, Halil
Sneiderman, Charles
Rindflesch, Thomas C.
TI A methodology for extending domain coverage in SemRep
SO JOURNAL OF BIOMEDICAL INFORMATICS
LA English
DT Article
DE Natural language processing application; Domain-independent ontology
development methodology; Semantic predications; UMLS knowledge sources
ID BIOMEDICAL TEXT; KNOWLEDGE; ONTOLOGY; SYSTEM
AB We describe a domain-independent methodology to extend SemRep coverage beyond the biomedical domain. SemRep, a natural language processing application originally designed for biomedical texts, uses the knowledge sources provided by the Unified Medical Language System (UMLS (c)). Ontological and terminological extensions to the system are needed in order to support other areas of knowledge. We extended SemRep's application by developing a semantic representation of a previously unsupported domain. This was achieved by adapting well-known ontology engineering phases and integrating them with the UMLS knowledge sources on which SemRep crucially-depends. While the process to extend SemRep coverage has been successfully applied in earlier projects, this paper presents in detail the step-wise approach we followed and the mechanisms implemented. A case study in the field of medical informatics illustrates how the ontology engineering phases have been adapted for optimal integration with the UMLS. We provide qualitative and quantitative results, which indicate the validity and usefulness of our methodology. Published by Elsevier Inc.
C1 [Rosemblat, Graciela; Shin, Dongwook; Kilicoglu, Halil; Sneiderman, Charles; Rindflesch, Thomas C.] NIH, Natl Lib Med, Lister Hill Ctr, Cognit Sci Branch, Bethesda, MD 20894 USA.
RP Rosemblat, G (reprint author), Natl Lib Med, Lister Hill Ctr, Bldg 38A,7S713B,8600 Rockville Pike, Bethesda, MD 20894 USA.
EM grosemblat@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Library of Medicine
FX This study was supported by the Intramural Research Program of the
National Institutes of Health, National Library of Medicine.
NR 41
TC 2
Z9 2
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1532-0464
EI 1532-0480
J9 J BIOMED INFORM
JI J. Biomed. Inform.
PD DEC
PY 2013
VL 46
IS 6
BP 1099
EP 1107
DI 10.1016/j.jbi.2013.08.005
PG 9
WC Computer Science, Interdisciplinary Applications; Medical Informatics
SC Computer Science; Medical Informatics
GA 266GU
UT WOS:000328012900014
PM 23973273
ER
PT J
AU Chawla, N
Arora, NK
AF Chawla, Neetu
Arora, Neeraj K.
TI Why do some patients prefer to leave decisions up to the doctor: lack of
self-efficacy or a matter of trust?
SO JOURNAL OF CANCER SURVIVORSHIP
LA English
DT Article
DE Cancer; Patient preferences; Patient decision support; Patient-provider
communication
ID CANCER SURVIVORS; PHYSICIAN SCALE; CENTERED CARE; PARTICIPATION;
INFORMATION; PERSPECTIVE; OUTCOMES; ROLES
AB Decision-making preferences among cancer survivors during their follow-up care remains understudied and limited research examines factors that underlie these preferences. The purpose of this study was to assess cancer patients' decision-making preferences during follow-up care, the role of trust and self-efficacy, and the effect of preferences on health outcomes.
Six hundred twenty-three bladder, leukemia, and colorectal cancer survivors were recruited to the Assessment of Patient Experiences of Cancer Care study between April 2003 and November 2004. Respondents were asked about their follow-up care experiences, including decision-making preferences, trust in physicians, self-efficacy, health-related quality of life (HRQOL), and health appraisal. Unadjusted mean scores of trust and self-efficacy measures by decision preference group were examined. Multinomial logistic and linear regressions were conducted to examine predictors of decision-making preferences and the impact of decision-making preferences on HRQOL and health appraisal.
While the majority of patients preferred shared decision-making (61.0 %), 16.1 % preferred to control their decisions and 22.1 % preferred physician control over decisions. Compared to the other groups, patients preferring physician control had greater trust in their physician (p < 0.001), similar self-efficacy for engaging in the decision-making process, and lower self-efficacy for taking responsibility over decisions (p < 0.001). There were no notable differences between decision-making groups on outcome measures.
Patients who prefer physicians to control decisions are as confident about participating in the decision-making process and experience similar health outcomes as those preferring greater decisional control. Physicians need to tailor their communication behavior to encourage participation and trust among all patients.
Findings from this study provide unique insights into the decision-making preferences of cancer patients during receipt of follow-up care, which remains an understudied phase of cancer care delivery. Results underscore the need for approaches to decision-making and patient engagement to become more nuanced and to encourage patients to participate in decision-making in ways they are most comfortable. Furthermore, physicians and health care professionals should foster environments that promote trust and clear communication regardless of patient decision-making styles.
C1 [Chawla, Neetu; Arora, Neeraj K.] NCI, Outcomes Res Branch, Appl Res Program, Div Canc Control & Populat Sci, Rockville, MD 20850 USA.
RP Chawla, N (reprint author), NCI, Outcomes Res Branch, Appl Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,3E450, Rockville, MD 20850 USA.
EM neetu.chawla@nih.gov; aroran@mail.nih.gov
FU National Cancer Institute [N01-PC-35136]
FX This paper reflects the personal opinions of Dr. Chawla and Dr. Arora
and does not convey any official position of the National Cancer
Institute. Funding for data collection was provided by the National
Cancer Institute as a contract to the Cancer Prevention Institute of
California (formerly known as the Northern California Cancer Center),
contract no. N01-PC-35136. Findings from this study were presented at
Academy Health Annual Research Meeting, June 24-26, 2012, Orlando, FL,
USA. The authors would like to acknowledge the Dr. Ingrid Oakley-Girvan
for her data collection efforts for this study.
NR 35
TC 11
Z9 11
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1932-2259
EI 1932-2267
J9 J CANCER SURVIV
JI J. Cancer Surviv.-Res. Pract.
PD DEC
PY 2013
VL 7
IS 4
BP 592
EP 601
DI 10.1007/s11764-013-0298-2
PG 10
WC Oncology; Social Sciences, Biomedical
SC Oncology; Biomedical Social Sciences
GA 259CK
UT WOS:000327504800009
PM 23892559
ER
PT J
AU Te Riele, ASJM
James, CA
Philips, B
Rastegar, N
Bhonsale, A
Groeneweg, JA
Murray, B
Tichnell, C
Judge, DP
Van der Heijden, JF
Cramer, MJM
Velthuis, BK
Bluemke, DA
Zimmerman, SL
Kamel, IR
Hauer, RNW
Calkins, H
Tandri, H
AF Te Riele, Anneline S. J. M.
James, Cynthia A.
Philips, Binu
Rastegar, Neda
Bhonsale, Aditya
Groeneweg, Judith A.
Murray, Brittney
Tichnell, Crystal
Judge, Daniel P.
Van der Heijden, Jeroen F.
Cramer, Maarten J. M.
Velthuis, Birgitta K.
Bluemke, David A.
Zimmerman, Stefan L.
Kamel, Ihab R.
Hauer, Richard N. W.
Calkins, Hugh
Tandri, Harikrishna
TI Mutation-Positive Arrhythmogenic Right Ventricular
Dysplasia/Cardiomyopathy: The Triangle of Dysplasia Displaced
SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
LA English
DT Article
DE arrhythmogenic right ventricular dysplasia; cardiomyopathy; magnetic
resonance imaging; electroanatomic mapping; ventricular tachcardia;
phenotype; genetics; implantable cardioverter defibrillator
ID TASK-FORCE CRITERIA; MAGNETIC-RESONANCE; HUMAN HEART; CARDIOMYOPATHY;
TACHYCARDIA; ABLATION; SUBSTRATE; FAMILIES; DISEASE
AB ARVD/C: The Triangle of Dysplasia Displaced
IntroductionThe traditional description of the Triangle of Dysplasia in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) predates genetic testing and excludes biventricular phenotypes.
Methods and ResultsWe analyzed Cardiac Magnetic Resonance (CMR) studies of 74 mutation-positive ARVD/C patients for regional abnormalities on a 5-segment RV and 17-segment LV model. The location of electroanatomic endo- and epicardial scar and site of successful VT ablation was recorded in 11 ARVD/C subjects. Among 54/74 (73%) subjects with abnormal CMR, the RV was abnormal in almost all (96%), and 52% had biventricular involvement. Isolated LV abnormalities were uncommon (4%). Dyskinetic basal inferior wall (94%) was the most prevalent RV abnormality, followed by basal anterior wall (87%) dyskinesis. Subepicardial fat infiltration in the posterolateral LV (80%) was the most frequent LV abnormality. Similar to CMR data, voltage maps revealed scar (<0.5 mV) in the RV basal inferior wall (100%), followed by the RV basal anterior wall (64%) and LV posterolateral wall (45%). All 16 RV VTs originated from the basal inferior wall (50%) or basal anterior wall (50%). Of 3 LV VTs, 2 localized to the posterolateral wall. In both modalities, RV apical involvement never occurred in isolation.
ConclusionMutation-positive ARVD/C exhibits a previously unrecognized characteristic pattern of disease involving the basal inferior and anterior RV, and the posterolateral LV. The RV apex is only involved in advanced ARVD/C, typically as a part of global RV involvement. These results displace the RV apex from the Triangle of Dysplasia, and provide insights into the pathophysiology of ARVD/C.
C1 [Te Riele, Anneline S. J. M.; Groeneweg, Judith A.; Van der Heijden, Jeroen F.; Cramer, Maarten J. M.; Hauer, Richard N. W.] Univ Med Ctr Utrecht, Dept Cardiol, Utrecht, Netherlands.
[Te Riele, Anneline S. J. M.; James, Cynthia A.; Philips, Binu; Bhonsale, Aditya; Murray, Brittney; Tichnell, Crystal; Judge, Daniel P.; Calkins, Hugh; Tandri, Harikrishna] Johns Hopkins Univ, Sch Med, Dept Med, Div Cardiol, Baltimore, MD 21205 USA.
[Rastegar, Neda; Bluemke, David A.; Zimmerman, Stefan L.; Kamel, Ihab R.] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
[Groeneweg, Judith A.; Hauer, Richard N. W.] Interuniv Cardiol Inst Netherlands, Utrecht, Netherlands.
[Velthuis, Birgitta K.] Univ Med Ctr Utrecht, Dept Radiol, Utrecht, Netherlands.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Tandri, H (reprint author), Johns Hopkins Univ Hosp, Div Cardiol, Dept Med, 600 N Wolfe St,Carnegie 565D, Baltimore, MD 21287 USA.
EM htandri1@jhmi.edu
OI te Riele, Anneline/0000-0003-1115-6193; Bluemke,
David/0000-0002-8323-8086
FU Dutch Heart Foundation; Alexandre Suerman Stipend; Interuniversity
Cardiology Institute of the Netherlands; National Heart, Lung, and Blood
Institute [K23HL093350]; St. Jude Medical Foundation; Medtronic Inc.;
Bogle Foundation; Healing Hearts Foundation; Campanella family;
Wilmerding Endowments; Dr. Francis P. Chiaramonte Private Foundation;
Medtronic; St. Jude Medical
FX The authors wish to acknowledge funding from the Dutch Heart Foundation
(to ASJMtR), the Alexandre Suerman Stipend (to ASJMtR), the
Interuniversity Cardiology Institute of the Netherlands (to JAG), the
National Heart, Lung, and Blood Institute (K23HL093350 to HT), the St.
Jude Medical Foundation, and Medtronic Inc. The Johns Hopkins ARVD/C
Program (ARVD. com) is supported by the Bogle Foundation, the Healing
Hearts Foundation, the Campanella family, and Wilmerding Endowments, and
the Dr. Francis P. Chiaramonte Private Foundation.; Dr. Calkins received
research support from Medtronic and St. Jude Medical. Other authors: No
disclosures.
NR 25
TC 29
Z9 29
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1045-3873
EI 1540-8167
J9 J CARDIOVASC ELECTR
JI J. Cardiovasc. Electrophysiol.
PD DEC
PY 2013
VL 24
IS 12
BP 1311
EP 1320
DI 10.1111/jce.12222
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 260OB
UT WOS:000327603100014
PM 23889974
ER
PT J
AU Yaniv, Y
Lakatta, EG
AF Yaniv, Yael
Lakatta, Edward G.
TI Pacemaker Gene Mutations, Bradycardia, Arrhythmias and the Coupled Clock
Theory
SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
LA English
DT Letter
ID AUTOMATICITY; CA(V)1.3
C1 [Yaniv, Yael; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Biomed Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Yaniv, Y (reprint author), NIA, Cardiovasc Sci Lab, Biomed Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
EM yanivy@nia.nih.gov
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
FU Intramural NIH HHS [Z99 AG999999]
NR 7
TC 5
Z9 6
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1045-3873
EI 1540-8167
J9 J CARDIOVASC ELECTR
JI J. Cardiovasc. Electrophysiol.
PD DEC
PY 2013
VL 24
IS 12
BP E28
EP E29
DI 10.1111/jce.12236
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 260OB
UT WOS:000327603100012
PM 24015891
ER
PT J
AU Canepa, M
Milaneschi, Y
Ameri, P
AlGhatrif, M
Leoncini, G
Spallarossa, P
Pontremoli, R
Brunelli, C
Strait, JB
Lakatta, EG
Ferrucci, L
AF Canepa, Marco
Milaneschi, Yuri
Ameri, Pietro
AlGhatrif, Majd
Leoncini, Giovanna
Spallarossa, Paolo
Pontremoli, Roberto
Brunelli, Claudio
Strait, James B.
Lakatta, Edward G.
Ferrucci, Luigi
TI Relationship Between Inter-Arm Difference in Systolic Blood Pressure and
Arterial Stiffness in Community-Dwelling Older Adults
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Article
ID CARDIOVASCULAR EVENTS; VASCULAR-DISEASE; HYPERTENSION; PREVALENCE;
STENOSIS; METAANALYSIS; ASSOCIATION; VARIABILITY; CANDIDATES
AB A significant inter-arm difference in systolic blood pressure (IADSBP) has recently been associated with worse cardiovascular outcomes. The authors hypothesized that part of this association is mediated by arterial stiffness, and examined the relationship between significant IADSBP and carotid-femoral pulse wave velocity (CF-PWV) in a sample from the Baltimore Longitudinal Study of Aging. Of 1045 participants, 50 (4.8%) had an IADSBP 10mm Hg at baseline, and 629 had completed data from 2 visits (for a total of 1704 visits during 8years). CF-PWV was significantly higher in patients with an IADSBP 10mm Hg (7.3 +/- 1.9 vs 8.2 +/- 2, P=.002). Compared with others, patients with IADSBP 10mm Hg also had higher body mass index, waist circumference, and triglycerides; higher prevalence of diabetes; and lower high-density lipoprotein (HDL) cholesterol (P<.001 for all). A significant association with IADSBP 10mm Hg was observed for CF-PWV in both cross-sectional (odds ratio [OR], 1.19; 95% confidence interval [CI], 1.06-1.87; P=.01) and longitudinal (OR, 1.15; 95% CI, 1.03-1.29; P=.01) multivariate analyses. Female sex, Caucasian race, high body mass index (plus diabetes and low HDL cholesterol only cross-sectionally) were other independent correlates of IADSBP 10mm Hg. Significant IADSBP is associated with increased arterial stiffness in community-dwelling older adults.
C1 [Canepa, Marco; Milaneschi, Yuri; Strait, James B.; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21225 USA.
[Canepa, Marco; AlGhatrif, Majd; Strait, James B.; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Human Cardiovasc Studies Unit, NIH, Baltimore, MD 21225 USA.
[Canepa, Marco; Ameri, Pietro; Leoncini, Giovanna; Spallarossa, Paolo; Pontremoli, Roberto; Brunelli, Claudio] Univ Genoa, Dept Internal Med, I-16126 Genoa, Italy.
[Milaneschi, Yuri] VU Univ Med Ctr GGZ InGeest, Dept Psychiat, Amsterdam, Netherlands.
[AlGhatrif, Majd] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
RP Canepa, M (reprint author), NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Harbor Hosp Ctr Room NM524,3001 South Hanover St, Baltimore, MD 21225 USA.
EM marco.canepa@nih.gov
FU NIH, National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging.
NR 31
TC 14
Z9 14
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1524-6175
EI 1751-7176
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD DEC
PY 2013
VL 15
IS 12
BP 880
EP 887
DI 10.1111/jch.12178
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 260YX
UT WOS:000327631700006
PM 24299691
ER
PT J
AU Margolis, KL
Davis, BR
Baimbridge, C
Ciocon, JO
Cuyjet, AB
Dart, RA
Einhorn, PT
Ford, CE
Gordon, D
Hartney, TJ
Haywood, LJ
Holtzman, J
Mathis, DE
Oparil, S
Probstfield, JL
Simpson, LM
Stokes, JD
Wiegmann, TB
Williamson, JD
AF Margolis, Karen L.
Davis, Barry R.
Baimbridge, Charles
Ciocon, Jerry O.
Cuyjet, Aloysius B.
Dart, Richard A.
Einhorn, Paula T.
Ford, Charles E.
Gordon, David
Hartney, Thomas J.
Haywood, L. Julian
Holtzman, Jordan
Mathis, David E.
Oparil, Suzanne
Probstfield, Jeffrey L.
Simpson, Lara M.
Stokes, John D.
Wiegmann, Thomas B.
Williamson, Jeff D.
CA ALLHAT Collaborative Res Grp
TI Author Response to Lipid-Lowering in African Americans in
ALLHAT-Optimism Bias?
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Letter
C1 [Margolis, Karen L.] Hlth Partners Inst Educ & Res, Minneapolis, MN USA.
[Davis, Barry R.; Baimbridge, Charles; Ford, Charles E.; Simpson, Lara M.] Univ Texas Sch Publ Hlth, Houston, TX USA.
[Ciocon, Jerry O.] Cleveland Clin Florida, Weston, FL USA.
[Cuyjet, Aloysius B.] Nassau Univ Med Ctr, E Meadow, NY USA.
[Dart, Richard A.] Marshfield Clin Res Fdn, Marshfield, WI USA.
[Einhorn, Paula T.; Gordon, David] NHLBI, Bethesda, MD 20892 USA.
[Hartney, Thomas J.] Vet Affairs Med Ctr Augusta, Augusta, GA USA.
[Haywood, L. Julian] LAC & USC Med Ctr, Keck Sch Med, Los Angeles, CA USA.
[Holtzman, Jordan] Vet Affairs Med Ctr, Minneapolis, MN USA.
[Mathis, David E.] Mercer Univ, Macon, GA 31207 USA.
[Oparil, Suzanne] Univ Alabama Birmingham, Birmingham, AL USA.
[Probstfield, Jeffrey L.] Univ Washington, Med Ctr, Seattle, WA 98195 USA.
[Stokes, John D.] Christie Clin, Champaign, IL USA.
[Wiegmann, Thomas B.] Vet Affairs Med Ctr Kansas City, Kansas City, MO USA.
[Williamson, Jeff D.] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
RP Margolis, KL (reprint author), Hlth Partners Inst Educ & Res, Minneapolis, MN USA.
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 1524-6175
EI 1751-7176
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD DEC
PY 2013
VL 15
IS 12
BP 941
EP 941
DI 10.1111/jch.12220
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 260YX
UT WOS:000327631700018
PM 24299695
ER
PT J
AU Gardell, AM
Yang, J
Sacchi, R
Fangue, NA
Hammock, BD
Kultz, D
AF Gardell, Alison M.
Yang, Jun
Sacchi, Romina
Fangue, Nann A.
Hammock, Bruce D.
Kueltz, Dietmar
TI Tilapia (Oreochromis mossambicus) brain cells respond to hyperosmotic
challenge by inducing myo-inositol biosynthesis
SO JOURNAL OF EXPERIMENTAL BIOLOGY
LA English
DT Article
DE osmoregulation; compatible osmolyte; myo-inositol; brain; tilapia
ID INDUCED PROLACTIN-RELEASE; CENTRAL-NERVOUS-SYSTEM; EEL
ANGUILLA-ANGUILLA; RAT-BRAIN; ORGANIC OSMOLYTES; MESSENGER-RNA; INOSITOL
COTRANSPORTER; ENVIRONMENTAL SALINITY; SEAWATER ACCLIMATION; CHRONIC
HYPOGLYCEMIA
AB This study aimed to determine the regulation of the de novo myo-inositol biosynthetic (MIB) pathway in Mozambique tilapia (Oreochromis mossambicus) brain following acute (25 ppt) and chronic (30, 60 and 90 ppt) salinity acclimations. The MIB pathway plays an important role in accumulating the compatible osmolyte, myo-inositol, in cells in response to hyperosmotic challenge and consists of two enzymes, myo-inositol phosphate synthase and inositol monophosphatase. In tilapia brain, MIB enzyme transcriptional regulation was found to robustly increase in a time (acute acclimation) or dose (chronic acclimation) dependent manner. Blood plasma osmolality and Na+ and Cl- concentrations were also measured and significantly increased in response to both acute and chronic salinity challenges. Interestingly, highly significant positive correlations were found between MIB enzyme mRNA and blood plasma osmolality in both acute and chronic salinity acclimations. Additionally, a mass spectrometry assay was established and used to quantify total myo-inositol concentration in tilapia brain, which closely mirrored the hyperosmotic MIB pathway induction. Thus, myo-inositol is a major compatible osmolyte that is accumulated in brain cells when exposed to acute and chronic hyperosmotic challenge. These data show that the MIB pathway is highly induced in response to environmental salinity challenge in tilapia brain and that this induction is likely prompted by increases in blood plasma osmolality. Because the MIB pathway uses glucose-6-phosphate as a substrate and large amounts of myo-inositol are being synthesized, our data also illustrate that the MIB pathway likely contributes to the high energetic demand posed by salinity challenge.
C1 [Gardell, Alison M.; Sacchi, Romina; Kueltz, Dietmar] Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA.
[Gardell, Alison M.; Yang, Jun; Hammock, Bruce D.; Kueltz, Dietmar] Univ Calif Davis, Superfund Res Program, NIEHS, Davis, CA 95616 USA.
[Yang, Jun; Hammock, Bruce D.] Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
[Yang, Jun; Hammock, Bruce D.] Univ Calif Davis, UCDMC Comprehens Canc Ctr, Davis, CA 95616 USA.
[Fangue, Nann A.] Univ Calif Davis, Davis, CA 95616 USA.
RP Gardell, AM (reprint author), Univ Calif Davis, Dept Anim Sci, 1 Shields Ave, Davis, CA 95616 USA.
EM amgardell@ucdavis.edu
FU NSF [IOS-1049780]; NIEHS Superfund Research Grant [P42 ES004699]; NIH;
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Grant [U24 DK097154]; West Coast Central Comprehensive Metabolomics
Resource Core Grant [WC3MRC]; NIEHS/UC Davis Superfund for a
Pre-doctoral Training Fellowship; NIEHS/UC Davis Superfund Enrichment
Activity Award; UC Davis Jastro-Shields Research Fellowship
FX Funding for this study was primarily provided by NSF Grant IOS-1049780
(to D.K.) and NIEHS Superfund Research Grant P42 ES004699 (to B.D.H. and
D.K.). This research was partially supported by NIH and the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Grant
U24 DK097154 (to B.D.H.) and through the West Coast Central
Comprehensive Metabolomics Resource Core Grant WC3MRC (to B.D.H.).
Additional support was provided by NIEHS/UC Davis Superfund for a
Pre-doctoral Training Fellowship, a NIEHS/UC Davis Superfund Enrichment
Activity Award and a UC Davis Jastro-Shields Research Fellowship (all to
A.M.G.). This content is solely the responsibility of the authors and
does not necessarily represent the official views of the National
Science Foundation (NSF) or the National Institutes of Health (NIH).
Deposited in PMC for release after 12 months.
NR 92
TC 9
Z9 9
U1 1
U2 13
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0022-0949
EI 1477-9145
J9 J EXP BIOL
JI J. Exp. Biol.
PD DEC
PY 2013
VL 216
IS 24
BP 4615
EP 4625
DI 10.1242/jeb.088906
PG 11
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 266YB
UT WOS:000328059000019
PM 24072790
ER
PT J
AU Murphy, MM
Spungen, JH
Barraj, LM
Bailey, RL
Dwyer-, JT
AF Murphy, Mary M.
Spungen, Judith H.
Barraj, Leila M.
Bailey, Regan L.
Dwyer-, Johanna T.
TI Revising the Daily Values May Affect Food Fortification and in Turn
Nutrient Intake Adequacy
SO JOURNAL OF NUTRITION
LA English
DT Article
ID DIETARY; LEVEL
AB The Nutrition Facts panel on food labels in the United States currently displays Daily Values (DVs) that are based on outdated RDAs. The FDA has indicated that it plans to update the DVs based on the newer Dietary Reference Intakes (DRIs), but there is controversy regarding the best method for calculating new DVs from the DRIs. To better understand the implications of DV revisions, assuming that manufacturers choose to maintain current label claims for micronutrients from voluntarily fortified foods, we modeled intake of 8 micronutrients using NHANES 2007-2008 data and 2 potential methods for calculating DVs: the population-weighted Estimated Average Requirement (EAR) and the population-coverage RDA. In each scenario, levels of fortified nutrients were adjusted to maintain the current %DV. Usual nutrient intakes and percentages with usual intakes less than the EAR were estimated for the U.S. population and subpopulations aged >= 4 y (n = 7976). For most nutrients, estimates of the percentage of the U.S. population with intakes below the EAR were similar regardless of whether the DV corresponded to the population-weighted EAR or the population-coverage RDA. Potential decreases were observed in adequacy of nutrients of concern for women of childbearing age, namely iron and folate (up to 9% and 3%, respectively), adequacy of calcium among children (up to 6%), and adequacy of vitamin A intakes in the total population (5%) assuming use of the population-weighted EAR compared with the population-coverage RDA for setting the DV. Results of this modeling exercise will help to inform decisions in revising the DVs.
C1 [Murphy, Mary M.; Spungen, Judith H.; Barraj, Leila M.] Exponent Inc, Washington, DC USA.
[Bailey, Regan L.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Dwyer-, Johanna T.] Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[Dwyer-, Johanna T.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Dwyer-, Johanna T.] Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
RP Murphy, MM (reprint author), Exponent Inc, Washington, DC USA.
EM mmurphy@exponent.com
OI Dwyer, Johanna/0000-0002-0783-1769
FU Fortification Committee of the International Life Sciences Institute,
North America, Washington, DC
FX Supported by the Fortification Committee of the International Life
Sciences Institute, North America, Washington, DC. This is a free access
article, distributed under terms
(http://www.nutrition.org/publications/guidelines-and-policies/license/)
that permit unrestricted noncommercial use, distribution, and
reproduction in any medium, provided the original work is properly cited
NR 28
TC 3
Z9 4
U1 0
U2 4
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3166
EI 1541-6100
J9 J NUTR
JI J. Nutr.
PD DEC
PY 2013
VL 143
IS 12
BP 1999
EP 2006
DI 10.3945/jn.113.181099
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 260CB
UT WOS:000327571500018
PM 24132571
ER
PT J
AU Ames, NJ
Peng, C
Powers, JH
Leidy, NK
Miller-Davis, C
Rosenberg, A
VanRaden, M
Wallen, GR
AF Ames, Nancy J.
Peng, Claudia
Powers, John H.
Leidy, Nancy Kline
Miller-Davis, Claiborne
Rosenberg, Alice
VanRaden, Mark
Wallen, Gwenyth R.
TI Beyond Intuition: Patient Fever Symptom Experience
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Fever; symptoms; qualitative research; content validity
ID MORTALITY
AB Context. Fever is an important sign of inflammation recognized by health care practitioners and family caregivers. However, few empirical data obtained directly from patients exist to support many of the long-standing assumptions about the symptoms of fever. Many of the literature-cited symptoms, including chills, diaphoresis, and malaise, have limited scientific bases, yet they often represent a major justification for antipyretic administration.
Objectives. To describe the patient experience of fever symptoms for the preliminary development of a fever assessment questionnaire.
Methods. Qualitative interviews were conducted with 28 inpatients, the majority (86%) with cancer diagnoses, who had a recorded temperature of >= 38 degrees C within approximately 12 hours before the interview. A semi-structured interview guide was used to elicit patient fever experiences. Thematic analyses were conducted by three independent research team members, and the data were verified through two rounds of consensus building.
Results. Eleven themes emerged. The participants reported experiences of feeling cold, weakness, warmth, sweating, nonspecific bodily sensations, gastrointestinal symptoms, headaches, emotional changes, achiness, respiratory symptoms, and vivid dreams/hallucinations.
Conclusion. Our data not only confirm long-standing symptoms of fever but also suggest new symptoms and a level of variability and complexity not captured by the existing fever literature. Greater knowledge of patients' fever experiences will guide more accurate assessment of symptoms associated with fever and the impact of antipyretic treatments on patient symptoms in this common condition. Results from this study are contributing to the content validity of a future instrument that will evaluate patient outcomes related to fever interventions. Published by Elsevier Inc. on behalf of U.S. Cancer Pain Relief Committee.
C1 [Ames, Nancy J.; Peng, Claudia; Miller-Davis, Claiborne; Wallen, Gwenyth R.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[VanRaden, Mark] NIAID, Bethesda, MD 20892 USA.
[Powers, John H.; Rosenberg, Alice] NCI, Clin Res Directorate CMRP, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Leidy, Nancy Kline] United BioSource Corp, Bethesda, MD USA.
RP Ames, NJ (reprint author), NIH, Ctr Clin, Bldg 10,Rm 3-5627,10 Ctr Dr, Bethesda, MD 20892 USA.
EM names@cc.nih.gov
FU National Institutes of Health Intramural Research Program; National
Institute of Allergy and Infectious Diseases; National Cancer Institute,
NIH [HHSN2612008 00001E]
FX Financial support for this project was provided by the National
Institutes of Health Intramural Research Program. This research also was
supported in part by the National Institute of Allergy and Infectious
Diseases.; SAIC funding statements: This project has been funded in
whole or in part with federal funds from the National Cancer Institute,
NIH, under Contract No. HHSN2612008 00001E. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor imply endorsement by the U.
S. government. The authors declare no conflicts of interest.
NR 20
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD DEC
PY 2013
VL 46
IS 6
BP 807
EP 816
DI 10.1016/j.jpainsymman.2013.02.012
PG 10
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 262WM
UT WOS:000327768600004
PM 23742739
ER
PT J
AU Aziz, NM
Grady, PA
Curtis, JR
AF Aziz, Noreen M.
Grady, Patricia A.
Curtis, J. Randall
TI Training and Career Development in Palliative Care and End-of-Life
Research: Opportunities for Development in the US
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Palliative care; end of life; research training
ID EVIDENCE-BASED RECOMMENDATIONS; INTENSIVE-CARE; MEDICAL-EDUCATION;
RANDOMIZED-TRIAL; UNITED-STATES; CANCER CARE; PROGRAMS; QUALITY;
COMMUNICATION; ADVANCE
AB There has been a dramatic increase in attention to the field of palliative care and end-of-life (PCEOL) research over the past 20 years. This increase is particularly notable in the development of palliative care clinical and educational programs. However, there remain important shortcomings in the evidence base to ensure access to and delivery of effective palliative care for patients with life-limiting illness and their families. Development of this evidence base will require that we train the next generation of researchers to focus on issues in PCEOL. The purpose of this article was to explore the current status of the recruitment, training, and retention of future investigators in PCEOL research in the U. S. and propose recommendations to move us forward. Some key contextual issues for developing and supporting this research workforce are articulated, along with timely and important research areas that will need to be addressed during research training and career development. We provide targeted key recommendations to facilitate the nurturing and support of the future research workforce that is needed to ensure the development and implementation of the science necessary for providing high-quality, evidence-based palliative care to all who need and desire it. (C) 2013 U. S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved.
C1 [Aziz, Noreen M.; Grady, Patricia A.] NINR, NIH, Bethesda, MD 20892 USA.
[Curtis, J. Randall] Univ Washington, Harborview Med Ctr, Div Pulm & Crit Care, Seattle, WA 98104 USA.
[Curtis, J. Randall] Univ Washington, Harborview Med Ctr, Dept Med, Palliat Care Ctr Excellence, Seattle, WA 98104 USA.
RP Curtis, JR (reprint author), Univ Washington, Harborview Med Ctr, UW Palliat Care Ctr Excellence, Div Pulm & Crit Care Med, Box 359762,325 9th Ave, Seattle, WA 98104 USA.
EM jrc@u.washington.edu
FU NINR
FX This work was supported by NINR. The opinions expressed in this
commentary are exclusively those of the authors and do not necessarily
reflect the opinions of the funding agency. The authors declare no
conflicts of interest.
NR 43
TC 1
Z9 1
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD DEC
PY 2013
VL 46
IS 6
BP 938
EP 946
DI 10.1016/j.jpainsymman.2013.02.008
PG 9
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 262WM
UT WOS:000327768600015
PM 23631858
ER
PT J
AU Ferreira, JN
Figueiredo, R
AF Ferreira, Joao N.
Figueiredo, Rui
TI Prevention and management of persistent idiopathic facial pain after
dental implant placement
SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION
LA English
DT Article
ID INFERIOR ALVEOLAR NERVE; OROFACIAL PAIN; POSTOPERATIVE PAIN; ANXIETY;
INJURY; SURGERY; NEUROPATHY; HYPNOSIS; TAXONOMY; PROPOSAL
C1 [Ferreira, Joao N.] Natl Inst Dent & Craniofacial Res, NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Figueiredo, Rui] Univ Barcelona, Sch Dent, Barcelona, Spain.
[Figueiredo, Rui] Inst Invest Biomed Bellvitge, Sch Dent, Barcelona, Spain.
RP Ferreira, JN (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Ctr Clin, 30 Convent Dr,Bldg 30,Room 429, Bethesda, MD 20892 USA.
EM andraderequicj@mail.nih.gov
RI Figueiredo, Rui/C-2428-2008; Ferreira, Joao/M-1517-2016
OI Figueiredo, Rui/0000-0002-2122-6530; Ferreira, Joao/0000-0002-4230-4593
FU Intramural Research Program of the National Institute of Dental and
Craniofacial Research, National Institutes of Health, Bethesda, Md
FX This study was supported in part by the Intramural Research Program of
the National Institute of Dental and Craniofacial Research, National
Institutes of Health, Bethesda, Md.
NR 27
TC 1
Z9 1
U1 1
U2 7
PU AMER DENTAL ASSOC
PI CHICAGO
PA 211 E CHICAGO AVE, CHICAGO, IL 60611 USA
SN 0002-8177
EI 1943-4723
J9 J AM DENT ASSOC
JI J. Am. Dent. Assoc.
PD DEC
PY 2013
VL 144
IS 12
BP 1358
EP 1361
PG 4
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 262JV
UT WOS:000327731900009
PM 24282265
ER
PT J
AU Jackson, SN
Woods, AS
AF Jackson, Shelley N.
Woods, Amina S.
TI Imaging of Noncovalent Complexes by MALDI-MS
SO JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY
LA English
DT Article
DE Noncovalent complexes; MALDI; Imaging; Electrostatic and hydrophobic
interactions; Matrix properties
ID ASSISTED-LASER-DESORPTION/IONIZATION; IONIZATION MASS-SPECTROMETRY;
PROTEIN COMPLEXES; STRANDED-DNA; PHOSPHATE; RECEPTOR; PEPTIDES;
ARGININE; SINGLE
AB Noncovalent interactions govern how molecules communicate. Mass spectrometry is an important and versatile tool for the analysis of noncovalent complexes (NCX). Electrospray mass spectrometry (ESI-MS) is the most widely used MS technique for the study of NCXs because of its softer ionization and easy compatibility with the solution phase of NCX mixtures. Matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) has also been used to study NCXs. However, successful analysis depends upon several experimental factors, such as matrix selection, solution pH, and instrumental parameters. In this study, we employ MALDI imaging mass spectrometry to investigate the location and formation of NCXs, involving both peptides and proteins, in a MALDI sample spot.
C1 [Jackson, Shelley N.; Woods, Amina S.] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Woods, AS (reprint author), NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM awoods@intra.nida.nih.gov
NR 40
TC 3
Z9 3
U1 0
U2 25
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1044-0305
EI 1879-1123
J9 J AM SOC MASS SPECTR
JI J. Am. Soc. Mass Spectrom.
PD DEC
PY 2013
VL 24
IS 12
BP 1950
EP 1956
DI 10.1007/s13361-013-0745-3
PG 7
WC Biochemical Research Methods; Chemistry, Analytical; Chemistry,
Physical; Spectroscopy
SC Biochemistry & Molecular Biology; Chemistry; Spectroscopy
GA 258LF
UT WOS:000327460100016
PM 24092630
ER
PT J
AU Nomani, F
Kamal, AK
AF Nomani, Fauzia
Kamal, Ayeesha Kamran
TI Granulocyte-Colony Stimulating factor for mobilizing bone marrow stem
cells in the Sub acute Stroke.How safe is the use of Granulocyte-colony
stimulating factor in sub-acute stroke? Isthis stem cell trial of
recovery enhancement beneficial?
SO JOURNAL OF THE PAKISTAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
C1 [Kamal, Ayeesha Kamran] Aga Khan Univ Hosp, Stroke Serv & Vasc Fellowship Program, Int Cerebrovasc Translat Clin Res Training Progra, Fogarty Int Ctr, Karachi, Pakistan.
Aga Khan Univ Hosp, Natl Inst Neurol Disorders & Stroke, Karachi, Pakistan.
RP Kamal, AK (reprint author), Aga Khan Univ Hosp, Stroke Serv & Vasc Fellowship Program, Int Cerebrovasc Translat Clin Res Training Progra, Fogarty Int Ctr, Karachi, Pakistan.
EM ayeesha.kamal@aku.edu
FU FIC NIH HHS [D43TW008660, D43 TW008660]
NR 1
TC 0
Z9 0
U1 0
U2 4
PU PAKISTAN MEDICAL ASSOC
PI KARACHI
PA PMA HOUSE, AGA KHAN III RD, KARACHI, 00000, PAKISTAN
SN 0030-9982
J9 J PAK MED ASSOC
JI J. Pak. Med. Assoc.
PD DEC
PY 2013
VL 63
IS 12
BP 1558
EP 1559
PG 2
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 263TL
UT WOS:000327830800027
PM 24397109
ER
PT J
AU Saw, J
Curtis, DJ
Hussey, DJ
Dobrovic, A
Aplan, PD
Slape, CI
AF Saw, Jesslyn
Curtis, David J.
Hussey, Damian J.
Dobrovic, Alexander
Aplan, Peter D.
Slape, Christopher I.
TI The fusion partner specifies the oncogenic potential of NUP98 fusion
proteins
SO LEUKEMIA RESEARCH
LA English
DT Article
DE NUP98; Homeobox; HOX; Leukemia; Translocation
ID MYELODYSPLASTIC SYNDROME; MYELOID-LEUKEMIA; GENE; LEUKEMOGENESIS;
EXPRESSION; TRANSFORMATION; TRANSCRIPTION; NUCLEOPORIN; NUP98-HOXA9;
HOXA9
AB NUP98 is among the most promiscuously translocated genes in hematological diseases. Among the 28 known fusion partners, there are two categories: homeobox genes and non-homeobox genes. The homeobox fusion partners are well-studied in animal models, resulting in HoxA cluster overexpression and hematological disease. The non-homeobox fusion partners are less well studied. We created transgenic animal models for three NUP98 fusion genes (one homeobox, two non-homeobox), and show that in this system, the NUP98-homeobox fusion promotes self-renewal and aberrant gene expression to a significantly greater extent. We conclude that homeobox partners create more potent NUP98 fusion oncogenes than do non-homeobox partners. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Saw, Jesslyn; Curtis, David J.; Slape, Christopher I.] Monash Univ, Australian Ctr Blood Dis, Cent Clin Sch, Div Blood Canc, Melbourne, Vic 3800, Australia.
[Hussey, Damian J.] Flinders Univ S Australia, Flinders Med Ctr, Dept Surg, Bedford Pk, SA 5042, Australia.
[Dobrovic, Alexander] Ludwig Inst Canc Res, Heidelberg, Vic, Australia.
[Dobrovic, Alexander] Univ Melbourne, Dept Pathol, Melbourne, Vic, Australia.
[Aplan, Peter D.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Slape, CI (reprint author), Monash Univ, Dept Biochem & Mol Biol, Bldg 77, Melbourne, Vic 3800, Australia.
EM christopher.slape@monash.edu
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016;
OI Slape, Christopher/0000-0002-8407-3092; Dobrovic,
Alexander/0000-0003-3414-112X
FU National Health and Medical Research Council of Australia; Cancer
Council of Victoria; National Institutes of Health, National Cancer
Institute
FX We thank Lionel Feigenbaum of the NCI Transgenic core facility for the
generation of the mice, animal facility staff for animal care, and Geza
Paukovics, Michael Thomson and Jeanne Le Massurier for flow cytometric
sorting. This research was supported by the National Health and Medical
Research Council of Australia, the Cancer Council of Victoria and the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute.
NR 25
TC 5
Z9 5
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
J9 LEUKEMIA RES
JI Leuk. Res.
PD DEC
PY 2013
VL 37
IS 12
BP 1668
EP 1673
DI 10.1016/j.leukres.2013.09.013
PG 6
WC Oncology; Hematology
SC Oncology; Hematology
GA 259PV
UT WOS:000327539700014
PM 24090997
ER
PT J
AU Qi, CF
Zhang, RH
Sun, JF
Li, ZY
Shin, DM
Wang, HS
Kovalchuk, AL
Sakai, T
Xiong, HB
Kon, N
Gu, W
Morse, HC
AF Qi, Chen-Feng
Zhang, Ruihua
Sun, Jiafang
Li, Zhaoyang
Shin, Dong-Mi
Wang, Hongsheng
Kovalchuk, Alexander L.
Sakai, Tomomi
Xiong, Huabao
Kon, Ning
Gu, Wei
Morse, Herbert C., III
TI Homeostatic defects in B cells deficient in the E3 ubiquitin ligase
ARF-BPI are restored by enhanced expression of MYC
SO LEUKEMIA RESEARCH
LA English
DT Article
DE ARF BP1; MYC; p53; B cell development
ID C-MYC; TUMOR-SUPPRESSOR; P53; PROLIFERATION; MICE; DIFFERENTIATION;
NEUROGENESIS; ACTIVATION; NEOPLASMS; ARF-BP1
AB The E3 ligase ARF-BP1 governs the balance of life and death decisions by directing the degradation of p53 and enhancing the transcriptional activity of MYC. We find B cells selectively deficient in ARF-BP1 have many defects in developing and mature B cells associated with increased expression of p53 and reduced expression of Myc. Overexpression of Myc results in suppression of p53 and complete reversal of defects induced by ARF-BP1 deficiency. These findings indicate that the dynamic balance between MYC and p53 required for normal B cell maturation and function is finely tuned and critically dependent on the activities of ARF-BP1. Published by Elsevier Ltd.
C1 [Qi, Chen-Feng; Sun, Jiafang; Shin, Dong-Mi; Wang, Hongsheng; Kovalchuk, Alexander L.; Sakai, Tomomi; Morse, Herbert C., III] NIAID, Virol & Cellular Immunol Sect, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Zhang, Ruihua; Xiong, Huabao; Kon, Ning] Mt Sinai Sch Med, Dept Med, Inst Immunol, New York, NY USA.
[Li, Zhaoyang] Univ Maryland Greenebaum Canc Ctr, Oncol Program, Baltimore, MD USA.
[Shin, Dong-Mi] Seoul Natl Univ, Dept Food & Nutr, Seoul, South Korea.
[Gu, Wei] Columbia Univ Coll Phys & Surg, Inst Canc Genet, New York, NY 10032 USA.
[Gu, Wei] Columbia Univ Coll Phys & Surg, Dept Pathol & Cell Biol, New York, NY 10032 USA.
RP Qi, CF (reprint author), NIAID, Immunogenet Lab, NIH, 5640 Fishers Lane,Room 1528, Rockville, MD 20852 USA.
EM cqi@niaid.nih.gov; hmorse@niaid.nih.gov
RI ZHANG, RUIHUA/G-8685-2014
FU NIH, National Institute of Allergy and Infectious Diseases; NIH
[RO1CA169246]
FX This work was supported in part by the Intramural Research Program of
the NIH, National Institute of Allergy and Infectious Diseases and NIH
grant RO1CA169246 to WG. We are indebted to Dr. Alfonso Macias for his
contributions to animal management and Dr. Zohreh Naghashfar for her
contributions to microarray studies.
NR 20
TC 1
Z9 1
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
J9 LEUKEMIA RES
JI Leuk. Res.
PD DEC
PY 2013
VL 37
IS 12
BP 1680
EP 1689
DI 10.1016/j.leukres.2013.09.009
PG 10
WC Oncology; Hematology
SC Oncology; Hematology
GA 259PV
UT WOS:000327539700016
PM 24199708
ER
PT J
AU Lesniak, WG
Mishra, MK
Jyoti, A
Balakrishnan, B
Zhang, F
Nance, E
Romero, R
Kannan, S
Kannan, RM
AF Lesniak, Wojciech G.
Mishra, Manoj K.
Jyoti, Arnar
Balakrishnan, Bindu
Zhang, Fan
Nance, Elizabeth
Romero, Roberto
Kannan, Sujatha
Kannan, Rangaramanujam M.
TI Biodistribution of Fluorescently Labeled PAMAM Dendrimers in Neonatal
Rabbits: Effect of Neuroinflammation
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE PAMAM dendrimer; biodistribution; brain uptake quantification; cellular
imaging; pharmacokinetics; neuroinflammation; cerebral palsy
ID IN-VIVO BIODISTRIBUTION; POLYAMIDOAMINE DENDRIMERS; COMPOSITE
NANODEVICES; MAGNETIC-RESONANCE; POLY(AMIDOAMINE) DENDRIMERS; TOXICITY
EVALUATION; CONTRAST AGENTS; SERUM-ALBUMIN; CANCER; NANOPARTICLES
AB Dendrimers are being explored in many preclinical studies as drug, gene, and imaging agent delivery systems. Understanding their detailed organ, tissue, cellular uptake, and retention can provide valuable insights into their effectiveness as delivery vehides and the associated toxicity. This work explores a fluorescence-quantification based assay that enables simultaneous quantitative biodistribution and imaging of dendrimers with a single agent. We have labeled an ethylenediamine-core generation-4 hydroxyl-terminated poly(amidoamine) (PAMAM) dendrimer using the fluorescent photostable, near-IR cyanine dye (Cy5) and performed quantitative and qualitative biodistribution of the dendrimer-Cy5 conjugates (D-Cy5) in healthy neonatal rabbits and neonatal rabbits with cerebral palsy (CP). The biodistribution of D-Cy5 and free Cy5 dye was evaluated in newborn rabbits, based on the developed quantification methods using fluorescence spectroscopy, high-performance liquid chromatography (HPLC), and size exclusion chromatography (SEC) and supported by microscopic imaging. The uptake was assessed in the brain, heart, liver, lungs, kidneys, blood serum, and urine. Results obtained based on these three independent methods are in good agreement and indicate the fast renal clearance of D-Cy5 and free Cy5 with relatively higher organs accumulation of the D-Cy5 conjugate. Following systemic administration, the D-Cy5 mainly accumulated in kidneys and bladder at 24 h. The quantitative biodistribution is in good agreement with previous studies based on radiolabeling. These methods for dendrimers quantification are easier and more practical, provide excellent sensitivity (reaching 0.1 ng per gram of tissue), and allow for quantification of dendrimers in different organs over longer time periods without concerns for radioactive decay, while also enabling tissue and cellular imaging in the same animal. In kits with fetal-neuroinflarnmation induced CP, there was a significantly higher uptake of D-Cy5 in the brain, while biodistribution in other organs was similar to that of healthy kits.
C1 [Lesniak, Wojciech G.; Mishra, Manoj K.; Zhang, Fan; Kannan, Rangaramanujam M.] Johns Hopkins Sch Med, Dept Ophthalmol, Ctr Nanomed, Baltimore, MD 21287 USA.
[Jyoti, Arnar; Balakrishnan, Bindu; Nance, Elizabeth; Kannan, Sujatha] Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21287 USA.
[Romero, Roberto] NICHD, Perinatol Res Branch, NIH, DHHS, Detroit, MI 48201 USA.
RP Kannan, RM (reprint author), Johns Hopkins Sch Med, Dept Ophthalmol, Ctr Nanomed, Baltimore, MD 21287 USA.
EM krangar1@jhmi.edu
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD), NIH; NICHD [R01HD069562-02]
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 (NICHD), NIH, and by
NICHD R01HD069562-02 (S.K).
NR 41
TC 23
Z9 23
U1 1
U2 29
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD DEC
PY 2013
VL 10
IS 12
BP 4560
EP 4571
DI 10.1021/mp400371r
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 263TS
UT WOS:000327831500017
PM 24116950
ER
PT J
AU Kachko, A
Loesgen, S
Shahzad-ul-Hussan, S
Tan, W
Zubkova, I
Takeda, K
Wells, F
Rubin, S
Bewley, CA
Major, ME
AF Kachko, Alla
Loesgen, Sandra
Shahzad-ul-Hussan, Syed
Tan, Wendy
Zubkova, Iryna
Takeda, Kazuyo
Wells, Frances
Rubin, Steven
Bewley, Carole A.
Major, Marian E.
TI Inhibition of Hepatitis C Virus by the Cyanobacterial Protein
Microcystis viridis Lectin: Mechanistic Differences between the
High-Mannose Specific Lectins MVL, CV-N, and GNA
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE hepatitis C; antiviral lectin; HCV entry inhibitor; cyanovirin-N (CV-N);
HCVcc; biolayer interferometry
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CARBOHYDRATE-BINDING AGENTS; REVEALS
EXTENDED MICROHETEROGENEITY; HIGH-AFFINITY BINDING; ANTI-HIV ACTIVITY;
CYANOVIRIN-N; ENVELOPE GLYCOPROTEINS; GALANTHUS-NIVALIS;
IMMUNE-RESPONSES; STRUCTURAL BASIS
AB Plant or microbial lectins are known to exhibit potent antiviral activities against viruses with glycosylated surface proteins, yet the mechanism(s) by which these carbohydrate-binding proteins exert their antiviral activities is not fully understood. Hepatitis C virus (HCV) is known to possess glycosylated envelope proteins (gpE1E2) and to be potently inhibited by lectins. Here, we tested in detail the antiviral properties of the newly discovered Microcystis viridis lectin (MVL) along with cyanovirin-N (CV-N) and Galanthus nivalis agglutinin (GNA) against cell culture HCV, as well as their binding properties toward viral particles, target cells, and recombinant HCV glycoproteins. Using infectivity assays, CV-N, MVL, and GNA inhibited HCV with IC50 values of 0.6 nM, 30.4 nM, and 11.1 nM, respectively. Biolayer interferometry analysis demonstrated a higher affinity of GNA to immobilized recombinant HCV glycoproteins compared to CV-N and MVL. Complementary studies, including fluorescence-activated cell sorting (FACS) analysis, confocal microscopy, and pre- and post-virus binding assays, showed a complex mechanism of inhibition for CV-N and MVL that includes both viral and cell association, while GNA functions by binding directly to the viral particle. Combinations of GNA with CV-N or MVL in HCV infection studies revealed synergistic inhibitory effects, which can be explained by different glycan recognition profiles of the mainly high-mannoside specific lectins, and supports the hypothesis that these lectins inhibit through different and complex modes of action. Our findings provide important insights into the mechanisms by which lectins inhibit HCV infection. Overall, the data suggest MVL and CV-N have the potential for toxicity due to interactions with cellular proteins while GNA may be a better therapeutic agent due to specificity for the HCV gpE1E2.
C1 [Kachko, Alla; Tan, Wendy; Zubkova, Iryna; Wells, Frances; Major, Marian E.] US FDA, Ctr Biol Evaluat & Res, Lab Hepatitis Viruses, Div Viral Prod, Bethesda, MD 20892 USA.
[Takeda, Kazuyo] US FDA, Ctr Biol Evaluat & Res, Microscopy & Imaging Core Facil, Bethesda, MD 20892 USA.
[Rubin, Steven] US FDA, Ctr Biol Evaluat & Res, Lab Method Dev, Div Viral Prod, Bethesda, MD 20892 USA.
[Loesgen, Sandra; Shahzad-ul-Hussan, Syed; Bewley, Carole A.] NIAID, Bioorgan Chem Lab, Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD 20892 USA.
[Shahzad-ul-Hussan, Syed] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Major, ME (reprint author), US FDA, Ctr Biol Evaluat & Res, Lab Hepatitis Viruses, Div Viral Prod, Bethesda, MD 20892 USA.
EM Marian.Major@fda.hhs.gov
FU Food and Drug Administration Intramural Research Program; Intramural
Research Program, National Institutes of Health (NIDDK); Intramural AIDS
Targeted Antiviral Program, Office of the Director (CAB)
FX The authors thank Drs. Alain Debrabant and Rana Nagatkatti, Center for
Biologics Evaluation and Research, FDA, for the usage of their Octet red
96 system. This work was supported by Food and Drug Administration
Intramural Research Program, the Intramural Research Program, National
Institutes of Health (NIDDK), and the Intramural AIDS Targeted Antiviral
Program, Office of the Director (CAB).
NR 57
TC 6
Z9 6
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD DEC
PY 2013
VL 10
IS 12
BP 4590
EP 4602
DI 10.1021/mp400399b
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 263TS
UT WOS:000327831500019
PM 24152340
ER
PT J
AU Rosenberg, HF
Foster, PS
AF Rosenberg, Helene F.
Foster, Paul S.
TI Eosinophil cytolysis and release of cell-free granules
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Letter
ID PIECEMEAL DEGRANULATION; SECRETION; MECHANISM
C1 [Rosenberg, Helene F.] NIAID, Inflammat Immunobiol Sect, NIH, Bethesda, MD 20892 USA.
[Foster, Paul S.] Univ Newcastle, Fac Hlth, Prior Res Ctr Asthma & Resp Dis, Hunter Med Res Inst, Newcastle, NSW 2300, Australia.
[Foster, Paul S.] Univ Newcastle, Fac Hlth, Sch Biomed Sci & Pharm, Newcastle, NSW 2300, Australia.
RP Rosenberg, HF (reprint author), NIAID, Inflammat Immunobiol Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM hrosenberg@niaid.nih.gov; paul.foster@newcastle.edu.au
NR 12
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD DEC
PY 2013
VL 13
IS 12
DI 10.1038/nri3341-c2
PG 1
WC Immunology
SC Immunology
GA 262EU
UT WOS:000327717900016
ER
PT J
AU Canepa, M
Strait, JB
Milaneschi, Y
AlGhatrif, M
Ramachandran, R
Makrogiannis, S
Moni, M
David, M
Brunelli, C
Lakatta, EG
Ferrucci, L
AF Canepa, M.
Strait, J. B.
Milaneschi, Y.
AlGhatrif, M.
Ramachandran, R.
Makrogiannis, S.
Moni, M.
David, M.
Brunelli, C.
Lakatta, E. G.
Ferrucci, L.
TI The relationship between visceral adiposity and left ventricular
diastolic function: Results from the Baltimore Longitudinal Study of
Aging
SO NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES
LA English
DT Article
DE Adiposity; Diastolic function; Triglycerides; Sex hormone-binding
globulin; Adipokines
ID ALL-CAUSE MORTALITY; HEART-DISEASE; OBESITY; ASSOCIATION; ADIPONECTIN;
STIFFNESS; ARTERIAL; LEPTIN; FAT
AB Background and aims: It is unclear whether subcutaneous and visceral fat are differentially correlated to the decline in left ventricular (LV) diastolic function with aging. This study sought to examine the hypothesis that age-related changes in the regional fat distribution account for changes in LV diastolic function and to explore potential mediators of this association.
Methods and results: In this cross-sectional study, we evaluated 843 participants of the Baltimore Longitudinal Study of Aging with echocardiogram, dual-energy X-ray absorptiometry (DEXA), abdominal computed tomography (CT) and blood tests performed at the same visit. LV diastolic function was assessed by parameters of LV relaxation (E/A ratio, Em and Em/Am ratio) and LV filling pressures (E/Em ratio). Total body fat was computed by DEXA, while visceral and subcutaneous fat were determined from abdominal CT. In multivariate models adjusted for demographics, cardiovascular risk factors, antihypertensive medications, physical activity and LV mass, both visceral and subcutaneous fat were associated with LV diastolic dysfunction. When both measures of adiposity were simultaneously included in the same model, only visceral fat was significantly associated with LV diastolic dysfunction. Triglycerides and sex-hormone binding globulin, but not adiponectin and leptin, were found to be significant mediators of the relationship between visceral fat and LV diastolic function, explaining 28-47% of the association. Bootstrapping analyses confirmed the significance of these findings.
Conclusions: Increased visceral adiposity is associated with LV diastolic dysfunction, possibly through a metabolic pathway involving blood lipids and ectopic fat accumulation rather than adipokines. Published by Elsevier B.V.
C1 [Canepa, M.; Strait, J. B.; Milaneschi, Y.; Ramachandran, R.; Makrogiannis, S.; David, M.; Ferrucci, L.] NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21225 USA.
[Canepa, M.; Strait, J. B.; AlGhatrif, M.; Moni, M.; Lakatta, E. G.] NIA, Lab Cardiovasc Sci, Human Cardiovasc Studies Unit, NIH, Baltimore, MD 21225 USA.
[Canepa, M.; Brunelli, C.] Univ Genoa, Res Ctr Cardiovasc Biol, Genoa, Italy.
[Milaneschi, Y.] VU Univ Med Center GGZ inGeest, Dept Psychiat, Amsterdam, Netherlands.
[AlGhatrif, M.] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
RP Canepa, M (reprint author), NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH,Harbor Hosp Ctr, 3001 S Hanover St, Baltimore, MD 21225 USA.
EM marco.canepa@nih.gov
FU NIH, National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging.
NR 31
TC 14
Z9 14
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0939-4753
EI 1590-3729
J9 NUTR METAB CARDIOVAS
JI Nutr. Metab. Carbiovasc. Dis.
PD DEC
PY 2013
VL 23
IS 12
BP 1263
EP 1270
DI 10.1016/j.numecd.2013.04.003
PG 8
WC Cardiac & Cardiovascular Systems; Endocrinology & Metabolism; Nutrition
& Dietetics
SC Cardiovascular System & Cardiology; Endocrinology & Metabolism;
Nutrition & Dietetics
GA 267EG
UT WOS:000328078900016
PM 23809149
ER
PT J
AU Epstein, MS
Ephros, HD
Epstein, JB
AF Epstein, Matthew S.
Ephros, Hillel D.
Epstein, Joel B.
TI Review of current literature and implications of RANKL inhibitors for
oral health care providers
SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY
LA English
DT Review
ID BONE-MINERAL DENSITY; POSTMENOPAUSAL WOMEN; MULTIPLE-MYELOMA;
BREAST-CANCER; OSTEOCLAST DIFFERENTIATION; PROSTATE-CANCER; JAW ONJ;
DENOSUMAB; OSTEONECROSIS; THERAPY
AB Bisphosphonates (BPs) were the first class of drugs commonly used to prevent skeletal-related events (SRE) in patients with osteoporosis, multiple myeloma (MM), or solid tumors with metastases to bone. A new alternative class of agents, receptor activator of nuclear factor kappa-B ligand (RANKL) inhibitors, are now available for use in these indications and have the potential to replace intravenous BPs. This paper presents a review of the current literature on denosumab and its association with osteonecrosis of the jaw (ONJ). Denosumab is a RANKL inhibitor that has recently been approved for the prevention of SRE for the same indications as BPs except for MM. Although the overall frequency of denosumab-related ONJ may be similar or higher than estimates of the occurrence rate of bisphosphonate-related ONJ, evidence continues to support appropriate planning and preventive care can reduce the likelihood of adverse effects, including osteonecrosis.
C1 [Epstein, Matthew S.; Ephros, Hillel D.] St Josephs Reg Med Ctr, Paterson, NJ USA.
[Ephros, Hillel D.] Seton Hall Univ, Sch Hlth & Med Sci, S Orange, NJ 07079 USA.
[Epstein, Joel B.] NCI, Div Otolaryngol & Head & Neck Surg, City Hope, Duarte, CA USA.
[Epstein, Joel B.] Cedars Sinai Hlth Syst, Los Angeles, CA USA.
RP Epstein, MS (reprint author), St Josephs Reg Med Ctr, 523 Washington St,Apt 2, Hoboken, NJ 07030 USA.
EM epsteinmatthew@gmail.com
NR 39
TC 9
Z9 9
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-4403
EI 1528-395X
J9 OR SURG OR MED OR PA
JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol.
PD DEC
PY 2013
VL 116
IS 6
BP E437
EP E442
DI 10.1016/j.oooo.2012.01.046
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 258BN
UT WOS:000327433200004
PM 22901640
ER
PT J
AU Webster, LR
Provan, PJ
Graham, DJ
Byth, K
Walker, RL
Davis, S
Salisbury, EL
Morey, AL
Ward, RL
Hawkins, NJ
Clarke, CL
Meltzer, PS
Balleine, RL
AF Webster, Lucy R.
Provan, Pamela J.
Graham, Dinny J.
Byth, Karen
Walker, Robert L.
Davis, Sean
Salisbury, Elizabeth L.
Morey, Adrienne L.
Ward, Robyn L.
Hawkins, Nicholas J.
Clarke, Christine L.
Meltzer, Paul S.
Balleine, Rosemary L.
TI Prohibitin expression is associated with high grade breast cancer but is
not a driver of amplification at 17q21.33
SO PATHOLOGY
LA English
DT Article
DE Breast cancer; genomic amplification; grade; prohibitin
ID COMPARATIVE GENOMIC HYBRIDIZATION; IN-SITU HYBRIDIZATION; REGION
POLYMORPHISM; CELL-LINES; ER STATUS; ARRAY; RISK; MYC; SENSITIVITY;
PROTEINS
AB Aims:In a study of ductal carcinoma in situ of the breast, we identified five genes at chromosome 17q21.33 that were over-expressed in high grade cases, and showed a correlation between expression and gene copy number. The aim of this study was to investigate potential drivers of genomic amplification at 17q21.33.Methods:Analysis of high resolution comparative genomic hybridisation and published data specified a minimum region of amplification at 17q21.33. Prohibitin (PHB) expression was examined by immunohistochemistry in 285 invasive breast cancers. Gene copy number was examined by fluorescence in situ hybridisation.Results:The minimum region of amplification at 17q21.33 included ten genes with PHB selected as a candidate driver. Increased PHB expression was associated with higher grade breast cancer and poorer survival. Amplification of PHB was detected in 13 of 235 cases (5.5%) but was not associated with PHB expression. PHB amplification was most common in the ERBB2+ breast cancer subtype, although high expression was most prevalent in basal-like and luminal B cancers.Conclusions:Amplification at 17q21.33 is a recurrent feature of breast cancer that forms part of a firestorm' pattern of genomic aberration. PHB is not a driver of amplification, however PHB may contribute to high grade breast cancer.
C1 [Webster, Lucy R.; Provan, Pamela J.; Graham, Dinny J.; Byth, Karen; Clarke, Christine L.; Balleine, Rosemary L.] Univ Sydney, Sydney Med Sch Westmead, Westmead, NSW 2145, Australia.
[Webster, Lucy R.; Provan, Pamela J.; Graham, Dinny J.; Clarke, Christine L.; Balleine, Rosemary L.] Westmead Inst Canc Res, Westmead, NSW, Australia.
[Webster, Lucy R.; Provan, Pamela J.; Graham, Dinny J.; Byth, Karen; Clarke, Christine L.; Balleine, Rosemary L.] Westmead Millennium Inst, Westmead, NSW, Australia.
[Salisbury, Elizabeth L.] Westmead Hosp, Inst Clin Pathol & Med Res, Westmead, NSW 2145, Australia.
[Webster, Lucy R.; Provan, Pamela J.; Clarke, Christine L.; Balleine, Rosemary L.] Western Sydney & Nepean Blue Mt Local Hlth Dist, Sydney West Canc Network, Westmead, NSW, Australia.
[Morey, Adrienne L.] St Vincents Hosp, Darlinghurst, NSW 2010, Australia.
[Ward, Robyn L.] Univ New S Wales, Prince Wales Clin Sch, Randwick, NSW, Australia.
[Hawkins, Nicholas J.] Univ New S Wales, Sch Med Sci, Randwick, NSW, Australia.
[Webster, Lucy R.] Charles Sturt Univ, Sch Biomed Sci, Wagga Wagga, NSW, Australia.
[Walker, Robert L.; Davis, Sean; Meltzer, Paul S.] NCI, Genet Branch, Bethesda, MD 20892 USA.
RP Balleine, RL (reprint author), Westmead Hosp, Inst Clin Pathol & Med Res, Westmead, NSW 2145, Australia.
EM rosemary.balleine@sydney.edu.au
RI Ward, Robyn/I-2313-2013; Hawkins, Nicholas/A-8461-2008;
OI Ward, Robyn/0000-0002-6877-8906; Hawkins, Nicholas/0000-0002-2204-3189;
Davis, Sean/0000-0002-8991-6458
FU Cure Cancer Australia Foundation; National Health and Medical Research
Council of Australia (NHMRC) [306700]; Cancer Institute New South Wales
(CINSW); University of Sydney
FX This work was supported by funding by the Cure Cancer Australia
Foundation, the National Health and Medical Research Council of
Australia (NHMRC; grant number 306700), the Cancer Institute New South
Wales (CINSW) and the University of Sydney Cancer Research Fund. RLB was
a CINSW Fellow. The authors state that there are no conflicts of
interest to disclose.
NR 37
TC 1
Z9 1
U1 1
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0031-3025
EI 1465-3931
J9 PATHOLOGY
JI Pathology
PD DEC
PY 2013
VL 45
IS 7
BP 629
EP 636
DI 10.1097/PAT.0000000000000004
PG 8
WC Pathology
SC Pathology
GA 261CF
UT WOS:000327640800001
PM 24247619
ER
PT J
AU Colon-Lopez, V
Banerjee, G
Gertz, AM
Ortiz, AP
Calo, W
Finney-Rutten, LJ
Colon-Ramos, U
Hesse, BW
Tortolero, G
AF Colon-Lopez, Vivian
Banerjee, Geetanjoli
Gertz, Alida Maria
Ortiz, Ana Patricia
Calo, William
Finney-Rutten, Lila J.
Colon-Ramos, Uriyoan
Hesse, Bradford W.
Tortolero, Guillermo
TI Behavioral Correlates of Fruit and Vegetable Intake in Puerto Rico:
Results from the Health Information National Trends Survey
SO PUERTO RICO HEALTH SCIENCES JOURNAL
LA English
DT Article
DE Puerto Rico; Fruit and Vegetable Intake Recommendations; Nutrition;
HINTS
ID NON-HISPANIC WHITES; UNITED-STATES; CANCER; CONSUMPTION; DISPARITIES;
PREVALENCE; BLACKS; RICANS
AB Objective: A diet high in fruit and vegetables (FV) is associated with a decreased risk for chronic diseases, such as cancer. Limited information exists regarding the factors associated with FV intake in persons living in Puerto Rico. The objective of this study was to examine sociodemographic, behavioral, and health-belief factors associated with dietary habits in Puerto Rico.
Methods: Secondary data analysis of adults aged 18 years and older from the Puerto Rico Health Information National Trends Survey (HINTS-PR) conducted in 2009. Multivariate logistic regression models were used to identify factors associated with meeting the established recommendations for FV consumption.
Results: Only 14.5% of the adults in Puerto Rico met the recommendations for daily FV intake, and the vast majority (90.9%) were unaware of current recommendations. Bivariate analyses demonstrated that being obese, having lower than a high school education, and not knowing the recommendations were significantly associated with not meeting these recommendations. In the multivariate logistic regression analysis, being obese (OR = 3.77; 95% CI = 1.41-10.08) and not being aware of the current dietary recommendations (OR = 9.26; 95% CI = 3.77-22.73) continued to be significantly associated with not meeting the FV intake recommendations.
Conclusion: The Puerto Rican population is far from meeting FV consumption recommendations, with prevalence estimates of consumption that are below the US median. Low FV intake might put the population in Puerto Rico at increased risk of developing cancer as well as a number of other chronic diseases that are secondary both to improper nutrition and to obesity.
C1 [Colon-Lopez, Vivian] Univ Puerto Rico, Grad Sch Publ Hlth, Dept Hlth Serv Adm, San Juan, PR 00936 USA.
[Colon-Lopez, Vivian; Banerjee, Geetanjoli; Ortiz, Ana Patricia; Tortolero, Guillermo] Univ Puerto Rico, Ctr Comprehens Canc, Canc Control & Populat Sci Program, San Juan, PR 00936 USA.
[Banerjee, Geetanjoli] Yale Univ, Sch Publ Hlth, Dept Epidemiol, New Haven, CT USA.
[Gertz, Alida Maria] Johns Hopkins Univ Hosp, Dept Internal Med, Baltimore, MD 21287 USA.
[Ortiz, Ana Patricia] Univ Puerto Rico, Grad Sch Publ Hlth, Dept Biostat & Epidemiol, San Juan, PR 00936 USA.
[Calo, William] Univ Texas Houston, Sch Publ Hlth, Div Management Policy & Community Hlth, Houston, TX USA.
[Finney-Rutten, Lila J.] Frederick Natl Canc Inst, SAIC Inc, Frederick, MD USA.
[Colon-Ramos, Uriyoan] George Washington Univ, Dept Global Hlth, Sch Publ Hlth & Hlth Serv, Washington, DC USA.
[Hesse, Bradford W.] NCI, Bethesda, MD 20892 USA.
RP Colon-Lopez, V (reprint author), Univ Puerto Rico, Sch Publ Hlth, Med Sci Campus,POB 36937, San Juan, PR 00936 USA.
EM vivian.colon@upr.edu
OI Hesse, Bradford/0000-0003-1142-1161
FU Centers for Disease Control and Prevention, Hispanic-Serving Health
Professions School [U50/325128-02]; National Institutes of Health,
National Cancer Institute [HHSN261200800001E]; Hispanic-Serving Health
Professions Schools; NCI
FX The project described herein was supported by the Centers for Disease
Control and Prevention, Hispanic-Serving Health Professions School
(U50/325128-02), and a grant from the National Institutes of Health,
National Cancer Institute (HHSN261200800001E). In addition, this study
could not have been accomplished without the help of the University of
Puerto Rico, Medical Sciences Campus, Comprehensive Cancer Center staff,
especially Lorena Gonzalez Sepulveda, epidemiology student; Lizbeth Del
Toro Mejias; and, finally, Adriana Font and Alexandra Acosta,
undergraduate research assistants from the University of Puerto Rico,
Rio Piedras Campus. We would like to thank the Hispanic-Serving Health
Professions Schools and the NCI, as well, for their financial support.
NR 24
TC 9
Z9 9
U1 0
U2 8
PU UNIV PUERTO RICO MEDICAL SCIENCES CAMPUS
PI SAN JUAN
PA OFFICE DEAN ACADEMIC AFFAIRS BOX 365067, SAN JUAN, PR 00936-5067 USA
SN 0738-0658
J9 P R HEALTH SCI J
JI P. R. Health Sci. J.
PD DEC
PY 2013
VL 32
IS 4
BP 194
EP 199
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 259PM
UT WOS:000327538800006
PM 24397217
ER
PT J
AU Pollack, AZ
Louis, GMB
Chen, Z
Peterson, CM
Sundaram, R
Croughan, MS
Sun, LP
Hediger, ML
Stanford, JB
Varner, MW
Palmer, CD
Steuerwald, AJ
Parsons, PJ
AF Pollack, Anna Z.
Louis, Germaine M. Buck
Chen, Zhen
Peterson, C. Matthew
Sundaram, Rajeshwari
Croughan, Mary S.
Sun, Liping
Hediger, Mary L.
Stanford, Joseph B.
Varner, Michael W.
Palmer, Christopher D.
Steuerwald, Amy J.
Parsons, Patrick J.
TI Trace elements and endometriosis: The ENDO Study
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Article
DE Arsenic; Cadmium; Chromium; Endometriosis; Lead; Metals; Mercury; Trace
elements
ID PLASMA-MASS SPECTROMETRY; OXIDATIVE STRESS; URINE CADMIUM; WOMEN;
EXPOSURE; MERCURY; LEAD; BLOOD; ASSOCIATION; CLASSIFICATION
AB There has been limited study of trace elements and endometriosis. Using a matched cohort design, 473 women aged 18-44 years were recruited into an operative cohort, along with 131 similarly aged women recruited into a population cohort. Endometriosis was defined as surgically visualized disease in the operative cohort, and magnetic resonance imaging diagnosed disease in the population cohort. Twenty trace elements in urine and three in blood were quantified using inductively coupled plasma mass spectrometry. Logistic regression estimated the adjusted odds (a0R) of endometriosis diagnosis for each element by cohort. No association was observed between any element and endometriosis in the population cohort. In the operative cohort, blood cadmium was associated with a reduced odds of diagnosis (aOR = 0.55; 95% CI: 0.31, 0.98), while urinary chromium and copper reflected an increased odds (aOR = 1.97; 95% CI: 1.21,3.19; aOR = 2.66; 95% CI: 1.26, 5.64, respectively). The varied associations underscore the need for continued research. Published by Elsevier Inc.
C1 [Pollack, Anna Z.; Louis, Germaine M. Buck; Chen, Zhen; Sundaram, Rajeshwari; Sun, Liping; Hediger, Mary L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Rockville, MD 20852 USA.
[Peterson, C. Matthew] Univ Utah, Div Reprod Endocrinol & Infertil, Dept Obstet & Gynecol, Salt Lake City, UT 84108 USA.
[Croughan, Mary S.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA 94110 USA.
[Croughan, Mary S.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94110 USA.
[Stanford, Joseph B.] Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT 84108 USA.
[Varner, Michael W.] Univ Utah, Dept Obstet & Gynecol, Div Maternal Fetal Med, Salt Lake City, UT 84132 USA.
[Palmer, Christopher D.; Steuerwald, Amy J.; Parsons, Patrick J.] New York State Dept Hlth, Lab Inorgan & Nucl Chem, Wadsworth Ctr, Albany, NY 12201 USA.
[Palmer, Christopher D.; Steuerwald, Amy J.; Parsons, Patrick J.] SUNY Albany, Dept Environm Hlth Sci, Albany, NY 12201 USA.
RP Pollack, AZ (reprint author), NICHD, NIH, 6100 Execut Blvd, Rockville, MD 20852 USA.
EM pollacka@mail.nih.gov
RI Varner, Michael/K-9890-2013;
OI Varner, Michael/0000-0001-9455-3973; Pollack, Anna/0000-0002-4313-3298;
Parsons, Patrick/0000-0001-9133-875X; Sundaram,
Rajeshwari/0000-0002-6918-5002; Buck Louis, Germaine/0000-0002-1774-4490
FU Intramural Research Program; Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD); National Institutes of
Health [NO1-DK-6-3428, NO1-DK-6-3427, 10001406-02]
FX Funded by the Intramural Research Program, Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD),
National Institutes of Health (Contracts NO1-DK-6-3428; NO1-DK-6-3427;
10001406-02; 10001406-02). Ethicon Endo-Surgery, LLC donated HARMONIC
(R) ACE 36P shears and scalpel blades through a signed Materials
Transfer Agreement with the University of Utah and NICHD. The authors
acknowledge the efforts of Dr. Anne M. Kennedy for reading the MRI
images.
NR 54
TC 11
Z9 11
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD DEC
PY 2013
VL 42
BP 41
EP 48
DI 10.1016/j.reprotox.2013.05.009
PG 8
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA 260BD
UT WOS:000327569100005
PM 23892002
ER
PT J
AU Sadowski, SM
He, M
Gesuwan, K
Gulati, N
Celi, F
Merino, MJ
Nilubol, N
Kebebew, E
AF Sadowski, Samira M.
He, Mei
Gesuwan, Krisana
Gulati, Neelam
Celi, Francesco
Merino, Maria J.
Nilubol, Naris
Kebebew, Electron
TI Prospective screening in familial nonmedullary thyroid cancer
SO SURGERY
LA English
DT Article
ID CARCINOMA; MANAGEMENT
AB Background. Approximately 8% of nonmedullary thyroid cancers are familial. The optimal age for screening in familial nonmedullary thyroid cancer (FNMTC) is unknown.
Methods. Kindreds with FNMTC (2 or more first-degree relatives affected) were screened prospectively with thyroid ultrasonography.
Results. Fifteen kindreds showed an overall prevalence of thyroid nodule(s) >= 5 mm of 44% at screening; 19% in the second generation, and 90% in the generation anterior to the index case. The youngest age of detection was 10 years for thyroid nodules and 18 years for thyroid cancer. Microcalcification of thyroid nodules at screening was associated with a greater risk of cancer (P < .05). Family members diagnosed with thyroid cancer by ultrasonographic screening were diagnosed at a younger age and had a lower rate of extra thyroidal invasion (P < .05).
Conclusion. In FNMTC, first-degree relatives 10 years or older, including the generation anterior to the index case, should have thyroid screening by ultrasonography, which may result in earlier diagnosis.
C1 [Sadowski, Samira M.; He, Mei; Gesuwan, Krisana; Gulati, Neelam; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Celi, Francesco] NCI, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Merino, Maria J.] NCI, Translat Surg Pathol Sect, Pathol Lab, 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 Center for Cancer Research, National Cancer Institute and National
Institute of Diabetes, Digestive, and Kidney Diseases, National
Institutes of Health
FX This research was supported by the intramural research program of the
Center for Cancer Research, National Cancer Institute and National
Institute of Diabetes, Digestive, and Kidney Diseases, National
Institutes of Health.
NR 16
TC 8
Z9 9
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6060
J9 SURGERY
JI Surgery
PD DEC
PY 2013
VL 154
IS 6
BP 1194
EP 1198
DI 10.1016/j.surg.2013.06.019
PG 5
WC Surgery
SC Surgery
GA 260BY
UT WOS:000327571200014
PM 23978593
ER
PT J
AU Patel, D
Boufraqech, M
Jain, M
Zhang, L
He, M
Gesuwan, K
Gulati, N
Nilubol, N
Fojo, T
Kebebew, E
AF Patel, Dhaval
Boufraqech, Myriem
Jain, Meenu
Zhang, Lisa
He, Mei
Gesuwan, Krisana
Gulati, Neelam
Nilubol, Nails
Fojo, Tito
Kebebew, Electron
TI M1R-34a and miR-483-5p are candidate serum biomarkers for adrenocortical
tumors
SO SURGERY
LA English
DT Article
ID MICRORNA; CANCER
AB Background. Nonfunctioning adrenal incidentalomas are common and many patients undergo adrenalectomy to exclude adrenocortical. carcinoma (ACC). Recent studies have shown dysregulated microRNA (miRNA) expression in ACC. The objective of this study was to determine the feasibility and diagnostic accuracy of measuring serum miRNAs in patients with benign and malignant adrenocortical neoplasms.
Method. Five miRNAs were selected from miRNA profiling studies in ACC (miR-let-7d, -34a, -195, -214, and 483-5p). Total miRNA was extracted from serum samples in patients with malignant and benign adrenal neoplasms. miRNAs levels w. ere measured by quantitative reverse transcript polymerase chain reaction and normalized to miR-16. To determine if miRNAs were secreted from ACC cells, we measured miRNA levels in culture.
Results. Serum samples from 22 patients with cortical adenomas and 17 patients with ACC were analyzed, and all 5 miRNAs were detected. We found greater levels of miR-34a (P =.001) and miR-4835p (P =.011) in patients with ACC. The area under the receiver operating characteristic curve was 0.81 for miR-34a and 0.74 for miR-438-5p. MiR-34a and miR-483-5p levels in ACC cells were greater in the supernatant at 48 hours compared with intracellular levels.
Conclusion. We show that dysregulated miRNAs in ACC are detectable in human serum samples. MiR34a and miR-483-5p are candidate serum biomarkers for distinguishing between benign and malignant adrenocortical tumors.
C1 [Patel, Dhaval; Boufraqech, Myriem; Jain, Meenu; Zhang, Lisa; He, Mei; Gesuwan, Krisana; Gulati, Neelam; Nilubol, Nails; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Fojo, Tito] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Patel, D (reprint author), NCI, Endocrine Oncol Branch, NIH, Clin Res Ctr, Bldg 10-CRC,Room 3-5840, Bethesda, MD 20892 USA.
EM pateldt@mail.nih.gov
RI Boufraqech, Myriem/E-4823-2016
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX Supported by the intramural research program of the Center for Cancer
Research, National Cancer Institute, National Institutes of Health.
NR 18
TC 24
Z9 27
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6060
J9 SURGERY
JI Surgery
PD DEC
PY 2013
VL 154
IS 6
BP 1224
EP 1228
DI 10.1016/j.surg.2013.06.022
PG 5
WC Surgery
SC Surgery
GA 260BY
UT WOS:000327571200022
PM 24238045
ER
PT J
AU Kaplan, SA
Lee, JY
O'Neill, EA
Meehan, AG
Kusek, JW
AF Kaplan, Steven A.
Lee, Jeannette Y.
O'Neill, Edward A.
Meehan, Alan G.
Kusek, John W.
TI Prevalence of low testosterone and its relationship to body mass index
in older men with lower urinary tract symptoms associated with benign
prostatic hyperplasia
SO AGING MALE
LA English
DT Article
DE Benign prostatic hyperplasia; lower urinary tract symptoms; Medical
Therapy of Prostatic Symptoms trial; testosterone deficiency
ID NUTRITION EXAMINATION SURVEY; HORMONE-BINDING GLOBULIN; LATE-ONSET
HYPOGONADISM; 3RD NATIONAL-HEALTH; MIDDLE-AGED MEN; METABOLIC SYNDROME;
ANDROGEN DEFICIENCY; ERECTILE DYSFUNCTION; REPLACEMENT THERAPY;
ELDERLY-MEN
AB Purpose: We examined the prevalence of low testosterone (LT) and its relationship with body mass index (BMI) in men with lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH), who were enrolled in a clinical trial of drug therapy, the Medical Therapy of Prostatic Symptoms (MTOPS) Study.
Materials and methods: MTOPS enrolled 3047 men, and of these, 1896 had total testosterone (TT) measured at baseline. LT was defined as a single measurement of TT of <5300 ng/dL.
Results: The overall prevalence of LT was 25.7%. Prevalence increased with increasing BMI; 14.7% among men who were normal weight (BMI <525 kg/m(2)) and 24.2% and 39.3% among overweight (BMI 25 to <530 kg/m(2)), and obese (baseline BMI >= 30 kg/m(2)) men, respectively.
Conclusions: LT was observed in about one in four MTOPS study participants with baseline TT measurements. The prevalence of LT increased markedly with increasing BMI. Our findings suggest a high prevalence of LT in obese men with LUTS/BPH. Physicians should be alert to the possibility of symptoms of hypogonadism in this population.
C1 [Kaplan, Steven A.] Weill Cornell Med Coll, New York, NY USA.
[Lee, Jeannette Y.] Univ Arkansas Med Sci, Dept Biostat, Little Rock, AR 72205 USA.
[O'Neill, Edward A.; Meehan, Alan G.] Merck & Co Inc, Whitehouse Stn, NJ USA.
[Kusek, John W.] NIDDK, Bethesda, MD 20892 USA.
RP Kaplan, SA (reprint author), Cornell Univ, Weill Cornell Med Coll, Inst Bladder & Prostate Hlth, 525 East 68th St F9 West,Box 261, New York, NY 10065 USA.
EM kaplans@med.cornell.edu
FU National Institute of Diabetes, Digestive and Kidney Diseases [U01
DK49977, U01 DK46416, U01 DK41418, U01 DK46429, U01 DK46431, U01
DK46437, U01 DK46468, U01 DK46472, U01 DK49880, U01 DK 49912, U01
DK49921, U01 DK49951, U01 DK49954, U01 DK49960, U01 DK49961, U01
DK49963, U01 DK49964, U01 DK49971, U01 DK49980]; National Center for
Minority Health and Health Disparities; NIH; Merck; Pfizer
FX S.A.K. has received compensation from Merck & Co., Inc. A.G.M. and
E.A.O. are employees of Merck Sharp & Dohme Corp., a subsidiary of Merck
& Co., Inc., Whitehouse Station, NJ, USA, and may hold stock/stock
options in the company. J.W.K. and J.Y.L. have no disclosures to report.
MTOPS was supported by the following cooperative agreements from the
National Institute of Diabetes, Digestive and Kidney Diseases: U01
DK49977, U01 DK46416, U01 DK41418, U01 DK46429, U01 DK46431, U01
DK46437, U01 DK46468, U01 DK46472, U01 DK49880, U01 DK 49912, U01
DK49921, U01 DK49951, U01 DK49954, U01 DK49960, U01 DK49961, U01
DK49963, U01 DK49964, U01 DK49971, U01 DK49980, as well as by the
National Center for Minority Health and Health Disparities, NIH.
Financial support and drug products for MTOPS were also provided by
Merck and Pfizer.
NR 35
TC 7
Z9 8
U1 1
U2 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1368-5538
EI 1473-0790
J9 AGING MALE
JI Aging Male
PD DEC
PY 2013
VL 16
IS 4
BP 169
EP 172
DI 10.3109/13685538.2013.844786
PG 4
WC Endocrinology & Metabolism; Urology & Nephrology
SC Endocrinology & Metabolism; Urology & Nephrology
GA 259CU
UT WOS:000327505800005
PM 24134648
ER
PT J
AU Wendler, D
AF Wendler, David
TI What Should Be Disclosed to Research Participants?
SO AMERICAN JOURNAL OF BIOETHICS
LA English
DT Article
DE informed consent; research; disclosure; risks
ID CLINICAL-TRIALS; HEALTH-CARE; SUPPORT; FRAMEWORK; CANCER; OHRP; VIEW
AB Debate surrounding the SUPPORT study highlights the absence of consensus regarding what information should be disclosed to potential research participants. Some commentators endorse the view that clinical research should be subject to high disclosure standards, even when it is testing standard-of-care interventions. Others argue that trials assessing standard-of-care interventions need to disclose only the information that is disclosed in the clinical care setting. To resolve this debate, it is important to identify the ethical concerns raised by clinical research and determine what consent process is needed to address them.
C1 NIH, Ctr Clin, Dept Bioeth, Bethesda, MD 20892 USA.
RP Wendler, D (reprint author), NIH, Ctr Clin, Dept Bioeth, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM dwendler@nih.gov
FU National Institutes of Health (NIH)
FX This work was funded by National Institutes of Health (NIH) intramural
research funds. However, the views expressed are the author's own. They
do not represent the position or policy of the NIH, the PHS, or the
DHHS. The author has no competing interests with respect to this
article.
NR 21
TC 11
Z9 11
U1 0
U2 5
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1526-5161
EI 1536-0075
J9 AM J BIOETHICS
JI Am. J. Bioeth.
PD DEC 1
PY 2013
VL 13
IS 12
BP 3
EP 8
DI 10.1080/15265161.2013.851578
PG 6
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 254HI
UT WOS:000327155300002
PM 24256522
ER
PT J
AU Resnik, DB
AF Resnik, David B.
TI What Are Reasonably Foreseeable Risks?
SO AMERICAN JOURNAL OF BIOETHICS
LA English
DT Editorial Material
ID SUPPORT; CONSENT
C1 [Resnik, David B.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Resnik, DB (reprint author), NIEHS, NIH, Mail Drop CU 03,Box 12233, Res Triangle Pk, NC 27709 USA.
EM resnikd@niehs.nih.gov
NR 9
TC 2
Z9 2
U1 0
U2 2
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1526-5161
EI 1536-0075
J9 AM J BIOETHICS
JI Am. J. Bioeth.
PD DEC 1
PY 2013
VL 13
IS 12
BP 29
EP 30
DI 10.1080/15265161.2013.849304
PG 2
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 254HI
UT WOS:000327155300010
PM 24256530
ER
PT J
AU Hidalgo, G
Ng, DK
Moxey-Mims, M
Minnick, ML
Blydt-Hansen, T
Warady, BA
Furth, SL
AF Hidalgo, Guillermo
Ng, Derek K.
Moxey-Mims, Marva
Minnick, Maria Lourdes
Blydt-Hansen, Tom
Warady, Bradley A.
Furth, Susan L.
TI Association of Income Level With Kidney Disease Severity and Progression
Among Children and Adolescents With CKD: A Report From the Chronic
Kidney Disease in Children (CKiD) Study
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Socioeconomic status; children; adolescents; chronic kidney disease;
progression; growth
ID GLOMERULAR-FILTRATION-RATE; STAGE RENAL-DISEASE; SOCIOECONOMIC
DISPARITIES; RACIAL-DIFFERENCES; UNITED-STATES; HEALTH; DIALYSIS; RACE;
US
AB Background: Among adults, lower socioeconomic status (SES) is a risk factor for chronic kidney disease (CKD), progression to end-stage renal disease, and poor health outcomes; but its impact on young people with CKD is not established.
Study Design: Prospective cohort study.
Settings & Participants: 572 children and adolescents aged 1-16 years with mild to moderate CKD residing in the United States and Canada who were enrolled in the Chronic Kidney Disease in Children (CKiD) Study.
Predictor: Self-reported annual household income category as a proxy measure for SES: >=$75,000 (high income), $30,000 to <$75,000 (middle income) and, <$30,000 (low income).
Outcomes & Measurements: Clinical characteristics and CKD severity at baseline (glomerular filtration rate [GFR] and comorbid conditions related to disease severity and management) and longitudinally (GFR decline and changes in blood pressure z scores and height z scores per year).
Results: At baseline, low and middle household incomes, compared to high income, were associated with minority race (39% and 20% vs 7%), lower maternal education (28% and 5% vs 1%), abnormal birth history (34% and 32% vs 21%), and having at least one clinical comorbid condition (66% and 64% vs 55%). Baseline median GFRs were similar across income categories (43-45 mL/min/1.73 m(2)). After adjusting for baseline differences, average GFR declines per year for the low-, middle-, and high-income categories were -2.3%, -2.7%, and -1.9%, respectively, and were not statistically significantly different among groups. Blood pressure control tended to improve in all groups (z score, -0.10 to -0.04) but higher income was associated with a faster improvement. Each group showed similar deficits in height at baseline. Height deficits diminished over time for participants from high-income families, but not among those from low-income families (z scores for height per year, 0.05 and -0.004, respectively; P = 0.03 for comparison of high and low income).
Limitations: Income is an imperfect measure for SES; CKiD participants are not representative of children and adolescents with CKD who are uninsured or not receiving care; statistical power to detect associations by income level is limited.
Conclusions: GFR decline was similar across income groups but better improvement in BP was observed among those with high income. Children and adolescents with CKD from lower income households are at higher risk of impaired growth. (C) 2013 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
C1 [Hidalgo, Guillermo] E Carolina Univ, Sch Med, Dept Pediat, Greenville, NC USA.
[Ng, Derek K.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Moxey-Mims, Marva] NIDDK, NIH, Bethesda, MD 20892 USA.
[Minnick, Maria Lourdes; Furth, Susan L.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Blydt-Hansen, Tom] Univ Manitoba, Winnipeg, MB, Canada.
[Warady, Bradley A.] Childrens Mercy Hosp, Kansas City, MO 64108 USA.
[Furth, Susan L.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Furth, SL (reprint author), Childrens Hosp Philadelphia, Div Nephrol, 3401 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM furths@email.chop.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK); Eunice Kennedy Shriver National Institute of Child Health and
Human Development; National Heart, Lung and Blood Institute
[U01-DK-66143, U01-DK-66174, U01-DK82194, U01-DK-66116]
FX Support: The CKiD Study is funded by the National Institute of Diabetes
and Digestive and Kidney Diseases (NIDDK); Dr Moxey-Mims serves as the
NIDDK project officer on the steering committee. The study received
additional funding from the Eunice Kennedy Shriver National Institute of
Child Health and Human Development and the National Heart, Lung and
Blood Institute. Grant numbers: U01-DK-66143, U01-DK-66174, U01-DK82194,
and U01-DK-66116.
NR 22
TC 13
Z9 13
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD DEC
PY 2013
VL 62
IS 6
BP 1087
EP 1094
DI 10.1053/j.ajkd.2013.06.013
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 259JS
UT WOS:000327523800012
PM 23932090
ER
PT J
AU Shea, N
Prasad, V
AF Shea, Neil
Prasad, Vinay
TI Response to the "Open Issues with Open Access Publication" Reply
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Shea, Neil] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Prasad, Vinay] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Shea, N (reprint author), Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
NR 3
TC 0
Z9 0
U1 0
U2 2
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 DEC
PY 2013
VL 126
IS 12
BP E45
EP E45
DI 10.1016/j.amjmed.2013.07.039
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 257OC
UT WOS:000327393300023
PM 24262747
ER
PT J
AU Powell, KE
Zimmerman, RK
Ahern, DK
Lewis, AL
Ramirez, AG
Atienza, A
Ayala, GX
Elder, JP
Calonge, N
Chin, M
Clymer, J
Fielding, J
Glanz, K
Goetzel, R
Green, LW
Grossman, D
Johnson, RL
Kumanyika, S
Orleans, T
Pronk, N
Ramirez, G
Remington, PL
Rimer, B
Hesse, BW
Frumkin, H
Jones, BH
Canham-Chervak, M
Kohatsu, ND
Harris, JR
Koo, D
Michener, L
Kottke, TE
Dickey, LL
Maibach, E
Mays, GP
Halverson, PK
McGinnis, JM
Barry, MA
Owen, N
Pronk, N
Sallis, JF
Stokols, D
Hall, KL
Felitti, VJ
Anda, RF
Butchart, A
Sethi, D
Pratt, M
Gruner, L
AF Powell, Kenneth E.
Zimmerman, Richard K.
Ahern, David K.
Lewis, Allison L.
Ramirez, Amelie G.
Atienza, Audie
Ayala, Guadalupe X.
Elder, John P.
Calonge, Ned
Chin, Marshall
Clymer, John
Fielding, Jonathan
Glanz, Karen
Goetzel, Ron
Green, Lawrence W.
Grossman, David
Johnson, Robert L.
Kumanyika, Shiriki
Orleans, Tracy
Pronk, Nico
Ramirez, Gilbert
Remington, Patrick L.
Rimer, Barbara
Hesse, Bradford W.
Frumkin, Howard
Jones, Bruce H.
Canham-Chervak, Michelle
Kohatsu, Neal D.
Harris, Jeffrey R.
Koo, Denise
Michener, Lloyd
Kottke, Thomas E.
Dickey, Larry L.
Maibach, Edward
Mays, Glen P.
Halverson, Paul K.
McGinnis, J. Michael
Barry, Michael A.
Owen, Neville
Pronk, Nico
Sallis, James F.
Stokols, Daniel
Hall, Kara L.
Felitti, Vincent J.
Anda, Robert F.
Butchart, Alexander
Sethi, Dinesh
Pratt, Michael
Gruner, Linda
TI Notes from the Field: Planting, Nurturing, and Watching Things Grow
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Editorial Material
ID ADVERSE CHILDHOOD EXPERIENCES; HEALTH COMMUNICATION APPLICATIONS;
UNDERGRADUATE PUBLIC-HEALTH; PHYSICAL-ACTIVITY INTERVENTIONS;
COMMUNITY-PREVENTIVE-SERVICES; BUILT ENVIRONMENT; POPULATION HEALTH;
HOUSEHOLD DYSFUNCTION; CLINICAL PREVENTION; NEIGHBORHOOD WALKABILITY
C1 [Zimmerman, Richard K.] Univ Pittsburgh, Sch Med, Dept Family Med & Clin Epidemiol, Pittsburgh, PA 15260 USA.
[Ahern, David K.] Brigham & Womens Hosp, Psychiat Hlth e Technol Initiat, Boston, MA 02115 USA.
[Lewis, Allison L.] Assoc Prevent Teaching & Res, Washington, DC USA.
[Ramirez, Amelie G.] Univ Texas Hlth Sci Ctr San Antonio, Inst Hlth Promot Res, San Antonio, TX USA.
[Atienza, Audie] NIH, Hlth Promot Res Branch, Bethesda, MD 20892 USA.
[Ayala, Guadalupe X.; Elder, John P.] San Diego State Univ, Grad Sch Publ Hlth, San Diego, CA 92182 USA.
[Hesse, Bradford W.] NCI, Hlth Commun & Informat Res Branch, Bethesda, MD 20892 USA.
[Frumkin, Howard] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
[Jones, Bruce H.; Canham-Chervak, Michelle] US Army Inst Publ Hlth, Injury Prevent Program, Aberdeen Proving Ground, MD USA.
[Harris, Jeffrey R.] Univ Washington, Hlth Promot Res Ctr, Seattle, WA 98195 USA.
[Koo, Denise] Ctr Dis Control & Prevent, Off Director, Sci Educ & Profess Dev Program Off, Atlanta, GA 30329 USA.
[Michener, Lloyd] Duke Univ, Med Ctr, Dept Community & Family Med, Duke Ctr Community Res, Durham, NC 27706 USA.
[Kottke, Thomas E.] HealthPartners, Populat Hlth, Minneapolis, MN USA.
[Maibach, Edward] George Mason Univ, Ctr Climate Change Commun, Fairfax, VA 22030 USA.
[Mays, Glen P.] Univ Kentucky, Lexington, KY 40506 USA.
[Halverson, Paul K.] Indiana Univ Purdue Univ Indianapolis, Fairbanks Sch Publ Hlth, Indianapolis, IN USA.
[Barry, Michael A.] Amer Coll Prevent Med, Washington, DC USA.
[Owen, Neville] Monash Univ, Baker IDI Heart & Diabet Inst, Clayton, Vic 3800, Australia.
[Owen, Neville] Univ Melbourne, Melbourne, Vic 3010, Australia.
[Owen, Neville] Univ Queensland, Brisbane, Qld 4072, Australia.
[Pronk, Nico] Harvard Univ, Sch Publ Hlth, HealthPartners, Cambridge, MA 02138 USA.
[Sallis, James F.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Stokols, Daniel] Univ Calif Irvine, Sch Sociol Ecol, Irvine, CA USA.
[Hall, Kara L.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Anda, Robert F.] ACE Interface, Fayetteville, GA USA.
[Butchart, Alexander] WHO, Dept Violence & Injury Prevent & Disabil, Geneva, Switzerland.
[Pratt, Michael] Ctr Dis Control & Prevent, Atlanta, GA 30329 USA.
RP Powell, KE (reprint author), Care of Seidman C, UCSD, AJPM Editorial Off, 9500 Gilman Dr, La Jolla, CA 92093 USA.
EM nekllewop@hotmail.com; zimmer@pitt.edu; dahern@partners.org;
ALL@aptrweb.org; ramirezag@uthscsa.edu; AtienzaA@mail.nih.gov;
ayala@mail.sdsu.edu; lwgreen@comcast.net; hesseb@mail.nih.gov;
frumkin@uw.edu; michelle.c.chervak.civ@mail.mil;
Neal.Kohatsu@dhcs.ca.gov; dkoo@cdc.gov; tkottke@comcast.net;
emaibach@gmu.edu; MMcGinnis@nas.edu; mbarry@acpm.org;
neville.owen@bakeridi.edu.au; nico.p.pronk@healthpartners.com;
jsallis@ucsd.edu; dstokols@uci.edu; VJFMDSDCA@mac.com; butcharta@who.int
NR 123
TC 0
Z9 0
U1 3
U2 20
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 DEC
PY 2013
VL 45
IS 6
BP 687
EP 702
DI 10.1016/j.amepre.2013.09.006
PG 16
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 258SG
UT WOS:000327478400007
ER
PT J
AU Vogel, AL
Hall, KL
Fiore, SM
Klein, JT
Bennett, LM
Gadlin, H
Stokols, D
Nebeling, LC
Wuchty, S
Patrick, K
Spotts, EL
Pohl, C
Riley, WT
Falk-Krzesinski, HJ
AF Vogel, Amanda L.
Hall, Kara L.
Fiore, Stephen M.
Klein, Julie T.
Bennett, L. Michelle
Gadlin, Howard
Stokols, Daniel
Nebeling, Linda C.
Wuchty, Stefan
Patrick, Kevin
Spotts, Erica L.
Pohl, Christian
Riley, William T.
Falk-Krzesinski, Holly J.
TI The Team Science Toolkit Enhancing Research Collaboration Through Online
Knowledge Sharing
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Editorial Material
C1 [Hall, Kara L.; Nebeling, Linda C.; Riley, William T.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Gadlin, Howard] NHLBI, Ctr Cooperat Resolut, NIH, Bethesda, MD 20892 USA.
[Bennett, L. Michelle] NHLBI, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Spotts, Erica L.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Falk-Krzesinski, Holly J.] Global Acad & Res Affairs, Chicago, IL USA.
[Fiore, Stephen M.] Univ Cent Florida, Dept Philosophy, Orlando, FL 32816 USA.
[Klein, Julie T.] Wayne State Univ, Dept English, Detroit, MI USA.
[Patrick, Kevin] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Pohl, Christian] Swiss Fed Inst Technol, Dept Environm Syst Sci, Zurich, Switzerland.
[Stokols, Daniel] Univ Calif Irvine, Sch Social Ecol, Irvine, CA USA.
[Vogel, Amanda L.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Clin Res Directorate CMRP, Rockville, MD 20850 USA.
[Wuchty, Stefan] Univ Miami, Dept Comp Sci, Miami, FL USA.
RP Vogel, AL (reprint author), Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Clin Res Directorate CMRP, 9609 Med Ctr Dr,Room 3E124, Rockville, MD 20850 USA.
EM vogelal@mail.nih.gov
OI Falk-Krzesinski, Holly/0000-0001-8112-2445; Fiore,
Stephen/0000-0003-3529-1322
NR 13
TC 14
Z9 14
U1 1
U2 30
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 DEC
PY 2013
VL 45
IS 6
BP 787
EP 789
DI 10.1016/j.amepre.2013.09.001
PG 3
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 258SG
UT WOS:000327478400021
PM 24237924
ER
PT J
AU Madeleine, MM
Finch, JL
Lynch, CF
Goodman, MT
Engels, EA
AF Madeleine, M. M.
Finch, J. L.
Lynch, C. F.
Goodman, M. T.
Engels, E. A.
TI HPV-Related Cancers After Solid Organ Transplantation in the United
States
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE HPV-related cancer; immunosuppression; organ transplant cohort;
Transplant Cancer Match Study
ID SQUAMOUS-CELL CARCINOMAS; HUMAN-PAPILLOMAVIRUS; CERVICAL-CANCER; SKIN
CANCERS; ANAL CANCER; RECIPIENTS; RISK; MALIGNANCY; WORLDWIDE; SIROLIMUS
AB Transplant recipients have elevated cancer risk including risk of human papillomavirus (HPV)-associated cancers of the cervix, anus, penis, vagina, vulva and oropharynx. We examined the incidence of HPV-related cancers in 187649 US recipients in the Transplant Cancer Match Study. Standardized incidence ratios (SIRs) compared incidence rates to the general population, and incidence rate ratios (IRRs) compared rates across transplant subgroups. We observed elevated incidence of HPV-related cancers (SIRs: in situ 3.3-20.3, invasive 2.2-7.3), except for invasive cervical cancer (SIR 1.0). Incidence increased with time since transplant for vulvar, anal and penile cancers (IRRs 2.1-4.6 for 5+ vs. <2 years). Immunophenotype, characterized by decreased incidence with HLA DRB1:13 and increased incidence with B:44, contributed to susceptibility at several sites. Use of specific immunosuppressive medications was variably associated with incidence; for example, tacrolimus, was associated with reduced incidence for some anogenital cancers (IRRs 0.4-0.7) but increased incidence of oropharyngeal cancer (IRR 2.1). Thus, specific features associated with recipient characteristics, transplanted organs and medications are associated with incidence of HPV-related cancers after transplant. The absence of increased incidence of invasive cervical cancer highlights the success of cervical screening in this population and suggests a need for screening for other HPV-related cancers.
C1 [Madeleine, M. M.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
[Madeleine, M. M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Finch, J. L.] Colorado Dept Publ Hlth & Environm, Colorado Cent Canc Registry, Denver, CO USA.
[Lynch, C. F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Goodman, M. T.] Cedars Sinai Med Ctr, Dept Biomed Sci, Los Angeles, CA 90048 USA.
[Engels, E. A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Madeleine, MM (reprint author), Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
EM mmadelei@fhcrc.org
FU Intramural Research Program of the National Cancer Institute; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: California [1U58 DP000807-01]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: Colorado
[U58 DP000848-04]; National Program of Cancer Registries of the Centers
for Disease Control and Prevention: Georgia [5U58DP000817-05]; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: Illinois [5658DP000805-04]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: Michigan
[5U58DP000812-03]; National Program of Cancer Registries of the Centers
for Disease Control and Prevention: New Jersey [5U58/DP000808-05];
National Program of Cancer Registries of the Centers for Disease Control
and Prevention: New York [U58DP0038789]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: North
Carolina [U58DP000832]; National Program of Cancer Registries of the
Centers for Disease Control and Prevention: Texas [5U58DP000824-04];
SEER Program of the National Cancer Institute: California
[HHSN261201000036C, HHSN261201000035C, HHSN261201000034C]; SEER Program
of the National Cancer Institute: Connecticut [HHSN261201000024C]; SEER
Program of the National Cancer Institute: Hawaii [HHSN261201000037C,
N01-PC-35137, N01-PC-35139]; SEER Program of the National Cancer
Institute: Iowa [HSN261201000032C, N01-PC-35143]; SEER Program of the
National Cancer Institute: New Jersey [HHSN261201000027C, N01-PC-54405];
SEER Program of the National Cancer Institute: Seattle-Puget Sound
[N01-PC-35142]; SEER Program of the National Cancer Institute: Utah
[HHSN261201000026C]; state of California; state of Colorado; state of
Connecticut; state of Illinois; state of Iowa; state of New Jersey;
state of New York (Cancer Surveillance Improvement Initiative)
[14-2491]; state of Texas; state of Washington; Fred Hutchinson Cancer
Research Center in Seattle, WA; General Funds from the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, Division of Cancer Epidemiology and Genetics
FX The authors gratefully acknowledge the support and assistance provided
by individuals at the Health Resources and Services Administration
(Monica Lin), the SRTR (Ajay Israni, Bertram Kasiske, Paul Newkirk, Jon
Snyder), and the following cancer registries: the states of California
(Tina Clarke), Colorado, Connecticut (Lou Gonsalves), Georgia (Rana
Bayakly), Hawaii, Iowa, Illinois (Lori Koch), Michigan (Glenn Copeland),
New Jersey (Xiaoling Niu), New York (Amy Kahn), North Carolina
(Chandrika Rao), Texas (Melanie Williams) and Utah (Janna Harrell), and
the Seattle-Puget Sound area of Washington (Margaret Madeleine). We also
thank analysts at Information Management Services for programming
support (David Castenson, Michael Curry, Ruth Parsons). The views
expressed in this paper are those of the authors and should not be
interpreted to reflect the views or policies of the National Cancer
Institute, Health Resources and Services Administration, SRTR, cancer
registries or their contractors. This research was supported in part by
the Intramural Research Program of the National Cancer Institute. During
the initial period when registry linkages were performed, the SRTR was
managed by Arbor Research Collaborative for Health in Ann Arbor, MI
(contract HHSH234200537009C); beginning in September 2010, the SRTR was
managed by Minneapolis Medical Research Foundation in Minneapolis, MN
(HHSH250201000018C). The following cancer registries were supported by
the National Program of Cancer Registries of the Centers for Disease
Control and Prevention: California (agreement 1U58 DP000807-01),
Colorado (U58 DP000848-04), Georgia (5U58DP000817-05), Illinois
(5658DP000805-04), Michigan (5U58DP000812-03), New Jersey
(5U58/DP000808-05), New York (U58DP0038789), North Carolina
(U58DP000832) and Texas (5U58DP000824-04). The following cancer
registries were supported by the SEER Program of the National Cancer
Institute: California (contracts HHSN261201000036C, HHSN261201000035C
and HHSN261201000034C), Connecticut (HHSN261201000024C), Hawaii
(HHSN261201000037C, N01-PC-35137 and N01-PC-35139), Iowa
(HSN261201000032C and N01-PC-35143), New Jersey (HHSN261201000027C and
N01-PC-54405), Seattle-Puget Sound (N01-PC-35142) and Utah
(HHSN261201000026C). Additional support was provided by the states of
California, Colorado, Connecticut, Illinois, Iowa, New Jersey, New York
(Cancer Surveillance Improvement Initiative 14-2491), Texas and
Washington, as well as the Fred Hutchinson Cancer Research Center in
Seattle, WA. This research was supported by General Funds from the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Division of Cancer Epidemiology and Genetics.
NR 30
TC 25
Z9 25
U1 0
U2 3
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 DEC
PY 2013
VL 13
IS 12
BP 3202
EP 3209
DI 10.1111/ajt.12472
PG 8
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 255JN
UT WOS:000327235300022
PM 24119294
ER
PT J
AU Colson, P
De Lamballerie, X
Yutin, N
Asgari, S
Bigot, Y
Bideshi, DK
Cheng, XW
Federici, BA
Van Etten, JL
Koonin, EV
La Scola, B
Raoult, D
AF Colson, Philippe
De Lamballerie, Xavier
Yutin, Natalya
Asgari, Sassan
Bigot, Yves
Bideshi, Dennis K.
Cheng, Xiao-Wen
Federici, Brian A.
Van Etten, James L.
Koonin, Eugene V.
La Scola, Bernard
Raoult, Didier
TI "Megavirales", a proposed new order for eukaryotic nucleocytoplasmic
large DNA viruses
SO ARCHIVES OF VIROLOGY
LA English
DT Article
ID GIANT VIRUSES; EVOLUTION; MIMIVIRUS; REPLICATION; FACTORIES; VACCINIA;
ORIGIN; GENES; HIGHLIGHTS; LINEAGE
AB The nucleocytoplasmic large DNA viruses (NCLDVs) comprise a monophyletic group of viruses that infect animals and diverse unicellular eukaryotes. The NCLDV group includes the families Poxviridae, Asfarviridae, Iridoviridae, Ascoviridae, Phycodnaviridae, Mimiviridae and the proposed family "Marseilleviridae". The family Mimiviridae includes the largest known viruses, with genomes in excess of one megabase, whereas the genome size in the other NCLDV families varies from 100 to 400 kilobase pairs. Most of the NCLDVs replicate in the cytoplasm of infected cells, within so-called virus factories. The NCLDVs share a common ancient origin, as demonstrated by evolutionary reconstructions that trace approximately 50 genes encoding key proteins involved in viral replication and virion formation to the last common ancestor of all these viruses. Taken together, these characteristics lead us to propose assigning an official taxonomic rank to the NCLDVs as the order "Megavirales", in reference to the large size of the virions and genomes of these viruses.
C1 [Colson, Philippe; La Scola, Bernard; Raoult, Didier] Aix Marseille Univ, IHU Med Infect, Fac Med & Pharm, Unite Rickettsies,URMITE UMR CNRS IRD INSERM U 72, F-13385 Marseille 05, France.
[Colson, Philippe; De Lamballerie, Xavier; La Scola, Bernard; Raoult, Didier] Ctr Hosp Univ Timone, Assistance Publ Hop Marseille, IHU Med, Fed Bacteriol Hyg Virol,Pole Malad Infect & Tropi, F-13385 Marseille 05, France.
[De Lamballerie, Xavier] Aix Marseille Univ, EHSP French Sch Publ Hlth, Inst Rech Dev, Fac Med,Unite Virus Emergents,UMR 190 Emergence P, F-13385 Marseille 05, France.
[Bigot, Yves] INRA, CNRS, UMR 7247, PRC UMR0085, Nouzilly, France.
[Yutin, Natalya; Koonin, Eugene V.] NIH, NCBI, Natl Lib Med, Bethesda, MD 20894 USA.
[Asgari, Sassan] Univ Queensland, Sch Biol Sci, St Lucia, Qld 4072, Australia.
Ctr INRA Nouzilly, UMR INRA CNRS 7247, PRC, F-37380 Nouzilly, France.
[Bideshi, Dennis K.] Univ Calif Riverside, Mol & Dev Biol, Riverside, CA 92521 USA.
[Cheng, Xiao-Wen] Miami Univ, Dept Microbiol, Oxford, OH 45056 USA.
[Federici, Brian A.] Univ Calif Riverside, Dept Entomol, Riverside, CA 92521 USA.
[Van Etten, James L.] Univ Nebraska, Dept Plant Pathol, Lincoln, NE 68583 USA.
[Van Etten, James L.] Univ Nebraska, Nebraska Ctr Virol, Lincoln, NE 68583 USA.
RP Raoult, D (reprint author), Aix Marseille Univ, IHU Med Infect, Fac Med & Pharm, Unite Rickettsies,URMITE UMR CNRS IRD INSERM U 72, 27 Blvd Jean Moulin, F-13385 Marseille 05, France.
EM didier.raoult@gmail.com
RI Colson, Philippe/P-6355-2014; LA SCOLA, Bernard/P-6477-2016
OI Colson, Philippe/0000-0001-6285-0308; LA SCOLA,
Bernard/0000-0001-8006-7704
FU US Department of Health and Human Services; NIH from the COBRE Program
of the National Center for Research Resources [P20 RR15635]
FX Natalya Yutin and Eugene V. Koonin are supported by intramural funds of
the US Department of Health and Human Services (to the National Library
of Medicine). James Van Etten is partially supported by NIH Grant P20
RR15635 from the COBRE Program of the National Center for Research
Resources.
NR 35
TC 78
Z9 78
U1 2
U2 36
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
EI 1432-8798
J9 ARCH VIROL
JI Arch. Virol.
PD DEC
PY 2013
VL 158
IS 12
BP 2517
EP 2521
DI 10.1007/s00705-013-1768-6
PG 5
WC Virology
SC Virology
GA 253XA
UT WOS:000327121600010
PM 23812617
ER
PT J
AU Prager, AJ
Peng, CR
Lita, E
McNally, D
Kaushal, A
Sproull, M
Compton, K
Dahut, WL
Figg, WD
Citrin, D
Camphausen, KA
AF Prager, Alisa J.
Peng, Cynthia R.
Lita, Elena
McNally, Debbie
Kaushal, Aradhana
Sproull, Mary
Compton, Kathryn
Dahut, William L.
Figg, William D.
Citrin, Deborah
Camphausen, Kevin A.
TI Urinary aHGF, IGFBP3 and OPN as diagnostic and prognostic biomarkers for
prostate cancer
SO BIOMARKERS IN MEDICINE
LA English
DT Article
DE biomarker; HGH; OPN; prostate cancer; urine
ID GROWTH-FACTOR-I; HEPATOCYTE GROWTH; BINDING PROTEIN-3; PLASMA
OSTEOPONTIN; FACTOR/SCATTER FACTOR; TMPRSS2-ERG FUSION; ANDROGEN
RECEPTOR; ANTIGEN LEVEL; CELLS; RISK
AB Aim: Serum PSA screening for prostate cancer (PCa) is controversial. Here, we identify three urinary biomarkers - aHGF, IGFBP3 and OPN - for PCa screening and prognostication. Methods: Urinary aHGF, OPN and IGFBP3 from healthy men (n = 19) and men with localized (n = 65) and metastatic (n = 36) PCa were quantified via ELISA. Mann-Whitney nonparametric t-test and the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analyses were used to analyze associations. Results: Mean aHGF and IGFBP3 levels were significantly elevated in PCa patients versus controls (p = 0.0006 and p = 0.0012, respectively), and the area under the curve of the receiver operating characteristic curve (indicator of diagnostic accuracy) for aHGF and IGFBP3 was 0.75 and 0.74, respectively. OPN levels were significantly higher in metastatic groups (p = 0.0060) versus localized and controls (area under the curve = 0.68). Conclusion: Urinary aHGF and IGFBP3 exhibit the capacity for diagnostic discrimination for PCa, whereas OPN may indicate presence of metastatic disease.
C1 [Prager, Alisa J.; Peng, Cynthia R.; Sproull, Mary; Citrin, Deborah; Camphausen, Kevin A.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Lita, Elena; McNally, Debbie; Kaushal, Aradhana] NCI, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Compton, Kathryn; Figg, William D.] NCI, Mol Pharmacol Sect, NIH, Bethesda, MD 20892 USA.
[Dahut, William L.] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Camphausen, KA (reprint author), NCI, Radiat Oncol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM camphauk@mail.nih.gov
RI Figg Sr, William/M-2411-2016
NR 56
TC 3
Z9 3
U1 0
U2 5
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1752-0363
EI 1752-0371
J9 BIOMARK MED
JI Biomark. Med.
PD DEC
PY 2013
VL 7
IS 6
BP 831
EP 841
DI 10.2217/bmm.13.112
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 255QB
UT WOS:000327253800003
PM 24266816
ER
PT J
AU Huang, CY
Qin, J
AF Huang, Chiung-Yu
Qin, Jing
TI Semiparametric estimation for the additive hazards model with
left-truncated and right-censored data
SO BIOMETRIKA
LA English
DT Article
DE Canadian Study of Health and Aging; Composite likelihood; Estimating
equation; Martingale; Prevalent sampling
ID NONPARAMETRIC-ESTIMATION; REGRESSION-MODELS; LIKELIHOOD; SURVIVAL
AB Survival data from prevalent cases collected under a cross-sectional sampling scheme are subject to left-truncation. When fitting an additive hazards model to left-truncated data, the conditional estimating equation method (Lin & Ying, 1994), obtained by modifying the risk sets to account for left-truncation, can be very inefficient, as the marginal likelihood of the truncation times is not used in the estimation procedure. In this paper, we use a pairwise pseudolikelihood to eliminate nuisance parameters from the marginal likelihood and, by combining the marginal pairwise pseudo-score function and the conditional estimating function, propose an efficient estimator for the additive hazards model. The proposed estimator is shown to be consistent and asymptotically normally distributed with a sandwich-type covariance matrix that can be consistently estimated. Simulation studies show that the proposed estimator is more efficient than its competitors. A data analysis illustrates application of the method.
C1 [Huang, Chiung-Yu] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Div Oncol Biostat & Bioinformat, Baltimore, MD 21205 USA.
[Qin, Jing] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Huang, CY (reprint author), Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Div Oncol Biostat & Bioinformat, Baltimore, MD 21205 USA.
EM cyhuang@jhmi.edu; jingqin@niaid.nih.gov
FU National Health Research and Development Program of Health Canada
Project; Pfizer Canada Incorporated through the Medical Research
Council/Pharmaceutical Manufacturers Association of Canada Health
Activity Program; Bayer Incorporated; British Columbia Health Research
Foundation
FX The authors thank Professors Christina Wolfson, Masoud Asgharian and Ian
McDowell for kindly sharing the Canadian Study of Health and Aging data.
The core study was funded by the National Health Research and
Development Program of Health Canada Project. Additional funding was
provided by Pfizer Canada Incorporated through the Medical Research
Council/Pharmaceutical Manufacturers Association of Canada Health
Activity Program, Bayer Incorporated, and the British Columbia Health
Research Foundation Projects. The authors also thank the referees,
associate editor, editor, and Dr. Dean Follmann for their comments,
which have helped to improve the presentation of this article. This work
was conducted when the first author was a mathematical statistician at
the National Institute of Allergy and Infectious Diseases.
NR 26
TC 2
Z9 3
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-3444
EI 1464-3510
J9 BIOMETRIKA
JI Biometrika
PD DEC
PY 2013
VL 100
IS 4
BP 877
EP 888
DI 10.1093/biomet/ast039
PG 12
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA 262DL
UT WOS:000327714200007
PM 26246622
ER
PT J
AU Vincent, DT
Ibrahim, YF
Espey, MG
Suzuki, YJ
AF Vincent, Duncan T.
Ibrahim, Yasmine F.
Espey, Michael Graham
Suzuki, Yuichiro J.
TI The role of antioxidants in the era of cardio-oncology
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE Antioxidants; Cancer; Cardioprotection; Cardiotoxicity; Chemotherapy;
Free radicals; Reactive oxygen species
ID ADVANCED BREAST-CANCER; CHRONIC DOXORUBICIN CARDIOTOXICITY;
ADRIAMYCIN-INDUCED CARDIOMYOPATHY; CISPLATIN-INDUCED CARDIOTOXICITY;
ACUTE LYMPHOBLASTIC-LEUKEMIA; NON-HODGKIN-LYMPHOMA; ALPHA-LIPOIC ACID;
VITAMIN-E; MITOCHONDRIAL TOXICITY; TAXANE CHEMOTHERAPIES
AB Although most chemotherapeutic drugs have the potential to exert cardiotoxicity, these drugs have been chosen for use in cancer treatment because survival and curability benefits outweigh the risk of these complications. Anthracyclines, for example, are a powerful class of chemotherapeutic agents; however, their use is restricted by dose-related cardiotoxicity. Experimental evidence strongly supports the role of reactive oxygen species in this process, suggesting that antioxidants may be effective in protecting the heart from toxicity. Clinical use of antioxidants to protect the heart during anthracycline chemotherapy has been controversial due to the potential for reduced cytotoxic efficacy toward cancer cells. Results from randomized clinical trials addressing whether antioxidants either reduce the incidence of clinical heart failure among patients undergoing anthracycline-based chemotherapy or reduce the response rates to anthracycline-based chemotherapy have been unclear. While anthracyclines are by far the most well-studied antitumor agents with cardiotoxic properties, evidence now shows that reactive oxygen species may play roles in cardiotoxicity induced by other chemotherapeutic agents such as cyclophosphamide, cisplatin, 5-fluorouracil, and trastuzumab. Thus, in the new era of combination therapy and long-term survival of cancer patients, the use of antioxidants to support cancer therapy should be revisited.
C1 [Vincent, Duncan T.; Ibrahim, Yasmine F.; Suzuki, Yuichiro J.] Georgetown Univ, Med Ctr, Dept Physiol & Pharmacol, Washington, DC 20057 USA.
[Espey, Michael Graham] NIDDK, Off Sci Director, Bethesda, MD 20892 USA.
RP Suzuki, YJ (reprint author), Georgetown Univ, Med Ctr, Dept Physiol & Pharmacol, 3900 Reservoir Rd NW, Washington, DC 20057 USA.
EM ys82@georgetown.edu
FU NHLBI NIH HHS [R01 HL072844]
NR 99
TC 8
Z9 10
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD DEC
PY 2013
VL 72
IS 6
BP 1157
EP 1168
DI 10.1007/s00280-013-2260-4
PG 12
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 257LX
UT WOS:000327387000001
PM 23959462
ER
PT J
AU Chudasama, Y
Daniels, TE
Gorrin, DP
Rhodes, SEV
Rudebeck, PH
Murray, EA
AF Chudasama, Yogita
Daniels, Teresa E.
Gorrin, Daniel P.
Rhodes, Sarah E. V.
Rudebeck, Peter H.
Murray, Elisabeth A.
TI The Role of the Anterior Cingulate Cortex in Choices based on Reward
Value and Reward Contingency
SO CEREBRAL CORTEX
LA English
DT Article
DE action-reversal; monkey; object-reversal; reward value
ID MEDIAL PREFRONTAL CORTEX; ORBITOFRONTAL CORTEX; RHESUS-MONKEY;
FRONTAL-CORTEX; MACAQUE MONKEY; REINFORCER DEVALUATION; DECISION-MAKING;
AMYGDALA; LESIONS; SELECTION
AB Although several studies have emphasized the role of the anterior cingulate cortex (ACC) in associating actions with reward value, its role in guiding choices on the basis of changes in reward value has not been assessed. Accordingly, we compared rhesus monkeys with ACC lesions and controls on object- and action-based reinforcer devaluation tasks. Monkeys were required to associate an object or an action with one of two reward outcomes, and we assessed the monkeys shift in choices of objects or actions after changes in the value of 1 outcome. No group differences emerged on either task. For comparison, we tested the same monkeys on their ability to make choices guided by reward contingency in object- and action-based reversal learning tasks. Monkeys with ACC lesions were impaired in using rewarded trials to sustain the selection of the correct object during object reversal learning. They were also impaired in using errors to guide choices in action reversal learning. These data indicate that the role of the ACC is not restricted to linking specific actions with reward outcomes, as previously reported. Instead, the data suggest a more general role for the ACC in using information about reward and nonreward to sustain effective choice behavior.
C1 [Chudasama, Yogita] McGill Univ, Dept Psychol, Montreal, PQ H3A 1B1, Canada.
[Daniels, Teresa E.; Gorrin, Daniel P.; Rhodes, Sarah E. V.; Rudebeck, Peter H.; Murray, Elisabeth A.] NIMH, Sect Neurobiol Learning & Memory, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
RP Chudasama, Y (reprint author), McGill Univ, Dept Psychol, 1205 Dr Penfield Ave, Montreal, PQ H3A 1B1, Canada.
EM yogita.chudasama@mcgill.ca
OI Rudebeck, Peter/0000-0002-1411-7555; Murray,
Elisabeth/0000-0003-1450-1642
FU Intramural Research Program of the National Institute of Mental Health
at the National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Mental Health at the National Institutes of
Health.
NR 58
TC 15
Z9 15
U1 2
U2 11
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
EI 1460-2199
J9 CEREB CORTEX
JI Cereb. Cortex
PD DEC
PY 2013
VL 23
IS 12
BP 2884
EP 2898
DI 10.1093/cercor/bhs266
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 258AY
UT WOS:000327431400010
PM 22944530
ER
PT J
AU Manzur, HE
Alvarez, J
Babul, C
Maldonado, PE
AF Manzur, Hachi E.
Alvarez, Joel
Babul, Cecilia
Maldonado, Pedro E.
TI Synchronization Across Sensory Cortical Areas by Electrical
Microstimulation is Sufficient for Behavioral Discrimination
SO CEREBRAL CORTEX
LA English
DT Article
DE coding; cortex; microstimulation; sensory; synchronization
ID CAT VISUAL-CORTEX; OSCILLATORY NEURONAL RESPONSES; STRIATE CORTEX;
INTRACORTICAL MICROSTIMULATION; GAMMA OSCILLATIONS; MOTOR CORTEX;
NEOCORTICAL NEURONS; CEREBRAL-CORTEX; OLFACTORY-BULB; AWAKE MACAQUE
AB The temporal correlation hypothesis proposes that cortical neurons engage in synchronized activity, thus configuring a general mechanism to account for a range of cognitive processes from perceptual binding to consciousness. However, most studies supporting this hypothesis have only provided correlational, but not causal evidence. Here, we used electrical microstimulation of the visual and somatosensory cortices of the rat in both hemispheres, to test whether rats could discriminate synchronous versus asynchronous patterns of stimulation applied to the same cortical sites. To disambiguate synchrony from other related parameters, our experiments independently manipulated the rate and intensity of stimulation, the spatial locations of stimulation, the exact temporal sequence of stimulation patterns, and the degree of synchrony across stimulation sites. We found that rats reliably distinguished between 2 microstimulation patterns, differing in the spatial arrangement of cortical sites stimulated synchronously. Also, their performance was proportional to the level of synchrony in the microstimulation patterns. We demonstrated that rats can recognize artificial current patterns containing precise synchronization features, thus providing the first direct evidence that artificial synchronous activity can guide behavior. Such precise temporal information can be used as feedback signals in machine interface arrangements.
C1 [Manzur, Hachi E.; Alvarez, Joel; Babul, Cecilia; Maldonado, Pedro E.] Univ Chile, Biomed Neurosci Inst, Santiago 8380453, Chile.
[Manzur, Hachi E.] NIA, Neural Circuits & Cognit Unit, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA.
[Maldonado, Pedro E.] Univ Chile, Fac Med, Program Physiol & Biophys, Casilla Santiago, Chile.
RP Maldonado, PE (reprint author), Univ Chile, Fac Med, Program Physiol & Biophys, Independencia 1027, Santiago 8380453, Chile.
EM pedro@neuro.med.uchile.cl
OI Maldonado, Pedro/0000-0001-9895-7684
FU Fondecyt [1090101]; Iniciativa Cientifica Milenio; Conicyt; Conciyt
Anillo [ACT 66]
FX This study was supported in part by Fondecyt 1090101 to P. M.,
Iniciativa Cientifica Milenio and a Conicyt Doctoral fellowship and
Conciyt Anillo ACT 66 to H. M.
NR 84
TC 2
Z9 2
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
EI 1460-2199
J9 CEREB CORTEX
JI Cereb. Cortex
PD DEC
PY 2013
VL 23
IS 12
BP 2976
EP 2986
DI 10.1093/cercor/bhs288
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 258AY
UT WOS:000327431400018
PM 22989583
ER
PT J
AU Jain, L
Raju, TNK
AF Jain, Lucky
Raju, Tonse N. K.
TI Late Preterm and Early Term Births Preface
SO CLINICS IN PERINATOLOGY
LA English
DT Editorial Material
ID MORTALITY; PREGNANCY
C1 [Jain, Lucky] Emory Univ, Sch Med, Atlanta, GA 30322 USA.
[Jain, Lucky] Childrens Healthcare Atlanta, Atlanta, GA 30322 USA.
[Raju, Tonse N. K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Jain, L (reprint author), Emory Univ, Sch Med, 2015 Uppergate Dr, Atlanta, GA 30322 USA.
EM ljain@emory.edu; rajut@mail.nih.gov
NR 5
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0095-5108
EI 1557-9840
J9 CLIN PERINATOL
JI Clin. Perinatol.
PD DEC
PY 2013
VL 40
IS 4
BP XIX
EP XX
DI 10.1016/j.clp.2013.07.013
PG 2
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 259XQ
UT WOS:000327560000002
PM 24182963
ER
PT J
AU Raju, TNK
AF Raju, Tonse N. K.
TI Moderately Preterm, Late Preterm and Early Term Infants: Research Needs
SO CLINICS IN PERINATOLOGY
LA English
DT Article
DE Preterm; Immaturity; Respiratory distress; Apnea; Hypothermia;
Hypoglycemia; Jaundice; Infection
ID RESPIRATORY MORBIDITY; NEONATAL OUTCOMES; COLD STRESS; BRAIN; RISK;
GESTATION; DELIVERY; FETUS
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, Bethesda, MD 20892 USA.
RP Raju, TNK (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, 6100 Execut Blvd,Room 4803, Bethesda, MD 20892 USA.
EM rajut@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]
NR 32
TC 9
Z9 9
U1 0
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0095-5108
EI 1557-9840
J9 CLIN PERINATOL
JI Clin. Perinatol.
PD DEC
PY 2013
VL 40
IS 4
BP 791
EP +
DI 10.1016/j.clp.2013.07.010
PG 8
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 259XQ
UT WOS:000327560000015
PM 24182962
ER
PT J
AU Alexander, VM
Choyke, PL
Kobayashi, H
AF Alexander, V. M.
Choyke, P. L.
Kobayashi, H.
TI Fluorescent Molecular Imaging: Technical Progress and Current
Preclinical and Clinical Applications in Urogynecologic Diseases
SO CURRENT MOLECULAR MEDICINE
LA English
DT Article
DE Gynecologic cancer; molecular imaging; near infrared; urologic cancer
ID TARGETED CONTRAST AGENT; IN-VIVO; INDOCYANINE GREEN; PROSTATE-CANCER;
OVARIAN-CANCER; QUANTUM DOTS; MONOCLONAL-ANTIBODY; INTRAOPERATIVE
ASSESSMENT; ADVERSE REACTIONS; PEPTIDE PROBES
AB Many molecular imaging probes have been developed in recent years that hold great promise for both diagnostic and therapeutic functions in urogynecologic disease. Historically, optical probe designs were based on either endogenous or exogenous fluorophores. More recently, organic fluorophore probes have been engineered to target specific tissues and emit fluorescence only upon binding to targets. Several different photochemical mechanisms of activation exist. This review presents a discussion of the history and development of molecular imaging probe designs and provides an overview of successful preclinical and clinical models employing molecular probes for in vivo imaging of urogynecologic cancers.
C1 [Alexander, V. M.; Choyke, P. L.; Kobayashi, H.] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Choyke, PL (reprint author), NCI, Mol Imaging Program, NIH, Bldg 10,Room B3B69,MSC 1088, Bethesda, MD 20892 USA.
EM pchoyke@mail.nih.gov
NR 97
TC 1
Z9 1
U1 1
U2 18
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1566-5240
EI 1875-5666
J9 CURR MOL MED
JI Curr. Mol. Med.
PD DEC
PY 2013
VL 13
IS 10
BP 1568
EP 1578
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 258GV
UT WOS:000327448200007
PM 24206135
ER
PT J
AU Bornstein, MH
Jager, J
Putnick, DL
AF Bornstein, Marc H.
Jager, Justin
Putnick, Diane L.
TI Sampling in developmental science: Situations, shortcomings, solutions,
and standards
SO DEVELOPMENTAL REVIEW
LA English
DT Article
DE Sampling; Methodology; Developmental science
ID SOCIOECONOMIC-STATUS; DEPRESSIVE SYMPTOMS; UNITED-STATES;
GENDER-DIFFERENCES; RACIAL-DIFFERENCES; FAMILY-STRUCTURE; PUBLIC-HEALTH;
SUBSTANCE USE; RACE; ADOLESCENCE
AB Sampling is a key feature of every study in developmental science. Although sampling has far-reaching implications, too little attention is paid to sampling. Here, we describe, discuss, and evaluate four prominent sampling strategies in developmental science: population-based probability sampling, convenience sampling, quota sampling, and homogeneous sampling. We then judge these sampling strategies by five criteria: whether they yield representative and generalizable estimates of a study's target population, whether they yield representative and generalizable estimates of subsamples within a study's target population, the recruitment efforts and costs they entail, whether they yield sufficient power to detect subsample differences, and whether they introduce "noise" related to variation in subsamples and whether that "noise" can be accounted for statistically. We use sample composition of gender, ethnicity, and socioeconomic status to illustrate and assess the four sampling strategies. Finally, we tally the use of the four sampling strategies in five prominent developmental science journals and make recommendations about best practices for sample selection and reporting. Published by Elsevier Inc.
C1 [Bornstein, Marc H.; Jager, Justin; Putnick, Diane L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Publ Hlth Serv, Bethesda, MD 20892 USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Rockledge 1,Suite 8030,6705 Rockledge Dr,MSC 7971, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
OI Putnick, Diane/0000-0002-6323-749X
FU Intramural NIH HHS [ZIA HD001119-27]
NR 46
TC 19
Z9 19
U1 2
U2 14
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0273-2297
EI 1090-2406
J9 DEV REV
JI Dev. Rev.
PD DEC
PY 2013
VL 33
IS 4
BP 357
EP 370
DI 10.1016/j.dr.2013.08.003
PG 14
WC Psychology, Developmental
SC Psychology
GA 256CE
UT WOS:000327286500004
PM 25580049
ER
PT J
AU Lipska, KJ
Inzucchi, SE
Van Ness, PH
Gill, TM
Kanaya, A
Strotmeyer, ES
Koster, A
Johnson, KC
Goodpaster, BH
Harris, T
De Rekeneire, N
AF Lipska, Kasia J.
Inzucchi, Silvio E.
Van Ness, Peter H.
Gill, Thomas M.
Kanaya, Alka
Strotmeyer, Elsa S.
Koster, Annemarie
Johnson, Karen C.
Goodpaster, Bret H.
Harris, Tamara
De Rekeneire, Nathalie
CA Health Abc Study
TI Elevated HbA(1c) and Fasting Plasma Glucose in Predicting Diabetes
Incidence Among Older Adults Are two better than one?
SO DIABETES CARE
LA English
DT Article
ID GLYCATED HEMOGLOBIN; ODDS RATIO; RISK; A1C; PERFORMANCE; HEALTH;
CLASSIFICATION; DIAGNOSIS; MARKER; COHORT
AB OBJECTIVETo determine which measuresimpaired fasting glucose (IFG), elevated HbA(1c), or bothbest predict incident diabetes in older adults.RESEARCH DESIGN AND METHODSFrom the Health, Aging, and Body Composition study, we selected individuals without diabetes, and we defined IFG (100-125 mg/dL) and elevated HbA(1c) (5.7-6.4%) per American Diabetes Association guidelines. Incident diabetes was based on self-report, use of antihyperglycemic medicines, or HbA(1c) 6.5% during 7 years of follow-up. Logistic regression analyses were adjusted for age, sex, race, site, BMI, smoking, blood pressure, and physical activity. Discrimination and calibration were assessed for models with IFG and with both IFG and elevated HbA(1c).RESULTSAmong 1,690 adults (mean age 76.5, 46% men, 32% black), 183 (10.8%) developed diabetes over 7 years. Adjusted odds ratios of diabetes were 6.2 (95% CI 4.4-8.8) in those with IFG (versus those with fasting plasma glucose [FPG] <100 mg/dL) and 11.3 (7.8-16.4) in those with elevated HbA(1c) (versus those with HbA(1c) <5.7%). When FPG and HbA(1c) were considered together, odds ratios were 3.5 (1.9-6.3) in those with IFG only, 8.0 (4.8-13.2) in those with elevated HbA(1c) only, and 26.2 (16.3-42.1) in those with both IFG and elevated HbA(1c) (versus those with normal FPG and HbA(1c)). Addition of elevated HbA(1c) to the model with IFG resulted in improved discrimination and calibration.CONCLUSIONSOlder adults with both IFG and elevated HbA(1c) have a substantially increased odds of developing diabetes over 7 years. Combined screening with FPG and HbA(1c) may identify older adults at very high risk for diabetes.
C1 [Lipska, Kasia J.; Inzucchi, Silvio E.] Yale Univ, Sch Med, Dept Internal Med, Endocrinol Sect, New Haven, CT 06510 USA.
[Van Ness, Peter H.; Gill, Thomas M.; De Rekeneire, Nathalie] Yale Univ, Sch Med, Dept Internal Med, Geriatr Sect, New Haven, CT 06510 USA.
[Kanaya, Alka] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Strotmeyer, Elsa S.; Goodpaster, Bret H.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Koster, Annemarie] Maastricht Univ, Dept Social Med, CAPHRI, Maastricht, Netherlands.
[Johnson, Karen C.] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[Goodpaster, Bret H.] Univ Pittsburgh, Grad Sch Publ Hlth, Div Endocrinol & Metab, Pittsburgh, PA USA.
[Harris, Tamara] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
RP Lipska, KJ (reprint author), Yale Univ, Sch Med, Dept Internal Med, Endocrinol Sect, New Haven, CT 06510 USA.
EM kasia.lipska@yale.edu
RI Strotmeyer, Elsa/F-3015-2014; Koster, Annemarie/E-7438-2010
FU National Institute on Aging (NIA) [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106]; NIA [R01-AG028050, T32AG1934, R03 AG045086,
K24AG021507]; National Institute of Nursing Research (NINR)
[R01-NR012459]; National Institutes of Health, NIA; Pepper Center Career
Development Award [P30 AG21342]
FX This research was supported by National Institute on Aging (NIA)
contracts N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106; NIA grant
R01-AG028050; and National Institute of Nursing Research (NINR) grant
R01-NR012459 and in part by the Intramural Research Program of the
National Institutes of Health, NIA. K.J.L. was supported by NIA training
grant T32AG1934 and is currently supported by the Pepper Center Career
Development Award (P30 AG21342) and the Grants for Early
Medical/Surgical Specialists' Transition to Aging Research (R03
AG045086) from the NIA. T. M. G. is the recipient of a Midcareer
Investigator Award in Patient-Oriented Research (K24AG021507) from the
NIA. The study was conducted at the Yale Claude D. Pepper Older
Americans Independence Center (P30AG21342).
NR 34
TC 13
Z9 15
U1 3
U2 9
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 DEC
PY 2013
VL 36
IS 12
BP 3923
EP 3929
DI 10.2337/dc12-2631
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255AL
UT WOS:000327211500039
PM 24135387
ER
PT J
AU Yau, RK
Strotmeyer, ES
Resnick, HE
Sellmeyer, DE
Feingold, KR
Cauley, JA
Vittinghoff, E
De Rekeneire, N
Harris, TB
Nevitt, MC
Cummings, SR
Shorr, RI
Schwartz, AV
AF Yau, Rebecca K.
Strotmeyer, Elsa S.
Resnick, Helaine E.
Sellmeyer, Deborah E.
Feingold, Kenneth R.
Cauley, Jane A.
Vittinghoff, Eric
De Rekeneire, Nathalie
Harris, Tamara B.
Nevitt, Michael C.
Cummings, Steven R.
Shorr, Ronald I.
Schwartz, Ann V.
TI Diabetes and Risk of Hospitalized Fall Injury Among Older Adults
SO DIABETES CARE
LA English
DT Article
ID BODY-COMPOSITION; ELDERLY RESIDENTS; GLYCEMIC CONTROL; FRACTURE RISK;
HEALTH ABC; WOMEN; MELLITUS; PREDICTORS; PEOPLE; TYPE-1
AB OBJECTIVETo determine whether older adults with diabetes are at increased risk of an injurious fall requiring hospitalization.RESEARCH DESIGN AND METHODSThe longitudinal Health, Aging, and Body Composition Study included 3,075 adults aged 70-79 years at baseline. Hospitalizations that included ICD-9-Clinical Modification codes for a fall and an injury were identified. The effect of diabetes with and without insulin use on the rate of first fall-related injury hospitalization was assessed using proportional hazards models.RESULTSAt baseline, 719 participants had diabetes, and 117 of them were using insulin. Of the 293 participants who were hospitalized for a fall-related injury, 71 had diabetes, and 16 were using insulin. Diabetes was associated with a higher rate of injurious fall requiring hospitalization (hazard ratio [HR] 1.48 [95% CI 1.12-1.95]) in models adjusted for age, race, sex, BMI, and education. In those participants using insulin, compared with participants without diabetes, the HR was 3.00 (1.78-5.07). Additional adjustment for potential intermediaries, such as fainting in the past year, standing balance score, cystatin C level, and number of prescription medications, accounted for some of the increased risk associated with diabetes (1.41 [1.05-1.88]) and insulin-treated diabetes (2.24 [1.24-4.03]). Among participants with diabetes, a history of falling, poor standing balance score, and A1C level 8% were risk factors for an injurious fall requiring hospitalization.CONCLUSIONSOlder adults with diabetes, in particular those using insulin, are at greater risk of an injurious fall requiring hospitalization than those without diabetes. Among those with diabetes, poor glycemic control may increase the risk of an injurious fall.
C1 [Yau, Rebecca K.] Ctr Dis Control & Prevent, Council State & Terr Epidemiologists Appl Epidemi, Atlanta, GA 30333 USA.
[Yau, Rebecca K.] Univ N Carolina, Injury Prevent Res Ctr, Chapel Hill, NC USA.
[Strotmeyer, Elsa S.; Cauley, Jane A.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Resnick, Helaine E.] Univ Maryland, Sch Med, Dept Geriatr, Baltimore, MD 21201 USA.
[Resnick, Helaine E.] Gerontol Res Educ & Training Ctr, Baltimore, MD USA.
[Resnick, Helaine E.] Resnick Chodorow & Associates, Silver Spring, MD USA.
[Sellmeyer, Deborah E.] Johns Hopkins Sch Med, Div Endocrinol, Baltimore, MD USA.
[Feingold, Kenneth R.] Univ Calif San Francisco, Dept Med, Div Endocrinol, San Francisco, CA USA.
[Vittinghoff, Eric; Nevitt, Michael C.; Schwartz, Ann V.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[De Rekeneire, Nathalie] Yale Univ, Sch Med, Dept Internal Med, Geriatr Sect, New Haven, CT 06510 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol, Bethesda, MD 20892 USA.
[Cummings, Steven R.] Calif Pacific Med Ctr Res Inst, San Francisco, CA USA.
[Shorr, Ronald I.] North Florida South Georgia Vet Hlth Syst, Ctr Geriatr Res Educ & Clin, Gainesville, FL USA.
[Shorr, Ronald I.] Univ Florida, Dept Aging & Geriatr, Gainesville, FL USA.
RP Yau, RK (reprint author), Ctr Dis Control & Prevent, Council State & Terr Epidemiologists Appl Epidemi, Atlanta, GA 30333 USA.
EM rebeccayau@unc.edu
RI Strotmeyer, Elsa/F-3015-2014;
OI Strotmeyer, Elsa/0000-0002-4093-6036; Cauley, Jane A/0000-0003-0752-4408
FU National Institute on Aging [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, R01-AG028050]; National Institute of Nursing Research
[R01-NR012459]; Applied Epidemiology Fellowship Program; Centers for
Disease Control and Prevention [5U38HM000414]; Intramural Research
Program of the National Institutes of Health, National Institute on
Aging
FX This research was supported by National Institute on Aging contracts
N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106; National Institute on
Aging grant R01-AG028050; and National Institute of Nursing Research
grant R01-NR012459. This research was also supported by an appointment
to the Applied Epidemiology Fellowship Program administered by the
Council of State and Territorial Epidemiologists and funded by Centers
for Disease Control and Prevention Cooperative Agreement number
5U38HM000414. This research was supported in part by the Intramural
Research Program of the National Institutes of Health, National
Institute on Aging.
NR 39
TC 16
Z9 17
U1 1
U2 19
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 DEC
PY 2013
VL 36
IS 12
BP 3985
EP 3991
DI 10.2337/dc13-0429
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255AL
UT WOS:000327211500047
PM 24130352
ER
PT J
AU Dize, L
West, S
Quinn, TC
Gaydos, CA
AF Dize, Laura
West, Sheila
Quinn, Thomas C.
Gaydos, Charlotte A.
TI Pooling ocular swab specimens from Tanzania for testing by Roche
Amplicor and Aptima Combo 2 assays for the detection of Chlamydia
trachomatis: accuracy and cost-savings
SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE
LA English
DT Article
DE Chlamydia trachomatis; Trachoma; Pooling; Cost-savings
ID NEISSERIA-GONORRHOEAE; RANDOMIZED-TRIAL; SAMPLES; URINE; INFECTION;
PROGRAMS; STRATEGY
AB Ocular swabs collected in Tanzania were evaluated by Amplicor CT PCR and Aptima Combo2 assays for the detection of Chlamydia trachomatis to determine if pooling could be used to reduce the cost of detection. Pooling would be an accurate method and has thus far resulted in a cost-savings of 62.2%. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Dize, Laura; West, Sheila; Quinn, Thomas C.; Gaydos, Charlotte A.] Johns Hopkins Univ, Div Infect Dis, Baltimore, MD 21218 USA.
[Dize, Laura; West, Sheila; Quinn, Thomas C.; Gaydos, Charlotte A.] Johns Hopkins Univ, Wilmer Eye Inst, Baltimore, MD 21218 USA.
[Quinn, Thomas C.] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
RP Dize, L (reprint author), Johns Hopkins Univ, Div Infect Dis, Baltimore, MD 21218 USA.
EM Ldize2@jhmi.edu
FU Intramural NIH HHS [ZIA AI000358-32]
NR 16
TC 7
Z9 7
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0732-8893
EI 1879-0070
J9 DIAGN MICR INFEC DIS
JI Diagn. Microbiol. Infect. Dis.
PD DEC
PY 2013
VL 77
IS 4
BP 289
EP 291
DI 10.1016/j.diagmicrobio.2013.08.005
PG 3
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 257WW
UT WOS:000327419500003
PM 24079951
ER
PT J
AU Whirledge, S
Cidlowski, JA
AF Whirledge, Shannon
Cidlowski, John A.
TI A Role for Glucocorticoids in Stress-Impaired Reproduction: Beyond the
Hypothalamus and Pituitary
SO ENDOCRINOLOGY
LA English
DT Review
ID BETA-HYDROXYSTEROID DEHYDROGENASE; RAT LEYDIG-CELLS;
GONADOTROPIN-RELEASING-HORMONE; MESSENGER-RIBONUCLEIC-ACID;
FOLLICLE-STIMULATING-HORMONE; IN-VITRO FERTILIZATION; TESTICULAR
GERM-CELLS; OVARIAN 11-BETA-HYDROXYSTEROID DEHYDROGENASE; INTRAUTERINE
GROWTH RESTRICTION; ENDOMETRIAL STROMAL CELLS
AB In addition to the well-characterized role of the sex steroid receptors in regulating fertility and reproduction, reproductive events are also mediated by the hypothalamic-pituitary-adrenal axis in response to an individual's environment. Glucocorticoid secretion in response to stress contributes to the well-characterized suppression of the hypothalamic-pituitary-gonadal axis through central actions in the hypothalamus and pituitary. However, both animal and in vitro studies indicate that other components of the reproductive system are also regulated by glucocorticoids. Furthermore, in the absence of stress, it appears that homeostatic glucocorticoid signaling plays a significant role in reproduction and fertility in all tissues comprising the hypothalamic-pituitary-gonadal axis. Indeed, as central regulators of the immune response, glucocorticoids are uniquely poised to integrate an individual's infectious, inflammatory, stress, nutritional, and metabolic status through glucocorticoid receptor signaling in target tissues. Endocrine signaling between tissues regulating the immune and stress response and those determining reproductive status provides an evolutionary advantage, facilitating the trade-off between reproductive investment and offspring fitness. This review focuses on the actions of glucocorticoids in tissues important for fertility and reproduction, highlighting recent studies that show glucocorticoid signaling plays a significant role throughout the hypothalamic-pituitary-gonadal axis and characterizing these effects as permissive or inhibitory in terms of facilitating reproductive success.
C1 [Whirledge, Shannon; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Cidlowski, JA (reprint author), NIEHS, NIH, MD F3-07,POB 12233, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences.
NR 251
TC 19
Z9 20
U1 4
U2 41
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD DEC
PY 2013
VL 154
IS 12
BP 4450
EP 4468
DI 10.1210/en.2013-1652
PG 19
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 259RY
UT WOS:000327545200004
PM 24064362
ER
PT J
AU Mok, K
Laaksovirta, H
Tienari, PJ
Peuralinna, T
Myllykangas, L
Chio, A
Traynor, BJ
Nalls, MA
Gurunlian, N
Shatunov, A
Restagno, G
Mora, G
Leigh, PN
Shaw, CE
Morrison, KE
Shaw, PJ
Al-Chalabi, A
Hardy, J
Orrell, RW
AF Mok, Kin
Laaksovirta, Hannu
Tienari, Pentti J.
Peuralinna, Terhi
Myllykangas, Liisa
Chio, Adriano
Traynor, Bryan J.
Nalls, Michael A.
Gurunlian, Nicole
Shatunov, Aleksey
Restagno, Gabriella
Mora, Gabriele
Leigh, P. Nigel
Shaw, Chris E.
Morrison, Karen E.
Shaw, Pamela J.
Al-Chalabi, Ammar
Hardy, John
Orrell, Richard W.
TI Homozygosity analysis in amyotrophic lateral sclerosis
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE amyotrophic lateral sclerosis; homozygosity; recessive
ID GENOME-WIDE ASSOCIATION; LINKAGE DISEQUILIBRIUM; HEXANUCLEOTIDE REPEAT;
SUPEROXIDE-DISMUTASE; MUTATIONS; ALS; POPULATION; GENE; TRAFFICKING;
PROTEIN
AB Amyotrophic lateral sclerosis (ALS) may appear to be familial or sporadic, with recognised dominant and recessive inheritance in a proportion of cases. Sporadic ALS may be caused by rare homozygous recessive mutations. We studied patients and controls from the UK and a multinational pooled analysis of GWAS data on homozygosity in ALS to determine any potential recessive variant leading to the disease. Six-hundred and twenty ALS and 5169 controls were studied in the UK cohort. A total of 7646 homozygosity segments with length <2 Mb were identified, and 3568 rare segments remained after filtering 'common' segments. The mean total of the autosomal genome with homozygosity segments was longer in ALS than in controls (unfiltered segments, P = 0.05). Two-thousand and seventeen ALS and 6918 controls were studied in the pooled analysis. There were more regions of homozygosity segments per case (P = 1 x 10(-5)), a greater proportion of cases harboured homozygosity (P = 2 x 10(-5))(,) a longer average length of segment (P = 1 x 10(-5)), a longer total genome coverage (P = 1 x 10(-5)), and a higher rate of these segments overlapped with RefSeq gene regions (P = 1 = 10 = 5), in ALS patients than controls. Positive associations were found in three regions. The most significant was in the chromosome 21 SOD1 region, and also chromosome 1 2.9-4.8 Mb, and chromosome 5 in the 65 Mb region. There are more than twenty potential genes in these regions. These findings point to further possible rare recessive genetic causes of ALS, which are not identified as common variants in GWAS.
C1 [Mok, Kin; Gurunlian, Nicole; Hardy, John; Orrell, Richard W.] UCL, Inst Neurol, Dept Mol Neurosci, Reta Lila Weston Res Labs, London NW3 2PF, England.
[Mok, Kin; Gurunlian, Nicole; Hardy, John; Orrell, Richard W.] UCL, Inst Neurol, Dept Clin Neurosci, London NW3 2PF, England.
[Laaksovirta, Hannu] Univ Helsinki, Cent Hosp, Biomedicum, Dept Neurol,Mol Neurol Res Program, Helsinki, Finland.
[Laaksovirta, Hannu; Tienari, Pentti J.; Peuralinna, Terhi; Traynor, Bryan J.; Nalls, Michael A.] NIA, Mol Genet Sect, NIH, Bethesda, MD 20892 USA.
[Laaksovirta, Hannu; Tienari, Pentti J.; Peuralinna, Terhi; Traynor, Bryan J.; Nalls, Michael A.] NIA, Neuromuscular Dis Res Grp, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Myllykangas, Liisa] Univ Helsinki, Dept Pathol, Haartman Inst, Helsinki, Finland.
[Myllykangas, Liisa] HUSLAB, Helsinki, Finland.
[Myllykangas, Liisa] Folkhalsan Inst Genet, Helsinki, Finland.
[Chio, Adriano] Univ Turin, Dept Neurosci, Turin, Italy.
[Chio, Adriano] Azienda Osped Univ San Giovanni Battista, Turin, Italy.
[Shatunov, Aleksey; Shaw, Chris E.; Al-Chalabi, Ammar] Kings Coll London, Med Res Council Ctr Neurodegenerat Res, Inst Psychiat, London WC2R 2LS, England.
[Restagno, Gabriella] Azienda Osped OIRM St Anna, Mol Genet Lab, Turin, Italy.
[Mora, Gabriele] Fdn Salvatore Mangeri, IRCCS Sci Inst Milan, Milan, Italy.
[Leigh, P. Nigel] Univ Sussex, Trafford Ctr Biomed Res, Brighton & Sussex Med Sch, Falmer, England.
[Morrison, Karen E.] Univ Birmingham, Sch Clin & Expt Med, Birmingham, W Midlands, England.
[Morrison, Karen E.] Univ Hosp Birmingham NHS Fdn Trust, Queen Elizabeth Hosp, Birmingham, W Midlands, England.
[Shaw, Pamela J.] Univ Sheffield, Dept Neurosci, Sheffield Inst Translat Neurosci SITraN, Sheffield, S Yorkshire, England.
RP Orrell, RW (reprint author), UCL, Inst Neurol, Dept Clin Neurosci, Rowland Hill St, London NW3 2PF, England.
EM r.orrell@ucl.ac.uk
RI Al-Chalabi, Ammar/E-5361-2010; Hardy, John/C-2451-2009; Traynor,
Bryan/G-5690-2010; Tienari, Pentti/A-4893-2012; Mok, Kin/F-5860-2012;
OI Al-Chalabi, Ammar/0000-0002-4924-7712; Chio, Adriano/0000-0001-9579-5341
FU NIH; National Institute on Aging [Z01-AG000949-02]; National Institute
of Neurological Disorders and Stroke; Extramural NIH grants
[R01AG031278, R01AG038791]; European Community [259867]; Motor Neurone
Disease Association of Great Britain; ALS Association; Angel Fund; ALS
Therapy Alliance; Wellcome Trust; Reta Lila Weston Foundation; MRC;
Microsoft Research Foundation; ALS Association, Helsinki University
Central Hospital; Finnish Academy, Ministero della Salute, Progetti
Finalizzati; Fondazione Vialli e Mauro for ALS; Federazione Italiana
Giuoco Calcio; NIHR specialist Biomedical Research Centre for Mental
Health at the South London and Maudsley NHS Foundation Trust (SLaM);
Institute of Psychiatry, King's College London; National Institute for
Health Research
FX This work was supported in part by the Intramural Research Programs of
the NIH, the National Institute on Aging (Z01-AG000949-02), and the
National Institute of Neurological Disorders and Stroke. Extramural NIH
grants R01AG031278 and R01AG038791 supported some family assessments.
The research leading to these results has received funding from the
European Community's Health Seventh Framework Programme (FP7/2007-2013)
under grant agreement no. 259867. We thank the Motor Neurone Disease
Association of Great Britain for several grants relating to this work
(RWO, AAC, PJS, HM), the ALS Association, The Angel Fund, the ALS
Therapy Alliance, and the Wellcome Trust (PJS) for support. This work
was also funded by the Reta Lila Weston Foundation, and by an MRC
returning scientist (JH) and fellowship (SPB) award, by Microsoft
Research Foundation, the ALS Association, Helsinki University Central
Hospital, the Finnish Academy, Ministero della Salute, Progetti
Finalizzati 2007, Fondazione Vialli e Mauro for ALS, and Federazione
Italiana Giuoco Calcio. The authors thank the NIHR specialist Biomedical
Research Centre for Mental Health at the South London and Maudsley NHS
Foundation Trust (SLaM) and the Institute of Psychiatry, King's College
London, and the National Institute for Health Research-funded University
College London / University College London Hospitals Biomedical Research
Centre.
NR 40
TC 10
Z9 10
U1 2
U2 6
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 DEC
PY 2013
VL 21
IS 12
BP 1429
EP 1435
DI 10.1038/ejhg.2013.59
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 257AK
UT WOS:000327355100017
PM 23612577
ER
PT J
AU DeCherney, AH
AF DeCherney, Alan H.
TI From partner's desk to iPad
SO FERTILITY AND STERILITY
LA English
DT Editorial Material
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP DeCherney, AH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD DEC
PY 2013
VL 100
IS 6
BP 1492
EP 1494
DI 10.1016/j.fertnstert.2013.10.004
PG 3
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 259NG
UT WOS:000327533000007
ER
PT J
AU Trabert, B
Lamb, EJ
Scoccia, B
Moghissi, KS
Westhoff, CL
Niwa, S
Brinton, LA
AF Trabert, Britton
Lamb, Emmet J.
Scoccia, Bert
Moghissi, Kamran S.
Westhoff, Carolyn L.
Niwa, Shelley
Brinton, Louise A.
TI Ovulation-inducing drugs and ovarian cancer risk: results from an
extended follow-up of a large United States infertility cohort
SO FERTILITY AND STERILITY
LA English
DT Article
DE Ovarian cancer; risk; infertility; clomiphene citrate; gonadotropins
ID FERTILITY DRUGS; WOMEN; STIMULATION; BREAST; TUMORS
AB Objective: To examine the relationship of ovulation-inducing drugs and ovarian cancer.
Design: Retrospective cohort study, with additional follow-up since initial report.
Setting: Five large reproductive endocrinology practices.
Patient(s): In a retrospective cohort of 9,825 women evaluated for infertility at five clinical sites in the United States between 1965 and 1988 with follow-up through 2010, we examined the relationship of ovulation-inducing drugs and ovarian cancer (n = 85).
Intervention(s): None.
Main Outcome Measure(s): Hazard rate ratios (RR) and 95% confidence intervals (CI) for ovarian cancer.
Result(s): Among women evaluated for infertility, there was no association of ovarian cancer risk with ever use of clomiphene citrate (CC) (adjusted RR 1.34, 95% CI 0.86-2.07) or gonadotropins (RR 1.00, 95% CI 0.48-2.08) and no evidence that any of several more detailed subgroups of usage were related to an increased risk with one exception: women who used CC and remained nulligravid did demonstrate much higher risks than those who successfully conceived compared with nonusers (respectively, RR 3.63, 95% CI 1.36-9.72 vs. RR 0.88, 95% CI 0.47-1.63).
Conclusion(s): Our overall results were reassuring and consistent with other studies. A reason for an association between CC use and ovarian cancer among persistently nulligravid women remains to be determined. Given the large and increasing number of women treated with ovulation-inducing drugs, the increased risk of ovarian cancer among the subset of women who remained nulligravid should be further monitored. (Fertil Steril (R) 2013;100:1660-6. (C)2013 by American Society for Reproductive Medicine.)
C1 [Trabert, Britton; Brinton, Louise A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Lamb, Emmet J.] Stanford Univ, Dept Obstet & Gynecol, Stanford, CA 94305 USA.
[Scoccia, Bert] Univ Illinois, Dept Obstet & Gynecol, Chicago, IL 60612 USA.
[Moghissi, Kamran S.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
[Westhoff, Carolyn L.] Columbia Univ, Dept Obstet & Gynecol, New York, NY USA.
[Niwa, Shelley] Westat Corp, Rockville, MD USA.
RP Trabert, B (reprint author), 9609 Med Ctr Dr,Room 7-E228,MSC 9774, Bethesda, MD 20892 USA.
EM britton.trabert@nih.gov
RI Brinton, Louise/G-7486-2015; Trabert, Britton/F-8051-2015
OI Brinton, Louise/0000-0003-3853-8562;
FU National Cancer Institute, National Institutes of Health
FX Supported by the intramural research program of the National Cancer
Institute, National Institutes of Health.
NR 21
TC 11
Z9 12
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD DEC
PY 2013
VL 100
IS 6
BP 1660
EP 1666
DI 10.1016/j.fertnstert.2013.08.008
PG 7
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 259NG
UT WOS:000327533000036
PM 24011610
ER
PT J
AU Filiberto, AC
Mumford, SL
Pollack, AZ
Zhang, CL
Yeung, EH
Schliep, KC
Perkins, NJ
Wactawski-Wende, J
Schisterman, EF
AF Filiberto, Amanda C.
Mumford, Sunni L.
Pollack, Anna Z.
Zhang, Cuilin
Yeung, Edwina H.
Schliep, Karen C.
Perkins, Neil J.
Wactawski-Wende, Jean
Schisterman, Enrique F.
TI Usual dietary isoflavone intake and reproductive function across the
menstrual cycle
SO FERTILITY AND STERILITY
LA English
DT Article
DE Isoflavone; anovulation; sex hormones; nutrition
ID HORMONE-BINDING GLOBULIN; PREMENOPAUSAL WOMEN; MEDITERRANEAN DIET; SOY
PROTEIN; POSTMENOPAUSAL WOMEN; US ADULTS; ADHERENCE; RISK; MEN;
METABOLITES
AB Objective: To assess the association of total isoflavone intake with ovulatory function, including sporadic anovulation in healthy premenopausal women.
Design: Prospective cohort study.
Setting: University.
Patient(s): Participants included 259 healthy regularly menstruating women aged 18-44 years.
Intervention(s): None.
Main Outcome Measure(s): Serum concentrations of E-2, free E-2, P, LH, FSH, and SHBG and sporadic anovulation in healthy premenopausal women.
Result(s): Isoflavone intake was not associated with E-2, free E-2, P, LH, and FSH concentrations. Consumption in the highest quartile (Q4: 1.6-78.8 mg/d) was significantly associated with greater SHBG concentrations (beta = 0.09; 95% confidence interval [CI] 0.02-0.16), compared with the first quartile (Q1: 0.0-0.3 mg/d).
Conclusion(s): Isoflavone intake was not associated with sporadic anovulation (Q4 vs. Q1: odds ratio 0.87, 95% CI 0.32-1.66). Dietary isoflavone intake among young premenopausal women was not related to sex hormone concentrations or anovulation, but was associated with minimally increased SHBG concentrations. These results suggest potential endocrine effects with no subsequent effects on ovulation, easing concerns regarding their impacts on fertility. (Fertil Steril (R) 2013;100:1727-34. (C)2013 by American Society for Reproductive Medicine.)
C1 [Filiberto, Amanda C.; Mumford, Sunni L.; Pollack, Anna Z.; Zhang, Cuilin; Yeung, Edwina H.; Schliep, Karen C.; Perkins, Neil J.; Schisterman, Enrique F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Rockville, MD 20852 USA.
[Schliep, Karen C.] Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT USA.
[Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, 6100 Execut Blvd,7B03M, Rockville, MD 20852 USA.
EM schistee@mail.nih.gov
RI Yeung, Edwina/F-5992-2015;
OI Yeung, Edwina/0000-0002-3851-2613; Perkins, Neil/0000-0002-6802-4733;
Pollack, Anna/0000-0002-4313-3298; Schisterman,
Enrique/0000-0003-3757-641X
FU Intramural Research Program at the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institute of
Health
FX Supported by the Intramural Research Program at the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
National Institute of Health.
NR 32
TC 2
Z9 2
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD DEC
PY 2013
VL 100
IS 6
BP 1727
EP 1734
DI 10.1016/j.fertnstert.2013.08.002
PG 8
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 259NG
UT WOS:000327533000046
PM 23998910
ER
PT J
AU Thompson, AJ
Scholz, SW
Singleton, AB
Hardwick, A
McFarland, NR
Okun, MS
AF Thompson, Amanda J.
Scholz, Sonja W.
Singleton, Andrew B.
Hardwick, Angela
McFarland, Nikolaus R.
Okun, Michael S.
TI Variability in clinical phenotypes of heterozygous and homozygous cases
of Parkin-related Parkinson's disease
SO INTERNATIONAL JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE Parkin; Parkinson's disease; levodopa-equivalent dose (LED);
dyskinesias; PARK 2
ID STIMULATION
AB Parkin mutations are a common cause of early-onset Parkinson's disease. To study the clinical features and treatment responses of patients with homozygous or heterozygous Parkin mutations, we performed a retrospective chart review in six early-onset parkinsonism patients with pathogenic Parkin mutations. The clinical phenotypes observed in this cohort, all drawn from different families, were variable. All patients had a slowly progressive form of parkinsonism that responded well to dopaminergic therapy with the exception of one advanced case. Homozygous patients had an earlier age at disease onset than heterozygous patients. Two of our patients underwent bilateral deep brain stimulation (DBS) of the subthalamic nucleus or globus pallidus leading to a sustained positive response. Our observations support an earlier age of onset for homozygous cases and possible beneficial effects of DBS in Parkin-related parkinsonism.
C1 [Thompson, Amanda J.; Hardwick, Angela; McFarland, Nikolaus R.; Okun, Michael S.] Univ Florida, Ctr Movement Disorders & Neurorestorat, Dept Neurol, Gainesville, FL 32607 USA.
[Thompson, Amanda J.; Hardwick, Angela; McFarland, Nikolaus R.; Okun, Michael S.] Univ Florida, Ctr Movement Disorders & Neurorestorat, Dept Neurosurg, Gainesville, FL 32607 USA.
[Scholz, Sonja W.] Georgetown Univ, Dept Neurosci, Washington, DC USA.
[Scholz, Sonja W.; Singleton, Andrew B.] NIH, Neurogenet Lab, Bethesda, MD 20892 USA.
RP Okun, MS (reprint author), Univ Florida, Ctr Movement Disorders & Neurorestorat, Dept Neurol, Gainesville, FL 32607 USA.
EM okun@neurology.ufl.edu
RI Singleton, Andrew/C-3010-2009;
OI McFarland, Nikolaus/0000-0002-8699-8857; Okun,
Michael/0000-0002-6247-9358; Scholz, Sonja/0000-0002-6623-0429
FU NIH; NPF; Michael J. Fox Foundation; Parkinson Alliance; Smallwood
Foundation; UF Foundation; USF CME office; PeerView; Vanderbilt
University; Medtronic; ANS/St. Jude
FX The authors alone are responsible for the content and writing of the
article. Dr. Okun serves as a consultant for the National Parkinson
Foundation, and has received research grants from NIH, NPF, the Michael
J. Fox Foundation, the Parkinson Alliance, Smallwood Foundation, and the
UF Foundation. Dr. Okun has previously received honoraria, but in the
past >36 months has received no support from industry including travel.
Dr. Okun has received royalties for publications with Demos, Manson, and
Cambridge (movement disorders books). Dr. Okun has participated in CME
activities on movement disorders sponsored by the USF CME office,
PeerView, and by Vanderbilt University. The institution and not Dr. Okun
receives grants from Medtronic and ANS/St. Jude, and the PI has no
financial interest in these grants. Dr. Okun has participated as a site
PI and/or co-I for several NIH, foundation, and industry sponsored
trials over the years but has not received honoraria.
NR 7
TC 0
Z9 0
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0020-7454
EI 1563-5279
J9 INT J NEUROSCI
JI Int. J. Neurosci.
PD DEC
PY 2013
VL 123
IS 12
BP 847
EP 849
DI 10.3109/00207454.2013.810626
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 255RV
UT WOS:000327258400004
PM 23767969
ER
PT J
AU Nichols, SL
Bethel, J
Garvie, PA
Patton, DE
Thornton, S
Kapogiannis, BG
Ren, WJ
Major-Wilson, H
Puga, A
Woods, SP
AF Nichols, Sharon L.
Bethel, James
Garvie, Patricia A.
Patton, Doyle E.
Thornton, Sarah
Kapogiannis, Bill G.
Ren, Weijia
Major-Wilson, Hanna
Puga, Ana
Woods, Steven P.
TI Neurocognitive Functioning in Antiretroviral Therapy-Naive Youth With
Behaviorally Acquired Human Immunodeficiency Virus
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE HIV; Adolescent; Neurocognitive functioning; Substance use;
HIV-associated neurocognitive disorder
ID HIV-INFECTION; NEUROPSYCHOLOGICAL IMPAIRMENT; MEDICATION ADHERENCE;
DISORDERS; MEMORY; INDIVIDUALS; ADOLESCENCE; HIV/AIDS; DEMENTIA; WORKING
AB Purpose: Youth living with human immunodeficiency virus (HIV) account for over one third of new HIV infections and are at high risk of adverse psychosocial, everyday living, and health outcomes. Human immunodeficiency virus-associated neurocognitive disorders (HAND) are known to affect health outcomes of HIV-infected adults even in the era of combination antiretroviral therapy. Thus, the current study aimed to characterize the prevalence and clinical correlates of HAND in youth living with HIV. Here, we report baseline neurocognitive data for behaviorally HIV-infected youth enrolled in a prospective study evaluating strategies of antiretroviral treatment initiation and use.
Methods: A total of 220 participants, age 18-24 years, who were naive to treatment (except for prevention of mother-to-child HIV transmission; n = 3), completed a comprehensive neurocognitive, substance use, and behavioral health assessment battery.
Results: Sixty-seven percent of youth met criteria for HAND (96.4% were asymptomatic and 3.5% were syndromic); deficits in episodic memory and fine-motor skills emerged as the most commonly affected ability areas. Multivariable models showed that lower CD4 count, longer time since HIV diagnosis, and high-risk alcohol use were uniquely associated with neurocognitive deficits.
Conclusions: Over two thirds of youth with behaviorally acquired HIV evidence neurocognitive deficits, which have modest associations with more advanced HIV disease as well as other factors. Research is needed to determine the impact of such neuropsychiatric morbidity on mental health and HIV disease treatment outcomes (e. g., nonadherence) and transition to independent living responsibilities in HIV-infected youth, as well as its long-term trajectory and possible responsiveness to cognitive rehabilitation and pharmacotherapy. (C) 2013 Society for Adolescent Health and Medicine. All rights reserved.
C1 [Nichols, Sharon L.] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
[Bethel, James; Thornton, Sarah; Ren, Weijia] Westat Corp, Rockville, MD USA.
[Patton, Doyle E.; Puga, Ana] Childrens Diagnost & Treatment Ctr Inc, Ft Lauderdale, FL USA.
[Kapogiannis, Bill G.] NIH, Bethesda, MD 20892 USA.
[Major-Wilson, Hanna] Univ Miami, Dept Pediat, Div Adolescent Med, Miami, FL 33152 USA.
[Woods, Steven P.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
RP Nichols, SL (reprint author), Univ Calif San Diego, Dept Neurosci, 9500 Gilman Dr,0935, La Jolla, CA 92093 USA.
EM slnichols@ucsd.edu
FU Adolescent Trials Network for HIV/AIDS Interventions (ATN) from the
National Institutes of Health through the National Institute of Child
Health and Human Development [U01-HD040533]; National Institutes of Drug
Abuse; National Institutes of Drug Abuse [R01 DA DA031017]; National
Institute of Allergy and Infectious Diseases (NIAID); Eunice Kennedy
Shriver National Institute of Child Health and Human Development
(NICHD); National Institute of Mental Health (NIMH) [U01 A1068632]; ATN
Coordinating Center at the University of Alabama at Birmingham
FX This work was supported by the Adolescent Trials Network for HIV/AIDS
Interventions (ATN; Grant U01-HD040533) from the National Institutes of
Health through the National Institute of Child Health and Human
Development (B. Kapogiannis, C. Worrell), with supplemental funding from
the National Institutes of Drug Abuse (N. Borek, D. Lawrence) and Mental
Health (P. Brouwers, S. Allison), and Grant R01 DA DA031017 from the
National Institutes of Drug Abuse. The protocol was co-endorsed by the
International Maternal Pediatric Adolescent AIDS Clinical Trials Group.
Support for the International Maternal Pediatric Adolescent AIDS
Clinical Trials Group (IMPAACT) was provided by the National Institute
of Allergy and Infectious Diseases (NIAID), the Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD), and
the National Institute of Mental Health (NIMH) [U01 A1068632]. The study
was scientifically reviewed by the ATN's Behavioral Leadership Group.
Network, scientific, and logistical support was provided by the ATN
Coordinating Center (C. Wilson, C. Partlow) at the University of Alabama
at Birmingham. Network operations and data management support was
provided by the ATN Data and Operations Center at Westat, Inc. (J.
Korelitz, B. Driver). Please note that listing in the acknowledgments
section does not imply endorsement of the findings and conclusions of
this article. The authors acknowledge the contribution of the
investigators and staff at the following ATN 071 and IMPAACT sites that
participated in this study (listed in order of Site Principal
Investigator, Study Coordinator, Psychologist): University of South
Florida (Patricia Emmanuel, M. D., Priscilla Julian, RN, Tiffany
Chenneville, Ph.D.); Children's Hospital of Los Angeles (Marvin Belzer,
M. D., Michelle Bradford, B. A., Anita Hamilton, Ph.D., ABPP-CN);
Children's National Medical Center (Lawrence D'Angelo, M. D., Connie
Trexler, RN, Donna Marschall, Ph.D.); University of Pennsylvania and the
Children's Hospital of Philadelphia (Mary Tanney, M. P. H., M.S.N.,
C.P.N.P., Linda Hawkins, M. S., Ed.D.; Jerilynn Radcliffe, Ph.D.);
Stroger Hospital and the CORE Center (Jaime Martinez, M. D., Kelly
Bojan, D.N.P., Harold Fuentes, Psy.D.); University Pediatric Hospital
(Irma Febo, M. D., Hazel Ayala-Flores, B.S.N., Nydia Scalley-Trifilio,
M. A.); Montefiore Medical Center (Donna Futterman, M. D., Elizabeth
Bruce, M. D., Erica Weiss, M. A.); Mount Sinai Medical Center,
Adolescent Health Center (John Steever, M. D., Mary Geiger, M. P. H.,
Marijane Lehr, Ph.D.); University of California, San Francisco (Barbara
Moscicki, M. D., Lisa Irish, B.S.N., Rita Jeremy, Ph.D.); Tulane Medical
Center (Sue Ellen Abdalian, M. D., Leslie Kozina, RN, Patricia Sirois,
Ph.D.); University of Maryland (Vicki Tepper, Ph.D., Reshma Gorle, M. P.
H., Terry Lee-Wilk, Ph.D.); University of Miami School of Medicine
(Lawrence Friedman, M. D., Donna Maturo, M.S.N., Anai Cuadra, Ph.D.);
Children's Diagnostic and Treatment Center (Ana Puga, M. D., Amy Inman,
B. S., Doyle Patton, Ph.D.); St Jude Children's Research Hospital
(Patricia Flynn, M. D., Mary Dillard, B.S.N, Patricia Garvie, Ph.D.,
Megan Wilkins, Ph.D.); Lurie Children's Hospital (Robert Garofalo, M.
D., M. P. H., Ann Sanders, M. P. H., Andrea Boyd, Ph.D.); University of
Southern California (Andrea Kovacs, M. D., Michelle Aranda, M. P. H.,
Maribel Mejia, Ph.D.); Children's Hospital of Michigan (Ellen Moore, M.
D., Ayanna Walters, RN, Salome Cockern, Ph.D.); Children's Hospital of
Denver (Elizabeth McFarland, M. D., Kerry Hahn, B. S.; , CCRP, Robin
McEvoy, Ph.D.); Howard University (Sohail Rana, M. D., Meseret Deressa,
M. P. H, Eshauna Padilla, M. A.); and Johns Hopkins University (Allison
George Agwu, M. D., Todd Noletto, M. P. H., Laura Margolis, Ph.D.). The
authors sincerely thank additional ATN 071 Protocol Team Members (Pim
Brouwers, Ph.D., Tiandong Li, Ph.D., Craig Wilson, M. D.), the ATN
Community Advisory Board, and the youth who participated in the study.
An oral presentation of portions of this study was made at the bi-annual
Adolescent Medicine Trials Network for HIV/AIDS Intervention Meeting in
Bethesda, Maryland, on April 11, 2011. The authors extend sincere
gratitude to Pim Brouwers, Ph.D., for his comments on earlier versions
of the manuscript, and Tiandong Li, Ph.D., for statistical analysis and
consultation.
NR 42
TC 11
Z9 11
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 DEC
PY 2013
VL 53
IS 6
BP 763
EP 771
DI 10.1016/j.jadohealth.2013.07.006
PG 9
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA 258TJ
UT WOS:000327481300015
PM 23972941
ER
PT J
AU Myers, VH
Mcvay, MA
Champagne, CM
Hollis, JF
Coughlin, JW
Funk, KL
Gullion, CM
Jerome, GJ
Loria, CM
Samuel-Hodge, CD
Stevens, VJ
Svetkey, LP
Brantley, PJ
AF Myers, Valerie H.
McVay, Megan A.
Champagne, Catherine M.
Hollis, Jack F.
Coughlin, Janelle W.
Funk, Kristine L.
Gullion, Christina M.
Jerome, Gerald J.
Loria, Catherine M.
Samuel-Hodge, Carmen D.
Stevens, Victor J.
Svetkey, Laura P.
Brantley, Phillip J.
TI Weight loss history as a predictor of weight loss: results from Phase I
of the weight loss maintenance trial
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Weight loss history; Previous weight; Weight loss method; Behavioral;
Lifestyle; Greatest weight loss
ID DIABETES PREVENTION PROGRAM; DIETARY-SUPPLEMENTS; PHYSICAL-ACTIVITY;
PRETREATMENT PREDICTORS; MISSING DATA; OBESITY; REDUCTION; WOMEN;
BEHAVIOR; INTERVENTIONS
AB Past studies have suggested that weight loss history is associated with subsequent weight loss. However, questions remain whether method and amount of weight lost in previous attempts impacts current weight loss efforts. This study utilized data from the Weight Loss Maintenance Trial to examine the association between weight loss history and weight loss outcomes in a diverse sample of high-risk individuals. Multivariate regression analysis was conducted to determine which specific aspects of weight loss history predict change in weight during a 6-month weight loss intervention. Greater weight loss was predicted by fewer previous weight loss attempts with assistance (p = 0.03), absence of previous dietary/herbal weight loss supplement use (p = 0.01), and greater maximum weight loss in previous attempts (p < 0.001). Future interventions may benefit from assessment of weight loss history and tailoring of interventions based on past weight loss behaviors and outcomes.
C1 [Myers, Valerie H.; McVay, Megan A.; Champagne, Catherine M.; Brantley, Phillip J.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
[Hollis, Jack F.; Funk, Kristine L.; Gullion, Christina M.; Stevens, Victor J.] Kaiser Permanente Ctr Hlth Res, Portland, OR 97227 USA.
[Coughlin, Janelle W.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21287 USA.
[Jerome, Gerald J.] Towson Univ, Towson, MD 21252 USA.
[Loria, Catherine M.] NHLBI, Bethesda, MD 20892 USA.
[Samuel-Hodge, Carmen D.] Univ N Carolina, Gillings Sch Publ Hlth, Chapel Hill, NC 27599 USA.
[Samuel-Hodge, Carmen D.] Univ N Carolina, Sch Med, Chapel Hill, NC 27599 USA.
[Svetkey, Laura P.] Duke Univ, Med Ctr, Durham, NC 27705 USA.
RP Myers, VH (reprint author), Louisiana State Univ Syst, Pennington Biomed Res Ctr, 6400 Perkins Rd, Baton Rouge, LA 70808 USA.
EM valerie.myers@pbrc.edu; meganamcvay@gmail.com;
catherine.champagne@pbrc.edu; Jack.Hollis@kpchr.org; jwilder3@jhmi.edu;
Kristine.Funk@kpchr.org; Christina.Gullion@kpchr.org;
GJerome@towson.edu; loriac@nih.gov; carmen_samuel@unc.edu;
victor.j.stevens@kpchr.org; svetk001@mc.duke.edu; brantlpj@pbrc.edu
OI Jerome, Gerald/0000-0003-0612-2626
FU NHLBI NIH HHS [5-U01 HL68920, 5-HL 68955, 5-U01 HL68676, 5-U01 HL68790,
U01 HL068676, U01 HL068734, U01 HL068790, U01 HL068920, U01 HL068955];
PHS HHS [5-U01 68734]
NR 35
TC 3
Z9 3
U1 1
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
EI 1573-3521
J9 J BEHAV MED
JI J. Behav. Med.
PD DEC
PY 2013
VL 36
IS 6
BP 574
EP 582
DI 10.1007/s10865-012-9450-0
PG 9
WC Psychology, Clinical
SC Psychology
GA 255BL
UT WOS:000327214100004
PM 22907176
ER
PT J
AU Peabody, NC
White, BH
AF Peabody, Nathan C.
White, Benjamin H.
TI Eclosion gates progression of the adult ecdysis sequence of Drosophila
SO JOURNAL OF EXPERIMENTAL BIOLOGY
LA English
DT Article
DE hormones; behavior; innate; circuit
ID IMAGINAL ECDYSIS; WING EXPANSION; INSECT ECDYSIS; BEHAVIORAL SEQUENCE;
DECISION NETWORK; CELL-DEATH; BURSICON; HORMONE; ROLES; MELANOGASTER
AB Animal behavior is often organized into stereotyped sequences that promote the goals of reproduction, development and survival. However, for most behaviors, the neural mechanisms that govern the order of execution of the motor programs within a sequence are poorly understood. An important model in understanding the hormonal determinants of behavioral sequencing is the ecdysis sequence, which is performed by insects at each developmental transition, or molt. The adult ecdysis sequence in Drosophila includes the emergence of the insect from the pupal case followed by expansion and hardening of the wings. Wing expansion is governed by the hormone bursicon, and stimulation of the bursicon-expressing neurons in newly eclosed flies induces rapid wing expansion. Here we show that that such stimulation delivered prior to eclosion has no immediate effect, but does cause rapid wing expansion after eclosion if the stimulus is delivered within 40 min of that event. We observe a similar delayed effect upon stimulation of a single pair of bursicon-expressing neurons previously identified as command neurons for wing expansion. We conclude that command neuron stimulation enables the motor output pathway for wing expansion, but that this pathway is blocked prior to eclosion. By manipulating the time of eclosion, we demonstrate that some physiological process tightly coupled to adult ecdysis releases the block on wing expansion. Eclosion thus serves as a behavioral checkpoint and complements hormonal mechanisms to ensure that wing expansion strictly follows eclosion in the ecdysis sequence.
C1 [Peabody, Nathan C.; White, Benjamin H.] NIMH, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP White, BH (reprint author), NIMH, Mol Biol Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM benjaminwhite@mail.nih.gov
FU Intramural Research Program of the National Institute of Mental Health
[1ZIA-MH-002800-07]
FX This research was supported by the Intramural Research Program of the
National Institute of Mental Health (Project 1ZIA-MH-002800-07 to B. H.
W.). Deposited in PMC for release after 12 months.
NR 25
TC 0
Z9 0
U1 0
U2 9
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0022-0949
EI 1477-9145
J9 J EXP BIOL
JI J. Exp. Biol.
PD DEC
PY 2013
VL 216
IS 23
BP 4395
EP 4402
DI 10.1242/jeb.091595
PG 8
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 258YZ
UT WOS:000327495900020
PM 24031052
ER
PT J
AU Slaughter, J
Wei, CS
Korzeniewski, SJ
Lu, Q
Beck, JS
Khoo, SK
Brovont, A
Maurer, J
Martin, D
Lenski, M
Paneth, N
AF Slaughter, Jaime
Wei, Changshuai
Korzeniewski, Steven J.
Lu, Qing
Beck, John S.
Khoo, Sok Kean
Brovont, Ariel
Maurer, Joel
Martin, Denny
Lenski, Madeleine
Paneth, Nigel
TI High correlations in gene expression between paired umbilical cord blood
and neonatal blood of healthy newborns on Guthrie cards
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE Archived newborn blood spots; genes and transcripts; genome-wide;
messenger RNAs; oligonucleotide microarrays
ID DISEASE; SPOTS
AB Objective: To examine the correlation in genes expressed in paired umbilical cord blood (UCB) and newborn blood (NB).
Method: Total mRNA and mRNA of three gene sets (inflammatory, hypoxia, and thyroidal response) was assessed using microarray in UCB and NB spotted on Guthrie cards from 7 mother/infant pairs.
Results: The average gene expression correlation between paired UCB and NB samples was 0.941 when all expressed genes were considered, and 0.949 for three selected gene sets.
Conclusion: The high correlation of UCB and NB gene expression suggest that either source may be useful for examining gene expression in the perinatal period.
C1 [Slaughter, Jaime; Wei, Changshuai; Lu, Qing; Brovont, Ariel; Lenski, Madeleine; Paneth, Nigel] Michigan State Univ, Coll Human Med, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Korzeniewski, Steven J.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Korzeniewski, Steven J.] NICHHD, Perinatal Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Beck, John S.; Khoo, Sok Kean] Van Andel Inst, Lab Microarray Technol, Grand Rapids, MI USA.
[Maurer, Joel; Martin, Denny] Michigan State Univ, Coll Human Med, Dept Obstet Gynecol & Reprod Biol, E Lansing, MI 48824 USA.
[Paneth, Nigel] Michigan State Univ, Coll Human Med, Dept Pediat & Human Dev, E Lansing, MI 48824 USA.
RP Paneth, N (reprint author), Michigan State Univ, 909 Fee Rd Room 218, E Lansing, MI 48824 USA.
EM paneth@msu.edu
RI Wei, Changshuai/A-7750-2015;
OI Wei, Changshuai/0000-0003-0148-6797; Slaughter-Acey,
Jaime/0000-0002-8897-1244
FU Wayne State University Perinatal Initiative; NIH [R01 NS055101]; [T32
HD046377]
FX The authors have no conflicts of interests. This research was supported
in part by the Wayne State University Perinatal Initiative and funded by
NIH R01 NS055101 to Dr. Paneth. Dr. Slaughter is funded by T32 HD046377.
NR 10
TC 2
Z9 2
U1 0
U2 4
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 DEC
PY 2013
VL 26
IS 18
BP 1765
EP 1767
DI 10.3109/14767058.2013.804050
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 256OA
UT WOS:000327321900001
PM 23668672
ER
PT J
AU Mehta, GU
Sheehan, JP
Vance, ML
AF Mehta, Gautam U.
Sheehan, Jason P.
Vance, Mary Lee
TI Effect of stereotactic radio surgery before bilateral adrenalectomy for
Cushing's disease on the incidence of Nelson's syndrome
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE adrenalectomy; Cushing's disease; Gamma Knife; Nelson's syndrome;
stereotactic radiosurgery; pituitary surgery
ID GAMMA-KNIFE SURGERY; PITUITARY-ADENOMAS; RADIOSURGERY; TUMOR
AB Object. Nelson's syndrome (NS) is a significant and frequent risk for patients with Cushing's disease (CD) who undergo bilateral adrenalectomy. A recent study has shown tumor progression in 47% of patients at risk for NS. The authors sought to define the rate of NS in patients who were treated with Gamma Knife stereotactic radiosurgery (GK SRS) prior to bilateral adrenalectomy.
Methods. Consecutive patients with CD who were treated with GK SRS after pituitary surgery but before bilateral adrenalectomy were included. Serial MRI sequences were analyzed to evaluate for pituitary tumor growth. Clinical evaluations were performed to screen for NS. Follow-up for adrenocorticotropic hormone levels and hormone studies of other pituitary axes was performed.
Results. Twenty consecutive patients were followed with neuroimaging and clinically for a median of 5.4 years (range 0.6-12 years). One patient (5%) developed pituitary tumor growth consistent with NS 9 months after adrenalectomy. By Kaplan-Meier analysis, progression-free survival was 94.7% at 1, 3, and 7 years. No predisposing factors were identified for the tumor progression. Two patients developed new pituitary dysfunction and no patient developed cranial neuropathy or visual deficit after GK SRS.
Conclusions. These findings suggest that GK SRS not only serves a role as second-line therapy for CD, but that it also provides prophylaxis for NS when used before bilateral adrenalectomy.
C1 [Mehta, Gautam U.; Sheehan, Jason P.] Univ Virginia Hlth Syst, Dept Neurosurg, Charlottesville, VA 22908 USA.
[Vance, Mary Lee] Univ Virginia Hlth Syst, Dept Med, Charlottesville, VA 22908 USA.
[Mehta, Gautam U.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Vance, ML (reprint author), Univ Virginia Hlth Syst, Dept Med, Charlottesville, VA 22908 USA.
EM mlv@virginia.edu
OI Mehta, Gautam/0000-0002-8009-6430
FU Intramural NIH HHS
NR 24
TC 10
Z9 10
U1 1
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
EI 1933-0693
J9 J NEUROSURG
JI J. Neurosurg.
PD DEC
PY 2013
VL 119
IS 6
BP 1493
EP 1497
DI 10.3171/2013.7.JNS13389
PG 5
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 257EU
UT WOS:000327367200021
PM 23952749
ER
PT J
AU Guo, F
Simons-Morton, BG
Klauer, SE
Ouimet, MC
Dingus, TA
Lee, SE
AF Guo, Feng
Simons-Morton, Bruce G.
Klauer, Sheila E.
Ouimet, Marie Claude
Dingus, Thomas A.
Lee, Suzanne E.
TI Variability in Crash and Near-Crash Risk among Novice Teenage Drivers: A
Naturalistic Study
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID SENSATION-SEEKING; DRIVING BEHAVIOR; PERSONALITY; PASSENGERS;
INVOLVEMENT; PERFORMANCE; EXPERIENCE; SIMULATOR
AB Objective Using video monitoring technologies, we investigated teenage driving risk variation during the first 18 months of independent driving.
Study design Driving data were collected on 42 teenagers whose vehicles were instrumented with sophisticated video and data recording devices. Surveys on demographic and personality characteristics were administered at baseline. Drivers were classified into 3 risk groups using a K-mean clustering method based on crash and near-crash (CNC) rate. The change in CNC rates over time was evaluated by mixed-effect Poisson models.
Results Compared with the first 3 months after licensure (first quarter), the CNC rate for participants during the third, fourth, and fifth quarters decreased significantly to 59%, 62%, and 48%, respectively. Three distinct risk groups were identified with CNC rates of 21.8 (high-risk), 8.3 (moderate-risk), and 2.1 (low-risk) per 10 000 km traveled. High-and low-risk drivers showed no significant change in CNC rates throughout the 18-month study period. CNC rates for moderate-risk drivers decreased substantially from 8.8 per 10 000 km in the first quarter to 0.8 and 3.2 in the fourth and fifth quarters, respectively. The 3 groups were not distinguishable with respect to personality characteristics.
Conclusion Teenage CNC rates varied substantially, with distinct high-, moderate-, and low-risk groups. Risk declined over time only in the moderate-risk group. The high-risk drivers appeared to be insensitive to experience, with CNC rates consistently high throughout the 18-month study period, and the moderate-risk group appeared to learn from experience.
C1 [Guo, Feng] Virginia Tech, Dept Stat, Blacksburg, VA 24061 USA.
[Guo, Feng; Klauer, Sheila E.; Dingus, Thomas A.; Lee, Suzanne E.] Virginia Tech, Transportat Inst, Blacksburg, VA 24061 USA.
[Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Bethesda, MD USA.
[Ouimet, Marie Claude] Univ Sherbrooke, Fac Med & Hlth Sci, Longueuil, PQ, Canada.
[Dingus, Thomas A.] Virginia Tech, Charles E Via Jr Dept Civil & Environm Engn, Blacksburg, VA 24061 USA.
RP Guo, F (reprint author), Virginia Tech, Transportat Inst, 3500 Transportat Res Plaza, Blacksburg, VA 24061 USA.
EM feng.guo@vt.edu
OI Simons-Morton, Bruce/0000-0003-1099-6617
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development [N01-HD-5-3405];
National Highway Traffic Safety Administration; career grant from the
Quebec Health Research Fund (Fonds de recherche du Quebec-Sante)
FX Supported by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development
(N01-HD-5-3405) and by the National Highway Traffic Safety
Administration. M.O. was supported by a career grant from the Quebec
Health Research Fund (Fonds de recherche du Quebec-Sante). The authors
declare no conflicts of interest.
NR 32
TC 6
Z9 6
U1 0
U2 11
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
EI 1097-6833
J9 J PEDIATR-US
JI J. Pediatr.
PD DEC
PY 2013
VL 163
IS 6
BP 1670
EP 1676
DI 10.1016/j.jpeds.2013.07.025
PG 7
WC Pediatrics
SC Pediatrics
GA 259RE
UT WOS:000327543200032
PM 23992677
ER
PT J
AU McGuire, PJ
Lee, HS
Summar, ML
AF McGuire, Peter J.
Lee, Hye-Seung
Summar, Marshall L.
CA Urea Cycle Disorders Consoritum
TI Infectious Precipitants of Acute Hyperammonemia Are Associated with
Indicators of Increased Morbidity in Patients with Urea Cycle Disorders
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID MULTICENTER; MANAGEMENT; MORTALITY
AB Objective To prospectively characterize acute hyperammonemic episodes in patients with urea cycle disorders (UCDs) in terms of precipitating factors, treatments, and use of medical resources.
Study design This was a prospective, longitudinal observational study of hyperammonemic episodes in patients with UCD enrolled in the National Institutes of Health-sponsored Urea Cycle Disorders Consortium Longitudinal Study. An acute hyperammonemic event was defined as plasma ammonia level >100 mu mol/L. Physician-reported data regarding the precipitating event and laboratory and clinical variables were recorded in a central database.
Results In our study population, 128 patients with UCD experienced a total of 413 hyperammonemia events. Most patients experienced between 1 and 3 (65%) or between 4 and 6 (23%) hyperammonemia events since study inception, averaging fewer than 1 event/year. The most common identifiable precipitant was infection (33%), 24% of which were upper/lower respiratory tract infections. Indicators of increased morbidity were seen with infection, including increased hospitalization rates (P = .02), longer hospital stays (+2.0 days; P = .003), and increased use of intravenous ammonia scavengers (+45%-52%; P = .003-.03).
Conclusion Infection is the most common precipitant of acute hyperammonemia in patients with UCD and is associated with indicators of increased morbidity (ie, hospitalization rate, length of stay, and use of intravenous ammonia scavengers). These findings suggest that the catabolic and immune effects of infection may be a target for clinical intervention in inborn errors of metabolism.
C1 [McGuire, Peter J.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Lee, Hye-Seung] Univ S Florida, Dept Pediat, Pediat Epidemiol Ctr, Tampa, FL 33620 USA.
[Summar, Marshall L.] Childrens Natl Med Ctr, Div Genet & Metab, Washington, DC 20010 USA.
RP McGuire, PJ (reprint author), NHGRI, NIH, 49 Convent Dr,Room 4A62, Bethesda, MD 20892 USA.
EM peter.mcguire@nih.gov
FU NIH
FX We wish to recognize the efforts of Dr Danuta Krotoski (National
Institutes of Health [NIH]) for programmatic support for the UCDC, and
Dr Mary Lou Oster-Granite (NIH) for scientific support. We also thank
Cindy LeMons (Executive Director, National Urea Cycle Disorders
Foundation) for support and direction, and Dr Les Biesecker (who is
funded by the NIH, serves as an advisor to the Illumina Corp, receives
royalties from Genentech Corp, and receives compensation for editorial
duties by Wiley-Blackwell Corp) for his guidance and the support of the
Physician Scientist Development Program at National Human Genome
Research Institute.
NR 13
TC 13
Z9 13
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
EI 1097-6833
J9 J PEDIATR-US
JI J. Pediatr.
PD DEC
PY 2013
VL 163
IS 6
BP 1705
EP U254
DI 10.1016/j.jpeds.2013.08.029
PG 7
WC Pediatrics
SC Pediatrics
GA 259RE
UT WOS:000327543200037
PM 24084106
ER
PT J
AU Kramer, RM
Zeng, YH
Sahni, N
Kueltzo, LA
Schwartz, RM
Srivastava, IK
Crane, L
Joshi, SB
Volkin, DB
Middaugh, CR
AF Kramer, Ryan M.
Zeng, Yuhong
Sahni, Neha
Kueltzo, Lisa A.
Schwartz, Richard M.
Srivastava, Indresh K.
Crane, Lindsey
Joshi, Sangeeta B.
Volkin, David B.
Middaugh, C. Russell
TI Development of a Stable Virus-Like Particle Vaccine Formulation against
Chikungunya Virus and Investigation of the Effects of Polyanions
SO JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Article
DE stabilization; thermal analysis; vaccines; particle size; physical
stability; physicochemical properties; preformulation; spectroscopy;
protein formulation
ID INDIAN-OCEAN; INFECTION; OUTBREAK; PH; TRAVELERS; DISEASES; COHORT;
FEVER
AB Chikungunya virus (CHIKV) is an alphavirus that infects millions of people every year, especially in the developing world. The selective expression of recombinant CHIKV capsid and envelope proteins results in the formation of self-assembled virus-like particles (VLPs) that have been shown to protect nonhuman primates against infection from multiple strains of CHIKV. This study describes the characterization, excipient screening, and optimization of CHIKV VLP solution conditions toward the development of a stable parenteral formulation. The CHIKV VLPs were found to be poorly soluble at pH 6 and below. Circular dichroism, intrinsic fluorescence, and static and dynamic light scattering measurements were therefore performed at neutral pH, and results consistent with the formation of molten globule structures were observed at elevated temperatures. A library of generally recognized as safe excipients was screened for their ability to physically stabilize CHIKV VLPs using a high-throughput turbidity-based assay. Sugars, sugar alcohols, and polyanions were identified as potential stabilizers and the concentrations and combinations of select excipients were optimized. The effects of polyanions were further studied, and while all polyanions tested stabilized CHIKV VLPs against aggregation, the effects of polyanions on conformational stability varied. (c) 2013 Wiley Periodicals, Inc. and the American Pharmacists Association J Pharm Sci 102:4305-4314, 2013
C1 [Kramer, Ryan M.; Zeng, Yuhong; Sahni, Neha; Crane, Lindsey; Joshi, Sangeeta B.; Volkin, David B.; Middaugh, C. Russell] Univ Kansas, Macromol & Vaccine Stabilizat Ctr, Dept Pharmaceut Chem, Lawrence, KS 66047 USA.
[Kueltzo, Lisa A.; Schwartz, Richard M.] NIAID, Vaccine Prod Program, Vaccine Res Ctr, NIH, Gaithersburg, MD 20878 USA.
[Srivastava, Indresh K.] Prot Sci Corp, Meriden, CT 06450 USA.
RP Middaugh, CR (reprint author), Univ Kansas, Macromol & Vaccine Stabilizat Ctr, Dept Pharmaceut Chem, Lawrence, KS 66047 USA.
EM Middaugh@Ku.Edu
FU National Cancer Institute, National Institutes of Health
[HHSN26120080001E]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract 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 U.S. Government.
NR 24
TC 11
Z9 11
U1 0
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3549
EI 1520-6017
J9 J PHARM SCI-US
JI J. Pharm. Sci.
PD DEC
PY 2013
VL 102
IS 12
BP 4305
EP 4314
DI 10.1002/jps.23749
PG 10
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology &
Pharmacy
SC Pharmacology & Pharmacy; Chemistry
GA 254UM
UT WOS:000327193300010
PM 24129946
ER
PT J
AU Sinha, BK
Kumar, A
Bhattacharjee, S
Espey, MG
Mason, RP
AF Sinha, Birandra K.
Kumar, Ashutosh
Bhattacharjee, Suchandra
Espey, Michael G.
Mason, Ronald P.
TI Effect of Nitric Oxide on the Anticancer Activity of the
Topoisomerase-Active Drugs Etoposide and Adriamycin in Human Melanoma
Cells
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID CISPLATIN-INDUCED APOPTOSIS; FREE-RADICAL FORMATION; BREAST TUMOR-CELLS;
CATALYZED METABOLISM; NITROGEN-OXIDES; O-DEMETHYLATION; CANCER CELLS;
DNA; CYTOTOXICITY; MACROPHAGES
AB Nitric oxide ((NO)-N-center dot) was originally identified as an innate cytotoxin. However, in tumors it can enhance resistance to chemotherapy and exacerbate cancer progression. Our previous studies indicated that (NO)-N-center dot/(NO)-N-center dot-derived species react with etoposide (VP-16) in vitro and form products that show significantly reduced activity toward HL60 cells and lipopolysaccharide (LPS)-induced macrophages. Here, we further confirm the hypothesis that (NO)-N-divided by generation contributes to VP-16 resistance by examining interactions of (NO)-N-center dot with VP-16 in inducible nitric-oxide synthase (iNOS)-expressing human melanoma A375 cells. Inhibition of iNOS catalysis by N-6-(1-iminoethyl)-L-lysine dihydrochloride (L-NIL) in human melanoma A375 cells reversed VP-16 resistance, leading to increased DNA damage and apoptosis. Furthermore, we found that coculturing A375 melanoma cells with LPS-induced macrophage RAW cells also significantly reduced VP-16 cytotoxicity and DNA damage in A375 cells. We also examined the interactions of (NO)-N-center dot with another topoisomerase active drug, Adriamycin, in A375 cells. In contrast, to VP-16, (NO)-N-center dot caused no significant modulation of cytotoxicity or Adriamycin-dependent apoptosis, suggesting that (NO)-N-center dot does not interact with Adriamycin. Our studies support the hypothesis that (NO)-N-center dot oxidative chemistry can detoxify VP-16 through direct nitrogen oxide radical attack. Our results provide insights into the pharmacology and anticancer mechanisms of VP-16 that may ultimately contribute to increased resistance, treatment failure, and induction of secondary leukemia in VP-16-treated patients.
C1 [Sinha, Birandra K.; Kumar, Ashutosh; Bhattacharjee, Suchandra; Mason, Ronald P.] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
[Espey, Michael G.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Sinha, BK (reprint author), NIEHS, Res Triangle Pk, NC 27709 USA.
EM sinha1@niehs.nih.gov
FU National Institutes of Health [National Institute of Environmental
Health Sciences]
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health [National Institute of
Environmental Health Sciences].
NR 59
TC 7
Z9 7
U1 0
U2 7
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 DEC
PY 2013
VL 347
IS 3
BP 607
EP 614
DI 10.1124/jpet.113.207928
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 258IQ
UT WOS:000327453200009
PM 24049059
ER
PT J
AU Oosthuyzen, W
Sime, NEL
Ivy, JR
Turtle, EJ
Street, JM
Pound, J
Bath, LE
Webb, DJ
Gregory, CD
Bailey, MA
Dear, JW
AF Oosthuyzen, Wilna
Sime, Nicole E. L.
Ivy, Jessica R.
Turtle, Emma J.
Street, Jonathan M.
Pound, John
Bath, Louise E.
Webb, David J.
Gregory, Christopher D.
Bailey, Matthew A.
Dear, James W.
TI Quantification of human urinary exosomes by nanoparticle tracking
analysis
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID VESICLES; CELLS; BIOMARKERS; DISCOVERY; DISTINCT; DISEASE
AB Exosomes are vesicles that are released from the kidney into urine. They contain protein and RNA from the glomerulus and all sections of the nephron and represent a reservoir for biomarker discovery. Current methods for the identification and quantification of urinary exosomes are time consuming and only semi-quantitative. Nanoparticle tracking analysis (NTA) counts and sizes particles by measuring their Brownian motion in solution. In this study, we applied NTA to human urine and identified particles with a range of sizes. Using antibodies against the exosomal proteins CD24 and aquaporin 2 (AQP2), conjugated to a fluorophore, we could identify a subpopulation of CD24- and AQP2-positive particles of characteristic exosomal size. Extensive pre-NTA processing of urine was not necessary. However, the intra-assay variability in the measurement of exosome concentration was significantly reduced when an ultracentrifugation step preceded NTA. Without any sample processing, NTA tracked exosomal AQP2 upregulation induced by desmopressin stimulation of kidney collecting duct cells. Nanoparticle tracking analysis was also able to track changes in exosomal AQP2 concentration that followed desmopressin treatment of mice and a patient with central diabetes insipidus. When urine was stored at room temperature, 4 degrees C or frozen, nanoparticle concentration was reduced; freezing at -80 degrees C with the addition of protease inhibitors produced the least reduction. In conclusion, with appropriate sample storage, NTA has potential as a tool for the characterization and quantification of extracellular vesicles in human urine.
C1 [Oosthuyzen, Wilna; Sime, Nicole E. L.; Ivy, Jessica R.; Turtle, Emma J.; Webb, David J.; Bailey, Matthew A.; Dear, James W.] Univ Edinburgh, British Heart Fdn Ctr Cardiovasc Sci, Queens Med Res Inst, Edinburgh EH16 4TJ, Midlothian, Scotland.
[Street, Jonathan M.] NIDDK, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD 20892 USA.
[Pound, John; Gregory, Christopher D.] Univ Edinburgh, MRC Ctr Inflammat Res, Queens Med Res Inst, Edinburgh EH16 4TJ, Midlothian, Scotland.
[Bath, Louise E.] Royal Hosp Sick Children, Natl Hlth Serv Lothian, Edinburgh Ctr Endocrinol, Edinburgh EH9 1LF, Midlothian, Scotland.
RP Dear, JW (reprint author), Univ Edinburgh, British Heart Fdn Ctr Cardiovasc Sci, Queens Med Res Inst, 47 Little France Crescent, Edinburgh EH16 4TJ, Midlothian, Scotland.
EM james.dear@ed.ac.uk
OI Gregory, Chris/0000-0002-7553-0132
FU British Heart Foundation Centre of Research Excellence Award; NHS
Research Scotland (NRS), through NHS Lothian; Diabetes Research and
Wellness Foundation; NC3R
FX The authors acknowledge the contribution of the British Heart Foundation
Centre of Research Excellence Award. J.W.D. acknowledges the financial
support of NHS Research Scotland (NRS), through NHS Lothian. Funding was
received from the Diabetes Research and Wellness Foundation and NC3R.
NR 16
TC 31
Z9 33
U1 4
U2 43
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3751
EI 1469-7793
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD DEC 1
PY 2013
VL 591
IS 23
BP 5833
EP 5842
DI 10.1113/jphysiol.2013.264069
PG 10
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 259FC
UT WOS:000327511800010
PM 24060994
ER
PT J
AU Detterbeck, FC
Asamura, H
Crowley, J
Falkson, C
Giaccone, G
Giroux, D
Huang, J
Kim, J
Kondo, K
Lucchi, M
Marino, M
Marom, EM
Nicholson, A
Okumura, M
Ruffini, E
van Schil, P
Stratton, K
AF Detterbeck, Frank C.
Asamura, Hisao
Crowley, John
Falkson, Conrad
Giaccone, Giuseppe
Giroux, Dori
Huang, James
Kim, Jhingook
Kondo, Kazuya
Lucchi, Marco
Marino, Mirella
Marom, Edith M.
Nicholson, Andrew
Okumura, Meinoshin
Ruffini, Enrico
van Schil, Paul
Stratton, Kelly
CA Staging Prognostic Factors Comm
TI The IASLC/ITMIG Thymic Malignancies Staging Project Development of a
Stage Classification for Thymic Malignancies
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Thymoma; Thymic carcinoma; Staging of stage classification
ID FORTHCOMING 7TH EDITION; IASLC LUNG-CANCER; INTERNATIONAL-ASSOCIATION;
TNM CLASSIFICATION; TUMORS; PROPOSALS; THYMOMAS; SYSTEM; NODE
AB The lack of an official-stage classification system for thymic malignancies is an issue that hampers progress in this rare disease. A collaborative effort by the International Association for the Study of Lung Cancer and the International Thymic Malignancies Interest Group is underway to develop proposals for such a system. A database of more than 10,000 cases worldwide has been assembled to provide a solid basis for analysis. This report outlines the structure of the effort and the process that has been designed.
C1 [Detterbeck, Frank C.] Yale Univ, Dept Thorac Surg, Yale New Haven Hosp, Sch Med, New Haven, CT 06510 USA.
[Asamura, Hisao; Stratton, Kelly] Natl Canc Ctr, Tokyo, Japan.
[Falkson, Conrad] Queens Univ, Kingston, ON K7L 3N6, Canada.
[Giaccone, Giuseppe] NCI, Bethesda, MD 20892 USA.
[Huang, James] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Kim, Jhingook] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
[Kondo, Kazuya] Univ Tokushima, Tokushima 770, Japan.
[Lucchi, Marco] Univ Pisa, Pisa, Italy.
[Marino, Mirella] Regina Elena Inst Canc Res, Rome, Italy.
[Marino, Mirella; Marom, Edith M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Nicholson, Andrew] Royal Brompton Hosp, London SW3 6LY, England.
[Okumura, Meinoshin] Osaka Univ, Osaka, Japan.
[Ruffini, Enrico] Univ Torino, Turin, Italy.
[van Schil, Paul] Univ Antwerp Hosp, Antwerp, Belgium.
RP Detterbeck, FC (reprint author), Yale Univ, Dept Surg, Div Thorac Surg, Sch Med, BB2 333 Cedar St, New Haven, CT 06510 USA.
EM frank.detterbeck@yale.edu
RI Spaggiari, Lorenzo/G-7915-2012; Kondo, Kazuya/J-9163-2012; Nowak,
Anna/B-2487-2013; Giaccone, Giuseppe/E-8297-2017;
OI Lim, Eric/0000-0002-9078-3226; Brunelli, Alessandro/0000-0002-6505-1656;
Nowak, Anna/0000-0002-9317-9526; Giaccone, Giuseppe/0000-0002-5023-7562;
Rami-Porta, Ramon/0000-0003-3366-7664; Van Schil,
Paul/0000-0002-1962-8821; Huang, James/0000-0001-5495-3577;
Bertolaccini, Luca/0000-0002-1153-3334; Venuta,
Federico/0000-0001-9296-877X; LUCCHI, MARCO/0000-0001-9909-6820
NR 18
TC 28
Z9 30
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD DEC
PY 2013
VL 8
IS 12
BP 1467
EP 1473
DI 10.1097/JTO.0000000000000017
PG 7
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 257XG
UT WOS:000327420500013
PM 24389429
ER
PT J
AU Shuch, B
Ricketts, CJ
Vocke, CD
Komiya, T
Middelton, LA
Kauffman, EC
Merino, MJ
Metwalli, AR
Dennis, P
Linehan, WM
AF Shuch, Brian
Ricketts, Christopher J.
Vocke, Cathy D.
Komiya, Takefumi
Middelton, Lindsay A.
Kauffman, Eric C.
Merino, Maria J.
Metwalli, Adam R.
Dennis, Phillip
Linehan, W. Marston
TI Germline PTEN Mutation Cowden Syndrome: An Underappreciated Form of
Hereditary Kidney Cancer
SO JOURNAL OF UROLOGY
LA English
DT Article
DE carcinoma, renal cell; hamartoma syndrome, multiple; genetic diseases,
inborn
ID RENAL-CELL CARCINOMA; HAMARTOMA-TUMOR-SYNDROME; GENETIC-BASIS; DISEASE;
FREQUENCY; COMPLEX
AB Purpose: Cowden syndrome is a hereditary cancer syndrome associated with a germline mutation in PTEN. Patients are predisposed to multiple malignancies including renal cell carcinoma.
Materials and Methods: Patients with Cowden syndrome were evaluated as part of a clinical protocol. Those with a history of renal cell carcinoma underwent review of clinical features, tumor characteristics and family history. Renal tumors were evaluated for loss of heterozygosity.
Results: Among 24 patients with Cowden syndrome 4 were identified with renal cell carcinoma (16.7%). Three patients had solitary tumors, 2 with papillary type I histology and 1 with clear cell histology. The fourth patient had bilateral, synchronous chromophobe tumors. No patients had a prior family history of renal cell carcinoma. All patients with renal cell carcinoma had dermatologic manifestations of Cowden syndrome and had macrocephaly. Loss of heterozygosity at the PTEN mutation was identified in 4 tumors (80%). No genotype-phenotype association was found, as the same mutation was identified in different renal cell carcinoma histologies.
Conclusions: Renal cell carcinoma is an underappreciated feature of Cowden syndrome. As most patients lack a prior family history or a distinctive renal cell carcinoma histology, recognition of the associated nonrenal features should target referral for genetic counseling. PTEN loss of heterozygosity is common in Cowden syndrome renal tumors. Because loss of PTEN can activate mTOR and mTOR inhibitors are Food and Drug Administration approved to treat renal cell carcinoma, these agents have clinical potential in renal cell carcinoma associated with Cowden syndrome.
C1 [Shuch, Brian; Ricketts, Christopher J.; Vocke, Cathy D.; Middelton, Lindsay A.; Kauffman, Eric C.; Metwalli, Adam R.; Linehan, W. Marston] NCI, Urol Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Merino, Maria J.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Komiya, Takefumi] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Dennis, Phillip] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
RP Linehan, WM (reprint author), NCI, Urol Oncol Branch, Bldg 10 CRC Room 1-5940, Bethesda, MD 20892 USA.
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research
FX Supported by the Intramural Research Program of the National Institutes
of Health, National Cancer Institute, Center for Cancer Research.
NR 29
TC 22
Z9 22
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2013
VL 190
IS 6
BP 1990
EP 1998
DI 10.1016/j.juro.2013.06.012
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 258EC
UT WOS:000327441000007
PM 23764071
ER
PT J
AU Diaz, AW
Hoang, AN
Turkbey, B
Hong, CW
Truong, H
Sterling, T
Rais-Bahrami, S
Siddiqui, MM
Stamatakis, L
Vourganti, S
Nix, J
Logan, J
Harris, C
Weintraub, M
Chua, C
Merino, MJ
Choyke, P
Wood, BJ
Pinto, PA
AF Diaz, Annerleim Walton
Hoang, Anthony N.
Turkbey, Baris
Hong, Cheng William
Hong Truong
Sterling, Todd
Rais-Bahrami, Soroush
Siddiqui, M. Minhaj
Stamatakis, Lambros
Vourganti, Srinivas
Nix, Jeffrey
Logan, Jennifer
Harris, Colette
Weintraub, Michael
Chua, Celene
Merino, Maria J.
Choyke, Peter
Wood, Bradford J.
Pinto, Peter A.
TI Can Magnetic Resonance-Ultrasound Fusion Biopsy Improve Cancer Detection
in Enlarged Prostates?
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostate; prostatic neoplasms; prostatic hyperplasia; magnetic resonance
imaging; ultrasonography
ID NEEDLE-BIOPSY; GLAND VOLUME; MRI; POPULATION; EXPERIENCE; GUIDANCE;
SYSTEM
AB Purpose: Patients with an enlarged prostate and suspicion of prostate cancer pose a diagnostic dilemma. The prostate cancer detection rate of systematic 12-core transrectal ultrasound guided biopsy is between 30% and 40%. For prostates greater than 40 cc this decreases to 30% or less. Magnetic resonance-ultrasound fusion biopsy has shown superior prostate cancer detection rates. We defined the detection rate of magnetic resonance-ultrasound fusion biopsy in men with an enlarged prostate gland.
Materials and Methods: We retrospectively analyzed the records of patients who underwent multiparametric prostate magnetic resonance imaging followed by magnetic resonance-ultrasound fusion biopsy at our institution. Whole prostate volumes were calculated using magnetic resonance imaging reconstructions. Detection rates were analyzed with respect to age, prostate specific antigen and whole prostate volumes. Multivariable logistic regression was used to assess these parameters as independent predictors of prostate cancer detection.
Results: We analyzed 649 patients with a mean +/- SD age of 61.8 +/- 7.9 years and a median prostate specific antigen of 6.65 ng/ml (IQR 4.35-11.0). Mean whole prostate volume was 58.7 +/- 34.3 cc. The overall detection rate of the magnetic resonance-ultrasound fusion platform was 55%. For prostates less than 40 cc the detection rate was 71.1% compared to 57.5%, 46.9%, 46.9% 33.3%, 36.4% and 30.4% for glands 40 to 54.9, 55 to 69.9, 70 to 84.9, 85 to 99.9, 100 to 114.9 and 115 cc or greater, respectively (p < 0.0001). Multivariable logistic regression showed a significant inverse association of magnetic resonance imaging volume with prostate cancer detection, controlling for age and prostate specific antigen.
Conclusions: Transrectal ultrasound guided and fusion biopsy cancer detection rates decreased with increasing prostate volume. However, magnetic resonance-ultrasound fusion biopsy had a higher prostate cancer detection rate compared to that of transrectal ultrasound guided biopsy in the literature. Magnetic resonance-ultrasound fusion biopsy represents a promising solution for patients with suspicion of prostate cancer and an enlarged prostate.
C1 [Diaz, Annerleim Walton; Hoang, Anthony N.; Hong Truong; Sterling, Todd; Rais-Bahrami, Soroush; Siddiqui, M. Minhaj; Stamatakis, Lambros; Vourganti, Srinivas; Nix, Jeffrey; Logan, Jennifer; Harris, Colette; Weintraub, Michael; Chua, Celene; Pinto, Peter A.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Turkbey, Baris; Choyke, Peter] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Hong, Cheng William; Wood, Bradford J.; Pinto, Peter A.] NCI, Ctr Intervent Oncol, NIH, Bethesda, MD 20892 USA.
[Merino, Maria J.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Pinto, PA (reprint author), NCI, Urol Oncol Branch, NIH, CRC, 10 Ctr Dr,MSC 1210,Bldg 10,Room 2W-5940, Bethesda, MD 20892 USA.
EM pintop@mail.nih.gov
OI Siddiqui, Mohummad/0000-0002-4484-6820; Rais-Bahrami,
Soroush/0000-0001-9466-9925
NR 29
TC 18
Z9 19
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2013
VL 190
IS 6
BP 2020
EP 2025
DI 10.1016/j.juro.2013.05.118
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 258EC
UT WOS:000327441000016
ER
PT J
AU Blasche, S
Wuchty, S
Rajagopala, SV
Uetz, P
AF Blasche, Sonja
Wuchty, Stefan
Rajagopala, Seesandra V.
Uetz, Peter
TI The Protein Interaction Network of Bacteriophage Lambda with Its Host,
Escherichia coli
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID C-TERMINAL DOMAIN; PHAGE-LAMBDA; RNA-POLYMERASE; DNA-REPLICATION;
DEPENDENT ACTIVATION; POINT MUTATIONS; FIS PROTEIN; IN-VIVO; INITIATION;
COMPLEX
AB Although most of the 73 open reading frames (ORFs) in bacteriophage lambda have been investigated intensively, the function of many genes in host-phage interactions remains poorly understood. Using yeast two-hybrid screens of all lambda ORFs for interactions with its host Escherichia coli, we determined a raw data set of 631 host-phage interactions resulting in a set of 62 high-confidence interactions after multiple rounds of retesting. These links suggest novel regulatory interactions between the E. coli transcriptional network and lambda proteins. Targeted host proteins and genes required for lambda infection are enriched among highly connected proteins, suggesting that bacteriophages resemble interaction patterns of human viruses. Lambda tail proteins interact with both bacterial fimbrial proteins and E. coli proteins homologous to other phage proteins. Lambda appears to dramatically differ from other phages, such as T7, because of its unusually large number of modified and processed proteins, which reduces the number of host-virus interactions detectable by yeast two-hybrid screens.
C1 [Blasche, Sonja] German Canc Res Ctr, Genom & Prote Core Facil, Heidelberg, Germany.
[Wuchty, Stefan] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Rajagopala, Seesandra V.] J Craig Venter Inst, Rockville, MD USA.
[Uetz, Peter] Virginia Commonwealth Univ, Ctr Study Biol Complex, Richmond, VA 23284 USA.
RP Uetz, P (reprint author), Virginia Commonwealth Univ, Ctr Study Biol Complex, Richmond, VA 23284 USA.
EM peter@uetz.us
RI Uetz, Peter/A-7119-2012;
OI Uetz, Peter/0000-0001-6194-4927; Rajagopala,
Seesandra/0000-0001-7176-5770
FU National Institutes of Health [R01GM79710]; European Union
[HEALTH-F3-2009-223101]; National Institutes of Health/Department of
Health and Human Services, Intramural Research program of the National
Library of Medicine
FX This project was partly funded by National Institutes of Health grant
R01GM79710 and the European Union (grant HEALTH-F3-2009-223101,
AntipathoGN). Research at the National Center for Biotechnology
Information was supported by the National Institutes of
Health/Department of Health and Human Services as part of the Intramural
Research program of the National Library of Medicine.
NR 67
TC 3
Z9 3
U1 6
U2 14
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 DEC
PY 2013
VL 87
IS 23
BP 12745
EP 12755
DI 10.1128/JVI.02495-13
PG 11
WC Virology
SC Virology
GA 254RG
UT WOS:000327183800023
PM 24049175
ER
PT J
AU Kerr, PJ
Rogers, MB
Fitch, A
DePasse, JV
Cattadori, IM
Twaddle, AC
Hudson, PJ
Tscharke, DC
Read, AF
Holmes, EC
Ghedin, E
AF Kerr, Peter J.
Rogers, Matthew B.
Fitch, Adam
DePasse, Jay V.
Cattadori, Isabella M.
Twaddle, Alan C.
Hudson, Peter J.
Tscharke, David C.
Read, Andrew F.
Holmes, Edward C.
Ghedin, Elodie
TI Genome Scale Evolution of Myxoma Virus Reveals Host-Pathogen Adaptation
and Rapid Geographic Spread
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ORYCTOLAGUS-CUNICULUS L; RABBIT FIBROMA VIRUS; EUROPEAN RABBITS; EASTERN
AUSTRALIA; PROTEIN; SEQUENCE; RECOMBINANT; POPULATIONS; VIRULENCE;
RESPONSES
AB The evolutionary interplay between myxoma virus (MYXV) and the European rabbit (Oryctolagus cuniculus) following release of the virus in Australia in 1950 as a biological control is a classic example of host-pathogen coevolution. We present a detailed genomic and phylogeographic analysis of 30 strains of MYXV, including the Australian progenitor strain Standard Laboratory Strain (SLS), 24 Australian viruses isolated from 1951 to 1999, and three isolates from the early radiation in Britain from 1954 and 1955. We show that in Australia MYXV has spread rapidly on a spatial scale, with multiple lineages cocirculating within individual localities, and that both highly virulent and attenuated viruses were still present in the field through the 1990s. In addition, the detection of closely related virus lineages at sites 1,000 km apart suggests that MYXV moves freely in geographic space, with mosquitoes, fleas, and rabbit migration all providing means of transport. Strikingly, despite multiple introductions, all modern viruses appear to be ultimately derived from the original introductions of SLS. The rapidity of MYXV evolution was also apparent at the genomic scale, with gene duplications documented in a number of viruses. Duplication of potential virulence genes may be important in increasing the expression of virulence proteins and provides the basis for the evolution of novel functions. Mutations leading to loss of open reading frames were surprisingly frequent and in some cases may explain attenuation, but no common mutations that correlated with virulence or attenuation were identified.
C1 [Kerr, Peter J.] CSIRO Ecosyst Sci, Canberra, ACT, Australia.
[Rogers, Matthew B.; Fitch, Adam; DePasse, Jay V.; Twaddle, Alan C.; Ghedin, Elodie] Univ Pittsburgh, Sch Med, Ctr Vaccine Res, Pittsburgh, PA 15260 USA.
[Rogers, Matthew B.; Ghedin, Elodie] Univ Pittsburgh, Sch Med, Dept Computat & Syst Biol, Pittsburgh, PA USA.
[Cattadori, Isabella M.; Hudson, Peter J.; Read, Andrew F.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Tscharke, David C.] Australian Natl Univ, Res Sch Biol, Canberra, ACT, Australia.
[Holmes, Edward C.] Univ Sydney, Sch Biol Sci, Marie Bashir Inst Infect Dis & Biosecur, Sydney, NSW 2006, Australia.
[Holmes, Edward C.] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Ghedin, E (reprint author), Univ Pittsburgh, Sch Med, Ctr Vaccine Res, Pittsburgh, PA 15260 USA.
EM elg21@pitt.edu
RI Tscharke, David/C-9133-2009;
OI Tscharke, David/0000-0001-6825-9172; Holmes, Edward/0000-0001-9596-3552
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health [R01 AI093804]; NHMRC Australia Fellowship; ARC
Future Fellowship
FX This work was funded in part by grant R01 AI093804 from the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. E.C.H. is funded by an NHMRC Australia Fellowship. D.C.T. is
funded by an ARC Future Fellowship.
NR 60
TC 16
Z9 16
U1 3
U2 46
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 DEC
PY 2013
VL 87
IS 23
BP 12900
EP 12915
DI 10.1128/JVI.02060-13
PG 16
WC Virology
SC Virology
GA 254RG
UT WOS:000327183800036
PM 24067966
ER
PT J
AU Breed, MW
Jordan, APO
Aye, PP
Sugimoto, C
Alvarez, X
Kuroda, MJ
Pahar, B
Keele, BF
Hoxie, JA
Lackner, AA
AF Breed, Matthew W.
Jordan, Andrea P. O.
Aye, Pyone P.
Sugimoto, Chie
Alvarez, Xavier
Kuroda, Marcelo J.
Pahar, Bapi
Keele, Brandon F.
Hoxie, James A.
Lackner, Andrew A.
TI A Single Amino Acid Mutation in the Envelope Cytoplasmic Tail Restores
the Ability of an Attenuated Simian Immunodeficiency Virus Mutant To
Deplete Mucosal CD4(+) T Cells
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ACUTE SIV INFECTION; GASTROINTESTINAL-TRACT; IMMUNE ACTIVATION; MASSIVE
INFECTION; VIRAL REPLICATION; RHESUS MACAQUES; HIV DISEASE; EXPRESSION;
OCCURS; HOSTS
AB Disruption of the conserved motif GYxxO in the simian immunodeficiency virus (SIV) SIVmac239 envelope (Env) cytoplasmic tail resulted in a virus (Delta GY) that exhibited a high plasma peak but uniquely failed to acutely deplete mucosal CD4(+) T cells. Here, we show that Delta GY containing a flanking S727P mutation that was acquired in Delta GY-infected macaques reacquired the ability to rapidly deplete CD4(+) T cells in lamina propria. This suggests that the GYxxO motif and S727P each contribute to SIV's targeting to mucosal tissues.
C1 [Breed, Matthew W.; Aye, Pyone P.; Sugimoto, Chie; Alvarez, Xavier; Kuroda, Marcelo J.; Pahar, Bapi; Lackner, Andrew A.] Tulane Natl Primate Res Ctr, Covington, LA USA.
[Jordan, Andrea P. O.; Hoxie, James A.] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
[Keele, Brandon F.] Frederick Natl Lab Canc Res, SAIC Frederick, Frederick, MD USA.
RP Lackner, AA (reprint author), Tulane Natl Primate Res Ctr, Covington, LA USA.
EM lackner@tulane.edu
OI Pahar, Bapi/0000-0003-1949-973X
FU National Institutes of Health [RR000164/P51OD011104, RR000168, RO1
AI074362, RO1 AI097059, AI045008, RR021309 (T32)]; National Cancer
Institute, National Institutes of Health [HHSN261200800001E]
FX This work was supported by National Institutes of Health grants
RR000164/P51OD011104 (TNPRC) and RR000168 (NEPRC), RO1 AI074362
(J.A.H.), RO1 AI097059 (M.J.K.), AI045008 (Penn CFAR), and RR021309
(T32) and was supported in part with federal funds from the National
Cancer Institute, National Institutes of Health, under contract
HHSN261200800001E.
NR 28
TC 2
Z9 2
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 DEC
PY 2013
VL 87
IS 23
BP 13048
EP 13052
DI 10.1128/JVI.02126-13
PG 5
WC Virology
SC Virology
GA 254RG
UT WOS:000327183800051
PM 24027336
ER
PT J
AU Balinsky, CA
Schmeisser, H
Ganesan, S
Singh, K
Pierson, TC
Zoon, KC
AF Balinsky, Corey A.
Schmeisser, Hana
Ganesan, Sundar
Singh, Kavita
Pierson, Theodore C.
Zoon, Kathryn C.
TI Nucleolin Interacts with the Dengue Virus Capsid Protein and Plays a
Role in Formation of Infectious Virus Particles
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID JAPANESE ENCEPHALITIS-VIRUS; SURFACE-EXPRESSED NUCLEOLIN; INHIBITS
HIV-INFECTION; N-TERMINAL REGION; CORE PROTEIN; NUCLEAR-LOCALIZATION;
ANTIPROLIFERATIVE ACTIVITY; ENDOPLASMIC-RETICULUM; VIRAL REPLICATION;
BINDING PROPERTY
AB Dengue virus (DENV) is a mosquito-transmitted flavivirus that can cause severe disease in humans and is considered a reemerging pathogen of significant importance to public health. The DENV capsid (C) protein functions as a structural component of the infectious virion; however, it may have additional functions in the virus replicative cycle. Here, we show that the DENV C protein interacts and colocalizes with the multifunctional host protein nucleolin (NCL). Furthermore, we demonstrate that this interaction can be disrupted by the addition of an NCL binding aptamer (AS1411). Knockdown of NCL with small interfering RNA (siRNA) or treatment of cells with AS1411 results in a significant reduction of viral titers after DENV infection. Western blotting and quantitative RT-PCR (qRT-PCR) analysis revealed no differences in viral RNA or protein levels at early time points postinfection, suggesting a role for NCL in viral morphogenesis. We support this hypothesis by showing that treatment with AS1411 alters the migration characteristics of the viral capsid, as visualized by native electrophoresis. Here, we identify a critical interaction between DENV C protein and NCL that represents a potential new target for the development of antiviral therapeutics.
C1 [Balinsky, Corey A.; Schmeisser, Hana; Zoon, Kathryn C.] NIAID, Cytokine Biol Sect, NIH, Bethesda, MD 20892 USA.
[Ganesan, Sundar] NIAID, Biol Imaging Sect, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
[Singh, Kavita] NIAID, Struct Biol Unit, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
[Pierson, Theodore C.] NIAID, Viral Pathogenesis Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Zoon, KC (reprint author), NIAID, Cytokine Biol Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kzoon@niaid.nih.gov
FU National Institutes of Health (NIH), National Institute of Allergy and
Infectious Diseases (NIAID)
FX This work was supported by the Intramural Research Program of the
National Institutes of Health (NIH), National Institute of Allergy and
Infectious Diseases (NIAID).
NR 82
TC 19
Z9 19
U1 1
U2 15
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 DEC
PY 2013
VL 87
IS 24
BP 13094
EP 13106
DI 10.1128/JVI.00704-13
PG 13
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300002
PM 24027323
ER
PT J
AU Kew, C
Lui, PY
Chan, CP
Liu, X
Au, SWN
Mohr, I
Jin, DY
Kok, KH
AF Kew, Chun
Lui, Pak-Yin
Chan, Chi-Ping
Liu, Xiang
Au, Shannon Wing Ngor
Mohr, Ian
Jin, Dong-Yan
Kok, Kin-Hang
TI Suppression of PACT-Induced Type I Interferon Production by Herpes
Simplex Virus 1 Us11 Protein
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID DOUBLE-STRANDED-RNA; BINDING-PROTEIN; RIG-I; ALPHA/BETA-INTERFERON; PKR
ACTIVATION; NS1 PROTEIN; INHIBITION; PATHWAY; PHOSPHORYLATION;
FACILITATE
AB Herpes simplex virus 1 (HSV-1) Us11 protein is a double-stranded RNA-binding protein that suppresses type I interferon production through the inhibition of the cytoplasmic RNA sensor RIG-I. Whether additional cellular mediators are involved in this suppression remains to be determined. In this study, we report on the requirement of cellular double-stranded RNA-binding protein PACT for Us11-mediated perturbation of type I interferon production. Us11 associates with PACT tightly to prevent it from binding with and activating RIG-I. The Us11-deficient HSV-1 was indistinguishable from the Us11-proficient virus in the suppression of interferon production when PACT was compromised. More importantly, HSV-1-induced activation of interferon production was abrogated in PACT knockout murine embryonic fibroblasts. Our findings suggest a new mechanism for viral evasion of innate immunity through which a viral double-stranded RNA-binding protein interacts with PACT to circumvent type I interferon production. This mechanism might also be used by other PACT-binding viral interferon-antagonizing proteins such as Ebola virus VP35 and influenza A virus NS1.
C1 [Kew, Chun; Lui, Pak-Yin; Chan, Chi-Ping; Jin, Dong-Yan; Kok, Kin-Hang] Univ Hong Kong, Li Ka Shing Fac Med, Dept Biochem, Pokfulam, Hong Kong, Peoples R China.
[Liu, Xiang] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Au, Shannon Wing Ngor] Chinese Univ Hong Kong, Fac Sci, Sch Life Sci, Shatin, Hong Kong, Peoples R China.
[Mohr, Ian] NYU, Sch Med, Dept Microbiol, Inst Canc, New York, NY 10016 USA.
RP Jin, DY (reprint author), Univ Hong Kong, Li Ka Shing Fac Med, Dept Biochem, Pokfulam, Hong Kong, Peoples R China.
EM dyjin@hku.hk; khkok@hku.hk
RI Liu, Xiang/F-5731-2014
FU Hong Kong Health and Medical Research Fund [10091202, 12111312]; Hong
Kong Research Grants Council [HKU7677/10 M, HKU1/CRF/11G]; SK Yee
Medical Research Fund
FX This work was supported by the Hong Kong Health and Medical Research
Fund (10091202 and 12111312), Hong Kong Research Grants Council
(HKU7677/10 M and HKU1/CRF/11G), and SK Yee Medical Research Fund
(2011).
NR 41
TC 16
Z9 16
U1 1
U2 9
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 DEC
PY 2013
VL 87
IS 24
BP 13141
EP 13149
DI 10.1128/JVI.02564-13
PG 9
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300007
PM 24067967
ER
PT J
AU Handisurya, A
Day, PM
Thompson, CD
Buck, CB
Pang, YYS
Lowy, DR
Schiller, JT
AF Handisurya, Alessandra
Day, Patricia M.
Thompson, Cynthia D.
Buck, Christopher B.
Pang, Yuk-Ying S.
Lowy, Douglas R.
Schiller, John T.
TI Characterization of Mus musculus Papillomavirus 1 Infection In Situ
Reveals an Unusual Pattern of Late Gene Expression and Capsid Protein
Localization
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MICROMYS-MINUTUS; MOUSE MODEL; VIRAL-DNA; DIFFERENTIATION; CARCINOMAS;
CLONING; BINDING; VIRUS; SKIN; NEUTRALIZATION
AB Full-length genomic DNA of the recently identified laboratory mouse papillomavirus 1 (MusPV1) was synthesized in vitro and was used to establish and characterize a mouse model of papillomavirus pathobiology. MusPV1 DNA, whether naked or encapsidated by MusPV1 or human papillomavirus 16 (HPV 16) capsids, efficiently induced the outgrowth of papillomas as early as 3 weeks after application to abraded skin on the muzzles and tails of athymic NCr nude mice. High concentrations of virions were extracted from homogenized papillomatous tissues and were serially passaged for > 10 generations. Neutralization by L1 antisera confirmed that infectious transmission was capsid mediated. Unexpectedly, the skin of the murine back was much less susceptible to virion-induced papillomas than the muzzle or tail. Although reporter pseudovirions readily transduced the skin of the back, infection with native MusPV1 resulted in less viral genome amplification and gene expression on the back, including reduced expression of the L1 protein and very low expression of the L2 protein, results that imply skin region-specific control of postentry aspects of the viral life cycle. Unexpectedly, L1 protein on the back was predominantly cytoplasmic, while on the tail the abundant L1 was cytoplasmic in the lower epithelial layers and nuclear in the upper layers. Nuclear localization of L1 occurred only in cells that coexpressed the minor capsid protein, L2. The pattern of L1 protein staining in the infected epithelium suggests that L1 expression occurs earlier in the MusPV1 life cycle than in the life cycle of high-risk HPV and that virion assembly is regulated by a previously undescribed mechanism.
C1 [Handisurya, Alessandra; Day, Patricia M.; Thompson, Cynthia D.; Buck, Christopher B.; Pang, Yuk-Ying S.; Lowy, Douglas R.; Schiller, John T.] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
RP Schiller, JT (reprint author), NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
EM schillej@mail.nih.gov
OI Buck, Christopher/0000-0003-3165-8094
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research; Austrian Science Fund FWF (Erwin Schroedinger
Fellowship project) [J3012-B13]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research, and the Austrian Science Fund FWF (Erwin Schroedinger
Fellowship project J3012-B13, to A.H.).
NR 44
TC 11
Z9 11
U1 0
U2 1
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 DEC
PY 2013
VL 87
IS 24
BP 13214
EP 13225
DI 10.1128/JVI.02162-13
PG 12
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300014
PM 24067981
ER
PT J
AU Chakrabarti, BK
Feng, Y
Sharma, SK
McKee, K
Hedestam, GBK
LaBranche, CC
Montefiori, DC
Mascola, JR
Wyatt, RT
AF Chakrabarti, Bimal K.
Feng, Yu
Sharma, Shailendra Kumar
McKee, Krisha
Hedestam, Gunilla B. Karlsson
LaBranche, Celia C.
Montefiori, David C.
Mascola, John R.
Wyatt, Richard T.
TI Robust Neutralizing Antibodies Elicited by HIV-1 JRFL Envelope
Glycoprotein Trimers in Nonhuman Primates
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; B-CELL RESPONSES; CD4-BINDING SITE; ENV
TRIMERS; CD4 BINDING; SUBTYPE-B; GP120; PROTEIN; TYPE-1; POTENT
AB Host cell-mediated proteolytic cleavage of the human immunodeficiency virus type 1 (HIV-1) gp160 precursor glycoprotein into gp120 and gp41 subunits is required to generate fusion-competent envelope glycoprotein (Env) spikes. The gp120-directed broadly neutralizing monoclonal antibodies (bNabs) isolated from HIV-infected individuals efficiently recognize fully cleaved JRFL Env spikes; however, nonneutralizing gp120-directed monoclonal antibodies isolated from infected or vaccinated subjects recognize only uncleaved JRFL spikes. Therefore, as an immunogen, cleaved spikes that selectively present desired neutralizing epitopes to B cells may elicit cross-reactive neutralizing antibodies. Accordingly, we inoculated nonhuman primates (NHPs) with plasmid DNA encoding transmembrane-anchored, cleaved JRFL Env or by electroporation (EP). Priming with DNA expressing soluble, uncleaved gp140 trimers was included as a comparative experimental group of NHPs. DNA inoculation was followed by boosts with soluble JRFL gp140 trimers, and control NHPs were inoculated with soluble JRFL protein trimers without DNA priming. In the TZM-bl assay, elicitation of neutralizing antibodies against HIV-1 tier 1 isolates was robust following the protein boost. Neutralization of tier 2 isolates was detected, but only in animals primed with plasmid DNA and boosted with trimeric protein. Using the more sensitive A3R5 assay, consistent neutralization of both clade B and C tier 2 isolates was detected from all regimens assessed in the current study, exceeding levels achieved by our previous vaccine regimens in primates. Together, these data suggest a potential advantage of B cell priming followed by a rest interval and protein boosting to present JRFL Env spikes to the immune system to better generate HIV-1 cross-clade neutralizing antibodies.
C1 [Chakrabarti, Bimal K.; Feng, Yu; Sharma, Shailendra Kumar; Wyatt, Richard T.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[McKee, Krisha; Mascola, John R.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Hedestam, Gunilla B. Karlsson] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden.
[LaBranche, Celia C.; Montefiori, David C.] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
[Wyatt, Richard T.] Scripps Res Inst, Scripps Ctr HIV AIDS Vaccine Immunol & Immunogen, La Jolla, CA 92037 USA.
RP Wyatt, RT (reprint author), Scripps Res Inst, IAVI Neutralizing Antibody Ctr, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
EM bchakrabarti@iavi.org; rwyatt@iavi.org
FU IAVI intramural research; NIH intramural research program; SIDA; Bill
and Melinda Gates Foundation; Scripps CHAVI-ID
FX This work was supported primarily by IAVI intramural research, as well
as by the NIH intramural research program, SIDA, The Bill and Melinda
Gates Foundation, and the Scripps CHAVI-ID.
NR 58
TC 33
Z9 33
U1 0
U2 12
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 DEC
PY 2013
VL 87
IS 24
BP 13239
EP 13251
DI 10.1128/JVI.01247-13
PG 13
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300016
PM 24067980
ER
PT J
AU Keller, PW
Huang, RK
England, MR
Waki, K
Cheng, NQ
Heymann, JB
Craven, RC
Freed, EO
Steven, AC
AF Keller, Paul W.
Huang, Rick K.
England, Matthew R.
Waki, Kayoko
Cheng, Naiqian
Heymann, J. Bernard
Craven, Rebecca C.
Freed, Eric O.
Steven, Alasdair C.
TI A Two-Pronged Structural Analysis of Retroviral Maturation Indicates
that Core Formation Proceeds by a Disassembly-Reassembly Pathway Rather
than a Displacive Transition
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID VIRUS CAPSID PROTEIN; HELICAL STRUCTURE; HIV-1 MATURATION; TERMINAL
DOMAIN; SPACER PEPTIDE; GAG PROTEIN; IMMUNODEFICIENCY; RESOLUTION;
CLEAVAGE; VIRIONS
AB Retrovirus maturation involves sequential cleavages of the Gag polyprotein, initially arrayed in a spherical shell, leading to formation of capsids with polyhedral or conical morphology. Evidence suggests that capsids assemble de novo inside maturing virions from dissociated capsid (CA) protein, but the possibility persists of a displacive pathway in which the CA shell remains assembled but is remodeled. Inhibition of the final cleavage between CA and spacer peptide SP1/SP blocks the production of mature capsids. We investigated whether retention of SP might render CA assembly incompetent by testing the ability of Rous sarcoma virus (RSV) CA-SP to assemble in vitro into icosahedral capsids. Capsids were indeed assembled and were indistinguishable from those formed by CA alone, indicating that SP was disordered. We also used cryo-electron tomography to characterize HIV-1 particles produced in the presence of maturation inhibitor PF-46396 or with the cleavage-blocking CA5 mutation. Inhibitor-treated virions have a shell that resembles the CA layer of the immature Gag shell but is less complete. Some CA protein is generated but usually not enough for a mature core to assemble. We propose that inhibitors like PF-46396 bind to the Gag lattice where they deny the protease access to the CA-SP1 cleavage site and prevent the release of CA. CA5 particles, which exhibit no cleavage at the CA-SP1 site, have spheroidal shells with relatively thin walls. It appears that this lattice progresses displacively toward a mature-like state but produces neither conical cores nor infectious virions. These observations support the disassembly- reassembly pathway for core formation.
C1 [Keller, Paul W.; Huang, Rick K.; Cheng, Naiqian; Heymann, J. Bernard; Steven, Alasdair C.] NIAMSD, Struct Biol Res Lab, NIH, Bethesda, MD 20892 USA.
[England, Matthew R.; Craven, Rebecca C.] Penn State Univ, Coll Med, Dept Microbiol & Immunol, Hershey, PA USA.
[Waki, Kayoko; Freed, Eric O.] NCI, Virus Cell Interact Sect, HIV Drug Resistance Program, Frederick, MD 21701 USA.
RP Steven, AC (reprint author), NIAMSD, Struct Biol Res Lab, NIH, Bethesda, MD 20892 USA.
EM stevena@mail.nih.gov
OI Heymann, Bernard/0000-0002-8872-5326
FU NIAMS; NCI; NIH [CA100322, 2 T32 CA60395]; PA Department of Health
FX This work was supported by the Intramural Research Programs of NIAMS and
NCI, by the NIH Intramural AIDS Targeted Antiviral Program, by NIH
CA100322, NIH training grant 2 T32 CA60395, and by the PA Department of
Health (R.C.C.).
NR 57
TC 31
Z9 31
U1 2
U2 11
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 DEC
PY 2013
VL 87
IS 24
BP 13655
EP 13664
DI 10.1128/JVI.01408-13
PG 10
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300053
PM 24109217
ER
PT J
AU Lee, PD
Mukherjee, S
Edeling, MA
Dowd, KA
Austin, SK
Manhart, CJ
Diamond, MS
Fremont, DH
Pierson, TC
AF Lee, Phong D.
Mukherjee, Swati
Edeling, Melissa A.
Dowd, Kimberly A.
Austin, S. Kyle
Manhart, Carolyn J.
Diamond, Michael S.
Fremont, Daved H.
Pierson, Theodore C.
TI The Fc Region of an Antibody Impacts the Neutralization of West Nile
Viruses in Different Maturation States
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID BORNE ENCEPHALITIS-VIRUS; PROTEIN DOMAIN-III; ENVELOPE PROTEIN;
DENGUE-VIRUS; CRYSTAL-STRUCTURE; MEMBRANE-FUSION; MEDIATED
NEUTRALIZATION; DISSEMINATED INFECTION; MONOCLONAL-ANTIBODY; REACTIVE
EPITOPES
AB Flavivirus-infected cells secrete a structurally heterogeneous population of viruses because of an inefficient virion maturation process. Flaviviruses assemble as noninfectious, immature virions composed of trimers of envelope (E) and precursor membrane (prM) protein heterodimers. Cleavage of prM is a required process during virion maturation, although this often remains incomplete for infectious virus particles. Previous work demonstrated that the efficiency of virion maturation could impact antibody neutralization through changes in the accessibility of otherwise cryptic epitopes on the virion. In this study, we show that the neutralization potency of monoclonal antibody (MAb) E33 is sensitive to the maturation state of West Nile virus (WNV), despite its recognition of an accessible epitope, the domain III lateral ridge (DIII-LR). Comprehensive epitope mapping studies with 166 E protein DIII-LR variants revealed that the functional footprint of MAb E33 on the E protein differs subtly from that of the well-characterized DIII-LR MAb E16. Remarkably, aromatic substitutions at E protein residue 306 ablated the maturation state sensitivity of E33 IgG, and the neutralization efficacy of E33 Fab fragments was not affected by changes in the virion maturation state. We propose that E33 IgG binding on mature virions orients the Fc region in a manner that impacts subsequent antibody binding to nearby sites. This Fc-mediated steric constraint is a novel mechanism by which the maturation state of a virion modulates the efficacy of the humoral immune response to flavivirus infection.
C1 [Lee, Phong D.; Mukherjee, Swati; Dowd, Kimberly A.; Manhart, Carolyn J.; Pierson, Theodore C.] NIAID, Viral Pathogenesis Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Fremont, Daved H.] Washington Univ, Sch Med, Dept Biochem & Mol Biophys, St Louis, MO 63110 USA.
[Edeling, Melissa A.; Austin, S. Kyle; Diamond, Michael S.; Fremont, Daved H.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
[Austin, S. Kyle; Diamond, Michael S.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA.
RP Pierson, TC (reprint author), NIAID, Viral Pathogenesis Sect, Viral Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM piersontc@niaid.nih.gov
FU Intramural Research Program of the National Institutes of Allergy and
Infectious Diseases
FX This work was funded by the Intramural Research Program of the National
Institutes of Allergy and Infectious Diseases.
NR 71
TC 10
Z9 10
U1 0
U2 9
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 DEC
PY 2013
VL 87
IS 24
BP 13729
EP 13740
DI 10.1128/JVI.02340-13
PG 12
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300059
PM 24109224
ER
PT J
AU Yoshida, T
Koyanagi, Y
Strebel, K
AF Yoshida, Takeshi
Koyanagi, Yoshio
Strebel, Klaus
TI Functional Antagonism of Rhesus Macaque and Chimpanzee BST-2 by HIV-1
Vpu Is Mediated by Cytoplasmic Domain Interactions
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; PIG-TAILED MACAQUES; TYPE-1 VPU;
CELL-SURFACE; TRANSMEMBRANE DOMAIN; PROTEIN INTERACTIONS; RESTRICTION
FACTOR; PARTICLE RELEASE; LIVING CELLS; MOLECULAR-CLONING
AB Human immunodeficiency virus type 1 (HIV-1) Vpu enhances the release of viral particles from infected cells by interfering with the function of BST-2/tetherin, a cellular protein inhibiting virus release. The Vpu protein encoded by NL4-3, a widely used HIV-1 laboratory strain, antagonizes human BST-2 but not monkey or murine BST-2, leading to the conclusion that BST-2 antagonism by Vpu is species specific. In contrast, we recently identified several primary Vpu isolates, such as Vpu of HIV-1DH12, capable of antagonizing both human and rhesus BST-2. Here we report that while Vpu interacts with human BST-2 primarily through their respective transmembrane domains, antagonism of rhesus BST-2 by Vpu involved an interaction of their cytoplasmic domains. Importantly, a Vpu mutant carrying two mutations in its transmembrane domain (A(14)L and W(22)A), rendering it incompetent for interaction with human BST-2, was able to interact with human BST-2 carrying the rhesus BST-2 cytoplasmic domain and partially neutralized the ability of this BST-2 variant to inhibit viral release. Bimolecular fluorescence complementation analysis to detect Vpu-BST-2 interactions suggested that the physical interaction of Vpu with rhesus or chimpanzee BST-2 involves a 5-residue motif in the cytoplasmic domain of BST-2 previously identified as important for the antagonism of monkey and great ape BST-2 by simian immunodeficiency virus (SIV) Nef. Thus, our study identifies a novel mechanism of antagonism of monkey and great ape BST-2 by Vpu that targets the same motif in BST-2 used by SIV Nef and might explain the expanded host range observed for Vpu isolates in our previous study.
C1 [Yoshida, Takeshi; Strebel, Klaus] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Koyanagi, Yoshio] Kyoto Univ, Inst Virus Res, Lab Viral Pathogenesis, Sakyo Ku, Kyoto 606, Japan.
RP Strebel, K (reprint author), NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
EM kstrebel@nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health; Ministry of Health,
Labor and Welfare of Japan [24115008, 24390112]
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health (K.S.) and by grants from the Grants in-Aid for
Scientific Research (24115008 and 24390112) and Research on HIV/AIDS
from the Ministry of Health, Labor and Welfare of Japan (to Y.K.).
NR 76
TC 2
Z9 3
U1 1
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 DEC
PY 2013
VL 87
IS 24
BP 13825
EP 13836
DI 10.1128/JVI.02567-13
PG 12
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300068
PM 24109238
ER
PT J
AU Rahmberg, AR
Neidermyer, WJ
Breed, MW
Alvarez, X
Midkiff, CC
Piatak, M
Lifson, JD
Evans, DT
AF Rahmberg, Andrew R.
Neidermyer, William J., Jr.
Breed, Matthew W.
Alvarez, Xavier
Midkiff, Cecily C.
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Evans, David T.
TI Tetherin Upregulation in Simian Immunodeficiency Virus-Infected Macaques
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PLASMACYTOID DENDRITIC CELLS; IN-VIVO; VPU; SIV; ADAPTATION; RESISTANCE;
RESPONSES; RELEASE; BST2
AB Here we show that simian immunodeficiency virus (SIV) infection of rhesus macaques results in rapid upregulation of tetherin (BST-2 or CD317) on peripheral blood lymphocytes, including the CD4(+) CCR5(+) T cell targets of virus infection, with a peak of induction that coincides with peak alpha interferon (IFN-alpha) levels in plasma, and that tetherin remains above baseline levels throughout chronic infection. These observations are consistent with a role for tetherin in innate immunity to immunodeficiency virus infection.
C1 [Rahmberg, Andrew R.; Neidermyer, William J., Jr.; Evans, David T.] Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Dept Microbiol & Immunobiol, Southborough, MA 01772 USA.
[Breed, Matthew W.; Alvarez, Xavier; Midkiff, Cecily C.] Tulane Natl Primate Res Ctr, Div Comparat Pathol, Covington, LA USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] SAIC Frederick, Natl Canc Inst Frederick, Frederick, MD USA.
RP Evans, DT (reprint author), Univ Wisconsin, Dept Pathol & Lab Med, Wisconsin Natl Primate Res Ctr, Madison, WI 53715 USA.
EM david_evans@hms.harvard.edu
FU Public Health Service [AI098485, AI087498, AI071306]; National
Institutes of Health [RR000164, RR000168/OD011103]; National Cancer
Institute, National Institutes of Health [HHSN261200800001E]
FX This work was supported by Public Health Service grants AI098485,
AI087498, and AI071306, National Institutes of Health grants RR000164
(TNPRC) and RR000168/OD011103, and, in part, federal funds from the
National Cancer Institute, National Institutes of Health, under contract
HHSN261200800001E.
NR 25
TC 7
Z9 8
U1 0
U2 1
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 DEC
PY 2013
VL 87
IS 24
BP 13917
EP 13921
DI 10.1128/JVI.01757-13
PG 5
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300078
PM 24109219
ER
PT J
AU Cai, YY
Yu, SQ
Mazur, S
Dong, L
Janosko, K
Zhang, TF
Muller, MA
Hensley, LE
Bavari, S
Jahrling, PB
Radoshitzky, SR
Kuhn, JH
AF Cai, Yingyun
Yu, Shuiqing
Mazur, Steven
Dong, Lian
Janosko, Krisztina
Zhang, Tengfei
Mueller, Marcel A.
Hensley, Lisa E.
Bavari, Sina
Jahrling, Peter B.
Radoshitzky, Sheli R.
Kuhn, Jens H.
TI Nonhuman Transferrin Receptor 1 Is an Efficient Cell Entry Receptor for
Ocozocoautla de Espinosa Virus
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HEMORRHAGIC-FEVER ARENAVIRUSES; LYMPHOCYTIC CHORIOMENINGITIS VIRUS;
JUNIN VIRUS; GLYCOPROTEINS; INFECTION; MEXICO; MICE
AB Ocozocoautla de Espinosa virus (OCEV) is a novel, uncultured arenavirus. We found that the OCEV glycoprotein mediates entry into grivet and bat cells through transferrin receptor 1 (TfR1) binding but that OCEV glycoprotein precursor (GPC)-pseudotyped retroviruses poorly entered 53 human cancer cell lines. Interestingly, OCEV and Tacaribe virus could use bat, but not human, TfR1. Replacing three human TfR1 amino acids with their bat ortholog counterparts transformed human TfR1 into an efficient OCEV and Tacaribe virus receptor.
C1 [Cai, Yingyun; Yu, Shuiqing; Mazur, Steven; Janosko, Krisztina; Zhang, Tengfei; Hensley, Lisa E.; Jahrling, Peter B.; Kuhn, Jens H.] NIAID, Integrated Res Facil Ft Detrick, NIH, Frederick, MD USA.
[Dong, Lian; Bavari, Sina; Radoshitzky, Sheli R.] US Army Med Res Inst Infect Dis, Frederick, MD USA.
[Mueller, Marcel A.] Univ Bonn, Inst Virol, Med Ctr, Bonn, Germany.
RP Kuhn, JH (reprint author), NIAID, Integrated Res Facil Ft Detrick, NIH, Frederick, MD USA.
EM sheli.r.radoshitzky.ctr@mail.mil; kuhnjens@mail.nih.gov
RI Kuhn, Jens H./B-7615-2011;
OI Kuhn, Jens H./0000-0002-7800-6045; Mueller, Marcel/0000-0003-2242-5117
FU NIAID [HHSN272200700016I]; Joint Science and Technology Office for
Chemical and Biological Defense [TMTI0048_09_RD_T]
FX Y.C. and J.H.K. performed this work as employees of Tunnell Consulting,
Inc., S. M. as an employee of MRI Global, T.Z. as an employee of
Lovelace, and S.Y. and K.J. as employees of Battelle Memorial Institute,
all under Battelle's prime contract with NIAID under contract number
HHSN272200700016I. This work was in part funded by the Joint Science and
Technology Office for Chemical and Biological Defense (proposal number
TMTI0048_09_RD_T to S.B.).
NR 27
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U1 1
U2 9
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 DEC
PY 2013
VL 87
IS 24
BP 13930
EP 13935
DI 10.1128/JVI.02701-13
PG 6
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300081
PM 24109228
ER
PT J
AU Zhu, ZY
Qin, HR
Chen, WZ
Zhao, Q
Shen, XY
Schutte, R
Wang, YP
Ofek, G
Streaker, E
Prabakaran, P
Fouda, GG
Liao, HX
Owens, J
Louder, M
Yang, YP
Klaric, KA
Moody, MA
Mascola, JR
Scott, JK
Kwong, PD
Montefiori, D
Haynes, BF
Tomaras, GD
Dimitrov, DS
AF Zhu, Zhongyu
Qin, Haiyan Rebekah
Chen, Weizao
Zhao, Qi
Shen, Xiaoying
Schutte, Robert
Wang, Yanping
Ofek, Gilad
Streaker, Emily
Prabakaran, Ponraj
Fouda, Genevieve G.
Liao, Hua-Xin
Owens, John
Louder, Mark
Yang, Yongping
Klaric, Kristina-Ana
Moody, M. Anthony
Mascola, John R.
Scott, Jamie K.
Kwong, Peter D.
Montefiori, David
Haynes, Barton F.
Tomaras, Georgia D.
Dimitrov, Dimiter S.
TI Cross-Reactive HIV-1-Neutralizing Human Monoclonal Antibodies Identified
from a Patient with 2F5-Like Antibodies (vol 85, pg 11401, 2011)
SO JOURNAL OF VIROLOGY
LA English
DT Correction
C1 [Zhu, Zhongyu] NCI, Frederick, MD 21701 USA.
Human Vaccine Inst, Durham, NC USA.
SAIC, Frederick, MD USA.
Vaccine Res Ctr, Bethesda, MD USA.
Simon Fraser Univ, Dept Mol Biol & Biochem, Burnaby, BC V5A 1S6, Canada.
Simon Fraser Univ, Fac Hlth Sci, Burnaby, BC V5A 1S6, Canada.
RP Zhu, ZY (reprint author), NCI, Frederick, MD 21701 USA.
RI Tomaras, Georgia/J-5041-2016
NR 1
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Z9 0
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 DEC
PY 2013
VL 87
IS 24
BP 13936
EP 13936
DI 10.1128/JVI.02726-13
PG 1
WC Virology
SC Virology
GA 258EZ
UT WOS:000327443300082
ER
PT J
AU Witkowski, B
Amaratunga, C
Khim, N
Sreng, S
Chim, P
Kim, S
Lim, P
Mao, S
Sopha, C
Sam, B
Anderson, JM
Duong, S
Chuor, CM
Taylor, WRJ
Suon, S
Mercereau-Puijalon, O
Fairhurst, RM
Menard, D
AF Witkowski, Benoit
Amaratunga, Chanaki
Khim, Nimol
Sreng, Sokunthea
Chim, Pheaktra
Kim, Saorin
Lim, Pharath
Mao, Sivanna
Sopha, Chantha
Sam, Baramey
Anderson, Jennifer M.
Duong, Socheat
Chuor, Char Meng
Taylor, Walter R. J.
Suon, Sella
Mercereau-Puijalon, Odile
Fairhurst, Rick M.
Menard, Didier
TI Novel phenotypic assays for the detection of artemisinin-resistant
Plasmodium falciparum malaria in Cambodia: in-vitro and ex-vivo
drug-response studies
SO LANCET INFECTIOUS DISEASES
LA English
DT Article
ID PARASITE CLEARANCE; WESTERN CAMBODIA; SUSCEPTIBILITY; SENSITIVITY;
ARTESUNATE; PROVINCE; RATES
AB Background Artemisinin resistance in Plasmodium falciparum lengthens parasite clearance half-life during artemisinin monotherapy or artemisinin-based combination therapy. Absence of in-vitro and ex-vivo correlates of artemisinin resistance hinders study of this phenotype. We aimed to assess whether an in-vitro ring-stage survival assay (RSA) can identify culture-adapted P falciparum isolates from patients with slow-clearing or fast-clearing infections, to investigate the stage-dependent susceptibility of parasites to dihydroaitemisinin in the in-vitro RSA, and to assess whether an ex-vivo RSA can identify artemisinin-resistant P falciparum infections.
Methods We culture-adapted parasites from patients with long and short parasite clearance half-lives from a study done in Pursat, Cambodia, in 2010 (registered with ClinicalTrials.gov, number NCT00341003) and used novel in-vitro survival assays to explore the stage-dependent susceptibility of slow-clearing and fast-clearing parasites to dihydroartemisinin. In 2012, we implemented the RSA in prospective parasite clearance studies in Pursat, Preah Vihear, and Ratanakiri, Cambodia (NCT01736319), to measure the ex-vivo responses of parasites from patients with malaria. Continuous variables were compared with the Mann-Whitney U test. Correlations were analysed with the Spearman correlation test.
Findings In-vitro survival rates of culture-adapted parasites from 13 slow-clearing and 13 fast-clearing infections differed significantly when assays were done on 0-3 h ring-stage parasites (10.88% vs 0"23%; p=0.007). Ex-vivo survival rates significantly correlated with in-vivo parasite clearance half-lives (n=30, r=0.74, 95% CI 0.50-0.87; p<0.0001).
Interpretation The in-vitro RSA of 0-3 h ring-stage parasites provides a platform for the molecular characterisation of artemisinin resistance. The ex-vivo RSA can be easily implemented where surveillance for artemisinin resistance is needed.
Funding Institut Pasteur du Cambodge and the Intramural Research Program, NIAID, NIH.
C1 [Witkowski, Benoit; Khim, Nimol; Chim, Pheaktra; Kim, Saorin; Lim, Pharath; Menard, Didier] Inst Pasteur Cambodge, Malaria Mol Epidemiol Unit, Phnom Penh, Cambodia.
[Amaratunga, Chanaki; Lim, Pharath; Anderson, Jennifer M.; Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Sreng, Sokunthea; Lim, Pharath; Duong, Socheat; Chuor, Char Meng; Suon, Sella] Natl Ctr Parasitol Entomol & Malaria Control, Phnom Penh, Cambodia.
[Mao, Sivanna] Sampov Mean Referral Hosp, Pursat, Cambodia.
[Sopha, Chantha] Makara 16 Referral Hosp, Preah Vihear, Cambodia.
[Sam, Baramey] Ratanakiri Referral Hosp, Ratanakiri, Cambodia.
[Taylor, Walter R. J.] Hop Cantonal Univ Geneva, Serv Med Int & Humanitaire, Geneva, Switzerland.
[Mercereau-Puijalon, Odile] Inst Pasteur, Parasite Mol Immunol Unit, Paris, France.
RP Menard, D (reprint author), Inst Pasteur Cambodge, 5 Blvd Monivong BP 983, Phnom Penh, Cambodia.
EM rfairhurst@niaid.nih.gov; dmenard@pasteur-kh.org
RI Menard, Didier/O-3294-2013
OI Menard, Didier/0000-0003-1357-4495
FU Institut Pasteur du Cambodge; NIAID, NIH; International Division,
Institut Pasteur; French Ministry of Foreign Affairs; Laboratoire
d'excellence IBEID (Agence Nationale de la Recherche, France)
FX Institut Pasteur du Cambodge and the Intramural Research Program, NIAID,
NIH.; We thank Robert Gwadz, Savuth Koeuth, Francois Nosten, Eng Ly
Pech, Thomas Wellems, and Chongjun Zhou for their efforts in support of
this work. This study was funded by the Intramural Research Program,
NIAID, NIH, and by grants from Institut Pasteur du Cambodge (Institut
Pasteur, International Division and Banque Natixis) and Laboratoire
d'excellence IBEID (Agence Nationale de la Recherche, France). BW is
supported by a postdoctoral fellowship from the International Division,
Institut Pasteur, and DM by the French Ministry of Foreign Affairs.
NR 34
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U1 25
U2 54
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 DEC
PY 2013
VL 13
IS 12
BP 1043
EP 1049
DI 10.1016/S1473-3099(13)70252-4
PG 7
WC Infectious Diseases
SC Infectious Diseases
GA 256AZ
UT WOS:000327283400026
PM 24035558
ER
PT J
AU Corbex, M
Harford, JB
AF Corbex, Marilys
Harford, Joe B.
TI Perspectives on breast cancer in Arab populations
SO LANCET ONCOLOGY
LA English
DT Letter
ID MIDDLE-INCOME COUNTRIES
C1 [Corbex, Marilys] Inst Trop Med, Dept Publ Hlth, B-2000 Antwerp, Belgium.
[Harford, Joe B.] NCI, Ctr Global Hlth, NIH, Rockville, MD 20850 USA.
RP Corbex, M (reprint author), Inst Trop Med, Dept Publ Hlth, B-2000 Antwerp, Belgium.
EM harfordj@mail.nih.gov
NR 5
TC 3
Z9 3
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2013
VL 14
IS 13
BP E582
EP E582
PG 1
WC Oncology
SC Oncology
GA 259PU
UT WOS:000327539600001
PM 24275130
ER
PT J
AU Mousoulis, C
Xu, X
Reiter, DA
Neu, CP
AF Mousoulis, Charilaos
Xu, Xin
Reiter, David A.
Neu, Corey P.
TI Single cell spectroscopy: Noninvasive measures of small-scale structure
and function
SO METHODS
LA English
DT Article
DE Spectroscopy; Single cells; Nuclear magnetic resonance; Fluorescence
microscopy; Atomic force microscopy
ID ATOMIC-FORCE MICROSCOPY; NUCLEAR-MAGNETIC-RESONANCE; RAMAN SCATTERING
MICROSCOPY; RESOLUTION NMR-SPECTROSCOPY; FLUORESCENCE MICROSCOPY; LIVE
CELLS; LIVING CELLS; ILLUMINATION MICROSCOPY; PROTEIN-PHOSPHORYLATION;
INFRARED-SPECTROSCOPY
AB The advancement of spectroscopy methods attained through increases in sensitivity, and often with the coupling of complementary techniques, has enabled real-time structure and function measurements of single cells. The purpose of this review is to illustrate, in light of advances, the strengths and the weaknesses of these methods. Included also is an assessment of the impact of the experimental setup and conditions of each method on cellular function and integrity. A particular emphasis is placed on noninvasive and nondestructive techniques for achieving single cell detection, including nuclear magnetic resonance, in addition to physical, optical, and vibrational methods. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Mousoulis, Charilaos; Xu, Xin; Neu, Corey P.] Purdue Univ, Weldon Sch Biomed Engn, W Lafayette, IN 47907 USA.
[Reiter, David A.] NIA, Lab Clin Invest, NIH, Baltimore, MD 21225 USA.
RP Neu, CP (reprint author), Purdue Univ, Weldon Sch Biomed Engn, W Lafayette, IN 47907 USA.
EM cpneu@purdue.edu
RI Xu, Xin/B-1975-2014
OI Xu, Xin/0000-0002-4876-5710
FU Showalter Trust Fund; Intramural program of the National Institutes of
Health (NIH), National Institute on Aging [NIH R21 AR064178]
FX This research was funded in part by the Showalter Trust Fund, the
Intramural program of the National Institutes of Health (NIH), National
Institute on Aging, and NIH R21 AR064178. The authors have no financial
conflicts of interest to declare.
NR 135
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U1 0
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-2023
EI 1095-9130
J9 METHODS
JI Methods
PD DEC 1
PY 2013
VL 64
IS 2
BP 119
EP 128
DI 10.1016/j.ymeth.2013.07.025
PG 10
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 260AM
UT WOS:000327567400005
PM 23886910
ER
PT J
AU Kidder, BL
Hu, GQ
Yu, ZX
Liu, CY
Zhao, KJ
AF Kidder, Benjamin L.
Hu, Gangqing
Yu, Zu-Xi
Liu, Chengyu
Zhao, Keji
TI Extended Self-Renewal and Accelerated Reprogramming in the Absence of
Kdm5b
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID EMBRYONIC STEM-CELLS; CORE TRANSCRIPTIONAL NETWORK; HISTONE DEMETHYLASE;
HUMAN GENOME; REGULATES PLURIPOTENCY; ACTIVE GENES; ES CELLS;
METHYLATION; MOUSE; EXPRESSION
AB Embryonic stem (ES) cell pluripotency is thought to be regulated in part by H3K4 methylation. However, it is unclear how H3K4 demethylation contributes to ES cell function and participates in induced pluripotent stem (iPS) cell reprogramming. Here, we show that KDM5B, which demethylates H3K4, is important for ES cell differentiation and presents a barrier to the reprogramming process. Depletion of Kdm5b leads to an extension in the self-renewal of ES cells in the absence of LIF. Transcriptome analysis revealed the persistent expression of pluripotency genes and underexpression of developmental genes during differentiation in the absence of Kdm5b, suggesting that KDM5B plays a key role in cellular fate changes. We also observed accelerated reprogramming of differentiated cells in the absence of Kdm5b, demonstrating that KDM5B is a barrier to the reprogramming process. Expression analysis revealed that mesenchymal master regulators associated with the epithelial-to-mesenchymal transition (EMT) are downregulated during reprogramming in the absence of Kdm5b. Moreover, global analysis of H3K4me3/2 revealed that enhancers of fibroblast genes are rapidly deactivated in the absence of Kdm5b, and genes associated with EMT lose H3K4me3/2 during the early reprogramming process. These findings provide functional insight into the role for KDM5B in regulating ES cell differentiation and as a barrier to the reprogramming process.
C1 [Kidder, Benjamin L.; Hu, Gangqing; Zhao, Keji] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Yu, Zu-Xi] NHLBI, Pathol Core Facil, NIH, Bethesda, MD 20892 USA.
[Liu, Chengyu] NHLBI, Transgen Core, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
RP Kidder, BL (reprint author), NHLBI, Syst Biol Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM benjamin.kidder@nih.gov; zhaok@nhlbi.nih.gov
RI HU, GANGQING/K-5849-2012
NR 54
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U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2013
VL 33
IS 24
BP 4793
EP 4810
DI 10.1128/MCB.00692-13
PG 18
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259RO
UT WOS:000327544200003
PM 24100015
ER
PT J
AU Lamichhane, TN
Mattijssen, S
Maraia, RJ
AF Lamichhane, Tek N.
Mattijssen, Sandy
Maraia, Richard J.
TI Human Cells Have a Limited Set of tRNA Anticodon Loop Substrates of the
tRNA Isopentenyltransferase TRIT1 Tumor Suppressor
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID SELENOCYSTEINE TRANSFER; LUNG-CANCER; RECOGNITION;
DIMETHYLALLYLTRANSFERASE; TRANSLATION; METHYLATION; EXPRESSION;
INHIBITION; NUCLEOSIDE; EFFICIENCY
AB Human TRIT1 is a tRNA isopentenyltransferase (IPTase) homologue of Escherichia coli MiaA, Saccharomyces cerevisiae Mod5, Schizosaccharomyces pombe Tit1, and Caenorhabditis elegans GRO-1 that adds isopentenyl groups to adenosine 37 (i6A37) of substrate tRNAs. Prior studies indicate that i6A37 increases translation fidelity and efficiency in codon-specific ways. TRIT1 is a tumor suppressor whose mutant alleles are associated with cancer progression. We report the systematic identification of i6A37-containing tRNAs in a higher eukaryote, performed using small interfering RNA knockdown and other methods to examine TRIT1 activity in HeLa cells. Although several potential substrates contained the IPTase recognition sequence A36A37-A38 in the anticodon loop, only tRNA(Ser)AGA, tRNA(Ser)CGA, tRNA(Ser)UGA, and selenocysteine tRNA with UCA (tRNA([Ser]Sec)UCA) contained i6A37. This subset is a significantly more restricted than that for two distant yeasts (S. cerevisiae and S. pombe), the only other organisms comprehensively examined. Unlike the fully i6A37-modified tRNAs for Ser, tRNA([Ser]Sec)UCA is partially (similar to 40%) modified. Exogenous selenium and other treatments that decreased the i6A37 content of tRNA([Ser]Sec)UCA led to increased levels of the tRNA([Ser]Sec)UCA. Of the human mitochondrion (mt)-encoded tRNAs with A36A37-A38, only mt tRNAs tRNASerUGA and tRNA(Trp)UCA contained detectable i6A37. Moreover, while tRNA(Ser) levels were unaffected by TRIT1 knockdown, the tRNA([Ser]Sec)UCA level was increased and the mt tRNA(Ser)UGA level was decreased, suggesting that TRIT1 may control the levels of some tRNAs as well as their specific activity.
C1 [Lamichhane, Tek N.; Mattijssen, Sandy; Maraia, Richard J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Maraia, Richard J.] US PHS, Commissioned Corps, Washington, DC USA.
RP Maraia, RJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
EM maraiar@mail.nih.gov
FU Intramural Research Program of the NICHD, NIH
FX This work was supported by the Intramural Research Program of the NICHD,
NIH.
NR 41
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U1 0
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2013
VL 33
IS 24
BP 4900
EP 4908
DI 10.1128/MCB.01041-13
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259RO
UT WOS:000327544200011
PM 24126054
ER
PT J
AU Zhang, XX
Sun, ZC
Guo, JX
Wang, Z
Wu, CX
Niu, G
Ma, Y
Kiesewetter, DO
Chen, XY
AF Zhang, Xiao-Xiang
Sun, Zhongchan
Guo, Jinxia
Wang, Zhe
Wu, Chenxi
Niu, Gang
Ma, Ying
Kiesewetter, Dale O.
Chen, Xiaoyuan
TI Comparison of F-18-labeled CXCR4 antagonist peptides for PET imaging of
CXCR4 expression
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Article
DE CXCR4; PET imaging; CXCR4 antagonist peptides; F-18-labeling
ID CHEMOKINE RECEPTOR CXCR4; CELL-DERIVED FACTOR-1;
POSITRON-EMISSION-TOMOGRAPHY; HIGH SELECTIVITY INDEXES; HUMAN CANCER
XENOGRAFTS; FACTOR-I; TUMOR; METASTASIS; LIGAND; T140
AB CXCR4 is overexpressed on tumor cells from many types of human cancers. A high level of CXCR4 expression often correlates with poor prognosis, chemotherapy resistance, and metastasis. The development of CXCR4-specific radiotracers for positron emission tomography (PET) imaging will allow in vivo evaluation of receptor expression level for diagnosis or therapeutic evaluation.
Two new F-18-labeled radiotracers based on an Ac-TC14012 peptide, [F-18]FP-Ac-TC14012 and [F-18]FB-Ac-TC14012, were synthesized and characterized. The affinities of the 2-fluoropropionate (FP)-conjugated or 4-fluorobenzoate (FB)-conjugated peptides to CXCR4-transfected Chinese hamster ovarian (CHO) cells were evaluated in a competitive binding assay with [I-125]CXCL12 radioligand. The cell uptake and retention of [F-18]FP-labeled and [F-18]FB-labeled peptides were measured. The tumor targetability and pharmacokinetics of these two tracers were also evaluated by microPET imaging and biodistribution studies.
The labeled peptides retained high binding affinity to CXCR4 and showed much higher uptake in CXCR4-positive CHO cells than in CXCR4-negative cells in vitro. The smaller and more hydrophilic [F-18]FP prosthetic group resulted in higher affinity and lower nonspecific cell uptake compared to the [F-18]FB-labeled peptide. Both radiotracers showed much higher accumulation in CXCR4-positive than CXCR4-negative tumor xenografts in mice and allowed clear visualization of CXCR4 expression by PET. Among the two, [F-18]FP-Ac-TC14012 showed higher tumor uptake and better tumor-to-background contrast. Unlike their N-terminal 4-F-benzoate analogs, these two tracers had minimal blood retention, likely due to reduced red blood cell binding. Metabolic organs, such as the liver and kidney, also showed high uptake. When blocked with low-dose cold peptide (10 mu g), the tumor uptake was significantly increased, most likely due to the increased concentration in blood circulation, as evidenced by decreased liver uptake.
These results demonstrate that the [F-18]FP-labeled Ac-TC14012 peptide with high tumor uptake, low nonspecific binding, and good tumor-to-background contrast promises [F-18]FP-Ac-TC14012 as a PET tracer for in vivo PET imaging of CXCR4 expression.
C1 [Zhang, Xiao-Xiang; Guo, Jinxia; Wang, Zhe; Wu, Chenxi; Niu, Gang; Ma, Ying; Kiesewetter, Dale O.; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
[Sun, Zhongchan] Fourth Mil Med Univ, Xijing Hosp, Dept Cardiol, Xian 710032, Shaanxi, Peoples R China.
[Sun, Zhongchan] Fourth Mil Med Univ, Xijing Hosp, Mol Imaging Program, Xian 710032, Shaanxi, Peoples R China.
[Guo, Jinxia; Wang, Zhe] Xiamen Univ, Sch Publ Hlth, Ctr Mol Imaging & Translat Med, Xiamen 361005, Peoples R China.
RP Kiesewetter, DO (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
EM dkiesewetter@mail.nih.gov; shawn.chen@nih.gov
FU Intramural Research Program of the National Institute of Biomedical
Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH);
National Research Council Research Associateship Award at NIH/NIBIB
FX We want to thank the Intramural Research Program of the National
Institute of Biomedical Imaging and Bioengineering (NIBIB), National
Institutes of Health (NIH) for the funding support. This work was
performed while X-X Zhang held a National Research Council Research
Associateship Award at NIH/NIBIB.
NR 41
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U1 0
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1536-1632
EI 1860-2002
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD DEC
PY 2013
VL 15
IS 6
BP 758
EP 767
DI 10.1007/s11307-013-0640-0
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 255CH
UT WOS:000327216300014
PM 23636490
ER
PT J
AU Zhang, XX
Sun, ZC
Guo, JX
Wang, Z
Wu, CX
Niu, G
Ma, Y
Kiesewetter, DO
Chen, XY
AF Zhang, Xiao-Xiang
Sun, Zhongchan
Guo, Jinxia
Wang, Zhe
Wu, Chenxi
Niu, Gang
Ma, Ying
Kiesewetter, Dale O.
Chen, Xiaoyuan
TI Comparison of F-18-labeled CXCR4 antagonist peptides for PET imaging of
CXCR4 expression (vol 15, pg 758, 2013)
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Correction
C1 [Zhang, Xiao-Xiang; Guo, Jinxia; Wang, Zhe; Wu, Chenxi; Niu, Gang; Ma, Ying; Kiesewetter, Dale O.; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
[Sun, Zhongchan] Fourth Mil Med Univ, Xijing Hosp, Dept Cardiol & Mol Imaging Program, Xian 710032, Shaanxi, Peoples R China.
[Guo, Jinxia; Wang, Zhe] Xiamen Univ, Sch Publ Hlth, Ctr Mol Imaging & Translat Med, Xiamen 361005, Peoples R China.
RP Kiesewetter, DO (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
EM dkiesewetter@mail.nih.gov; shawn.chen@nih.gov
NR 1
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PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1536-1632
EI 1860-2002
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD DEC
PY 2013
VL 15
IS 6
BP 788
EP 788
DI 10.1007/s11307-013-0650-y
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 255CH
UT WOS:000327216300018
ER
PT J
AU Antonioli, L
Blandizzi, C
Pacher, P
Hasko, G
AF Antonioli, Luca
Blandizzi, Corrado
Pacher, Pal
Hasko, Gyoergy
TI Immunity, inflammation and cancer: a leading role for adenosine
SO NATURE REVIEWS CANCER
LA English
DT Review
ID REGULATORY T-CELLS; ENDOTHELIAL GROWTH-FACTOR; ACTIVATED PROTEIN-KINASE;
TUMOR-ASSOCIATED MACROPHAGES; HUMAN-MELANOMA CELLS; NF-KAPPA-B;
CL-IB-MECA; NUCLEOSIDE TRANSPORTER FAMILY; RECEPTOR MEDIATES APOPTOSIS;
SYNERGISTIC UP-REGULATION
AB Cancer is a complex disease that is dictated by both cancer cell-intrinsic and cell-extrinsic processes. Adenosine is an ancient extracellular signalling molecule that can regulate almost all aspects of tissue function. As such, several studies have recently highlighted a crucial role for adenosine signalling in regulating the various aspects of cell-intrinsic and cell-extrinsic processes of cancer development. This Review critically discusses the role of adenosine and its receptors in regulating the complex interplay among immune, inflammatory, endothelial and cancer cells during the course of neoplastic disease.
C1 [Antonioli, Luca; Blandizzi, Corrado] Univ Pisa, Dept Clin & Expt Med, I-56126 Pisa, Italy.
[Antonioli, Luca; Hasko, Gyoergy] Rutgers New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA.
[Antonioli, Luca; Hasko, Gyoergy] Rutgers New Jersey Med Sch, Ctr Immun & Inflammat, Newark, NJ 07103 USA.
[Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Labs Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Hasko, Gyoergy] Univ Debrecen, Med & Hlth Sci Ctr, Dept Med Chem, H-4032 Debrecen, Hungary.
RP Hasko, G (reprint author), Rutgers New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA.
EM haskoge@njms.rutgers.edu
RI Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU US National Institutes of Health (NIH) [R01GM66189]; Hungarian
Scientific Research Fund grants (Orszagos Tudomanyos Kutatasi
Alapprogramok (OTKA)) [CK 78275, K 109178]; NIH, the National Institute
on Alcohol Abuse and Alcoholism; Nexus award "Marcello Tonini";
Inflammatory Bowel Disease (IBD) Research Foundation
FX This work was supported by US National Institutes of Health (NIH) grant
R01GM66189 (to G. H.), Hungarian Scientific Research Fund grants
(Orszagos Tudomanyos Kutatasi Alapprogramok (OTKA)) CK 78275 (to G. H.)
and K 109178 (to G. H.), the Intramural Research Program of the NIH, the
National Institute on Alcohol Abuse and Alcoholism (to P. P.), the Nexus
award "Marcello Tonini" (to L. A.) and by the Inflammatory Bowel Disease
(IBD) Research Foundation (mini grant 2012) (to L.A.).
NR 215
TC 106
Z9 111
U1 10
U2 71
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-175X
EI 1474-1768
J9 NAT REV CANCER
JI Nat. Rev. Cancer
PD DEC
PY 2013
VL 13
IS 12
BP 842
EP 857
DI 10.1038/nrc3613
PG 16
WC Oncology
SC Oncology
GA 259RA
UT WOS:000327542800008
PM 24226193
ER
PT J
AU Morgan, IG
Cotch, MF
AF Morgan, Ian G.
Cotch, Mary Frances
TI Birth Order and Myopia: What are the Messages to Readers?
SO OPHTHALMIC EPIDEMIOLOGY
LA English
DT Editorial Material
ID REFRACTIVE ERROR; VISUAL IMPAIRMENT; SOUTHERN CHINA; CHILDREN;
ADOLESCENCE
C1 [Morgan, Ian G.] Australian Natl Univ, Res Sch Biol, Canberra, ACT, Australia.
[Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
RP Morgan, IG (reprint author), Australian Natl Univ, Res Sch Biol, Canberra, ACT, Australia.
EM ian.morgan@anu.edu.au
RI Morgan, Ian/D-1190-2009;
OI Morgan, Ian/0000-0002-4548-3574; Cotch, Mary Frances/0000-0002-2046-4350
FU Intramural NIH HHS [Z99 EY999999]
NR 17
TC 2
Z9 2
U1 0
U2 5
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0928-6586
EI 1744-5086
J9 OPHTHAL EPIDEMIOL
JI Ophthalmic Epidemiol.
PD DEC
PY 2013
VL 20
IS 6
BP 333
EP 334
DI 10.3109/09286586.2013.860994
PG 2
WC Ophthalmology
SC Ophthalmology
GA 256OC
UT WOS:000327322100001
PM 24229068
ER
PT J
AU Dalal, MD
Morgans, CW
Duvoisin, RM
Gamboa, EA
Jeffrey, BG
Garg, SJ
Chan, CC
Sen, HN
AF Dalal, Monica D.
Morgans, Catherine W.
Duvoisin, Robert M.
Gamboa, Elizabeth A.
Jeffrey, Brett G.
Garg, Sunir J.
Chan, Chi-Chao
Sen, H. Nida
TI Diagnosis of Occult Melanoma Using Transient Receptor Potential
Melastatin 1 (TRPM1) Autoantibody Testing A Novel Approach
SO OPHTHALMOLOGY
LA English
DT Article
ID UNKNOWN PRIMARY SITE; BIPOLAR CELLS; CUTANEOUS MELANOMA; RETINOPATHY MAR
AB Purpose: To report the first case of melanoma-associated retinopathy (MAR) and underlying occult melanoma diagnosed based on the presence of serum transient receptor potential melastatin 1 (TRPM1) autoantibodies.
Design: Interventional case report with basic science correlation.
Participants: One patient with MAR.
Intervention: Testing for the presence of serum TRPM1 autoantibodies.
Main Outcome Measures: Diagnosis of an occult melanoma involving the axillary lymph nodes (unknown primary site) and MAR based on the presence of TRPM1 autoantibodies in the patient's serum.
Results: The patient's clinical exam was remarkable for mild intraocular inflammation in both eyes and retinal hemorrhages with an apparent choroidal neovascularization in the left eye, which was confirmed by fluorescein angiography and indocyanine green angiography testing. Humphrey visual field 30-2 SITA-fast (Humphrey Visual Field Analyzer, Carl Zeiss Meditec, Inc, Dublin, CA) demonstrated diffuse depression in both eyes out of proportion to the clinical exams, prompting electroretinography testing that revealed an electronegative response. Dark-adapted thresholds were markedly elevated and mediated by cones. Due to concern for MAR, a systemic work-up for melanoma was performed by the primary care physician that was unrevealing. Given our continued clinical suspicion for MAR, the patient's serum was sent for evaluation for TRPM1 autoantibodies. The patient's serum applied to normal human retina exhibited positivity in the inner nuclear layer. Application of the patient's serum to wild-type and TRPM1 knockout mouse retina revealed strongly labeled bipolar cells in the wild-type retina, but not in the TRPM1 knockout retina, indicating TRPM1-dependent immunoreactivity. The antigen was confirmed as TRPM1 by labeling of TRPM1-transfected human embryonic kidney 293 cells. Additional systemic work-up prompted by this finding resulted in identification of an occult metastatic melanoma involving the axillary lymph nodes with an unknown primary site. The patient underwent surgical excision of the occult melanoma without evidence of other sites of metastases. He also received intravenous immunoglobulin therapy and his vision has stabilized.
Conclusions: This is the first reported case of a melanoma-associated retinopathy diagnosed utilizing the innovative approach of testing for serum TRPM1 autoantibodies. (C) 2013 by the American Academy of Ophthalmology.
C1 [Dalal, Monica D.; Jeffrey, Brett G.; Chan, Chi-Chao; Sen, H. Nida] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Morgans, Catherine W.; Duvoisin, Robert M.; Gamboa, Elizabeth A.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97201 USA.
[Garg, Sunir J.] Wills Eye Inst, Retina Serv, Philadelphia, PA USA.
RP Sen, HN (reprint author), NEI, NIH, 10 Ctr Dr,Room 10D42, Bethesda, MD 20892 USA.
EM senh@nei.nih.gov
FU National Eye Institute Intramural Research Program, Bethesda, Maryland
FX Supported by the National Eye Institute Intramural Research Program,
Bethesda, Maryland. The sponsor or funding organization had no role in
the design or conduct of this research.
NR 19
TC 5
Z9 6
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
EI 1549-4713
J9 OPHTHALMOLOGY
JI Ophthalmology
PD DEC
PY 2013
VL 120
IS 12
BP 2560
EP 2564
DI 10.1016/j.ophtha.2013.07.037
PG 5
WC Ophthalmology
SC Ophthalmology
GA 255OL
UT WOS:000327249600040
PM 24053997
ER
PT J
AU Domalpally, A
Danis, RP
White, J
Narkar, A
Clemons, T
Ferris, F
Chew, E
AF Domalpally, Amitha
Danis, Ronald P.
White, James
Narkar, Ashwini
Clemons, Traci
Ferris, Fredrick
Chew, Emily
TI Circularity Index as a Risk Factor for Progression of Geographic Atrophy
SO OPHTHALMOLOGY
LA English
DT Article
ID OPTICAL COHERENCE TOMOGRAPHY; RETINAL-PIGMENT EPITHELIUM; MACULAR
DEGENERATION; NATURAL-HISTORY; CLINICAL-TRIALS; EYE DISEASE; AREA
AB Objective: To develop a parameter that can assess the relative rate of progression of geographic atrophy (GA) based on the hypothesis that noncircular configuration of the atrophic lesion may be a risk factor for enlargement.
Design: Cohort study.
Participants: Digitized color photographs of 593 eyes with GA from the Age-Related Eye Disease Study (AREDS).
Methods: A novel parameter called the "Geographic Atrophy Circularity Index" (GACI) was developed on the basis of area and perimeter measurements to categorize the irregularity of the shape of GA. The GACI ranges from 0.0 to 1.0 and is categorized into 3 groups: 0.25 (very irregular), 0.25 to <0.75 (partly irregular), and >= 0.75 (circular). Main Outcome Measures: Growth rate of GA.
Results: The mean growth rate in the 3 categories was 0.40 (+/- 0.18), 0.36 (+/- 0.30), and 0.21 (+/- 0.22) mm/year, respectively (P<0.001). By adjusting for known confounders, baseline area, duration of GA, and configuration, GACI categories were significantly associated with increased growth rate of GA (P<0.001).
Conclusions: The GACI was associated with the progression rate of GA and may be a useful measure for clinical trial eligibility. The association also suggests that enlargement of GA may be related to the extent of the junctional zone of damaged retinal pigment epithelium, which increases with noncircularity for a given GA area. (C) 2013 by the American Academy of Ophthalmology.
C1 [Domalpally, Amitha; Danis, Ronald P.; White, James; Narkar, Ashwini] Univ Wisconsin, Fundus Photograph Reading Ctr, Madison, WI USA.
[Ferris, Fredrick; Chew, Emily] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Clemons, Traci] EMMES Corp, Rockville, MD USA.
RP Danis, RP (reprint author), Fundus Photograph Reading Ctr, 8010 Excelsior Dr,Suite 100, Madison, WI 53717 USA.
EM rdanis@rc.ophth.wisc.edu
RI Domalpally, Amitha/B-2367-2015
NR 16
TC 9
Z9 9
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
EI 1549-4713
J9 OPHTHALMOLOGY
JI Ophthalmology
PD DEC
PY 2013
VL 120
IS 12
BP 2666
EP 2671
DI 10.1016/j.ophtha.2013.07.047
PG 6
WC Ophthalmology
SC Ophthalmology
GA 255OL
UT WOS:000327249600053
PM 24206616
ER
PT J
AU Groninger, H
AF Groninger, Hunter
TI Regarding a definition of the palliative care patient
SO PALLIATIVE MEDICINE
LA English
DT Letter
ID PAIN
C1 NIH, Pain & Palliat Care Serv, Ctr Clin, Bethesda, MD 20892 USA.
RP Groninger, H (reprint author), NIH, Pain & Palliat Care Serv, Ctr Clin, Room 2-1733, Bethesda, MD 20892 USA.
EM hunter.groninger@nih.gov
NR 4
TC 1
Z9 1
U1 0
U2 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-2163
EI 1477-030X
J9 PALLIATIVE MED
JI Palliat. Med.
PD DEC
PY 2013
VL 27
IS 10
BP 952
EP 953
DI 10.1177/0269216313493220
PG 2
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Medicine, General & Internal
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; General & Internal Medicine
GA 254FA
UT WOS:000327148800009
PM 24259476
ER
PT J
AU Fox, MA
Panessiti, MG
Moya, PR
Tolliver, TJ
Chen, K
Shih, JC
Murphy, DL
AF Fox, M. A.
Panessiti, M. G.
Moya, P. R.
Tolliver, T. J.
Chen, K.
Shih, J. C.
Murphy, D. L.
TI Mutations in monoamine oxidase (MAO) genes in mice lead to
hypersensitivity to serotonin-enhancing drugs: implications for drug
side effects in humans
SO PHARMACOGENOMICS JOURNAL
LA English
DT Article
DE 5-hydroxy-L-tryptophan (5-HTP); monoamine oxidase (MAO) A/B-knockout
mice; serotonin syndrome; tramadol
ID TRANSPORTER (SERT)-DEFICIENT MICE; KNOCK-OUT MICE; DEFICIENT MICE;
FUNCTIONAL POLYMORPHISM; PROMOTER POLYMORPHISM; REUPTAKE INHIBITOR;
BRAIN-SEROTONIN; POINT MUTATION; TRAMADOL; ASSOCIATION
AB A possible side effect of serotonin-enhancing drugs is the serotonin syndrome, which can be lethal. Here we examined possible hypersensitivity to two such drugs, the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP) and the atypical opioid tramadol, in mice lacking the genes for both monoamine oxidase A (MAOA) and MAOB. MAOA/B-knockout (KO) mice displayed baseline serotonin syndrome behaviors, and these behavioral responses were highly exaggerated following 5-HTP or tramadol versus baseline and wild-type (WT) littermates. Compared with MAOA/B-WT mice, baseline tissue serotonin levels were increased similar to 2.6-3.9-fold in MAOA/B-KO mice. Following 5-HTP, serotonin levels were further increased similar to 4.5-6.2-fold in MAOA/B-KO mice. These exaggerated responses are in line with the exaggerated responses following serotonin-enhancing drugs that we previously observed in mice lacking the serotonin transporter (SERT). These findings provide a second genetic mouse model suggestive of possible human vulnerability to the serotonin syndrome in individuals with lesser-expressing MAO or SERT polymorphisms that confer serotonergic system changes.
C1 [Fox, M. A.; Panessiti, M. G.; Moya, P. R.; Tolliver, T. J.; Murphy, D. L.] NIMH, LCS, NIH, Bethesda, MD 20892 USA.
[Chen, K.; Shih, J. C.] Univ So Calif, Sch Pharm, Dept Pharmacol & Pharmaceut Sci, Los Angeles, CA USA.
[Shih, J. C.] Univ So Calif, Keck Sch Med, Dept Cell & Neurobiol, Los Angeles, CA 90033 USA.
RP Fox, MA (reprint author), NIMH, LCS, NIH, 10 Ctr Dr,Bldg 10-3D41,MSC 1264, Bethesda, MD 20892 USA.
EM mfox@mail.nih.gov
FU NIMH; NIH, NIMH [RO1-MH39085]; Boyd and Elsie Welin Professorship
FX This research was supported by the NIMH Intramural Research Program and
by NIH, NIMH RO1-MH39085 and the Boyd and Elsie Welin Professorship to
JCS.
NR 73
TC 2
Z9 2
U1 2
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1470-269X
EI 1473-1150
J9 PHARMACOGENOMICS J
JI Pharmacogenomics J.
PD DEC
PY 2013
VL 13
IS 6
BP 551
EP 557
DI 10.1038/tpj.2012.35
PG 7
WC Genetics & Heredity; Pharmacology & Pharmacy
SC Genetics & Heredity; Pharmacology & Pharmacy
GA 258HJ
UT WOS:000327449700011
PM 22964922
ER
PT J
AU Rao, M
AF Rao, Mahendra
TI Anthony Atala (ed): Progenitor and Stem Cell Technologies and Therapies
SO STEM CELL REVIEWS AND REPORTS
LA English
DT Editorial Material
C1 NIH, Ctr Regenerat Med, Bethesda, MD 20892 USA.
RP Rao, M (reprint author), NIH, Ctr Regenerat Med, Bldg 10, Bethesda, MD 20892 USA.
EM mahendra.rao@nih.gov
NR 0
TC 0
Z9 0
U1 1
U2 5
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1550-8943
EI 1558-6804
J9 STEM CELL REV REP
JI Stem Cell Rev. Rep.
PD DEC
PY 2013
VL 9
IS 6
BP 873
EP 873
DI 10.1007/s12015-013-9471-2
PG 1
WC Cell & Tissue Engineering; Cell Biology; Medicine, Research &
Experimental
SC Cell Biology; Research & Experimental Medicine
GA 257LT
UT WOS:000327386500012
ER
PT J
AU Alberts, MJ
Wechsler, LR
Jensen, MEL
Latchaw, RE
Crocco, TJ
George, MG
Baranski, J
Bass, RR
Ruff, RL
Huang, J
Mancini, B
Gregory, T
Gress, D
Emr, M
Warren, M
Walker, MD
AF Alberts, Mark J.
Wechsler, Lawrence R.
Jensen, Mary E. Lee
Latchaw, Richard E.
Crocco, Todd J.
George, Mary G.
Baranski, James
Bass, Robert R.
Ruff, Robert L.
Huang, Judy
Mancini, Barbara
Gregory, Tammy
Gress, Daryl
Emr, Marian
Warren, Margo
Walker, Michael D.
TI Formation and Function of Acute Stroke-Ready Hospitals Within a Stroke
System of Care Recommendations From the Brain Attack Coalition
SO STROKE
LA English
DT Article
DE acute stroke; cerebrovascular disease; stroke
ID ACUTE ISCHEMIC-STROKE; TISSUE-PLASMINOGEN ACTIVATOR; EMERGENCY
MEDICAL-SERVICES; NORTH-CAROLINA STROKE; POLICY STATEMENT;
GUIDELINES-STROKE; PILOT PROJECT; UNITED-STATES; ASSOCIATION; CENTERS
AB Background and Purpose Many patients with an acute stroke live in areas without ready access to a Primary or Comprehensive Stroke Center. The formation of care facilities that meet the needs of these patients might improve their care and outcomes and guide them and emergency responders to such centers within a stroke system of care.
Methods The Brain Attack Coalition conducted an electronic search of the English medical literature from January 2000 to December 2012 to identify care elements and processes shown to be beneficial for acute stroke care. We used evidence grading and consensus paradigms to synthesize recommendations for Acute Stroke-Ready Hospitals (ASRHs).
Results Several key elements for an ASRH were identified, including acute stroke teams, written care protocols, involvement of emergency medical services and emergency department, and rapid laboratory and neuroimaging testing. Unique aspects include the use of telemedicine, hospital transfer protocols, and drip and ship therapies. Emergent therapies include the use of intravenous tissue-type plasminogen activator and the reversal of coagulopathies. Although many of the care elements are similar to those of a Primary Stroke Center, compliance rates of 67% are suggested in recognition of the staffing, logistical, and financial challenges faced by rural facilities.
Conclusions ASRHs will form the foundation for acute stroke care in many settings. Recommended elements of an ASRH build on those proven to improve care and outcomes at Primary Stroke Centers. The ASRH will be a key component for patient care within an evolving stroke system of care.
C1 [Alberts, Mark J.] Univ Texas Southwestern, Dept Neurol & Neurotherapeut, Dallas, TX USA.
[Wechsler, Lawrence R.] Univ Pittsburgh, Dept Neurol, Pittsburgh, PA 15260 USA.
[Jensen, Mary E. Lee] Univ Virginia, Dept Radiol & Med Imaging, Charlottesville, VA USA.
[Gress, Daryl] Univ Virginia, Dept Neurol, Charlottesville, VA USA.
[Latchaw, Richard E.] UC Davis Med Ctr, Dept Radiol, Davis, CA USA.
[Crocco, Todd J.] W Virginia Univ, Dept Emergency Med, Morgantown, WV 26506 USA.
[George, Mary G.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Baranski, James] Natl Stroke Assoc, Englewood, CO USA.
[Bass, Robert R.] Natl Assoc EMS Officials, Falls Church, VA USA.
[Ruff, Robert L.] VA Med Ctr, Dept Neurol, Cleveland, OH USA.
[Huang, Judy] Johns Hopkins Univ Hosp, Dept Neurosurg, Baltimore, MD 21287 USA.
[Mancini, Barbara] Inova Inc, San Diego, CA USA.
[Gregory, Tammy] Amer Heart Assoc, Dallas, TX USA.
[Emr, Marian; Warren, Margo; Walker, Michael D.] NINDS, Bethesda, MD 20892 USA.
RP Alberts, MJ (reprint author), Univ Texas SW Med Ctr Dallas, Dept Neurol & Neurotherapeut, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM Mark.Alberts@UTSouthwestern.edu
NR 58
TC 14
Z9 15
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD DEC
PY 2013
VL 44
IS 12
BP 3382
EP 3393
DI 10.1161/STROKEAHA.113.002285
PG 12
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 257LR
UT WOS:000327386300309
PM 24222046
ER
PT J
AU Meltzer, JA
Chu, R
Braun, AR
AF Meltzer, J. A.
Chu, R.
Braun, A. R.
TI Detection and Quantification of Functional Lesions from Slowing in
Resting-State MEG
SO STROKE
LA English
DT Meeting Abstract
CT Canadian Stroke Congress
CY OCT 17-20, 2013
CL Montreal, CANADA
C1 [Meltzer, J. A.] Baycrest, Rotman Res Inst, Toronto, ON, Canada.
[Chu, R.] Univ Toronto, Toronto, ON, Canada.
[Braun, A. R.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD DEC
PY 2013
VL 44
IS 12
BP E177
EP E178
PG 2
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 257LR
UT WOS:000327386300022
ER
PT J
AU Palesch, YY
Martin, RH
Hill, MD
Tamariz, D
Jauch, EC
Weng, Y
Speiser, JL
Woolson, RF
Barsan, WG
Moy, CS
Ginsberg, MD
AF Palesch, Y. Y.
Martin, R. H.
Hill, M. D.
Tamariz, D.
Jauch, E. C.
Weng, Y.
Speiser, J. L.
Woolson, R. F.
Barsan, W. G.
Moy, C. S.
Ginsberg, M. D.
TI Meta-analysis of Albumin in Acute Stroke (ALIAS) Parts 1 and 2 Trials
SO STROKE
LA English
DT Meeting Abstract
CT Canadian Stroke Congress
CY OCT 17-20, 2013
CL Montreal, CANADA
C1 [Palesch, Y. Y.; Martin, R. H.; Jauch, E. C.; Weng, Y.; Speiser, J. L.; Woolson, R. F.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Hill, M. D.] Univ Calgary, Calgary, AB, Canada.
[Tamariz, D.; Ginsberg, M. D.] Univ Miami, Miami, FL USA.
[Barsan, W. G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Moy, C. S.] NINDS, Bethesda, MD 20892 USA.
RI Hill, Michael/C-9073-2012
OI Hill, Michael/0000-0002-6269-1543
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD DEC
PY 2013
VL 44
IS 12
BP E209
EP E209
PG 1
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 257LR
UT WOS:000327386300185
ER
PT J
AU Castaneto, MS
Barnes, AJ
Scheidweiler, KB
Schaffer, M
Rogers, KK
Stewart, D
Huestis, MA
AF Castaneto, Marisol S.
Barnes, Allan J.
Scheidweiler, Karl B.
Schaffer, Michael
Rogers, Kristen K.
Stewart, Deborah
Huestis, Marilyn A.
TI Identifying Methamphetamine Exposure in Children
SO THERAPEUTIC DRUG MONITORING
LA English
DT Article
DE hair; urine; oral fluid; drug-exposed children; methamphetamine
ID ORAL FLUID; MENTAL-HEALTH; HAIR SAMPLES; LABORATORIES; MANUFACTURE;
COCAINE; URINE; ABUSE; MDMA; AMPHETAMINE
AB Objective:Methamphetamine (MAMP) use, distribution, and manufacture remain a serious public health and safety problem in the United States, and children environmentally exposed to MAMP face a myriad of developmental, social, and health risks, including severe abuse and neglect necessitating child protection involvement. It is recommended that drug-endangered children receive medical evaluation and care with documentation of overall physical and mental conditions and have urine drug testing. The primary aim of this study was to determine the best biological matrix to detect MAMP, amphetamine (AMP), methylenedioxymethamphetamine (MDMA), methylenedioxyamphetamine (MDA), and 3,4-methylenedioxyethylamphetamine (MDEA) in environmentally exposed children.Methods:Ninety-one children, environmentally exposed to household MAMP intake, were medically evaluated at the Child and Adolescent Abuse Resource and Evaluation Diagnostic and Treatment Center at the University of California, Davis Children's Hospital. MAMP, AMP, MDMA, MDA, and MDEA were quantified in urine and oral fluid (OF) by gas chromatography mass spectrometry and in hair by liquid chromatography tandem mass spectrometry.Results:Overall drug detection rates in OF, urine, and hair were 6.9%, 22.1%, and 77.8%, respectively. Seventy children (79%) tested positive for 1 or more drugs in 1 or more matrices. MAMP was the primary analyte detected in all 3 biological matrices. All positive OF (n = 5), and 18 of 19 positive urine specimens also had a positive hair test.Conclusions:Hair analysis offered a more sensitive tool for identifying MAMP, AMP, and MDMA environmental exposure in children than urine or OF testing. A negative urine or hair test does not exclude the possibility of drug exposure, but hair testing provided the greatest sensitivity for identifying drug-exposed children.
C1 [Castaneto, Marisol S.; Barnes, Allan J.; Scheidweiler, Karl B.; Huestis, Marilyn A.] NIDA, IRP, NIH, Baltimore, MD 21224 USA.
[Schaffer, Michael] Psychemed Corp, Culver City, CA USA.
[Rogers, Kristen K.] Calif Dept Publ Hlth, Data Benchmark & Evaluat Sect, Maternal Child & Adolescent Hlth Div, Sacramento, CA USA.
[Stewart, Deborah] Calif State Univ Chico, Student Hlth Serv, Chico, CA 95929 USA.
RP Huestis, MA (reprint author), NIDA, IRP, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mhuestis@nida.nih.gov
FU National Institutes on Drug Abuse
FX Supported by the Intramural Research Program, National Institutes on
Drug Abuse and National Institutes of Health, University of California,
Davis, Psychemedics, Corporation (hair testing and results).
NR 39
TC 3
Z9 3
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0163-4356
EI 1536-3694
J9 THER DRUG MONIT
JI Ther. Drug Monit.
PD DEC
PY 2013
VL 35
IS 6
BP 823
EP 830
DI 10.1097/FTD.0b013e31829685b2
PG 8
WC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology
SC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology
GA 256LQ
UT WOS:000327312200012
PM 24263642
ER
PT J
AU Gonzales, JM
Law, SHW
AF Gonzales, John M., Jr.
Law, Sheran Hiu Wan
TI Feed and Feeding Regime Affect Growth Rate and Gonadosomatic Index of
Adult Zebrafish (Danio Rerio)
SO ZEBRAFISH
LA English
DT Article
ID TILAPIA OREOCHROMIS-NILOTICUS; BASS DICENTRARCHUS-LABRAX; VARYING
DIETARY-PROTEIN; FATTY-ACID-COMPOSITION; REPRODUCTIVE-PERFORMANCE;
CLARIAS-GARIEPINUS; NILE TILAPIA; BROODSTOCK NUTRITION;
HAMILTON-BUCHANAN; FEMALE ZEBRAFISH
AB A 5-week study was conducted to evaluate commercially available Artemia, Ziegler zebrafish diet, and Calamac diet fed in five different feeding regimes on the growth and reproductive development of 7-month-old zebrafish. Zebrafish were fed to satiation three times daily during the normal work week and twice daily during the weekend and holidays. Zebrafish in dietary groups CCC (Calamac three times daily) and CCA (Calamac twice daily, Artemia once daily) had a significantly (p<0.05) greater weight gain and specific growth rate as compared to all other dietary groups. Male zebrafish in dietary group 5 had significantly larger gonadosomatic index (GSI) values than all other groups, while female zebrafish in dietary group CCC had significantly larger GSI values than all other groups. No differences in the fatty acid content of female gonads were detected. Zebrafish fed solely Artemia had the greatest weight loss and lowest GSI values. Preliminary evidence of protein sparing in zebrafish is reported. Collectively, this study sheds more light into the effects of the use of commercially available feeds and feeding regime on the rearing of zebrafish.
C1 [Gonzales, John M., Jr.; Law, Sheran Hiu Wan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Gonzales, JM (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, 6 Ctr Dr, Bethesda, MD 20892 USA.
EM gonzaljo@mail.nih.gov
FU American Association for the Laboratory Animal Science; Intramural
Research Program of the NIH, Eunice Kennedy Shriver National Institute
of Child Health and Human Development
FX We would like to thank Dr. Igor Dawid for the use of fish, laboratory
space, manuscript review, and other resources made available during the
course of this study. We would also like to thank the Charles River
aquatics husbandry staff at the NICHD for their involvement with this
study. We would like to thank Mr. Dennis Barnard for his input and
review of the manuscript. We also appreciate all the comments provided
by the reviewers in completing this manuscript. This work was supported
by grants for Laboratory Animal Science (GLAS) from the American
Association for the Laboratory Animal Science. This research was party
supported by the Intramural Research Program of the NIH, Eunice Kennedy
Shriver National Institute of Child Health and Human Development.
NR 62
TC 4
Z9 4
U1 1
U2 23
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1545-8547
EI 1557-8542
J9 ZEBRAFISH
JI Zebrafish
PD DEC 1
PY 2013
VL 10
IS 4
BP 532
EP 540
DI 10.1089/zeb.2013.0891
PG 9
WC Developmental Biology; Zoology
SC Developmental Biology; Zoology
GA 255DH
UT WOS:000327219100011
PM 23902461
ER
PT J
AU Choi, SE
Fu, T
Seok, S
Kim, DH
Yu, E
Lee, KW
Kang, Y
Li, XL
Kemper, B
Kemper, JK
AF Choi, Sung-E
Fu, Ting
Seok, Sunmi
Kim, Dong-Hyun
Yu, Eunkyung
Lee, Kwan-Woo
Kang, Yup
Li, Xiaoling
Kemper, Byron
Kemper, Jongsook K.
TI Elevated microRNA-34a in obesity reduces NAD(+) levels and SIRT1
activity by directly targeting NAMPT
SO AGING CELL
LA English
DT Article
DE deacetylation; diabetes; miR-34a; resveratrol; sirtuins; steatosis
ID METABOLIC DISEASE; RESVERATROL; SIRTUINS; DIET; PROTECTS; BIOSYNTHESIS;
INHIBITION; ACTIVATION; EXPRESSION; PATHWAY
AB SIRT1 is an NAD(+)-dependent deacetylase that is implicated in prevention of many age-related diseases including metabolic disorders. As SIRT1 deacetylase activity is dependent on NAD(+) levels and the development of compounds that directly activate SIRT1 has been controversial, indirectly activating SIRT1 through enhancing NAD(+) bioavailability has received increasing attention. NAD(+) levels are reduced in obesity and the aged, but the underlying mechanisms remain unclear. We recently showed that hepatic microRNA-34a (miR-34a), which is elevated in obesity, directly targets and decreases SIRT1 expression. Here, we further show that miR-34a reduces NAD(+) levels and SIRT1 activity by targeting NAMPT, the rate-limiting enzyme for NAD(+) biosynthesis. A functional binding site for miR-34a is present in the 3 UTR of NAMPT mRNA. Hepatic overexpression of miR-34a reduced NAMPT/NAD(+) levels, increased acetylation of the SIRT1 target transcriptional regulators, PGC-1, SREBP-1c, FXR, and NF-B, and resulted in obesity-mimetic outcomes. The decreased NAMPT/NAD(+) levels were independent of miR-34a effects on SIRT1 levels as they were also observed in SIRT1 liver-specific knockout mice. Further, the miR-34a-mediated decreases were reversed by treatment with the NAD(+) intermediate, nicotinamide mononucleotide. Conversely, antagonism of miR-34a in diet-induced obese mice restored NAMPT/NAD(+) levels and alleviated steatosis, inflammation, and glucose intolerance. Anti-miR-34a-mediated increases in NAD(+) levels were attenuated when NAMPT was downregulated. Our findings reveal a novel function of miR-34a in reducing both SIRT1 expression and activity in obesity. The miR-34a/NAMPT axis presents a potential target for treating obesity- and aging-related diseases involving SIRT1 dysfunction like steatosis and type 2 diabetes.
C1 [Choi, Sung-E; Fu, Ting; Seok, Sunmi; Kim, Dong-Hyun; Yu, Eunkyung; Kemper, Byron; Kemper, Jongsook K.] Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
[Lee, Kwan-Woo] Ajou Univ, Sch Med, Dept Endocrinol & Metab, Suwon 442749, South Korea.
[Kang, Yup] Ajou Univ, Sch Med, Inst Med Sci, Suwon 442749, South Korea.
[Li, Xiaoling] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
RP Kemper, JK (reprint author), Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
EM jongsook@illinois.edu
FU Korean Health 21 R&D Project, Ministry of Health and Welfare [A102065];
MRC [2012-051426]; National Institutes of Health [DK62777, DK95842];
American Diabetes Association
FX This study was supported by a grant from the Korean Health 21 R&D
Project, Ministry of Health and Welfare (A102065) to K. W. Lee and a
grant from MRC 2012-051426 to Y. Kang, and grants from National
Institutes of Health (DK62777 and DK95842) and a Basic Science Award
from the American Diabetes Association to J. K. Kemper.
NR 42
TC 54
Z9 56
U1 1
U2 28
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD DEC
PY 2013
VL 12
IS 6
BP 1062
EP 1072
DI 10.1111/acel.12135
PG 11
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 255AN
UT WOS:000327211700013
PM 23834033
ER
PT J
AU Tembhare, PR
Marti, G
Wiestner, A
Degheidy, H
Farooqui, M
Kreitman, RJ
Jasper, GA
Yuan, CM
Liewehr, D
Venzon, D
Stetler-Stevenson, M
AF Tembhare, Prashant R.
Marti, Gerald
Wiestner, Adrian
Degheidy, Heba
Farooqui, Mohammed
Kreitman, Robert J.
Jasper, Gregory A.
Yuan, Constance M.
Liewehr, David
Venzon, David
Stetler-Stevenson, Maryalice
TI Quantification of Expression of Antigens Targeted by Antibody-Based
Therapy in Chronic Lymphocytic Leukemia
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Chronic lymphocytic leukemia; Antibody therapy; Rituximab; Alemtuzumab;
Quantitative flow cytometry
ID QUANTITATIVE FLOW-CYTOMETRY; IMMUNOTOXIN RFB4(DSFV)-PE38 BL22; B-CELL
LEUKEMIAS; PHASE-I TRIAL; CD20 EXPRESSION; LYMPHOPROLIFERATIVE
DISORDERS; ALEMTUZUMAB CAMPATH-1H; RESIDUAL DISEASE; RITUXIMAB;
FLUDARABINE
AB Objectives: Anti-CD20 (rituximab), anti-CD52 (alemtuzumab), anti-CD22 (BL22, HA22), and anti-CD25 (Oncotac) are therapeutic options that are the mainstay or in preclinical development for the treatment of chronic lymphocytic leukemia (CLL). Studies suggest that levels of surface antigen expression may affect response to monoclonal antibody-based therapy.
Methods: Using the flow cytometric Quantibrite method (BD Biosciences, San Jose, CA) to determine antibodies bound per cell, we quantified the levels of surface expression of CD20, CD22, CD25, and CD52 in CLL cells from 28 untreated patients.
Results: The CLL cells in all cases expressed CD20, CD22, and CD52 but 4 (14%) cases were negative for CD25. Although the ranking of levels of expression from highest to lowest was CD52, CD20, CD22, and CD25, the level of antigen expression on any specific case could not be accurately predicted.
Conclusions: Quantification of antigens might be useful in evaluating new antigens to target for therapy and may provide a systematic approach to selecting individualized therapy in CLL. (C) American Society for Clinical Pathology
C1 [Tembhare, Prashant R.; Jasper, Gregory A.; Yuan, Constance M.; Stetler-Stevenson, Maryalice] NCI, Flow Cytometry Unit, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Kreitman, Robert J.] NCI, Lab Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Liewehr, David; Venzon, David] NCI, Biostat & Data Management Sect, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Marti, Gerald; Degheidy, Heba] US FDA, Ctr Biol Evaluat & Res, Silver Spring, MD USA.
[Wiestner, Adrian; Farooqui, Mohammed] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Stetler-Stevenson, M (reprint author), NCI, Flow Cytometry Unit, Pathol Lab, Ctr Canc Res,NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM stetler@mail.nih.gov
FU Intramural NIH HHS [Z01 BC011104-01]
NR 31
TC 6
Z9 7
U1 0
U2 6
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD DEC
PY 2013
VL 140
IS 6
BP 813
EP 818
DI 10.1309/AJCPYFQ4XMGJD6TI
PG 6
WC Pathology
SC Pathology
GA 255ZX
UT WOS:000327280400007
PM 24225748
ER
PT J
AU Godfrey, CC
Michelow, PM
Godard, M
Sahasrabuddhe, VV
Darden, J
Firnhaber, CS
Wetherall, NT
Bremer, J
Coombs, RW
Wilkin, T
AF Godfrey, Catherine C.
Michelow, Pamela M.
Godard, Mandana
Sahasrabuddhe, Vikrant V.
Darden, Janice
Firnhaber, Cynthia S.
Wetherall, Neal T.
Bremer, James
Coombs, Robert W.
Wilkin, Timothy
CA A5282 Study Team
TI Improving Diagnostic Capability for HPV Disease Internationally Within
the NIH-NIAID Division of AIDS Clinical Trial Networks
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE External quality assurance; EQA; HPV; Cervical pathology; Cervical
cytology; Histopathology; HPV DNA testing
ID SQUAMOUS INTRAEPITHELIAL LESIONS; EXTERNAL QUALITY-ASSURANCE;
CERVICAL-CANCER PREVENTION; HIV-INFECTED WOMEN; DEVELOPING-COUNTRIES;
POSITIVE WOMEN; MORTALITY; CYTOLOGY; RISK; INDIA
AB Objectives: To evaluate an external quality assurance (EQA) program for the laboratory diagnosis of human papillomavirus (HPV) disease that was established to improve international research capability within the Division of AIDS at the National Institute of Allergy and Infectious Disease supported Adult AIDS Clinical Trials Group network.
Methods: A three-component EQA scheme was devised comprising assessments of diagnostic accuracy of cytotechnologists and pathologists using available EQA panels, review of quality and accuracy of clinical slides from local sites by an outside expert, and HPV DNA detection using a commercially available HPV test kit.
Results: Seven laboratories and 17 pathologists in Africa, India, and South America participated EQA scores were suboptimal for EQA proficiency testing panels in three of seven laboratories. There was good agreement between the local laboratory and the central reader 70% of the time (90% confidence interval, 42%-98%). Performance on the College of American Pathologists' HPV DNA testing panel was successful in all laboratories tested
Conclusions: The prequalifying EQA round identified correctable issues that will improve the laboratory diagnosis of HPV-related cervical disease at the participating international study sites and will provide a mechanism for ongoing education and continuous quality improvement. American Society for Clinical Pathology
C1 [Godfrey, Catherine C.] NIAID, NIH, Bethesda, MD 20892 USA.
[Michelow, Pamela M.] Univ Witwatersrand, Fac Hlth Sci, Cytol Unit, Johannesburg, South Africa.
[Michelow, Pamela M.] Natl Hlth Lab Serv, Johannesburg, South Africa.
[Godard, Mandana] Johns Hopkins Univ, Patient Safety Monitoring Int Labs SMILE, Baltimore, MD USA.
[Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Vanderbilt Inst Global Hlth, Nashville, TN 37235 USA.
[Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
[Darden, Janice] Social & Sci Syst, Silver Spring, MD USA.
[Firnhaber, Cynthia S.] Univ Witwatersrand, Fac Hlth Sci, Dept Internal Med, Clin HIV Res Unit, Johannesburg, South Africa.
[Firnhaber, Cynthia S.] Right Care, Johannesburg, South Africa.
[Wetherall, Neal T.] HJF DAIDS, Bethesda, MD USA.
[Bremer, James] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Coombs, Robert W.] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA.
[Coombs, Robert W.] Univ Washington, Dept Med, Seattle, WA USA.
[Wilkin, Timothy] Weill Cornell Med Coll, Div Infect Dis, New York, NY USA.
RP Godfrey, CC (reprint author), NIAID, NIH, 6700 B Rockledge Dr, Bethesda, MD 20892 USA.
EM Cgodfrey@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases [UM1 AI068636, UM1
AI069463-07, AI38858]
FX The project described was supported by award numbers UM1 AI068636
(C.S.F., R.W.C., and T. W.), UM1 AI069463-07 (C.S.F.), AI38858 (C.S.F.,
R.W.C., and T.W), AI27757 (R.W.C.) from the National Institute of
Allergy and Infectious Diseases and supported by National Institute of
Mental Health and National Institute of Dental and Craniofacial
Research. This project has been funded in whole or in part with federal
funds from the National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Department of Health and Human Services,
under contract numbers HHSN2722008000I4C (NT. W), HHSN272201300004C
(MG.), and HHSN272201200023C (J.B). 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.
NR 31
TC 3
Z9 3
U1 0
U2 1
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD DEC
PY 2013
VL 140
IS 6
BP 881
EP 889
DI 10.1309/AJCPIBIS19QIYHJY
PG 9
WC Pathology
SC Pathology
GA 255ZX
UT WOS:000327280400016
PM 24225757
ER
PT J
AU Shah, MT
Zonderman, AB
Waldstein, SR
AF Shah, Mauli T.
Zonderman, Alan B.
Waldstein, Shari R.
TI Sex and Age Differences in the Relation of Depressive Symptoms With
Blood Pressure
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
DE age factors; blood pressure; depressive symptoms; hypertension;
longitudinal studies; older adults; repeated measures; sex factors;
women
ID CARDIOVASCULAR-DISEASE; RISK-FACTORS; HEART-DISEASE; LATE-LIFE; CES-D;
HYPERTENSION; ANXIETY; WOMEN; METAANALYSIS; MODELS
AB BACKGROUND
Longitudinal associations between depressive symptoms and blood pressure have been inconsistent. Most studies have examined incident hypertension as an outcome, and few have examined effect modification.
METHODS
This study examined moderating influences of sex and age on coincident trajectories of depressive symptoms and blood pressure among 2,087 participants from the Baltimore Longitudinal Study of Aging (aged 19-97 years; 53% men; 74% white). Participants underwent clinical blood pressure measurement and completed the Center for Epidemiological Studies-Depression (CES-D) scale on up to 14 occasions (mean = 3.8; SD = 2.6) over up to 29 years (mean = 7.8; SD = 6.4). CES-D was log-transformed (CES-D(log)) for analyses.
RESULTS
Mixed-effects regression revealed that prospective relations of CESD(log) to diastolic blood pressure differed by age in women (b = 0.095; P = 0.001) but not men; greater CES-D(log) attenuated the expected age-related decline in diastolic blood pressure. Across all testing sessions, greater CES-D(log) was associated significantly with higher average systolic blood pressure for women (b = 2.238; P = 0.006) but not men. Age-stratified analyses showed that greater CES-D(log) was associated significantly with higher average systolic (b = 3.348; P = 0.02) and diastolic (b = 1.730; P < 0.03) blood pressure for older adults (>= 58.8 years at first visit). In the younger age cohort, sex moderated the relation of CES-D(log) to systolic blood pressure (b = -3.563; P = 0.007); greater CES-D(log) in women, but lesser CES-D(log) in men, was associated with higher systolic blood pressure.
CONCLUSIONS
Results demonstrate sex and age differences in the relation between depressive symptoms and blood pressure. Findings suggest the potential importance of preventing, detecting, and lowering depressive symptoms to prevent hypertension among women and older adults.
C1 [Shah, Mauli T.; Waldstein, Shari R.] Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA.
[Shah, Mauli T.; Zonderman, Alan B.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Waldstein, Shari R.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
RP Shah, MT (reprint author), Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA.
EM maulishah@umbc.edu
OI Zonderman, Alan B/0000-0002-6523-4778
FU Intramural NIH HHS
NR 40
TC 7
Z9 8
U1 0
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0895-7061
EI 1941-7225
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD DEC
PY 2013
VL 26
IS 12
BP 1413
EP 1420
DI 10.1093/ajh/hpt135
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 251IW
UT WOS:000326922700008
PM 23959543
ER
PT J
AU George, MD
Wine, RN
Lackford, B
Kissling, GE
Akiyama, SK
Olden, K
Roberts, JD
AF George, Margaret D.
Wine, Robert N.
Lackford, Brad
Kissling, Grace E.
Akiyama, Steven K.
Olden, Kenneth
Roberts, John D.
TI p38 mitogen-activated protein kinase interacts with vinculin at focal
adhesions during fatty acid-stimulated cell adhesion
SO BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE
LA English
DT Article
DE p38 MAP kinase; vinculin; signal transduction; arachidonic acid; cell
adhesion
ID BREAST-CARCINOMA CELLS; HEAT-SHOCK PROTEINS; COLLAGEN TYPE-IV;
ARACHIDONIC-ACID; MAP KINASE; TYROSINE PHOSPHORYLATION; TUMOR
MICROENVIRONMENT; INTEGRIN ACTIVATION; MATRIX ADHESION; CANCER-CELLS
AB Arachidonic acid stimulates cell adhesion by activating alpha 2 beta 1 integrins in a process that depends on protein kinases, including p38 mitogen activated protein kinase. Here, we describe the interaction of cytoskeletal components with key signaling molecules that contribute to the spreading of, and morphological changes in, arachidonic acid-treated MDA-MB-435 human breast carcinoma cells. Arachidonic acid-treated cells showed increased attachment and spreading on collagen type IV, as measured by electric cell-substrate impedance sensing. Fatty acid-treated cells displayed short cortical actin filaments associated with an increased number of beta 1 integrin-containing pseudopodia, whereas untreated cells displayed elongated stress fibers and fewer clusters of beta 1 integrins. Confocal microscopy of arachidonic acid-treated cells showed that vinculin and phospho-p38 both appeared enriched in pseudopodia and at the tips of actin filaments, and fluorescence ratio imaging indicated the increase was specific for the phospho-(active) form of p38. Immunoprecipitates of phospho-p38 from extracts of arachidonic acid-treated cells contained vinculin, and GST-vinculin fusion proteins carrying the central region of vinculin bound phospho-p38, whereas fusion proteins expressing the terminal portions of vinculin did not. These data suggest that phospho-p38 associates with particular domains on critical focal adhesion proteins that are involved in tumor cell adhesion and spreading, and that this association can be regulated by factors in the tumor microenvironment.
C1 [George, Margaret D.; Wine, Robert N.; Lackford, Brad; Kissling, Grace E.; Akiyama, Steven K.; Olden, Kenneth; Roberts, John D.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Roberts, JD (reprint author), NIEHS, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM roberts1@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences
FX We thank Dr. Kris DeMali of the University of Iowa and Dr. Keith
Burridge of the University of North Carolina at Chapel Hill for
providing the GST-vinculin DNA constructs. We thank Drs. Alex Merrick
and David Miller of NIEHS for providing critical advice on the
manuscript. We are grateful to Jeff Reece, Jeff Tucker, and Agnes
Janoshazi for help with the confocal microscopy and to Toni Smith for
carrying out initial spreading assays. This research was supported (in
part) by the Intramural Research Program of the NIH, National Institute
of Environmental Health Sciences.
NR 102
TC 1
Z9 1
U1 0
U2 9
PU CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
PI OTTAWA
PA 1200 MONTREAL ROAD, BUILDING M-55, OTTAWA, ON K1A 0R6, CANADA
SN 0829-8211
EI 1208-6002
J9 BIOCHEM CELL BIOL
JI Biochem. Cell Biol.
PD DEC
PY 2013
VL 91
IS 6
BP 404
EP 418
DI 10.1139/bcb-2013-0013
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 254DC
UT WOS:000327142700013
PM 24219282
ER
PT J
AU Avigan, D
Hari, P
Battiwalla, M
Bishop, MR
Giralt, SA
Hardy, NM
Kroger, N
Wayne, AS
Hsu, KC
AF Avigan, David
Hari, Parameswaran
Battiwalla, Minoo
Bishop, Michael R.
Giralt, Sergio A.
Hardy, Nancy M.
Kroeger, Nicolaus
Wayne, Alan S.
Hsu, Katharine C.
TI Proceedings from the National Cancer Institute's Second International
Workshop on the Biology, Prevention, and Treatment of Relapse after
Hematopoietic Stem Cell Transplantation: Part II. Autologous
Transplantation-Novel Agents and Immunomodulatory Strategies
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Relapse; Hematopoietic stem cell transplantation; Autologous;
Allogeneic; Multiple myeloma
ID ACUTE MYELOID-LEUKEMIA; NATURAL-KILLER-CELLS; MINIMAL RESIDUAL DISEASE;
WT1 PEPTIDE VACCINATION; ACUTE MYELOGENOUS LEUKEMIA; EARLY LYMPHOCYTE
RECOVERY; CYTOTOXIC T-LYMPHOCYTES; NEWLY-DIAGNOSED MYELOMA;
MULTIPLE-MYELOMA; DENDRITIC CELLS
AB In the National Cancer Institute's Second International Workshop on the Biology, Prevention, and Treatment of Relapse after Hematopoietic Stem Cell Transplantation, the Scientific/Educational Session on Autologous Transplantation addressed the role of novel agents and immunomodulatory strategies in management of relapse after autologous hematopoietic stem cell transplantation (AHSCT). Concepts were illustrated through in-depth discussion of multiple myeloma, with broader discussion of areas relevant for relapse of other malignancies as well as in the setting of allogeneic transplantation. Dr. Hari provided an overview of the epidemiology of relapse after AHSCT in multiple myeloma, addressing clinical patterns, management implications, and treatment options at relapse, highlighting the implications of novel therapeutic agents in initial, maintenance, and relapse treatment. Dr. Avigan discussed current concepts in tumor vaccine design, including whole cell and antigen-specific strategies, use of an AHSCT platform to reverse tumor-associated immunosuppression and tolerance, and combining vaccines with immunomodulatory agents to promote establishment of durable antitumor immunity. Dr. Hsu reviewed the immunogenetics of natural killer (NK) cells and general NK biology, the clinical importance of autologous NK activity (eg, lymphoma and neuroblastoma), the impact of existing therapies on promotion of NK cell activity (eg, immunomodulatory drugs, monoclonal antibodies), and strategies for enhancing autologous and allogeneic NK cell effects through NK cell gene profiling. Published by Elsevier Inc. on behalf of American Society for Blood and Marrow Transplantation.
C1 [Avigan, David] Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Hematol Malignancies Bone Marrow Transplant Progr, Boston, MA 02215 USA.
[Hari, Parameswaran] Med Coll Wisconsin, Div Hematol & Oncol, Milwaukee, WI 53226 USA.
[Battiwalla, Minoo] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bishop, Michael R.] Univ Chicago, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Giralt, Sergio A.; Hsu, Katharine C.] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
[Hardy, Nancy M.] NCI, Expt Transplantat Immunol Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
[Kroeger, Nicolaus] Univ Med Ctr Hamburg Eppendorf, Dept Stem Cell Transplantat, Hamburg, Germany.
[Wayne, Alan S.] NCI, Pediat Oncol Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
[Wayne, Alan S.] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles, Current Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90033 USA.
RP Hardy, NM (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Hatfield Clin Res Ctr, 10 Ctr Dr,Room 3E-3330, Bethesda, MD 20892 USA.
EM hardyn@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute, Center for Cancer Research; National Heart,
Lung and Blood Institute
FX Financial disclosure: Supported in part by the Intramural Research
Program of the National Institutes of Health, National Cancer Institute,
Center for Cancer Research, and National Heart, Lung and Blood
Institute.
NR 97
TC 4
Z9 4
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD DEC
PY 2013
VL 19
IS 12
BP 1661
EP 1669
DI 10.1016/j.bbmt.2013.08.011
PG 9
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 257CL
UT WOS:000327361100003
PM 24018393
ER
PT J
AU Pedone, C
Scarlata, S
Napoli, N
Lauretani, F
Bandinelli, S
Ferrucci, L
Incalzi, RA
AF Pedone, Claudio
Scarlata, Simone
Napoli, Nicola
Lauretani, Fulvio
Bandinelli, Stefania
Ferrucci, Luigi
Incalzi, Raffaele Antonelli
TI Relationship Between Bone Cross-Sectional Area and Indices of Peripheral
Artery Disease
SO CALCIFIED TISSUE INTERNATIONAL
LA English
DT Article
DE Bone cross-sectional area; Peripheral artery disease; Osteoporosis;
Atherosclerosis; Women; Elderly
ID MINERAL DENSITY; VITAMIN-D; POSTMENOPAUSAL WOMEN; CORONARY-ARTERY;
CARDIOVASCULAR-DISEASE; AORTIC CALCIUM; FRACTURE RISK; ATHEROSCLEROSIS;
CALCIFICATION; OSTEOPOROSIS
AB Most studies on the relationship between bone mineral density and atherosclerosis have used dual-energy X-ray absorptiometry, but this method is relatively insensitive to bone geometry. The aim of this study was to investigate the relationship between bone area and indices of carotid and peripheral atherosclerosis. We studied 841 persons aged 65 years or older (women = 444, mean age 73.8 years; men = 397, mean age = 75.3 years) enrolled in the InCHIANTI study and free from active malignancies, chronic use of bisphosphonates or steroids, and estrogen replacement therapy. The tibial cortical and total cross-sectional area (CSA) were measured by peripheral quantitative computed tomography and their ratio was calculated (cortical/total cross-sectional area ratio, cCSA/tCSA); carotid plaques were screened by echography, and peripheral artery disease (PAD) was defined as an ankle/brachial index < 0.9 or presence of intermittent claudication. No association between cCSA/tCSA and atherosclerosis was observed in men. In women, lower cCSA/tCSA was associated with both carotid plaques [odds ratio (OR) for lowest vs. best quartile = 2.09, 95 % confidence interval (CI) 1.2-3.68] and PAD (OR = 3.43, 95 % CI 1.58-8.12). After correction for potential confounders (age since menopause, body mass index, Parathyroid hormone, vitamin D, leptin, DHEA-S, testosterone, physical activity, chronic obstructive pulmonary disease, and reduced renal function), the association was not confirmed. According to partial logistic regression, the carotid plaque-cCSA/tCSA association, but not the PAD-cCSA/tCSA association, was mostly dependent on years since menopause. In women the association between osteoporosis and carotid plaques likely reflects hormonal deprivation, whereas that between osteoporosis and PAD seems multifactorial in origin.
C1 [Pedone, Claudio; Scarlata, Simone; Incalzi, Raffaele Antonelli] Campus Biomed Univ & Teaching Hosp, Area Geriatr, I-00128 Rome, Italy.
[Napoli, Nicola] Campus Biomed Univ & Teaching Hosp, Div Endocrinol, I-00128 Rome, Italy.
[Lauretani, Fulvio] Univ Hosp Parma, Geriatr & Rehabil Dept, Geriatr Unit, Parma, Italy.
[Lauretani, Fulvio] Univ Hosp Parma, Geriatr & Rehabil Dept, Lab Movement Anal, Parma, Italy.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Rehabil Unit, Florence, Italy.
[Ferrucci, Luigi] NIA, Longitudinal Study Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[Incalzi, Raffaele Antonelli] San Raffaele Cittadella Carita Fdn, Taranto, Italy.
RP Pedone, C (reprint author), Campus Biomed Univ & Teaching Hosp, Area Geriatr, Via Alvaro Portillo 200, I-00128 Rome, Italy.
EM c.pedone@unicampus.it
RI Scarlata, Simone/G-6490-2010; Lauretani, Fulvio/K-5115-2016
OI Scarlata, Simone/0000-0002-2704-2708; Napoli,
Nicola/0000-0002-3091-8205; Pedone, Claudio/0000-0003-1847-9032;
Lauretani, Fulvio/0000-0002-5287-9972
NR 36
TC 2
Z9 2
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0171-967X
EI 1432-0827
J9 CALCIFIED TISSUE INT
JI Calcif. Tissue Int.
PD DEC
PY 2013
VL 93
IS 6
BP 508
EP 516
DI 10.1007/s00223-013-9782-y
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 253HH
UT WOS:000327074400004
PM 23995829
ER
PT J
AU Caliendo, AM
Gilbert, DN
Ginocchio, CC
Hanson, KE
May, L
Quinn, TC
Tenover, FC
Alland, D
Blaschke, AJ
Bonomo, RA
Carroll, KC
Ferraro, MJ
Hirschhorn, LR
Joseph, WP
Karchmer, T
MacIntyre, AT
Reller, LB
Jackson, AF
AF Caliendo, Angela M.
Gilbert, David N.
Ginocchio, Christine C.
Hanson, Kimberly E.
May, Larissa
Quinn, Thomas C.
Tenover, Fred C.
Alland, David
Blaschke, Anne J.
Bonomo, Robert A.
Carroll, Karen C.
Ferraro, Mary Jane
Hirschhorn, Lisa R.
Joseph, W. Patrick
Karchmer, Tobi
MacIntyre, Ann T.
Reller, L. Barth
Jackson, Audrey F.
CA IDSA
TI Better Tests, Better Care: Improved Diagnostics for Infectious Diseases
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
DE diagnostics; rapid diagnostics; point-of-care testing; molecular
diagnostics; clinical microbiology; infectious diseases
ID DESORPTION IONIZATION-TIME; POLYMERASE-CHAIN-REACTION; FLIGHT
MASS-SPECTROMETRY; VENTILATOR-ASSOCIATED PNEUMONIA; BLOOD-STREAM
INFECTIONS; PEDIATRIC EMERGENCY-DEPARTMENT; RESPIRATORY-TRACT
INFECTIONS; HUMAN SEPTIC SHOCK; CHLAMYDIA-TRACHOMATIS;
PATIENT-MANAGEMENT
AB In this IDSA policy paper, we review the current diagnostic landscape, including unmet needs and emerging technologies, and assess the challenges to the development and clinical integration of improved tests. To fulfill the promise of emerging diagnostics, IDSA presents recommendations that address a host of identified barriers. Achieving these goals will require the engagement and coordination of a number of stakeholders, including Congress, funding and regulatory bodies, public health agencies, the diagnostics industry, healthcare systems, professional societies, and individual clinicians.
C1 [Caliendo, Angela M.] Brown Univ, Dept Med, Alpert Med Sch, Providence, RI 02912 USA.
[Gilbert, David N.] Providence Portland Med Ctr, Div Infect Dis, Portland, OR USA.
[Gilbert, David N.] Oregon Hlth & Sci Univ, Dept Med, Portland, OR 97201 USA.
[Ginocchio, Christine C.] North Shore LIJ Labs, Div Infect Dis Diagnost, Lake Success, NY USA.
[Ginocchio, Christine C.] Hofstra North Shore LIJ Sch Med, Dept Pathol & Lab Med, Hempstead, NY USA.
[Ginocchio, Christine C.] Hofstra North Shore LIJ Sch Med, Dept Mol Med, Hempstead, NY USA.
[Hanson, Kimberly E.] Univ Utah, Dept Med, Salt Lake City, UT 84112 USA.
[Hanson, Kimberly E.] Univ Utah, Dept Pathol, Salt Lake City, UT USA.
[May, Larissa] George Washington Univ, Dept Emergency Med, Washington, DC USA.
[Quinn, Thomas C.] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Quinn, Thomas C.] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
[Tenover, Fred C.] Cepheid, Sunnyvale, CA USA.
[Alland, David] Rutgers State Univ, Rutgers New Jersey Med Sch, Dept Med, Ctr Emerging Pathogens, Newark, NJ USA.
[Blaschke, Anne J.] Univ Utah, Sch Med, Dept Pediat, Div Pediat Infect Dis, Salt Lake City, UT USA.
[Bonomo, Robert A.] Louis Stokes Cleveland Dept Vet Affairs Med Ctr, Res Serv, Cleveland, OH USA.
[Bonomo, Robert A.] Case Western Reserve Univ, Sch Med, Dept Med, Cleveland, OH 44106 USA.
[Bonomo, Robert A.] Case Western Reserve Univ, Sch Med, Dept Pharmacol, Cleveland, OH 44106 USA.
[Bonomo, Robert A.] Case Western Reserve Univ, Sch Med, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA.
[Carroll, Karen C.] Johns Hopkins Univ, Sch Med, Dept Pathol, Div Med Microbiol, Baltimore, MD 21205 USA.
[Carroll, Karen C.] Johns Hopkins Univ, Sch Med, Dept Med, Div Infect Dis, Baltimore, MD 21205 USA.
[Ferraro, Mary Jane] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Ferraro, Mary Jane] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Hirschhorn, Lisa R.] Harvard Univ, Sch Med, Dept Global Hlth & Social Med, Boston, MA USA.
[Hirschhorn, Lisa R.] JSI Res & Training Inst, Boston, MA USA.
[Joseph, W. Patrick] Siemens Clin Lab, Berkeley, CA USA.
[Joseph, W. Patrick] Genom Hlth, Redwood City, CA USA.
[Joseph, W. Patrick] XDx Lab, San Francisco, CA USA.
[Joseph, W. Patrick] Tethys Biosci, Emeryville, CA USA.
[Karchmer, Tobi] Becton Dickinson & Co, Sparks, MD USA.
[MacIntyre, Ann T.] Nova SE Univ, Dept Internal Med, Ft Lauderdale, FL 33314 USA.
[Reller, L. Barth] Duke Univ, Sch Med, Dept Med, Durham, NC 27706 USA.
[Reller, L. Barth] Duke Univ, Sch Med, Dept Pathol, Durham, NC 27706 USA.
[Jackson, Audrey F.] Infect Dis Soc Amer, Arlington, VA 22209 USA.
RP Jackson, AF (reprint author), Infect Dis Soc Amer, 1300 Wilson Blvd,Ste 300, Arlington, VA 22209 USA.
EM ajackson@idsociety.org
FU IDSA
FX This supplement is sponsored by IDSA. The policy paper was developed by
IDSA's Diagnostics Task Force through discussion and deliberation over
several months, and the authors thank all who provided input and
interesting discussion during that time. The authors extend special
thanks to Drs Johan S. Bakken and Janet Nicholson for careful review of
the manuscript.
NR 82
TC 103
Z9 104
U1 2
U2 27
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD DEC 1
PY 2013
VL 57
SU 3
BP S139
EP S170
DI 10.1093/cid/cit578
PG 32
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 251XB
UT WOS:000326965600001
PM 24200831
ER
PT J
AU Krause, BR
Remaley, AT
AF Krause, Brian R.
Remaley, Alan T.
TI Reconstituted HDL for the acute treatment of acute coronary syndrome
SO CURRENT OPINION IN LIPIDOLOGY
LA English
DT Review
DE acute coronary syndrome; apoA-I; cholesterol; high density lipoprotein;
reverse cholesterol transport
ID HIGH-DENSITY-LIPOPROTEIN; APOLIPOPROTEIN-A-I; LECITHIN-CHOLESTEROL
ACYLTRANSFERASE; RANDOMIZED CONTROLLED-TRIAL; LANDSCHUTZ ASCITES-CELLS;
INTRAVASCULAR ULTRASOUND; ATHEROSCLEROTIC LESIONS; PLAQUE STABILIZATION;
ENDOTHELIAL FUNCTION; PLASMA-LIPOPROTEINS
AB Purpose of reviewNew therapeutic strategies are needed for the rapid stabilization of acute coronary syndrome (ACS) patients by treating nonculprit lesions. Reconstituted HDL (rHDL), which is apoA-I combined with phospholipids, is currently being tested in clinical trials for this purpose and is the subject of this review.Recent findingsAt least four different formulations (SRC-rHDL, CSL-111, CSL-112 and ETC-216) have been tested in clinical trials. The various rHDL preparations have been shown to be effective in the rapid mobilization of excess cholesterol from cells and in regressing atherosclerotic plaques in animal models. Two of the rHDL agents, namely ETC-216 and CSL-111, have been shown to be effective after only a few treatments in reducing plaque volume in ACS patients, as assessed by intravascular ultrasound, but no clinical trials assessing clinical endpoints have yet been completed.SummaryrHDL is a promising new potential therapy for ACS patients, but much work remains to be done, and there are many unresolved questions. Progress in developing rHDL into a therapy will depend on improving our understanding of their mechanism of action, determining the optimum formulation and delivery and how to monitor rHDL therapy.
C1 [Krause, Brian R.] AlphaCore Pharma, Ann Arbor, MI USA.
[Remaley, Alan T.] NHLBI, Lipoprot Metab Sect, Cardiopulm Branch, NIH, Bethesda, MD 20892 USA.
RP Remaley, AT (reprint author), NIH, Bldg 10,Rm 2C-433, Bethesda, MD USA.
EM aremaley1@cc.nih.gov
FU intramural National Heart, Lung, and Blood Institute of the NIH,
Bethesda, MD
FX Research support for one of the authors (A. R.) comes from the
intramural National Heart, Lung, and Blood Institute of the NIH,
Bethesda, MD.
NR 92
TC 24
Z9 25
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0957-9672
EI 1473-6535
J9 CURR OPIN LIPIDOL
JI Curr. Opin. Lipidology
PD DEC
PY 2013
VL 24
IS 6
BP 480
EP 486
DI 10.1097/MOL.0000000000000020
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Peripheral
Vascular Disease
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Cardiovascular System & Cardiology
GA 251VJ
UT WOS:000326959100004
PM 24184938
ER
PT J
AU Howard, BV
Rossouw, JE
AF Howard, Barbara V.
Rossouw, Jacques E.
TI Estrogens and cardiovascular disease risk revisited: the Women's Health
Initiative
SO CURRENT OPINION IN LIPIDOLOGY
LA English
DT Review
DE cardiovascular disease; CVD risk factors; hormone therapy; Women's
Health Initiative
ID CORONARY-HEART-DISEASE; POSTMENOPAUSAL HORMONE-THERAPY; CONJUGATED
EQUINE ESTROGENS; RANDOMIZED CONTROLLED-TRIAL; PERIPHERAL
ARTERIAL-DISEASE; PLUS PROGESTIN; REPLACEMENT THERAPY; VENOUS
THROMBOSIS; EVENTS; ATHEROSCLEROSIS
AB Purpose of reviewIn 2002 and 2004, the Women's Health Initiative found no evidence that hormone therapy with estrogen or estrogen with progestin (E+P) protected against cardiovascular disease (CVD). Since then, further analyses have been performed. This review summarizes current analyses on the effects of hormone therapy on CVD and CVD risk factors.Recent findingsThe negative effects of hormone therapy vary by the type of CVD event. Estrogen alone and E+P show consistent effects on CVD, but E+P has more impact on coronary heart disease (CHD) and venous thromboembolism. Women of all ethnicities, including those who are obese, have diabetes, or are taking daily aspirin or statins remain at risk for adverse effects from hormone therapy. Although younger women or more recently menopausal women taking hormone therapy may be at relatively lower risk for CHD and myocardial infarction, they remain at risk for stroke, venous thromboembolism and peripheral artery disease. Adverse effects are enhanced in older women with menopausal symptoms. Although hormone therapy lowers LDL cholesterol and lipoprotein (a) and raises high-density lipoprotein cholesterol, it has adverse effects on triglyceride, lipoprotein composition, and inflammatory and hemostatic markers. Baseline metabolic syndrome and high LDL cholesterol increase the CHD risk with hormone therapy. Analyses of discontinuation data in the estrogen-alone and E+P trials suggest that the adverse effects of hormone therapy on CVD are reversible.SummaryRecent analyses do not justify postmenopausal hormone therapy for CVD prevention. Further research on the role of hormone therapy-induced changes in CVD risk factors along with genetic studies may increase understanding and aid in developing safer therapies for menopausal symptoms.
C1 [Howard, Barbara V.] MedStar Hlth Res Inst, Hyattsville, MD 20782 USA.
[Howard, Barbara V.] Georgetown Howard Univ Ctr Clin & Translat Sci, Washington, DC USA.
[Rossouw, Jacques E.] NHLBI, Bethesda, MD 20892 USA.
RP Howard, BV (reprint author), MedStar Hlth Res Inst, 6525 Belcrest Rd,Suite 700, Hyattsville, MD 20782 USA.
EM Barbara.V.Howard@MedStar.net
FU National Heart, Lung, and Blood Institute, National Institutes of
Health; U.S. Department of Health and Human Services [HHSN268201100046C,
HHSN268201100001C, HHSN268201100002C, HHSN268201100003C,
HHSN268201100004C, HHSN271201100004C]
FX This research was funded by the National Heart, Lung, and Blood
Institute, National Institutes of Health, U.S. Department of Health and
Human Services through contracts HHSN268201100046C, HHSN268201100001C,
HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and
HHSN271201100004C. We thank Rachel Schaperow, MedStar Health Research
Institute, for editing the manuscript.; The Women's Health Initiative is
funded by the National Heart, Lung, and Blood Institute, National
Institutes of Health, U.S. Department of Health and Human Services,
through contracts HHSN268201100046C, HHSN268201100001C,
HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and
HHSN271201100004C.
NR 35
TC 16
Z9 18
U1 1
U2 49
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0957-9672
EI 1473-6535
J9 CURR OPIN LIPIDOL
JI Curr. Opin. Lipidology
PD DEC
PY 2013
VL 24
IS 6
BP 493
EP 499
DI 10.1097/MOL.0000000000000022
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Peripheral
Vascular Disease
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Cardiovascular System & Cardiology
GA 251VJ
UT WOS:000326959100006
PM 24184944
ER
PT J
AU Lo Surdo, JL
Millis, BA
Bauer, SR
AF Lo Surdo, Jessica L.
Millis, Bryan A.
Bauer, Steven R.
TI Automated microscopy as a quantitative method to measure differences in
adipogenic differentiation in preparations of human mesenchymal stromal
cells
SO CYTOTHERAPY
LA English
DT Article
DE adipogenesis; bone marrow stromal cell; mesenchymal stromal cell;
microscopy
ID HUMAN BONE-MARROW; ADULT STEM-CELLS; IN-VITRO; OSTEOGENIC
DIFFERENTIATION; ADIPOSE-TISSUE; PROGENITOR CELLS; EXPANSION;
POPULATIONS; PRECURSORS; CULTURES
AB Background aims. Multipotent stromal cells, also called mesenchymal stromal cells (MSCs), are potentially valuable as a cellular therapy because of their differentiation and immunosuppressive properties. As the result of extensive heterogeneity of MSCs, quantitative approaches to measure differentiation capacity between donors and passages on a per-cell basis are needed. Methods. Human bone marrow-derived MSCs were expanded to passages P3, P5 and P7 from eight different donors and were analyzed for colony-forming unit capacity (CPU), cell size, surface marker expression and forward/side-scatter analysis by flow cytometry. Adipogenic differentiation potential was quantified with the use of automated microscopy. Percentage of adipogenesis was determined by quantifying nuclei and Nile red positive adipocytes after automated image acquisition. Results. MSCs varied in expansion capacity and increased in average cell diameter with passage. CFU capacity decreased with passage and varied among cell lines within the same passage. The number of adipogenic precursors varied between cell lines, ranging from 0.5% to 13.6% differentiation at P3. Adipogenic capacity decreased significantly with increasing passage. MSC cell surface marker analysis revealed no changes caused by passaging or donor differences. Conclusions. We measured adipogenic differentiation on a per-cell basis with high precision and accuracy with the use of automated fluorescence microscopy. We correlated these findings with other quantitative bioassays to better understand the role of donor variability and passaging on CPU, cell size and adipogenic differentiation capacity in vitro. These quantitative approaches provide valuable tools to measure MSC quality and measure functional biological differences between donors and cell passages that are not revealed by conventional MSC cell surface marker analysis.
C1 [Lo Surdo, Jessica L.; Bauer, Steven R.] Off Cellular Tissue & Gene Therapies, Div Cellular & Gene Therapies, FDA Ctr Biol Evaluat & Res, Bethesda, MD USA.
[Millis, Bryan A.] NIDCD, NIH, Sect Struct Cell Biol, Bethesda, MD USA.
RP Bauer, SR (reprint author), US FDA, Ctr Biol Evaluat & Res, NIH Bldg 29B HFM 740,Room 2NN10, Bethesda, MD 20892 USA.
EM steven.bauer@fda.hhs.gov
OI Bauer, Steven/0000-0003-2831-846X
FU Jessica Lo Surdo's appointment to the Research Participation Program at
the Center for Biologics Evaluation and Research; US Food and Drug
Administration; Food and Drug Administration Modernizing Science grant
program; Biomedical Advanced Research and Development Authority grant;
Medical Countermeasures Initiative; Division of Cell and Gene Therapies
FX The authors would like to acknowledge Eva Rudikoff for her assistance in
growing the MSCs and Drs Brenton McCright, Deborah Hursh and Patrick
Lynch for reviewing the manuscript. This project was supported in part
by Jessica Lo Surdo's appointment to the Research Participation Program
at the Center for Biologics Evaluation and Research administered by the
Oak Ridge Institute for Science and Education through US Department of
Education and US Food and Drug Administration. This work was also
supported in part by the Food and Drug Administration Modernizing
Science grant program, a Biomedical Advanced Research and Development
Authority grant, a grant from the Medical Countermeasures Initiative and
research funds from the Division of Cell and Gene Therapies.
NR 62
TC 16
Z9 17
U1 0
U2 6
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1465-3249
EI 1477-2566
J9 CYTOTHERAPY
JI Cytotherapy
PD DEC
PY 2013
VL 15
IS 12
BP 1527
EP 1540
DI 10.1016/j.jcyt.2013.04.010
PG 14
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology; Hematology; Medicine, Research & Experimental
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
& Experimental Medicine
GA 254ME
UT WOS:000327169000010
PM 23992827
ER
PT J
AU Yamben, IF
Rachel, RA
Shatadal, S
Copeland, NG
Jenkins, NA
Warming, S
Griep, AE
AF Yamben, Idella F.
Rachel, Rivka A.
Shatadal, Shalini
Copeland, Neal G.
Jenkins, Nancy A.
Warming, Soren
Griep, Anne E.
TI Scrib is required for epithelial cell identity and prevents epithelial
to mesenchymal transition in the mouse
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE Scrib; PDZ proteins; Lens development; Epithelial to mesenchymal
transition; Cell adhesion; Cell polarity
ID GROWTH-FACTOR-BETA; PROLIFERATION CONTROL; SUBCAPSULAR CATARACT; TUMOR
SUPPRESSORS; POLARITY MODULE; E-CADHERIN; TGF-BETA; LENS; CANCER;
EXPRESSION
AB The integrity and function of epithelial tissues depend on the establishment and maintenance of defining characteristics of epithelial cells, cell-cell adhesion and cell polarity. Disruption of these characteristics can lead to the loss of epithelial identity through a process called epithelial to mesenchymal transition (EMT), which can contribute to pathological conditions such as tissue fibrosis and invasive cancer. In invertebrates, the epithelial polarity gene scrib plays a critical role in establishing and maintaining cell adhesion and polarity. In this study we asked if the mouse homolog, Scrib, is required for establishment and/or maintenance of epithelial identity in vivo. To do so, we conditionally deleted Scrib in the head ectoderm tissue that gives rise to both the ocular lens and the corneal epithelium. Deletion of Scrib in the lens resulted in a change in epithelial cell shape from cuboidal to flattened and elongated. Early in the process, the cell adhesion protein, E-cadherin, and apical polarity protein, ZO-1, were downregulated and the myofibroblast protein, alpha SMA, was upregulated, suggesting EMT was occurring in the Scrib deficient lenses. Correlating temporally with the upregulation of alpha SMA, Smad3 and Smad4, TGF beta signaling intermediates, accumulated in the nucleus and Snail, a TGF beta target and transcriptional repressor of the gene encoding E-cadherin, was upregulated. Pax6, a lens epithelial transcription factor required to maintain lens epithelial cell identity also was downregulated. Loss of Scrib in the corneal epithelium also led to molecular changes consistent with EMT, suggesting that the effect of Scrib deficiency was not unique to the lens. Together, these data indicate that mammalian Scrib is required to maintain epithelial identity and that loss of Scrib can culminate in EMT, mediated, at least in part, through TCF beta signaling. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Yamben, Idella F.; Shatadal, Shalini; Griep, Anne E.] Univ Wisconsin, Dept Cell & Regenerat Biol, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[Rachel, Rivka A.; Copeland, Neal G.; Jenkins, Nancy A.; Warming, Soren] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Griep, AE (reprint author), Univ Wisconsin, Dept Cell & Regenerat Biol, Sch Med & Publ Hlth, Madison, WI 53706 USA.
EM aegriep@wisc.edu
FU NIH [GM07215, EY09091, CA98428, CA14520, EY016665]
FX The authors thank Ruth Ashery-Padan for generously providing the LeCre
mice. The authors also thank Lance Roderick of the Keck Imaging
Facility, Toshi Kinoshita of the Pathology Department Histology Core,
the McArdle Laboratories Histology Core and Denis Lee and Susan Moran of
the McArdle Laboratories. The authors thank Angela Verdoni and Aki Ikeda
for guidance with the cornea experiments. The authors thank Paul Lambert
for helpful discussions and his critical reading of the manuscript
I.F.Y. was supported by the NIH training Grant GM07215. This work was
supported by NIH Grants EY09091, CA98428, CA14520, and EY016665.
NR 66
TC 14
Z9 14
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
EI 1095-564X
J9 DEV BIOL
JI Dev. Biol.
PD DEC 1
PY 2013
VL 384
IS 1
BP 41
EP 52
DI 10.1016/j.ydbio.2013.09.027
PG 12
WC Developmental Biology
SC Developmental Biology
GA 251AV
UT WOS:000326901100004
PM 24095903
ER
PT J
AU Chin, LMK
Heigenhauser, GJF
Paterson, DH
Kowalchuk, JM
AF Chin, Lisa M. K.
Heigenhauser, George J. F.
Paterson, Donald H.
Kowalchuk, John M.
TI Effect of voluntary hyperventilation with supplemental CO2 on pulmonary
O-2 uptake and leg blood flow kinetics during moderate-intensity
exercise
SO EXPERIMENTAL PHYSIOLOGY
LA English
DT Article
ID RESPIRATORY MUSCLE WORK; INDUCED HYPOCAPNIC ALKALOSIS; NEAR-INFRARED
SPECTROSCOPY; OXYGEN-UPTAKE KINETICS; PRIOR HEAVY EXERCISE;
FEMORAL-ARTERY; PHOSPHOCREATINE KINETICS; SUBMAXIMAL EXERCISE; MAXIMAL
EXERCISE; GAS-EXCHANGE
AB New findings center dot What is the central question of this study? Voluntary hyperventilation that induces hypocapnic alkalosis (HYPO) is associated with slowed adaptation of O-2 uptake and leg blood flow during moderate exercise; however, it is unknown whether hypocapnia, alkalosis and/or the hyperventilation manoeuvre is related to these observations.
center dot What is the main finding and its importance? We included a condition with the same work of breathing as HYPO, but the fall in CO2 was prevented by the addition of higher CO2 to the inspirate (normocapnia). This condition demonstrated that hypocapnia/alkalosis was responsible for the slower leg blood flow response; however, the act of hyperventilation itself also had a role to play in the slower O-2 uptake kinetics.
Pulmonary O-2 uptake ((V) over dot(O2P)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 +/- 6 years old; mean +/- SD) performed alternate-leg kneeextension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P-ET,(CO2)) similar to 40 mmHg], i. e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; P-ET,P-CO2 similar to 20 mmHg), i. e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; P-ET,P-CO2 similar to 40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (similar to 5%). The. (V)over dot(O2P) was measured breath by breath usingmass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 (V)over dot(O2P) kinetics (tau(V)over dot(O2P)) was different (P < 0.05) amongst all three conditions (CON, 19 +/- 7 s; HYPO, 43 +/- 17 s; and NORMO, 30 +/- 8 s), while LBF kinetics (tLBF) was slower (P < 0.05) in HYPO (31 +/- 9s) compared with both CON (19 +/- 3 s) and NORMO (20 +/- 6 s). Similar to previous findings, HYPO was associated with slower. (V) over dot(O2P) and LBF kinetics compared with CON. In the present study, preventing the fall in end-tidal P-CO2 (NORMO) restored LBF kinetics, but not. (V) over dot(O2P) kinetics, which remained ` slowed' relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower. (V) over dot(O2P) kinetics observed during HYPO.
C1 [Chin, Lisa M. K.; Paterson, Donald H.; Kowalchuk, John M.] Univ Western Ontario, Sch Kinesiol, London, ON N6A 5B9, Canada.
[Kowalchuk, John M.] Univ Western Ontario, Dept Physiol & Pharmacol, London, ON N6A 5B9, Canada.
[Chin, Lisa M. K.] George Mason Univ, Dept Rehabil Sci, Fairfax, VA 22030 USA.
[Chin, Lisa M. K.] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Heigenhauser, George J. F.] McMaster Univ, Dept Med, Hamilton, ON, Canada.
RP Kowalchuk, JM (reprint author), Univ Western Ontario, Sch Kinesiol, Canadian Ctr Act & Aging, Arthur & Sonia Labatt Hlth Sci Bldg,Room 411C, London, ON N6A 5B9, Canada.
EM jkowalch@uwo.ca
RI Chin, Lisa/O-4706-2014
OI Chin, Lisa/0000-0002-0178-739X
FU Natural Sciences and Engineering Research Council of Canada (NSERC);
Western's Graduate Thesis Research Fund; National Institutes of Health
FX This study was supported by Natural Sciences and Engineering Research
Council of Canada (NSERC) grants. Additional support was provided to L.
M. K. C. by Western's Graduate Thesis Research Fund and by intramural
funds from the National Institutes of Health.
NR 32
TC 3
Z9 3
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0958-0670
EI 1469-445X
J9 EXP PHYSIOL
JI Exp. Physiol.
PD DEC 1
PY 2013
VL 98
IS 12
BP 1668
EP 1682
DI 10.1113/expphysiol.2013.074021
PG 15
WC Physiology
SC Physiology
GA 254KF
UT WOS:000327163100004
PM 23975901
ER
PT J
AU Singh, TP
Lee, CH
Farber, JM
AF Singh, Tej Pratap
Lee, Chang Hoon
Farber, Joshua M.
TI Chemokine receptors in psoriasis
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE chemokine receptors; cytokines; inflammation; psoriasis
ID REGULATORY T-CELLS; PLASMACYTOID DENDRITIC CELLS; INFLAMMATORY PROTEIN
3-ALPHA; EXTRACELLULAR TRAP FORMATION; MESSENGER-RNA EXPRESSION;
NECROSIS-FACTOR-ALPHA; DRAINING LYMPH-NODES; HUMAN TH17 CELLS; SKIN
INFLAMMATION; ATOPIC-DERMATITIS
AB Introduction: Psoriasis is a prevalent immune-mediated disease involving primarily the skin. Infiltrating leukocytes play key roles in driving the disease. Along with an array of adhesion proteins, leukocyte trafficking into tissue is controlled by chemoattractants, including chemokines, and their receptors. This review summarizes the data on roles for the chemokine system in psoriasis in order to highlight opportunities for inhibiting this system for therapeutic benefit.
Areas covered: The review covers the roles of various leukocyte subsets in psoriasis, focusing on the chemokine receptors that are thought to be responsible for the trafficking of these cells into tissue. The review also discusses in some detail the significance of the IL-23/IL-17/IL-22 cytokine axis in disease.
Expert opinion: Many of the new therapies developed for psoriasis are antibodies to neutralize cytokines that have pleiotropic functions in host defense. Inhibiting chemokine receptors can be accomplished using small molecules, and would be expected to block inflammation while resulting in more limited immunosuppression. There has been limited success to date in treating inflammatory disease with chemokine receptor antagonists, which has often been ascribed to the system's redundancy. Other factors may also be important, however, including sub-optimal choices of targets based on incomplete understandings of disease pathogenesis.
C1 [Singh, Tej Pratap; Lee, Chang Hoon; Farber, Joshua M.] NIAID, NIH, Lab Mol Immunol, Inflammat Biol Sect, Bethesda, MD 20892 USA.
RP Farber, JM (reprint author), NIAID, NIH, Lab Mol Immunol, Inflammat Biol Sect, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jfarber@niaid.nih.gov
FU Intramural Research Program of the DIR, NIAID, NIH
FX The authors have no relevant financial interests. This work was
supported by the Intramural Research Program of the DIR, NIAID, NIH.
NR 223
TC 7
Z9 8
U1 1
U2 19
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD DEC
PY 2013
VL 17
IS 12
BP 1405
EP 1422
DI 10.1517/14728222.2013.838220
PG 18
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 255QT
UT WOS:000327255600003
PM 24070343
ER
PT J
AU Corona, A
Masaoka, T
Tocco, G
Tramontano, E
Le Grice, SFJ
AF Corona, Angela
Masaoka, Takashi
Tocco, Graziella
Tramontano, Enzo
Le Grice, Stuart F. J.
TI Active site and allosteric inhibitors of the ribonuclease H activity of
HIV reverse transcriptase
SO FUTURE MEDICINAL CHEMISTRY
LA English
DT Review
ID SMALL-MOLECULE INHIBITORS; CELL-BASED ASSAYS; RNASE-H; DNA-POLYMERASE;
DUAL INHIBITORS; INTEGRASE INHIBITORS; STRAND TRANSFER; STRUCTURAL
BASIS; DIKETO ACID; VIRUS
AB Despite the wealth of information available for the reverse transcriptase (RT)-associated ribonuclease H (RNaseH) domain of lentiviruses, gammaretroviruses and long terminal repeat containing retrotransposons, exploiting this information in the form of an RNaseH inhibitor with high specificity and low cellular toxicity has been disappointing. However, it is now becoming increasingly evident that the two-subunit HIV-1 RT is a highly versatile enzyme, undergoing major structural alterations in order to interact with, position and ultimately hydrolyze the RNA component of an RNA/DNA hybrid. Thus, in addition to targeting the RNaseH active site, identifying small molecules that bind elsewhere and disrupt catalysis allosterically by impairing conformational flexibility is gaining increased attention. This review summarizes current progress towards development of both active site and allosteric RNaseH inhibitors.
C1 [Corona, Angela; Tramontano, Enzo] Univ Cagliari, Dept Life & Environm Sci, Unit Biomed, I-09124 Cagliari, Italy.
[Masaoka, Takashi; Le Grice, Stuart F. J.] NCI, RT Biochem Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Tocco, Graziella] Univ Cagliari, Dept Life & Environm Sci, Unit Drug Sci, I-09124 Cagliari, Italy.
RP Le Grice, SFJ (reprint author), NCI, RT Biochem Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA.
EM legrices@mail.nih.gov
RI Tramontano, Enzo/B-4919-2012; Corona, Angela/G-7327-2014
OI Tramontano, Enzo/0000-0002-4849-0980; Corona, Angela/0000-0002-6630-8636
FU RAS [LR 7/2007 CRP-24915]; MIUR PRIN; Ministero dell 'Universita, dell'
Istruzione e della Ricerca MIUR - PRIN; Fondazione Banco di Sardegna;
Intramural Research Program of the National Cancer Institute, NIH,
Department of Health and Human Services, USA
FX A Corona and E Tramontano were supported by RAS grant LR 7/2007
CRP-24915 and MIUR PRIN 2012, G Tocco by Ministero dell 'Universita,
dell' Istruzione e della Ricerca MIUR - PRIN 2008 and Fondazione Banco
di Sardegna, and T Masaoka and SFJ Le Grice by the Intramural Research
Program of the National Cancer Institute, NIH, Department of Health and
Human Services, USA. The authors have no other relevant affiliations or
financial involvement with any organization or entity with a financial
interest in or financial conflict with the subject matter or materials
discussed in the manuscript apart from those disclosed. No writing
assistance was utilized in the production of this manuscript.
NR 62
TC 16
Z9 16
U1 0
U2 22
PU FUTURE SCI LTD
PI LONDON
PA UNITED HOUSE, 2 ALBERT PL, LONDON, N3 1QB, ENGLAND
SN 1756-8919
EI 1756-8927
J9 FUTURE MED CHEM
JI Future Med. Chem.
PD DEC
PY 2013
VL 5
IS 18
BP 2127
EP 2139
DI 10.4155/fmc.13.178
PG 13
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 255EO
UT WOS:000327222400007
PM 24261890
ER
PT J
AU Wu, JC
Pfeiffer, RM
Gail, MH
AF Wu, Jincao
Pfeiffer, Ruth M.
Gail, Mitchell H.
TI Strategies for Developing Prediction Models From Genome-Wide Association
Studies
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE GWAS; risk prediction; discriminatory accuracy; ROC curve; AUC;
probability of correct classification
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; COMPLEX DISEASES; RISK PREDICTION;
WINNERS CURSE; GENETIC RISK; CANCER-RISK; ODDS RATIOS; SUSCEPTIBILITY;
PROSTATE
AB Genome-wide association studies (GWASs) have identified hundreds of single nucleotide polymorphisms (SNPs) associated with complex human diseases. However, risk prediction models based on them have limited discriminatory accuracy. It has been suggested that including many such SNPs can improve predictive performance. Here, we studied various aspects of model building to improve discriminatory accuracy, as measured by the area under the receiver operating characteristic curve (AUC), including: (1) How well does a one-phase procedure that selects SNPs and estimates odds ratios on the same data perform? (2) How should training data be allocated between SNP selection (Phase 1) and estimation (Phase 2) in a two-phase procedure? (3) Should SNP selection be based on P-value thresholding or ranking P-values? (4) How many SNPs should be selected? and (5) Is multivariate estimation preferred to univariate estimation in the presence of linkage disequilibrium (LD)? We used realistic estimates of the distributions of genetic effect sizes, allele frequencies, and LD patterns based on GWAS data for Crohn's disease and prostate cancer. Theory and simulations were used to estimate AUC. Empirical risk models based on 10,000 cases and controls had considerably lower AUC than theoretically achievable. The most critical aspect of prediction model building was initial SNP selection. The single-phase procedure achieved higher AUC than the two-phase procedure. Multivariate estimation did not perform as well as univariate (marginal) estimation. For complex diseases and samples of 10,000 or fewer cases and controls, one should limit the number of SNPs to tens or hundreds.
C1 [Wu, Jincao; Pfeiffer, Ruth M.; Gail, Mitchell H.] NCI, Div Canc Epidemiol & Genet, Biostat Branch, Rockville, MD 20850 USA.
RP Wu, JC (reprint author), NCI, Div Canc Epidemiol & Genet, Biostat Branch, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM jincao.wu@nih.gov
FU National Cancer Institute, Division of Cancer Epidemiology, and Genetics
FX This work was supported by the intramural research program of the
National Cancer Institute, Division of Cancer Epidemiology, and
Genetics. We thank Drs. Ju-Hyun Park and Nilanjan Chatterjee for
providing the formulas for the conditional densities of log odds ratios
per allele given minor allele frequency, leading to the distributions in
Supplementary Fig. S1. We thank Dr. Charles Kooperberg for providing the
Crohn's disease data with imputed genotypes from Kooperberg et al.
[2010] and the Welcome Trust Case Control Consortium for access to the
data. We thank the reviewers for helpful comments that improved the
paper.
NR 27
TC 7
Z9 8
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD DEC
PY 2013
VL 37
IS 8
BP 768
EP 777
DI 10.1002/gepi.21762
PG 10
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 251ZZ
UT WOS:000326975300002
PM 24166696
ER
PT J
AU Chen, HS
Pfeiffer, RM
Zhang, SP
AF Chen, Huann-Sheng
Pfeiffer, Ruth M.
Zhang, Shunpu
TI A Powerful Method for Combining P-Values in Genomic Studies
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE association study; gene set; permutation test; Simes test
ID TRUNCATED PRODUCT; MULTIPLE; VARIANTS; CANCER
AB After genetic regions have been identified in genomewide association studies (GWAS), investigators often follow up with more targeted investigations of specific regions. These investigations typically are based on single nucleotide polymorphisms (SNPs) with dense coverage of a region. Methods are thus needed to test the hypothesis of any association in given genetic regions. Several approaches for combining P-values obtained from testing individual SNP hypothesis tests are available. We recently proposed a sequential procedure for testing the global null hypothesis of no association in a region. When this global null hypothesis is rejected, this method provides a list of significant hypotheses and has weak control of the family-wise error rate. In this paper, we devise a permutation-based version of the test that accounts for correlations of tests based on SNPs in the same genetic region. Based on simulated data, the method has correct control of the type I error rate and higher or comparable power to other tests.
C1 [Chen, Huann-Sheng] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Pfeiffer, Ruth M.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Zhang, Shunpu] Univ Nebraska, Dept Stat, Lincoln, NE USA.
RP Chen, HS (reprint author), NCI, Div Canc Control & Populat Sci, NIH, 9609 Med Ctr Dr,Room 4E348,MSC 9765, Bethesda, MD 20892 USA.
EM chenh6@mail.nih.gov
NR 18
TC 3
Z9 3
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD DEC
PY 2013
VL 37
IS 8
BP 814
EP 819
DI 10.1002/gepi.21755
PG 6
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 251ZZ
UT WOS:000326975300006
PM 23959976
ER
PT J
AU Yu, B
Zheng, Y
Alexander, D
Manolio, TA
Alonso, A
Nettleton, JA
Boerwinkle, E
AF Yu, Bing
Zheng, Yan
Alexander, Danny
Manolio, Teri A.
Alonso, Alvaro
Nettleton, Jennifer A.
Boerwinkle, Eric
TI Genome-Wide Association Study of a Heart Failure Related Metabolomic
Profile Among African Americans in the Atherosclerosis Risk in
Communities (ARIC) Study
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE African Americans; heart failure; genome-wide association; metabolomics
ID CHRONIC KIDNEY-DISEASE; OXIDATIVE STRESS; CARDIOVASCULAR-DISEASE;
EPIDEMIOLOGY; SYSTEMS; ADULTS
AB Both the prevalence and incidence of heart failure (HF) are increasing, especially among African Americans, but no large-scale, genome-wide association study (GWAS) of HF-related metabolites has been reported. We sought to identify novel genetic variants that are associated with metabolites previously reported to relate to HF incidence. GWASs of three metabolites identified previously as risk factors for incident HF (pyroglutamine, dihydroxy docosatrienoic acid, and X-11787, being either hydroxy-leucine or hydroxy-isoleucine) were performed in 1,260 African Americans free of HF at the baseline examination of the Atherosclerosis Risk in Communities (ARIC) study. A significant association on chromosome 5q33 (rs10463316, MAF = 0.358, P-value = 1.92 x 10(-10)) was identified for pyroglutamine. One region on chromosome 2p13 contained a nonsynonymous substitution in N-acetyltransferase 8 (NAT8) was associated with X-11787 (rs13538, MAF = 0.481, P-value = 1.71 x 10(-23)). The smallest P-value for dihydroxy docosatrienoic acid was rs4006531 on chromosome 8q24 (MAF = 0.400, P-value = 6.98 x 10(-7)). None of the above SNPs were individually associated with incident HF, but a genetic risk score (GRS) created by summing the most significant risk alleles from each metabolite detected 11% greater risk of HF per allele. In summary, we identified three loci associated with previously reported HF-related metabolites. Further use of metabolomics technology will facilitate replication of these findings in independent samples.
C1 [Yu, Bing; Zheng, Yan; Nettleton, Jennifer A.; Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Div Epidemiol Human Genet & Environm Sci, Houston, TX 77030 USA.
[Alexander, Danny] Metabolon Inc, Durham, NC USA.
[Manolio, Teri A.] NHGRI, Div Genom Med, Bethesda, MD 20892 USA.
[Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Boerwinkle, Eric] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
RP Boerwinkle, E (reprint author), Univ Texas Houston, Ctr Human Genet, Sch Publ Hlth, 1200 Herman Pressler E-447, Houston, TX 77030 USA.
EM Eric.Boerwinkle@uth.tmc.edu
RI Alonso, Alvaro/A-4917-2010
OI Alonso, Alvaro/0000-0002-2225-8323
FU National Heart, Lung, and Blood Institute [HHSN268201100005C,
HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
HHSN268201100009C, HHSN268201100010C, HHSN268201100011C,
HHSN268201100012C, R01HL087641, R01HL59367, R01HL086694]; National Human
Genome Research Institute [U01HG004402]; National Institutes of Health
[HHSN268200625226C, UL1RR025005]
FX The 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 grant U01HG004402; and National
Institutes of Health contract HHSN268200625226C. Infrastructure was
partly supported by Grant Number UL1RR025005, a component of the
National Institutes of Health and NIH Roadmap for Medical Research.
NR 37
TC 11
Z9 11
U1 3
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD DEC
PY 2013
VL 37
IS 8
BP 840
EP 845
DI 10.1002/gepi.21752
PG 6
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 251ZZ
UT WOS:000326975300009
PM 23934736
ER
PT J
AU Stephens, SH
Hartz, SM
Hoft, NR
Saccone, NL
Corley, RC
Hewitt, JK
Hopfer, CJ
Breslau, N
Coon, H
Chen, XN
Ducci, F
Dueker, N
Franceschini, N
Frank, J
Han, YH
Hansel, NN
Jiang, CH
Korhonen, T
Lind, PA
Liu, J
Lyytikainen, LP
Michel, M
Shaffer, JR
Short, SE
Sun, JZ
Teumer, A
Thompson, JR
Vogelzangs, N
Vink, JM
Wenzlaff, A
Wheeler, W
Yang, BZ
Aggen, SH
Balmforth, AJ
Baumeister, SE
Beaty, TH
Benjamin, DJ
Bergen, AW
Broms, U
Cesarini, D
Chatterjee, N
Chen, JC
Cheng, YC
Cichon, S
Couper, D
Cucca, F
Dick, D
Foroud, T
Furberg, H
Giegling, I
Gillespie, NA
Gu, FY
Hall, AS
Haellfors, J
Han, S
Hartmann, AM
Heikkilae, K
Hickie, IB
Hottenga, JJ
Jousilahti, P
Kaakinen, M
Kaehoenen, M
Koellinger, PD
Kittner, S
Konte, B
Landi, MT
Laatikainen, T
Leppert, M
Levy, SM
Mathias, RA
McNeil, DW
Medland, SE
Montgomery, GW
Murray, T
Nauck, M
North, KE
Pare, PD
Pergadia, M
Ruczinski, I
Salomaa, V
Viikari, J
Willemsen, G
Barnes, KC
Boerwinkle, E
Boomsma, DI
Caporaso, N
Edenberg, HJ
Francks, C
Gelernter, J
Grabe, HJ
Hops, H
Jarvelin, MR
Johannesson, M
Kendler, KS
Lehtimaeki, T
Magnusson, PKE
Marazita, ML
Marchini, J
Mitchell, BD
Noethen, MM
Penninx, BW
Raitakari, O
Rietschel, M
Rujescu, D
Samani, NJ
Schwartz, AG
Shete, S
Spitz, M
Swan, GE
Volzke, H
Veijola, J
Wei, QY
Amos, C
Cannon, DS
Grucza, R
Hatsukami, D
Heath, A
Johnson, EO
Kaprio, J
Madden, P
Martin, NG
Stevens, VL
Weiss, RB
Kraft, P
Bierut, LJ
Ehringer, MA
AF Stephens, Sarah H.
Hartz, Sarah M.
Hoft, Nicole R.
Saccone, Nancy L.
Corley, Robin C.
Hewitt, John K.
Hopfer, Christian J.
Breslau, Naomi
Coon, Hilary
Chen, Xiangning
Ducci, Francesca
Dueker, Nicole
Franceschini, Nora
Frank, Josef
Han, Younghun
Hansel, Nadia N.
Jiang, Chenhui
Korhonen, Tellervo
Lind, Penelope A.
Liu, Jason
Lyytikaeinen, Leo-Pekka
Michel, Martha
Shaffer, John R.
Short, Susan E.
Sun, Juzhong
Teumer, Alexander
Thompson, John R.
Vogelzangs, Nicole
Vink, Jacqueline M.
Wenzlaff, Angela
Wheeler, William
Yang, Bao-Zhu
Aggen, Steven H.
Balmforth, Anthony J.
Baumeister, Sebastian E.
Beaty, Terri H.
Benjamin, Daniel J.
Bergen, Andrew W.
Broms, Ulla
Cesarini, David
Chatterjee, Nilanjan
Chen, Jingchun
Cheng, Yu-Ching
Cichon, Sven
Couper, David
Cucca, Francesco
Dick, Danielle
Foroud, Tatiana
Furberg, Helena
Giegling, Ina
Gillespie, Nathan A.
Gu, Fangyi
Hall, Alistair S.
Haellfors, Jenni
Han, Shizhong
Hartmann, Annette M.
Heikkilae, Kauko
Hickie, Ian B.
Hottenga, Jouke Jan
Jousilahti, Pekka
Kaakinen, Marika
Kaehoenen, Mika
Koellinger, Philipp D.
Kittner, Stephen
Konte, Bettina
Landi, Maria-Teresa
Laatikainen, Tiina
Leppert, Mark
Levy, Steven M.
Mathias, Rasika A.
McNeil, Daniel W.
Medland, Sarah E.
Montgomery, Grant W.
Murray, Tanda
Nauck, Matthias
North, Kari E.
Pare, Peter D.
Pergadia, Michele
Ruczinski, Ingo
Salomaa, Veikko
Viikari, Jorma
Willemsen, Gonneke
Barnes, Kathleen C.
Boerwinkle, Eric
Boomsma, Dorret I.
Caporaso, Neil
Edenberg, Howard J.
Francks, Clyde
Gelernter, Joel
Grabe, Hans Joergen
Hops, Hyman
Jarvelin, Marjo-Riitta
Johannesson, Magnus
Kendler, Kenneth S.
Lehtimaeki, Terho
Magnusson, Patrik K. E.
Marazita, Mary L.
Marchini, Jonathan
Mitchell, Braxton D.
Noethen, Markus M.
Penninx, Brenda W.
Raitakari, Olli
Rietschel, Marcella
Rujescu, Dan
Samani, Nilesh J.
Schwartz, Ann G.
Shete, Sanjay
Spitz, Margaret
Swan, Gary E.
Voelzke, Henry
Veijola, Juha
Wei, Qingyi
Amos, Chris
Cannon, Dale S.
Grucza, Richard
Hatsukami, Dorothy
Heath, Andrew
Johnson, Eric O.
Kaprio, Jaakko
Madden, Pamela
Martin, Nicholas G.
Stevens, Victoria L.
Weiss, Robert B.
Kraft, Peter
Bierut, Laura J.
Ehringer, Marissa A.
TI Distinct Loci in the CHRNA5/CHRNA3/CHRNB4 Gene Cluster Are Associated
With Onset of Regular Smoking
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE CHRNA5; CHRNA3; CHRNB4; meta-analysis; nicotine; smoke
ID SUBSTANCE-USE DISORDERS; HIGH-SCHOOL-STUDENTS; NICOTINE DEPENDENCE;
LUNG-CANCER; CIGARETTE-SMOKING; YOUNG-ADULTS; EARLY AGE;
ENVIRONMENTAL-INFLUENCES; SUSCEPTIBILITY LOCUS; QUANTITATIVE TRAITS
AB Neuronal nicotinic acetylcholine receptor (nAChR) genes (CHRNA5/CHRNA3/CHRNB4) have been reproducibly associated with nicotine dependence, smoking behaviors, and lung cancer risk. Of the few reports that have focused on early smoking behaviors, association results have been mixed. This meta-analysis examines early smoking phenotypes and SNPs in the gene cluster to determine: (1) whether the most robust association signal in this region (rs16969968) for other smoking behaviors is also associated with early behaviors, and/or (2) if additional statistically independent signals are important in early smoking. We focused on two phenotypes: age of tobacco initiation (AOI) and age of first regular tobacco use (AOS). This study included 56,034 subjects (41 groups) spanning nine countries and evaluated five SNPs including rs1948, rs16969968, rs578776, rs588765, and rs684513. Each dataset was analyzed using a centrally generated script. Meta-analyses were conducted from summary statistics. AOS yielded significant associations with SNPs rs578776 (beta = 0.02, P = 0.004), rs1948 (beta = 0.023, P = 0.018), and rs684513 (beta = 0.032, P = 0.017), indicating protective effects. There were no significant associations for the AOI phenotype. Importantly, rs16969968, the most replicated signal in this region for nicotine dependence, cigarettes per day, and cotinine levels, was not associated with AOI (P = 0.59) or AOS (P = 0.92). These results provide important insight into the complexity of smoking behavior phenotypes, and suggest that association signals in the CHRNA5/A3/B4 gene cluster affecting early smoking behaviors may be different from those affecting the mature nicotine dependence phenotype.
C1 [Stephens, Sarah H.; Dueker, Nicole; Cheng, Yu-Ching; Mitchell, Braxton D.] Univ Maryland, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[Hartz, Sarah M.; Saccone, Nancy L.; Pergadia, Michele; Grucza, Richard; Heath, Andrew; Madden, Pamela; Bierut, Laura J.] Washington Univ Sch Med, Dept Psychiat, St Louis, MO USA.
[Hoft, Nicole R.; Corley, Robin C.; Hewitt, John K.; Hopfer, Christian J.; Ehringer, Marissa A.] Univ Colorado, Inst Behav Genet, Boulder, CO 80309 USA.
[Breslau, Naomi] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Coon, Hilary; Leppert, Mark; Cannon, Dale S.; Weiss, Robert B.] Univ Utah Sch Med, Dept Psychiat, Salt Lake City, UT USA.
[Chen, Xiangning; Aggen, Steven H.; Chen, Jingchun; Dick, Danielle; Gillespie, Nathan A.; Kendler, Kenneth S.] Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA USA.
[Ducci, Francesca] Univ London, Kings Coll London, Inst Psychiat, London SW3 6LX, England.
[Ducci, Francesca] St Georges Univ, Dept Mental Hlth, London, England.
[Ducci, Francesca; Couper, David] Univ Pisa, Dept Psychiat Neurobiol Pharmacol & Biotechnol, Pisa, Italy.
[Franceschini, Nora; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Frank, Josef; Rietschel, Marcella] Heidelberg Univ, Clin Fac Mannheim, Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, Mannheim, Germany.
[Han, Younghun; Shete, Sanjay; Spitz, Margaret; Wei, Qingyi; Amos, Chris] MD Anderson, Dept Epidemiol, Houston, TX USA.
[Hansel, Nadia N.; Beaty, Terri H.; Mathias, Rasika A.; Murray, Tanda; Ruczinski, Ingo; Barnes, Kathleen C.] Johns Hopkins Univ, Div Pulm & Crit Care Med, Baltimore, MD USA.
[Jiang, Chenhui; Yang, Bao-Zhu; Han, Shizhong; Gelernter, Joel] Yale Univ Sch Med, Dept Psychiat, New Haven, CT USA.
[Korhonen, Tellervo; Broms, Ulla; Haellfors, Jenni; Heikkilae, Kauko; Kaprio, Jaakko] Univ Helsinki, Dept Publ Hlth, Hjelt Inst, Helsinki, Finland.
[Lind, Penelope A.; Medland, Sarah E.; Montgomery, Grant W.; Martin, Nicholas G.] Queensland Inst Med Res, Dept Epidemiol, Brisbane, Qld 4006, Australia.
[Liu, Jason; Marchini, Jonathan] Univ Oxford, Dept Stat, Oxford OX1 3TG, England.
[Lyytikaeinen, Leo-Pekka; Lehtimaeki, Terho] Tampere Univ Hosp, Dept Clin Chem, Fimlab Labs, FIN-33521 Tampere, Finland.
[Lyytikaeinen, Leo-Pekka; Lehtimaeki, Terho] Univ Tampere Sch Med, Tampere, Finland.
[Michel, Martha; Bergen, Andrew W.; Swan, Gary E.] SRI Int, Ctr Hlth Sci, Menlo Pk, CA 94025 USA.
[Shaffer, John R.; Marazita, Mary L.] Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA.
[Short, Susan E.] Brown Univ, Dept Sociol, Providence, RI 02912 USA.
[Sun, Juzhong; Stevens, Victoria L.] Amer Canc Soc, Dept Epidemiol Res, Atlanta, GA 30329 USA.
[Teumer, Alexander; Baumeister, Sebastian E.; Nauck, Matthias; Grabe, Hans Joergen; Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Univ Med Greifswald, Greifswald, Germany.
[Thompson, John R.] Univ Leicester, Dept Hlth Sci, Leicester, Leics, England.
[Vogelzangs, Nicole; Penninx, Brenda W.] Vrije Univ Amsterdam Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
[Vink, Jacqueline M.; Hottenga, Jouke Jan; Willemsen, Gonneke; Boomsma, Dorret I.] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
[Wenzlaff, Angela; Schwartz, Ann G.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Wheeler, William] NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Balmforth, Anthony J.; Hall, Alistair S.] Univ Leeds, Fac Med & Hlth, LIGHT Res Inst, Leeds, W Yorkshire, England.
[Benjamin, Daniel J.] Cornell Univ, Dept Econ, Ithaca, NY 14853 USA.
[Cesarini, David] NYU, Dept Econ, New York, NY 10003 USA.
[Chatterjee, Nilanjan; Gu, Fangyi] NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Cichon, Sven] Res Ctr Juelich, Life & Brain Ctr, Dept Genom, Inst Neurosci & Med Struct & Funct Org Brain Geno, Julich, Germany.
[Cichon, Sven] Univ Bonn, Life & Brain Ctr, Bonn, Germany.
[Cichon, Sven] Univ Bonn, Inst Human Genet, Bonn, Germany.
[Cucca, Francesco] CNR, Ist Ric Genet & Biomed, Cagliari, Italy.
[Foroud, Tatiana; Edenberg, Howard J.] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Furberg, Helena] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Giegling, Ina; Hartmann, Annette M.; Konte, Bettina; Rujescu, Dan] Univ Munich LMU, Dept Psychiat, Munich, Germany.
[Hickie, Ian B.] Univ Sydney, Brain & Mind Res Inst, Sydney, NSW 2006, Australia.
[Jousilahti, Pekka; Laatikainen, Tiina; Salomaa, Veikko] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Kaakinen, Marika; Veijola, Juha] Univ Oulu, Inst Hlth Sci, SF-90100 Oulu, Finland.
[Kaakinen, Marika; Veijola, Juha] Univ Oulu, Bioctr Oulu, SF-90100 Oulu, Finland.
[Kaehoenen, Mika] Tampere Univ Hosp, Dept Clin Physiol, Tampere, Finland.
[Kaehoenen, Mika] Univ Tampere Sch Med, Tampere, Finland.
[Koellinger, Philipp D.] Erasmus Univ, Dept Appl Econ, Rotterdam, Netherlands.
[Kittner, Stephen] Univ Maryland Sch Med, Baltimore Vet Affairs Med Ctr, Dept Neurol, Baltimore, MD USA.
[Landi, Maria-Teresa; Caporaso, Neil] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Levy, Steven M.] Univ Iowa, Dept Prevent & Community Dent, Iowa City, IA USA.
[Levy, Steven M.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[McNeil, Daniel W.] W Virginia Univ, Dept Psychol & Dent Practice & Rural Hlth, Morgantown, WV 26506 USA.
[Pare, Peter D.] Univ British Columbia, Dept Med, Vancouver, BC, Canada.
[Viikari, Jorma] Turku Univ Hosp, Dept Med, FIN-20520 Turku, Finland.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Human Genet Ctr, Houston, TX 77030 USA.
[Francks, Clyde] Max Planck Inst Psycholinguist, Dept MPI Psycholinguist, Nijmegen, Netherlands.
[Hops, Hyman] Oregon Res Inst, Eugene, OR 97403 USA.
[Jarvelin, Marjo-Riitta] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Biostat, MRC Hlth Protect Agcy HPA Ctr Environm & Hlth, Sch Publ Hlth, London SW7 2AZ, England.
[Jarvelin, Marjo-Riitta] Univ Oulu, Inst Hlth Sci, SF-90100 Oulu, Finland.
[Jarvelin, Marjo-Riitta] Univ Oulu, Bioctr Oulu, SF-90100 Oulu, Finland.
[Jarvelin, Marjo-Riitta] Oulu Univ Hosp, Unit Primary Care, Oulu, Finland.
[Jarvelin, Marjo-Riitta] Natl Inst Hlth & Welf, Dept Children & Young People & Families, Oulu, Finland.
[Johannesson, Magnus] Stockholm Sch Econ, Dept Econ, S-11383 Stockholm, Sweden.
[Magnusson, Patrik K. E.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Noethen, Markus M.] Univ Bonn, Inst Human Genet, Life & Brain Ctr, Dept Genom, Bonn, Germany.
[Raitakari, Olli] Turku Univ Hosp, Dept Clin Physiol & Nucl Med, Turku, Finland.
[Raitakari, Olli] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Samani, Nilesh J.] Univ Leicester, Dept Cardiovasc Sci, Leicester NIHR Biomed Res Unit Cardiovasc Dis, Leicester, Leics, England.
[Hatsukami, Dorothy] Univ Minnesota, Dept Psychiat, Minneapolis, MN 55455 USA.
[Johnson, Eric O.] RTI Int, Dept Behav Hlth Epidemiol, Res Triangle Pk, NC USA.
[Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
RP Ehringer, MA (reprint author), 1480 30th St, Boulder, CO 80303 USA.
EM Marissa.Ehringer@colorado.edu
RI Cichon, Sven/B-9618-2014; Johannesson, Magnus/E-9680-2011; Gu,
Fangyi/I-5957-2014; Medland, Sarah/C-7630-2013; Montgomery,
Grant/B-7148-2008; Cichon, Sven/H-8803-2013; Lyytikainen,
Leo-Pekka/C-8544-2016; Magnusson, Patrik/C-4458-2017;
OI Lind, Penelope/0000-0002-3887-2598; Grucza, Richard/0000-0002-8191-6875;
Bergen, Andrew/0000-0002-1237-7644; Korhonen,
Tellervo/0000-0003-2838-3085; Jarvelin,
Marjo-Riitta/0000-0002-2149-0630; Nothen, Markus/0000-0002-8770-2464;
Hartz, Sarah/0000-0002-5429-3799; Edenberg, Howard/0000-0003-0344-9690;
Mitchell, Braxton/0000-0003-4920-4744; Kaprio,
Jaakko/0000-0002-3716-2455; Martin, Nicholas/0000-0003-4069-8020;
Cichon, Sven/0000-0002-9475-086X; Johannesson,
Magnus/0000-0001-8759-6393; Medland, Sarah/0000-0003-1382-380X;
Montgomery, Grant/0000-0002-4140-8139; Cichon, Sven/0000-0002-9475-086X;
Lyytikainen, Leo-Pekka/0000-0002-7200-5455; Kaakinen,
Marika/0000-0002-9228-0462; Koellinger, Philipp/0000-0001-7413-0412;
Cesarini, David/0000-0002-0043-009X
FU NIH [R01 DA12690, R01 DA12849, K01 DA24758, R01 AA11330, R01 AA017535,
R01 AA07535, R01 AA07728, R01 AA13320, R01AA13321, R01 AA14041, R01
AA11998, R01 AA17688, R01DA012854, K02DA021237, UL1RR024992, R01
DA021913, P60 DA011015, K01 DA19498, R21 DA027070, K02 AA018755, U01
DA020830, R01HL089651-01, N01-AG1-2109, K07 CA118412, R01 DA03706, U01
HG004436]; Australian National Health and Research Council [241944,
339462, 389927, 389875, 389891, 389892, 389938, 442915, 442981, 464914,
496739, 552485, 552498]; Australian Research Council [A7960034,
A79906588, A79801419, APP1009839, DP0770096, DP0212016, DP0343921,
FT110100548]; Germany Federal Ministry for Education and Research [BMBF
NGNF-2, BMBF IG MooDS 01GS08144, 01GS08147]; Alfried Krupp von Bohlen
und Halbach-Stiftung; 5th Framework Programme (FP-5); GenomEUtwin
Project [QLG2-CT-2002-01254]; University of California Tobacco-Related
Disease Research Program [7PT2000-2004]; Academy of Finland [134309,
126925, 121584, 124282, 129378, 117787, 129494, 41071]; Center of
Excellence in Complex Diseases); University Hospital Oulu (Oulu,
Finland); Tampere and Turku University Hospital Medical Funds [9M048,
9N035]; Juho Vainio Foundation; Finnish Foundation for Cardiovascular
Diseases; Paavo Nurmi Foundation; Finnish Foundation of Cardiovascular
Research; Finnish Cultural Foundation; Tampere Tuberculosis Foundation;
Emil Aaltonen Foundation; Social Insurance Institution of Finland;
NARSAD Young Investigator Award; Welcome Trust; British Heart
Foundation; National Institute for Health Research; Academy of Finland
Center of Excellence in Complex Disease Genetics; Global Research Awards
for Nicotine Dependence (GRAND); SALVE Program; NIHR Academic Clinical
Fellowship at the Division of Mental Health, StGeorge's, University of
London, UK; Medical Research Service; Baltimore Geriatrics Research,
Education, and Clinical Center of the Department of Veterans Affairs;
European Commission; Genome EU twin Project under the European
Commission Programme Quality of Life and Management of the Living
Resources of Fifth Framework Programme; Swedish Research Council;
Swedish Council for Working Life and Social Research; Swedish Foundation
for Strategic Research; Swedish Heart and Lung Foundation; Ragnar
Soderberg Foundation; Jan Wallander and Tom Hedelius Foundation; Federal
Ministry of Education and Research [01ZZ9603, 01ZZ0103, 01ZZ0403,
03ZIK012]; Ministry of Cultural Affairs and the Social Ministry of the
Federal State of Mecklenburg-West Pomerania; Siemens Healthcare,
Erlangen, Germany; Federal State of Mecklenburg-West Pomerania;
Netherlands Organization for Scientific Research (NWO); CMSB: Center for
Medical Systems Biology (NWO Genomics); Spinozapremie [SPI
56-464-14192]; VU University Centre for Neurogenomics and Cognitive
Research (CNCR); Genomewide analyses of European twin and population
cohorts [EU/QLRT-2001-01254]; European Research Council: Genetics of
Mental Illness [ERC 230374]; Beyond the Genetics of Addiction [ERC
284167]; Mary Beryl Patch Turnbull Scholar Program; N.I.H [R01 NS45012,
U01 NS069208, P01 CA089392, R01 DA12854, R01 CA060691, N01-PC35146, R01
CA87895, P01 AG005842, T32 AG000186, K99R00 DA023549, R01 DA026911, KL2
RR024994, K08 DA032680, P30 DK-072488, U01 HG004738, R01 DE12101]
FX NIH Grants R01 DA12690, R01 DA12849, K01 DA24758, R01 AA11330, R01
AA017535, R01 AA07535, R01 AA07728, R01 AA13320, R01AA13321, R01
AA14041, R01 AA11998, R01 AA17688, R01DA012854, K02DA021237,
UL1RR024992, R01 DA021913, P60 DA011015, K01 DA19498, R21 DA027070, K02
AA018755, U01 DA020830, R01HL089651-01, N01-AG1- 2109, K07 CA118412, R01
DA03706, U01 HG004436, R01 NS45012, U01 NS069208, P01 CA089392, R01
DA12854, R01 CA060691, N01-PC35146, R01 CA87895, P01 AG005842, T32
AG000186, K99R00 DA023549, R01 DA026911, KL2 RR024994, K08 DA032680, P30
DK-072488, U01 HG004738, R01 DE12101; Australian National Health and
Research Council (241944, 339462, 389927, 389875, 389891, 389892,
389938, 442915, 442981, 464914, 496739, 552485, 552498); Australian
Research Council (A7960034, A79906588, A79801419, APP1009839, DP0770096,
DP0212016, DP0343921, and FT110100548); Germany Federal Ministry for
Education and Research (project grants BMBF NGNF-2; BMBF NGFNplus; BMBF
IG MooDS 01GS08144 and 01GS08147); Alfried Krupp von Bohlen und
Halbach-Stiftung; 5th Framework Programme (FP-5); GenomEUtwin Project
(QLG2-CT-2002-01254); 7PT2000-2004, from the University of California
Tobacco-Related Disease Research Program; Academy of Finland (project
grants 134309, 126925, 121584, 124282, 129378, 117787, 129494, 41071 and
The Center of Excellence in Complex Diseases); University Hospital Oulu
(Oulu, Finland); Tampere and Turku University Hospital Medical Funds
(project grants 9M048 and 9N035); Juho Vainio Foundation; Finnish
Foundation for Cardiovascular Diseases; Paavo Nurmi Foundation; Finnish
Foundation of Cardiovascular Research; Finnish Cultural Foundation;
Tampere Tuberculosis Foundation and Emil Aaltonen Foundation (T. L.);
Social Insurance Institution of Finland; NARSAD Young Investigator
Award; Welcome Trust; British Heart Foundation; National Institute for
Health Research; Academy of Finland Center of Excellence in Complex
Disease Genetics; Global Research Awards for Nicotine Dependence
(GRAND); SALVE Program; NIHR Academic Clinical Fellowship at the
Division of Mental Health, StGeorge's, University of London, UK; Medical
Research Service and the Baltimore Geriatrics Research, Education, and
Clinical Center of the Department of Veterans Affairs; The European
Commission; Genome EU twin Project under the European Commission
Programme Quality of Life and Management of the Living Resources of
Fifth Framework Programme; the Swedish Research Council; the Swedish
Council for Working Life and Social Research; the Swedish Foundation for
Strategic Research; the Swedish Heart and Lung Foundation; the Ragnar
Soderberg Foundation; the Jan Wallander and Tom Hedelius Foundation;
Federal Ministry of Education and Research (grants 01ZZ9603, 01ZZ0103,
01ZZ0403, and 03ZIK012); The Ministry of Cultural Affairs and the Social
Ministry of the Federal State of Mecklenburg-West Pomerania; joint grant
from Siemens Healthcare, Erlangen, Germany and the Federal State of
Mecklenburg-West Pomerania. For the NTR study (www.tweelingregister.org)
funding was obtained from the Netherlands Organization for Scientific
Research (NWO); CMSB: Center for Medical Systems Biology (NWO Genomics);
Spinozapremie (SPI 56-464-14192); the VU University Centre for
Neurogenomics and Cognitive Research (CNCR); Genomewide analyses of
European twin and population cohorts (EU/QLRT-2001-01254); the European
Research Council: Genetics of Mental Illness (ERC 230374) and Beyond the
Genetics of Addiction (ERC 284167). KCB was supported in part by the
Mary Beryl Patch Turnbull Scholar Program.
NR 78
TC 14
Z9 14
U1 2
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD DEC
PY 2013
VL 37
IS 8
BP 846
EP 859
DI 10.1002/gepi.21760
PG 14
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 251ZZ
UT WOS:000326975300010
PM 24186853
ER
PT J
AU Kubo, A
Cook, MB
Shaheen, NJ
Vaughan, TL
Whiteman, DC
Murray, L
Corley, DA
AF Kubo, Ai
Cook, Michael Blaise
Shaheen, Nicholas J.
Vaughan, Thomas L.
Whiteman, David C.
Murray, Liam
Corley, Douglas A.
TI Sex-specific associations between body mass index, waist circumference
and the risk of Barrett's oesophagus: a pooled analysis from the
international BEACON consortium
SO GUT
LA English
DT Article
DE Barrett's Oesophagus; Obesity; Gastroesophageal Reflux Disease;
Nutrition
ID GASTROESOPHAGEAL-REFLUX DISEASE; GROWTH-FACTOR-I; METABOLIC SYNDROME;
ABDOMINAL OBESITY; GASTRIC CARDIA; ESOPHAGOGASTRIC JUNCTION;
BREAST-CANCER; ADENOCARCINOMA; METAANALYSIS; HYPERINSULINEMIA
AB Objective Barrett's oesophagus is a precursor lesion of oesophageal adenocarcinoma, a cancer that, in the USA, has increased in incidence over 600% during the past 40years. Barrett's oesophagus and oesophageal adenocarcinoma are much more common among men than among women; this finding is unexplained and most earlier studies lacked sufficient numbers of women to evaluate sex-specific risk factors. We leveraged the power of an international consortium to assess sex-specific relationships between body mass index (BMI), abdominal circumference and Barrett's oesophagus.
Design Four case-control studies provided a total of 1102 cases (316 women, 786 men) and 1400 population controls (436 women, 964 men) for analysis. Study-specific estimates, generated using individual participant data, were combined using random effects meta-analysis.
Results Waist circumference was significantly associated with Barrett's oesophagus, even after adjustment for BMI; persons in the highest versus the lowest quartiles of waist circumference had approximately 125% and 275% increases in the odds of Barrett's oesophagus among men and women, respectively (OR 2.24, 95% CI 1.08 to 4.65, I-2=57; OR 3.75, 95% CI 1.47 to 9.56, I-2=0). In contrast, there was no evidence of a significant association between BMI and the risk of Barrett's oesophagus, with or without adjustment for waist circumference.
Conclusions Waist circumference, independent of BMI, was found to be a risk factor for Barrett's oesophagus among both men and women. Future studies examining the biological mechanisms of this association will extend our knowledge regarding the pathogenesis of Barrett's oesophagus.
C1 [Kubo, Ai; Corley, Douglas A.] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
[Cook, Michael Blaise] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Shaheen, Nicholas J.] Univ N Carolina, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Vaughan, Thomas L.] Fred Hutchinson Canc Res Ctr, Dept Epidemiol, Seattle, WA 98104 USA.
[Whiteman, David C.] Queensland Inst Med Res, Dept Populat & Canc Studies, Brisbane, Qld 4006, Australia.
[Murray, Liam] Sch Med, Belfast, Antrim, North Ireland.
RP Kubo, A (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94612 USA.
EM ai.kubo@kp.org
RI Cook, Michael/A-5641-2009; Whiteman, David/P-2728-2014
OI Cook, Michael/0000-0002-0533-7302; Whiteman, David/0000-0003-2563-9559
FU National Institutes of Health [RO1 DK63616, 1R21DK077742, K23DK59311,
R03DK75842]; intramural program of the National Institutes of Health;
Ireland-Northern Ireland cooperation research project; Northern Ireland
Research and Development Office; Health Research Board, Ireland (FINBAR)
[RES/1699/01N/S]; Study of Digestive Health [NCI RO1 CA 001833]; Study
of Reflux Disease [NCI R01 CA72866]; Established Investigator Award in
Cancer Prevention and Control [K05 CA124911, KR021183]
FX This work was supported by the National Institutes of Health RO1 DK63616
(AK and DAC); 1R21DK077742 (AK, NJS and DAC); K23DK59311 and R03DK75842
(NJS); the intramural program of the National Institutes of Health
(MBC); an Ireland-Northern Ireland cooperation research project grant
sponsored by the Northern Ireland Research and Development Office and
the Health Research Board, Ireland (FINBAR) (LM: RES/1699/01N/S); the
Study of Digestive Health, NCI RO1 CA 001833 (DCW); the Study of Reflux
Disease, NCI R01 CA72866 (TLV) and the Established Investigator Award in
Cancer Prevention and Control, K05 CA124911 (TLV, Kaiser Permanente
Community Benefit Grant (KR021183)).
NR 47
TC 51
Z9 51
U1 0
U2 5
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 DEC
PY 2013
VL 62
IS 12
BP 1684
EP 1691
DI 10.1136/gutjnl-2012-303753
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 250TH
UT WOS:000326877200005
PM 23355549
ER
PT J
AU Xin, HW
Ambe, CM
Hari, DM
Wiegand, GW
Miller, TC
Chen, JQ
Anderson, AJ
Ray, S
Mullinax, JE
Koizumi, T
Langan, RC
Burka, D
Herrmann, MA
Goldsmith, PK
Stojadinovic, A
Rudloff, U
Thorgeirsson, SS
Avital, I
AF Xin, Hong-Wu
Ambe, Chenwi M.
Hari, Danielle M.
Wiegand, Gordon W.
Miller, Tyler C.
Chen, Jin-Qiu
Anderson, Andrew J.
Ray, Satyajit
Mullinax, John E.
Koizumi, Tomotake
Langan, Russell C.
Burka, Douglas
Herrmann, Michelle A.
Goldsmith, Paul K.
Stojadinovic, Alexander
Rudloff, Udo
Thorgeirsson, Snorri S.
Avital, Itzhak
TI Label-retaining liver cancer cells are relatively resistant to sorafenib
SO GUT
LA English
DT Article
DE Cancer; Cell Proliferation; Drug Resistance; Hepatocellular Carcinoma;
Stem Cells
ID ADVANCED HEPATOCELLULAR-CARCINOMA; MULTIKINASE INHIBITOR;
MYELOID-LEUKEMIA; STEM-CELLS; PROLIFERATION; APOPTOSIS; DIVISION
AB Objective The standard therapy for advanced hepatocellular carcinoma (HCC) is sorafenib, with most patients experiencing disease progression within 6months. Label-retaining cancer cells (LRCC) represent a novel subpopulation of cancer stem cells (CSC). The objective was to test whether LRCC are resistant to sorafenib.
Methods We tested human HCC derived LRCC and non-LRCC before and after treatment with sorafenib.
Results LRCC derived from human HCC are relatively resistant to sorafenib. The proportion of LRCC in HCC cell lines is increased after sorafenib while the general population of cancer cells undergoes growth suppression. We show that LRCC demonstrate improved viability and toxicity profiles, and reduced apoptosis, over non-LRCC. We show that after treatment with sorafenib, LRCC upregulate the CSC marker aldehyde dehydrogenase 1 family, wingless-type MMTV-integration-site family, cell survival and proliferation genes, and downregulate apoptosis, cell cycle arrest, cell adhesion and stem cells differentiation genes. This phenomenon was accompanied by non-uniform activation of specific isoforms of the sorafenib target proteins extracellular-signal-regulated kinases and v-akt-murine-thymoma-viral-oncogene homologue (AKT) in LRCC but not in non-LRCC. A molecular pathway map for sorafenib treated LRCC is proposed.
Conclusions Our results suggest that HCC derived LRCC are relatively resistant to sorafenib. Since LRCC can generate tumours with as few as 10 cells, our data suggest a potential role for these cells in disease recurrence. Further investigation of this phenomenon might provide novel insights into cancer biology, cancer recurrence and drug resistance with important implications for the development of novel cancer therapies based on targeting LRCC.
C1 [Xin, Hong-Wu; Ambe, Chenwi M.; Hari, Danielle M.; Wiegand, Gordon W.; Miller, Tyler C.; Anderson, Andrew J.; Ray, Satyajit; Mullinax, John E.; Koizumi, Tomotake; Langan, Russell C.; Burka, Douglas; Rudloff, Udo; Avital, Itzhak] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Chen, Jin-Qiu; Herrmann, Michelle A.; Goldsmith, Paul K.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Stojadinovic, Alexander] Walter Reed Natl Mil Med Ctr, Div Surg Oncol, Dept Surg, Bethesda, MD USA.
[Stojadinovic, Alexander; Avital, Itzhak] Uniformed Serv Univ Hlth Sci, Dept Surg, Bethesda, MD 20814 USA.
[Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Avital, Itzhak] Bon Secours Canc Inst, Richmond, VA 23230 USA.
RP Thorgeirsson, SS (reprint author), NCI, Ctr Excellence Integrat Canc Biol & Genom, Expt Carcinogenesis Lab, Ctr Canc Res,NIH, 37 Convent Dr MSC 4262,Bldg 37,Room 4146A, Bethesda, MD 20892 USA.
EM snorri_thorgeirsson@nih.gov; itzhak.avital@gmail.com
RI Mullinax, John/L-2509-2014
FU NIH/National Cancer Institute, NCI [1ZIABC011005]
FX The NIH/National Cancer Institute, NCI intramural grant 1ZIABC011005.
NR 22
TC 21
Z9 21
U1 1
U2 8
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 DEC
PY 2013
VL 62
IS 12
BP 1777
EP 1786
DI 10.1136/gutjnl-2012-303261
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 250TH
UT WOS:000326877200016
PM 23411027
ER
PT J
AU Liu, QY
Pittaluga, S
Davies-Hill, T
Raffeld, M
Xi, LQ
Jaffe, ES
AF Liu, Qingyan
Pittaluga, Stefania
Davies-Hill, Theresa
Raffeld, Mark
Xi, Liqiang
Jaffe, Elaine S.
TI Increased CD5-positive polyclonal B cells in Castleman disease: a
diagnostic pitfall
SO HISTOPATHOLOGY
LA English
DT Letter
C1 [Liu, Qingyan; Pittaluga, Stefania; Davies-Hill, Theresa; Raffeld, Mark; Xi, Liqiang; Jaffe, Elaine S.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Liu, QY (reprint author), NCI, Pathol Lab, Bldg 10, Bethesda, MD 20892 USA.
OI Jaffe, Elaine/0000-0003-4632-0301
FU Intramural NIH HHS [ZIA BC011070-05]
NR 8
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0309-0167
EI 1365-2559
J9 HISTOPATHOLOGY
JI Histopathology
PD DEC
PY 2013
VL 63
IS 6
BP 877
EP 880
DI 10.1111/his.12213
PG 4
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 252PB
UT WOS:000327018300015
PM 24033372
ER
PT J
AU Leoyklang, P
Suphapeetiporn, K
Srichomthong, C
Tongkobpetch, S
Fietze, S
Dorward, H
Cullinane, AR
Gahl, WA
Huizing, M
Shotelersuk, V
AF Leoyklang, Petcharat
Suphapeetiporn, Kanya
Srichomthong, Chalurmpon
Tongkobpetch, Siraprapa
Fietze, Stefanie
Dorward, Heidi
Cullinane, Andrew R.
Gahl, William A.
Huizing, Marjan
Shotelersuk, Vorasuk
TI Disorders with similar clinical phenotypes reveal underlying genetic
interaction: SATB2 acts as an activator of the UPF3B gene
SO HUMAN GENETICS
LA English
DT Article
ID CLEFT-PALATE; MESSENGER-RNA; MENTAL-RETARDATION; PROTEIN; EXPRESSION;
MUTATIONS; COMPLEX; NUCLEUS; DECAY; DIFFERENTIATION
AB Two syndromic cognitive impairment disorders have very similar craniofacial dysmorphisms. One is caused by mutations of SATB2, a transcription regulator and the other by heterozygous mutations leading to premature stop codons in UPF3B, encoding a member of the nonsense-mediated mRNA decay complex. Here we demonstrate that the products of these two causative genes function in the same pathway. We show that the SATB2 nonsense mutation in our patient leads to a truncated protein that localizes to the nucleus, forms a dimer with wild-type SATB2 and interferes with its normal activity. This suggests that the SATB2 nonsense mutation has a dominant negative effect. The patient's leukocytes had significantly decreased UPF3B mRNA compared to controls. This effect was replicated both in vitro, where siRNA knockdown of SATB2 in HEK293 cells resulted in decreased UPF3B expression, and in vivo, where embryonic tissue of Satb2 knockout mice showed significantly decreased Upf3b expression. Furthermore, chromatin immunoprecipitation demonstrates that SATB2 binds to the UPF3B promoter, and a luciferase reporter assay confirmed that SATB2 expression significantly activates gene transcription using the UPF3B promoter. These findings indicate that SATB2 activates UPF3B expression through binding to its promoter. This study emphasizes the value of recognizing disorders with similar clinical phenotypes to explore underlying mechanisms of genetic interaction.
C1 [Leoyklang, Petcharat] Chulalongkorn Univ, Program Biomed Sci, Fac Grad Sch, Bangkok, Thailand.
[Leoyklang, Petcharat; Suphapeetiporn, Kanya; Srichomthong, Chalurmpon; Tongkobpetch, Siraprapa; Shotelersuk, Vorasuk] Chulalongkorn Univ, Fac Med, Dept Pediat, Ctr Excellence Med Genet, Bangkok 10330, Thailand.
[Leoyklang, Petcharat; Suphapeetiporn, Kanya; Srichomthong, Chalurmpon; Tongkobpetch, Siraprapa; Shotelersuk, Vorasuk] King Chulalongkorn Mem Hosp, Thai Red Cross Soc, Excellence Ctr Med Genet, Bangkok, Thailand.
[Leoyklang, Petcharat; Dorward, Heidi; Cullinane, Andrew R.; Gahl, William A.; Huizing, Marjan] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Suphapeetiporn, Kanya] King Chulalongkorn Mem Hosp, Dept Pediat, Div Med Genet & Metab, Bangkok 10330, Thailand.
[Fietze, Stefanie] Max Planck Inst Immunobiol & Epigenet, Dept Cellular & Mol Immunol, D-79108 Freiburg, Germany.
RP Huizing, M (reprint author), NHGRI, Med Genet Branch, NIH, 10 Ctr Dr,Bldg 10,Room 10C103, Bethesda, MD 20892 USA.
EM kanya.su@chula.ac.th; mhuizing@mail.nih.gov
FU Royal Golden Jubilee Ph.D. Program [PHD/0026/2549]; Intramural Research
Program of the National Human Genome Research Institute, National
Institutes of Health, Bethesda, MD, USA; Thailand Research Fund;
Ratchadapiseksomphot Fund [RES560530177-HR]; Chulalongkorn University
Centenary Academic Development Project [CU56-HR05]; Higher Education
Research Promotion and National Research University Project of Thailand,
Office of the Higher Education Commission [HR1163A]
FX We like to thank Drs. Gergana Dobreva and Rudolph Grosschedl (Max Planck
Institution for Immunobiology and Epigenetics, Freiburg, Germany) for
kindly providing the pfos-luc-Wt SATB2 plasmid and Satb2 knockout mice.
This study was supported by the Royal Golden Jubilee Ph.D. Program to PL
(Grant No PHD/0026/2549); the Intramural Research Program of the
National Human Genome Research Institute, National Institutes of Health,
Bethesda, MD, USA; The Thailand Research Fund; Ratchadapiseksomphot Fund
(RES560530177-HR), Chulalongkorn University Centenary Academic
Development Project (CU56-HR05), and the Higher Education Research
Promotion and National Research University Project of Thailand, Office
of the Higher Education Commission (HR1163A).
NR 35
TC 9
Z9 9
U1 3
U2 9
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 DEC
PY 2013
VL 132
IS 12
BP 1383
EP 1393
DI 10.1007/s00439-013-1345-9
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 251LE
UT WOS:000326929500006
PM 23925499
ER
PT J
AU Dumitrescu, L
Carty, CL
Franceschini, N
Hindorff, LA
Cole, SA
Buzkova, P
Schumacher, FR
Eaton, CB
Goodloe, RJ
Duggan, DJ
Haessler, J
Cochran, B
Henderson, BE
Cheng, I
Johnson, KC
Carlson, CS
Love, SA
Brown-Gentry, K
Nato, AQ
Quibrera, M
Shohet, RV
Ambite, JL
Wilkens, LR
Le Marchand, L
Haiman, CA
Buyske, S
Kooperberg, C
North, KE
Fornage, M
Crawford, DC
AF Dumitrescu, Logan
Carty, Cara L.
Franceschini, Nora
Hindorff, Lucia A.
Cole, Shelley A.
Buzkova, Petra
Schumacher, Fredrick R.
Eaton, Charles B.
Goodloe, Robert J.
Duggan, David J.
Haessler, Jeff
Cochran, Barbara
Henderson, Brian E.
Cheng, Iona
Johnson, Karen C.
Carlson, Chris S.
Love, Shelly-Anne
Brown-Gentry, Kristin
Nato, Alejandro Q.
Quibrera, Miguel
Shohet, Ralph V.
Ambite, Jose Luis
Wilkens, Lynne R.
Le Marchand, Loic
Haiman, Christopher A.
Buyske, Steven
Kooperberg, Charles
North, Kari E.
Fornage, Myriam
Crawford, Dana C.
TI No evidence of interaction between known lipid-associated genetic
variants and smoking in the multi-ethnic PAGE population
SO HUMAN GENETICS
LA English
DT Article
AB Genome-wide association studies (GWAS) have identified many variants that influence high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and/or triglycerides. However, environmental modifiers, such as smoking, of these known genotype-phenotype associations are just recently emerging in the literature. We have tested for interactions between smoking and 49 GWAS-identified variants in over 41,000 racially/ethnically diverse samples with lipid levels from the Population Architecture Using Genomics and Epidemiology (PAGE) study. Despite their biological plausibility, we were unable to detect significant SNP x smoking interactions.
C1 [Dumitrescu, Logan; Goodloe, Robert J.; Brown-Gentry, Kristin; Crawford, Dana C.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN 37232 USA.
[Carty, Cara L.; Haessler, Jeff; Carlson, Chris S.; Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Franceschini, Nora; Love, Shelly-Anne; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Hindorff, Lucia A.] NHGRI, Off Populat Genom, Bethesda, MD 20892 USA.
[Cole, Shelley A.] Texas Biomed Res Inst, Dept Genet, San Antonio, TX USA.
[Buzkova, Petra] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Schumacher, Fredrick R.; Henderson, Brian E.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Eaton, Charles B.] Brown Univ, Dept Family Med, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Duggan, David J.] Translat Genom Sci Inst, Phoenix, AZ USA.
[Cochran, Barbara] Baylor Coll Med, Houston, TX 77030 USA.
[Cheng, Iona; Wilkens, Lynne R.; Le Marchand, Loic] Univ Hawaii, Canc Res Ctr, Honolulu, HI 96813 USA.
[Johnson, Karen C.] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[Nato, Alejandro Q.; Buyske, Steven] Rutgers State Univ, Dept Genet, Piscataway, NJ USA.
[Quibrera, Miguel] Univ N Carolina, Gillings Sch Publ Hlth, Chapel Hill, NC USA.
[Shohet, Ralph V.] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96822 USA.
[Ambite, Jose Luis] Univ So Calif, Inst Informat Sci, Marina Del Rey, CA 90292 USA.
[Buyske, Steven] Rutgers State Univ, Dept Stat, Piscataway, NJ USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Div Epidemiol Human Genet & Environm Sci, Sch Publ Hlth, Houston, TX 77030 USA.
[Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Inst Mol Med, Houston, TX 77030 USA.
[Crawford, Dana C.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
RP Crawford, DC (reprint author), Vanderbilt Univ, Ctr Human Genet Res, 2215 Garland Ave,515B Light Hall, Nashville, TN 37232 USA.
EM logan.dumitrescu@chgr.mc.vanderbilt.edu; crawford@chgr.mc.vanderbilt.edu
RI Nato, Alejandro/J-3880-2016;
OI Nato, Alejandro/0000-0002-8745-9046; Buyske, Steven/0000-0001-8539-5416
FU National Human Genome Research Institute (NHGRI); CALiCo [U01HG004803];
EAGLE [U01HG004798]; MEC [U01HG004802]; WHI [U01HG004790]; Coordinating
Center [U01HG004801]; NHGRI ARRA; NHGRI PAGE [U01HG004803, U01HG004798,
U01HG004802, U01HG004790]; NHLBI [N01-HV-48195, U01 HL65520, U01
HL41642, U01 HL41652, U01 HL41654, U01 HL65521]; Centers for Disease
Control and Prevention; National Cancer Institute [R37CA54281, R01 CA63,
P01CA33619, U01CA136792, U01CA98758]; National Heart, Lung, and Blood
Institute; NIH; U.S. Department of Health and Human Services
[N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115,
32118-32119, 32122, 42107-26, 42129-32, 44221]; National Heart, Lung,
and Blood Institute [HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN 268201100009C,
HHSN268201100010C, HHSN268201100011C, HHSN268201100012C]; National
Institutes of Health, National Heart, Lung and Blood Institute
[N01-HC-95095, N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050,
N01-HC-45134, N01-HC-05187, N01-HC-45205]; National Heart, Lung, and
Blood Institute (NHLBI) [HHSN268201200036C, N01-HC-85239, N01-HC-85079,
N01-HC-85080, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084,
N01-HC-85085, N01-HC-85086, N01-HC-35129, N01 HC-15103, N01 HC-55222,
N01-HC-75150, N01-HC-45133, HL080295]; National Institute on Aging (NIA)
[AG-023629, AG-15928, AG-20098, AG-027058]
FX 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. The
"Epidemiologic Architecture for Genes Linked to Environment (EAGLE)" is
funded through the NHGRI PAGE program (U01HG004798 and its NHGRI ARRA
supplement). Genotyping services for select NHANES III SNPs presented
here were also provided by the Johns Hopkins University under federal
contract number (N01-HV-48195) from NHLBI. The study participants were
derived from the National Health and Nutrition Examination Surveys
(NHANES), and these studies are supported by the Centers for Disease
Control and Prevention. The findings and conclusions in this report are
those of the authors and do not necessarily represent the views of the
Centers for Disease Control and Prevention. The Multiethnic Cohort study
(MEC) characterization 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 CA63, 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; NIH; and U.S.
Department of Health and Human Services through contracts N01WH22110,
24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122,
42107-26, 42129-32, and 44221. 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
studies contributed to this manuscript and are 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, HHSN 268201100009C,
HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C. The
Coronary Artery Risk Development in Young Adults (CARDIA) study is
supported by the following National Institutes of Health, National
Heart, Lung and Blood Institute contracts: N01-HC-95095; N01-HC-48047;
N01-HC-48048; N01-HC-48049; N01-HC-48050; N01-HC-45134; N01-HC-05187;
and N01-HC-45205. The Cardiovascular Health Study (CHS) is supported by
contracts HHSN268201200036C, N01-HC-85239, N01-HC-85079 through
N01-HC-85086, N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150,
N01-HC-45133, and grant 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 through AG-023629, AG-15928, AG-20098, and
AG-027058 from the National Institute on Aging (NIA). The Strong Heart
Study (SHS) is supported by NHLBI grants U01 HL65520, U01 HL41642, U01
HL41652, U01 HL41654, and U01 HL65521. The opinions expressed in this
paper are those of the author(s) and do not necessarily reflect the
views of the Indian Health Service. Assistance with phenotype
harmonization, SNP selection and annotation, data cleaning, data
management, integration and dissemination, and general study
coordination were provided by the PAGE Coordinating Center (U01HG004801
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 7
TC 1
Z9 1
U1 0
U2 2
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 DEC
PY 2013
VL 132
IS 12
BP 1427
EP 1431
DI 10.1007/s00439-013-1375-3
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 251LE
UT WOS:000326929500010
PM 24100633
ER
PT J
AU Sergeev, YV
Vitale, S
Sieving, PA
Vincent, A
Robson, AG
Moore, AT
Webster, AR
Holder, GE
AF Sergeev, Yuri V.
Vitale, Susan
Sieving, Paul A.
Vincent, Ajoy
Robson, Anthony G.
Moore, Anthony T.
Webster, Andrew R.
Holder, Graham E.
TI Molecular modeling indicates distinct classes of missense variants with
mild and severe XLRS phenotypes
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID X-LINKED RETINOSCHISIS; PROTEIN DISULFIDE-ISOMERASE; JUVENILE
RETINOSCHISIS; B-WAVE; ENDOPLASMIC-RETICULUM; GENE-THERAPY; A-WAVE;
MUTATIONS; DOMAIN; ELECTRORETINOGRAM
AB X-linked retinoschisis (XLRS) is a vitreo-retinal degeneration caused by mutations in the RS1 gene which encodes the protein retinoschisin (RS1), required for the structural and functional integrity of the retina. Data are presented from a group of 38 XLRS patients from Moorfields Eye Hospital (London, UK) who had one of 18 missense mutations in RS1. Patients were grouped based on mutation severity predicted by molecular modeling: mild (class I), moderate (intermediate) and severe (class II). Most patients had an electronegative scotopic bright flash electroretinogram (ERG) (reduced b/a-wave ratio) in keeping with predominant inner retinal dysfunction. An association between the type of structural RS1 alterations and the severity of b/a-wave reduction was found in all but the oldest group of patients, significant in patients aged 15-30 years. Severe RS1 missense changes were associated with a lower ERG b/a ratio than were mild changes, suggesting that the extent of inner retinal dysfunction is influenced by the effect of the mutations on protein structure. The majority of class I mutations showed no changes involving cysteine residues. Class II mutations caused severe perturbations due to the removal or insertion of cysteine residues or due to changes in the hydrophobic core. The ERG b/a ratio in intermediate cases was abnormal but showed significant variability, possibly related to the role of praline or arginine residues. We also conducted a second study, using a completely independent cohort, to indicate a genotype-ERG phenotype correlation.
C1 [Sergeev, Yuri V.] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
[Vitale, Susan] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Sieving, Paul A.] NEI, NIH, Bethesda, MD 20892 USA.
[Vincent, Ajoy; Robson, Anthony G.; Holder, Graham E.] Moorfields Eye Hosp, Dept Electrophysiol, London, England.
[Robson, Anthony G.; Moore, Anthony T.; Webster, Andrew R.; Holder, Graham E.] UCL, Inst Ophthalmol, London, England.
RP Sergeev, YV (reprint author), NEI, OGVFB, Bldg 10,Rm 5B47,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sergeevy@nei.nih.gov
OI Vincent, Ajoy/0000-0001-6446-3846
FU National Institutes of Health [Z01-EY000476-01, Z01-DC000065-08];
Foundation Fighting Blindness (USA); National Institute for Health
Research UK (NIHR) Biomedical Research Centre based at Moorfields Eye
Hospital NHS Foundation Trust; UCL Institute of Ophthalmology
FX This work was supported by National Institutes of Health
(Z01-EY000476-01 to Y.V.S., and Z01-DC000065-08 to P.A.S.) and
Foundation Fighting Blindness (USA), and was partly funded by the
National Institute for Health Research UK (NIHR) Biomedical Research
Centre based at Moorfields Eye Hospital NHS Foundation Trust and UCL
Institute of Ophthalmology.
NR 60
TC 6
Z9 7
U1 1
U2 4
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 DEC 1
PY 2013
VL 22
IS 23
BP 4756
EP 4767
DI 10.1093/hmg/ddt329
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 251ZD
UT WOS:000326973000010
PM 23847049
ER
PT J
AU Miura, K
Takashima, E
Deng, BB
Tullo, G
Diouf, A
Moretz, SE
Nikolaeva, D
Diakite, M
Fairhurst, RM
Fay, MP
Long, CA
Tsuboi, T
AF Miura, Kazutoyo
Takashima, Eizo
Deng, Bingbing
Tullo, Gregory
Diouf, Ababacar
Moretz, Samuel E.
Nikolaeva, Daria
Diakite, Mahamadou
Fairhurst, Rick M.
Fay, Michael P.
Long, Carole A.
Tsuboi, Takafumi
TI Functional Comparison of Plasmodium falciparum Transmission-Blocking
Vaccine Candidates by the Standard Membrane-Feeding Assay
SO INFECTION AND IMMUNITY
LA English
DT Article
ID CELL-FREE SYSTEM; MALARIA; ANTIBODIES; ANTIGEN; DISCOVERY; PROTEINS;
PFS230; TRIAL; STAGE
AB Recently, there has been a renewed interest in the development of transmission-blocking vaccines (TBV) against Plasmodium falciparum malaria. While several candidate TBVs have been reported, studies directly comparing them in functional assays are limited. To this end, recombinant proteins of TBV candidates Pfs25, Pfs230, and PfHAP2 were expressed in the wheat germ cell-free expression system. Outbred CD-1 mice were immunized twice with the antigens. Two weeks after the second immunization, IgG levels were measured by enzyme-linked immunosorbent assay (ELISA), and IgG functionality was assessed by the standard membrane-feeding assay (SMFA) using cultured P. falciparum NF54 gametocytes and Anopheles stephensi mosquitoes. All three recombinant proteins elicited similar levels of antigen-specific IgG judged by ELISA. When IgGs purified from pools of immune serum were tested at 0.75 mg/ml in the SMFA, all three IgGs showed 97 to 100% inhibition in oocyst intensity compared to control IgG. In two additional independent SMFA evaluations, anti-Pfs25, anti-Pfs230, and anti-PfHAP2 IgGs inhibited oocyst intensity in a dose-dependent manner. When all three data sets were analyzed, anti-Pfs25 antibody showed significantly higher inhibition than the other two antibodies (P < 0.001 for both), while there was no significant difference between the other two (P = 0.15). A proportion of plasma samples collected from adults living in an area of malaria endemicity in Mali recognized Pfs230 and PfHAP2. This is the first study showing that the HAP2 protein of P. falciparum can induce transmission-blocking antibody. The current study supports the possibility of using this system for a comparative study with multiple TBV candidates.
C1 [Miura, Kazutoyo; Deng, Bingbing; Tullo, Gregory; Diouf, Ababacar; Moretz, Samuel E.; Nikolaeva, Daria; Fairhurst, Rick M.; Long, Carole A.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Takashima, Eizo; Tsuboi, Takafumi] Ehime Univ, Div Malaria Res, Proteosci Ctr, Matsuyama, Ehime, Japan.
[Diakite, Mahamadou] Univ Bamako, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Fay, Michael P.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Tsuboi, Takafumi] Ehime Univ, Venture Business Lab, Matsuyama, Ehime, Japan.
RP Tsuboi, T (reprint author), Ehime Univ, Div Malaria Res, Proteosci Ctr, Matsuyama, Ehime, Japan.
EM clong@niaid.nih.gov; tsuboi@ccr.ehime-u.ac.jp
OI Fay, Michael P./0000-0002-8643-9625
FU National Institute of Allergy and Infectious Diseases, NIH; PATH Malaria
Vaccine Initiative; MEXT KAKENHI [23117008]; JSPS KAKENHI in Japan
[23406007]
FX This study was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, NIH, the PATH
Malaria Vaccine Initiative, and MEXT KAKENHI (23117008) and JSPS KAKENHI
(23406007) in Japan.
NR 22
TC 26
Z9 27
U1 3
U2 15
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD DEC
PY 2013
VL 81
IS 12
BP 4377
EP 4382
DI 10.1128/IAI.01056-13
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 253EU
UT WOS:000327066100005
PM 24042109
ER
PT J
AU Tremblay, JM
Mukherjee, J
Leysath, CE
Debatis, M
Ofori, K
Baldwin, K
Boucher, C
Peters, R
Beamer, G
Sheoran, A
Bedenice, D
Tzipori, S
Shoemaker, CB
AF Tremblay, Jacqueline M.
Mukherjee, Jean
Leysath, Clinton E.
Debatis, Michelle
Ofori, Kwasi
Baldwin, Karen
Boucher, Courtney
Peters, Rachel
Beamer, Gillian
Sheoran, Abhineet
Bedenice, Daniela
Tzipori, Saul
Shoemaker, Charles B.
TI A Single VHH-Based Toxin-Neutralizing Agent and an Effector Antibody
Protect Mice against Challenge with Shiga Toxins 1 and 2
SO INFECTION AND IMMUNITY
LA English
DT Article
ID HEMOLYTIC-UREMIC SYNDROME; ESCHERICHIA-COLI; MONOCLONAL-ANTIBODIES;
SYSTEMIC COMPLICATIONS; ENDOTHELIAL-CELLS; IMMUNE-COMPLEXES;
BINDING-AGENTS; INFECTION; RECEPTOR; ASSOCIATION
AB Shiga toxin-producing Escherichia coli (STEC) is a major cause of severe food-borne disease worldwide, and two Shiga toxins, Stx1 and Stx2, are primarily responsible for the serious disease consequence, hemolytic-uremic syndrome (HUS). Here we report identification of a panel of heavy-chain-only antibody (Ab) VH (VHH) domains that neutralize Stx1 and/or Stx2 in cell-based assays. VHH heterodimer toxin-neutralizing agents containing two linked Stx1-neutralizing VHHs or two Stx2-neutralizing VHHs were generally much more potent at Stx neutralization than a pool of the two-component monomers tested in cell-based assays and in vivo mouse models. We recently reported that clearance of toxins can be promoted by coadministering a VHH-based toxin-neutralizing agent with an antitag monoclonal antibody (MAb), called the "effector Ab," that indirectly decorates each toxin molecule with four Ab molecules. Decoration occurs because the Ab binds to a common epitopic tag present at two sites on each of the two VHH heterodimer molecules that bind to each toxin molecule. Here we show that coadministration of effector Ab substantially improved the efficacy of Stx toxin-neutralizing agents to prevent death or kidney damage in mice following challenge with Stx1 or Stx2. A single toxin-neutralizing agent consisting of a double-tagged VHH heterotrimer-one Stx1-specific VHH, one Stx2-specific VHH, and one Stx1/Stx2 cross-specific VHH-was effective in preventing all symptoms of intoxication from Stx1 and Stx2 when coadministered with effector Ab. Overall, the availability of simple, defined, recombinant proteins that provide cost-effective protection against HUS opens up new therapeutic approaches to managing disease.
C1 [Tremblay, Jacqueline M.; Mukherjee, Jean; Debatis, Michelle; Ofori, Kwasi; Baldwin, Karen; Boucher, Courtney; Peters, Rachel; Beamer, Gillian; Sheoran, Abhineet; Bedenice, Daniela; Tzipori, Saul; Shoemaker, Charles B.] Tufts Cummings Sch Vet Med, Dept Infect Dis & Global Hlth, North Grafton, MA 01536 USA.
[Leysath, Clinton E.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Shoemaker, CB (reprint author), Tufts Cummings Sch Vet Med, Dept Infect Dis & Global Hlth, North Grafton, MA 01536 USA.
EM charles.shoemaker@tufts.edu
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Department of Health and Human Services
[N01-AI-30050, U54 AI057159]
FX This project has been supported in part with federal funds from the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Department of Health and Human Services, under
contract number N01-AI-30050 and award number U54 AI057159.
NR 40
TC 22
Z9 22
U1 2
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD DEC
PY 2013
VL 81
IS 12
BP 4592
EP 4603
DI 10.1128/IAI.01033-13
PG 12
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 253EU
UT WOS:000327066100028
PM 24082082
ER
PT J
AU Magill, SS
Klompas, M
Balk, R
Burns, SM
Deutschman, CS
Diekema, D
Fridkin, S
Greene, L
Guh, A
Gutterman, D
Hammer, B
Henderson, D
Hess, DR
Hill, NS
Horan, T
Kollef, M
Levy, M
Septimus, E
VanAntwerpen, C
Wright, D
Lipsett, P
AF Magill, Shelley S.
Klompas, Michael
Balk, Robert
Burns, Suzanne M.
Deutschman, Clifford S.
Diekema, Daniel
Fridkin, Scott
Greene, Linda
Guh, Alice
Gutterman, David
Hammer, Beth
Henderson, David
Hess, Dean R.
Hill, Nicholas S.
Horan, Teresa
Kollef, Marin
Levy, Mitchell
Septimus, Edward
VanAntwerpen, Carole
Wright, Don
Lipsett, Pamela
TI Developing a New, National Approach to Surveillance for
Ventilator-Associated Events: Executive Summary
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
C1 [Magill, Shelley S.; Fridkin, Scott; Guh, Alice; Horan, Teresa] Ctr Dis Control & Prevent, Div Healthcare Qual Promot, Atlanta, GA 30329 USA.
[Klompas, Michael] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
[Klompas, Michael] Harvard Univ, Pilgrim Hlth Care Inst, Boston, MA USA.
[Klompas, Michael] Brigham & Womens Hosp, Infect Control Dept, Boston, MA 02115 USA.
[Klompas, Michael] Soc Healthcare Epidemiol Amer, Arlington, VA USA.
[Balk, Robert] Rush Univ, Sch Med, Div Pulm & Crit Care Med, Chicago, IL 60612 USA.
[Balk, Robert; Burns, Suzanne M.; Deutschman, Clifford S.; Gutterman, David; Hammer, Beth; Hill, Nicholas S.; Kollef, Marin; Levy, Mitchell; Lipsett, Pamela] Amer Thorac Soc, Soc Crit Care Med, Amer Coll Chest Phys, Crit Care Soc Collaborat Amer Assoc Crit Care Nur, Philadelphia, PA USA.
[Burns, Suzanne M.] Univ Virginia, Sch Nursing Crit & Acute Care, Charlottesville, VA USA.
[Deutschman, Clifford S.] Univ Penn, Perelman Sch Med, Dept Anesthesiol & Crit Care, Philadelphia, PA 19104 USA.
[Diekema, Daniel] Univ Iowa, Carver Coll Med, Div Infect Dis, Iowa City, IA USA.
[Diekema, Daniel] Healthcare Infect Control Practices Advisory Comm, Surveillance Working Grp, Atlanta, GA USA.
[Greene, Linda] Rochester Gen Hlth Syst, Infect Prevent & Control Dept, Rochester, NY USA.
[Greene, Linda] Assoc Profess Infect Control & Epidemiol, Washington, DC USA.
[Gutterman, David] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
[Hammer, Beth] Zablocki VA Med Ctr, Dept Cardiol, Milwaukee, WI USA.
[Henderson, David] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Hess, Dean R.] Massachusetts Gen Hosp, Dept Resp Care, Boston, MA 02114 USA.
[Hess, Dean R.] Harvard Univ, Sch Med, Dept Anesthesia, Boston, MA 02115 USA.
[Hess, Dean R.] Amer Assoc Resp Care, Irving, TX USA.
[Hill, Nicholas S.] Tufts Med Ctr, Div Pulm & Crit Care Med, Boston, MA USA.
[Kollef, Marin] Washington Univ, Div Pulm & Crit Care Med, St Louis, MO USA.
[Levy, Mitchell] Brown Univ, Warren Alpert Med Sch, Rhode Isl Hosp, Div Pulm Crit Care & Sleep, Providence, RI 02912 USA.
[Septimus, Edward] Texas A&M Hlth Sci Ctr, Dept Internal Med, College Stn, TX USA.
[Septimus, Edward] Infect Dis Soc Amer, Arlington, VA USA.
[VanAntwerpen, Carole] New York State Dept Hlth, Bur Healthcare Assoc Infect, Albany, NY USA.
[VanAntwerpen, Carole] Council State & Terr Epidemiologists, Atlanta, GA USA.
[Wright, Don] US Dept HHS, Off Dis Prevent & Hlth Promot, Washington, DC 20201 USA.
[Lipsett, Pamela] Johns Hopkins Univ, Sch Med, Dept Surg Anesthesiol & Crit Care Med, Baltimore, MD USA.
RP Magill, SS (reprint author), Ctr Dis Control & Prevent, Div Healthcare Qual Promot, 1600 Clifton Rd,MS A-24, Atlanta, GA 30329 USA.
EM smagill@cdc.gov
FU Centers for Disease Control and Prevention (CDC)
FX Financial support. The work described herein was supported by the
Centers for Disease Control and Prevention (CDC).
NR 2
TC 4
Z9 5
U1 0
U2 1
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 DEC 1
PY 2013
VL 34
IS 12
BP 1239
EP 1243
DI 10.1086/673463
PG 5
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 252AJ
UT WOS:000326976300001
PM 24225607
ER
PT J
AU Kim, H
Crago, E
Kim, M
Sherwood, P
Conley, Y
Poloyac, S
Kerr, M
AF Kim, Hyungsuk
Crago, Elizabeth
Kim, Mirim
Sherwood, Paula
Conley, Yvette
Poloyac, Samuel
Kerr, Mary
TI Cerebral vasospasm after sub-arachnoid hemorrhage as a clinical
predictor and phenotype for genetic association study
SO INTERNATIONAL JOURNAL OF STROKE
LA English
DT Article
DE brain; genetic disorders; hemorrhage; ischaemic stroke; risk factors;
sub-arachnoid hemorrhage
ID INTRACRANIAL ANEURYSMS; POLYMORPHISM; RISK; DEFINITION; INFARCTION;
RELATIVES; MUTATION; REGION; PAIN
AB BackgroundA typology of cerebral vasospasm has been proposed based on distinct clinical manifestations: delayed cerebral ischemia, symptomatic vasospasm', angiographic vasospasm, and transcranial Doppler vasospasm. We examined each distinct clinical manifestation in a nonparametric genetic association study.
AimsThe purpose of this study was to examine and compare each four distinct acute clinical manifestations and test its perspectives in genetic association studies.
MethodsTwo hundred forty-five Caucasian patients with sub-arachnoid hemorrhage were evaluated for these four distinct clinical manifestations along with 906600 single-nucleotide polymorphisms across the human genome.
ResultsThe four clinical manifestations were significantly associated with each other as P-values ranged from 331x10(-4) to 810x10(-15). Transcranial Doppler vasospasm showed significant genetic association with single nucleotide polymorphism (SNP) (rs999662, P=339x10(-8)). Statistical P-value of rs999662 in association with delayed cerebral ischemia, symptomatic vasospasm', and angiographic vasospasm was 00017, 00017, and 019, respectively.
ConclusionsDespite different criteria for each of the four clinical manifestations, they are significantly associated with each other. Our results suggest transcranial Doppler vasospasm may be an appropriate intermediate but still clinically relevant phenotype for genetic association studies. Association with SNP rs999662 indicates a potential role for the region containing the solute carrier family 12 member 3 (SLC12A3) gene in transcranial Doppler vasospasm following sub-arachnoid hemorrhage.
C1 [Kim, Hyungsuk; Kim, Mirim; Kerr, Mary] NINR, NIH, Bethesda, MD 20892 USA.
[Crago, Elizabeth; Sherwood, Paula; Conley, Yvette; Poloyac, Samuel] Univ Pittsburgh, Sch Nursing, Dept Hlth Promot & Dev, Pittsburgh, PA 15261 USA.
[Crago, Elizabeth; Sherwood, Paula; Conley, Yvette; Poloyac, Samuel] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15261 USA.
RP Kim, H (reprint author), NIH, 9 Mem Dr B9 Rm 1W121, Bethesda, MD 20892 USA.
EM kimhy@mail.nih.gov
FU National Institutes of Health
FX This research was funded by National Institutes of Health.
NR 27
TC 4
Z9 4
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1747-4930
EI 1747-4949
J9 INT J STROKE
JI Int. J. Stroke
PD DEC
PY 2013
VL 8
IS 8
BP 620
EP 625
DI 10.1111/j.1747-4949.2012.00823.x
PG 6
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 255RN
UT WOS:000327257600009
PM 22568564
ER
PT J
AU Leviton, A
Allred, EN
Dammann, O
Engelke, S
Fichorova, RN
Hirtz, D
Kuban, KCK
Ment, LR
O'shea, TM
Paneth, N
Shah, B
Schreiber, MD
AF Leviton, Alan
Allred, Elizabeth N.
Dammann, Olaf
Engelke, Stephen
Fichorova, Raina N.
Hirtz, Deborah
Kuban, Karl C. K.
Ment, Laura R.
O'shea, T. Michael
Paneth, Nigel
Shah, Bhavesh
Schreiber, Michael D.
CA ELGAN Study Investigators
TI Systemic Inflammation, Intraventricular Hemorrhage, and White Matter
Injury
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article
DE premature; hemorrhage; brain injuries; acute; inflammation; white matter
ID LOW-BIRTH-WEIGHT; LOW GESTATIONAL-AGE; BLOOD PROTEIN CONCENTRATIONS;
CRANIAL ULTRASOUND LESIONS; EXTREMELY PRETERM INFANTS; BRAIN-DAMAGE;
HISTOLOGIC CHARACTERISTICS; MAGNETIC-RESONANCE; PREMATURE-INFANTS;
PLACENTA
AB To see if the systemic inflammation profile of 123 infants born before the 28th week of gestation who had intraventricular hemorrhage without white matter injury differed from that of 68 peers who had both lesions, we compared both groups to 677 peers who had neither. Cranial ultrasound scans were read independently by multiple readers until concordance. The concentrations of 25 proteins were measured with multiplex arrays using an electrochemiluminescence system. Infants who had both hemorrhage and white matter injury were more likely than others to have elevated concentrations of C-reactive protein and interleukin 8 on days 1, 7, and 14, and elevated concentrations of serum amyloid A and tumor necrosis factor- on 2 of these days. Intraventricular hemorrhage should probably be viewed as 2 entities: hemorrhage alone and hemorrhage with white matter injury. Each entity is associated with inflammation, but the combination has a stronger inflammatory signal than hemorrhage alone.
C1 [Leviton, Alan; Allred, Elizabeth N.] Childrens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Leviton, Alan; Allred, Elizabeth N.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Allred, Elizabeth N.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Dammann, Olaf] Tufts Univ, Sch Med, Dept Publ Hlth & Community Med, Boston, MA 02111 USA.
[Engelke, Stephen] E Carolina Univ, Brody Sch Med, Dept Pediat, Greenville, NC USA.
[Fichorova, Raina N.] Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02115 USA.
[Fichorova, Raina N.] Harvard Univ, Sch Med, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02115 USA.
[Hirtz, Deborah] NINDS, Off Clin Res, Bethesda, MD 20892 USA.
[Kuban, Karl C. K.] Boston Med Ctr, Dept Pediat, Boston, MA USA.
[Kuban, Karl C. K.] Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA.
[Kuban, Karl C. K.] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Ment, Laura R.] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA.
[Ment, Laura R.] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06520 USA.
[O'shea, T. Michael] Wake Forest Univ, Bowman Gray Sch Med, Dept Pediat, Winston Salem, NC 27103 USA.
[Paneth, Nigel] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Paneth, Nigel] Michigan State Univ, Dept Pediat & Human Dev, E Lansing, MI 48824 USA.
[Shah, Bhavesh] Baystate Med Ctr, Div Newborn Med, Springfield, MA USA.
[Schreiber, Michael D.] Univ Chicago, Comer Childrens Hosp, Dept Pediat, Chicago, IL 60637 USA.
RP Leviton, A (reprint author), Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA.
EM alan.leviton@childrens.harvard.edu
RI Fichorova, Raina/G-9969-2014
FU National Institute of Neurological Disorders and Stroke
[5U01NS040069-05]; National Institute of Child Health and Human
Development [5P30HD018655-28]
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: This study was
supported by a cooperative agreement with the National Institute of
Neurological Disorders and Stroke (5U01NS040069-05) and a center grant
award from the National Institute of Child Health and Human Development
(5P30HD018655-28).
NR 42
TC 9
Z9 10
U1 0
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0883-0738
EI 1708-8283
J9 J CHILD NEUROL
JI J. Child Neurol.
PD DEC
PY 2013
VL 28
IS 12
BP 1637
EP 1645
DI 10.1177/0883073812463068
PG 9
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 250NQ
UT WOS:000326859900012
PM 23112243
ER
PT J
AU Mariotto, AB
Wang, ZQ
Klabunde, CN
Cho, H
Das, B
Feuer, EJ
AF Mariotto, Angela B.
Wang, Zhuoqiao
Klabunde, Carrie N.
Cho, Hyunsoon
Das, Barnali
Feuer, Eric J.
TI Life tables adjusted for comorbidity more accurately estimate noncancer
survival for recently diagnosed cancer patients
SO JOURNAL OF CLINICAL EPIDEMIOLOGY
LA English
DT Article
DE Life expectancy; Comorbidity; Cancer; Health-adjusted age; Survival;
Life tables; SEER-Medicare
ID PROSTATE-CANCER; RADICAL PROSTATECTOMY; BREAST-CANCER; CANDIDATES;
RADIOTHERAPY; PREDICTION; MORTALITY; MODELS
AB Objectives: To provide cancer patients and clinicians with more accurate estimates of a patient's life expectancy with respect to noncancer mortality, we estimated comorbidity-adjusted life tables and health-adjusted age.
Study Design and Setting: Using data from the Surveillance Epidemiology and End Results Medicare database, we estimated comorbidity scores that reflect the health status of people who are 66 years of age and older in the year before cancer diagnosis. Noncancer survival by comorbidity score was estimated for each age, race, and sex. Health-adjusted age was estimated by systematically comparing the noncancer survival models with US life tables.
Results: Comorbidity, cancer status, sex, and race are all important predictors of noncancer survival; however, their relative impact on noncancer survival decreases as age increases. Survival models by comorbidity better predicted noncancer survival than the US life tables. The health-adjusted age and national life tables can be consulted to provide an approximate estimate of a person's life expectancy, for example, the health-adjusted age of a black man aged 75 years with no comorbidities is 67 years, giving him a life expectancy of 13 years.
Conclusion: The health-adjusted age and the life tables adjusted by age, race, sex, and comorbidity can provide important information to facilitate decision making about treatment for cancer and other conditions. Published by Elsevier Inc.
C1 [Mariotto, Angela B.; Klabunde, Carrie N.; Cho, Hyunsoon; Das, Barnali; Feuer, Eric J.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Wang, Zhuoqiao] Informat Management Serv Inc, Beltsville, MD 20705 USA.
[Das, Barnali] Westat Corp, Rockville, MD 20850 USA.
RP Mariotto, AB (reprint author), NCI, Surveillance Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr 4E602, Bethesda, MD 20892 USA.
EM mariotta@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 27
TC 12
Z9 14
U1 1
U2 7
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 DEC
PY 2013
VL 66
IS 12
BP 1376
EP 1385
DI 10.1016/j.jclinepi.2013.07.002
PG 10
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 250MP
UT WOS:000326857200010
PM 24035494
ER
PT J
AU Shenai, S
Amisano, D
Ronacher, K
Kriel, M
Banada, PP
Song, T
Lee, M
Joh, JS
Winter, J
Thayer, R
Via, LE
Kim, S
Barry, CE
Walzl, G
Alland, D
AF Shenai, Shubhada
Amisano, Danielle
Ronacher, Katharina
Kriel, Magdalena
Banada, Padmapriya P.
Song, Taeksun
Lee, Myungsun
Joh, Joon Sung
Winter, Jill
Thayer, Rich
Via, Laura E.
Kim, Soyeon
Barry, Clifton E., III
Walzl, Gerhard
Alland, David
TI Exploring Alternative Biomaterials for Diagnosis of Pulmonary
Tuberculosis in HIV-Negative Patients by Use of the GeneXpert MTB/RIF
Assay
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID POLYMERASE-CHAIN-REACTION; EXHALED BREATH CONDENSATE;
MYCOBACTERIUM-TUBERCULOSIS; XPERT MTB/RIF; PERIPHERAL-BLOOD; RIFAMPICIN
RESISTANCE; PCR ASSAY; URINE; DNA; SALIVA
AB The utility of the GeneXpert MTB/RIF (Xpert) assay for detection of Mycobacterium tuberculosis in sputum samples has been extensively studied. However, the performance of the Xpert assay as applied to other readily accessible body fluids such as exhaled breath condensate (EBC), saliva, urine, and blood has not been established. We used the Xpert assay to test EBC, saliva, urine, and blood samples from HIV-negative, smear-and culture-positive pulmonary tuberculosis (TB) patients for the presence of M. tuberculosis. To compare the ability of the assay to perform bacterial load measurements on sputum samples with versus without sample processing, the assay was also performed on paired direct and processed sputum samples from each patient. The Xpert assay detected M. tuberculosis in none of the 26 EBC samples (sensitivity, 0.0%; 95% confidence interval [ 95% CI], 0.0%, 12.9%), 10 of the 26 saliva samples (sensitivity, 38.5%; 95% CI, 22.4%, 57.5%), 1 of 26 urine samples (sensitivity, 3.8%; 95% CI, 0.7%, 18.9%), and 2 of 24 blood samples (sensitivity, 8.3%; 95% CI, 2.3%, 25.8%). For bacterial load measurements in the different types of sputum samples, the cycle thresholds of the two M. tuberculosis-positive sputum types were well correlated (Spearman correlation of 0.834). This study demonstrates that the Xpert assay should not be routinely used to detect M. tuberculosis in EBC, saliva, urine, or blood samples from HIV-negative patients suspected of having pulmonary tuberculosis. As a test of bacterial load, the assay produced similar results when used to test direct versus processed sputum samples. Sputum remains the optimal sample type for diagnosing pulmonary tuberculosis in HIV-negative patients with the Xpert assay.
C1 [Shenai, Shubhada; Amisano, Danielle; Banada, Padmapriya P.; Alland, David] Rutgers Biomed & Hlth Sci, New Jersey Med Sch, Ctr Infect Dis, Newark, NJ 07103 USA.
[Ronacher, Katharina; Kriel, Magdalena; Walzl, Gerhard] Univ Stellenbosch, Fac Med & Hlth Sci, DST NRF Ctr Excellence Biomed TB Res, Cape Town, South Africa.
[Ronacher, Katharina; Kriel, Magdalena; Walzl, Gerhard] Univ Stellenbosch, Fac Med & Hlth Sci, MRC Ctr Mol & Cellular Biol, Div Mol Biol & Human Genet,Dept Biomed Sci, Cape Town, South Africa.
[Song, Taeksun; Lee, Myungsun] Int TB Res Ctr, Chang Won, South Korea.
[Joh, Joon Sung] Natl Med Ctr, Seoul, South Korea.
[Winter, Jill; Thayer, Rich] Catalysis Fdn Hlth, Emeryville, CA USA.
[Via, Laura E.; Barry, Clifton E., III] NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Kim, Soyeon] Rutgers Biomed & Hlth Sci, New Jersey Med Sch, Dept Prevent Med & Community Hlth, Newark, NJ USA.
RP Alland, D (reprint author), Rutgers Biomed & Hlth Sci, New Jersey Med Sch, Ctr Infect Dis, Newark, NJ 07103 USA.
EM allandda@njms.rutgers.edu
RI Barry, III, Clifton/H-3839-2012; Ronacher, Katharina/N-9603-2016;
OI Ronacher, Katharina/0000-0002-6371-1462; Via, Laura/0000-0001-6074-9521;
banada, padmapriya/0000-0002-5217-6142; Walzl,
Gerhard/0000-0003-2487-125X
FU Bill and Melinda Gates Foundation; Intramural Research Program of the
NIAID, NIH
FX This work was supported in part by the Bill and Melinda Gates Foundation
through a grant to the Catalysis Foundation for Health and in part by
the Intramural Research Program of the NIAID, NIH (C. E. Barry).
NR 42
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Z9 10
U1 1
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0095-1137
EI 1098-660X
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD DEC
PY 2013
VL 51
IS 12
BP 4161
EP 4166
DI 10.1128/JCM.01743-13
PG 6
WC Microbiology
SC Microbiology
GA 254EL
UT WOS:000327147100043
PM 24108610
ER
PT J
AU Ritzwoller, DP
Glasgow, RE
Sukhanova, AY
Bennett, GG
Warner, ET
Greaney, ML
Askew, S
Goldman, J
Emmons, KM
Colditz, GA
AF Ritzwoller, Debra P.
Glasgow, Russell E.
Sukhanova, Anna Y.
Bennett, Gary G.
Warner, Erica T.
Greaney, Mary L.
Askew, Sandy
Goldman, Julie
Emmons, Karen M.
Colditz, Graham A.
CA Be Fit Be Well Study Investigators
TI Economic Analyses of the Be Fit Be Well Program: A Weight Loss Program
for Community Health Centers
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE weight loss; RCT; pragmatic trial; cost; cost-effectiveness; health
disparities
ID UNITED-STATES; CARDIOVASCULAR RISK; ETHNIC DISPARITIES; CLINICAL-TRIALS;
OBESE-PATIENTS; PRIMARY-CARE; MANAGEMENT; ADULTS; INTERVENTIONS;
PATTERNS
AB BACKGROUND: The U.S. Preventive Services Task Force has released new guidelines on obesity, urging primary care physicians to provide obese patients with intensive, multi-component behavioral interventions. However, there are few studies of weight loss in real world nonacademic primary care, and even fewer in largely racial/ethnic minority, low-income samples.
To evaluate the recruitment, intervention and replications costs of a 2-year, moderate intensity weight loss and blood pressure control intervention.
A comprehensive cost analysis was conducted, associated with a weight loss and hypertension management program delivered in three community health centers as part of a pragmatic randomized trial.
Three hundred and sixty-five high risk, low-income, inner city, minority (71 % were Black/African American and 13 % were Hispanic) patients who were both hypertensive and obese.
Measures included total recruitment costs and intervention costs, cost per participant, and incremental costs per unit reduction in weight and blood pressure.
Recruitment and intervention costs were estimated $2,359 per participant for the 2-year program. Compared to the control intervention, the cost per additional kilogram lost was $2,204 /kg, and for blood pressure, $621 /mmHg. Sensitivity analyses suggest that if the program was offered to a larger sample and minor modifications were made, the cost per participant could be reduced to the levels of many commercially available products.
The costs associated with the Be Fit Be Well program were found to be significantly more expensive than many commercially available products, and much higher than the amount that the Centers for Medicare and Medicaid reimburse physicians for obesity counseling. However, given the serious and costly health consequences associated with obesity in high risk, multimorbid and socioeconomically disadvantaged patients, the resources needed to provide interventions like those described here may still prove to be cost-effective with respect to producing long-term behavior change.
C1 [Ritzwoller, Debra P.; Sukhanova, Anna Y.] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO 80237 USA.
[Glasgow, Russell E.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Bennett, Gary G.] Duke Univ, Dept Psychol & Neurosci, Durham, NC USA.
[Bennett, Gary G.; Askew, Sandy] Duke Univ, Duke Global Hlth Inst, Durham, NC USA.
[Warner, Erica T.; Colditz, Graham A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Warner, Erica T.; Greaney, Mary L.; Goldman, Julie; Emmons, Karen M.] Dana Farber Canc Inst, Div Populat Sci, Ctr Community Based Res, Boston, MA 02115 USA.
[Emmons, Karen M.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Dept Surg, Div Publ Hlth Sci,Alvin J Siteman Canc Ctr, St Louis, MO 63110 USA.
RP Ritzwoller, DP (reprint author), Kaiser Permanente Colorado, Inst Hlth Res, POB 378066, Denver, CO 80237 USA.
EM Debra.Ritzwoller@kp.org
RI Colditz, Graham/A-3963-2009
OI Colditz, Graham/0000-0002-7307-0291
FU National Heart Lung Blood Institute [UO1-HL087071]; Foundation for
Barnes-Jewish Hospital; National Cancer Institute [5T32CA009001-36];
[K22CA126992]; [K05CA124415-04]; [P30CA091842]
FX This work was supported in part by grant funding from the National Heart
Lung Blood Institute (UO1-HL087071). G. Bennett was supported by
K22CA126992.; K. Emmons was supported by K05CA124415-04. G. Colditz was
supported in part by P30CA091842 and the Foundation for Barnes-Jewish
Hospital. E. Warner was supported by grant 5T32CA009001-36 from the
National Cancer Institute.
NR 45
TC 7
Z9 7
U1 0
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD DEC
PY 2013
VL 28
IS 12
BP 1581
EP 1588
DI 10.1007/s11606-013-2492-3
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 253YY
UT WOS:000327127700012
PM 23733374
ER
PT J
AU Maruthur, NM
Ma, Y
Delahanty, LM
Nelson, JA
Aroda, V
White, NH
Marrero, D
Brancati, FL
Clark, JM
AF Maruthur, Nisa M.
Ma, Yong
Delahanty, Linda M.
Nelson, Julie A.
Aroda, Vanita
White, Neil H.
Marrero, David
Brancati, Frederick L.
Clark, Jeanne M.
CA Diabet Prevention Program Res Grp
TI Early Response to Preventive Strategies in the Diabetes Prevention
Program
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE diabetes prevention; diabetes risk; type 2 diabetes
ID IMPAIRED GLUCOSE-TOLERANCE; LIFE-STYLE INTERVENTION; WEIGHT-LOSS;
METFORMIN; MELLITUS; THERAPY; TRIAL
AB BACKGROUND: Recommendations for diabetes prevention in patients with prediabetes include lifestyle modification and metformin. However, the significance of early weight loss and glucose measurements when monitoring response to these proven interventions is unknown.
To quantify the relationship between early measures of weight and glucose and subsequent diabetes in patients undergoing diabetes prevention interventions.
Analysis of results from a randomized controlled trial in 27 academic medical centers in the United States.
3,041 adults with hyperglycemia randomized to lifestyle (n = 1,018), metformin (n = 1,036), or placebo (n = 987) with complete follow-up in The Diabetes Prevention Program.
Independent variables were weight loss at 6 and 12 months; fasting glucose (FG) at 6 months; hemoglobin A1c (HbA1c) at 6 months; and post-load glucose at 12 months. The main outcome was time to diabetes diagnosis.
After 6 months, 604 participants developed diabetes in the lifestyle (n = 140), metformin (n = 206), and placebo (n = 258) arms over 2.7 years. In the lifestyle arm, 6-month weight loss predicted decreased diabetes risk in a graded fashion: adjusted HR (95 % CI) 0.65 (0.35-1.22), 0.62 (0.33-1.18), 0.46 (0.24-0.87), 0.34 (0.18-0.64), and 0.15 (0.07-0.30) for 0-< 3 %, 3-< 5 %, 5-< 7 %, 7-< 10 %, and a parts per thousand yen10 % weight loss, respectively (reference: weight gain). Attainment of optimal 6-month FG and HbA1c and 12-month post-load glucose predicted > 60 % lower diabetes risk across arms. We found a significant interaction between 6-month weight loss and FG in the lifestyle arm (P = 0.038).
Weight and glucose at 6 and 12 months strongly predict lower subsequent diabetes risk with a lifestyle intervention; lower FG predicts lower risk even with substantial weight loss. Early reduction in glycemia is a stronger predictor of future diabetes risk than weight loss for metformin. We offer the first evidence to guide clinicians in making interval management decisions for high-risk patients undertaking measures to prevent diabetes.
C1 [Maruthur, Nisa M.; Brancati, Frederick L.; Clark, Jeanne M.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Maruthur, Nisa M.; Brancati, Frederick L.; Clark, Jeanne M.] Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Ma, Yong] George Washington Univ, Rockville, MD 20852 USA.
[Delahanty, Linda M.] Massachusetts Gen Hosp, Diabet Res Ctr, Boston, MA 02114 USA.
[Delahanty, Linda M.] Harvard Univ, Sch Med, Boston, MA USA.
[Nelson, Julie A.] NIDDK, Southwest Amer Indian Ctr Arizona, Phoenix, AZ USA.
[Aroda, Vanita] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[White, Neil H.] Washington Univ, Sch Med, St Louis, MO USA.
[Marrero, David] Regenstrief Inst Hlth Care, Indianapolis, IN 46202 USA.
[Marrero, David] Indiana Univ Sch Med, Diabet Translat Res Ctr, Indianapolis, IN 46202 USA.
[Brancati, Frederick L.; Clark, Jeanne M.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
RP Maruthur, NM (reprint author), George Washington Univ, Ctr Biostat, Diabet Prevent Program Coordinating Ctr, 6110 Execut Blvd,Suite 750, Rockville, MD 20852 USA.
EM dppmail@biostat.bsc.gwu.edu
FU NIH/NCCR [1KL2RR025006-01]
FX Dr. Maruthur was supported by NIH/NCCR grant 1KL2RR025006-01.
NR 16
TC 10
Z9 11
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD DEC
PY 2013
VL 28
IS 12
BP 1629
EP 1636
DI 10.1007/s11606-013-2548-4
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 253YY
UT WOS:000327127700018
PM 23860722
ER
PT J
AU Irvin, VL
Nichols, JF
Hofstetter, CR
Ojeda, VD
Song, YJ
Kang, S
Hovell, MF
AF Irvin, Veronica L.
Nichols, Jeanne F.
Hofstetter, C. Richard
Ojeda, Victoria D.
Song, Yoon Ju
Kang, Sunny
Hovell, Melbourne F.
TI Osteoporosis and Milk Intake Among Korean Women in California:
Relationship with Acculturation to US Lifestyle
SO JOURNAL OF IMMIGRANT AND MINORITY HEALTH
LA English
DT Article
DE Osteoporosis; Milk; Acculturation; Asian; Korean; Women's health
ID AMERICAN; DESCENT
AB The Korean population in the US increased by a third between 2000 and 2010. Korean women in the US report low calcium intake and relatively high rate of fractures. However, little is known about the prevalence of osteoporosis among Korean American women. This paper examined the relationship between prevalence of osteoporosis and milk consumption, and their relationship with acculturation among a representative sample of immigrant California women of Korean descent. Bilingual telephone surveys were conducted from a probability sample (N = 590) in 2007. Lower acculturation significantly related to lower milk consumption for women during the age periods of 12-18 and 19-34 years. Acculturation was related to higher prevalence of osteoporosis among post-menopausal, but not pre-menopausal Korean women in California. Future research should include larger cohorts, objective measures of osteoporosis, other sources of calcium specific to Korean cuisine, and assessment of bone-loading physical activity.
C1 [Irvin, Veronica L.; Nichols, Jeanne F.; Hofstetter, C. Richard; Kang, Sunny; Hovell, Melbourne F.] San Diego State Univ, Ctr Behav Epidemiol & Community Hlth, Grad Sch Publ Hlth, San Diego, CA 92123 USA.
[Irvin, Veronica L.] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
[Irvin, Veronica L.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Nichols, Jeanne F.] San Diego State Univ, Sch Exercise & Nutrit Sci, San Diego, CA 92183 USA.
[Hofstetter, C. Richard] San Diego State Univ, Dept Polit Sci, San Diego, CA 92182 USA.
[Ojeda, Victoria D.] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Song, Yoon Ju] Catholic Univ Korea, Sch Human Ecol, Wonmi Gu 420743, Bucheon Si, South Korea.
RP Irvin, VL (reprint author), San Diego State Univ, Ctr Behav Epidemiol & Community Hlth, Grad Sch Publ Hlth, 9245 Sky Pk Court,Suite 230, San Diego, CA 92123 USA.
EM veronica.irvin@nih.gov; mhovell@cbeachsdsu.org
FU Intramural NIH HHS; NCI NIH HHS [R01CA105199, R01 CA105199,
R01CA138192]; NIDA NIH HHS [K01 DA025504, K01DA025504]
NR 14
TC 1
Z9 1
U1 1
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1912
EI 1557-1920
J9 J IMMIGR MINOR HEALT
JI J. Immigr. Minor. Health
PD DEC
PY 2013
VL 15
IS 6
BP 1119
EP 1124
DI 10.1007/s10903-013-9774-z
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 250WT
UT WOS:000326888100015
PM 23338905
ER
PT J
AU Cox, CJ
Sharma, M
Leckman, JF
Zuccolo, J
Zuccolo, A
Kovoor, A
Swedo, SE
Cunningham, MW
AF Cox, Carol J.
Sharma, Meenakshi
Leckman, James F.
Zuccolo, Jonathan
Zuccolo, Amir
Kovoor, Abraham
Swedo, Susan E.
Cunningham, Madeleine W.
TI Brain Human Monoclonal Autoantibody from Sydenham Chorea Targets
Dopaminergic Neurons in Transgenic Mice and Signals Dopamine D2
Receptor: Implications in Human Disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID AUTOIMMUNE NEUROPSYCHIATRIC DISORDERS; OBSESSIVE-COMPULSIVE SYMPTOMS;
BETA-D-GLUCOSAMINE; STREPTOCOCCAL-M-PROTEINS; GROUP-A STREPTOCOCCI;
RHEUMATIC-FEVER; BASAL GANGLIA; CLINICAL DESCRIPTION; ANTIBODY-RESPONSE;
TIC DISORDERS
AB How autoantibodies target the brain and lead to disease in disorders such as Sydenham chorea (SC) is not known. SC is characterized by autoantibodies against the brain and is the main neurologic manifestation of streptococcal-induced rheumatic fever. Previously, our novel SC-derived mAb 24.3.1 was found to recognize streptococcal and brain Ags. To investigate in vivo targets of human mAb 24.3.1, V-H/V-L genes were expressed in B cells of transgenic (Tg) mice as functional chimeric human V-H 24.3.1mouse C-region IgG1(a) autoantibody. Chimeric human-mouse IgG1 a autoantibody colocalized with tyrosine hydroxylase in the basal ganglia within dopaminergic neurons in vivo in V-H 24.3.1 Tg mice. Both human mAb 24.3.1 and IgG1(a) in Tg sera were found to react with human dopamine D2 receptor (D2R). Reactivity of chorea-derived mAb 24.3.1 or SC IgG with D2R was confirmed by dose-dependent inhibitory signaling of D2R as a potential consequence of targeting dopaminergic neurons, reaction with surface-exposed FLAG epitope-tagged D2R, and blocking of Ab reactivity by an extracellular D2R peptide. IgG from SC and a related subset of streptococcal-associated behavioral disorders called " pediatric autoimmune neuropsychiatric disorder associated with streptococci "(PANDAS) with small choreiform movements reacted in ELISA with D2R. Reaction with FLAG-tagged D2R distinguished SC from PANDAS, whereas sera from both SC and PANDAS induced inhibitory signaling of D2R on transfected cells comparably to dopamine. In this study, we define a mechanism by which the brain may be altered by Ab in movement and behavioral disorders.
C1 [Cox, Carol J.; Zuccolo, Jonathan; Zuccolo, Amir; Cunningham, Madeleine W.] Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Biomed Res Ctr, Oklahoma City, OK 73104 USA.
[Sharma, Meenakshi; Kovoor, Abraham] Univ Rhode Isl, Dept Biomed & Pharmacol Sci, Coll Pharm, Kingston, RI 02881 USA.
[Leckman, James F.] Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT 06519 USA.
[Leckman, James F.; Swedo, Susan E.] Yale Univ, Dept Pediat, Sch Med, New Haven, CT 06519 USA.
[Leckman, James F.] Yale Univ, Dept Psychiat, Sch Med, New Haven, CT 06519 USA.
[Swedo, Susan E.] NIMH, Pediat & Dev Neurosci Branch, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Cunningham, MW (reprint author), Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Biomed Res Ctr, Room 217,975 NE 10th St, Oklahoma City, OK 73104 USA.
EM madeleine-cunningham@ouhsc.edu
FU National Heart, Lung, and Blood Institute [HL35280, HL56267]; National
Institute of Mental Health; Oklahoma Center for Advancement of Science
and Technology
FX This work was supported by Grants HL35280 and HL56267 from the National
Heart, Lung, and Blood Institute, a supplement from the National
Institute of Mental Health, and a grant from the Oklahoma Center for
Advancement of Science and Technology. M.W.C. is the recipient of a
National Institutes of Health Merit Award. J.F.L. receives grant support
from Grifols and the National Institutes of Mental Health Intramural
program for a randomized clinical trial of i.v. Ig treatment for
children with pediatric autoimmune neuropsychiatric disorder associated
with streptococci being conducted at the National Institutes of Health
Clinical Center under the leadership of S.E.S
NR 81
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Z9 26
U1 9
U2 14
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 DEC 1
PY 2013
VL 191
IS 11
BP 5524
EP 5541
DI 10.4049/jimmunol.1102592
PG 18
WC Immunology
SC Immunology
GA 254QO
UT WOS:000327180600020
PM 24184556
ER
PT J
AU Wu, LT
Blazer, DG
Gersing, KR
Burchett, B
Swartz, MS
Mannelli, P
AF Wu, Li-Tzy
Blazer, Dan G.
Gersing, Kenneth R.
Burchett, Bruce
Swartz, Marvin S.
Mannelli, Paolo
CA NIDA AAPI Workgrp
TI Comorbid substance use disorders with other Axis I and II mental
disorders among treatment-seeking Asian Americans, Native
Hawaiians/Pacific Islanders, and mixed-race people
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Asian Americans; Comorbidity; Mixed-race; Native Hawaiians; Pacific
islanders; Substance use disorder
ID NATIONAL EPIDEMIOLOGIC SURVEY; UNITED-STATES; DRUG-USE;
PERSONALITY-DISORDERS; PSYCHIATRIC-DISORDERS; LIFETIME PREVALENCE;
ETHNIC-DIFFERENCES; SURVEY REPLICATION; HEALTH-SERVICES; ALCOHOL
AB Little is known about behavioral healthcare needs of Asian Americans (AAs), Native Hawaiians/Pacific Islanders (NHs/PIs), and mixed-race people (MRs) the fastest growing segments of the U.S. population. We examined substance use disorder (SUD) prevalences and comorbidities among AAs, NHs/PIs, and MRs (N = 4572) in a behavioral health electronic health record database. DSM-IV diagnoses among patients aged 1-90 years who accessed behavioral healthcare from 11 sites were systematically captured: SUD, anxiety, mood, personality, adjustment, childhood-onset, cognitive/dementia, dissociative, eating, factitious, impulse-control, psychotic/schizophrenic, sleep, and somatoform diagnoses. Of all patients, 15.0% had a SUD. Mood (60%), anxiety (312%), adjustment (30.9%), and disruptive (attention deficit-hyperactivity, conduct, oppositional defiant, disruptive behavior diagnosis, 22.7%) diagnoses were more common than others (psychotic 14.2%, personality 133%, other childhood-onset 11.4%, impulse-control 6.6%, cognitive 2.8%, eating 2.2%, iomatoform 2.1%). Less than 1% of children aged <12 years had SUD. Cannabis diagnosis was the primary SUD affecting adolescents aged 12-17. MRs aged 35-49 years had the highest prevalence of cocaine diagnosis. Controlling for age at first visit, sex, treatment setting, length of treatment, and number of comorbid diagnoses, NHs/Pls and MRs were about two times more likely than AAs to have >= 2 SUDs. Regardless of race/ethnicity, personality diagnosis was comorbid with SUD. NHs/Pls with a mood diagnosis had elevated odds of having SUD. Findings present the most comprehensive patterns of mental diagnoses available for treatment-seeking AAs, NHs/Pls, and MRs in the real-world medical setting. In-depth research is needed to elucidate intraracial and interracial differences in treatment needs. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Wu, Li-Tzy; Blazer, Dan G.; Gersing, Kenneth R.; Burchett, Bruce; Swartz, Marvin S.; Mannelli, Paolo] Duke Univ, Sch Med, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27710 USA.
[NIDA AAPI Workgrp] Natl Inst Drug Abuse Asian Amer & Pacific Islande, Bethesda, MD USA.
RP Wu, LT (reprint author), Duke Univ, Sch Med, Med Ctr, Dept Psychiat & Behav Sci, Box 3903, Durham, NC 27710 USA.
EM litzy.wu@duke.edu
FU U.S. National Institute on Drug Abuse; National Institute on Minority
Health and Health Disparities of the National Institutes of Health
[R01MD007658, HHSN271200900499P, R01DA019623, R01DA019901, R33DA027503];
Duke University Department of Psychiatry and Behavioral Sciences
FX This work was made possible by research support from the U.S. National
Institute on Drug Abuse and National Institute on Minority Health and
Health Disparities of the National Institutes of Health (R01MD007658,
HHSN271200900499P, R01DA019623, R01DA019901, R33DA027503 to Li-Tzy Wu)
and by Duke University Department of Psychiatry and Behavioral Sciences.
The sponsoring agency had no further role in the study design and
analysis, the writing of the report, or the decision to submit the paper
for publication. The opinions expressed in this paper are solely those
of the authors.
NR 53
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U1 4
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
EI 1879-1379
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD DEC
PY 2013
VL 47
IS 12
BP 1940
EP 1948
DI 10.1016/j.jpsychires.2013.08.022
PG 9
WC Psychiatry
SC Psychiatry
GA 253ST
UT WOS:000327110300015
PM 24060266
ER
PT J
AU Lau, MWL
Ferre-D'Amare, AR
AF Lau, Matthew W. L.
Ferre-D'Amare, Adrian R.
TI An in vitro evolved glmS ribozyme has the wild-type fold but loses
coenzyme dependence
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID SELF-CLEAVING RIBOZYMES; ACTIVE-SITE GUANINE; ACID-BASE CATALYSIS;
HAIRPIN RIBOZYME; HAMMERHEAD RIBOZYME; STRUCTURAL BASIS; SMALL
MOLECULES; RNA; RIBOSWITCH; BINDING
AB Uniquely among known ribozymes, the glmS ribozyme-riboswitch requires a small-molecule coenzyme, glucosamine-6-phosphate (GlcN6P). Although consistent with its gene-regulatory function, the use of GlcN6P is unexpected because all of the other characterized self-cleaving ribozymes use RNA functional groups or divalent cations for catalysis. To determine what active site features make this ribozyme reliant on GlcN6P and to evaluate whether it might have evolved from a coenzyme-independent ancestor, we isolated a GlcN6P-independent variant through in vitro selection. Three active site mutations suffice to generate a highly reactive RNA that adopts the wild-type fold but uses divalent cations for catalysis and is insensitive to GlcN6P. Biochemical and crystallographic comparisons of wild-type and mutant ribozymes show that a handful of functional groups fine-tune the RNA to be either coenzyme or cation dependent. These results indicate that a few mutations can confer new biochemical activities on structured RNAs. Thus, families of structurally related ribozymes with divergent function may exist.
C1 [Lau, Matthew W. L.; Ferre-D'Amare, Adrian R.] NHLBI, Bethesda, MD 20892 USA.
RP Ferre-D'Amare, AR (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA.
EM adrian.ferre@nih.gov
FU Croucher Foundation; US National Heart, Lung and Blood
Institute-National Institutes of Health
FX We thank the staff at beamlines 5.0.1 and 5.0.2 of the Advanced Light
Source and of 12-ID (BESSRC CAT) of the Advanced Photon Source for
crystallographic and SAXS data collection support, respectively; X. Fang
and Y.-X. Wang for access to SAXS beam-time; D.-Y. Lee and R. Levine for
access to MS; J. Sellers for access to a rapid quench apparatus; N.
Baird for performing analysis of SAXS data; K. Deigan, J. Posakony and
J. Zhang for discussions; and an anonymous referee for motivating the
phosphorothioate interference analysis of glmSAAG and
glmSUAG. M. W. L. L. was a recipient of the Croucher
Foundation Fellowship. This work was supported in part by the intramural
program of the US National Heart, Lung and Blood Institute-National
Institutes of Health.
NR 60
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U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
EI 1552-4469
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD DEC
PY 2013
VL 9
IS 12
BP 805
EP +
DI 10.1038/NCHEMBIO.1360
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 253ZR
UT WOS:000327130000012
PM 24096303
ER
PT J
AU Jelicic, K
Cimbro, R
Nawaz, F
Huang, DW
Zheng, X
Yang, J
Lempicki, RA
Pascuccio, M
Van Ryk, D
Schwing, C
Hiatt, J
Okwara, N
Wei, DL
Roby, G
David, A
Hwang, IY
Kehrl, JH
Arthos, J
Cicala, C
Fauci, AS
AF Jelicic, Katija
Cimbro, Raffaello
Nawaz, Fatima
Huang, Da Wei
Zheng, Xin
Yang, Jun
Lempicki, Richard A.
Pascuccio, Massimiliano
Van Ryk, Donald
Schwing, Catherine
Hiatt, Joseph
Okwara, Noreen
Wei, Danlan
Roby, Gregg
David, Antonio
Hwang, Il Young
Kehrl, John H.
Arthos, James
Cicala, Claudia
Fauci, Anthony S.
TI The HIV-1 envelope protein gp120 impairs B cell proliferation by
inducing TGF-beta 1 production and FcRL4 expression
SO NATURE IMMUNOLOGY
LA English
DT Article
ID GROWTH-FACTOR-BETA; VIRUS TYPE-1 INFECTION; INTEGRIN ALPHA(4)BETA(7);
HUMORAL IMMUNITY; DENDRITIC CELLS; IGA PRODUCTION; T-CELLS; RESPONSES;
TISSUE; INDIVIDUALS
AB The humoral immune response after acute infection with HIV-1 is delayed and ineffective. The HIV-1 envelope protein gp120 binds to and signals through integrin alpha(4)beta(7) on T cells. We found that gp120 also bound to and signaled through alpha(4)beta(7) on naive B cells, which resulted in an abortive proliferative response. In primary B cells, signaling by gp120 through alpha(4)beta(7) resulted in increased expression of the immunosuppressive cytokine TGF-beta 1 and FcRL4, an inhibitory receptor expressed on B cells. Coculture of B cells with HIV-1-infected autologous CD4(+) T cells also increased the expression of FcRL4 by B cells. Our findings indicated that in addition to mediating chronic activation of the immune system, viral proteins contributed directly to HIV-1-associated B cell dysfunction. Our studies identify a mechanism whereby the virus may subvert the early HIV-1-specific humoral immune response.
C1 [Jelicic, Katija; Cimbro, Raffaello; Nawaz, Fatima; Pascuccio, Massimiliano; Van Ryk, Donald; Schwing, Catherine; Hiatt, Joseph; Okwara, Noreen; Wei, Danlan; Roby, Gregg; Hwang, Il Young; Kehrl, John H.; Arthos, James; Cicala, Claudia; Fauci, Anthony S.] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Cimbro, Raffaello; Zheng, Xin; Yang, Jun; Lempicki, Richard A.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Nawaz, Fatima] NYU, Sch Med, Sackler Inst Grad Biomed Sci, New York, NY USA.
[Huang, Da Wei] Sci Applicat Int Corp, Lab Immunopathogenesis & Bioinformat, Frederick, MD USA.
[David, Antonio] Univ Messina, Dept Internal Med, Fac Med, Messina, Italy.
RP Cicala, C (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM ccicala@niaid.nih.gov
RI Lempicki, Richard/E-1844-2012;
OI Lempicki, Richard/0000-0002-7059-409X; Hiatt, Joseph/0000-0002-8015-9614
FU Intramural Research Program of the US National Institutes of Health
(National Institute of Allergy and Infectious Diseases)
FX We thank C. Derdeyn for HIV sequence information; A. Introini for
suggestions; and J. Weddle and A. Weddle for assistance with figure
preparation. Supported by the Intramural Research Program of the US
National Institutes of Health (National Institute of Allergy and
Infectious Diseases).
NR 59
TC 29
Z9 30
U1 3
U2 20
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 DEC
PY 2013
VL 14
IS 12
BP 1256
EP +
DI 10.1038/ni.2746
PG 12
WC Immunology
SC Immunology
GA 254FG
UT WOS:000327149400011
PM 24162774
ER
PT J
AU Huang, L
Goldsmith, J
Reiss, PT
Reich, DS
Crainiceanu, CM
AF Huang, Lei
Goldsmith, Jeff
Reiss, Philip T.
Reich, Daniel S.
Crainiceanu, Ciprian M.
TI Bayesian scalar-on-image regression with application to association
between intracranial DTI and cognitive outcomes
SO NEUROIMAGE
LA English
DT Article
DE Multiple sclerosis; Diffusion tensor imaging; Ising prior; Binary Markov
random field
ID GENERALIZED LINEAR-MODELS; MULTIPLE-SCLEROSIS; FMRI DATA; FRACTIONAL
ANISOTROPY; VARIABLE SELECTION; WHITE-MATTER; MEAN DIFFUSIVITY;
QUANTITATIVE MRI; CORPUS-CALLOSUM; TRACTOGRAPHY
AB Diffusion tensor imaging (DTI) measures water diffusion within white matter, allowing for in vivo quantification of brain pathways. These pathways often subserve specific functions, and impairment of those functions is often associated with imaging abnormalities. As a method for predicting clinical disability from DTI images, we propose a hierarchical Bayesian "scalar-on-image" regression procedure. Our procedure introduces a latent binary map that estimates the locations of predictive voxels and penalizes the magnitude of effect sizes in these voxels, thereby resolving the ill-posed nature of the problem. By inducing a spatial prior structure, the procedure yields a sparse association map that also maintains spatial continuity of predictive regions. The method is demonstrated on a simulation study and on a study of association between fractional anisotropy and cognitive disability in a cross-sectional sample of 135 multiple sclerosis patients. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Huang, Lei; Reich, Daniel S.; Crainiceanu, Ciprian M.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
[Goldsmith, Jeff] Columbia Univ, Dept Biostat, Mailman Sch Publ Hlth, New York, NY USA.
[Reiss, Philip T.] NYU, Sch Med, Dept Child & Adolescent Psychiat, New York, NY USA.
[Reiss, Philip T.] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA.
[Reich, Daniel S.] NINDS, Translat Neuroradiol Unit, Neuroimmunol Branch, Bethesda, MD 20892 USA.
[Reich, Daniel S.] Johns Hopkins Sch Med, Dept Radiol, Baltimore, MD USA.
[Reich, Daniel S.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
RP Huang, L (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
EM lehuang@jhsph.edu
RI Reich, Daniel/E-5701-2010;
OI Reich, Daniel/0000-0002-2628-4334; Reiss, Philip/0000-0002-8491-7080
FU National Institute of Neurological Disorders and Stroke; National
Institutes of Health
FX This work was partially supported by the Intramural Research Program of
the National Institute of Neurological Disorders and Stroke, National
Institutes of Health.
NR 56
TC 6
Z9 6
U1 1
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD DEC
PY 2013
VL 83
BP 210
EP 223
DI 10.1016/j.neuroimage.2013.06.020
PG 14
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 251TN
UT WOS:000326953700020
PM 23792220
ER
PT J
AU Nasr, S
Devaney, KJ
Tootell, RBH
AF Nasr, Shahin
Devaney, Kathryn J.
Tootell, Roger B. H.
TI Spatial encoding and underlying circuitry in scene-selective cortex
SO NEUROIMAGE
LA English
DT Article
ID PARAHIPPOCAMPAL PLACE AREA; SHORT-TERM-MEMORY; PARIETAL CORTEX;
VISUAL-CORTEX; RETROSPLENIAL CORTEX; PERCEPTUAL DECISION; CORTICAL
REGIONS; GLOBAL SIGNAL; OBJECT; NAVIGATION
AB Three cortical areas (Retro-Splenial Cortex (RSC), Transverse Occipital Sulcus (TOS) and Parahippocampal Place Area (PPA)) respond selectively to scenes. However, their wider role in spatial encoding and their functional connectivity remain unclear. Using fMRI, first we tested the responses of these areas during spatial comparison tasks using dot targets on white noise. Activity increased during task performance in both RSC and TOS, but not in PPA. However, the amplitude of task-driven activity and behavioral measures of task demand were correlated only in RSC. A control experiment showed that none of these areas were activated during a comparable shape comparison task.
Secondly, we analyzed functional connectivity of these areas during the resting state. Results revealed a significant connection between RSC and frontal association areas (known to be involved in perceptual decision-making). In contrast, TOS showed functional connections dorsally with the Inferior Parietal Sulcus, and ventrally with the Lateral Occipital Complex - but not with RSC and/or frontal association areas. Moreover, RSC and TOS showed differentiable functional connections with the anterior-medial and posterior-lateral parts of PPA, respectively. These results suggest two parallel pathways for spatial encoding, including RSC and TOS respectively. Only the RSC network was involved in active spatial comparisons. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Nasr, Shahin; Devaney, Kathryn J.; Tootell, Roger B. H.] Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Tootell, Roger B. H.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
RP Nasr, S (reprint author), Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, 149 13th St, Charlestown, MA 02129 USA.
EM shahin@ranr.mgh.harvard.edu
FU National Institutes of Health (NIH) [R01 MH67529, R01 EY017081];
Martinos Center for Biomedical Imaging; NCRR; MIND Institute; NIMH
Intramural Research Program
FX We thank Drs. A. Afraz, R Rajimehr and M. Vaziri for review and
suggestions on the manuscript This study was supported by National
Institutes of Health (NIH Grants R01 MH67529 and R01 EY017081 to RBHT),
the Martinos Center for Biomedical Imaging, the NCRR, the MIND
Institute, and the NIMH Intramural Research Program.
NR 61
TC 16
Z9 16
U1 1
U2 14
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 DEC
PY 2013
VL 83
BP 892
EP 900
DI 10.1016/j.neuroimage.2013.07.030
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 251TN
UT WOS:000326953700082
PM 23872156
ER
PT J
AU Raznahan, A
Probst, F
Palmert, MR
Giedd, JN
Lerch, JP
AF Raznahan, Armin
Probst, Frank
Palmert, Mark R.
Giedd, Jay N.
Lerch, Jason P.
TI High resolution whole brain imaging of anatomical variation in XO, XX,
and XY mice
SO NEUROIMAGE
LA English
DT Article
DE Sex chromosomes; Aneuploidy; Sex differences; Brain development
ID ORIGIN ALLELIC EXPRESSION; MUS-MUSCULUS L; TURNER-SYNDROME; MOUSE-BRAIN;
COGNITIVE FUNCTION; SEX-DIFFERENCES; CHROMOSOME; GENE; MRI; TESTOSTERONE
AB The capacity of sex to modify behavior in health and illness may stem from biological differences between males and females. One such difference - fundamental to the biological definition of sex - is inequality of X chromosome dosage. Studies of Turner Syndrome (TS) suggest that X-monosomy profoundly alters mammalian brain development. However, use of TS as a model for X chromosome haploinsufficiency is complicated by karyotypic mosaicism, background genetic heterogeneity and ovarian dysgenesis. Therefore, to better isolate X chromosome effects on brain development and identify how these overlap with normative sex differences, we used wholebrain structural imaging to study X-monosomic mice (free of mosaicism and ovarian dysgenesis) alongside their karyotypical normal male and female littermates. We demonstrate that murine X-monosomy (XO) causes (i) accentuation of XX vs XY differences in a set of sexually dimorphic structures including classical foci of sexhormone action, such as the bed nucleus of the stria terminal and medial amygdala, (ii) parietal and striatal abnormalities that recapitulate those reported TS, and (iii) abnormal development of brain systems relevant for domains of altered cognition and emotion in both murine and human X-monosomy. Our findings suggest an unexpected role frit X-linked genes in shaping sexually dimorphic brain development, and an evolutionarily conserved influence of X-linked genes on both cortical and subcortical development in mammals. Furthermore, our murine findings highlight the bed nucleus of the stria terminalis and periaqueductal gray matter as novel neuroanatomical candidates for closer study in TS. Integration of these data with existing genomic knowledge generates a set of novel, testable hypotheses regarding candidate mechanisms for each observed pattern of anatomical variation across XO,)0( and XY groups.. Published by Elsevier Inc.
C1 [Raznahan, Armin; Giedd, Jay N.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
[Probst, Frank] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Palmert, Mark R.] Hosp Sick Children, Div Endocrinol, Toronto, ON M5G 1X8, Canada.
[Palmert, Mark R.] Univ Toronto, Dept Pediat, Toronto, ON, Canada.
[Palmert, Mark R.] Univ Toronto, Dept Physiol, Toronto, ON, Canada.
[Lerch, Jason P.] Hosp Sick Children Hosp, Mouse Imaging Ctr, Toronto, ON, Canada.
[Lerch, Jason P.] Hosp Sick Children Hosp, Program Neurosci & Mental, Toronto, ON, Canada.
[Lerch, Jason P.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
RP Raznahan, A (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM raznahana@mail.nih.gov
RI Giedd, Jay/J-9644-2015
OI Giedd, Jay/0000-0003-2002-8978
FU National Institutes of Health; Institute of Health Research; Burroughs
Wellcome Fund
FX This study was funded through the National Institutes of Health,
Institute of Health Research. FJP holds a Career Award for Medical
Scientists from the Burroughs Wellcome Fund. We thank Monica J Justice
for the use of laboratory space and reagents; and Christine Laliberte,
Shoshana Spring and Dr. Miriam Friedel for their assistance with data
acquisition and processing.
NR 47
TC 12
Z9 12
U1 1
U2 10
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 DEC
PY 2013
VL 83
BP 962
EP 968
DI 10.1016/j.neuroimage.2013.07.052
PG 7
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 251TN
UT WOS:000326953700088
PM 23891883
ER
PT J
AU Chen, M
Carass, A
Oh, J
Nair, G
Pham, DL
Reich, DS
Prince, JL
AF Chen, Min
Carass, Aaron
Oh, Jiwon
Nair, Govind
Pham, Dzung L.
Reich, Daniel S.
Prince, Jerry L.
TI Automatic magnetic resonance spinal cord segmentation with topology
constraints for variable fields of view
SO NEUROIMAGE
LA English
DT Article
DE Atlas construction; Topology-preserving segmentation; Digital
homeomorphism; Spinal cord segmentation; Magnetic resonance imaging
ID GRADIENT VECTOR FLOW; MULTIPLE-SCLEROSIS; CT IMAGES; MR-IMAGES;
SEMIAUTOMATIC SEGMENTATION; DISEASE PROGRESSION; ATROPHY; ARTIFACTS;
DISABILITY; REGISTRATION
AB Spinal cord segmentation is an important step in the analysis of neurological diseases such as multiple sclerosis. Several studies have shown correlations between disease progression and metrics relating to spinal cord atrophy and shape changes. Current practices primarily involve segmenting the spinal cord manually or semiautomatically, which can be inconsistent and time-consuming for large datasets. An automatic method that segments the spinal cord and cerebrospinal fluid from magnetic resonance images is presented. The method uses a deformable atlas and topology constraints to produce results that are robust to noise and artifacts. The method is designed to be easily extended to new data with different modalities, resolutions, and fields of view. Validation was performed on two distinct datasets. The first consists of magnetization transfer-prepared T2*-weighted gradient-echo MRI centered only on the cervical vertebrae (CI-CS). The second consists of TI-weighted MRI that covers both the cervical and portions of the thoracic vertebrae (C1-T4). Results were found to be highly accurate in comparison to manual segmentations. A pilot study was carried out to demonstrate the potential utility of this new method for research and clinical studies of multiple sclerosis. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Chen, Min; Carass, Aaron; Prince, Jerry L.] Johns Hopkins Univ, Dept Elect & Comp Engn, Baltimore, MD 21218 USA.
[Oh, Jiwon; Reich, Daniel S.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
[Chen, Min; Nair, Govind; Reich, Daniel S.] NINDS, Translat Neuroradiol Unit, Bethesda, MD 20892 USA.
[Pham, Dzung L.] Ctr Neurosci & Regenerat Med, Image Proc Core, Bethesda, MD USA.
RP Chen, M (reprint author), Johns Hopkins Univ, Dept Elect & Comp Engn, 105 Barton Hall,3400 N Charles St, Baltimore, MD 21218 USA.
EM mchen55@jhu.edu; aaron_carass@jhu.edu; jioh@jhsph.edu;
govindnib@gmail.com; dzung.pham@nih.gov; reichds@ninds.nih.gov;
prince@jhu.edu
RI Reich, Daniel/E-5701-2010;
OI Reich, Daniel/0000-0002-2628-4334; Carass, Aaron/0000-0003-4939-5085
FU NIH/NINDS [R01-N5070906]; Intramural Research Program of NINDS; National
MS Society (NMSS)
FX Funding for this work was supported in part by NIH/NINDS grant
R01-N5070906, the Intramural Research Program of NINDS, and the National
MS Society (NMSS).
NR 48
TC 21
Z9 21
U1 0
U2 7
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 DEC
PY 2013
VL 83
BP 1051
EP 1062
DI 10.1016/j.neuroimage.2013.07.060
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 251TN
UT WOS:000326953700097
PM 23927903
ER
PT J
AU Feligioni, M
Mattson, M
Nistico, R
AF Feligioni, Marco
Mattson, Mark P.
Nistico, Robert
TI SUMOylation in Neuroplasticity and Neurological Disorders
SO NEUROMOLECULAR MEDICINE
LA English
DT Editorial Material
C1 [Feligioni, Marco] European Brain Res Inst, Rome, Italy.
[Mattson, Mark P.] NIA, Natl Inst Hlth, Intramural Res Program, Bethesda, MD 20892 USA.
[Nistico, Robert] IRCSS Santa Lucia Fdn, Rome, Italy.
[Nistico, Robert] Sapienza Univ Rome, Rome, Italy.
RP Feligioni, M (reprint author), European Brain Res Inst, Rome, Italy.
EM m.feligioni@ebri.it
OI Nistico, Robert/0000-0003-3433-9232
NR 9
TC 0
Z9 0
U1 1
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1535-1084
EI 1559-1174
J9 NEUROMOL MED
JI Neuromol. Med.
PD DEC
PY 2013
VL 15
IS 4
BP 637
EP 638
DI 10.1007/s12017-013-8267-5
PG 2
WC Neurosciences
SC Neurosciences & Neurology
GA 250XV
UT WOS:000326891000001
PM 24354012
ER
PT J
AU Lee, YJ
Hallenbeck, JM
AF Lee, Yang-ja
Hallenbeck, John M.
TI SUMO and Ischemic Tolerance
SO NEUROMOLECULAR MEDICINE
LA English
DT Review
DE SUMO; Ischemia; Hibernation; ULMs; miR-200; miR-182; Hypothermia
ID ARCTIC GROUND-SQUIRRELS; FOCAL CEREBRAL-ISCHEMIA; UBIQUITIN-LIKE
PROTEIN; SUMO2/3-CONJUGATED PROTEINS; MAMMALIAN HIBERNATION; MODIFIER
CONJUGATION; NUCLEAR ACCUMULATION; GLUCOSE DEPRIVATION; IN-VITRO;
SUMOYLATION
AB Hibernating squirrels slow blood flow to a crawl, but sustain no damage to brain or other tissues. This phenomenon provides an excellent model of natural tolerance to ischemia. Small ubiquitin-like modifier (SUMO) is a 100-residue peptide that modifies other proteins by being attached to the epsilon amino group of specific lysine residues. The discovery of massive SUMOylation (by both SUMO-1 and SUMO-2/3) occurring in the brains of 13-lined ground squirrels (Ictidomys tridecemlineatus) during hibernation torpor had opened the door to the studies on SUMO and ischemic tolerance reviewed here. Ischemic stress was shown to increase the levels of SUMO conjugation, especially SUMO-2/3, mostly during reperfusion in animal models and during restoration of oxygen and glucose in cell culture systems. Over-expression or depletion of SUMOs and/or Ubc9 (the SUMO E2 conjugating enzyme) increases or decreases (respectively) the levels of SUMO conjugates. Elevated global SUMO conjugations were shown to cytoprotect from ischemic insults; conversely, depressed SUMOylation sensitized cells. Global protein conjugation not only by SUMOs, but also by other ubiquitin-like modifiers (ULMs) including NEDD8, ISG15, UFM1 and FUB1 was shown to be significantly increased in the brains of hibernating ground squirrels during torpor. These increases in multiple ULM conjugations may orchestrate the cellular events in hibernating ground squirrels that induce a state of natural tolerance through their multipronged effects. Certain miRNAs such as the miR-200 family and the miR-182 family were shown, at least partly, to control the levels of these ULM conjugations. Lowering the levels of these miRNAs leads to an increase in global SUMOylation/ULM conjugation, thereby providing the tolerance to ischemia. This suggests that these miRNAs may be good targets for therapeutic intervention in stroke.
C1 [Lee, Yang-ja; Hallenbeck, John M.] NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA.
RP Lee, YJ (reprint author), NINDS, Stroke Branch, NIH, Bldg10,Rm5B06,MSC 1401,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wicknery@ninds.nih.gov
FU Intramural Research Program of the NINDS/NIH
FX This research was supported by the Intramural Research Program of the
NINDS/NIH. The authors thank to all colleagues and collaborators
involved in this work including Shinichi Miyake, Hideaki Wakita, David
McMullen, Yongshan Mou, Paola Castri, Dace Klimanis, Joliet Bembry,
Dragan Maric, Kory Johnson, Sungyoung Auh, Yoshiaki Azuma, and Mary
Dasso.
NR 72
TC 12
Z9 13
U1 2
U2 10
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1535-1084
EI 1559-1174
J9 NEUROMOL MED
JI Neuromol. Med.
PD DEC
PY 2013
VL 15
IS 4
BP 771
EP 781
DI 10.1007/s12017-013-8239-9
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 250XV
UT WOS:000326891000010
PM 23775726
ER
PT J
AU Murphy, E
Hou, LP
Maher, BS
Woldehawariat, G
Kassem, L
Akula, N
Laje, G
McMahon, FJ
AF Murphy, Eleanor
Hou, Liping
Maher, Brion S.
Woldehawariat, Girma
Kassem, Layla
Akula, Nirmala
Laje, Gonzalo
McMahon, Francis J.
TI Race, Genetic Ancestry and Response to Antidepressant Treatment for
Major Depression
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Pharmacology; Genetics; Ethnicity; African Americans; SSRI
ID STAR-ASTERISK-D; CITALOPRAM TREATMENT; TREATMENT OUTCOMES;
AFRICAN-AMERICANS; ASSOCIATION; POPULATION; ANXIETY; BLACK; TRIAL;
PHARMACOGENETICS
AB The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) Study revealed poorer antidepressant treatment response among black compared with white participants. This racial disparity persisted even after socioeconomic and baseline clinical factors were taken into account. Some studies have suggested genetic contributions to this disparity, but none have attempted to disentangle race and genetic ancestry. Here we used genome-wide single-nucleotide polymorphism (SNP) data to examine independent contributions of race and genetic ancestry to citalopram response. Secondary data analyses included 1877 STAR*D participants who completed an average of 10 weeks of citalopram treatment and provided DNA samples. Participants reported their race as White (n = 1464), black (n = 299) or other/mixed (n = 114). Genetic ancestry was estimated by multidimensional scaling (MDS) analyses of about 500 000 SNPs. Ancestry proportions were estimated by STRUCTURE. Structural equation modeling was used to examine the direct and indirect effects of observed and latent predictors of response, defined as change in the Quick Inventory of Depressive Symptomatology (QIDS) score from baseline to exit. Socioeconomic and baseline clinical factors, race, and anxiety significantly predicted response, as previously reported. However, direct effects of race disappeared in all models that included genetic ancestry. Genetic African ancestry predicted lower treatment response in all models. Although socioeconomic and baseline clinical factors drive racial differences in antidepressant response, genetic ancestry, rather than self-reported race, explains a significant fraction of the residual differences. Larger samples would be needed to identify the specific genetic mechanisms that may be involved, but these findings underscore the importance of including more African-American patients in drug trials.
C1 [Murphy, Eleanor; Hou, Liping; Woldehawariat, Girma; Kassem, Layla; Akula, Nirmala; Laje, Gonzalo; McMahon, Francis J.] NIMH, Human Genet Branch, Intramural Res Program, NIH,US Dept HHS, Bethesda, MD 20892 USA.
[Maher, Brion S.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
RP Murphy, E (reprint author), NIMH, Human Genet Branch, Intramural Res Program, NIH,US Dept HHS, 35 Convent Dr,Bldg 35,Porter Bldg,RM 1A-209, Bethesda, MD 20892 USA.
EM eleanor.murphy@nih.gov
RI Laje, Gonzalo/L-2654-2014; Hou, Liping/G-1648-2011;
OI Laje, Gonzalo/0000-0003-2763-3329; Hou, Liping/0000-0003-3972-245X;
McMahon, Francis/0000-0002-9469-305X
FU NIMH [MH-072802]
FX STAR*D genotyping was supported by NIMH grant MH-072802 to the
Department of Psychiatry and Institute for Human Genetics, University of
California, San Francisco (Steven P Hamilton, principal investigator),
whom we thank for making their genotyping data available through the
NIMH Center for Genomic Studies of Mental Disorders
(www.nimhgenetics.org). The Sequenced Treatment Alternatives to Relieve
Depression (STAR*D) Study is registered at www.clinicaltrials.gov with
identifier number NCT00021528.
NR 44
TC 9
Z9 9
U1 0
U2 13
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 DEC
PY 2013
VL 38
IS 13
BP 2598
EP 2606
DI 10.1038/npp.2013.166
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 251VD
UT WOS:000326958100005
PM 23827886
ER
PT J
AU Chefer, VI
Backman, CM
Gigante, ED
Shippenberg, TS
AF Chefer, Vladimir I.
Baeckman, Cristina M.
Gigante, Eduardo D.
Shippenberg, Toni S.
TI Kappa Opioid Receptors on Dopaminergic Neurons Are Necessary for
Kappa-Mediated Place Aversion
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Kappa-opioid receptor; conditioned place aversion; dopamine
ID NUCLEUS-ACCUMBENS SHELL; VENTRAL TEGMENTAL AREA; SELECTIVE DELETION;
SALVINORIN-A; ACTIVATION; COCAINE; MICE; INHIBITION; PREFERENCE; SYSTEMS
AB Kappa-opioid receptor (KOR) agonists have dysphoric properties in humans and are aversive in rodents. This has been attributed to the activation of KORs within the mesolimbic dopamine (DA) system. However, the role of DA in KOR-mediated aversion and stress remains divisive as recent studies have suggested that activation of KORs on serotonergic neurons may be sufficient to mediate aversive behaviors. To address this question, we used conditional knock-out (KO) mice with KORs deleted on DA neurons (DAT(Cre/wt)/KORloxp/loxp, or DATCre-KOR KO). In agreement with previous findings, control mice (DAT(Cre/wt)/KORwt/wt or WT) showed conditioned place aversion (CPA) to the systemically administered KOR agonist U69,593. In contrast, DATCre-KOR KO mice did not exhibit CPA with this same agonist. In addition, in vivo microdialysis showed that systemic U69,593 decreased overflow of DA in the nucleus accumbens (NAc) in WT mice, but had no effect in DATCre-KOR KO mice. Intra- ventral tegmental area (VTA) delivery of KORs using an adeno-associated viral gene construct, resulted in phenotypic rescue of the KOR-mediated NAc DA response and aversive behavior in DATCre-KOR KO animals. These results provide evidence that KORs on VTA DA neurons are necessary to mediate KOR-mediated aversive behavior. Therefore, our data, along with recent findings, suggest that the neuronal mechanisms of KOR-mediated aversive behavior may include both dopaminergic and serotonergic components.
C1 [Chefer, Vladimir I.; Baeckman, Cristina M.; Gigante, Eduardo D.; Shippenberg, Toni S.] NIDA, Integrat Neurosci Sect, Integrat Neurosci Branch, Baltimore, MD 21221 USA.
RP Chefer, VI (reprint author), NIDA, Behav Neurosci Sect, IRP, 251 Bayview Blvd,RM 8A721, Baltimore, MD 21221 USA.
EM vchefer@intra.nida.nih.gov
FU National Institute on Drug Abuse Intramural Research Program
FX This work was supported by the National Institute on Drug Abuse
Intramural Research Program. We thank Dr Carl Lupica for his helpful
editorial comments and suggestions; and Dr Jennifer Whistler for
providing KORloxp mice.
NR 41
TC 26
Z9 26
U1 0
U2 4
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 DEC
PY 2013
VL 38
IS 13
BP 2623
EP 2631
DI 10.1038/npp.2013.171
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 251VD
UT WOS:000326958100008
PM 23921954
ER
PT J
AU Brady, LS
Herkenham, M
AF Brady, Linda S.
Herkenham, Miles
TI Candace B Pert Obituary
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Biographical-Item
C1 [Brady, Linda S.] NIMH, Div Neurosci & Basic Behav Sci, Bethesda, MD 20892 USA.
[Herkenham, Miles] NIMH, Funct Neuroanat Sect, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
RP Brady, LS (reprint author), NIMH, Div Neurosci & Basic Behav Sci, Bethesda, MD 20892 USA.
EM lbrady@mail.nih.gov; herkenh@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
IS 13
BP 2730
EP 2730
DI 10.1038/npp.2013.269
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 251VD
UT WOS:000326958100021
ER
PT J
AU Barrett, JE
Bergman, J
Katz, JL
Morse, WH
AF Barrett, James E.
Bergman, Jack
Katz, Jonathan L.
Morse, W. H.
TI Peter B Dews Obituary
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Biographical-Item
C1 [Barrett, James E.] Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
[Bergman, Jack; Morse, W. H.] Harvard Univ, Sch Med, Boston, MA USA.
[Katz, Jonathan L.] NIDA, Baltimore, MD USA.
RP Barrett, JE (reprint author), Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
EM james.barrett@drexelmed.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
IS 13
BP 2733
EP 2733
DI 10.1038/npp.2013.276
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 251VD
UT WOS:000326958100023
ER
PT J
AU Persoskie, A
Nelson, WL
AF Persoskie, Alexander
Nelson, Wendy L.
TI Just Blowing Smoke? Social Desirability and Reporting of Intentions to
Quit Smoking
SO NICOTINE & TOBACCO RESEARCH
LA English
DT Article
ID SENSITIVE QUESTIONS; DATA-COLLECTION; CESSATION; MODE; CONSUMPTION;
NONRESPONSE; VALIDITY; ADULTS; HEALTH; SCORES
AB Introduction: Do cigarette smokers really want to quit smoking or do they simply say they do in order to placate others and avoid criticism? In surveys of smokers, stated quit intentions and reports of quit attempts may be biased by social desirability concerns. This makes it difficult to interpret large-scale state and national surveys of smoking behavior that collect data through telephone and face-to-face interviews, methods that tend to evoke high levels of socially desirable responding.
Methods: The 2007 Health Information National Trends Survey used a dual-frame design to query smokers' quit intentions and past quit attempts in 1 of 2 ways: A self-administered mail survey (low pressure for socially desirable responding; n = 563), or an interviewer-administered telephone survey (high pressure for socially desirable responding; n = 499). Estimates derived from the 2 formats were compared to test for social desirability effects.
Results: In both survey modes, approximately two thirds of smokers reported seriously considering quitting in the next 6 months (mail: 64.9%; telephone: 68.9%), and approximately half reported making a quit attempt in the past year (mail: 54.9%; telephone: 52.3%). Neither difference approached significance in logistic regressions controlling for demographics (ps > .24).
Conclusions: It appears that a large proportion of smokers in the United States aspire to live smoke-free lives and are not simply responding in a socially desirable manner to deflect criticism in an antismoking social climate. Future research should (1) replicate this study with greater statistical power, (2) examine the possible effects of survey context (e. g., health survey vs. smoking pleasure survey), and (3) explore survey mode effects in specific subpopulations.
C1 [Persoskie, Alexander; Nelson, Wendy L.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Persoskie, A (reprint author), NCI, Basic Biobehav & Psychol Sci Branch, Behav Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM persoskieai@mail.nih.gov
NR 32
TC 6
Z9 6
U1 2
U2 7
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 DEC
PY 2013
VL 15
IS 12
BP 2088
EP 2093
DI 10.1093/ntr/ntt101
PG 6
WC Substance Abuse; Public, Environmental & Occupational Health
SC Substance Abuse; Public, Environmental & Occupational Health
GA 252BD
UT WOS:000326978400017
PM 23884318
ER
PT J
AU Siberry, GK
Abzug, MJ
Nachman, S
AF Siberry, George K.
Abzug, Mark J.
Nachman, Sharon
CA Panel Prevention Treatment Opportu
TI Executive Summary: 2013 Update of the Guidelines for the Prevention and
Treatment of Opportunistic Infections in HIV-exposed and HIV-infected
Children
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; RECONSTITUTION INFLAMMATORY SYNDROME;
UNITED-STATES; HAART ERA; VIRUS; INFANTS; TUBERCULOSIS; TRANSMISSION;
ADOLESCENTS; MORTALITY
C1 [Siberry, George K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, NIH, Bethesda, MD 20892 USA.
[Abzug, Mark J.] Univ Colorado, Sch Med, Dept Pediat, Aurora, CO USA.
[Abzug, Mark J.] Childrens Hosp Colorado, Aurora, CO USA.
[Nachman, Sharon] Stony Brook Long Isl Childrens Hosp, Dept Pediat, Stony Brook, NY USA.
RP Siberry, GK (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, NIH, 6100 Execut,Blvd,Off 4B11H, Bethesda, MD 20892 USA.
EM siber-ryg@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]
NR 17
TC 0
Z9 0
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
EI 1532-0987
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD DEC
PY 2013
VL 32
IS 12
BP 1303
EP 1307
DI 10.1097/INF.0000000000000080
PG 5
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 254UH
UT WOS:000327192800012
PM 24569304
ER
PT J
AU D'Angio, CT
Murray, TE
Li, L
Heyne, RJ
O'Shea, TM
Schelonka, RL
Shankaran, S
Duara, S
Goldberg, RN
Stoll, BJ
Stevenson, DK
Vohr, BR
Phelps, DL
Carlo, WA
Pichichero, ME
Das, A
Higgins, RD
AF D'Angio, Carl T.
Murray, Theresa E.
Li, Lei
Heyne, Roy J.
O'Shea, T. Michael
Schelonka, Robert L.
Shankaran, Seetha
Duara, Shahnaz
Goldberg, Ronald N.
Stoll, Barbara J.
Stevenson, David K.
Vohr, Betty R.
Phelps, Dale L.
Carlo, Waldemar A.
Pichichero, Michael E.
Das, Abhik
Higgins, Rosemary D.
CA NICHD Neonatal Res Network
TI Immunogenicity of Haemophilus influenzae Type b Protein Conjugate
Vaccines in Very Low Birth Weight Infants
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Letter
ID PREMATURE
C1 [D'Angio, Carl T.; Phelps, Dale L.] Univ Rochester, Sch Med & Dent, Dept Pediat, Rochester, NY 14642 USA.
[Murray, Theresa E.] Spotsylvania Reg Med Ctr, Fredericksburg, VA USA.
[Li, Lei] RTI Int, Social Stat & Environm Sci Unit, Res Triangle Pk, NC USA.
[Heyne, Roy J.] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
[O'Shea, T. Michael] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
[Schelonka, Robert L.] Oregon Hlth & Sci Univ, Div Neonatol, Portland, OR USA.
[Shankaran, Seetha] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Duara, Shahnaz] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Goldberg, Ronald N.] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
[Stoll, Barbara J.] Emory Univ, Sch Med, Dept Pediat, Childrens Healthcare Atlanta, Atlanta, GA USA.
[Stevenson, David K.] Stanford Univ, Sch Med, Dept Pediat, Div Neonatal & Dev Med,Lucile Packard Childrens H, Palo Alto, CA 94304 USA.
[Vohr, Betty R.] Brown Univ, Women & Infants Hosp, Dept Pediat, Providence, RI 02908 USA.
[Carlo, Waldemar A.] Univ Alabama Birmingham, Div Neonatol, Birmingham, AL USA.
[Pichichero, Michael E.] Rochester Gen Hosp, Rochester, NY 14621 USA.
[Das, Abhik] RTI Int, Social Stat & Environm Sci Unit, Rockville, MD USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP D'Angio, CT (reprint author), Univ Rochester, Sch Med & Dent, Dept Pediat, Rochester, NY 14642 USA.
FU NCRR NIH HHS [M01 RR007122, M01 RR016587, M01 RR16587, M01 RR30, M01
RR32, M01 RR39, M01 RR44, M01 RR633, M01 RR70, M01 RR7122]; NICHD NIH
HHS [U10 HD036790, U10 HD021385, U10 HD021397, U10 HD027851, U10
HD027880, U10 HD034216, U10 HD040492, U10 HD040498, U10 HD040521, U10
HD040689, U10 HD068263, U10 HD21397, U10 HD27851, U10 HD27880, U10
HD36790, U10 HD40492, U10 HD40689, U10HD21385, U10HD34216, U10HD40498,
U10HD40521]
NR 6
TC 0
Z9 0
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
EI 1532-0987
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD DEC
PY 2013
VL 32
IS 12
BP 1400
EP 1402
DI 10.1097/01.inf.0000437263.04493.7c
PG 3
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 254UH
UT WOS:000327192800035
PM 24569312
ER
PT J
AU Tabarani, CM
Bonville, CA
Suryadevara, M
Branigan, P
Wang, DL
Huang, DN
Rosenberg, HF
Domachowske, JB
AF Tabarani, Christy M.
Bonville, Cynthia A.
Suryadevara, Manika
Branigan, Patrick
Wang, Dongliang
Huang, Danning
Rosenberg, Helene F.
Domachowske, Joseph B.
TI Novel Inflammatory Markers, Clinical Risk Factors and Virus Type
Associated With Severe Respiratory Syncytial Virus Infection
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE respiratory syncytial virus; innate immunity; illness severity;
hepatocyte growth factor
ID HEPATOCYTE GROWTH-FACTOR; DISEASE SEVERITY; GENE POLYMORPHISMS; TRACT
INFECTION; BRONCHIOLITIS; CHILDREN; INFANTS; POPULATION; RECEPTOR;
PROTEIN-1-ALPHA
AB Background: Virus-induced inflammation contributes to respiratory syncytial virus (RSV) pathogenesis. We sought to determine the specific mediators that are associated with more severe illness in young children.
Methods: Children 5 years of age seen in our emergency department for respiratory symptoms from September 1998 to May 2008 were eligible for enrollment. Nasopharyngeal wash samples were collected from all eligible patients, and clinical data were recorded. Individuals were included in this study if nasopharyngeal wash samples were positive for RSV only. Patients enrolled in the study were stratified by disease severity, defined as mild (not hospitalized), moderate (hospitalized) or severe (requiring intensive care unit stay). Concentrations of individual inflammatory biomarkers in nasopharyngeal wash fluids were determined using the Luminex human 30-plex assay.
Results: Eight hundred fifty-one patients met study criteria: 268 (31.5%) with mild, 503 (59.1%) with moderate and 80 (9.4%) with severe illness. As expected, illness severity was directly associated with young age, prematurity, heart or lung disease, infection with RSV group A and elevated concentrations of interleukin (IL)-2R, IL-6, CXCL8, tumor necrosis factor-, interferon-, CCL3, CCL4 and CCL2. In addition, we report several novel and mechanistically important inflammatory biomarkers of severe RSV disease, including IL-1, IL1-RA, IL-7, epidermal growth factor and hepatocyte growth factor.
Conclusions: In a large, longitudinal study (10 years, 851 enrolled patients) limited to RSV infection only, in which well-known risk factors are confirmed, we identified 5 novel biomarkers specifically of severe disease. These markers may ultimately serve to elucidate disease mechanisms.
C1 [Tabarani, Christy M.; Bonville, Cynthia A.; Suryadevara, Manika; Domachowske, Joseph B.] Upstate Golisano Childrens Hosp, Dept Pediat, Syracuse, NY 13210 USA.
[Branigan, Patrick] Centocor Inc, Infect Dis Res, Radnor, PA USA.
[Wang, Dongliang; Huang, Danning] SUNY Upstate Med Univ, Dept Publ Hlth & Prevent Med, Syracuse, NY 13210 USA.
[Rosenberg, Helene F.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
RP Domachowske, JB (reprint author), Upstate Golisano Childrens Hosp, 1 Childrens Circle, Syracuse, NY 13210 USA.
EM domachoj@upstate.edu
OI Branigan, Patrick/0000-0001-9741-9067
FU Children's Miracle Network of Central New York; National Institute of
Allergy and Infectious Diseases, Division of Intramural Research
[Z01-AI000943]
FX Funded by the Children's Miracle Network of Central New York (to J.B.D.)
and the National Institute of Allergy and Infectious Diseases, Division
of Intramural Research (Z01-AI000943 to H. F. R.). P. B. is employed by
the Infectious Disease Research Division at Centocor, Radnor, PA. The
authors have no other funding or conflicts of interest to disclose.
NR 42
TC 15
Z9 15
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
EI 1532-0987
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD DEC
PY 2013
VL 32
IS 12
BP E437
EP E442
DI 10.1097/INF.0b013e3182a14407
PG 6
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 254UH
UT WOS:000327192800004
PM 23804121
ER
PT J
AU Johnson, EO
Calogero, AE
Konstandi, M
Kamilaris, TC
La Vignera, S
Chrousos, GP
AF Johnson, Elizabeth O.
Calogero, Aldo E.
Konstandi, Maria
Kamilaris, Themis C.
La Vignera, Sandro
Chrousos, George P.
TI Effects of experimentally induced hyperthyroidism on central
hypothalamic-pituitary-adrenal axis function in rats: in vitro and in
situ studies (vol 16, pg 275, 2013)
SO PITUITARY
LA English
DT Correction
C1 [Johnson, Elizabeth O.] Univ Athens, Sch Med, Dept Anat, GR-11527 Athens, Greece.
[Calogero, Aldo E.] Univ Catania, Osped Garibaldi, Dept Biomed Sci, Sect Endocrinol Androl & Internal Med, Catania, Italy.
[Konstandi, Maria] Univ Ioannina, Sch Med, Dept Pharmacol, GR-45110 Ioannina, Greece.
[Kamilaris, Themis C.] NICHHD, Dev Endocrinol Branch, Bethesda, MD 20892 USA.
[La Vignera, Sandro] Univ Catania, Dept Internal Med & Syst Dis, Sect Endocrinol Androl & Internal Med, Catania, Italy.
[Chrousos, George P.] Univ Athens, Sch Med, Dept Pediat 1, GR-11527 Athens, Greece.
RP Johnson, EO (reprint author), Univ Athens, Sch Med, Dept Anat, 75 Mikras Asias Str, GR-11527 Athens, Greece.
EM elizabethojohnson@gmail.com
NR 1
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1386-341X
EI 1573-7403
J9 PITUITARY
JI Pituitary
PD DEC
PY 2013
VL 16
IS 4
BP 554
EP 554
DI 10.1007/s11102-012-0458-9
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 250XZ
UT WOS:000326891400017
ER
PT J
AU Haller, J
Goldberg, SR
Pelczer, KG
Aliczki, M
Panlilio, LV
AF Haller, Jozsef
Goldberg, Steven R.
Pelczer, Katalin Gyimesine
Aliczki, Mano
Panlilio, Leigh V.
TI The effects of anandamide signaling enhanced by the FAAH inhibitor
URB597 on coping styles in rats
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Behavior; Endocannabinoid; FAAH; URB597; Context; Coping; Rats
ID ENDOCANNABINOID SYSTEM; PLASMA-CORTICOSTERONE; STRESS; ACID; BEHAVIOR;
MEMORY; RESPONSES; DOPAMINE; ANXIETY; MODULATION
AB Rationale Coping styles are fundamental characteristics of behavior that affect susceptibility to, and resilience during, mental and physical illness. Shifts from passive to active coping are considered therapeutic goals in many stress-related disorders, but the neural control of coping is poorly understood. Based on earlier findings, we hypothesized that coping styles are influenced by endocannabinoids.
Here, we tested whether FAAH inhibition by URB597 affects behaviors aimed at controlling a critical situation and the degree to which environmental stimuli influence behavior i.e., we studied the impact of URB597 on the two main attributes of coping styles.
Rats were tested in the tail-pinch test of coping and in the elevated plus-maze test that was performed under highly divergent conditions.
Under the effects of URB597, rats focused their behavior more on the discomfort-inducing clamp in the tail-pinch test, i.e., they coped with the challenge more actively. In the elevated plus-maze, URB597-treated rats demonstrated an autonomous behavioral control by reducing both "wariness" induced by aversive conditions and "carelessness" resulting from favorable conditions.
URB597 treatment-induced behavioral changes indicated a shift towards active coping with challenges. This behavioral change appears compatible with the previously suggested role of endocannabinoids in emotional homeostasis. Albeit further studies are required to characterize the role of endocannabinoids in coping, these findings suggest that the enhancement of endocannabinoid signaling may become a therapeutic option in emotional disorders characterized by passive coping (e.g., anxiety and depression) and in physical diseases where active coping is therapeutically desirable.
C1 [Haller, Jozsef; Pelczer, Katalin Gyimesine; Aliczki, Mano] Inst Expt Med, Dept Behav Neurobiol, Budapest, Hungary.
[Goldberg, Steven R.; Panlilio, Leigh V.] Natl Inst Drug Abuse, NIH, Biomed Res Ctr,Preclin Pharmacol Sect, Dept Hlth & Human Serv,Intramural Res Program, Baltimore, MD USA.
RP Haller, J (reprint author), Inst Expt Med, Dept Behav Neurobiol, Budapest, Hungary.
EM haller@koki.hu
OI Haller, Jozsef/0000-0002-1953-3726
FU OTKA [K101645]; National Institute on Drug Abuse, National Institutes of
Health, Department of Health and Human Services
FX This research was made possible by grants from OTKA (Hungarian
Scientific Research Fund) grant no. K101645 to JH and was also supported
by the Intramural Research Program of the National Institute on Drug
Abuse, National Institutes of Health, Department of Health and Human
Services to SRG, and LVP.
NR 41
TC 7
Z9 7
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD DEC
PY 2013
VL 230
IS 3
BP 353
EP 362
DI 10.1007/s00213-013-3161-2
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 253MF
UT WOS:000327090500003
PM 23743650
ER
PT J
AU Bjork, K
Tronci, V
Thorsell, A
Tanda, G
Hirth, N
Heilig, M
Hansson, AC
Sommer, WH
AF Bjork, Karl
Tronci, Valeria
Thorsell, Annika
Tanda, Gianluigi
Hirth, Natalie
Heilig, Markus
Hansson, Anita C.
Sommer, Wolfgang H.
TI beta-Arrestin 2 knockout mice exhibit sensitized dopamine release and
increased reward in response to a low dose of alcohol
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Arrestin; Opioid; Dopamine; Alcohol; Reward; Nucleus accumbens
ID OPIOID RECEPTOR GENE; NUCLEUS-ACCUMBENS; VENTRAL PALLIDUM; DEPENDENCE;
BETA-ARRESTIN-2; POLYMORPHISM; ASSOCIATION; NALTREXONE; MORPHINE;
COCAINE
AB Rationale The rewarding effects of alcohol have been attributed to interactions between opioid and dopaminergic system within the mesolimbic reward pathway. We have previously shown that ablation of beta-arrestin 2 (Arrb2), a crucial regulator of mu-opioid receptor function, attenuates alcohol-induced hyperlocomotion and c-fos activation in the nucleus accumbens.
Here, we further investigated the role of Arrb2 in modulating alcohol-induced dopamine (DA) release and conditioned place preference (CPP). We also assessed the functional importance of Arrb2 for mu-opioid receptor surface expression and signaling following an acute alcohol challenge.
Alcohol-evoked (0.375, 0.75, and 1.5 g/kg intraperitoneally) DA release was measured by in vivo microdialysis in the shell of nucleus accumbens. Reward was assessed by the CPP paradigm. Receptor function was assessed by mu-receptor binding and [S-35]GTP-gamma-S autoradiography.
In Arrb2 knockout mice accumbal DA levels reach maximum response at a lower dose compared to wild-type (wt) animals. In line with these results, Arrb2 knockout mice display increased CPP for alcohol as compared to wt mice. Finally, Arrb2 mutant mice display increased mu-opioid receptor signaling in the ventral and dorsal striatum and amygdala in response to a low dose of alcohol, indicating impaired desensitization mechanisms in these mice.
Our results show that Arrb2 modulates the response to low doses of alcohol on various levels including mu-opioid receptor signaling, DA release, and reward. They also reveal a clear dissociation between the effects of Arrb2 on psychomotor and reward behaviors.
C1 [Bjork, Karl] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Tronci, Valeria; Tanda, Gianluigi] NIDA, Psychobiol Sect, NIH, Baltimore, MD USA.
[Bjork, Karl; Thorsell, Annika; Heilig, Markus; Hansson, Anita C.; Sommer, Wolfgang H.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Thorsell, Annika] Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.
[Hirth, Natalie; Hansson, Anita C.; Sommer, Wolfgang H.] Heidelberg Univ, Inst Psychopharmacol, Cent Inst Mental Hlth, Med Fac Mannheim, Mannheim, Germany.
[Bjork, Karl] L8 01 Karolinska Univ Hosp, Karolinska Inst, Ctr Mol Med, Sect Translat Neuropharmacol, S-17176 Stockholm, Sweden.
RP Bjork, K (reprint author), L8 01 Karolinska Univ Hosp, Karolinska Inst, Ctr Mol Med, Sect Translat Neuropharmacol, S-17176 Stockholm, Sweden.
EM karl.bjork@ki.se
RI Tanda, Gianluigi/B-3318-2009;
OI Tanda, Gianluigi/0000-0001-9526-9878; Heilig, Markus/0000-0003-2706-2482
FU Svenska Stiftelsen for Medicinsk Forskning; Deutsche
Forschungsgemeinschaft (DFG) [HA 6102/1]; NIAAA; NIDA, National
Institutes of Health, Department of Health and Human Services
FX KB was supported by a grant from Svenska Stiftelsen for Medicinsk
Forskning. NH and ACH were supported by a grant from the "Deutsche
Forschungsgemeinschaft" (DFG, HA 6102/1). This report was also funded by
the Intramural Research Programs of NIAAA and NIDA, National Institutes
of Health, Department of Health and Human Services.
NR 43
TC 6
Z9 6
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD DEC
PY 2013
VL 230
IS 3
BP 439
EP 449
DI 10.1007/s00213-013-3166-x
PG 11
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 253MF
UT WOS:000327090500010
PM 23779257
ER
PT J
AU Hsu, ER
Williams, DE
DiJoseph, LG
Schnell, JD
Finstad, SL
Lee, JSH
Greenspan, EJ
Corrigan, JG
AF Hsu, Elizabeth R.
Williams, Duane E.
DiJoseph, Leo G.
Schnell, Joshua D.
Finstad, Samantha L.
Lee, Jerry S. H.
Greenspan, Emily J.
Corrigan, James G.
TI Piloting an approach to rapid and automated assessment of a new research
initiative: Application to the National Cancer Institute's Provocative
Questions initiative
SO RESEARCH EVALUATION
LA English
DT Article
ID TECHNOLOGY; NOVELTY
AB Funders of biomedical research are often challenged to understand how a new funding initiative fits within the agency's portfolio and the larger research community. While traditional assessment relies on retrospective review by subject matter experts, it is now feasible to design portfolio assessment and gap analysis tools leveraging administrative and grant application data that can be used for early and continued analysis. We piloted such methods on the National Cancer Institute's Provocative Questions (PQ) initiative to address key questions regarding diversity of applicants; whether applicants were proposing new avenues of research; and whether grant applications were filling portfolio gaps. For the latter two questions, we defined measurements called focus shift and relevance, respectively, based on text similarity scoring. We demonstrate that two types of applicants were attracted by the PQs at rates greater than or on par with the general National Cancer Institute applicant pool: those with clinical degrees and new investigators. Focus shift scores tended to be relatively low, with applicants not straying far from previous research, but the majority of applications were found to be relevant to the PQ the application was addressing. Sensitivity to comparison text and inability to distinguish subtle scientific nuances are the primary limitations of our automated approaches based on text similarity, potentially biasing relevance and focus shift measurements. We also discuss potential uses of the relevance and focus shift measures including the design of outcome evaluations, though further experimentation and refinement are needed for a fuller understanding of these measures before broad application.
C1 [Hsu, Elizabeth R.; Finstad, Samantha L.; Corrigan, James G.] NCI, Off Sci Planning & Assessment, Bethesda, MD 20892 USA.
[Williams, Duane E.; DiJoseph, Leo G.; Schnell, Joshua D.] Thomson Reuters, Rockville, MD 20850 USA.
[Lee, Jerry S. H.; Greenspan, Emily J.] NCI, Ctr Strateg Sci Initiat, Bethesda, MD 20892 USA.
RP Hsu, ER (reprint author), NCI, Off Sci Planning & Assessment, Bethesda, MD 20892 USA.
EM hsuel@mail.nih.gov
RI Lee, Jerry/K-4553-2014; Schnell, Joshua/J-4000-2012;
OI Schnell, Joshua/0000-0001-9241-7441; Finstad,
Samantha/0000-0002-3460-6428
NR 24
TC 0
Z9 0
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0958-2029
EI 1471-5449
J9 RES EVALUAT
JI Res. Evaluat.
PD DEC
PY 2013
VL 22
IS 5
BP 272
EP 284
DI 10.1093/reseval/rvt024
PG 13
WC Information Science & Library Science
SC Information Science & Library Science
GA 250UT
UT WOS:000326882300002
ER
PT J
AU Basner, JE
Theisz, KI
Jensen, US
Jones, CD
Ponomarev, I
Sulima, P
Jo, K
Eljanne, M
Espey, MG
Franca-Koh, J
Hanlon, SE
Kuhn, NZ
Nagahara, LA
Schnell, JD
Moore, NM
AF Basner, Jodi E.
Theisz, Katrina I.
Jensen, Unni S.
Jones, C. David
Ponomarev, Ilya
Sulima, Pawel
Jo, Karen
Eljanne, Mariam
Espey, Michael G.
Franca-Koh, Jonathan
Hanlon, Sean E.
Kuhn, Nastaran Z.
Nagahara, Larry A.
Schnell, Joshua D.
Moore, Nicole M.
TI Measuring the evolution and output of cross-disciplinary collaborations
within the NCI Physical Sciences-Oncology Centers Network
SO RESEARCH EVALUATION
LA English
DT Article
ID TEAM SCIENCE; TRANSDISCIPLINARY RESEARCH; SCIENTIFIC COLLABORATION;
INTERDISCIPLINARY; INTEGRATION
AB Development of effective quantitative indicators and methodologies to assess the outcomes of cross-disciplinary collaborative initiatives has the potential to improve scientific program management and scientific output. This article highlights an example of a prospective evaluation that has been developed to monitor and improve progress of the National Cancer Institute Physical Sciences-Oncology Centers (PS-OC) program. Study data, including collaboration information, was captured through progress reports and compiled using the web-based analytic database: Interdisciplinary Team Reporting, Analysis, and Query Resource. Analysis of collaborations was further supported by data from the Thomson Reuters Web of Science database, MEDLINE database, and a web-based survey. Integration of novel and standard data sources was augmented by the development of automated methods to mine investigator pre-award publications, assign investigator disciplines, and distinguish cross-disciplinary publication content. The results highlight increases in cross-disciplinary authorship collaborations from pre- to post-award years among the primary investigators and confirm that a majority of cross-disciplinary collaborations have resulted in publications with cross-disciplinary content that rank in the top third of their field. With these evaluation data, PS-OC Program officials have provided ongoing feedback to participating investigators to improve center productivity and thereby facilitate a more successful initiative. Future analysis will continue to expand these methods and metrics to adapt to new advances in research evaluation and changes in the program.
C1 [Theisz, Katrina I.] Kelly Govt Solut, Rockville, MD 20852 USA.
[Theisz, Katrina I.; Jo, Karen; Eljanne, Mariam; Espey, Michael G.; Franca-Koh, Jonathan; Hanlon, Sean E.; Kuhn, Nastaran Z.; Nagahara, Larry A.; Moore, Nicole M.] NCI, Off Phys Sci Oncol, Ctr Strateg Sci Initiat, Off Director, Bethesda, MD 20892 USA.
RP Moore, NM (reprint author), NCI, Off Phys Sci Oncol, Ctr Strateg Sci Initiat, Off Director, Bethesda, MD 20892 USA.
EM nicole.moore@nih.gov
RI Ponomarev, Ilya/F-5183-2010; Schnell, Joshua/J-4000-2012
OI Ponomarev, Ilya/0000-0002-8584-6034; Schnell, Joshua/0000-0001-9241-7441
NR 19
TC 6
Z9 6
U1 7
U2 39
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0958-2029
EI 1471-5449
J9 RES EVALUAT
JI Res. Evaluat.
PD DEC
PY 2013
VL 22
IS 5
BP 285
EP 297
DI 10.1093/reseval/rvt025
PG 13
WC Information Science & Library Science
SC Information Science & Library Science
GA 250UT
UT WOS:000326882300003
ER
PT J
AU Terracciano, A
Piras, MG
Lobina, M
Mulas, A
Meirelles, O
Sutin, AR
Chan, W
Sanna, S
Uda, M
Crisponi, L
Schlessinger, D
AF Terracciano, Antonio
Piras, Maria Grazia
Lobina, Monia
Mulas, Antonella
Meirelles, Osorio
Sutin, Angelina R.
Chan, Wayne
Sanna, Serena
Uda, Manuela
Crisponi, Laura
Schlessinger, David
TI Genetics of serum BDNF: Meta-analysis of the Val66Met and genome-wide
association study
SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Brain-derived neurotrophic factor ( BDNF); serum; Val66Met; NTRK3; GWAS
ID MILD COGNITIVE IMPAIRMENT; NEUROTROPHIC FACTOR; MAJOR DEPRESSION;
PERSONALITY-TRAITS; MOOD DISORDERS; POLYMORPHISM; VARIANTS; NTRK3;
PROGRESSION; NEUROTICISM
AB Objectives. Lower levels of serum brain derived neurotrophic factor (BDNF) is one of the best known biomarkers of depression. To identify genetic variants associated with serum BDNF, we tested the Val66Met (rs6265) functional variant and conducted a genome-wide association scan (GWAS). Methods. In a community-based sample (N = 2054; aged 19-101, M = 51, SD = 15) from Sardinia, Italy, we measured serum BDNF concentration and conducted a GWAS. Results. We estimated the heritability of serum BDNF to be 0.48 from sib-pairs. There was no association between serum BDNF and Val66Met in the SardiNIA sample and in a meta-analysis of published studies (k = 13 studies, total n = 4727, P = 0.92). Although no genome-wide significant associations were identified, some evidence of association was found in the BDNF gene (rs11030102, P = 0.001) and at two loci (rs7170215, P = 4.8 x 10 (5) and rs11073742 P = 1.2 x 10 (5)) near and within NTRK3 gene, a neurotrophic tyrosine kinase receptor. Conclusions. Our study and meta-analysis of the literature indicate that the BDNF Val66Met variant is not associated with serum BDNF, but other variants in the BDNF and NTRK3 genes might regulate the level of serum BDNF.
C1 [Terracciano, Antonio; Meirelles, Osorio; Sutin, Angelina R.; Chan, Wayne; Schlessinger, David] NIA, NIH, DHHS, Baltimore, MD 21224 USA.
[Piras, Maria Grazia; Lobina, Monia; Mulas, Antonella; Sanna, Serena; Uda, Manuela; Crisponi, Laura] CNR, Ist Ric Genet & Biomed, Cagliari, Italy.
RP Terracciano, A (reprint author), NIA, NIH, DHHS, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM terraccianoa@mail.nih.gov
OI Mulas, Antonella/0000-0002-6856-1483; piras, maria
grazia/0000-0001-9004-0900; Lobina, Monia/0000-0003-3620-3160; Chan,
Wayne/0000-0001-5061-1713; sanna, serena/0000-0002-3768-1749
FU Intramural Research Program of the NIH, National Institute on Aging
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute on Aging.
NR 49
TC 19
Z9 20
U1 1
U2 13
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1562-2975
EI 1814-1412
J9 WORLD J BIOL PSYCHIA
JI World J. Biol. Psychiatry
PD DEC
PY 2013
VL 14
IS 8
BP 583
EP 589
DI 10.3109/15622975.2011.616533
PG 7
WC Psychiatry
SC Psychiatry
GA 256JT
UT WOS:000327307100005
PM 22047184
ER
PT J
AU Bigdeli, TB
Maher, BS
Zhao, ZM
Sun, JC
Medeiros, H
Akula, N
McMahon, FJ
Carvalho, C
Ferreira, SR
Azevedo, MH
Knowles, JA
Pato, MT
Pato, CN
Fanous, AH
AF Bigdeli, T. Bernard
Maher, Brion S.
Zhao, Zhongming
Sun, Jingchun
Medeiros, Helena
Akula, Nirmala
McMahon, Francis J.
Carvalho, Celia
Ferreira, Susana R.
Azevedo, Maria H.
Knowles, James A.
Pato, Michele T.
Pato, Carlos N.
Fanous, Ayman H.
TI Association Study of 83 Candidate Genes for Bipolar Disorder in
Chromosome 6q Selected Using an Evidence-Based Prioritization Algorithm
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE bipolar disorder; 6q; genetic association; gene-based association
ID LINKAGE DISEQUILIBRIUM; SUSCEPTIBILITY LOCUS; SCHIZOPHRENIA; POPULATION;
PEDIGREES; GENETICS; SCAN; HETEROGENEITY; METAANALYSIS; FAMILIES
AB BackgroundPrior genome-scans of bipolar disorder have revealed chromosome 6q22 as a promising candidate region. However, linkage disequilibrium (LD) mapping studies have yet to identify replicated susceptibility loci.
MethodsWe analyzed 1,422 LD-tagging single nucleotide polymorphisms (SNPs) in 83 genes to test single-marker and locus-wide evidence of association with bipolar disorder in the NIMH Genetics Initiative bipolar pedigrees and the Portuguese Island Collection (PIC) (N=1,093 in 528 informative pairs). Both studies previously demonstrated significant evidence of linkage to 6q. SNPs were genotyped using an Illumina iSelect genotyping array which employs the Infinium assay. Evidence of single-marker association was assessed using the generalized disequilibrium test (GDT). Empirical estimates of gene-wide significance were obtained by permutation (via 100,000 gene-dropping simulations) of Fisher's combined test of P-values for each locus.
ResultsNo single variant yielded significant experiment-wide evidence of association, for either the combined sample or in each subsample. Our gene-dropping simulations identified nominally significant gene-wide associations with multiple loci, of which NT5DC1 in the NIMH subsample and CCNC in the PIC were the strongest candidates. However, no one gene consistently exceeded empirical significance criteria in both independent samples or survived Bonferroni correction for the number of genes tested.
ConclusionsUsing a gene-based approach to family-based association, we identified gene-wide associations with several genes, though no single locus was significantly associated with bipolar disorder in both cohorts. This suggests that chromosome 6q may harbor multiple susceptibility loci or that complex patterns of LD in this region may confound approaches based on common SNPs. Published 2013. This article is a U.S. Government work and is in the public domain in the USA
C1 [Bigdeli, T. Bernard; Fanous, Ayman H.] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA.
[Maher, Brion S.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mental Hlth, Baltimore, MD USA.
[Zhao, Zhongming; Sun, Jingchun] Vanderbilt Univ, Med Ctr, Dept Psychiat, Vanderbilt, TN USA.
[Zhao, Zhongming; Sun, Jingchun] Vanderbilt Univ, Med Ctr, Dept Biomed Informat, Vanderbilt, TN USA.
[Zhao, Zhongming; Sun, Jingchun] Vanderbilt Univ, Med Ctr, Dept Canc Biol, Vanderbilt, TN USA.
[Medeiros, Helena; Knowles, James A.; Pato, Michele T.; Pato, Carlos N.; Fanous, Ayman H.] Univ So Calif, Keck Sch Med, Dept Psychiat, Los Angeles, CA 90033 USA.
[Akula, Nirmala; McMahon, Francis J.] NIMH, Human Genet Branch, Intramural Res Program, NIH,US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Carvalho, Celia] Univ Azores, Dept Sci Educ, Azores, Portugal.
[Ferreira, Susana R.] Dept Psychiat, Sao Miguel, Azores, Portugal.
[Azevedo, Maria H.] Univ Coimbra, Dept Psychiat, Coimbra, Portugal.
[Fanous, Ayman H.] Washington VA Med Ctr, Mental Hlth Serv Line, Washington, DC USA.
[Fanous, Ayman H.] Georgetown Univ, Sch Med, Dept Psychiat, Washington, DC USA.
RP Fanous, AH (reprint author), VA Med Ctr, Psychiat Genet Res Program, 50 Irving St NW, Washington, DC 20422 USA.
EM ayman.fanous@va.gov
OI de Oliveira Barreto Coimbra Carvalho, Celia Maria/0000-0003-4453-8139;
McMahon, Francis/0000-0002-9469-305X
FU Department of Veterans Affairs Merit Review Program; US National
Institute of Health [AA017437]; NARSAD Maltz Investigator Award
[5R01MH085548-05]
FX Grant sponsor: Department of Veterans Affairs Merit Review Program;
Grant sponsor: US National Institute of Health; Grant number: AA017437;
Grant sponsor: NARSAD Maltz Investigator Award; Grant number:
5R01MH085548-05.
NR 43
TC 2
Z9 2
U1 2
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4841
EI 1552-485X
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD DEC
PY 2013
VL 162
IS 8
BP 898
EP 906
DI 10.1002/ajmg.b.32200
PG 9
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 246AE
UT WOS:000326506700013
PM 24123842
ER
PT J
AU Coughlin, JW
Gullion, CM
Brantley, PJ
Stevens, VJ
Bauck, A
Champagne, CM
Dalcin, AT
Funk, KL
Hollis, JF
Jerome, GJ
Lien, LF
Loria, CM
Myers, VH
Appel, LJ
AF Coughlin, J. W.
Gullion, C. M.
Brantley, P. J.
Stevens, V. J.
Bauck, A.
Champagne, C. M.
Dalcin, A. T.
Funk, K. L.
Hollis, J. F.
Jerome, G. J.
Lien, L. F.
Loria, C. M.
Myers, V. H.
Appel, L. J.
TI Behavioral Mediators of Treatment Effects in the Weight Loss Maintenance
Trial
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Obesity; Weight maintenance; Weight regain; Behavioral strategies;
Mediators
ID RANDOMIZED CLINICAL-TRIALS; PHYSICAL-ACTIVITY; DIETARY PATTERNS;
BODY-MASS; ADULTS; INTERVENTION; MODERATORS; PREVENTION; GAIN; FAT
AB The Weight Loss Maintenance Trial tested strategies for maintenance of weight loss. Personal contact was superior to interactive technology and self-directed conditions.
We aimed to identify behavioral mediators of the superior effect of personal contact vs. interactive technology and of personal contact vs. self-directed arms.
Overweight/obese adults at risk for cardiovascular disease (n = 1,032) who lost at least 4 kg were randomized to personal contact, interactive technology, or self-directed. After 30 months, 880 participants had data on weight and behavioral strategies.
Reported increase of intake of fruits and vegetables and physical activity and more frequent self-weighing met criteria as mediators of the better outcome of personal contact vs. interactive technology. Increased intake of fruits and vegetables, more frequent self-weighing, and decreased dessert consumption were mediators of the difference between personal contact vs. self-directed.
Inducing changes in the identified behaviors might yield better outcomes in future weight loss maintenance trials.
(ClinicalTrials.gov number NCT00054925).
C1 [Coughlin, J. W.; Dalcin, A. T.; Appel, L. J.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21287 USA.
[Gullion, C. M.; Stevens, V. J.; Bauck, A.; Funk, K. L.; Hollis, J. F.] Kaiser Permanente Ctr Hlth Res, Oakland, CA USA.
[Brantley, P. J.; Champagne, C. M.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Jerome, G. J.] Towson Univ, Towson, MD USA.
[Lien, L. F.] Duke Univ, Med Ctr, Durham, NC USA.
[Loria, C. M.] NHLBI, Bethesda, MD 20892 USA.
[Myers, V. H.] Klein Buendel Inc, Golden, CO USA.
RP Coughlin, JW (reprint author), Johns Hopkins Univ, Sch Med, 600 North Wolfe St,Meyer 101, Baltimore, MD 21287 USA.
EM jwilder3@jhmi.edu
OI Jerome, Gerald/0000-0003-0612-2626
FU NHLBI NIH HHS [5-U01 HL68790, 5-U01 HL68676, 5-U01 HL68920, 5U01
HL68734, HL68955, U01 HL068676, U01 HL068734, U01 HL068790, U01
HL068920, U01 HL068955]
NR 37
TC 11
Z9 11
U1 1
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
EI 1532-4796
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD DEC
PY 2013
VL 46
IS 3
BP 369
EP 381
DI 10.1007/s12160-013-9517-3
PG 13
WC Psychology, Multidisciplinary
SC Psychology
GA 248HX
UT WOS:000326690300014
PM 23813320
ER
PT J
AU Usategui, A
Criado, G
Izquierdo, E
Del Rey, MJ
Carreira, PE
Ortiz, P
Leonard, WJ
Pablos, JL
AF Usategui, Alicia
Criado, Gabriel
Izquierdo, Elena
Del Rey, Manuel J.
Carreira, Patricia E.
Ortiz, Pablo
Leonard, Warren J.
Pablos, Jose L.
TI A profibrotic role for thymic stromal lymphopoietin in systemic
sclerosis
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Article
DE Systemic Sclerosis; Autoimmunity; Cytokines; Fibroblasts
ID BLEOMYCIN-INDUCED SCLERODERMA; AIRWAY EPITHELIAL-CELLS; INDUCED SKIN
FIBROSIS; FACTOR T-BET; MAST-CELLS; PULMONARY-FIBROSIS; GENE-EXPRESSION;
UP-REGULATION; ANIMAL-MODEL; LUNG-DISEASE
AB Objetive Systemic sclerosis (SSc) is an autoimmune disease characterised by progressive fibrosis. Although SSc shares pathogenetic features with other autoimmune diseases, the participation of profibrotic Th2 cytokines is unique to SSc, but the mechanisms of Th2 skewing are unknown. We have analysed the expression and function of thymic stromal lymphopoietin (TSLP), a central regulator of Th2-mediated allergic inflammation, in human SSc, primary lung fibrosis and in a mouse model of scleroderma.
Methods TSLP expression was analysed by immunohistochemistry in human SSc skin, primary lung fibrosis and mouse bleomycin-induced skin fibrosis, and by quantitative RT-PCR in mouse skin and cultured fibroblasts. The regulation of TSLP expression by specific toll-like receptors (TLR)-2, -3 and -4 agonists was analysed in human dermal fibroblast cultures. The role of TSLP in skin fibrosis and local cytokine expression was analysed in TSLP receptor (TSLPR)-deficient mice.
Results TSLP was overexpressed by epithelial cells, mast cells and fibroblasts in human SSc skin and lung fibrosis, and in the bleomycin model of scleroderma. In cultured human and mouse skin fibroblasts, TSLP expression was inducible by activation of TLR, particularly TLR3. In TSLPR-deficient mice, bleomycin-induced fibrosis was significantly reduced in parallel with significantly reduced local expression of IL-13.
Conclusions These data provide the first evidence of TSLP overexpression in SSc and other non-allergic fibrotic conditions, and demonstrate a profibrotic role that is potentially meditated by specific changes in the local cytokine milieu. Thus, modulating TSLP may have antifibrotic therapeutic implications.
C1 [Usategui, Alicia; Criado, Gabriel; Izquierdo, Elena; Del Rey, Manuel J.; Carreira, Patricia E.; Pablos, Jose L.] Inst Invest Hosp 12 Octubre I 12, Serv Reumatol, Madrid, Spain.
[Ortiz, Pablo] Inst Invest Hosp 12 Octubre I 12, Serv Dermatol, Madrid, Spain.
[Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Leonard, Warren J.] NHLBI, Ctr Immunol, NIH, Bethesda, MD 20892 USA.
RP Pablos, JL (reprint author), Hosp 12 Octubre, Serv Reumatol, E-28041 Madrid, Spain.
EM jlpablos@h12o.es
RI Del Rey, Manuel /O-6114-2014; Usategui, Alicia/O-6476-2014;
OI Del Rey, Manuel /0000-0002-8180-1584; Criado,
Gabriel/0000-0003-4824-0890
FU Fondo de Investigacion Sanitaria [PI08/0316, PI12/439, RIER
RD12/09/016]; Division of Intramural Research National Heart, Lung, and
Blood Institute, National Institutes of Health
FX This work was supported by Fondo de Investigacion Sanitaria through
grants PI08/0316 and PI12/439 and RIER RD12/09/016 and by the Division
of Intramural Research National Heart, Lung, and Blood Institute,
National Institutes of Health.
NR 44
TC 14
Z9 15
U1 1
U2 8
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD DEC
PY 2013
VL 72
IS 12
BP 2018
EP 2023
DI 10.1136/annrheumdis-2012-202279
PG 6
WC Rheumatology
SC Rheumatology
GA 250TJ
UT WOS:000326877500025
PM 23413283
ER
PT J
AU Kelly, PA
Viding, E
Wallace, GL
Schaer, M
De Brito, SA
Robustelli, B
McCrory, EJ
AF Kelly, Philip A.
Viding, Essi
Wallace, Gregory L.
Schaer, Marie
De Brito, Stephane A.
Robustelli, Briana
McCrory, Eamon J.
TI Cortical Thickness, Surface Area, and Gyrification Abnormalities in
Children Exposed to Maltreatment: Neural Markers of Vulnerability?
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Child abuse; cortical thickness; local gyrification; maltreatment;
psychopathology; surface area
ID POSTTRAUMATIC-STRESS-DISORDER; HUMAN CEREBRAL-CORTEX; ANTERIOR CINGULATE
CORTEX; MAGNETIC-RESONANCE IMAGES; GRAY-MATTER VOLUME; CHILDHOOD
MALTREATMENT; ORBITOFRONTAL CORTEX; MAJOR DEPRESSION; REDUCED VOLUME;
VISUAL-CORTEX
AB Background: Childhood maltreatment has been shown to significantly elevate the risk of psychiatric disorder. Previous neuroimaging studies of children exposed to maltreatment have reported atypical neural structure in several regions, including the prefrontal cortex and temporal lobes. These studies have exclusively investigated volumetric differences rather than focusing on genetically and developmentally distinct indices of brain structure.
Methods: Here we used surface-based methods to examine cortical thickness, surface area, and local gyrification in a community sample of children with documented experiences of abuse (n = 22) and a group of carefully matched nonmaltreated peers (n = 21).
Results: Reduced cortical thickness in the maltreated compared with the nonmaltreated group was observed in an extended cluster that incorporated the anterior cingulate, superior frontal gyrus, and orbitofrontal cortex. In addition, reduced cortical surface area was observed within the parcellated regions of the left middle temporal area and lingual gyrus. Local gyrification deficits within the maltreated group were located within two clusters, the lingual gyrus and the insula extending into pars opercularis.
Conclusions: This is the first time structural abnormalities in the anterior cingulate and lingual gyrus have been detected in children exposed to maltreatment. Surface-based methods seem to capture subtle, previously undetected, morphological abnormalities associated with maltreatment. We suggest that these approaches detect developmental precursors of brain volume differences seen in adults with histories of abuse. Because the reported regions are implicated in several clinical disorders, they might constitute biological markers of vulnerability, linking exposure to early adversity and psychiatric risk.
C1 [Kelly, Philip A.; Viding, Essi; McCrory, Eamon J.] UCL, Div Psychol & Language Sci, London WC1H 0AP, England.
[Viding, Essi] UCL, Inst Cognit Neurosci, London WC1H 0AP, England.
[Kelly, Philip A.; McCrory, Eamon J.] Anna Freud Ctr, London, England.
[De Brito, Stephane A.] Univ Birmingham, Sch Psychol, Birmingham, W Midlands, England.
[Wallace, Gregory L.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Schaer, Marie] Univ Geneva, Dept Psychiat, Geneva, Switzerland.
RP McCrory, EJ (reprint author), UCL, Div Psychol & Language Sci, 26 Bedford Way, London WC1H 0AP, England.
EM e.mccrory@ucl.ac.uk
OI De Brito, Stephane/0000-0002-9082-6185; Wallace,
Gregory/0000-0003-0329-5054
FU United Kingdom Economic and Social Research Council [RES-061-250189]
FX This work was supported by a grant from the United Kingdom Economic and
Social Research Council (RES-061-250189) to EMC.
NR 68
TC 32
Z9 32
U1 3
U2 16
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 DEC 1
PY 2013
VL 74
IS 11
BP 845
EP 852
DI 10.1016/j.biopsych.2013.06.020
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 252CJ
UT WOS:000326981800010
PM 23954109
ER
PT J
AU Maggio, M
Lauretani, F
Ceda, GP
De Vita, F
Bondi, G
Corsonello, A
Cattabiani, C
Lattanzio, F
Ruggiero, C
Nouvenne, A
Meschi, T
Bandinelli, S
Ferrucci, L
AF Maggio, Marcello
Lauretani, Fulvio
Ceda, Gian Paolo
De Vita, Francesca
Bondi, Giuliana
Corsonello, Andrea
Cattabiani, Chiara
Lattanzio, Fabrizia
Ruggiero, Carmelinda
Nouvenne, Antonio
Meschi, Tiziana
Bandinelli, Stefania
Ferrucci, Luigi
TI Use of proton pump inhibitors is associated with lower trabecular bone
density in older individuals
SO BONE
LA English
DT Article
DE Bone mineral density; Trabecular bone mineral density; Proton pump
inhibitors; InCHIANTI Study; Elderly
ID COMMUNITY-ACQUIRED PNEUMONIA; CLOSTRIDIUM-DIFFICILE INFECTION;
ACID-SUPPRESSIVE DRUGS; MINERAL DENSITY; HIP FRACTURE; POSTMENOPAUSAL
WOMEN; RISK; OSTEOPOROSIS; METAANALYSIS; OMEPRAZOLE
AB Proton pump inhibitors (PPIs) are highly effective in the treatment of upper gastrointestinal acid-related conditions and are fast becoming one of the most frequently prescribed treatments in adult or older persons. Recent data show that long-term use of PPIs in older subjects is associated with important undesirable effects, including a higher risk of osteoporotic fractures. The mechanisms of this association are unclear and the relationship between the use of PPIs and parameters of bone mass and geometry has never been fully explored.
This study investigates the relationship between the chronic use of PPIs and the parameters of bone mass (cortical and trabecular bone mineral density - vBMDc and vBMDt) and bone geometry (cortical and trabecular cross sectional area - tCSA and cCSA) in older individuals.
The study population consisted of 1038 subjects (452 men and 586 women) 65 years or older, selected from the InCHIANTI study, with complete information on computerized tomography performed at tibial level (pQCT) and on medications. Participants were classified as PPI users and nonusers based on self-report of PPI use over the last 15 days, with PPI users (36 subjects, 14 men and 22 women) making up 3.4% of the study population (mean age 75.7 +/- 7.4 years). The relationship between use of PPIs and pQCT bone parameters was tested by multivariate linear regression analysis adjusted for age, sex and several clinical factors and/or statistically confounding variables identified by partial correlation coefficient and Spearman partial rank order correlation coefficients, as appropriate (age, sex, EMI, caloric intake, IGF-1, IL-6, calcium, estradiol, bioavailable testosterone, vitamin D, parathyroid hormone, cross-sectional muscle area, and level of physical activity). PPI users showed age- and sex-adjusted lower vBMDt than nonusers (180.5 +/- 54.8 vs. 207.9 +/- 59.4, p = 0.001). The inverse association between PPI use and vBMDt remained almost unchanged after adjustment for multiple confounders. There was no statistically significant difference in vBMDc, tCSA and cCSA between PPI users and nonusers. In community dwelling older persons, the use of PPIs is inversely associated with vBMDt, an early marker of the osteoporotic process. These findings suggest that PPI use might increase the risk of fractures in older subjects through its detrimental effects on trabecular bone. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Maggio, Marcello; Ceda, Gian Paolo; Bondi, Giuliana; Meschi, Tiziana] Univ Parma, Sect Geriatr, Dept Clin & Expt Med, I-43126 Parma, PR, Italy.
[Maggio, Marcello; Lauretani, Fulvio; Ceda, Gian Paolo; De Vita, Francesca; Nouvenne, Antonio; Meschi, Tiziana] Univ Hosp Parma, Geriatr Rehabil Dept, I-43126 Parma, PR, Italy.
[Corsonello, Andrea] INRCA, Unit Geriatr Pharmacoepidemiol, Contrada Muoio Piccolo Snc, I-87100 Cosenza, CS, Italy.
[Lattanzio, Fabrizia] INRCA Ancona, Sci Direct, I-60124 Ancona, AN, Italy.
[Ruggiero, Carmelinda] Univ Perugia, Sch Med, Inst Gerontol & Geriatr, Dept Clin & Expt Med, I-06100 Perugia, PG, Italy.
[Bandinelli, Stefania] Local Hlth Agcy, Geriatr Unit, I-50122 Florence, FI, Italy.
[Ferrucci, Luigi] NIA, NIH, Baltimore, MD 21224 USA.
RP Maggio, M (reprint author), Univ Parma, Sect Geriatr, Dept Clin & Expt Med, Via Gramsci 14, I-43126 Parma, PR, Italy.
EM marcellomaggio2001@yahoo.it
RI Lauretani, Fulvio/K-5115-2016; meschi, tiziana/K-5032-2016;
OI Lauretani, Fulvio/0000-0002-5287-9972; meschi,
tiziana/0000-0002-7538-6863; Ceda, Gian Paolo/0000-0002-9648-8295;
Nouvenne, Antonio/0000-0002-2680-2242
FU Italian Ministry of Health [ICS 110.1/RS97.71]; US National Institute on
Aging [N01-AG-916413, N01-AG-821336]; Intramural Research Program of the
US National Institute on Aging [263 MD 9164 13, 263 MD 821336]; Italian
Ministry of Health and Emilia Romagna Region [RF-2010-2312659]
FX The InCHIANTI Study was supported as a "targeted project" (ICS
110.1/RS97.71) by the Italian Ministry of Health and in part by the US
National Institute on Aging (Contracts N01-AG-916413 and N01-AG-821336),
and by the Intramural Research Program of the US National Institute on
Aging (Contracts 263 MD 9164 13 and 263 MD 821336) and by grant
RF-2010-2312659 from the Italian Ministry of Health and Emilia Romagna
Region. None of the sponsoring institutions interfered with the
collection, analysis, presentation, or interpretation of the data
reported here.
NR 52
TC 14
Z9 16
U1 0
U2 19
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 DEC
PY 2013
VL 57
IS 2
BP 437
EP 442
DI 10.1016/j.bone.2013.09.014
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 250JB
UT WOS:000326848000016
PM 24076021
ER
PT J
AU Palmore, TN
Henderson, DK
AF Palmore, Tara N.
Henderson, David K.
TI Managing Transmission of Carbapenem-Resistant Enterobacteriaceae in
Healthcare Settings: A View From the Trenches
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
DE carbapenem-resistant enterobacteriaceae; whole genome sequencing;
isolation; transmission; multidrug resistance
ID HYDROGEN-PEROXIDE VAPOR; KLEBSIELLA-PNEUMONIAE; ACINETOBACTER-BAUMANNII;
HANDWASHING SINKS; K. PNEUMONIAE; UNIT PATIENTS; OUTBREAK; DISINFECTION;
EPIDEMIOLOGY; BACTERIA
AB In 2011, the National Institutes of Health Clinical Center experienced a cluster of infection and colonization caused by carbapenem-resistant Klebsiella pneumoniae among profoundly immunocompromised inpatients. This manuscript describes the approach and interventions that were implemented in an attempt to curtail the cluster. Interventions employed included engagement of all stakeholders involved in care of at-risk patients; detailed and frequent communication with hospital staff about issues relating to the outbreak; aggressive microbial surveillance; use of techniques that facilitate rapid identification of resistant organisms; rapid characterization of resistance mechanisms; whole-genome sequencing of outbreak isolates to characterize the spread and to investigate mechanisms of healthcare-associated spread; implementation of enhanced contact precautions for all infected or colonized patients; geographic and personnel cohorting; daily chlorhexidine gluconate baths; dedicating equipment to be used solely for cohorted patients and aggressive decontamination of equipment that had to be reused on uncohorted patients; monitoring adherence to infection control precautions, including unwavering attention to adherence to appropriate hand hygiene procedures; and attention to the details of environmental decontamination. In addition, the manuscript discusses some of the challenges associated with managing such an event, as well as a few of the unanticipated consequences associated with the aftermath of the case cluster.
C1 Hosp Epidemiol Serv, Bethesda, MD USA.
NIH, Ctr Clin, Off Deputy Director Clin Care, Bethesda, MD 20892 USA.
RP Henderson, DK (reprint author), NIH, Ctr Clin, 10 Ctr Dr,Bldg 10,Rm 6-1480, Bethesda, MD 20892 USA.
EM dkh@nih.gov
NR 40
TC 31
Z9 31
U1 3
U2 17
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD DEC 1
PY 2013
VL 57
IS 11
BP 1593
EP 1599
DI 10.1093/cid/cit531
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 247XK
UT WOS:000326657000017
PM 23934166
ER
PT J
AU Blanchet, EM
Martucci, V
Millo, C
Chen, CC
Herscovitch, P
Pacak, K
AF Blanchet, Elise M.
Martucci, Victoria
Millo, Corina
Chen, Clara C.
Herscovitch, Peter
Pacak, Karel
TI Multitracer PET imaging of bone metastases from paraganglioma:
peripheral halo of uptake on F-18-FLT PET mismatching with central
uptake of F-18-FDOPA, F-18-fluorodopamine, and F-18-FDG
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Editorial Material
C1 [Blanchet, Elise M.; Martucci, Victoria; Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, CRC, Bethesda, MD 20892 USA.
[Millo, Corina; Herscovitch, Peter] NIH, PET Dept, Warren Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Chen, Clara C.] NIH, Dept Nucl Med, Warren Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Pacak, K (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, CRC, Bldg 10,1 East,10 Ctr Dr,MSC 1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
FU Intramural NIH HHS [ZIA HD008735-12]
NR 3
TC 1
Z9 1
U1 0
U2 2
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 DEC
PY 2013
VL 40
IS 12
BP 1928
EP 1929
DI 10.1007/s00259-013-2507-7
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 248HZ
UT WOS:000326690600020
PM 23880966
ER
PT J
AU Muscillo, M
Fratini, M
Graffeo, R
Sanguinetti, M
Martella, V
Green, KY
Della Libera, S
La Rosa, G
AF Muscillo, M.
Fratini, M.
Graffeo, R.
Sanguinetti, M.
Martella, V.
Green, K. Y.
Della Libera, S.
La Rosa, Giuseppina
TI GIV Noroviruses in Wastewaters and in Stool Specimens from Hospitalized
Patients
SO FOOD AND ENVIRONMENTAL VIROLOGY
LA English
DT Article
DE Norovirus genogroup IV; Nested PCR; Real-time PCR; Sewage; Stool samples
ID GENOGROUP IV NOROVIRUSES; NORWALK-LIKE VIRUSES; GENETIC DIVERSITY;
WASTE-WATER; MOLECULAR CHARACTERIZATION; TREATMENT PLANTS; ENTERIC
VIRUSES; JAPAN; GASTROENTERITIS; OUTBREAKS
AB Noroviruses (NoVs) are important human pathogens associated with foodborne and waterborne gastroenteritis. These viruses are genetically highly heterogeneous, with more than forty genotypes within three genogroups (GI, GII, and GIV) identified in humans. However, the vast majority of human infections are associated with variants of a unique genotype, GII.4. Aside from these NoV strains of epidemiological relevance, NoV strains of genogroup GIV (Alphatron-like) are reported in a sporadic fashion and their overall prevalence in the community is unknown and this likely reflects the lack of specific diagnostic tools. We analyzed raw sewages collected from 32 wastewater treatment plants distributed throughout Italy (307 samples) and stool specimens collected from hospitalized patients with clinical signs of diarrhea of unknown etiology (285 samples). By using specific qualitative and quantitative RT-PCR assays, 21.8 % of the sewage samples and 3.2 % of the stool specimens tested positive for GIV NoVs. The number of genome copies in fecal samples ranged from 5.08 x 10(4) to 1.73x 10(6)/g of feces. Sequence analysis showed limited genetic variability in human GIV viruses. The presence of GIV NoV both in sewage and in clinical samples confirms that not only GI and GII NoVs but also GIV strains are circulating in humans. Monitoring of GIV NoV is recommended in order to understand the dynamics of circulation in human populations, environmental contamination, and potential health risks.
C1 [Muscillo, M.; Fratini, M.; Della Libera, S.; La Rosa, Giuseppina] Ist Super Sanita, Dept Environm & Primary Prevent, I-00161 Rome, Italy.
[Graffeo, R.; Sanguinetti, M.] Univ Cattolica Sacro Cuore, Ist Microbiol, Policlin A Gemelli, Rome, Italy.
[Martella, V.] Univ Aldo Moro, Dipartimento Sanita Pubbl & Zootecnia, Bari, Italy.
[Green, K. Y.] NIAID, Infect Dis Lab, NIH, DHHS, Bethesda, MD 20892 USA.
RP La Rosa, G (reprint author), Ist Super Sanita, Dept Environm & Primary Prevent, Viale Regina Elena 299, I-00161 Rome, Italy.
EM giuseppina.larosa@iss.it
RI La Rosa, Giuseppina/I-8532-2016; Martella, Vito/K-3146-2016;
OI La Rosa, Giuseppina/0000-0002-2657-100X; Martella,
Vito/0000-0002-5740-6947; Sanguinetti, Maurizio/0000-0002-9780-7059
FU Italian-American Project "Assessing the Impact of GIV Norovirus on Human
Health: a Molecular Epidemiological Investigation on Environmental and
Clinical Samples as a Basis for the Design of Novel Diagnostic Tools for
an Emerging Pathogen"; Grant "Calicivirus nei carnivori e nell'uomo:
caratterizzazione molecolare, epidemiologia, implicazioni
zoonosiche"-PRIN
FX This study was financed by the joint Italian-American Project "Assessing
the Impact of GIV Norovirus on Human Health: a Molecular Epidemiological
Investigation on Environmental and Clinical Samples as a Basis for the
Design of Novel Diagnostic Tools for an Emerging Pathogen," and
partially by the Grant "Calicivirus nei carnivori e nell'uomo:
caratterizzazione molecolare, epidemiologia, implicazioni
zoonosiche"-PRIN 2008. We thank Professor Herbert W. Virgin, Washington
University (St. Louis, Missouri, United States) for providing the murine
NoV stain used as sample process control. We gratefully acknowledge for
wastewater sample collection: 1-2. E. Lorenzi, L. Meucci, M. Deceglie
(SMAT Spa, Torino), E. Garrou, M. Morello, G. Mantovani (ARPA Piemonte,
Torino); 3-4. G. Manassero (Arpa Valle d'Aosta), A. Martello (Corpo
Forestale Valdostano); 5. W. Bodini, C. Amadasi (Vettabbia Spa, Milano);
6. L. Boscolo (Amiacque Spa, Milano); 7. M. Tomasoni, D. Monteverdi (A2A
Spa, Brescia); 8-9. M. Poli, M. Dekas (Eco Center Spa AG, Bolzano), W.
Strobl, E. Scarperi (APPA, Bolzano); 10-11. L. Bruni, G. Gatti, L.
Tomasi, G. Cimadon (APPA, Trento); 12-13. P. Parati, E. Dell'Andrea, G.
Gambillara (Arpa Veneto, Venezia); 14-15. S. Gaiter, L. Sola (ARPA
Liguria, Genova); 16. F.Cornia, M. A. Corvaglia, P. Albertelli (ARPA
Emilia Romagna, Bologna); 17. A. Gambaccioni, M. Razzolini (Publiacqua
S. p. A. Firenze); 18. E. Renna, G. Saltalamacchia, M. Lucarini (ARPA
Umbria, Perugia); 19-20. C. Mengarelli, Trimboli (ARPA Marche, Ancona);
21-24. C. Gala, R. Tomassini (Arpalazio, Roma), G. Ranalletta (ACEA ATO2
S. p. A., Roma); 25. E. Rufolo, R. Martino (ARPA Campania, Sezione
provinciale di Napoli); 26-27. G. Assennato, G. Blonda, (Regione Puglia,
Direzione Scientifica), V. Perrino, M. Mariani (ARPA Puglia, Bari); 28.
R. Vita, R. Masotti, R. Martoccia (ARPA Basilicata, Potenza); 29. F.
Pedulla, G. Belmusto (ARPA Calabria, Reggio Calabria); 30. L. Librici G.
Abbate (ARPA Sicilia, Palermo); 31-32. M. G. Mulas, G. Campus (Regione
Sardegna), A. M. Mereu, M. Secci (ARPA Sardegna, Cagliari).
NR 39
TC 15
Z9 15
U1 1
U2 19
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1867-0334
EI 1867-0342
J9 FOOD ENVIRON VIROL
JI Food Environ. Virol.
PD DEC
PY 2013
VL 5
IS 4
BP 194
EP 202
DI 10.1007/s12560-013-9121-5
PG 9
WC Environmental Sciences; Microbiology; Virology
SC Environmental Sciences & Ecology; Microbiology; Virology
GA 248IE
UT WOS:000326691400002
ER
PT J
AU Singh, UP
Singh, NP
Guan, HB
Busbee, B
Price, RL
Taub, DD
Mishra, MK
Fayad, R
Nagarkatti, M
Nagarkatti, PS
AF Singh, Udai P.
Singh, Narendra P.
Guan, Hongbing
Busbee, Brandon
Price, Robert L.
Taub, Dennis D.
Mishra, Manoj K.
Fayad, Raja
Nagarkatti, Mitzi
Nagarkatti, Prakash S.
TI Leptin antagonist ameliorates chronic colitis in IL-10(-/-) mice
SO IMMUNOBIOLOGY
LA English
DT Article
DE Inflammation; Inflammatory bowel disease (IBD); Leptin; Antagonist;
Pegylated; Ulcerative colitis (UC); Crohn's disease (CD)
ID INFLAMMATORY-BOWEL-DISEASE; REGULATORY T-CELLS; TGF-BETA; INTESTINAL
INFLAMMATION; CROHNS-DISEASE; CUTTING EDGE; AUTOIMMUNE
ENCEPHALOMYELITIS; ULCERATIVE-COLITIS; STAT3 ACTIVATION; IMMUNE-RESPONSE
AB Background: Although the etiology of two major forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC) are unknown and evidence suggests that chronic intestinal inflammation is caused by an excessive immune response to mucosal antigens. Previous studies support the role for TGF-beta 1 through 3 in the initiation and maintenance of tolerance via the induction of regulatory T cells (Tregs) to control intestinal inflammation. Leptin, a satiety hormone produced primarily by adipose tissue, has been shown to increase during colitis progression and is believed to contribute to disease genesis and/or progression.
Aim: We investigated the ability of a pegylated leptin antagonist (PG-MLA) to ameliorate the development of chronic experimental colitis.
Results: Compared to vehicle control animals, PG-MLA treatment of mice resulted in an (1) attenuated clinical score; (2) reversed colitis-associated pathogenesis including a decrease in body weight; (3) reduced systemic and mucosal inflammatory cytokine expression; (4) increased insulin levels and (5) enhanced systemic and mucosal Tregs and CD39(+) Tregs in mice with chronic colitis. The percentage of systemic and mucosal TGF-beta 1, -beta 2 and -beta 3 expressing CD4(+) T cells were augmented after PG-MLA treatment. The activation of STAT1 and STAT3 and the expression of Smad7 were also reduced after PG-MLA treatment in the colitic mice. These findings clearly suggest that PG-MLA treatment reduces intestinal Smad7 expression, restores TGF-beta 1-3 signaling and reduces STAT1/STAT3 activation that may increase the number of Tregs to ameliorate chronic colitis.
Conclusion: This study clearly links inflammation with the metabolic hormone leptin suggesting that nutritional status influences immune tolerance through the induction of functional Tregs. Inhibiting leptin activity through PG-MLA might provide a new and novel therapeutic strategy for the treatment of IBD. Published by Elsevier GmbH.
C1 [Singh, Udai P.; Singh, Narendra P.; Guan, Hongbing; Busbee, Brandon; Nagarkatti, Mitzi; Nagarkatti, Prakash S.] Univ S Carolina, Sch Med, Columbia, SC 29208 USA.
[Price, Robert L.] Univ S Carolina, Dept Cell & Dev Biol, Columbia, SC 29208 USA.
[Taub, Dennis D.] NIA, Lab Mol Biol & Immunol, IRP, NIH, Baltimore, MD 21224 USA.
[Mishra, Manoj K.] Alabama State Univ, Dept Math & Sci, Montgomery, AL 36104 USA.
[Fayad, Raja] Univ S Carolina, Arnold Sch Publ Hlth, Dept Exercise Sci, Columbia, SC 29208 USA.
RP Singh, UP (reprint author), Univ S Carolina, Dept Pathol Microbiol & Immunol, Columbia, SC 29208 USA.
EM Udai.singh@uscmed.sc.edu
OI Nagarkatti, Mitzi/0000-0002-5977-5615
FU NIH [R56 DK087836, R01 AT006888, R01 ES019313, R01 MH094755, P01
AT003961]; University of South Carolina School of Medicine; National
Institute on Aging, NIH
FX This work was supported, in part by NIH grants R56 DK087836, R01
AT006888, R01 ES019313, R01 MH094755, P01 AT003961, Research and
Development Funds from the University of South Carolina School of
Medicine and Intramural Program of the National Institute on Aging, NIH.
NR 70
TC 14
Z9 15
U1 0
U2 9
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD DEC
PY 2013
VL 218
IS 12
BP 1439
EP 1451
DI 10.1016/j.imbio.2013.04.020
PG 13
WC Immunology
SC Immunology
GA 250NF
UT WOS:000326858800001
PM 23726523
ER
PT J
AU Anderson, TK
Nelson, MI
Kitikoon, P
Swenson, SL
Korslund, JA
Vincent, AL
AF Anderson, Tavis K.
Nelson, Martha I.
Kitikoon, Pravina
Swenson, Sabrina L.
Korslund, John A.
Vincent, Amy L.
TI Population dynamics of cocirculating swine influenza A viruses in the
United States from 2009 to 2012
SO INFLUENZA AND OTHER RESPIRATORY VIRUSES
LA English
DT Article; Proceedings Paper
CT 2nd ISIRV International Symposium on Neglected Influenza Viruses
CY MAR 07-08, 2013
CL Dublin, IRELAND
DE Epidemiology; influenza A virus; surveillance; swine; vaccines; zoonotic
diseases
ID GENETIC-CHARACTERIZATION; MAXIMUM-LIKELIHOOD; H3N2 VIRUS; PIGS;
TRANSMISSION; REASSORTMENT; EVOLUTION; HUMANS; SEASONALITY; INFECTIONS
AB BackgroundUnderstanding the ecology and evolution of influenza A viruses (IAV) in mammalian hosts is critical to reduce disease burden in production animals and lower zoonotic infection risk in humans. Recent advances in influenza surveillance in US swine populations allow for timely epidemiological, phylogenetic, and virological analyses that monitor emergence of novel viruses and assess changes in viral population dynamics.
MethodsTo better understand IAV in the North American swine population, we undertook a phylogenetic analysis of 1075 HA, 1049 NA, and 1040M sequences of IAV isolated from US swine during 2009-2012 through voluntary and anonymous submissions to the US Department of Agriculture IAV swine surveillance system.
ResultsAnalyses revealed changes in population dynamics among multiple clades of A/H1N1, A/H3N2, and A/H1N2 cocirculating in US swine populations during 2009-2012. Viral isolates were categorized into one of seven genetically and antigenically distinct hemagglutinin lineages: H1, H1, H1, H11, H12, H1pdm09, and H3 cluster IV. There was an increase in occurrence of H11 in samples submitted, with a concurrent decrease in H1pdm09. H3 cluster IV exhibited increasing diversification, warranting a re-evaluation of phylogenetic nomenclature criteria. Although H3N2 represented 25% of identified viruses, this subtype was reported in increasing proportion of sequenced isolates since late 2011.
ConclusionsSurveillance and reporting of IAV in US swine have increased since 2009, and we demonstrate a period of expanded viral diversity. These data may be used to inform intervention strategies of vaccine and diagnostic updates and changes in swine health management.
C1 [Anderson, Tavis K.; Kitikoon, Pravina; Vincent, Amy L.] USDA ARS, Virus & Prion Res Unit, Natl Anim Dis Ctr, Ames, IA 50010 USA.
[Nelson, Martha I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Swenson, Sabrina L.] USDA APHIS, Natl Vet Serv Labs, Ames, IA USA.
[Korslund, John A.] USDA APHIS, Ctr Epidemiol & Anim Hlth, Riverdale, MD USA.
RP Vincent, AL (reprint author), USDA ARS, Virus & Prion Res Unit, NADC, 1920 Dayton Ave,POB 70, Ames, IA 50010 USA.
EM amy.vincent@ars.usda.gov
OI Anderson, Tavis/0000-0002-3138-5535
FU Supplemental Appropriations Act
FX We are grateful to the pork producers, swine veterinarians, and
laboratories for participating in the USDA Influenza Virus Surveillance
System for swine. Funding was provided from the Supplemental
Appropriations Act of 2009 for pandemic influenza preparedness and
response to the Department of Health and Human Services, as well as base
funding to the USDA-ARS and USDA-APHIS-VS. Disclaimer: Mention of trade
names or commercial products in this article is solely for the purpose
of providing specific information and does not imply recommendation or
endorsement by the US Department of Agriculture. USDA is an equal
opportunity provider and employer.
NR 55
TC 28
Z9 28
U1 1
U2 25
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 DEC
PY 2013
VL 7
SU S4
SI SI
BP 42
EP 51
DI 10.1111/irv.12193
PG 10
WC Infectious Diseases; Virology
SC Infectious Diseases; Virology
GA 250YC
UT WOS:000326891700008
PM 24224819
ER
PT J
AU Schelman, WR
Traynor, AM
Holen, KD
Kolesar, JM
Attia, S
Hoang, T
Eickhoff, J
Jiang, ZS
Alberti, D
Marnocha, R
Reid, JM
Ames, MM
McGovern, RM
Espinoza-Delgado, I
Wright, JJ
Wilding, G
Bailey, HH
AF Schelman, William R.
Traynor, Anne M.
Holen, Kyle D.
Kolesar, Jill M.
Attia, Steven
Hoang, Tien
Eickhoff, Jens
Jiang, Zhisheng
Alberti, Dona
Marnocha, Rebecca
Reid, Joel M.
Ames, Matthew M.
McGovern, Renee M.
Espinoza-Delgado, Igor
Wright, John J.
Wilding, George
Bailey, Howard H.
TI A phase I study of vorinostat in combination with bortezomib in patients
with advanced malignancies
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE SAHA; Vorinostat; PS-341; Bortezomib; Phase I
ID HISTONE DEACETYLASE INHIBITOR; SUBEROYLANILIDE HYDROXAMIC ACID; CANCER
CELLS; PROTEASOME INHIBITORS; INDUCED APOPTOSIS; MULTIPLE-MYELOMA;
DOWN-REGULATION; LEUKEMIA CELLS; LUNG-CANCER; BCR-ABL
AB Background A phase I study to assess the maximum-tolerated dose (MTD), dose-limiting toxicity (DLT), pharmacokinetics (PK) and antitumor activity of vorinostat in combination with bortezomib in patients with advanced solid tumors. Methods Patients received vorinostat orally once daily on days 1-14 and bortezomib intravenously on days 1, 4, 8 and 11 of a 21-day cycle. Starting dose (level 1) was vorinostat (400 mg) and bortezomib (0.7 mg/m(2)). Bortezomib dosing was increased using a standard phase I dose-escalation schema. PKs were evaluated during cycle 1. Results Twenty-three patients received 57 cycles of treatment on four dose levels ranging from bortezomib 0.7 mg/m(2) to 1.5 mg/m(2). The MTD was established at vorinostat 400 mg daily and bortezomib 1.3 mg/m(2). DLTs consisted of grade 3 fatigue in three patients (1 mg/m(2),1.3 mg/m(2) and 1.5 mg/m(2)) and grade 3 hyponatremia in one patient (1.5 mg/m(2)). The most common grade 1/2 toxicities included nausea (60.9 %), fatigue (34.8 %), diaphoresis (34.8 %), anorexia (30.4 %) and constipation (26.1 %). Objective partial responses were observed in one patient with NSCLC and in one patient with treatment-refractory soft tissue sarcoma. Bortezomib did not affect the PKs of vorinostat; however, the Cmax and AUC of the acid metabolite were significantly increased on day 2 compared with day 1. Conclusions This combination was generally well-tolerated at doses that achieved clinical benefit. The MTD was established at vorinostat 400 mg daily x 14 days and bortezomib 1.3 mg/m(2) on days 1, 4, 8 and 11 of a 21-day cycle.
C1 [Schelman, William R.; Traynor, Anne M.; Holen, Kyle D.; Kolesar, Jill M.; Attia, Steven; Hoang, Tien; Eickhoff, Jens; Jiang, Zhisheng; Alberti, Dona; Marnocha, Rebecca; Wilding, George; Bailey, Howard H.] Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53792 USA.
[Espinoza-Delgado, Igor; Wright, John J.] NCI, Clin Treatment Evaluat Program, Bethesda, MD 20892 USA.
[Reid, Joel M.; Ames, Matthew M.; McGovern, Renee M.] Mayo Clin, Ctr Canc, Rochester, MN USA.
RP Schelman, WR (reprint author), Univ Wisconsin, Carbone Canc Ctr, 600 Highland Ave,K6-568 CSC, Madison, WI 53792 USA.
EM wrs@medicine.wisc.edu
FU NCI [UO1 CA062491]; CTEP Translational Research Initiative; Clinical and
Translational Science Award, National Center for Research Resources, NIH
[1UL 1RR025011]; Mayo Clinic [U01 CA69912]; CTEP Translational Research
Initiative-Support Subcontracts, Correlative Studies Core Laboratory for
SAHA Phase I and Phase II Clinical Protocols (Mayo Clinic),
SAIC-FREDERICK, INC. [23XS026]
FX UO1 CA062491, Early Clinical Trials of Anti-Cancer Agents with Phase I
Emphasis, NCI; CTEP Translational Research Initiative, Contract; 1UL
1RR025011, Clinical and Translational Science Award, National Center for
Research Resources, NIH; U01 CA69912, Phase I Trials of Anticancer
Agents (Mayo Clinic); and 23XS026, CTEP Translational Research
Initiative-Support Subcontracts, Correlative Studies Core Laboratory for
SAHA Phase I and Phase II Clinical Protocols (Mayo Clinic),
SAIC-FREDERICK, INC.
NR 37
TC 9
Z9 9
U1 2
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD DEC
PY 2013
VL 31
IS 6
BP 1539
EP 1546
DI 10.1007/s10637-013-0029-6
PG 8
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 247FT
UT WOS:000326602500015
PM 24114121
ER
PT J
AU Alexander, J
Kwon, HT
Strecher, R
Bartholomew, J
AF Alexander, James
Kwon, Harry T.
Strecher, Rachael
Bartholomew, Jill
TI Multicultural Media Outreach: Increasing Cancer Information Coverage in
Minority Communities
SO JOURNAL OF CANCER EDUCATION
LA English
DT Article
DE Cancer health disparities; Ethnic media; Minority and underserved;
Cancer education
AB Ethnic media can serve as an opportunity for cancer education and outreach to minority communities. The National Cancer Institute developed the Multicultural Media Outreach (MMO) program which utilizes an integrated approach of both traditional and social media to disseminate evidence-based cancer education information for minority communities. The MMO program is the contact point for multicultural media outlets seeking evidence-based cancer information, education materials, minority spokespersons, and news tailored to minority communities affected by cancer health disparities. MMO developed LifelinesA (R), a cancer education series that addresses cancer prevention, treatment, survivorship, clinical trials, and other cancer-related topics for African American, Hispanic, Asian American, American Indian, and Alaska Native audiences. LifelinesA (R) content is disseminated through traditional media (radio, print, and television) as well as social media (web, Twitter, YouTube, and RSS feed). This article describes the MMO program and lessons learned to date.
C1 [Alexander, James; Kwon, Harry T.; Strecher, Rachael; Bartholomew, Jill] NCI, Off Commun & Educ, NIH, Bethesda, MD 20892 USA.
RP Kwon, HT (reprint author), NCI, Off Commun & Educ, NIH, 9609 Med Ctr Dr,Room 2E532,MSC 9760, Bethesda, MD 20892 USA.
EM harry.kwon@nih.gov
NR 9
TC 5
Z9 5
U1 2
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0885-8195
EI 1543-0154
J9 J CANCER EDUC
JI J. Cancer Educ.
PD DEC
PY 2013
VL 28
IS 4
BP 744
EP 747
DI 10.1007/s13187-013-0534-5
PG 4
WC Oncology; Education, Scientific Disciplines; Public, Environmental &
Occupational Health
SC Oncology; Education & Educational Research; Public, Environmental &
Occupational Health
GA 242ZQ
UT WOS:000326286200023
PM 23963725
ER
PT J
AU Sarkin, AJ
Tally, SR
Wooldridge, JS
Choi, K
Shieh, M
Kaplan, RM
AF Sarkin, Andrew J.
Tally, Steven R.
Wooldridge, Jennalee S.
Choi, Kyle
Shieh, Marian
Kaplan, Robert M.
TI Gender Differences in Adapting Driving Behavior to Accommodate Visual
Health Limitations
SO JOURNAL OF COMMUNITY HEALTH
LA English
DT Article
DE Driving; Gender; Cataracts; Visual acuity; Public safety
ID MOTOR-VEHICLE CRASH; OLDER DRIVERS; CATARACT-SURGERY; FUNCTION
QUESTIONNAIRE; SELF-REGULATION; UNITED-STATES; RISK; EYE; IMPAIRMENT;
ADULTS
AB This study investigated whether men and women are equally likely to adapt their driving behaviors in response to visual limitations. Participants were 376 (222 women and 154 men) pre-surgical cataract patients from the Shiley Eye Center in La Jolla, California. All participants completed the National Eye Institute Visual Functioning Questionnaire, which assesses self-reported visual symptoms, functional limitations, and behaviors including driving during the day, at night, or in difficult conditions. Visual acuity was assessed using the log of the minimal angle of resolution (LogMAR) scale. There were no significant differences in LogMAR visual acuity between men and women who reported either that they stopped driving at night because of visual impairment or reported having no difficulty driving at night. Of participants who reported having difficulty driving at night, mean weighted LogMAR scores indicated significantly better visual acuity for women than men. There were no significant differences in LogMAR visual acuity between women and men in any of the difficult driving condition categories. Significantly more women than men reported that they stopped driving in difficult conditions because of eyesight, despite the lack of gender differences in visual acuity for this sample. We found no evidence that cataract disease had different effects on the visual acuity of older adult men and women. However, there was a significant difference between genders in self-reported driving behavior. It is possible that some women are more cautious or have less need to drive. However, failing to adapt driving behaviors to accommodate visual limitations may represent a potential behavioral public health risk for men.
C1 [Sarkin, Andrew J.; Tally, Steven R.; Wooldridge, Jennalee S.; Choi, Kyle; Shieh, Marian] Univ Calif San Diego, Hlth Serv Res Ctr, San Diego, CA 92093 USA.
[Kaplan, Robert M.] NIH, Dept Rehabil Med, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Sarkin, AJ (reprint author), Univ Calif San Diego, Hlth Serv Res Ctr, 9500 Gilman Dr 0994, San Diego, CA 92093 USA.
EM asarkin@ucsd.edu
NR 36
TC 3
Z9 3
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0094-5145
EI 1573-3610
J9 J COMMUN HEALTH
JI J. Community Health
PD DEC
PY 2013
VL 38
IS 6
BP 1175
EP 1181
DI 10.1007/s10900-013-9730-9
PG 7
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 248IW
UT WOS:000326693600024
PM 23852327
ER
PT J
AU Clark, K
Vendt, B
Smith, K
Freymann, J
Kirby, J
Koppel, P
Moore, S
Phillips, S
Maffitt, D
Pringle, M
Tarbox, L
Prior, F
AF Clark, Kenneth
Vendt, Bruce
Smith, Kirk
Freymann, John
Kirby, Justin
Koppel, Paul
Moore, Stephen
Phillips, Stanley
Maffitt, David
Pringle, Michael
Tarbox, Lawrence
Prior, Fred
TI The Cancer Imaging Archive (TCIA): Maintaining and Operating a Public
Information Repository
SO JOURNAL OF DIGITAL IMAGING
LA English
DT Article
DE TCIA; NBIA; Cancer imaging; Image archive; Biomedical image analysis;
Cancer detection
AB The National Institutes of Health have placed significant emphasis on sharing of research data to support secondary research. Investigators have been encouraged to publish their clinical and imaging data as part of fulfilling their grant obligations. Realizing it was not sufficient to merely ask investigators to publish their collection of imaging and clinical data, the National Cancer Institute (NCI) created the open source National Biomedical Image Archive software package as a mechanism for centralized hosting of cancer related imaging. NCI has contracted with Washington University in Saint Louis to create The Cancer Imaging Archive (TCIA)-an open-source, open-access information resource to support research, development, and educational initiatives utilizing advanced medical imaging of cancer. In its first year of operation, TCIA accumulated 23 collections (3.3 million images). Operating and maintaining a high-availability image archive is a complex challenge involving varied archive-specific resources and driven by the needs of both image submitters and image consumers. Quality archives of any type (traditional library, PubMed, refereed journals) require management and customer service. This paper describes the management tasks and user support model for TCIA.
C1 [Clark, Kenneth; Vendt, Bruce; Smith, Kirk; Koppel, Paul; Moore, Stephen; Phillips, Stanley; Maffitt, David; Pringle, Michael; Tarbox, Lawrence; Prior, Fred] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, St Louis, MO 63110 USA.
[Freymann, John; Kirby, Justin] SAIC Frederick Inc, Clin Res Directorate, CMRP, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
RP Clark, K (reprint author), Washington Univ, Sch Med, Mallinckrodt Inst Radiol, ERL 510 South Kingshighway Blvd, St Louis, MO 63110 USA.
EM clarkk@mir.wustl.edu
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Image Archive Hosting; [10XS220: SAIC-F]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract No. 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
Washington University component is funded by SUBCONTRACT 10XS220: SAIC-F
(PI: Prior) Image Archive Hosting.
NR 23
TC 66
Z9 66
U1 1
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0897-1889
EI 1618-727X
J9 J DIGIT IMAGING
JI J. Digit. Imaging
PD DEC
PY 2013
VL 26
IS 6
BP 1045
EP 1057
DI 10.1007/s10278-013-9622-7
PG 13
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 248KR
UT WOS:000326698800008
PM 23884657
ER
PT J
AU Schwartz, LM
Castle, PE
Follansbee, S
Borgonovo, S
Fetterman, B
Tokugawa, D
Lorey, TS
Sahasrabuddhe, VV
Luhn, P
Gage, JC
Darragh, TM
Wentzensen, N
AF Schwartz, Lauren M.
Castle, Philip E.
Follansbee, Stephen
Borgonovo, Sylvia
Fetterman, Barbara
Tokugawa, Diane
Lorey, Thomas S.
Sahasrabuddhe, Vikrant V.
Luhn, Patricia
Gage, Julia C.
Darragh, Teresa M.
Wentzensen, Nicolas
TI Risk Factors for Anal HPV Infection and Anal Precancer in HIV-Infected
Men Who Have Sex With Men
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
DE anal cancer; human papillomavirus (HPV); human immunodeficiency virus
(HIV); men who have sex with men (MSM); anal intraepithelial neoplasia
(AIN)
ID HUMAN-PAPILLOMAVIRUS INFECTION; INTRAEPITHELIAL NEOPLASIA;
ANTIRETROVIRAL THERAPY; CANCER PRECURSORS; HOMOSEXUAL-MEN;
UNITED-STATES; END-POINTS; PREVALENCE; EPIDEMIOLOGY; METAANALYSIS
AB Background. Carcinogenic human papillomaviruses (HPVs) cause a large proportion of anal cancers. Human immunodeficiency virus (HIV)-infected men who have sex with men (MSM) are at increased risk of HPV infection and anal cancer compared with HIV-negative men. We evaluated risk factors for HPV infection and anal precancer in a population of HIV-infected MSM.
Methods. Our study included 305 MSM at an HIV/AIDS clinic in the Kaiser Permanente Northern California Health Maintenance Organization. Logistic regression was used to estimate associations of risk factors comparing men without anal HPV infection; men with anal HPV infection, but no precancer; and men with anal precancer.
Results. Low CD4 count (<350 cells/mm(3)) and previous chlamydia infection were associated with an increased risk of carcinogenic HPV infection (odds ratio [OR], 3.65; 95% confidence interval [CI], 1.28-10.40 and OR, 4.24; 95% CI, 1.16-15.51, respectively). History of smoking (OR, 2.71 95% CI, 1.43-5.14), duration, recency, and dose of smoking increased the risk of anal precancer among carcinogenic HPV-positive men but had no association with HPV infection.
Conclusions. We found distinct risk factors for anal HPV infection and anal precancer. Risk factors for HPV infection and anal precancer are similar to established risk factors for cervical cancer progression.
C1 [Schwartz, Lauren M.; Sahasrabuddhe, Vikrant V.; Luhn, Patricia; Gage, Julia C.; Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Castle, Philip E.] Global Canc Initiat Inc, Chestertown, MD USA.
[Follansbee, Stephen; Borgonovo, Sylvia] Kaiser Permanente Med Ctr, San Francisco, CA USA.
[Fetterman, Barbara; Tokugawa, Diane; Lorey, Thomas S.] Kaiser Permanente, TPMG Reg Lab, Berkeley, CA USA.
[Darragh, Teresa M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Wentzensen, N (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 5024, Rockville, MD 20852 USA.
EM wentzenn@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute.
NR 39
TC 18
Z9 18
U1 1
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD DEC 1
PY 2013
VL 208
IS 11
BP 1768
EP 1775
DI 10.1093/infdis/jit374
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 247WQ
UT WOS:000326654300007
PM 23908478
ER
PT J
AU Sourial, N
Bergman, H
Karunananthan, S
Wolfson, C
Payette, H
Gutierrez-Robledo, LM
Beland, F
Fletcher, JD
Guralnik, J
AF Sourial, Nadia
Bergman, Howard
Karunananthan, Sathya
Wolfson, Christina
Payette, Helene
Gutierrez-Robledo, Luis Miguel
Beland, Franois
Fletcher, John D.
Guralnik, Jack
TI Implementing Frailty Into Clinical Practice: A Cautionary Tale
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Frailty; Epidemiology; Functional performance; Risk factors; Outcomes
ID ELDERLY-PATIENTS; MAJOR MORBIDITY; CARDIAC-SURGERY; OLDER-ADULTS; GAIT
SPEED; ROC CURVE; MORTALITY; OUTCOMES; WOMEN; RISK
AB Little is known about the contribution of frailty in improving patient-level prediction beyond readily available clinical information. The objective of this study is to compare the predictive ability of 129 combinations of seven frailty markers (cognition, energy, mobility, mood, nutrition, physical activity, and strength) and quantify their contribution to predictive accuracy beyond age, sex, and number of chronic diseases.
Two cohorts from the Established Populations for Epidemiologic Studies of the Elderly were used. The model with the best predictive fit in predicting 6-year incidence of disability was determined using the Akaike Information Criterion. Predictive accuracy was measured by the C statistic.
Incident disability was 23% in one cohort and 20% in the other cohort. The best model in each cohort was found to be a model including between five and seven frailty markers including cognition, mobility, nutrition, physical activity, and strength. Predictive accuracy of the 129 models ranged from 0.73 to 0.77 across both cohorts. Adding frailty markers to age, sex, and chronic disease increased predictive accuracy by up to 3% in both cohorts (p < .001). The contribution of frailty increased up to 9% in the oldest age group.
Adding frailty markers provided a modest increase in patient-level prediction of disability. Such a modest increase may still be worthwhile because while age, sex, and the number of chronic diseases are not modifiable, frailty may be. Further studies examining the contribution of frailty in improving prediction are needed before adopting frailty as a prognostic tool.
C1 [Sourial, Nadia; Bergman, Howard; Karunananthan, Sathya; Beland, Franois; Fletcher, John D.] Jewish Gen Hosp, SOLIDAGE, McGill Univ Univ Montreal Res Grp Frailty & Aging, Ctr Clin Epidemiol, Montreal, PQ, Canada.
[Bergman, Howard] McGill Univ, Dept Family Med, Montreal, PQ H2W LS4, Canada.
[Bergman, Howard; Beland, Franois] McGill Univ, Div Geriatr Med, Jewish Gen Hosp, Montreal, PQ H2W LS4, Canada.
[Bergman, Howard; Beland, Franois] Univ Montreal, Dept Hlth Adm, Montreal, PQ H3C 3J7, Canada.
[Karunananthan, Sathya; Wolfson, Christina] McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H2W LS4, Canada.
[Wolfson, Christina] McGill Univ, Ctr Hlth, Res Inst, Montreal, PQ H2W LS4, Canada.
[Payette, Helene] Univ Sherbrooke, Res Ctr Aging, Hlth & Social Serv Ctr, Quebec City, PQ, Canada.
[Payette, Helene] Univ Sherbrooke, Univ Inst Geriatr Sherbrooke, Quebec City, PQ, Canada.
[Guralnik, Jack] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[Guralnik, Jack] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
RP Bergman, H (reprint author), McGill Univ, Dept Family Med, 515-517 Pine Ave West, Montreal, PQ H2W LS4, Canada.
EM howard.bergman@mcgill.ca
FU Solidage Research Group and Dr. Joseph Kaufmann Chair in Geriatric
Medicine, McGill University; Canadian Initiative on Frailty and Aging;
Canadian Institutes of Health Research (CIHR) International Opportunity
Program Development [68739]; CIHR team grant in frailty and aging
[82945]; Fonds de la recherche en sante du Quebec
FX This study was supported by grants from the Solidage Research Group and
Dr. Joseph Kaufmann Chair in Geriatric Medicine, McGill University; the
Canadian Initiative on Frailty and Aging; the Canadian Institutes of
Health Research (CIHR) International Opportunity Program Development
(68739); the CIHR team grant in frailty and aging (82945); and the Fonds
de la recherche en sante du Quebec.
NR 40
TC 33
Z9 33
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 DEC
PY 2013
VL 68
IS 12
BP 1505
EP 1511
DI 10.1093/gerona/glt053
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 248DX
UT WOS:000326675000006
PM 23640761
ER
PT J
AU Hirt, C
Weitmann, K
Schuler, F
Kiefer, T
Rabkin, CS
Hoffmann, W
Dolken, G
AF Hirt, Carsten
Weitmann, Kerstin
Schueler, Frank
Kiefer, Thomas
Rabkin, Charles S.
Hoffmann, Wolfgang
Doelken, Gottfried
TI Circulating t(14;18)-positive cells in healthy individuals: association
with age and sex but not with smoking
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE Follicular lymphoma; t(14;18); lymphomagenesis; healthy individuals
ID NON-HODGKINS-LYMPHOMA; OCCUPATIONAL RISK-FACTORS; B-CELLS; T(14/18)
TRANSLOCATIONS; BCL-2/IGH REARRANGEMENT; FOLLICULAR LYMPHOMA;
CIGARETTE-SMOKING; PERIPHERAL-BLOOD; CARRYING CELLS; UNITED-STATES
AB t(14;18)-positive cells can be detected not only in patients with follicular lymphoma (FL) but also in healthy individuals (HIs). We used epidemiological data and blood samples of the population-based Study of Health in Pomerania (SHIP) to analyze associations of FL risk factors and t(14; 18)-positive cells in HIs. Buffy coat samples from 4152 study participants were tested by real-time polymerase chain reaction (PCR) for t(14; 18)-positive cells. Of 3966 evaluable subjects, 1526 were t(14; 18)-PCR positive [38.5%, median 3.9 t(14; 18)-positive per million nucleated cells, range 0.6-9299]. In multivariable analyses, age and sex but not parameters of smoking exposure were significantly associated with t(14; 18) prevalence (logistic regression, p < 0.001). Multivariable analyses of t(14; 18)-frequency showed a positive association with age but not with sex or smoking. These age and sex associations in HIs require careful control in future studies of t(14; 18) as a potential biomarker of lymphoma risk.
C1 [Hirt, Carsten; Schueler, Frank; Kiefer, Thomas; Doelken, Gottfried] Univ Med, Dept Hematol & Oncol, Greifswald, Germany.
[Weitmann, Kerstin; Hoffmann, Wolfgang] Univ Med, Inst Community Med, Greifswald, Germany.
[Rabkin, Charles S.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Hirt, C (reprint author), Ernst Moritz Arndt Univ Greifswald, Med Ctr, Dept Hematol & Oncol, Ferdinand Sauerbruchstr, D-17475 Greifswald, Germany.
EM hirtonko@uni-greifswald.de
FU German Federal Ministry of Education and Research (BMBF) [01ZZ96030,
01ZZ0701]; Ministry for Education, Research, and Cultural Affairs;
Ministry for Social Affairs of the Federal State of Mecklenburg-West
Pomerania
FX SHIP is part of the Community Medicine Net
(http://www.medizin.uni-greifswald.de/icm) of the University of
Greifswald, which is funded by grants from the German Federal Ministry
of Education and Research (BMBF, grant 01ZZ96030, 01ZZ0701); the
Ministry for Education, Research, and Cultural Affairs; and the Ministry
for Social Affairs of the Federal State of Mecklenburg-West Pomerania.
NR 34
TC 4
Z9 4
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
EI 1029-2403
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD DEC
PY 2013
VL 54
IS 12
BP 2678
EP 2684
DI 10.3109/10428194.2013.788177
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 247QK
UT WOS:000326633700021
PM 23527525
ER
PT J
AU Bagci, U
Udupa, JK
Mendhiratta, N
Foster, B
Xu, ZY
Yao, JH
Chen, XJ
Mollura, DJ
AF Bagci, Ulas
Udupa, Jayaram K.
Mendhiratta, Neil
Foster, Brent
Xu, Ziyue
Yao, Jianhua
Chen, Xinjian
Mollura, Daniel J.
TI Joint segmentation of anatomical and functional images: Applications in
quantification of lesions from PET, PET-CT, MRI-PET, and MRI-PET-CT
images
SO MEDICAL IMAGE ANALYSIS
LA English
DT Article
DE Simultaneous segmentation; PET segmentation; Random Walk; MRI-PET
Co-segmentation; PET-CT Co-segmentation
ID CELL LUNG-CANCER; POSITRON-EMISSION-TOMOGRAPHY; TARGET VOLUME
DELINEATION; FDG-PET; THRESHOLD SEGMENTATION; TUMOR VOLUME;
INTEROBSERVER VARIABILITY; ACTIVE CONTOURS; F-18-FDG PET; NECK-CANCER
AB We present a novel method for the joint segmentation of anatomical and functional images. Our proposed methodology unifies the domains of anatomical and functional images, represents them in a product lattice, and performs simultaneous delineation of regions based on random walk image segmentation. Furthermore, we also propose a simple yet effective object/background seed localization method to make the proposed segmentation process fully automatic. Our study uses PET, PET-CT, MRI-PET, and fused MRI-PET-CT scans (77 studies in all) from 56 patients who had various lesions in different body regions. We validated the effectiveness of the proposed method on different PET phantoms as well as on clinical images with respect to the ground truth segmentation provided by clinicians. Experimental results indicate that the presented method is superior to threshold and Bayesian methods commonly used in PET image segmentation, is more accurate and robust compared to the other PET-CT segmentation methods recently published in the literature, and also it is general in the sense of simultaneously segmenting multiple scans in real-time with high accuracy needed in routine clinical use. Published by Elsevier B.V.
C1 [Bagci, Ulas; Mollura, Daniel J.] NIH, Ctr Infect Dis Imaging, Bethesda, MD 20892 USA.
[Bagci, Ulas; Mendhiratta, Neil; Foster, Brent; Xu, Ziyue; Yao, Jianhua; Mollura, Daniel J.] NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Udupa, Jayaram K.] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Mendhiratta, Neil] NYU, Sch Med, New York, NY USA.
[Chen, Xinjian] Soochow Univ, Sch Elect & Informat Engn, Suzhou, Peoples R China.
RP Bagci, U (reprint author), NIH, Dept Radiol & Imaging Sci, Bldg 10, Bethesda, MD 20892 USA.
EM ulasbagci@gmail.com
RI Xy, Ziyue/K-9438-2014; Chen, Xinjian/E-8592-2016
OI Xy, Ziyue/0000-0002-5728-6869; Bagci, Ulas/0000-0001-7379-6829;
FU Center for Infectious Disease Imaging (CIDI); National Institutes of
Allergy and Infectious Diseases (NIAID); National Institutes of
Bio-imaging and Bioengineering (NIBIB) at the National Institutes of
Health (NIH)
FX This research is supported by the Center for Infectious Disease Imaging
(CIDI), the Intramural Program of the National Institutes of Allergy and
Infectious Diseases (NIAID), and the National Institutes of Bio-imaging
and Bioengineering (NIBIB) at the National Institutes of Health (NIH).
We thank Kristine S. Evers for her editing of this manuscript.
NR 72
TC 46
Z9 47
U1 3
U2 33
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1361-8415
EI 1361-8423
J9 MED IMAGE ANAL
JI Med. Image Anal.
PD DEC
PY 2013
VL 17
IS 8
BP 929
EP 945
DI 10.1016/j.media.2013.05.004
PG 17
WC Computer Science, Artificial Intelligence; Computer Science,
Interdisciplinary Applications; Engineering, Biomedical; Radiology,
Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Radiology, Nuclear Medicine & Medical
Imaging
GA 247YX
UT WOS:000326662000005
PM 23837967
ER
PT J
AU Yotter, RA
Doshi, J
Clark, V
Sojkova, J
Zhou, Y
Wong, DF
Ferrucci, L
Resnick, SM
Davatzikos, C
AF Yotter, Rachel A.
Doshi, Jimit
Clark, Vanessa
Sojkova, Jitka
Zhou, Yun
Wong, Dean F.
Ferrucci, Luigi
Resnick, Susan M.
Davatzikos, Christos
TI Memory decline shows stronger associations with estimated spatial
patterns of amyloid deposition progression than total amyloid burden
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Amyloid; PiB; PET; CVLT; Cognition
ID PITTSBURGH COMPOUND-B; PRECLINICAL ALZHEIMERS-DISEASE; MILD COGNITIVE
IMPAIRMENT; REFERENCE TISSUE MODEL; A-BETA DEPOSITION; NONDEMENTED
INDIVIDUALS; ELDERLY SUBJECTS; OLDER-ADULTS; PET; PIB
AB The development of amyloid imaging compounds has allowed in vivo imaging of amyloid deposition. In this study, we examined the spatial patterns of amyloid deposition throughout the brain using Pittsburgh Compound Blue (C-11-PiB) positron emission tomography data from the Baltimore Longitudinal Study of Aging. We used a new methodology that allowed us to approximate spatial patterns of the temporal progression of amyloid plaque deposition from cross-sectional data. Our results are consistent with patterns of progression known from autopsy studies, with frontal and precuneus regions affected early and occipital and sensorimotor cortices affected later in disease progression-here, disease progression means lower-to-higher total amyloid burden. Furthermore, we divided participants into subgroups based on longitudinal change in memory performance, and demonstrated significantly different spatial patterns of the estimated progression of amyloid deposition between these subgroups. Our results indicate that the spatial pattern of amyloid deposition is related to cognitive performance and may be more informative than a biomarker reflecting total amyloid burden, the use of which is the current practice. This finding has broad implications for our understanding of the relationship between cognitive decline/resilience and amyloid deposition, as well as for the use of amyloid imaging as a biomarker in research and clinical applications. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Yotter, Rachel A.; Doshi, Jimit; Clark, Vanessa; Davatzikos, Christos] Univ Penn, Dept Radiol, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.
[Sojkova, Jitka; Resnick, Susan M.] NIA, Lab Behav Neurosci, Baltimore, MD 21224 USA.
[Sojkova, Jitka; Zhou, Yun; Wong, Dean F.] Johns Hopkins Sch Med, Dept Radiol, Baltimore, MD USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
RP Yotter, RA (reprint author), Univ Penn, Dept Radiol, Sect Biomed Image Anal, 3600 Market St,Suite 380, Philadelphia, PA 19104 USA.
EM rachel.yotter@uphs.upenn.edu
FU National Institutes of Health (NIH) [NIA-R01-14971]; Intramural Research
Program of the NIH, National Institute on Aging (NIA); NIA Research and
Development Contract [HHSN-260-2004-00012C]
FX This research was supported in part by National Institutes of Health
(NIH) grant NIA-R01-14971, by the Intramural Research Program of the
NIH, National Institute on Aging (NIA), and by NIA Research and
Development Contract HHSN-260-2004-00012C. R.A.Y. received support from
an NIH T-32 Training Grant. We thank the staff of the Johns Hopkins PET
facility for their efforts and the BLSA participants for their
participation.
NR 44
TC 15
Z9 15
U1 2
U2 13
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 DEC
PY 2013
VL 34
IS 12
BP 2835
EP 2842
DI 10.1016/j.neurobiolaging.2013.05.030
PG 8
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 247XQ
UT WOS:000326657800015
PM 23859610
ER
PT J
AU Jawad, S
Liu, BY
Agron, E
Nussenblatt, RB
Sen, HN
AF Jawad, Shayma
Liu, Baoying
Agron, Elvira
Nussenblatt, Robert B.
Sen, H. Nida
TI Elevated Serum Levels of Interleukin-17A in Uveitis Patients
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE Cytokine; interleukin 17; serum; Th17; uveitis
ID 1ST INTERNATIONAL WORKSHOP; BEHCETS-DISEASE; ANKYLOSING-SPONDYLITIS;
T-CELLS; EXPRESSION; IL-17; CYTOKINE; IL-23; AUTOIMMUNITY; ASSOCIATION
AB Purpose: T helper 17 cells (Th17) are one of the main pathogenic effectors in autoimmune uveitis, and IL-17A is the signature cytokine of Th17 cells. This study aims to assess serum IL-17A levels in patients with autoimmune uveitis and evaluate associations between IL-17A levels and disease characteristics.
Methods: Serum IL-17A levels from 87 autoimmune uveitis patients and 60 healthy controls were assessed using an enzyme-linked immunosorbent assay. Among this cohort, 9 patients were followed longitudinally for IL-17A levels during active and inactive stages of their disease.
Results: Median serum IL-17A levels were higher among uveitis patients compared to controls (p<0.0001). Moreover, IL-17A levels were elevated among uveitis patients with active disease compared to those with inactive disease (p = 0.0202). Among the 9 patients followed longitudinally, IL-17A levels were elevated during active disease compared to the inactive stage (p = 0.0078).
Conclusions: Serum IL-17A levels are elevated in uveitis patients, particularly in active uveitis.
C1 [Jawad, Shayma; Liu, Baoying; Nussenblatt, Robert B.; Sen, H. Nida] NEI, Clin Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Agron, Elvira] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
RP Sen, HN (reprint author), Immunol Lab, Bldg 10,Room 10N109,10 Ctr Dr, Bethesda, MD 20814 USA.
EM hatice.sen@nih.gov
FU Laboratory of Immunology; National Eye Institute
FX We would like to thank the Laboratory of Immunology and National Eye
Institute Intramural Research Program for their support.
NR 33
TC 8
Z9 8
U1 1
U2 8
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0927-3948
EI 1744-5078
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PD DEC
PY 2013
VL 21
IS 6
BP 434
EP 439
DI 10.3109/09273948.2013.815786
PG 6
WC Ophthalmology
SC Ophthalmology
GA 252EG
UT WOS:000326987300003
PM 23957503
ER
PT J
AU Cesta, MF
Hard, GC
Boyce, JT
Ryan, MJ
Chan, PC
Sills, RC
AF Cesta, Mark F.
Hard, Gordon C.
Boyce, John T.
Ryan, Michael J.
Chan, Po C.
Sills, Robert C.
TI Complex Histopathologic Response in Rat Kidney to Oral beta-myrcene: An
Unusual Dose-related Nephrosis and Low-dose Alpha2u-Globulin Nephropathy
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE kidney; nephropathy; beta-myrcene; alpha2u-globulin; rat
ID HYALINE DROPLET NEPHROPATHY; ALPHA-2U-GLOBULIN; ASSOCIATION; CPN
AB Oral gavage studies with -myrcene in male F344 rats showed a complex renal pathology comprising both alpha2u-globulin (2u-g) nephropathy, an unusual nephrosis involving the outer stripe of outer medulla (OSOM), and an increased incidence of renal tubule tumors by 2 years. In the 90-day and 2-year studies, respectively, 2u-g nephropathy and linear papillary mineralization were observed in males at the two lower doses but were absent from the high dose. Nephrosis was characterized by dilation of the S3 tubules, nuclear enlargement (including karyomegaly), and luminal pyknotic cells, all in the outermost OSOM. Nephrosis was minimal at the higher doses in the 90-day study, but progressed to a severe grade in males dosed with 1,000 mg/kg for 2 years. Renal tubule tumors developed in treated groups with incidences up to 30% in the 250 and 500 mg/kg male dose groups. Tumors at the lower doses in males may have been associated with 2u-g nephropathy, while those at higher doses in both sexes may have been due to the nephrosis. Because -myrcene induced a complex spectrum of renal pathology, the 2u-g nephropathy mechanism cannot be the sole mechanism of carcinogenesis in these rats.
C1 [Cesta, Mark F.; Chan, Po C.; Sills, Robert C.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Boyce, John T.] Beechy Ridge Toxpath, Clay, WV USA.
[Ryan, Michael J.] Battelle Columbus, Columbus, OH USA.
RP Cesta, MF (reprint author), NIEHS, Natl Toxicol Program, 111 TW Alexander Dr,Rm B337,POB 12233,MD B3-06, Res Triangle Pk, NC 27709 USA.
EM cesta@niehs.nih.gov
FU Division of the National Toxicology Program of the National Institutes
of Health (NIH), National Institute of Environmental Health Sciences
(NIEHS), Research Triangle Park, NC; NIEHS, NIH [NO1-ES-95435]
FX This work was supported by the Division of the National Toxicology
Program of the National Institutes of Health (NIH), National Institute
of Environmental Health Sciences (NIEHS), Research Triangle Park, NC.
However, the statements, opinions, or conclusions contained herein do
not necessarily represent the statements, opinions, or conclusions of
NIEHS, NIH, or the U. S. Government. Dr Hard's efforts in this project
were supported, in part, by Federal funds from the NIEHS, NIH, under
contract NO1-ES-95435 to Experimental Pathology Laboratories Inc.,
Research Triangle Park, NC. The authors wish to thank Ms. Natasha
Clayton and Mr. David Olson for preparing the immunohistochemical
stains, and Drs. David Malarkey and Kyathanahalli Janardhan for their
review of this article.
NR 16
TC 2
Z9 2
U1 0
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2013
VL 41
IS 8
BP 1068
EP 1077
DI 10.1177/0192623313482057
PG 10
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 248CI
UT WOS:000326670900003
PM 23531794
ER
PT J
AU Sanford, BJ
Emerson, SU
Purcell, RH
Engle, RE
Dryman, BA
Cecere, TE
Buechner-Maxwell, V
Sponenberg, DP
Meng, XJ
AF Sanford, B. J.
Emerson, S. U.
Purcell, R. H.
Engle, R. E.
Dryman, B. A.
Cecere, T. E.
Buechner-Maxwell, V.
Sponenberg, D. P.
Meng, X. J.
TI Serological Evidence for a Hepatitis E Virus-Related Agent in Goats in
the United States
SO TRANSBOUNDARY AND EMERGING DISEASES
LA English
DT Article
DE hepatitis E virus; animal reservoir; goat; prospective study;
experimental infection; neutralizing antibodies
ID CROSS-SPECIES INFECTION; ANTI-HEV ANTIBODIES; TRANSPLANT RECIPIENTS;
ZOONOTIC TRANSMISSION; NEUROLOGIC DISORDERS; DOMESTIC-ANIMALS;
RHESUS-MONKEYS; BLOOD-DONORS; PIG-LIVER; WILD RATS
AB Hepatitis E virus (HEV) causes an important public health disease in many developing countries and is also endemic in some industrialized countries. In addition to humans, strains of HEV have been genetically identified from pig, chicken, rat, mongoose, deer, rabbit and fish. While the genotypes 1 and 2 HEV are restricted to humans, the genotypes 3 and 4 HEV are zoonotic and infect humans and other animal species. As a part of our ongoing efforts to search for potential animal reservoirs for HEV, we tested goats from Virginia for evidence of HEV infection and showed that 16% (13/80) of goat sera from Virginia herds were positive for IgG anti-HEV. Importantly, we demonstrated that neutralizing antibodies to HEV were present in selected IgG anti-HEV positive goat sera. Subsequently, in an attempt to genetically identify the HEV-related agent from goats, we conducted a prospective study in a closed goat herd with known anti-HEV seropositivity and monitored a total of 11 kids from the time of birth until 14weeks of age for evidence of HEV infection. Seroconversion to IgG anti-HEV was detected in seven of the 11 kids, although repeated attempts to detect HEV RNA by a broad-spectrum nested RT-PCR from the faecal and serum samples of the goats that had seroconverted were unsuccessful. In addition, we also attempted to experimentally infect laboratory goats with three well-characterized mammalian strains of HEV but with no success. The results indicate that a HEV-related agent is circulating and maintained in the goat population in Virginia and that the goat HEV is likely genetically very divergent from the known HEV strains.
C1 [Sanford, B. J.; Dryman, B. A.; Cecere, T. E.; Buechner-Maxwell, V.; Sponenberg, D. P.; Meng, X. J.] Virginia Tech, Coll Vet Med, Dept Biomed Sci & Pathobiol, Ctr Mol Med & Infect Dis,Virginia Polytech Inst &, Blacksburg, VA USA.
[Emerson, S. U.; Purcell, R. H.; Engle, R. E.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Meng, XJ (reprint author), Virginia Polytech Inst & State Univ, Coll Vet Med, Dept Biomed Sci & Pathobiol, 1981 Kraft Dr, Blacksburg, VA 24060 USA.
EM xjmeng@vt.edu
RI Meng, X.J./B-8769-2009; Cecere, Thomas/N-9266-2016
OI Meng, X.J./0000-0002-2739-1334;
FU Intramural Research Program of the National Institutes of Health,
National Institute of Allergy and Infectious Diseases; NIH intramural
contract [HHSN272200800962P]; NIH [AI065546, AI050611]
FX This study was supported in part by the Intramural Research Program of
the National Institutes of Health, National Institute of Allergy and
Infectious Diseases and by a NIH intramural contract (HHSN272200800962P)
and in part by extramural grants from NIH (AI065546 and AI050611). We
thank Pete Jobst, Marlice Vonck, Pam Mohr and Shannon Viers at the
Virginia Tech Animal Facility for their assistance.
NR 61
TC 10
Z9 10
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1865-1674
EI 1865-1682
J9 TRANSBOUND EMERG DIS
JI Transbound. Emerg. Dis.
PD DEC
PY 2013
VL 60
IS 6
BP 538
EP 545
DI 10.1111/tbed.12001
PG 8
WC Infectious Diseases; Veterinary Sciences
SC Infectious Diseases; Veterinary Sciences
GA 248JU
UT WOS:000326696500006
PM 22909079
ER
PT J
AU Shi, M
Lemey, P
Brar, MS
Suchard, MA
Murtaugh, MP
Carman, S
D'Allaire, S
Delisle, B
Lambert, ME
Gagnon, CA
Ge, L
Qu, YH
Yoo, D
Holmes, EC
Leung, FCC
AF Shi, Mang
Lemey, Philippe
Brar, Manreetpal Singh
Suchard, Marc A.
Murtaugh, Michael P.
Carman, Susy
D'Allaire, Sylvie
Delisle, Benjamin
Lambert, Marie-Eve
Gagnon, Carl A.
Ge, Li
Qu, Yihan
Yoo, Dongwan
Holmes, Edward C.
Leung, Frederick Chi-Ching
TI The spread of Type 2 Porcine Reproductive and Respiratory Syndrome Virus
(PRRSV) in North America: A phylogeographic approach
SO VIROLOGY
LA English
DT Article
DE Phylogeography; PRRSV; Evolution; Recombination; Molecular epidemiology
ID RECOMBINATION; SEQUENCES; EVOLUTIONARY; PHYLOGENIES; MODELS
AB The emergence and spread of Type 2 Porcine Reproductive and Respiratory Syndrome virus (Type 2 PRRSV) in North America is heavily influenced by the multiple site production system used in the hog industry. However, it is unclear how anthropogenic factors such has this have shaped the current spatial distribution of PRRSV genotypes. We employed Bayesian phylogeographic analyses of 7040 ORF5 sequences to reveal the recent geographical spread of Type 2 PRRSV in North America. The directions and intensities in our inferred virus traffic network closely mirror the hog transportation. Most notably, we reveal multiple viral introductions from Canada into the United States causing a major shift in virus genetic composition in the Midwest USA that went unnoticed by the regular surveillance and field epidemiological studies. Overall, these findings provide important insights into the dynamics of Type 2 PRRSV evolution and spread that will facilitate programs for control and prevention. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Shi, Mang; Holmes, Edward C.] Univ Sydney, Sch Biol Sci, Sydney Emerging Infect & Biosecur Inst, Sydney, NSW 2006, Australia.
[Shi, Mang; Holmes, Edward C.] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia.
[Lemey, Philippe] Katholieke Univ Leuven, Rega Inst, Dept Microbiol & Immunol, B-3000 Louvain, Belgium.
[Brar, Manreetpal Singh; Leung, Frederick Chi-Ching] Univ Hong Kong, Sch Biol Sci, Hong Kong, Hong Kong, Peoples R China.
[Suchard, Marc A.] Univ Calif Los Angeles, Jonathan & Karin Fielding Sch Publ Hlth, Dept Biostat, Los Angeles, CA USA.
[Suchard, Marc A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Biomath, Los Angeles, CA 90095 USA.
[Suchard, Marc A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
[Murtaugh, Michael P.] Univ Minnesota, Dept Vet & Biomed Sci, St Paul, MN 55108 USA.
[Carman, Susy; Ge, Li] Univ Guelph, Lab Serv Div, Hlth Anim Lab, Guelph, ON N1H 6R8, Canada.
[D'Allaire, Sylvie; Delisle, Benjamin; Lambert, Marie-Eve; Gagnon, Carl A.] Univ Montreal, Fac Med Vet, St Hyacinthe, PQ J2S 7C6, Canada.
[Qu, Yihan] Univ Sydney, Fac Agr & Environm, Sydney, NSW 2006, Australia.
[Yoo, Dongwan] Univ Illinois, Coll Vet Med, Urbana, IL 61801 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Leung, Frederick Chi-Ching] Nanjing Agr Univ, Bioinformat Ctr, Nanjing, Jiangsu, Peoples R China.
RP Leung, FCC (reprint author), Univ Hong Kong, Sch Biol Sci, Hong Kong, Hong Kong, Peoples R China.
EM fcleung@hkucc.hku.hk
RI Gagnon, Carl/A-9239-2015;
OI Holmes, Edward/0000-0001-9596-3552
FU Research Grant Council of the Hong Kong Government [GRF770612]; HKU
Strategic Research Theme of Infection and Immunology; European
Community's Seventh Framework Programme [278433]; ERC [260864];
International Postgraduate Research Scholarship from the University of
Sydney; NHMRC Australia
FX This work was supported by grants from the Research Grant Council of the
Hong Kong Government (GRF770612) and HKU Strategic Research Theme of
Infection and Immunology to FCL and from the European Community's
Seventh Framework Programme (FP7/2007-2013) under Grant Agreement no.
278433 and ERC (Grant agreement no. 260864) to PL. MS is supported by an
International Postgraduate Research Scholarship from the University of
Sydney, while ECH is supported by an NHMRC Australia Fellowship. Special
thanks are given to Kay Faaberg, National Animal Disease Center, Ames,
IA, and Trevor Wennblom, University of Minnesota, Minneapolis, MN, for
database maintenance.
NR 27
TC 13
Z9 13
U1 2
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 146
EP 154
DI 10.1016/j.virol.2013.08.028
PG 9
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500016
PM 24210109
ER
PT J
AU Cortes-Malagon, EM
Bonilla-Delgado, J
Diaz-Chavez, J
Hidalgo-Miranda, A
Romero-Cordoba, S
Uren, A
Celik, H
McCormick, M
Munguia-Moreno, JA
Ibarra-Sierra, E
Escobar-Herrera, J
Lambert, PF
Mendoza-Villanueva, D
Bermudez-Cruz, RM
Gariglio, P
AF Cortes-Malagon, Enoc M.
Bonilla-Delgado, Jose
Diaz-Chavez, Jose
Hidalgo-Miranda, Alfredo
Romero-Cordoba, Sandra
Ueren, Aykut
Celik, Haydar
McCormick, Matthew
Munguia-Moreno, Jose A.
Ibarra-Sierra, Eloisa
Escobar-Herrera, Jaime
Lambert, Paul F.
Mendoza-Villanueva, Daniel
Bermudez-Cruz, Rosa M.
Gariglio, Patricio
TI Gene expression profile regulated by the HPV16 E7 oncoprotein and
estradiol in cervical tissue
SO VIROLOGY
LA English
DT Article
DE HPV16 E7; 17 beta-estradiol; Microarrays; Cervix; Carcinogenesis; K14E7
ID HUMAN-PAPILLOMAVIRUS TYPE-16; ESTROGEN-RECEPTOR-ALPHA; SQUAMOUS-CELL
CARCINOMA; TRANSGENIC MOUSE MODEL; INTRAEPITHELIAL NEOPLASIA;
EPITHELIAL-CELLS; HUMAN KERATINOCYTES; DIAGNOSTIC MARKERS;
PERIPHERAL-BLOOD; UP-REGULATION
AB The HPV16 E7 oncoprotein and 17 beta-estradiol are important factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. Here, we assessed the global gene expression profiles induced by the HPV16 E7 oncoprotein and/or 17 beta-estradiol in cervical tissue of FvB and K14E7 transgenic mice. We found that the most dramatic changes in gene expression occurred in K14E7 and FvB groups treated with 17 beta-estradiol. A large number of differentially expressed genes involved in the immune response were observed in 17 beta-estradiol treated groups. The E7 oncoprotein mainly affected the expression of genes involved in cellular metabolism. Our microarray data also identified differentially expressed genes that have not previously been reported in cervical cancer. The identification of genes regulated by E7 and 17 beta-estradiol, provides the basis for further studies on their role in cervical carcinogenesis. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Cortes-Malagon, Enoc M.; Munguia-Moreno, Jose A.; Bermudez-Cruz, Rosa M.; Gariglio, Patricio] Ctr Invest & Estudios Avanzados Cinvestav, Dept Genet & Mol Biol, Mexico City 07360, DF, Mexico.
[Escobar-Herrera, Jaime] Ctr Invest & Estudios Avanzados Cinvestav, Dept Cell Biol, Mexico City 07360, DF, Mexico.
[Cortes-Malagon, Enoc M.; Bonilla-Delgado, Jose] Hosp Juarez Mexico, Res Unit, Mexico City 07760, DF, Mexico.
[Diaz-Chavez, Jose] UNAM Inst Nacl Cancerol INCan, Unit Biomed Res Canc, Mexico City 14080, DF, Mexico.
[Hidalgo-Miranda, Alfredo; Romero-Cordoba, Sandra] Inst Nacl Med Genom INMEGEN, Oncogen Dept, Mexico City 14610, DF, Mexico.
[Ueren, Aykut; Celik, Haydar; McCormick, Matthew] Georgetown Univ, Dept Oncol, Lombardi Comprehens Canc Ctr, Med Ctr, Washington, DC 20057 USA.
[Ibarra-Sierra, Eloisa] Inst Estatal Cancerol, Res Lab, Acapulco 39570, Guerrero, Mexico.
[Lambert, Paul F.] Univ Wisconsin, McArdle Lab Canc Res, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[Mendoza-Villanueva, Daniel] NCI, Lab Cell & Dev Signaling, Frederick, MD 21702 USA.
RP Gariglio, P (reprint author), Ctr Invest & Estudios Avanzados Cinvestav, Dept Genet & Mol Biol, Av Inst Politecn Nacl 2508, Mexico City 07360, DF, Mexico.
EM enoc.cortes@salud.gob.mx; jose.bonilla@salud.gob.mx;
josediaz030178@hotmail.com; ahidalgo@inmegen.gob.mx;
sromero_cordoba@hotmail.com; au26@georgetown.edu; hc547@georgetown.edu;
mjm444@georgetown.edu; antoniomgeminis@yahoo.com.mx;
eibarra@cinvestav.mx; moemras@yahoo.com; plambert@wisc.edu;
daniel.mendozavillanueva@nih.gov; roberm@cinvestav.mx;
vidal@cinvestav.mx
RI Hidalgo-Miranda, Alfredo/B-2123-2010; Romero-Cordoba, Sandra
Lorena/A-2246-2014
OI Hidalgo-Miranda, Alfredo/0000-0003-2315-3977; Romero-Cordoba, Sandra
Lorena/0000-0002-5591-696X
FU Intramural Research Program of the NIH; NCI; CONACYT; NIH [R01CA120847,
P01CA022443]; [ICYT326/11]
FX The authors would like to thank to Raul Mojica (INMEGEN), Laura Uribe
Figueroa (INMEGEN), Enrique Garcia Villa, Elizabeth Alvarez Rios,
Rodolfo Ocadiz Delgado and Lauro Macias Gonzales for technical support.
P.G. was supported by grants from the ICYT326/11 to perform this work.
This research was supported in part by the Intramural Research Program
of the NIH, NCI and CONACYT (D.M.V.). P.F.L. was supported by grants
from the NIH: R01CA120847 and P01CA022443. This study was performed in
partial fulfillment of the requirement for the doctoral degree of
E.M.C.M. in Biomedical Sciences at Universidad Nacional Autonoma de
Mexico.
NR 76
TC 11
Z9 12
U1 1
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 155
EP 165
DI 10.1016/j.virol.2013.08.036
PG 11
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500017
PM 24210110
ER
PT J
AU Song, HF
Sidney, J
Wiseman, RW
Josleyn, N
Cohen, M
Blaney, JE
Jahrling, PB
Sette, A
AF Song, Haifeng
Sidney, John
Wiseman, Roger W.
Josleyn, Nicole
Cohen, Melanie
Blaney, Joseph E.
Jahrling, Peter B.
Sette, Alessandro
TI Characterizing monkeypox virus specific CD8+T cell epitopes in rhesus
macaques
SO VIROLOGY
LA English
DT Article
DE Monkeypox virus; Rhesus; T cell epitopes; CD8+T cells; Bioinformatics
analysis; Peptides; Elispot
ID SIMIAN IMMUNODEFICIENCY VIRUS; I MOLECULE MAMU-A-ASTERISK-01; VACCINIA
VIRUS; LETHAL MONKEYPOX; SMALLPOX VACCINE; IMMUNE-RESPONSE; PEPTIDE
BINDING; INFECTION; CHALLENGE; PROTECTS
AB To characterize T cell epitopes in monkeypox virus (MPXV) infected rhesus macaques, we utilized IFN gamma Elispot assay to screen 400 predicted peptides from 20 MPXV proteins. Two peptides from the F8L protein, an analog of E9L protein in vaccinia, were found to elicit CD8+ T cell responses. Prediction and in vitro MHC binding analyses suggest that one is restricted by Mamu-A1*001 and another by Mamu-A1*002. The Mamu-A1*002 epitope is completely identical in all reported sequences for variola, vaccinia, cowpox and MPXV. The Mamu-A1*001 epitope is conserved in MPXV and vaccinia, and has one residue substitution (V6 > I) in some cowpox sequences and all variola sequences. Given CD8(+) T-cell epitopes from E9L were also identified in humans and mice, our data suggested that F8L/E9L may be a dominant pox viral protein for CD8+ T cell responses, and may be considered as a target when designing vaccines that target pox-specific T cell responses. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Song, Haifeng; Josleyn, Nicole; Cohen, Melanie; Jahrling, Peter B.] NIAID, Integrated Res Facil, NIH, Frederick, MD 21702 USA.
[Sidney, John; Sette, Alessandro] La Jolla Inst Allergy & Immunol, Div Vaccine Discovery, La Jolla, CA 92037 USA.
[Wiseman, Roger W.] Univ Wisconsin, Wisconsin Natl Primate Res Ctr, Madison, WI USA.
[Blaney, Joseph E.; Jahrling, Peter B.] NIAID, Emerging Viral Pathogens Sect, NIH, Frederick, MD 21702 USA.
RP Song, HF (reprint author), NIAID, Integrated Res Facil, NIH, Frederick, MD 21702 USA.
EM songhai@mail.nih.gov; alex@liai.org
FU Intramural NIH HHS [Z99 AI999999]; NIAID NIH HHS [HHSN272200700016I];
PHS HHS [HHSN272200700016I]
NR 34
TC 0
Z9 0
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 181
EP 186
DI 10.1016/j.virol.2013.09.003
PG 6
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500020
PM 24210113
ER
PT J
AU Gill, RB
Bowman, JJ
Krogmann, T
Wollenberg, K
Asher, DM
Cohen, JI
AF Gill, Rachel B.
Bowman, J. Jason
Krogmann, Tammy
Wollenberg, Kurt
Asher, David M.
Cohen, Jeffrey I.
TI Coding potential of UL/b ' from the initial source of rhesus
cytomegalovirus Strain 68-1
SO VIROLOGY
LA English
DT Article
DE Human cytomegalovirus; Rhesus cytomegalovirus; Cercopithecine
herpesvirus: macacine herpesvirus 3; Cynomolgus macaque cytomegalovirus;
UL/b '
ID ENDOTHELIAL-CELLS; ANTIBODY-RESPONSE; IN-VITRO; MACAQUES; COMPLEX;
INFECTION; ENCODES; GENES; REPLICATION; CHEMOKINE
AB Rhesus cytomegalovirus (RhCMV) 68-1 is the prototypic strain of RhCMV that has been used for pathogenesis and vaccine development. We determined the complete sequence of the RhCMV 68-1 UL/b' region directly from the original urine from which RhCMV 68-1 was isolated in 1968, and compared it to other RhCMVs. The laboratory passaged RhCMV 68-1 has inversions, deletions, and stop codons in UL/b' that are absent in the original isolate and other low passage RhCMV isolates. Fourteen of the 17 open reading frames (ORFs) in 68-1 UL/b' in the original isolate share >95% amino acid identity with low passage RhCMV. The original isolate retains 6 ORFs that encode alpha-chemokine-like proteins, including RhUL146 and RhUL146b that share only 92% and 81% amino acid identity, respectively, with a contemporary low passage RhCMV isolate. Identification of the original RhCMV 68-1 UL/b' sequence is important for using RhCMV 68-1 in pathogenesis and vaccine studies. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Gill, Rachel B.; Bowman, J. Jason; Krogmann, Tammy; Cohen, Jeffrey I.] NIH, Med Virol Sect, Infect Dis Lab, Bethesda, MD 20892 USA.
[Wollenberg, Kurt] NIH, Bioinformat & Computat Biosci Branch, Bethesda, MD 20892 USA.
[Asher, David M.] US FDA, Lab Bacterial & Transmissible Spongiform Encephal, Div Emerging & Transfus Transmitted Dis, Rockville, MD 20852 USA.
RP Cohen, JI (reprint author), NIH, Infect Dis Lab, Bldg 50,Rm 6134,50 South Dr,MSC1807, Bethesda, MD 20892 USA.
EM jcohen@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases
FX This study was supported by the intramural research program of the
National Institute of Allergy and Infectious Diseases. We thank Anita
Mora and Heather Murphy of Rocky Mountain Laboratories (NIAID) for their
assistance with artwork, Yanmei Wang for assistance with viral DNA
quantification, and Peter Barry for advice with sequencing.
NR 44
TC 1
Z9 1
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 208
EP 212
DI 10.1016/j.virol.2013.08.026
PG 5
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500023
PM 24210116
ER
PT J
AU Yang, ZL
Maruri-Avidal, L
Sisler, J
Stuart, CA
Moss, B
AF Yang, Zhilong
Maruri-Avidal, Liliana
Sisler, Jerry
Stuart, Carey A.
Moss, Bernard
TI Cascade regulation of vaccinia virus gene expression is modulated by
multistage promoters
SO VIROLOGY
LA English
DT Article
DE Poxvirus transcription; mRNA Synthesis; Consensus promoter sequence;
Regulation of gene expression
ID EARLY TRANSCRIPTION FACTOR; INTERMEDIATE-STAGE GENES; GENOME-WIDE
ANALYSIS; PROTEIN INTERACTIONS; MUTATIONAL ANALYSIS; DNA-REPLICATION;
BINDING PROTEIN; IN-VITRO; H5R GENE; PURIFICATION
AB Vaccinia virus contains similar to 200 genes classified temporally as early, intermediate or late. We analyzed 53 intermediate promoters to determine whether any have dual late promoter activity. Our strategy involved (i) construction of a cell line that stably expressed the three late transcription factors, (ii) infection with a vaccinia virus mutant that expresses RNA polymerase but neither intermediate nor late transcription factors, and (iii) transfection with plasmids containing a luciferase reporter regulated by an intermediate promoter. After confirming the specificity of the system for late promoters, we found that many intermediate promoters had late promoter activity, the strength of which correlated with a TAAAT at the initiator site and T-content from positions -12 to -8 of the coding strand. In contrast, intermediate promoter activity correlated with the A-content from positions -22 to -14. The sequence correlations were confirmed by altering the specificities of strict intermediate and late promoters. Published by Elsevier Inc.
C1 [Yang, Zhilong; Maruri-Avidal, Liliana; Sisler, Jerry; Stuart, Carey A.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU Division of Intramural Research, NIAID, NIH
FX We thank Catherine Cotter for maintenance of cell cultures, Yan Xiang
for antibody to the A14 protein, members of our laboratory for helpful
discussions, and the NIAID Biological Imaging Section for help with
confocal microscopy. Research support was provided by the Division of
Intramural Research, NIAID, NIH.
NR 33
TC 3
Z9 4
U1 2
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 213
EP 220
DI 10.1016/j.virol.2013.09.007
PG 8
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500024
PM 24210117
ER
PT J
AU Vargas-Inchaustegui, DA
Xiao, P
Hogg, AE
Demberg, T
McKinnon, K
Venzon, D
Brocca-Cofano, E
DiPasquale, J
Lee, EM
Hudacik, L
Pal, R
Sui, YJ
Berzofsky, JA
Liu, LD
Langermann, S
Robert-Guroff, M
AF Vargas-Inchaustegui, Diego A.
Xiao, Peng
Hogg, Alison E.
Demberg, Thorsten
McKinnon, Katherine
Venzon, David
Brocca-Cofano, Egidio
DiPasquale, Janet
Lee, Eun M.
Hudacik, Lauren
Pal, Ranajit
Sui, Yongjun
Berzofsky, Jay A.
Liu, Linda
Langermann, Solomon
Robert-Guroff, Marjorie
TI Immune targeting of PD-1(hi) expressing cells during and after
antiretroviral therapy in SIV-infected rhesus macaques
SO VIROLOGY
LA English
DT Article
DE PD-1; Treg; ART; Immunomodulation; Viremia
ID CHRONIC VIRAL-INFECTION; CD8(+) T-CELLS; SIMIAN IMMUNODEFICIENCY;
HIV-INFECTION; FOLLICULAR HELPER; TREG CELLS; BLOCKADE; RESPONSES;
VACCINATION; CD4(+)
AB High-level T cell expression of PD-1 during Sly infection is correlated with impaired proliferation and function. We evaluated the phenotype and distribution of T cells and Tregs during antiretroviral therapy plus PD-1 modulation (using a B7-DC-Ig fusion protein) and post-ART. Chronically Sly-infected rhesus macaques received: 11 weeks of ART (Group A); 11 weeks of ART plus B7-DC-Ig (Group B); 11 weeks of ART plus B7-DC-Ig, then 12 weeks of B7-DC-Ig alone (Group C). Continuous B7-DC-Ig treatment (Group C) decreased rebound viremia post-ART compared to pre-ART levels, associated with decreased PD-1(hi) expressing T cells and Tregs in PBMCs, and PD-1(hi) Tregs in lymph nodes. It transiently decreased expression of Ki67 and alpha(4)beta(7) in PBMC CD4(+) and CD8(+) Tregs for up to 8 weeks post-ART and maintained Ag-specific T-cell responses at low levels. Continued immune modulation targeting PD-1(hi) cells during and post-ART helps maintain lower viremia, keeps a favorable T cell/Treg repertoire and modulates antigen-specific responses. Published by Elsevier Inc.
C1 [Vargas-Inchaustegui, Diego A.; Xiao, Peng; Hogg, Alison E.; Demberg, Thorsten; McKinnon, Katherine; Brocca-Cofano, Egidio; DiPasquale, Janet; Sui, Yongjun; Berzofsky, Jay A.; Robert-Guroff, Marjorie] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Lee, Eun M.; Hudacik, Lauren; Pal, Ranajit] Adv Biosci Labs Inc, Rockville, MD 20850 USA.
[Liu, Linda] Amplimmune Inc, Gaithersburg, MD 20878 USA.
RP Robert-Guroff, M (reprint author), NCI, NIH, 41 Medlars Dr,Bldg 41,Room D804, Bethesda, MD 20892 USA.
EM guroffm@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute
FX We gratefully acknowledge the animal caretakers at Advanced BioScience
Laboratories, Inc., for their expert care of our rhesus macaques and
collection of serial samples. The following reagents were obtained
through the NIH Nonhuman Primate Reagent Resource: Alpha-4/beta-7-APC
and CD4-Qdot 655. The following reagent was obtained through the AIDS
Research and Reference Reagent Program, Division of AIDS, NIAID, NIH:
SIVmac239 Gag peptides, Complete Set. This research was supported by the
Intramural Research Program of the NIH, National Cancer Institute.
NR 68
TC 6
Z9 6
U1 0
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 274
EP 284
DI 10.1016/j.virol.2013.09.015
PG 11
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500031
PM 24210124
ER
PT J
AU Zhang, LM
Alter, HJ
Wang, HP
Jia, SZ
Wang, E
Marincola, FM
Shih, JWK
Wang, RY
AF Zhang, Lumin
Alter, Harvey J.
Wang, Haiping
Jia, Shuaizheng
Wang, Ena
Marincola, Francesco M.
Shih, James W. -K.
Wang, Richard Y.
TI The modulation of hepatitis C virus 1a replication by PKR is dependent
on NF-kB mediated interferon beta response in Huh7.5.1 cells (vol 438,
pg 28, 2013)
SO VIROLOGY
LA English
DT Correction
C1 [Zhang, Lumin; Alter, Harvey J.; Wang, Ena; Marincola, Francesco M.; Wang, Richard Y.] NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Wang, Ena; Marincola, Francesco M.] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
[Wang, Haiping] Acad Mil Med Sci, Affiliated Hosp, Dept Transfus Med, Beijing, Peoples R China.
[Jia, Shuaizheng] Beijing Inst Transfus Med, Beijing, Peoples R China.
[Shih, James W. -K.] Xiamen Univ, Natl Inst Diagnost & Vaccine Dev Infect Dis, Xiamen, Peoples R China.
RP Wang, RY (reprint author), NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM rwang@cc.nih.gov
RI zhang, lumin/R-3456-2016
NR 1
TC 0
Z9 0
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC
PY 2013
VL 447
IS 1-2
BP 339
EP 339
DI 10.1016/j.virol.2013.08.007
PG 1
WC Virology
SC Virology
GA 246QF
UT WOS:000326553500038
ER
PT J
AU Robert, V
Vu, D
Amor, AB
van de Wiele, N
Brouwer, C
Jabas, B
Szoke, S
Dridi, A
Triki, M
ben Daoud, S
Chouchen, O
Vaas, L
de Cock, A
Stalpers, JA
Stalpers, D
Verkley, GJM
Groenewald, M
dos Santos, FB
Stegehuis, G
Li, W
Wu, LH
Zhang, R
Ma, JC
Zhou, MM
Gorjon, SP
Eurwilaichitr, L
Ingsriswang, S
Hansen, K
Schoch, C
Robbertse, B
Irinyi, L
Meyer, W
Cardinali, G
Hawksworth, DL
Taylor, JW
Crous, PW
AF Robert, Vincent
Duong Vu
Amor, Ammar Ben Hadj
van de Wiele, Nathalie
Brouwer, Carlo
Jabas, Bernard
Szoke, Szaniszlo
Dridi, Ahmed
Triki, Maher
ben Daoud, Samy
Chouchen, Oussema
Vaas, Lea
de Cock, Arthur
Stalpers, Joost A.
Stalpers, Dora
Verkley, Gerard J. M.
Groenewald, Marizeth
dos Santos, Felipe Borges
Stegehuis, Gerrit
Li, Wei
Wu, Linhuan
Zhang, Run
Ma, Juncai
Zhou, Miaomiao
Gorjon, Sergio Perez
Eurwilaichitr, Lily
Ingsriswang, Supawadee
Hansen, Karen
Schoch, Conrad
Robbertse, Barbara
Irinyi, Laszlo
Meyer, Wieland
Cardinali, Gianluigi
Hawksworth, David L.
Taylor, John W.
Crous, Pedro W.
TI MycoBank gearing up for new horizons
SO IMA FUNGUS
LA English
DT Article
DE MycoBank; EUBOLD identification services; Forum; Fungi; International
Nucleotide Sequence Database Collaboration; Next Generation Sequencing;
Nomenclature; Registration; Repositories; Typification
AB MycoBank, a registration system for fungi established in 2004 to capture all taxonomic novelties, acts as a coordination hub between repositories such as Index Fungorum and Fungal Names. Since January 2013, registration of fungal names is a mandatory requirement for valid publication under the International Code of Nomenclature for algae, fungi and plants (ICN). This review explains the database innovations that have been implemented over the past few years, and discusses new features such as advanced queries, registration of typification events (MBT numbers for lecto, epi- and neotypes), the multi-lingual database interface, the nomenclature discussion forum, annotation system, and web services with links to third parties. MycoBank has also introduced novel identification services, linking DNA sequence data to numerous related databases to enable intelligent search queries. Although MycoBank fills an important void for taxon registration, challenges for the future remain to improve links between taxonomic names and DNA data, and to also introduce a formal system for naming fungi known from DNA sequence data only. To further improve the quality of MycoBank data, remote access will now allow registered mycologists to act as MycoBank curators, using Citrix software.
C1 [Robert, Vincent; Duong Vu; Amor, Ammar Ben Hadj; van de Wiele, Nathalie; Brouwer, Carlo; Jabas, Bernard; Szoke, Szaniszlo; Dridi, Ahmed; Triki, Maher; ben Daoud, Samy; Chouchen, Oussema; Vaas, Lea; de Cock, Arthur; Stalpers, Joost A.; Stalpers, Dora; Verkley, Gerard J. M.; Groenewald, Marizeth; dos Santos, Felipe Borges; Stegehuis, Gerrit; Zhou, Miaomiao] CBS KNAW Fungal Biodivers Ctr, Uppsalalaan 8, NL-3584 CT Utrecht, Netherlands.
[Li, Wei; Wu, Linhuan; Zhang, Run; Ma, Juncai] Chinese Acad Sci, Inst Microbiol, Beijing 100101, Peoples R China.
[Gorjon, Sergio Perez] Univ Salamanca, Salamanca 37007, Spain.
[Eurwilaichitr, Lily; Ingsriswang, Supawadee] Natl Ctr Genet Engn & Biotechnol BIOTEC, Klongluang 12120, Pathumthani, Thailand.
[Hansen, Karen] Swedish Museum Nat Hist S, Dept Cryptogam Bot, S-10405 Stockholm, Sweden.
[Schoch, Conrad; Robbertse, Barbara] NIH, Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Irinyi, Laszlo; Meyer, Wieland] Univ Sydney, Marie Bashir Inst Infect Dis & Biosecur, Res Lab,Ctr Infect Dis & Microbiol,Westmead Hosp, Westmead Millennium Inst,Sydney Med Sch, Sydney, NSW, Australia.
[Irinyi, Laszlo; Meyer, Wieland] Westmead Hosp, Sydney, NSW, Australia.
[Cardinali, Gianluigi] Univ Perugia, Dip Biol Appl, I-06121 Perugia, Italy.
[Hawksworth, David L.] Univ Complutense Madrid, Fac Farm, Dept Biol Vegetal 2, E-28040 Madrid, Spain.
[Hawksworth, David L.] Nat Hist Museum, Dept Life Sci, London SW7 5BD, England.
[Hawksworth, David L.] Royal Bot Gardens, Mycol Sect, Richmond TW9 3DS, Surrey, England.
[Taylor, John W.] Univ Calif Berkeley, Dept Plant & Microbial Biol, Berkeley, CA 94720 USA.
RP Robert, V (reprint author), CBS KNAW Fungal Biodivers Ctr, Uppsalalaan 8, NL-3584 CT Utrecht, Netherlands.
EM v.robert@cbs.knaw.nl
RI Crous, Pedro/H-1489-2012; Groenewald, Marizeth/G-4976-2012;
OI Crous, Pedro/0000-0001-9085-8825; Groenewald,
Marizeth/0000-0003-0835-5925; Meyer, Wieland/0000-0001-9933-8340
FU European Commission's Seventh Framework Program for Research and
Technological Development; "Fonds Economische Structuurversterking"
(FES) of the Dutch Ministry of Education, Culture and Science (OCW);
Australian NH MRC [APP1031952]; Intramural Research Program of the NIH,
National Library of Medicine
FX The MycoBank software developments were partially made within the
framework of the Indexing for Life (i4Life) project, a European
e-Infrastructure project co-funded by the European Commission's Seventh
Framework Program for Research and Technological Development.; Some data
entries were made possible thanks to the EMbaRC project also supported
by the European Commission's Seventh Framework Program for Research and
Technological Development; Parts of the developments were done in the
framework of the "Inversteringproject NCB" supported by the "Fonds
Economische Structuurversterking" (FES) of the Dutch Ministry of
Education, Culture and Science (OCW).; Parts of the developments were
also done in the framework of the "DNA barcoding of pathogenic fungi as
the basis for the development of novel standardized diagnostic",
Australian NH& MRC grant # APP1031952 to WM and VR.; CLS acknowledges
support from the Intramural Research Program of the NIH, National
Library of Medicine.
NR 16
TC 13
Z9 13
U1 0
U2 7
PU INT MYCOLOGICAL ASSOC
PI BERKELEY
PA C/O J TAYLOR, DEPT PLANT & MICROBIAL BIOLOGY, BERKELEY, CA 94720 USA
SN 2210-6340
EI 2210-6359
J9 IMA FUNGUS
JI IMA Fungus
PD DEC
PY 2013
VL 4
IS 2
BP 371
EP 379
DI 10.5598/imafungus.2013.04.02.16
PG 9
WC Mycology
SC Mycology
GA V46UH
UT WOS:000209908600035
PM 24563843
ER
PT J
AU Reid, BC
AF Reid, Britt C.
TI Visual Screening for Oral Cancer May Reduce Oral Cancer Mortality in
High-risk Adult Populations Through Early Diagnosis and Treatment
SO JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
LA English
DT Editorial Material
C1 NCI, Modifiable Risk Factors Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Reid, BC (reprint author), NCI, Modifiable Risk Factors Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Room 4E128, Bethesda, MD 20892 USA.
EM reidbr@mail.nih.gov
NR 9
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1532-3382
J9 J EVID-BASED DENT PR
JI J. Evid.-Based Dent. Pract.
PD DEC
PY 2013
VL 13
IS 4
BP 174
EP 176
DI 10.1016/j.jebdp.2013.10.013
PG 3
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA V37RY
UT WOS:000209294100013
PM 24237744
ER
PT J
AU Pavlova, O
Ieva, R
Bernstein, HD
AF Pavlova, Olga
Ieva, Raffaele
Bernstein, Harris D.
TI Monitoring the Assembly of a Secreted Bacterial Virulence Factor Using
Site-specific Crosslinking
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Immunology; Issue 82; Autotransporters; Bam complex; Molecular
chaperones; protein-protein interactions; Site-specific
photocrosslinking
AB This article describes a method to detect and analyze dynamic interactions between a protein of interest and other factors in vivo. Our method is based on the amber suppression technology that was originally developed by Peter Schultz and colleagues(1). An amber mutation is first introduced at a specific codon of the gene encoding the protein of interest. The amber mutant is then expressed in E. coli together with genes encoding an amber suppressor tRNA and an amino acyl-tRNA synthetase derived from Methanococcus jannaschii. Using this system, the photo activatable amino acid analog p-benzoylphenylalanine (Bpa) is incorporated at the amber codon. Cells are then irradiated with ultraviolet light to covalently link the Bpa residue to proteins that are located within 3-8 angstrom. Photocrosslinking is performed in combination with pulse-chase labeling and immunoprecipitation of the protein of interest in order to monitor changes in protein-protein interactions that occur over a time scale of seconds to minutes. We optimized the procedure to study the assembly of a bacterial virulence factor that consists of two independent domains, a domain that is integrated into the outer membrane and a domain that is translocated into the extracellular space, but the method can be used to study many different assembly processes and biological pathways in both prokaryotic and eukaryotic cells. In principle interacting factors and even specific residues of interacting factors that bind to a protein of interest can be identified by mass spectrometry.
C1 [Pavlova, Olga; Ieva, Raffaele; Bernstein, Harris D.] NIDDK, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
RP Bernstein, HD (reprint author), NIDDK, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
EM harris_bernstein@nih.gov
RI Ieva, Raffaele/J-9207-2014
OI Ieva, Raffaele/0000-0002-3405-0650
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases.
NR 17
TC 0
Z9 0
U1 2
U2 3
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD DEC
PY 2013
IS 82
AR UNSP e51217
DI 10.3791/51217
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36RR
UT WOS:000209229000068
PM 24378574
ER
PT J
AU Tacher, V
Lin, M
Bhagat, N
Jaoudeh, NA
Radaelli, A
Noordhoek, N
Carelsen, B
Wood, BJ
Geschwind, JF
AF Tacher, Vania
Lin, MingDe
Bhagat, Nikhil
Jaoudeh, Nadine Abi
Radaelli, Alessandro
Noordhoek, Niels
Carelsen, Bart
Wood, Bradford J.
Geschwind, Jean-Francois
TI Dual-phase Cone-beam Computed Tomography to See, Reach, and Treat
Hepatocellular Carcinoma during Drug-eluting Beads Transarterial
Chemoembolization
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Medicine; Issue 82; Carcinoma; Hepatocellular; Tomography; X-Ray
Computed; Surgical Procedures; Minimally Invasive; Digestive System
Diseases; Diagnosis; Therapeutics; Surgical Procedures; Operative;
Equipment and Supplies; Transarterial chemo-embolization; Hepatocellular
carcinoma; Dual-phase cone-beam computed tomography; 3D roadmap;
Drug-Eluting Beads
AB The advent of cone-beam computed tomography (CBCT) in the angiography suite has been revolutionary in interventional radiology. CBCT offers 3 dimensional (3D) diagnostic imaging in the interventional suite and can enhance minimally-invasive therapy beyond the limitations of 2D angiography alone. The role of CBCT has been recognized in transarterial chemo-embolization (TACE) treatment of hepatocellular carcinoma (HCC). The recent introduction of a CBCT technique: dual-phase CBCT (DP-CBCT) improves intra-arterial HCC treatment with drug-eluting beads (DEB-TACE). DP-CBCT can be used to localize liver tumors with the diagnostic accuracy of multi-phasic multidetector computed tomography (M-MDCT) and contrast enhanced magnetic resonance imaging (CE-MRI) (See the tumor), to guide intra-arterially guidewire and microcatheter to the desired location for selective therapy (Reach the tumor), and to evaluate treatment success during the procedure (Treat the tumor). The purpose of this manuscript is to illustrate how DP-CBCT is used in DEB-TACE to see, reach, and treat HCC.
C1 [Tacher, Vania; Bhagat, Nikhil; Geschwind, Jean-Francois] Johns Hopkins Univ Hosp, Russell H Morgan Dept Radiol & Radiol Sci, Div Vasc & Intervent Radiol, Baltimore, MD 21287 USA.
[Lin, MingDe] Philips Res North Amer, CIITS, Andover, MA 01810 USA.
[Jaoudeh, Nadine Abi; Wood, Bradford J.] NIH, Ctr Intervent Oncol, Intervent Radiol Sect, Bethesda, MD USA.
RP Lin, M (reprint author), Philips Res North Amer, CIITS, Andover, MA 01810 USA.
EM ming.lin@philips.com
FU NIH/NCI [R01 CA160771, P30 CA006973]; Philips Research North America,
Briarcliff Manor, NY, USA; French Society of Radiology (SFR)
FX The authors wish to acknowledge the financial support of NIH/NCI R01
CA160771, P30 CA006973, Philips Research North America, Briarcliff
Manor, NY, USA and the French Society of Radiology (SFR).
NR 26
TC 0
Z9 0
U1 0
U2 0
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD DEC
PY 2013
IS 82
AR UNSP e50795
DI 10.3791/50795
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36RR
UT WOS:000209229000024
ER
PT J
AU Amara, SG
AF Amara, Susan G.
TI The Activation of Intracellular Signaling Systems by Amphetamines: A
Potential Role for Trace Amine Receptors
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Amara, Susan G.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 6.3
BP S11
EP S11
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100022
ER
PT J
AU Augier, E
Damadzic, R
Singley, E
Pincus, A
Heilig, M
AF Augier, Eric
Damadzic, Ruslan
Singley, Erick
Pincus, Alexandra
Heilig, Markus
TI Reduced Motivation to Consume Alcohol after an Extended Access
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE alcohol; addiction; self-administration; extended access; amygdala
C1 [Augier, Eric; Damadzic, Ruslan; Singley, Erick; Pincus, Alexandra; Heilig, Markus] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
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 DEC
PY 2013
VL 38
SU 2
MA T68
BP S312
EP S313
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100512
ER
PT J
AU Baker, MB
Lindell, S
Yuan, QP
Zhou, ZF
Higley, JD
Suomi, S
Barr, C
AF Baker, Maggie B.
Lindell, Stephen
Yuan, Qiaoping
Zhou, Zhifeng
Higley, J. Dee
Suomi, Stephen
Barr, Christina
TI Disruption of Early Maternal Care Results in Epigenetic Regulation of
the Oxytocin Receptor (OXTR) Gene in Rhesus Macaques
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE oxytocin; stress; epigenetic; macaque; Chip-SEQ
C1 [Baker, Maggie B.; Lindell, Stephen; Yuan, Qiaoping; Zhou, Zhifeng; Higley, J. Dee; Suomi, Stephen; Barr, Christina] NIAAA, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T210
BP S414
EP S414
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100653
ER
PT J
AU Barbier, E
Tapocik, J
Johnstone, AL
Schank, J
Zhou, ZF
Yuan, QP
Goldman, D
Wahlestedt, C
Heilig, M
AF Barbier, Estelle
Tapocik, Jenica
Johnstone, Andrea L.
Schank, Jesse
Zhou, Zhifeng
Yuan, Qiaoping
Goldman, David
Wahlestedt, Claes
Heilig, Markus
TI The Methyltransferase PRDM2 Regulates Escalated Alcohol Consumption
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE alcohol dependence; epigenetic; histone methyltransferase
C1 [Barbier, Estelle; Tapocik, Jenica; Johnstone, Andrea L.; Schank, Jesse; Zhou, Zhifeng; Yuan, Qiaoping; Goldman, David; Wahlestedt, Claes; Heilig, Markus] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
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 DEC
PY 2013
VL 38
SU 2
MA T95
BP S330
EP S330
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100539
ER
PT J
AU Baumann, MH
AF Baumann, Michael H.
TI Effects of Newly-emerging Synthetic Cathinone Derivatives on Monoamine
Transporter Function in Rats
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Baumann, Michael H.] NIDA, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 2
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 DEC
PY 2013
VL 38
SU 2
MA 16.2
BP S23
EP S23
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100044
ER
PT J
AU Berman, RA
McAdams, H
Greenstein, D
Gogtay, N
Rapoport, JL
AF Berman, Rebecca A.
McAdams, Harrison
Greenstein, Deanna
Gogtay, Nitin
Rapoport, Judith L.
TI Distinct Patterns of Functional Connectivity in Patients with
Childhood-Onset Schizophrenia, Their Unaffected Siblings, and Healthy
Controls
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE fMRI; resting-state; psychosis; cortex
C1 [Berman, Rebecca A.; McAdams, Harrison; Greenstein, Deanna; Gogtay, Nitin; Rapoport, Judith L.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M110
BP S181
EP S182
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100320
ER
PT J
AU Bossert, JM
AF Bossert, Jennifer M.
TI Role of Ventral Medial Prefrontal Cortex (mPFC) and Its Projections to
Accumbens Shell on Context-induced Reinstatement of Heroin Seeking in
Rats
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Bossert, Jennifer M.] NIDA, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 45.4
BP S77
EP S78
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100155
ER
PT J
AU Brotman, MA
Deveney, CM
Thomas, LA
Hinton, K
Yi, J
Pine, DS
Leibenluft, E
AF Brotman, Melissa A.
Deveney, Christen M.
Thomas, Laura A.
Hinton, Kendra
Yi, Jennifer
Pine, Daniel S.
Leibenluft, Ellen
TI Parametric Modulation of Neural Activity during Face Emotion Processing
in Unaffected Youth at Familial Risk for Bipolar Disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE fMRI; bipolar disorder; youth at familial risk; face emotion
C1 [Brotman, Melissa A.; Deveney, Christen M.; Thomas, Laura A.; Hinton, Kendra; Yi, Jennifer; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Bethesda, MD 20892 USA.
RI Brotman, Melissa/H-7409-2013
NR 0
TC 1
Z9 1
U1 0
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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 DEC
PY 2013
VL 38
SU 2
MA M39
BP S132
EP S133
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100249
ER
PT J
AU Colvis, C
AF Colvis, Christine
TI NCATS/NIH-Industry Pilot Program on Drug Repositioning
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Colvis, Christine] Natl Ctr Adv Translat Sci, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 44.2
BP S75
EP S75
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100149
ER
PT J
AU Dickinson, D
Straub, R
Trampush, JW
Gao, Y
Feng, NP
Ursini, G
Bigos, K
Kolachana, B
Hashimoto, R
Takeda, M
Rujescu, D
Callicott, JH
Hyde, TM
Berman, KF
Kleinman, JE
Weinberger, DR
AF Dickinson, Dwight
Straub, Richard
Trampush, Joey W.
Gao, Yuan
Feng, Ningping
Ursini, Gianluca
Bigos, Kristin
Kolachana, Bhaskar
Hashimoto, Ryota
Takeda, Masatoshi
Rujescu, Dan
Callicott, Joseph H.
Hyde, Thomas M.
Berman, Karen F.
Kleinman, Joel E.
Weinberger, Daniel R.
TI Association of SCN2A Variants with Cognitive Ability in Schizophrenia,
and Additional Support from Analyses of Unaffected Siblings, Independent
Schizophrenia Samples, fMRI, and mRNA Expression in Brain
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE SCN2A; schizophrenia; cognition; GWAS; fMRI; RNA sequencing
C1 [Dickinson, Dwight; Straub, Richard; Trampush, Joey W.; Gao, Yuan; Feng, Ningping; Ursini, Gianluca; Bigos, Kristin; Kolachana, Bhaskar; Hashimoto, Ryota; Takeda, Masatoshi; Rujescu, Dan; Callicott, Joseph H.; Hyde, Thomas M.; Berman, Karen F.; Kleinman, Joel E.; Weinberger, Daniel R.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
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U1 1
U2 1
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 DEC
PY 2013
VL 38
SU 2
MA W80
BP S486
EP S487
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100756
ER
PT J
AU Driver, DI
Greenstein, D
Farmer, M
Rapoport, JL
Gogtay, N
AF Driver, David I.
Greenstein, Deanna
Farmer, Madison
Rapoport, Judith L.
Gogtay, Nitin
TI Premorbid Impairments in Childhood-onset Schizophrenia
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE childhood-onset schizophrenia; premorbid impairments
C1 [Driver, David I.; Greenstein, Deanna; Farmer, Madison; Rapoport, Judith L.; Gogtay, Nitin] NIMH, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
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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 DEC
PY 2013
VL 38
SU 2
MA T188
BP S399
EP S400
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100631
ER
PT J
AU Eisenberg, DP
Masdeu, JC
Kohn, P
Kolachana, BS
Weinberger, DR
Berman, KF
AF Eisenberg, Daniel P.
Masdeu, Joseph C.
Kohn, Philip
Kolachana, Bhaskar S.
Weinberger, Daniel R.
Berman, Karen F.
TI Impact of DOPA Decarboxylase Genetic Variation on Its In Vivo Enzymatic
Activity in Humans
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE DOPA decarboxylase; DDC; dopamine; gene; PET
C1 [Eisenberg, Daniel P.; Masdeu, Joseph C.; Kohn, Philip; Kolachana, Bhaskar S.; Weinberger, Daniel R.; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/S-4342-2016
NR 0
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U1 0
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M32
BP S127
EP S128
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100242
ER
PT J
AU Enoch, MA
Hodgkinson, CA
Gorodetsky, E
Marietta, C
Roy, A
Goldman, D
AF Enoch, Mary-Anne
Hodgkinson, Colin A.
Gorodetsky, Elena
Marietta, Cheryl
Roy, Alec
Goldman, David
TI Haplotype and SNP Variation in Genes Implicated in GABA Synthesis,
Synaptic Transmission and Re-uptake are Predictors for Alcoholism
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE GABA; GAD1; GPHN; GABBR1; SLC6A1
C1 [Enoch, Mary-Anne; Hodgkinson, Colin A.; Gorodetsky, Elena; Marietta, Cheryl; Roy, Alec; Goldman, David] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 2
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 DEC
PY 2013
VL 38
SU 2
MA W55
BP S470
EP S470
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100733
ER
PT J
AU Furey, ML
Szczepanik, J
Nugent, AC
Brutsche, N
Luckenbaugh, D
Zarate, CA
AF Furey, Maura L.
Szczepanik, Joanna
Nugent, Allison C.
Brutsche, Nancy
Luckenbaugh, David
Zarate, Carlos A.
TI Neural Response in Visual Cortex to Emotional Stimuli Predicts Clinical
Outcome Across Rapid Antidepressant Agents
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE ketamine; scopolamine; biomarker
C1 [Furey, Maura L.; Szczepanik, Joanna; Nugent, Allison C.; Brutsche, Nancy; Luckenbaugh, David; Zarate, Carlos A.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T181
BP S395
EP S396
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100624
ER
PT J
AU Gogtay, N
AF Gogtay, Nitin
TI Vulnerability or Resilience? Brain Developmental Studies in
Non-Psychotic Siblings of Childhood Onset Schizophrenia Patients
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Gogtay, Nitin] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
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 DEC
PY 2013
VL 38
SU 2
MA 7.4
BP S13
EP S13
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100027
ER
PT J
AU Goswami, S
Mishra, S
Hoon, M
Mannes, A
Iadarola, M
AF Goswami, Samridhi
Mishra, Santosh
Hoon, Mark
Mannes, Andrew
Iadarola, Michael
TI Analysis of the Pain Transcriptome Using RNA-Seq
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE gene expression transcriptome RNA Seq pain analgesia
C1 [Goswami, Samridhi; Mishra, Santosh; Hoon, Mark; Mannes, Andrew; Iadarola, Michael] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T127
BP S352
EP S352
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100571
ER
PT J
AU Gregory, MD
Kippenhan, JS
Mervis, C
Sottile, M
Czarapata, J
Roe, K
Xiao, E
Tong, YX
Kolachana, BS
Weinberger, DR
Mattay, VS
Berman, KF
AF Gregory, Michael D.
Kippenhan, J. Shane.
Mervis, Carolyn
Sottile, Melanie
Czarapata, Jasmin
Roe, Katherine
Xiao, Ena
Tong, Yunxia
Kolachana, Bhaskar S.
Weinberger, Daniel R.
Mattay, Venkata S.
Berman, Karen F.
TI Functional Connectivity of the Intraparietal Sulcus Is Affected by Both
Copy Number and Sequence Variation of the Williams Syndrome Gene LIMK1
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Williams syndrome; LIMK1; intraparietal sulcus; fMRI; connectivity
C1 [Gregory, Michael D.; Kippenhan, J. Shane.; Mervis, Carolyn; Sottile, Melanie; Czarapata, Jasmin; Roe, Katherine; Xiao, Ena; Tong, Yunxia; Kolachana, Bhaskar S.; Weinberger, Daniel R.; Mattay, Venkata S.; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M144
BP S206
EP S207
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100354
ER
PT J
AU Grodin, EN
Momenan, R
AF Grodin, Erica N.
Momenan, Reza
TI Morphometric and Volumetric Subcortical Differences in Alcoholics with
and without Comorbid Drug Use Disorders
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE subcortical; morphometry; substance-abuse; alcoholism
C1 [Grodin, Erica N.; Momenan, Reza] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M116
BP S185
EP S186
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100326
ER
PT J
AU Guerrieri, G
Ben Dor, R
Smith, L
Thompson, K
Martinez, P
Rubinow, D
Schmidt, P
AF Guerrieri, Gioia
Ben Dor, Rivka
Smith, Leslie
Thompson, Karla
Martinez, Pedro
Rubinow, David
Schmidt, Peter
TI The Hypothalamic-Pituitary-Adrenal Axis, Reproductive Aging, and
Depression: Results of Cortisol and ACTH Response to Dex/CRH testing in
Women with and without Perimenopause-related Depression
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE perimenopause; depression; HPA-axis; cortisol; ACTH
C1 [Guerrieri, Gioia; Ben Dor, Rivka; Smith, Leslie; Thompson, Karla; Martinez, Pedro; Rubinow, David; Schmidt, Peter] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T195
BP S404
EP S405
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100638
ER
PT J
AU Hall, FS
Houston-Ludlam, A
Lin, ZC
Uhl, G
AF Hall, Frank S.
Houston-Ludlam, Alexandra
Lin, Zhicheng
Uhl, George
TI The Effects of Gene Knockout of the Vesicular Monoamine Transporter 2
(VMAT2; SLC18A2) and the Dopamine Transporter (DAT; SLC3A6) on Ethanol
Consumption and Escalation in Mice
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE alcoholism; pharmacogenetics; dopamine transporter; vesicular monoamine
transporter; escalation
C1 [Hall, Frank S.; Houston-Ludlam, Alexandra; Lin, Zhicheng; Uhl, George] NIDA, Baltimore, MD USA.
RI Hall, Frank/C-3036-2013
OI Hall, Frank/0000-0002-0822-4063
NR 0
TC 0
Z9 0
U1 1
U2 1
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 DEC
PY 2013
VL 38
SU 2
MA W193
BP S565
EP S565
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100868
ER
PT J
AU Huang, MC
Schwandt, ML
Chester, JA
Kirchhoff, AM
Kao, CF
Liang, TB
Tapocik, J
Ramchandani, VA
George, DT
Hodgkinson, CA
Goldman, D
Heilig, M
AF Huang, Ming-Chyi
Schwandt, Melanie L.
Chester, Julie A.
Kirchhoff, Aaron M.
Kao, Chung-Feng
Liang, Tiebing
Tapocik, Jenica
Ramchandani, Vijay A.
George, David T.
Hodgkinson, Colin A.
Goldman, David
Heilig, Markus
TI FKBP5 Moderates Alcohol Withdrawal Severity: Human Genetic Association
and Functional Validation in Knockout
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE FKBP5 gene; alcohol withdrawal severity; HPA axis; humans; mice
C1 [Huang, Ming-Chyi; Schwandt, Melanie L.; Chester, Julie A.; Kirchhoff, Aaron M.; Kao, Chung-Feng; Liang, Tiebing; Tapocik, Jenica; Ramchandani, Vijay A.; George, David T.; Hodgkinson, Colin A.; Goldman, David; Heilig, Markus] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W54
BP S469
EP S470
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100732
ER
PT J
AU Innis, R
AF Innis, Robert
TI Binding of 11C-(R)-rolipram to Phosphodiesterase 4 is Downregulated in
Major Depressive Disorder and Normalized with Antidepressant Treatment
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Innis, Robert] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 54.1
BP S95
EP S95
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100188
ER
PT J
AU Jabbi, M
Chen, Q
Turner, N
White, M
Kippenhan, JS
Kohn, P
Dickinson, D
Kolachana, B
Mattay, V
Weinberger, DR
Berman, K
AF Jabbi, Mbemba
Chen, Qiang
Turner, Nicholas
White, Michael
Kippenhan, J. Shane
Kohn, Philip
Dickinson, Dwight
Kolachana, Bhaskar
Mattay, Venkata
Weinberger, Daniel R.
Berman, Karen
TI Variation in the Williams Syndrome GTF2i Gene and Anxiety-proneness
Interactively Predict DLPFC Response to Aversive Social Stimuli in
Humans
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE genetics; anxiety proneness; GTF2i; DLPFC response
C1 [Jabbi, Mbemba; Chen, Qiang; Turner, Nicholas; White, Michael; Kippenhan, J. Shane; Kohn, Philip; Dickinson, Dwight; Kolachana, Bhaskar; Mattay, Venkata; Weinberger, Daniel R.; Berman, Karen] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 DEC
PY 2013
VL 38
SU 2
MA W81
BP S487
EP S487
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100757
ER
PT J
AU Johanna, JM
Davis, M
Leibenluft, E
Fox, N
Shechner, T
Pine, DS
Nelson, E
AF Johanna, Jarcho M.
Davis, Megan
Leibenluft, Ellen
Fox, Nathan
Shechner, Tomer
Pine, Daniel S.
Nelson, Eric
TI Dysregulated Neural Response to Social Evaluation in Bullied
Adolescents: A Potential Mechanism that Promotes Risk for Social Anxiety
Disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE fMRI; peer victimization; adolescence; social evaluation
C1 [Johanna, Jarcho M.; Davis, Megan; Leibenluft, Ellen; Fox, Nathan; Shechner, Tomer; Pine, Daniel S.; Nelson, Eric] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 4
U2 6
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 DEC
PY 2013
VL 38
SU 2
MA M48
BP S139
EP S139
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100258
ER
PT J
AU Kim, SW
Fowler, J
Skolnick, P
Kang, Y
Kim, D
Volkow, ND
AF Kim, Sung Won
Fowler, Joanna
Skolnick, Phil
Kang, Yeona
Kim, Dohyun
Volkow, Nora D.
TI Buspirone Blocks Dopamine D3 Receptors in the Non-human Primate Brain
when Administered Orally
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE addiction; treatment; striatum; pallidum; buspirone; D3 receptors
C1 [Kim, Sung Won; Fowler, Joanna; Skolnick, Phil; Kang, Yeona; Kim, Dohyun; Volkow, Nora D.] NIDA, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M139
BP S203
EP S203
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100349
ER
PT J
AU Kopin, IJ
Sullivan, P
Goldstein, DS
AF Kopin, Irwin J.
Sullivan, Patti
Goldstein, David S.
TI Key Role of Decreased Vesicular Uptake in the Profound Myocardial
Norepinephrine Depletion in Parkinson's Disease
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Norepinephrine; Dopamine; VMAT; myocardium; MAO
C1 [Kopin, Irwin J.; Sullivan, Patti; Goldstein, David S.] NINDS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M23
BP S121
EP S122
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100233
ER
PT J
AU Kunii, Y
Hyde, TM
Deep-Soboslay, A
Weinberger, DR
Kleinman, JE
Lipska, B
AF Kunii, Yasuto
Hyde, Thomas M.
Deep-Soboslay, Amy
Weinberger, Daniel R.
Kleinman, Joel E.
Lipska, Barbara
TI Expression of CHRNA7 and the Chimeric Gene CHRFAM7A are Altered in the
Postmortem Dorsolateral Prefrontal Cortex in Major Psychiatric Disorders
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE prefrontal cortex; human; nicotinic receptor; postmortem; SNP; genetic
C1 [Kunii, Yasuto; Hyde, Thomas M.; Deep-Soboslay, Amy; Weinberger, Daniel R.; Kleinman, Joel E.; Lipska, Barbara] NIMH, Bethesda, MD 20892 USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M28
BP S125
EP S125
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100238
ER
PT J
AU Leggio, L
Schwandt, ML
Oot, EN
Dias, AA
Ramchandani, VA
AF Leggio, Lorenzo
Schwandt, Melanie L.
Oot, Emily N.
Dias, Alexandra A.
Ramchandani, Vijay A.
TI Fasting-induced Increase in Plasma Ghrelin is Blunted by Intravenous
Alcohol Administration: A Within-subject Placebo-controlled Study
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE alcohol; ghrelin; insulin; GLP-1; PYY; intravenous alcohol
administration
C1 [Leggio, Lorenzo; Schwandt, Melanie L.; Oot, Emily N.; Dias, Alexandra A.; Ramchandani, Vijay A.] NIDA, NIAAA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T200
BP S407
EP S408
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100643
ER
PT J
AU Lehmann, M
Herkenham, M
AF Lehmann, Michael
Herkenham, Miles
TI Acute but Not Chronic Psychosocial Stress Alters the Density and
Immune-phenotype of Microglia in Mouse Stress-responsive Brain Regions
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE microglia; mouse; psychosocial-stress; immune; cytokines; prefrontal
cortex
C1 [Lehmann, Michael; Herkenham, Miles] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T87
BP S325
EP S325
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100531
ER
PT J
AU Leibenluft, E
AF Leibenluft, Ellen
TI Neural Mechanisms of Frustration in Chronically Irritable Youth
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Leibenluft, Ellen] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 14.3
BP S20
EP S21
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100039
ER
PT J
AU Lovinger, D
AF Lovinger, David
TI Chronic Ethanol Exposure Increases Output from the Sensorimotor Striatum
in Mouse and Monkey Models via Changes in Neuronal Excitability and
Synaptic Transmission
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Lovinger, David] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 47.3
BP S81
EP S82
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100162
ER
PT J
AU Mann, C
Durkee, C
Grodin, EN
Ramchandani, VA
Momenan, R
AF Mann, Claire
Durkee, Caitlin
Grodin, Erica N.
Ramchandani, Vijay A.
Momenan, Reza
TI Measuring the Effects of Acute Alcohol Infusion on Human Brain
Metabolites: An MR Spectroscopy Study
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE MRS; ethanol; glutamate; alcoholism
C1 [Mann, Claire; Durkee, Caitlin; Grodin, Erica N.; Ramchandani, Vijay A.; Momenan, Reza] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M30
BP S126
EP S127
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100240
ER
PT J
AU Marenco, S
Zhang, Y
Slagle, A
Kuo, S
Meyer, C
Sethi, A
Barnett, AS
Shen, J
Weinberger, DR
Berman, KF
AF Marenco, Stefano
Zhang, Yan
Slagle, Anna
Kuo, Susie
Meyer, Christian
Sethi, Adhiraaj
Barnett, Alan S.
Shen, Jun
Weinberger, Daniel R.
Berman, Karen F.
TI Glutamate Levels Determined with Magnetic Resonance Spectroscopy (MRS)
in the Medial Prefrontal Cortex of Patients with Psychosis as Compared
to Healthy Volunteers
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE glutamate; MRS; schizophrenia; aging
C1 [Marenco, Stefano; Zhang, Yan; Slagle, Anna; Kuo, Susie; Meyer, Christian; Sethi, Adhiraaj; Barnett, Alan S.; Shen, Jun; Weinberger, Daniel R.; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
RI Marenco, Stefano/A-2409-2008
OI Marenco, Stefano/0000-0002-2488-2365
NR 0
TC 0
Z9 0
U1 1
U2 1
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 DEC
PY 2013
VL 38
SU 2
MA M94
BP S171
EP S172
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100304
ER
PT J
AU Martinez, P
Nieman, LK
Morrow, L
Cintron, D
Thompson, K
Rubinow, D
Schmidt, P
AF Martinez, Pedro
Nieman, Lynnette K.
Morrow, Leslie
Cintron, Dahima
Thompson, Karla
Rubinow, David
Schmidt, Peter
TI Therapeutic Benefits of Dutasteride, a 5 Alpha-reductase Type I
Inhibitor, in PMDD: Results of a Pilot Study
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE premenstrual mood disorders (PMDD); 5-alpha reductase; allopregnanolone;
progesterone; dutasteride
C1 [Martinez, Pedro; Nieman, Lynnette K.; Morrow, Leslie; Cintron, Dahima; Thompson, Karla; Rubinow, David; Schmidt, Peter] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T194
BP S403
EP S404
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100637
ER
PT J
AU McHugh, MJ
Catherine, D
Jacquelyn, B
Salmeron, BJ
Devous, MD
Briggs, RW
Walker, NR
Adinoff, B
Stein, EA
AF McHugh, Meredith J.
Catherine, Demers
Jacquelyn, Braud
Salmeron, Betty J.
Devous, Michael D.
Briggs, Richard W.
Walker, N. Robrina
Adinoff, Bryon
Stein, Elliot A.
TI Cortico-amygdala Coupling as a Marker of Early Relapse Risk in
Cocaine-addicted Individuals
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE cocaine addiction; amygdala; connectivity; relapse
C1 [McHugh, Meredith J.; Catherine, Demers; Jacquelyn, Braud; Salmeron, Betty J.; Devous, Michael D.; Briggs, Richard W.; Walker, N. Robrina; Adinoff, Bryon; Stein, Elliot A.] NIDA IRP, Baltimore, MD USA.
RI Salmeron, Betty Jo/M-1793-2016
OI Salmeron, Betty Jo/0000-0003-1699-9333
NR 0
TC 0
Z9 0
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 DEC
PY 2013
VL 38
SU 2
MA M131
BP S196
EP S197
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100341
ER
PT J
AU Merikangas, KR
AF Merikangas, Kathleen Ries
TI Comorbidity of Medical and Psychiatric Disorders in the
Neurodevelopmental Genomics Cohort Study
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Merikangas, Kathleen Ries] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
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 DEC
PY 2013
VL 38
SU 2
MA 49.3
BP S86
EP S86
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100170
ER
PT J
AU Phillip, S
Sharp, W
Rapoport, JL
AF Phillip, Shaw
Sharp, Wendy
Rapoport, Judith L.
TI Abnormalities in Striato-pallidal-thalamic Surface Morphology as an
Endophenotype for Obsessive-Compulsive Disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Obsesssive-Compulsive Disorder; Striatum; Thalamus; Systems
Neuroscience; Endophenotype
C1 [Phillip, Shaw; Sharp, Wendy; Rapoport, Judith L.] NHGRI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M207
BP S250
EP S251
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100416
ER
PT J
AU Prabhakaran, R
Rasetti, R
Xiao, E
Kolachana, BS
Weinberger, DR
Mattay, VS
Berman, KF
AF Prabhakaran, Ranjani
Rasetti, Roberta
Xiao, Ena
Kolachana, Bhaskar S.
Weinberger, Daniel R.
Mattay, Venkata S.
Berman, Karen F.
TI Variation in Serotonin Transporter Gene Predicts Neural Activation in a
Response Inhibition Task
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE serotonin transporter gene; response inhibition; fMRI; flanker task;
individual differences
C1 [Prabhakaran, Ranjani; Rasetti, Roberta; Xiao, Ena; Kolachana, Bhaskar S.; Weinberger, Daniel R.; Mattay, Venkata S.; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W39
BP S459
EP S460
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100717
ER
PT J
AU Qin, HD
Samuels, J
Wang, Y
Nestadt, G
Yao, Y
AF Qin, Haide
Samuels, Jack
Wang, Ying
Nestadt, Gerald
Yao, Yin
TI New Insight into Genetic Mechanism Underlying the Treatment Effect of
Obsessive-Compulsive Disorder Using SSRIs
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE selective serotonin reuptake inhibitors (SSRIs) obsessive-compulsive
disorder (OCD) pharmacogenomics GWAS study family-based design
C1 [Qin, Haide; Samuels, Jack; Wang, Ying; Nestadt, Gerald; Yao, Yin] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W83
BP S488
EP S488
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100759
ER
PT J
AU Raznahan, A
Phillip, S
Liv, C
Greenstein, D
Lerch, J
Chakravarty, M
Giedd, J
AF Raznahan, Armin
Phillip, Shaw
Liv, Clasen
Greenstein, Deanna
Lerch, Jason
Chakravarty, Mallar
Giedd, Jay
TI The Spatiotempotal Organization of Subcortical Anatomy in Human
Development
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Development; MRI; subcortex; WGCNA
C1 [Raznahan, Armin; Phillip, Shaw; Liv, Clasen; Greenstein, Deanna; Lerch, Jason; Chakravarty, Mallar; Giedd, Jay] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
RI Giedd, Jay/J-9644-2015
OI Giedd, Jay/0000-0003-2002-8978
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M38
BP S132
EP S132
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100248
ER
PT J
AU Resnick, SM
Bilgel, M
An, Y
Thambisetty, M
Kraut, M
Zhou, Y
Wong, DF
AF Resnick, Susan M.
Bilgel, Murat
An, Yang
Thambisetty, Madhav
Kraut, Michael
Zhou, Yun
Wong, Dean F.
TI Longitudinal Change in Amyloid Deposition, Measured by PET and 11-C-PiB,
in Older Adults
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE amyloid imaging; PET-PiB; preclinical Alzheimer's disease; aging;
longitudinal studies
C1 [Resnick, Susan M.; Bilgel, Murat; An, Yang; Thambisetty, Madhav; Kraut, Michael; Zhou, Yun; Wong, Dean F.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M119
BP S188
EP S188
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100329
ER
PT J
AU Robinson, OJ
AF Robinson, Oliver J.
TI The Impact of Induced Anxiety on Ventral Striatal Response to Aversive
and Appetitive Prediction Error Signals
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Robinson, Oliver J.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 19.4
BP S29
EP S29
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100056
ER
PT J
AU Rubinstein, D
Eisenberg, DP
Carver, FW
Weinberger, DR
Coppola, R
Berman, KF
AF Rubinstein, Dani
Eisenberg, Daniel P.
Carver, Frederick W.
Weinberger, Daniel R.
Coppola, Richard
Berman, Karen F.
TI Reduced Prefrontal Gamma Band Power in Patients with Schizophrenia
Studied with MEG During Working Memory
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Magnetoencephalography; Working; memory; Schizophrenia Gamma
C1 [Rubinstein, Dani; Eisenberg, Daniel P.; Carver, Frederick W.; Weinberger, Daniel R.; Coppola, Richard; Berman, Karen F.] NIMH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/S-4342-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M156
BP S214
EP S215
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100366
ER
PT J
AU Schank, JR
King, C
Cheng, KJ
Rice, KC
Weinshenker, D
Schroeder, JP
Heilig, M
AF Schank, Jesse R.
King, Courtney
Cheng, Kejun
Rice, Kenner C.
Weinshenker, David
Schroeder, Jason P.
Heilig, Markus
TI The Neurokinin-1 Receptor Mediates Stress-induced Reinstatement to
Alcohol and Cocaine Seeking
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE stress; reinstatement; neurokinin; cocaine; alcohol
C1 [Schank, Jesse R.; King, Courtney; Cheng, Kejun; Rice, Kenner C.; Weinshenker, David; Schroeder, Jason P.; Heilig, Markus] NIAAA, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W154
BP S539
EP S540
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100829
ER
PT J
AU Sibley, DR
Free, RB
Chun, LN
Moritz, A
Miller, B
Doyle, T
Conroy, J
Padron, A
Meade, J
Xiao, JB
Han, Y
Duan, LH
Ferrer, M
Javitch, J
Southall, N
Marugan, J
AF Sibley, David R.
Free, R. Benjamin
Chun, Lani
Moritz, Amy
Miller, Brittney
Doyle, Trevor
Conroy, Jennie
Padron, Adrian
Meade, Julie
Xiao, Jingbo
Han, Yang
Duan, Lihua
Ferrer, Marc
Javitch, Jonathan
Southall, Noel
Marugan, Juan
TI Discovery and Characterization of a G Protein-biased Agonist That
Inhibits beta-arrestin Recruitment to the D2 Dopamine Receptor
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE dopamine receptor; functional-selectivity; biased-agonism; cAMP;
beta-arrestin D2
C1 [Sibley, David R.; Free, R. Benjamin; Chun, Lani; Moritz, Amy; Miller, Brittney; Doyle, Trevor; Conroy, Jennie; Padron, Adrian; Meade, Julie; Xiao, Jingbo; Han, Yang; Duan, Lihua; Ferrer, Marc; Javitch, Jonathan; Southall, Noel; Marugan, Juan] NINDS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W163
BP S545
EP S546
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100838
ER
PT J
AU Spagnolo, P
Kwako, L
Momenan, R
Schwandt, ML
Ramchandani, VA
Hommer, DW
George, DT
Heilig, M
AF Spagnolo, Primavera
Kwako, Laura
Momenan, Reza
Schwandt, Melanie L.
Ramchandani, Vijay A.
Hommer, Daniel W.
George, David T.
Heilig, Markus
TI Effects of Neurokinin 1 Receptor Antagonism on Brain Response to
Emotional Visual Stimuli in Comorbid Alcohol Dependence and
Posttraumatic Stress Disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE PTSD; alcoholism; NK1 antagonism; vmPFC
C1 [Spagnolo, Primavera; Kwako, Laura; Momenan, Reza; Schwandt, Melanie L.; Ramchandani, Vijay A.; Hommer, Daniel W.; George, David T.; Heilig, Markus] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T165
BP S383
EP S384
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100608
ER
PT J
AU Stangl, BL
Schwandt, ML
Kwako, LE
Yan, J
Zametkin, M
Ramchandani, VA
AF Stangl, Bethany L.
Schwandt, Melanie L.
Kwako, Laura E.
Yan, Jia
Zametkin, Molly
Ramchandani, Vijay A.
TI Adverse Childhood Experiences Predict Heavier Drinking and Greater
Alcohol Intake During Intravenous (IV) Alcohol Self-Administration in
Non-Dependent Drinkers
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE childhood trauma; CTQ; IV alcohol; CASE; self-administration
C1 [Stangl, Bethany L.; Schwandt, Melanie L.; Kwako, Laura E.; Yan, Jia; Zametkin, Molly; Ramchandani, Vijay A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W133
BP S524
EP S525
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100809
ER
PT J
AU Tapocik, J
Schank, JR
Mayo, C
King, C
Koenig, J
Heilig, M
Elmer, GI
AF Tapocik, Jenica
Schank, Jesse R.
Mayo, Cheryl
King, Courtney
Koenig, Jim
Heilig, Markus
Elmer, Greg I.
TI Comorbidity of PTSD and Alcoholism: A Rat Model of PTSD Leads to
Escalated Ethanol Consumption
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE PTSD; alcoholism; predator exposure; two bottle choice; learned
helplessness
C1 [Tapocik, Jenica; Schank, Jesse R.; Mayo, Cheryl; King, Courtney; Koenig, Jim; Heilig, Markus; Elmer, Greg I.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T14
BP S280
EP S281
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100460
ER
PT J
AU Tomasi, D
Wang, GJ
Caparelli, E
Volkow, ND
AF Tomasi, Dardo
Wang, Gene-Jack
Caparelli, Elisabeth
Volkow, Nora D.
TI Brain Activation to Natural Cues and Drug Cues and Dopamine Receptors in
Cocaine Addicts
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Addiction; fMRI; cocaine; PET; dopamine
C1 [Tomasi, Dardo; Wang, Gene-Jack; Caparelli, Elisabeth; Volkow, Nora D.] NIH, Fulton, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M36
BP S130
EP S131
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100246
ER
PT J
AU Tseng, WL
Deveney, CM
Guyer, AE
Yi, J
Espy, K
Wakschlag, L
Towbin, K
Leibenluft, E
Brotman, MA
AF Tseng, Wan-Ling
Deveney, Christen M.
Guyer, Amanda E.
Yi, Jennifer
Espy, Kimberly
Wakschlag, Lauren
Towbin, Kenneth
Leibenluft, Ellen
Brotman, Melissa A.
TI Responses to Blocked Goal Attainment in Preschoolers at Risk for Bipolar
Disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE Bipolar disorder; Risk factor; Irritability; Preschoolers; Frustration
C1 [Tseng, Wan-Ling; Deveney, Christen M.; Guyer, Amanda E.; Yi, Jennifer; Espy, Kimberly; Wakschlag, Lauren; Towbin, Kenneth; Leibenluft, Ellen; Brotman, Melissa A.] NIMH, NIH, Bethesda, MD 20892 USA.
RI Brotman, Melissa/H-7409-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M194
BP S241
EP S242
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100403
ER
PT J
AU Nguyen, TV
Schmidt, P
Kippenhan, JS
Sottile, M
Ekuta, V
Kolachana, BS
Verchinski, BA
Mattay, VS
Kleinman, JE
Lipska, B
Weinberger, DR
Berman, KF
AF Tuong-Vi Nguyen
Schmidt, Peter
Kippenhan, J. Shane
Sottile, Melanie
Ekuta, Victor
Kolachana, Bhaskar S.
Verchinski, Beth A.
Mattay, Venkata S.
Kleinman, Joel E.
Lipska, Barbara
Weinberger, Daniel R.
Berman, Karen F.
TI Sex Steroid Receptor Gene Expression Correlates with the Expression of
Neurodevelopmental Genes and Modulates Gray Matter Volume in the Human
Brain
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE estrogen receptor; progesterone receptor; estradiol; progesterone;
development
C1 [Tuong-Vi Nguyen; Schmidt, Peter; Kippenhan, J. Shane; Sottile, Melanie; Ekuta, Victor; Kolachana, Bhaskar S.; Verchinski, Beth A.; Mattay, Venkata S.; Kleinman, Joel E.; Lipska, Barbara; Weinberger, Daniel R.; Berman, Karen F.] NIH, Bethesda, MD 20892 USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA T209
BP S413
EP S414
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100652
ER
PT J
AU Uhl, G
Hall, FS
Ranscht, B
Uetani, N
Drgonova, J
AF Uhl, George
Hall, Frank S.
Ranscht, Barbara
Uetani, Noriko
Drgonova, Jana
TI Genes Harboring Addiction-related Variants Alter Dose-response
Relationships for Stimulant Reward
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE cocaine; amphetamine; knockout mouse; translational reserach; polygenic
disorder
C1 [Uhl, George; Hall, Frank S.; Ranscht, Barbara; Uetani, Noriko; Drgonova, Jana] NIDA, Baltimore, MD USA.
RI Hall, Frank/C-3036-2013
OI Hall, Frank/0000-0002-0822-4063
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M16
BP S116
EP S117
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100226
ER
PT J
AU Umhau, JC
Zhou, WY
Thada, S
Herscovitch, P
Salem, N
Hibbeln, JR
Hirvonen, J
Rapoport, S
AF Umhau, John C.
Zhou, Weiyin
Thada, Shantalaxmi
Herscovitch, Peter
Salem, Norman, Jr.
Hibbeln, Joseph R.
Hirvonen, Jussi
Rapoport, Stanley
TI Non-smoking Chronic Alcoholics Following Withdrawal Show Increased
Cerebral Blood Flow and Altered Brain Docosahexaenoic (DHA) Metabolism
on Partial Volume Error-corrected PET
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE chronic alcoholism; positron emission tomography; cerebral blood flow;
docosahexaenoic acid; brain
C1 [Umhau, John C.; Zhou, Weiyin; Thada, Shantalaxmi; Herscovitch, Peter; Salem, Norman, Jr.; Hibbeln, Joseph R.; Hirvonen, Jussi; Rapoport, Stanley] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M40
BP S133
EP S134
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100250
ER
PT J
AU Volkow, ND
AF Volkow, Nora D.
TI Unmotivated? Signatures of Blunted Dopaminergic Responsiveness in
Chronic Marijuana Abuse
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Volkow, Nora D.] NIDA, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA 39.4
BP S67
EP S67
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100131
ER
PT J
AU Yan, J
Stangl, BL
Reimers, MA
Schwandt, ML
Sun, H
Hodgkinson, CA
Goldman, D
Hommer, DW
George, DT
Kendler, KS
Heilig, M
Ramchandani, VA
AF Yan, Jia
Stangl, Bethany L.
Reimers, Mark A.
Schwandt, Melanie L.
Sun, Hui
Hodgkinson, Colin A.
Goldman, David
Hommer, Daniel W.
George, David T.
Kendler, Kenneth S.
Heilig, Markus
Ramchandani, Vijay A.
TI Genetic Pathway Analyses of the Endocannabinoid System in a Sample of
Social Drinkers and Treatment-Seeking Alcoholics
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE alcohol dependence; pathway analysis; endocannabinoid system; genetics
C1 [Yan, Jia; Stangl, Bethany L.; Reimers, Mark A.; Schwandt, Melanie L.; Sun, Hui; Hodgkinson, Colin A.; Goldman, David; Hommer, Daniel W.; George, David T.; Kendler, Kenneth S.; Heilig, Markus; Ramchandani, Vijay A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W97
BP S498
EP S499
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100773
ER
PT J
AU Yao, Y
Xu, MY
Murphy, E
Wang, H
McMahon, FJ
AF Yao, Yin
Xu, Mengyuan
Murphy, Eleanor
Wang, Harold
McMahon, Francis J.
TI A Mixture Model Estimate of Time to Antidepressant Drug-Effect in
Association with Covariates Using the STAR(star)D Sample
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE drug effect; drug onset; major depression; anxiety; association
C1 [Yao, Yin; Xu, Mengyuan; Murphy, Eleanor; Wang, Harold; McMahon, Francis J.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA M193
BP S241
EP S241
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100402
ER
PT J
AU Yuan, QP
Yeo, S
Zhou, ZF
Hodgkinson, CA
Goldman, D
AF Yuan, Qiaoping
Yeo, Seungeun
Zhou, Zhifeng
Hodgkinson, Colin A.
Goldman, David
TI Differential Allelic Expression and cis-Regulatory Sites at Human
Neuronal Genes
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
DE human; expression; regulation; genetics
C1 [Yuan, Qiaoping; Yeo, Seungeun; Zhou, Zhifeng; Hodgkinson, Colin A.; Goldman, David] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2013
VL 38
SU 2
MA W67
BP S477
EP S478
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V40KI
UT WOS:000209477100744
ER
PT J
AU Sanchez, MA
Rabin, BA
Gaglio, B
Henton, M
Elzarrad, MK
Purcell, P
Glasgow, RE
AF Sanchez, Michael A.
Rabin, Borsika A.
Gaglio, Bridget
Henton, Michelle
Elzarrad, M. Khair
Purcell, Peyton
Glasgow, Russell E.
TI A systematic review of eHealth cancer prevention and control
interventions: new technology, same methods and designs?
SO TRANSLATIONAL BEHAVIORAL MEDICINE
LA English
DT Review
DE eHealth; Pragmatic trials; Systematic review; Design; PRECIS; External
validity; RE-AIM framework
AB There has been a recent surge of eHealth programs in cancer and other content areas, but few reviews have focused on the methodologies and designs employed in these studies. We conducted a systematic review of studies on eHealth interventions on cancer prevention and control published between 2001 and 2010 applying the Pragmatic Explanatory Continuum Indicator Summary (PRECIS) criteria and external validity components from the Reach Effectiveness Adoption Implementation Maintenance (RE-AIM) framework. We identified 113 studies that focused on cancer prevention and control of eHealth interventions. Most studies fell midway along the explanatory/pragmatic trial continuum, but few reported on various practical feasibility criteria for translation. Despite vast interest in cancer eHealth and the applied nature of this field, few studies considered key external validity issues. There is a need for use of alternative pragmatic study designs and transparent reporting of external validity components to produce more rapid and generalizable results.
C1 [Sanchez, Michael A.; Elzarrad, M. Khair] NCI, Bethesda, MD 20892 USA.
[Rabin, Borsika A.; Henton, Michelle] Kaiser Permanente Colorado, CRN Canc Commun Res Ctr, Denver, CO USA.
[Gaglio, Bridget] Kaiser Permanente Midatlantic States, Midatlantic Permanente Res Inst, Rockville, MD USA.
[Elzarrad, M. Khair] NCI, US FDA, Interagency Oncol Task Force IOTF Fellowship Canc, Bethesda, MD 20892 USA.
[Purcell, Peyton] SAIC Frederick Inc, CMRP, Clin Res Directorate, Natl Lab Canc Res, Frederick, MD USA.
RP Sanchez, MA (reprint author), NCI, Bethesda, MD 20892 USA.
EM sanchezgarciama@mail.nih.gov
FU National Cancer Institute Centers of Excellence in Cancer Communication
Research [P20CA137219]; National Cancer Institute; National Institutes
of Health [HHSN261200800001E]
FX The preparation of this manuscript was partially funded through the
National Cancer Institute Centers of Excellence in Cancer Communication
Research (award number P20CA137219). This project has been funded, in
whole or in part, with federal funds from the National Cancer Institute,
the National Institutes of Health, under contract no. HHSN261200800001E.
The content of this publication does not necessarily reflect the views
or policies of the Department of Health and Human Services, nor does it
mention of trade names, commercial products, or organizations implying
endorsement by the US government. The opinions expressed are those of
the authors and do not necessarily reflect those of the National Cancer
Institute.
NR 31
TC 8
Z9 8
U1 3
U2 6
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1869-6716
EI 1613-9860
J9 TRANSL BEHAV MED
JI Transl. Behav. Med.
PD DEC
PY 2013
VL 3
IS 4
BP 392
EP 401
DI 10.1007/s13142-013-0224-1
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA V39LR
UT WOS:000209413000008
PM 24294327
ER
PT J
AU Michino, M
Donthamsetti, P
Beuming, T
Banala, A
Duan, LH
Roux, T
Han, Y
Trinquet, E
Newman, AH
Javitch, JA
Shi, L
AF Michino, Mayako
Donthamsetti, Prashant
Beuming, Thijs
Banala, Ashwini
Duan, Lihua
Roux, Thomas
Han, Yang
Trinquet, Eric
Newman, Amy Hauck
Javitch, Jonathan A.
Shi, Lei
TI A Single Glycine in Extracellular Loop 1 Is the Critical Determinant for
Pharmacological Specificity of Dopamine D2 and D3 Receptors
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; FUNCTIONALIZED LINKING CHAINS; EXCHANGE
MOLECULAR-DYNAMICS; BINDING-SITE CREVICE; TRANSMEMBRANE SEGMENT;
STRUCTURAL BIOLOGY; CRYSTAL-STRUCTURES; LIGAND-BINDING; BETA-HAIRPIN;
SELECTIVITY
AB Subtype-selective agents for the dopamine D3 receptor (D3R) have been considered as potential medications for drug addiction and other neuropsychiatric disorders. Medicinal chemistry efforts have led to the discovery of 4-phenylpiperazine derivatives that are >100-fold selective for the dopamine D3 receptor over dopamine D2 receptor (D2R), despite high sequence identity (78% in the transmembrane domain). Based on the recent crystal structure of D3R, we demonstrated that the 4-phenylpiperazine moiety in this class of D3R-selective compounds binds to the conserved orthosteric binding site, whereas the extended aryl amide moiety is oriented toward a divergent secondary binding pocket (SBP). In an effort to further characterize molecular determinants of the selectivity of these compounds, we modeled their binding modes in D3R and D2R by comparative ligand docking and molecular dynamics simulations. We found that the aryl amide moiety in the SBP differentially induces conformational changes in transmembrane segment 2 and extracellular loop 1 (EL1), which amplify the divergence of the SBP in D3R and D2R. Receptor chimera and site-directed mutagenesis studies were used to validate these binding modes and to identify a divergent glycine in EL1 as critical to D3R over D2R subtype selectivity. A better understanding of drug-dependent receptor conformations such as these is key to the rational design of compounds targeting a specific receptor among closely related homologs, and may also lead to discovery of novel chemotypes that exploit subtle differences in protein conformations.
C1 [Michino, Mayako; Shi, Lei] Cornell Univ, Weill Med Coll, Inst Computat Biomed, Dept Physiol & Biophys, New York, NY 10021 USA.
[Donthamsetti, Prashant; Duan, Lihua; Han, Yang; Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
[Donthamsetti, Prashant; Duan, Lihua; Han, Yang; Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Dept Pharmacol, New York, NY 10032 USA.
[Donthamsetti, Prashant; Duan, Lihua; Han, Yang; Javitch, Jonathan A.] New York State Psychiat Inst & Hosp, Div Mol Therapeut, New York, NY 10032 USA.
[Beuming, Thijs] Schrodinger Inc, New York, NY USA.
[Banala, Ashwini; Newman, Amy Hauck] NIDA, Med Chem Sect, Mol Targets & Medicat Discovery Branch, Intramural Res Program,NIH, Baltimore, MD USA.
[Roux, Thomas; Trinquet, Eric] Cisbio Bioassays, Codolet, France.
RP Shi, L (reprint author), Weill Cornell Med Coll, Dept Physiol & Biophys, 1300 York Ave,Box 75, New York, NY 10065 USA.
EM jaj2@columbia.edu; les2007@med.cornell.edu
FU Ranger at the Texas Advanced Computing Center [TG-MCB090022]
FX Computations were performed on the Ranger at the Texas Advanced
Computing Center [Project Number TG-MCB090022].
NR 47
TC 23
Z9 23
U1 0
U2 15
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
EI 1521-0111
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD DEC
PY 2013
VL 84
IS 6
BP 854
EP 864
DI 10.1124/mol.113.087833
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 248GX
UT WOS:000326687200007
PM 24061855
ER
PT J
AU Leddy, MA
Anderson, BL
Schulkin, J
AF Leddy, Meaghan A.
Anderson, Britta L.
Schulkin, Jay
TI Cognitive-behavioral therapy and decision science
SO NEW IDEAS IN PSYCHOLOGY
LA English
DT Article
DE Cognitive-behavioral therapy; Decision science; Judgment; Decision
making; Biases
ID GENERALIZED ANXIETY DISORDER; RANDOMIZED CONTROLLED-TRIAL;
MOOD-CONGRUENT JUDGMENT; FOLLOW-UP; ANTIDEPRESSANT MEDICATION;
PSYCHOLOGICAL TREATMENTS; DEPRESSED-PATIENTS; MAJOR DEPRESSION; RATIONAL
CHOICE; HINDSIGHT BIAS
AB In recent decades cognitive-behavioral therapy (CBT) and decision science (DS) have emerged within the field of psychological science. Though these are two vastly different areas of study, they are similar in that they address human information processing, cognition, behavior, and the link between them. In this article, we provide brief summaries of CBT and decision science, discuss their similarities and differences, and discuss how future research can identify ways in which these fields can inform each other. Several CBT techniques that might be of use to the efforts of the decision science field to prevent cognitive biases are suggested. Research that integrates these two fields may lead to the improvement of both. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Leddy, Meaghan A.; Anderson, Britta L.] VA Connecticut Healthcare Syst, West Haven, CT 06516 USA.
[Leddy, Meaghan A.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06510 USA.
[Schulkin, Jay] Amer Coll Obstetricians & Gynecologists, Res Dept, Washington, DC 20024 USA.
[Schulkin, Jay] Georgetown Univ, Med Ctr, Dept Neurosci, Washington, DC 20007 USA.
[Schulkin, Jay] NIMH, Behav Endocrinol Branch, Bethesda, MD 20892 USA.
RP Schulkin, J (reprint author), Georgetown Univ, Med Ctr, Dept Neurosci, 3970 Reservoir Rd NW, Washington, DC 20007 USA.
EM anderson.britta.l@gmail.com; jschulkin@acog.org
NR 91
TC 1
Z9 1
U1 3
U2 17
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0732-118X
EI 1873-3522
J9 NEW IDEAS PSYCHOL
JI New Ideas Psychol.
PD DEC
PY 2013
VL 31
IS 3
BP 173
EP 183
DI 10.1016/j.newideapsych.2013.01.001
PG 11
WC Psychology, Multidisciplinary; Psychology, Experimental
SC Psychology
GA 244AI
UT WOS:000326359100001
ER
PT J
AU Hall, FS
Drgonova, J
Jain, S
Uhl, GR
AF Hall, F. Scott
Drgonova, Jana
Jain, Siddharth
Uhl, George R.
TI Implications of genome wide association studies for addiction: Are our a
priori assumptions all wrong?
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Addiction; Drug abuse; Genome-wide association study; Linkage;
Transgenic; Knockout; Genetics
ID MU-OPIOID-RECEPTOR; TRANSPORTER KNOCKOUT MICE; D-2 DOPAMINE-RECEPTOR;
PREPULSE INHIBITION DEFICITS; CONDITIONED PLACE PREFERENCE;
SMOKING-CESSATION SUCCESS; SINGLE-NUCLEOTIDE POLYMORPHISMS; AND/OR
SEROTONIN TRANSPORTERS; SUBSTANCE USE DISORDERS; ALCOHOL DEPENDENCE
AB Substantial genetic contributions to addiction vulnerability are supported by data from twin studies, linkage studies, candidate gene association studies and, more recently, Genome Wide Association Studies (GWAS). Parallel to this work, animal studies have attempted to identify the genes that may contribute to responses to addictive drugs and addiction liability, initially focusing upon genes for the targets of the major drugs of abuse. These studies identified genes/proteins that affect responses to drugs of abuse; however, this does not necessarily mean that variation in these genes contributes to the genetic component of addiction liability. One of the major problems with initial linkage and candidate gene studies was an a priori focus on the genes thought to be involved in addiction based upon the known contributions of those proteins to drug actions, making the identification of novel genes unlikely. The GWAS approach is systematic and agnostic to such a priori assumptions. From the numerous GWAS now completed several conclusions may be drawn: (1) addiction is highly polygenic; each allelic variant contributing in a small, additive fashion to addiction vulnerability; (2) unexpected, compared to our a priori assumptions, classes of genes are most important in explaining addiction vulnerability; (3) although substantial genetic heterogeneity exists, there is substantial convergence of GWAS signals on particular genes. This review traces the history of this research; from initial transgenic mouse models based upon candidate gene and linkage studies, through the progression of GWAS for addiction and nicotine cessation, to the current human and transgenic mouse studies post-GWAS. Published by Elsevier Inc.
C1 [Hall, F. Scott; Drgonova, Jana; Jain, Siddharth; Uhl, George R.] NIDA, Mol Neurobiol Branch, Intramural Res Program, Baltimore, MD 21224 USA.
RP Hall, FS (reprint author), NIDA, Mol Neurobiol Branch, 333 Cassell Dr, Baltimore, MD 21224 USA.
EM shall@intra.nida.nih.gov
RI Hall, Frank/C-3036-2013;
OI Hall, Frank/0000-0002-0822-4063; Drgonova, Jana/0000-0002-4623-8466
FU National Institute on Drug Abuse
FX This work was supported by intramural funding from the National
Institute on Drug Abuse.
NR 184
TC 11
Z9 13
U1 7
U2 55
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD DEC
PY 2013
VL 140
IS 3
BP 267
EP 279
DI 10.1016/j.pharmthera.2013.07.006
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 244WZ
UT WOS:000326422200005
PM 23872493
ER
PT J
AU Camfield, L
Masae, A
McGregor, JA
Promphaking, B
AF Camfield, Laura
Masae, Awae
McGregor, J. Allister
Promphaking, Buapun
TI Cultures of Aspiration and Poverty? Aspirational Inequalities in
Northeast and Southern Thailand
SO SOCIAL INDICATORS RESEARCH
LA English
DT Article
DE Aspirations; Subjective wellbeing; Thailand; Inequality; Adaptation;
Poverty
ID CONSUMPTION; WOMEN; HAPPINESS
AB The paper provides micro-level evidence of rising inequality in Thailand, using data from an intensive study of seven communities in Northeast and Southern Thailand. This inequality affects participants' material and subjective wellbeing, their aspirations, and the extent to which they feel these are realised. The paper argues that adaptation, expressed as reduced aspirations, could explain why the effect of material poverty on people's satisfaction with their lives is small. The reduction in attainment of aspirations linked to socio-economic status suggests that a small, but constant group of people are being excluded from a shift in the societal consensus over what constitutes a good life.
C1 [Camfield, Laura] Univ E Anglia, Dept Int Dev, Norwich NR4 7TJ, Norfolk, England.
[Masae, Awae] NIDA, Sch Social & Environm Dev, Bangkok, Thailand.
[Promphaking, Buapun] Khon Kaen Univ, Khon Kaen, Thailand.
RP Camfield, L (reprint author), Univ E Anglia, Dept Int Dev, Norwich NR4 7TJ, Norfolk, England.
EM l.camfield@uea.ac.uk
OI Camfield, Laura/0000-0002-0165-9857
NR 58
TC 1
Z9 1
U1 1
U2 14
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0303-8300
EI 1573-0921
J9 SOC INDIC RES
JI Soc. Indic. Res.
PD DEC
PY 2013
VL 114
IS 3
BP 1049
EP 1072
DI 10.1007/s11205-012-0189-3
PG 24
WC Social Sciences, Interdisciplinary; Sociology
SC Social Sciences - Other Topics; Sociology
GA 244QZ
UT WOS:000326405800017
ER
PT J
AU Kuo, CC
Moon, K
Thayer, KA
Navas-Acien, A
AF Kuo, Chin-Chi
Moon, Katherine
Thayer, Kristina A.
Navas-Acien, Ana
TI Environmental Chemicals and Type 2 Diabetes: An Updated Systematic
Review of the Epidemiologic Evidence
SO CURRENT DIABETES REPORTS
LA English
DT Review
DE Systematic review; Environmental chemicals; Diabetes; Arsenic; Cadmium;
Mercury; Persistent organic pollutants; Bisphenol A; Phthalates; Type 2
diabetes; Epidemiology
ID PERSISTENT ORGANIC POLLUTANTS; POLYCHLORINATED BIPHENYL EXPOSURE;
URINARY PHTHALATE METABOLITES; CAPACITOR MANUFACTURING PLANT;
BISPHENOL-A CONCENTRATIONS; OPERATION RANCH HAND; ARSENIC EXPOSURE;
INSULIN-RESISTANCE; NATIONAL-HEALTH; ENDOCRINE DISRUPTOR
AB The burden of diabetes is increasing globally. Identifying novel preventable risk factors is an urgent need. In 2011, the U.S. National Toxicological Program (NTP) conducted a workshop to evaluate the epidemiologic and experimental evidence on the relationship of environmental chemicals with obesity, diabetes, and metabolic syndrome. Although the evidence was insufficient to establish causality, the NTP workshop review identified an overall positive association between some environmental chemicals and diabetes. In the present systematic review, our objective was to summarize the epidemiological research published since the NTP workshop. We identified a total of 29 articles (7 on arsenic, 3 on cadmium, 2 on mercury, 11 on persistent organic pollutants, 3 on phthalates, and 4 on bisphenol A), including 7 prospective studies. Considering consistency, temporality, strength, dose-response relationship, and biological plausibility (confounding), we concluded that the evidence is suggestive but not sufficient for a relationship between arsenic and persistent organic pollutants and is insufficient for mercury, phthalates, and bisphenol A. For cadmium, the epidemiologic evidence does not seem to suggest an association with diabetes. Important research questions include the need for additional prospective studies and the evaluation of the dose-response relationship, the role of joint exposures, and effect modification with other comorbidities and genetic variants.
C1 [Kuo, Chin-Chi; Moon, Katherine; Navas-Acien, Ana] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Kuo, Chin-Chi; Moon, Katherine; Navas-Acien, Ana] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA.
[Kuo, Chin-Chi; Moon, Katherine; Navas-Acien, Ana] Johns Hopkins Med Inst, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21205 USA.
[Thayer, Kristina A.] NIEHS, Off Hlth Assessment & Translat, Div Natl Toxicol Program, NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Kuo, CC (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
EM ckuo@jhsph.edu; kmoon@jhsph.edu; thayer@niehs.nih.gov; anavas@jhsph.edu
RI Tuomisto, Jouko/J-7450-2012
FU National Institute of Environmental Health Sciences [R01ES021367,
P30ES03819]; National Heart Lung and Blood Institute [R01HL090863]
FX Supported by grants from the National Institute of Environmental Health
Sciences (R01ES021367, P30ES03819) and the National Heart Lung and Blood
Institute (R01HL090863).
NR 123
TC 60
Z9 63
U1 6
U2 74
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1534-4827
EI 1539-0829
J9 CURR DIABETES REP
JI Curr. Diabetes Rep.
PD DEC
PY 2013
VL 13
IS 6
BP 831
EP 849
DI 10.1007/s11892-013-0432-6
PG 19
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 241SR
UT WOS:000326188500009
PM 24114039
ER
PT J
AU Ramakrishnan, B
Moncrief, AJ
Davis, TA
Holland, LA
Qasba, PK
AF Ramakrishnan, Boopathy
Moncrief, Anthony J.
Davis, Tyler A.
Holland, Lisa A.
Qasba, Pradman K.
TI Investigations on beta 1,4-galactosyltransferase I using 6-sulfo-GlcNAc
as an acceptor sugar substrate
SO GLYCOCONJUGATE JOURNAL
LA English
DT Article
DE beta 1,4-galactosyltransferase; Acceptor specificity; 6-sulfo-GlcNAc;
Crystal structure; Capillary electrophoresis
ID ALPHA-LACTALBUMIN; CRYSTAL-STRUCTURE; N-ACETYLGLUCOSAMINE; LACTOSE
SYNTHETASE; GALACTOSYLTRANSFERASE; GLYCOSYLTRANSFERASES; REVEALS;
COMPLEX; PROTEIN; MUTANT
AB 6-sulfate modified N-acetylglucosamine (6-sulfo-GlcNAc) is often found as part of many biologically important carbohydrate epitopes such as 6-sulfo-Le(X). In these epitopes, the 6-sulfo-GlcNAc moiety is extended by a galactose sugar in a beta 1-4 linkage. The beta 4GalT1 enzyme transfers galactose (Gal) from UDP-Gal to N-acetylglucosamine (GlcNAc) in the presence of manganese. Here we report that the beta 4GalT1 enzyme transfers Gal to the 6-sulfo-GlcNAc and 4-methylumbelliferyl-6-sulfo-N-acetyl-beta-D-glucosaminide (6-sulfo-beta GlcNAc-MU) acceptor substrates, although with very low efficiency. To understand the effect that the 6-sulfate group on the GlcNAc acceptor has on the catalytic activity of the beta 4GalT1 molecule, we have determined the crystal structure of the catalytic domain of bovine beta 4GalT1 mutant enzyme M344H-beta 4GalT1 complex with the 6-sulfo-GlcNAc molecule. In the crystal structure, the 6-sulfo-GlcNAc is bound to the protein in a way that is similar to the GlcNAc molecule. However, the 6-sulfate group engages in additional interactions with the hydrophobic region, residues 276-285, of the protein molecule, and this group is found wedged between the aromatic side chains of Phe-280 and Trp314 residues. Since the side chain of the Trp314 residue undergoes conformational changes during the catalytic cycle of the enzyme, molecular interaction between Trp314 and the 6-sulfate group might hinder this conformational change. Therefore, the lack of a favorable binding environment, together with hindrance to the conformational changes, might be responsible for the poor catalytic activity.
C1 [Ramakrishnan, Boopathy; Qasba, Pradman K.] NCI, Struct Glycobiol Sect, Basic Sci Lab, Frederick, MD 21702 USA.
[Ramakrishnan, Boopathy] SAIC Frederick Inc, Basic Res Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Moncrief, Anthony J.; Davis, Tyler A.; Holland, Lisa A.] W Virginia Univ, C Eugene Bennett Dept Chem, Morgantown, WV 26506 USA.
RP Qasba, PK (reprint author), NCI, Struct Glycobiol Sect, Basic Sci Lab, POB B, Frederick, MD 21702 USA.
EM qasbapr@helix.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; National Science Foundation [1003907]; Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract HHSN261200800001E. We acknowledge support for T. A. D. from the
National Science Foundation (Cooperative Agreement 1003907). 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. This research was supported [in part] by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 32
TC 1
Z9 1
U1 4
U2 11
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0282-0080
EI 1573-4986
J9 GLYCOCONJUGATE J
JI Glycoconjugate J.
PD DEC
PY 2013
VL 30
IS 9
BP 835
EP 842
DI 10.1007/s10719-013-9488-4
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 241TB
UT WOS:000326189600003
PM 23942731
ER
PT J
AU Ftacek, P
Nelson, V
Szu, SC
AF Ftacek, Peter
Nelson, Victor
Szu, Shousun C.
TI Immunochemical characterization of synthetic hexa-, octa- and
decasaccharide conjugate vaccines for Vibrio cholerae O:1 Serotype Ogawa
with emphasis on antigenic density and chain length
SO GLYCOCONJUGATE JOURNAL
LA English
DT Article
DE Neoglyco conjugate; Cholera vaccine; Immunogenicity; Vibriocidal
ID SHIGELLA-DYSENTERIAE TYPE-1; ORAL CHOLERA; BACTERICIDAL ANTIBODIES;
IMMUNE-RESPONSES; FAMILY CONTACTS; PROTEIN CARRIER; EAST PAKISTAN;
FIELD-TRIAL; LIPOPOLYSACCHARIDE; POLYSACCHARIDE
AB Cholera remains to be a global health problem without suitable vaccines for endemic control or outbreak relief. Here we describe a new parenteral vaccine based on neoglyco-conjugate of synthetic fragments of O-specific polysaccharide (O-SP) of Vibrio cholerae O1, serotype Ogawa. Hexa-, octa- and decasaccharides of the O-SP with carboxylic acid at the reducing end were chemically synthesized and conjugated to tetanus toxoid (TT). The conjugates prepared by a novel linking scheme consisted of 17-atom linker of hydrazide and alkyl bonds elicited robust serum IgG anti-LPS responses with vibriocidal activities in mice. There is a length dependence in immune response with decasaccharide conjugates elicited the highest anti-LPS IgG. There seems to be an indication that regardless of the carbohydrate chain length, a molar ratio of 230 +/- 10 monosaccharide units per TT induced high antibody response. The conjugates also elicited cross-reactive antibodies to serotype Inaba. The formulation of the proposed cholera conjugate vaccine, similar to other licensed polysaccharide vaccine, is suitable for children immunization. A parenteral cholera vaccine could overcome the diminishing immunogenicity in most of oral vaccines due to the gastrointestinal complexity and environmental enteropathy in children living in impoverished environment and could be considered for global cholera immunization.
C1 [Ftacek, Peter; Nelson, Victor; Szu, Shousun C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Szu, SC (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bldg 6,Room 1A06,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM szunih@gmail.com
FU Intramural Research at the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health
FX This work was supported fully by the Intramural Research at the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health. The authors have no conflict
interest to disclose.
NR 72
TC 1
Z9 1
U1 1
U2 14
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0282-0080
EI 1573-4986
J9 GLYCOCONJUGATE J
JI Glycoconjugate J.
PD DEC
PY 2013
VL 30
IS 9
BP 871
EP 880
DI 10.1007/s10719-013-9491-9
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 241TB
UT WOS:000326189600006
PM 23955520
ER
PT J
AU Staats, KA
Van Helleputte, L
Jones, AR
Bento-Abreu, A
Van Hoecke, A
Shatunov, A
Simpson, CL
Lemmens, R
Jaspers, T
Fukami, K
Nakamura, Y
Brown, RH
Van Damme, P
Liston, A
Robberecht, W
Al-Chalabi, A
Van Den Bosch, L
AF Staats, Kim A.
Van Helleputte, Lawrence
Jones, Ashley R.
Bento-Abreu, Andre
Van Hoecke, Annelies
Shatunov, Aleksey
Simpson, Claire L.
Lemmens, Robin
Jaspers, Tom
Fukami, Kiyoko
Nakamura, Yoshikazu
Brown, Robert H., Jr.
Van Damme, Philip
Liston, Adrian
Robberecht, Wim
Al-Chalabi, Ammar
Van Den Bosch, Ludo
TI Genetic ablation of phospholipase C delta 1 increases survival in
SOD1(G93A) mice
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE Amyotrophic lateral sclerosis; Phospholipase C delta 1; Neurogenetics;
SOD1-G93A mice; Excitotoxicity; Motor neuron disease; Nuclear shrinkage
ID AMYOTROPHIC-LATERAL-SCLEROSIS; GENOME-WIDE ASSOCIATION; MOTOR-NEURON
DEGENERATION; TRANSGENIC MOUSE MODEL; HEXANUCLEOTIDE REPEAT; MUTATIONS;
SUSCEPTIBILITY; DISEASE; C-DELTA-1; ALS
AB Amyotrophic Lateral Sclerosis (ALS) is a devastating progressive neurodegenerative disease, resulting in selective motor neuron degeneration and paralysis. Patients die approximately 3-5 years after diagnosis. Disease pathophysiology is multifactorial, including excitotoxicity, but is not yet fully understood. Genetic analysis has proven fruitful in the past to further understand genes modulating the disease and increase knowledge of disease mechanisms. Here, we revisit a previously performed microsatellite analysis in ALS and focus on another hit, PLCD1, encoding phospholipase C delta 1 (PLC delta 1), to investigate its role in ALS. PLC delta 1 may contribute to excitotoxicity as it increases inositol 1,4,5-trisphosphate (IP3) formation, which releases calcium from the endoplasmic reticulum through IP3 receptors. We find that expression of PLC delta 1 is increased in ALS mouse spinal cord and in neurons from ALS mice. Furthermore, genetic ablation of this protein in ALS mice significantly increases survival, but does not affect astrogliosis, microgliosis, aggregation or the amount of motor neurons at end stage compared to ALS mice with PLC delta 1. Interestingly, genetic ablation of PLC delta 1 prevents nuclear shrinkage of motor neurons in ALS mice at end stage. These results indicate that PLCD1 contributes to ALS and that PLC delta 1 may be a new target for future studies. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Jones, Ashley R.; Shatunov, Aleksey; Al-Chalabi, Ammar] Kings Coll London, Inst Psychiat, Dept Clin Neurosci, London, England.
[Simpson, Claire L.] NHGRI, Inherited Dis Res Branch, US Natl Inst Hlth, Baltimore, MD USA.
[Fukami, Kiyoko; Nakamura, Yoshikazu] Tokyo Univ Pharm & Life Sci, Lab Genome & Biosignal, Hachioji, Tokyo 19203, Japan.
[Brown, Robert H., Jr.] Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA USA.
[Liston, Adrian] VIB, Autoimmune Genet Lab, Louvain, Belgium.
[Liston, Adrian] Katholieke Univ Leuven, Dept Microbiol & Immunol, Louvain, Belgium.
EM kim.staats@vib-kuleuven.be; Lawrence.vanhelleputte@vib-kuleuven.be;
ashley.ajones@kcl.ac.uk; Andre.BentoAbreu@vib-kuleuven.be;
avanhoecke@neuro.mpg.de; aleksey.shatunov@kcLac.uk;
claire.simpson@nih.gov; robin.lemmens@vib-kuleuven.be;
tom.jaspers@vib-kuleuven.be; kfukami@ls.toyaku.ac.jp;
ynakamur@toyaku.ac.jp; robertbrown@umassmed.edu;
philip.vandamme@vib-kuleuven.be; adriandiston@vib-kuleuven.be;
wim.robberecht@vib-kuleuven.be; ammar.al-chalabi@kcl.ac.uk;
ludo.vandenbosch@vib-kuleuven.be
RI Al-Chalabi, Ammar/E-5361-2010; Van Damme, Philip/A-6464-2009; Liston,
Adrian/G-8606-2013
OI Al-Chalabi, Ammar/0000-0002-4924-7712; Van Damme,
Philip/0000-0001-6384-0611; Liston, Adrian/0000-0002-6272-4085
FU ALS Association; Motor Neurone Disease Association of England, Wales and
Northern Ireland; NIHR Dementia Biomedical Research Unit at South
London; Maudsley NHS Foundation Trust; King's College London; "Fund for
Scientific Research Flanders" (FWO-Vlaanderen); University of Leuven (KU
Leuven); Belgian Government (Interuniversity Attraction Poles, programme
of the Belgian Federal Science Policy Office) [P7/16]; ALS Therapy
Alliance; Angel Fund; European Community [259867]; National Human Genome
Research Institute, National Institutes of Health
FX MC thanks the ALS Association and Motor Neurone Disease Association of
England, Wales and Northern Ireland for support. He receives salary
support from the NIHR Dementia Biomedical Research Unit at South London
and Maudsley NHS Foundation Trust and King's College London. This work
was supported by grants from the "Fund for Scientific Research Flanders"
(FWO-Vlaanderen), the University of Leuven (KU Leuven), the Belgian
Government (Interuniversity Attraction Poles, programme P7/16 of the
Belgian Federal Science Policy Office), the ALS Therapy Alliance, the
Angel Fund and the European Community's Health Seventh Framework
Programme (FP7/2007-2013 under grant agreement 259867). PVD and RL hold
a clinical investigatorship of the FWO-Vlaanderen. WR is supported
through the E von Behring Chair for Neuromuscular and Neurodegenerative
Disorders. CLS is funded by the Intramural Research Program of the
National Human Genome Research Institute, National Institutes of Health.
The views expressed are those of the authors and not necessarily those
of the National Health Service, the NIHR, or the Department of Health.
NR 48
TC 6
Z9 7
U1 2
U2 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD DEC
PY 2013
VL 60
BP 11
EP 17
DI 10.1016/j.nbd.2013.08.006
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 239ZO
UT WOS:000326064700002
PM 23969236
ER
PT J
AU Lopez-Dominguez, JA
Khraiwesh, H
Gonzalez-Reyes, JA
Lopez-Lluch, G
Navas, P
Ramsey, JJ
de Cabo, R
Buron, MI
Villalba, JM
AF Alberto Lopez-Dominguez, Jose
Khraiwesh, Husam
Antonio Gonzalez-Reyes, Jose
Lopez-Lluch, Guillermo
Navas, Placido
Ramsey, Jon Jay
de Cabo, Rafael
Buron, Maria Isabel
Villalba, Jose M.
TI Dietary fat modifies mitochondrial and plasma membrane apoptotic
signaling in skeletal muscle of calorie-restricted mice
SO AGE
LA English
DT Article
DE Apoptotic signaling; Calorie restriction; Dietary fat; Sarcopenia;
Skeletal muscle
ID AGE-RELATED ALTERATIONS; COENZYME-Q; OXIDATIVE STRESS; ACID-COMPOSITION;
LIFE-SPAN; EICOSAPENTAENOIC ACID; GASTROCNEMIUS-MUSCLE; REGULATORY
PROTEINS; ANTIOXIDANT SYSTEM; PLANTARIS MUSCLE
AB Calorie restriction decreases skeletal muscle apoptosis, and this phenomenon has been mechanistically linked to its protective action against sarcopenia of aging. Alterations in lipid composition of membranes have been related with the beneficial effects of calorie restriction. However, no study has been designed to date to elucidate if different dietary fat sources with calorie restriction modify apoptotic signaling in skeletal muscle. We show that a 6-month calorie restriction decreased the activity of the plasma membrane neutral sphingomyelinase, although caspase-8/10 activity was not altered, in young adult mice. Lipid hydroperoxides, Bax levels, and cytochrome c and AIF release/accumulation into the cytosol were also decreased, although caspase-9 activity was unchanged. No alterations in caspase-3 and apoptotic index (DNA fragmentation) were observed, but calorie restriction improved structural features of gastrocnemius fibers by increasing cross-sectional area and decreasing circularity of fibers in cross sections. Changing dietary fat with calorie restriction produced substantial alterations of apoptotic signaling. Fish oil augmented the protective effect of calorie restriction decreasing plasma membrane neutral sphingomyelinase, Bax levels, caspase-8/10, and -9 activities, while increasing levels of the antioxidant coenzyme Q at the plasma membrane, and potentiating the increase of cross-sectional area and the decrease of fiber circularity in cross sections. Many of these changes were not found when we used lard. Our data support that dietary fish oil with calorie restriction produces a cellular anti-apoptotic environment in skeletal muscle with a downregulation of components involved in the initial stages of apoptosis engagement, both at the plasma membrane and the mitochondria.
C1 [Alberto Lopez-Dominguez, Jose; Khraiwesh, Husam; Antonio Gonzalez-Reyes, Jose; Buron, Maria Isabel; Villalba, Jose M.] Univ Cordoba, Dept Biol Celular Fisiol & Inmunol, Cordoba 14014, Spain.
[Lopez-Lluch, Guillermo; Navas, Placido] Univ Pablo Olavide CSIC, CABD, Seville, Spain.
[Lopez-Lluch, Guillermo; Navas, Placido] CIBERER Inst Salud Carlos III, Seville, Spain.
[Ramsey, Jon Jay] Univ Calif Davis, VM Mol Biosci, Davis, CA 95616 USA.
[de Cabo, Rafael] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
RP Villalba, JM (reprint author), Univ Cordoba, Dept Biol Celular Fisiol & Inmunol, Campus Excelencia Agroalimentario CeiA3,Edificio, Cordoba 14014, Spain.
EM jmvillalba@uco.es
RI Gonzalez-Reyes, Jose A/K-1367-2014; Lopez-Lluch, Guillermo/N-4742-2014;
de Cabo, Rafael/J-5230-2016;
OI Gonzalez-Reyes, Jose A/0000-0003-1918-5490; Lopez-Lluch,
Guillermo/0000-0001-9830-8502; de Cabo, Rafael/0000-0002-3354-2442; ,
rafael/0000-0003-2830-5693
FU NIH [1R01AG028125-01A1]; Ministerio de Economia y Competitividad
[BFU2011-23578]; Junta de Andalucia Proyectos de Excelencia
[P09-CVI-4887]; Junta de Andalucia Proyectos Internacionales grant;
Junta de Andalucia [BIO-276]; University of Cordoba [BIO-276]; Spanish
Ministerio de Educacion; Agencia Espanola de Cooperacion Internacional
al Desarrollo
FX This work was supported by NIH grant 1R01AG028125-01A1 (to JJR, PN and
JMV), Ministerio de Economia y Competitividad BFU2011-23578 (to JMV),
Junta de Andalucia Proyectos de Excelencia grant P09-CVI-4887 (to JMV),
Junta de Andalucia Proyectos Internacionales grant (to JMV), and BIO-276
(Junta de Andalucia and the University of Cordoba, to JMV). JALD was
funded by a predoctoral fellowship of the Spanish Ministerio de
Educacion. HK was funded by a predoctoral fellowship of the Agencia
Espanola de Cooperacion Internacional al Desarrollo.
NR 60
TC 7
Z9 7
U1 0
U2 13
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0161-9152
EI 1574-4647
J9 AGE
JI Age
PD DEC
PY 2013
VL 35
IS 6
BP 2027
EP 2044
DI 10.1007/s11357-012-9492-9
PG 18
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 240MK
UT WOS:000326100600001
PM 23179253
ER
PT J
AU Pizzarelli, F
Maas, R
Dattolo, P
Tripepi, G
Michelassi, S
D'Arrigo, G
Mieth, M
Bandinelli, S
Ferrucci, L
Zoccali, C
AF Pizzarelli, Francesco
Maas, Renke
Dattolo, Pietro
Tripepi, Giovanni
Michelassi, Stefano
D'Arrigo, Graziella
Mieth, Maren
Bandinelli, Stefania
Ferrucci, Luigi
Zoccali, Carmine
TI Asymmetric dimethylarginine predicts survival in the elderly
SO AGE
LA English
DT Article
DE ADMA; Elderly; Cardiovascular risk factor; Survival; Population study
ID NITRIC-OXIDE SYNTHASE; CORONARY-HEART-DISEASE; L-ARGININE PARADOX;
CARDIOVASCULAR RISK; ENDOTHELIAL DYSFUNCTION; CELL SENESCENCE; ADMA;
HUMANS; MORTALITY; PLASMA
AB Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase implicated in several age-related biological mechanisms such as telomere shortening and cell senescence. We tested the hypothesis that ADMA blood level is an independent predictor of mortality in elderly. This is a longitudinal population-based cohort study. Participants are a representative cohort of 1,025 men and women (age range 65-102 years) living in Chianti area, Tuscany, Italy. The plasma ADMA was measured by liquid chromatography-tandem mass spectrometry. During the follow-up (95 +/- 32 months), 384 individuals died, of whom 141 (37 %) died of cardiovascular (CV) causes. In adjusted analyses, the plasma ADMA was the strongest predictor of all-cause mortality (HR (0.1 mu Mol/L) 1.26, 95 % CI 1.10-1.44, P < 0.001) with a non-significant trend for CV mortality (HR 1.22, P = 0.07). The predictive effect of the ADMA level on mortality was statistically significant among participants with low to low-normal l-arginine levels (a parts per thousand currency sign60 mu Mol/L), but not in those with l-arginine > 60 mu Mol/L. Notwithstanding the association of ADMA with all-cause mortality was robust, this biomarker failed to add predictive power to a simple model based on the risk factors in the elderly (area under the ROC curve 0.85 +/- 0.01 vs. 0.84 +/- 0.01). ADMA is a strong independent predictor of mortality in the older population, and l-arginine modifies the effect of ADMA on survival. The mechanisms for this association should be targeted by future studies.
C1 [Pizzarelli, Francesco; Dattolo, Pietro; Michelassi, Stefano] SM Annunziata Hosp, Nephrol Unit, I-50011 Florence, Italy.
[Maas, Renke; Mieth, Maren] Univ Erlangen Nurnberg, Inst Expt & Klin Pharmakol & Toxikol, D-91054 Erlangen, Germany.
[Tripepi, Giovanni; D'Arrigo, Graziella; Zoccali, Carmine] Osped Riuniti Reggio Calabria, CNR, IBIM, Reggio Di Calabria, Italy.
[Tripepi, Giovanni; D'Arrigo, Graziella; Zoccali, Carmine] Osped Riuniti Reggio Calabria, Nephrol Transplant Unit, Reggio Di Calabria, Italy.
[Bandinelli, Stefania] SM Annunziata Hosp, Geriatr Unit, I-50011 Florence, Italy.
[Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
RP Pizzarelli, F (reprint author), SM Annunziata Hosp, Nephrol Unit, Via Antella 58, I-50011 Florence, Italy.
EM fpizzarelli@yahoo.com; pierodattolo@tin.it
OI Zoccali, Carmine/0000-0002-6616-1996
NR 32
TC 14
Z9 14
U1 0
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0161-9152
EI 1574-4647
J9 AGE
JI Age
PD DEC
PY 2013
VL 35
IS 6
BP 2465
EP 2475
DI 10.1007/s11357-013-9523-1
PG 11
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 240MK
UT WOS:000326100600036
PM 23584888
ER
PT J
AU Liyanage, NPM
Dassanayake, RP
Kuszynski, CA
Duhamel, GE
AF Liyanage, Namal P. M.
Dassanayake, Rohana P.
Kuszynski, Charles A.
Duhamel, Gerald E.
TI Contribution of Helicobacter hepaticus Cytolethal Distending Toxin
Subunits to Human Epithelial Cell Cycle Arrest and Apoptotic Death in
vitro
SO HELICOBACTER
LA English
DT Article
DE apoptosis; CDT; cell cycle arrest; Helicobacter hepaticus
ID HUMAN T-CELLS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS;
HAEMOPHILUS-DUCREYI; ESCHERICHIA-COLI; CAMPYLOBACTER-JEJUNI; BACTERIAL
GENOTOXIN; B6C3F(1) MICE; G(2) ARREST; DNA-DAMAGE; ANNEXIN-V
AB BackgroundCytolethal distending toxin (CDT) is the only known virulence factor found in H.hepaticus, the cause of chronic typhlocolitis and hepatitis leading to colonic and hepatocellular carcinomas in mice. Interaction of the tripartite polypeptide CdtA, CdtB, and CdtC subunits produced by H.hepaticus CDT (HhepCDT) causes cell cycle arrest and apoptotic death of cultured cells; however, the contribution of individual subunit to these processes has not been investigated.
Materials and MethodsThe temporal relationship between cell cycle and apoptotic death of human epithelial HeLa and INT407 cells intoxicated with HhepCDT holotoxin or reconstituted recombinant HhepCDT was compared by flow cytometry. The genotoxic activity of individual and combinations of recombinant HhepCDT protein subunits or increasing concentrations of individual recombinant HhepCDT protein subunits transfected into HeLa cells was assessed at 72hours post-treatment by flow cytometry.
ResultsSimilar time course of HhepCDT-induced G(2)/M cell cycle arrest and apoptotic death was found with both cell lines which reached a maximum at 72hours. The presence of all three HhepCDT subunits was required for maximum cell cycle arrest and apoptosis of both cell lines. Transfection of HeLa cells with HhepCdtB, but not with HhepCdtA or HhepCdtC, resulted in a dose-dependent G(2)/M arrest and apoptotic death.
ConclusionAll three subunits of HhepCDT are required for maximum epithelial cell cycle arrest and progression to apoptotic death, and HhepCdtB subunit alone is necessary and sufficient for epithelial cell genotoxicity.
C1 [Liyanage, Namal P. M.; Dassanayake, Rohana P.; Duhamel, Gerald E.] Univ Nebraska, Sch Vet Med & Biomed Sci, Lincoln, NE USA.
[Kuszynski, Charles A.] Univ Nebraska Med Ctr, Coll Med, Dept Pathol & Microbiol, Omaha, NE USA.
[Liyanage, Namal P. M.] NCI, Vaccine Branch, Bethesda, MD 20892 USA.
[Dassanayake, Rohana P.] Washington State Univ, Dept Vet Microbiol & Pathol, Pullman, WA 99164 USA.
RP Duhamel, GE (reprint author), Cornell Univ, Dept Biomed Sci, Coll Vet Med, T4 012A Vet Res Tower, Ithaca, NY 14850 USA.
EM ged36@cornell.edu
FU NIH/NIAID [RO3 AI059532]
FX We thank ShiHong Gill in the School of Veterinary Medicine and
Biomedical Sciences at the University of Nebraska-Lincoln for her
excellent technical assistance with flow cytometry. This study was
funded in part by the NIH/NIAID grant RO3 AI059532 to GED.
NR 67
TC 6
Z9 7
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-4389
EI 1523-5378
J9 HELICOBACTER
JI Helicobacter
PD DEC
PY 2013
VL 18
IS 6
BP 433
EP 443
DI 10.1111/hel.12084
PG 11
WC Gastroenterology & Hepatology; Microbiology
SC Gastroenterology & Hepatology; Microbiology
GA 238YK
UT WOS:000325988100005
PM 23895367
ER
PT J
AU Zou, QH
Ross, TJ
Gu, H
Geng, XJ
Zuo, XN
Hong, LE
Gao, JH
Stein, EA
Zang, YF
Yang, YH
AF Zou, Qihong
Ross, Thomas J.
Gu, Hong
Geng, Xiujuan
Zuo, Xi-Nian
Hong, L. Elliot
Gao, Jia-Hong
Stein, Elliot A.
Zang, Yu-Feng
Yang, Yihong
TI Intrinsic Resting-State Activity Predicts Working Memory Brain
Activation and Behavioral Performance
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE resting-state fMRI; ALFF; N-back working memory; load dependency;
behavior
ID FUNCTIONAL CONNECTIVITY; VISUAL-CORTEX; INTERINDIVIDUAL DIFFERENCES;
PREFRONTAL CORTEX; MOTOR CORTEX; DEFAULT MODE; TASK; FMRI; MRI;
VARIABILITY
AB Although resting-state brain activity has been demonstrated to correspond with task-evoked brain activation, the relationship between intrinsic and evoked brain activity has not been fully characterized. For example, it is unclear whether intrinsic activity can also predict task-evoked deactivation and whether the rest-task relationship is dependent on task load. In this study, we addressed these issues on 40 healthy control subjects using resting-state and task-driven [N-back working memory (WM) task] functional magnetic resonance imaging data collected in the same session. Using amplitude of low-frequency fluctuation (ALFF) as an index of intrinsic resting-state activity, we found that ALFF in the middle frontal gyrus and inferior/superior parietal lobules was positively correlated with WM task-evoked activation, while ALFF in the medial prefrontal cortex, posterior cingulate cortex, superior frontal gyrus, superior temporal gyrus, and fusiform gyrus was negatively correlated with WM task-evoked deactivation. Further, the relationship between the intrinsic resting-state activity and task-evoked activation in lateral/superior frontal gyri, inferior/superior parietal lobules, superior temporal gyrus, and midline regions was stronger at higher WM task loads. In addition, both resting-state activity and the task-evoked activation in the superior parietal lobule/precuneus were significantly correlated with the WM task behavioral performance, explaining similar portions of intersubject performance variance. Together, these findings suggest that intrinsic resting-state activity facilitates or is permissive of specific brain circuit engagement to perform a cognitive task, and that resting activity can predict subsequent task-evoked brain responses and behavioral performance. Hum Brain Mapp 34:3204-3215, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Zou, Qihong; Ross, Thomas J.; Gu, Hong; Geng, Xiujuan; Stein, Elliot A.; Yang, Yihong] NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
[Zou, Qihong; Gao, Jia-Hong] Peking Univ, MRI Res Ctr, Beijing 100871, Peoples R China.
[Zou, Qihong; Gao, Jia-Hong] Peking Univ, Beijing City Key Lab Med Phys & Engn, Beijing 100871, Peoples R China.
[Zou, Qihong; Zang, Yu-Feng] Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
[Zuo, Xi-Nian] Chinese Acad Sci, Inst Psychol, Lab Funct Connectome & Dev, Key Lab Behav Sci, Beijing 100101, Peoples R China.
[Zuo, Xi-Nian] Chinese Acad Sci, Inst Psychol, Magnet Resonance Imaging Res Ctr, Beijing 100101, Peoples R China.
[Hong, L. Elliot] Univ Maryland, Sch Med, Dept Psychiat, Maryland Psychiat Res Ctr, Baltimore, MD 21201 USA.
[Gao, Jia-Hong] Univ Chicago, Brain Res Imaging Ctr, Chicago, IL 60637 USA.
[Zang, Yu-Feng] Hangzhou Normal Univ, Affiliated Hosp, Ctr Cognit & Brain Disorders, Hangzhou, Zhejiang, Peoples R China.
RP Yang, YH (reprint author), NIDA, Neuroimaging Res Branch, NIH, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM zangyf@gmail.com; yihongyang@intra.nida.nih.gov
RI ZANG, Yu-Feng/J-1558-2012;
OI ZANG, Yu-Feng/0000-0003-1833-8010; Ross, Thomas/0000-0002-7745-3572;
Zuo, Xi-Nian/0000-0001-9110-585X
FU Intramural Research Program of the National Institute on Drug Abuse
(NIDA); National Institutes of Health (NIH); Natural Science Foundation
of China [81020108022]; China's National Strategic Basic Research
Program (973) [2012CB720700]
FX Contract grant sponsors: Intramural Research Program of the National
Institute on Drug Abuse (NIDA) and National Institutes of Health (NIH);
Contract grant sponsor: Natural Science Foundation of China; Contract
grant number: 81020108022; Contract grant sponsor: China's National
Strategic Basic Research Program (973); Contract grant number:
2012CB720700.
NR 52
TC 56
Z9 58
U1 3
U2 28
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 DEC
PY 2013
VL 34
IS 12
BP 3204
EP 3215
DI 10.1002/hbm.22136
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 240BC
UT WOS:000326068700008
PM 22711376
ER
PT J
AU Montalvo, V
Quigley, L
Vistica, BP
Boelte, KC
Nugent, LF
Takai, T
McVicar, DW
Gery, I
AF Montalvo, Vanessa
Quigley, Laura
Vistica, Barbara P.
Boelte, Kimberly C.
Nugent, Lindsey F.
Takai, Toshiyuki
McVicar, Daniel W.
Gery, Igal
TI Environmental factors determine DAP12 deficiency to either enhance or
suppress immunopathogenic processes
SO IMMUNOLOGY
LA English
DT Article
DE cytokines; lymphoid cells; ocular inflammation; TREM-2
ID EXPERIMENTAL AUTOIMMUNE UVEITIS; MYELOID CELLS (TREM)-2; TOLL-LIKE
RECEPTOR; INFLAMMATORY RESPONSES; AMPLIFIES INFLAMMATION;
DAP12-DEFICIENT MICE; CUTTING EDGE; FCR-GAMMA; ACTIVATION; DISEASE
AB DNAX-activation protein 12 (DAP12), a transmembrane adapter, plays a major role in transducing activation signals in natural killer cells and various myeloid cells. Quantitative RT-PCR detected in normal mouse eyes considerable levels of DAP12 and multiple DAP12-coupled receptors, in particular TREM-1, Clec5a and SIRPb1. The role of DAP12 and its receptors in experimental autoimmune diseases has been controversial. Here, we analysed the effect of DAP12 deficiency on the capacity of mice to mount immunopathogenic cellular responses to the uveitogenic ocular antigen and interphotoreceptor retinoid-binding protein (IRBP), and to develop experimental autoimmune uveitis (EAU). Surprisingly, sequential analysis of EAU in mice deficient in DAP12 in two different animal facilities at first revealed enhanced disease as compared with wild-type mice, but when these mice were re-derived into a second, cleaner, animal facility, the response of control mice was essentially unchanged, whereas the DAP12 null mice were markedly hyporesponsive relative to controls in the new facility. Accordingly, when stimulated in vitro with IRBP, lymphocytes from the DAP12-deficient mice housed in the two facilities proliferated and produced opposite profiles of pro-inflammatory and anti-inflammatory cytokines, compared with their controls. These findings therefore demonstrate that the effects of DAP12 deficiency on development of autoimmune disease are dramatically affected by environmental factors.
C1 [Montalvo, Vanessa; Vistica, Barbara P.; Nugent, Lindsey F.; Gery, Igal] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Quigley, Laura; Boelte, Kimberly C.; McVicar, Daniel W.] NCI, Canc & Inflammat Program, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
[Takai, Toshiyuki] Tohoku Univ, Inst Dev Aging & Canc, Dept Expt Immunol, Sendai, Miyagi 980, Japan.
RP Gery, I (reprint author), NEI, NIH, Bldg 10,Room 10N208, Bethesda, MD 20892 USA.
EM geryi@nei.nih.gov
RI McVicar, Daniel/G-1970-2015
FU Intramural Research Programs of the National Eye Institute; Intramural
Research Program of the Center for Cancer Research of the National
Cancer Institute
FX This work was supported by the Intramural Research Programs of the
National Eye Institute and the Intramural Research Program of the Center
for Cancer Research of the National Cancer Institute. The authors are
grateful to Dr Wayne Yokoyama of Washington University, St Louis, for
the gift of DAP12-deficient mice on the C57BL/6 background. We thank Dr
Robert Fariss, Biological Imagining Core, NEI, for digitized microscopy
and Mehak K. Aziz and Osato Ogbeifun for superb professional help. V.M,
L.Q., B.P.V., K.C.B. and L.F.N. performed the experimental work and
contributed to the interpretation of data and preparation of the
manuscript. T.T. generated the DAP12-deficient mice. D.W.M. and I.G.
designed the experiments, contributed to data interpretation and wrote
the paper.
NR 37
TC 3
Z9 3
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2013
VL 140
IS 4
BP 475
EP 482
DI 10.1111/imm.12158
PG 8
WC Immunology
SC Immunology
GA 240GB
UT WOS:000326081900009
PM 23906311
ER
PT J
AU Lee, JH
Cheng, KT
Malinin, V
Li, ZL
Yao, ZS
Lee, SJ
Gould, CM
Olivier, KN
Chen, C
Perkins, WR
Paik, CH
AF Lee, Jae-Ho
Cheng, Kenneth T.
Malinin, Vladimir
Li, Zhili
Yao, Zhengsheng
Lee, Sung-Jin
Gould, Christine M.
Olivier, Kenneth N.
Chen, Clara
Perkins, Walter R.
Paik, Chang H.
TI Tc-99m-labeled therapeutic inhaled amikacin loaded liposomes
SO JOURNAL OF LIPOSOME RESEARCH
LA English
DT Article
DE Tc-99m-labeled liposome-encapsulated amikacin; radiolabeling; size
exclusion analysis
ID GEL EXCLUSION CHROMATOGRAPHY; CYSTIC-FIBROSIS PATIENTS;
PSEUDOMONAS-AERUGINOSA; GAMMA-SCINTIGRAPHY; LUNG DEPOSITION; IN-VITRO;
CLEARANCE; PERFORMANCE; VOLUNTEERS; TOBRAMYCIN
AB The radiolabeling of the liposome surface can be a useful tool for in vivo tracking of therapeutic drug loaded liposomes. We investigated radiolabeling therapeutic drug (i.e. an antibiotic, amikacin) loaded liposomes with Tc-99m, nebulization properties of Tc-99m-labeled liposomal amikacin for inhalation (Tc-99m-LAI), and its stability by size exclusion low-pressure liquid chromatography (LPLC). LAI was reacted with Tc-99m using SnCl2 dissolved in ascorbic acid as a reducing agent for 10 min at room temperature. The labeled products were then purified by anion exchange resin. The purified Tc-99m-LAI in 1.5% NaCl solution was incubated at 4 degrees C to assess its stability by LPLC. The purified Tc-99m-LAI was subjected to studies with a clinically used nebulizer (PARI eFlow (R)) and the Anderson Cascade Impactor (ACI). The use of ascorbic acid at 0.91 mM resulted in a quantitative labeling efficiency. The LPLC profile showed that the liposomal peak of LAI detected by a UV monitor at both 200 nm and 254 nm overlapped with the radioactivity peak of Tc-99m-LAI, indicating that Tc-99m-LAI is suitable for tracing LAI. The ACI study demonstrated that the aerosol droplet size distribution determined gravimetrically was similar to that determined by radioactivity. The liposome surface labeling method using SnCl2 in 0.91 mM ascorbic acid produced Tc-99m-LAI with a high labeling efficiency and stability that are adequate to evaluate the deposition and clearance of inhaled LAI in the lung by gamma scintigraphy.
C1 [Lee, Jae-Ho; Cheng, Kenneth T.; Yao, Zhengsheng; Lee, Sung-Jin; Chen, Clara; Paik, Chang H.] NIH, Radiopharmaceut Lab, Div Nucl Med, Dept Radiol & Imaging Sci,Warren G Magnuson Clin, Bethesda, MD 20892 USA.
[Malinin, Vladimir; Li, Zhili; Perkins, Walter R.] Insmed Inc, Monmouth Jct, NJ 08852 USA.
[Gould, Christine M.; Olivier, Kenneth N.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Lee, JH (reprint author), NIH, Radiopharmaceut Lab, Div Nucl Med, Dept Radiol & Imaging Sci,Warren G Magnuson Clin, Bldg 10, Bethesda, MD 20892 USA.
EM leejaeho@mail.nih.gov
FU National Institute of Allergy and Infectious Diseases; Clinical Center
of the NIH
FX This research was supported in part by the intramural research programs
of the National Institute of Allergy and Infectious Diseases and the
Clinical Center of the NIH.
NR 33
TC 4
Z9 4
U1 0
U2 13
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0898-2104
EI 1532-2394
J9 J LIPOSOME RES
JI J. Liposome Res.
PD DEC
PY 2013
VL 23
IS 4
BP 336
EP 342
DI 10.3109/08982104.2013.819889
PG 7
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 232VM
UT WOS:000325522500009
PM 23879241
ER
PT J
AU Koethe, Y
Widemann, BC
Hajjar, F
Wood, BJ
Venkatesan, AM
AF Koethe, Yilun
Widemann, Brigitte C.
Hajjar, Fouad
Wood, Bradford J.
Venkatesan, Aradhana M.
TI PET-Guided Biopsy With Needle Navigation Facilitates Diagnosis of
Angiosarcoma in Neurofibromatosis Type 1
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE FDG-PET; image guided biopsy; malignant peripheral neural sheath tumor;
neurofibromatosis type 1; plexiform neurofibroma
ID NERVE SHEATH TUMORS; TOMOGRAPHY FDG-PET
AB Malignant degeneration frequently arises from preexisting plexiform neurofibroma in patients with neurofibromatosis type 1 (NF1). Image guided biopsy for diagnostic purposes, such as with CT guidance, can be technically challenging in these patients, as CT cannot distinguish malignant from benign areas within the same tumor. Navigation with multi-modality (PET, CT, and ultrasound) image fusion facilitated the successful biopsy and diagnosis of angiosarcoma arising from a pelvic neurofibroma in a patient with NF1. Successful targeting assisted treatment selection in this case. This novel navigation technique may facilitate the otherwise difficult diagnosis of malignancy in patients with NF1. Pediatr Blood Cancer 2013;60:E166-E169. (c) 2013 Wiley Periodicals, Inc.
C1 [Koethe, Yilun; Wood, Bradford J.; Venkatesan, Aradhana M.] NIH, Ctr Intervent Oncol, Bethesda, MD 20892 USA.
[Koethe, Yilun; Wood, Bradford J.; Venkatesan, Aradhana M.] NIH, Bethesda, MD 20892 USA.
[Koethe, Yilun] Duke Univ, Sch Med, Durham, NC USA.
[Widemann, Brigitte C.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Hajjar, Fouad] Florida Hosp, Childrens Ctr Canc & Blood Dis, Orlando, FL USA.
RP Venkatesan, AM (reprint author), NIH, Ctr Intervent Oncol Radiol & Imaging Sci, 10 Ctr Dr,Bldg 10 CRC,Room 1C369,MSC 1182, Bethesda, MD 20892 USA.
EM venkatesana@cc.nih.gov
FU Intramural Research program of the NIH; NIH Clinical Center; National
Cancer Institute
FX This research was supported in part by the Intramural Research program
of the NIH, by the NIH Clinical Center and by the National Cancer
Institute.
NR 9
TC 2
Z9 2
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2013
VL 60
IS 12
BP E166
EP E169
DI 10.1002/pbc.24668
PG 4
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 232HX
UT WOS:000325484900005
PM 23922330
ER
PT J
AU Ghirlando, R
Felsenfeld, G
AF Ghirlando, Rodolfo
Felsenfeld, Gary
TI Physical Chemistry of Nucleic Acids and Their Complexes
SO BIOPOLYMERS
LA English
DT Review
DE DNA; chromatin; polynucleotide structures
ID RICH HISTONE KERNEL; CHROMATIN-STRUCTURE; NEUTRAL PH; TRANSCRIBING
POLYMERASE; POLYRIBOADENYLIC ACID; NUCLEOSOME STRUCTURE; RNA-POLYMERASE;
TRANSCRIPTION; DNA; CONFORMATION
AB Studies of the physical properties of nucleic acids began almost immediately following the discovery of the DNA structure. Early investigations focused on the stability and specificity of multi-strand polynucleotide complexes, then gradually on their interaction with other molecules, particularly proteins. As molecular and structural biology expanded to provide detailed information about biochemical mechanisms, physical studies eventually acquired the additional constraint that they should be relevant to functioning biological systems. We describe work in our laboratory that began with investigations of relatively simple questions about the role of electrostatic interactions in the stabilization of multi-strand nucleic acid structures, and evolved to studies of chromatin structure in vitro and within the nucleus. Published 2013 Wiley Periodicals, Inc*. Biopolymers 99: 910-915, 2013.
C1 [Ghirlando, Rodolfo; Felsenfeld, Gary] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Felsenfeld, G (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM gary.felsenfeld@nih.gov
FU National Institutes of Health, National Institute of Diabetes, Digestive
and Kidney Diseases
FX Contract grant sponsor: Intramural Research Program, National Institutes
of Health, National Institute of Diabetes, Digestive and Kidney Diseases
NR 46
TC 3
Z9 3
U1 2
U2 37
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-3525
J9 BIOPOLYMERS
JI Biopolymers
PD DEC
PY 2013
VL 99
IS 12
SI SI
BP 910
EP 915
DI 10.1002/bip.22311
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 227DS
UT WOS:000325089800002
PM 23765314
ER
PT J
AU Lynch, SM
Major, JM
Cawthon, R
Weinstein, SJ
Virtamo, J
Lan, Q
Rothman, N
Albanes, D
Stolzenberg-Solomon, RZ
AF Lynch, Shannon M.
Major, Jacqueline M.
Cawthon, Richard
Weinstein, Stephanie J.
Virtamo, Jarmo
Lan, Qing
Rothman, Nathaniel
Albanes, Demetrius
Stolzenberg-Solomon, Rachael Z.
TI A prospective analysis of telomere length and pancreatic cancer in the
alpha-tocopherol beta-carotene cancer (ATBC) prevention study
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE pancreatic cancer; telomere length; biomarker; epidemiology
ID COHORT-CONSORTIUM PANSCAN; MULTIPLEX QUANTITATIVE PCR; BODY-MASS INDEX;
POOLED-ANALYSIS; INTRAEPITHELIAL NEOPLASIA; CIGARETTE-SMOKING; ALCOHOL
INTAKE; MALE SMOKERS; RISK; CELLS
AB Smoking and diabetes, consistent risk factors for pancreatic cancer, are also factors that influence telomere length maintenance. To test whether telomere length is associated with pancreatic cancer risk, we conducted a nested case-control study in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort of male smokers, aged 50-69 years at baseline. Between 1992 and 2004, 193 incident cases of pancreatic adenocarcinoma occurred (mean follow-up from blood draw: 6.3 years) among participants with whole blood samples available for telomere length assays. For these cases and 660 controls, we calculated odds ratios (OR) and 95% confidence intervals using unconditional logistic regression, adjusting for age, number of years smoked regularly, and history of diabetes mellitus. Telomere length was categorized into quartiles (shortest to longest) and analyzed as both a categorical and a continuous normal variable (reported per 0.2 unit increase in telomere length). All statistical tests were two-sided. Longer telomere length was significantly associated with increased pancreatic cancer risk (continuous OR = 1.26 95% CI = 1.09-1.46; highest quartile compared to lowest, OR = 1.57, 95% CI = 1.01-2.43, p-trend = 0.007). This association remained for subjects diagnosed within the first five years of blood draw (continuous OR = 1.46, 95% CI = 1.19-1.79 highest quartile OR = 2.92, 95% CI = 1.47-5.77, p-trend = 0.002), but not those diagnosed greater than five years after blood draw (continuous OR = 1.03, 95% CI = 0.85-1.22; highest quartile OR = 1.04, 95% CI = 0.60-1.79). This is the first prospective study to suggest an association between longer blood leukocyte telomere length and increased pancreatic cancer risk.
What's new? This is the first prospective study to examine the association between blood leukocyte telomere length and pancreatic cancer. In tumor, longer telomeres have been observed in advanced pancreatic cancer and risk factors for pancreatic cancer (cigarette smoke and diabetes) are known to affect telomere length. Based on a nested case-control study in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort of male smokers, here the authors found that longer blood leukocyte telomeres were significantly associated with increased pancreatic cancer risk. The results add insight into the role of telomeres in pancreatic cancer, a disease that can benefit from the identification of early detection markers.
C1 [Lynch, Shannon M.; Major, Jacqueline M.; Weinstein, Stephanie J.; Albanes, Demetrius; Stolzenberg-Solomon, Rachael Z.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lynch, Shannon M.] Univ Penn, Ctr Clin Epidemiol & Biostat, Ctr Genet & Complex Traits, Philadelphia, PA 19104 USA.
[Cawthon, Richard] Univ Utah, Dept Human Genet, Salt Lake City, UT USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Lan, Qing; Rothman, Nathaniel] NCI, Ocupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Lynch, SM (reprint author), Univ Penn, Ctr Clin Epidemiol & Biostat, Ctr Genet & Complex Traits, Philadelphia, PA 19104 USA.
EM lynchsh@mail.med.upenn.edu
RI Albanes, Demetrius/B-9749-2015
NR 54
TC 22
Z9 22
U1 1
U2 38
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 1
PY 2013
VL 133
IS 11
BP 2672
EP 2680
DI 10.1002/ijc.28272
PG 9
WC Oncology
SC Oncology
GA 227DA
UT WOS:000325087600017
PM 23674344
ER
PT J
AU Rosenberg, AS
Roivainen, M
Hovi, T
Liu, Q
Murphy, PM
AF Rosenberg, A. S.
Roivainen, M.
Hovi, T.
Liu, Q.
Murphy, P. M.
TI CCR5 Deficiency and Severe Polio Infection in the 1984 Outbreak in
Finland
SO JOURNAL OF MEDICAL VIROLOGY
LA English
DT Article
DE poliovirus; CCR5delta32; neuropathology
ID NILE-VIRUS-INFECTION; CHEMOKINE RECEPTORS; POLIOMYELITIS
AB CCR5, a leukocyte chemoattractant receptor for chemokines CCL3, CCL4, and CCL5, promotes innate and adaptive immune responses by mediating leukocyte trafficking within lymph nodes and to peripheral tissues and is also known as a co-receptor for HIV cell entry. Homozygous inheritance of a complete loss-of-function mutation in CCR5 (CCR532/CCR532) is associated with symptomatic neuroinflammatory disease in humans with West Nile and Tickborne Encephalitis flavivirus infections. This study sought to establish whether CCR5 deficiency could also be a determinant of clinical outcome after infection by poliovirus which results in central nervous system damage in only a small proportion of cases. We analyzed serum samples from seven patients and 79 controls, collected during the 1984-1985 polio outbreak in Finland, where CCR532 is relatively common in the general population. The results excluded CCR5 deficiency as the sole determinant of severe neurologic disease after poliovirus infection in this population. J. Med. Virol. 85:2139-2140, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Rosenberg, A. S.] US FDA, Div Therapeut Prot, Off Biotechnol Prod, CDER, Silver Spring, MD USA.
[Roivainen, M.; Hovi, T.] Natl Inst Hlth & Welf THL, Dept Infect Dis Surveillance & Control, Virol Unit, Helsinki, Finland.
[Liu, Q.; Murphy, P. M.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Rosenberg, AS (reprint author), US FDA, Div Therapeut Prot, Off Biotechnol Prod, CDER, Silver Spring, MD USA.
EM amy.rosenberg@fda.hhs.gov
NR 10
TC 0
Z9 0
U1 0
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0146-6615
J9 J MED VIROL
JI J. Med. Virol.
PD DEC
PY 2013
VL 85
IS 12
BP 2139
EP 2140
DI 10.1002/jmv.23739
PG 2
WC Virology
SC Virology
GA 227ZE
UT WOS:000325153400012
PM 24037958
ER
PT J
AU Shen, XP
Liu, YX
Zhang, EZ
Bhamidipati, P
AF Shen, Xipeng
Liu, Yixun
Zhang, Eddy Z.
Bhamidipati, Poornima
TI An Infrastructure for Tackling Input-Sensitivity of GPU Program
Optimizations
SO INTERNATIONAL JOURNAL OF PARALLEL PROGRAMMING
LA English
DT Article
DE GPU; Program Optimizations; Empirical Search; CUDA; G-ADAPT; Cross-input
Adaptation
ID GENERATION; FEEDBACK
AB Graphic processing units (GPU) have become increasingly adopted for the enhancement of computing throughput. However, the development of a high-quality GPU application is challenging, due to the large optimization space and complex unpredictable effects of optimizations on GPU program performance. Many recent efforts have been employing empirical search-based auto-tuners to tackle the problem, but few of them have concentrated on the influence of program inputs on the optimizations. In this paper, based on a set of CUDA and OpenCL kernels, we report some evidences on the importance for auto-tuners to adapt to program input changes, and present a framework, G-ADAPT+, to address the influence by constructing cross-input predictive models for automatically predicting the (near-)optimal configurations for an arbitrary input to a GPU program. G-ADAPT+ is based on source-to-source compilers, specifically, Cetus and ROSE. It supports the optimizations of both CUDA and OpenCL programs.
C1 [Shen, Xipeng] Coll William & Mary, Dept Comp Sci, Williamsburg, VA 23185 USA.
[Liu, Yixun] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Zhang, Eddy Z.] Rutgers State Univ, Dept Comp Sci, New Brunswick, NJ 08901 USA.
[Bhamidipati, Poornima] Capital One, Williamsburg, VA 23185 USA.
RP Shen, XP (reprint author), Coll William & Mary, Dept Comp Sci, Williamsburg, VA 23185 USA.
EM xshen@cs.wm.edu; yixun.liu@nih.gov; eddy.zhengzhang@cs.rutgers.edu;
poornimabhamidipati@gmail.com
FU National Science Foundation [0720499, 0811791, CAREER 0954015];
Department of Energy
FX This material is based upon work supported by the National Science
Foundation under Grant No. 0720499 and 0811791 and CAREER 0954015, along
with the Early Career Grant from the Department of Energy. Any opinions,
findings, and conclusions or recommendations expressed in this material
are those of the authors and do not necessarily reflect the views of the
National Science Foundation or the Department of Energy.
NR 31
TC 2
Z9 2
U1 0
U2 13
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0885-7458
J9 INT J PARALLEL PROG
JI Int. J. Parallel Program.
PD DEC
PY 2013
VL 41
IS 6
SI SI
BP 855
EP 869
DI 10.1007/s10766-012-0236-3
PG 15
WC Computer Science, Theory & Methods
SC Computer Science
GA 195TK
UT WOS:000322726300007
ER
PT J
AU Frierson, GM
Howard, EN
DeFina, LF
Powell-Wiley, TM
Willis, BL
AF Frierson, Georita M.
Howard, Erica N.
DeFina, Laura F.
Powell-Wiley, Tiffany M.
Willis, Benjamin L.
TI EFFECT OF RACE AND SOCIOECONOMIC STATUS ON CARDIOVASCULAR RISK FACTOR
BURDEN: THE COOPER CENTER LONGITUDINAL STUDY
SO ETHNICITY & DISEASE
LA English
DT Article
DE Socioeconomic Status; Racial/ethnic Minorities; Preventive Medicine;
Cardiovascular Risk Factors
ID ALL-CAUSE MORTALITY; RACIAL DISPARITIES; AFRICAN-AMERICANS;
PHYSICAL-FITNESS; CARDIORESPIRATORY FITNESS; INCOME INEQUALITY; HEALTH;
MEN; PREVALENCE; STRESS
AB Objectives: This study examines the prevalence of cardiovascular risk factors and chronic disease burden among African Americans compared to Caucasians in a population of higher socioeconomic status.
Design: The current study is a cross-sectional, secondary data analysis of the Cooper Center Longitudinal Study.
Setting: Patients with a medical examination from 1970-2010 at the Cooper Clinic.
Participants: 762 African Americans and 40,051 Caucasians who met the criteria.
Outcome Measures: Racial differences in cardiovascular risk factors/burden of disease between African Americans and Caucasians.
Results: African Americans had higher prevalence of evaluated cardiovascular risk factors than did Caucasians after controlling for obesity, tobacco use, and physical fitness. Caucasians had greater likelihood of no risk factors while African Americans were more likely to have all three risk factors. Race was typically predictive of cardiovascular risk factors in African Americans compared to Caucasians.
Conclusions: Findings suggest that health differences persist despite greater socioeconomic status, and further investigations of biopsychosocial causes are warranted. (Ethn Dis. 2013;23[1]:35-42)
C1 [Frierson, Georita M.] Howard Univ, Dept Psychol, Washington, DC 20059 USA.
[Howard, Erica N.; DeFina, Laura F.; Willis, Benjamin L.] Cooper Inst, Dallas, TX USA.
[Powell-Wiley, Tiffany M.] NHLBI, Cardiovasc Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Frierson, GM (reprint author), Howard Univ, Dept Psychol, CB Powell Bldg, Washington, DC 20059 USA.
EM georitafrierson@gmail.com
FU Intramural NIH HHS [Z99 HL999999]
NR 58
TC 5
Z9 5
U1 1
U2 249
PU INT SOC HYPERTENSION BLACKS-ISHIB
PI ATLANTA
PA 100 AUBURN AVE NE STE 401, ATLANTA, GA 30303-2527 USA
SN 1049-510X
J9 ETHNIC DIS
JI Ethn. Dis.
PD WIN
PY 2013
VL 23
IS 1
BP 35
EP 42
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 069VH
UT WOS:000313464700007
PM 23495620
ER
PT J
AU Holland, RJ
Paulisch, R
Cao, Z
Keefer, LK
Saavedra, JE
Donzelli, S
AF Holland, Ryan J.
Paulisch, Rika
Cao, Zhao
Keefer, Larry K.
Saavedra, Joseph E.
Donzelli, Sonia
TI Enzymatic generation of the NO/HNO-releasing IPA/NO anion at controlled
rates in physiological media using beta-galactosidase
SO NITRIC OXIDE-BIOLOGY AND CHEMISTRY
LA English
DT Article
DE IPA/NO; Prodrug; Nitroxyl; Diazeniumdiolate; Gal-IPA/NO;
beta-Galactosidase
ID NITROXYL HNO DONORS; NITRIC-OXIDE; DIAZENIUMDIOLATE; CHEMISTRY; NO;
PRODRUGS
AB We introduce a strategy for generating mixtures of nitric oxide (NO) and nitroxyl (HNO) at tunable rates in physiological media. The approach involves converting a spontaneously HNO/NO-generating ion to a caged (prodrug) form that is essentially stable in neutral media, but that can be activated for HNO/NO release by adding an enzyme capable of efficiently opening the cage to regenerate the ion. By judiciously choosing the enzyme, substrate, and reaction conditions, unwanted scavenging of the HNO and NO by the protein can be minimised and the catalytic efficiency of the enzyme can be maintained. We illustrate this approach with a proof-of-concept study wherein the prodrug is Gal-IPA/NO, a diazeniumdiolate of structure iPrHN-N(O)=NOR, with R = beta-D-galactosyl. Escherichia coli-derived beta-D-galactosidase at concentrations of 1.9-15 nM hydrolysed 56 mu M substrate with half-lives of 140-19 mm, respectively, producing the IPA/NO anion (iPrHN-N(O)=NO-, half-life similar to 3 mm), which in turn spontaneously hydrolysed to mixtures of HNO with NO. Using saturating substrate concentrations furnished IPA/NO generation rates that were directly proportional to enzyme concentration. Consistent with these data, the enzyme/substrate combination applied to ventricular myocytes isolated from wild-type mouse hearts resulted not only in a significant positive inotropic effect, but also rescued the cells from the negative inotropy, hypercontractions, and occasional cell death seen with the enzyme alone. This mechanism represents an alternate approach for achieving controlled fluxes of NO/HNO to investigate their biological actions. (C) 2013 Published by Elsevier Inc.
C1 [Holland, Ryan J.; Keefer, Larry K.] NCI, Biol Chem Lab, Drug Design Sect, Frederick, MD 21702 USA.
[Paulisch, Rika; Donzelli, Sonia] Univ Med Ctr Hamburg Eppendorf, Dept Expt Pharmacol & Toxicol, D-20246 Hamburg, Germany.
[Cao, Zhao; Saavedra, Joseph E.] Frederick Natl Lab Canc Res, SAIC Frederick, Basic Res Program, Ft Detrick, MD 21702 USA.
RP Holland, RJ (reprint author), NCI, Biol Chem Lab, Drug Design Sect, Frederick, MD 21702 USA.
EM hollandrj@mail.nih.gov
RI Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research; National Cancer Institute [HHSN261200800001E]
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 with Federal funds from the National Cancer
Institute under Contract HHSN261200800001E to SAIC. We thank Dr. Sergey
Tarasov and Ms. Marzena A. Dyba of the Biophysics Resource in the
Structural Biophysics Laboratory, NCI-Frederick, for assistance with the
high resolution mass spectrometry studies. We gratefully acknowledge Mr.
John Klose for assistance with the NMR experiments.
NR 28
TC 3
Z9 3
U1 3
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1089-8603
EI 1089-8611
J9 NITRIC OXIDE-BIOL CH
JI Nitric Oxide-Biol. Chem.
PD NOV 30
PY 2013
VL 35
BP 131
EP 136
DI 10.1016/j.niox.2013.10.003
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 270IP
UT WOS:000328312400017
PM 24126017
ER
PT J
AU Salunke, S
Brandys, B
Giacoia, G
Tuleu, C
AF Salunke, Smita
Brandys, Barbara
Giacoia, George
Tuleu, Catherine
TI The STEP (Safety and Toxicity of Excipients for Paediatrics) database:
Part 2-The pilot version
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Article
DE Excipients; Children; Database; Toxicity; Adverse effects; Chemicals
ID PROPYLENE-GLYCOL; EXPOSURE; MEDICINES
AB The screening and careful selection of excipients is a critical step in paediatric formulation development as certain excipients acceptable in adult formulations, may not be appropriate for paediatric use. While there is extensive toxicity data that could help in better understanding and highlighting the gaps in toxicity studies, the data are often scattered around the information sources and saddled with incompatible data types and formats.
This paper is the second in a series that presents the update on the Safety and Toxicity of Excipients for Paediatrics ("STEP") database being developed by Eu-US PFIs, and describes the architecture data fields and functions of the database. The STEP database is a user designed resource that compiles the safety and toxicity data of excipients that is scattered over various sources and presents it in one freely accessible source. Currently, in the pilot database data from over 2000 references/10 excipients presenting preclinical, clinical, regulatory information and toxicological reviews, with references and source links. The STEP database allows searching "FOR" excipients and "BY" excipients. This dual nature of the STEP database, in which toxicity and safety information can be searched in both directions, makes it unique from existing sources. If the pilot is successful, the aim is to increase the number of excipients in the existing database so that a database large enough to be of practical research use will be available. It is anticipated that this source will prove to be a useful platform for data management and data exchange of excipient safety information. (C) 2013 Elsevier B. V. All rights reserved.
C1 [Salunke, Smita; Tuleu, Catherine] UCL Sch Pharm, Dept Pharmaceut, London WC1N 1AX, England.
[Salunke, Smita; Tuleu, Catherine] UCL Sch Pharm, Ctr Paediat Pharm Res, London WC1N 1AX, England.
[Brandys, Barbara] NIH, Natl Inst Hlth NIH Lib, Div Lib Serv, Off Res Serv, Bethesda, MD 20892 USA.
[Giacoia, George] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, OPPB, NIH, Bethesda, MD USA.
RP Salunke, S (reprint author), UCL Sch Pharm, Dept Pharmaceut, 29-39 Brunswick Sq, London WC1N 1AX, England.
EM S.Salunke@ucl.ac.uk
OI tuleu, catherine/0000-0001-8384-357X
FU European Union [261060]
FX The research leading to these results has received funding from the
European Union Seventh Framework Programme FP7/2007-2013 under grant
agreement no. 261060.
NR 27
TC 19
Z9 20
U1 1
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD NOV 30
PY 2013
VL 457
IS 1
BP 310
EP 322
DI 10.1016/j.ijpharm.2013.09.013
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 248FU
UT WOS:000326681800033
PM 24070789
ER
PT J
AU Chen, BJ
Qin, J
AF Chen, Baojiang
Qin, Jing
TI A new estimation with minimum trace of asymptotic covariance matrix for
incomplete longitudinal data with a surrogate process
SO STATISTICS IN MEDICINE
LA English
DT Article
DE longitudinal data; missing data; optimal; surrogate outcome
ID DOUBLY ROBUST ESTIMATION; MISSING DATA; END-POINTS; REGRESSION-MODELS;
INFERENCE; IMPUTATION; TRIALS
AB Missing data is a very common problem in medical and social studies, especially when data are collected longitudinally. It is a challenging problem to utilize observed data effectively. Many papers on missing data problems can be found in statistical literature. It is well known that the inverse weighted estimation is neither efficient nor robust. On the other hand, the doubly robust (DR) method can improve the efficiency and robustness. As is known, the DR estimation requires a missing data model (i.e., a model for the probability that data are observed) and a working regression model (i.e., a model for the outcome variable given covariates and surrogate variables). Because the DR estimating function has mean zero for any parameters in the working regression model when the missing data model is correctly specified, in this paper, we derive a formula for the estimator of the parameters of the working regression model that yields the optimally efficient estimator of the marginal mean model (the parameters of interest) when the missing data model is correctly specified. Furthermore, the proposed method also inherits the DR property. Simulation studies demonstrate the greater efficiency of the proposed method compared with the standard DR method. A longitudinal dementia data set is used for illustration. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Chen, Baojiang] Univ Nebraska Med Ctr, Dept Biostat, Omaha, NE 68198 USA.
[Qin, Jing] NIAID, NIH, Bethesda, MD 20892 USA.
RP Chen, BJ (reprint author), Univ Nebraska Med Ctr, Dept Biostat, Omaha, NE 68198 USA.
EM baojiang.chen@unmc.edu
FU National Institute on Aging [U01AG016976]
FX Dr. Chen were supported in part by the National Institute on Aging grant
U01AG016976. This paper presents the findings and conclusions of the
authors.
NR 28
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD NOV 30
PY 2013
VL 32
IS 27
BP 4763
EP 4780
DI 10.1002/sim.5875
PG 18
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 238QT
UT WOS:000325963300006
PM 23744541
ER
PT J
AU Hu, JX
Hu, K
Liu, T
Stern, MK
Mistry, R
Challiss, RAJ
Costanzi, S
Wess, J
AF Hu, Jianxin
Hu, Kelly
Liu, Tong
Stern, Matthew K.
Mistry, Rajendra
Challiss, R. A. John
Costanzi, Stefano
Wess, Juergen
TI Novel Structural and Functional Insights into M-3 Muscarinic Receptor
Dimer/Oligomer Formation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Cholinergic Receptor; G Protein-coupled Receptors (GPCR);
Neurotransmitter Receptors; Receptor Structure-function; Site-directed
Mutagenesis
ID PROTEIN-COUPLED RECEPTOR; CRYSTAL-STRUCTURE; ACETYLCHOLINE-RECEPTORS;
OPIOID RECEPTOR; NATIVE MEMBRANES; MOLECULAR-BASIS; DRUG DISCOVERY;
RHODOPSIN; ACTIVATION; TRANSDUCIN
AB Background: G protein-coupled receptors (GPCRs) exist in dimeric/oligomeric arrays but the structural basis underling this phenomenon is not well understood. Results: The M-3 muscarinic receptor, a prototypic GPCR, can form multiple, structurally distinct dimeric species. Conclusion: GPCRs may exist in a dynamic equilibrium of multiple dimers or oligomers. Significance: Our findings may facilitate efforts to target GPCR dimers for therapeutic purposes.
Class A G protein-coupled receptors (GPCRs) are able to form homodimers and/or oligomeric arrays. We recently proposed, based on bioluminescence resonance energy transfer studies with the M-3 muscarinic receptor (M3R), a prototypic class A GPCR, that the M3R is able to form multiple, structurally distinct dimers that are probably transient in nature (McMillin, S. M., Heusel, M., Liu, T., Costanzi, S., and Wess, J. (2011) J. Biol. Chem. 286, 28584-28598). To provide more direct experimental support for this concept, we employed a disulfide cross-linking strategy to trap various M3R dimeric species present in a native lipid environment (transfected COS-7 cells). Disulfide cross-linking studies were carried out with many mutant M3Rs containing single cysteine (Cys) substitutions within two distinct cytoplasmic M3R regions, the C-terminal portion of the second intracellular loop (i2) and helix H8 (H8). The pattern of cross-links that we obtained, in combination with molecular modeling studies, was consistent with the existence of two structurally distinct M3R dimer interfaces, one involving i2/i2 contacts (TM4-TM5-i2 interface) and the other one characterized by H8-H8 interactions (TM1-TM2-H8 interface). Specific H8-H8 disulfide cross-links led to significant impairments in M3R-mediated G protein activation, suggesting that changes in the structural orientation or mobility of H8 are critical for efficient receptor-G protein coupling. Our findings provide novel structural and functional insights into the mechanisms involved in M3R dimerization (oligomerization). Because the M3R shows a high degree of sequence similarity with many other class A GPCRs, our findings should be of considerable general interest.
C1 [Hu, Jianxin; Hu, Kelly; Liu, Tong; Stern, Matthew K.; Wess, Juergen] NIDDK, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Mistry, Rajendra; Challiss, R. A. John] Univ Leicester, Dept Cell Physiol & Pharmacol, Leicester LE1 9HN, Leics, England.
[Costanzi, Stefano] Amer Univ, Dept Chem, Washington, DC 20016 USA.
[Costanzi, Stefano] Amer Univ, Ctr Behav Neurosci, Washington, DC 20016 USA.
RP Wess, J (reprint author), Bldg 8A,Rm B1A-05,8 Ctr Dr MSC 0810, Bethesda, MD 20892 USA.
EM jwess@helix.nih.gov
OI Costanzi, Stefano/0000-0003-3183-7332; Challiss,
John/0000-0001-5506-2848
FU National Institutes of Health, NIDDK; American University
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, NIDDK, and the American University.
NR 51
TC 12
Z9 12
U1 3
U2 12
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 29
PY 2013
VL 288
IS 48
BP 34777
EP 34790
DI 10.1074/jbc.M113.503714
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 291FH
UT WOS:000329812800046
PM 24133207
ER
PT J
AU Belugin, S
Diogenes, AR
Patil, MJ
Ginsburg, E
Henry, MA
Akopian, AN
AF Belugin, Sergei
Diogenes, Anibal R.
Patil, Mayur J.
Ginsburg, Erika
Henry, Michael A.
Akopian, Armen N.
TI Mechanisms of Transient Signaling via Short and Long Prolactin Receptor
Isoforms in Female and Male Sensory Neurons
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE Neuroendocrinology; Pain; PI3-kinase (PI3K); Prolactin; Protein Kinase C
(PKC)
ID PROTEIN-KINASE-C; DELTA-OPIOID-RECEPTOR; MESSENGER-RNA;
PHOSPHATIDYLINOSITOL 3-KINASE; INFLAMMATORY HYPERALGESIA; TRIGEMINAL
NOCICEPTORS; FUNCTIONAL COMPETENCE; INHIBITORY-ACTION; TRP CHANNELS;
SHORT-FORM
AB Background: Prolactin regulates the activity of nociceptors in pain conditions. Results: Prolactin regulation of sensory neurons is acute and mediated via PI3K and PKCE following activation of prolactin receptor short isoform. Prolactin receptor short isoform actions are inhibited by the long isoform. Conclusion: Prolactin receptor short isoform mediates transient sensitization of nociceptors. Significance: The proposed mechanism could underlie prolactin involvement in hyperalgesia/pain.
Prolactin (PRL) regulates activity of nociceptors and causes hyperalgesia in pain conditions. PRL enhances nociceptive responses by rapidly modulating channels in nociceptors. The molecular mechanisms underlying PRL-induced transient signaling in neurons are not well understood. Here we use a variety of cell biology and pharmacological approaches to show that PRL transiently enhanced capsaicin-evoked responses involve protein kinase C E (PKCE) or phosphatidylinositol 3-kinase (PI3K) pathways in female rat trigeminal (TG) neurons. We next reconstituted PRL-induced signaling in a heterologous expression system and TG neurons from PRL receptor (PRLR)-null mutant mice by expressing rat PRLR-long isoform (PRLR-L), PRLR-short isoform (PRLR-S), or a mix of both. Results show that PRLR-S, but not PRLR-L, is capable of mediating PRL-induced transient enhancement of capsaicin responses in both male and female TG neurons. However, co-expression of PRLR-L with PRLR-S (1:1 ratio) leads to the inhibition of the transient PRL actions. Co-expression of PRLR-L deletion mutants with PRLR-S indicated that the cytoplasmic site adjacent to the trans-membrane domain of PRLR-L was responsible for inhibitory effects of PRLR-L. Furthermore, in situ hybridization and immunohistochemistry data indicate that in normal conditions, PRLR-L is expressed mainly in glia with little expression in rat sensory neurons (3-5%) and human nerves. The predominant PRLR form in TG neurons/nerves from rats and humans is PRLR-S. Altogether, PRL-induced transient signaling in sensory neurons is governed by PI3K or PKCE, mediated via the PRLR-S isoform, and transient effects mediated by PRLR-S are inhibited by presence of PRLR-L in these cells.
C1 [Belugin, Sergei; Diogenes, Anibal R.; Henry, Michael A.; Akopian, Armen N.] Univ Texas Hlth Sci Ctr San Antonio, Dept Endodont, San Antonio, TX 78229 USA.
[Patil, Mayur J.; Akopian, Armen N.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
[Ginsburg, Erika] NCI, NIH, Bethesda, MD 20892 USA.
RP Akopian, AN (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Endodont, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM akopian@uthscsa.edu
OI Belugin, Sergei/0000-0001-9006-7732
FU National Institutes of Health [DE017696]; Intramural Research Program of
the NCI/National Institutes of Health
FX This work was supported, in whole or in part, by National Institutes of
Health Grant DE017696 (to A.N.A.) and by the Intramural Research Program
of the NCI/National Institutes of Health (to E.G.).
NR 63
TC 5
Z9 5
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 29
PY 2013
VL 288
IS 48
BP 34943
EP 34955
DI 10.1074/jbc.M113.486571
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 291FH
UT WOS:000329812800060
PM 24142695
ER
PT J
AU Falivelli, G
Lisabeth, EM
de la Torre, ER
Perez-Tenorio, G
Tosato, G
Salvucci, O
Pasquale, EB
AF Falivelli, Giulia
Lisabeth, Erika Mathes
de la Torre, Elena Rubio
Perez-Tenorio, Gizeh
Tosato, Giovanna
Salvucci, Ombretta
Pasquale, Elena B.
TI Attenuation of Eph Receptor Kinase Activation in Cancer Cells by
Coexpressed Ephrin Ligands
SO PLOS ONE
LA English
DT Article
ID TYROSINE KINASE; LUNG-CANCER; THERAPEUTIC TARGET; A LIGANDS; CIS;
SUPPRESSES; EXPRESSION; MUTATIONS; PATHWAY; GROWTH
AB The Eph receptor tyrosine kinases mediate juxtacrine signals by interacting "in trans" with ligands anchored to the surface of neighboring cells via a GPI-anchor (ephrin-As) or a transmembrane segment (ephrin-Bs), which leads to receptor clustering and increased kinase activity. Additionally, soluble forms of the ephrin-A ligands released from the cell surface by matrix metalloproteases can also activate EphA receptor signaling. Besides these trans interactions, recent studies have revealed that Eph receptors and ephrins coexpressed in neurons can also engage in lateral "cis" associations that attenuate receptor activation by ephrins in trans with critical functional consequences. Despite the importance of the Eph/ephrin system in tumorigenesis, Eph receptor-ephrin cis interactions have not been previously investigated in cancer cells. Here we show that in cancer cells, coexpressed ephrin-A3 can inhibit the ability of EphA2 and EphA3 to bind ephrins in trans and become activated, while ephrin-B2 can inhibit not only EphB4 but also EphA3. The cis inhibition of EphA3 by ephrin-B2 implies that in some cases ephrins that cannot activate a particular Eph receptor in trans can nevertheless inhibit its signaling ability through cis association. We also found that an EphA3 mutation identified in lung cancer enhances cis interaction with ephrin-A3. These results suggest a novel mechanism that may contribute to cancer pathogenesis by attenuating the tumor suppressing effects of Eph receptor signaling pathways activated by ephrins in trans.
C1 [Falivelli, Giulia; Lisabeth, Erika Mathes; de la Torre, Elena Rubio; Perez-Tenorio, Gizeh; Pasquale, Elena B.] Sanford Burnham Med Res Inst, San Diego, CA 92101 USA.
[Tosato, Giovanna; Salvucci, Ombretta] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Pasquale, Elena B.] Univ Calif San Diego, Dept Pathol, San Diego, CA 92103 USA.
[Falivelli, Giulia] Univ Bologna, Dept Pharmacol, Bologna, Italy.
RP Pasquale, EB (reprint author), Sanford Burnham Med Res Inst, San Diego, CA 92101 USA.
EM elenap@sanfordburnham.org
FU National Institutes of Health [P01CA138390, P01HD025938, T32CA121949];
Tobacco-Related Disease Research Program [18XT-0099, 20FT-0076]; Spanish
Foundation for Science and Technology; Swedish Research Council [Dnr
2009-7360]
FX This work was supported by National Institutes of Health grants
P01CA138390 and P01HD025938, grant 18XT-0099 from the Tobacco-Related
Disease Research Program (E.B.P.), a postdoctoral fellowship from the
Spanish Foundation for Science and Technology (FECYT, E. R. T.),
National Institutes of Health postdoctoral training grant T32CA121949
and postdoctoral fellowship 20FT-0076 from the Tobacco-Related Disease
Research Program (E.M.L.), and postdoctoral fellowship Dnr 2009-7360
from the Swedish Research Council (G. P.). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 51
TC 19
Z9 19
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 29
PY 2013
VL 8
IS 11
AR e81445
DI 10.1371/journal.pone.0081445
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261MX
UT WOS:000327670300032
PM 24348920
ER
PT J
AU Trost, B
Kindrachuk, J
Maattanen, P
Napper, S
Kusalik, A
AF Trost, Brett
Kindrachuk, Jason
Maeaettaenen, Pekka
Napper, Scott
Kusalik, Anthony
TI PIIKA 2: An Expanded, Web-Based Platform for Analysis of Kinome
Microarray Data
SO PLOS ONE
LA English
DT Article
ID PROTEIN-KINASE; PEPTIDE CHIPS; R-PACKAGE; EXPRESSION; TUMORS; SUBSTRATE;
TESTS; SITE
AB Kinome microarrays are comprised of peptides that act as phosphorylation targets for protein kinases. This platform is growing in popularity due to its ability to measure phosphorylation-mediated cellular signaling in a high-throughput manner. While software for analyzing data from DNA microarrays has also been used for kinome arrays, differences between the two technologies and associated biologies previously led us to develop Platform for Intelligent, Integrated Kinome Analysis (PIIKA), a software tool customized for the analysis of data from kinome arrays. Here, we report the development of PIIKA 2, a significantly improved version with new features and improvements in the areas of clustering, statistical analysis, and data visualization. Among other additions to the original PIIKA, PIIKA 2 now allows the user to: evaluate statistically how well groups of samples cluster together; identify sets of peptides that have consistent phosphorylation patterns among groups of samples; perform hierarchical clustering analysis with bootstrapping; view false negative probabilities and positive and negative predictive values for t-tests between pairs of samples; easily assess experimental reproducibility; and visualize the data using volcano plots, scatterplots, and interactive three-dimensional principal component analyses. Also new in PIIKA 2 is a web-based interface, which allows users unfamiliar with command-line tools to easily provide input and download the results. Collectively, the additions and improvements described here enhance both the breadth and depth of analyses available, simplify the user interface, and make the software an even more valuable tool for the analysis of kinome microarray data. Both the web-based and stand-alone versions of PIIKA 2 can be accessed via http://saphire.usask.ca.
C1 [Trost, Brett; Kusalik, Anthony] Univ Saskatchewan, Dept Comp Sci, Saskatoon, SK S7N 0W0, Canada.
[Trost, Brett; Kindrachuk, Jason] NIAID, Emerging Viral Pathogens Sect, NIH, Frederick, MD USA.
[Maeaettaenen, Pekka; Napper, Scott] Univ Saskatchewan, Vaccine & Infect Dis Org, Saskatoon, SK, Canada.
[Napper, Scott] Univ Saskatchewan, Dept Biochem, Saskatoon, SK S7N 0W0, Canada.
RP Trost, B (reprint author), Univ Saskatchewan, Dept Comp Sci, Saskatoon, SK S7N 0W0, Canada.
EM brett.trost@usask.ca
RI Trost, Brett/K-4127-2016;
OI Trost, Brett/0000-0003-4863-7273; Kindrachuk, Jason/0000-0002-3305-7084
FU Natural Sciences and Engineering Research Council of Canada (NSERC);
Genome Canada; Intramural Research Program of the National Institutes of
Health /National Institute of Allergy and Infectious Diseases
FX This work was supported in part by the Natural Sciences and Engineering
Research Council of Canada (NSERC) (http://www.nserc-crsng.gc.ca),
Genome Canada (http://www.genomecanada.ca), and the Intramural Research
Program of the National Institutes of Health /National Institute of
Allergy and Infectious Diseases (http://www.niaid.nih.gov). The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 30
TC 12
Z9 12
U1 1
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 29
PY 2013
VL 8
IS 11
AR e80837
DI 10.1371/journal.pone.0080837
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261MX
UT WOS:000327670300017
PM 24312246
ER
PT J
AU Carrington, M
Bashirova, AA
McLaren, PJ
AF Carrington, Mary
Bashirova, Arman A.
McLaren, Paul J.
TI On stand by: host genetics of HIV control
SO AIDS
LA English
DT Editorial Material
DE genome-wide association study; host genetics; human leukocyte antigen
ID MAJOR HISTOCOMPATIBILITY COMPLEX; HLA-C EXPRESSION; GENOME-WIDE
ASSOCIATION; NUMBER VARIANT ASSAYS; CLASS-I; MESSENGER-RNA; AIDS;
INFECTION; RECOMBINATION; POLYMORPHISM
AB The impact of host genetic variation on determining the differential outcomes after HIV infection has been studied by two approaches: targeting of candidate genes and genome-wide association studies (GWASs). The overlap in genetic variants that has been identified by these two means has essentially been restricted to variants near to the human leukocyte antigen (HLA) class I genes, although variation in the CCR5 locus, which was first shown to have an effect on HIV outcomes using the candidate gene approach, does reach significance genome-wide when very large samples sizes (i.e. thousands) are used in GWAS. Overall, many of the variants identified by the candidate gene approach are likely to be spurious, as no additional variants apart from a novel variant near the HLA-C gene have been consistently identified by GWAS. Variants with low frequency and/or low impact on HIV outcomes are likely to exist in the genome and there could be many of them, but these are not identifiable, given current GWAS sample sizes. Several loci centrally involved in the immune response, including the immunoglobulin genes, T-cell receptor loci, or leukocyte receptor complex, are either poorly covered on the GWAS chips or difficult to interpret due to their repetitive nature and/or the presence of insertion/deletion polymorphisms in the region. These loci warrant further interrogation, but genetic characterization of these regions across a range of individuals will first be required. Finally, synergistic interactions between loci may affect outcome after infection, as suggested by associations of specific, functionally relevant HLA and killer cell immunoglobulin-like receptor variants with HIV disease outcomes, and these require further consideration as well.
C1 [Carrington, Mary; Bashirova, Arman A.] SAIC Frederick Inc, Canc & Inflammat Program, Expt Immunol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Carrington, Mary; Bashirova, Arman A.] Ragon Inst MGH & Harvard, Boston, MA USA.
[McLaren, Paul J.] Ecole Polytech Fed Lausanne, Sch Life Sci, CH-1015 Lausanne, Switzerland.
[McLaren, Paul J.] Univ Hosp Ctr, Inst Microbiol, Lausanne, Switzerland.
[McLaren, Paul J.] Univ Lausanne, Lausanne, Switzerland.
[McLaren, Paul J.] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.
RP Carrington, M (reprint author), SAIC Frederick Inc, Frederick Natl Lab Canc Res, POB B,Bldg 560, Frederick, MD 21702 USA.
EM carringm@mail.nih.gov
FU Intramural NIH HHS; PHS HHS [HHSN261200800001E]
NR 53
TC 4
Z9 4
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
EI 1473-5571
J9 AIDS
JI Aids
PD NOV 28
PY 2013
VL 27
IS 18
BP 2831
EP 2839
DI 10.1097/01.aids.0000432536.85335.c8
PG 9
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 295PQ
UT WOS:000330128400002
PM 25119688
ER
PT J
AU Coghill, AE
Newcomb, PA
Madeleine, MM
Richardson, BA
Mutyaba, I
Okuku, F
Phipps, W
Wabinga, H
Orem, J
Casper, C
AF Coghill, Anna E.
Newcomb, Polly A.
Madeleine, Margaret M.
Richardson, Barbra A.
Mutyaba, Innocent
Okuku, Fred
Phipps, Warren
Wabinga, Henry
Orem, Jackson
Casper, Corey
TI Contribution of HIV infection to mortality among cancer patients in
Uganda
SO AIDS
LA English
DT Article
DE cancer in Africa; cancer survival; HIV; immunosuppression; Uganda
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ORGAN TRANSPLANT RECIPIENTS;
NON-HODGKIN-LYMPHOMA; T-CELL RESPONSES; ACTIVE-ANTIRETROVIRAL-THERAPY;
AIDS-DEFINING MALIGNANCIES; UNITED-STATES; KAPOSIS-SARCOMA;
KIDNEY-TRANSPLANTATION; TUMOR IMMUNOGENICITY
AB Objective:HIV infection is associated with cancer risk. This relationship has resulted in a growing cancer burden, especially in resource-limited countries where HIV is highly prevalent. Little is known, however, about how HIV affects cancer survival in these settings. We therefore investigated the role of HIV in cancer survival in Uganda.Design:Retrospective cohort (N=802).Methods:Eligible cancer patients were residents of Kyadondo County, at least 18 years of age at cancer diagnosis, and diagnosed between 2003 and 2010 with one of the following: breast cancer, cervical cancer, non-Hodgkin's lymphoma, Hodgkin's lymphoma, or esophageal cancer. Patients were classified as HIV-infected at cancer diagnosis based on a documented positive HIV antibody test, medical history indicating HIV infection, or an HIV clinic referral letter. The primary outcome, vital status at 1 year following cancer diagnosis, was abstracted from the medical record or determined through linkage to the national hospice database. The risk of death during the year after cancer diagnosis was compared between cancer patients with and without evidence of HIV infection using Cox proportional hazards regression.Results:HIV-infected cancer patients in Uganda experienced a more than two-fold increased risk of death during the year following cancer diagnosis compared to HIV-uninfected cancer patients [hazard ratio 2.28; 95% confidence interval (CI) 1.61-3.23]. This association between HIV and 1-year cancer survival was observed for both cancers with (hazard ratio 1.56; 95% CI 1.04-2.34) and without (hazard ratio 2.68; 95% CI 1.20-5.99) an infectious cause.Conclusion:This study demonstrates the role of HIV in cancer survival for both cancers with and without an infectious cause in a resource-limited, HIV-endemic setting.
C1 [Coghill, Anna E.; Newcomb, Polly A.; Madeleine, Margaret M.; Richardson, Barbra A.; Phipps, Warren; Orem, Jackson; Casper, Corey] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Coghill, Anna E.; Newcomb, Polly A.; Madeleine, Margaret M.; Richardson, Barbra A.; Phipps, Warren; Casper, Corey] Univ Washington, Seattle, WA 98195 USA.
[Coghill, Anna E.] NCI, Bethesda, MD USA.
[Mutyaba, Innocent; Okuku, Fred; Phipps, Warren; Orem, Jackson; Casper, Corey] UCI Hutchinson Canc Ctr Alliance, Kampala, Uganda.
[Wabinga, Henry] Kampala Canc Registry, Kampala, Uganda.
RP Coghill, AE (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Rockville, MD 20892 USA.
EM anna.coghill@nih.gov
FU National Cancer Institute at the National Institutes of Health [T32
CA09168, R03 CA153371]
FX This work was supported by the National Cancer Institute at the National
Institutes of Health (T32 CA09168, R03 CA153371).
NR 77
TC 12
Z9 12
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
EI 1473-5571
J9 AIDS
JI Aids
PD NOV 28
PY 2013
VL 27
IS 18
BP 2933
EP 2942
DI 10.1097/01.aids.0000433236.55937.cb
PG 10
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 295PQ
UT WOS:000330128400012
PM 23921614
ER
PT J
AU Song, JY
Jaffe, ES
AF Song, Joo Y.
Jaffe, Elaine S.
TI HHV-8-positive but EBV-negative primary effusion lymphoma
SO BLOOD
LA English
DT Editorial Material
C1 [Song, Joo Y.] Univ Calif Davis, Davis, CA 95616 USA.
[Jaffe, Elaine S.] Natl Canc Inst, Bethesda, MD USA.
RP Song, JY (reprint author), Univ Calif Davis, Davis, CA 95616 USA.
RI Song, Joo/E-5356-2016;
OI Song, Joo/0000-0003-3497-2513; Jaffe, Elaine/0000-0003-4632-0301
NR 0
TC 2
Z9 2
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 28
PY 2013
VL 122
IS 23
BP 3712
EP 3712
DI 10.1182/blood-2013-07-515882
PG 1
WC Hematology
SC Hematology
GA 290EA
UT WOS:000329735000008
PM 24427809
ER
PT J
AU Assie, G
Libe, R
Espiard, S
Rizk-Rabin, M
Guimier, A
Luscap, W
Barreau, O
Lefevre, L
Sibony, M
Guignat, L
Rodriguez, S
Perlemoine, K
Rene-Corail, F
Letourneur, F
Trabulsi, B
Poussier, A
Chabbert-Buffet, N
Borson-Chazot, F
Groussin, L
Bertagna, X
Stratakis, CA
Ragazzon, B
Bertherat, J
AF Assie, Guillaume
Libe, Rossella
Espiard, Stephanie
Rizk-Rabin, Marthe
Guimier, Anne
Luscap, Windy
Barreau, Olivia
Lefevre, Lucile
Sibony, Mathilde
Guignat, Laurence
Rodriguez, Stephanie
Perlemoine, Karine
Rene-Corail, Fernande
Letourneur, Franck
Trabulsi, Bilal
Poussier, Alix
Chabbert-Buffet, Nathalie
Borson-Chazot, Francoise
Groussin, Lionel
Bertagna, Xavier
Stratakis, Constantine A.
Ragazzon, Bruno
Bertherat, Jerome
TI ARMC5 Mutations in Macronodular Adrenal Hyperplasia with Cushing's
Syndrome
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID GASTRIC-INHIBITORY POLYPEPTIDE; ADRENOCORTICAL TUMORS; GENE-EXPRESSION;
FREQUENT; PROTEIN; RECEPTORS; HYPERCORTISOLISM; PATHWAY; DISEASE;
CANCERS
AB BackgroundCorticotropin-independent macronodular adrenal hyperplasia may be an incidental finding or it may be identified during evaluation for Cushing's syndrome. Reports of familial cases and the involvement of both adrenal glands suggest a genetic origin of this condition.
MethodsWe genotyped blood and tumor DNA obtained from 33 patients with corticotropin-independent macronodular adrenal hyperplasia (12 men and 21 women who were 30 to 73 years of age), using single-nucleotide polymorphism arrays, microsatellite markers, and whole-genome and Sanger sequencing. The effects of armadillo repeat containing 5 (ARMC5) inactivation and overexpression were tested in cell-culture models.
ResultsThe most frequent somatic chromosome alteration was loss of heterozygosity at 16p (in 8 of 33 patients for whom data were available [24%]). The most frequent mutation identified by means of whole-genome sequencing was in ARMC5, located at 16p11.2. ARMC5 mutations were detected in tumors obtained from 18 of 33 patients (55%). In all cases, both alleles of ARMC5 carried mutations: one germline and the other somatic. In 4 patients with a germline ARMC5 mutation, different nodules from the affected adrenals harbored different secondary ARMC5 alterations. Transcriptome-based classification of corticotropin-independent macronodular adrenal hyperplasia indicated that ARMC5 mutations influenced gene expression, since all cases with mutations clustered together. ARMC5 inactivation decreased steroidogenesis in vitro, and its overexpression altered cell survival.
ConclusionsSome cases of corticotropin-independent macronodular adrenal hyperplasia appear to be genetic, most often with inactivating mutations of ARMC5, a putative tumor-suppressor gene. Genetic testing for this condition, which often has a long and insidious prediagnostic course, might result in earlier identification and better management. (Funded by Agence Nationale de la Recherche and others.)
C1 [Assie, Guillaume; Libe, Rossella; Espiard, Stephanie; Rizk-Rabin, Marthe; Guimier, Anne; Luscap, Windy; Barreau, Olivia; Lefevre, Lucile; Rodriguez, Stephanie; Perlemoine, Karine; Rene-Corail, Fernande; Letourneur, Franck; Groussin, Lionel; Bertagna, Xavier; Ragazzon, Bruno; Bertherat, Jerome] Inst Cochin, INSERM Unite 1016, CNRS, UMR 8104, Paris, France.
[Assie, Guillaume; Espiard, Stephanie; Guimier, Anne; Barreau, Olivia; Lefevre, Lucile; Sibony, Mathilde; Perlemoine, Karine; Rene-Corail, Fernande; Groussin, Lionel; Bertagna, Xavier; Bertherat, Jerome] Univ Paris 05, Fac Med Paris Descartes, Sorbonne Paris Cite, Paris, France.
[Assie, Guillaume; Libe, Rossella; Barreau, Olivia; Guignat, Laurence; Groussin, Lionel; Bertagna, Xavier; Bertherat, Jerome] Referral Ctr Rare Adrenal Dis, Dept Endocrinol, Paris, France.
[Sibony, Mathilde] Hop Cochin, AP HP, Dept Pathol, F-75674 Paris, France.
[Chabbert-Buffet, Nathalie] Hop Tenon, Dept Obstet & Gynecol, Unit Endocrinol, F-75970 Paris, France.
[Trabulsi, Bilal] Ctr Hosp, Ctr Bretagne, Unit Endocrinol, Noyal Pontivy, France.
[Poussier, Alix] Hotel Dieu Creusot, Unit Endocrinol, Le Creusot, France.
[Borson-Chazot, Francoise] Grp Hosp Est, Dept Endocrinol Lyon Est, Bron, France.
[Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD USA.
[Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Endocrinol Inter Inst, Training Program, NIH, Bethesda, MD USA.
RP Bertherat, J (reprint author), Hop Cochin, Serv Malad Endocriniennes & Metab, Ctr Reference Malad Rares Surrenale, 27 Rue Faubourg St Jacques, F-75014 Paris, France.
EM jerome.bertherat@cch.aphp.fr
RI Ragazzon, Bruno/E-6541-2017;
OI Ragazzon, Bruno/0000-0001-9476-4973; Borson-Chazot,
Francoise/0000-0003-2515-7840
FU Agence Nationale de la Recherche [ANR-10-Blan-1136];
Corticomedullosurrenale Tumeur Endocrine Network (Programme Hospitalier
de Recherche Clinique grant) [AOM95201]; Assistance Publique-Hopitaux de
Paris (Clinical Research Center) [Genhyper P061006]; Institut National
du Cancer [Recherche Translationelle 2009-RT-02]; Seventh Framework
Program of the European Commission [F2-2010-259735]; INSERM (Contrat
d'Interface); Conny-Maeva Charitable Foundation; intramural program of
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX Supported in part by grants from Agence Nationale de la Recherche
(ANR-10-Blan-1136), Corticomedullosurrenale Tumeur Endocrine Network
(Programme Hospitalier de Recherche Clinique grant AOM95201), Assistance
Publique-Hopitaux de Paris (Clinical Research Center Grant Genhyper
P061006), Institut National du Cancer (Recherche Translationelle
2009-RT-02), the Seventh Framework Program of the European Commission
(F2-2010-259735), INSERM (Contrat d'Interface, to Dr. Assie), the
Conny-Maeva Charitable Foundation, and the intramural program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development.
NR 29
TC 82
Z9 85
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 NOV 28
PY 2013
VL 369
IS 22
BP 2105
EP 2114
DI 10.1056/NEJMoa1304603
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 258OB
UT WOS:000327467500008
PM 24283224
ER
PT J
AU Patnaik, S
Marugan, JJ
Liu, K
Zheng, W
Southall, N
Dehdashti, SJ
Thorsell, A
Heilig, M
Bell, L
Zook, M
Eskay, B
Brimacombe, KR
Austin, CP
AF Patnaik, Samarjit
Marugan, Juan J.
Liu, Ke
Zheng, Wei
Southall, Noel
Dehdashti, Seameen J.
Thorsell, Annika
Heilig, Markus
Bell, Lauren
Zook, Michelle
Eskay, Bob
Brimacombe, Kyle R.
Austin, Christopher P.
TI Structure-Activity Relationship of Imidazopyridinium Analogues as
Antagonists of Neuropeptide S Receptor
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID BIOLOGICAL-ACTIVITY; FOOD-INTAKE; DISCOVERY; BRAIN; AROUSAL; SYSTEM;
POTENT; RATS; MICE
AB The discovery and characterization of a novel chemical series of phosphorothioyl-containing imidazopyridines as potent neuropeptide S receptor antagonists is presented. The synthesis of analogues and their structure-activity relationship with respect to the Gq, Gs, and ERK pathways is detailed. The pharmacokinetics and in vivo efficacy of a potent analogue in a food intake rodent model are also included, underscoring its potential therapeutic value for the treatment of sleep, anxiety, and addiction disorders.
C1 [Patnaik, Samarjit; Marugan, Juan J.; Liu, Ke; Zheng, Wei; Southall, Noel; Dehdashti, Seameen J.; Brimacombe, Kyle R.; Austin, Christopher P.] NIH, Natl Ctr Adv Translat Sci, Rockville, MD 20850 USA.
[Thorsell, Annika; Heilig, Markus; Bell, Lauren; Zook, Michelle; Eskay, Bob] NIAAA, NIH, Bethesda, MD 20892 USA.
RP Marugan, JJ (reprint author), 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;
Heilig, Markus/0000-0003-2706-2482; Thorsell, Annika/0000-0003-3535-3845
FU Molecular Libraries Initiative of the National Institutes of Health
Roadmap for Medical Research; Intramural Research Programs of the
National Institute on Alcohol Abuse and Alcoholism, NIH
FX This research was supported by the Molecular Libraries Initiative of the
National Institutes of Health Roadmap for Medical Research and the
Intramural Research Programs of the National Institute on Alcohol Abuse
and Alcoholism, NIH. We thank Dr. Reinscheid for generously providing
the NPSR clone originally used to generate the CHO-NPSR cell line; Sam
Michael for assistance in robotic screening; and William Leister, Paul
Shinn, Jeremy Smith, Danielle van Leer, and James Bougie for compound
management.
NR 37
TC 7
Z9 7
U1 0
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 NOV 28
PY 2013
VL 56
IS 22
BP 9045
EP 9056
DI 10.1021/jm400904m
PG 12
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 263ML
UT WOS:000327812600008
PM 24171469
ER
PT J
AU Xu, R
Zanotti-Fregonara, P
Zoghbi, SS
Gladding, RL
Woock, AE
Innis, RB
Pike, VW
AF Xu, Rong
Zanotti-Fregonara, Paolo
Zoghbi, Sami S.
Gladding, Robert L.
Woock, Alicia E.
Innis, Robert B.
Pike, Victor W.
TI Synthesis and Evaluation in Monkey of
[F-18]4-Fluoro-N-methyl-N-(4-(6-(methylannino)pyrimidin-4-yl)thiazol-2-y
l)benzamide ([F-18]FIMX): A Promising Radioligand for PET Imaging of
Brain Metabotropic Glutamate Receptor 1 (mGluR1)
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; DIARYLIODONIUM-SALTS; IN-VIVO; EXTRUSION
REACTIONS; R2I-F IODINE(III); FREE-FRACTION; AB-INITIO;
RADIOFLUORINATION; TOSYLATES; LIGAND
AB We sought to develop a PET radioligand that would be useful for imaging human brain metabotropic subtype 1 receptors (mGluR1) in neuropsychiatric disorders and in drug development. 4-Fluoro-N-methyl-N-(4-(6(methylamino)pyrimidin-4-yOthiazol-2-ylbenzamide (FIMX, 11) was identified as having favorable properties for development as a PET radioligand. We developed a method for preparing [F-18]11 in useful radiochemical yield and in high specific activity from [18F]fluoride ion and an N-Boc-protected (phenyl)aryliodonium salt precursor (15). In baseline experiments in rhesus monkey, [F-18 ]11 gave high brain radioactivity uptake, reflecting the expected distribution of mGluR1 with notably high uptake in cerebellum, which became 47% lower by 120 min after radioligand injection. Pharmacological challenges demonstrated that a very high proportion of the radioactivity in monkey brain was bound specifically and reversibly to mGluRl. [F-18]11 is concluded to be an effective PET radioligand for imaging mGluR1 in monkey brain and therefore merits further evaluation in human subjects.
C1 [Xu, Rong; Zanotti-Fregonara, Paolo; Zoghbi, Sami S.; Gladding, Robert L.; Woock, Alicia E.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
RP Pike, VW (reprint author), NIMH, Mol Imaging Branch, NIH, Bldg 10,Room B3 C346A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM pikev@mail.nih.gov
FU project officer Jamie Driscol (NIMH), at the University of North
Carolina at Chapel Hill [NO1MH32004]
FX This work is support by the Intramural Research Program of NIMH. We
thank the NIH Clinical PET Center (Director Dr. P. Herscovitch) for
radioisotope production and the PDSP for performing binding assays. The
PDSP is directed by Bryan L. Roth, Ph.D., with project officer Jamie
Driscol (NIMH), at the University of North Carolina at Chapel Hill
(contract no. NO1MH32004).
NR 55
TC 11
Z9 11
U1 0
U2 15
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 NOV 28
PY 2013
VL 56
IS 22
BP 9146
EP 9155
DI 10.1021/jm4012017
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 263ML
UT WOS:000327812600016
PM 24147864
ER
PT J
AU Romagnoli, R
Baraldi, PG
Lopez-Cara, C
Preti, D
Tabrizi, MA
Balzarini, J
Bassetto, M
Brancale, A
Fu, XH
Gao, Y
Li, J
Zhang, SZ
Hamel, E
Bortolozzi, R
Basso, G
Viola, G
AF Romagnoli, Romeo
Baraldi, Pier Giovanni
Lopez-Cara, Carlota
Preti, Delia
Tabrizi, Mojgan Aghazadeh
Balzarini, Jan
Bassetto, Marcella
Brancale, Andrea
Fu, Xian-Hua
Gao, Yang
Li, Jun
Zhang, Su-Zhan
Hamel, Ernest
Bortolozzi, Roberta
Basso, Giuseppe
Viola, Giampietro
TI Concise Synthesis and Biological Evaluation of 2-Aroyl-5-Amino
Benzo[b]thiophene Derivatives As a Novel Class of Potent Antimitotic
Agents
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID COMBRETASTATIN A-4 PHOSPHATE; CELL-DEATH; ANTICANCER AGENTS;
MESSENGER-RNA; TUBULIN; APOPTOSIS; CANCER; COLCHICINE; BINDING;
MICROTUBULES
AB The biological importance of microtubules make them an interesting target for the synthesis of antitumor agents. The 2(3',4',5'-trimethoxybenzoyl)-5-aminobenzo[b]thiophene moiety was identified as a novel scaffold for the preparation of potent inhibitors of microtubule polymerization acting through the colchicine site of tubulin. The position of the methoxy group on the benzo[b]thiophene was important for maximal antiproliferative activity. Structure-activity relationship analysis established that the best activities were obtained with amino and methoxy groups placed at the C-5 and C-7 positions, respectively. Compounds 3c-e showed more potent inhibition of tubulin polymerization than combretastatin A-4 and strong binding to the colchicine site. These compounds also demonstrated substantial antiproliferative activity, with IC50 values ranging from 2.6 to 18 nM in a variety of cancer cell lines. Importantly, compound 3c (50 mg/kg), significantly inhibited the growth of the human osteosarcoma MNNG/HOS xenograft in nude mice.
C1 [Romagnoli, Romeo; Baraldi, Pier Giovanni; Lopez-Cara, Carlota; Preti, Delia; Tabrizi, Mojgan Aghazadeh] Univ Ferrara, Dipartimento Sci Chim & Farmaceut, I-44121 Ferrara, Italy.
[Balzarini, Jan] Catholic Univ Louvain, Rega Inst Med Res, Lab Virol & Chemotherapy, B-3000 Louvain, Belgium.
[Bassetto, Marcella; Brancale, Andrea] Cardiff Univ, Sch Pharm & Pharmaceut Sci, Cardiff CF10 3NB, S Glam, Wales.
[Fu, Xian-Hua; Gao, Yang; Li, Jun; Zhang, Su-Zhan] Zhejiang Univ, Inst Canc, Key Lab Canc Prevent & Intervent, China Natl Minist Educ,Sch Med,Affiliated Hosp 2, Hangzhou 310009, Zhejiang, Peoples R China.
[Hamel, Ernest] NCI, Screening Technol Branch, Dev Therapeut Program,NIH, Div Canc Treatment & Diag,Frederick Natl Lab Canc, Frederick, MD 21702 USA.
[Bortolozzi, Roberta; Basso, Giuseppe; Viola, Giampietro] Univ Padua, Lab Oncoematol, Dipartimento Salute Donna & Bambino, I-35131 Padua, Italy.
RP Romagnoli, R (reprint author), Univ Ferrara, Dipartimento Sci Chim & Farmaceut, I-44121 Ferrara, Italy.
EM rmr@unife.it; pgb@unife.it; giampietro.violal@unipd.it
RI Aghazadeh Tabrizi, Mojgan/I-9169-2014; Viola, Giampietro/I-4095-2012;
Brancale, Andrea/N-9445-2014; Bortolozzi, Roberta/D-4950-2015; preti,
delia/G-9916-2015; Romagnoli, Romeo/G-9887-2015; LOPEZ-CARA, LUISA
CARLOTA/F-9686-2014; Baraldi, Pier Giovanni/B-7933-2017;
OI Viola, Giampietro/0000-0001-9329-165X; Brancale,
Andrea/0000-0002-9728-3419; Bortolozzi, Roberta/0000-0002-3357-4815;
preti, delia/0000-0002-1075-3781; LOPEZ-CARA, LUISA
CARLOTA/0000-0003-1142-6448; Bassetto, Marcella/0000-0002-2491-5868;
BASSO, GIUSEPPE/0000-0002-2634-9302
FU GOA (Krediet) of the KU Leuven [10/14]
FX Jan Balzarini is funded by GOA (Krediet no. 10/14) of the KU Leuven. We
gratefully acknowledge Alberto Casolari and Lizette van Berckelaer for
their excellent technical assistance.
NR 54
TC 20
Z9 20
U1 1
U2 16
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 NOV 28
PY 2013
VL 56
IS 22
BP 9296
EP 9309
DI 10.1021/jm4013938
PG 14
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 263ML
UT WOS:000327812600027
PM 24164557
ER
EF