FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Ehrman, JK
Kraus, WE
Piner, LW
Leifer, ES
Saval, MA
Keteyian, SJ
Brawner, CA
AF Ehrman, Jonathan K.
Kraus, William E.
Piner, Lucy W.
Leifer, Eric S.
Saval, Matthew A.
Keteyian, Steven J.
Brawner, Clinton A.
TI Oxygen Uptake Efficiency Slope (oues): Maximal Vs. Submaximal
Calculation Methods
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the American-College-of-Sports-Medicine
CY MAY 28-JUN 01, 2013
CL Indianapolis, IN
SP Amer Coll Sports Med
C1 [Ehrman, Jonathan K.] Henry Ford, Detroit, MI USA.
[Kraus, William E.; Piner, Lucy W.] Duke Univ, Med Ctr, Durham, NC USA.
[Leifer, Eric S.] NIH, Bethesda, MD 20892 USA.
[Saval, Matthew A.; Keteyian, Steven J.; Brawner, Clinton A.] Henry Ford Hlth Syst, Detroit, MI 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 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2013
VL 45
IS 5
SU 1
MA 2431
BP 573
EP 574
PG 2
WC Sport Sciences
SC Sport Sciences
GA 300ND
UT WOS:000330469704323
ER
PT J
AU Hudson, G
Nalls, M
Evans, JR
Breen, DP
Winder-Rhodes, S
Morrison, KE
Morris, HR
Williams-Gray, CH
Barker, RA
Singleton, AB
Hardy, J
Wood, NE
Burn, DJ
Chinnery, PF
AF Hudson, Gavin
Nalls, Mike
Evans, Jonathan R.
Breen, David P.
Winder-Rhodes, Sophie
Morrison, Karen E.
Morris, Huw R.
Williams-Gray, Caroline H.
Barker, Roger A.
Singleton, Andrew B.
Hardy, John
Wood, Nicholas E.
Burn, David J.
Chinnery, Patrick F.
TI Two-stage association study and meta-analysis of mitochondrial DNA
variants in Parkinson disease
SO NEUROLOGY
LA English
DT Article
ID ALPHA-SYNUCLEIN; COMPLEX I; ALZHEIMERS-DISEASE; RISK; HAPLOGROUPS;
POLYMORPHISMS; POPULATION; MUTATIONS; EXPOSURE; PEPTIDE
AB Objectives: Previous associations between mitochondrial DNA (mtDNA) and idiopathic Parkinson disease (PD) have been inconsistent and contradictory. Our aim was to resolve these inconsistencies and determine whether mtDNA has a significant role in the risk of developing PD.
Methods: Two-stage genetic association study of 138 common mtDNA variants in 3,074 PD cases and 5,659 ethnically matched controls followed by meta-analysis of 6,140 PD cases and 13,280 controls.
Results: In the association study, m.2158T>C and m.11251A>G were associated with a reduced risk of PD in both the discovery and replication cohorts. None of the common European mtDNA haplogroups were consistently associated with PD, but pooling of discovery and replication cohorts revealed a protective association with "super-haplogroup" JT. In the meta-analysis, there was a reduced risk of PD with haplogroups J, K, and T and super-haplogroup JT, and an increase in the risk of PD with super-haplogroup H.
Conclusions: In a 2-stage association study of mtDNA variants and PD, we confirm the reduced risk of PD with super-haplogroup JT and resolve this at the J1b level. Meta-analysis explains the previous inconsistent associations that likely arise through sampling effects. The reduced risk of PD with haplogroups J, K, and T is mirrored by an increased risk of PD in super-haplogroup HV, which increases survival after sepsis. Antagonistic pleiotropy between mtDNA haplogroups may thus be shaping the genetic landscape in humans, leading to an increased risk of PD in later life.
C1 [Hudson, Gavin; Chinnery, Patrick F.] Newcastle Univ, Inst Med Genet, Wellcome Ctr Mitochondrial Res, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Nalls, Mike; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Evans, Jonathan R.; Breen, David P.; Winder-Rhodes, Sophie; Williams-Gray, Caroline H.] Univ Cambridge, Dept Clin Neurosci, Cambridge, England.
[Morrison, Karen E.; Barker, Roger A.] Univ Birmingham, Dept Neurosci, Birmingham, W Midlands, England.
[Morris, Huw R.] Cardiff Univ, Sch Med, MRC, Ctr Neuropsychiat Genet & Genom, Cardiff, Wales.
[Hardy, John; Wood, Nicholas E.] UCL, Inst Neurol, Dept Mol Neurosci, London, England.
[Burn, David J.] Newcastle Univ, Inst Ageing & Hlth, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
RP Chinnery, PF (reprint author), Newcastle Univ, Inst Med Genet, Wellcome Ctr Mitochondrial Res, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
EM patrick.chinnery@ncl.ac.uk
RI Hardy, John/C-2451-2009; Singleton, Andrew/C-3010-2009; Hudson,
Gavin/E-7117-2017
FU Wellcome Centre for Mitochondrial Research; Medical Research Council
(UK) Translational Muscle Centre; UK NIHR Biomedical Research Centre for
Ageing and Age-Related Disease; NIHR Dementia Biomedical Research Unit;
National Institute on Aging, NIH, Department of Health and Human
Services [Z01 AG000949-06]; Parkinson's UK; Raymond and Beverly Sackler
studentship
FX G.H. is a Parkinson's UK Senior Fellow. P. F. C. is a Wellcome Trust
Senior Fellow in Clinical Science and an NIHR Senior Investigator also
receives funding from the Wellcome Centre for Mitochondrial Research,
the Medical Research Council (UK) Translational Muscle Centre, the UK
NIHR Biomedical Research Centre for Ageing and Age-Related Disease, and
NIHR Dementia Biomedical Research Unit awards to the Newcastle upon Tyne
Foundation Hospitals NHS Trust. M.N. and A. S. are supported in part by
the Intramural Research Program of the National Institute on Aging, NIH,
Department of Health and Human Services, project number Z01 AG000949-06.
D. P. B. is supported by Parkinson's UK and has been the recipient of a
Raymond and Beverly Sackler studentship.
NR 30
TC 37
Z9 37
U1 2
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD MAY
PY 2013
VL 80
IS 22
BP 2042
EP 2048
DI 10.1212/WNL.0b013e318294b434
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 300LX
UT WOS:000330466500016
PM 23645593
ER
PT J
AU Izhak, L
Berzofsky, JA
Terabe, M
AF Izhak, Liat
Berzofsky, Jay A.
Terabe, Masaki
TI Balance is a key for happiness
SO ONCOIMMUNOLOGY
LA English
DT Editorial Material
DE immune regulation; immunosuppression; NKT cells; regulatory T cells;
tumor immunology
ID T-CELL FUNCTION; TUMOR-IMMUNITY; NKT CELLS; VACCINATION; CANCER
AB Eliminating one immunosuppressive mechanism is rarely sufficient to overcome cancer. One of reasons underlying this fact is that whether regulatory T cells (Tregs) or type II natural killer T (NKT) cells dominate immunosuppression depends on the mutual interactions between the latter and their type I counterparts. thus, the balance among three immunomodulatory cell types dictates whether eliminating Tregs relieves or not immunosuppression.
C1 [Izhak, Liat; Berzofsky, Jay A.; Terabe, Masaki] NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Terabe, M (reprint author), NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM terabe@mail.nih.gov
NR 10
TC 2
Z9 2
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2162-4011
EI 2162-402X
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PD MAY
PY 2013
VL 2
IS 5
AR e24211
DI 10.4161/onci.24211
PG 2
WC Oncology; Immunology
SC Oncology; Immunology
GA 301HQ
UT WOS:000330523800022
ER
PT J
AU Shive, HR
AF Shive, H. R.
TI Zebrafish Models for Human Cancer
SO VETERINARY PATHOLOGY
LA English
DT Article
DE animal disease models; cancer; genetic modification; zebrafish
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; RECOMBINATION ACTIVATING GENE-1; REGULATED
TRANSGENIC ZEBRAFISH; CAUSES GENOME INSTABILITY; ZINC-FINGER NUCLEASES;
LI-FRAUMENI SYNDROME; NERVE SHEATH TUMORS; GERM-CELL TUMORS;
DANIO-RERIO; ADULT ZEBRAFISH
AB For decades, the advancement of cancer research has relied on in vivo models for examining key processes in cancer pathogenesis, including neoplastic transformation, progression, and response to therapy. These studies, which have traditionally relied on rodent models, have engendered a vast body of scientific literature. Recently, experimental cancer researchers have embraced many new and alternative model systems, including the zebrafish (Danio rerio). The general benefits of the zebrafish model for laboratory investigation, such as cost, size, fecundity, and generation time, were quickly superseded by the discovery that zebrafish are amenable to a wide range of investigative techniques, many of which are difficult or impossible to perform in mammalian models. These advantages, coupled with the finding that many aspects of carcinogenesis are conserved in zebrafish as compared with humans, have firmly established a unique niche for the zebrafish model in comparative cancer research. This article introduces methods for generating cancer models in zebrafish and reviews a range of models that have been developed for specific cancer types.
C1 NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Shive, HR (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM shiveh@mail.nih.gov
FU US National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX This work was supported by the Intramural Research Program of the US
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 119
TC 7
Z9 7
U1 4
U2 22
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0300-9858
EI 1544-2217
J9 VET PATHOL
JI Vet. Pathol.
PD MAY
PY 2013
VL 50
IS 3
BP 468
EP 482
DI 10.1177/0300985812467471
PG 15
WC Pathology; Veterinary Sciences
SC Pathology; Veterinary Sciences
GA 298BJ
UT WOS:000330298600017
PM 23203679
ER
PT J
AU Twenhafel, NA
Mattix, ME
Johnson, JC
Robinson, CG
Pratt, WD
Cashman, KA
Wahl-Jensen, V
Terry, C
Olinger, GG
Hensley, LE
Honko, AN
AF Twenhafel, N. A.
Mattix, M. E.
Johnson, J. C.
Robinson, C. G.
Pratt, W. D.
Cashman, K. A.
Wahl-Jensen, V.
Terry, C.
Olinger, G. G.
Hensley, L. E.
Honko, A. N.
TI Pathology of Experimental Aerosol Zaire Ebolavirus Infection in Rhesus
Macaques
SO VETERINARY PATHOLOGY
LA English
DT Article
DE aerosol; animal model; ebolavirus; filovirus; macaque; rhesus; Zaire;
Zaire ebolavirus
ID FIBROBLASTIC RETICULAR CELLS; HEMORRHAGIC-FEVER VIRUSES; AFRICAN-GREEN
MONKEYS; NIEMANN-PICK C1; DENDRITIC CELLS; NONHUMAN-PRIMATES; ALVEOLAR
MACROPHAGES; CYNOMOLGUS MACAQUES; MARBURG VIRUSES; NITRIC-OXIDE
AB There is limited knowledge of the pathogenesis of human ebolavirus infections and no reported human cases acquired by the aerosol route. There is a threat of ebolavirus as an aerosolized biological weapon, and this study evaluated the pathogenesis of aerosol infection in 18 rhesus macaques. Important and unique findings include early infection of the respiratory lymphoid tissues, early fibrin deposition in the splenic white pulp, and perivasculitis and vasculitis in superficial dermal blood vessels of haired skin with rash. Initial infection occurred in the respiratory lymphoid tissues, fibroblastic reticular cells, dendritic cells, alveolar macrophages, and blood monocytes. Virus spread to regional lymph nodes, where significant viral replication occurred. Virus secondarily infected many additional blood monocytes and spread from the respiratory tissues to multiple organs, including the liver and spleen. Viremia, increased temperature, lymphocytopenia, neutrophilia, thrombocytopenia, and increased alanine aminotransferase, aspartate aminotransferase, g-glutamyl transpeptidase, total bilirubin, serum urea nitrogen, creatinine, and hypoalbuminemia were measurable mid to late infection. Infection progressed rapidly with whole-body destruction of lymphoid tissues, hepatic necrosis, vasculitis, hemorrhage, and extravascular fibrin accumulation. Hypothermia and thrombocytopenia were noted in late stages with the development of disseminated intravascular coagulation and shock. This study provides unprecedented insight into pathogenesis of human aerosol Zaire ebolavirus infection and suggests development of a medical countermeasure to aerosol infection will be a great challenge due to massive early infection of respiratory lymphoid tissues. Rhesus macaques may be used as a model of aerosol infection that will allow the development of lifesaving medical countermeasures under the Food and Drug Administration's animal rule.
C1 [Twenhafel, N. A.; Mattix, M. E.; Johnson, J. C.; Robinson, C. G.; Pratt, W. D.; Cashman, K. A.; Terry, C.; Olinger, G. G.; Hensley, L. E.; Honko, A. N.] USAMRIID, Ft Detrick, MD USA.
[Wahl-Jensen, V.] NIAID, Integrated Res Facil Frederick, NIH, Frederick, MD USA.
RP Twenhafel, NA (reprint author), US Army, Med Res Inst Infect Dis, Div Pathol, 1425 Porter St, Ft Detrick, MD 21702 USA.
EM nancy.twenhafel@us.army.mil
OI Olinger, Gene/0000-0001-7338-0292; Johnson, Joshua/0000-0002-5677-3841;
Honko, Anna/0000-0001-9165-148X
NR 82
TC 31
Z9 32
U1 0
U2 12
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0300-9858
EI 1544-2217
J9 VET PATHOL
JI Vet. Pathol.
PD MAY
PY 2013
VL 50
IS 3
BP 514
EP 529
DI 10.1177/0300985812469636
PG 16
WC Pathology; Veterinary Sciences
SC Pathology; Veterinary Sciences
GA 298BJ
UT WOS:000330298600021
PM 23262834
ER
PT J
AU Boyle, MC
Boyle, MH
AF Boyle, M. C.
Boyle, M. H.
CA Sixth Rodent Pathology Course Comm
TI Meeting Report: Urinary Pathology; Sixth Research Triangle Park Rodent
Pathology Course
SO VETERINARY PATHOLOGY
LA English
DT Editorial Material
DE rodent pathology; toxicologic pathology; urinary pathology; kidney;
mouse model; biomarker; rat; mouse
ID UROTHELIAL CARCINOMA; 2 STRAINS; MALE-RAT; EXPRESSION; VASCULITIS;
BLADDER; SYSTEM; CANCER
AB Urinary system toxicity is a significant concern to pathologists in the hazard identification, drug and chemical safety evaluation, and diagnostic service industries worldwide. There are myriad known human and animal urinary system toxicants, and investigatory renal toxicology and pathology is continually evolving. The system-specific Research Triangle Park (RTP) Rodent Pathology Course biennially serves to update scientists on the latest research, laboratory techniques, and debates. The Sixth RTP Rodent Pathology Course, Urinary Pathology, featured experts from the government, pharmaceutical, academic, and diagnostic arenas sharing the state of the science in urinary pathology. Speakers presented on a wide range of topics including background lesions, treatment-related non-neoplastic and neoplastic lesions, transgenic rodent models of human disease, diagnostic imaging, biomarkers, and molecular analyses. These seminars were accompanied by case presentation sessions focused on usual and unusual lesions, grading schemes, and tumors.
C1 [Boyle, M. C.] NIEHS, Natl Toxicol Program, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
[Boyle, M. H.] Integrated Syst Lab, Res Triangle Pk, NC USA.
RP Boyle, MC (reprint author), NIEHS, Natl Toxicol Program, Cellular & Mol Pathol Branch, 111 TW Alexander Dr,POB 12233,Mail Drop B3-06, Res Triangle Pk, NC 27709 USA.
EM boylemc@niehs.nih.gov
OI Everitt, Jeffrey/0000-0003-0273-6284
FU Integrated Laboratory Systems for Molly Boyle
FX The author(s) declared receipt of the following financial support for
the research, authorship, and/or publication of this article: Financial
support was provided by Integrated Laboratory Systems for Molly Boyle to
attend the meeting and contribute to this meeting report.
NR 29
TC 0
Z9 0
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0300-9858
EI 1544-2217
J9 VET PATHOL
JI Vet. Pathol.
PD MAY
PY 2013
VL 50
IS 3
BP 563
EP 568
DI 10.1177/0300985813480217
PG 6
WC Pathology; Veterinary Sciences
SC Pathology; Veterinary Sciences
GA 298BJ
UT WOS:000330298600027
PM 23645617
ER
PT J
AU Vezina, HE
Park, JG
Wallis, CL
Bartlett, JA
Kumarasamy, N
Stevens, WS
Klingman, KL
Ribaudo, HJ
Katzenstein, DA
AF Vezina, Heather E.
Park, Jeong-Gun
Wallis, Carole L.
Bartlett, John A.
Kumarasamy, Nagalingeswaran
Stevens, Wendy S.
Klingman, Karin L.
Ribaudo, Heather J.
Katzenstein, David A.
CA A5230 Team
TI Lopinavir Population Pharmacokinetics in HIV-infected Patients from
Resource-limited Settings Receiving Second-line Treatment with
Lopinavir/Ritonavir Monotherapy in AIDS Clinical Trials Group (ACTG)
Study 5230
SO JOURNAL OF PHARMACOKINETICS AND PHARMACODYNAMICS
LA English
DT Meeting Abstract
C1 [Vezina, Heather E.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Park, Jeong-Gun; Ribaudo, Heather J.] Harvard Univ, Stat Data Anal Ctr, Boston, MA 02115 USA.
[Wallis, Carole L.] Lancet Labs, Johannesburg, South Africa.
[Bartlett, John A.] Duke Univ, Med Ctr, Durham, NC USA.
[Bartlett, John A.] Kilimanjaro Christian Med Ctr, Moshi, Tanzania.
[Kumarasamy, Nagalingeswaran] YRG CARE Med Ctr, Chennai, Tamil Nadu, India.
[Stevens, Wendy S.] Univ Witwatersrand, Johannesburg, South Africa.
[Klingman, Karin L.] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Katzenstein, David A.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
NR 2
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1567-567X
EI 1573-8744
J9 J PHARMACOKINET PHAR
JI J. Pharmacokinet. Pharmacodyn.
PD MAY
PY 2013
VL 40
SU 1
BP S31
EP S32
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 295OS
UT WOS:000330126000026
ER
PT J
AU Cotten, M
Lam, TT
Watson, SJ
Palser, AL
Petrova, V
Grant, P
Pybus, OG
Rambaut, A
Guan, Y
Pillay, D
Kellam, P
Nastouli, E
AF Cotten, Matthew
Lam, Tommy T.
Watson, Simon J.
Palser, Anne L.
Petrova, Velislava
Grant, Paul
Pybus, Oliver G.
Rambaut, Andrew
Guan, Yi
Pillay, Deenan
Kellam, Paul
Nastouli, Eleni
TI Full-Genome Deep Sequencing and Phylogenetic Analysis of Novel Human
Betacoronavirus
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN CORONAVIRUS OC43; MAXIMUM-LIKELIHOOD; SARS CORONAVIRUS; BATS;
TRANSMISSION; ALGORITHMS; DIVERSITY; ALIGNMENT; CHINA; TIME
AB A novel betacoronavirus associated with lethal respiratory and renal complications was recently identified in patients from several countries in the Middle East. We report the deep genome sequencing of the virus directly from a patient's sputum sample. Our high-throughput sequencing yielded a substantial depth of genome sequence assembly and showed the minority viral variants in the specimen. Detailed phylogenetic analysis of the virus genome (England/Qatar/2012) revealed its close relationship to European bat coronaviruses circulating among the bat species of the Vespertilionidae family. Molecular clock analysis showed that the 2 human infections of this betacoronavirus in June 2012 (EMC/2012) and September 2012 (England/Qatar/2012) share a common virus ancestor most likely considerably before early 2012, suggesting the human diversity is the result of multiple zoonotic events.
C1 [Cotten, Matthew; Watson, Simon J.; Palser, Anne L.; Petrova, Velislava; Kellam, Paul] Wellcome Trust Sanger Inst, Hinxton, England.
[Lam, Tommy T.; Pybus, Oliver G.] Univ Oxford, Oxford, England.
[Pillay, Deenan; Kellam, Paul] UCL, London, England.
[Grant, Paul; Nastouli, Eleni] Univ Coll London Hosp, London, England.
[Rambaut, Andrew] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Rambaut, Andrew] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Guan, Yi] Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
RP Kellam, P (reprint author), Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Cambridge CB10 1SA, England.
EM pk5@sanger.ac.uk
RI Lam, Tommy Tsan-Yuk/D-4837-2012;
OI Pybus, Oliver/0000-0002-8797-2667; Rambaut, Andrew/0000-0003-4337-3707
FU Wellcome Trust; European Community [223498, 278433]
FX This work was supported by the Wellcome Trust and the European
Community's Seventh Framework Programme (FP7/2007-2013) under the
project EMPERIE, European Community grant agreement number 223498 and
under the project PREDEMICS, grant agreement number 278433.
NR 31
TC 58
Z9 64
U1 0
U2 20
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 MAY
PY 2013
VL 19
IS 5
BP 736
EP 742
DI 10.3201/eid1905.130057
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 268LX
UT WOS:000328173400005
PM 23693015
ER
PT J
AU Levinson, J
Bogich, TL
Olival, KJ
Epstein, JH
Johnson, CK
Karesh, W
Daszak, P
AF Levinson, Jordan
Bogich, Tiffany L.
Olival, Kevin J.
Epstein, Jonathan H.
Johnson, Christine K.
Karesh, William
Daszak, Peter
TI Targeting Surveillance for Zoonotic Virus Discovery
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID HOST-RANGE; EMERGENCE; PATHOGENS; DISEASES; MAMMALS; RISK
AB We analyzed a database of mammal virus associations to ask whether surveillance targeting diseased animals is the best strategy to identify potentially zoonotic pathogens. Although a mixed healthy and diseased animal surveillance strategy is generally best, surveillance of apparently healthy animals would likely maximize zoonotic virus discovery potential for bats and rodents.
C1 [Levinson, Jordan; Bogich, Tiffany L.; Olival, Kevin J.; Epstein, Jonathan H.; Karesh, William; Daszak, Peter] EcoHlth Alliance, New York, NY 10001 USA.
[Bogich, Tiffany L.] NIH, Bethesda, MD 20892 USA.
[Bogich, Tiffany L.] Princeton Univ, Ecol & Evolutionary Biol Dept, Princeton, NJ 08544 USA.
[Johnson, Christine K.] Univ Calif Davis, Sch Vet Med, Davis, CA 95616 USA.
RP Daszak, P (reprint author), EcoHlth Alliance, 460 W 34th St,17th Flr, New York, NY 10001 USA.
EM daszak@ecohealthalliance.org
OI Bogich, Tiffany/0000-0002-8143-5289
FU United States Agency for International Development (USAID) Emerging
Pandemic Threats PREDICT program; NIAID [R01 AI079231]; Research and
Policy for Infectious Disease Dynamics (RAPIDD) program of the Science
and Technology Directorate; US Department of Homeland Security; Fogarty
International Center, National Institutes of Health (NIH); NIH Fogarty
American Recovery and Reinvestment Act award [3R01TW005869-06S10]
FX This study was funded in part by the generous support of the American
people through the United States Agency for International Development
(USAID) Emerging Pandemic Threats PREDICT program, a NIAID non-biodefene
emerging infectious disease research opportunities award R01 AI079231
(to P.D.); the Research and Policy for Infectious Disease Dynamics
(RAPIDD) program of the Science and Technology Directorate; the US
Department of Homeland Security; the Fogarty International Center,
National Institutes of Health (NIH) (to T.L.B.); and an NIH Fogarty
American Recovery and Reinvestment Act award (3R01TW005869-06S10; to
K.J.O).
NR 18
TC 13
Z9 13
U1 1
U2 20
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 MAY
PY 2013
VL 19
IS 5
BP 743
EP 747
DI 10.3201/eid1905.121042
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 268LX
UT WOS:000328173400006
PM 23647732
ER
PT J
AU Weinberg, A
Muresan, P
Fenton, T
Richardson, K
Dominguez, T
Bloom, A
Petzold, E
Anthony, P
Cunningham, CK
Spector, SA
Nachman, S
Siberry, GK
Handelsman, E
Flynn, PM
AF Weinberg, Adriana
Muresan, Petronella
Fenton, Terence
Richardson, Kelly
Dominguez, Teresa
Bloom, Anthony
Petzold, Elizabeth
Anthony, Patricia
Cunningham, Coleen K.
Spector, Stephen A.
Nachman, Sharon
Siberry, George K.
Handelsman, Edward
Flynn, Patricia M.
CA IMPAACTT P1088 Study Team
TI High proportions of regulatory B and T cells are associated with
decreased cellular responses to pH1N1 influenza vaccine in HIV-infected
children and youth (IMPAACT P1088)
SO HUMAN VACCINES & IMMUNOTHERAPEUTICS
LA English
DT Article
DE HIV infection; influenza vaccine; cell-mediated immunity; regulatory T
cells; regulatory B cells
ID BLOOD MONONUCLEAR-CELLS; GRANZYME-B; IMMUNE-RESPONSES; OLDER-ADULTS;
H1N1 2009; PROTECTION; IMMUNOGENICITY; LIVE; INDIVIDUALS; SAFETY
AB HIV-infected individuals have poor responses to inactivated influenza vaccines. To evaluate the potential role of regulatory T (Treg) and B cells (Breg), we analyzed their correlation with humoral and cell-mediated immune (CMI) responses to pandemic influenza (pH1N1) monovalent vaccine in HIV-infected children and youth. Seventy-four HIV-infected, 4- to 25-y old participants in a 2-dose pH1N1 vaccine study had circulating and pH1N1-stimulated Treg and Breg measured by flow cytometry at baseline, post-dose 1 and post-dose 2. Concomitantly, CMI was measured by ELISPOT and flow cytometry; and antibodies by hemagglutination inhibition (HAI). At baseline, most of the participants had pH1N1-specific IFN ELISPOT responses, whose magnitude positively correlated with the baseline pH1N1, but not with seasonal H1N1 HAI titers. pH1N1-specific IFN ELISPOT responses did not change post-dose 1 and significantly decreased post-dose 2. In contrast, circulating CD4+CD25+% and CD4+FOXP3+% Treg increased after vaccination. The decrease in IFN ELISPOT results was marginally associated with higher pH1N1-specific CD19+FOXP3+ and CD4+TGF+% Breg and Treg, respectively. In contrast, increases in HAI titers post-dose 1 were associated with significantly higher circulating CD19+CD25+% post-dose 1, whereas increases in IFN ELISPOT results post-dose 1 were associated with higher circulating CD4+/C8+CD25+FOXP3+%. In conclusion, in HIV-infected children and youth, influenza-specific Treg and Breg may contribute to poor responses to vaccination. However, robust humoral and CMI responses to vaccination may result in increased circulating Treg and/or Breg, establishing a feed-back mechanism.
C1 [Weinberg, Adriana; Richardson, Kelly; Dominguez, Teresa] Univ Colorado Denver, Div Infect Dis, Dept Pediat, Aurora, CO 80045 USA.
[Muresan, Petronella] Harvard Univ, Sch Publ Hlth, Frontier Sci & Technol Res Fdn, Boston, MA 02115 USA.
[Fenton, Terence] Harvard Univ, Sch Publ Hlth, Stat & Data Anal Ctr, Boston, MA 02115 USA.
[Bloom, Anthony] Frontier Sci & Technol Res Fdn Inc, Amherst, NY USA.
[Petzold, Elizabeth] Int Maternal Pediat Adolescent AIDS Clin Trials G, Durham, NC USA.
[Anthony, Patricia] Univ So Calif, Child & Adolescent Virol Res Lab, Los Angeles, CA USA.
[Cunningham, Coleen K.] Duke Univ, Med Ctr, Duke Hosp, Durham, NC USA.
[Spector, Stephen A.] Univ Calif San Diego, Div Infect Dis, Dept Pediat, San Diego, CA 92103 USA.
[Nachman, Sharon] SUNY Stony Brook, Dept Pediat, Stony Brook, NY 11794 USA.
[Siberry, George K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediatr Adolescent & Maternal AIDS Branch, NIH, Bethesda, MD USA.
[Handelsman, Edward] DAIDS, NIAID, HIV Res Branch NIH, Bethesda, MD USA.
[Flynn, Patricia M.] St Jude Childrens Res Hosp, Dept Infect Dis, Memphis, TN 38105 USA.
RP Weinberg, A (reprint author), Univ Colorado Denver, Div Infect Dis, Dept Pediat, Aurora, CO 80045 USA.
EM adriana.weinberg@ucdenver.edu
FU National Institute of Allergy and Infectious Diseases (NIAID) [U01
AI068632]; Eunice Kennedy Shriver National Institute of Child Health and
Human Development (NICHD); National Institute of Mental Health (NIMH)
[AI068632]; National Institute of Allergy and Infectious Diseases
(NIAID); NICHD International and Domestic Pediatric and Maternal HIV
Clinical Trials Network; NICHD [N01-DK-9-001/HHSN267200800001C]; [U01
AI41110]; [1 U01 AI068616]
FX Overall support for the International Maternal Pediatric Adolescent AIDS
Clinical Trials Group (IMPAACT) was provided by the National Institute
of Allergy and Infectious Diseases (NIAID) [U01 AI068632], the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD) and the National Institute of Mental Health (NIMH) [AI068632].
The content is solely the responsibility of the authors and does not
necessarily represent the official views of the NIH. This work was
supported by the Statistical and Data Analysis Center at Harvard School
of Public Health, under the National Institute of Allergy and Infectious
Diseases cooperative agreement #5 U01 AI41110 with the Pediatric AIDS
Clinical Trials Group (PACTG) and #1 U01 AI068616 with the IMPAACT
Group. Support of the sites was provided by the National Institute of
Allergy and Infectious Diseases (NIAID) and the NICHD International and
Domestic Pediatric and Maternal HIV Clinical Trials Network funded by
NICHD (contract number N01-DK-9-001/HHSN267200800001C).
NR 43
TC 5
Z9 5
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2164-5515
EI 2164-554X
J9 HUM VACC IMMUNOTHER
JI Human Vaccines Immunother.
PD MAY 1
PY 2013
VL 9
IS 5
BP 957
EP 968
DI 10.4161/hv.23774
PG 12
WC Biotechnology & Applied Microbiology; Immunology
SC Biotechnology & Applied Microbiology; Immunology
GA 259SD
UT WOS:000327545700004
PM 23370281
ER
PT J
AU Nguyen, CM
Levy, AJ
AF Nguyen, Chien M.
Levy, Alan J.
TI Cohesive fracture of plane orthotropic layers
SO INTERNATIONAL JOURNAL OF SOLIDS AND STRUCTURES
LA English
DT Article
DE Layers; Orthotropy; Debonding; Cohesion; Interface; Defect; Integral
equation; Fracture; Elasticity
ID FRP-CONCRETE INTERFACE; DECOHESION; DELAMINATION; COMPOSITES; SPECIMENS;
FAILURE; BEAMS
AB Crack-like cohesive defect propagation within a plane orthotropic linear elastic layer is considered by assuming that the defect, and its growth under load, can be modeled as the evolving separation along a straight, predetermined nonlinear, nonuniform Needleman-type cohesive interface. The analysis exploits a general form of orthotropy rescaling originally developed for the displacement boundary value problem by Krenk (1979). It is shown that when the material is degenerate orthotropic (i.e., rho = 1, rho is the orthotropic shear parameter) rescaling enables the determination of solutions from isotropic ones and, when the material is fully orthotropic, rescaling allows for solutions to be obtained from problems with the simpler cubic symmetry. (These are well known attributes of linear static sharp crack analysis, which depend on an alternative form of rescaling the traction boundary value problem (Suo, 1990; Suo et al, 1991).) The procedure is demonstrated by obtaining degenerate orthotropic response from isotropic solutions recently obtained by the authors in an investigation of both solitary as well as multiple cohesive defect interaction problems in layered systems under arbitrary loading (Nguyen and Levy, 2009, 2011). In order to obtain fully orthotropic solutions via rescaling, a novel integral equation formulation is developed based on exact infinitesimal strain elasticity solutions for rectangular domains composed of cubically symmetric media and subject to arbitrary loading. Explicit results are obtained for the simple edge notch bend configuration, chosen so as to shed light on the mechanisms of defect propagation in orthotropic layers. It is demonstrated that increasing the orthotropic stiffness ratio can precipitate a quasi-brittle defect growth response. Furthermore, it is well known that in a number of technically important problem geometries and loadings, static sharp crack solutions are only weakly dependent on shear parameter rho enabling the estimation of fully orthotropic behavior from isotropic solutions (Suo et al, 1991). This result is shown to be true for nonlinear cohesive fracture analysis of the edge notch bend configuration analyzed in this study. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Nguyen, Chien M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Levy, Alan J.] Syracuse Univ, Dept Mech & Aerosp Engn, Syracuse, NY 13244 USA.
RP Levy, AJ (reprint author), Syracuse Univ, Dept Mech & Aerosp Engn, Syracuse, NY 13244 USA.
EM ajlevy@syr.edu
NR 24
TC 0
Z9 0
U1 1
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0020-7683
EI 1879-2146
J9 INT J SOLIDS STRUCT
JI Int. J. Solids Struct.
PD MAY 1
PY 2013
VL 50
IS 9
BP 1266
EP 1284
DI 10.1016/j.ijsolstr.2012.12.024
PG 19
WC Mechanics
SC Mechanics
GA 250MZ
UT WOS:000326858200007
ER
PT J
AU Ghany, MG
Liang, TJ
AF Ghany, Marc G.
Liang, T. Jake
TI Current and Future Therapies for Hepatitis C Virus Infection REPLY
SO GLOBAL PUBLIC HEALTH
LA English
DT Letter
C1 [Ghany, Marc G.; Liang, T. Jake] NIH, Bethesda, MD 20892 USA.
RP Ghany, MG (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM jliang@nih.gov
NR 4
TC 0
Z9 0
U1 0
U2 1
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1744-1692
EI 1744-1706
J9 GLOB PUBLIC HEALTH
JI Glob. Public Health
PD MAY 1
PY 2013
VL 8
IS 5
BP 679
EP 680
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 243XE
UT WOS:000326350900024
ER
PT J
AU Kelly, AC
Wickner, RB
AF Kelly, Amy C.
Wickner, Reed B.
TI Saccharomyces cerevisiae A sexy yeast with a prion problem
SO PRION
LA English
DT Editorial Material
DE outcross; fitness; evolutionary constraint; effective population size
ID ESCHERICHIA-COLI; SUP35 PROTEIN; ENVIRONMENTAL-STRESS; POPULATION
GENOMICS; NATURAL-SELECTION; GENETIC-VARIATION; SPECIES BARRIERS;
MUTATOR ALLELES; WILD YEASTS; PSI+ PRION
AB Yeast prions are infectious proteins that spread exclusively by mating. The frequency of prions in the wild therefore largely reflects the rate of spread by mating counterbalanced by prion growth slowing effects in the host. We recently showed that the frequency of outcross mating is about 1% of mitotic doublings with 23-46% of total matings being outcrosses. These findings imply that even the mildest forms of the [PSI+], [URE3] and [PIN+] prions impart > 1% growth/survival detriment on their hosts. Our estimate of outcrossing suggests that Saccharomyces cerevisiae is far more sexual than previously thought and would therefore be more responsive to the adaptive effects of natural selection compared with a strictly asexual yeast. Further, given its large effective population size, a growth/survival detriment of > 1% for yeast prions should strongly select against prion-infected strains in wild populations of Saccharomyces cerevisiae.
C1 [Kelly, Amy C.; Wickner, Reed B.] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Wickner, RB (reprint author), NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
EM wickner@helix.nih.gov
FU Intramural NIH HHS
NR 60
TC 6
Z9 6
U1 0
U2 9
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD MAY 1
PY 2013
VL 7
IS 3
BP 215
EP 220
DI 10.4161/pri.24845
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 246BJ
UT WOS:000326510900005
PM 23764836
ER
PT J
AU Henson, JM
Derlega, VJ
Pearson, MR
Ferrer, R
Holmes, K
AF Henson, James M.
Derlega, Valerian J.
Pearson, Matthew R.
Ferrer, Rebecca
Holmes, Karen
TI AFRICAN AMERICAN STUDENTS' RESPONSES TO RACIAL DISCRIMINATION: HOW
RACE-BASED REJECTION SENSITIVITY AND SOCIAL CONSTRAINTS ARE RELATED TO
PSYCHOLOGICAL REACTIONS
SO JOURNAL OF SOCIAL AND CLINICAL PSYCHOLOGY
LA English
DT Article
ID PERCEIVED DISCRIMINATION; MENTAL-HEALTH; ETHNIC DISCRIMINATION;
INTRUSIVE THOUGHTS; STRESS; PATTERNS; STIGMA; CANCER; BLACK
AB We examined the association between two individual differences (race-based rejection sensitivity and social constraints in talking about racism with family, friends, and/or intimate partners) and psychological reactions to an incident of racial discrimination. Participants were 551 African American undergraduates from either a predominantly white university (PWU) or a historically black university (HBU). Race-based rejection sensitivity (RS-Race) predicted higher negative affect and lower forgiveness for the perpetrator. Social constraints predicted higher negative affect and (marginally) lower forgiveness. There was also an interaction between social constraints and RS-Race: RS-Race was strongly negatively related to positive affect and forgiveness among participants with low social constraints but essentially unrelated among those with high social constraints. Thought intrusions (that might prolong the memory of the prejudicial event) also mediated the effects of RS-Race and social constraints on negative affect and forgiveness. The results document how individual differences are associated with reactions to being the target of racial discrimination in day-to-day interactions.
C1 [Henson, James M.; Derlega, Valerian J.; Pearson, Matthew R.] Old Dominion Univ, Norfolk, VA 23529 USA.
[Ferrer, Rebecca] NCI, Bethesda, MD 20892 USA.
[Holmes, Karen] Norfolk State Univ, Norfolk, VA USA.
RP Henson, JM (reprint author), Old Dominion Univ, Dept Psychol, Norfolk, VA 23529 USA.
EM jhenson@odu.edu; vderlega@odu.edu
NR 42
TC 9
Z9 9
U1 4
U2 14
PU GUILFORD PUBLICATIONS INC
PI NEW YORK
PA 72 SPRING STREET, NEW YORK, NY 10012 USA
SN 0736-7236
J9 J SOC CLIN PSYCHOL
JI J. Soc. Clin. Psychol.
PD MAY
PY 2013
VL 32
IS 5
BP 504
EP 529
PG 26
WC Psychology, Clinical; Psychology, Social
SC Psychology
GA 236YK
UT WOS:000325835200003
ER
PT J
AU Bhattacharyya, S
Kurdziel, K
Wei, L
Riffle, L
Kaur, G
Hill, GC
Jacobs, PM
Tatum, JL
Doroshow, JH
Kalen, JD
AF Bhattacharyya, Sibaprasad
Kurdziel, Karen
Wei, Ling
Riffle, Lisa
Kaur, Gurmeet
Hill, G. Craig
Jacobs, Paula M.
Tatum, James L.
Doroshow, James H.
Kalen, Joseph D.
TI Zirconium-89 labeled panitumumab: a potential immuno-PET probe for
HER1-expressing carcinomas
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; POSITRON-EMISSION-TOMOGRAPHY; HUMAN
MONOCLONAL-ANTIBODY; ABX-EGF; COLORECTAL-CANCER; PHARMACOKINETICS;
INHIBITOR; THERAPY; MICE
AB Introduction: Anti-HER1 monoclonal antibody (mAb), panitumumab (Vectibix) is a fully human mAb approved by the FDA for the treatment of epidermal growth factor receptor (EGFR, HER1)-expressing colorectal cancers. By combining the targeted specificity of panitumumab with the quantitative in vivo imaging capabilities of PET, we evaluated the potential of Zr-89-DFO-panitumumab PET/CT imaging and performed non-invasive, in vivo imaging of HER1 expression and estimated human dosimetry.
Methods: Panitumumab was radiolabeled with Zr-89 using a derivative of desferrioxamine (DFO-Bz-NCS) and with In-111 using CHX-A" DTPA as bifunctional chelators. Comparative biodistribution/dosimetry of both radiotracers was performed in non-tumor bearing athymic nude mice (n=2 females and n=2 males) over 1-week following i.v. injection of either using Zr-89-DFO-panitumumab or In-111-CHX-A"-DTPA-panitumumab. Micro-PET/CT imaging of female athymic nude mice bearing human breast cancer tumors (n=5 per tumor group) with variable HER1-expression very low (BT-474), moderate (MDA-MB-231), and very high (MDA-MB-468) was performed at over 1 week following i.v. injection of Zr-89-DFO-panitumumab.
Results: Radiochemical yield and purity of Zr-89-Panitumumab was >70% and >98% respectively with specific activity 150 +/- 10 MBq/mg of panitumumab in a similar to 4 hr synthesis time. Biodistribution of In-111-CHX-A" DTPA-panitumumab and Zr-89-DFO-panitumumab in athymic non-tumor bearing nude mice displayed similar percent injected dose per gram of tissue with prominent accumulation of both tracers in the lymph nodes, a known clearance mechanism of panitumumab. Also exhibited was prolonged blood pool with no evidence of targeted accumulation in any organ. Human radiation dose estimates showed similar biodistributions with estimated human effective doses of 0.578 and 0.183 mSv/MBq for Zr-89-DFO-panitumumab and In-111-CHX-A"DTPA-panitumumab, respectively. Given the potential quantitative and image quality advantages of PET, imaging of tumor bearing mice was only performed using Zr-89-DFO-panitumumab. Immuno-PET imaging of Zr-89-DFO-panitumumab in mice bearing breast cancer xenograft tumors with variable HER1 expression showed high tumor uptake (SUV >7) in the MDA-MB-468 high HER1-expressing mice and a strong correlation between HER1-expression level and tumor uptake (R-2 = 0.857, P < .001).
Conclusions: Zr-89-DFO-panitumumab can prepared with high radiochemical purity and specific activity. Zr-89-DFO-panitumumab microPET/CT showed uptake corresponding to HER-1 expression. Due to poor clearance, initial dosimetry estimates suggest that only a low dose Zr-89-DFO-panitumumab shows favorable human dosimetry; however due to high tumor uptake, the use of Zr-89-DFO-panitumumab is expected to be clinically feasible. Published by Elsevier Inc.
C1 [Bhattacharyya, Sibaprasad; Wei, Ling] SAIC Frederick, FNLCR, ADRD, Frederick, MD 21702 USA.
[Kurdziel, Karen] NCI, NIH, CCR, Mol Imaging Program, Bethesda, MD USA.
[Riffle, Lisa; Kalen, Joseph D.] SAIC Frederick, Small Anim Imaging Program, LASP, Frederick, MD 21702 USA.
[Kaur, Gurmeet] Frederick Natl Lab Canc Res, DCTD, Frederick, MD USA.
[Hill, G. Craig] SAIC Frederick, Clin Res Directorate, CMRP, Frederick, MD USA.
[Jacobs, Paula M.; Tatum, James L.; Doroshow, James H.] NCI, DCTD, Canc Imaging Program, Bethesda, MD USA.
RP Bhattacharyya, S (reprint author), SAIC Frederick, FNLCR, ADRD, Frederick, MD 21702 USA.
EM bhattacharyyas2@mail.nih.gov
OI Kalen, Joseph/0000-0002-7163-4604
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract 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.
Authors are grateful to Dr. Lawrence Szajek of cyclotron facility at NIH
Bethesda for providing 89Zr-oxalate.
NR 31
TC 15
Z9 15
U1 3
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
EI 1872-9614
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD MAY
PY 2013
VL 40
IS 4
BP 451
EP 457
DI 10.1016/j.nucmedbio.2013.01.007
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 237BI
UT WOS:000325842800004
PM 23454247
ER
PT J
AU Karabanov, AN
Chao, CC
Paine, R
Hallett, M
AF Karabanov, Anke Ninija
Chao, Chi-Chao
Paine, Rainer
Hallett, Mark
TI Mapping Different Intra-Hemispheric Parietal-Motor Networks Using Twin
Coil TMS
SO BRAIN STIMULATION
LA English
DT Article
DE Twin-coil TMS; Intra-parietal sulcus; Primary motor cortex;
Intra-hemispheric connectivity
ID TRANSCRANIAL MAGNETIC STIMULATION; HUMAN POSTERIOR PARIETAL; VENTRAL
PREMOTOR CORTEX; FUNCTIONAL INTERPLAY; HUMANS; CONNECTIONS; PRECISION;
AREAS; ACTIVATION; PATHWAYS
AB Background: Accumulating evidence suggests anatomical and functional differences in connectivity between the anterior and posterior parts of the inferior-parietal lobule (IPL) and the frontal motor areas.
Objective/Hypothesis: This study investigates whether different intra-hemispheric parietal-motor interactions can be observed along the anterior posterior axis of the IPL in the resting human brain.
Methods: We use a twin coil transcranial magnetic stimulation technique to test intra-hemispheric interactions between three points adjacent to the intra-parietal sulcus (anterior, central, posterior) and the ipsilateral primary motor cortex (M1) at rest in both hemispheres.
Results: We found that stimulation of the anterior IPL resulted in an inhibition of the ipsilateral M1 in both hemispheres. Stimulation of the central and posterior IPL resulted in a facilitatory effect on ipsilateral M1 in the left but not for the right hemisphere. Additionally we show that there is considerable inter-subject variability concerning the optimal parietal facilitatory and inhibitory position.
Conclusions: The IPL has distinct inhibitory and facilitatory connections to the ipsilateral M1 Whereas inhibitory connections are observed in both hemispheres, facilitatory connections are asymmetric. These parietal-motor networks may represent the basis for the functional differences between these regions in reaching and grasping tasks and mirror the functional asymmetry observed in the motor system. From a practical point of view, we note that the inter-subject variability means that future TMS studies of the parietal area might consider a hot-spot localization similar to the procedures commonly used for M1. Published by Elsevier Inc.
C1 [Karabanov, Anke Ninija; Chao, Chi-Chao; Paine, Rainer; Hallett, Mark] NINDS, NIH, Bethesda, MD 20892 USA.
[Karabanov, Anke Ninija] Univ Copenhagen, Hvidovre Hosp, Danish Res Ctr Magnet Resonance, DK-2650 Hvidovre, Denmark.
[Karabanov, Anke Ninija] Univ Copenhagen, Dept Exercise & Sport Sci, Copenhagen, Denmark.
RP Karabanov, AN (reprint author), Univ Copenhagen, Hvidovre Hosp, Danish Res Ctr Magnet Resonance, Dept MR,Sect 340, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark.
EM ankenk@drcmr.dk
OI Chao, Chi-Chao/0000-0001-6499-5789; Karabanov, Anke
Ninija/0000-0003-1874-393X
FU National Institute of Neurological Disorders and Stroke Intramural
Program
FX This work was supported by the National Institute of Neurological
Disorders and Stroke Intramural Program.
NR 33
TC 10
Z9 10
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1935-861X
EI 1876-4754
J9 BRAIN STIMUL
JI Brain Stimul.
PD MAY
PY 2013
VL 6
IS 3
BP 384
EP 389
DI 10.1016/j.brs.2012.08.002
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 234VF
UT WOS:000325671700023
PM 22939165
ER
PT J
AU Apostolova, E
You, DK
Xue, ZY
Antani, S
Demner-Fushman, D
Thoma, GR
AF Apostolova, Emilia
You, Daekeun
Xue, Zhiyun
Antani, Sameer
Demner-Fushman, Dina
Thoma, George R.
TI Image retrieval from scientific publications: Text and image content
processing to separate multipanel figures
SO JOURNAL OF THE AMERICAN SOCIETY FOR INFORMATION SCIENCE AND TECHNOLOGY
LA English
DT Article
DE automatic indexing; information retrieval; image retrieval
ID SEARCH
AB Images contained in scientific publications are widely considered useful for educational and research purposes, and their accurate indexing is critical for efficient and effective retrieval. Such image retrieval is complicated by the fact that figures in the scientific literature often combine multiple individual subfigures (panels). Multipanel figures are in fact the predominant pattern in certain types of scientific publications. The goal of this work is to automatically segment multipanel figuresa necessary step for automatic semantic indexing and in the development of image retrieval systems targeting the scientific literature. We have developed a method that uses the image content as well as the associated figure caption to: (1) automatically detect panel boundaries; (2) detect panel labels in the images and convert them to text; and (3) detect the labels and textual descriptions of each panel within the captions. Our approach combines the output of image-content and text-based processing steps to split the multipanel figures into individual subfigures and assign to each subfigure its corresponding section of the caption. The developed system achieved precision of 81% and recall of 73% on the task of automatic segmentation of multipanel figures.
C1 [Apostolova, Emilia; You, Daekeun; Xue, Zhiyun; Antani, Sameer; Demner-Fushman, Dina; Thoma, George R.] Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD 20894 USA.
RP Apostolova, E (reprint author), Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM emilia.aposto@gmail.com; youd@mail.nih.gov; xuez@mail.nih.gov;
santani@mail.nih.gov; ddemner@mail.nih.gov; gthoma@mail.nih.gov
OI Antani, Sameer/0000-0002-0040-1387
FU National Library of Medicine, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Library of Medicine, National Institutes of Health. We would
like to thank the ImageCLEF organizers and the Radiological Society of
North America (RSNA), publisher of Radiology and RadioGraphics, for
making the database available for the experiments under the ImageCLEF
medical image retrieval task.
NR 23
TC 9
Z9 9
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1532-2882
EI 1532-2890
J9 J AM SOC INF SCI TEC
JI J. Am. Soc. Inf. Sci. Technol.
PD MAY
PY 2013
VL 64
IS 5
BP 893
EP 908
DI 10.1002/asi.22810
PG 16
WC Computer Science, Information Systems; Information Science & Library
Science
SC Computer Science; Information Science & Library Science
GA 238GE
UT WOS:000325930600003
ER
PT J
AU Jeong, W
Doroshow, JH
Kummar, S
AF Jeong, Woondong
Doroshow, James H.
Kummar, Shivaani
TI United States Food and Drug Administration approved oral kinase
inhibitors for the treatment of malignancies
SO CURRENT PROBLEMS IN CANCER
LA English
DT Article
ID CELL LUNG-CANCER; CHRONIC MYELOID-LEUKEMIA; PHASE-III TRIAL;
GASTROINTESTINAL STROMAL TUMORS; DIAGNOSED CHRONIC-PHASE; LAPATINIB PLUS
CAPECITABINE; PLACEBO-CONTROLLED PHASE-3; ADVANCED BREAST-CANCER;
DOUBLE-BLIND; IMATINIB MESYLATE
C1 [Jeong, Woondong] NCI, Div Canc Treatment & Diag, Adv Dev Therapeut Training Program, Bethesda, MD 20892 USA.
[Doroshow, James H.] NCI, Bethesda, MD 20892 USA.
[Kummar, Shivaani] NCI, Off Director, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Jeong, W (reprint author), NCI, Div Canc Treatment & Diag, Adv Dev Therapeut Training Program, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z99 CA999999]
NR 82
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 0147-0272
EI 1535-6345
J9 CURR PROB CANCER
JI Curr. Probl. Cancer
PD MAY-JUN
PY 2013
VL 37
IS 3
BP 110
EP 144
DI 10.1016/j.currproblcancer.2013.06.001
PG 35
WC Oncology
SC Oncology
GA 215PH
UT WOS:000324222200002
PM 23972982
ER
PT J
AU Squarize, CH
Castilho, RM
Abrahao, AC
Molinolo, A
Lingen, MW
Gutkind, JS
AF Squarize, Cristiane H.
Castilho, Rogerio M.
Abrahao, Aline C.
Molinolo, Alfredo
Lingen, Mark W.
Gutkind, J. Silvio
TI PTEN Deficiency Contributes to the Development and Progression of Head
and Neck Cancer
SO NEOPLASIA
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; GENE-EXPRESSION; TUMOR SUPPRESSION; TONGUE
CANCER; MOUSE MODELS; ORAL-CANCER; K-RAS; MUTATIONS; CARCINOGENESIS;
IDENTIFICATION
AB The sequencing of the head and neck cancer has provided a blueprint of the most frequent genetic alterations in this cancer type. They include inactivating mutations in Notch, p53, and p16(ink4a) tumor suppressor genes, in addition to nonoverlapping activating mutations of the PIK3CA and RAS oncogenes or inactivation of the tumor suppressor gene PTEN. Notably, these genetic alterations, along with epigenetic changes, result in increased activity of phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway, which is present in most head and neck squamous cell carcinomas (HNSCCs). Moreover, we show here that approximately 30% of HNSCCs exhibit reduced PTEN expression. We challenged the biologic relevance of this finding by combining the intraoral administration of a tobacco surrogate, 4-nitroquinoline 1-oxide, with a genetically defined animal model displaying reduced PTEN expression, achieved by the conditional deletion of Pten using the keratin promoter 14 CRE-lox system. This provided a specific genetic and environmentally defined animal model for HNSCC that resulted in the rapid development of oral-specific carcinomas. Under these experimental conditions, control mice did not develop HNSCC lesions. In contrast, most mice harboring Pten deficiency developed multiple SCC lesions in the lateral border and ventral part of the tongue and floor of the mouth, which are the preferred anatomic sites for human HNSCC. Overall, our study highlights the likely clinical relevance of reduced PTEN expression and/or inactivation in HNSCC progression, while the combined Pten deletion with exposure to tobacco carcinogens or their surrogates may provide a unique experimental model system to study novel molecular targeted treatments for HNSCC patients.
C1 [Squarize, Cristiane H.; Castilho, Rogerio M.] Univ Michigan, Dept Periodont & Oral Med, Lab Epithelial Biol, Ann Arbor, MI 48109 USA.
[Abrahao, Aline C.] Univ Fed Rio de Janeiro, Sch Dent, Dept Pathol & Oral Diag, Rio De Janeiro, RJ, Brazil.
[Molinolo, Alfredo; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
[Lingen, Mark W.] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
RP Squarize, CH (reprint author), Univ Michigan, 1011 N Univ Ave,Room 3210, Ann Arbor, MI 48109 USA.
EM csquariz@umich.edu
RI Abrahao, Aline/G-1863-2012
OI Abrahao, Aline/0000-0002-3397-3234
FU Intramural Research Program, National Institute of Dental and
Craniofacial Research, National Institutes of Health (NIH); University
of Michigan Comprehensive Cancer Center [P50-CA97248]; (University of
Michigan Head and Neck, Specialized Programs of Research Excellence)
from the NIH/National Cancer Institute; Coordenacao de Aperfeicoamento
de Pessoal de Nivel Superior (Brasilia, DF, Brazil)
FX This work was supported by the Intramural Research Program, National
Institute of Dental and Craniofacial Research, National Institutes of
Health (NIH) and the University of Michigan Comprehensive Cancer Center
through grant P50-CA97248 (University of Michigan Head and Neck,
Specialized Programs of Research Excellence) from the NIH/National
Cancer Institute. A.C.A. was supported by Coordenacao de Aperfeicoamento
de Pessoal de Nivel Superior (Brasilia, DF, Brazil).
NR 52
TC 28
Z9 32
U1 0
U2 8
PU NEOPLASIA PRESS
PI ANN ARBOR
PA 1150 W MEDICAL CENTER DR, MSRB III, RM 9303, ANN ARBOR, MI 48109-0648
USA
SN 1522-8002
J9 NEOPLASIA
JI Neoplasia
PD MAY
PY 2013
VL 15
IS 5
BP 461
EP 471
DI 10.1593/neo.121024
PG 11
WC Oncology
SC Oncology
GA 219DT
UT WOS:000324486500001
PM 23633918
ER
PT J
AU Mohammed, A
Janakiram, NB
Brewer, M
Vedala, K
Steele, VE
Rao, CV
AF Mohammed, Altaf
Janakiram, Naveena B.
Brewer, Misty
Vedala, Krishna
Steele, Vernon E.
Rao, Chinthalapally V.
TI Multitargeted Low-Dose GLAD Combination Chemoprevention: A Novel and
Promising Approach to Combat Colon Carcinogenesis
SO NEOPLASIA
LA English
DT Article
ID EPIDERMAL-GROWTH-FACTOR; FAMILIAL ADENOMATOUS POLYPOSIS; ABERRANT CRYPT
FOCI; COLORECTAL-CANCER; FACTOR RECEPTOR; MIN MOUSE; CYCLOOXYGENASE-2
INHIBITOR; INTESTINAL CARCINOGENESIS; REDUCTASE INHIBITOR; PREVENTION
AB Preclinical studies have shown that gefitinib, licofelone, atorvastatin, and alpha- difluoromethylornithine (GLAD) are promising colon cancer chemopreventive agents. Because low-dose combination regimens can offer potential additive or synergistic effects without toxicity, GLAD combination was tested for toxicity and chemopreventive efficacy for suppression of intestinal tumorigenesis in adenomatous polyposis coli (APC)(Min/+) mice. Six-week-old wild-type and APC(Min/+) mice were fed modified American Institute of Nutrition 76A diets with or without GLAD (25 + 50 + 50 + 500 ppm) for 14 weeks. Dietary GLAD caused no signs of toxicity based on organ pathology and liver enzyme profiles. GLAD feeding strongly inhibited (80-83%, P < .0001) total intestinal tumor multiplicity and size in APC(Min/+) mice (means +/- SEM tumors for control vs GLAD were 67.1 +/- 5.4 vs 11.3 +/- 1.1 in males and 72.3 +/- 8.9 vs 14.5 +/- 2.8 in females). Mice fed GLAD had >95% fewer polyps with sizes of >2 mm compared with control mice and showed 75% and 85% inhibition of colonic tumors in males and females, respectively. Molecular analyses of polyps suggested that GLAD exerts efficacy by inhibiting cell proliferation, inducing apoptosis, decreasing beta-catenin and caveolin-1 levels, increasing caspase-3 cleavage and p21, and modulating expression profile of inflammatory cytokines. These observations demonstrate that GLAD, a novel cocktail of chemopreventive agents at very low doses, suppresses intestinal tumorigenesis in APC(Min/+) mice with no toxicity. This novel strategy to prevent colorectal cancer is an important step in developing agents with high efficacy without unwanted side effects.
C1 [Mohammed, Altaf; Janakiram, Naveena B.; Brewer, Misty; Vedala, Krishna; Rao, Chinthalapally V.] Univ Oklahoma, Hlth Sci Ctr, PC Stephenson Canc Ctr, Dept Med,Hematol Oncol Sect,Ctr Canc Prevent & Dr, Oklahoma City, OK 73104 USA.
[Steele, Vernon E.] NCI, Chemoprevent Agent Dev Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Rao, CV (reprint author), Univ Oklahoma, Hlth Sci Ctr, Ctr Canc Prevent & Drug Dev, 975 NE 10th St,BRC Bldg 2,Room 1203, Oklahoma City, OK 73104 USA.
EM cv-rao@ouhsc.edu
FU National Cancer Institute [N01CN-53300]; Kerley Cade Endowed Chair
FX We acknowledge support from the National Cancer Institute (N01CN-53300)
and Kerley Cade Endowed Chair in supporting this study.
NR 49
TC 7
Z9 7
U1 0
U2 4
PU NEOPLASIA PRESS
PI ANN ARBOR
PA 1150 W MEDICAL CENTER DR, MSRB III, RM 9303, ANN ARBOR, MI 48109-0648
USA
SN 1522-8002
J9 NEOPLASIA
JI Neoplasia
PD MAY
PY 2013
VL 15
IS 5
BP 481
EP +
DI 10.1593/neo.13282
PG 12
WC Oncology
SC Oncology
GA 219DT
UT WOS:000324486500003
PM 23633920
ER
PT J
AU Leung, JM
Sin, DD
AF Leung, Janice M.
Sin, Don D.
TI Biomarkers in airway diseases
SO CANADIAN RESPIRATORY JOURNAL
LA English
DT Review
DE Airway disease; Asthma; Biomarkers; Chronic obstructive pulmonary
disease
ID OBSTRUCTIVE PULMONARY-DISEASE; EXHALED NITRIC-OXIDE; RANDOMIZED
CONTROLLED-TRIAL; ASTHMA; EXACERBATIONS; PROTEIN; COUNTS; COPD
AB The inherent limitations of spirometry and clinical history have prompted clinicians and scientists to search for surrogate markers of airway diseases. Although few biomarkers have been widely accepted into the clinical armamentarium, the authors explore three sources of biomarkers that have shown promise as indicators of disease severity and treatment response. In asthma, exhaled nitric oxide measurements can predict steroid responsiveness and sputum eosinophil counts have been used to titrate anti-inflammatory therapies. In chronic obstructive pulmonary disease, inflammatory plasma biomarkers, such as fibrinogen, club cell secretory protein-16 and surfactant protein D, can denote greater severity and predict the risk of exacerbations. While the multitude of disease phenotypes in respiratory medicine make biomarker development especially challenging, these three may soon play key roles in the diagnosis and management of airway diseases.
C1 [Leung, Janice M.] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Sin, Don D.] St Pauls Hosp, UBC James Hogg Res Ctr, Vancouver, BC V6Z 1Y6, Canada.
[Sin, Don D.] Univ British Columbia, Dept Med, Div Resp Med, Vancouver, BC, Canada.
RP Leung, JM (reprint author), NIH, Dept Crit Care Med, 10 Ctr Dr,Room 2C145, Bethesda, MD 20892 USA.
EM janice.leung@nih.gov
NR 21
TC 9
Z9 9
U1 0
U2 4
PU PULSUS GROUP INC
PI OAKVILLE
PA 2902 S SHERIDAN WAY, OAKVILLE, ONTARIO L6J 7L6, CANADA
SN 1198-2241
J9 CAN RESPIR J
JI Can. Respir. J.
PD MAY-JUN
PY 2013
VL 20
IS 3
BP 180
EP 182
PG 3
WC Respiratory System
SC Respiratory System
GA 207JM
UT WOS:000323594700013
PM 23762888
ER
PT J
AU Deziel, NC
Ward, MH
Bell, EM
Whitehead, TP
Gunier, RB
Friesen, MC
Nuckols, JR
AF Deziel, Nicole C.
Ward, Mary H.
Bell, Erin M.
Whitehead, Todd P.
Gunier, Robert B.
Friesen, Melissa C.
Nuckols, John R.
TI Temporal Variability of Pesticide Concentrations in Homes and
Implications for Attenuation Bias in Epidemiologic Studies
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE dust; environmental exposure; pesticides; reliability
ID CHILDHOOD LEUKEMIA; PRENATAL EXPOSURE; CHLORPYRIFOS; CALIFORNIA; CANCER;
DUST; RISK; LYMPHOMA; CHILDREN; HOUSE
AB BACKGROUND: Residential pesticide exposure has been linked to adverse health outcomes in adults and children. High-quality exposure estimates are critical for confirming these associations. Past epidemiologic studies have used one measurement of pesticide concentrations in carpet dust to characterize an individual's average long-term exposure. If concentrations vary over time, this approach could substantially misclassify exposure and attenuate risk estimates.
OBJECTIVES: We assessed the repeatability of pesticide concentrations in carpet dust samples and the potential attenuation bias in epidemiologic studies relying on one sample.
METHODS: We collected repeated carpet dust samples (median = 3; range, 1-7) from 21 homes in Fresno County, California, during 2003-2005. Dust was analyzed for 13 pesticides using gas chromatography-mass spectrometry. We used mixed-effects models to estimate between-and within-home variance. For each pesticide, we computed intraclass correlation coefficients (ICCs) and the estimated attenuation of regression coefficients in a hypothetical case-control study collecting a single dust sample.
RESULTS: The median ICC was 0.73 (range, 0.37-0.95), demonstrating higher between-home than within-home variability for most pesticides. The expected magnitude of attenuation bias associated with using a single dust sample was estimated to be < 30% for 7 of the 13 compounds evaluated.
CONCLUSIONS: For several pesticides studied, use of one dust sample to represent an exposure period of approximately 2 years would not be expected to substantially attenuate odds ratios. Further study is needed to determine if our findings hold for longer exposure periods and for other pesticides.
C1 [Deziel, Nicole C.; Ward, Mary H.; Friesen, Melissa C.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Bell, Erin M.] Univ Albany, Sch Publ Hlth, Dept Environm Hlth Sci, Rensselaer, NY USA.
[Whitehead, Todd P.; Gunier, Robert B.] Univ Calif Berkeley, Sch Publ Hlth, Dept Environm Hlth Sci, Berkeley, CA 94720 USA.
[Nuckols, John R.] Colorado State Univ, Dept Environm & Radiol Hlth Sci, Ft Collins, CO USA.
RP Deziel, NC (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 8005, Bethesda, MD 20892 USA.
EM dezielnc@mail.nih.gov
RI Friesen, Melissa/A-5362-2009;
OI Gunier, Robert/0000-0001-5485-9919
FU National Cancer Institute (NCI) [R01CA092683]; NCI; National Institutes
of Health [7590-S-04, 7590-S-01]; NCI Division of Cancer Epidemiology
and Genetics; Colorado State University
FX This study was funded by the National Cancer Institute (NCI) through
research grant R01CA092683 (J.R.N.) and, in part, by the Intramural
Research Program of the NCI and the National Institutes of Health
(subcontracts 7590-S-04, 7590-S-01). J.R.N. was also supported, in part,
through an Intergovernmental Personnel Agreement between the NCI
Division of Cancer Epidemiology and Genetics and Colorado State
University.
NR 37
TC 5
Z9 5
U1 1
U2 20
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD MAY
PY 2013
VL 121
IS 5
BP 565
EP 571
DI 10.1289/ehp.1205811
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 208UX
UT WOS:000323707300019
PM 23462689
ER
PT J
AU Leiding, JW
Marciano, BE
Zerbe, CS
DeRavin, SS
Malech, HL
Holland, SM
AF Leiding, Jennifer W.
Marciano, Beatriz E.
Zerbe, Christa S.
DeRavin, Suk See
Malech, Harry L.
Holland, Steven M.
TI Diabetes, Renal and Cardiovascular Disease in p47(phox-/-) Chronic
Granulomatous Disease
SO JOURNAL OF CLINICAL IMMUNOLOGY
LA English
DT Article
DE Chronic granulomatous disease; p47phox; diabetes; kidney; renal
ID NADPH OXIDASE; GLOMERULONEPHRITIS; AMYLOIDOSIS; CHILDHOOD; FAILURE
AB Chronic granulomatous disease is a rare immunodeficiency due to defects in the phagocyte NADPH oxidase. The X-linked form (gp91(phox) deficiency) accounts for about 70 % of cases; autosomal recessive p47(phox) deficiency accounts for about 25 % of cases. We identified a 10 % incidence of diabetes in p47(phox) deficient CGD, but none in X-linked CGD. Renal and cardiovascular diseases were also higher in p47(phox) deficiency. p47(phox) deficient CGD has noninfectious morbidities distinct from those in X-linked CGD.
C1 [Leiding, Jennifer W.; Marciano, Beatriz E.; Zerbe, Christa S.; Holland, Steven M.] NIH, Labs Clin Infect Dis, Bethesda, MD 20892 USA.
[DeRavin, Suk See; Malech, Harry L.] NIAID, NIH, Bethesda, MD USA.
[Leiding, Jennifer W.] Univ S Florida, Dept Pediat, Div Allergy Immunol & Rheumatol, St Petersburg, FL 33701 USA.
RP Holland, SM (reprint author), NIH, Labs Clin Infect Dis, CRC B3-4141 MSC 1684, Bethesda, MD 20892 USA.
EM smh@nih.gov
OI Malech, Harry/0000-0001-5874-5775
FU Division of Intramural Research, NIAID, NIH
FX This work supported by the Division of Intramural Research, NIAID, NIH.
NR 31
TC 7
Z9 8
U1 0
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0271-9142
J9 J CLIN IMMUNOL
JI J. Clin. Immunol.
PD MAY
PY 2013
VL 33
IS 4
BP 725
EP 730
DI 10.1007/s10875-013-9871-8
PG 6
WC Immunology
SC Immunology
GA 201FC
UT WOS:000323125100003
PM 23386289
ER
PT J
AU Fuss, IJ
Friend, J
Yang, ZQ
He, JP
Hooda, L
Boyer, J
Xi, LQ
Raffeld, M
Kleiner, DE
Heller, T
Strober, W
AF Fuss, Ivan J.
Friend, Julia
Yang, Zhiqiong
He, Jian Ping
Hooda, Lubna
Boyer, James
Xi, Liqiang
Raffeld, Mark
Kleiner, David E.
Heller, Theo
Strober, Warren
TI Nodular Regenerative Hyperplasia in Common Variable Immunodeficiency
SO JOURNAL OF CLINICAL IMMUNOLOGY
LA English
DT Article
DE CVID; NRH; autoimmune; liver; hypertension; cytokine
ID IMMUNE-DEFICIENCY; LIVER; DISEASE; ABNORMALITIES; INFECTION
AB Purpose Patients with Common Variable Immunodeficiency (CVID) are subject to the development of a liver disease syndrome known as nodular regenerative hyperplasia (NRH). The purpose of this study was to define the characteristics and course of this complication of CVID.
Methods CVID patients were evaluated by retrospective and prospective clinical course review. Liver biopsy specimens were evaluated for evidence of NRH and studied via RT-PCR for cytokine analysis.
Results NRH in our CVID patient population occurred in approximately 5% of the 261 patients in our total CVID study group, initially presenting in most cases with an elevated alkaline phosphatase level. While in some patients the disease remained static, in a larger proportion a more severe disease developed characterized by portal hypertension, the latter leading to hypersplenism with neutropenia and thrombocytopenia and, in some cases, to ascites. In addition, a substantial proportion of patients either developed or presented initially with an autoimmune hepatitis-like (AIH-like) liver disease that resulted in severe liver dysfunction and, in most cases to death due to infections. The liver histologic findings in these AIH-like patients were characterized by underlying NRH pattern with superimposed interface hepatitis, lymphocytic infiltration and fibrosis. Immunologic studies of biopsies of NRH patients demonstrated the presence of infiltrating T cells producing IFN-gamma, suggesting that the NRH is due to an autoimmune process.
Conclusion Overall, these studies provide evidence that NRH may not be benign but, can be a severe and potentially fatal disease complication of CVID that merits close monitoring and intervention.
C1 [Fuss, Ivan J.; Friend, Julia; Yang, Zhiqiong; Hooda, Lubna; Strober, Warren] NIAID, Mucosal Immun Sect, NIH, Bethesda, MD 20892 USA.
[Hooda, Lubna] Frederick Natl Lab Canc Res, Clin Res Directorate CMRP, SAIC Frederick Inc, Frederick, MD 21702 USA.
[He, Jian Ping] NIAID, Mucosal Immunobiol Sect, NIH, Bethesda, MD 20892 USA.
[Boyer, James] Yale Univ, Div Digest Dis, Bethesda, MD USA.
[Xi, Liqiang; Raffeld, Mark; Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Fuss, Ivan J.] NIAID, Mucosal Immun Sect, Host Def Lab, Bethesda, MD 20892 USA.
RP Fuss, IJ (reprint author), NIAID, Mucosal Immun Sect, Host Def Lab, CRC Bldg Rm 5W-3864, Bethesda, MD 20892 USA.
EM ifuss@niaid.nih.gov
OI Kleiner, David/0000-0003-3442-4453
FU NIAID, NCI, National Institutes of Health
FX Funding is from the intramural program of the NIAID, NCI, National
Institutes of Health. None of the authors has any financial
relationships with industries that have an interest in the subject
matter or materials discussed in the manuscript.
NR 24
TC 19
Z9 19
U1 0
U2 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0271-9142
J9 J CLIN IMMUNOL
JI J. Clin. Immunol.
PD MAY
PY 2013
VL 33
IS 4
BP 748
EP 758
DI 10.1007/s10875-013-9873-6
PG 11
WC Immunology
SC Immunology
GA 201FC
UT WOS:000323125100006
PM 23420139
ER
PT J
AU Anderson, K
Sung, H
Mayer-Barber, K
Beura, L
Vezys, V
Barber, D
Masopust, D
AF Anderson, Kristin
Sung, Heungsup
Mayer-Barber, Katrin
Beura, Lalit
Vezys, Vaiva
Barber, Daniel
Masopust, David
TI Methods for defining vascular and parenchymal leukocyte populations:
implications for characterizing innate and adaptive immune responses in
non-lymphoid tissue
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Anderson, Kristin; Sung, Heungsup; Beura, Lalit; Vezys, Vaiva; Masopust, David] Univ Minnesota, Ctr Immunol, Minneapolis, MN USA.
[Mayer-Barber, Katrin; Barber, Daniel] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3281
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103206
ER
PT J
AU Anderson, S
Li, HC
Huehn, A
Cooley, S
Miller, J
AF Anderson, Stephen
Li, Hongchuan
Huehn, Andrew
Cooley, Sarah
Miller, Jeffrey
TI Characterization of a weakly expressed KIR2DL1 allele supports a
positive role for the KIR distal promoter in proximal KIR promoter
activation.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Anderson, Stephen; Li, Hongchuan] SAIC Frederick Inc, Canc & Inflammat Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Anderson, Stephen; Li, Hongchuan; Huehn, Andrew] NCI, Expt Immunol Lab, Frederick, MD 21701 USA.
[Cooley, Sarah; Miller, Jeffrey] Univ Minnesota, Div Hematol Oncol & Transplantat, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1357
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101106
ER
PT J
AU Asefa, B
Jett, C
Janosko, K
Bernbaum, J
Dodd, L
Johnson, R
AF Asefa, Ben
Jett, Catherine
Janosko, Krisztina
Bernbaum, John
Dodd, Lori
Johnson, Reed
TI Defining the immune correlates of pathogenicity of Simian Hemorrhagic
Fever virus in Rhesus macaques
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Asefa, Ben; Jett, Catherine; Janosko, Krisztina; Bernbaum, John; Dodd, Lori; Johnson, Reed] NIAID, Integrated Res Facil, IRF, NIH, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6314
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108150
ER
PT J
AU Atasoy, U
Gubin, M
Calaluce, R
Magee, J
Martindale, J
Gorospe, M
Casolaro, V
Stellato, C
AF Atasoy, Ulus
Gubin, Matthew
Calaluce, Robert
Magee, Joseph
Martindale, Jennifer
Gorospe, Myriam
Casolaro, Vincenzo
Stellato, Cristiana
TI The RNA-binding protein HuR coordinately regulates GATA-3 and Th2
cytokine gene expression in dose dependent manner
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Atasoy, Ulus; Gubin, Matthew; Calaluce, Robert; Magee, Joseph] Univ Missouri, Columbia, MO USA.
[Martindale, Jennifer; Gorospe, Myriam] NIA, NIH, Baltimore, MD 21224 USA.
[Casolaro, Vincenzo; Stellato, Cristiana] Johns Hopkins, Baltimore, MD USA.
RI Casolaro, Vincenzo/E-9144-2010; Stellato, Cristiana/P-3001-2015
OI Casolaro, Vincenzo/0000-0001-9810-0488; Stellato,
Cristiana/0000-0002-1294-8355
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 462
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108099
ER
PT J
AU Barski, A
Cuddapah, S
Kartashov, A
Imamichi, H
Lane, C
Zhao, KJ
AF Barski, Artem
Cuddapah, Suresh
Kartashov, Andrey
Imamichi, Hiromi
Lane, Clifford
Zhao, Keji
TI Rapid recall ability of memory T cells is associated with epigenetic
gene poising (P1134)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Barski, Artem; Kartashov, Andrey] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Cuddapah, Suresh] NYU, New York, NY USA.
[Barski, Artem; Cuddapah, Suresh; Zhao, Keji] NHLBI, NIH, Bethesda, MD 20892 USA.
[Imamichi, Hiromi; Lane, Clifford] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100134
ER
PT J
AU Bergamaschi, C
Valentin, A
Kulkarni, V
Bear, J
Rosati, M
Alicea, C
Sowder, R
Chertova, E
Lifson, J
Felber, B
Pavlakis, G
AF Bergamaschi, Cristina
Valentin, Antonio
Kulkarni, Viraj
Bear, Jenifer
Rosati, Margherita
Alicea, Candido
Sowder, Raymond
Chertova, Elena
Lifson, Jeffrey
Felber, Barbara
Pavlakis, George
TI Comparison of pharmacokinetics and biological activity of two IL-15
heterodimeric forms in mice and macaques
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Bergamaschi, Cristina; Valentin, Antonio; Kulkarni, Viraj; Bear, Jenifer; Rosati, Margherita; Alicea, Candido; Felber, Barbara; Pavlakis, George] Frederick Natl Lab Canc Res, Ctr Canc Res, Vaccine Branch, Frederick, MD USA.
[Sowder, Raymond; Chertova, Elena; Lifson, Jeffrey] Frederick Natl Lab Canc Res, SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6356
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108192
ER
PT J
AU Biancotto, A
Liu, Y
Pelletier, M
Goldbach-Mansky, R
McCoy, JP
AF Biancotto, Angelique
Liu, Yin
Pelletier, Martin
Goldbach-Mansky, Raphaela
McCoy, J. Philip
TI Abnormal neutrophils present in peripheral blood of Chronic Atypical
Neutrophilic Dermatosis with Lipodystrophy and Elevated Temperature
(CANDLE) syndrome patients
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Biancotto, Angelique; McCoy, J. Philip] NHLBI, CHI, NIH, Bethesda, MD 20892 USA.
[Liu, Yin; Pelletier, Martin; Goldbach-Mansky, Raphaela] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4173
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104241
ER
PT J
AU Boularan, C
Kehrl, J
AF Boularan, Cedric
Kehrl, John
TI Role of heterotrimeric G-protein exchange factor Ric-8A in B cell
development and asymmetric cell division
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Boularan, Cedric; Kehrl, John] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1465
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101187
ER
PT J
AU Bowman, K
Holz, L
Rehermann, B
AF Bowman, Kathryn
Holz, Lauren
Rehermann, Barbara
TI Antigen-specific natural killer cell cytokine production in chronic
hepatitis C infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Bowman, Kathryn; Holz, Lauren; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6062
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987107157
ER
PT J
AU Caldwell, H
Olivares-Zavaleta, N
Carmody, A
Whitmire, B
Kari, L
AF Caldwell, Harlan
Olivares-Zavaleta, Norma
Carmody, Aaron
Whitmire, Bill
Kari, Laszlo
TI T cell correlates of solid protective immunity following immunization of
macaques with a live-attenuated trachoma vaccine
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Caldwell, Harlan; Olivares-Zavaleta, Norma; Carmody, Aaron; Whitmire, Bill; Kari, Laszlo] NIAID, NIH, Hamilton, MT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4403
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105217
ER
PT J
AU Cardone, M
Dzutsev, A
Li, HC
Gerosa, F
Winkler-Pickett, R
Provezza, L
Riboldi, E
Orr, S
Steinhagen, F
Wewers, M
McVicar, D
Anderson, S
Goldszmid, R
Lyakh, L
Trinchieri, G
AF Cardone, Marco
Dzutsev, Amiran
Li, Hongchuan
Gerosa, Franca
Winkler-Pickett, Robin
Provezza, Lisa
Riboldi, Elena
Orr, Selinda
Steinhagen, Folkert
Wewers, Mark
McVicar, Daniel
Anderson, Stephen
Goldszmid, Romina
Lyakh, Lyudmila
Trinchieri, Giorgio
TI IL-1 and IFN-gamma differentially program human dendritic cells exposed
to beta-glucan via IkappaB-zeta regulation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Cardone, Marco; Dzutsev, Amiran; Li, Hongchuan; Winkler-Pickett, Robin; Riboldi, Elena; Orr, Selinda; Steinhagen, Folkert; McVicar, Daniel; Anderson, Stephen; Goldszmid, Romina; Lyakh, Lyudmila; Trinchieri, Giorgio] NCI, Canc & Inflammat Program, NIH, Frederick, MD 21701 USA.
[Dzutsev, Amiran; Li, Hongchuan; Anderson, Stephen] SAIC Frederick Inc, Basic Sci Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Gerosa, Franca; Provezza, Lisa] Univ Verona, Dept Pathol, Immunol Sect, I-37100 Verona, Italy.
[Wewers, Mark] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6279
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108116
ER
PT J
AU Caspi, R
Chen, J
Silver, P
Horai, R
Mattapallil, M
Zhou, R
Chong, WP
AF Caspi, Rachel
Chen, Jun
Silver, Phyllis
Horai, R.
Mattapallil, Mary
Zhou, Ru
Chong, WaiPo
TI Reciprocal interaction between NK cells and DCs regulates the Th17
response by controlling the innate IFN-gamma/IL-27 axis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Caspi, Rachel; Chen, Jun; Silver, Phyllis; Horai, R.; Mattapallil, Mary; Zhou, Ru; Chong, WaiPo] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4067
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104136
ER
PT J
AU Chen, GB
Solokina, A
Oelke, M
Madara, K
Wersto, R
Schneck, J
Weng, NP
AF Chen, Guobing
Solokina, Arina
Oelke, Mathias
Madara, Karen
Wersto, Robert
Schneck, Jonathan
Weng, Nan-ping
TI Comparative analysis of CD8 T cell response to cytomegalovirus or
influenza virus in healthy human adults
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Chen, Guobing; Solokina, Arina; Weng, Nan-ping] NIA, Lab Mol Biol & Immunol, Baltimore, MD 21224 USA.
[Oelke, Mathias; Schneck, Jonathan] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Madara, Karen] NIA, Clin Core Unit, Baltimore, MD 21224 USA.
[Wersto, Robert] NIA, Flow Cytometry Unit, Baltimore, MD 21224 USA.
RI Chen, Guobing/D-9572-2012
OI Chen, Guobing/0000-0002-2401-6168
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3002
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102179
ER
PT J
AU Chen, X
Willette-Brown, J
Wu, XQ
Howard, OMZ
Hu, YL
Oppenheim, J
AF Chen, Xin
Willette-Brown, Jami
Wu, Xueqiang
Howard, O. M. Zack
Hu, Yinling
Oppenheim, Joost
TI IKKalpha is critical for the maintenance of a normal pool of regulatory
T cells and for the expansion of both regulatory and effector T cells
(P1095)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Chen, Xin] SAIC Frederick Inc, Basic Sci Program, Frederick, MD USA.
[Willette-Brown, Jami; Hu, Yinling] NCI, Expt Immunol Lab, Frederick, MD 21701 USA.
[Wu, Xueqiang; Howard, O. M. Zack; Oppenheim, Joost] NCI, Mol Immunoregulat Lab, Frederick, MD 21701 USA.
RI Howard, O M Zack/B-6117-2012; Chen, Xin/I-6601-2015
OI Howard, O M Zack/0000-0002-0505-7052; Chen, Xin/0000-0002-2628-4027
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100095
ER
PT J
AU Chen, YQ
Liu, Y
Huang, Y
Yee, C
McBride, A
Morasso, M
Bowcock, A
Lowes, M
Goldbach-Mansky, R
AF Chen, Yongqing
Liu, Yin
Huang, Yan
Yee, Carole
McBride, Alison
Morasso, Maria
Bowcock, Anne
Lowes, Michelle
Goldbach-Mansky, Raphaela
TI Immune activating effects of stimulation of TLR agonists and cytokines
on keratinocytes from a patient with a CARD14 mediated pustular
psoriasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Chen, Yongqing; Liu, Yin; Huang, Yan; Goldbach-Mansky, Raphaela] NIAMS, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD USA.
[Yee, Carole] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[McBride, Alison] NIAID, DNA Tumor Virus Sect, NIH, Bethesda, MD 20892 USA.
[Morasso, Maria] NIAMS, Dev Skin Biol Sect, NIH, Bethesda, MD USA.
[Bowcock, Anne] Washington Univ, St Louis, MO USA.
[Lowes, Michelle] Rockefeller Univ, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6283
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108120
ER
PT J
AU Chodisetti, SB
Jain, S
Agrewala, J
AF Chodisetti, Sathi Babu
Jain, Shweta
Agrewala, Javed
TI Cooperation of CD86 signaling with TLR-2 in the activation of resting B
cells: a novel BCR independent pathway of stimulating B cells (P1126)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Chodisetti, Sathi Babu; Jain, Shweta; Agrewala, Javed] Inst Microbial Technol, Immunol Lab, Chandigarh, India.
[Jain, Shweta] NIH, Lab Immunogenet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100126
ER
PT J
AU Edwards, J
Unutmaz, D
Shevach, E
AF Edwards, Justin
Unutmaz, Derya
Shevach, Ethan
TI Regulation of the expression of GARP/latent-TGF-beta 1 complexes on
mouse regulatory T cells and their role in Th17 differentiation.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Edwards, Justin; Shevach, Ethan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Unutmaz, Derya] NYU, Sch Med, Dept Microbiol, New York, NY 10016 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1033
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100033
ER
PT J
AU Felices, M
Lenvik, T
Ankarlo, D
Curtsinger, J
Cooley, S
Tolar, J
Blazar, B
Anderson, S
Miller, J
AF Felices, Martin
Lenvik, Todd
Ankarlo, Dave
Curtsinger, Julie
Cooley, Sarah
Tolar, Jakub
Blazar, Bruce
Anderson, Stephen
Miller, Jeffrey
TI Natural killer cell education results in prolonged survival through a
cytokine receptor balance mediated mechanism
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Felices, Martin; Lenvik, Todd; Ankarlo, Dave; Curtsinger, Julie; Cooley, Sarah; Tolar, Jakub; Blazar, Bruce; Miller, Jeffrey] Univ Minnesota, Minneapolis, MN USA.
[Anderson, Stephen] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1435
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101166
ER
PT J
AU Gerner, M
Kastenmuller, W
Germain, R
AF Gerner, Michael
Kastenmuller, Wolfgang
Germain, Ronald
TI The role of lymphoid micro-architecture in dendritic cell-mediated
antigen capture and initiation of cellular adaptive immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Gerner, Michael; Kastenmuller, Wolfgang; Germain, Ronald] NIAID, LSB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P5200
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987107061
ER
PT J
AU Gomez-Rodriguez, J
Wohlfert, E
Handon, R
Wu, J
Belkaid, Y
Schwartzberg, P
AF Gomez-Rodriguez, Julio
Wohlfert, Elizabeth
Handon, Robin
Wu, Julie
Belkaid, Yasmine
Schwartzberg, Pamela
TI Cross-talk between T cell receptor and cytokine signaling is mediated by
Itk: implications for the balance between Th17 and regulatory T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Gomez-Rodriguez, Julio; Handon, Robin; Schwartzberg, Pamela] NHGRI, NIH, Bethesda, MD 20892 USA.
[Wohlfert, Elizabeth; Belkaid, Yasmine] NIAID, NIH, Bethesda, MD 20892 USA.
[Wu, Julie] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1141
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100141
ER
PT J
AU Ha, HL
Siebenlist, U
AF Ha, Hye-Lin
Siebenlist, Ulrich
TI The adaptor protein CIKS/Act1 is essential for imiquimod-induced
psoriasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Ha, Hye-Lin; Siebenlist, Ulrich] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6269
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108106
ER
PT J
AU Heikamp, E
Patel, C
Collins, S
Waickman, A
Scharma, A
Naray-Fejes-Toth, A
Fejes-Toth, G
Sen, J
Horton, M
Powell, J
AF Heikamp, Emily
Patel, Chirag
Collins, Sam
Waickman, Adam
Scharma, Archna
Naray-Fejes-Toth, Aniko
Fejes-Toth, Geza
Sen, Jyoti
Horton, Maureen
Powell, Jonathan
TI mTOR regulates CD4 and CD8 effector T cell differentiation via serum-
and glucocorticoid-regulated kinase 1
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Heikamp, Emily; Patel, Chirag; Collins, Sam; Waickman, Adam; Horton, Maureen; Powell, Jonathan] Johns Hopkins Sch Med, Baltimore, MD USA.
[Scharma, Archna; Sen, Jyoti] NIA, NIH, Baltimore, MD 21224 USA.
[Naray-Fejes-Toth, Aniko; Fejes-Toth, Geza] Dartmouth Coll, Geisel Sch Med, Hanover, NH 03755 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1161
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100161
ER
PT J
AU Herz, J
McGavern, D
AF Herz, Jasmin
McGavern, Dorian
TI Therapeutic clearance of the virally infected nervous system is mediated
by noncytopathic T cell interactions with resident myeloid cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Herz, Jasmin; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4220
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105037
ER
PT J
AU Janelsins, B
Valdez, P
Munford, R
Lu, MF
Datta, S
AF Janelsins, Brian
Valdez, Patricia
Munford, Robert
Lu, Mingfang
Datta, Sandip
TI Persistent exposure to endogenous LPS programs colonic lamina propria
dendritic cells to impair CD4+Th17 immunity in vivo
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Janelsins, Brian; Valdez, Patricia; Datta, Sandip] NIAID, Bacterial Pathogenesis Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Munford, Robert; Lu, Mingfang] NIAID, Antibacterial Host Def Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3225
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103151
ER
PT J
AU Jiang, CC
Zhao, ML
Hobbie, K
Herbert, R
Diaz, M
AF Jiang, Chuancang
Zhao, Ming-Lang
Hobbie, Kristen
Herbert, Ronald
Diaz, Marilyn
TI Anti-nuclear IgM antibodies protect against lymphoma/lymphocytic
leukemia
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Jiang, Chuancang; Zhao, Ming-Lang; Diaz, Marilyn] NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Hobbie, Kristen] Integrated Syst Lab Inc, Res Triangle Pk, NC USA.
[Herbert, Ronald] NIEHS, Cellular & Mol Pathol Branch, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P2219
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102166
ER
PT J
AU Kang, S
Fedoriw, G
Jiang, CC
Diaz, M
Vilen, BJ
AF Kang, SunAh
Fedoriw, George
Jiang, Chuancang
Diaz, Marilyn
Vilen, Barbara J.
TI IgG immune complexes promote systemic lupus erythematosus by elevating
BAFF and inducing T cell infiltration into the glomeruli
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Kang, SunAh; Vilen, Barbara J.] Univ N Carolina, Chapel Hill, NC USA.
[Fedoriw, George] Univ N Carolina, Canc Hosp, Chapel Hill, NC USA.
[Jiang, Chuancang; Diaz, Marilyn] NIEHS, Somat Hypermutat Grp, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4036
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104105
ER
PT J
AU Kielczewski, J
Horai, R
Caspi, R
AF Kielczewski, Jennifer
Horai, Reiko
Caspi, Rachel
TI Tertiary lymphoid tissue with germinal centers and T follicular helper
cells in immunologically privileged retinas of mice with chronic
autoimmune uveitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Kielczewski, Jennifer; Horai, Reiko; Caspi, Rachel] NEI, LI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4172
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104240
ER
PT J
AU Klatt, N
Canary, L
Vinton, C
Morcock, D
Estes, J
Brenchley, J
AF Klatt, Nichole
Canary, Lauren
Vinton, Carol
Morcock, David
Estes, Jacob
Brenchley, Jason
TI Rate of AIDS progression is associated with gastrointestinal dysfunction
in SIV-infected pigtail macaques
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Klatt, Nichole; Canary, Lauren; Vinton, Carol; Brenchley, Jason] NIAID, LMM, NIH, Bethesda, MD 20892 USA.
[Klatt, Nichole] Univ Washington, Dept Pharmaceut, Seattle, WA 98195 USA.
[Morcock, David; Estes, Jacob] Frederick Natl Lab Canc Res, SAIC Frederick Inc, AIDS & Canc & Virus Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3045
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102222
ER
PT J
AU Koh, Y
Nemazee, D
Rickert, R
Radic, M
Cascalho, M
Casellas, R
Theofilopoulos, A
Kono, D
AF Koh, Yi
Nemazee, David
Rickert, Robert
Radic, Marko
Cascalho, Marilia
Casellas, Rafael
Theofilopoulos, Argyrios
Kono, Dwight
TI FLEx-autoAb transgenic mice, a novel mouse model for studying peripheral
tolerance to B cells that acquire self-reactivity following somatic
hypermutation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Koh, Yi; Nemazee, David; Theofilopoulos, Argyrios; Kono, Dwight] Scripps Res Inst, La Jolla, CA 92037 USA.
[Rickert, Robert] Sanford Burnham Med Res Inst, La Jolla, CA USA.
[Radic, Marko] Univ Tennessee, Dept Microbiol Immunol & Biochem, Memphis, TN USA.
[Cascalho, Marilia] Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
[Casellas, Rafael] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4034
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104103
ER
PT J
AU Kole, H
Scott, B
Bolland, S
AF Kole, Hemanta
Scott, Bethany
Bolland, Silvia
TI Understanding lupus pathology in Fc gamma RIIB-/-yaa mice:
autoantibodies and autoantigens
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Kole, Hemanta; Scott, Bethany; Bolland, Silvia] NIAID, AFGS LIG, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4008
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104077
ER
PT J
AU Kraus, Z
Dutta, M
Schwartzberg, P
AF Kraus, Zachary
Dutta, Mala
Schwartzberg, Pamela
TI Ly108 enhances PLZF expression in developing thymocytes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Kraus, Zachary; Dutta, Mala; Schwartzberg, Pamela] NHGRI, GDRB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 5243
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987106015
ER
PT J
AU Kyle, R
Robinson, M
Plunkett, C
Mearns, H
Ochiai, S
Tang, SC
Forbes-Blom, E
Chen, X
Paul, W
Le Gros, G
AF Kyle, Ryan
Robinson, Marcus
Plunkett, Catherine
Mearns, Helen
Ochiai, Sotaro
Tang, Shiau Choot
Forbes-Blom, Elizabeth
Chen, Xi
Paul, William
Le Gros, Graham
TI Spatial and temporal regulation of interleukin 4 and interleukin 13
expression identified by dual reporter mice. (P1129)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Kyle, Ryan; Robinson, Marcus; Plunkett, Catherine; Ochiai, Sotaro; Tang, Shiau Choot; Forbes-Blom, Elizabeth; Le Gros, Graham] Malaghan Inst Med Res, Wellington, New Zealand.
[Mearns, Helen] Singapore Immunol Network SIgN, Singapore, Singapore.
[Chen, Xi; Paul, William] NIAID, Cytokine Biol Unit, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RI Le Gros, Graham/C-6725-2011
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100129
ER
PT J
AU Le Saout, C
Hasley, R
Imamichi, H
Tcheung, L
Luckey, M
Smith, M
Hu, ZH
Sneller, M
Rehm, C
Lane, H
Catalfamo, M
AF Le Saout, Cecile
Hasley, Rebecca
Imamichi, Hiromi
Tcheung, Lueng
Luckey, Megan
Smith, Mindy
Hu, Zonghui
Sneller, Michael
Rehm, Catherine
Lane, H.
Catalfamo, Marta
TI Lymphopenia modulates levels of STAT1 expression leading to enhanced CD4
T cell responsiveness to Type-I IFN
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Le Saout, Cecile; Hasley, Rebecca; Imamichi, Hiromi; Tcheung, Lueng; Smith, Mindy; Sneller, Michael; Rehm, Catherine; Lane, H.; Catalfamo, Marta] NIAID, Lab Immunoregulat, NIH, Bethesda, MD 20892 USA.
[Luckey, Megan] NCI, Expt Immunol Branch, CCR, NIH, Bethesda, MD 20892 USA.
[Hu, Zonghui] NIAID, Biostat Res Branch, DCR, NIH, Bethesda, MD 20892 USA.
RI Davis, Megan/F-5339-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6272
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108109
ER
PT J
AU Li, FY
Chaigne-Delalande, B
O'Connor, G
Lukacs, M
Zheng, LX
Shatzer, A
Matthews, H
Su, H
Cohen, J
Uzel, G
Lenardo, M
AF Li, Feng-Yen
Chaigne-Delalande, Benjamin
O'Connor, Geraldine
Lukacs, Marshall
Zheng, Lixin
Shatzer, Amber
Matthews, Helen
Su, Helen
Cohen, Jeffrey
Uzel, Gulbu
Lenardo, Michael
TI Intracellular free Mg2+is required to maintain NKG2D expression
necessary for controlling EBV infection in XMEN disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Li, Feng-Yen] UCSF, San Francisco, CA USA.
[Li, Feng-Yen; Chaigne-Delalande, Benjamin; Lukacs, Marshall; Zheng, Lixin; Shatzer, Amber; Matthews, Helen; Su, Helen; Cohen, Jeffrey; Uzel, Gulbu; Lenardo, Michael] NIAID, NIH, Bethesda, MD 20892 USA.
[O'Connor, Geraldine] NCI, NIH, Frederick, MD 21701 USA.
RI Su, Helen/H-9541-2015
OI Su, Helen/0000-0002-5582-9110
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3028
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102205
ER
PT J
AU Li, WQ
Xiao, Z
Ravichandran, S
Collins, J
Veenstra, T
Durum, S
AF Li, Wenqing
Xiao, Zhen
Ravichandran, Sarangan
Collins, Jack
Veenstra, Timothy
Durum, Scott
TI Lysine dimethylation in the BH4 domain of Bcl-2 and functional
significance
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Li, Wenqing; Durum, Scott] NCI, Canc & Inflammat Program, CCR, NIH, Frederick, MD 21701 USA.
[Xiao, Zhen; Veenstra, Timothy] NCI, Lab Prote & Analyt Technol, SAIC Frederick Inc, NIH, Frederick, MD 21701 USA.
[Ravichandran, Sarangan; Collins, Jack] NCI, Adv Biomed Comp Ctr, Informat Syst Program, SAIC Frederick Inc,NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1306
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101055
ER
PT J
AU Li, YF
Wang, AJ
Grinchuk, V
Smith, A
Ramalingam, T
Wynn, T
Urban, J
Shea-Donohue, T
Zhao, AP
AF Li, Yanfei
Wang, Anjiang
Grinchuk, Viktoriya
Smith, Allen
Ramalingam, Thirumalai
Wynn, Thomas
Urban, Joseph
Shea-Donohue, Terez
Zhao, Aiping
TI Mice deficient in IL-25 are less susceptible to dextran sulfate
sodium-induced colitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Li, Yanfei; Wang, Anjiang; Grinchuk, Viktoriya; Shea-Donohue, Terez; Zhao, Aiping] Univ Maryland, Sch Med, Med & Mucosal Biol Res Ctr, Baltimore, MD 21201 USA.
[Smith, Allen; Urban, Joseph] USDA, DGIL, BHNRC, Beltsville, MD 20705 USA.
[Ramalingam, Thirumalai; Wynn, Thomas] NIAID, NIH, Bethesda, MD 20892 USA.
[Wang, Anjiang] Nanchang Univ, Affiliated Hosp 1, Nanchang, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3270
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103195
ER
PT J
AU Lieberman, M
Lehrer, A
Humphreys, T
Johns, L
Wong, TA
Olinger, G
Dye, J
Carrion, R
Patterson, J
Marzi, A
Feldmann, H
AF Lieberman, Michael
Lehrer, Axel
Humphreys, Tom
Johns, Lisa
Wong, Teri-Ann
Olinger, Gene
Dye, John
Carrion, Ricardo
Patterson, Jean
Marzi, Andrea
Feldmann, Heinz
TI Recombinant Ebolavirus antigens from insect cells are potent immunogens
inducing cellular and humoral immunity in rodents and non-human primates
and provide protection against virus challenge
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Lieberman, Michael] Lieberman Consulting, Honolulu, HI USA.
[Lehrer, Axel; Johns, Lisa; Wong, Teri-Ann] PanThera Biopharma LLC, Aiea, HI USA.
[Humphreys, Tom] Univ Hawaii, Honolulu, HI 96822 USA.
[Olinger, Gene; Dye, John] US Army Med Res Inst Infect Dis, Ft Detrick, MD USA.
[Carrion, Ricardo; Patterson, Jean] Texas Biomed Res Inst, San Antonio, TX USA.
[Marzi, Andrea; Feldmann, Heinz] NIAID, NIH, Hamilton, MT USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4325
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105140
ER
PT J
AU Liu, J
Kim, SH
Cao, S
Peppers, G
Graham, B
AF Liu, Jie
Kim, Sung-Han
Cao, Shirley
Peppers, Gretchen
Graham, Barney
TI Virus-specific Tregs are terminally differentiated upon peripheral
activation and dependent on thymic output after both primary and
secondary infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Liu, Jie; Kim, Sung-Han; Cao, Shirley; Peppers, Gretchen; Graham, Barney] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1035
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100035
ER
PT J
AU Liu, WL
Sugui, J
Li, HZ
Kwon-Chung, K
Rodgers, G
AF Liu, Wenli
Sugui, Jancy
Li, Hongzhen
Kwon-Chung, Kyung
Rodgers, Griffin
TI Deletion of OLFM4 rescues defective host defense against Staphylococcus
aureus, but not Aspergillus fumigatus in murine X-linked chronic
granulomatous disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Liu, Wenli; Li, Hongzhen; Rodgers, Griffin] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Sugui, Jancy; Kwon-Chung, Kyung] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1259
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101008
ER
PT J
AU Lo, B
Schaffer, A
Paik, D
Davis, J
Price, S
Rao, K
Lenardo, M
AF Lo, Bernice
Schaeffer, Alejandro
Paik, Daniel
Davis, Joie
Price, Susan
Rao, Koneti
Lenardo, Michael
TI Identifying modifier genes in Autoimmune Lymphoproliferative Syndrome
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Lo, Bernice; Paik, Daniel; Lenardo, Michael] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Schaeffer, Alejandro] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Davis, Joie; Price, Susan; Rao, Koneti] NIAID, ALPS Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4084
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104153
ER
PT J
AU Mani, R
Frissora, F
Mao, YC
Chiang, CL
Mo, XK
Jarjoura, D
Baskar, S
Rader, C
Lee, R
Lee, LJ
Chen, CS
Byrd, J
Muthusamy, N
AF Mani, Rajeswaran
Frissora, Frank
Mao, Yicheng
Chiang, Chi-ling
Mo, Xiaokui
Jarjoura, David
Baskar, Sivasubramanian
Rader, Christoph
Lee, Robert
Lee, L. James
Chen, Ching-Shih
Byrd, John
Muthusamy, Natarajan
TI OSU-2S: a novel non-immunosuppressive FTY720 derivative mediates potent
cytotoxic activity through PKC dependent phosphorylation of tumor
suppressor SHP1 and down modulation of Tcl1 oncogene in chronic
lymphocytic leukemia
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Mani, Rajeswaran; Frissora, Frank; Mao, Yicheng; Chiang, Chi-ling; Chen, Ching-Shih; Byrd, John; Muthusamy, Natarajan] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Mani, Rajeswaran; Chen, Ching-Shih; Byrd, John; Muthusamy, Natarajan] Ohio State Univ, Coll Vet Med, Columbus, OH 43210 USA.
[Mo, Xiaokui; Jarjoura, David] Ohio State Univ, Ctr Biostat, Columbus, OH 43210 USA.
[Baskar, Sivasubramanian] NCI, Pediat Oncol Branch, CCR, NIH, Bethesda, MD 20892 USA.
[Rader, Christoph] Scripps Res Inst, Jupiter, FL USA.
[Mao, Yicheng; Lee, Robert; Chen, Ching-Shih; Byrd, John] Ohio State Univ, Coll Pharm, Columbus, OH 43210 USA.
[Lee, L. James] Ohio State Univ, Columbus, OH 43210 USA.
[Byrd, John; Muthusamy, Natarajan] Ohio State Univ, Dept Internal Med, Div Hematol, Columbus, OH 43210 USA.
RI Mani, Rajeswaran/Q-2762-2015
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P2120
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102069
ER
PT J
AU Marquardt, N
Ivarsson, M
Blom, K
Braun, M
Gonzalez, V
Falconer, K
Sandberg, J
Michaelsson, J
AF Marquardt, Nicole
Ivarsson, Martin
Blom, Kim
Braun, Monika
Gonzalez, Veronica
Falconer, Karolin
Sandberg, Johan
Michaelsson, Jakob
TI Function and regulation of human NK cells in an acute viral infection
model
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Marquardt, Nicole; Ivarsson, Martin; Blom, Kim; Braun, Monika; Gonzalez, Veronica; Falconer, Karolin; Sandberg, Johan; Michaelsson, Jakob] Karolinska Inst, Dept Med, Stockholm, Sweden.
[Gonzalez, Veronica] NIDDK, NIH, Bethesda, MD USA.
RI Marquardt, Nicole/K-2942-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6127
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987107218
ER
PT J
AU Mattmiller, S
Sordillo, L
Carlson, B
AF Mattmiller, Sarah
Sordillo, Lorraine
Carlson, Bradley
TI Selenoprotein activity alters eicosanoid biosynthesis in macrophages
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Mattmiller, Sarah; Sordillo, Lorraine] Michigan State Univ, E Lansing, MI 48824 USA.
[Carlson, Bradley] NCI, Sect Mol Biol Selenium, Lab Canc Prevent, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P5042
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987106154
ER
PT J
AU McFarland, A
Steinhagen, F
Rodriguez, L
Tewary, P
Jarret, A
Savan, R
Klinman, D
AF McFarland, Adelle
Steinhagen, Folkert
Rodriguez, Luis
Tewary, Poonam
Jarret, Abigail
Savan, Ram
Klinman, Dennis
TI IRF-5 and NF-kappa B p50 co-regulate IFN-beta and IL-6 expression in
TLR9-stimulated human plasmacytoid dendritic cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [McFarland, Adelle; Jarret, Abigail; Savan, Ram] Univ Washington, Dept Immunol, Seattle, WA 98195 USA.
[Steinhagen, Folkert; Klinman, Dennis] Frederick Natl Lab Canc Res, Canc & Inflammat Program, Frederick, MD USA.
[Rodriguez, Luis] SAIC Frederick Inc, Lab Prote & Analyt Technol, Frederick, MD USA.
[Tewary, Poonam] Frederick Natl Lab Canc Res, Mol Immunoregulat Lab, Frederick, MD USA.
[Steinhagen, Folkert] Univ Hosp Bonn, Dept Anaesthesiol & Intens Care Med, Bonn, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1363
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101112
ER
PT J
AU McGavern, D
Gossa, S
AF McGavern, Dorian
Gossa, Selamawit
TI MMP-8 mediates vascular breakdown during viral infection of the nervous
system (P6368)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [McGavern, Dorian; Gossa, Selamawit] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 21610
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108204
ER
PT J
AU Metidji, A
Punkosdy, G
Shevach, E
AF Metidji, Amina
Punkosdy, George
Shevach, Ethan
TI Interferon alpha/beta receptor signaling plays a critical role in
regulatory T cell development and function (P1093)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Metidji, Amina; Punkosdy, George; Shevach, Ethan] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100093
ER
PT J
AU Meylan, F
Hawley, E
Barron, L
Barlow, J
Penumetcha, P
Richard, A
Chen, X
Paul, W
Wynn, T
McKenzie, A
Siegel, R
AF Meylan, Francoise
Hawley, Eric
Barron, Luke
Barlow, Jillian
Penumetcha, Pallavi
Richard, Arianne
Chen, Xi
Paul, William
Wynn, Thomas
McKenzie, Andrew
Siegel, Richard
TI The TL1A-IL13 axis: a novel pathway for Type 2 immunity mediated by
innate lymphocytes independent of helminth infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Meylan, Francoise; Hawley, Eric; Penumetcha, Pallavi; Richard, Arianne; Siegel, Richard] NIAMS, Autoimmun Branch, Immunoregulat Grp, NIH, Bethesda, MD USA.
[Barron, Luke; Wynn, Thomas] NIAID, Immunopathogenesis Sect, LPD, NIH, Bethesda, MD 20892 USA.
[Barlow, Jillian; McKenzie, Andrew] MRC, Mol Biol Lab, Cambridge CB2 2QH, England.
[Chen, Xi; Paul, William] NIAID, Cytokine Biol Sect, LI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6264
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108101
ER
PT J
AU Muthusamy, N
Mao, YC
Frissora, F
Mani, R
Wang, J
Wu, Y
Yu, B
Baskar, S
Rader, C
Phelphs, M
Chen, CS
Lee, R
Lee, L
Byrd, J
AF Muthusamy, Natarajan
Mao, Yicheng
Frissora, Frank
Mani, Rajeswaran
Wang, Jiang
Wu, Yun
Yu, Bo
Baskar, Sivasubramanian
Rader, Christoph
Phelphs, Mitch
Chen, Ching-Shih
Lee, Robert
Lee, L.
Byrd, John
TI ROR1 directed delivery of FTY720 derivative OSU-2S mediates potent
cytotoxic activity against chronic lymphocytic leukemia but not normal B
cells in-vitro and in ROR1 expressing transgenic CLL mouse model in-vivo
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Muthusamy, Natarajan; Frissora, Frank; Mani, Rajeswaran; Byrd, John] Ohio State Univ, Dept Internal Med, Div Hematol, Columbus, OH 43210 USA.
[Mao, Yicheng; Wu, Yun; Phelphs, Mitch; Lee, Robert] Ohio State Univ, Coll Pharm, Div Pharmaceut, Columbus, OH 43210 USA.
[Muthusamy, Natarajan; Frissora, Frank; Wang, Jiang; Yu, Bo; Phelphs, Mitch; Chen, Ching-Shih; Lee, Robert; Lee, L.; Byrd, John] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Lee, L.] Ohio State Univ, Ctr Affordable Nanoengn Polymer Biomed Devices, Columbus, OH 43210 USA.
[Baskar, Sivasubramanian] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Rader, Christoph] Scripps Res Inst, Dept Canc Biol, Jupiter, FL USA.
[Rader, Christoph] Scripps Res Inst, Dept Mol Therapeut, Jupiter, FL USA.
[Chen, Ching-Shih] Ohio State Univ, Coll Pharm, Div Med Chem, Columbus, OH 43210 USA.
[Yu, Bo; Lee, L.] Ohio State Univ, Dept Chem & Biomol Engn, Columbus, OH 43210 USA.
RI Mani, Rajeswaran/Q-2762-2015
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3275
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103200
ER
PT J
AU Myles, I
Fontecella, N
Valdez, P
Vithayathil, P
Naik, S
Belkaid, Y
Ouyang, WJ
Datta, S
AF Myles, Ian
Fontecella, Natalia
Valdez, Patricia
Vithayathil, Paul
Naik, Shruti
Belkaid, Yasmine
Ouyang, Wenjun
Datta, Sandip
TI IL-20 receptor signaling inhibits cutaneous IL-1 beta and IL-17A
production to promote methicillin-resistant Staphylococcus aureus
infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Myles, Ian; Fontecella, Natalia; Valdez, Patricia; Vithayathil, Paul; Naik, Shruti; Belkaid, Yasmine; Ouyang, Wenjun; Datta, Sandip] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6350
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108186
ER
PT J
AU Myles, I
Fontecella, N
Janelsins, B
Vithayathil, P
Segre, J
Datta, S
AF Myles, Ian
Fontecella, Natalia
Janelsins, Brian
Vithayathil, Paul
Segre, Julia
Datta, Sandip
TI The lard legacy: parental dietary fat intake alters offspring microbiome
and immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Myles, Ian; Fontecella, Natalia; Janelsins, Brian; Vithayathil, Paul; Segre, Julia; Datta, Sandip] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 7
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3359
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104034
ER
PT J
AU Noubade, R
Wong, K
Ota, N
Rutz, S
Valdez, P
Peng, I
Sebrell, A
Caplazi, P
DeVoss, J
Soriano, R
Modrusan, Z
Hackney, J
Sai, T
Ouyang, WJ
AF Noubade, Rajkumar
Wong, Kit
Ota, Neko
Rutz, Sascha
Valdez, Patricia
Peng, Ivan
Sebrell, Andrew
Caplazi, Patrick
DeVoss, Jason
Soriano, Robert
Modrusan, Zora
Hackney, Jason
Sai, Tao
Ouyang, Wenjun
TI NRROS negatively regulates the production of reactive oxygen species in
phagocytes during host defense and autoimmunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Noubade, Rajkumar; Wong, Kit; Ota, Neko; Rutz, Sascha; Peng, Ivan; Sebrell, Andrew; Caplazi, Patrick; DeVoss, Jason; Soriano, Robert; Modrusan, Zora; Hackney, Jason; Sai, Tao; Ouyang, Wenjun] Genentech Inc, San Francisco, CA 94080 USA.
[Valdez, Patricia] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1339
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101088
ER
PT J
AU Omenetti, S
Brogi, M
Garg, R
Goodman, W
Klinman, D
Pinzani, M
Pizarro, T
AF Omenetti, Sara
Brogi, Marco
Garg, Rekha
Goodman, Wendy
Klinman, Dennis
Pinzani, Massimo
Pizarro, Theresa
TI Essential role for Toll-like receptor 9 in the pathogenesis of liver
inflammation in a murine model of Crohn's disease-like ileitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Omenetti, Sara; Brogi, Marco; Garg, Rekha; Goodman, Wendy; Pinzani, Massimo; Pizarro, Theresa] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
[Omenetti, Sara; Pizarro, Theresa] Univ Florence, DENOThe Ctr Excellence, Florence, Italy.
[Klinman, Dennis] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Pinzani, Massimo] Univ Col London, Inst Liver & Digest Hlth, London, England.
[Pinzani, Massimo; Pizarro, Theresa] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3147
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103073
ER
PT J
AU Parish, S
Izhak, L
Xia, Z
Suzuki, M
Terabe, M
Berzofsky, J
AF Parish, Stanley
Izhak, Liat
Xia, Zheng
Suzuki, Motoshi
Terabe, Masaki
Berzofsky, Jay
TI Identification of sulfatide reactive type II NKT cells using CD1d dimers
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Parish, Stanley; Izhak, Liat; Xia, Zheng; Terabe, Masaki; Berzofsky, Jay] NCI, NIH, Bethesda, MD 20892 USA.
[Suzuki, Motoshi] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3291
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103216
ER
PT J
AU Park, SH
Park, H
Pan, W
Rehermann, B
AF Park, Su-Hyung
Park, Heiyoung
Pan, Warren
Rehermann, Barbara
TI Development of genetically engineered TCR-transduced T cells for
immunotherapy of chronic hepatitis B and C virus infections
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Park, Su-Hyung; Park, Heiyoung; Pan, Warren; Rehermann, Barbara] NIDDK, Immunol Sect, LDB, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4222
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105039
ER
PT J
AU Pavlakis, G
Bergamaschi, C
Valentin, A
Kulkarni, V
Bear, J
Rosati, M
Alicea, C
Sowder, R
Chertova, E
Lifson, J
Felber, B
AF Pavlakis, George
Bergamaschi, Cristina
Valentin, Antonio
Kulkarni, Viraj
Bear, Jenifer
Rosati, Margherita
Alicea, Candido
Sowder, Raymond
Chertova, Elena
Lifson, Jeffrey
Felber, Barbara
TI Pharmacokinetics and immunological effects of human IL-15/IL-15R alpha
heterodimeric complexes in macaques and comparison to single-chain IL-15
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Pavlakis, George; Bergamaschi, Cristina; Valentin, Antonio; Kulkarni, Viraj; Bear, Jenifer; Rosati, Margherita; Alicea, Candido; Felber, Barbara] Frederick Natl Lab Canc Res, Vaccine Branch, Ctr Canc Res, Frederick, MD USA.
[Sowder, Raymond; Chertova, Elena; Lifson, Jeffrey] Frederick Natl Lab Canc Res, AIDS & Canc Virus Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 11517
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108079
ER
PT J
AU Punkosdy, G
Shevach, E
AF Punkosdy, George
Shevach, Ethan
TI Foxp3+regulatory T cells consist of rapidly dividing and quiescent
subpopulations
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Punkosdy, George; Shevach, Ethan] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1179
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100179
ER
PT J
AU Ragheb, J
Bushar, N
AF Ragheb, Jack
Bushar, Nicholas
TI CD40L at the interface of the innate and adaptive immune responses.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Ragheb, Jack; Bushar, Nicholas] NIH, Immunol Lab, US FDA, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P5206
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987107067
ER
PT J
AU Ramaswamy, M
Cruz, A
Barden, M
Siegel, R
AF Ramaswamy, Madhu
Cruz, Anthony
Barden, Mary
Siegel, Richard
TI The death receptor Fas mediates a non-apoptotic signaling cascade in
apoptosis resistant CD4+T cells via the MAPK pathway.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Ramaswamy, Madhu; Cruz, Anthony; Barden, Mary; Siegel, Richard] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1304
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101053
ER
PT J
AU Rieder, S
Shevach, E
AF Rieder, Sadiye
Shevach, Ethan
TI The role of Eos in T cell function (P1059)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Rieder, Sadiye; Shevach, Ethan] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100059
ER
PT J
AU Roediger, B
Kyle, R
Yip, K
Sumaria, N
Guy, T
Mitchell, A
Tay, S
Jain, R
Forbes-Blom, E
Chen, X
Tong, P
Bolton, H
Paul, W
de St Groth, BF
Grimbaldeston, M
Le Gros, G
Weninger, W
AF Roediger, Ben
Kyle, Ryan
Yip, Kwok
Sumaria, Nital
Guy, Thomas
Mitchell, Andrew
Tay, Szun
Jain, Rohit
Forbes-Blom, Elizabeth
Chen, Xi
Tong, Philip
Bolton, Holly
Paul, William
de St Groth, Barbara Fazekas
Grimbaldeston, Michele
Le Gros, Graham
Weninger, Wolfgang
TI Cutaneous immuno-surveillance and regulation of inflammation by group 2
innate lymphoid cells (P6374)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Roediger, Ben; Sumaria, Nital; Guy, Thomas; Mitchell, Andrew; Tay, Szun; Jain, Rohit; Tong, Philip; Bolton, Holly; de St Groth, Barbara Fazekas; Weninger, Wolfgang] Centenary Inst, Sydney, NSW, Australia.
[Kyle, Ryan; Forbes-Blom, Elizabeth; Le Gros, Graham] Malaghan Inst, Wellington, New Zealand.
[Yip, Kwok; Grimbaldeston, Michele] Ctr Canc Biol, Adelaide, NSW, Australia.
[Chen, Xi; Paul, William] Natl Inst Allerg Dis, Bethesda, MD USA.
[de St Groth, Barbara Fazekas; Weninger, Wolfgang] Univ Sydney, Sydney, NSW 2006, Australia.
[Weninger, Wolfgang] Royal Prince Alfred Hosp, Sydney, NSW, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 2013
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108210
ER
PT J
AU Sarangi, P
Wahl, L
Vega, S
Yamada, Y
AF Sarangi, Pranita
Wahl, Larry
Vega, Susana
Yamada, Yoshihiko
TI Fibulin-7, a member of the extracellular matrix fibulin family,
regulates immune cell migration and function (P5124)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Sarangi, Pranita; Wahl, Larry; Vega, Susana; Yamada, Yoshihiko] NIDCR, Lab Cell & Dev Biol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 5816
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987106236
ER
PT J
AU Scheuermann, R
Finak, G
Ramey, J
Taghiyar, J
Stanton, R
Brandes, A
De Jager, P
Qiu, P
McCoy, J
Hafler, D
Maecker, H
Mosmann, T
Brinkman, R
Gottardo, R
AF Scheuermann, Richard
Finak, Greg
Ramey, John
Taghiyar, Jafar
Stanton, Rick
Brandes, Aaron
De Jager, Philip
Qiu, Peng
McCoy, J.
Hafler, David
Maecker, Holden
Mosmann, Tim
Brinkman, Ryan
Gottardo, Raphael
TI FlowCAP: comparison of automated and manual gating of standardized
lyoplate flow cytometry data
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Scheuermann, Richard; Stanton, Rick] J Craig Venter Inst, San Diego, CA USA.
[Finak, Greg; Ramey, John; Gottardo, Raphael] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Taghiyar, Jafar; Brinkman, Ryan] British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada.
[Brandes, Aaron; De Jager, Philip] Harvard Univ, Broad Inst, Program Med & Populat Genet, Cambridge, MA 02138 USA.
[Qiu, Peng] Univ Texas MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA.
[McCoy, J.] NHLBI, Ctr Human Immunol, Bethesda, MD 20892 USA.
[Hafler, David] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA.
[Maecker, Holden] Stanford Univ, Sch Med, Inst Immun Transplantat & Infect, Palo Alto, CA 94304 USA.
[Mosmann, Tim] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
RI Brinkman, Ryan/B-1108-2008
OI Brinkman, Ryan/0000-0002-9765-2990
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3374
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104049
ER
PT J
AU Schountz, T
Haddock, E
Feldmann, H
Prescott, J
AF Schountz, Tony
Haddock, Elaine
Feldmann, Heinz
Prescott, Joseph
TI Predominant Th2 cytokine gene expression in lymph node cell cultures
from Andes virus-infected deer mice (Peromyscus maniculatus)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Schountz, Tony] Univ No Colorado, Greeley, CO 80639 USA.
[Haddock, Elaine; Feldmann, Heinz; Prescott, Joseph] NIAID, Rocky Mt Labs, Virol Lab, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6316
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108152
ER
PT J
AU Seedhom, M
David, A
Bennink, J
Yewdell, J
AF Seedhom, Mina
David, Alexandre
Bennink, Jack
Yewdell, Jonathan
TI The RiboPuroMycylation method reveals surprising protein synthesis in
bone marrow T cells within a day of vaccinia virus infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Seedhom, Mina; David, Alexandre; Bennink, Jack; Yewdell, Jonathan] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3385
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104060
ER
PT J
AU Shen, W
Li, WQ
Feigenbaum, L
Hixon, J
Durum, S
AF Shen, Wei
Li, Wenqing
Feigenbaum, Lionel
Hixon, Julie
Durum, Scott
TI Plasticity in the differentiation of IL-22 producing cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Shen, Wei; Li, Wenqing; Hixon, Julie; Durum, Scott] NCI, Lab Mol Immunoregulat, NIH, Frederick, MD 21701 USA.
[Feigenbaum, Lionel] NCI, Lab Anim Sci Program, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P6265
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108102
ER
PT J
AU Singh, U
Singh, N
Busbee, B
Guan, HB
Price, R
Taub, D
Mishra, M
Nagarkatti, M
Nagarkatti, P
AF Singh, Udai
Singh, Narendra
Busbee, Brandon
Guan, Hongbing
Price, Robert
Taub, Dennis
Mishra, Manoj
Nagarkatti, Mitzi
Nagarkatti, Prakash
TI Leptin antagonist reduces STAT1/3 activation, lessens Smad7 expression,
restores TGF-beta 1 signaling and induces regulatory T cells (Tregs) to
ameliorate chronic colitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Singh, Udai; Singh, Narendra; Busbee, Brandon; Guan, Hongbing; Price, Robert; Nagarkatti, Mitzi; Nagarkatti, Prakash] Univ S Carolina, Columbia, SC 29208 USA.
[Taub, Dennis] NIA IRP, Lab Mol Biol & Immunol, Baltimore, MD USA.
[Mishra, Manoj] Alabama State Univ, Dept Math & Sci, Montgomery, AL 36101 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4208
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105025
ER
PT J
AU Smith, M
Hurley, A
Karpova, T
Hasley, R
Belkina, N
Shaw, S
Balenga, N
Druey, K
Nickel, E
Packard, B
Imamichi, H
Hu, ZH
McNally, J
Higgins, J
Sneller, M
Lane, H
Catalfamo, M
AF Smith, Mindy
Hurley, Amanda
Karpova, Tatiana
Hasley, Rebecca
Belkina, Natalya
Shaw, Stephen
Balenga, Nariman
Druey, Kirk
Nickel, Erin
Packard, Beverly
Imamichi, Hiromi
Hu, Zonghui
McNally, James
Higgins, Jeanette
Sneller, Michael
Lane, Henry
Catalfamo, Marta
TI Enhanced effector function of CD8+T cells through thrombin activation of
protease-activated receptor 1
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Smith, Mindy; Hurley, Amanda; Hasley, Rebecca; Nickel, Erin; Imamichi, Hiromi; Sneller, Michael; Lane, Henry; Catalfamo, Marta] NIAID, CMRS, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Balenga, Nariman; Druey, Kirk] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Hu, Zonghui] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Karpova, Tatiana; McNally, James] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
[Belkina, Natalya; Shaw, Stephen] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Packard, Beverly] OncoImmunin, Gaithersburg, MD USA.
[Higgins, Jeanette] SAIC Frederick Inc, AIDS Monitoring Labs, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 588
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987106220
ER
PT J
AU Song, HF
Josleyn, N
Janosko, K
Skinner, J
Reeves, RK
Cohen, M
Blaney, J
Jahrling, P
AF Song, Haifeng
Josleyn, Nicole
Janosko, Krisztina
Skinner, Jeff
Reeves, R. Keith
Cohen, Melanie
Blaney, Joe
Jahrling, Peter
TI Monkeypox virus infection of rhesus macaques induces massive expansion
of NK cells, but suppresses NK cell function
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Song, Haifeng; Josleyn, Nicole; Janosko, Krisztina; Cohen, Melanie; Jahrling, Peter] NIAID, IRF, NIH, Frederick, MD USA.
[Blaney, Joe; Jahrling, Peter] NIAID, EVPS, NIH, Frederick, MD USA.
[Skinner, Jeff] NIAID, CBS, BCBB, NIH, Frederick, MD USA.
[Reeves, R. Keith] Harvard Univ, Sch Med, NEPRC, Southborough, MA 01772 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4369
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105183
ER
PT J
AU Spolski, R
Li, P
Liao, W
Wang, L
Leonard, W
AF Spolski, Rosanne
Li, Peng
Liao, Wei
Wang, Lu
Leonard, Warren
TI Elucidation of the mechanism of cell type specific IRF-4-mediated
transcription in CD4+T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Spolski, Rosanne; Li, Peng; Liao, Wei; Wang, Lu; Leonard, Warren] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1081
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100081
ER
PT J
AU Tegla, C
Cudrici, C
Nguyen, V
Danoff, J
Vlaicu, S
Rus, V
Badea, T
Rus, H
AF Tegla, Cosmin
Cudrici, Cornelia
Vinh Nguyen
Danoff, Jacob
Vlaicu, Sonia
Rus, Violeta
Badea, Tudor
Rus, Horea
TI Characterization of the in vivo function of RGC-32 in T-cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Tegla, Cosmin; Rus, Horea] VA Maryland Hlth Care Sys, Res Serv, Baltimore, MD USA.
[Tegla, Cosmin; Cudrici, Cornelia; Vinh Nguyen; Danoff, Jacob; Vlaicu, Sonia; Rus, Violeta; Rus, Horea] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Badea, Tudor] NEI, Retinal Circuit Dev & Genet Unit, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1151
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100151
ER
PT J
AU Thomas, E
Noureddin, M
Rotman, Y
Liang, TJ
AF Thomas, Emmanuel
Noureddin, Mazen
Rotman, Yaron
Liang, T. Jake
TI Mechanism of induction and genotype-phenotype correlation of IL28B and
ISG expression in HCV-infected primary human hepatocytes and liver
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Thomas, Emmanuel] Univ Miami, Miami, FL USA.
[Noureddin, Mazen; Rotman, Yaron; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1383
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101132
ER
PT J
AU Thomas, L
Long, E
AF Thomas, Louis
Long, Eric
TI NK cell licensing modulates NK cell conjugation to target cells via
altered activation receptor function
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Thomas, Louis; Long, Eric] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1063
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100063
ER
PT J
AU Tsuchiya, K
Hernandez-Cuellar, E
Hara, H
Fang, RD
Sakai, S
Kawamura, I
Mitsuyama, M
AF Tsuchiya, Kohsuke
Hernandez-Cuellar, Eduardo
Hara, Hideki
Fang, Rendong
Sakai, Shunsuke
Kawamura, Ikuo
Mitsuyama, Masao
TI Nitric oxide inhibits the NLRP3 inflammasome
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Tsuchiya, Kohsuke; Hernandez-Cuellar, Eduardo; Hara, Hideki; Fang, Rendong; Sakai, Shunsuke; Kawamura, Ikuo; Mitsuyama, Masao] Kyoto Univ, Grad Sch Med, Kyoto, Japan.
[Sakai, Shunsuke] NIAID, Lymphocyte Biol Unit T, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1270
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101019
ER
PT J
AU Vo, M
Holz, L
Benseler, V
McGuffog, C
Hilton, D
McCaughan, G
Bowen, D
Bertolino, P
AF Vo, Michelle
Holz, Lauren
Benseler, Volker
McGuffog, Claire
Hilton, Douglas
McCaughan, Geoffrey
Bowen, David
Bertolino, Patrick
TI The magnitude of acute hepatitis is more limited by regulation of
cytokine signalling than apoptosis of liver-infiltrating effector CD8 T
cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Vo, Michelle; Holz, Lauren; Benseler, Volker; McGuffog, Claire; McCaughan, Geoffrey; Bowen, David; Bertolino, Patrick] Centenary Inst, Camperdown, NSW, Australia.
[Holz, Lauren] NIH, Liver Dis Branch, Bethesda, MD 20892 USA.
[Benseler, Volker] Univ Regensburg, Dept Surg, D-93053 Regensburg, Germany.
[Hilton, Douglas] Walter & Eliza Hall Inst Med Res, Mol Med Div, Melbourne, Vic 3050, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4174
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104242
ER
PT J
AU Wang, HS
Jain, S
Sun, JF
Morse, H
AF Wang, Hongsheng
Jain, Shweta
Sun, Jiafang
Morse, Herbert, III
TI IRF8 regulates lymphoid-myeloid lineage priming and commitment defined
by an IRF8-EGFP reporter mouse
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Wang, Hongsheng; Jain, Shweta; Sun, Jiafang; Morse, Herbert, III] NIAID, Immunogenet Lab, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4374
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987105188
ER
PT J
AU Wang, YC
Sui, YJ
Steel, J
Morris, J
Berzofsky, J
AF Wang, Yichuan
Sui, Yongjun
Steel, Jason
Morris, John
Berzofsky, Jay
TI Vaginal type-II mucosa acts as an inductive site during the generation
of primary CD8+T cell mucosal immune responses
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Wang, Yichuan; Sui, Yongjun; Berzofsky, Jay] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Steel, Jason; Morris, John] Univ Cincinnati, Dept Med, Div Hematol Oncol, Cincinnati, OH 45221 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3186
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103112
ER
PT J
AU Wang, ZY
Mathiarasu, A
Hong, P
Xu, Y
Li, AQ
Bluth, M
Lum, L
Huang, BH
Romero, R
Cerutti, A
Chen, K
AF Wang, Zhao-Yuan
Mathiarasu, Aditya
Hong, Peng
Xu, Yi
Li, Aiqun
Bluth, Martin
Lum, Lawrence
Huang, Bihui
Romero, Roberto
Cerutti, Andrea
Chen, Kang
TI Defective induction of regulatory B cells by decidua stromal cells
underlies the pathogenesis of preterm birth
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Wang, Zhao-Yuan; Mathiarasu, Aditya; Bluth, Martin; Lum, Lawrence; Chen, Kang] Wayne State Univ, Detroit, MI USA.
[Wang, Zhao-Yuan; Mathiarasu, Aditya; Xu, Yi; Romero, Roberto; Chen, Kang] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Detroit, MI USA.
[Hong, Peng] Suny Downstate Med Ctr, New York, NY USA.
[Li, Aiqun] New York Stem Cell Fdn, New York, NY USA.
[Bluth, Martin; Lum, Lawrence; Chen, Kang] Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
[Huang, Bihui] Yale Univ, New Haven, CT USA.
[Cerutti, Andrea] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P3213
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987103139
ER
PT J
AU Watanabe, M
Hodes, R
AF Watanabe, Masashi
Hodes, Richard
TI Cell type specific role of B7 for Ag-specific T and B cell activation
and differentiation in T-dependent antibody response in vivo
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Watanabe, Masashi; Hodes, Richard] NCI, EIB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1017
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100019
ER
PT J
AU Weindel, C
Richey, L
Bolland, S
Huber, B
AF Weindel, Chi
Richey, Lauren
Bolland, Silvia
Huber, Brigitte
TI Autophagy: a dichotomous player in Toll-like receptor 7-mediated
autoimmunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Weindel, Chi; Huber, Brigitte] Tufts Univ, Sackler Sch Grad Biomed Sci, Grad Program Genet, Boston, MA 02111 USA.
[Richey, Lauren] Tufts Univ, Div Lab Anim Med, Boston, MA 02111 USA.
[Huber, Brigitte] Tufts Univ, Sackler Sch Grad Biomed Sci, Dept Pathol, Boston, MA 02111 USA.
[Bolland, Silvia] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P4073
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987104142
ER
PT J
AU Weitzel, R
Fitzhugh, C
Phang, O
Hsieh, M
Tisdale, J
AF Weitzel, R.
Fitzhugh, Courtney
Phang, Oswald
Hsieh, Matthew
Tisdale, John
TI Nonmyeloablative conditioning employing busulfan and sirolimus permits
donor-dominant stable chimerism in a murine model of haploidentical
allogeneic stem cell transplantation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Weitzel, R.; Fitzhugh, Courtney; Phang, Oswald; Hsieh, Matthew; Tisdale, John] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P2192
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102141
ER
PT J
AU Weitzel, R
Biancotto, A
Fitzhugh, C
McCoy, P
Hsieh, M
Tisdale, J
AF Weitzel, R.
Biancotto, Angelique
Fitzhugh, Courtney
McCoy, Philip
Hsieh, Matthew
Tisdale, John
TI Characterization of lymphocytes emerging early after nonmyeloablative
conditioning and hematopoietic stem cell transplant supported with
sirolimus
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Weitzel, R.; Fitzhugh, Courtney; Hsieh, Matthew; Tisdale, John] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Biancotto, Angelique; McCoy, Philip] NIH, Ctr Human Immunol & Inflammat, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P2186
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987102135
ER
PT J
AU Wessel, A
Hsu, A
Zilberman-Rudenko, J
Goldbach-Mansky, R
Siegel, R
Hanson, E
AF Wessel, Alex
Hsu, Amy
Zilberman-Rudenko, Jevgenia
Goldbach-Mansky, Raphaela
Siegel, Richard
Hanson, Eric
TI Inflammatory disease and impaired antiviral immunity due to unbalanced
NF-kB and IRF3 activation result from a de novo human NEMO mutation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Wessel, Alex; Zilberman-Rudenko, Jevgenia; Siegel, Richard; Hanson, Eric] NIAMS, NIH, Autoimmun Branch, Bethesda, MD USA.
[Hsu, Amy] NIAID, NIH, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Goldbach-Mansky, Raphaela] NIAMS, NIH, Pediat Translat Res Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1415
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987101157
ER
PT J
AU West, E
Rochman, Y
Kashyap, M
Li, P
Spolski, R
Leonard, W
AF West, Erin
Rochman, Yrina
Kashyap, Mohit
Li, Peng
Spolski, Rosanne
Leonard, Warren
TI Direct actions of TSLP on CD4+T cells are important for in vivo Th2-type
responses
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [West, Erin; Rochman, Yrina; Kashyap, Mohit; Li, Peng; Spolski, Rosanne; Leonard, Warren] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 11522
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108089
ER
PT J
AU Yoshimi, R
Watanabe, R
Tsukahara, T
Hama, M
Ihata, A
Ueda, A
Takeno, M
Morse, H
Ozato, K
Ishigatsubo, Y
AF Yoshimi, Ryusuke
Watanabe, Reikou
Tsukahara, Toshinori
Hama, Maasa
Ihata, Atsushi
Ueda, Atsuhisa
Takeno, Mitsuhiro
Morse, Herbert, III
Ozato, Keiko
Ishigatsubo, Yoshiaki
TI The E3 ubiquitin ligase TRIM21 forms a complex with p62 and TRAF6 and
promotes degradation of TRAF6
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Yoshimi, Ryusuke; Watanabe, Reikou; Tsukahara, Toshinori; Hama, Maasa; Ihata, Atsushi; Ueda, Atsuhisa; Takeno, Mitsuhiro; Ishigatsubo, Yoshiaki] Yokohama City Univ, Grad Sch Med, Dept Internal Med & Clin Immunol, Yokohama, Kanagawa 232, Japan.
[Morse, Herbert, III] NIAID, Lab Immunopathol, NIH, Rockville, MD USA.
[Yoshimi, Ryusuke; Ozato, Keiko] NICHHD, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P1176
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987100176
ER
PT J
AU Zhang, GX
Yan, YP
Ding, XL
Li, K
Ciric, B
Yang, JX
Wu, S
Xu, H
Chen, WJ
Lovett-Racke, A
Rostami, A
AF Zhang, Guang-Xian
Yan, Yaping
Ding, Xiaoli
Li, Ke
Ciric, Bogoljub
Yang, Jingxian
Wu, Shuai
Xu, Hui
Chen, Wanjun
Lovett-Racke, Amy
Rostami, Abdolmohamad
TI IFN-gamma signaling in astrocytes and microglia has opposite roles in
CNS autoimmunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Zhang, Guang-Xian; Yan, Yaping; Ding, Xiaoli; Li, Ke; Ciric, Bogoljub; Yang, Jingxian; Wu, Shuai; Xu, Hui; Rostami, Abdolmohamad] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Chen, Wanjun] OIIB, Mucosal Immunol Sect, NIH, Bethesda, MD USA.
[Lovett-Racke, Amy] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA P5170
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987107031
ER
PT J
AU Zoon, K
Fey, S
Horowitz, J
Fischer, E
Balinsky, C
Miyake, K
Bekisz, J
Snow, A
Schmeisser, H
AF Zoon, Kathryn
Fey, Samuel
Horowitz, Julie
Fischer, Elizabeth
Balinsky, Corey
Miyake, Kotaro
Bekisz, Joseph
Snow, Andrew
Schmeisser, Hana
TI Induction of autophagy by Type I interferon in human cancer cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the American-Association-of-Immunologists
CY MAY 03-07, 2013
CL Honolulu, HI
SP Amer Assoc Immunologists
C1 [Zoon, Kathryn; Fey, Samuel; Horowitz, Julie; Fischer, Elizabeth; Balinsky, Corey; Miyake, Kotaro; Bekisz, Joseph; Schmeisser, Hana] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Snow, Andrew] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2013
VL 190
MA 1154
PG 1
WC Immunology
SC Immunology
GA 199ID
UT WOS:000322987108054
ER
PT J
AU Schmeisser, H
Fey, SB
Horowitz, J
Fischer, ER
Balinsky, CA
Miyake, K
Bekisz, J
Snow, AL
Zoon, KC
AF Schmeisser, Hana
Fey, Samuel B.
Horowitz, Julie
Fischer, Elizabeth R.
Balinsky, Corey A.
Miyake, Kotaro
Bekisz, Joseph
Snow, Andrew L.
Zoon, Kathryn C.
TI Type I interferons induce autophagy in certain human cancer cell lines
SO AUTOPHAGY
LA English
DT Article
DE autophagy; human cancer cells; type I interferon; MTORC1; signal
transduction; AKT; PI3K
ID MESSENGER-RNA TRANSLATION; PLASMACYTOID DENDRITIC CELLS; P70 S6 KINASE;
PHOSPHATIDYLINOSITOL 3-KINASE; TRANSCRIPTIONAL ACTIVATOR; NUCLEAR
TRANSLOCATION; PROMOTES SURVIVAL; DEFENSE-MECHANISM; STIMULATED GENES;
DAUDI CELLS
AB Autophagy is an evolutionarily conserved cellular recycling mechanism that occurs at a basal level in all cells. It can be further induced by various stimuli including starvation, hypoxia, and treatment with cytokines such as IFNG/IFN and TGFB/TGF. Type I IFNs are proteins that induce an antiviral state in cells. They also have antiproliferative, proapoptotic and immunomodulatory activities. We investigated whether type I IFN can also induce autophagy in multiple human cell lines. We found that treatment with IFNA2c/IFN2c and IFNB/IFN induces autophagy by 24 h in Daudi B cells, as indicated by an increase of autophagy markers MAP1LC3-II, ATG12-ATG5 complexes, and a decrease of SQSTM1 expression. An increase of MAP1LC3-II was also detected 48 h post-IFNA2c treatment in HeLa S3, MDA-MB-231, T98G and A549 cell lines. The presence of autophagosomes in selected cell lines exposed to type I IFN was confirmed by electron microscopy analysis. Increased expression of autophagy markers correlated with inhibition of MTORC1 in Daudi cells, as well as inhibition of cancer cell proliferation and changes in cell cycle progression. Concomitant blockade of either MTOR or PI3K-AKT signaling in Daudi and T98G cells treated with IFNA2c increased the level of MAP1LC3-II, indicating that the PI3K-AKT-MTORC1 signaling pathway may modulate IFN-induced autophagy in these cells. Taken together, our findings demonstrated a novel function of type I IFN as an inducer of autophagy in multiple cell lines.
C1 [Schmeisser, Hana; Fey, Samuel B.; Horowitz, Julie; Balinsky, Corey A.; Miyake, Kotaro; Bekisz, Joseph; Zoon, Kathryn C.] NIAID, NIH, Cytokine Biol Sect, Bethesda, MD 20892 USA.
[Fischer, Elizabeth R.] NIAID, NIH, Rocky Mt Labs, Res Technol Sect, Hamilton, MT USA.
[Snow, Andrew L.] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA.
RP Zoon, KC (reprint author), NIAID, NIH, Cytokine Biol Sect, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kzoon@niaid.nih.gov
OI Snow, Andrew/0000-0002-8728-6691
FU Intramural Research Program of the NIH (NIAID)
FX We thank Drs. J. Hartley, D. Esposito and W. Gillette (NCI/SAIC) for
expression and purification of IFNA2c, Drs. H. Young (NCI), M. Lotze
(University of Pittsburgh), M. Lenardo (NIAID), Li Yu (NIAID), F.
Schmeisser (FDA), D. Jankovic (NIAID), G. Fabozzi (FDA), N. Lai and L.L.
Chan (Nexcelom Bioscience LLC) for reviewing the manuscript and valuable
discussions. This research was supported by the Intramural Research
Program of the NIH (NIAID).
NR 66
TC 23
Z9 25
U1 1
U2 9
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 MAY 1
PY 2013
VL 9
IS 5
BP 683
EP 696
DI 10.4161/auto.23921
PG 14
WC Cell Biology
SC Cell Biology
GA 201WQ
UT WOS:000323174100006
PM 23419269
ER
PT J
AU Martin, TJ
Peer, CJ
Figg, WD
AF Martin, Timothy J.
Peer, Cody J.
Figg, William D.
TI Uncovering the genetic landscape driving castration-resistant prostate
cancer
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE castration-resistant prostate cancer; mutations; genetics
ID MUTATION
AB Identification of the mechanisms that drive progression of metastatic castration-resistant prostate cancer (CRPC) has fostered interest since early androgen studies in the 1940s. Little knowledge has surfaced about the role mutations play in prostate cancer development. A group at the Michigan Center for Translation Pathology studied exomes of lethal, metastatic CRPC and documented the overall mutation rates. In classifying these mutations, the monoclonal cause of CRPC was recognized. Nine identified genes showed significant mutations. Six of these genes had previously been reported as mutated in prostate cancer. The analysis also found significantly mutated androgen receptor (AR) cofactors and linked proteins, including FOXA1 and MLL2. Another finding concerned an aberration in CHD1. Prostate cancers with deletions or mutations in CHD1 showed a strong correlation with ETS gene family fusion negative prostate cancers (96%). In profiling these exomes, this group provides an original method to identify deletions and mutations that drive CRPC progression.
C1 [Martin, Timothy J.; Peer, Cody J.; Figg, William D.] NCI, Clin Pharmacol Program, Med Oncol Branch, Off Clin Director, Bethesda, MD 20892 USA.
RP Figg, WD (reprint author), NCI, Clin Pharmacol Program, Med Oncol Branch, Off Clin Director, Bethesda, MD 20892 USA.
EM wdfigg@helix.nih.gov
RI Figg Sr, William/M-2411-2016
NR 10
TC 1
Z9 1
U1 1
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD MAY 1
PY 2013
VL 14
IS 5
BP 399
EP 400
DI 10.4161/cbt.24426
PG 2
WC Oncology
SC Oncology
GA 201WW
UT WOS:000323174700003
PM 23917376
ER
PT J
AU Gorfinkel, IS
Aoki, F
McNeil, S
Dionne, M
Shafran, SD
Zickler, P
Halperin, S
Langley, J
Bellamy, A
Schulte, J
Heineman, T
Belshe, R
AF Gorfinkel, I. S.
Aoki, F.
McNeil, S.
Dionne, M.
Shafran, S. D.
Zickler, P.
Halperin, S.
Langley, J.
Bellamy, A.
Schulte, J.
Heineman, T.
Belshe, R.
TI Seroprevalence of HSV-1 and HSV-2 antibodies in Canadian women screened
for enrolment in a herpes simplex virus vaccine trial
SO INTERNATIONAL JOURNAL OF STD & AIDS
LA English
DT Article
DE Herpes simplex 1; Herpes simplex 2; HSV-1; HSV-2; seroprevalence;
Canadian women; Herpevac Trial for Women; herpes virus; Sexually
transmitted infection; STI
ID GENITAL HERPES; GLYCOPROTEIN-G; RISK-FACTORS; COLLEGE-STUDENTS; NEONATAL
HERPES; WESTERN-BLOT; TYPE-2 HSV-2; INFECTION; PREVALENCE; CHILDREN
AB Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) infections continue to be among the most common and unrecognized sexually transmitted infections in the world. Although treatable, HSV-1 and HSV-2 infections remain incurable. Hence, there is interest in the development of a vaccine to prevent genital herpes. As part of a multicentre, randomized, placebo-controlled trial to test such a vaccine, healthy women 18-30 years were enrolled as volunteers in several Canadian centres between 2005 and 2007. This study reports the seroprevalence of HSV-1 and HSV-2 antibodies in this group. A total of 2694 adult female volunteers in Canada with no known history of herpes simplex were screened for HSV antibodies using Western blot assay (the gold standard for diagnosis of HSV) for potential participation in a randomized, double-blind efficacy field trial of a herpes simplex vaccine. This trial provides a unique opportunity to examine the prevalence of antibodies to HSV-1 and of antibodies to HSV-2 in women with no known history of herpes simplex infection. The prevalence of antibodies to HSV-1 and to HSV-2 is compared with that found in previous Canadian studies that focused on a more general population. The overall seroprevalence of antibody to HSV-1 was 43%; that of HSV-2 was 2.5% and seropositivity to both was 2%. The prevalence of antibody to both HSV-1 and to HSV-2 increased with age. Seronegativity to both HSV-1 and HSV-2 was 56% in participating centres with populations under 250,000 and 46% in participating centres with populations over 250,000. Significant racial differences in seropositivity to HSV-1 and to HSV-2 were noted. The likelihood of participants being seropositive to HSV-1 and to HSV-2 was found to increase with age and to positively correlate with the population of the city in which they resided. Hypotheses are proposed to account for differences in racial seropositivity to HSV-1 and to HSV-2.
C1 [Gorfinkel, I. S.] Prime Hlth Res Corp, Toronto, ON, Canada.
[Aoki, F.] Univ Manitoba, Winnipeg, MB, Canada.
[Dionne, M.] Dept Sante Publ, Quebec City, PQ, Canada.
[Shafran, S. D.] Univ Alberta Hosp, Edmonton, AB T6G 2B7, Canada.
[Zickler, P.] TASC CMX Res Serv Inc, Surrey, England.
[Halperin, S.; Langley, J.] Dalhousie Univ, Canadian Ctr Vaccinol, IWK Hlth Ctr, Halifax, NS, Canada.
[Halperin, S.; Langley, J.] Dalhousie Univ, Capital Hlth, Halifax, NS, Canada.
[Bellamy, A.] EMMES Corp, Rockville, MD USA.
[Schulte, J.] NIAID, NIH, Bethesda, MD 20892 USA.
[Heineman, T.] GlaxoSmithKline Inc, King Of Prussia, PA USA.
[Belshe, R.] St Louis Univ, Div Infect Dis Allergy & Immunol, St Louis, MO 63103 USA.
RP Gorfinkel, IS (reprint author), Prime Hlth Res Corp, 1849 Yonge St,Suite 516, Toronto, ON, Canada.
EM hannah_marie33@hotmail.com
NR 35
TC 3
Z9 4
U1 1
U2 8
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND
SN 0956-4624
J9 INT J STD AIDS
JI Int. J. STD AIDS
PD MAY
PY 2013
VL 24
IS 5
BP 345
EP 349
DI 10.1177/0956462412472822
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 198EF
UT WOS:000322904200003
PM 23970700
ER
PT J
AU Koonin, EV
Makarova, KS
AF Koonin, Eugene V.
Makarova, Kira S.
TI CRISPR-Cas: Evolution of an RNA-based adaptive immunity system in
prokaryotes
SO RNA BIOLOGY
LA English
DT Article
DE CRISPR-Cas; adaptive immunity; innate immunity; programmed cell death;
dormancy; RRM domain
ID SHORT PALINDROMIC REPEATS; SEQUENCE-SPECIFIC ENDORIBONUCLEASES;
BIOCHEMICAL-CHARACTERIZATION; BACTERIAL IMMUNITY; CRYSTAL-STRUCTURE;
ESCHERICHIA-COLI; DNA; PROTEIN; COMPLEX; CLEAVAGE
AB The CRISPR-Cas (clustered regularly interspaced short palindromic repeats, CRISPR-associated genes) is an adaptive immunity system in bacteria and archaea that functions via a distinct self-non-self recognition mechanism that is partially analogous to the mechanism of eukaryotic RNA interference (RNAi). The CRISPR-Cas system incorporates fragments of virus or plasmid DNA into the CRISPR repeat cassettes and employs the processed transcripts of these spacers as guide RNAs to cleave the cognate foreign DNA or RNA. The Cas proteins, however, are not homologous to the proteins involved in RNAi and comprise numerous, highly diverged families. The majority of the Cas proteins contain diverse variants of the RNA recognition motif (RRM), a widespread RNA-binding domain. Despite the fast evolution that is typical of the cas genes, the presence of diverse versions of the RRM in most Cas proteins provides for a simple scenario for the evolution of the three distinct types of CRISPR-cas systems. In addition to several proteins that are directly implicated in the immune response, the cas genes encode a variety of proteins that are homologous to prokaryotic toxins that typically possess nuclease activity. The predicted toxins associated with CRISPR-Cas systems include the essential Cas2 protein, proteins of COG1517 that, in addition to a ligand-binding domain and a helix-turn-helix domain, typically contain different nuclease domains and several other predicted nucleases. The tight association of the CRISPR-Cas immunity systems with predicted toxins that, upon activation, would induce dormancy or cell death suggests that adaptive immunity and dormancy/suicide response are functionally coupled. Such coupling could manifest in the persistence state being induced and potentially providing conditions for more effective action of the immune system or in cell death being triggered when immunity fails.
C1 [Koonin, Eugene V.; Makarova, Kira S.] NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
RP Koonin, EV (reprint author), NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bldg 10, Bethesda, MD 20892 USA.
EM koonin@ncbi.nlm.nih.gov
FU intramural program of the United States Department of Health and Human
Services
FX The authors' research is supported by the intramural program of the
United States Department of Health and Human Services (to National
Library of Medicine).
NR 70
TC 54
Z9 62
U1 3
U2 35
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1547-6286
J9 RNA BIOL
JI RNA Biol.
PD MAY 1
PY 2013
VL 10
IS 5
SI SI
BP 679
EP 686
DI 10.4161/rna.24022
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 201XS
UT WOS:000323176900005
PM 23439366
ER
PT J
AU Strizzi, L
Margaryan, NV
Gilgur, A
Hardy, KM
Normanno, N
Salomon, DS
Hendrix, MJC
AF Strizzi, Luigi
Margaryan, Naira V.
Gilgur, Alina
Hardy, Katharine M.
Normanno, Nicola
Salomon, David S.
Hendrix, Mary J. C.
TI The significance of a Cripto-1-positive subpopulation of human melanoma
cells exhibiting stem cell-like characteristics
SO CELL CYCLE
LA English
DT Article
DE Cripto-1; melanoma; tumorigenicity; aggressiveness; recurrence; target
ID HUMAN-MALIGNANT MELANOMA; CRIPTO-1; EXPRESSION; GROWTH; ENHANCEMENT;
PHENOTYPE
AB Cripto-1 (CR-1) protein function differs according to cellular or extracellular expression. In this study, we explore the significance of cell surface CR-1 expression in human melanoma cells. Cell surface CR-1-expressing human melanoma cells (CR1-CS+) were selected by fluorescence-activated cell sorting (FACS) and grown in vitro and in vivo in nude mice to study their growth characteristics. The CR1-CS+ melanoma cells were found to express increased levels of Oct4, MDR-1 and activated c-Src compared with cells lacking this subpopulation (CR1-CS-) or unsorted cells, used as control. CR1-CS+ show reduced proliferation rates and diminished spherical colony formation compared with control cells when cultured in vitro. Orthotopic injections of CR1-CS+ in nude mice formed slow growing tumors with histologic variability across different areas of the CR1-CS+ xenografts. CR-1-expressing cells from first generation CR1-CS+ tumors showed significantly increased tumor-forming rate and aggressiveness following subsequent transplants in nude mice. These data demonstrate that within a heterogeneous melanoma cell population there resides a slow proliferating, cell surface CR-1-expressing subpopulation capable of giving rise to a fast growing, aggressive progeny that may contribute to disease recurrence and progression.
C1 [Strizzi, Luigi; Margaryan, Naira V.; Gilgur, Alina; Hardy, Katharine M.; Hendrix, Mary J. C.] Northwestern Univ, Feinberg Sch Med, Ann & Robert H Lurie Childrens Hosp, Chicago Res Ctr, Chicago, IL 60611 USA.
[Normanno, Nicola] INT Fdn Pascale, Cell Biol & Biotherapy Unit, Naples, Italy.
[Salomon, David S.] NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
RP Strizzi, L (reprint author), Northwestern Univ, Feinberg Sch Med, Ann & Robert H Lurie Childrens Hosp, Chicago Res Ctr, Chicago, IL 60611 USA.
EM lstrizzi@luriechildrens.org
OI Normanno, Nicola/0000-0002-7158-2605
FU Eisenberg Research Scholar Grant; Italian Association for Cancer
Research (AIRC); National Institutes of Health Intramural Funding; NIH
[R37CA59702, RO1CA121205]
FX This work was supported by the following: Eisenberg Research Scholar
Grant to L. Strizzi; Italian Association for Cancer Research (AIRC) to
N. Normanno; National Institutes of Health Intramural Funding to D.S.
Salomon; NIH grants R37CA59702 and RO1CA121205 to M.J.C. Hendrix.
NR 24
TC 7
Z9 7
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD MAY 1
PY 2013
VL 12
IS 9
BP 1450
EP 1456
DI 10.4161/cc.24601
PG 7
WC Cell Biology
SC Cell Biology
GA 196FJ
UT WOS:000322758600019
PM 23574716
ER
PT J
AU Xu, JH
Luo, FJ
Zhang, Z
Xue, L
Wu, XS
Chiang, HC
Shin, W
Wu, LG
AF Xu, Jianhua
Luo, Fujun
Zhang, Zhen
Xue, Lei
Wu, Xin-Sheng
Chiang, Hsueh-Cheng
Shin, Wonchul
Wu, Ling-Gang
TI SNARE Proteins Synaptobrevin, SNAP-25, and Syntaxin Are Involved in
Rapid and Slow Endocytosis at Synapses
SO CELL REPORTS
LA English
DT Article
ID KISS-AND-RUN; SYNAPTIC-VESICLE ENDOCYTOSIS; ADRENAL CHROMAFFIN CELLS;
CENTRAL-NERVOUS-SYSTEM; RETINAL BIPOLAR CELLS; NEUROTRANSMITTER RELEASE;
GLUTAMATERGIC SYNAPSE; SINGLE NANOPARTICLES; CALCIUM-DEPENDENCE; DYNAMIC
CONTROL
AB Rapid endocytosis, which takes only a few seconds, is widely observed in secretory cells. Although it is more efficient in recycling vesicles than in slow clathrin-mediated endocytosis, its underlying mechanism, thought to be clathrin independent, is largely unclear. Here, we report that cleavage of three SNARE proteins essential for exocytosis, including synaptobrevin, SNAP-25, and syntaxin, inhibited rapid endocytosis at the calyx of Held nerve terminal, suggesting the involvement of the three SNARE proteins in rapid endocytosis. These SNARE proteins were also involved in slow endocytosis. In addition, SNAP-25 and syntaxin facilitated vesicle mobilization to the readily releasable pool, most likely via their roles in endocytosis and/or exocytosis. We conclude that both rapid and slow endocytosis share the involvement of SNARE proteins. The dual role of three SNARE proteins in exo- and endocytosis suggests that SNARE proteins may be molecular substrates contributing to the exocytosis-endocytosis coupling, which maintains exocytosis in secretory cells.
C1 [Xu, Jianhua; Luo, Fujun; Zhang, Zhen; Xue, Lei; Wu, Xin-Sheng; Chiang, Hsueh-Cheng; Shin, Wonchul; Wu, Ling-Gang] NINDS, Bethesda, MD 20892 USA.
[Xu, Jianhua] Georgia Hlth Sci Univ, Inst Mol Med & Genet, Augusta, GA 30912 USA.
[Xu, Jianhua] Georgia Hlth Sci Univ, Dept Neurol, Augusta, GA 30912 USA.
RP Wu, LG (reprint author), NINDS, 35 Convent Dr,Bldg 35,Room 2B-1012, Bethesda, MD 20892 USA.
EM wul@ninds.nih.gov
RI Luo, Fujun/I-1016-2013;
OI Xu, Jianhua/0000-0003-0084-8856
FU National Institute of Neurological Disorders and Stroke Intramural
Research Program
FX We thank Dr. Peter Wen for reading of the manuscript. This work was
supported by the National Institute of Neurological Disorders and Stroke
Intramural Research Program.
NR 42
TC 25
Z9 25
U1 2
U2 14
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAY
PY 2013
VL 3
IS 5
BP 1414
EP 1421
DI 10.1016/j.celrep.2013.03.010
PG 8
WC Cell Biology
SC Cell Biology
GA 184NY
UT WOS:000321899300012
PM 23643538
ER
PT J
AU Yang, MY
Hilton, MB
Seaman, S
Haines, DC
Nagashima, K
Burks, CM
Tessarollo, L
Ivanova, PT
Brown, HA
Umstead, TM
Floros, J
Chroneos, ZC
Croix, BS
AF Yang, Mi Young
Hilton, Mary Beth
Seaman, Steven
Haines, Diana C.
Nagashima, Kunio
Burks, Christina M.
Tessarollo, Lino
Ivanova, Pavlina T.
Brown, H. Alex
Umstead, Todd M.
Floros, Joanna
Chroneos, Zissis C.
Croix, Brad St.
TI Essential Regulation of Lung Surfactant Homeostasis by the Orphan G
Protein-Coupled Receptor GPR116
SO CELL REPORTS
LA English
DT Article
ID PULMONARY ALVEOLAR PROTEINOSIS; LIPID-ACCUMULATION; IDENTIFICATION;
MICE; DIFFERENTIATION; THERAPY; DOMAIN; GENES; CELLS; GPCRS
AB GPR116 is an orphan seven-pass transmembrane receptor whose function has been unclear. Global disruption of the Gpr116 gene in mice revealed an unexpected, critical role for this receptor in lung surfactant homeostasis, resulting in progressive accumulation of surfactant lipids and proteins in the alveolar space, labored breathing, and a reduced lifespan. GPR116 expression analysis, bone marrow transplantation studies, and characterization of conditional knockout mice revealed that GPR116 expression in ATII cells is required for maintaining normal surfactant levels. Aberrant packaging of surfactant proteins with lipids in the Gpr116 mutant mice resulted in compromised surfactant structure, function, uptake, and processing. Thus, GPR116 plays an indispensable role in lung surfactant homeostasis with important ramifications for the understanding and treatment of lung surfactant disorders.
C1 [Yang, Mi Young; Hilton, Mary Beth; Seaman, Steven; Croix, Brad St.] NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, Ctr Canc Res, Ft Detrick, MD 21702 USA.
[Hilton, Mary Beth] NCI, SAIC Frederick, Frederick Natl Lab Canc Res, Ft Detrick, MD 21702 USA.
[Tessarollo, Lino] NCI, Neural Dev Sect, MCGP, CCR, Ft Detrick, MD 21702 USA.
[Nagashima, Kunio] NCI, Electron Microscopy Lab, Adv Technol Program, SAIC Frederick,FNLCR, Ft Detrick, MD 21702 USA.
[Haines, Diana C.; Burks, Christina M.] NCI, Vet Pathol Sect, Pathol Histotechnol Lab, SAIC Frederick,FNLCR, Ft Detrick, MD 21702 USA.
[Ivanova, Pavlina T.; Brown, H. Alex] Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA.
[Ivanova, Pavlina T.; Brown, H. Alex] Vanderbilt Univ, Med Ctr, Vanderbilt Inst Chem Biol, Nashville, TN 37232 USA.
[Umstead, Todd M.; Floros, Joanna; Chroneos, Zissis C.] Penn State Univ, Coll Med, Dept Pediat, Hershey, PA 17033 USA.
[Umstead, Todd M.; Floros, Joanna; Chroneos, Zissis C.] Penn State Univ, Coll Med, Ctr Host Def Inflammat & Lung Dis Res, Hershey, PA 17033 USA.
[Floros, Joanna] Penn State Univ, Coll Med, Dept Obstet & Gynecol, Hershey, PA 17033 USA.
RP Croix, BS (reprint author), NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, Ctr Canc Res, Ft Detrick, MD 21702 USA.
EM stcroix@ncifcrf.gov
FU Center for Cancer Research Intramural Program, National Cancer Institute
(NCI), National Institutes of Health, a part of the U.S. Department of
Health and Human Services; NCI [HHSN261200800001E, NIH HL34788]; NIGMS
[U54 GM069338]
FX This manuscript is dedicated to the memory of our dear friend and
colleague Dr. Jo Rae Wright, who provided helpful advice and SFTPC-GFP
mice for these studies. We thank Brigid L.M. Hogan and Jason R. Rock for
providing SFTPC-Cre mice. This research was supported by the Center for
Cancer Research Intramural Program, National Cancer Institute (NCI),
National Institutes of Health, a part of the U.S. Department of Health
and Human Services, and with federal funds from the NCI under contract
nos. HHSN261200800001E and NIH HL34788. The content of this publication
does not necessarily reflect the views or policies of the DHHS, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government. Partial support for the lipidomic
analysis was provided by an award from the NIGMS (U54 GM069338 to
H.A.B.).
NR 21
TC 17
Z9 18
U1 1
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAY
PY 2013
VL 3
IS 5
BP 1457
EP 1464
DI 10.1016/j.celrep.2013.04.019
PG 8
WC Cell Biology
SC Cell Biology
GA 184NY
UT WOS:000321899300017
PM 23684610
ER
PT J
AU Klemm, RW
Norton, JP
Cole, RA
Li, CS
Park, SH
Crane, MM
Li, LY
Jin, D
Boye-Doe, A
Liu, TY
Shibata, Y
Lu, H
Rapoport, TA
Farese, RV
Blackstone, C
Guo, Y
Mak, HY
AF Klemm, Robin W.
Norton, Justin P.
Cole, Ronald A.
Li, Chen S.
Park, Seong H.
Crane, Matthew M.
Li, Liying
Jin, Diana
Boye-Doe, Alexandra
Liu, Tina Y.
Shibata, Yoko
Lu, Hang
Rapoport, Tom A.
Farese, Robert V., Jr.
Blackstone, Craig
Guo, Yi
Mak, Ho Yi
TI A Conserved Role for Atlastin GTPases in Regulating Lipid Droplet Size
SO CELL REPORTS
LA English
DT Article
ID HEREDITARY SPASTIC PARAPLEGIA; ENDOPLASMIC-RETICULUM; TRIACYLGLYCEROL
SYNTHESIS; CAENORHABDITIS-ELEGANS; HOMOTYPIC FUSION; ER; DROSOPHILA;
MEMBRANES; ENZYMES; ASSOCIATION
AB Lipid droplets (LDs) are the major fat storage organelles in eukaryotic cells, but how their size is regulated is unknown. Using genetic screens in C. elegans for LD morphology defects in intestinal cells, we found that mutations in atlastin, a GTPase required for homotypic fusion of endoplasmic reticulum (ER) membranes, cause not only ER morphology defects, but also a reduction in LD size. Similar results were obtained after depletion of atlastin or expression of a dominant-negative mutant, whereas overexpression of atlastin had the opposite effect. Atlastin depletion in Drosophila fat bodies also reduced LD size and decreased triglycerides in whole animals, sensitizing them to starvation. In mammalian cells, co-overexpression of atlastin-1 and REEP1, a paralog of the ER tubule-shaping protein DP1/REEP5, generates large LDs. The effect of atlastin-1 on LD size correlates with its activity to promote membrane fusion in vitro. Our results indicate that atlastin-mediated fusion of ER membranes is important for LD size regulation.
C1 [Klemm, Robin W.; Boye-Doe, Alexandra; Liu, Tina Y.; Shibata, Yoko; Rapoport, Tom A.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Norton, Justin P.; Cole, Ronald A.; Li, Chen S.; Li, Liying; Mak, Ho Yi] Stowers Inst Med Res, Kansas City, MO 64110 USA.
[Park, Seong H.; Blackstone, Craig] Natl Inst Neurol Disorders & Stroke, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Crane, Matthew M.; Lu, Hang] Georgia Inst Technol, Sch Chem & Biomol Engn, Atlanta, GA 30332 USA.
[Jin, Diana] Univ Minnesota, Dept Biochem, Minneapolis, MN 55455 USA.
[Farese, Robert V., Jr.] Univ Calif San Francisco, Gladstone Inst Cardiovasc Dis, San Francisco, CA 94158 USA.
[Farese, Robert V., Jr.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94158 USA.
[Farese, Robert V., Jr.] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94158 USA.
[Guo, Yi] Mayo Clin, Dept Biochem & Mol Biol, Rochester, MN 55905 USA.
[Guo, Yi] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
[Mak, Ho Yi] Univ Kansas, Med Ctr, Dept Mol & Integrat Physiol, Kansas City, KS 66160 USA.
RP Guo, Y (reprint author), Mayo Clin, Dept Biochem & Mol Biol, Rochester, MN 55905 USA.
EM guo.yi@mayo.edu; hym@stowers.org
RI Klemm, Robin/C-5463-2014;
OI Klemm, Robin/0000-0003-2313-8240; Mak, Ho Yi/0000-0002-1500-5328
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke, NIH; Mayo Clinic New Investigator Startup Fund;
Richard F. Emslander Career Development Award; National Institutes of
Health [R01-GM099844, R01AG035317, R01GM088333]; National Science
Foundation grant [CBET 0954578]; Stowers Institute for Medical Research
FX We thank Sabrina Caldwell for the initial mapping of altn-1 alleles, and
the Stowers Institute Microscopy Center for assistance with imaging. We
thank the Mayo Clinic Microscopy and Cell Analysis Core Facility for
assistance with TEM and CARS applications. We thank the Nikon Imaging
Center at Harvard Medical School for help. This work was supported by
the Intramural Research Program of the National Institute of
Neurological Disorders and Stroke, NIH (C.B.), a Mayo Clinic New
Investigator Startup Fund and Richard F. Emslander Career Development
Award (Y.G.), the National Institutes of Health grants R01-GM099844
(R.V.F.), R01AG035317 (H.L.), R01GM088333 (H.L.), the National Science
Foundation grant CBET 0954578 (H.L.), and the Stowers Institute for
Medical Research (H.Y.M.). T.A.R. is a Howard Hughes Medical Institute
investigator. Author contributions: Mak lab: Figures 1, 2, S1, and S2;
Rapoport lab: Figures 4 (except C), S4; Guo and Farese labs: Figures 3
and S3; Blackstone lab: Figure 4C. Genetic screens were conducted in the
Mak and Lu labs. R.W.K., T.A.R., Y.G., and H.Y.M. wrote the manuscript.
NR 34
TC 29
Z9 31
U1 1
U2 22
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAY
PY 2013
VL 3
IS 5
BP 1465
EP 1475
DI 10.1016/j.celrep.2013.04.015
PG 11
WC Cell Biology
SC Cell Biology
GA 184NY
UT WOS:000321899300018
PM 23684613
ER
PT J
AU Bellodi, C
McMahon, M
Contreras, A
Juliano, D
Kopmar, N
Nakamura, T
Maltby, D
Burlingame, A
Savage, SA
Shimamura, A
Ruggero, D
AF Bellodi, Cristian
McMahon, Mary
Contreras, Adrian
Juliano, Dayle
Kopmar, Noam
Nakamura, Tomoka
Maltby, David
Burlingame, Alma
Savage, Sharon A.
Shimamura, Akiko
Ruggero, Davide
TI H/ACA Small RNA Dysfunctions in Disease Reveal Key Roles for Noncoding
RNA Modifications in Hematopoietic Stem Cell Differentiation
SO CELL REPORTS
LA English
DT Article
ID SMALL NUCLEOLAR RNAS; LINKED DYSKERATOSIS-CONGENITA; RIBOSOMAL-RNA;
MASS-SPECTROMETRY; PSEUDOURIDINE SYNTHASE; SMALL NUCLEAR; MUTATIONS;
CANCER; EXPRESSION; GENE
AB Noncoding RNAs control critical cellular processes, although their contribution to disease remains largely unexplored. Dyskerin associates with hundreds of H/ACA small RNAs to generate a multitude of functionally distinct ribonucleoproteins (RNPs). The DKC1 gene, encoding dyskerin, is mutated in the multisystem disorder X-linked dyskeratosis congenita (X-DC). A central question is whether DKC1 mutations affect the stability of H/ACA RNPs, including those modifying ribosomal RNA (rRNA). We carried out comprehensive profiling of dyskerin-associated H/ACA RNPs, revealing remarkable heterogeneity in the expression and function of subsets of H/ACA small RNAs in X-DC patient cells. Using a mass spectrometry approach, we uncovered single-nucleotide perturbations in dyskerin-guided rRNA modifications, providing functional readouts of small RNA dysfunction in X-DC. In addition, we identified that, strikingly, the catalytic activity of dyskerin is required for accurate hematopoietic stem cell differentiation. Altogether, these findings reveal that small noncoding RNA dysfunctions may contribute to the pleiotropic manifestation of human disease.
C1 [Bellodi, Cristian; McMahon, Mary; Contreras, Adrian; Juliano, Dayle; Kopmar, Noam; Ruggero, Davide] UCSF Helen Diller Comprehens Canc Ctr, Sch Med, San Francisco, CA 94115 USA.
[Bellodi, Cristian; McMahon, Mary; Contreras, Adrian; Juliano, Dayle; Kopmar, Noam; Ruggero, Davide] UCSF Helen Diller Comprehens Canc Ctr, Dept Urol, San Francisco, CA 94115 USA.
[Maltby, David; Burlingame, Alma] Univ Calif San Francisco, Dept Pharmaceut Chem, San Francisco, CA 94143 USA.
[Savage, Sharon A.] NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, Rockville, MD 20892 USA.
[Nakamura, Tomoka; Shimamura, Akiko] Seattle Childrens Hosp, Fred Hutchinson Canc Res Ctr, Seattle, WA 98105 USA.
[Nakamura, Tomoka; Shimamura, Akiko] Univ Washington, Seattle, WA 98105 USA.
RP Ruggero, D (reprint author), UCSF Helen Diller Comprehens Canc Ctr, Sch Med, San Francisco, CA 94115 USA.
EM davide.ruggero@ucsf.edu
RI Savage, Sharon/B-9747-2015
OI 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; NIH
NIGMS [8P41GM103481]; Howard Hughes Medical Institute [NIH R01DK098057,
NIH R01HL085572, NIH 3R01HL085572-05S1]
FX We thank M. Barna for critical discussion and reading of this
manuscript, K. Tong for editing the manuscript, the Fujimori laboratory
for technical support and equipment, J. Johl for technical assistance,
and Lizette Caballero and the UCSF BMT Laboratory for their generous
assistance. We also thank Drs. B.P. Alter and N. Giri at the National
Cancer Institute for clinical characterization of patients and
biospecimen collection. We are grateful to the patients for their
valuable contributions to this study. C.B. is a fellow of the Leukemia &
Lymphoma Society and the Aplastic Anemia & MDS International Foundation.
D.R. is a Leukemia & Lymphoma Society Scholar. This work was supported,
in part, by the intramural research program of the Division of Cancer
Epidemiology and Genetics, National Cancer Institute, National
Institutes of Health (S.S.). This work is supported by NIH NIGMS
8P41GM103481 and Howard Hughes Medical Institute (A.B.), NIH R01DK098057
(D.R.), NIH R01HL085572 (D.R.), and NIH 3R01HL085572-05S1 (D.R.).
NR 48
TC 33
Z9 33
U1 1
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAY
PY 2013
VL 3
IS 5
BP 1493
EP 1502
DI 10.1016/j.celrep.2013.04.030
PG 10
WC Cell Biology
SC Cell Biology
GA 184NY
UT WOS:000321899300021
PM 23707062
ER
PT J
AU Sharma, P
Yamada, S
Lualdi, M
Dasso, M
Kuehn, MR
AF Sharma, Prashant
Yamada, Satoru
Lualdi, Margaret
Dasso, Mary
Kuehn, Michael R.
TI Senp1 Is Essential for Desumoylating Sumo1-Modified Proteins but
Dispensable for Sumo2 and Sumo3 Deconjugation in the Mouse Embryo
SO CELL REPORTS
LA English
DT Article
ID TOPOISOMERASE-II; STRUCTURAL BASIS; NUCLEAR-BODIES; PROTEASE; PATHWAY;
SUMOYLATION; SPECIFICITY; UBIQUITIN; COMPLEX; ENZYMES
AB Posttranslational modification with small ubiquitin-like modifier (Sumo) regulates numerous cellular and developmental processes. Sumoylation is dynamic with deconjugation by Sumo-specific proteases (Senps) regulating steady-state levels. Different Senps are found in distinct subcellular domains, which may limit their deconjugation activity to colocalizing Sumo-modified proteins. In vitro, Senps can discriminate between the different Sumo paralogs: Sumo1 versus the highly related Sumo2 and Sumo3 (Sumo2/3), which can form poly-Sumo chains. However, a full understanding of Senp specificity in vivo is still lacking. Here, using biochemical and genetic approaches, we establish that Senp1 has an essential, nonredundant function to desumoylate Sumo1-modified proteins during mouse embryonic development. Senp1 specificity for Sumo1 conjugates represents an intrinsic function and not simply a product of colocalization. In contrast, Senp1 has only a limited role in Sumo2/3 desumoylation, although it may regulate Sumo1-mediated termination of poly-Sumo2/3 chains.
C1 [Sharma, Prashant; Kuehn, Michael R.] NCI, Lab Prot Dynam & Signaling, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Yamada, Satoru] Osaka Univ, Dept Periodontol, Grad Sch Dent, Suita, Osaka 5650871, Japan.
[Lualdi, Margaret] SAIC Frederick, Lab Anim Sci Program, Frederick, MD 21702 USA.
[Dasso, Mary] NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Kuehn, MR (reprint author), NCI, Lab Prot Dynam & Signaling, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
EM mkuehn@mail.nih.gov
RI Kuehn, Michael/A-4573-2014;
OI Kuehn, Michael/0000-0002-7703-9160; Dasso, Mary/0000-0002-5410-1371
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health
FX We thank Dr. Lionel Feigenbaum and the Transgenic Mouse Model Laboratory
for generation of germline chimeric mice from XG001 ES cells; Dr.
Stephen Goff for HA-Sumo retroviral vectors; Dr. Jadranka Loncarek for
assistance with quantification; and Drs. Ira Daar and Allan Weissman for
comments on the manuscript. This work was supported by the Intramural
Research Program of the National Cancer Institute, National Institutes
of Health. The content of this publication does not necessarily reflect
the views or policies of the Department of Health and Human Services and
nor does mention of trade names, commercial products, or organizations
imply endorsement by the U.S. Government.
NR 42
TC 19
Z9 19
U1 2
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAY
PY 2013
VL 3
IS 5
BP 1640
EP 1650
DI 10.1016/j.celrep.2013.04.016
PG 11
WC Cell Biology
SC Cell Biology
GA 184NY
UT WOS:000321899300033
PM 23684609
ER
PT J
AU Nakahashi, H
Kwon, KRK
Resch, W
Vian, L
Dose, M
Stavreva, D
Hakim, O
Pruett, N
Nelson, S
Yamane, A
Qian, J
Dubois, W
Welsh, S
Phair, RD
Pugh, BF
Lobanenkov, V
Hager, GL
Casellas, R
AF Nakahashi, Hirotaka
Kwon, Kyong-Rim Kieffer
Resch, Wolfgang
Vian, Laura
Dose, Marei
Stavreva, Diana
Hakim, Ofir
Pruett, Nathanael
Nelson, Steevenson
Yamane, Arito
Qian, Jason
Dubois, Wendy
Welsh, Scott
Phair, Robert D.
Pugh, B. Franklin
Lobanenkov, Victor
Hager, Gordon L.
Casellas, Rafael
TI A Genome-wide Map of CTCF Multivalency Redefines the CTCF Code
SO CELL REPORTS
LA English
DT Article
ID PROTEIN-DNA INTERACTIONS; EMBRYONIC STEM-CELLS; REGULATORY ELEMENTS;
BINDING PROTEIN; ZINC FINGERS; GENE; CHROMATIN; TRANSCRIPTION; SITES;
IDENTIFICATION
AB The "CTCF code" hypothesis posits that CTCF pleiotropic functions are driven by recognition of diverse sequences through combinatorial use of its 11 zinc fingers (ZFs). This model, however, is supported by in vitro binding studies of a limited number of sequences. To study CTCF multivalency in vivo, we define ZF binding requirements at similar to 50,000 genomic sites in primary lymphocytes. We find that CTCF reads sequence diversity through ZF clustering. ZFs 4-7 anchor CTCF to similar to 80% of targets containing the core motif. Nonconserved flanking sequences are recognized by ZFs 1-2 and ZFs 8-11 clusters, which also stabilize CTCF broadly. Alternatively, ZFs 9-11 associate with a second phylogenetically conserved upstream motif at similar to 15% of its sites. Individually, ZFs increase overall binding and chromatin residence time. Unexpectedly, we also uncovered a conserved downstream DNA motif that destabilizes CTCF occupancy. Thus, CTCF associates with a wide array of DNA modules via combinatorial clustering of its 11 ZFs.
C1 [Nakahashi, Hirotaka; Kwon, Kyong-Rim Kieffer; Resch, Wolfgang; Vian, Laura; Dose, Marei; Pruett, Nathanael; Nelson, Steevenson; Yamane, Arito; Qian, Jason; Casellas, Rafael] NIAMS, Bethesda, MD 20892 USA.
[Dubois, Wendy; Casellas, Rafael] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Stavreva, Diana; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
[Hakim, Ofir] Bar Ilan Univ, Mina & Everard Goodman Fac Life Sci, IL-5290002 Ramat Gan, Israel.
[Welsh, Scott] Peconic LLC, State Coll, PA 16803 USA.
[Phair, Robert D.] Integrat Bioinformat Inc, Mountain View, CA 94024 USA.
[Pugh, B. Franklin] Penn State Univ, Dept Biochem & Mol Biol, Ctr Eukaryot Gene Regulat, University Pk, PA 16802 USA.
[Lobanenkov, Victor] NIAID, Immunopathol Lab, NIH, Rockville, MD 20852 USA.
RP Resch, W (reprint author), NIAMS, Bethesda, MD 20892 USA.
EM wresch@mail.nih.gov; casellar@mail.nih.gov
OI Dose, Marei/0000-0001-5394-9779; Lobanenkov, Victor/0000-0001-6665-3635
FU Intramural Research Program of NIAMS, NIH; NCI, NIH; American-Italian
Cancer Foundation postdoctoral research fellowship
FX We thank G. Gutierrez from the NIAMS genomics facility for technical
assistance and Ethan Tyler for designing Figure 7C. This work was
supported in part by the Intramural Research Program of NIAMS and NCI,
NIH. The study made use of the high-performance computational
capabilities of the Biowulf Linux cluster at the NIH
(http://biowulf.nih.gov) and the resources of NCI's High-Throughput
Imaging Facility. L.V. was supported in part by an American-Italian
Cancer Foundation postdoctoral research fellowship.
NR 56
TC 76
Z9 77
U1 2
U2 19
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD MAY
PY 2013
VL 3
IS 5
BP 1678
EP 1689
DI 10.1016/j.celrep.2013.04.024
PG 12
WC Cell Biology
SC Cell Biology
GA 184NY
UT WOS:000321899300036
PM 23707059
ER
PT J
AU Wang, XY
Yu, H
Linnoila, RI
Li, L
Li, D
Mo, B
Okano, H
Penalva, LOF
Glazer, RI
AF Wang, Xiao-Yang
Yu, Huina
Linnoila, R. Ilona
Li, Laodong
Li, Dangyu
Mo, Biwen
Okano, Hideyuki
Penalva, Luiz O. F.
Glazer, Robert I.
TI Musashi1 as a potential therapeutic target and diagnostic marker for
lung cancer
SO ONCOTARGET
LA English
DT Article
DE Musashi1; lung cancer; shRNA; beta-catenin; notch; numb
ID RNA-BINDING PROTEIN; STEM-CELLS; MESSENGER-RNA; POOR-PROGNOSIS;
EXPRESSION; WNT; IDENTIFICATION; CARCINOGENESIS; PROLIFERATION;
TRANSLATION
AB Lung cancer remains one of the leading causes of cancer-related deaths worldwide with a 5-year survival rate of less than 20%. One approach to improving survival is the identification of biomarkers to detect early stage disease. In this study, we investigated the potential of the stem cell and progenitor cell marker, Musashi1 (Msi1), as a diagnostic marker and potential therapeutic target for lung cancer. Functional studies in A549 bronchioalveolar carcinoma and NCI-H520 squamous cell carcinoma cells revealed that Msi1 was enriched in spheroid cultures of tumor cells and in the CD133+ cell population. Downregulation of Msi1 by lentivirus-mediated expression of an Msi1 shRNA reduced spheroid colony proliferation. Growth inhibition was associated with reduced nuclear localization of beta-catenin and inhibition of the processing of intracellular Notch. In primary lung cancer, Msi1 protein expression was elevated in 86% of 202 tissue microarray specimens, and Msi1 mRNA was increased in 80% of 118 bronchoscopic biopsies, including metastatic disease, but was rarely detected in adjacent normal lung tissue and in non-malignant diseased tissue. Msi1 was expressed in a diffuse pattern in most tumor subtypes, except in squamous cell carcinomas, where it appeared in a focal pattern in 50% of specimens. Thus, Msi1 is a sensitive and specific diagnostic marker for all lung cancer subtypes.
C1 [Wang, Xiao-Yang; Linnoila, R. Ilona] NCI, Cell & Canc Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Yu, Huina; Li, Laodong; Mo, Biwen] Guilin Med Univ Hosp, Div Resp Dis, Guilin, Guangxi, Peoples R China.
[Li, Dangyu] Guilin Med Univ Hosp, Nan Xi Shan Hosp, Div Resp Dis, Guilin, Guangxi, Peoples R China.
[Okano, Hideyuki] Keio Univ, Dept Physiol, Tokyo, Japan.
[Penalva, Luiz O. F.] Univ Texas Hlth Sci Ctr San Antonio, Dept Cell & Struct Biol, Childrens Canc Res Inst, San Antonio, TX 78229 USA.
[Glazer, Robert I.] Georgetown Univ, Dept Oncol, Washington, DC 20007 USA.
[Glazer, Robert I.] Lombardi Comprehens Canc Ctr, Washington, DC USA.
RP Glazer, RI (reprint author), Georgetown Univ, Dept Oncol, Washington, DC 20007 USA.
EM glazerr@georgetown.edu
RI Hidokano, Hideyuki/J-5973-2013
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute [2012003]; Guangxi Health Department; Uniting
Against Lung Cancer, New York, NY
FX This work was supported by Intramural Research Program of the National
Institutes of Health, National Cancer Institute, Key Research Project
Grant 2012003, Guangxi Health Department, and a grant from Uniting
Against Lung Cancer, New York, NY.
NR 43
TC 12
Z9 13
U1 0
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 MAY
PY 2013
VL 4
IS 5
BP 739
EP 750
PG 12
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 193RU
UT WOS:000322580000010
PM 23715514
ER
PT J
AU Klorin, G
Rozenblum, E
Glebov, O
Walker, RL
Park, Y
Meltzer, PS
Kirsch, IR
Kaye, FJ
Roschke, AV
AF Klorin, Geula
Rozenblum, Ester
Glebov, Oleg
Walker, Robert L.
Park, Yoonsoo
Meltzer, Paul S.
Kirsch, Ilan R.
Kaye, Frederic J.
Roschke, Anna V.
TI Integrated high-resolution array CGH and SKY analysis of homozygous
deletions and other genomic alterations present in malignant
mesothelioma cell lines
SO CANCER GENETICS
LA English
DT Article
DE Malignant mesothelioma; oligonucleotide array CGH; spectral karyotyping;
homozygous deletions; tumor suppressors
ID CIRCULAR BINARY SEGMENTATION; COPY-NUMBER CHANGES; PLEURAL MESOTHELIOMA;
TUMOR-SUPPRESSOR; KARYOTYPIC COMPLEXITY; EPITHELIOID-TYPE; GENE; CANCER;
HYBRIDIZATION; MUTATIONS
AB High-resolution oligonucleotide array comparative genomic hybridization (aCGH) and spectral karyotyping (SKY) were applied to a panel of malignant mesothelioma (MMt) cell lines. SKY has not been applied to MMt before, and complete karyotypes are reported based on the integration of SKY and aCGH results. A whole genome search for homozygous deletions (HDs) produced the largest set of recurrent and non-recurrent HDs for MMt (52 recurrent HDs in 10 genomic regions; 36 non-recurrent HDs). For the first time, LINGO2, RBFOX1/A2BP1, RPL29, DUSP7, and CCSER1/FAM190A were found to be homozygously deleted in MMt, and some of these genes could be new tumor suppressor genes for MMt. Integration of SKY and aCGH data allowed reconstruction of chromosomal rearrangements that led to the formation of HDs. Our data imply that only with acquisition of structural and/or numerical karyotypic instability can MMt cells attain a complete loss of tumor suppressor genes located in 9p21.3, which is the most frequently homozygously deleted region. Tetraploidization is a late event in the karyotypic progression of MMt cells, after HDs in the 9p21.3 region have already been acquired.
C1 [Klorin, Geula; Rozenblum, Ester; Glebov, Oleg; Walker, Robert L.; Park, Yoonsoo; Meltzer, Paul S.; Kirsch, Ilan R.; Kaye, Frederic J.; Roschke, Anna V.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Klorin, Geula] Rambam Hlth Care Campus, Haifa, Israel.
[Kaye, Frederic J.] Univ Florida, Dept Med, Gainesville, FL USA.
RP Roschke, AV (reprint author), NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM roschkea@mail.nih.gov
FU Intramural NIH HHS [Z01 BC010930-01, Z99 CA999999, ZIC BC010930-05]
NR 59
TC 8
Z9 9
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2210-7762
EI 2210-7770
J9 CANCER GENET-NY
JI Cancer Genet.
PD MAY
PY 2013
VL 206
IS 5
BP 191
EP 205
DI 10.1016/j.cancergen.2013.04.006
PG 15
WC Oncology; Genetics & Heredity
SC Oncology; Genetics & Heredity
GA 190NS
UT WOS:000322348100006
PM 23830731
ER
PT J
AU Shiozaki, AA
Senra, T
Arteaga, E
Martinelli, M
Pita, CG
Avila, LFR
Parga, JR
Mady, C
Kalil, R
Bluemke, DA
Rochitte, CE
AF Shiozaki, Afonso Akio
Senra, Tiago
Arteaga, Edmund
Martinelli Filho, Martino
Pita, Cristiane Guedes
Avila, Luis Francisco R.
Parga Filho, Jose Rodrigues
Mady, Charles
Kalil-Filho, Roberto
Bluemke, David A.
Rochitte, Carlos Eduardo
TI Myocardial fibrosis detected by cardiac CT predicts ventricular
fibrillation/ventricular tachycardia events in patients with
hypertrophic cardiomyopathy
SO JOURNAL OF CARDIOVASCULAR COMPUTED TOMOGRAPHY
LA English
DT Article
DE Hypertrophic cardiomyopathy; Myocardial fibrosis; Ventricular
arrhythmias; Delayed enhancement cardiac computed tomography;
Implantable cardiac defibrillator
ID CARDIOVASCULAR MAGNETIC-RESONANCE; LATE GADOLINIUM ENHANCEMENT; BINDING
PROTEIN-C; IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS; MULTIDETECTOR
COMPUTED-TOMOGRAPHY; CORONARY-ARTERY-DISEASE; SUDDEN-DEATH; DELAYED
ENHANCEMENT; PROGNOSTIC-SIGNIFICANCE; ALPHA-TROPOMYOSIN
AB Background: Myocardial fibrosis (MF) occurs in up to 80% of subjects with asymptomatic or mildly symptomatic hypertrophic cardiomyopathy (HCM) and can constitute an arrhythmogenic substrate for re-entrant, life-threatening ventricular arrhythmias in predisposed persons.
Objective: The aim was to investigate whether MF detected by delayed enhancement cardiac CT is predictive of ventricular tachycardia (VT) and fibrillation (VF) that require appropriate therapy by an implantable cardioverter defibrillator (ICD) in patients with HCM.
Methods: Twenty-six patients with HCM with previously (for at least 1 year) implanted ICD underwent MF evaluation by cardiac CT. MF was quantified by myocardial delayed enhanced cardiac CT. Data on ICD firing were recorded every 3 months after ICD implantation. Risk factors for sudden cardiac death in patients with HCM were evaluated in all patients.
Results: MF was present in 25 of 26 patients (96%) with mean fibrosis mass of 20.5 +/- 15.8 g. Patients with appropriate ICD shocks for VF/VT had significantly greater MF mass than patients without (29.10 +/- 19.13 g vs 13.57 +/- 8.31 g; P = .01). For a MF mass of at least 18 g, sensitivity and specificity for appropriate ICD firing were 73% (95% CI, 49%-88%) and 71% (95% CI, 56%-81%), respectively. Kaplan-Meier curves indicated a significantly greater VF/VT event rate in patients with MF mass >= 18 g than in patients with MF <18 g (P = .02). In the Cox regression analysis, the amount of MF was independently associated with VF/VT in ICD-stored electrograms.
Conclusion: The mass of MF detected by cardiac CT in patients with HCM at high risk of sudden death was associated with appropriate ICD firings. (C) 2013 Society of Cardiovascular Computed Tomography. All rights reserved.
C1 [Shiozaki, Afonso Akio; Senra, Tiago; Avila, Luis Francisco R.; Parga Filho, Jose Rodrigues; Kalil-Filho, Roberto; Rochitte, Carlos Eduardo] Univ Sao Paulo, Sch Med, Heart Inst InCor, Cardiovasc Magnet Resonance & Computed Tomog Sect, Sao Paulo, Brazil.
[Arteaga, Edmund; Mady, Charles] Univ Sao Paulo, Sch Med, Heart Inst InCor, Cardiomyopathy Unit, Sao Paulo, Brazil.
[Martinelli Filho, Martino; Pita, Cristiane Guedes] Univ Sao Paulo, Sch Med, Heart Inst InCor, Pacemaker Clin, Sao Paulo, Brazil.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Rochitte, CE (reprint author), Univ Sao Paulo, Sch Med, Heart Inst InCor, Cardiovasc Magnet Resonance & Computed Tomog Sect, Sao Paulo, Brazil.
EM rochitte@incor.usp.br
RI Arteaga-Fernandez, Edmundo/D-3276-2012; Mady, Charles/C-8870-2012;
Martinelli, Martino/D-9785-2012; Kalil Filho, Roberto/D-4994-2014;
OI Arteaga-Fernandez, Edmundo/0000-0002-1588-5492; Mady,
Charles/0000-0002-8838-199X; Martinelli, Martino/0000-0003-4440-8078;
Bluemke, David/0000-0002-8323-8086
FU FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo)
[07/58876-8]; Zerbini Foundation; Brazilian Society of Cardiology
(Sociedade Brasileira de Cardiologia)
FX This work was supported by FAPESP (Fundacao de Amparo a Pesquisa do
Estado de Sao Paulo) Grant-in-aid no. 07/58876-8, Zerbini Foundation,
and Brazilian Society of Cardiology (Sociedade Brasileira de
Cardiologia) partially supported Dr Shiozaki.
NR 57
TC 14
Z9 16
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1934-5925
J9 J CARDIOVASC COMPUT
JI J. Cardiovasc. Comput. Tomogr.
PD MAY-JUN
PY 2013
VL 7
IS 3
BP 173
EP 181
DI 10.1016/j.jcct.2013.04.002
PG 9
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 187DU
UT WOS:000322097900005
PM 23849490
ER
PT J
AU Hall, KD
AF Hall, Kevin D.
TI Diet Versus Exercise in "The Biggest Loser" Weight Loss Competition
SO OBESITY
LA English
DT Article
ID RESTING METABOLIC-RATE; FAT-FREE MASS; BODY-COMPOSITION
AB Background: Obesity experts have criticized The Biggest Loser television show for its portrayal of an unrealistic intervention that raises false expectations for weight loss. However, the magnitude of the diet and exercise intervention has not been previously quantified.
Design and Methods: Using a validated computational model of metabolism, I quantified the diet and exercise intervention by integrating data on energy expenditure, body weight and fat mass collected during The Biggest Loser competition.
Results: Participant body mass index, weight, and percent body fat at baseline were 48.7 +/- 10.1 kg/m(2), 144.9 +/- 39.4 kg, and 49 +/- 6% (mean +/- SD), respectively. During the first phase of the competition when the contestants were isolated in a boot camp environment, the average rate of weight loss was 0.4 +/- 0.1 kg/d and decreased to 0.19 +/- 0.1 kg/d after returning home. Total weight loss was 58.2 +/- 26 kg with 81.6 +/- 8.4% coming from body fat. The computer simulations closely matched these data and calculated that average energy intake decreased by 65% during the first phase to 1300 kcal/d while participating in 3.1 h/d of vigorous exercise. After returning home, energy intake increased to 1900 kcal/d and vigorous exercise decreased to 1.1 h/d. Simulation of diet alone resulted in 34 kg of weight loss with 65% coming from body fat, whereas exercise alone resulted in a loss of 27 kg with 102% from fat.
Conclusion: The intense diet and exercise intervention during The Biggest Loser competition were not sustainable. However, a relatively modest permanent lifestyle intervention of 20% caloric restriction and 20 min/d of vigorous exercise could maintain the massive weight loss.
C1 NIDDK, NIH, Bethesda, MD 20892 USA.
RP Hall, KD (reprint author), NIDDK, NIH, Bethesda, MD 20892 USA.
EM kevinh@niddk.nih.gov
RI Biguzzi, Felipe/E-4724-2015
FU NIH, National Institute of Diabetes & Digestive & Kidney Diseases
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Diabetes & Digestive & Kidney Diseases.
NR 13
TC 13
Z9 15
U1 0
U2 22
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD MAY
PY 2013
VL 21
IS 5
BP 957
EP 959
DI 10.1002/oby.20065
PG 3
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 187AR
UT WOS:000322088300014
PM 23404767
ER
PT J
AU Pavlatou, MG
Vickers, KC
Varma, S
Malek, R
Sampson, M
Remaley, AT
Gold, PW
Skarulis, MC
Kino, T
AF Pavlatou, Maria G.
Vickers, Kasey C.
Varma, Sudhir
Malek, Rana
Sampson, Maureen
Remaley, Alan T.
Gold, Philip W.
Skarulis, Monica C.
Kino, Tomoshige
TI Circulating Cortisol-Associated Signature of Glucocorticoid-related Gene
Expression in Subcutaneous Fat of Obese Subjects
SO OBESITY
LA English
DT Article
ID STRESS SYSTEM; TRANSCRIPTIONAL ACTIVITY; INSULIN-RESISTANCE; METABOLIC
SYNDROME; RECEPTOR; INFLAMMATION; MODEL; DEPRESSION; REGULATOR;
INTERACTS
AB Objective: Serum cortisol concentrations fluctuate in a circadian fashion, and glucocorticoids exert strong effects on adipose tissue and induce obesity through the glucocorticoid receptor.
Design and Methods: To examine the impact of physiologic levels of circulating cortisol on subcutaneous adipose tissue, 25 overweight and obese subjects were employed, and their serum levels of morning (AM) and evening (PM) cortisol, AM/PM cortisol ratios, and 24-h urinary-free cortisol (UFC) were compared with their clinical parameters, serum cytokine levels, and mRNA expression of 93 receptor action-regulating and 93 glucocorticoid-responsive genes in abdominal subcutaneous fat.
Results and Conclusions: AM cortisol levels did not correlate with mRNA expression of the all genes examined, whereas PM cortisol levels, AM/PM cortisol ratios, and 24-h UFC were associated with distinct sets of these genes. Body mass index did not significantly correlate with the four cortisol parameters employed. These results suggest that physiologic levels of AM serum cortisol do not solely represent biological effects of circulating cortisol on the expression of glucocorticoid-related genes in subcutaneous adipose tissue, whereas PM levels, amplitude, and net amounts of the diurnally fluctuating serum cortisol have distinct effects. Through the genes identified in this study, glucocorticoids appear to influence intermediary metabolism, energy balance, inflammation, and local circadian rythmicity in subcutaneous fat. Our results may also explain in part the development of metabolic abnormality and obesity in subjects under stress or patients with melancholic/atypical depression who demonstrate elevated levels of PM serum cortisol.
C1 [Pavlatou, Maria G.; Kino, Tomoshige] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Mol Hormone Act, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
[Pavlatou, Maria G.; Gold, Philip W.] NIMH, Clin Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA.
[Vickers, Kasey C.; Sampson, Maureen; Remaley, Alan T.] Natl Inst Heart Lung & Blood Inst, Lipoprot Metab Sect, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Varma, Sudhir] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
[Malek, Rana; Skarulis, Monica C.] NIDDK, Clin Endocrine Sect, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
RP Kino, T (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Mol Hormone Act, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
EM kinot@mail.nih.gov
RI Varma, Sudhir/N-8763-2014
OI Varma, Sudhir/0000-0002-4096-4782
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Heart, Lung and Blood Institute; National
Institute of Allergy and Inflammatory Diseases; National Institute of
Diabetes and Digestive and Kidney Diseases; National Institute of Mental
Health, National Institutes of Health; NIH NHLBI Intramural Research
Program; NIH [KHL113039A]
FX This study was funded by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Heart, Lung and Blood Institute, National
Institute of Allergy and Inflammatory Diseases, National Institute of
Diabetes and Digestive and Kidney Diseases and the National Institute of
Mental Health, National Institutes of Health. We thank Drs. A.H.
DeCherney, Program in Reproductive and Adult Endocrinology, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, and G.P. Chrousos, 1st Department of Pediatrics, Athens
University Medical School, for valuable discussion at the time of
starting this study and for editing the manuscript, respectively. K.C.V.
is supported by NIH NHLBI Intramural Research Program and NIH
KHL113039A.
NR 40
TC 4
Z9 4
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD MAY
PY 2013
VL 21
IS 5
BP 960
EP 967
DI 10.1002/oby.20073
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 187AR
UT WOS:000322088300015
PM 23784897
ER
PT J
AU McClain, J
Hsu, F
Brown, E
Burke, G
Carr, J
Harris, T
Kritchevsky, S
Szklo, M
Tracy, R
Ding, J
AF McClain, Jill
Hsu, Fang
Brown, Elizabeth
Burke, Gregory
Carr, John
Harris, Tamara
Kritchevsky, Stephen
Szklo, Moyses
Tracy, Russell
Ding, Jingzhong
TI Pericardial Adipose Tissue and Coronary Artery Calcification in the
Multi-Ethnic Study of Atherosclerosis (MESA)
SO OBESITY
LA English
DT Article
ID EPICARDIAL FAT THICKNESS; DISEASE RISK-FACTORS; COMPUTED-TOMOGRAPHY;
ETHNIC-DIFFERENCES; METABOLIC SYNDROME; AFRICAN-AMERICAN; YOUNG-ADULTS;
BODY-MASS; CALCIUM; HEART
AB Objective: To examine the relationship of pericardial adipose tissue (PAT) with coronary artery calcification in the Multi-Ethnic Study of Atherosclerosis.
Design and Methods: The baseline cohort comprised 6,814 Caucasian (38%), African-American (28%), Chinese American (12%), and Hispanic (22%) adults aged 45-84, without known clinical cardiovascular disease. Cardiac CT was used to measure PAT (cm(3)) and calcification (Agatston score). We examined cross-sectional associations of PAT with the presence (score > 0) and severity (continuous score if > 0) of calcification using prevalence ratio (PR) (n = 6,672) and linear regression (n = 3,362), respectively. Main models were adjusted for age, age(2), gender, race/ethnicity, field site, smoking, physical activity, alcohol, and education.
Results: PAT volume (adjusted for age, height, weight, and site) was greatest in Chinese males, whereas Black males had less PAT than all but Black females. PAT was associated with presence [PR per standard deviation (SD): 1.06 (95% CI: 1.04, 1.08)] and severity [difference in log Agatston score per SD: 0.15 (0.09, 0.21)] of calcification, but neither association varied by race/ethnicity. Adjustment for generalized adiposity attenuated but did not eliminate the associations. With further adjustment for traditional risk factors and inflammatory markers, only the association with severity remained statistically significant [PR: 1.02 (1.00, 1.04); difference: 0.10 (0.03, 0.17)]. Heterogeneity by sex was observed for the presence of calcification (PR in men: 1.04; in women: 1.08; P for interaction < 0.0001).
Conclusion: PAT was associated with the presence and severity of coronary artery calcification in this cohort, but neither association varied by race/ethnicity.
C1 [McClain, Jill; Kritchevsky, Stephen; Ding, Jingzhong] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Hsu, Fang] Wake Forest Sch Med, Dept Biostatist Sci, Winston Salem, NC USA.
[Brown, Elizabeth] Univ Washington, Dept Biostatist, Seattle, WA 98195 USA.
[Burke, Gregory] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
[Carr, John] Wake Forest Sch Med, Dept Radiol, Winston Salem, NC USA.
[Harris, Tamara] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Szklo, Moyses] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Szklo, Moyses] Johns Hopkins Univ, Dept Med Cardiol, Baltimore, MD USA.
[Tracy, Russell] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA.
[Tracy, Russell] Univ Vermont, Coll Med, Dept Biochem, Burlington, VT 05405 USA.
RP McClain, J (reprint author), Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
EM jillmccl@wakehealth.edu
RI Carr, John/A-1938-2012;
OI Carr, John/0000-0002-4398-8237; Kritchevsky, Stephen/0000-0003-3336-6781
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95160,
N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165,
N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, R01-HL-085323]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95169 and by grant R01-HL-085323 from the National Heart, Lung,
and Blood Institute.
NR 41
TC 7
Z9 7
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD MAY
PY 2013
VL 21
IS 5
BP 1056
EP 1063
DI 10.1002/oby.20090
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 187AR
UT WOS:000322088300029
PM 23784910
ER
PT J
AU Weber, M
Killgore, WDS
Rosso, IM
Britton, JC
Schwab, ZJ
Weiner, MR
Simon, NM
Pollack, MH
Rauch, SL
AF Weber, Mareen
Killgore, William D. S.
Rosso, Isabelle M.
Britton, Jennifer C.
Schwab, Zachary J.
Weiner, Melissa R.
Simon, Naomi M.
Pollack, Mark H.
Rauch, Scott L.
TI Voxel-based morphometric gray matter correlates of posttraumatic stress
disorder
SO JOURNAL OF ANXIETY DISORDERS
LA English
DT Article
DE Magnetic resonance imaging; Chronic post-traumatic stress disorder;
Prefrontal cortex; Hippocampus; Amygdala
ID SMALLER HIPPOCAMPAL VOLUME; STRUCTURAL BRAIN ABNORMALITIES; MEDIAL
PREFRONTAL CORTEX; ADMINISTERED PTSD SCALE; ANTERIOR CINGULATE;
BASOLATERAL AMYGDALA; ANXIETY DISORDER; HUMAN EMOTION; CHILD-ABUSE;
GREY-MATTER
AB Posttraumatic stress disorder (PTSD) is associated with functional abnormalities within a neurocircuitry that includes the hippocampus, amygdala, and medial prefrontal cortex. Evidence of structural abnormalities within these regions, and their association with PTSD severity and symptom burden is, however, sparse. The present study evaluated the relation between indices of gray matter volume and PTSD symptom severity using voxel-based morphometry. Fifteen individuals meeting DSM-IV criteria for PTSD completed the Clinician Administered PTSD Scale and underwent structural magnetic resonance imaging. Greater PTSD severity and avoidance/numbing were correlated with increased gray matter volume of the right amygdala-hippocampal complex. Greater hyper-arousal was associated with reduced gray matter volume in the left superior medial frontal gyrus. Findings are consistent with current neurocircuitry models of PTSD, which posit that the disorder is associated with structural and functional variance within this distributed network. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Weber, Mareen; Killgore, William D. S.; Rosso, Isabelle M.; Schwab, Zachary J.; Rauch, Scott L.] Harvard Univ, McLean Hosp, Sch Med, Belmont, MA 02478 USA.
[Britton, Jennifer C.] NIMH, Bethesda, MD 20892 USA.
[Weiner, Melissa R.] Yale Univ, New Haven, CT USA.
[Simon, Naomi M.; Pollack, Mark H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Killgore, WDS (reprint author), Harvard Univ, Social Cognit & Affect Neurosci Lab, McLean Hosp, Sch Med, 115 Mill St, Belmont, MA 02478 USA.
EM mweber@mclean.harvard.edu; killgore@mclean.harvard.edu
RI Britton, Jennifer/J-4501-2013;
OI Killgore, William/0000-0002-5328-0208
FU NIMH NIH HHS [R01 MH70730-01A2, R01 MH070730]
NR 65
TC 14
Z9 16
U1 3
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0887-6185
J9 J ANXIETY DISORD
JI J. Anxiety Disord.
PD MAY
PY 2013
VL 27
IS 4
BP 413
EP 419
DI 10.1016/j.janxdis.2013.04.004
PG 7
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 184IJ
UT WOS:000321883000007
PM 23746489
ER
PT J
AU Cole, TG
Contois, JH
Csako, G
McConnell, JP
Remaley, AT
Devaraj, S
Hoefner, DM
Mallory, T
Sethi, AA
Warnick, GR
AF Cole, Thomas G.
Contois, John H.
Csako, Gyorgy
McConnell, Joseph P.
Remaley, Alan T.
Devaraj, Sridevi
Hoefner, Daniel M.
Mallory, Tonya
Sethi, Amar A.
Warnick, G. Russell
TI Association of Apolipoprotein B and Nuclear Magnetic Resonance
Spectroscopy-Derived LDL Particle Number with Outcomes in 25 Clinical
Studies: Assessment by the AACC Lipoprotein and Vascular Diseases
Division Working Group on Best Practices
SO CLINICAL CHEMISTRY
LA English
DT Article
ID LOW-DENSITY-LIPOPROTEIN; CHEMISTRY STANDARDIZATION PROJECT; ION MOBILITY
ANALYSIS; NON-HDL CHOLESTEROL; CARDIOVASCULAR-DISEASE; METABOLIC
SYNDROME; INTERNATIONAL FEDERATION; DCCT/EDIC COHORT; DOUBLE-BLIND;
RISK-FACTORS
AB BACKGROUND: The number of circulating LDL particles is a strong indicator of future cardiovascular disease (CVD) events, even superior to the concentration of LDL cholesterol. Atherogenic (primarily LDL) particle number is typically determined either directly by the serum concentration of apolipoprotein B (apo B) or indirectly by nuclear magnetic resonance (NMR) spectroscopy of serum to obtain NMR-derived LDL particle number (LDL-P).
CONTENT: To assess the comparability of apo B and LDL-P, we reviewed 25 clinical studies containing 85 outcomes for which both biomarkers were determined. In 21 of 25 (84.0%) studies, both apo B and LDL-P were significant for at least 1 outcome. Neither was significant for any outcome in only 1 study (4.0%). In 50 of 85 comparisons (58.8%), both apo B and LDL-P had statistically significant associations with the clinical outcome, whereas in 17 comparisons (20.0%) neither was significantly associated with the outcome. In 18 comparisons (21.1%) there was discordance between apo B and LDL-P.
CONCLUSIONS: In most studies, both apo B and LDL-P were comparable in association with clinical outcomes. The biomarkers were nearly equivalent in their ability to assess risk for CVD and both have consistently been shown to be stronger risk factors than LDL-C. We support the adoption of apo B and/or LDL-P as indicators of atherogenic particle numbers into CVD risk screening and treatment guidelines. Currently, in the opinion of this Working Group on Best Practices, apo B appears to be the preferable biomarker for guideline adoption because of its availability, scalability, standardization, and relatively low cost. (C) 2013 American Association for Clinical Chemistry
C1 [Cole, Thomas G.] Thom Cole Consulting LLC, St Louis, MO 63122 USA.
[Contois, John H.] Sun Diagnost LLC, New Gloucester, ME USA.
[Csako, Gyorgy; Remaley, Alan T.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
[McConnell, Joseph P.; Hoefner, Daniel M.; Mallory, Tonya; Warnick, G. Russell] Hlth Diagnost Lab Inc, Richmond, VA USA.
[Devaraj, Sridevi] Texas Childrens Hosp, Dept Clin Chem, Houston, TX 77030 USA.
[Sethi, Amar A.] Pacific Biomarkers Inc, Seattle, WA USA.
RP Cole, TG (reprint author), Thom Cole Consulting LLC, 594 Gederson Lane, St Louis, MO 63122 USA.
EM tgchol@aol.com
NR 56
TC 43
Z9 43
U1 0
U2 6
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD MAY
PY 2013
VL 59
IS 5
BP 752
EP 770
DI 10.1373/clinchem.2012.196733
PG 19
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 179UU
UT WOS:000321547700011
ER
PT J
AU Sacks, DB
AF Sacks, David B.
TI 2011 Consensus Meeting on the Worldwide Standardization of Hemoglobin
A(1c) Measurement
SO CLINICAL CHEMISTRY
LA English
DT News Item
C1 [Sacks, David B.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
RP Sacks, DB (reprint author), Dept Lab Med, Bldg 10,Rm 2C306,10 Ctr Dr, Bethesda, MD 20892 USA.
EM sacksdb@mail.nih.gov
OI Sacks, David/0000-0003-3100-0735
FU Intramural NIH HHS
NR 1
TC 1
Z9 1
U1 0
U2 1
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD MAY
PY 2013
VL 59
IS 5
BP 857
EP 858
DI 10.1373/clinchem.2013.204800
PG 3
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 179UU
UT WOS:000321547700025
PM 23757768
ER
PT J
AU Bachran, C
Morley, T
Abdelazim, S
Fattah, RJ
Liu, SH
Leppla, SH
AF Bachran, Christopher
Morley, Thomas
Abdelazim, Suzanne
Fattah, Rasem J.
Liu, Shihui
Leppla, Stephen H.
TI Anthrax Toxin-Mediated Delivery of the Pseudomonas Exotoxin A Enzymatic
Domain to the Cytosol of Tumor Cells via Cleavable Ubiquitin Fusions
SO MBIO
LA English
DT Article
ID END RULE PATHWAY; LETHAL FACTOR; DIPHTHERIA-TOXIN; RECOMBINANT
IMMUNOTOXINS; SELECTIVE CYTOTOXICITY; PROTECTIVE ANTIGEN;
MAMMALIAN-CELLS; PROTEIN; INHIBITION; TRANSLOCATION
AB Anthrax toxin proteins from Bacillus anthracis constitute a highly efficient system for delivering cytotoxic enzymes to the cytosol of tumor cells. However, exogenous proteins delivered to the cytosol of cells are subject to ubiquitination on lysines and proteasomal degradation, which limit their potency. We created fusion proteins containing modified ubiquitins with their C-terminal regions fused to the Pseudomonas exotoxin A catalytic domain (PEIII) in order to achieve delivery and release of PEIII to the cytosol. Fusion proteins in which all seven lysines of wild-type ubiquitin were retained while the site cleaved by cytosolic deubiquitinating enzymes (DUBs) was removed were nontoxic, apparently due to rapid ubiquitination and proteasomal degradation. Fusion proteins in which all lysines of wild-type ubiquitin were substituted by arginine had high potency, exceeding that of a simple fusion lacking ubiquitin. This variant was less toxic to nontumor tissues in mice than the fusion protein lacking ubiquitin and was very efficient for tumor treatment in mice. The potency of these proteins was highly dependent on the number of lysines retained in the ubiquitin domain and on retention of the C-terminal ubiquitin sequence cleaved by DUBs. It appears that rapid cytosolic release of a cytotoxic enzyme (e.g., PEIII) that is itself resistant to ubiquitination is an effective strategy for enhancing the potency of tumor-targeting toxins.
IMPORTANCE Bacterial toxins typically have highly efficient mechanisms for cellular delivery of their enzymatic components. Cytosolic delivery of therapeutic enzymes and drugs is an important topic in molecular medicine. We describe anthrax toxin fusion proteins containing ubiquitin as a cytosolic cleavable linker that improves the delivery of an enzyme to mammalian cells. The ubiquitin linker allowed modulation of potency in cells and in mice. This effective strategy for enhancing the intracellular potency of an enzyme may be useful for the cytosolic delivery and release of internalized drugs.
C1 [Bachran, Christopher; Morley, Thomas; Abdelazim, Suzanne; Fattah, Rasem J.; Liu, Shihui; Leppla, Stephen H.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Leppla, SH (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM sleppla@niaid.nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases (NIAID), Bethesda, MD
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases (NIAID), Bethesda,
MD.
NR 44
TC 8
Z9 8
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 2150-7511
J9 MBIO
JI mBio
PD MAY-JUN
PY 2013
VL 4
IS 3
AR e00201-13
DI 10.1128/mBio.00201-13
PG 9
WC Microbiology
SC Microbiology
GA 174WK
UT WOS:000321187400013
PM 23631917
ER
PT J
AU Singh, A
Panting, RJ
Varma, A
Saijo, T
Waldron, KJ
Jong, A
Ngamskulrungroj, P
Chang, YC
Rutherford, JC
Kwon-Chung, KJ
AF Singh, Arpita
Panting, Robert J.
Varma, Ashok
Saijo, Tomomi
Waldron, Kevin J.
Jong, Ambrose
Ngamskulrungroj, Popchai
Chang, Yun C.
Rutherford, Julian C.
Kwon-Chung, Kyung J.
TI Factors Required for Activation of Urease as a Virulence Determinant in
Cryptococcus neoformans
SO MBIO
LA English
DT Article
ID KLEBSIELLA-AEROGENES UREASE; CENTRAL-NERVOUS-SYSTEM;
SCHIZOSACCHAROMYCES-POMBE; ALCALIGENES-EUTROPHUS; ACCESSORY PROTEINS;
CRYSTAL-STRUCTURE; NICKEL-BINDING; IDENTIFICATION; BRAIN; GENE
AB Urease in Cryptococcus neoformans plays an important role in fungal dissemination to the brain and causing meningoencephalitis. Although urea is not required for synthesis of apourease encoded by URE1, the available nitrogen source affected the expression of URE1 as well as the level of the enzyme activity. Activation of the apoenzyme requires three accessory proteins, Ure4, Ure6, and Ure7, which are homologs of the bacterial urease accessory proteins UreD, UreF, and UreG, respectively. A yeast two-hybrid assay showed positive interaction of Ure1 with the three accessory proteins encoded by URE4, URE6, and URE7. Metalloproteomic analysis of cryptococcal lysates using inductively coupled plasma mass spectrometry (ICP-MS) and a biochemical assay of urease activity showed that, as in many other organisms, urease is a metallocentric enzyme that requires nickel transported by Nic1 for its catalytic activity. The Ure7 accessory protein (bacterial UreG homolog) binds nickel likely via its conserved histidine-rich domain and appears to be responsible for the incorporation of Ni2+ into the apourease. Although the cryptococcal genome lacks the bacterial UreE homolog, Ure7 appears to combine the functions of bacterial UreE and UreG, thus making this pathogen more similar to that seen with the plant system. Brain invasion by the ure1, ure7, and nic1 mutant strains that lack urease activity was significantly less effective in a mouse model. This indicated that an activated urease and not the Ure1 protein was responsible for enhancement of brain invasion and that the factors required for urease activation in C. neoformans resemble those of plants more than those of bacteria.
IMPORTANCE Cryptococcus neoformans is the major fungal agent of meningoencephalitis in humans. Although urease is an important factor for cryptococcal brain invasion, the enzyme activation system has not been studied. We show that urease is a nickel-requiring enzyme whose activity level is influenced by the type of available nitrogen source. C. neoformans contains all the bacterial urease accessory protein homologs and nickel transporters except UreE, a nickel chaperone. Cryptococcal Ure7 (a homolog of UreG) apparently functions as both the bacterial UreG and UreE in activating the Ure1 apoenzyme. The cryptococcal urease accessory proteins Ure4, Ure6, and Ure7 interacted with Ure1 in a yeast two-hybrid assay, and deletion of any one of these not only inactivated the enzyme but also reduced the efficacy of brain invasion. This is the first study showing a holistic picture of urease in fungi, clarifying that urease activity, and not Ure1 protein, contributes to pathogenesis in C. neoformans
C1 [Singh, Arpita; Varma, Ashok; Saijo, Tomomi; Ngamskulrungroj, Popchai; Chang, Yun C.; Kwon-Chung, Kyung J.] NIAID, Mol Microbiol Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Panting, Robert J.; Waldron, Kevin J.; Rutherford, Julian C.] Newcastle Univ, Sch Med, Inst Cell & Mol Biosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Jong, Ambrose] Univ So Calif, Keck Sch Med, Div Hematol Oncol, Saban Res Inst,Childrens Hosp Los Angeles, Los Angeles, CA 90033 USA.
[Ngamskulrungroj, Popchai] Mahidol Univ, Dept Microbiol, Bangkok, Thailand.
RP Rutherford, JC (reprint author), Newcastle Univ, Sch Med, Inst Cell & Mol Biosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
EM Julian.Rutherford@newcastle.ac.uk; june_kwon-chung@nih.gov
RI Waldron, Kevin/J-2368-2016
OI Waldron, Kevin/0000-0002-5577-7357
FU Intramural Research Program of the U.S. National Institute of Allergy
and Infectious Diseases, National Institutes of Health; Research
Councils United Kingdom Academic Fellowship; Marie Curie International
Re-Integration Grant; Biotechnology and Biological Sciences Research
Council; Royal Society [RG100365]; Newcastle University Faculty of
Medical Sciences
FX This study was supported by the Intramural Research Program of the U.S.
National Institute of Allergy and Infectious Diseases, National
Institutes of Health (K.J.K.-C.), and by the Research Councils United
Kingdom Academic Fellowship and Marie Curie International Re-Integration
Grant to J.C.R. R.J.P. was supported by a Biotechnology and Biological
Sciences Research Council studentship. Funding from the Royal Society
(RG100365) and from Newcastle University Faculty of Medical Sciences
supported K.J.W. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 53
TC 12
Z9 12
U1 1
U2 11
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 2150-7511
J9 MBIO
JI mBio
PD MAY-JUN
PY 2013
VL 4
IS 3
AR e00220-13
DI 10.1128/mBio.00220-13
PG 11
WC Microbiology
SC Microbiology
GA 174WK
UT WOS:000321187400016
PM 23653445
ER
PT J
AU Lim, CW
Sen, PK
Peddada, SD
AF Lim, Changwon
Sen, Pranab K.
Peddada, Shyamal D.
TI Robust Analysis of High Throughput Screening (HTS) Assay Data
SO TECHNOMETRICS
LA English
DT Article
DE Dose-response study; False discovery rate (FDR); Heteroscedasticity;
Hill model; M-estimation procedure; Nonlinear regression model; Power;
Toxicology
ID FALSE DISCOVERY RATE
AB Quantitative high throughput screening (qHTS) assays use cells or tissues to screen thousands of compounds in a short period of time. Data generated from qHTS assays are then evaluated using nonlinear regression models, such as the Hill model, and decisions regarding toxicity are made using the estimates of the parameters of the model. For any given compound, the variability in the observed response may either be constant across dose groups (homoscedasticity) or vary with dose (heteroscedasticity). Since thousands of compounds are simultaneously evaluated in a qHTS assay, it is not practically feasible for an investigator to perform residual analysis to determine the variance structure before performing statistical inferences on each compound. Since it is well known that the variance structure plays an important role in the analysis of linear and nonlinear regression models, it is therefore important to have practically useful and easy to interpret methodology that is robust to the variance structure. Furthermore, given the number of chemicals that are investigated in the qHTS assay, outliers and influential observations are not uncommon. In this article, we describe preliminary test estimation (PTE)-based methodology that is robust to the variance structure as well as any potential outliers and influential observations. Performance of the proposed methodology is evaluated in terms of false discovery rate (FDR) and power using a simulation study mimicking a real qHTS data. Of the two methods currently in use, our simulations studies suggest that one is extremely conservative with very small power in comparison to the proposed PTE-based method whereas the other method is very liberal. In contrast, the proposed PTE-based methodology achieves a better control of FDR while maintaining good power. The proposed methodology is illustrated using a dataset obtained from the National Toxicology Program (NTP). Additional information, simulation results, data, and computer code are available online as supplementary materials.
C1 [Lim, Changwon] Loyola Univ, Dept Math & Stat, Chicago, IL 60660 USA.
[Sen, Pranab K.] Univ N Carolina, Dept Stat & Operat Res, Chapel Hill, NC 27599 USA.
[Sen, Pranab K.] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
[Peddada, Shyamal D.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Lim, CW (reprint author), Loyola Univ, Dept Math & Stat, Chicago, IL 60660 USA.
EM clim2@luc.edu; pksen@bios.unc.edu; peddada@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences [Z01 ES101744-04]
FX This research was supported, in part, by the Intramural Research Program
of the NIH, National Institute of Environmental Health Sciences [Z01
ES101744-04]. This work was initiated while Dr. Lim was a post-doctoral
research fellow at NIEHS under the supervision of Dr. Peddada. We thank
Drs. Kissling and Shockely, the editor, the associate editor, and the
two anonymous referees for several helpful comments that led to
substantial improvement in the content and presentation of the article.
NR 13
TC 4
Z9 4
U1 1
U2 8
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 732 N WASHINGTON ST, ALEXANDRIA, VA 22314-1943 USA
SN 0040-1706
J9 TECHNOMETRICS
JI Technometrics
PD MAY
PY 2013
VL 55
IS 2
BP 150
EP U73
DI 10.1080/00401706.2012.749166
PG 22
WC Statistics & Probability
SC Mathematics
GA 181WA
UT WOS:000321699200004
PM 23908557
ER
PT J
AU Schulz-Menger, J
Bluemke, DA
Bremerich, J
Flamm, SD
Fogel, MA
Friedrich, MG
Kim, RJ
von Knobelsdorff-Brenkenhoff, F
Kramer, CM
Pennell, DJ
Plein, S
Nagel, E
AF Schulz-Menger, Jeanette
Bluemke, David A.
Bremerich, Jens
Flamm, Scott D.
Fogel, Mark A.
Friedrich, Matthias G.
Kim, Raymond J.
von Knobelsdorff-Brenkenhoff, Florian
Kramer, Christopher M.
Pennell, Dudley J.
Plein, Sven
Nagel, Eike
TI Standardized image interpretation and post processing in cardiovascular
magnetic resonance: Society for Cardiovascular Magnetic Resonance (SCMR)
Board of Trustees Task Force on Standardized Post Processing
SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE
LA English
DT Article
DE Magnetic resonance imaging; Heart; Recommendations; Image
interpretation; Post processing
ID STATE FREE PRECESSION; CORONARY-ARTERY-DISEASE; EXTRACELLULAR CONTRAST
AGENT; DIFFUSE MYOCARDIAL FIBROSIS; IRON-OVERLOADED THALASSEMIA;
INVESTIGATE OPTIMAL METHODS; BASE-LINE CORRECTION; QUANTITATIVE
ASSESSMENT; BLOOD-FLOW; VOLUME MEASUREMENTS
AB With mounting data on its accuracy and prognostic value, cardiovascular magnetic resonance (CMR) is becoming an increasingly important diagnostic tool with growing utility in clinical routine. Given its versatility and wide range of quantitative parameters, however, agreement on specific standards for the interpretation and post-processing of CMR studies is required to ensure consistent quality and reproducibility of CMR reports. This document addresses this need by providing consensus recommendations developed by the Task Force for Post Processing of the Society for Cardiovascular MR (SCMR). The aim of the task force is to recommend requirements and standards for image interpretation and post processing enabling qualitative and quantitative evaluation of CMR images. Furthermore, pitfalls of CMR image analysis are discussed where appropriate.
C1 [Schulz-Menger, Jeanette; von Knobelsdorff-Brenkenhoff, Florian] Charite, Working Grp Cardiovasc Magnet Resonance, Expt & Clin Res Ctr, Charite Med Fac & Max Delbrueck Ctr Mol Med, D-13353 Berlin, Germany.
[Schulz-Menger, Jeanette; von Knobelsdorff-Brenkenhoff, Florian] Charite, Dept Cardiol & Nephrol, HELIOS Klinikum Berlin Buch, D-13353 Berlin, Germany.
[Kramer, Christopher M.] Univ Virginia Hlth Syst, Dept Med, Charlottesville, VA USA.
[Kramer, Christopher M.] Univ Virginia Hlth Syst, Dept Radiol, Charlottesville, VA USA.
[Kramer, Christopher M.] Univ Virginia Hlth Syst, Cardiovasc Imaging Ctr, Charlottesville, VA USA.
[Flamm, Scott D.] Cleveland Clin, Imaging Inst, Cleveland, OH 44106 USA.
[Flamm, Scott D.] Cleveland Clin, Inst Heart & Vasc, Cleveland, OH 44106 USA.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Plein, Sven] Univ Leeds, Leeds Inst Genet Hlth & Therapeut, Leeds, W Yorkshire, England.
[Plein, Sven] Univ Leeds, Leeds Multidisciplinary Cardiovasc Res Ctr, Leeds, W Yorkshire, England.
[Kim, Raymond J.] Duke Univ, Univ Med Ctr, Duke Cardiovasc Magnet Resonance Ctr, Durham, NC USA.
[Kim, Raymond J.] Duke Univ, Dept Med, Univ Med Ctr, Durham, NC USA.
[Kim, Raymond J.] Duke Univ, Dept Radiol, Univ Med Ctr, Durham, NC 27710 USA.
[Friedrich, Matthias G.] Univ Montreal, CMR Ctr, Montreal Heart Inst, Dept Cardiol, Montreal, PQ, Canada.
[Pennell, Dudley J.] Royal Brompton Hosp, London SW3 6LY, England.
[Pennell, Dudley J.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Fogel, Mark A.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Dept Radiol, Philadelphia, PA 19104 USA.
[Bremerich, Jens] Univ Basel Hosp, Dept Radiol, CH-4031 Basel, Switzerland.
[Nagel, Eike] Kings Coll London, Dept Cardiovasc Imaging, Div Imaging Sci & Biomed Engn, London WC2R 2LS, England.
RP Schulz-Menger, J (reprint author), Charite, Working Grp Cardiovasc Magnet Resonance, Expt & Clin Res Ctr, Charite Med Fac & Max Delbrueck Ctr Mol Med, D-13353 Berlin, Germany.
EM jeanette.schulz-menger@charite.de
RI Nagel, Eike/C-6903-2008;
OI Nagel, Eike/0000-0002-6044-950X; Bremerich, Jens/0000-0002-1002-8483;
Bluemke, David/0000-0002-8323-8086
FU Siemens Healthcare; Else Kroner-Fresenius-Stiftung, Germany; Siemens
Medical Solutions and Philips Healthcare; Philips Healthcare; Siemens
Medical Solutions; HeartIT, LLC; Canadian Foundation for Innovation;
Fonds de Recherche Sante Quebec Matthias; NIHR Cardiovascular Biomedical
Research Unit of Royal Brompton & Harefield NHS Foundation Trust;
Imperial College; Siemens to develop functional fetal cardiac MR; NIH;
Edwards Life Sciences - CMR Core lab for COMPASSION trial; Kereos -
Medical Monitor for P19 imaging agent; Department of Health via the
National Institute for Health Research (NIHR) comprehensive Biomedical
Research Centre; NHS Foundation Trust; King's College London; King's
College Hospital NHS Foundation Trust; Centre of Excellence in Medical
Engineering; Wellcome Trust; EPSRC [WT 088641/Z/09/Z]; British Heart
Foundation [RE/08/003]; Philips HealthcareGrant; Bayer Healthcare
FX Christopher M. Kramer: Dr. Kramer acknowledges research support from
Siemens Healthcare; Florian von Knobelsdorff-Brenkenhoff: Dr. von
Knobelsdorff-Brenkenhoff acknowledges research support from the Else
Kroner-Fresenius-Stiftung, Germany; Scott D. Flamm: Dr. Flamm
acknowledges institutional grant/research support from Siemens Medical
Solutions and Philips Healthcare, and acts as a Consultant/Advisory
Board Member for Bayer Healthcare and Circle Cardiovascular, Inc.; David
A. Bluemke: -; Sven Plein: Dr. Plein acknowledges research support from
Philips Healthcare Raymond J. Kim: 1) Dr. RJ Kim is an inventor on a
United States patent, owned by Northwestern University, concerning the
use of contrast-enhanced MRI to detect myocardial viability. 2) Dr. RJ
Kim has an education grant from Siemens Medical Solutions. 3) Dr. RJ Kim
is a co-founder of HeartIT, LLC; Matthias G. Friedrich: Dr. Friedrich is
partially funded by the Canadian Foundation for Innovation and the Fonds
de Recherche Sante Quebec Matthias G. Friedrich: Matthias G. Friedrich
is on the board of directors and shareholder of Circle Cardiovascular
Imaging Inc., the manufacturer of a CMR-post processing and evaluation
software; Dudley J. Pennell: This work was supported by the NIHR
Cardiovascular Biomedical Research Unit of Royal Brompton & Harefield
NHS Foundation Trust and Imperial College.; Mark A. Fogel: Two NIH RO1
grants, grant from Siemens to develop functional fetal cardiac MR, grant
from Edwards Life Sciences - CMR Core lab for COMPASSION trial and
Kereos - Medical Monitor for P19 imaging agent.; Jens Bremerich: -; Eike
Nagel: Dr. Nagel acknowledges financial support from the Department of
Health via the National Institute for Health Research (NIHR)
comprehensive Biomedical Research Centre award to Guy's & St Thomas' NHS
Foundation Trust in partnership with King's College London and King's
College Hospital NHS Foundation Trust; the Centre of Excellence in
Medical Engineering funded by the Wellcome Trust and EPSRC under grant
number WT 088641/Z/09/Z; Funded by the British Heart Foundation award
RE/08/003. Grant support from Philips HealthcareGrant support from Bayer
Healthcare.
NR 69
TC 165
Z9 167
U1 2
U2 13
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1097-6647
J9 J CARDIOVASC MAGN R
JI J. Cardiov. Magn. Reson.
PD MAY 1
PY 2013
VL 15
AR 35
DI 10.1186/1532-429X-15-35
PG 19
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 172ZP
UT WOS:000321047100001
PM 23634753
ER
PT J
AU Mallajosyula, SS
Adams, KM
Barchi, JJ
MacKerell, AD
AF Mallajosyula, Sairam S.
Adams, Kristie M.
Barchi, Joseph J.
MacKerell, Alexander D.
TI Conformational Determinants of the Activity of Antiproliferative Factor
Glycopeptide
SO JOURNAL OF CHEMICAL INFORMATION AND MODELING
LA English
DT Article
ID INTERSTITIAL CYSTITIS PATIENTS; BLADDER EPITHELIAL-CELLS; ATOM
FORCE-FIELD; MOLECULAR-DYNAMICS; LIQUID WATER; PROTEINS; CHARMM;
SIMULATION; PEPTIDES; SOLVENT
AB The antiproliferative factor (APF) involved in interstitial cystitis is a glycosylated nonapeptide (TVPAAVVVA) containing a sialylated core 1 alpha-O-disaccharide linked to the N-terminal threonine. The chemical structure of APF was deduced using spectroscopic techniques and confirmed using total synthesis. The synthetic APF provided a platform to study amino acid modifications and their effect on APF activity, based on which a structure-activity relationship (SAR) for APF activity was previously proposed. However, this SAR model could not explain the change in activity associated with minor alterations in the peptide sequence. Presented is computational analysis of 14 APF derivatives to identify structural trends from which a more detailed SAR is obtained. The APF activity is found to be dictated by the close interplay between carbohydrate-peptide and peptide-peptide interactions. The former involves hydrogen bond and hydrophobic interactions, and the latter is dominated by hydrophobic interactions. The highly flexible hydrophobic peptide adopts collapsed conformations separated by low energy barriers. APF activity correlates with hydrophobic clustering associated with amino acids 4A, 6V, and 8V. Peptide conformations are highly sensitive to single point mutations, which explain the experimental trends. The presented SAR will act as a guide for lead optimization of more potent APF analogues of potential therapeutic utility.
C1 [Mallajosyula, Sairam S.; MacKerell, Alexander D.] Univ Maryland, Dept Pharmaceut Sci, Baltimore, MD 21201 USA.
[Adams, Kristie M.; Barchi, Joseph J.] NCI, Biol Chem Lab, Mol Discovery Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP MacKerell, AD (reprint author), Univ Maryland, Dept Pharmaceut Sci, 20 Penn St HSF 2, Baltimore, MD 21201 USA.
EM alex@outerbanks.umaryland.edu
RI Barchi Jr., Joseph/N-3784-2014;
OI MacKerell, Alex/0000-0001-8287-6804
FU NIH [GM070855]
FX Financial support from the NIH (GM070855) is acknowledged. The modified
REPDSTR module to perform periodic boundary simulations with CHARMM
c36a2 was kindly provided by Prof. Benoit Roux and Dr. Wei Jiang
(University of Chicago).
NR 40
TC 8
Z9 8
U1 0
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9596
J9 J CHEM INF MODEL
JI J. Chem Inf. Model.
PD MAY
PY 2013
VL 53
IS 5
BP 1127
EP 1137
DI 10.1021/ci400147s
PG 11
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Computer Science,
Information Systems; Computer Science, Interdisciplinary Applications
SC Pharmacology & Pharmacy; Chemistry; Computer Science
GA 154DD
UT WOS:000319650800011
PM 23627670
ER
PT J
AU Byeon, IJL
Ahn, J
Mitra, M
Byeon, CH
Hercik, K
Hritz, J
Charlton, LM
Levin, JG
Gronenborn, AM
AF Byeon, In-Ja L.
Ahn, Jinwoo
Mitra, Mithun
Byeon, Chang-Hyeock
Hercik, Kamil
Hritz, Jozef
Charlton, Lisa M.
Levin, Judith G.
Gronenborn, Angela M.
TI NMR structure of human restriction factor APOBEC3A reveals substrate
binding and enzyme specificity
SO NATURE COMMUNICATIONS
LA English
DT Article
ID SINGLE-STRANDED-DNA; CRYSTAL-STRUCTURE; CYTIDINE DEAMINASE; CATALYTIC
DOMAIN; LINE-1 RETROTRANSPOSITION; HIV-1 RESTRICTION; FOREIGN DNA;
NUCLEAR-DNA; HUMAN-CELLS; PROTEINS
AB Human APOBEC3A is a single-stranded DNA cytidine deaminase that restricts viral pathogens and endogenous retrotransposons, and has a role in the innate immune response. Furthermore, its potential to act as a genomic DNA mutator has implications for a role in carcinogenesis. A deeper understanding of APOBEC3A's deaminase and nucleic acid-binding properties, which is central to its biological activities, has been limited by the lack of structural information. Here we report the nuclear magnetic resonance solution structure of APOBEC3A and show that the critical interface for interaction with single-stranded DNA substrates includes residues extending beyond the catalytic centre. Importantly, by monitoring deaminase activity in real time, we find that A3A displays similar catalytic activity on APOBEC3A-specific TT (C) under barA- or A3G-specific CC (C) under barA-containing substrates, involving key determinants immediately 5' of the reactive C. Our results afford novel mechanistic insights into APOBEC3A-mediated deamination and provide the structural basis for further molecular studies.
C1 [Byeon, In-Ja L.; Ahn, Jinwoo; Byeon, Chang-Hyeock; Hritz, Jozef; Charlton, Lisa M.; Gronenborn, Angela M.] Univ Pittsburgh, Sch Med, Dept Biol Struct, Pittsburgh, PA 15261 USA.
[Byeon, In-Ja L.; Ahn, Jinwoo; Byeon, Chang-Hyeock; Charlton, Lisa M.; Gronenborn, Angela M.] Univ Pittsburgh, Sch Med, Pittsburgh Ctr HIV Prot Interact, Pittsburgh, PA 15261 USA.
[Mitra, Mithun; Hercik, Kamil; Levin, Judith G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Viral Gene Regulat, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Gronenborn, AM (reprint author), Univ Pittsburgh, Sch Med, Dept Biol Struct, 3501 5th Ave, Pittsburgh, PA 15261 USA.
EM amg100@pitt.edu
RI Mitra, Mithun/A-2133-2015; Hritz, Jozef/J-6887-2015;
OI Hritz, Jozef/0000-0002-4512-9241; Gronenborn, Angela
M/0000-0001-9072-3525
FU International Outgoing Fellowship of the European Community
[PIOF-GA-2009-235902]; National Institutes of Health NIGMS
[P50GM082251]; Intramural Research Program at the National Institutes of
Health, Eunice Kennedy Shriver National Institute of Child Health and
Human Development
FX We thank Maria DeLucia for help with A3A purification, Doug Bevan and
Phil Greer for computer technical support and Michael J Delk for NMR
instrumental support. J.H. acknowledges financial support by an
International Outgoing Fellowship of the European Community program
'Support for training and career development of researchers (Marie
Curie)', under Contract No. PIOF-GA-2009-235902. This work was supported
in part by the National Institutes of Health NIGMS Grant P50GM082251
(A.M.G.) and the Intramural Research Program at the National Institutes
of Health, Eunice Kennedy Shriver National Institute of Child Health and
Human Development (M.M., K.H. and J.G.L.).
NR 58
TC 56
Z9 57
U1 1
U2 17
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 MAY
PY 2013
VL 4
AR 1890
DI 10.1038/ncomms2883
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 166WI
UT WOS:000320589900086
PM 23695684
ER
PT J
AU Gutierrez-Uzquiza, A
Colon-Gonzalez, F
Leonard, TA
Canagarajah, BJ
Wang, HB
Mayer, BJ
Hurley, JH
Kazanietz, MG
AF Gutierrez-Uzquiza, Alvaro
Colon-Gonzalez, Francheska
Leonard, Thomas A.
Canagarajah, Bertram J.
Wang, HongBin
Mayer, Bruce J.
Hurley, James H.
Kazanietz, Marcelo G.
TI Coordinated activation of the Rac-GAP beta 2-chimaerin by an atypical
proline-rich domain and diacylglycerol
SO NATURE COMMUNICATIONS
LA English
DT Article
ID PROTEIN-KINASE-C; ADAPTER PROTEIN; SH3 DOMAIN; AUTOINHIBITORY MECHANISM;
SUBCELLULAR-LOCALIZATION; STRUCTURAL INSIGHT; SURFACE-RECEPTORS;
TERMINAL TAIL; BINDING-SITE; PXXP MOTIF
AB Chimaerins, a family of GTPase activating proteins for the small G-protein Rac, have been implicated in development, neuritogenesis and cancer. These Rac-GTPase activating proteins are regulated by the lipid second messenger diacylglycerol generated by tyrosine kinases such as the epidermal growth factor receptor. Here we identify an atypical proline-rich motif in chimaerins that binds to the adaptor protein Nck1. Unlike most Nck1 partners, chimaerins bind to the third SH3 domain of Nck1. This association is mediated by electrostatic interactions of basic residues within the Pro-rich motif with acidic clusters in the SH3 domain. Epidermal growth factor promotes the binding of beta 2-chimaerin to Nck1 in the cell periphery in a diacylglycerol-dependent manner. Moreover, beta 2-chimaerin translocation to the plasma membrane and its peripheral association with Rac1 requires Nck1. Our studies underscore a coordinated mechanism for beta 2-chimaerin activation that involves lipid interactions via the C1 domain and protein-protein interactions via the N-terminal proline-rich region.
C1 [Gutierrez-Uzquiza, Alvaro; Colon-Gonzalez, Francheska; Wang, HongBin; Kazanietz, Marcelo G.] Univ Penn, Dept Pharmacol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Leonard, Thomas A.; Canagarajah, Bertram J.; Hurley, James H.] NIH, Mol Biol Lab, Bethesda, MD 20892 USA.
[Mayer, Bruce J.] Univ Connecticut, Ctr Hlth, Dept Genet & Dev Biol, Farmington, CT 06030 USA.
RP Kazanietz, MG (reprint author), Univ Penn, Dept Pharmacol, Perelman Sch Med, Philadelphia, PA 19104 USA.
EM marcelog@upenn.edu
RI Leonard, Thomas/A-5143-2013
OI Leonard, Thomas/0000-0001-6853-666X
FU NIH [CA74197, CA139120, CA82258]; NIDDK; EMBO
FX This work was supported by NIH Grants CA74197 (M.G.K.), CA139120
(M.G.K.), CA82258 (B.J.M.), and the Intramural Programme of the NIDDK
(J.H.H.). T.A.L. was supported in part by an EMBO long-term fellowship.
NR 56
TC 1
Z9 1
U1 1
U2 6
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 MAY
PY 2013
VL 4
AR 1849
DI 10.1038/ncomms2834
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 166WI
UT WOS:000320589900045
PM 23673634
ER
PT J
AU Liu, H
Kim, SY
Fu, YL
Wu, XF
Ng, L
Swaroop, A
Forrest, D
AF Liu, Hong
Kim, Soo-Young
Fu, Yulong
Wu, Xuefeng
Ng, Lily
Swaroop, Anand
Forrest, Douglas
TI An isoform of retinoid-related orphan receptor beta directs
differentiation of retinal amacrine and horizontal interneurons
SO NATURE COMMUNICATIONS
LA English
DT Article
ID CELL-FATE; PHOTORECEPTOR DEVELOPMENT; MOUSE RETINA; TRANSCRIPTIONAL
REGULATION; MAMMALIAN RETINA; HORMONE-RECEPTOR; ROR-BETA; PTF1A; GENE;
EXPRESSION
AB Amacrine and horizontal interneurons integrate visual information as it is relayed through the retina from the photoreceptors to the ganglion cells. The early steps that generate these interneuron networks remain unclear. Here we show that a distinct retinoid-related orphan nuclear receptor beta 1 (ROR beta 1) isoform encoded by the retinoid-related orphan nuclear receptor beta gene (Rorb) is critical for both amacrine and horizontal cell differentiation in mice. A fluorescent protein cassette targeted into Rorb revealed RORb1 as a novel marker of immature amacrine and horizontal cells and of undifferentiated, dividing progenitor cells. ROR beta 1-deficient mice lose expression of pancreas-specific transcription factor 1a (Ptf1a) but retain forkhead box n4 factor (Foxn4), two early-acting factors necessary for amacrine and horizontal cell generation. ROR beta 1 and Foxn4 synergistically induce Ptf1a expression, suggesting a central role for ROR beta 1 in a transcriptional hierarchy that directs this interneuron differentiation pathway. Moreover, ectopic ROR beta 1 expression in neonatal retina promotes amacrine cell differentiation.
C1 [Liu, Hong; Fu, Yulong; Wu, Xuefeng; Ng, Lily; Forrest, Douglas] NIDDK, Lab Endocrinol & Receptor Biol, NIH, Bethesda, MD 20892 USA.
[Kim, Soo-Young; Swaroop, Anand] NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
RP Forrest, D (reprint author), NIDDK, Lab Endocrinol & Receptor Biol, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM forrestd@niddk.nih.gov
RI kim, soo-young/G-2365-2014
OI kim, soo-young/0000-0003-3632-8246
FU NIDDK intramural research program at the NIH; NEI intramural research
program at the NIH; KaroBio Foundation
FX We thank C. Stewart for W9.5 ES cells, M. Capecchi for plasmid pACN, D.
Kim, T. Badea and M. Ma for advice and assistance and K. Kelley for
blastocyst injections. This work was supported by the NIDDK and NEI
intramural research programs at the NIH and a grant from the KaroBio
Foundation.
NR 44
TC 18
Z9 20
U1 0
U2 6
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 MAY
PY 2013
VL 4
AR 1813
DI 10.1038/ncomms2793
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 166WI
UT WOS:000320589900009
PM 23652001
ER
PT J
AU Mine, KL
Shulzhenko, N
Yambartsev, A
Rochman, M
Sanson, GFO
Lando, M
Varma, S
Skinner, J
Volfovsky, N
Deng, T
Brenna, SMF
Carvalho, CRN
Ribalta, JCL
Bustin, M
Matzinger, P
Silva, IDCG
Lyng, H
Gerbase-DeLima, M
Morgun, A
AF Mine, Karina L.
Shulzhenko, Natalia
Yambartsev, Anatoly
Rochman, Mark
Sanson, Gerdine F. O.
Lando, Malin
Varma, Sudhir
Skinner, Jeff
Volfovsky, Natalia
Deng, Tao
Brenna, Sylvia M. F.
Carvalho, Carmen R. N.
Ribalta, Julisa C. L.
Bustin, Michael
Matzinger, Polly
Silva, Ismael D. C. G.
Lyng, Heidi
Gerbase-DeLima, Maria
Morgun, Andrey
TI Gene network reconstruction reveals cell cycle and antiviral genes as
major drivers of cervical cancer
SO NATURE COMMUNICATIONS
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS ONCOPROTEINS; GENOMIC INSTABILITY; NATURAL-HISTORY;
UTERINE CERVIX; HPV INFECTION; EXPRESSION; CARCINOMAS; INTERFERON; GAIN;
3Q
AB Although human papillomavirus was identified as an aetiological factor in cervical cancer, the key human gene drivers of this disease remain unknown. Here we apply an unbiased approach integrating gene expression and chromosomal aberration data. In an independent group of patients, we reconstruct and validate a gene regulatory meta-network, and identify cell cycle and antiviral genes that constitute two major subnetworks upregulated in tumour samples. These genes are located within the same regions as chromosomal amplifications, most frequently on 3q. We propose a model in which selected chromosomal gains drive activation of antiviral genes contributing to episomal virus elimination, which synergizes with cell cycle dysregulation. These findings may help to explain the paradox of episomal human papillomavirus decline in women with invasive cancer who were previously unable to clear the virus.
C1 [Mine, Karina L.; Shulzhenko, Natalia; Sanson, Gerdine F. O.; Gerbase-DeLima, Maria; Morgun, Andrey] Inst Imunogenet Assoc Fundo Incent Pesquisa IGEN, Sao Paulo, Brazil.
[Mine, Karina L.; Gerbase-DeLima, Maria] Univ Fed Sao Paulo, Dept Pediat, Sao Paulo, Brazil.
[Shulzhenko, Natalia; Matzinger, Polly; Morgun, Andrey] NIAID, Cellular & Mol Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Shulzhenko, Natalia; Morgun, Andrey] Oregon State Univ, Coll Pharm, Corvallis, OR 97331 USA.
[Yambartsev, Anatoly] Univ Sao Paulo, Inst Math & Stat, Dept Stat, Sao Paulo, Brazil.
[Rochman, Mark; Deng, Tao; Bustin, Michael] NCI, Prot Sect, Lab Metab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Lando, Malin; Lyng, Heidi] Norwegian Radium Hosp, Dept Radiat Biol, Oslo, Norway.
[Varma, Sudhir; Skinner, Jeff] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
[Volfovsky, Natalia] SAIC Frederick Inc, Adv Biomed Comp Ctr, Frederick, MD USA.
[Brenna, Sylvia M. F.] Univ Cidade Sao Paulo UNICID, Sch Med, Sao Paulo, Brazil.
[Carvalho, Carmen R. N.; Ribalta, Julisa C. L.; Silva, Ismael D. C. G.] Univ Fed Sao Paulo, Dept Gynecol, Sao Paulo, Brazil.
RP Morgun, A (reprint author), Inst Imunogenet Assoc Fundo Incent Pesquisa IGEN, Sao Paulo, Brazil.
EM andriy.morgun@oregonstate.edu
RI Varma, Sudhir/N-8763-2014; Deng, Tao/J-2031-2015; Gerbase-DeLima,
Maria/K-2515-2015; Bustin, Michael/G-6155-2015;
OI Varma, Sudhir/0000-0002-4096-4782; Skinner, Jeff/0000-0001-5697-0442
FU FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo), Brazil;
AFIP (Associacao Fundo de Incentivo Psicofarmacologia), Sao Paulo,
Brazil; Intramural Research Program of the NIAID, NIH; Oregon State
University, OR, USA
FX We thank Richard Simon, Ronald Germain, Yuri Kotliarov, Amiran Dzutsev
for helpful discussions and suggestions; Constantin Vasilyev for help
with matching ambiguous gene locations in databases; Tim Myers and the
staff of NIAID microarray facility for excellent technical support. This
research was partially supported by FAPESP (Fundacao de Amparo a
Pesquisa do Estado de Sao Paulo), Brazil; AFIP (Associacao Fundo de
Incentivo Psicofarmacologia), Sao Paulo, Brazil; and Intramural Research
Program of the NIAID, NIH; startup funds for A.M. from Oregon State
University, OR, USA.
NR 55
TC 22
Z9 25
U1 0
U2 16
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 MAY
PY 2013
VL 4
AR 1806
DI 10.1038/ncomms2693
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 166WI
UT WOS:000320589900002
PM 23651994
ER
PT J
AU Pelosi, E
Omari, S
Michel, M
Ding, J
Amano, T
Forabosco, A
Schlessinger, D
Ottolenghi, C
AF Pelosi, Emanuele
Omari, Shakib
Michel, Marc
Ding, Jun
Amano, Tomokazu
Forabosco, Antonino
Schlessinger, David
Ottolenghi, Chris
TI Constitutively active Foxo3 in oocytes preserves ovarian reserve in mice
SO NATURE COMMUNICATIONS
LA English
DT Article
ID MENOPAUSAL TRANSITION; TRANSCRIPTION FACTORS; MOUSE OVARY; EXPRESSION;
GROWTH; FOLLICLES; CANCER; GENES; CELLS; AGE
AB During female reproductive life, ovarian follicle reserve is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. Here we show that overexpression of constitutively active FOXO3 can increase ovarian reproductive capacity in mice. We find increased follicle numbers and decreased gonadotropin levels in aging FOXO3-transgenic mice compared with wild-type littermates, suggesting maintenance of a greater ovarian reserve. Based on cumulative progeny in aging animals, we find 31-49% increased fertility in transgenic females. The gene expression profile of Foxo3-/- knockout ovaries appears older than that of wild-type littermates, and the transgene induces a younger-looking profile, restoring much of the wild-type transcriptome. This is the first gain-of-function model of augmented reproductive reserve in mice, thus emphasizing the role of Foxo3 as a guardian of the ovarian follicle pool in mammals and a potential determinant of the onset of menopause.
C1 [Pelosi, Emanuele; Omari, Shakib; Michel, Marc; Ding, Jun; Amano, Tomokazu; Schlessinger, David] NIA, Genet Lab, NIH, IRP, Baltimore, MD 21224 USA.
[Forabosco, Antonino] Cante Montevecchio Assoc, Genom Res Ctr, I-61032 Fano, PU, Italy.
[Ottolenghi, Chris] Univ Paris 05, INSERM, Unite UMR S 747, F-75270 Paris 06, France.
RP Pelosi, E (reprint author), NIA, Genet Lab, NIH, IRP, 251 Bayview Blvd,Room 10B014, Baltimore, MD 21224 USA.
EM pelosie@mail.nih.gov
RI Amano, Tomokazu/F-9720-2013;
OI Pelosi, Emanuele/0000-0003-1890-9821
FU National Institute on Aging, NIH
FX We would like to thank the NIA Comparative Medicine Section for service
with breeding, genotyping and handling of the mice here analysed. We
also thank K. Gold for help with follicle count. We are grateful to E.
Lehrmann and Y. Zhang for technical assistance with the microarray
experiments; M. Ko, R. Nagaraja and P. Western for discussion. This
research was supported by the Intramural Research Program of the
National Institute on Aging, NIH.
NR 29
TC 18
Z9 20
U1 1
U2 12
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 MAY
PY 2013
VL 4
AR 1843
DI 10.1038/ncomms2861
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 166WI
UT WOS:000320589900039
PM 23673628
ER
PT J
AU Pittaluga, S
AF Pittaluga, Stefania
TI Viral-associated lymphoid proliferations
SO SEMINARS IN DIAGNOSTIC PATHOLOGY
LA English
DT Article
DE Lymphoid proliferation; EBV; Chronic active EBV; HHV6
ID EPSTEIN-BARR-VIRUS; CELL LYMPHOPROLIFERATIVE DISORDERS; ACUTE
INFECTIOUS-MONONUCLEOSIS; HUMAN-HERPESVIRUS 6; EBV INFECTION; DISEASE;
PATHOGENESIS; TONSILS; ADULTS; STATES
AB The histological spectrum of viral-associated lymphoid proliferations is quite broad, ranging from reactive lymphadenitis to atypical proliferations mimicking classical Hodgkin lymphoma or non-Hodgkin lymphoma. Virally associated reactive lesions can appear quite alarming on histological examination, because of direct (cytopathic) and indirect viral-induced changes eliciting a polymorphic cellular host response. In addition, the atypical lymphoid proliferation may show aberrant phenotypic features as well as restricted/clonal gene immunoglobulin or T-cell receptor rearrangements, further complicating the interpretation. In order to achieve an accurate diagnosis, it is important to be aware of the clinical history, including family history and ethnic background, clinical presentation, symptoms, and extent of the disease. Among the clinical data, particular emphasis should be placed on serology and viral load studies, and the use of immunosuppressive drugs. The clinical course and outcome vary greatly, from an indolent, self-limited to aggressive clinical course, blurring at times the distinction between neoplastic and reactive proliferations. It is now recognized that immunosenescence also plays a significant role in the development of these viral-associated lymphoid proliferations, and new entities have been described in recent years. In this review we discuss mostly Epstein-Barr virus-associated viral proliferations that may be confused with lymphomas, which the practicing pathologist may encounter. Published by Elsevier Inc.
C1 [Pittaluga, Stefania] NCI, Hematopathol Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Pittaluga, S (reprint author), NCI, Hematopathol Sect, Pathol Lab, 10 Ctr Dr,MSC 1500, Bethesda, MD 20892 USA.
EM stefpitt@mail.nih.gov
FU Intramural Research Program, National Cancer Institute, NIH
FX Supported in part by the Intramural Research Program, National Cancer
Institute, NIH.
NR 33
TC 4
Z9 5
U1 0
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0740-2570
J9 SEMIN DIAGN PATHOL
JI Semin. Diagn. Pathol.
PD MAY
PY 2013
VL 30
IS 2
BP 130
EP 136
DI 10.1053/j.semdp.2012.08.009
PG 7
WC Medical Laboratory Technology; Pathology
SC Medical Laboratory Technology; Pathology
GA 172AR
UT WOS:000320972800004
PM 23537914
ER
PT J
AU Quick, VM
Byrd-Bredbenner, C
Neumark-Sztainers, D
AF Quick, Virginia M.
Byrd-Bredbenner, Carol
Neumark-Sztainers, Dianne
TI Chronic Illness and Disordered Eating: A Discussion of the Literature
SO ADVANCES IN NUTRITION
LA English
DT Review
ID DEPENDENT DIABETES-MELLITUS; QUALITY-OF-LIFE; IRRITABLE-BOWEL-SYNDROME;
POUCH-ANAL ANASTOMOSIS; PERCEIVED BODY-IMAGE; CYSTIC-FIBROSIS;
ANOREXIA-NERVOSA; GLYCEMIC CONTROL; CELIAC-DISEASE; CROHNS-DISEASE
AB This paper describes the prevalence of eating disorders and disordered eating behaviors, the reasons why these practices are endorsed, and the potential consequences in youths and young adults with selected diet-related chronic health conditions (DRCHCs) and provides recommendations for eating disorder prevention interventions and research efforts. Although it remains unclear whether the prevalence of eating disorders is higher in those with DRCHCs compared with the general population, overall findings suggest that young people with DRCHCs may be at risk of endorsing disordered eating behaviors that may lead to diagnosis of an eating disorder and other health problems over the course of their treatment. Thus, health care providers should be aware that young people with DRCHCs may be at risk of eating disorders and carefully monitor psychological changes and the use of unhealthy weight control methods. It is also important to develop and evaluate theory-based interventions and disease-specific eating disorder risk screening tools that are effective in halting the progression of eating disorders and negative health outcomes in young people with chronic health conditions.
C1 [Quick, Virginia M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, DHHS, Bethesda, MD 20892 USA.
[Byrd-Bredbenner, Carol] Rutgers State Univ, Dept Nutr Sci, New Brunswick, NJ 08903 USA.
[Neumark-Sztainers, Dianne] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
RP Quick, VM (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, DHHS, Bethesda, MD 20892 USA.
EM gingermguick@gmail.com
RI Byrd-Bredbenner, Carol/F-8064-2015;
OI Byrd-Bredbenner, Carol/0000-0002-8010-3987; Quick,
Virginia/0000-0002-4338-963X; Neumark-Sztainer,
Dianne/0000-0001-9435-1669
FU Kappa Omicron Nu Research Fellowship; Eunice Kennedy Shriver National
Institute of Child Health and Human Development Intramural Research
Training Award
FX Kappa Omicron Nu Research Fellowship and the Eunice Kennedy Shriver
National Institute of Child Health and Human Development Intramural
Research Training Award to V. M. Quick.
NR 115
TC 14
Z9 15
U1 3
U2 27
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 2161-8313
J9 ADV NUTR
JI Adv. Nutr.
PD MAY
PY 2013
VL 4
IS 3
BP 277
EP 286
DI 10.3945/an.112.003608
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 167LC
UT WOS:000320632500002
PM 23674793
ER
PT J
AU Zhang, XZ
Bullard, KM
Cotch, MF
Wilson, MR
Rovner, BW
McGwin, G
Owsley, C
Barker, L
Crews, JE
Saaddine, JB
AF Zhang, Xinzhi
Bullard, Kai McKeever
Cotch, Mary Frances
Wilson, M. Roy
Rovner, Barry W.
McGwin, Gerald, Jr.
Owsley, Cynthia
Barker, Lawrence
Crews, John E.
Saaddine, Jinan B.
TI Association Between Depression and Functional Vision Loss in Persons 20
Years of Age or Older in the United States, NHANES 2005-2008
SO JAMA OPHTHALMOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; REPORTED VISUAL FUNCTION; DUAL SENSORY LOSS; MACULAR
DEGENERATION; ELDERLY-PATIENTS; SELF-MANAGEMENT; MOOD DISORDERS;
PRIME-MD; IMPAIRMENT; ADULTS
AB Importance: This study provides further evidence from a national sample to generalize the relationship between depression and vision loss to adults across the age spectrum. Better recognition of depression among people reporting reduced ability to perform routine activities of daily living due to vision loss is warranted.
Objectives: To estimate, in a national survey of US adults 20 years of age or older, the prevalence of depression among adults reporting visual function loss and among those with visual acuity impairment. The relationship between depression and vision loss has not been reported in a nationally representative sample of US adults. Previous studies have been limited to specific cohorts and predominantly focused on the older population.
Design: The National Health and Nutrition Examination Survey (NHANES) 2005-2008.
Setting: Across-sectional, nationally representative sample of adults, with prevalence estimates weighted to represent the civilian, noninstitutionalized US population.
Participants: A total of 10 480 US adults 20 years of age or older.
Main Outcome Measures: Depression, as measured by the 9-item Patient Health Questionnaire depression scale, and vision loss, as measured by visual function using a questionnaire and by visual acuity at examination.
Results: In 2005-2008, the estimated crude prevalence of depression (9-item Patient Health Questionnaire score of >= 10) was 11.3% (95% CI, 9.7%-13.2%) among adults with self-reported visual function loss and 4.8% (95% CI, 4.0%-5.7%) among adults without. The estimated prevalence of depression was 10.7% (95% CI, 8.0%-14.3%) among adults with presenting visual acuity impairment (visual acuity worse than 20/40 in the better-seeing eye) compared with 6.8% (95% CI, 5.8%-7.8%) among adults with normal visual acuity. After controlling for age, sex, race/ethnicity, marital status, living alone or not, education, income, employment status, health insurance, body mass index, smoking, binge drinking, general health status, eyesight worry, and major chronic conditions, self-reported visual function loss remained significantly associated with depression (overall odds ratio, 1.9 [95% CI, 1.6-2.3]), whereas the association between presenting visual acuity impairment and depression was no longer statistically significant.
Conclusions and Relevance: Self-reported visual function loss, rather than loss of visual acuity, is significantly associated with depression. Health professionals should be aware of the risk of depression among persons reporting visual function loss.
C1 [Zhang, Xinzhi] Natl Inst Minor Hlth & Hlth Dispar, Div Data Management & Sci Reporting, NIH, Bethesda, MD 20892 USA.
[Cotch, Mary Frances] NEI, NIH, Bethesda, MD 20892 USA.
[Bullard, Kai McKeever; Barker, Lawrence; Crews, John E.; Saaddine, Jinan B.] Ctr Dis Control & Prevent, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA.
[Rovner, Barry W.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Psychiat, Philadelphia, PA 19107 USA.
[Rovner, Barry W.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Neurol, Philadelphia, PA 19107 USA.
[McGwin, Gerald, Jr.; Owsley, Cynthia] Univ Alabama Birmingham, Dept Ophthalmol, Birmingham, AL USA.
RP Zhang, XZ (reprint author), Natl Inst Minor Hlth & Hlth Dispar, Div Data Management & Sci Reporting, NIH, 6707 Democracy Blvd,Ste 800, Bethesda, MD 20892 USA.
EM xinzhi.zhang@nih.gov
OI Cotch, Mary Frances/0000-0002-2046-4350
FU National Center for Health Statistics of the CDC; Division of Diabetes
Translation of the CDC [05FED47304]; National Eye Institute/National
Institutes of Health [ZIAEY000402]
FX This study was supported by the National Center for Health Statistics of
the CDC. Funding for the NHANES retinal component was provided by
intra-agency agreement 05FED47304 from the Division of Diabetes
Translation of the CDC. Funding for the vision component was provided by
Intramural Research Program award ZIAEY000402 from the National Eye
Institute/National Institutes of Health.
NR 72
TC 31
Z9 32
U1 4
U2 9
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6165
EI 2168-6173
J9 JAMA OPHTHALMOL
JI JAMA Ophthalmol.
PD MAY
PY 2013
VL 131
IS 5
BP 573
EP 581
DI 10.1001/jamaophthalmol.2013.2597
PG 9
WC Ophthalmology
SC Ophthalmology
GA 163JY
UT WOS:000320333300002
PM 23471505
ER
PT J
AU de Moura, TR
Oliveira, F
Carneiro, MW
Miranda, JC
Clarencio, J
Barral-Netto, M
Brodskyn, C
Barral, A
Ribeiro, JMC
Valenzuela, JG
de Oliveira, CI
AF de Moura, Tatiana R.
Oliveira, Fabiano
Carneiro, Marcia W.
Miranda, Jose Carlos
Clarencio, Jorge
Barral-Netto, Manoel
Brodskyn, Claudia
Barral, Aldina
Ribeiro, Jose M. C.
Valenzuela, Jesus G.
de Oliveira, Camila I.
TI Functional Transcriptomics of Wild-Caught Lutzomyia intermedia Salivary
Glands: Identification of a Protective Salivary Protein against
Leishmania braziliensis Infection
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID SAND FLY VECTOR; CUTANEOUS LEISHMANIASIS; VISCERAL LEISHMANIASIS;
SEQUENCE ALIGNMENT; CIMEX-LECTULARIUS; INFANTUM-CHAGASI; BED BUG;
LONGIPALPIS; MAXADILAN; IMMUNITY
AB Background: Leishmania parasites are transmitted in the presence of sand fly saliva. Together with the parasite, the sand fly injects salivary components that change the environment at the feeding site. Mice immunized with Phlebotomus papatasi salivary gland (SG) homogenate are protected against Leishmania major infection, while immunity to Lutzomyia intermedia SG homogenate exacerbated experimental Leishmania braziliensis infection. In humans, antibodies to Lu. intermedia saliva are associated with risk of acquiring L. braziliensis infection. Despite these important findings, there is no information regarding the repertoire of Lu. intermedia salivary proteins.
Methods and Findings: A cDNA library from the Salivary Glands (SGs) of wild-caught Lu. intermedia was constructed, sequenced, and complemented by a proteomic approach based on 1D SDS PAGE and mass/mass spectrometry to validate the transcripts present in this cDNA library. We identified the most abundant transcripts and proteins reported in other sand fly species as well as novel proteins such as neurotoxin-like proteins, peptides with ML domain, and three small peptides found so far only in this sand fly species. DNA plasmids coding for ten selected transcripts were constructed and used to immunize BALB/c mice to study their immunogenicity. Plasmid Linb-11-coding for a 4.5-kDa protein-induced a cellular immune response and conferred protection against L. braziliensis infection. This protection correlated with a decreased parasite load and an increased frequency of IFN-c-producing cells.
Conclusions: We identified the most abundant and novel proteins present in the SGs of Lu. intermedia, a vector of cutaneous leishmaniasis in the Americas. We also show for the first time that immunity to a single salivary protein from Lu. intermedia can protect against cutaneous leishmaniasis caused by L. braziliensis.
C1 [de Moura, Tatiana R.; Carneiro, Marcia W.; Miranda, Jose Carlos; Clarencio, Jorge; Barral-Netto, Manoel; Brodskyn, Claudia; Barral, Aldina; de Oliveira, Camila I.] Fundacao Oswaldo Cruz FIOCRUZ, Ctr Pesquisas Goncalo Moniz, Salvador, BA, Brazil.
[Oliveira, Fabiano; Valenzuela, Jesus G.] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Barral-Netto, Manoel; Brodskyn, Claudia; Barral, Aldina] Univ Fed Bahia, Salvador, BA, Brazil.
[Barral-Netto, Manoel; Brodskyn, Claudia; Barral, Aldina; de Oliveira, Camila I.] Inst Nacl Ciencia & Tecnol Invest Imunol III INCT, Salvador, BA, Brazil.
[Ribeiro, Jose M. C.] NIAID, Vector Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RP de Moura, TR (reprint author), Univ Fed Sergipe, Ctr Ciencias Biol & Saude, Aracaju, Sergipe, Brazil.
EM jvalenzuela@niaid.nih.gov; camila@bahia.fiocruz.br
RI de Oliveira, Camila/B-4358-2009; Oliveira, Fabiano/B-4251-2009; Ribeiro,
Jose/J-7011-2015; DE MOURA, TATIANA/L-4556-2016;
OI de Oliveira, Camila/0000-0002-7868-5164; Oliveira,
Fabiano/0000-0002-7924-8038; DE MOURA, TATIANA/0000-0002-7442-4434;
Barral Netto, Manoel/0000-0002-5823-7903; Ribeiro,
Jose/0000-0002-9107-0818
FU Intramural Research Program of the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, USA; Fundacao de Amparo a Pesquisa da Bahia
(FAPESB); Conselho Nacional de Desenvolvimento Cientifico e Tecnologico
(CNPq), Brazil
FX This work was funded in part by the Intramural Research Program of the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, USA, and by the
Fundacao de Amparo a Pesquisa da Bahia (FAPESB) and Conselho Nacional de
Desenvolvimento Cientifico e Tecnologico (CNPq), Brazil. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 47
TC 16
Z9 16
U1 0
U2 19
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 MAY
PY 2013
VL 7
IS 5
AR e2242
DI 10.1371/journal.pntd.0002242
PG 16
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 158SW
UT WOS:000319994400042
PM 23717705
ER
PT J
AU Kari, L
Bakios, LE
Goheen, MM
Bess, LN
Watkins, HS
Southern, TR
Song, LH
Whitmire, WM
Olivares-Zavaleta, N
Caldwell, HD
AF Kari, Laszlo
Bakios, Lauren E.
Goheen, Morgan M.
Bess, Leah N.
Watkins, Heather S.
Southern, Timothy R.
Song, Lihua
Whitmire, William M.
Olivares-Zavaleta, Norma
Caldwell, Harlan D.
TI Antibody Signature of Spontaneous Clearance of Chlamydia trachomatis
Ocular Infection and Partial Resistance against Re-challenge in a
Nonhuman Primate Trachoma Model
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID OUTER-MEMBRANE PROTEIN; PROTECTIVE IMMUNITY; MURIDARUM INFECTION;
VACCINATION; IDENTIFICATION; IMMUNIZATION; ANTIGENS; STRAINS; GENOME;
CELLS
AB Background: Chlamydia trachomatis is the etiological agent of trachoma the world's leading cause of infectious blindness. Here, we investigate whether protracted clearance of a primary infection in nonhuman primates is attributable to antigenic variation or related to the maturation of the anti-chlamydial humoral immune response specific to chlamydial antigens.
Methodology/Principal Findings: Genomic sequencing of organisms isolated throughout the protracted primary infection revealed that antigenic variation was not related to the inability of monkeys to efficiently resolve their infection. To explore the maturation of the humoral immune response as a possible reason for delayed clearance, sera were analyzed by radioimmunoprecipitation using intrinsically radio-labeled antigens prepared under non-denaturing conditions. Antibody recognition was restricted to the antigenically variable major outer membrane protein (MOMP) and a few antigenically conserved antigens. Recognition of MOMP occurred early post-infection and correlated with reduction in infectious ocular burdens but not with infection eradication. In contrast, antibody recognition of conserved antigens, identified as PmpD, Hsp60, CPAF and Pgp3, appeared late and correlated with infection eradication. Partial immunity to re-challenge was associated with a discernible antibody recall response against all antigens. Antibody recognition of PmpD and CPAF was destroyed by heat treatment while MOMP and Pgp3 were partially affected, indicating that antibody specific to conformational epitopes on these proteins may be important to protective immunity.
Conclusions/Significance: Our findings suggest that delayed clearance of chlamydial infection in NHP is not the result of antigenic variation but rather a consequence of the gradual maturation of the C. trachomatis antigen-specific humoral immune response. However, we cannot conclude that antibodies specific for these proteins play the primary role in host protective immunity as they could be surrogate markers of T cell immunity. Collectively, our results argue that an efficacious subunit trachoma vaccine might require a combination of these antigens delivered in their native conformation.
C1 [Kari, Laszlo; Bakios, Lauren E.; Goheen, Morgan M.; Bess, Leah N.; Watkins, Heather S.; Southern, Timothy R.; Song, Lihua; Whitmire, William M.; Olivares-Zavaleta, Norma; Caldwell, Harlan D.] NIAID, Intracellular Parasites Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
RP Kari, L (reprint author), NIAID, Intracellular Parasites Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
EM hcaldwell@niaid.nih.gov
FU Division of Intramural Research, NIAID, NIH
FX This work was funded by the Division of Intramural Research, NIAID, NIH.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 28
TC 2
Z9 2
U1 0
U2 7
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 MAY
PY 2013
VL 7
IS 5
AR e2248
DI 10.1371/journal.pntd.0002248
PG 8
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 158SW
UT WOS:000319994400048
PM 23738030
ER
PT J
AU Coate, TM
Kelley, MW
AF Coate, Thomas M.
Kelley, Matthew W.
TI Making connections in the inner ear: Recent insights into the
development of spiral ganglion neurons and their connectivity with
sensory hair cells
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Spiral ganglion; Cochlea; Afferent; Hair cell; Auditory; Deafness
ID AXON GUIDANCE; MAMMALIAN COCHLEA; EXPRESSION PATTERNS; NEURITE
OUTGROWTH; AUDITORY SYSTEMS; GENE-EXPRESSION; MOLECULAR-BASIS;
NERVOUS-SYSTEM; MOUSE; INNERVATION
AB In mammals, auditory information is processed by the hair cells (HCs) located in the cochlea and then rapidly transmitted to the CNS via a specialized cluster of bipolar afferent connections known as the spiral ganglion neurons (SGNs). Although many anatomical aspects of SGNs are well described, the molecular and cellular mechanisms underlying their genesis, how they are precisely arranged along the cochlear duct, and the guidance mechanisms that promote the innervation of their hair cell targets are only now being understood. Building upon foundational studies of neurogenesis and neurotrophins, we review here new concepts and technologies that are helping to enrich our understanding of the development of the nervous system within the inner ear. Published by Elsevier Ltd.
C1 [Coate, Thomas M.; Kelley, Matthew W.] Natl Inst Deafness & Other Commun Disorders, Lab Cochlear Dev, NIH, Bethesda, MD USA.
RP Coate, TM (reprint author), 35 Convent Dr, Bethesda, MD 20892 USA.
EM coatet@nidcd.nih.gov
FU Intramural NIH HHS [Z99 DC999999]
NR 107
TC 19
Z9 20
U1 0
U2 10
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD MAY
PY 2013
VL 24
IS 5
BP 460
EP 469
DI 10.1016/j.semcdb.2013.04.003
PG 10
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 166YJ
UT WOS:000320596800012
PM 23660234
ER
PT J
AU Howdeshell, KL
Shelby, MD
Walker, VR
AF Howdeshell, K. L.
Shelby, M. D.
Walker, V. R.
TI Summary of National Toxicology Monograph on Developmental Effects of
Cancer Chemotherapy Administered during Pregnancy
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Howdeshell, K. L.; Shelby, M. D.; Walker, V. R.] NIEHS, Res Triangle Pk, NC 27709 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 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD MAY
PY 2013
VL 97
IS 5
SI SI
BP 288
EP 288
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100037
ER
PT J
AU Inselman, AL
Nakamura, N
Mcintyre, B
Foster, PMD
Harrouk, W
Hansen, DK
AF Inselman, A. L.
Nakamura, N.
Mcintyre, B.
Foster, P. M. D.
Harrouk, W.
Hansen, D. K.
TI Preliminary Results from Prenatal Toxicity Study of Oxybenzone in Rats
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Inselman, A. L.; Nakamura, N.; Hansen, D. K.] US FDA, NCTR, Jefferson, AR USA.
[Mcintyre, B.; Foster, P. M. D.] NIEHS, NTP, Res Triangle Pk, NC 27709 USA.
[Harrouk, W.] US FDA, CDER, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 8
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 MAY
PY 2013
VL 97
IS 5
SI SI
BP 313
EP 313
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100081
ER
PT J
AU Miller, RK
Stodgell, CJ
Katzman, PJ
Friedman, AE
Jamerson, D
Friedman, MR
Salamone, L
Ruffolo, LI
Weidenborner, P
Aagaard-Tillery, K
Culhane, J
Wadlinger, S
Pacholski, M
Kent, MA
Green, L
Wapner, R
Torres, C
Perou, J
Landrigan, P
Chen, J
Lambertini, L
Littman, L
Sheffield, P
Golden, A
Gilbert, J
Lendor, C
Allen, S
Schadt, E
Dudley, J
Leuthner, S
Szabo, S
Salafia, CM
Dalton, JL
Misra, D
Thiex, N
Gutzman, K
Martin, A
Specker, B
Hobbs, C
Maccleod, S
Walker, CK
Swanson, J
Holliday, C
Butler, J
Li, A
Dassanayake, RMAPS
Nanes, J
Xia, Y
Murray, JC
Busch, TD
Rigdon, J
Darrah, TH
Campbell, E
Dole, N
Thorp, J
Eucker, B
Bell, C
Clark, EB
Varner, MW
Taggart, E
Billy, J
Stradling, S
Leavitt, J
Bell, W
Waterfall, S
O'Brien, B
Layton, M
Todd, D
Wilson, K
Durkin, MS
Sandoval, MN
Kasten, C
Moye, J
AF Miller, R. K.
Stodgell, C. J.
Katzman, P. J.
Friedman, A. E.
Jamerson, D.
Friedman, M. R.
Salamone, L.
Ruffolo, L., I
Weidenborner, P.
Aagaard-Tillery, K.
Culhane, J.
Wadlinger, S.
Pacholski, M.
Kent, M. A.
Green, L.
Wapner, R.
Torres, C.
Perou, J.
Landrigan, P.
Chen, J.
Lambertini, L.
Littman, L.
Sheffield, P.
Golden, A.
Gilbert, J.
Lendor, C.
Allen, S.
Schadt, E.
Dudley, J.
Leuthner, S.
Szabo, S.
Salafia, C. M.
Dalton, J. L.
Misra, D.
Thiex, N.
Gutzman, K.
Martin, A.
Specker, B.
Hobbs, C.
Maccleod, S.
Walker, C. K.
Swanson, J.
Holliday, C.
Butler, J.
Li, A.
Dassanayake, R. M. A. P. S.
Nanes, J.
Xia, Y.
Murray, J. C.
Busch, T. D.
Rigdon, J.
Darrah, T. H.
Campbell, E.
Dole, N.
Thorp, J.
Eucker, B.
Bell, C.
Clark, E. B.
Varner, M. W.
Taggart, E.
Billy, J.
Stradling, S.
Leavitt, J.
Bell, W.
Waterfall, S.
O'Brien, B.
Layton, M.
Todd, D.
Wilson, K.
Durkin, M. S.
Sandoval, M-N
Kasten, C.
Moye, J.
CA Natl Children's Study Placental Re
TI Use of the Human Placenta As a Biomarker for Environmental Exposures and
Clinical, Genetics/Epigenetic, Morphological, and Systems Biology
Assessments in the National Children's Study (NCS)
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Miller, R. K.; Stodgell, C. J.; Katzman, P. J.; Friedman, A. E.; Jamerson, D.; Friedman, M. R.; Salamone, L.; Ruffolo, L., I; Weidenborner, P.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Aagaard-Tillery, K.] Baylor Coll Med, Houston, TX 77030 USA.
[Culhane, J.; Wadlinger, S.; Pacholski, M.; Kent, M. A.; Green, L.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Wapner, R.; Torres, C.; Perou, J.] Columbia Univ, New York, NY USA.
[Landrigan, P.; Chen, J.; Lambertini, L.; Littman, L.; Sheffield, P.; Golden, A.; Gilbert, J.; Lendor, C.; Allen, S.; Schadt, E.; Dudley, J.] Icahn Sch Med Mt Sinai, New York, NY USA.
[Leuthner, S.; Szabo, S.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Salafia, C. M.; Dalton, J. L.; Misra, D.] Placental Analyt Inc, Larchmont, NY USA.
[Thiex, N.; Gutzman, K.; Martin, A.; Specker, B.] S Dakota State Univ, Brookings, SD 57007 USA.
[Hobbs, C.; Maccleod, S.] Univ Arkansas, Little Rock, AR 72204 USA.
[Walker, C. K.] Univ Calif Davis, Davis, CA 95616 USA.
[Swanson, J.; Holliday, C.; Butler, J.] Univ Calif Irvine, Irvine, CA USA.
[Li, A.; Dassanayake, R. M. A. P. S.; Nanes, J.; Xia, Y.] Univ Illinois, Chicago, IL USA.
[Murray, J. C.; Busch, T. D.; Rigdon, J.] Univ Iowa, Iowa City, IA USA.
[Darrah, T. H.; Campbell, E.] Univ Massachusetts, Boston, MA 02125 USA.
[Darrah, T. H.] Duke Univ, Durham, NC USA.
[Dole, N.; Thorp, J.; Eucker, B.; Bell, C.] Univ N Carolina, Chapel Hill, NC USA.
[Clark, E. B.; Varner, M. W.; Taggart, E.; Billy, J.; Stradling, S.; Leavitt, J.; Bell, W.; Waterfall, S.] Univ Utah, Salt Lake City, UT USA.
[O'Brien, B.; Layton, M.; Todd, D.; Wilson, K.] Westat Corp, Rockville, MD USA.
[Durkin, M. S.; Sandoval, M-N] Univ Wisconsin, Madison, WI USA.
[Kasten, C.; Moye, J.; Natl Children's Study Placental Re] NIH, Natl Childrens Study, Bethesda, MD 20892 USA.
RI Durkin, Maureen/B-7834-2015;
OI Li, An/0000-0002-8476-8783
NR 0
TC 0
Z9 0
U1 1
U2 13
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 MAY
PY 2013
VL 97
IS 5
SI SI
BP 330
EP 331
PG 2
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100113
ER
PT J
AU Stodgell, CJ
Salamone, L
Katzman, PK
Ruffolo, LI
Murray, J
Busch, T
Culhane, J
Wadlinger, S
Landrigan, P
Littman, L
Hiex, N
Specker, B
Swanson, J
Dole, N
Eucker, B
Clark, EB
Varner, M
Taggart, E
Moye, J
Miller, RK
AF Stodgell, C. J.
Salamone, L.
Katzman, P. K.
Ruffolo, L., I
Murray, J.
Busch, T.
Culhane, J.
Wadlinger, S.
Landrigan, P.
Littman, L.
Hiex, N.
Specker, B.
Swanson, J.
Dole, N.
Eucker, B.
Clark, E. B.
Varner, M.
Taggart, E.
Moye, J.
Miller, R. K.
TI Gene Expression in Human Placenta from the National Children's Study
(NCS)
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Stodgell, C. J.; Salamone, L.; Katzman, P. K.; Ruffolo, L., I; Murray, J.; Busch, T.; Culhane, J.; Wadlinger, S.; Landrigan, P.; Littman, L.; Hiex, N.; Specker, B.; Swanson, J.; Dole, N.; Eucker, B.; Clark, E. B.; Varner, M.; Taggart, E.; Moye, J.; Miller, R. K.] Natl Childrens Study Placenta Consortium, Bethesda, MD USA.
[Stodgell, C. J.; Salamone, L.; Katzman, P. K.; Ruffolo, L., I; Miller, R. K.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Murray, J.; Busch, T.] Univ Iowa, Sch Med, Iowa City, IA 52242 USA.
[Culhane, J.; Wadlinger, S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Landrigan, P.; Littman, L.] Icahn Sch Med Mt Sinai, New York, NY USA.
[Hiex, N.; Specker, B.] S Dakota State Univ, Brookings, SD 57007 USA.
[Swanson, J.] Univ Calif Irvine, Irvine, CA USA.
[Dole, N.; Eucker, B.] Univ N Carolina, Chapel Hill, NC USA.
[Clark, E. B.; Varner, M.; Taggart, E.] Univ Utah, Salt Lake City, UT USA.
[Moye, J.] NIH, Natl Childrens Study, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD MAY
PY 2013
VL 97
IS 5
SI SI
BP 331
EP 331
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100114
ER
PT J
AU Darrah, TH
White, AM
Campbell, ME
Miller, RK
Stodgell, CJ
Katzman, PJ
Ruffolo, L
Weidenborner, P
Culhane, J
Wadlinger, S
Landrigan, P
Littman, L
Thiex, N
Specker, B
Swanson, J
Dole, N
Eucker, B
Clark, EB
Varner, M
Taggart, E
Moye, J
AF Darrah, T. H.
White, A. M.
Campbell, M. E.
Miller, R. K.
Stodgell, C. J.
Katzman, P. J.
Ruffolo, L.
Weidenborner, P.
Culhane, J.
Wadlinger, S.
Landrigan, P.
Littman, L.
Thiex, N.
Specker, B.
Swanson, J.
Dole, N.
Eucker, B.
Clark, E. B.
Varner, M.
Taggart, E.
Moye, J.
TI Understanding the Trace Metal Composition of Human Placenta from the
National Children's Study (NCS)
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [White, A. M.; Campbell, M. E.; Miller, R. K.; Stodgell, C. J.; Katzman, P. J.; Ruffolo, L.; Weidenborner, P.; Culhane, J.; Wadlinger, S.; Landrigan, P.; Littman, L.; Thiex, N.; Specker, B.; Swanson, J.; Dole, N.; Eucker, B.; Clark, E. B.; Varner, M.; Taggart, E.; Moye, J.] Natl Childrens Study Placenta Consortium, Bethesda, MD USA.
[Darrah, T. H.; White, A. M.; Campbell, M. E.] Duke Univ, Nicholas Sch Environm, Durham, NC 27708 USA.
[Darrah, T. H.] UUMass Boston, Environm Earth & Ocean Sci, Boston, MA USA.
[Miller, R. K.; Stodgell, C. J.; Katzman, P. J.; Ruffolo, L.; Weidenborner, P.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Culhane, J.; Wadlinger, S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Landrigan, P.; Littman, L.] Icahn Sch Med Mt Sinai, New York, NY USA.
[Thiex, N.; Specker, B.] S Dakota State Univ, Brookings, SD 57007 USA.
[Swanson, J.] Univ Calif Irvine, Irvine, CA USA.
[Dole, N.; Eucker, B.] Univ N Carolina, Chapel Hill, NC USA.
[Clark, E. B.; Varner, M.; Taggart, E.] Univ Utah, Salt Lake City, UT USA.
[Moye, J.] NIH, Natl Childrens Study, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 11
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 MAY
PY 2013
VL 97
IS 5
SI SI
BP 332
EP 332
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100115
ER
PT J
AU Salafia, CM
Dalton, JL
Misra, D
Stodgell, CJ
Katzman, PJ
Ruffolo, LI
Culhane, J
Wadlinger, S
Torres, C
Landrigan, P
Littman, L
Sheffield, P
Leuthner, S
Szabo, S
Thiex, N
Specker, B
Swanson, J
Dole, N
Thorp, J
Eucker, B
Clark, EB
Varner, MW
Taggart, E
Durkin, MS
Sandoval, MN
Moye, J
Miller, RK
AF Salafia, C. M.
Dalton, J. L.
Misra, D.
Stodgell, C. J.
Katzman, P. J.
Ruffolo, L., I
Culhane, J.
Wadlinger, S.
Torres, C.
Landrigan, P.
Littman, L.
Sheffield, P.
Leuthner, S.
Szabo, S.
Thiex, N.
Specker, B.
Swanson, J.
Dole, N.
Thorp, J.
Eucker, B.
Clark, E. B.
Varner, M. W.
Taggart, E.
Durkin, M. S.
Sandoval, M-N
Moye, J.
Miller, R. K.
CA Natl Children's Study Placental Re
TI The Chorionic Surface Vascular Network in Human Placenta: Quantifying
Structure to Estimate Gestational Stressors and Life Course Risks,
Autism Spectrum Disorder (ASD) As a Model for Future Analyses: National
Children's Study and EARLI
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Salafia, C. M.; Dalton, J. L.; Misra, D.; Stodgell, C. J.; Katzman, P. J.; Ruffolo, L., I; Culhane, J.; Wadlinger, S.; Torres, C.; Landrigan, P.; Littman, L.; Sheffield, P.; Leuthner, S.; Szabo, S.; Thiex, N.; Specker, B.; Swanson, J.; Dole, N.; Thorp, J.; Eucker, B.; Clark, E. B.; Varner, M. W.; Taggart, E.; Durkin, M. S.; Sandoval, M-N; Moye, J.; Miller, R. K.; Natl Children's Study Placental Re] Natl Childrens Study Placenta Consortium, Bethesda, MD USA.
[Salafia, C. M.; Dalton, J. L.; Misra, D.] Placental Analyt Inc, Larchmont, NY USA.
[Stodgell, C. J.; Katzman, P. J.; Ruffolo, L., I; Miller, R. K.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Culhane, J.; Wadlinger, S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Torres, C.] Columbia Univ, New York, NY USA.
[Landrigan, P.; Littman, L.; Sheffield, P.] Icahn Sch Med Mt Sinai, New York, NY USA.
[Leuthner, S.; Szabo, S.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Thiex, N.; Specker, B.] S Dakota State Univ, Brookings, SD 57007 USA.
[Swanson, J.] Univ Calif Irvine, Irvine, CA USA.
[Dole, N.; Thorp, J.; Eucker, B.] Univ N Carolina, Chapel Hill, NC USA.
[Clark, E. B.; Varner, M. W.; Taggart, E.] Univ Utah, Salt Lake City, UT USA.
[Durkin, M. S.; Sandoval, M-N] Univ Wisconsin, Madison, WI USA.
[Moye, J.] NIH, Natl Childrens Study, Bethesda, MD 20892 USA.
RI Durkin, Maureen/B-7834-2015
NR 0
TC 0
Z9 0
U1 0
U2 5
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 MAY
PY 2013
VL 97
IS 5
SI SI
BP 333
EP 333
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100117
ER
PT J
AU Stanko, JP
Kissling, GE
Fenton, SE
AF Stanko, J. P.
Kissling, G. E.
Fenton, S. E.
TI A Novel Quantitative Method for the Comparison of Mammary Gland
Development in Multiple Strains of Rat
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Meeting Abstract
C1 [Stanko, J. P.; Fenton, S. E.] NIEHS, Natl Toxicol Program Lab, Res Triangle Pk, NC 27709 USA.
[Kissling, G. E.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD MAY
PY 2013
VL 97
IS 5
SI SI
BP 345
EP 345
PG 1
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 171MB
UT WOS:000320932100140
ER
PT J
AU Muallem, S
Verkhratsky, A
AF Muallem, Shmuel
Verkhratsky, Alexei
TI The art of physiology in the hands of the master The Calcium community
celebrates the 70th birthday of Ole Holger Petersen
SO CELL CALCIUM
LA English
DT Editorial Material
ID CAT SUBMANDIBULAR GLAND; ACINAR CELL-MEMBRANES; ENDOPLASMIC-RETICULUM;
SECRETORY POTENTIALS; CA2+; POTASSIUM; RELEASE; SODIUM; STORE;
ACTIVATION
C1 [Muallem, Shmuel] Natl Inst Dent & Craniofacial Res, Epithelial Signaling & Transport Sect, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Verkhratsky, Alexei] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England.
RP Muallem, S (reprint author), Natl Inst Dent & Craniofacial Res, Epithelial Signaling & Transport Sect, Mol Physiol & Therapeut Branch, NIH, Bldg 10,Room 1N-113, Bethesda, MD 20892 USA.
EM Shmuel.muallem@nig.gov; Alexej.Verkhratsky@manchester.ac.uk
RI Verkhratsky, Alexei/J-4527-2013
OI Verkhratsky, Alexei/0000-0003-2592-9898
NR 25
TC 1
Z9 1
U1 0
U2 1
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0143-4160
J9 CELL CALCIUM
JI Cell Calcium
PD MAY-JUN
PY 2013
VL 53
IS 5-6
BP 303
EP 306
DI 10.1016/j.ceca.2013.05.001
PG 4
WC Cell Biology
SC Cell Biology
GA 167LZ
UT WOS:000320634800001
PM 23710829
ER
PT J
AU Medic, N
Desai, A
Olivera, A
Abramowitz, J
Birnbaumer, L
Beaven, MA
Gilfillan, AM
Metcalfe, DD
AF Medic, Nevenka
Desai, Avanti
Olivera, Ana
Abramowitz, Joel
Birnbaumer, Lutz
Beaven, Michael A.
Gilfillan, Alasdair M.
Metcalfe, Dean D.
TI Knockout of the Trpc1 gene reveals that TRPC1 can promote recovery from
anaphylaxis by negatively regulating mast cell TNF-alpha production
SO CELL CALCIUM
LA English
DT Article
DE Anaphylaxis; Calcium; Degranulation; Fc epsilon RI; JUN; KIT; Mast
cells; NFAT; SCF; TNF-alpha; TRPC1
ID FC-EPSILON-RI; SMOOTH-MUSCLE-CELLS; OPERATED CA2+ ENTRY; CALCIUM-ENTRY;
BONE-MARROW; ACTIVATION; RECEPTOR; CHANNEL; RESPONSES; DEGRANULATION
AB Antigen-mediated mast cell (MC) degranulation is the critical early event in the induction of allergic reactions. Transient receptor potential channels (TRPC), particularly TRPC1, are thought to contribute to. such MC activation. To explore the contribution of TRPC1 in MC-driven allergic reactions, we examined antigen-mediated anaphylaxis in Trpc1(-/-) and WT mice, and TRPC1 involvement in the activation of MCs derived from the bone marrow (BMMCs) of these mice. In vivo, we observed a similar induction of passive systemic anaphylaxis in the Tipc1(-/-) mice compared to WT controls. Nevertheless, there was delayed recovery from this response in Trpc1(-/-) mice. Furthermore, contrary to expectations, Trpc1(-/-) BMMCs responded to antigen with enhanced calcium signaling but with little defect in degranulation or associated signaling. In contrast, antigen-mediated production of TNF-alpha, and other cytokines, was enhanced in the Trpc1(-/-) BMMCs, as were calcium-dependent events required for these responses. Additionally, circulating levels of TNF-alpha in response to antigen were preferentially elevated in the Tipc1(-/-) mice, and administration of an anti-TNF-alpha antibody blocked the delay in recovery from anaphylaxis in these mice. These data thus provide evidence that, in this model, TRPC1 promotes recovery from the anaphylactic response by repressing antigen-mediated TNF-alpha release from MCs. Published by Elsevier Ltd.
C1 [Medic, Nevenka; Desai, Avanti; Gilfillan, Alasdair M.; Metcalfe, Dean D.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Olivera, Ana] NIAMSD, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
[Birnbaumer, Lutz; Beaven, Michael A.] NIEHS, Neurobiol Lab, Res Triangle Pk, NC 27709 USA.
[Beaven, Michael A.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Metcalfe, DD (reprint author), NIAID, Lab Allerg Dis, NIH, Bldg 10,Room 11C207,10 Ctr Dr MSC 1881, Bethesda, MD 20892 USA.
EM dmetcalfe@niaid.nih.gov
RI Abramowitz, Joel/A-2620-2015
FU Intramural Research programs within NIAID; NHLBI; NIAMS; NIEHS
[Z01-ES101864]
FX Research in the authors' laboratories was supported by funding from the
Intramural Research programs within NIAID (N.M., A.D., A.M.G., D.D.M.),
the NHLBI (M.A.B), the NIAMS (A.O.) and NIEHS (project Z01-ES101864 to
L.B.).
NR 56
TC 8
Z9 8
U1 3
U2 5
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0143-4160
J9 CELL CALCIUM
JI Cell Calcium
PD MAY-JUN
PY 2013
VL 53
IS 5-6
BP 315
EP 326
DI 10.1016/j.ceca.2013.02.001
PG 12
WC Cell Biology
SC Cell Biology
GA 167LZ
UT WOS:000320634800003
PM 23489970
ER
PT J
AU Paukner, A
Bower, S
Simpson, EA
Suomi, SJ
AF Paukner, Annika
Bower, Seth
Simpson, Elizabeth A.
Suomi, Stephen J.
TI Sensitivity to First-Order Relations of Facial Elements in Infant Rhesus
Macaques
SO INFANT AND CHILD DEVELOPMENT
LA English
DT Article
DE rhesus macaque; infant; face perception; first order relations; eye
tracking
AB Faces are visually attractive to both human and nonhuman primates. Human neonates are thought to have a broad template for faces at birth and prefer face-like to non-face-like stimuli. To better compare developmental trajectories of face processing phylogenetically, here, we investigated preferences for face-like stimuli in infant rhesus macaques using photographs of real faces. We presented infant macaques aged 15-25days with human, macaque and abstract faces with both normal and linear arrangements of facial features and measured infants' gaze durations, number of fixations and latency to look to each face using eye-tracking technology. There was an overall preference for normal over linear facial arrangements for abstract and monkey faces but not human faces. Moreover, infant macaques looked less at monkey faces than at abstract or human faces. These results suggest that species and facial configurations affect face processing in infant macaques, and we discuss potential explanations for these findings. Further, carefully controlled studies are required to ascertain whether infant macaques' face template can be considered as broad as human infants' face template. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Paukner, Annika; Bower, Seth; Simpson, Elizabeth A.; Suomi, Stephen J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, Poolesville, MD USA.
[Simpson, Elizabeth A.] Univ Parma, Dipartimento Neurosci, I-43100 Parma, Italy.
RP Paukner, A (reprint author), NIH, Anim Ctr, POB 529, Poolesville, MD 20837 USA.
EM pauknera@mail.nih.gov
OI Simpson, Elizabeth/0000-0003-2715-2533
FU Intramural NIH HHS [Z99 HD999999]; NICHD NIH HHS [P01 HD064653]
NR 0
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1522-7227
J9 INFANT CHILD DEV
JI Infant Child Dev.
PD MAY-JUN
PY 2013
VL 22
IS 3
BP 320
EP 330
DI 10.1002/icd.1793
PG 11
WC Psychology, Developmental
SC Psychology
GA 161DW
UT WOS:000320172900007
PM 23997657
ER
PT J
AU Beveridge, R
Fox, J
Higgins, SA
Kohn, M
Mahoney, JJ
Newcomer, LN
von Eschenbach, A
AF Beveridge, Roy
Fox, John
Higgins, Susan A.
Kohn, Martin
Mahoney, John J.
Newcomer, Lee N.
von Eschenbach, Andrew
TI The Changing Oncology Landscape: Evolution or Revolution?
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
AB Complex challenges face all players in the oncology landscape, from health care policy leaders and third-party payers, to practicing physicians and nurses, to patients and their families. In these unsteady economic times, possible answers proposed by some may represent part of the problem to others. A distinguished panel assembled at the NCCN 18th Annual Conference: Advancing the Standard of Cancer Care to explore the changing oncology landscape. This article is the synopsis of that discussion, with panelists shedding light on such issues as the astronomic cost of medical care, the need for clinicians to think outside the formulary, and the therapeutic decision-making process in the new world of "big data."
C1 [Beveridge, Roy] US Oncol, The Woodlands, TX USA.
[Beveridge, Roy] US Oncol Network, The Woodlands, TX USA.
[Beveridge, Roy] Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06520 USA.
[Higgins, Susan A.] Yale Univ, Sch Med, Div Obstet & Gynecol, New Haven, CT 06520 USA.
[Higgins, Susan A.] Smilow Canc Hosp, Multidisciplinary Gynecol Dis Team Unit, New Haven, CT USA.
[Higgins, Susan A.] Therapeut Radiol Residency Training Program, New Haven, CT USA.
IBM Res Corp, Care Delivery Syst, San Jose, CA USA.
[Kohn, Martin] Pitney Bowes Inc, Stamford, CT USA.
[Mahoney, John J.] UnitedHlth Grp, Minneapolis, MN USA.
[Newcomer, Lee N.] Pk Nicollet Hlth Serv, St Louis Pk, MN USA.
[Newcomer, Lee N.] Samaritan Hlth Initiat Inc, Montgomery, TX USA.
[von Eschenbach, Andrew] US FDA, Rockville, MD 20857 USA.
[von Eschenbach, Andrew] NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 3
U2 11
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD MAY
PY 2013
VL 11
IS 5.5
SI SI
BP 636
EP 638
PG 3
WC Oncology
SC Oncology
GA 159TX
UT WOS:000320071300003
PM 23704232
ER
PT J
AU Wilson, DM
Bohr, VA
AF Wilson, David M., III
Bohr, Vilhelm A.
TI Special Issue on the segmental progeria Cockayne syndrome Introduction
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Editorial Material
ID DNA-DAMAGE; REPAIR; PROTEIN; DEFECT
C1 [Wilson, David M., III; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, IRP, NIH, Baltimore, MD 21224 USA.
RP Wilson, DM (reprint author), NIA, Lab Mol Gerontol, IRP, NIH, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM wilsonda@mail.nih.gov
FU Intramural NIH HHS [ZIA AG000751-06]
NR 13
TC 2
Z9 2
U1 0
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD MAY-JUN
PY 2013
VL 134
IS 5-6
SI SI
BP 159
EP 160
DI 10.1016/j.mad.2013.04.002
PG 2
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 163RE
UT WOS:000320353800001
PM 23584053
ER
PT J
AU Aamann, MD
Muftuoglu, M
Bohr, VA
Stevnsner, T
AF Aamann, Maria D.
Muftuoglu, Meltem
Bohr, Vilhelm A.
Stevnsner, Tinna
TI Multiple interaction partners for Cockayne syndrome proteins:
Implications for genome and transcriptome maintenance
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article
DE Cockayne syndrome; Protein interactions; DNA repair deficiency;
Transcription deficiency; Mitochondria
ID SYNDROME GROUP-B; BASE EXCISION-REPAIR; RNA-POLYMERASE-II; UV-SENSITIVE
SYNDROME; OXIDATIVE DNA-DAMAGE; COUPLING FACTOR CSB/ERCC6; CSB PROTEIN;
MITOCHONDRIAL-DNA; POLY(ADP-RIBOSE) POLYMERASE-1; CANCER PREDISPOSITION
AB Cockayne syndrome (CS) is characterized by progressive multisystem degeneration and is classified as a segmental premature aging syndrome. The majority of CS cases are caused by defects in the CS complementation group B (CSB) protein and the rest are mainly caused by defects in the CS complementation group A (CSA) protein. Cells from CS patients are sensitive to UV light and a number of other DNA damaging agents including various types of oxidative stress. The cells also display transcription deficiencies, abnormal apoptotic response to DNA damage, and DNA repair deficiencies. Herein we have critically reviewed the current knowledge about known protein interactions of the CS proteins. The review focuses on the participation of the CSB and CSA proteins in many different protein interactions and complexes, and how these interactions inform us about pathways that are defective in the disease. (c) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Aamann, Maria D.; Stevnsner, Tinna] Aarhus Univ, Dept Mol Biol & Genet, Danish Ctr Mol Gerontol, DK-8000 Aarhus C, Denmark.
[Aamann, Maria D.; Stevnsner, Tinna] Aarhus Univ, Dept Mol Biol & Genet, Danish Aging Res Ctr, DK-8000 Aarhus C, Denmark.
[Muftuoglu, Meltem] Koc Univ, Sch Med, Dept Biochem, TR-34450 Istanbul, Turkey.
[Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Stevnsner, T (reprint author), Aarhus Univ, Dept Mol Biol & Genet, Danish Ctr Mol Gerontol, CF Mollers Alle 3,Bldg 1130, DK-8000 Aarhus C, Denmark.
EM tvs@mb.au.dk
FU Intramural Program at the National Institutes on Aging, National
Institutes of Health; Velux Foundation; NovoNordic Foundation
FX We acknowledge support from the Intramural Program at the National
Institutes on Aging, National Institutes of Health, the Velux Foundation
and the NovoNordic Foundation.
NR 92
TC 10
Z9 10
U1 1
U2 11
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD MAY-JUN
PY 2013
VL 134
IS 5-6
SI SI
BP 212
EP 224
DI 10.1016/j.mad.2013.03.009
PG 13
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 163RE
UT WOS:000320353800007
PM 23583689
ER
PT J
AU Scheibye-Knudsen, M
Croteau, DL
Bohr, VA
AF Scheibye-Knudsen, Morten
Croteau, Deborah L.
Bohr, Vilhelm A.
TI Mitochondrial deficiency in Cockayne syndrome
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article
DE Cockayne syndrome; Mitochondria; Aging; Transcription; DNA repair
ID SYNDROME GROUP-B; BASE EXCISION-REPAIR; TRANSCRIPTION-COUPLED REPAIR;
COENZYME-A DEHYDROGENASE; DNA DEPLETION SYNDROME; RNA-POLYMERASE-II;
OXIDATIVE STRESS; SACCHAROMYCES-CEREVISIAE; SENSORY NEUROPATHY;
METABOLIC SYNDROME
AB Cockayne syndrome is a rare inherited disorder characterized by accelerated aging, cachectic dwarfism and many other features. Recent work has implicated mitochondrial dysfunction in the pathogenesis of this disease. This is particularly interesting since mitochondrial deficiencies are believed to be important in the aging process. In this review, we discuss recent findings of mitochondrial pathology in Cockayne syndrome and suggest possible mechanisms for the mitochondrial dysfunction. Published by Elsevier Ireland Ltd.
C1 [Scheibye-Knudsen, Morten; Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Bethesda, MD 20892 USA.
RP Bohr, VA (reprint author), 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM borhv@mail.nih.gov
OI Scheibye-Knudsen, Morten/0000-0002-6637-1280
FU Intramural Research Program of the NIH, National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the NIH, National Institute on Aging.
NR 107
TC 16
Z9 16
U1 3
U2 11
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD MAY-JUN
PY 2013
VL 134
IS 5-6
SI SI
BP 275
EP 283
DI 10.1016/j.mad.2013.02.007
PG 9
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 163RE
UT WOS:000320353800014
PM 23435289
ER
PT J
AU Blumberg, S
Lloyd-Smith, JO
AF Blumberg, Seth
Lloyd-Smith, James O.
TI Inference of R-0 and Transmission Heterogeneity from the Size
Distribution of Stuttering Chains
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID BINOMIAL DISPERSION PARAMETER; MAXIMUM-LIKELIHOOD-ESTIMATION; ACUTE
RESPIRATORY SYNDROME; INFECTIOUS-DISEASES; MEASLES ELIMINATION;
BRANCHING-PROCESS; RISK-FACTORS; EMERGENCE; OUTBREAKS; MONKEYPOX
AB For many infectious disease processes such as emerging zoonoses and vaccine-preventable diseases, 07.0% or insulin use, and blood pressure or cholesterol not at levels recommended by expert consensus panel or medicine to achieve recommended levels. Generalized estimating equations assessed within-study arm relationships of elevated BDI score (>= 11) or ADM use with subsequent year CVD risk status, controlled for demographic variables, CVD history, diabetes duration, and prior CVD risk status.
RESULTS-Prior year elevated BDI was associated with subsequent CVD risk factor positive status for the DSE arm (A1C [odds ratio 1.30 (95% CI 1.09-1.56)]; total cholesterol [0.80 (0.65-1.00)]; i.e., protective from high total cholesterol) and the ILI arm (HDL [1.40 (1.12-1.75)], triglyceride [1.28 (1.00-1.64)]). Prior year ADM use predicted subsequent elevated CVD risk status for the DSE arm (HDL [1.24 (1.03-1.50)], total cholesterol [1.28 (1.05-1.57)], current smoking [1.73 (1.04-2.88)1) and for the ILI arm (A1C [1.25 (1.08-1.46)], HDL [1.32 (1.11-1.58)], triglycerides [1.75 (1.43-2.14)], systolic blood pressure [1.39 (1.11-1.74)], and obesity [1.46 (1.22-2.18)]).
CONCLUSIONS-Aggressive monitoring of CVD risk in diabetic patients with depressive symptoms or who are treated with ADM may be warranted.
C1 [Rubin, Richard R.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Rubin, Richard R.] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA.
[Peyrot, Mark] Loyola Univ Maryland, Dept Sociol, Baltimore, MD USA.
[Gaussoin, Sarah A.; Espeland, Mark A.] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
[Williamson, Don] Pennington Biomed Res Ctr, Div Clin Obes & Metab, Baton Rouge, LA USA.
[Faulconbridge, Lucy F.; Wadden, Thomas A.] Univ Penn, Dept Psychiat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Ewing, Linda] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA.
[Safford, Monika] Univ Alabama Birmingham, Sch Med, Dept Med, Birmingham, AL USA.
[Evans-Hudnall, Gina] Michael E DeBakey VA Med Ctr, Houston VA Hlth Serv Res & Dev Ctr Excellence, Houston, TX USA.
[Evans-Hudnall, Gina] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Wing, Rena R.] Brown Univ, Dept Psychiat & Human Behav, Providence, RI 02912 USA.
[Knowler, William C.] NIDDK, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ USA.
RP Peyrot, M (reprint author), Loyola Univ Maryland, Dept Sociol, Baltimore, MD USA.
EM mpeyrot@loyola.edu
FU Department of Health and Human Services through the National Institutes
of Health (NIH) [DK-57136, DK-57149, DK56990, DK-57177, DK-57171,
DK-57151, DK-57182, DK-57131, DK-57002, DK-57078, DK-57154, DK-57178,
DK-57219, DK-57008, DK-57135, DK-56992]; 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; Intramural Research
Program of the National Institute of Diabetes and Digestive and Kidney
Diseases; Johns Hopkins Medical Institutions Bay-view General Clinical
Research Center [M01-RR-02719]; Massachusetts General Hospital
Mallinckrodt General Clinical Research Center [M01-RR-01066]; University
of Colorado Health Sciences Center General Clinical Research Center [M01
RR00051]; Clinical Nutrition Research Unit [P30 DK48520]; University of
Tennessee at Memphis General Clinical Research Center [M01RR00211-40];
University of Pittsburgh General Clinical Research Center
[M01RR000056-44]; NIH [DK-046204]; University of Washington/VA Puget
Sound Health Care System Medical Research Service, Department of
Veterans Affairs
FX This study is supported by the Department of Health and Human Services
through the following cooperative agreements from the National
Institutes of Health (NIH): DK-57136, DK-57149, DK56990, DK-57177,
DK-57171, DK-57151, DK-57182, DK-57131, DK-57002, DK-57078, DK-57154,
DK-57178, DK-57219, DK-57008, DK-57135, and DK-56992. 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. This
research was supported in part by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases. The
Indian Health Service (IHS) provided personnel, medical oversight, and
use of facilities. The opinions expressed in this article are those of
the authors and do not necessarily reflect the views of the IHS or other
funding sources. Additional support was received from The Johns Hopkins
Medical Institutions Bay-view General Clinical Research Center
(M01-RR-02719); the Massachusetts General Hospital Mallinckrodt General
Clinical Research Center (M01-RR-01066); the University of Colorado
Health Sciences Center General Clinical Research Center (M01 RR00051)
and Clinical Nutrition Research Unit (P30 DK48520); the University of
Tennessee at Memphis General Clinical Research Center (M01RR00211-40);
the University of Pittsburgh General Clinical Research Center
(M01RR000056-44) and NIH Grant DK-046204; and the University of
Washington/VA Puget Sound Health Care System Medical Research Service,
Department of Veterans Affairs.
NR 34
TC 13
Z9 13
U1 2
U2 18
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1088
EP 1094
DI 10.2337/dc12-1871
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100005
PM 23359362
ER
PT J
AU Gadgil, MD
Appel, LJ
Yeung, E
Anderson, CAM
Sacks, FM
Miller, ER
AF Gadgil, Meghana D.
Appel, Lawrence J.
Yeung, Edwina
Anderson, Cheryl A. M.
Sacks, Frank M.
Miller, Edgar R., III
TI The Effects of Carbohydrate, Unsaturated Fat, and Protein Intake on
Measures of Insulin Sensitivity
SO DIABETES CARE
LA English
DT Article
ID TYPE-2 DIABETES-MELLITUS; LIFE-STYLE INTERVENTION;
CORONARY-HEART-DISEASE; APOLIPOPROTEIN C-III; BETA-CELL FUNCTION;
GLUCOSE-TOLERANCE; RISK-FACTORS; CARDIOVASCULAR RISK; MEDITERRANEAN
DIET; OMNIHEART TRIAL
AB OBJECTIVE-Impaired insulin sensitivity increases the risk of cardiovascular disease. Although calorie restriction and weight loss increase insulin sensitivity, the effects of modifying macronutrient composition on insulin sensitivity are uncertain. The purpose of this study is to determine the effects on insulin sensitivity of a carbohydrate-rich diet (CARB; similar to the Dietary Approaches to Stop Hypertension [DASH] diet), a protein-rich diet (PROT; protein predominantly from plant sources), and an unsaturated fat rich diet (UNSAT; predominantly monounsaturated).
RESEARCH DESIGN AND METHODS-This study was a randomized, controlled, three-period, crossover feeding study. The study participants were 164 individuals with prehypertension or stage 1 hypertension without diabetes. Diets were administered for 6 weeks each, with a washout period between diets of 2-4 weeks. Weight was held constant throughout the study. For our primary outcome, we calculated the quantitative insulin sensitivity check index (QUICKI) using the end-of-period fasting serum glucose and insulin. QUICKI is a validated measure of insulin sensitivity. The primary analyses used generalized estimating equations.
RESULTS-At baseline, mean (SD) BMI was 30.2 (6.1) kg/m(2), and mean (SD) QUICKI was 0.35 (0.04). The UNSAT diet increased QUICKI by 0.005, more than the CARB diet (P = 0.04). PROT had no significant effect compared with CARB.
CONCLUSIONS-A diet that partially replaces carbohydrate with unsaturated fat may improve insulin sensitivity in a population at risk for cardiovascular disease. Given the well-recognized challenges of sustaining weight loss, our results suggest an alternative approach for improving insulin sensitivity.
C1 [Gadgil, Meghana D.; Appel, Lawrence J.; Miller, Edgar R., III] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Appel, Lawrence J.; Anderson, Cheryl A. M.; Miller, Edgar R., III] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Appel, Lawrence J.; Anderson, Cheryl A. M.; Miller, Edgar R., III] Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Yeung, Edwina] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Epidemiol Branch, Bethesda, MD USA.
[Sacks, Frank M.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Sacks, Frank M.] Harvard Univ, Sch Med, Channing Lab, Dept Med, Boston, MA 02115 USA.
[Sacks, Frank M.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Gadgil, MD (reprint author), Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
EM mgadgil2@jhmi.edu
RI Yeung, Edwina/F-5992-2015
OI Yeung, Edwina/0000-0002-3851-2613
FU National Heart, Lung, and Blood Institute [T32-HL-007180]; Optimal
Macronutrient Intake to Prevent Heart Disease from the National
Institutes of Health [HL-67098, DK-63214, HL-68712, RR-02635];
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health
FX Funding for this study was provided by grants from the National Heart,
Lung, and Blood Institute (T32-HL-007180) and the Optimal Macronutrient
Intake to Prevent Heart Disease (HL-67098, DK-63214, HL-68712, and
RR-02635) from the National Institutes of Health. E.H.Y. was supported
by the Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, National
Institutes of Health.
NR 41
TC 26
Z9 26
U1 0
U2 10
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1132
EP 1137
DI 10.2337/dc12-0869
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100012
PM 23223345
ER
PT J
AU Jensen, MK
Bartz, TM
Mukamal, KJ
Djousse, L
Kizer, JR
Tracy, RP
Zieman, SJ
Rimm, EB
Sscovick, DS
Shlipak, M
Ix, JH
AF Jensen, Majken K.
Bartz, Traci M.
Mukamal, Kenneth J.
Djousse, Luc
Kizer, Jorge R.
Tracy, Russell P.
Zieman, Susan J.
Rimm, Eric B.
Siscovick, David S.
Shlipak, Michael
Ix, Joachim H.
TI Fetuin-A, Type 2 Diabetes, and Risk of Cardiovascular Disease in Older
Adults The Cardiovascular Health Study
SO DIABETES CARE
LA English
DT Article
ID ALPHA(2)-HEREMANS-SCHMID GLYCOPROTEIN/FETUIN-A; RECEPTOR TYROSINE
KINASE; INSULIN-RESISTANCE; ASSOCIATION; INHIBITOR; SERUM;
CALCIFICATION; MORTALITY; DIALYSIS; MELLITUS
AB OBJECTIVE-Fetuin-A, a hepatic secretory protein that simultaneously inhibits arterial calcification and insulin action, is associated with type 2 diabetes, but its association with cardiovascular disease (CVD) is uncertain. Preliminary studies suggest that the association of fetuin-A with CVD might differ among individuals with or without type 2 diabetes.
RESEARCH DESIGN AND METHODS-This was a prospective study of 3,810 community-living individuals older than 65 years (511 with type 2 diabetes) and free of CVD in 1992 when fetuin-A levels were measured. Participants were followed-up for incident CVD through June 2008.
RESULTS-Mean age was 75 years, and 61% were women; 1,456 participants had an incident CVD event (248 among individuals with type 2 diabetes). The association of fetuin-A with CVD was modified by type 2 diabetes (P interaction = 0.02). Higher fetuin-A was associated with lower CVD risk among persons without type 2 diabetes [hazard ratio per SD 0.1 g/L higher fetuin-A, 0.93 (95% Cl, 0.88-0.99)], whereas a trend in the opposite direction was observed among individuals with type 2 diabetes, although it was not statistically significant [1.07 (0.93 1.22)]. Among individuals without type 2 diabetes, similar effect modification was observed by obesity and insulin resistance. Consistently, higher fetuin-A was associated with lower CVD risk only in the subgroups without obesity or with HOMA-IR below the median [0.91 (0.85-0.97) and 0.87 (0.79-0.95), respectively].
CONCLUSIONS-The association of fetuin-A with risk of CVD differs among elderly individuals with and without insulin resistance or type 2 diabetes.
C1 [Jensen, Majken K.; Rimm, Eric B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Bartz, Traci M.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Djousse, Luc] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Aging, Boston, MA USA.
[Djousse, Luc] Boston Vet Affairs Healthcare Syst, Boston, MA USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Epidemiol, Bronx, NY 10467 USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Populat Hlth, Bronx, NY 10467 USA.
[Tracy, Russell P.] Univ Vermont, Colchester Res Facil, Dept Pathol, Colchester, VT USA.
[Zieman, Susan J.] NIA, NIH, Bethesda, MD 20892 USA.
[Rimm, Eric B.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA USA.
[Siscovick, David S.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Siscovick, David S.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Shlipak, Michael] Univ Calif San Francisco, San Francisco Vet Affairs Med Ctr, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Shlipak, Michael] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Shlipak, Michael] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
[Shlipak, Michael] Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA.
[Ix, Joachim H.] Univ Calif San Diego, Vet Affairs San Diego Healthcare Syst, Nephrol Sect, San Diego, CA 92103 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Nephrol, San Diego, CA 92103 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Prevent Med, San Diego, CA 92103 USA.
RP Jensen, MK (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
EM mkjensen@hsph.harvard.edu
RI Djousse, Luc/F-5033-2017
OI Djousse, Luc/0000-0002-9902-3047
FU National Heart, Lung, and Blood Institute (NHLBI) [R01 HL094555]; NHLBI
[N01 HC-85079, N01 HC-85080, N01 HC-85081, N01 HC-85082, N01 HC-85083,
N01 HC-85084, N01 HC-85085, N01HC-85086, N01-HC-35129, N01 HC-15103, N01
HC-55222, N01 HC-75150, N01 HC-54133, N01-HC85239, U01 HL080295]
FX The study was supported by a National Heart, Lung, and Blood Institute
(NHLBI) grant (R01 HL094555). The CHS was supported by contract numbers
N01 HC-85079 through N01HC-85086, N01-HC-35129, N01 HC-15103, N01
HC-55222, N01 HC-75150, N01 HC-54133, and N01-HC85239, and grant number
U01 HL080295 from the NHLBI, with additional contributions from the
National Institute of Neurologic Disorders and Stroke. This material is
the result of work supported with resources of the VA San Diego
Healthcare System.
NR 31
TC 39
Z9 41
U1 1
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1222
EP 1228
DI 10.2337/dc12-1591
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100026
PM 23250801
ER
PT J
AU Reis, JP
Hankinson, AL
Loria, CM
Lewis, CE
Powell-Wiley, T
Wei, GS
Liu, K
AF Reis, Jared P.
Hankinson, Arlene L.
Loria, Catherine M.
Lewis, Cora E.
Powell-Wiley, Tiffany
Wei, Gina S.
Liu, Kiang
TI Duration of Abdominal Obesity Beginning in Young Adulthood and Incident
Diabetes Through Middle Age The CARDIA Study
SO DIABETES CARE
LA English
DT Article
ID BODY-MASS INDEX; ARTERIAL-HYPERTENSION; METABOLIC SYNDROME;
UNITED-STATES; WEIGHT CHANGE; RISK-FACTOR; MELLITUS; FAT; MEN;
HYPERLIPIDEMIA
AB OBJECTIVE-To examine whether the duration of abdominal obesity determined prospectively using measured waist circumference (WC) is associated with the development of new-onset diabetes independent of the degree of abdominal adiposity.
RESEARCH DESIGN AND METHODS-The Coronary Artery Risk Development in Young Adults Study is a multicenter, community-based, longitudinal cohort study of 5,115 white and black adults aged 18-30 years in 1985 to 1986. Years spent abdominally obese were calculated for participants without abdominal obesity (WC >102 cm in men and >88 cm in women) or diabetes at baseline (n = 4,092) and was based upon repeat measurements conducted 2, 5, 7, 10, 15, 20, and 25 years later.
RESULTS-Over 25 years, 392 participants developed incident diabetes. Overall, following adjustment for demographics, family history of diabetes, study center, and time varying WC, energy intake, physical activity, smoking, and alcohol, each additional year of abdominal obesity was associated with a 4% higher risk of developing diabetes [hazard ratio (HR) 1.04 (95% Cl 1.02-1.07)]. However, a quadratic model best represented the data. HRs for 0, 1-5, 6-10, 11-15, 16-20, and >20 years of abdominal obesity were 1.00 (referent), 2.06 (1.43-2.98), 3.45 (2.28-5.22), 3.43 (2.28-5.22), 2.80 (1.73-4.54), and 2.91 (1.60-5.29), respectively; P-quadratic < 0.001.
CONCLUSIONS-Longer duration of abdominal obesity was associated with substantially higher risk for diabetes independent of the degree of abdominal adiposity. Preventing or at least delaying the onset of abdominal obesity in young adulthood may lower the risk of developing diabetes through middle age.
C1 [Reis, Jared P.; Loria, Catherine M.; Wei, Gina S.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Hankinson, Arlene L.; Liu, Kiang] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Lewis, Cora E.] Univ Alabama Birmingham, Dept Med, Div Prevent Med, Birmingham, AL 35294 USA.
[Powell-Wiley, Tiffany] NHLBI, Cardiovasc & Pulm Branch, Bethesda, MD 20892 USA.
[Powell-Wiley, Tiffany] NCI, Appl Res Program, Div Canc Control & Populat Studies, Bethesda, MD 20892 USA.
RP Reis, JP (reprint author), NHLBI, Div Cardiovasc Sci, Bldg 10, Bethesda, MD 20892 USA.
EM reisjp@mail.nih.gov
FU National Heart, Lung, and Blood Institute (NHLBI); University of Alabama
at Birmingham [N01-HC-95095, N01-HC-48047]; Kaiser Foundation Research
Institute [N01-HC-48050]; Northwestern University [N01-HC-48049];
University of Minnesota [N01-HC-48048]; Division of Intramural Research
of the NHLBI
FX The CARDIA Study is conducted and supported by the National Heart, Lung,
and Blood Institute (NHLBI) in collaboration with the University of
Alabama at Birmingham (N01-HC-95095 and N01-HC-48047), Kaiser Foundation
Research Institute (N01-HC-48050), Northwestern University
(N01-HC-48049), and the University of Minnesota (N01-HC-48048). T.P.-W.
is supported by the Division of Intramural Research of the NHLBI.
NR 30
TC 17
Z9 18
U1 0
U2 3
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1241
EP 1247
DI 10.2337/dc12-1714
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100029
PM 23248193
ER
PT J
AU Gerstein, HC
Ambrosius, WT
Danis, R
Ismail-Beigi, F
Cushman, W
Calles, J
Banerji, M
Schubart, U
Chew, EY
AF Gerstein, Hertzel C.
Ambrosius, Walter T.
Danis, Ronald
Ismail-Beigi, Faramarz
Cushman, William
Calles, Jorge
Banerji, MaryAnn
Schubart, Ulrich
Chew, Emily Y.
CA ACCORD Study Grp
TI Diabetic Retinopathy, Its Progression, and Incident Cardiovascular
Events in the ACCORD Trial
SO DIABETES CARE
LA English
DT Article
ID ATHEROSCLEROSIS RISK; VASA VASORUM; DISEASE; MORTALITY; TYPE-1;
COMPLICATIONS; COMMUNITIES; MELLITUS
AB OBJECTIVE-Both the presence of diabetic retinopathy and its severity are significantly associated with future cardiovascular (CV) events. Whether its progression is also linked to incident CV outcomes hasn't been assessed.
RESEARCH DESIGN AND METHODS-The relationship between retinopathy, its 4-year progression, and CV outcomes (CV death or nonfatal myocardial infarction or stroke) was analyzed in participants in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial who also participated in the ACCORD Eye Study. Retinopathy was classified as either none, mild, moderate, or severe, and worsening was classified as a <2-step, 2-3-step, or >3-step change (that included incident laser therapy or vitrectomy).
RESULTS-Participants (n = 3,433) of mean age 61 years had baseline retinal photographs (seven stereoscopic fields). Compared with no retinopathy, the adjusted HRs (95% CI) for the CV outcome rose from 1.49 (1.12-1.97) for mild retinopathy to 2.35 (1.47-3.76) for severe retinopathy. A subset of 2,856 was evaluated for progression of diabetic retinopathy at 4 years. The hazard of the primary outcome increased by 38% (1.38 [1.10-1.74]) for every category of change in retinopathy severity. Additional adjustment for the baseline and follow-up levels of A1C, systolic blood pressure, and lipids either individually or together rendered the relationships between worsening and CV outcomes nonsignificant.
CONCLUSIONS-Both the severity of retinopathy and its progression are determinants of incident CV outcomes. The retina may provide an anatomical index of the effect of metabolic and hemodynamic factors on future CV outcomes.
C1 [Gerstein, Hertzel C.] McMaster Univ & Hamilton Hlth Sci, Dept Med, Hamilton, ON, Canada.
[Gerstein, Hertzel C.] McMaster Univ & Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada.
[Ambrosius, Walter T.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Danis, Ronald] Univ Wisconsin, Sch Med & Publ Hlth, Dept Ophthalmol & Visual Sci, Madison, WI USA.
[Ismail-Beigi, Faramarz] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Ismail-Beigi, Faramarz] Cleveland VA Med Ctr, Cleveland, OH USA.
[Cushman, William] Memphis Vet Affairs Med Ctr, Memphis, TN USA.
[Calles, Jorge] Metrohlth Syst, Cleveland, OH USA.
[Calles, Jorge] Case Western Reserve Univ Sch Med, Cleveland, OH USA.
[Banerji, MaryAnn] Suny Downstate Med Ctr, Brooklyn, NY 11203 USA.
[Banerji, MaryAnn] Kings Country Hosp Ctr, Brooklyn, NY USA.
[Schubart, Ulrich] North Bronx Healthcare Network, Bronx, NY USA.
[Schubart, Ulrich] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Chew, Emily Y.] NEI, NIH, Bethesda, MD 20892 USA.
RP Gerstein, HC (reprint author), McMaster Univ & Hamilton Hlth Sci, Dept Med, Hamilton, ON, Canada.
EM gerstein@mcmaster.ca
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX The Department of Ophthalmology and Visual Sciences (School of Medicine
and Public Health, University of Wisconsin) is funded by the National
Institute of Diabetes and Digestive and Kidney Diseases as a reading
center for fundus photographs.
NR 20
TC 24
Z9 25
U1 1
U2 9
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1266
EP 1271
DI 10.2337/dc12-1311
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100033
PM 23238658
ER
PT J
AU Jakicic, JM
Egan, CM
Fabricatore, AN
Gaussoin, SA
Glasser, SP
Hesson, LA
Knowler, WC
Lang, W
Regensteiner, JG
Ribisl, PM
Ryan, DH
AF Jakicic, John M.
Egan, Caitlin M.
Fabricatore, Anthony N.
Gaussoin, Sarah A.
Glasser, Stephen P.
Hesson, Louise A.
Knowler, William C.
Lang, Wei
Regensteiner, Judith G.
Ribisl, Paul M.
Ryan, Donna H.
CA Look AHEAD Res Grp
TI Four-Year Change in Cardiorespiratory Fitness and Influence on Glycemic
Control in Adults With Type 2 Diabetes in a Randomized Trial The Look
AHEAD Trial
SO DIABETES CARE
LA English
DT Article
ID LIFE-STYLE INTERVENTION; ALL-CAUSE MORTALITY; CARDIOVASCULAR-DISEASE
MORTALITY; BODY-MASS INDEX; WEIGHT-LOSS; PHYSICAL-ACTIVITY;
RISK-FACTORS; WOMEN; MEN; OVERWEIGHT
AB OBJECTIVE-To examine an intensive lifestyle intervention (ILI) compared with diabetes support and education (DSE) on 4-year change in fitness and physical activity (PA), and to examine the effect of change in fitness and PA, adjusting for potential confounders, on glycemic control in the Look AHEAD Trial.
RESEARCH DESIGN AND METHODS-Subjects were overweight/obese adults with type 2 diabetes mellitus (T2DM) with available fitness data at 4 years (n = 3,942).This clinical trial randomized subjects to DSE or ILI. DSE subjects received standard care plus information related to diet, PA, and social support three times per year. ILL subjects received weekly intervention contact for 6 months, which was reduced over the 4-year period, and were prescribed diet and PA. Measures included weight, fitness, PA, and HbA(1c).
RESULTS-The difference in percent fitness change between ILI and DSE at 4 years was significant after adjustment for baseline fitness and change in weight (3.70 vs. 0.94%; P < 0.01). At 4 years, PA increased by 348 (1,562) kcal/week in ILI vs. 105 (1,309) kcal/week in DSE (P < 0.01). Fitness change at 4 years was inversely related to change in HbA(1c) after adjustment for clinical site, treatment, baseline HbA(1c), prescribed diabetes medication, baseline fitness, and weight change (P < 0.01). Change in PA was not related to change in HbA(1c).
CONCLUSIONS-A 4-year ILI increased fitness and PA in overweight/obese individuals with T2DM. Change in fitness was associated with improvements in glycemic control, which provides support for interventions to improve fitness in adults with T2DM.
C1 [Jakicic, John M.] Univ Pittsburgh, Dept Hlth & Phys Act, Phys Act & Weight Management Res Ctr, Pittsburgh, PA 15260 USA.
[Egan, Caitlin M.] Miriam Hosp, Weight Control & Diabet Res Ctr, Providence, RI 02906 USA.
[Fabricatore, Anthony N.] Univ Penn, Weight & Eating Disorders Program, Philadelphia, PA 19104 USA.
[Gaussoin, Sarah A.; Lang, Wei] Wake Forest Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Glasser, Stephen P.] Univ Alabama Birmingham, Birmingham, AL USA.
[Hesson, Louise A.] Univ Penn, Philadelphia, PA 19104 USA.
[Knowler, William C.] NIDDKD, Southwest Amer Indian Ctr, NIH, Phoenix, AZ USA.
[Regensteiner, Judith G.] Univ Colorado, Div Gen Internal Med, Denver, CO 80202 USA.
[Ribisl, Paul M.] Wake Forest Univ, Dept Hlth & Exercise Sci, Winston Salem, NC 27109 USA.
[Ryan, Donna H.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
RP Jakicic, JM (reprint author), Univ Pittsburgh, Dept Hlth & Phys Act, Phys Act & Weight Management Res Ctr, Pittsburgh, PA 15260 USA.
EM jjakicic@pitt.edu
OI Glasser, Stephen/0000-0001-9620-6406
FU BodyMedia, Inc.; 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; Department of
Veterans Affairs; Johns Hopkins Bayview General Clinical Research Center
[M01RR02719]; Massachusetts General Hospital Mallinckrodt General
Clinical Research Center; Massachusetts Institute of Technology General
Clinical Research Center [M01RR01066]; University of Colorado Health
Sciences Center General Clinical Research Center [M01RR00051]; Clinical
Nutrition Research Unit [P30 DK48520]; University of Tennessee at
Memphis General Clinical Research Center [M01RR0021140]; University of
Pittsburgh General Clinical Research Center (GCRC) [M01RR000056];
Clinical Translational Research Center (CTRC); Clinical & Translational
Science Award [UL1 RR 024153]; National Institutes of Health [DK
046204]; Frederic C. Banter General Clinical Research Center
[M01RR01346]
FX J.M.J. is supported by grants from BodyMedia, Inc.; has been paid by
Nestle Nutrition Institute for lectures and manuscript preparation; and
is a member of the Scientific Advisory Board for Alere Wellbeing. A.N.F.
is employed by and has stock options with Nutrisystem, Inc. 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; the Centers for Disease Control
and Prevention; and the Department of Veterans Affairs. This research
was supported in part by the Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases. The Indian
Health Service (IHS) provided personnel, medical oversight, and use of
facilities.; Additional support was received from The Johns Hopkins
Bayview General Clinical Research Center (M01RR02719); the Massachusetts
General Hospital Mallinckrodt General Clinical Research Center and the
Massachusetts Institute of Technology General Clinical Research Center
(M01RR01066); the University of Colorado Health Sciences Center General
Clinical Research Center (M01RR00051) and Clinical Nutrition Research
Unit (P30 DK48520); the University of Tennessee at Memphis General
Clinical Research Center (M01RR0021140); the University of Pittsburgh
General Clinical Research Center (GCRC) (M01RR000056), the Clinical
Translational Research Center (CTRC) funded by the Clinical &
Translational Science Award (UL1 RR 024153) and a National Institutes of
Health grant (DK 046204); and the Frederic C. Banter General Clinical
Research Center (M01RR01346).
NR 20
TC 24
Z9 24
U1 0
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1297
EP 1303
DI 10.2337/dc12-0712
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100038
PM 23223405
ER
PT J
AU Chakkera, HA
Weil, EJ
Pham, PT
Pomeroy, J
Knowler, WC
AF Chakkera, Harini A.
Weil, E. Jennifer
Phuong-Thu Pham
Pomeroy, Jeremy
Knowler, William C.
TI Can New-Onset Diabetes After Kidney Transplant Be Prevented?
SO DIABETES CARE
LA English
DT Review
ID IMPAIRED GLUCOSE-TOLERANCE; BODY-MASS INDEX;
RANDOMIZED-CONTROLLED-TRIAL; RENAL-ALLOGRAFT RECIPIENTS; LIFE-STYLE
INTERVENTION; HEMODIALYSIS-PATIENTS; INSULIN SENSITIVITY;
PHYSICAL-ACTIVITY; FASTING GLUCOSE; MELLITUS
AB Because the negative consequences of new-onset diabetes mellitus after transplantation (NODAT) diminish the significant gains of kidney transplantation, it is imperative to develop clinical interventions to reduce the incidence of NODAT. In this review, we discuss whether intensive lifestyle interventions that delay or prevent type 2 diabetes mellitus may decrease the incidence of NODAT. We examine the literature pertaining to incidence and timing of onset of NODAT, as well as the risk factors and pathophysiology that NODAT shares with type 2 diabetes mellitus, namely pathways related to increased insulin resistance and decreased insulin secretion. Our central hypothesis is that NODAT results from the same metabolic risk factors that underlie type 2 diabetes mellitus. These risk factors are altered and enhanced by transplantation, "tipping" some transplant recipients with seemingly normal glucose homeostasis before transplant toward the development of NODAT. We describe the diabetogenic properties of transplant immunosuppressive drugs. We describe novel methods of prevention that are being explored, including resting the pancreatic beta-cells by administration of basal insulin during the period immediately after transplant. On the basis of the current evidence, we propose that intensive lifestyle modification, adapted for individuals with chronic kidney disease or end-stage renal disease, as well as resting pancreatic beta-cells during the immediate postoperative period, may lower the incidence of NODAT.
C1 [Chakkera, Harini A.] Mayo Clin, Div Transplantat, Phoenix, AZ USA.
[Weil, E. Jennifer; Pomeroy, Jeremy; Knowler, William C.] NIDDKD, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ USA.
[Phuong-Thu Pham] Univ Calif Los Angeles, Dept Internal Med, Hlth Syst, Los Angeles, CA USA.
[Phuong-Thu Pham] Univ Calif Los Angeles, Dept Nephrol, Hlth Syst, Los Angeles, CA USA.
RP Chakkera, HA (reprint author), Mayo Clin, Div Transplantat, Phoenix, AZ USA.
EM chakkera.harini@mayo.edu
NR 61
TC 26
Z9 29
U1 1
U2 9
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1406
EP 1412
DI 10.2337/dc12-2067
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100052
PM 23613600
ER
PT J
AU Song, YQ
Wang, L
Pittas, AG
Del Gobbo, LC
Zhang, CL
Manson, JE
Hu, FB
AF Song, Yiqing
Wang, Lu
Pittas, Anastassios G.
Del Gobbo, Liana C.
Zhang, Cuilin
Manson, JoAnn E.
Hu, Frank B.
TI Blood 25-Hydroxy Vitamin D Levels and Incident Type 2 Diabetes
SO DIABETES CARE
LA English
DT Article
ID DOSE-RESPONSE DATA; METABOLIC SYNDROME; GLUCOSE-TOLERANCE; D
SUPPLEMENTATION; CONTROLLED-TRIAL; SERUM 25(OH)D; D DEFICIENCY; US
ADULTS; RISK; METAANALYSIS
AB OBJECTIVE-To quantitatively assess the strength and shape of the association between blood 25-hydroxy vitamin D [25(OH)D] levels and incident risk of type 2 diabetes.
RESEARCH DESIGN AND METHODS-A systematic search of the MEDLINE and Embase databases and a hand search of references from original reports were conducted up to 31 October 2012. Prospective observational studies that assessed the association between blood levels of 25(OH)D and risk of incident type 2 diabetes were included for meta-analysis. DerSimonian and Laird's random-effects model was used. A quadratic spline regression analysis was used to examine the shape of the association with a generalized least-squares trend test performed for the dose-response relation.
RESULTS-A total of 21 prospective studies involving 76,220 participants and 4,996 incident type 2 diabetes cases were included for meta-analysis. Comparing the highest to the lowest category of 25(OH)D levels, the summary relative risk for type 2 diabetes was 0.62 (95% CI 0.54-0.70). A spline regression model showed that higher 25(OH)D levels were monotonically associated with a lower diabetes risk. This inverse association did not differ by sex, duration of follow-up, study sample size, diabetes diagnostic criteria, or 25(OH)D assay method. A linear trend analysis showed that each 10 nmol/L increment in 25(OH)D levels was associated with a 4% lower risk of type 2 diabetes (95% CI 3-6; P for linear trend < 0.0001).
CONCLUSIONS-Our meta-analysis showed an inverse and significant association between circulating 25(OH)D levels and risk of type 2 diabetes across a broad range of blood 25(OH)D levels in diverse populations.
C1 [Song, Yiqing; Wang, Lu; Manson, JoAnn E.] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.
[Song, Yiqing; Wang, Lu; Manson, JoAnn E.; Hu, Frank B.] Harvard Univ, Sch Med, Boston, MA USA.
[Pittas, Anastassios G.] Tufts Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA USA.
[Del Gobbo, Liana C.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD USA.
[Manson, JoAnn E.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Hu, Frank B.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
RP Song, YQ (reprint author), Brigham & Womens Hosp, Dept Med, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA.
EM ysong3@rics.bwh.harvard.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[R01-DK-58845, R01-DK-088078]; National Institutes of Health (NIH);
NIDDK [R01-DK-76092, U34-DK-91958]; Office of the Director-NIH; NIH
Office of Dietary Supplements; NIH/Eunice Kennedy Shriver National
Institute of Child Health & Human Development; NIH
FX This work was supported by grants R01-DK-58845 and R01-DK-088078 (to
Y.S.) from the National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK) and the National Institutes of Health (NIH). Y.S. is
the Principal Investigator of an ancillary study (R01-DK-088078)
investigating diabetes prevention in the VITamin D and OmegA-3 TriaL
(VITAL). A.G.P. was supported by grants R01-DK-76092 and U34-DK-91958
from the NIDDK, the Office of the Director-NIH, and the NIH Office of
Dietary Supplements. C.Z. was supported by the Intramural Research
Program of the NIH/Eunice Kennedy Shriver National Institute of Child
Health & Human Development. J.E.M. is the Principal Investigator of the
parent VITAL study, a large-scale randomized trial of vitamin D and
omega-3 fatty acids for the prevention of cancer and cardiovascular
disease and funded by the NIH.
NR 42
TC 113
Z9 120
U1 3
U2 21
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2013
VL 36
IS 5
BP 1422
EP 1428
DI 10.2337/dc12-0962
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 155WW
UT WOS:000319782100054
PM 23613602
ER
PT J
AU Behrens, G
Fischer, B
Kohler, S
Park, Y
Hollenbeck, AR
Leitzmann, MF
AF Behrens, Gundula
Fischer, Beate
Kohler, Simone
Park, Yikyung
Hollenbeck, Albert R.
Leitzmann, Michael F.
TI Healthy lifestyle behaviors and decreased risk of mortality in a large
prospective study of U.S. women and men
SO EUROPEAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE Waist circumference; Physical activity; Smoking; Diet; Lifestyle;
Mortality
ID ALL-CAUSE MORTALITY; RETIRED-PERSONS DIET; PHYSICAL-ACTIVITY;
MEDITERRANEAN DIET; CARDIOVASCULAR-DISEASE; PROSPECTIVE COHORT; 10-YEAR
MORTALITY; AMERICAN-ASSOCIATION; NATIONAL-INSTITUTES; METABOLIC SYNDROME
AB Adiposity, insufficient physical activity, cigarette smoking, and poor diet have all been related independently to increased chronic disease risk, but their joint impact on overall health remains unclear. In a cohort of 170,672 women and men aged 51-71 years at baseline in 1996/1997 and followed-up through 2009, we investigated the individual and joint impact of four low-risk lifestyle factors: abdominal leanness (waist circumference < 88 cm in women and < 102 cm in men); recommended physical activity level (30 min or more of moderate exercise at least 5 times per week or 20 min or more of vigorous exercise at least 3 times per week); long-term non-smoking (never-smoker or quit smoking more than 10 years ago); and healthy diet (Mediterranean diet score within the upper two sex-specific quintiles). During 2,126,089 person-years of follow-up, 20,903 participants died. In multivariate Cox models, statistically significant decreased risks of mortality were observed for the low-risk factors abdominal leanness (relative risk (RR) = 0.86; 95 % confidence interval (CI) = 0.83-0.89), physical activity (RR = 0.86; 95 % CI = 0.84-0.89), non-smoking (RR = 0.43; 95 % CI = 0.42-0.45), and healthy diet (RR = 0.86; 95 % CI = 0.83-0.88). The larger the number of low-risk lifestyle factors, the lower was the mortality risk. The RR comparing adherence to all versus none of the factors was 0.27 (95 % CI = 0.25-0.29). We estimate that 33 % (95 % CI = 30-35 %) of deaths in our cohort were premature and could have been avoided if all study participants had adhered to all low-risk factors.
C1 [Behrens, Gundula; Fischer, Beate; Kohler, Simone; Leitzmann, Michael F.] Univ Regensburg, Med Ctr, Dept Epidemiol & Prevent Med, D-93053 Regensburg, Germany.
[Park, Yikyung] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Behrens, G (reprint author), Univ Regensburg, Med Ctr, Dept Epidemiol & Prevent Med, Franz Josef Strauss Allee 11, D-93053 Regensburg, Germany.
EM Gundula.Behrens@klinik.uni-regensburg.de
OI Behrens, Gundula/0000-0002-9355-6491; Park, Yikyung/0000-0002-6281-489X
NR 66
TC 22
Z9 22
U1 2
U2 21
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0393-2990
J9 EUR J EPIDEMIOL
JI Eur. J. Epidemiol.
PD MAY
PY 2013
VL 28
IS 5
BP 361
EP 372
DI 10.1007/s10654-013-9796-9
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 158UC
UT WOS:000319998000001
PM 23532745
ER
PT J
AU Li, LS
Simonsick, EM
Ferrucci, L
Lin, FR
AF Li, Lingsheng
Simonsick, Eleanor M.
Ferrucci, Luigi
Lin, Frank R.
TI Hearing loss and gait speed among older adults in the United States
SO GAIT & POSTURE
LA English
DT Article
DE Gait speed; Hearing loss; Epidemiology; Older adults
ID NUTRITION-EXAMINATION-SURVEY; VESTIBULAR FUNCTION; EXECUTIVE FUNCTION;
BODY-COMPOSITION; NATIONAL-HEALTH; COGNITION; AGE; ASSOCIATION;
PREVALENCE; DECLINE
AB Background: Previous studies have suggested that hearing loss, which is highly prevalent but undertreated in older adults, may be associated with gait and physical functioning. Determining if hearing loss is independently associated with gait speed is critical toward understanding whether hearing rehabilitative interventions could help mitigate declines in physical functioning in older adults.
Methods: We analyzed cross-sectional data from the 1999 to 2002 cycles of the National Health and Nutritional Examination Survey during which participants 50-69 years (n = 1180) underwent hearing and gait speed assessments. Hearing was defined by a pure tone average of hearing thresholds at 0.5-4 kHz tones in the better-hearing ear. Gait speed was obtained in a timed 20-ft (6.1 m) walk. Linear and logistic regression models were used to examine the association between hearing loss and gait speed while adjusting for demographic and cardiovascular risk factors. Analyses incorporated sampling weights to yield results generalizable to the U.S. population.
Results: In a model adjusted for demographic and cardiovascular risk factors, a hearing loss was associated with slower gait speed (-0.05 m/s per 25 dB of hearing loss [95% CI: -0.09 to -0.02]) and an increased odds of having a gait speed < 1.0 m/s (OR = 2.0 per 25 dB of hearing loss, 95% CI: 1.2-3.3). The reduction in gait speed associated with a 25 dB hearing loss was equivalent to that associated with an age difference of approximately 12 years.
Conclusions: Greater hearing loss is independently associated with slower gait speed. Further studies investigating the mechanistic basis of this association and whether hearing rehabilitative interventions could affect gait and physical functioning are needed. (C) 2012 Elsevier B. V. All rights reserved.
C1 [Li, Lingsheng; Lin, Frank R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
[Li, Lingsheng; Lin, Frank R.] Johns Hopkins Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD USA.
[Simonsick, Eleanor M.; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[Lin, Frank R.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
RP Lin, FR (reprint author), Johns Hopkins Ctr Aging & Hlth, 2024 E Monument St,Suite 2-700, Baltimore, MD 21205 USA.
EM flin1@jhmi.edu
FU National Institute on Deafness and Other Communication Disorders
[1K23DC011279]; Triological Society/American College of Surgeons
Clinician Scientist Award; Eleanor Schwartz Charitable Foundation;
National Institute on Aging
FX This work was supported by the National Institute on Deafness and Other
Communication Disorders (1K23DC011279 to F.L.), a Triological
Society/American College of Surgeons Clinician Scientist Award (F.L.),
the Eleanor Schwartz Charitable Foundation (F.L.), and the intramural
research program of the National Institute on Aging (E.S., L.F.).
NR 29
TC 17
Z9 17
U1 1
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0966-6362
J9 GAIT POSTURE
JI Gait Posture
PD MAY
PY 2013
VL 38
IS 1
BP 25
EP 29
DI 10.1016/j.gaitpost.2012.10.006
PG 5
WC Neurosciences; Orthopedics; Sport Sciences
SC Neurosciences & Neurology; Orthopedics; Sport Sciences
GA 157NZ
UT WOS:000319906300005
PM 23177614
ER
PT J
AU Mathews, DC
Zarate, CA
AF Mathews, Daniel C.
Zarate, Carlos A., Jr.
TI Current Status of Ketamine and Related Compounds for Depression
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Editorial Material
ID D-ASPARTATE ANTAGONIST; RESISTANT MAJOR DEPRESSION; ADD-ON TRIAL;
BIPOLAR DEPRESSION; DOUBLE-BLIND; ANTIDEPRESSANT ACTIONS; DISORDER;
RECEPTORS; MEMANTINE; INFUSION
C1 NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
US Dept HHS, Bethesda, MD USA.
RP Zarate, CA (reprint author), CRC, Unit Southeast 7, 10 Ctr Dr,Room 7-3445, Bethesda, MD 20892 USA.
EM zaratec@mail.nih.gov
FU Intramural NIH HHS [ZIA MH002857-08]
NR 40
TC 9
Z9 9
U1 0
U2 11
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD MAY
PY 2013
VL 74
IS 5
BP 516
EP 517
DI 10.4088/JCP.13ac08382
PG 2
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 157IW
UT WOS:000319890800008
PM 23759454
ER
PT J
AU Bouchard, DR
Porneala, B
Janssen, I
Langlois, MF
Baillargeon, JP
Fox, CS
Meigs, JB
D'Agostino, RB
Pencina, M
Hivert, MF
AF Bouchard, Danielle R.
Porneala, Bianca
Janssen, Ian
Langlois, Marie-France
Baillargeon, Jean-Patrice
Fox, Caroline S.
Meigs, James B.
D'Agostino, Ralph B., Sr.
Pencina, Michael
Hivert, Marie-France
TI Risk of type 2 diabetes and cumulative excess weight exposure in the
Framingham Offspring Study
SO JOURNAL OF DIABETES AND ITS COMPLICATIONS
LA English
DT Article
DE Adults; Aging; BMI; Diagnosis; Epidemiology
ID OBESE WOMEN; PACK-YEAR; MELLITUS; DURATION; BMI; HYPERTENSION;
ASSOCIATION; PREVENTION; PREVALENCE; PATTERNS
AB Aim: Mid-life obesity is associated with T2D risk. However, less is known about the cumulative effect of obesity during adulthood.
Methods: Framingham Offspring Study participants who had an examination at 35 +/- 2 years and were initially free of T2D were included in this study (N=1026). A cumulative excess weight (CEW) score (year*kg/m(2)) was calculated until T2D diagnostic or the end of follow-up.
Results: Eighty-four individuals (8.2%) developed T2D over 20 +/- 6 years. Mean CEW scores were 118.+/- 114.6 year*kg/m(2) in individuals who developed T2D and 30.2 +/- 91.4 year*kg/m(2) in those who did not develop T2D (P<0.01). T2D risk was doubled for each standard deviation increase in the CEW score (OR=1.99 [1.64-2.40]; P<0.001). However, CEW score was only significantly associated with T2D incidence for participants with a baseline BMI<25 kg/m(2) (OR=2.13 [136-336]; P<0.001).
Conclusions: Accumulating weight between the mid-thirties to the mid-fifties increases the risk of developing T2D. However, BMI in mid-thirties remains a stronger predictor of T2D risk. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Bouchard, Danielle R.] Univ Manitoba, Fac Kinesiol & Recreat Management, Winnipeg, MB, Canada.
[Bouchard, Danielle R.] Hlth Leisure & Human Performance Res Inst, Winnipeg, MB, Canada.
[Porneala, Bianca] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
[Janssen, Ian] Queens Univ, Dept Community Hlth Epidemiol, Kingston, ON, Canada.
[Janssen, Ian] Queens Univ, Sch Kinesiol & Hlth Studies, Kingston, ON, Canada.
[Langlois, Marie-France; Baillargeon, Jean-Patrice; Hivert, Marie-France] Univ Sherbrooke, Dept Med, Div Endocrinol, Sherbrooke, PQ J1K 2R1, Canada.
[Langlois, Marie-France; Baillargeon, Jean-Patrice; Hivert, Marie-France] CHU Sherbrooke, Etienne LeBel Clin Res Ctr, Sherbrooke, PQ J1H 5N4, Canada.
[Fox, Caroline S.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Fox, Caroline S.] Brigham Womens Hosp, Dept Endocrinol, Boston, MA USA.
[Meigs, James B.; Hivert, Marie-France] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
[D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Pencina, Michael] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
RP Hivert, MF (reprint author), Dept Med, Div Endocrinol, Sherbrooke, PQ J1H 5N4, Canada.
EM Marie-France.Hivert@USherbrooke.ca
RI Janssen, Ian/B-7700-2009
FU TheNational Heart, Lung, and Blood Institute (NHLBI); Fonds de Recherche
du Quebec-Sante (FRQ-S); Canadian Diabetes Association (CDA); FRQ-S;
NIDDK [K24 DK080140]
FX TheNational Heart, Lung, and Blood Institute (NHLBI) supported the
Framingham study. The NHLBI had no role in the design and conduct of the
study; the collection, analysis, and interpretation of the data; or the
preparation of the manuscript.; MFH is supported by a Scholar Award
(junior 1 level) from the Fonds de Recherche du Quebec-Sante (FRQ-S) and
was awarded a Canadian Diabetes Association (CDA) Clinician Scientist
award. MFL is the recipient of an FRQ-S National Researcher Award. JPB
is the recipient of an FRQ-S Senior Award. JBM is supported by NIDDK K24
DK080140.
NR 32
TC 4
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 1056-8727
J9 J DIABETES COMPLICAT
JI J. Diabetes Complications
PD MAY-JUN
PY 2013
VL 27
IS 3
BP 214
EP 218
DI 10.1016/j.jdiacomp.2012.11.009
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 158YR
UT WOS:000320011600004
PM 23312789
ER
PT J
AU Marais, BJ
Lonnroth, K
Lawn, SD
Migliori, GB
Mwaba, P
Glaziou, P
Bates, M
Colagiuri, R
Zijenah, L
Swaminathan, S
Memish, ZA
Pletschette, M
Hoelscher, M
Abubakar, I
Hasan, R
Zafar, A
Pantaleo, G
Craig, G
Kim, P
Maeurer, M
Schito, M
Zumla, A
AF Marais, Ben J.
Loennroth, Knut
Lawn, Stephen D.
Migliori, Giovanni Battista
Mwaba, Peter
Glaziou, Philippe
Bates, Matthew
Colagiuri, Ruth
Zijenah, Lynn
Swaminathan, Soumya
Memish, Ziad A.
Pletschette, Michel
Hoelscher, Michael
Abubakar, Ibrahim
Hasan, Rumina
Zafar, Afia
Pantaleo, Guiseppe
Craig, Gill
Kim, Peter
Maeurer, Markus
Schito, Marco
Zumla, Alimuddin
TI Tuberculosis comorbidity with communicable and non-communicable
diseases: integrating health services and control efforts
SO LANCET INFECTIOUS DISEASES
LA English
DT Article
ID SUB-SAHARAN AFRICA; HIV-INFECTED INFANTS; DIABETES-MELLITUS;
RISK-FACTORS; SOCIAL DETERMINANTS; ANTIRETROVIRAL THERAPY; MATERNAL
MORTALITY; DEVELOPING-COUNTRIES; TREATMENT OUTCOMES; INCOME COUNTRIES
AB Recent data for the global burden of disease reflect major demographic and lifestyle changes, leading to a rise in noncommunicable diseases. Most countries with high levels of tuberculosis face a large comorbidity burden from both non-communicable and communicable diseases. Traditional disease-specific approaches typically fail to recognise common features and potential synergies in integration of care, management, and control of non-communicable and communicable diseases. In resource-limited countries, the need to tackle a broader range of overlapping comorbid diseases is growing. Tuberculosis and HIV/AIDS persist as global emergencies. The lethal interaction between tuberculosis and HIV coinfection in adults, children, and pregnant women in sub-Saharan Africa exemplifies the need for well integrated approaches to disease management and control. Furthermore, links between diabetes mellitus, smoking, alcoholism, chronic lung diseases, cancer, immunosuppressive treatment, malnutrition, and tuberculosis are well recognised. Here, we focus on interactions, synergies, and challenges of integration of tuberculosis care with management strategies for non-communicable and communicable diseases without eroding the functionality of existing national programmes for tuberculosis. The need for sustained and increased funding for these initiatives is greater than ever and requires increased political and funder commitment.
C1 [Marais, Ben J.] Univ Sydney, Sydney Emerging Infect & Biosecur Inst, Sydney, NSW 2006, Australia.
[Marais, Ben J.] Univ Sydney, Sydney Med Sch, Childrens Hosp Westmead, Sydney, NSW 2006, Australia.
[Loennroth, Knut; Glaziou, Philippe] WHO, StopTB Dept, CH-1211 Geneva, Switzerland.
[Lawn, Stephen D.] Univ London London Sch Hyg & Trop Med, Fac Infect & Trop Dis, London WC1E 7HT, England.
[Lawn, Stephen D.] Univ Cape Town, Fac Hlth Sci, Inst Infect Dis & Mol Med, Desmond Tutu HIV Ctr, ZA-7925 Cape Town, South Africa.
[Migliori, Giovanni Battista] WHO Collaborating Ctr TB & Lung Dis, Fdn S Maugeri, Care & Res Inst, Tradate, Italy.
[Mwaba, Peter; Bates, Matthew; Zumla, Alimuddin] Univ Zambia Univ Coll London Med Sch UNZA UCLMS, Res & Training Project, Univ Teaching Hosp, Lusaka, Zambia.
[Mwaba, Peter] Minist Hlth, Lusaka, Zambia.
[Zijenah, Lynn] Univ Zimbabwe, Coll Hlth Sci, Harare, Zimbabwe.
[Colagiuri, Ruth] Univ Sydney, Boden Inst Obes Nutr Exercise & Eating Disorders, Hlth & Sustainabil Unit, Sydney, NSW 2006, Australia.
[Swaminathan, Soumya] Natl Inst Res TB, Madras, Tamil Nadu, India.
[Memish, Ziad A.] Minist Hlth, Riyadh, Saudi Arabia.
[Memish, Ziad A.] Alfaisal Univ, Coll Med, Riyadh, Saudi Arabia.
[Pletschette, Michel] Univ Zurich, Inst Med Microbiol, Zurich, Switzerland.
[Hoelscher, Michael] Klinikum Univ Munich, Dept Infect Dis & Trop Med, Munich, Germany.
[Hasan, Rumina; Zafar, Afia] Aga Khan Univ Hosp, Dept Pathol & Microbiol, Karachi, Pakistan.
[Abubakar, Ibrahim] Hlth Protect Agcy, London, England.
[Abubakar, Ibrahim] UCL, Dept Infect & Populat Hlth, Ctr Infect Dis Epidemiol, London, England.
[Pantaleo, Guiseppe] Univ Lausanne, Univ Lausanne Hosp, Div Immunol & Allergy, Lausanne, Switzerland.
[Craig, Gill] City Univ London, Sch Hlth Sci, London EC1V 0HB, England.
[Kim, Peter] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Maeurer, Markus] Karolinska Inst, Div Therapeut Immunol LabMed & Microbiol Tumor &, Stockholm, Sweden.
[Maeurer, Markus] Karolinska Hosp, Ctr Allogene Stem Cell Transplantat, S-10401 Stockholm, Sweden.
[Schito, Marco] NIAID, Henry M Jackson Fdn, Div Aids, NIH, Bethesda, MD 20892 USA.
[Bates, Matthew; Zumla, Alimuddin] UCL, Div Infect & Immun, Ctr Clin Microbiol, London, England.
RP Zumla, A (reprint author), UCL, Royal Free Hosp, Ctr Clin Microbiol, London NW3 2PF, England.
EM a.zumla@ucl.ac.uk
RI Hoelscher, Michael/D-3436-2012; Lonnroth, Knut/L-2339-2014; Hasan,
Rumina/F-4420-2015; Pantaleo, Giuseppe/K-6163-2016;
OI Lonnroth, Knut/0000-0001-5054-8240; Glaziou,
Philippe/0000-0002-0649-1272; Abubakar, Ibrahim/0000-0002-0370-1430;
Zumla, Alimuddin/0000-0002-5111-5735; Migliori, Giovanni
Battista/0000-0002-2597-574X
FU Australian NHMRC for creation of a Centre of Research Excellence in
Tuberculosis; European and Developing Countries Clinical Trials
Partnership, Netherlands (grant REMOX); European and Developing
Countries Clinical Trials Partnership, Netherlands (grant PANACEA);
European and Developing Countries Clinical Trials Partnership,
Netherlands (grant TB-NEAT); UK Medical Research Council; UBS Optimus
Foundation, Switzerland; University College London Hospitals (UCLH)
Comprehensive Biomedical Research Centre; UCLH National Health Service
Foundation Trust, London, UK; National Institute of Allergies and
Infectious Diseases, National Institutes of Health, Department of Health
and Human Services, Bethesda, MD, USA [HHSN272200800014C]; Wellcome
Trust, London, UK
FX We acknowledge support from: the Australian NHMRC for creation of a
Centre of Research Excellence in Tuberculosis (BJM); the European and
Developing Countries Clinical Trials Partnership, Netherlands (grants
REMOX [AZu, MH, PM], PANACEA [AZu, MM], and TB-NEAT [MM, MH, PM, MB,
AZu]); the UK Medical Research Council (AZu, MB, PM); UBS Optimus
Foundation, Switzerland (PM, AZu, MM); University College London
Hospitals (UCLH) Comprehensive Biomedical Research Centre, and UCLH
National Health Service Foundation Trust, London, UK (AZu); the National
Institute of Allergies and Infectious Diseases, National Institutes of
Health, Department of Health and Human Services, Bethesda, MD, USA
(contract no HHSN272200800014C [MS]); and the Wellcome Trust, London, UK
(SDL). The authors alone are responsible for the views expressed in this
publication. The opinions expressed here do not reflect the official
policies of the US Department of Health and Human Services or the
authors' national governments, nor does mention of trade names,
commercial practices, or organisations imply endorsement by the US
Government or the authors' national governments. KL and PG are staff
members of the World Health Organization. The views expressed in this
publication do not necessarily represent the decisions or policies of
the World Health Organization.
NR 125
TC 76
Z9 77
U1 4
U2 30
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1473-3099
EI 1474-4457
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD MAY
PY 2013
VL 13
IS 5
BP 436
EP 448
DI 10.1016/S1473-3099(13)70015-X
PG 13
WC Infectious Diseases
SC Infectious Diseases
GA 152LY
UT WOS:000319534400026
PM 23531392
ER
PT J
AU Wells, WA
Boehme, CC
Cobelens, FGJ
Daniels, C
Dowdy, D
Gardiner, E
Gheuens, J
Kim, P
Kimerling, ME
Kreiswirth, B
Lienhardt, C
Mdluli, K
Pai, M
Perkins, MD
Peter, T
Zignol, M
Zumla, A
Schito, M
AF Wells, William A.
Boehme, Catharina C.
Cobelens, Frank G. J.
Daniels, Colleen
Dowdy, David
Gardiner, Elizabeth
Gheuens, Jan
Kim, Peter
Kimerling, Michael E.
Kreiswirth, Barry
Lienhardt, Christian
Mdluli, Khisi
Pai, Madhukar
Perkins, Mark D.
Peter, Trevor
Zignol, Matteo
Zumla, Alimuddin
Schito, Marco
TI Alignment of new tuberculosis drug regimens and drug susceptibility
testing: a framework for action
SO LANCET INFECTIOUS DISEASES
LA English
DT Article
ID MYCOBACTERIUM-TUBERCULOSIS; RESISTANT TUBERCULOSIS; FLUOROQUINOLONE
RESISTANCE; PULMONARY TUBERCULOSIS; BACTERICIDAL ACTIVITY;
NATIONAL-SURVEY; DIAGNOSIS; PYRAZINAMIDE; MTB/RIF; IMPLEMENTATION
AB New tuberculosis drug regimens are creating new priorities for drug susceptibility testing (DST) and surveillance. To minimise turnaround time, rapid DST will need to be prioritised, but developers of these assays will need better data about the molecular mechanisms of resistance. Efforts are underway to link mutations with drug resistance and to develop strain collections to enable assessment of new diagnostic assays. In resource-limited settings, DST might not be appropriate for all patients with tuberculosis. Surveillance data and modelling will help country stakeholders to design appropriate DST algorithms and to decide whether to change drug regimens. Finally, development of practical DST assays is needed so that, in countries where surveillance and modelling show that DST is advisable, these assays can be used to guide clinical decisions for individual patients. If combined judiciously during both development and implementation, new tuberculosis regimens and new DST assays have enormous potential to improve patient outcomes and reduce the burden of disease.
C1 [Wells, William A.; Gardiner, Elizabeth; Mdluli, Khisi] Global Alliance TB Drug Dev, New York, NY USA.
[Boehme, Catharina C.; Perkins, Mark D.] Fdn Innovat New Diagnost, Geneva, Switzerland.
[Cobelens, Frank G. J.] Univ Amsterdam, Acad Med Ctr, Dept Global Hlth, NL-1105 AZ Amsterdam, Netherlands.
[Cobelens, Frank G. J.] Amsterdam Inst Global Hlth & Dev, Amsterdam, Netherlands.
[Daniels, Colleen] Treatment Act Grp, New York, NY USA.
[Dowdy, David] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Gheuens, Jan; Kimerling, Michael E.] Bill & Melinda Gates Fdn, Seattle, WA USA.
[Kim, Peter] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Kreiswirth, Barry] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
[Lienhardt, Christian; Zignol, Matteo] WHO, Stop TB Dept, CH-1211 Geneva, Switzerland.
[Pai, Madhukar] McGill Univ, Dept Epidemiol & Biostat, Montreal, PQ, Canada.
[Peter, Trevor] Clinton Hlth Access Initiat, Boston, MA USA.
[Zumla, Alimuddin] UCL, Div Infect & Immun, Ctr Clin Microbiol, London, England.
[Zumla, Alimuddin] Univ Zambia Univ Coll London Med Sch UNZA UCLMS, Res & Training Project, Univ Teaching Hosp, Lusaka, Zambia.
[Schito, Marco] NIAID, Henry M Jackson Fdn, Div Aids, NIH, Bethesda, MD 20892 USA.
RP Schito, M (reprint author), NIAID, NIH, 6700B Rockledge Dr, Bethesda, MD 20817 USA.
EM schitom@niaid.nih.gov
OI Zumla, Alimuddin/0000-0002-5111-5735
FU National Institute of Allergies and Infectious Diseases, National
Institutes of Health, Department of Health and Human Services
[HHSN272200800014C]; Bill & Melinda Gates Foundation; European
Commission; Irish Aid; National Institute of Allergy and Infectious
Diseases; UK Department for International Development; UNITAID; US
Agency for International Development; US Food and Drug Administration
FX This project has been funded in part with federal funds from the
National Institute of Allergies and Infectious Diseases, National
Institutes of Health, Department of Health and Human Services, under
contract number HHSN272200800014C. TB Alliance is funded by the Bill &
Melinda Gates Foundation, European Commission, Irish Aid, National
Institute of Allergy and Infectious Diseases, UK Department for
International Development, UNITAID, US Agency for International
Development, and the US Food and Drug Administration. The opinions
expressed herein are those of the authors and do not reflect the
official policies of the US Department of Health and Human Services or
the authors' national governments, nor does mention of trade names,
commercial practices, or organisations imply endorsement by the US
Government or the authors' national governments.
NR 62
TC 32
Z9 34
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1473-3099
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD MAY
PY 2013
VL 13
IS 5
BP 449
EP 458
DI 10.1016/S1473-3099(13)70025-2
PG 10
WC Infectious Diseases
SC Infectious Diseases
GA 152LY
UT WOS:000319534400027
PM 23531393
ER
PT J
AU Kononenko, AV
Lee, NCO
Earnshaw, WC
Kouprina, N
Larionov, V
AF Kononenko, Artem V.
Lee, Nicholas C. O.
Earnshaw, William C.
Kouprina, Natalay
Larionov, Vladimir
TI Re-engineering an alphoid(tetO)-HAC-based vector to enable
high-throughput analyses of gene function
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID HUMAN ARTIFICIAL CHROMOSOME; TRANSFORMATION-ASSOCIATED RECOMBINATION;
CONDITIONAL CENTROMERE; STEM-CELLS; GENOMIC LOCI; HAC VECTOR; CLONING;
DNA; EXPRESSION; TRANSGENE
AB Human artificial chromosome (HAC)-based vectors represent an alternative technology for gene delivery and expression with a potential to overcome the problems caused by the use of viral-based vectors. The recently developed alphoid(tetO)-HAC has an advantage over other HAC vectors because it can be easily eliminated from cells by inactivation of the HAC kinetochore via binding of tTS chromatin modifiers to its centromeric tetO sequences. This provides unique control for phenotypes induced by genes loaded into the alphoid(tetO)-HAC. However, inactivation of the HAC kinetochore requires transfection of cells by a retrovirus vector, a step that is potentially mutagenic. Here, we describe an approach to re-engineering the alphoid(tetO)-HAC that allows verification of phenotypic changes attributed to expression of genes from the HAC without a transfection step. In the new HAC vector, a tTS-EYFP cassette is inserted into a gene-loading site along with a gene of interest. Expression of the tTS generates a self-regulating fluctuating heterochromatin on the alphoid(tetO)-HAC that induces fast silencing of the genes on the HAC without significant effects on HAC segregation. This silencing of the HAC-encoded genes can be readily recovered by adding doxycycline. The newly modified alphoid(tetO)-HAC-based system has multiple applications in gene function studies.
C1 [Kononenko, Artem V.; Lee, Nicholas C. O.; Kouprina, Natalay; Larionov, Vladimir] NCI, Labs Mol Pharmacol, Bethesda, MD 20892 USA.
[Earnshaw, William C.] Univ Edinburgh, Wellcome Trust Ctr Cell Biol, Edinburgh EH9 3JR, Midlothian, Scotland.
RP Larionov, V (reprint author), NCI, Labs Mol Pharmacol, Bethesda, MD 20892 USA.
EM larionov@mail.nih.gov
RI Lee, Nicholas/F-3668-2015;
OI lee, nicholas/0000-0003-2628-6599
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, USA; Wellcome Trust [073915]; Intramural
funds of the US Department of Health and Human Services
FX Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, USA (to V.L.); Wellcome Trust of which
W.C.E. is a Principal Research Fellow [073915]. Funding for open access
charge: Intramural funds of the US Department of Health and Human
Services (to National Library of Medicine).
NR 51
TC 5
Z9 5
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD MAY
PY 2013
VL 41
IS 10
AR e107
DI 10.1093/nar/gkt205
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 156FG
UT WOS:000319806600004
PM 23558748
ER
PT J
AU Saba, NS
Dang, D
Saba, J
Cao, C
Janbain, M
Maalouf, B
Safah, H
AF Saba, Nakhle S.
Dang, Daniella
Saba, Jowana
Cao, Christine
Janbain, Maissaa
Maalouf, Bassam
Safah, Hana
TI Bortezomib in Plasmablastic Lymphoma: A Case Report and Review of the
Literature
SO ONKOLOGIE
LA English
DT Review
DE Lymphoma; PBL; HIV infection; Proteasome inhibitor; Multiple myeloma
ID ACTIVE ANTIRETROVIRAL THERAPY; B-CELL LYMPHOMAS; ORAL-CAVITY; PROTEASOME
INHIBITION; HIV; CHEMOTHERAPY; INFECTION; DISEASE; PATIENT
AB Background: Plasmablastic lymphoma (PBL) is an aggressive subtype of non-Hodgkin's lymphoma (NHL). While classically associated with the human immunodeficiency virus (HIV), cases of PBL in immunocompetent patients have been increasingly described. PBL shares common morphological and innmunohistochemical features with diffuse large B-cell lymphoma (DLBCL) and multiple myeloma (MM). Due to the rarity of PBL, there is no current consensual standard therapy available. As a result, PBL treatment is mirrored after aggressive NHL regimens. One of the newly emerged therapeutic options for PBL is bortezomib, which is a proteasome inhibitor and a cornerstone in MM therapy. In recently published cases, bortezomib has shown promising results in PBL. Case Report: In this report, we describe a patient with HIV-negative PBL who dramatically responded to bortezomib after failing several other lines of therapy. We also review 4 other, similar cases reported in the literature. Results and Conclusion: We conclude that bortezomib resulted in rapid and dramatical responses regardless of the line of therapy. Although most of these responses were not sustained, bortezomib represents a new therapeutic option for PBL that should be further explored in larger clinical trials.
C1 [Saba, Nakhle S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Saba, Nakhle S.; Janbain, Maissaa; Maalouf, Bassam; Safah, Hana] Tulane Univ, Dept Internal Med, Sect Hematol & Med Oncol, New Orleans, LA 70112 USA.
[Dang, Daniella] Univ Minnesota, Dept Therapeut Radiol & Radiat Oncol, Minneapolis, MN USA.
[Saba, Jowana] Lebanese Univ, Sch Med, Fac Med, Beirut, Lebanon.
[Cao, Christine] Tulane Univ, Dept Internal Med, New Orleans, LA 70118 USA.
RP Safah, H (reprint author), Tulane Univ, Dept Internal Med, Sect Hematol & Med Oncol, 1430 Tulane Ave,SL34, New Orleans, LA 70112 USA.
EM hsafah@tulane.edu
NR 23
TC 19
Z9 21
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0378-584X
J9 ONKOLOGIE
JI Onkologie
PD MAY
PY 2013
VL 36
IS 5
BP 287
EP 291
DI 10.1159/000350325
PG 5
GA 156UC
UT WOS:000319848400008
PM 23689224
ER
PT J
AU Ngo, VK
Rubinstein, A
Ganju, V
Kanellis, P
Loza, N
Rabadan-Diehl, C
Daar, AS
AF Ngo, Victoria K.
Rubinstein, Adolfo
Ganju, Vijay
Kanellis, Pamela
Loza, Nasser
Rabadan-Diehl, Cristina
Daar, Abdallah S.
TI Grand Challenges: Integrating Mental Health Care into the
Non-Communicable Disease Agenda
SO PLOS MEDICINE
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY IMPROVEMENT STRATEGIES;
COLLABORATIVE CARE; LOW-INCOME; SCALE-UP; DEPRESSION; DISORDERS;
OUTCOMES; INTERVENTION; SERVICES
C1 [Ngo, Victoria K.] RAND Corp, Santa Monica, CA USA.
[Rubinstein, Adolfo] Univ Buenos Aires, Inst Clin Effectiveness & Hlth Policy, Buenos Aires, DF, Argentina.
[Kanellis, Pamela; Daar, Abdallah S.] Grand Challenges Canada, Toronto, ON, Canada.
[Loza, Nasser] Behman Psychiat Hosp, Cairo, Egypt.
[Rabadan-Diehl, Cristina] NHLBI, Bethesda, MD 20892 USA.
[Daar, Abdallah S.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Daar, Abdallah S.] Univ Toronto, Dept Surg, Toronto, ON, Canada.
[Daar, Abdallah S.] Univ Stellenbosch, Wallenberg Res Ctr, Stellenbosch Inst Adv Study STIAS, ZA-7600 Stellenbosch, South Africa.
RP Ngo, VK (reprint author), RAND Corp, Santa Monica, CA USA.
EM vngo@rand.org
FU NIMH NIH HHS [R34 MH094648]
NR 45
TC 35
Z9 35
U1 1
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1676
J9 PLOS MED
JI PLos Med.
PD MAY
PY 2013
VL 10
IS 5
AR e1001443
DI 10.1371/journal.pmed.1001443
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 154JK
UT WOS:000319670900018
PM 23690753
ER
PT J
AU Blaney, JE
Marzi, A
Willet, M
Papaneri, AB
Wirblich, C
Feldmann, F
Holbrook, M
Jahrling, P
Feldmann, H
Schnell, MJ
AF Blaney, Joseph E.
Marzi, Andrea
Willet, Mallory
Papaneri, Amy B.
Wirblich, Christoph
Feldmann, Friederike
Holbrook, Michael
Jahrling, Peter
Feldmann, Heinz
Schnell, Matthias J.
TI Antibody Quality and Protection from Lethal Ebola Virus Challenge in
Nonhuman Primates Immunized with Rabies Virus Based Bivalent Vaccine
SO PLOS PATHOGENS
LA English
DT Article
ID TYPE-1 GAG; SAD B19; GLYCOPROTEIN; VECTOR; LIVE; IMMUNOGENICITY;
INFECTION; MORTALITY; RESPONSES; ENVELOPE
AB We have previously described the generation of a novel Ebola virus (EBOV) vaccine platform based on (a) replication-competent rabies virus (RABV), (b) replication-deficient RABV, or (c) chemically inactivated RABV expressing EBOV glycoprotein (GP). Mouse studies demonstrated safety, immunogenicity, and protective efficacy of these live or inactivated RABV/EBOV vaccines. Here, we evaluated these vaccines in nonhuman primates. Our results indicate that all three vaccines do induce potent immune responses against both RABV and EBOV, while the protection of immunized animals against EBOV was largely dependent on the quality of humoral immune response against EBOV GP. We also determined if the induced antibodies against EBOV GP differ in their target, affinity, or the isotype. Our results show that IgG1-biased humoral responses as well as high levels of GP-specific antibodies were beneficial for the control of EBOV infection after immunization. These results further support the concept that a successful EBOV vaccine needs to induce strong antibodies against EBOV. We also showed that a dual vaccine against RABV and filoviruses is achievable; therefore addressing concerns for the marketability of this urgently needed vaccine.
C1 [Blaney, Joseph E.; Papaneri, Amy B.; Jahrling, Peter] NIAID, Emerging Viral Pathogens Sect, NIH, Bethesda, MD 20892 USA.
[Marzi, Andrea; Feldmann, Friederike; Feldmann, Heinz] NIAID, Virol Lab, Div Intramural Res, NIH, Hamilton, MT USA.
[Willet, Mallory; Wirblich, Christoph; Schnell, Matthias J.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Microbiol & Immunol, Philadelphia, PA 19107 USA.
[Holbrook, Michael; Jahrling, Peter] NIAID, Integrated Res Facil, NIH, Ft Detrick, MD USA.
[Schnell, Matthias J.] Thomas Jefferson Univ, Jefferson Med Coll, Jefferson Vaccine Ctr, Philadelphia, PA 19107 USA.
RP Blaney, JE (reprint author), NIAID, Emerging Viral Pathogens Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM Matthias.schnell@jefferson.edu
OI Papaneri, Amy/0000-0003-2144-2441
FU National Institute of Allergy and Infectious Diseases (NIAID) Division
of Intramural Research; NIAID [R01AI105204]
FX This study was supported in part by the National Institute of Allergy
and Infectious Diseases (NIAID) Division of Intramural Research and the
grant R01AI105204 by NIAID to MJS. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript
NR 39
TC 34
Z9 37
U1 1
U2 35
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003389
DI 10.1371/journal.ppat.1003389
PG 13
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800058
PM 23737747
ER
PT J
AU Chen, Y
Tascon, I
Neunuebel, MR
Pallara, C
Brady, J
Kinch, LN
Fernandez-Recio, J
Rojas, AL
Machner, MP
Hierro, A
AF Chen, Yang
Tascon, Igor
Neunuebel, M. Ramona
Pallara, Chiara
Brady, Jacqueline
Kinch, Lisa N.
Fernandez-Recio, Juan
Rojas, Adriana L.
Machner, Matthias P.
Hierro, Aitor
TI Structural Basis for Rab1 De-AMPylation by the Legionella pneumophila
Effector SidD
SO PLOS PATHOGENS
LA English
DT Article
ID PROTEIN-PROTEIN DOCKING; SMALL GTPASE RAB1; GDI DISPLACEMENT;
PHOSPHATASE 2C; BINDING; TRANSFERASE; RECRUITMENT; RESOLUTION;
MECHANISM; SYSTEM
AB The covalent attachment of adenosine monophosphate (AMP) to proteins, a process called AMPylation (adenylylation), has recently emerged as a novel theme in microbial pathogenesis. Although several AMPylating enzymes have been characterized, the only known virulence protein with de-AMPylation activity is SidD from the human pathogen Legionella pneumophila. SidD de-AMPylates mammalian Rab1, a small GTPase involved in secretory vesicle transport, thereby targeting the host protein for inactivation. The molecular mechanisms underlying Rab1 recognition and de-AMPylation by SidD are unclear. Here, we report the crystal structure of the catalytic region of SidD at 1.6 angstrom resolution. The structure reveals a phosphatase-like fold with additional structural elements not present in generic PP2C-type phosphatases. The catalytic pocket contains a binuclear metal-binding site characteristic of hydrolytic metalloenzymes, with strong dependency on magnesium ions. Subsequent docking and molecular dynamics simulations between SidD and Rab1 revealed the interface contacts and the energetic contribution of key residues to the interaction. In conjunction with an extensive structure-based mutational analysis, we provide in vivo and in vitro evidence for a remarkable adaptation of SidD to its host cell target Rab1 which explains how this effector confers specificity to the reaction it catalyses.
C1 [Chen, Yang; Neunuebel, M. Ramona; Brady, Jacqueline; Machner, Matthias P.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
[Tascon, Igor; Rojas, Adriana L.; Hierro, Aitor] CIC BioGUNE, Struct Biol Unit, Derio, Spain.
[Pallara, Chiara; Fernandez-Recio, Juan] Barcelona Supercomp Ctr, Joint BSC IRB Res Program Computat Biol, Barcelona, Spain.
[Kinch, Lisa N.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Hierro, Aitor] Basque Fdn Sci, IKERBASQUE, Bilbao, Spain.
RP Chen, Y (reprint author), Peking Univ, Hlth Sci Ctr, Beijing 100871, Peoples R China.
EM machnerm@mail.nih.gov; ahierro@cicbiogune.es
RI Hierro, Aitor/F-9998-2011; Rojas, Adriana/G-2403-2011; Machner,
Matthias/G-2758-2015; Pallara, Chiara/F-9441-2016; SGIKER,
Cienciometria/A-5759-2012;
OI Hierro, Aitor/0000-0002-7721-1581; Rojas, Adriana/0000-0002-7358-3505;
Pallara, Chiara/0000-0003-3005-343X; Machner,
Matthias/0000-0002-6971-7451; Fernandez-Recio, Juan/0000-0002-3986-7686
FU Carlos III Health Institute [PI081739, PI11/00121]; Basque Government
[PI2011-26]; Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development;
[BIO2010-22324]
FX This research was supported by the Carlos III Health Institute grants
PI081739 and PI11/00121, the Basque Government grant PI2011-26 (to AH),
the Grant BIO2010-22324 (to JF-R) and the Intramural Research Program of
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development (to MPM). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 48
TC 8
Z9 9
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003382
DI 10.1371/journal.ppat.1003382
PG 14
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800054
PM 23696742
ER
PT J
AU Lu, MF
Varley, AW
Munford, RS
AF Lu, Mingfang
Varley, Alan W.
Munford, Robert S.
TI Persistently Active Microbial Molecules Prolong Innate Immune Tolerance
In Vivo
SO PLOS PATHOGENS
LA English
DT Article
ID NF-KAPPA-B; BACTERIAL LIPOPOLYSACCHARIDES; ENDOTOXIN TOLERANCE;
PHAGOCYTIC-CELLS; LIPID-A; POLYMORPHONUCLEAR LEUCOCYTES; INFLAMMATORY
RESPONSES; ACYLOXYACYL HYDROLASE; MURINE MACROPHAGES; GENE-EXPRESSION
AB Measures that bolster the resolution phase of infectious diseases may offer new opportunities for improving outcome. Here we show that inactivation of microbial lipopolysaccharides (LPS) can be required for animals to recover from the innate immune tolerance that follows exposure to Gram-negative bacteria. When wildtype mice are exposed to small parenteral doses of LPS or Gram-negative bacteria, their macrophages become reprogrammed (tolerant) for a few days before they resume normal function. Mice that are unable to inactivate LPS, in contrast, remain tolerant for several months; during this time they respond sluggishly to Gram-negative bacterial challenge, with high mortality. We show here that prolonged macrophage reprogramming is maintained in vivo by the persistence of stimulatory LPS molecules within the cells' in vivo environment, where naive cells can acquire LPS via cell-cell contact or from the extracellular fluid. The findings provide strong evidence that inactivation of a stimulatory microbial molecule can be required for animals to regain immune homeostasis following parenteral exposure to bacteria. Measures that disable microbial molecules might enhance resolution of tissue inflammation and help restore innate defenses in individuals recovering from many different infectious diseases.
C1 [Lu, Mingfang; Munford, Robert S.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Varley, Alan W.] Univ Texas SW Med Ctr Dallas, Div Infect Dis, Dept Internal Med, Dallas, TX 75390 USA.
RP Lu, MF (reprint author), NIAID, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM Lum3@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, Bethesda, MD; NIH [RO1 AI18188]
FX This study was funded by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, Bethesda, MD, and by NIH
Grant RO1 AI18188 to University of Texas Southwestern Medical Center,
Dallas, TX. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 75
TC 10
Z9 10
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003339
DI 10.1371/journal.ppat.1003339
PG 16
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800017
PM 23675296
ER
PT J
AU Nayak, D
Johnson, KR
Heydari, S
Roth, TL
Zinselmeyer, BH
McGavern, DB
AF Nayak, Debasis
Johnson, Kory R.
Heydari, Sara
Roth, Theodore L.
Zinselmeyer, Bernd H.
McGavern, Dorian B.
TI Type I Interferon Programs Innate Myeloid Dynamics and Gene Expression
in the Virally Infected Nervous System
SO PLOS PATHOGENS
LA English
DT Article
ID LYMPHOCYTIC CHORIOMENINGITIS VIRUS; DENDRITIC CELLS; IMMUNE RECOGNITION;
ANTIVIRAL RESPONSE; MICROGLIAL CELLS; MOUSE-BRAIN; T-CELLS; MICE;
RECEPTOR; VIVO
AB Viral infections of central nervous system (CNS) often trigger inflammatory responses that give rise to a wide range of pathological outcomes. The CNS is equipped with an elaborate network of innate immune sentinels (e.g. microglia, macrophages, dendritic cells) that routinely serve as first responders to these infections. The mechanisms that underlie the dynamic programming of these cells following CNS viral infection remain undefined. To gain insights into this programming, we utilized a combination of genomic and two-photon imaging approaches to study a pure innate immune response to a noncytopathic virus (lymphocytic choriomeningitis virus) as it established persistence in the brain. This enabled us to evaluate how global gene expression patterns were translated into myeloid cell dynamics following infection. Two-photon imaging studies revealed that innate myeloid cells mounted a vigorous early response to viral infection characterized by enhanced vascular patrolling and a complete morphological transformation. Interestingly, innate immune activity subsided over time and returned to a quasi-normal state as the virus established widespread persistence in the brain. At the genomic level, early myeloid cell dynamics were associated with massive changes in CNS gene expression, most of which declined over time and were linked to type I interferon signaling (IFN-I). Surprisingly, in the absence of IFN-I signaling, almost no differential gene expression was observed in the nervous system despite increased viral loads. In addition, two-photon imaging studies revealed that IFN-I receptor deficient myeloid cells were unresponsive to viral infection and remained in a naive state. These data demonstrate that IFN-I engages non-redundant programming responsible for nearly all innate immune activity in the brain following a noncytopathic viral infection. This Achilles' heel could explain why so many neurotropic viruses have acquired strategies to suppress IFN-I.
C1 [Nayak, Debasis; Johnson, Kory R.; Heydari, Sara; Roth, Theodore L.; Zinselmeyer, Bernd H.; McGavern, Dorian B.] NINDS, NIH, Bethesda, MD 20892 USA.
RP McGavern, DB (reprint author), NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM mcgavernd@mail.nih.gov
OI McGavern, Dorian/0000-0001-9568-545X; Roth, Theodore/0000-0002-3970-9573
FU NIH
FX This work was supported by the NIH intramural program. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 59
TC 19
Z9 19
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003395
DI 10.1371/journal.ppat.1003395
PG 17
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800062
PM 23737750
ER
PT J
AU Orr, SJ
Burg, AR
Chan, T
Quigley, L
Jones, GW
Ford, JW
Hodge, D
Razzook, C
Sarhan, J
Jones, YL
Whittaker, GC
Boelte, KC
Lyakh, L
Cardone, M
O'Connor, GM
Tan, CY
Li, HC
Anderson, SK
Jones, SA
Zhang, WG
Taylor, PR
Trinchieri, G
McVicar, DW
AF Orr, Selinda J.
Burg, Ashley R.
Chan, Tim
Quigley, Laura
Jones, Gareth W.
Ford, Jill W.
Hodge, Deborah
Razzook, Catherine
Sarhan, Joseph
Jones, Yava L.
Whittaker, Gillian C.
Boelte, Kimberly C.
Lyakh, Lyudmila
Cardone, Marco
O'Connor, Geraldine M.
Tan, Cuiyan
Li, Hongchuan
Anderson, Stephen K.
Jones, Simon A.
Zhang, Weiguo
Taylor, Philip R.
Trinchieri, Giorgio
McVicar, Daniel W.
TI LAB/NTAL Facilitates Fungal/PAMP-induced IL-12 and IFN-gamma Production
by Repressing beta-Catenin Activation in Dendritic Cells
SO PLOS PATHOGENS
LA English
DT Article
ID NF-KAPPA-B; COLONY-STIMULATING FACTOR; NECROSIS-FACTOR-ALPHA; ADAPTER
PROTEIN LAB; CANDIDA-ALBICANS; HOST-DEFENSE; TRANSPLANT RECIPIENTS;
SYSTEMIC CANDIDIASIS; DEFICIENT MICE; HUMAN DECTIN-1
AB Fungal pathogens elicit cytokine responses downstream of immunoreceptor tyrosine-based activation motif (ITAM)-coupled or hemilTAM-containing receptors and TLRs. The Linker for Activation of B cells/Non-T cell Activating Linker (LAB/NTAL) encoded by Lat2, is a known regulator of ITAM-coupled receptors and TLR-associated cytokine responses. Here we demonstrate that LAB is involved in anti-fungal immunity. We show that Lat2(-/-) mice are more susceptible to C. albicans infection than wild type (WT) mice. Dendritic cells (DCs) express LAB and we show that it is basally phosphorylated by the growth factor M-CSF or following engagement of Dectin-2, but not Dectin-1. Our data revealed a unique mechanism whereby LAB controls basal and fungal/pathogen-associated molecular patterns (PAMP)-induced nuclear beta-catenin levels. This in turn is important for controlling fungal/PAMP-induced cytokine production in DCs. C. albicans- and LPS-induced IL-12 and IL-23 production was blunted in Lat2(-/-) DCs. Accordingly, Lat2(-/-) DCs directed reduced Th1 polarization in vitro and Lat2(-/-) mice displayed reduced Natural Killer (NK) and T cell-mediated IFN-gamma production in vivo/ex vivo. Thus our data define a novel link between LAB and beta-catenin nuclear accumulation in DCs that facilitates IFN-gamma responses during antifungal immunity. In addition, these findings are likely to be relevant to other infectious diseases that require IL-12 family cytokines and an IFN-gamma response for pathogen clearance.
C1 [Orr, Selinda J.; Burg, Ashley R.; Chan, Tim; Quigley, Laura; Ford, Jill W.; Hodge, Deborah; Razzook, Catherine; Sarhan, Joseph; Whittaker, Gillian C.; Boelte, Kimberly C.; Lyakh, Lyudmila; Cardone, Marco; O'Connor, Geraldine M.; Li, Hongchuan; Anderson, Stephen K.; Trinchieri, Giorgio; McVicar, Daniel W.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Orr, Selinda J.; Jones, Gareth W.; Jones, Simon A.; Taylor, Philip R.] Cardiff Univ, Sch Med, Inst Infect & Immun, Cardiff CF10 3AX, S Glam, Wales.
[Jones, Yava L.] Purdue Univ, Sch Vet Med, Dept Comparat Pathobiol, W Lafayette, IN 47907 USA.
[Tan, Cuiyan] NEI, Expt Immunol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Li, Hongchuan; Anderson, Stephen K.] NCI, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Zhang, Weiguo] Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA.
RP Orr, SJ (reprint author), Cardiff Univ, Sch Med, Inst Infect & Immun, Cardiff CF10 3AX, S Glam, Wales.
EM mcvicard@mail.nih.gov
RI Anderson, Stephen/B-1727-2012; McVicar, Daniel/G-1970-2015
OI Anderson, Stephen/0000-0002-7856-4266;
FU National Cancer Institute (NCI), NIH [HHSN261200800001E]; Intramural
Research Program of the NIH, NCI, Center for Cancer Research; Medical
Research Council UK (MRC) [G0601617]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute (NCI), NIH, under contract
HHSN261200800001E. This research was supported by the Intramural
Research Program of the NIH, NCI, Center for Cancer Research and in part
by the Medical Research Council UK (MRC) (G0601617). The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 58
TC 10
Z9 10
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003357
DI 10.1371/journal.ppat.1003357
PG 15
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800034
PM 23675302
ER
PT J
AU Schmitz, I
Schneider, C
Frohlich, A
Frebel, H
Christ, D
Leonard, WJ
Sparwasser, T
Oxenius, A
Freigang, S
Kopf, M
AF Schmitz, Iwana
Schneider, Christoph
Froehlich, Anja
Frebel, Helge
Christ, Daniel
Leonard, Warren J.
Sparwasser, Tim
Oxenius, Annette
Freigang, Stefan
Kopf, Manfred
TI IL-21 Restricts Virus-driven Treg Cell Expansion in Chronic LCMV
Infection
SO PLOS PATHOGENS
LA English
DT Article
ID REGULATORY T-CELLS; CHRONIC VIRAL-INFECTION; LYMPHOCYTIC
CHORIOMENINGITIS VIRUS; TRANSCRIPTION FACTOR FOXP3; PERSISTENCE IN-VIVO;
DISEASE PROGRESSION; IMMUNE-RESPONSES; HEPATITIS-C; EFFECTOR
DIFFERENTIATION; TRANSGENIC MICE
AB Foxp3(+) regulatory T (Treg) cells are essential for the maintenance of immune homeostasis and tolerance. During viral infections, Treg cells can limit the immunopathology resulting from excessive inflammation, yet potentially inhibit effective antiviral T cell responses and promote virus persistence. We report here that the fast-replicating LCMV strain Docile triggers a massive expansion of the Treg population that directly correlates with the size of the virus inoculum and its tendency to establish a chronic, persistent infection. This Treg cell proliferation was greatly enhanced in IL-21R(-/-) mice and depletion of Treg cells partially rescued defective CD8(+) T cell cytokine responses and improved viral clearance in some but not all organs. Notably, IL-21 inhibited Treg cell expansion in a cell intrinsic manner. Moreover, experimental augmentation of Treg cells driven by injection of IL-2/anti-IL-2 immune complexes drastically impaired the functionality of the antiviral T cell response and impeded virus clearance. As a consequence, mice became highly susceptible to chronic infection following exposure to low virus doses. These findings reveal virus-driven Treg cell proliferation as potential evasion strategy that facilitates T cell exhaustion and virus persistence. Furthermore, they suggest that besides its primary function as a direct survival signal for antiviral CD8(+) T cells during chronic infections, IL-21 may also indirectly promote CD8(+) T cell poly-functionality by restricting the suppressive activity of infection-induced Treg cells.
C1 [Schmitz, Iwana; Schneider, Christoph; Froehlich, Anja; Freigang, Stefan; Kopf, Manfred] Swiss Fed Inst Technol, Dept Biol, Inst Mol Hlth Sci, Zurich, Switzerland.
[Frebel, Helge; Oxenius, Annette] Swiss Fed Inst Technol, Dept Biol, Inst Microbiol, Zurich, Switzerland.
[Christ, Daniel] Garvan Inst Med Res, Sydney, NSW, Australia.
[Christ, Daniel] Univ New S Wales, Fac Med, St Vincents Clin Sch, Sydney, NSW, Australia.
[Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Leonard, Warren J.] NHLBI, Ctr Immunol, NIH, Bethesda, MD 20892 USA.
[Sparwasser, Tim] TWINCORE Ctr Expt & Clin Infect Res, Inst Infect Immunol, Hannover, Germany.
RP Schmitz, I (reprint author), Swiss Fed Inst Technol, Dept Biol, Inst Mol Hlth Sci, Zurich, Switzerland.
EM stefan.freigang@biol.ethz.ch; manfred.kopf@ethz.ch
RI Oxenius, Annette/G-7794-2015;
OI Freigang, Stefan/0000-0003-4438-7828
FU Swiss National Science Foundation [310030-124922/1]; Division of
Intramural Research, National Heart, Lung, and Blood Institute, NIH
FX This research was supported by a grant from the Swiss National Science
Foundation (310030-124922/1; to MK). WJL is supported by the Division of
Intramural Research, National Heart, Lung, and Blood Institute, NIH. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 74
TC 26
Z9 26
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003362
DI 10.1371/journal.ppat.1003362
PG 14
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800039
PM 23696736
ER
PT J
AU Taylor, SM
Cerami, C
Fairhurst, RM
AF Taylor, Steve M.
Cerami, Carla
Fairhurst, Rick M.
TI Hemoglobinopathies: Slicing the Gordian Knot of Plasmodium falciparum
Malaria Pathogenesis
SO PLOS PATHOGENS
LA English
DT Review
ID SICKLE-CELL TRAIT; ERYTHROCYTE-MEMBRANE PROTEIN-1; RED-BLOOD-CELLS;
NITRIC-OXIDE PRODUCTION; CHONDROITIN SULFATE-A; CEREBRAL MALARIA;
INFECTED ERYTHROCYTES; ANTIBODY-RESPONSES; AFRICAN CHILDREN; HEME
OXYGENASE-1
AB Plasmodium falciparum malaria kills over 500,000 children every year and has been a scourge of humans for millennia. Owing to the co-evolution of humans and P. falciparum parasites, the human genome is imprinted with polymorphisms that not only confer innate resistance to falciparum malaria, but also cause hemoglobinopathies. These genetic traits-including hemoglobin S (HbS), hemoglobin C (HbC), and alpha-thalassemia- are the most common monogenic human disorders and can confer remarkable degrees of protection from severe, life-threatening falciparum malaria in African children: the risk is reduced 70% by homozygous HbC and 90% by heterozygous HbS (sickle-cell trait). Importantly, this protection is principally present for severe disease and largely absent for P. falciparum infection, suggesting that these hemoglobinopathies specifically neutralize the parasite's in vivo mechanisms of pathogenesis. These hemoglobin variants thus represent a "natural experiment'' to identify the cellular and molecular mechanisms by which P. falciparum produces clinical morbidity, which remain partially obscured due to the complexity of interactions between this parasite and its human host. Multiple lines of evidence support a restriction of parasite growth by various hemoglobinopathies, and recent data suggest this phenomenon may result from host microRNA interference with parasite metabolism. Multiple hemoglobinopathies mitigate the pathogenic potential of parasites by interfering with the export of P. falciparum erythrocyte membrane protein 1 (PfEMP1) to the surface of the host red blood cell. Few studies have investigated their effects upon the activation of the innate and adaptive immune systems, although recent murine studies suggest a role for heme oxygenase1 in protection. Ultimately, the identification of mechanisms of protection and pathogenesis can inform future therapeutics and preventive measures. Hemoglobinopathies slice the "Gordian knot'' of host and parasite interactions to confer malaria protection, and offer a translational model to identify the most critical mechanisms of P. falciparum pathogenesis.
C1 [Taylor, Steve M.] Duke Univ, Med Ctr, Div Infect Dis & Int Hlth, Durham, NC 27708 USA.
[Taylor, Steve M.; Cerami, Carla] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
RP Taylor, SM (reprint author), Duke Univ, Med Ctr, Div Infect Dis & Int Hlth, Durham, NC 27708 USA.
EM steve.taylor@duke.edu
OI Cerami, Carla/0000-0002-7634-0955
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health; NIAID [K08AI100924]; National Institute of Child
Health and Human Development [U01HD061235]
FX This research was supported in part by the Intramural Research Program
of the National Institute of Allergy and Infectious Diseases, National
Institutes of Health (RMF), the NIAID under award number K08AI100924
(SMT), and the National Institute of Child Health and Human Development
under award number U01HD061235 (CC). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 115
TC 26
Z9 27
U1 4
U2 26
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003327
DI 10.1371/journal.ppat.1003327
PG 10
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800008
PM 23696730
ER
PT J
AU Vega, CG
Bok, M
Vlasova, AN
Chattha, KS
Gomez-Sebastian, S
Nunez, C
Alvarado, C
Lasa, R
Escribano, JM
Garaicoechea, LL
Fernandez, F
Bok, K
Wigdorovitz, A
Saif, LJ
Parreno, V
AF Vega, Celina G.
Bok, Marina
Vlasova, Anastasia N.
Chattha, Kuldeep S.
Gomez-Sebastian, Silvia
Nunez, Carmen
Alvarado, Carmen
Lasa, Rodrigo
Escribano, Jose M.
Garaicoechea, Lorena L.
Fernandez, Fernando
Bok, Karin
Wigdorovitz, Andres
Saif, Linda J.
Parreno, Viviana
TI Recombinant Monovalent Llama-Derived Antibody Fragments (VHH) to
Rotavirus VP6 Protect Neonatal Gnotobiotic Piglets against Human
Rotavirus-Induced Diarrhea
SO PLOS PATHOGENS
LA English
DT Article
ID FED COLOSTRUM SUPPLEMENTS; VIRUS-LIKE PARTICLES; IMMUNE-RESPONSES;
BOVINE ROTAVIRUS; MONOCLONAL-ANTIBODIES; NEUTRALIZING ACTIVITY;
VACCINATION PROGRAMS; MATERNAL ANTIBODIES; NASAL IMMUNIZATION; CONFER
PROTECTION
AB Group A Rotavirus (RVA) is the leading cause of severe diarrhea in children. The aims of the present study were to determine the neutralizing activity of VP6-specific llama-derived single domain nanoantibodies (VHH nanoAbs) against different RVA strains in vitro and to evaluate the ability of G6P[1] VP6-specific llama-derived single domain nanoantibodies (VHH) to protect against human rotavirus in gnotobiotic (Gn) piglets experimentally inoculated with virulent Wa G1P[8] rotavirus. Supplementation of the daily milk diet with 3B2 VHH clone produced using a baculovirus vector expression system (final ELISA antibody -Ab- titer of 4096; virus neutralization -VN- titer of 256) for 9 days conferred full protection against rotavirus associated diarrhea and significantly reduced virus shedding. The administration of comparable levels of porcine IgG Abs only protected 4 out of 6 of the animals from human RVA diarrhea but significantly reduced virus shedding. In contrast, G6P[1]-VP6 rotavirus-specific IgY Abs purified from eggs of hyperimmunized hens failed to protect piglets against human RVA-induced diarrhea or virus shedding when administering similar quantities of Abs. The oral administration of VHH nanoAb neither interfered with the host's isotype profiles of the Ab secreting cell responses to rotavirus, nor induced detectable host Ab responses to the treatment in serum or intestinal contents. This study shows that the oral administration of rotavirus VP6-VHH nanoAb is a broadly reactive and effective treatment against rotavirus-induced diarrhea in neonatal pigs. Our findings highlight the potential value of a broad neutralizing VP6-specific VHH nanoAb as a treatment that can complement or be used as an alternative to the current strain-specific RVA vaccines. Nanobodies could also be scaled-up to develop pediatric medication or functional food like infant milk formulas that might help treat RVA diarrhea.
C1 [Vega, Celina G.; Bok, Marina; Garaicoechea, Lorena L.; Fernandez, Fernando; Wigdorovitz, Andres; Parreno, Viviana] INTA Castelar, Ctr Invest Ciencias Vet & Agron, Inst Virol, Buenos Aires, DF, Argentina.
[Vlasova, Anastasia N.; Chattha, Kuldeep S.; Saif, Linda J.] Ohio State Univ, Ohio Agr Res & Dev Ctr, Food Anim Hlth Res Program, Dept Vet Prevent Med, Wooster, OH 44691 USA.
[Gomez-Sebastian, Silvia; Nunez, Carmen; Alvarado, Carmen; Lasa, Rodrigo] Univ Politecn Madrid, Alternat Gene Express SL ALGENEX, Ctr Empresarial Parque Cient & Tecnol, Madrid, Spain.
[Escribano, Jose M.] Inst Nacl Invest & Tecnol Agr & Alimentaria INIA, Dept Biotecnol, Madrid, Spain.
[Bok, Karin] NIAID, Caliciviruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Vega, CG (reprint author), INTA Castelar, Ctr Invest Ciencias Vet & Agron, Inst Virol, Buenos Aires, DF, Argentina.
EM saif.2@osu.edu; vparreno@cnia.inta.gov.ar
RI Vlasova, Anastasia/C-2062-2016
FU Instituto Nacional de Tecnologia Agropecuaria (INTA, Argentina); Ohio
State University; Intramural Research Program of the National Institutes
of Health; National Institute of Allergy and Infectious Diseases;
international research collaboration, Basic Biomedical (FIRCA-BB) [R03];
Fogarty International Center, National Institutes of Health, USA, FIRCA
[60014561]
FX This research was funded in part by intramural funds from Instituto
Nacional de Tecnologia Agropecuaria (INTA, Argentina), The Ohio State
University, the Intramural Research Program of the National Institutes
of Health, National Institute of Allergy and Infectious Diseases, and an
international research collaboration, Basic Biomedical (FIRCA-BB) (R03).
International collaborative funds were provided by Fogarty International
Center, National Institutes of Health, USA, FIRCA Grant #60014561.
NR 91
TC 14
Z9 15
U1 1
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003334
DI 10.1371/journal.ppat.1003334
PG 17
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800013
PM 23658521
ER
PT J
AU Yukl, SA
Boritz, E
Busch, M
Bentsen, C
Chun, TW
Douek, D
Eisele, E
Haase, A
Ho, YC
Hutter, G
Justement, JS
Keating, S
Lee, TH
Li, PL
Murray, D
Palmer, S
Pilcher, C
Pillai, S
Price, RW
Rothenberger, M
Schacker, T
Siliciano, J
Siliciano, R
Sinclair, E
Strain, M
Wong, J
Richman, D
Deeks, SG
AF Yukl, Steven A.
Boritz, Eli
Busch, Michael
Bentsen, Christopher
Chun, Tae-Wook
Douek, Daniel
Eisele, Evelyn
Haase, Ashley
Ho, Ya-Chi
Huetter, Gero
Justement, J. Shawn
Keating, Sheila
Lee, Tzong-Hae
Li, Peilin
Murray, Danielle
Palmer, Sarah
Pilcher, Christopher
Pillai, Satish
Price, Richard W.
Rothenberger, Meghan
Schacker, Timothy
Siliciano, Janet
Siliciano, Robert
Sinclair, Elizabeth
Strain, Matt
Wong, Joseph
Richman, Douglas
Deeks, Steven G.
TI Challenges in Detecting HIV Persistence during Potentially Curative
Interventions: A Study of the Berlin Patient
SO PLOS PATHOGENS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; CD4(+)
T-CELLS; FOLLICULAR DENDRITIC CELLS; DEFECTIVE VIRAL GENOMES; LOW-LEVEL
VIREMIA; CCR5 DELTA 32; LYMPHOID-TISSUE; REPLICATION-COMPETENT; LATENT
RESERVOIR
AB There is intense interest in developing curative interventions for HIV. How such a cure will be quantified and defined is not known. We applied a series of measurements of HIV persistence to the study of an HIV-infected adult who has exhibited evidence of cure after allogeneic hematopoietic stem cell transplant from a homozygous CCR5 Delta 32 donor. Samples from blood, spinal fluid, lymph node, and gut were analyzed in multiple laboratories using different approaches. No HIV DNA or RNA was detected in peripheral blood mononuclear cells (PBMC), spinal fluid, lymph node, or terminal ileum, and no replication-competent virus could be cultured from PBMCs. However, HIV RNA was detected in plasma (2 laboratories) and HIV DNA was detected in the rectum (1 laboratory) at levels considerably lower than those expected in ART-suppressed patients. It was not possible to obtain sequence data from plasma or gut, while an X4 sequence from PBMC did not match the pre-transplant sequence. HIV antibody levels were readily detectable but declined over time; T cell responses were largely absent. The occasional, low-level PCR signals raise the possibility that some HIV nucleic acid might persist, although they could also be false positives. Since HIV levels in well-treated individuals are near the limits of detection of current assays, more sensitive assays need to be developed and validated. The absence of recrudescent HIV replication and waning HIV-specific immune responses five years after withdrawal of treatment provide proof of a clinical cure.
C1 [Yukl, Steven A.; Li, Peilin; Pillai, Satish; Wong, Joseph] San Francisco VA Med Ctr SFVA, San Francisco, CA USA.
[Yukl, Steven A.; Li, Peilin; Pillai, Satish; Wong, Joseph] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Boritz, Eli; Douek, Daniel] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Busch, Michael; Keating, Sheila; Lee, Tzong-Hae] BSRI, San Francisco, CA USA.
[Bentsen, Christopher] Biorad Labs, Redmond, WA USA.
[Chun, Tae-Wook; Justement, J. Shawn; Murray, Danielle] NIAID, NIH, Bethesda, MD 20892 USA.
[Eisele, Evelyn; Ho, Ya-Chi; Siliciano, Janet; Siliciano, Robert] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Haase, Ashley; Rothenberger, Meghan; Schacker, Timothy] Univ Minnesota, Minneapolis, MN USA.
[Huetter, Gero] Heidelberg Univ, Inst Transfus Med & Immunol, Mannheim, Germany.
[Palmer, Sarah] Swedish Inst Infect Dis Control, Dept Diagnost & Vaccinol, Solna, Sweden.
[Palmer, Sarah] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Solna, Sweden.
[Pilcher, Christopher; Sinclair, Elizabeth; Deeks, Steven G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Price, Richard W.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Siliciano, Robert] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA.
[Strain, Matt; Richman, Douglas] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Strain, Matt; Richman, Douglas] Vet Affairs San Diego Healthcare Syst, San Diego, CA USA.
RP Yukl, SA (reprint author), San Francisco VA Med Ctr SFVA, San Francisco, CA USA.
EM sdeeks@php.ucsf.edu
OI Keating, Sheila/0000-0002-8324-3694
FU Foundation for AIDS Research (amFAR); Delaney AIDS Research Enterprise
(DARE) [U19AI0961090]; Department of Veterans Affairs [1 IK2
CX000520-01]; Intramural Research Program of the NIAID; National
Institutes of Health [AI 080193, AI69432, AI047745, AI74621, AI306214,
AI096113]; NIMH [R21 MH096619]; James Pendleton Charitable Trust; NIAID
[P01 AI071713, R01 AI087145, K24 AI069994]; Consortium for the
Performance of HIV Incidence Assays (CEPHIA); Bill and Melinda Gates
Foundation; UCSF/Gladstone Institute of Virology & Immunology CFAR [P30
AI027763]; UCSF Clinical and Translational Research Institute Clinical
Research Center [UL1 RR024131]; Gen-Probe; Bio-Rad Laboratories, Inc.
FX This work was primarily supported by the Foundation for AIDS Research
(amFAR). Additional support was provided by the Delaney AIDS Research
Enterprise (DARE, U19AI0961090), the Department of Veterans Affairs (1
IK2 CX000520-01), the Intramural Research Program of the NIAID, the NIH
Office of AIDS Research, the Collaboratory for AIDS Research on
Eradication (CARE) from the National Institutes of Health (awards AI
080193, AI69432, AI047745, AI74621, AI306214 [CFAR], and AI096113), the
NIMH (R21 MH096619), and the James Pendleton Charitable Trust. UCSF
Options study work was supported by NIAID (P01 AI071713) and the
Consortium for the Performance of HIV Incidence Assays (CEPHIA), with
funding from the Bill and Melinda Gates Foundation. The UCSF SCOPE
cohort was also supported by NIAID (R01 AI087145, K24 AI069994), the
UCSF/Gladstone Institute of Virology & Immunology CFAR (P30 AI027763),
and the UCSF Clinical and Translational Research Institute Clinical
Research Center (UL1 RR024131). The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.; Michael Busch has consulted for Gen-Probe (now owned by
Hologic), which provided support for some of the virologic measurements
performed in this study. Christopher Bentsen is currently employed by
Bio-Rad Laboratories, Inc. and received salary, benefits and stock. He
oversaw the testing of samples in this paper with FDA approved tests
from Bio-Rad. These relationships do not alter our adherence to all PLoS
Pathogens policies on sharing data and materials.
NR 56
TC 103
Z9 104
U1 6
U2 40
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD MAY
PY 2013
VL 9
IS 5
AR e1003347
DI 10.1371/journal.ppat.1003347
PG 13
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 159GE
UT WOS:000320032800025
PM 23671416
ER
PT J
AU Cannons, JL
Lu, KT
Schwartzberg, PL
AF Cannons, Jennifer L.
Lu, Kristina T.
Schwartzberg, Pamela L.
TI T follicular helper cell diversity and plasticity
SO TRENDS IN IMMUNOLOGY
LA English
DT Review
DE T follicular helper cells; Bcl-6; histone modification; T cell
plasticity
ID CENTER B-CELL; GERMINAL CENTER FORMATION; CXC CHEMOKINE RECEPTOR-5;
FACTOR BATF CONTROLS; HYPER-IGE SYNDROME; GENE-EXPRESSION; TRANSCRIPTION
FACTOR; MOLECULAR-MECHANISMS; TH2 DIFFERENTIATION; EPIGENETIC CONTROL
AB CD4(+) T helper (Th) cells play an instrumental role in orchestrating adaptive immune responses to invading pathogens through their ability to differentiate into specialized effector subsets. Part of this customized response requires the development of T follicular helper (Tfh) cells, which provide help to B cells for the generation of germinal centers (GCs) and long-term protective humoral responses. Although initially viewed as terminally differentiated, we now recognize that Th cell subsets, including Tfh cells, display substantial flexibility and overlap in their characteristics. In this review, we highlight advances in our understanding of Tfh cell development, cytokine production, and the potential plasticity that allows Tfh cells to possess characteristics of other effector Th cell populations.
C1 [Cannons, Jennifer L.; Lu, Kristina T.; Schwartzberg, Pamela L.] NIH, Natl Hunrian Genome Res Inst, Bethesda, MD 20892 USA.
RP Schwartzberg, PL (reprint author), NIH, Natl Hunrian Genome Res Inst, Bethesda, MD 20892 USA.
EM pams@mail.nih.gov
FU Intramural NIH HHS [Z99 HG999999, ZIA HG000123-13, ZIA HG000123-14, ZIA
HG000123-15]
NR 96
TC 43
Z9 50
U1 0
U2 22
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4906
J9 TRENDS IMMUNOL
JI Trends Immunol.
PD MAY
PY 2013
VL 34
IS 5
BP 200
EP 207
DI 10.1016/j.it.2013.01.001
PG 8
WC Immunology
SC Immunology
GA 159UO
UT WOS:000320073000002
PM 23395212
ER
PT J
AU Kiyatkin, EA
Wakabayashi, KT
Lenoir, M
AF Kiyatkin, Eugene A.
Wakabayashi, Ken T.
Lenoir, Magalie
TI Physiological Fluctuations in Brain Temperature as a Factor Affecting
Electrochemical Evaluations of Extracellular Glutamate and Glucose in
Behavioral Experiments
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Review
DE Brain metabolism; amperometry; enzyme-based sensors; glutamate; glucose;
neuronal activity; cerebral blood flow
ID FREELY MOVING RATS; PREOPTIC-ANTERIOR HYPOTHALAMUS; LOCALIZED
THERMAL-CHANGES; NATURAL AROUSING STIMULI; CENTRAL-NERVOUS-SYSTEM;
CEREBRAL-BLOOD-FLOW; NUCLEUS-ACCUMBENS; RAPID CHANGES; SUPRACHIASMATIC
NUCLEUS; MICROELECTRODE ARRAYS
AB The rate of any chemical reaction or process occurring in the brain depends on temperature. While it is commonly believed that brain temperature is a stable, tightly regulated homeostatic parameter, it fluctuates within 1-4 degrees C following exposure to salient arousing stimuli and neuroactive drugs, and during different behaviors. These temperature fluctuations should affect neural activity and neural functions, but the extent of this influence on neurochemical measurements in brain tissue of freely moving animals remains unclear. In this Review, we present the results of amperometric evaluations of extracellular glutamate and glucose in awake, behaving rats and discuss how naturally occurring fluctuations in brain temperature affect these measurements. While this temperature contribution appears to be insignificant for glucose because its extracellular concentrations are large, it is a serious factor for electrochemical evaluations of glutamate, which is present in brain tissue at much lower levels, showing smaller phasic fluctuations. We further discuss experimental strategies for controlling the nonspecific chemical and physical contributions to electrochemical currents detected by enzyme-based biosensors to provide greater selectivity and reliability of neurochemical measurements in behaving animals.
C1 [Kiyatkin, Eugene A.; Wakabayashi, Ken T.; Lenoir, Magalie] NIDA, In Vivo Electrophysiol Unit, Behav Neurosci Branch, Intramural Res Program,NIH,DHHS, Baltimore, MD 21224 USA.
RP Kiyatkin, EA (reprint author), NIDA, In Vivo Electrophysiol Unit, Behav Neurosci Branch, Intramural Res Program,NIH,DHHS, 333 Cassell Dr, Baltimore, MD 21224 USA.
EM ekiyatki@intra.nida.nih.gov
FU National Institute on Drug Abuse - Intramural Research Program, NIH
FX Supported by the National Institute on Drug Abuse - Intramural Research
Program, NIH.
NR 126
TC 19
Z9 19
U1 1
U2 18
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1948-7193
J9 ACS CHEM NEUROSCI
JI ACS Chem. Neurosci.
PD MAY
PY 2013
VL 4
IS 5
BP 652
EP 665
DI 10.1021/cn300232m
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA 148ND
UT WOS:000319250400003
PM 23448428
ER
PT J
AU Dauter, Z
AF Dauter, Zbigniew
TI On optimal placement of molecules in the unit cell
SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY
LA English
DT Article
ID SPACE-GROUPS; NORMALIZERS
AB There are currently no rules for a unified, standard way of placing macromolecular structures in the crystal lattice. An analysis of all possible symmetry-equivalent representations of molecular structures in various space groups leads to the concept of the anti-Cheshire symmetry and suggests that the center of a unique structural motif can always be placed within the selected asymmetric unit of the anti-Cheshire cell. The placement of structures according to this suggestion will ensure uniformity of presentation of all structurally equivalent Protein Data Bank models and will therefore diminish the possibility of confusing less crystallographically knowledgeable users of the PDB. The anti-Cheshire cells and their asymmetric units are defined and tabulated for all 65 space groups relevant to macromolecular crystallography that exhibit only rotational symmetry operations.
C1 NCI, Synchrotron Radiat Res Sect, MCL, Argonne Natl Lab, Argonne, IL 60439 USA.
RP Dauter, Z (reprint author), NCI, Synchrotron Radiat Res Sect, MCL, Argonne Natl Lab, Argonne, IL 60439 USA.
EM dauter@anl.gov
NR 11
TC 2
Z9 2
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0907-4449
J9 ACTA CRYSTALLOGR D
JI Acta Crystallogr. Sect. D-Biol. Crystallogr.
PD MAY
PY 2013
VL 69
SI SI
BP 872
EP 878
DI 10.1107/S0907444913002722
PN 5
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Crystallography
SC Biochemistry & Molecular Biology; Biophysics; Crystallography
GA 134UK
UT WOS:000318240200023
PM 23633598
ER
PT J
AU Grossman, CI
Purcell, DW
Rotheram-Borus, MJ
Veniegas, R
AF Grossman, Cynthia I.
Purcell, David W.
Rotheram-Borus, Mary Jane
Veniegas, Rosemary
TI Opportunities for HIV Combination Prevention to Reduce Racial and Ethnic
Health Disparities
SO AMERICAN PSYCHOLOGIST
LA English
DT Article
DE HIV prevention; HIV care; HIV testing; health disparities
ID US EMERGENCY-DEPARTMENTS; FOR-DISEASE-CONTROL; AFRICAN-AMERICAN;
ANTIRETROVIRAL THERAPY; POSTEXPOSURE PROPHYLAXIS; MEDICATION ADHERENCE;
CONSPIRACY BELIEFS; HIV/AIDS TREATMENT; LIMITED KNOWLEDGE; UNITED-STATES
AB Despite advances in HIV prevention and care, African Americans and Latino Americans remain at much higher risk of acquiring HIV, are more likely to be unaware of their HIV-positive status, are less likely to be linked to and retained in care, and are less likely to have suppressed viral load than are Whites. The first National HIV/AIDS Strategy (NHAS) has reducing these disparities as one of its three goals by encouraging the implementation of combination high-impact HIV intervention strategies. Federal agencies have expanded their collaborations in order to decrease HIV-related disparities through better implementation of data-driven decision making; integration and consolidation of the continuum of HIV care; and the reorganization of relationships among public health agencies, researchers, community-based organizations, and HIV advocates. Combination prevention, the integration of evidence-based and impactful behavioral, biomedical, and structural intervention strategies to reduce HIV incidence, provides the tools to address the HIV epidemic. Unfortunately, health disparities exist at every step along the HIV testing-to-care continuum. This provides an opportunity and a challenge to everyone involved in HIV prevention and care to understand and address health disparities as an integral part of ending the HIV epidemic in the United States. To further reduce health disparities, successful implementation of NHAS and combination prevention strategies will require multidisciplinary teams, including psychologists with diverse cultural backgrounds and experiences, to successfully engage groups at highest risk for HIV and those already infected with HIV. In order to utilize the comprehensive care continuum, psychologists and behavioral scientists have a role to play in reconceptualizing the continuum of care, conducting research to address health disparities, and creating community mobilization strategies.
C1 [Grossman, Cynthia I.] NIMH, Div AIDS Res, Bethesda, MD 20892 USA.
[Purcell, David W.] Ctr Dis Control & Prevent, Div HIV AIDS Prevent, Atlanta, GA USA.
[Rotheram-Borus, Mary Jane] Univ Calif Los Angeles, Ctr Community Hlth, Los Angeles, CA 90024 USA.
[Veniegas, Rosemary] Univ Calif Los Angeles, Dept Family Med, Los Angeles, CA 90024 USA.
RP Rotheram-Borus, MJ (reprint author), Univ Calif Los Angeles, Ctr Community Hlth, 10920 Wilshire Blvd,Suite 350, Los Angeles, CA 90024 USA.
EM cchpublications@mednet.ucla.edu
OI Purcell, David/0000-0001-8125-5168
FU Intramural CDC HHS [CC999999]; NCATS NIH HHS [UL1 TR000124,
UL1TR000124]; NIAID NIH HHS [5P30AI028697, P30 AI028697]; NIMH NIH HHS
[P30 MH058107, MH58107]
NR 77
TC 7
Z9 7
U1 4
U2 9
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0003-066X
J9 AM PSYCHOL
JI Am. Psychol.
PD MAY-JUN
PY 2013
VL 68
IS 4
SI SI
BP 237
EP 246
DI 10.1037/a0032711
PG 10
WC Psychology, Multidisciplinary
SC Psychology
GA 146FS
UT WOS:000319075900004
PM 23688091
ER
PT J
AU Taylor, KC
Carty, CL
Dumitrescu, L
Buzkova, P
Cole, SA
Hindorff, L
Schumacher, FR
Wilkens, LR
Shohet, RV
Quibrera, PM
Johnson, KC
Henderson, BE
Haessler, J
Franceschini, N
Eaton, CB
Duggan, DJ
Cochran, B
Cheng, I
Carlson, CS
Brown-Gentry, K
Anderson, G
Ambite, JL
Haiman, C
Le Marchand, L
Kooperberg, C
Crawford, DC
Buyske, S
North, KE
Fornage, M
AF Taylor, Kira C.
Carty, Cara L.
Dumitrescu, Logan
Buzkova, Petra
Cole, Shelley A.
Hindorff, Lucia
Schumacher, Fred R.
Wilkens, Lynne R.
Shohet, Ralph V.
Quibrera, P. Miguel
Johnson, Karen C.
Henderson, Brian E.
Haessler, Jeff
Franceschini, Nora
Eaton, Charles B.
Duggan, David J.
Cochran, Barbara
Cheng, Iona
Carlson, Chris S.
Brown-Gentry, Kristin
Anderson, Garnet
Ambite, Jose Luis
Haiman, Christopher
Le Marchand, Loic
Kooperberg, Charles
Crawford, Dana C.
Buyske, Steven
North, Kari E.
Fornage, Myriam
CA PAGE Study
TI Investigation of gene-by-sex interactions for lipid traits in diverse
populations from the population architecture using genomics and
epidemiology study
SO BMC GENETICS
LA English
DT Article
DE Lipids; Genetics; Cardiovascular disease; Heterogeneity; Sex-specific
effect; Association study
ID DENSITY-LIPOPROTEIN CHOLESTEROL; CORONARY-ARTERY-DISEASE; WIDE
ASSOCIATION; CARDIOVASCULAR-DISEASE; PLASMA TRIGLYCERIDES; METABOLIC
SYNDROME; APOLIPOPROTEIN A5; SERUM-LIPIDS; GENDER; RISK
AB Background: High-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) levels are influenced by both genes and the environment. Genome-wide association studies (GWAS) have identified similar to 100 common genetic variants associated with HDL-C, LDL-C, and/or TG levels, mostly in populations of European descent, but little is known about the modifiers of these associations. Here, we investigated whether GWAS-identified SNPs for lipid traits exhibited heterogeneity by sex in the Population Architecture using Genomics and Epidemiology (PAGE) study.
Results: A sex-stratified meta-analysis was performed for 49 GWAS-identified SNPs for fasting HDL-C, LDL-C, and ln (TG) levels among adults self-identified as European American (25,013). Heterogeneity by sex was established when p(het) < 0.001. There was evidence for heterogeneity by sex for two SNPs for ln(TG) in the APOA1/C3/A4/A5/BUD13 gene cluster: rs28927680 (p(het) = 7.4x10(-7)) and rs3135506 (p(het) = 4.3x10(-4)), one SNP in PLTP for HDL levels (rs7679; p(het) = 9.9x10(-4)), and one in HMGCR for LDL levels (rs12654264; p(het) = 3.1x10(-5)). We replicated heterogeneity by sex in five of seventeen loci previously reported by genome-wide studies (binomial p = 0.0009). We also present results for other racial/ethnic groups in the supplementary materials, to provide a resource for future meta-analyses.
Conclusions: We provide further evidence for sex-specific effects of SNPs in the APOA1/C3/A4/A5/BUD13 gene cluster, PLTP, and HMGCR on fasting triglyceride levels in European Americans from the PAGE study. Our findings emphasize the need for considering context-specific effects when interpreting genetic associations emerging from GWAS, and also highlight the difficulties in replicating interaction effects across studies and across racial/ethnic groups.
C1 [Taylor, Kira C.; Quibrera, P. Miguel; Franceschini, Nora; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27515 USA.
[Taylor, Kira C.] Univ Louisville, Sch Publ Hlth & Informat Sci, Dept Epidemiol & Populat Hlth, Louisville, KY 40292 USA.
[Carty, Cara L.; Haessler, Jeff; Carlson, Chris S.; Anderson, Garnet; Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Dumitrescu, Logan; Brown-Gentry, Kristin; Crawford, Dana C.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN USA.
[Buzkova, Petra] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Cole, Shelley A.] Texas Biomed Res Inst, Dept Genet, San Antonio, TX USA.
[Hindorff, Lucia] NHGRI, Off Populat Genom, NIH, Bethesda, MD 20892 USA.
[Schumacher, Fred R.; Henderson, Brian E.; Haiman, Christopher; Le Marchand, Loic] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Wilkens, Lynne R.] Univ Hawaii, Univ Hawaii Canc Ctr, Program Epidemiol, Honolulu, HI 96822 USA.
[Shohet, Ralph V.] Univ Hawaii, John A Burns Sch Med, Dept Med, Cardiovasc Res Ctr, Honolulu, HI 96822 USA.
[Johnson, Karen C.] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[Henderson, Brian E.] Univ So Calif, Zilkha Neurogenet Inst, Los Angeles, CA USA.
[Eaton, Charles B.] Brown Univ, Alpert Med Sch, Dept Family Med & Community Hlth, Providence, RI 02912 USA.
[Duggan, David J.] Translat Genom Res Inst, Integrated Canc Genom Div, Phoenix, AZ USA.
[Cochran, Barbara] Baylor Coll Med, Sponsored Programs, Houston, TX 77030 USA.
[Cheng, Iona] Univ Hawaii, Canc Res Ctr, Honolulu, HI 96813 USA.
[Ambite, Jose Luis] Univ So Calif, Inst Informat Sci, Los Angeles, CA USA.
[Crawford, Dana C.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
[Buyske, Steven] Rutgers State Univ, Dept Stat & Biostat, Piscataway, NJ USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Fornage, Myriam] Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, Div Epidemiol Human Genet & Environm Sci, Houston, TX USA.
[Fornage, Myriam] Univ Texas Houston, Hlth Sci Ctr, Inst Mol Med, Houston, TX USA.
RP Taylor, KC (reprint author), Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27515 USA.
EM kctayl04@louisville.edu
OI Buyske, Steven/0000-0001-8539-5416
FU NHGRI NIH HHS [U01 HG004790]
NR 48
TC 8
Z9 8
U1 1
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2156
J9 BMC GENET
JI BMC Genet.
PD MAY 1
PY 2013
VL 14
AR 33
DI 10.1186/1471-2156-14-33
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 155NT
UT WOS:000319755800001
PM 23634756
ER
PT J
AU Luo, JC
Nijveen, H
Attwood, T
Judge, D
Pongor, S
Landsman, D
Bishop, M
AF Luo, Jingchu
Nijveen, Harm
Attwood, Teresa
Judge, David
Pongor, Sandor
Landsman, David
Bishop, Martin
TI Obituary: In memory of Jack Leunissen
SO BRIEFINGS IN BIOINFORMATICS
LA English
DT Biographical-Item
C1 [Luo, Jingchu] Peking Univ, Coll Life Sci, Beijing, Peoples R China.
[Luo, Jingchu] Peking Univ, Ctr Bioinformat, Beijing, Peoples R China.
[Nijveen, Harm] Univ Wageningen & Res Ctr, NL-6700 HB Wageningen, Netherlands.
[Attwood, Teresa] Univ Manchester, Fac Life Sci, Manchester M13 9PL, Lancs, England.
[Attwood, Teresa] Univ Manchester, Sch Comp Sci, Manchester M13 9PL, Lancs, England.
[Judge, David] Univ Cambridge, Cambridge CB2 1TN, England.
[Landsman, David] NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Luo, JC (reprint author), Peking Univ, Coll Life Sci, Beijing, Peoples R China.
RI Nijveen, Harm/L-2272-2014;
OI Nijveen, Harm/0000-0002-9167-4945; Bishop, Martin/0000-0003-3357-1531;
Landsman, David/0000-0002-9819-6675
NR 1
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1467-5463
J9 BRIEF BIOINFORM
JI Brief. Bioinform.
PD MAY
PY 2013
VL 14
IS 3
BP 261
EP 262
DI 10.1093/bib/bbt036
PG 2
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 150ZC
UT WOS:000319429400001
PM 23696635
ER
PT J
AU Lerit, DA
Smyth, JT
Rusan, NM
AF Lerit, Dorothy A.
Smyth, Jeremy T.
Rusan, Nasser M.
TI Organelle asymmetry for proper fitness, function, and fate
SO CHROMOSOME RESEARCH
LA English
DT Article
DE Centrosome; Asymmetric; Organelle; Mitosis; Stem cell
ID STEM-CELL DIVISION; MESSENGER-RNA LOCALIZATION; SPINDLE POLE BODY;
DROSOPHILA-NEUROBLASTS; ENDOPLASMIC-RETICULUM; CENTROSOME SIZE; BUDDING
YEAST; GAMMA-TUBULIN; SACCHAROMYCES-CEREVISIAE; PERICENTRIOLAR MATERIAL
AB During cellular division, centrosomes are tasked with building the bipolar mitotic spindle, which partitions the cellular contents into two daughter cells. While every cell will receive an equal complement of chromosomes, not every organelle is symmetrically passaged to the two progeny in many cell types. In this review, we highlight the conservation of nonrandom centrosome segregation in asymmetrically dividing stem cells, and we discuss how the asymmetric function of centrosomes could mediate nonrandom segregation of organelles and mRNA. We propose that such a mechanism is critical for insuring proper cell fitness, function, and fate.
C1 [Lerit, Dorothy A.; Smyth, Jeremy T.; Rusan, Nasser M.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
RP Rusan, NM (reprint author), NHLBI, Cell Biol & Physiol Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM Nasser@nih.gov
RI Rusan, Nasser/P-3511-2016
FU Intramural NIH HHS [ZIA HL006126-03]
NR 86
TC 7
Z9 7
U1 0
U2 10
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0967-3849
J9 CHROMOSOME RES
JI Chromosome Res.
PD MAY
PY 2013
VL 21
IS 3
SI SI
BP 271
EP 286
DI 10.1007/s10577-013-9350-3
PG 16
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 150YQ
UT WOS:000319428100008
PM 23681659
ER
PT J
AU Klar, AJS
Bonaduce, MJ
AF Klar, Amar J. S.
Bonaduce, Michael J.
TI Unbiased segregation of fission yeast chromosome 2 strands to daughter
cells
SO CHROMOSOME RESEARCH
LA English
DT Article
DE Asymmetric cell division mechanism; Somatic DNA strand segregation;
Yeast mating-type switching; Cell differentiation
ID MATING-TYPE CASSETTES; DNA STRANDS; SCHIZOSACCHAROMYCES-POMBE;
EPIGENETIC INHERITANCE; CHROMATID SEGREGATION; S-POMBE; MECHANISM;
DIVISION; GENES; RECOMBINATION
AB The base complementarity feature (Watson and Crick in Nature 171(4356):737-738, 1953) and the rule of semi-conservative mode of DNA replication (Messelson and Stahl in Proc Natl Acad Sci U S A 44:671-682, 1958) dictate that two identical replicas of the parental chromosome are produced during replication. In principle, the inherent strand sequence differences could generate nonequivalent daughter chromosome replicas if one of the two strands were epigenetically imprinted during replication to effect silencing/expression of developmentally important genes. Indeed, inheritance of such a strand- and site-specific imprint confers developmental asymmetry to fission yeast sister cells by a phenomenon called mating/cell-type switching. Curiously, location of DNA strands with respect to each other at the centromere is fixed, and as a result, their selected segregation to specific sister chromatid copies occurs in eukaryotic cells. The yeast system provides a unique opportunity to determine the significance of such biased strand distribution to sister chromatids. We determined whether the cylindrical-shaped yeast cell distributes the specific chromosomal strand to the same cellular pole in successive cycles of cell division. By observing the pattern of recurrent mating-type switching in progenies of individual cells by microscopic analyses, we found that chromosome 2 strands are distributed by the random mode in successive cell divisions. We also exploited unusual "hotspot" recombination features of this system to investigate whether there is selective segregation of strands such that oldest Watson-containing strands co-segregate in the diploid cell at mitosis. Our data suggests that chromosome 2 strands are segregated independently to those of the homologous chromosome.
C1 [Klar, Amar J. S.; Bonaduce, Michael J.] NCI, Gene Regulat & Chromosome Biol Lab, Ctr Natl Canc Res, NIH, Frederick, MD 21702 USA.
RP Klar, AJS (reprint author), NCI, Gene Regulat & Chromosome Biol Lab, Ctr Natl Canc Res, NIH, Bldg 539,Room 154, Frederick, MD 21702 USA.
EM klara@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
FX We thank our laboratory colleagues Sharon Moore, Stephan Sauer, and Ken
Ishikawa for discussions and for critical reading of the manuscript. The
Intramural Research Program of the National Cancer Institute, National
Institutes of Health, supports our research.
NR 54
TC 0
Z9 0
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0967-3849
EI 1573-6849
J9 CHROMOSOME RES
JI Chromosome Res.
PD MAY
PY 2013
VL 21
IS 3
SI SI
BP 297
EP 309
DI 10.1007/s10577-013-9352-1
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 150YQ
UT WOS:000319428100010
PM 23681661
ER
PT J
AU Sauer, S
Burkett, SS
Lewandoski, M
Klar, AJS
AF Sauer, Stephan
Burkett, Sandra S.
Lewandoski, Mark
Klar, Amar J. S.
TI A CO-FISH assay to assess sister chromatid segregation patterns in
mitosis of mouse embryonic stem cells
SO CHROMOSOME RESEARCH
LA English
DT Article
DE Asymmetric cell division mechanism; somatic strand segregation; mouse
stem cell biology and cell differentiation
ID MAMMALIAN-CELLS; BROMODEOXYURIDINE MUTAGENESIS; DNA STRANDS; DIVISION;
DEOXYCYTIDINE; REPLICATION; YEAST; PCR
AB Sister chromatids contain identical DNA sequence but are chiral with respect to both their helical handedness and their replication history. Emerging evidence from various model organisms suggests that certain stem cells segregate sister chromatids nonrandomly to either maintain genome integrity or to bias cellular differentiation in asymmetric cell divisions. Conventional methods for tracing of old vs. newly synthesized DNA strands generally lack resolution for individual chromosomes and employ halogenated thymidine analogs with profound cytotoxic effects on rapidly dividing cells. Here, we present a modified chromosome orientation fluorescence in situ hybridization (CO-FISH) assay, where identification of individual chromosomes and their replication history is achieved in subsequent hybridization steps with chromosome-specific DNA probes and PNA telomere probes. Importantly, we tackle the issue of BrdU cytotoxicity and show that our method is compatible with normal mouse ES cell biology, unlike a recently published related protocol. Results from our CO-FISH assay show that mitotic segregation of mouse chromosome 7 is random in ES cells, which contrasts previously published results from our laboratory and settles a controversy. Our straightforward protocol represents a useful resource for future studies on chromatid segregation patterns of in vitro-cultured cells from distinct model organisms.
C1 [Sauer, Stephan; Klar, Amar J. S.] NIH, Gene Regulat & Chromosome Biol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Burkett, Sandra S.] NIH, Mol Cytogenet Sect, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Sauer, Stephan; Lewandoski, Mark] NIH, Canc & Dev Biol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Klar, Amar J. S.] NCI, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Klar, AJS (reprint author), NCI, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res, NIH, Bldg 539,Room 154, Frederick, MD 21702 USA.
EM klara@mail.nih.gov
FU National Cancer Institute, National Institutes of Health; International
Human Frontier Science Organization [HFSP LT000444/2009]
FX We thank our laboratory colleagues Sharon Moore and Ken Ishikawa for
helpful discussions. We would like to thank Dr. Jonathan Keller for
sharing his laboratory space and reagents and for helpful comments. Dr.
Stephen Lockett, Kim Peifley, and Alla Brafman (Office of the Director)
provided outstanding support with Confocal microscope set up and
imaging. Kathleen Noer, Guity Mohammadi and Roberta Matthai (Cancer and
Inflammation Program) provided help with flow cytometry. The Intramural
Research Program of the National Cancer Institute, National Institutes
of Health, supports our research. Stephan Sauer is recipient of a
long-term fellowship by the International Human Frontier Science
Organization (HFSP LT000444/2009).
NR 34
TC 6
Z9 6
U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0967-3849
J9 CHROMOSOME RES
JI Chromosome Res.
PD MAY
PY 2013
VL 21
IS 3
SI SI
BP 311
EP 328
DI 10.1007/s10577-013-9358-8
PG 18
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 150YQ
UT WOS:000319428100011
PM 23681662
ER
PT J
AU Vitiello, B
AF Vitiello, Benedetto
TI How Effective are the Current Treatments for Children Diagnosed with
Manic/Mixed Bipolar Disorder?
SO CNS DRUGS
LA English
DT Editorial Material
ID CONTROLLED-TRIAL; RISPERIDONE; ADOLESCENTS; MANIA
C1 NIMH, Bethesda, MD 20892 USA.
RP Vitiello, B (reprint author), NIMH, Room 7147,6001 Execut Blvd, Bethesda, MD 20892 USA.
EM bvitiell@mail.nih.gov
NR 11
TC 0
Z9 0
U1 0
U2 3
PU ADIS INT LTD
PI AUCKLAND
PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW
ZEALAND
SN 1172-7047
J9 CNS DRUGS
JI CNS Drugs
PD MAY
PY 2013
VL 27
IS 5
BP 331
EP 333
DI 10.1007/s40263-013-0060-3
PG 3
WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 149CW
UT WOS:000319296600001
PM 23640534
ER
PT J
AU Berger, VW
AF Berger, Vance W.
TI What do non-randomized trials offer above and beyond randomized trials?
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Letter
DE Observational studies; Randomized trials; Selection bias; Validity
ID CLINICAL-TRIALS
C1 [Berger, Vance W.] NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
[Berger, Vance W.] UMBC, Bethesda, MD 20892 USA.
RP Berger, VW (reprint author), NCI, Biometry Res Grp, Executive Plaza North,Suite 3131,6130 Executive, Bethesda, MD 20892 USA.
EM vb78c@nih.gov
NR 7
TC 2
Z9 2
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD MAY
PY 2013
VL 35
IS 1
BP 168
EP 169
DI 10.1016/j.cct.2013.03.008
PG 2
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 153YD
UT WOS:000319637800020
PM 23545076
ER
PT J
AU Popuri, V
Tadokoro, T
Croteau, DL
Bohr, VA
AF Popuri, Venkateswarlu
Tadokoro, Takashi
Croteau, Deborah L.
Bohr, Vilhelm A.
TI Human RECQL5: Guarding the crossroads of DNA replication and
transcription and providing backup capability
SO CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Review
DE Base excision repair; DNA replication; homologous recombination; RecQ
helicases; transcription
ID RNA-POLYMERASE-II; WERNER-SYNDROME PROTEIN; CELL-CYCLE PROGRESSION;
MAINTAINS GENOMIC STABILITY; BASE EXCISION-REPAIR; STRAND BREAK REPAIR;
S-PHASE CHECKPOINT; HOMOLOGOUS RECOMBINATION; HUMAN RECQ5-BETA; HELICASE
ACTIVITY
AB DNA helicases are ubiquitous enzymes that catalyze unwinding of duplex DNA and function in all metabolic processes in which access to single-stranded DNA is required, including DNA replication, repair, recombination and RNA transcription. RecQ helicases are a conserved family of DNA helicases that display highly specialized and vital roles in the maintenance of genome stability. Mutations in three of the five human RecQ helicases, BLM, WRN and RECQL4 are associated with the genetic disorders Bloom syndrome, Werner syndrome and Rothmund-Thomson syndrome that are characterized by chromosomal instability, premature aging and predisposition to cancer. The biological role of human RECQL5 is only partially understood and RECQL5 has not yet been associated with any human disease. Illegitimate recombination and replication stress are hallmarks of human cancers and common instigators for genomic instability and cell death. Recql5 knockout mice are cancer prone and show increased chromosomal instability. Recql5-deficient mouse embryonic fibroblasts are sensitive to camptothecin and display elevated levels of sister chromatid exchanges. Unlike other human RecQ helicases, RECQL5 is recruited to single-stranded DNA breaks and is also proposed to play an essential role in RNA transcription. Here, we review the established roles of RECQL5 at the cross roads of DNA replication, recombination and transcription, and propose that human RECQL5 provides important backup functions in the absence of other DNA helicases.
C1 [Popuri, Venkateswarlu; Tadokoro, Takashi; Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
FU National Institute on Aging, NIH [AG000726-20]
FX The authors declare no conflict of interest. This work was supported by
funds from the Intramural Research Program of the National Institute on
Aging, NIH, AG000726-20.
NR 110
TC 10
Z9 10
U1 0
U2 13
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1040-9238
J9 CRIT REV BIOCHEM MOL
JI Crit. Rev. Biochem. Mol. Biol.
PD MAY-JUN
PY 2013
VL 48
IS 3
BP 289
EP 299
DI 10.3109/10409238.2013.792770
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 155JE
UT WOS:000319743000004
PM 23627586
ER
PT J
AU Paolicchi, E
Crea, F
Farrar, WL
Green, JE
Danesi, R
AF Paolicchi, Elisa
Crea, Francesco
Farrar, William L.
Green, Jeffrey E.
Danesi, Romano
TI Histone lysine demethylases in breast cancer
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Histone lysine demethylase; KDM3B; KDM5A; KDM6A; Polycomb; Breast cancer
ID CELLULAR-DIFFERENTIATION; GENE; PROTEIN; FAMILY; REPRESSOR; CELLS; MYC
AB Histone lysine demethylases (KDMs) have been recently discovered in mammals and have been nicknamed "erasers" for their ability to remove methyl groups from histone substrates. In cancer cells, KDMs can activate or repress gene transcription, behaving as oncogenes or tumor suppressors depending upon the cellular context. In order to investigate the potential role of KDMs in Breast Cancer (BC), we queried the Oncomine database and determined that the expression of KDMs correlates with BC prognosis. High expression of KDM3B and KDM5A is associated with a better prognosis (no recurrence after mastectomy p = 0.005 and response to docetaxel p = 0.005); conversely, KDM6A is overexpressed in BC patients with an unfavorable prognosis (mortality at 1 year, p = 8.65E-7). Our findings suggest that KDMs could be potential targets for BC therapy. Further, altering the interactions between KDMs and Polycomb Group genes (PcG) may provide novel avenues for therapy that specifically targets these genes in BC. Published by Elsevier Ireland Ltd.
C1 [Paolicchi, Elisa; Green, Jeffrey E.] NCI, Transgen Oncogenesis & Genom Sect, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Paolicchi, Elisa; Crea, Francesco; Danesi, Romano] Univ Pisa, Div Pharmacol, Dept Internal Med, I-56100 Pisa, Italy.
[Farrar, William L.] NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21701 USA.
RP Green, JE (reprint author), NCI, Transgen Oncogenesis & Genom Sect, Lab Canc Biol & Genet, Bldg 37,Room 4054,37 Convent Dr, Bethesda, MD 20892 USA.
EM jegreen@nih.gov
RI Crea, Francesco /I-8383-2015;
OI Paolicchi, Elisa/0000-0001-6101-7576; Crea,
Francesco/0000-0002-4903-2973
FU Federal funds from the National Cancer Institute, National Institutes of
Health [N01-CO-12400]; Intramural Research Program of the NIH, Center
for Cancer Research, National Cancer Institute; Italian MIUR
[20084TA5KL_004]; Ministero dell'Istruzione dell'Universita' e della
Ricerca, Rome (PRIN)
FX This publication has been supported in part by Federal funds from the
National Cancer Institute, National Institutes of Health, under contract
No. N01-CO-12400, by the Intramural Research Program of the NIH, Center
for Cancer Research, National Cancer Institute and by the Italian MIUR
project 20084TA5KL_004 to RD. 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 US Government.
Partially supported by Ministero dell'Istruzione dell'Universita' e
della Ricerca, Rome (PRIN 2008) to RD (Epigenetic manipulation and
reversal of resistance to Irinotecan in human colorectal cancer cell
lines).
NR 26
TC 16
Z9 17
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1040-8428
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD MAY
PY 2013
VL 86
IS 2
BP 97
EP 103
DI 10.1016/j.critrevonc.2012.11.008
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 137VQ
UT WOS:000318466700001
PM 23266085
ER
PT J
AU Brady, BL
Muljo, SA
AF Brady, Brenna L.
Muljo, Stefan A.
TI RNA decay tolerizes MCPIP1 (Zc3h12a) keeps inflammation in check by
cleaving 3 ' UTRs
SO IMMUNOLOGY AND CELL BIOLOGY
LA English
DT Editorial Material
ID DEGRADATION; ACTIVATION; MICE
C1 [Brady, Brenna L.; Muljo, Stefan A.] NIAID, Integrat Immunobiol Unit, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Brady, BL (reprint author), NIAID, Integrat Immunobiol Unit, Immunol Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM Stefan.Muljo@nih.gov
RI Muljo, Stefan/F-5671-2015
OI Muljo, Stefan/0000-0003-1013-446X
NR 11
TC 2
Z9 3
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0818-9641
J9 IMMUNOL CELL BIOL
JI Immunol. Cell Biol.
PD MAY-JUN
PY 2013
VL 91
IS 5
BP 331
EP 332
DI 10.1038/icb.2013.19
PG 2
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA 152BS
UT WOS:000319505200001
PM 23628803
ER
PT J
AU Kintu, K
Andrew, P
Musoke, P
Richardson, P
Asiimwe-Kateera, B
Nakyanzi, T
Wang, L
Fowler, MG
Emel, L
Ou, SS
Baglyos, L
Gurunathan, S
Zwerski, S
Jackson, JB
Guay, L
AF Kintu, Kenneth
Andrew, Philip
Musoke, Philippa
Richardson, Paul
Asiimwe-Kateera, Brenda
Nakyanzi, Teopista
Wang, Lei
Fowler, Mary Glenn
Emel, Lynda
Ou, San-San
Baglyos, Lynn
Gurunathan, Sanjay
Zwerski, Sheryl
Jackson, Jay Brooks
Guay, Laura
TI Feasibility and Safety of ALVAC-HIV vCP1521 Vaccine in HIV-Exposed
Infants in Uganda: Results From the First HIV Vaccine Trial in Infants
in Africa
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article; Proceedings Paper
CT AIDS Vaccine 2010
CY SEP 28-OCT 01, 2010
CL Atlanta, GA
DE HIV vaccine; ALVAC; infants; Africa; breast milk transmission
ID TO-CHILD TRANSMISSION; HIV-1-INFECTED WOMEN; CANARYPOX VACCINE; DOSE
NEVIRAPINE; PREVENTION; IMMUNOGENICITY; INFECTION; PROPHYLAXIS;
COMBINATION; VOLUNTEERS
AB Background: The development of a safe and effective vaccine against HIV type 1 for the prevention of mother-to-child transmission of HIV would significantly advance the goal of eliminating HIV infection in children. Safety and feasibility results from phase 1, randomized, double-blind, placebo-controlled trial of ALVAC-HIV vCP1521 in infants born to HIV type 1-infected women in Uganda are reported.
Methods: HIV-exposed infants were enrolled at birth and randomized (4:1) to receive vaccine or saline placebo intramuscular injections at birth, 4, 8, and 12 weeks of age. Vaccine reactogenicity was assessed at vaccination and days 1 and 2 postvaccination. Infants were followed until 24 months of age. HIV infection status was determined by HIV DNA polymerase chain reaction.
Results: From October 2006 to May 2007, 60 infants (48 vaccine and 12 placebo) were enrolled with 98% retention at 24 months. One infant was withdrawn, but there were no missed visits or vaccinations among the 59 infants retained. Immune responses elicited by diphtheria, polio, hepatitis B, haemophilus influenzae type B, and measles vaccination were similar in the 2 arms. The vaccine was well tolerated with no severe or life-threatening reactogenicity events. Adverse events were equally distributed across both study arms. Four infants were diagnosed as HIV infected [3 at birth (2 vaccine and 1 placebo) and 1 in vaccine arm at 2 weeks of age].
Conclusion: The ALVAC-HIV vCP1521 vaccination was feasible and safe in infants born to HIV-infected women in Uganda. The conduct of high-quality infant HIV vaccine trials is achievable in Africa.
C1 [Kintu, Kenneth; Musoke, Philippa; Asiimwe-Kateera, Brenda; Nakyanzi, Teopista] Makerere Univ Johns Hopkins Univ Res Collaborat, Kampala, Uganda.
[Andrew, Philip] Family Hlth Int 360, Res Triangle Pk, NC USA.
[Richardson, Paul; Fowler, Mary Glenn; Jackson, Jay Brooks] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Wang, Lei; Emel, Lynda; Ou, San-San] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Baglyos, Lynn; Gurunathan, Sanjay] Sanofi Pasteur, Sch Publ Hlth & Hlth Serv, Swiftwater, PA USA.
[Zwerski, Sheryl] NIAID, Dept Prevent Sci, Div AIDS, Bethesda, MD 20892 USA.
[Guay, Laura] George Washington Univ, Sch Publ Hlth & Hlth Serv, Washington, DC USA.
RP Kintu, K (reprint author), Makerere Univ Johns Hopkins Univ Res Collaborat, POB 23491, Kampala, Uganda.
EM kkintu@mujhu.org
FU NIAID NIH HHS [U01 AI046749, U01AI46749, U01 AI048054, UM1 AI068632, U01
AI068632, U01 AI48054, U01 AI069530, U01AI068632]
NR 32
TC 11
Z9 11
U1 1
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD MAY 1
PY 2013
VL 63
IS 1
BP 1
EP 8
DI 10.1097/QAI.0b013e31827f1c2d
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 146SW
UT WOS:000319112200010
PM 23221981
ER
PT J
AU Kreitchmann, R
Best, BM
Wang, J
Stek, A
Caparelli, E
Watts, DH
Smith, E
Shapiro, DE
Rossi, S
Burchett, SK
Hawkins, E
Byroads, M
Cressey, TR
Mirochnick, M
AF Kreitchmann, Regis
Best, Brookie M.
Wang, Jiajia
Stek, Alice
Caparelli, Edmund
Watts, D. Heather
Smith, Elizabeth
Shapiro, David E.
Rossi, Steve
Burchett, Sandra K.
Hawkins, Elizabeth
Byroads, Mark
Cressey, Tim R.
Mirochnick, Mark
TI Pharmacokinetics of an Increased Atazanavir Dose With and Without
Tenofovir During the Third Trimester of Pregnancy
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
ID RITONAVIR-BOOSTED ATAZANAVIR; LOPINAVIR EXPOSURE; NELFINAVIR;
PARAMETERS; SAQUINAVIR; INDINAVIR; ADULTS; WOMEN
AB Background: Reduced atazanavir exposure has been demonstrated during pregnancy with standard atazanavir/ritonavir dosing. We studied an increased dose during the third trimester of pregnancy.
Methods: International Maternal Pediatric Adolescent AIDS Clinical Trials Group 1026s is a prospective, nonblinded, pharmacokinetic study of HIV-infected pregnant women taking antiretrovirals for clinical indications, including 2 cohorts (with or without tenofovir) receiving atazanavir/ritonavir 300/100 mg once daily during the second trimester, 400/100 mg during the third trimester, and 300/100 mg postpartum (PP). Intensive steady-state 24-hour pharmacokinetic profiles were performed. Atazanavir concentrations were measured by high-performance liquid chromatography. Pharmacokinetic targets were the 10th percentile atazanavir area under the concentration versus time curve (AUC) (29.4 mu g.hr(-1).mL(-1).) in nonpregnant adults on standard dose and 0.15 mu g/mL, minimum trough concentration.
Results: Atazanavir pharmacokinetic data were available for 37 women without tenofovir, 35 with tenofovir; median (range) pharmacokinetic parameters are presented for second trimester, third trimester, and PP and number who met target/total.
Atazanavir Without Tenofovir: AUC 30.5 (9.19-93.8), 45.7 (11-88.3), and 48.8 (9.9-112.2) mu g.hr(-1).mL(-1), and 8/14, 29/37, and 27/34 met target. C-24 h was 0.49 (0.09-4.09), 0.71 (0.14-2.09), and 0.90 (0.05-2.73) mu g/mL; 13/14, 36/37, and 29/34 met target.
Atazanavir With Tenofovir: AUC 26.2 (6.8-60.9) (P < 0.05 compared with PP), 37.7 (0.72-88.2) (P, 0.05 compared with PP), and 58.6 (6-149) mu g.hr(-1).mL(-1), and 7/17, 23/32, and 27/29 met target. C24-h was 0.44 (0.12-1.06) (P < 0.05 compared with PP), 0.57 (0.02-2.06) (P < 0.05 compared with PP), and 1.26 (0.095.43) mg/mL; 7/17, 23/32, and 27/29 met target. Atazanavir/ritonavir was well tolerated with no unanticipated adverse events.
Conclusions: Atazanavir/ritonavir increased to 400/100 mg provides adequate atazanavir exposure during the third trimester and should be considered during the second trimester.
C1 [Kreitchmann, Regis] Irmandade Santa Casa Misericordia Porto Alegre, HIV AIDS Res Dept, Porto Alegre, RS, Brazil.
[Best, Brookie M.; Caparelli, Edmund; Rossi, Steve] Univ Calif San Diego, Dept Pediat, Rady Childrens Hosp San Diego, San Diego, CA 92103 USA.
[Best, Brookie M.; Caparelli, Edmund] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, San Diego, CA 92103 USA.
[Wang, Jiajia; Shapiro, David E.] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Stek, Alice] Univ So Calif, Sch Med, Dept Obstet & Gynecol, Los Angeles, CA 90033 USA.
[Watts, D. Heather] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, Bethesda, MD USA.
[Smith, Elizabeth] NIAID, Bethesda, MD 20892 USA.
[Burchett, Sandra K.] Childrens Hosp Boston, Boston, MA USA.
[Hawkins, Elizabeth] Social & Sci Syst Inc, IMPAACT Operat Off, Silver Spring, MD USA.
[Byroads, Mark] Frontier Sci & Technol Res, Amherst, NY USA.
[Cressey, Tim R.] Chiang Mai Univ, Fac Associated Med Sci, Program HIV Prevent & Treatment, Dept Med Technol, Chiang Mai 50000, Thailand.
[Cressey, Tim R.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Cressey, Tim R.] IRD, Marseille, France.
[Mirochnick, Mark] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Kreitchmann, R (reprint author), Av Lucas de Oliveira 1937-202, BR-90460001 Porto Alegre, RS, Brazil.
EM regis.kr@terra.com.br
FU International Maternal Pediatric Adolescent AIDS Clinical Trials Group
(IMPAACT); National Institute of Allergy and Infectious Diseases (NIAID)
[U01 AI068632]; Eunice Kennedy Shriver National Institute of Child
Health and Human Development (NICHD); National Institute of Mental
Health (NIMH) NIAID cooperative agreement [U01 AI41110]; Pediatric AIDS
Clinical Trials Group (PACTG) [1 U01 AI068616]; IMPAACT Group; NIAID;
NICHD International and Domestic Pediatric and Maternal HIV Clinical
Trials Network; NICHD [N01-DK-9-001/HHSN267200800001C]
FX Overall support for the International Maternal Pediatric Adolescent AIDS
Clinical Trials Group (IMPAACT) was provided by the National Institute
of Allergy and Infectious Diseases (NIAID) [U01 AI068632], the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD), and the National Institute of Mental Health (NIMH) [AI068632].
This work was supported by the Statistical and Data Management Center at
Harvard School of Public Health, under the NIAID cooperative agreement
#5 U01 AI41110 with the Pediatric AIDS Clinical Trials Group (PACTG) and
#1 U01 AI068616 with the IMPAACT Group. Support of the sites was
provided by the NIAID the NICHD International and Domestic Pediatric and
Maternal HIV Clinical Trials Network funded by NICHD (contract number
N01-DK-9-001/HHSN267200800001C).
NR 22
TC 12
Z9 12
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD MAY 1
PY 2013
VL 63
IS 1
BP 59
EP 66
DI 10.1097/QAI.0b013e318289b4d2
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 146SW
UT WOS:000319112200018
PM 23392467
ER
PT J
AU Richardson, BA
Kelly, C
Ramjee, G
Fleming, T
Makanani, B
Roberts, S
Musara, P
Mkandawire, N
Moench, T
Coletti, A
Soto-Torres, L
Karim, SA
AF Richardson, Barbra A.
Kelly, Cliff
Ramjee, Gita
Fleming, Thomas
Makanani, Bonus
Roberts, Sarah
Musara, Petina
Mkandawire, Nkhafwire
Moench, Thomas
Coletti, Anne
Soto-Torres, Lydia
Karim, Salim A.
CA IIPTN 035 Study Team
TI Appropriateness of Hydroxyethylcellulose Gel as a Placebo Control in
Vaginal Microbicide Trials: A Comparison of the Two Control Arms of HPTN
035
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article; Proceedings Paper
CT International Conference on Microbicides
CY MAY 22-25, 2010
CL Pittsburgh, PA
DE HIV prevention; vaginal microbicide; placebo; women; sexually
transmitted infections
ID RANDOMIZED CONTROLLED-TRIAL; HIV PREVENTION; LUBRICANT GEL;
TRANSMISSION; INFECTION; DIAPHRAGM
AB Objective: To compare the 2 control arms of HPTN 035 [a hydroxyethylcellulose (HEC) gel control arm and a no-gel control arm] to assess the behavioral effects associated with gel use and direct causal effects of the HEC gel on sexually transmitted infections (STIs), pregnancy, and genital safety.
Design: Randomized trial with 1 blinded (HEC gel) and 1 openlabel (no-gel) control arms.
Methods: HIV-uninfected, sexually active women were randomized into the HEC gel arm (n = 771) and into the no-gel arm (n = 772) in 5 countries. Participants in the HEC gel arm were instructed to insert the study gel intravaginally,1 hour before each vaginal sex act. Data on sexual behavior, adherence, safety, pregnancy, and STIs were collected quarterly for 12-30 months of follow-up.
Results: During follow-up, mean reported condom use in the past week was significantly higher in the no-gel arm (81% versus 70%, P < 0.001). There were no significant differences, after adjusting for this differential condom use, between the 2 arms in the rates of genital safety events, pregnancy outcomes, or STIs, including HIV-1.
Conclusions: In this large randomized trial, we found no significant differences between the no-gel and HEC gel arms in the rates of genital safety events, pregnancy outcomes, or STIs. These results aid interpretation of the results of previous vaginal microbicide trials that used the HEC gel as a control. The HEC gel is suitable as a control for ongoing and future vaginal microbicide studies.
C1 [Richardson, Barbra A.; Fleming, Thomas] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Kelly, Cliff] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Ramjee, Gita] MRC, HIV Prevent Res Unit, Tygerberg, South Africa.
[Makanani, Bonus] Johns Hopkins Univ Res Project, Dept Obstet & Gynecol, Blantyre, Malawi.
[Roberts, Sarah] Univ Alabama Birmingham, Birmingham, AL USA.
[Musara, Petina] UZ UCSF Res Programme, Harare, Zimbabwe.
[Mkandawire, Nkhafwire] UNC Project, Lilongwe, Malawi.
[Moench, Thomas] ReProtect Inc, Baltimore, MD USA.
[Coletti, Anne] Family Hlth Int, Res Triangle Pk, NC 27709 USA.
[Soto-Torres, Lydia] Natl Inst Allergy & Infect Dis, Bethesda, MD USA.
[Karim, Salim A.] Univ KwaZulu Natal, CAPRISA, Durban, South Africa.
RP Richardson, BA (reprint author), Univ Washington, MS359909,325 9th Ave, Seattle, WA 98104 USA.
EM bar-brar@u.washington.edu
RI Abdool Karim, Salim Safurdeen/N-5947-2013
OI Abdool Karim, Salim Safurdeen/0000-0002-4986-2133
FU NCATS NIH HHS [UL1 TR000454]; NIAID NIH HHS [U01 AI046749, U01 AI068633,
U01AI068633, U01AI46749, UM1 AI068615]
NR 20
TC 5
Z9 5
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD MAY 1
PY 2013
VL 63
IS 1
BP 120
EP 125
DI 10.1097/QAI.0b013e31828607c5
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 146SW
UT WOS:000319112200026
PM 23334506
ER
PT J
AU Rajapakse, N
Berzon, R
Linde, S
Coulouris, N
Artiles, L
Heppner, E
AF Rajapakse, Nishadi
Berzon, Richard
Linde, Sarah
Coulouris, Natasha
Artiles, Ligia
Heppner, Eliza
TI Untitled
SO JOURNAL OF HEALTH CARE FOR THE POOR AND UNDERSERVED
LA English
DT Editorial Material
C1 [Rajapakse, Nishadi; Berzon, Richard; Artiles, Ligia] Natl Inst Minor Hlth & Hlth Dispar, Div Sci Programs, NIH, Bethesda, MD 20892 USA.
[Linde, Sarah] HRSA, Off Administrator, Rockville, MD USA.
[Coulouris, Natasha; Heppner, Eliza] HRSA, Off Planning Anal & Evaluat, Rockville, MD USA.
RP Rajapakse, N (reprint author), Natl Inst Minor Hlth & Hlth Dispar, Div Sci Programs, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
21218-4363 USA
SN 1049-2089
J9 J HEALTH CARE POOR U
JI J. Health Care Poor Underserved
PD MAY
PY 2013
VL 24
IS 2
SU S
BP XIII
EP XV
PG 3
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 151VB
UT WOS:000319487300003
PM 23727977
ER
PT J
AU Lee, PR
Raymond, GV
AF Lee, Paul R.
Raymond, Gerald V.
TI Child Neurology: Zellweger syndrome
SO NEUROLOGY
LA English
DT Editorial Material
ID PEROXISOME BIOGENESIS DISORDERS; MUTATION; GENE
C1 [Lee, Paul R.] NINDS, NIH, Bethesda, MD 20892 USA.
[Raymond, Gerald V.] Johns Hopkins Sch Med, Kennedy Krieger Inst, Div Neurogenet, Baltimore, MD USA.
RP Lee, PR (reprint author), NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM Paul.lee@nih.gov
FU Intramural NIH HHS
NR 10
TC 9
Z9 11
U1 0
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD MAY
PY 2013
VL 80
IS 20
BP E207
EP E210
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 148NI
UT WOS:000319251000001
PM 23671347
ER
PT J
AU Gong, J
Hsu, L
Harrison, T
King, IB
Sturup, S
Song, XL
Duggan, D
Liu, Y
Hutter, C
Chanock, SJ
Eaton, CB
Marshall, JR
Peters, U
AF Gong, Jian
Hsu, Li
Harrison, Tabitha
King, Irena B.
Sturup, Stefan
Song, Xiaoling
Duggan, David
Liu, Yan
Hutter, Carolyn
Chanock, Stephen J.
Eaton, Charles B.
Marshall, James R.
Peters, Ulrike
TI Genome-Wide Association Study of Serum Selenium Concentrations
SO NUTRIENTS
LA English
DT Article
DE selenium; serum; selenoprotein; genome-wide association study; AGA;
NEIL3; SLC39A11
ID PROSTATE-CANCER RISK; SELENOPROTEIN-P; GENETIC-VARIATION; OXIDATIVE
STRESS; HUMAN HEALTH; METAANALYSIS; DEFICIENCY; POLYMORPHISMS; SEQUENCE;
DISEASES
AB Selenium is an essential trace element and circulating selenium concentrations have been associated with a wide range of diseases. Candidate gene studies suggest that circulating selenium concentrations may be impacted by genetic variation; however, no study has comprehensively investigated this hypothesis. Therefore, we conducted a two-stage genome-wide association study to identify genetic variants associated with serum selenium concentrations in 1203 European descents from two cohorts: the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening and the Women's Health Initiative (WHI). We tested association between 2,474,333 single nucleotide polymorphisms (SNPs) and serum selenium concentrations using linear regression models. In the first stage (PLCO) 41 SNPs clustered in 15 regions had p < 1 x 10(-5). None of these 41 SNPs reached the significant threshold (p = 0.05/15 regions = 0.003) in the second stage (WHI). Three SNPs had p < 0.05 in the second stage (rs1395479 and rs1506807 in 4q34.3/AGA-NEIL3; and rs891684 in 17q24.3/SLC39A11) and had p between 2.62 x 10(-7) and 4.04 x 10(-7) in the combined analysis (PLCO + WHI). Additional studies are needed to replicate these findings. Identification of genetic variation that impacts selenium concentrations may contribute to a better understanding of which genes regulate circulating selenium concentrations.
C1 [Gong, Jian; Hsu, Li; Harrison, Tabitha; Song, Xiaoling; Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Hsu, Li] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[King, Irena B.] Univ New Mexico, Dept Internal Med, Albuquerque, NM 87131 USA.
[Sturup, Stefan] Univ Copenhagen, Dept Pharm, DK-2100 Copenhagen, Denmark.
[Duggan, David] Translat Genom Res Inst, Phoenix, AZ 85004 USA.
[Liu, Yan] Stephens & Associates, Carrollton, TX 75006 USA.
[Hutter, Carolyn] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Eaton, Charles B.] Brown Univ, Mem Hosp Rhode Isl, Ctr Primary Care & Prevent, Pawtucket, RI 02860 USA.
[Marshall, James R.] Roswell Pk Canc Inst, Dept Hlth Behav, Buffalo, NY 14263 USA.
[Peters, Ulrike] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
RP Peters, U (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
EM jgong@fhcrc.org; lih@fhcrc.org; tharriso@fhcrc.org; IKing@salud.unm.edu;
stefan.sturup@sund.ku.dk; xsong2@fhcrc.org; dduggan@tgen.org;
yliu@stephens-associates.com; huttercm@mail.nih.gov;
hanocks@mail.nih.gov; Charles_Eaton@mhri.org;
James.Marshall@RoswellPark.org; upeters@fhcrc.org
FU National Institutes of Health, Genes, Environment and Health Initiative
[NIH GEI] [Z01 CP 010200]; intramural resources of the National Cancer
Institute; National Cancer Institute, National Heart, Lung, and Blood
Institute, NIH, United States Department of Health and Human Services
[R01 CA120582, R01 CA127943, N01WH22110, 24152, 32100-2, 32105-6,
32108-9, 32111-13, 32115, 2118-32119, 32122, 42107-26, 42129-32, 44221]
FX For WHI, we thank the study participants of the Women's Health
Initiative Observational Study and the study staff. This study was
funded by the National Cancer Institute, National Heart, Lung, and Blood
Institute, NIH, United States Department of Health and Human Services
(R01 CA120582, R01 CA127943, N01WH22110, 24152, 32100-2, 32105-6,
32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, and
44221).; For PLCO, we thank Christine Berg and Philip Prorok, Division
of Cancer Prevention, National Cancer Institute, the Screening Center
investigators and staff or the Prostate, Lung, Colorectal, and Ovarian
(PLCO), Cancer Screening Trial, Tom Riley and staff, Information
Management Services, Inc., Barbara O'Brien and staff, Westat, Inc., and
Bill Kopp, Wen Shao, and staff, SAIC-Frederick. Most importantly, we
acknowledge the study participants for their contributions to making
this study possible. Funding for this work was provided through the
National Institutes of Health, Genes, Environment and Health Initiative
[NIH GEI] (Z01 CP 010200). The human subjects participating in the GWAS
are derived from the Prostate, Lung, Colon and Ovarian Screening Trial
and the study is supported by intramural resources of the National
Cancer Institute. Assistance with genotype cleaning, as well as with
general study coordination, was provided by the Gene Environment
Association Studies, GENEVA Coordinating Center (U01 HG004446).
Assistance with data cleaning was provided by the National Center for
Biotechnology Information. Funding support for genotyping, which was
performed at the Johns Hopkins University Center for Inherited Disease
Research, was provided by the NIH GEI (U01 HG 004438).
NR 57
TC 1
Z9 1
U1 0
U2 5
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2072-6643
J9 NUTRIENTS
JI Nutrients
PD MAY
PY 2013
VL 5
IS 5
BP 1706
EP 1718
DI 10.3390/nu5051706
PG 13
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 151CW
UT WOS:000319439200016
PM 23698163
ER
PT J
AU Creswell, JD
Dutcher, JM
Klein, WMP
Harris, PR
Levine, JM
AF Creswell, J. David
Dutcher, Janine M.
Klein, William M. P.
Harris, Peter R.
Levine, John M.
TI Self-Affirmation Improves Problem-Solving under Stress
SO PLOS ONE
LA English
DT Article
ID PSYCHOLOGICAL STRESS; ACHIEVEMENT GAP; INTELLECTUAL-PERFORMANCE;
STEREOTYPE THREAT; WORKING-MEMORY; RESPONSES; INSIGHT; FLEXIBILITY;
DISCOVERY; AROUSAL
AB High levels of acute and chronic stress are known to impair problem-solving and creativity on a broad range of tasks. Despite this evidence, we know little about protective factors for mitigating the deleterious effects of stress on problem-solving. Building on previous research showing that self-affirmation can buffer stress, we tested whether an experimental manipulation of self-affirmation improves problem-solving performance in chronically stressed participants. Eighty undergraduates indicated their perceived chronic stress over the previous month and were randomly assigned to either a self-affirmation or control condition. They then completed 30 difficult remote associate problem-solving items under time pressure in front of an evaluator. Results showed that self-affirmation improved problem-solving performance in underperforming chronically stressed individuals. This research suggests a novel means for boosting problem-solving under stress and may have important implications for understanding how self-affirmation boosts academic achievement in school settings.
C1 [Creswell, J. David] Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA.
[Dutcher, Janine M.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
[Klein, William M. P.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Harris, Peter R.] Univ Sheffield, Dept Psychol, Sheffield S10 2TN, S Yorkshire, England.
[Levine, John M.] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
RP Creswell, JD (reprint author), Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA.
EM creswell@cmu.edu
FU National Science Foundation [924387]; Pittsburgh Life Sciences
Greenhouse Opportunity Fund
FX This research was supported by the National Science Foundation under
Grant #924387 and the Pittsburgh Life Sciences Greenhouse Opportunity
Fund. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 38
TC 9
Z9 9
U1 6
U2 33
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 MAY 1
PY 2013
VL 8
IS 5
AR e62593
DI 10.1371/journal.pone.0062593
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 147KY
UT WOS:000319167000060
PM 23658751
ER
PT J
AU Nagy, NT
Chakraborty, S
Harami, GM
Sellers, JR
Sakamoto, T
Kovacs, M
AF Nagy, Nikolett T.
Chakraborty, Saikat
Harami, Gabor M.
Sellers, James R.
Sakamoto, Takeshi
Kovacs, Mihaly
TI A Subdomain Interaction at the Base of the Lever Allosterically Tunes
the Mechanochemical Mechanism of Myosin 5a
SO PLOS ONE
LA English
DT Article
ID VITRO MOTILITY ASSAY; HAND-OVER-HAND; MUSCLE-CONTRACTION; MOTOR DOMAIN;
IN-VITRO; PROCESSIVE TRANSLOCATION; ACTOMYOSIN SUBFRAGMENT-1;
CONFORMATIONAL STATES; TRYPTOPHAN RESIDUE; PHOSPHATE RELEASE
AB The motor domain of myosin is the core element performing mechanochemical energy transduction. This domain contains the actin and ATP binding sites and the base of the force-transducing lever. Coordinated subdomain movements within the motor are essential in linking the ATPase chemical cycle to translocation along actin filaments. A dynamic subdomain interface located at the base of the lever was previously shown to exert an allosteric influence on ATP hydrolysis in the non-processive myosin 2 motor. By solution kinetic, spectroscopic and ensemble and single-molecule motility experiments, we determined the role of a class-specific adaptation of this interface in the mechanochemical mechanism of myosin 5a, a processive intracellular transporter. We found that the introduction of a myosin 2-specific repulsive interaction into myosin 5a via the I67K mutation perturbs the strong-binding interaction of myosin 5a with actin, influences the mechanism of ATP binding and facilitates ATP hydrolysis. At the same time, the mutation abolishes the actin-induced activation of ADP release and, in turn, slows down processive motility, especially when myosin experiences mechanical drag exerted by the action of multiple motor molecules bound to the same actin filament. The results highlight that subtle structural adaptations of the common structural scaffold of the myosin motor enable specific allosteric tuning of motor activity shaped by widely differing physiological demands.
C1 [Nagy, Nikolett T.; Harami, Gabor M.; Kovacs, Mihaly] Eotvos Lorand Univ, Dept Biochem, ELTE MTA Eotvos Lorand Univ Hungarian Acad Sci, Momentum Motor Enzymol Res Grp, Budapest, Hungary.
[Chakraborty, Saikat; Sakamoto, Takeshi] Wayne State Univ, Dept Phys & Astron, Detroit, MI 48202 USA.
[Sellers, James R.] NHLBI, Lab Mol Physiol, Bethesda, MD 20892 USA.
RP Kovacs, M (reprint author), Eotvos Lorand Univ, Dept Biochem, ELTE MTA Eotvos Lorand Univ Hungarian Acad Sci, Momentum Motor Enzymol Res Grp, Budapest, Hungary.
EM kovacsm@elte.hu
RI Kovacs, Mihaly/A-6841-2011
FU National Institutes of Health [R00HL089350]; TAMOP Grant
[4.2.1/B-09/1/KMR-2010-0003]; Human Frontier Science Program
[RGY0072/2010]; "Momentum" Program of the Hungarian Academy of Sciences
[LP2011-006/2011]
FX This work was supported by National Institutes of Health K99/R00 Career
grant (R00HL089350) to T.S.; and TAMOP Grant
(4.2.1/B-09/1/KMR-2010-0003), the Human Frontier Science Program
(RGY0072/2010) and the "Momentum" Program of the Hungarian Academy of
Sciences (LP2011-006/2011) to M.K. M.K. is a Bolyai Fellow of the
Hungarian Academy of Sciences. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 40
TC 0
Z9 0
U1 0
U2 13
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 MAY 1
PY 2013
VL 8
IS 5
AR e62640
DI 10.1371/journal.pone.0062640
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 147KY
UT WOS:000319167000065
PM 23650521
ER
PT J
AU Parvathaneni, S
Stortchevoi, A
Sommers, JA
Brosh, RM
Sharma, S
AF Parvathaneni, Swetha
Stortchevoi, Alexei
Sommers, Joshua A.
Brosh, Robert M., Jr.
Sharma, Sudha
TI Human RECQ1 Interacts with Ku70/80 and Modulates DNA End-Joining of
Double-Strand Breaks
SO PLOS ONE
LA English
DT Article
ID DEPENDENT PROTEIN-KINASE; REPAIR PATHWAY CHOICE; CELL-FREE-EXTRACTS;
HOMOLOGOUS RECOMBINATION; WERNER PROTEIN; KU PROTEIN; POLY(ADP-RIBOSE)
POLYMERASE-1; VERTEBRATE CELLS; MAMMALIAN-CELLS; APLF C2ORF13
AB Genomic instability is a known precursor to cancer and aging. The RecQ helicases are a highly conserved family of DNA-unwinding enzymes that play key roles in maintaining genome stability in all living organisms. Human RecQ homologs include RECQ1, BLM, WRN, RECQ4, and RECQ5 beta, three of which have been linked to diseases with elevated risk of cancer and growth defects (Bloom Syndrome and Rothmund-Thomson Syndrome) or premature aging (Werner Syndrome). RECQ1, the first RecQ helicase discovered and the most abundant in human cells, is the least well understood of the five human RecQ homologs. We have previously described that knockout of RECQ1 in mice or knockdown of its expression in human cells results in elevated frequency of spontaneous sister chromatid exchanges, chromosomal instability, increased load of DNA damage and heightened sensitivity to ionizing radiation. We have now obtained evidence implicating RECQ1 in the nonhomologous end-joining pathway of DNA double-strand break repair. We show that RECQ1 interacts directly with the Ku70/80 subunit of the DNA-PK complex, and depletion of RECQ1 results in reduced end-joining in cell free extracts. In vitro, RECQ1 binds and unwinds the Ku70/80-bound partial duplex DNA substrate efficiently. Linear DNA is co-bound by RECQ1 and Ku70/80, and DNA binding by Ku70/80 is modulated by RECQ1. Collectively, these results provide the first evidence for an interaction of RECQ1 with Ku70/80 and a role of the human RecQ helicase in double-strand break repair through nonhomologous end-joining.
C1 [Parvathaneni, Swetha; Stortchevoi, Alexei; Sharma, Sudha] Howard Univ, Coll Med, Dept Biochem & Mol Biol, Washington, DC 20059 USA.
[Sommers, Joshua A.; Brosh, Robert M., Jr.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Sharma, S (reprint author), Howard Univ, Coll Med, Dept Biochem & Mol Biol, Washington, DC 20059 USA.
EM sudha.sharma@howard.edu
OI Sharma, Sudha/0000-0003-2765-2482
FU NIH/NIGMS [5SC1GM093999-04]; NIH Intramural Research Program; National
Institute on Aging; NIH/NIMHD [G12MD007597]
FX This work is supported by NIH/NIGMS grant 5SC1GM093999-04 (to SS) and
the NIH Intramural Research Program, National Institute on Aging (to
RB). Howard University College of Medicine core facilities are supported
by the NIH/NIMHD under Award Number G12MD007597. The content is solely
the responsibility of the authors and does not necessarily represent the
official views of the NIH. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 78
TC 18
Z9 18
U1 1
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 1
PY 2013
VL 8
IS 5
AR e62481
DI 10.1371/journal.pone.0062481
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 147KY
UT WOS:000319167000050
PM 23650516
ER
PT J
AU Csordas, A
Wang, R
Rios, D
Reisinger, F
Foster, JM
Slotta, DJ
Vizcaino, JA
Hermjakob, H
AF Csordas, Attila
Wang, Rui
Rios, Daniel
Reisinger, Florian
Foster, Joseph M.
Slotta, Douglas J.
Vizcaino, Juan Antonio
Hermjakob, Henning
TI From Peptidome to PRIDE: Public proteomics data migration at a large
scale
SO PROTEOMICS
LA English
DT Article
DE Bioinformatics; Discontinuation; Mass spectrometry proteomics databases;
Peptidome; PRIDE
ID MASS-SPECTROMETRY; PROTEIN; IDENTIFICATIONS; TOOLS
AB The PRIDE database, developed and maintained at the European Bioinformatics Institute (EBI), is one of the most prominent data repositories dedicated to high throughput MS-based proteomics data. Peptidome, developed by the National Center for Biotechnology Information (NCBI) as a sibling resource to PRIDE, was discontinued due to funding constraints in April 2011. A joint effort between the two teams was started soon after the Peptidome closure to ensure that data were not lost to the wider proteomics community by exporting it to PRIDE. As a result, data in the low terabyte range have been migrated from Peptidome to PRIDE and made publicly available under experiment accessions 17900-18271, representing 54 projects, approximate to 53 million mass spectra, approximate to 10 million peptide identifications, approximate to 650000 protein identifications, approximate to 1.1 million biologically relevant protein modifications, and 28 species, from more than 30 different labs.
C1 [Csordas, Attila; Wang, Rui; Rios, Daniel; Reisinger, Florian; Foster, Joseph M.; Vizcaino, Juan Antonio; Hermjakob, Henning] EBI, EMBL Outstn, Cambridge, England.
[Slotta, Douglas J.] NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
RP Csordas, A (reprint author), EBI, EMBL Outstn, Wellcome Trust Genome Campus, Cambridge, England.
EM acsordas@ebi.ac.uk
OI Vizcaino, Juan Antonio/0000-0002-3905-4335; Hermjakob,
Henning/0000-0001-8479-0262
FU Wellcome Trust [WT085949MA]; EMBL; EU FP7 LipidomicNet [202272];
ProteomeXchange [260558]; BBSRC "PRIDE Converter" grant [BB/I024204/1];
BBSRC CASE studentship; BBSRC; Philips; NIH, National Library of
Medicine
FX The PRIDE database is supported by the Wellcome Trust [grant number
WT085949MA] and EMBL core funding. J.A.V. is supported by the EU FP7
LipidomicNet [grant number 202272] and ProteomeXchange [grant number
260558]. R. W. is supported by the BBSRC "PRIDE Converter" grant
[reference BB/I024204/1]. J.M.F. is supported by a BBSRC CASE
studentship funded by the BBSRC and Philips. DJS was supported by the
Intramural Research Program of the NIH, National Library of Medicine.
NR 13
TC 5
Z9 5
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1615-9853
J9 PROTEOMICS
JI Proteomics
PD MAY
PY 2013
VL 13
IS 10-11
SI SI
BP 1692
EP 1695
DI 10.1002/pmic.201200514
PG 4
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 156NJ
UT WOS:000319828700016
PM 23533138
ER
PT J
AU Horowitz, LM
Snyder, D
Ludi, E
Rosenstein, DL
Kohn-Godbout, J
Lee, L
Cartledge, T
Farrar, A
Pao, M
AF Horowitz, Lisa M.
Snyder, Deborah
Ludi, Erica
Rosenstein, Donald L.
Kohn-Godbout, Julie
Lee, Laura
Cartledge, Tannia
Farrar, Adrienne
Pao, Maryland
TI Ask Suicide-Screening Questions to Everyone in Medical Settings: The
asQ'em Quality Improvement Project
SO PSYCHOSOMATICS
LA English
DT Article
ID EMERGENCY-DEPARTMENT; PEDIATRIC EMERGENCY; ADOLESCENT SUICIDE; RISK;
CANCER; IDEATION; HEART; SOUL
AB Suicide in hospital settings is a frequently reported sentinel event to the Joint Commission (JC). Since 1995, over 1,000 inpatient deaths by suicide have been reported to the JC; 25% occurred in non-behavioral health settings. Lack of proper "assessment" was the leading root cause for 80% of hospital suicides. This paper describes the "Ask Suicide-Screening Questions to Everyone in Medical Settings (asQ'em)" Quality Improvement Project. We aimed to pilot a suicide screening tool and determine feasibility of screening in terms of prevalence, impact on unit worlflow, impact on mental health resources, and patient/nurse acceptance. Methods: We piloted the asQ'em two-item screening instrument that assesses suicidal thoughts and behaviors, designed specifically for nurses to administer to medical patients. Educational in-services were conducted. A convenience sample of adult patients, 18 years or older, from three selected inpatient units in the National Institutes of Health Clinical Center, participated. Results: A total of 331 patients were screened; 13 (4%) patients screened "positive" for suicide risk and received further evaluation. No patient had acute suicidal thoughts or required an observational monitor. Screening took approximately 2 minutes; 87% of patients reported feeling comfortable with screening; 81% of patients, 75% of nurses, and 100% of social workers agreed that all patients in hospitals should be screened for suicide risk. Discussion: Nurses can feasibly screen hospitalized medical/surgical patients for suicide risk with a two-item screening instrument. Patients, nurses, and social workers rated their experience of screening as positive and supported the idea of universal suicide screening in the hospital.
C1 [Horowitz, Lisa M.; Snyder, Deborah; Ludi, Erica; Pao, Maryland] NIMH, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Kohn-Godbout, Julie; Lee, Laura; Cartledge, Tannia] NIH, Dept Nursing, Ctr Clin, Bethesda, MD 20892 USA.
[Farrar, Adrienne] NIH, Dept Social Work, Ctr Clin, Bethesda, MD 20892 USA.
[Rosenstein, Donald L.] Univ N Carolina, Comprehens Canc Support Program, Chapel Hill, NC USA.
RP Horowitz, LM (reprint author), NIMH, Clin Res Ctr, Bldg 10,Room 6-5362, Bethesda, MD 20892 USA.
EM horowitzl@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Institute of Mental Health; NIH Clinical Center Nursing
Department
FX The Quality Improvement Project described in this article was supported
by the Intramural Research Program of the National Institutes of Health
and the National Institute of Mental Health; and by the NIH Clinical
Center Nursing Department.
NR 26
TC 9
Z9 10
U1 1
U2 16
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD MAY-JUN
PY 2013
VL 54
IS 3
BP 239
EP 247
PG 9
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 151WQ
UT WOS:000319491500005
PM 23398908
ER
PT J
AU Gifford, WD
Pfaff, SL
Macfarlan, TS
AF Gifford, Wesley D.
Pfaff, Samuel L.
Macfarlan, Todd S.
TI Transposable elements as genetic regulatory substrates in early
development
SO TRENDS IN CELL BIOLOGY
LA English
DT Review
DE transposon; endogenous retrovirus; evolution; development; placentation;
gene regulation
ID EMBRYONIC STEM-CELLS; RETROVIRUS-LIKE ELEMENTS; MURINE ENDOGENOUS
RETROVIRUS; EARLY MOUSE EMBRYOS; MUERV-L; RECOMBINATION HOTSPOTS; L1
RETROTRANSPOSITION; RESTRICTION GENE; DNA METHYLATION; CYTOSINE
METHYLATION
AB The abundance and ancient origins of transposable elements (TEs) in eukaryotic genomes has spawned research into the potential symbiotic relationship between these elements and their hosts. In this review, we introduce the diversity of TEs, discuss how distinct classes are uniquely regulated in development, and describe how they appear to have been coopted for the purposes of gene regulation and the orchestration of a number of processes during early embryonic development. Although young, active TEs play an important role in somatic tissues and evolution, we focus mostly on the contributions of the older, fixed elements in mammalian genomes. We also discuss major challenges inherent in the study of TEs and contemplate future experimental approaches to further investigate how they coordinate developmental processes.
C1 [Gifford, Wesley D.; Pfaff, Samuel L.] Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA.
[Gifford, Wesley D.; Pfaff, Samuel L.] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA.
[Macfarlan, Todd S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Program Genom Differentiat, Bethesda, MD 20892 USA.
RP Macfarlan, TS (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Program Genom Differentiat, Bldg 6B,Room 2B-211, Bethesda, MD 20892 USA.
EM todd.macfarlan@nih.gov
OI Macfarlan, Todd/0000-0003-2495-9809
FU ARCS Award; Rose Hills Foundation; Chapman Foundation; NINDS; CIRM;
Marshall Heritage Foundation
FX The authors thank Igor Dawid, Karl Pfeifer, and Carson Miller for
critical reading of the manuscript. W.D.G is supported by an ARCS Award,
the Rose Hills Foundation, and the Chapman Foundation. S.L.P. is the
Benjamin H. Lewis Chair in Neurobiology and an Investigator of the
Howard Hughes Medical Institute and his research is supported by NINDS,
CIRM, and The Marshall Heritage Foundation. T.S.M is an Earl Stadtman
Investigator at the Eunice Kennedy Shriver National Institute of Child
Health and Human Development.
NR 86
TC 31
Z9 35
U1 2
U2 31
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0962-8924
J9 TRENDS CELL BIOL
JI Trends Cell Biol.
PD MAY
PY 2013
VL 23
IS 5
BP 218
EP 226
DI 10.1016/j.tcb.2013.01.001
PG 9
WC Cell Biology
SC Cell Biology
GA 149GP
UT WOS:000319307300003
PM 23411159
ER
PT J
AU Jin, TC
Huang, M
Smith, P
Jiang, JS
Xiao, TS
AF Jin, Tengchuan
Huang, Mo
Smith, Patrick
Jiang, Jiansheng
Xiao, T. Sam
TI The structure of the CARD8 caspase-recruitment domain suggests its
association with the FIIND domain and procaspases through adjacent
surfaces
SO ACTA CRYSTALLOGRAPHICA SECTION F-STRUCTURAL BIOLOGY AND CRYSTALLIZATION
COMMUNICATIONS
LA English
DT Article
ID KAPPA-B ACTIVATION; INFLAMMATORY-BOWEL-DISEASE; CROHNS-DISEASE;
CONTAINING PROTEIN; NO ASSOCIATION; TUCAN; APOPTOSIS; NALP3;
SUPERFAMILY; MUTATION
AB CARD8 plays crucial roles in regulating apoptotic and inflammatory signaling pathways through the association of its caspase-recruitment domain (CARD) with those of procaspase-9 and procaspase-1. The CARD8 CARD has also been predicted to form an intramolecular complex with its FIIND domain. Here, the first crystal structure of the CARD8 CARD is reported; it adopts a six-helix bundle fold with a unique conformation of the alpha 6 helix that is described here for the first time. The surface of the CARD8 CARD displays a prominent acidic patch at its alpha 2, alpha 3 and alpha 5 helices that may interact with the procaspase-9 CARD, whereas an adjacent charged surface at its alpha 3 and alpha 4 helices may associate with the CARD8 FIIND domain without interfering with the CARD-CARD interaction. This suggests that the function of CARD8 may be regulated by both intramolecular and intermolecular interactions involving electrostatic attractions.
C1 [Jin, Tengchuan; Huang, Mo; Smith, Patrick; Jiang, Jiansheng; Xiao, T. Sam] NIAID, Struct Immunobiol Unit, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Xiao, TS (reprint author), NIAID, Struct Immunobiol Unit, Immunol Lab, NIH, 4 Mem Dr, Bethesda, MD 20892 USA.
EM xiaot@niaid.nih.gov
RI Xiao, Tsan/I-7616-2013; Xiao, Tsan/A-8590-2010; Jin,
Tengchuan/B-5883-2014
OI Xiao, Tsan/0000-0001-9688-475X; Jin, Tengchuan/0000-0002-1395-188X
FU National Cancer Institute [Y1-CO-1020]; National Institute of General
Medical Sciences [Y1-GM-1104]; US Department of Energy
[DE-AC02-06CH11357]; Division of Intramural Research, National Institute
of Allergy and Infectious Diseases, NIH
FX The authors thank the beamline scientists at the GM/CA-CAT, Advanced
Photon Source, which is funded by federal funds from the National Cancer
Institute (Y1-CO-1020) and the National Institute of General Medical
Sciences (Y1-GM-1104), for their support. Use of the Advanced Photon
Source was supported by the US Department of Energy under contract No.
DE-AC02-06CH11357. We are grateful to Dr Weichenberger (EURAC) for
providing the coordinates of the CARD8 model. TSX is supported by the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, NIH. The authors declare no conflict of interest.
NR 30
TC 5
Z9 6
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1744-3091
J9 ACTA CRYSTALLOGR F
JI Acta Crystallogr. F-Struct. Biol. Cryst. Commun.
PD MAY
PY 2013
VL 69
BP 482
EP 487
DI 10.1107/S1744309113010075
PN 5
PG 6
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Crystallography
SC Biochemistry & Molecular Biology; Biophysics; Crystallography
GA 148YO
UT WOS:000319285100003
PM 23695559
ER
PT J
AU Lakatta, EG
Yaniv, Y
Maltsev, VA
AF Lakatta, Edward G.
Yaniv, Yael
Maltsev, Victor A.
TI Minding the gaps that link intrinsic circadian clock within the heart to
its intrinsic ultradian pacemaker clocks. Focus on "The cardiomyocyte
molecular clock, regulation of Scn5a, and arrhythmia susceptibility"
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Editorial Material
ID PACEMAKER CELLS; CALCIUM; SYSTEM; DISRUPTION; CONDUCTION; CHANNELS
C1 [Lakatta, Edward G.; Yaniv, Yael; Maltsev, Victor A.] NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Lakatta, EG (reprint author), NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM lakattae@grc.nia.nih.gov
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
FU Intramural NIH HHS
NR 19
TC 3
Z9 3
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6143
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD MAY
PY 2013
VL 304
IS 10
BP C941
EP C944
DI 10.1152/ajpcell.00072.2013
PG 4
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 144VR
UT WOS:000318969900003
PM 23485714
ER
PT J
AU Konstandi, M
Cheng, J
Gonzalez, FJ
AF Konstandi, Maria
Cheng, Jie
Gonzalez, Frank J.
TI Sex steroid hormones regulate constitutive expression of Cyp2e1 in
female mouse liver
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE Cyp2e1; 17 beta-estradiol; progesterone; estrous cycle; mice
ID MESSENGER-RIBONUCLEIC-ACID; GROWTH-HORMONE; RAT-LIVER;
ESTROGEN-RECEPTOR; GENE-EXPRESSION; BETA-CATENIN; CYTOCHROME P4502E1;
NUCLEAR RECEPTORS; NITRIC-OXIDE; CHLORZOXAZONE 6-HYDROXYLATION
AB CYP2E1 is of paramount toxicological significance because it metabolically activates a large number of low-molecular-weight toxicants and carcinogens. In this context, factors that interfere with Cyp2e1 regulation may critically affect xenobiotic toxicity and carcinogenicity. The aim of this study was to investigate the role of female steroid hormones in the regulation of CYP2E1, as estrogens and progesterone are the bases of contraceptives and hormonal replacement therapy in menopausal women. Interestingly, a fluctuation in the hepatic expression pattern of Cyp2e1 was revealed in the different phases of the estrous cycle of female mice, with higher Cyp2e1 expression at estrus (E) and lower at methestrus (ME), highly correlated with that in plasma gonadal hormone levels. Depletion of sex steroids by ovariectomy repressed Cyp2e1 expression to levels similar to those detected in males and cyclic females at ME. Hormonal supplementation brought Cyp2e1 expression back to levels detected at E. The role of progesterone appeared to be more prominent than that of 17 beta-estradiol. Progester-one-induced Cyp2e1 upregulation could be attributed to inactivation of the insulin/PI3K/Akt/FOXO1 signaling pathway. Tamoxifen, an anti-estrogen, repressed Cyp2e1 expression potentially via activation of the PI3K/Akt/FOXO1 and GH/STAT5b-linked pathways. The sex steroid hormone-related changes in hepatic Cyp2e1 expression were highly correlated with those observed in Hnf-1 alpha, beta-catenin, and Srebp-1c. In conclusion, female steroid hormones are clearly involved in the regulation of CYP2E1, thus affecting the metabolism of a plethora of toxicants and carcinogenic agents, conditions that may trigger several pathologies or exacerbate the outcomes of various pathophysiological states.
C1 [Konstandi, Maria] Univ Ioannina, Sch Med, Dept Pharmacol, GR-45110 Ioannina, Greece.
[Konstandi, Maria; Cheng, Jie; Gonzalez, Frank J.] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
RP Konstandi, M (reprint author), Univ Ioannina, Sch Med, Dept Pharmacol, GR-45110 Ioannina, Greece.
EM mkonstan@cc.uoi.gr
FU National Cancer Institute Intramural program
FX This study was supported in part by the National Cancer Institute
Intramural program.
NR 84
TC 8
Z9 8
U1 1
U2 8
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD MAY
PY 2013
VL 304
IS 10
BP E1118
EP E1128
DI 10.1152/ajpendo.00585.2012
PG 11
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 144VL
UT WOS:000318969100010
PM 23548611
ER
PT J
AU Ravits, J
Appel, S
Baloh, RH
Barohn, R
Brooks, BR
Elman, L
Floeter, MK
Henderson, C
Lomen-Hoerth, C
Macklis, JD
McCluskey, L
Mitsumoto, H
Przedborski, S
Rothstein, J
Trojanowski, JQ
van den Berg, LH
Ringel, S
AF Ravits, John
Appel, Stanley
Baloh, Robert H.
Barohn, Richard
Brooks, Benjamin Rix
Elman, Lauren
Floeter, Mary Kay
Henderson, Christopher
Lomen-Hoerth, Catherine
Macklis, Jeffrey D.
McCluskey, Leo
Mitsumoto, Hiroshi
Przedborski, Serge
Rothstein, Jeffrey
Trojanowski, John Q.
van den Berg, Leonard H.
Ringel, Steven
TI Deciphering amyotrophic lateral sclerosis: What phenotype,
neuropathology and genetics are telling us about pathogenesis
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE ALS; PLS; PMA; motor neuron disease; FTD
ID MOTOR-NEURON DISEASE; PROGRESSIVE-MUSCULAR-ATROPHY; FRONTOTEMPORAL LOBAR
DEGENERATION; PRION-LIKE PROPAGATION; VERTICAL GAZE PALSY;
SUPEROXIDE-DISMUTASE; CORTICOSPINAL TRACT; CLINICAL-FEATURES;
NATURAL-HISTORY; MUTANT SOD1
AB Amyotrophic lateral sclerosis (ALS) is characterized phenotypically by progressive weakness and neuropathologically by loss of motor neurons. Phenotypically, there is marked heterogeneity. Typical ALS has mixed upper motor neuron (UMN) and lower motor neuron (LMN) involvement. Primary lateral sclerosis has predominant UMN involvement. Progressive muscular atrophy has predominant LMN involvement. Bulbar and limb ALS have predominant regional involvement. Frontotemporal dementia has significant cognitive and behavioral involvement. These phenotypes can be so distinctive that they would seem to have differing biology. However, they cannot be distinguished, at least neuropathologically or genetically. In sporadic ALS (SALS), they are mostly characterized by ubiquitinated cytoplasmic inclusions of TDP-43. In familial ALS (FALS), where phenotypes are indistinguishable from SALS and similarly heterogeneous, each mutated gene has its own genetic and molecular signature. Overall, since the same phenotypes can have multiple causes including different gene mutations, there must be multiple molecular mechanisms causing ALS - and ALS is a syndrome. Since, however, multiple phenotypes can be caused by one single gene mutation, a single molecular mechanism can cause heterogeneity. What the mechanisms are remain unknown, but active propagation of the pathology neuroanatomically seems to be a principal component. Leading candidate mechanisms include RNA processing, cell-cell interactions between neurons and non-neuronal neighbors, focal seeding from a misfolded protein that has prion-like propagation, and fatal errors introduced during neurodevelopment of the motor system. If fundamental mechanisms could be identified and understood, ALS therapy could rationally target progression and stop the disease - a goal that seems increasingly achievable.
C1 [Ravits, John] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
[Appel, Stanley] Methodist Res Inst, Houston, TX USA.
[Baloh, Robert H.] Cedars Sinai Med Ctr, Dept Neurol, Los Angeles, CA 90048 USA.
[Baloh, Robert H.] Cedars Sinai Med Ctr, Regenerat Med Inst, Los Angeles, CA 90048 USA.
[Barohn, Richard] Univ Kansas, Med Ctr, Dept Neurol, Kansas City, KS 66103 USA.
[Brooks, Benjamin Rix] Univ N Carolina, Sch Med, Carolinas Med Ctr, Dept Neurol, Charlotte, NC 28223 USA.
[Elman, Lauren; McCluskey, Leo] Penn Hosp, Dept Neurol, Philadelphia, PA 19107 USA.
[Floeter, Mary Kay] NINDS, NIH, Motor Neuron Ctr, Bethesda, MD USA.
[Henderson, Christopher] Columbia Univ, Med Ctr, New York, NY USA.
[Lomen-Hoerth, Catherine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Macklis, Jeffrey D.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Mitsumoto, Hiroshi; Przedborski, Serge] Columbia Univ, Med Ctr, Dept Neurol, New York, NY USA.
[Rothstein, Jeffrey] Johns Hopkins Univ, Med Ctr, Dept Neurol, Dept Neurosci, Baltimore, MD 21218 USA.
[Trojanowski, John Q.] Univ Penn, Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA.
[van den Berg, Leonard H.] Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Dept Neurol, Utrecht, Netherlands.
[Ringel, Steven] Univ Colorado, Sch Med, Dept Neurol, Denver, CO USA.
RP Ravits, J (reprint author), Univ Calif San Diego, Dept Neurosci, 9500 Gilman Dr,MC 0624, La Jolla, CA 92093 USA.
EM jravits@ucsd.edu
FU NIA NIH HHS [P01 AG032953]; NINDS NIH HHS [R01 NS075672]
NR 128
TC 39
Z9 40
U1 1
U2 20
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
SU 1
BP 5
EP 18
DI 10.3109/21678421.2013.778548
PG 14
WC Clinical Neurology
SC Neurosciences & Neurology
GA 145KH
UT WOS:000319014100002
PM 23678876
ER
PT J
AU Turner, MR
Bowser, R
Bruijn, L
Dupuis, L
Ludolph, A
McGrath, M
Manfredi, G
Maragakis, N
Miller, RG
Pullman, SL
Rutkove, SB
Shaw, PJ
Shefner, J
Fischbeck, KH
AF Turner, Martin R.
Bowser, Robert
Bruijn, Lucie
Dupuis, Luc
Ludolph, Albert
McGrath, Michael
Manfredi, Giovanni
Maragakis, Nicholas
Miller, Robert G.
Pullman, Seth L.
Rutkove, Seward B.
Shaw, Pamela J.
Shefner, Jeremy
Fischbeck, Kenneth H.
TI Mechanisms, models and biomarkers in amyotrophic lateral sclerosis
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE ALS; biomarkers; pathogenesis; neuroimaging; neurophysiology
ID ELECTRICAL-IMPEDANCE MYOGRAPHY; MOTOR-NEURON DISEASE; TRANSCRANIAL
MAGNETIC STIMULATION; SUPEROXIDE-DISMUTASE MUTATION;
POSITRON-EMISSION-TOMOGRAPHY; GLUTAMATE TRANSPORTER EAAT2;
CEREBROSPINAL-FLUID; OXIDATIVE STRESS; FAMILIAL ALS; MUTANT SOD1
AB The last 30 years have seen a major advance in the understanding of the clinical and pathological heterogeneity of amyotrophic lateral sclerosis (ALS), and its overlap with frontotemporal dementia. Multiple, seemingly disparate biochemical pathways converge on a common clinical syndrome characterized by progressive loss of upper and lower motor neurons. Pathogenic themes in ALS include excitotoxicity, oxidative stress, mitochondrial dysfunction, neuroinflammation, altered energy metabolism, and most recently RNA mis-processing. The transgenic rodent, overexpressing mutant superoxide dismutase-1, is now only one of several models of ALS pathogenesis. The nematode, fruit fly and zebrafish all offer fresh insight, and the development of induced pluripotent stem cell-derived motor neurons holds promise for the screening of candidate therapeutics. The lack of useful biomarkers in ALS contributes to diagnostic delay, and the inability to stratify patients by prognosis may be an important factor in the failure of therapeutic trials. Biomarkers sensitive to disease activity might lessen reliance on clinical measures and survival as trial endpoints and reduce study length. Emerging proteomic markers of neuronal loss and glial activity in cerebrospinal fluid, a cortical signature derived from advanced structural and functional MRI, and the development of more sensitive measurements of lower motor neuron physiology are leading a new phase of biomarker-driven therapeutic discovery.
C1 [Turner, Martin R.] Univ Oxford, Nuffield Dept Clin Neurosci, Oxford OX1 2JD, England.
[Bowser, Robert] Barrow Neurol Inst, Div Neurol, Phoenix, AZ 85013 USA.
[Bruijn, Lucie] ALS Assoc, Natl Off, Washington, DC USA.
[Dupuis, Luc] INSERM U692, Strasbourg, France.
[Dupuis, Luc] Univ Strasbourg, Strasbourg, France.
[Dupuis, Luc; Ludolph, Albert] Univ Ulm, Dept Neurol, D-89069 Ulm, Germany.
[McGrath, Michael] UCSF, San Francisco, CA USA.
[Manfredi, Giovanni] Cornell Univ, Weill Med Coll, Dept Neurol & Neurosci, New York, NY 10021 USA.
[Maragakis, Nicholas] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
[Miller, Robert G.] Calif Pacific Med Ctr, Forbes Norris ALS Res Ctr, San Francisco, CA USA.
[Pullman, Seth L.] Columbia Univ, New York, NY USA.
[Rutkove, Seward B.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Shaw, Pamela J.] Univ Sheffield, Dept Neurosci, Sheffield Inst Translat Neurosci, Sheffield S10 2TN, S Yorkshire, England.
[Shefner, Jeremy] SUNY Upstate Med Univ, Dept Neurol, Syracuse, NY 13210 USA.
[Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
RP Turner, MR (reprint author), John Radcliffe Hosp, West Wing Level 3, Oxford OX3 9DU, England.
EM martin.turner@ndcn.ox.ac.uk
RI Dupuis, Luc/A-6981-2012;
OI Turner, Martin/0000-0003-0267-3180
FU Medical Research Council; Motor Neurone Disease Association UK Lady
Edith Wolfson Fellowship; MND Association; European Community
FX MRT is supported by the Medical Research Council and Motor Neurone
Disease Association UK Lady Edith Wolfson Fellowship. PJS is supported
by the MND Association, the Medical Research Council and the European
Community 7th Framework Programme.
NR 148
TC 45
Z9 48
U1 2
U2 42
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
SU 1
BP 19
EP 32
DI 10.3109/21678421.2013.778554
PG 14
WC Clinical Neurology
SC Neurosciences & Neurology
GA 145KH
UT WOS:000319014100003
PM 23678877
ER
PT J
AU Factor-Litvak, P
Al-Chalabi, A
Ascherio, A
Bradley, W
Chio, A
Garruto, R
Hardiman, O
Kamel, F
Kasarskis, E
McKee, A
Nakano, I
Nelson, LM
Eisen, A
AF Factor-Litvak, Pam
Al-Chalabi, Ammar
Ascherio, Alberto
Bradley, Walter
Chio, Adriano
Garruto, Ralph
Hardiman, Orla
Kamel, Freya
Kasarskis, Edward
McKee, Ann
Nakano, Imaharu
Nelson, Lorene M.
Eisen, Andrew
TI Current pathways for epidemiological research in amyotrophic lateral
sclerosis
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE ALS; population based study; case-control study; center based;
multicenter study; Guamanian ALS
ID MOTOR-NEURON DISEASE; PARKINSONISM-DEMENTIA COMPLEX; CHRONIC TRAUMATIC
ENCEPHALOPATHY; CAPTURE-RECAPTURE METHODOLOGY; C9ORF72 REPEAT EXPANSION;
VITAMIN-E INTAKE; KII PENINSULA; NEURODEGENERATIVE DISEASE; PROSPECTIVE
COHORT; CLINICAL-FEATURES
AB Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disease. The current status of the epidemiology, challenges to its study, and novel study design options are discussed in this paper. We focus on recent results from large-scale population based prospective studies, case-control studies and population based registries, risk factors, and neuropathologic findings in chronic traumatic encephalomyelopathy. We identify areas of interest for future research, including time-trends in the incidence and prevalence of ALS; the meaning of lifetime risk; the phenotypic description of ALS; the definition of familial versus sporadic ALS, syndromic aspects of ALS; specific risk factors such as military service, life style factors such as smoking, the use of statins, and the presence of beta-N-methylamino-L-alanine (BMAA), an excitotoxic amino acid derivative possibly produced by cyanobacteria found in almost every terrestrial and aquatic habitat; the emergence and disappearance of an endemic ALS in areas of the Pacific; and gene-environment interactions in the etiology of ALS. To move the epidemiology forward, we suggest using well-characterized cohorts of newly diagnosed ALS patients to identify risk and prognostic factors; storing biological material for future studies; building on the National ALS Registry as a resource of future studies; working in multidisciplinary consortia; and addressing the possible early life etiology of ALS.
C1 [Factor-Litvak, Pam] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
[Al-Chalabi, Ammar] Kings Coll London, Inst Psychiat, Dept Clin Neurosci, London WC2R 2LS, England.
[Ascherio, Alberto] Harvard Univ, Sch Publ Hlth, Dept Epidemiol & Nutr, Boston, MA 02115 USA.
[Bradley, Walter] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
[Chio, Adriano] Univ Turin, Dept Neurosci, Turin, Italy.
[Chio, Adriano] AOU San Giovanni Battista, Turin, Italy.
[Garruto, Ralph] SUNY Binghamton, Dept Anthropol, Binghamton, NY USA.
[Garruto, Ralph] SUNY Binghamton, Dept Biol Sci, Binghamton, NY USA.
[Hardiman, Orla] Trinity Coll Dublin, Dept Neurol, Dublin, Ireland.
[Kamel, Freya] NIEHS, Chron Dis Epidemiol Grp, NIH, Res Triangle Pk, NC 27709 USA.
[Kasarskis, Edward] Univ Kentucky, Dept Neurol, Lexington, KY 40536 USA.
[Kasarskis, Edward] VA Med Ctr, Lexington, KY USA.
[McKee, Ann] Boston Univ, Sch Med, Dept Neurol & Pathol, Boston, MA 02118 USA.
[Nakano, Imaharu] Jichi Med Univ, Dept Med, Dept Neurol, Mibu, Tochigi, Japan.
[Nelson, Lorene M.] Stanford Univ, Div Epidemiol, Dept Hlth Res & Policy, Sch Med, Stanford, CA USA.
[Eisen, Andrew] Univ British Columbia, Dept Neurol, Vancouver, BC V5Z 1M9, Canada.
RP Factor-Litvak, P (reprint author), Mailman Sch Publ Hlth, Dept Epidemiol, 722 West 168th St,Room 1614, New York, NY 10032 USA.
EM prf1@columbia.edu
RI Al-Chalabi, Ammar/E-5361-2010;
OI Al-Chalabi, Ammar/0000-0002-4924-7712; Chio,
Adriano/0000-0001-9579-5341; Kamel, Freya/0000-0001-5052-6615; Hardiman,
Orla/0000-0003-2610-1291
FU Biogen Idec; Sanofi-Aventis; Knopp Biosciences; Pfizer
FX The International ALS Conference was in part funded by Biogen Idec,
Sanofi-Aventis, Knopp Biosciences, and Pfizer, which also in part
supported the publication of this supplement. All authors received
reimbursement for attending the meeting.
NR 76
TC 19
Z9 19
U1 1
U2 22
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
SU 1
BP 33
EP 43
DI 10.3109/21678421.2013.778565
PG 11
WC Clinical Neurology
SC Neurosciences & Neurology
GA 145KH
UT WOS:000319014100004
PM 23678878
ER
PT J
AU Sherman, AV
Gubitz, AK
Al-Chalabi, A
Bedlack, R
Berry, J
Conwit, R
Harris, BT
Horton, DK
Kaufmann, P
Leitner, ML
Miller, R
Shefner, J
Vonsattel, JP
Mitsumoto, H
AF Sherman, Alexander V.
Gubitz, Amelie K.
Al-Chalabi, Ammar
Bedlack, Richard
Berry, James
Conwit, Robin
Harris, Brent T.
Horton, D. Kevin
Kaufmann, Petra
Leitner, Melanie L.
Miller, Robert
Shefner, Jeremy
Vonsattel, Jean Paul
Mitsumoto, Hiroshi
TI Infrastructure resources for clinical research in amyotrophic lateral
sclerosis
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE Amyotrophic lateral sclerosis (ALS); motor neuron disease (MND);
clinical research infrastructure; North America; Europe
ID NEURON DISEASE; STEM-CELLS; ALS; EPIDEMIOLOGY
AB Clinical trial networks, shared clinical databases, and human biospecimen repositories are examples of infrastructure resources aimed at enhancing and expediting clinical and/or patient oriented research to uncover the etiology and pathogenesis of amyotrophic lateral sclerosis (ALS), a rapidly progressive neurodegenerative disease that leads to the paralysis of voluntary muscles. The current status of such infrastructure resources, as well as opportunities and impediments, were discussed at the second Tarrytown ALS meeting held in September 2011. The discussion focused on resources developed and maintained by ALS clinics and centers in North America and Europe, various clinical trial networks, U. S. government federal agencies including the National Institutes of Health (NIH), the Agency for Toxic Substances and Disease Registry (ATSDR) and the Centers for Disease Control and Prevention (CDC), and several voluntary disease organizations that support ALS research activities. Key recommendations included 1) the establishment of shared databases among individual ALS clinics to enhance the coordination of resources and data analyses; 2) the expansion of quality-controlled human biospecimen banks; and 3) the adoption of uniform data standards, such as the recently developed Common Data Elements (CDEs) for ALS clinical research. The value of clinical trial networks such as the Northeast ALS (NEALS) Consortium and the Western ALS (WALS) Consortium was recognized, and strategies to further enhance and complement these networks and their research resources were discussed.
C1 [Sherman, Alexander V.] Massachusetts Gen Hosp, NCRI, Boston, MA 02114 USA.
[Gubitz, Amelie K.; Conwit, Robin; Kaufmann, Petra] NINDS, NIH, Bethesda, MD 20892 USA.
[Al-Chalabi, Ammar] Kings Coll London, Inst Psychiat, Dept Clin Neurosci, London WC2R 2LS, England.
[Bedlack, Richard] Duke Inst Brain Sci, Sch Med, Div Neurol, Durham, NC USA.
[Berry, James] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Harris, Brent T.] Georgetown Univ, Med Ctr, Dept Neurol, Washington, DC 20007 USA.
[Horton, D. Kevin] Agcy Tox Subst & Dis Registry, Div Toxicol & Human Hlth Sci, Atlanta, GA USA.
[Leitner, Melanie L.] Prize4Life, Cambridge, MA USA.
[Miller, Robert] Calif Pacific Med Ctr, Forbes Norris MDA ALS Res Ctr, San Francisco, CA USA.
[Shefner, Jeremy] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY 13210 USA.
[Vonsattel, Jean Paul] Columbia Univ, New York Presbyterian Hosp, Med Ctr, Dept Pathol & Cell Biol, New York, NY USA.
[Mitsumoto, Hiroshi] Columbia Univ, Dept Neurol, Med Ctr, Eleanor & Lou Gehrig MDA ALS Res Ctr, New York, NY USA.
RP Sherman, AV (reprint author), Massachusetts Gen Hosp, 13th St,Bldg 149, Charlestown, MA 02129 USA.
EM avsherman@partners.org
RI Al-Chalabi, Ammar/E-5361-2010
OI Al-Chalabi, Ammar/0000-0002-4924-7712
NR 22
TC 7
Z9 7
U1 0
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
EI 2167-9223
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
SU 1
BP 53
EP 61
DI 10.3109/21678421.2013.779058
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 145KH
UT WOS:000319014100006
PM 23678880
ER
PT J
AU Chad, DA
Bidichandani, S
Bruijn, L
Capra, JD
Dickie, B
Ferguson, J
Figlewicz, D
Forsythe, M
Kaufmann, P
Kirshner, A
Monti, W
AF Chad, David A.
Bidichandani, Sanjay
Bruijn, Lucie
Capra, J. Donald
Dickie, Brian
Ferguson, John
Figlewicz, Denise
Forsythe, Melissa
Kaufmann, Petra
Kirshner, Annette
Monti, William
TI Funding agencies and disease organizations: Resources and
recommendations to facilitate ALS clinical research
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE ALS; funding agencies; patient voluntary organizations
AB Ten groups presented their perspectives on facilitating clinical research in ALS including four federal agencies, four disease organizations, one foundation and one advocacy group. The federal agencies (National Institute of Neurological Disorders and Stroke, National Institute of Environmental Health Sciences, Office of Rare Diseases Research, Department of Defense) encourage fostering a team approach between pre-clinical and clinical research investigators, coordinating with patient groups in the early phases of clinical studies, enhancing private and public partnerships, and investigating the interplay between genetic susceptibility and environmental exposure. The disease organizations (Muscular Dystrophy Association, ALS Association, ALS Society of Canada, and the Motor Neurone Disease Association UK) support fellowship training programs to develop ALS clinician scientists, and encourage work on the epidemiology of ALS, on genetic and epigenetic mechanisms that are relevant to ALS pathogenesis, on developing ALS registries and biobanks, and building bridges of collaboration among study groups. The Foundation supports innovative projects, including stem-cell research, and Patient Advocacy is committed to supporting excellence in ALS research and patient care, and believes strongly in enhancing communication between patients and members of the research community.
C1 [Chad, David A.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Dickie, Brian] Motor Neuron Dis Assoc, Northampton, England.
[Ferguson, John] NIH, Off Rare Dis Res, Bethesda, MD 20892 USA.
[Figlewicz, Denise] ALS Soc Canada, Bethesda, MD USA.
[Forsythe, Melissa] USA, Med Res & Mat Command, Congressionally Directed Med Res Programs Off, Bethesda, MD USA.
[Kaufmann, Petra] NINDS, NIH, Bethesda, MD 20892 USA.
[Kirshner, Annette] NIEHS, NIH, Bethesda, MD USA.
[Monti, William] ALS Advocacy, New York, NY USA.
RP Chad, DA (reprint author), Neuromuscular Diagnost Ctr, 165 Cambridge St,Suite 820,CPZ 8, Boston, MA 02114 USA.
EM dchad@partners.org
NR 0
TC 1
Z9 1
U1 0
U2 9
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
SU 1
BP 62
EP 66
DI 10.3109/21678421.2013.778588
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 145KH
UT WOS:000319014100007
PM 23678881
ER
PT J
AU Hsu, HS
Benjauthrit, V
Wei, Q
Huang, YH
Zhou, QF
Shung, KK
AF Hsu, Hsiu-Sheng
Benjauthrit, Vatcharee
Wei, Qiang
Huang, Yuhong
Zhou, Qifa
Shung, K. Kirk
TI Silver doped 0.9PMN-PT-0.1PZT composite films for very high frequency
ultrasonic transducer applications
SO APPLIED PHYSICS A-MATERIALS SCIENCE & PROCESSING
LA English
DT Article
ID PIEZOELECTRIC PROPERTIES
AB A series of silver doping concentration into the 0.9PMN-PT-0.1PZT (PMN-PT-PZT) films via the composite sol-gel technique were prepared. The crystallographic properties and microstructures of PMN-PT-PZT films with the silver dopant were investigated. Additionally, the effect of silver doping on dielectric and ferroelectric properties was examined. The results show that in general, the dielectric permittivity and remnant polarization increase as the silver doping concentration is increased. The PMN-PT-PZT+ 2.5 mol% Ag film exhibits a dielectric constant of 3,610 at 1 kHz and a remnant polarization of 57.6 mu C/cm(2) at room temperature. From this silver doped film, very high frequency ultrasonic needle transducers were fabricated and evaluated. The representative transducer had the center frequency of 225 MHz with a -6 dB bandwidth of 29 % (65 MHz) and 62 dB insertion loss. The performance of this transducer is comparable to other composite sol-gel films transducer. The results suggest that this silver-doped PMN-PT-PZT film is a promising candidate as an alternative piezoelectric film for very high frequency transducer applications.
C1 [Hsu, Hsiu-Sheng; Benjauthrit, Vatcharee; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
[Hsu, Hsiu-Sheng; Benjauthrit, Vatcharee; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
[Hsu, Hsiu-Sheng] Univ So Calif, Mork Family Dept Chem Engn & Mat Sci, Los Angeles, CA 90089 USA.
[Wei, Qiang; Huang, Yuhong] Chemat Technol Inc, Northridge, CA 91324 USA.
RP Zhou, QF (reprint author), Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
EM qifazhou@usc.edu
FU NIH [P41-EB218, R01-EB12058]; NSF SBIR Phase II [1026215]
FX This work has been supported by NIH P41-EB218, NIH R01-EB12058, and NSF
SBIR Phase II 1026215.
NR 17
TC 1
Z9 1
U1 1
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0947-8396
J9 APPL PHYS A-MATER
JI Appl. Phys. A-Mater. Sci. Process.
PD MAY
PY 2013
VL 111
IS 2
BP 459
EP 463
DI 10.1007/s00339-013-7558-x
PG 5
WC Materials Science, Multidisciplinary; Physics, Applied
SC Materials Science; Physics
GA 146BW
UT WOS:000319064800017
PM 23814408
ER
PT J
AU Chan, HW
Aslam, A
Lee, CH
Jones, L
Wynne, K
Wright, G
Crack, L
Macpherson, T
Stauss, H
Price, DR
Ogg, GS
AF Chan, H. W.
Aslam, A.
Lee, C. H.
Jones, L.
Wynne, K.
Wright, G.
Crack, L.
Macpherson, T.
Stauss, H.
Price, D. R.
Ogg, G. S.
TI The role of Der p 1 specific T cells in atopic eczema
SO AUSTRALASIAN JOURNAL OF DERMATOLOGY
LA English
DT Meeting Abstract
C1 [Chan, H. W.; Aslam, A.; Lee, C. H.; Jones, L.; Crack, L.; Macpherson, T.; Ogg, G. S.] Weatherall Inst Mol Med, MRC Human Immunol Unit, Oxford, England.
[Chan, H. W.; Macpherson, T.; Ogg, G. S.] Churchill Hosp, Dept Dermatol, Oxford OX3 7LJ, England.
[Lee, C. H.] Johns Hopkins Univ Hosp, Dept Dermatol, Baltimore, MD 21287 USA.
[Wynne, K.; Price, D. R.] Cardiff Univ, Dept Infect Immun & Biochem, Sch Med, Cardiff CF10 3AX, S Glam, Wales.
[Wright, G.; Stauss, H.] UCL, Ctr Rheumatol, London, England.
[Price, D. R.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-8380
J9 AUSTRALAS J DERMATOL
JI Australas. J. Dermatol.
PD MAY
PY 2013
VL 54
SU 2
SI SI
BP 13
EP 14
PG 2
WC Dermatology
SC Dermatology
GA 146YK
UT WOS:000319131900042
ER
PT J
AU Sano, K
Nakajima, T
Miyazaki, K
Ohuchi, Y
Ikegami, T
Choyke, PL
Kobayashi, H
AF Sano, Kohei
Nakajima, Takahito
Miyazaki, Kiminori
Ohuchi, Yuya
Ikegami, Takashi
Choyke, Peter L.
Kobayashi, Hisataka
TI Short PEG-Linkers Improve the Performance of Targeted, Activatable
Monoclonal Antibody-Indocyanine Green Optical Imaging Probes
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID HUMAN CANCER; VIVO; TUMORS; PEGYLATION; PROTEIN; GFP
AB The ability to switch optical imaging probes from the quenched (off) to the active state (on) has greatly improved target to background ratios. The optimal activation efficiency of an optical probe depends on complete quenching before activation and complete dequenching after activation. For instance, monoclonal antibody-indocyanine green (mAb-ICG) conjugates, which are promising agents for clinical translation, are normally quenched, but can be activated when bound to a cell surface receptor and internalized However, the small fraction of commonly used ICG derivative (ICG-Sulfo-OSu) can bind noncovalently to its mAb and is, thus, gradually released from the mAb leading to relatively high background signal especially in the liver and the abdomen. In this study, we re engineered a mAb-ICG conjugate, (Panitumumab-ICG) using bifunctional ICG derivatives (ICG-PEG4-Sulfo-OSu and ICG-PEG8-Sulfo-OSu) with short polyethylene glycol (PEG) linkers. Higher covalent binding (70-86%) was observed using the bifunctional ICG with short PEG linkers resulting in less in vivo noncovalent dissociation. Panitumumab-ICG conjugates with short PEG linkers were able to detect human epidermal growth factor receptor 1 (EGFR)-positive tumors with high tumor-to-background ratios (15.8 and 6.9 for EGFR positive tumor-to-negative tumor and tumor-to-liver ratios, respectively, at 3 d postinjection).
C1 [Sano, Kohei; Nakajima, Takahito; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Miyazaki, Kiminori; Ohuchi, Yuya; Ikegami, Takashi] Dojindo Labs, Mashikimachi, Kumamoto 8612202, Japan.
RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM Kobayash@mail.nih.gov
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research. We would like to thank T. Ido and M. Ishiyama (Dojindo
Molecular Technologies, Inc.) for their support.
NR 23
TC 23
Z9 24
U1 1
U2 31
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD MAY
PY 2013
VL 24
IS 5
BP 811
EP 816
DI 10.1021/bc400050k
PG 6
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 148NC
UT WOS:000319250300007
PM 23600922
ER
PT J
AU Sanda, T
Tyner, JW
Gutierrez, A
Ngo, VN
Glover, J
Chang, BH
Yost, A
Ma, WX
Fleischman, AG
Zhou, WJ
Yang, YD
Kleppe, M
Ahn, Y
Tatarek, J
Kelliher, MA
Neuberg, DS
Levine, RL
Moriggl, R
Muller, M
Gray, NS
Jamieson, CHM
Weng, AP
Staudt, LM
Druker, BJ
Look, AT
AF Sanda, Takaomi
Tyner, Jeffrey W.
Gutierrez, Alejandro
Ngo, Vu N.
Glover, Jason
Chang, Bill H.
Yost, Arla
Ma, Wenxue
Fleischman, Angela G.
Zhou, Wenjun
Yang, Yandan
Kleppe, Maria
Ahn, Yebin
Tatarek, Jessica
Kelliher, Michelle A.
Neuberg, Donna S.
Levine, Ross L.
Moriggl, Richard
Mueller, Mathias
Gray, Nathanael S.
Jamieson, Catriona H. M.
Weng, Andrew P.
Staudt, Louis M.
Druker, Brian J.
Look, A. Thomas
TI TYK2-STAT1-BCL2 Pathway Dependence in T-cell Acute Lymphoblastic
Leukemia
SO CANCER DISCOVERY
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; ACTIVATING MUTATIONS; KINASE INHIBITOR;
LUNG-CANCER; INTERLEUKIN-10; BCL-2; RECEPTOR; LYMPHOMA; TARGETS; JAK1
AB Targeted molecular therapy has yielded remarkable outcomes in certain cancers, but specific therapeutic targets remain elusive for many others. As a result of two independent RNA interference (RNAi) screens, we identified pathway dependence on a member of the Janus-activated kinase (JAK) tyrosine kinase family, TYK2, and its downstream effector STAT1, in T-cell acute lymphoblastic leukemia (T-ALL). Gene knockdown experiments consistently showed TYK2 dependence in both T-ALL primary specimens and cell lines, and a small-molecule inhibitor of JAK activity induced T-ALL cell death. Activation of this TYK2-STAT1 pathway in T-ALL cell lines occurs by gain-of-function TYK2 mutations or activation of interleukin (IL)-10 receptor signaling, and this pathway mediates T-ALL cell survival through upregulation of the antiapoptotic protein BCL2. These findings indicate that in many T-ALL cases, the leukemic cells are dependent upon the TYK2-STAT1-BCL2 pathway for continued survival, supporting the development of molecular therapies targeting TYK2 and other components of this pathway.
SIGNIFICANCE: In recent years, "pathway dependence" has been revealed in specific types of human cancer, which can be important because they pinpoint proteins that are particularly vulnerable to antitumor-targeted inhibition (so-called Achilles' heel proteins). Here, we use RNAi technology to identify a novel oncogenic pathway that involves aberrant activation of the TYK2 tyrosine kinase and its downstream substrate, STAT1, which ultimately promotes T-ALL cell survival through the upregulation of BCL2 expression. Cancer Discov; 3(5); 564-77. (C) 2013 AACR.
C1 [Sanda, Takaomi; Gutierrez, Alejandro; Ahn, Yebin; Look, A. Thomas] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02215 USA.
[Zhou, Wenjun; Gray, Nathanael S.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Neuberg, Donna S.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
[Gutierrez, Alejandro; Look, A. Thomas] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Tatarek, Jessica; Kelliher, Michelle A.] Univ Massachusetts, Sch Med, Dept Canc Biol, Worcester, MA USA.
[Tyner, Jeffrey W.; Fleischman, Angela G.; Druker, Brian J.] Oregon Hlth & Sci Univ, Knight Canc Inst, Div Hematol & Med Oncol, Portland, OR 97239 USA.
[Glover, Jason; Chang, Bill H.] Oregon Hlth & Sci Univ, Dept Pediat, Div Pediat Hematol & Oncol, Portland, OR 97239 USA.
[Druker, Brian J.] Howard Hughes Med Inst, Portland, OR USA.
[Ngo, Vu N.] City Hope Natl Med Ctr, Beckman Res Inst, Div Hematopoiet Stem Cell & Leukemia Res, Duarte, CA 91010 USA.
[Ma, Wenxue] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Ma, Wenxue; Jamieson, Catriona H. M.] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Yost, Arla; Weng, Andrew P.] BC Canc Agcy, Terry Fox Lab, Dept Pathol, Vancouver, BC, Canada.
[Yang, Yandan; Staudt, Louis M.] NCI, Metab Branch, Bethesda, MD 20892 USA.
[Kleppe, Maria; Levine, Ross L.] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10021 USA.
[Moriggl, Richard] Univ Vet Med Vienna, Ludwig Boltzmann Inst Canc Res, Vienna, Austria.
[Mueller, Mathias] Univ Vet Med Vienna, Inst Anim Breeding & Genet, Vienna, Austria.
RP Look, AT (reprint author), Dana Farber Canc Inst, Dept Pediat Oncol, Mayer Bldg,Rm 630,450 Brookline Ave, Boston, MA 02215 USA.
EM drukerb@ohsu.edu; thomas_look@dfci.harvard.edu
RI Kleppe, Maria/C-6341-2014; Weng, Andrew/I-5015-2014;
OI Fleischman, Angela/0000-0002-3701-6079; Chang, Bill/0000-0003-3783-1820;
Moriggl, Richard/0000-0003-0918-9463; Kleppe, Maria/0000-0002-4372-6704;
Gutierrez, Alejandro/0000-0002-0249-9007; Tyner,
Jeffrey/0000-0002-2133-0960
FU William Lawrence and Blanche Hughes Fund; Leukemia & Lymphoma Society;
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; National Cancer Institute [4R00CA151457-03];
Oregon Clinical and Translational Research Institute (OCTRI) from the
National Center for Research Resources (NRCC), a component of the NIH
[UL1 RR024140]; NIH Roadmap for Medical Research; NIH [NCI 1K99CA157951,
NCI 1K08CA133103]; Children's Leukemia Research Association; Japan
Society for the Promotion of Science; Oregon Child Health Research
Center; Austrian Science Fund FWF [SFB F28]; NCI [5P01CA109901, NCI
5P01CA68484]; Alex's Lemonade Stand Foundation Bridge grant; European
Molecular Biology Organization (EMBO) long-term fellowship; CIHR/Terry
Fox Foundation; California Institute for Regenerative Medicine (CIRM)
[TR21789, RN2-00910-1, DR1-01430]; Leichtag Family Foundation; Ratner
Family Foundation; [5P30CA069533]
FX This work was supported in part by the William Lawrence and Blanche
Hughes Fund, the Leukemia & Lymphoma Society, and the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research. J.W. Tyner is supported by grants from the National
Cancer Institute (4R00CA151457-03) and the Oregon Clinical and
Translational Research Institute (OCTRI), grant number UL1 RR024140 from
the National Center for Research Resources (NRCC), a component of the
NIH, and the NIH Roadmap for Medical Research. T. Sanda is supported by
NIH grant NCI 1K99CA157951, Children's Leukemia Research Association,
and the Japan Society for the Promotion of Science. A. Gutierrez is
supported by NIH grant NCI 1K08CA133103 and is a scholar of the American
Society of Hematology-Amos Medical Faculty Development Program. B.H.
Chang is supported by the Oregon Child Health Research Center and is a
St. Baldrick's Scholar. R. Moriggl and M. Muller are supported by grant
SFB F28 of the Austrian Science Fund FWF. A.T. Look and D.S. Neuberg are
supported by NCI grants 5P01CA109901 and NCI 5P01CA68484, and A.T. Look
is supported by an Alex's Lemonade Stand Foundation Bridge grant. B.J.
Druker is an investigator of the Howard Hughes Medical Institute and
principal investigator of the OHSU cancer center support grant
5P30CA069533. M. Kleppe is supported by the European Molecular Biology
Organization (EMBO) long-term fellowship. R.L. Levine is a Scholar of
the Leukemia and Lymphoma Society. A. Yost and A.P. Weng are supported
by a CIHR/Terry Fox Foundation program project grant. W. Ma and C.H.M.
Jamieson are supported by the California Institute for Regenerative
Medicine (CIRM) grants (TR21789; RN2-00910-1; DR1-01430) as well as the
Leichtag Family Foundation and the Ratner Family Foundation.
NR 47
TC 42
Z9 42
U1 0
U2 10
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD MAY
PY 2013
VL 3
IS 5
BP 564
EP 577
DI 10.1158/2159-8290.CD-12-0504
PG 14
WC Oncology
SC Oncology
GA 147ZI
UT WOS:000319210600027
PM 23471820
ER
PT J
AU Shneiderman, B
Plaisant, C
Hesse, BW
AF Shneiderman, Ben
Plaisant, Catherine
Hesse, Bradford W.
TI Improving Healthcare with Interactive Visualization
SO COMPUTER
LA English
DT Article
AB Visualization and visual analytics researchers can contribute substantial technological advances to support the reliable, effective, safe, and validated systems required for personal health, clinical healthcare, and public health policymaking.
C1 [Shneiderman, Ben] Univ Maryland, Dept Comp Sci, College Pk, MD 20742 USA.
[Shneiderman, Ben] Univ Maryland, Human Comp Interact Lab, College Pk, MD 20742 USA.
[Plaisant, Catherine] Univ Maryland, Human Comp Interact Lab, Inst Adv Comp Studies, College Pk, MD 20742 USA.
[Hesse, Bradford W.] NCI, Hlth Commun & Informat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Shneiderman, B (reprint author), Univ Maryland, Dept Comp Sci, College Pk, MD 20742 USA.
EM ben@cs.umd.edu; plaisant@cs.umd.edu; hesseb@mail.nih.gov
OI Hesse, Bradford/0000-0003-1142-1161
FU Oracle Health Sciences, the National Institutes of Health [RC 1
CA147489-02]; Office of the National Coordinator for Health Information
Technology [10510592]
FX mWe thank Wolfgang Aigner, Silvia Miksch, Jennifer Preece, Alexander
Rind, Matt Ward, the anonymous reviewers, and the editors of this
special issue for their comments on earlier drafts. We appreciate the
support of Oracle Health Sciences, the National Institutes of Health
(grant RC 1 CA147489-02: Interactive Exploration of Temporal Patterns in
Electronic Health Records), and grant no. 10510592 for Patient-Centered
Cognitive Support under the Strategic Health IT Advanced Research
Projects Program (SHARP) from the Office of the National Coordinator for
Health Information Technology.
NR 14
TC 18
Z9 19
U1 3
U2 15
PU IEEE COMPUTER SOC
PI LOS ALAMITOS
PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1314 USA
SN 0018-9162
J9 COMPUTER
JI Computer
PD MAY
PY 2013
VL 46
IS 5
BP 58
EP 66
PG 9
WC Computer Science, Hardware & Architecture; Computer Science, Software
Engineering
SC Computer Science
GA 145RO
UT WOS:000319034700009
ER
PT J
AU Grant, LM
Kleiner, DE
Conjeevaram, HS
Vuppalanchi, R
Lee, WM
AF Grant, Lafaine M.
Kleiner, David E.
Conjeevaram, Hari S.
Vuppalanchi, Raj
Lee, William M.
TI Clinical and Histological Features of Idiosyncratic Acute Liver Injury
Caused by Temozolomide
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Temozolomide toxicity; Temozolomide hepatotoxicity; Drug-induced liver
injury; Temozolomide hepatitis
ID TRIAL; GLIOBLASTOMA; MULTICENTER; DACARBAZINE; RATIONALE; MELANOMA;
THERAPY
C1 [Grant, Lafaine M.; Lee, William M.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA.
[Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
[Conjeevaram, Hari S.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Vuppalanchi, Raj] Indiana Univ, Indianapolis, IN 46204 USA.
RP Grant, LM (reprint author), Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM lafaine.grant@utsouthwestern.edu
OI Vuppalanchi, Raj/0000-0003-0637-1577; Kleiner, David/0000-0003-3442-4453
FU National Institute of Diabetes and Digestive and Kidney Disease;
National Institutes of Health (NIH); National Cancer Institute, NIH
FX Patients were participants in the Drug-Induced Liver Injury Network,
which is funded as a cooperative agreement by the National Institute of
Diabetes and Digestive and Kidney Disease and National Institutes of
Health (NIH). This research was also supported by the Intramural
Research Program of the National Cancer Institute, NIH. We acknowledge
referral to the study registry from Dr. Abdullah Mubarak of The Liver
Institute at Methodist Dallas Medical Center.
NR 17
TC 6
Z9 6
U1 1
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD MAY
PY 2013
VL 58
IS 5
BP 1415
EP 1421
DI 10.1007/s10620-012-2493-9
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 149VU
UT WOS:000319350300039
PM 23212393
ER
PT J
AU Liu, F
Xue, ZQ
Deng, SH
Kun, X
Luo, XG
Patrylo, PR
Rose, GM
Cai, HB
Struble, RG
Cai, Y
Yan, XX
AF Liu, Fei
Xue, Zhi-Qin
Deng, Si-Hao
Kun, Xiong
Luo, Xue-Gang
Patrylo, Peter R.
Rose, Gregory M.
Cai, Huaibin
Struble, Robert G.
Cai, Yan
Yan, Xiao-Xin
TI -Secretase binding sites in aged and Alzheimer's disease human cerebrum:
the choroid plexus as a putative origin of CSF A
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE -amyloid; -secretase; AD biomarker; anti-A therapy; BACE1
ID CEREBROSPINAL FLUID SYSTEM; MILD COGNITIVE IMPAIRMENT;
AMYLOID-BETA-PEPTIDES; GAMMA-SECRETASE; A-BETA; BETA-SECRETASE-1
ELEVATION; NEUROFIBRILLARY TANGLES; TERMINAL FRAGMENTS; SENILE PLAQUES;
CELL BIOLOGY
AB Deposition of -amyloid (A) peptides, cleavage products of -amyloid precursor protein (APP) by -secretase-1 (BACE1) and -secretase, is a neuropathological hallmark of Alzheimer's disease (AD). -Secretase inhibition is a therapeutical anti-A approach, although changes in the enzyme's activity in AD brain are unclear. Cerebrospinal fluid (CSF) A peptides are thought to derive from brain parenchyma and thus may serve as biomarkers for assessing cerebral amyloidosis and anti-A efficacy. The present study compared active -secretase binding sites with A deposition in aged and AD human cerebrum, and explored the possibility of A production and secretion by the choroid plexus (CP). The specific binding density of [3H]-L-685,458, a radiolabeled high-affinity -secretase inhibitor, in the temporal neocortex and hippocampal formation was similar for AD and control cases with similar ages and post-mortem delays. The CP in post-mortem samples exhibited exceptionally high [3H]-L-685,458 binding density, with the estimated maximal binding sites (Bmax) reduced in the AD relative to control groups. Surgically resected human CP exhibited APP, BACE1 and presenilin-1 immunoreactivity, and -site APP cleavage enzymatic activity. In primary culture, human CP cells also expressed these amyloidogenic proteins and released A40 and A42 into the medium. Overall, our results suggest that -secretase activity appears unaltered in the cerebrum in AD and is not correlated with regional amyloid plaque pathology. The CP appears to be a previously unrecognised non-neuronal contributor to CSF A, probably at reduced levels in AD.
C1 [Liu, Fei] Cent S Univ, Xiangya Hosp 3, Dept Neurosurg, Changsha 410013, Hunan, Peoples R China.
[Xue, Zhi-Qin; Deng, Si-Hao; Kun, Xiong; Luo, Xue-Gang; Cai, Yan; Yan, Xiao-Xin] Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
[Xue, Zhi-Qin] Xinjiang Med Univ, Dept Anat, Urumqi, Xinjiang, Peoples R China.
[Patrylo, Peter R.; Rose, Gregory M.; Struble, Robert G.] So Illinois Univ, Ctr Integrated Res Cognit & Neural Sci, Carbondale, IL 62901 USA.
[Cai, Huaibin] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Yan, XX (reprint author), Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
EM yanxiaoxin@csu.edu.cn
RI Cai, Huaibin/H-3359-2013
OI Cai, Huaibin/0000-0002-8596-6108
FU SIU School of Medicine (CRC); National Natural Science Foundation of
China [81171091, 81171160]; Intramural research program of National
Institute on Aging, NIH [Z01-IAAG000944-04]
FX This study was supported by the SIU School of Medicine (CRC grant to
X.X.Y.), the National Natural Science Foundation of China (no. 81171091
to X.X.Y. and no. 81171160 to X. G. L.) and the Intramural research
program of National Institute on Aging, NIH (Z01-IAAG000944-04 to H.
C.). We thank Dr Robert Fazio at Vitrax, California, USA for producing
tritiated L-685,458, Dr Yue-Ming Li for providing some cold
gamma-secretase inhibitors, and Dr Samuel Gandy for providing the PS1
antibody.
NR 74
TC 6
Z9 6
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD MAY
PY 2013
VL 37
IS 10
BP 1714
EP 1725
DI 10.1111/ejn.12159
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 148AK
UT WOS:000319213900016
PM 23432732
ER
PT J
AU Zhang, L
Yu, Z
Muranski, P
Palmer, DC
Restifo, NP
Rosenberg, SA
Morgan, RA
AF Zhang, L.
Yu, Z.
Muranski, P.
Palmer, D. C.
Restifo, N. P.
Rosenberg, S. A.
Morgan, R. A.
TI Inhibition of TGF-beta signaling in genetically engineered tumor
antigen-reactive T cells significantly enhances tumor treatment efficacy
SO GENE THERAPY
LA English
DT Article
DE adoptive T-cell therapy; antigen-specific T cell; TGF-beta
ID GROWTH-FACTOR-BETA; ANTITUMOR-ACTIVITY; BREAST-CANCER; ESTABLISHED
MELANOMA; AUTOIMMUNE-DISEASE; SOLUBLE BETAGLYCAN; II RECEPTOR;
DIFFERENTIATION; IMMUNOTHERAPY; LYMPHOCYTES
AB Transforming growth factor beta (TGF-beta) is a cytokine with complex biological functions that may involve tumor promotion or tumor suppression. It has been reported that multiple types of tumors secrete TGF-beta, which can inhibit tumor-specific cellular immunity and may represent a major obstacle to the success of tumor immunotherapy. In this study, we sought to enhance tumor immunotherapy using genetically modified antigen-specific T cells by interfering with TGF-beta signaling. We constructed three gamma-retroviral vectors, one that expressed TGF-beta-dominant-negative receptor II (DNRII) or two that secreted soluble TGF-beta receptors: soluble TGF-beta receptor II (sRII) and the sRII fused with mouse IgG Fc domain (sRIIFc). We demonstrated that T cells genetically modified with these viral vectors were resistant to exogenous TGF-beta-induced smad-2 phosphorylation in vitro. The functionality of antigen-specific T cells engineered to resist TGF-beta signaling was further evaluated in vivo using the B16 melanoma tumor model. Antigen-specific CD8+ T cells (pmel-1) or CD4+ T cells (tyrosinase-related protein-1) expressing DNRII dramatically improved tumor treatment efficacy. There was no enhancement in the B16 tumor treatment using cells secreting soluble receptors. Our data support the potential application of the blockade of TGF-beta signaling in tumor-specific T cells for cancer immunotherapy.
C1 [Zhang, L.; Yu, Z.; Palmer, D. C.; Restifo, N. P.; Rosenberg, S. A.; Morgan, R. A.] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Muranski, P.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Morgan, RA (reprint author), NCI, Surg Branch, Ctr Canc Res, NIH, 10 Ctr Dr,Bldg 10,CRC 3W-3864, Bethesda, MD 20892 USA.
EM rmorgan@mail.nih.gov
RI Palmer, Douglas/B-9454-2008;
OI Palmer, Douglas/0000-0001-5018-5734; Restifo, Nicholas
P./0000-0003-4229-4580
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, and Center for Cancer Research
FX We thank Dr Lalage Wakefield for kindly providing TGF-beta DNRII vector
and help in explaining data. FACS laboratory and the TIL laboratory in
the Surgery Branch, National Cancer Institute provide technical support
and maintenance of tumor cells from patients. This work is supported by
the Intramural Research Program of the National Institutes of Health,
National Cancer Institute, and Center for Cancer Research.
NR 40
TC 19
Z9 19
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0969-7128
J9 GENE THER
JI Gene Ther.
PD MAY
PY 2013
VL 20
IS 5
BP 575
EP 580
DI 10.1038/gt.2012.75
PG 6
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 143EM
UT WOS:000318849300013
PM 22972494
ER
PT J
AU Garcia-Closas, M
Gail, MH
Kelsey, KT
Ziegler, RG
AF Garcia-Closas, Montserrat
Gail, Mitchell H.
Kelsey, Karl T.
Ziegler, Regina G.
TI Searching for Blood DNA Methylation Markers of Breast Cancer Risk and
Early Detection
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID MICROARRAY; VALIDATION; EPIGENOME; DISEASE; GENOME
C1 [Garcia-Closas, Montserrat] Inst Canc Res, Div Genet & Epidemiol, London SW3 6JB, England.
[Garcia-Closas, Montserrat] Breakthrough Breast Canc Res Ctr, London, England.
[Gail, Mitchell H.; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Kelsey, Karl T.] Brown Univ, Sch Med, Dept Epidemiol, Providence, RI 02912 USA.
RP Ziegler, RG (reprint author), NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Execut Plaza S 8098, Bethesda, MD 20892 USA.
EM regina.ziegler@nih.gov
RI Kelsey, Karl/I-1252-2014; Garcia-Closas, Montserrat /F-3871-2015
OI Garcia-Closas, Montserrat /0000-0003-1033-2650
FU Intramural NIH HHS
NR 16
TC 3
Z9 3
U1 0
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 10
BP 678
EP 680
DI 10.1093/jnci/djt090
PG 3
WC Oncology
SC Oncology
GA 149JS
UT WOS:000319315700003
PM 23578855
ER
PT J
AU Madan, RA
Shah, AA
Dahut, WL
AF Madan, Ravi A.
Shah, Avni A.
Dahut, William L.
TI Is It Time to Reevaluate Definitive Therapy in Prostate Cancer?
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID EXTERNAL-BEAM RADIATION; PHASE-III TRIAL; RADICAL PROSTATECTOMY;
ANDROGEN-DEPRIVATION; RANDOMIZED-TRIAL; DOSE-RESPONSE; ANTIGEN ERA;
RADIOTHERAPY; TERM; MORTALITY
C1 [Madan, Ravi A.; Shah, Avni A.; Dahut, William L.] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Dahut, WL (reprint author), NCI, Ctr Canc Res, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM dahutw@mail.nih.gov
NR 22
TC 4
Z9 4
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 10
BP 683
EP 685
DI 10.1093/jnci/djt094
PG 4
WC Oncology
SC Oncology
GA 149JS
UT WOS:000319315700006
PM 23615688
ER
PT J
AU Lin, SH
George, TJ
Ben-Josef, E
Bradley, J
Choe, KS
Edelman, MJ
Guha, C
Krishnan, S
Lawrence, TS
Le, QT
Lu, B
Mehta, M
Peereboom, D
Sarkaria, J
Seong, J
Wang, DA
Welliver, MX
Coleman, CN
Vikram, B
Yoo, S
Chung, CH
AF Lin, Steven H.
George, Thomas J.
Ben-Josef, Edgar
Bradley, Jeffrey
Choe, Kevin S.
Edelman, Martin J.
Guha, Chandan
Krishnan, Sunil
Lawrence, Theodore S.
Quynh-Thu Le
Lu, Bo
Mehta, Minesh
Peereboom, David
Sarkaria, Jann
Seong, Jinsil
Wang, Dian
Welliver, Meng X.
Coleman, C. Norman
Vikram, Bhadrasain
Yoo, Stephen
Chung, Christine H.
CA Natl Canc Inst
TI Opportunities and Challenges in the Era of Molecularly Targeted Agents
and Radiation Therapy
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID CELL LUNG-CANCER; KINASE INHIBITOR; CETUXIMAB; MODELS; DRUGS
AB The first annual workshop for preclinical and clinical development of radiosensitizers took place at the National Cancer Institute on August 8-9, 2012. Radiotherapy is one of the most commonly applied and effective oncologic treatments for solid tumors. It is well recognized that improved clinical efficacy of radiotherapy would make a substantive impact in clinical practice and patient outcomes. Advances in genomic technologies and high-throughput drug discovery platforms have brought a revolution in cancer treatment by providing molecularly targeted agents for various cancers. Development of predictive biomarkers directed toward specific subsets of cancers has ushered in a new era of personalized therapeutics. The field of radiation oncology stands to gain substantial benefit from these advances given the concerted effort to integrate this progress into radiation therapy. This workshop brought together expert clinicians and scientists working in various disease sites to identify the exciting opportunities and expected challenges in the development of molecularly targeted agents in combination with radiation therapy.
C1 [Lin, Steven H.; Krishnan, Sunil] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA.
[George, Thomas J.] Univ Florida, Coll Med, Div Hematol Oncol, Gainesville, FL USA.
[Ben-Josef, Edgar] Hosp Univ Penn, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
[Bradley, Jeffrey] Washington Univ, Dept Radiat Oncol, St Louis, MO USA.
[Choe, Kevin S.] Univ Texas SW Med Ctr Dallas, Dept Radiat Oncol, Dallas, TX 75390 USA.
[Edelman, Martin J.] Univ Maryland, Med Ctr, Dept Med, Baltimore, MD 21201 USA.
[Guha, Chandan] Montefiore Med Ctr, Albert Einstein Coll Med, Dept Radiat Oncol, Bronx, NY 10467 USA.
[Lawrence, Theodore S.] Univ Michigan, Dept Radiat Oncol, Ann Arbor, MI 48109 USA.
[Quynh-Thu Le] Stanford Univ, Dept Radiat Oncol, Sch Med, Stanford, CA 94305 USA.
[Lu, Bo] Thomas Jefferson Univ, Dept Radiat Oncol, Med Ctr, Philadelphia, PA 19107 USA.
[Mehta, Minesh] Northwestern Univ, Dept Radiat Oncol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Peereboom, David] Cleveland Clin, Dept Brain Tumor, Cleveland, OH 44106 USA.
[Peereboom, David] Cleveland Clin, Neurooncol Ctr, Cleveland, OH 44106 USA.
[Sarkaria, Jann] Mayo Clin, Dept Radiat Oncol, Rochester, MN USA.
[Seong, Jinsil] Yonsei Univ, Coll Med, Dept Radiat Oncol, Seoul, South Korea.
[Wang, Dian] Med Coll Wisconsin, Dept Radiat Oncol, Milwaukee, WI 53226 USA.
[Welliver, Meng X.] Ohio State Univ, Ctr Comprehens Canc, Dept Radiat Oncol, Columbus, OH 43210 USA.
[Coleman, C. Norman] NIH, Radiat Oncol Branch, Bethesda, MD 20892 USA.
[Vikram, Bhadrasain; Yoo, Stephen] NCI, Radiat Res Program, Rockville, MD USA.
[Chung, Christine H.] Johns Hopkins Sidney Kimmel Comprehens Canc Ctr, Dept Oncol, Baltimore, MD 21231 USA.
RP Lin, SH (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, 1515 Holcombe Blvd,Unit 097, Houston, TX 77030 USA.
EM shlin@madanderson.org; cchung11@jhmi.edu
OI mehta, minesh/0000-0002-4812-5713
FU NCI NIH HHS [1R01CA161585-01A1, CA016672, P30 CA016672, P30CA130810, P50
CA130810, R01CA138723]; NIDCR NIH HHS [1R21DE021167A1-01]
NR 23
TC 26
Z9 26
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 10
BP 686
EP 693
DI 10.1093/jnci/djt055
PG 8
WC Oncology
SC Oncology
GA 149JS
UT WOS:000319315700007
PM 23503600
ER
PT J
AU Xu, ZL
Bolick, SCE
DeRoo, LA
Weinberg, CR
Sandler, DP
Taylor, JA
AF Xu, Zongli
Bolick, Sophia C. E.
DeRoo, Lisa A.
Weinberg, Clarice R.
Sandler, Dale P.
Taylor, Jack A.
TI Epigenome-wide Association Study of Breast Cancer Using Prospectively
Collected Sister Study Samples
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID PERIPHERAL-BLOOD DNA; METHYLATION PROFILES; GENETIC-VARIANTS; BRCA1
PROMOTER; OVARIAN-CANCER; CASE COHORT; RISK; MODEL; ATM
AB Background Previous studies have suggested DNA methylation in blood is a potential epigenetic marker of cancer risk, but this has not been evaluated on a genome-wide scale in prospective studies for breast cancer.
Methods We measured DNA methylation at 27 578 CpGs in blood samples from 298 women who developed breast cancer 0 to 5 years after enrollment in the Sister Study cohort and compared them with a random sample of 612 cohort women who remained cancer free. We also genotyped women for nine common polymorphisms associated with breast cancer.
Results We identified 250 differentially methylated CpGs (dmCpGs) between case subjects and noncase subjects (false discovery rate [FDR] Q < 0.05). Of these dmCpGs, 75.2% were undermethylated in case subjects relative to noncase subjects. Women diagnosed within 1 year of blood draw had small but consistently greater divergence from noncase subjects than did women diagnosed at more than 1 year. Gene set enrichment analysis identified Kyoto Encyclopedia of Genes and Genomes cancer pathways at the recommended FDR of Q less than 0.25. Receiver operating characteristic analysis estimated a prediction accuracy of 65.8% (95% confidence interval = 61.0% to 70.5%) for methylation, compared with 56.0% for the Gail model and 58.8% for genome-wide association study polymorphisms. The prediction accuracy of just five dmCpGs (64.1%) was almost as good as the larger panel and was similar (63.1%) when replicated in a small sample of 81 women with diverse ethnic backgrounds.
Conclusions Methylation profiling of blood holds promise for breast cancer detection and risk prediction.
C1 [Xu, Zongli; DeRoo, Lisa A.; Sandler, Dale P.; Taylor, Jack A.] NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Bolick, Sophia C. E.; Taylor, Jack A.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Weinberg, Clarice R.] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
RP Taylor, JA (reprint author), NIEHS, MD A3-05,111 TW Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
EM taylor@niehs.nih.gov
OI xu, zongli/0000-0002-9034-8902; taylor, jack/0000-0001-5303-6398;
Sandler, Dale/0000-0002-6776-0018
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01 ES044005, Z01
ES044032, Z01 ES049033]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences (Z01 ES044005, Z01 ES044032, and Z01 ES049033).
NR 31
TC 47
Z9 47
U1 0
U2 8
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-J. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 10
BP 694
EP 700
DI 10.1093/jnci/djt045
PG 7
WC Oncology
SC Oncology
GA 149JS
UT WOS:000319315700008
PM 23578854
ER
PT J
AU Xu, H
Yang, WJ
Perez-Andreu, V
Devidas, M
Fan, YP
Cheng, C
Pei, DQ
Scheet, P
Burchard, EG
Eng, C
Huntsman, S
Torgerson, DG
Dean, M
Winick, NJ
Martin, PL
Camitta, BM
Bowman, WP
Willman, CL
Carroll, WL
Mullighan, CG
Bhojwani, D
Hunger, SP
Pui, CH
Evans, WE
Relling, MV
Loh, ML
Yang, JJ
AF Xu, Heng
Yang, Wenjian
Perez-Andreu, Virginia
Devidas, Meenakshi
Fan, Yiping
Cheng, Cheng
Pei, Deqing
Scheet, Paul
Burchard, Esteban Gonzalez
Eng, Celeste
Huntsman, Scott
Torgerson, Dara G.
Dean, Michael
Winick, Naomi J.
Martin, Paul L.
Camitta, Bruce M.
Bowman, W. Paul
Willman, Cheryl L.
Carroll, William L.
Mullighan, Charles G.
Bhojwani, Deepa
Hunger, Stephen P.
Pui, Ching-Hon
Evans, William E.
Relling, Mary V.
Loh, Mignon L.
Yang, Jun J.
TI Novel Susceptibility Variants at 10p12.31-12.2 for Childhood Acute
Lymphoblastic Leukemia in Ethnically Diverse Populations
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GENETIC POLYMORPHISMS; MISSING HERITABILITY;
CANCER INCIDENCE; COMMON VARIANTS; RISK; DISEASE; COMPLEX; LOCI;
CONTRIBUTES
AB Background Acute lymphoblastic leukemia (ALL) is the most common cancer in children and the incidence of ALL varies by ethnicity. Although accumulating evidence indicates inherited predisposition to ALL, the genetic basis of ALL susceptibility in diverse ancestry has not been comprehensively examined.
Methods We performed a multiethnic genome-wide association study in 1605 children with ALL and 6661 control subjects after adjusting for population structure, with validation in three replication series of 845 case subjects and 4316 control subjects. Association was tested by two-sided logistic regression.
Results A novel ALL susceptibility locus at 10p12.31-12.2 (BMI1-PIP4K2A, rs7088318, P = 1.1 x 10(-11)) was identified in the genome-wide association study, with independent replication in European Americans, African Americans, and Hispanic Americans (P = .001, .009, and .04, respectively). Association was also validated at four known ALL susceptibility loci: ARID5B, IKZF1, CEBPE, and CDKN2A/2B. Associations at ARID5B, IKZF1, and BMI1-PIP4K2A variants were consistent across ethnicity, with multiple independent signals at IKZF1 and BMI1-PIP4K2A loci. The frequency of ARID5B and BMI1-PIP4K2A variants differed by ethnicity, in parallel with ethnic differences in ALL incidence. Suggestive evidence for modifying effects of age on genetic predisposition to ALL was also observed. ARID5B, IKZF1, CEBPE, and BMI1-PIP4K2A variants cumulatively conferred strong predisposition to ALL, with children carrying six to eight copies of risk alleles at a ninefold (95% confidence interval = 6.9 to 11.8) higher ALL risk relative to those carrying zero to one risk allele at these four single nucleotide polymorphisms.
Conclusions These findings indicate strong associations between inherited genetic variation and ALL susceptibility in children and shed new light on ALL molecular etiology in diverse ancestry.
C1 [Xu, Heng; Yang, Wenjian; Perez-Andreu, Virginia; Evans, William E.; Relling, Mary V.; Yang, Jun J.] St Jude Childrens Res Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA.
[Fan, Yiping] St Jude Childrens Res Hosp, Dept Computat Biol, Memphis, TN 38105 USA.
[Cheng, Cheng; Pei, Deqing] St Jude Childrens Res Hosp, Dept Biostat, Memphis, TN 38105 USA.
[Mullighan, Charles G.] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Bhojwani, Deepa; Pui, Ching-Hon] St Jude Childrens Res Hosp, Dept Oncol, Memphis, TN 38105 USA.
[Devidas, Meenakshi] Univ Florida, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
[Scheet, Paul] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Burchard, Esteban Gonzalez; Eng, Celeste; Huntsman, Scott; Torgerson, Dara G.] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci & Med, San Francisco, CA 94143 USA.
[Loh, Mignon L.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA.
[Dean, Michael] NCI, Expt Immunol Lab, Frederick, MD 21701 USA.
[Winick, Naomi J.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Martin, Paul L.] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
[Camitta, Bruce M.] Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA.
[Bowman, W. Paul] Cook Childrens Med Ctr, Ft Worth, TX USA.
[Willman, Cheryl L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Carroll, William L.] NYU, Inst Canc, New York, NY USA.
[Hunger, Stephen P.] Univ Colorado, Sch Med, Aurora, CO USA.
[Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
RP Yang, JJ (reprint author), St Jude Childrens Res Hosp, MS 313,262 Danny Thomas Pl, Memphis, TN 38105 USA.
EM jun.yang@stjude.org
RI Yang, Jun/B-6976-2008; Dean, Michael/G-8172-2012;
OI Yang, Jun/0000-0002-0770-9659; Dean, Michael/0000-0003-2234-0631;
Mullighan, Charles/0000-0002-1871-1850; Bhojwani,
Deepa/0000-0002-7559-7927
FU National Institutes of Health [CA156449, CA21765, CA36401, CA98543,
CA114766, CA98413, CA140729, U01GM92666]; Intramural Program of the
National Cancer Institute; American Lebanese Syrian Associated Charities
(ALSAC); Jeffrey Pride Foundation; National Childhood Cancer Foundation;
American Society of Hematology; Alex Lemonade Stand Foundation for
Childhood Cancer; Order of St. Francis Foundation
FX This work was supported by the National Institutes of Health (grant
numbers CA156449, CA21765, CA36401, CA98543, CA114766, CA98413,
CA140729, and U01GM92666), in part by the Intramural Program of the
National Cancer Institute, and by the American Lebanese Syrian
Associated Charities (ALSAC).; Genome-wide genotyping of COG P9904/P9905
samples was performed by the Center for Molecular Medicine with the
generous financial support from the Jeffrey Pride Foundation and the
National Childhood Cancer Foundation. S.P. Hunger is the Ergen Family
Chair in Pediatric Cancer, and J.J. Yang is supported by the American
Society of Hematology Scholar Award, Alex Lemonade Stand Foundation for
Childhood Cancer Young Investigator Grant, and by the Order of St.
Francis Foundation.
NR 50
TC 67
Z9 68
U1 1
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 10
BP 733
EP 742
DI 10.1093/jnci/djt042
PG 10
WC Oncology
SC Oncology
GA 149JS
UT WOS:000319315700013
PM 23512250
ER
PT J
AU Hirahara, K
Poholek, A
Vahedi, G
Laurence, A
Kanno, Y
Milner, JD
O'Shea, JJ
AF Hirahara, Kiyoshi
Poholek, Amanda
Vahedi, Golnaz
Laurence, Arian
Kanno, Yuka
Milner, Joshua D.
O'Shea, John J.
TI Mechanisms underlying helper T-cell plasticity: Implications for
immune-mediated disease
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE T-cell plasticity; asthma; allergic disease; epigenetics; histone
modification; therapy
ID GENOME-WIDE ASSOCIATION; ANTI-INTERLEUKIN-17 MONOCLONAL-ANTIBODY;
TRANSCRIPTION FACTOR GATA-3; IFN-GAMMA PROMOTER; TH17 CELLS;
ALLERGIC-ASTHMA; IN-VIVO; AIRWAY HYPERRESPONSIVENESS;
MOLECULAR-MECHANISMS; LINEAGE COMMITMENT
AB CD4 helper T cells are critical for proper immune cell homeostasis and host defense but are also major contributors to immune and inflammatory disease. Arising from a simple biphasic model of differentiation (ie, T(H)1 and T(H)2 cells). A bewildering number of fates seem possible for helper T cells. To what extent different helper cell subsets maintain their characteristic gene expression profiles or exhibit functional plasticity is a hotly debated topic. In this review we will discuss how the expression of "signature cytokines'' and "master regulator'' transcription factors do not neatly conform to a simple helper T-cell paradigm. Although this might seem confusing, the good news is that the newly recognized complexity fits better with our understanding of immunopathogenesis. Finally, we will discuss factors, including epigenetic regulation and metabolic alterations, that contribute to helper cell specificity and plasticity.
C1 [Hirahara, Kiyoshi; Poholek, Amanda; Vahedi, Golnaz; Laurence, Arian; Kanno, Yuka; O'Shea, John J.] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
[Milner, Joshua D.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
RP O'Shea, JJ (reprint author), 10 Ctr Dr,Bldg 10,Rm 13C103, Bethesda, MD 20892 USA.
EM osheajo@mail.nih.gov
RI Kanno, Yuka/B-5802-2013; Laurence, Arian/A-8770-2009; Hirahara,
Kiyoshi/E-2460-2017;
OI Laurence, Arian/0000-0003-0942-8292; Hirahara,
Kiyoshi/0000-0002-9128-9449; Kanno, Yuka/0000-0001-5668-9319
FU National Institutes of Health (NIH)/National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS); JSPS; NIH; PRAT
FX Supported by the National Institutes of Health (NIH)/National Institute
of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Intramural
Research Program, the JSPS Research Fellowship for Japanese Biomedical
and Behavioral Researchers at the NIH (to K.H.), and PRAT (to A.P.).
NR 201
TC 57
Z9 57
U1 1
U2 13
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD MAY
PY 2013
VL 131
IS 5
BP 1276
EP 1287
DI 10.1016/j.jaci.2013.03.015
PG 12
WC Allergy; Immunology
SC Allergy; Immunology
GA 144AU
UT WOS:000318912200002
PM 23622118
ER
PT J
AU Cai, LS
Liow, JS
Hurtle, B
Morse, CL
Gladding, RL
Qu, BX
Diaz-Arastia, R
Innis, RB
Pike, VW
AF Cai Lisheng
Liow, Jeih-San
Hurtle, Bryan
Morse, Cheryl L.
Gladding, Robert L.
Qu Bao-Xi
Diaz-Arastia, Ramon
Innis, Robert B.
Pike, Victor W.
TI Pegylated derivatives of THK523 as candidate PET radioligands for
tangle-abundant human brain disease: synthesis, in vitro binding, and
monkey PET imaging
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
ID ALZHEIMERS-DISEASE
C1 [Cai Lisheng; Liow, Jeih-San; Hurtle, Bryan; Morse, Cheryl L.; Gladding, Robert L.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD USA.
[Qu Bao-Xi; Diaz-Arastia, Ramon] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
NR 4
TC 0
Z9 0
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P231
BP S318
EP S318
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100319
ER
PT J
AU Chun, JH
Lu, SY
Pike, VW
AF Chun, Joong-Hyun
Lu Shuiyu
Pike, Victor W.
TI Microfluidic investigation of the radiofluorination of diaryliodonium
tosylates in aqueous DMF using F-18-fluoride ion in target water and
without cryptand K 2.2.2
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Chun, Joong-Hyun; Lu Shuiyu; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA O016
BP S16
EP S16
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100017
ER
PT J
AU Hong, J
Wilson, AA
Pike, VW
AF Hong, Jinsoo
Wilson, Alan A.
Pike, Victor W.
TI Simple instrumentation for producing [C-11]isocyanates and application
to synthesis of [C-11]CURB
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Hong, Jinsoo; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Wilson, Alan A.] Ctr Addict & Mental Hlth, Toronto, ON, Canada.
NR 1
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P380
BP S467
EP S467
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100468
ER
PT J
AU Lang, LX
Guo, JX
Ma, Y
Niu, G
Kiesewetter, DO
Chen, XY
AF Lang Lixin
Guo Jinxia
Ma Ying
Niu Gang
Kiesewetter, Dale O.
Chen Xiaoyuan
TI Radiolabeling peptides with [F-18]fluoroalkyl sulfonates through the
tyrosine residue
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Lang Lixin; Guo Jinxia; Ma Ying; Niu Gang; Kiesewetter, Dale O.; Chen Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
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 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P057
BP S144
EP S144
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100145
ER
PT J
AU Lu, SY
Zhang, Y
Kalin, J
Liow, JS
Gladding, RL
Innis, RB
Kozikowski, AP
Pike, VW
AF Lu Shuiyu
Zhang Yi
Kalin, Jay
Liow, Jeih-San
Gladding, Robert L.
Innis, Robert B.
Kozikowski, Alan P.
Pike, Victor W.
TI Synthesis and evaluation of [methyl-C-11]KB631-a candidate radioligand
for histone deacetylase isozyme 6 (HDAC6)
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Lu Shuiyu; Zhang Yi; Liow, Jeih-San; Gladding, Robert L.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Kalin, Jay; Kozikowski, Alan P.] Univ Illinois, Dept Med Chem & Pharmacognosy, Chicago, IL USA.
NR 3
TC 0
Z9 0
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P232
BP S319
EP S319
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100320
ER
PT J
AU Simeon, FG
Yi, Z
Morse, CL
Yoo, CH
Gladding, RL
Fujita, M
Innis, RB
Pike, VW
AF Simeon, Fabrice G.
Yi Zhang
Morse, Cheryl L.
Yoo, Chul H.
Gladding, Robert L.
Fujita, Masahiro
Innis, Robert B.
Pike, Victor W.
TI Labeling of FPEB with carbon-11 for evaluation as an mGluR5 radioligand
in monkey with PET
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Simeon, Fabrice G.; Yi Zhang; Morse, Cheryl L.; Yoo, Chul H.; Gladding, Robert L.; Fujita, Masahiro; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P242
BP S329
EP S329
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100330
ER
PT J
AU Simeon, FG
Lu, SY
Culligan, WJ
Jin, YY
Bao, XF
Pike, VW
AF Simeon, Fabrice G.
Lu Shuiyu
Culligan, William J.
Jin Yanyan
Bao Xiaofeng
Pike, Victor W.
TI Generic syntheses of candidate C-11-labeled brain histamine subtype 3
receptor radioligands
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
ID RADIOSYNTHESIS
C1 [Simeon, Fabrice G.; Lu Shuiyu; Culligan, William J.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Jin Yanyan; Bao Xiaofeng] Nanjing Univ Sci & Technol, Dept Biochem Engn, Nanjing, Jiangsu, Peoples R China.
RI Bao, Xiaofeng/K-5278-2013
NR 4
TC 0
Z9 0
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA O-078
BP S78
EP S78
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100079
ER
PT J
AU Telu, S
Xu, R
Liow, JS
Gladding, RL
Zoghbi, SS
Guillon, CD
Fabio, KM
Lu, SF
Heindel, N
Simon, N
Brownstein, MJ
Innis, RB
Pike, VW
AF Telu, Sanjay
Xu Rong
Liow, Jeih-San
Gladding, Robert L.
Zoghbi, Sami S.
Guillon, Christophe D.
Fabio, Karine M.
Lu Shifang
Heindel, Ned
Simon, Neal
Brownstein, Michael J.
Innis, Robert B.
Pike, Victor W.
TI Labeling of the high-affinity vasopressin subtype 1a receptor ligand,
AVN778, with carbon-11 and evaluation as a candidate PET radioligand in
monkey
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
ID ANTAGONISTS
C1 [Telu, Sanjay; Xu Rong; Liow, Jeih-San; Gladding, Robert L.; Zoghbi, Sami S.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Guillon, Christophe D.; Lu Shifang; Simon, Neal; Brownstein, Michael J.] Azevan Pharmaceut Inc, Bethlehem, PA USA.
[Guillon, Christophe D.; Fabio, Karine M.; Heindel, Ned] Lehigh Univ, Dept Chem, Bethlehem, PA 18015 USA.
[Lu Shifang; Simon, Neal] Lehigh Univ, Dept Biol Sci, Bethlehem, PA 18015 USA.
NR 4
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P240
BP S327
EP S327
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100328
ER
PT J
AU Telu, S
Xu, R
Liow, JS
Gladding, RL
Innis, RB
Pike, VW
AF Telu, Sanjay
Xu Rong
Liow, Jieh-San
Gladding, Robert L.
Innis, Robert B.
Pike, Victor W.
TI Syntheses and evaluation of two candidate C-11-labeled ligands for
imaging brain oxytocin receptors
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Telu, Sanjay; Xu Rong; Liow, Jieh-San; Gladding, Robert L.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P239
BP S326
EP S326
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100327
ER
PT J
AU Xu, R
Zanotti-Fregonara, P
Gladding, RL
Zoghbi, SS
Innis, RB
Pike, VW
AF Xu Rong
Zanotti-Fregonara, Paolo
Gladding, Robert L.
Zoghbi, Sami S.
Innis, Robert B.
Pike, Victor W.
TI [F-18]FIMX - a promising PET radioligand for imaging brain mGluR1
receptors: synthesis and early evaluation in monkey
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Xu Rong; Zanotti-Fregonara, Paolo; Gladding, Robert L.; Zoghbi, Sami S.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P241
BP S328
EP S328
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100329
ER
PT J
AU Yue, XY
Kiesewetter, DO
Chen, XY
AF Yue Xuyi
Kiesewetter, Dale O.
Chen Xiaoyuan
TI Development of a new F-18-radiolabeled thiol-specific prosthetic group
using a two-step one-pot strategy
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Yue Xuyi; Kiesewetter, Dale O.; Chen Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P085
BP S172
EP S172
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100173
ER
PT J
AU Yue, XY
Kiesewetter, DO
Guo, JX
Sun, ZC
Zhang, XX
Zhu, L
Niu, G
Ma, Y
Chen, XY
AF Yue Xuyi
Kiesewetter, Dale O.
Guo Jinxia
Sun Zhongchan
Zhang Xiaoxiang
Zhu Lei
Niu Gang
Ma Ying
Chen Xiaoyuan
TI Development of a new thiol site-specific prosthetic group and its
conjugation with [Cys(40)]-exendin-4 for insulinoma targeting
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
C1 [Yue Xuyi; Kiesewetter, Dale O.; Guo Jinxia; Sun Zhongchan; Zhang Xiaoxiang; Zhu Lei; Niu Gang; Ma Ying; Chen Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA O010
BP S10
EP S10
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100011
ER
PT J
AU Zhang, Y
Zanotti-Fregonara, P
Jenko, K
Gladding, RL
Zoghbi, SS
Fujita, M
Milite, C
Castellano, S
Taliani, S
Martini, C
Innis, RB
Da Settimo, F
Pike, VW
AF Zhang Yi
Zanotti-Fregonara, Paolo
Jenko, Kimberly
Gladding, Robert L.
Zoghbi, Sami S.
Fujita, Masahiro
Milite, Ciro
Castellano, Sabrina
Taliani, Sabrina
Martini, Claudia
Innis, Robert B.
Da Settimo, Federico
Pike, Victor W.
TI Synthesis and evaluation of new TSPO PET radioligands with low
sensitivity to human genotype
SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS
LA English
DT Meeting Abstract
ID TRANSLOCATOR PROTEIN; LIGANDS; BINDING; AFFINITY
C1 [Zhang Yi; Zanotti-Fregonara, Paolo; Jenko, Kimberly; Gladding, Robert L.; Zoghbi, Sami S.; Fujita, Masahiro; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Milite, Ciro; Castellano, Sabrina; Taliani, Sabrina] Univ Salerno, Dept Pharmaceut Sci, Fisciano, SA, Italy.
[Martini, Claudia; Da Settimo, Federico] Univ Pisa, Dept Med Chem, Pisa, Italy.
RI Castellano, Sabrina/B-7635-2011; Da Settimo, Federico/M-1451-2015
OI Da Settimo, Federico/0000-0002-7897-7917
NR 5
TC 0
Z9 0
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0362-4803
J9 J LABELLED COMPD RAD
JI J. Label. Compd. Radiopharm.
PD MAY
PY 2013
VL 56
SU 1
MA P233
BP S320
EP S320
PG 1
WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry,
Analytical
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 140ZD
UT WOS:000318694100321
ER
PT J
AU Sterling, K
Yang, W
Teal, V
Navaneethan, SD
Ojo, A
Reilly, M
Glenn, M
Rosas, S
Guzman, N
Cuevas, M
Fischer, M
Lustigova, E
Master, S
Xie, DW
Appleby, D
Joffe, M
Kusek, J
Feldman, H
Raj, DS
Wing, MR
AF Sterling, Kevin
Yang, Wei
Teal, Valerie
Navaneethan, Sankar D.
Ojo, Akinlolu
Reilly, Muredach
Glenn, Melanie
Rosas, Sylvia
Guzman, Nicolas
Cuevas, Magda
Fischer, Michael
Lustigova, Eva
Master, Stephen
Xie, Dawei
Appleby, Dina
Joffe, Marshall
Kusek, John
Feldman, Harold
Raj, Dominic S.
Wing, Maria R.
TI THE INFLUENCE OF RACE AND ETHNICITY ON THE ASSOCIATION BETWEEN BODY
COMPOSITION AND INFLAMMATION IN PATIENTS WITH CHRONIC KIDNEY DISEASE:
FINDINGS FROM THE CRIC STUDY
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Meeting Abstract
CT 50th European-Renal-Association -
European-Dialysis-and-Transplant-Association Congress
CY MAY 18-21, 2013
CL Istanbul, TURKEY
SP European Renal Assoc (ERA), European Dialysis & Transplant Assoc (EDTA)
C1 [Sterling, Kevin; Guzman, Nicolas; Raj, Dominic S.; Wing, Maria R.] George Washington Univ, Washington, DC USA.
[Yang, Wei; Teal, Valerie; Reilly, Muredach; Glenn, Melanie; Rosas, Sylvia; Cuevas, Magda; Master, Stephen; Xie, Dawei; Appleby, Dina; Joffe, Marshall; Feldman, Harold] Univ Penn, Philadelphia, PA 19104 USA.
[Teal, Valerie] Cleveland Clin, Cleveland, OH 44106 USA.
[Ojo, Akinlolu] Univ Michigan, Ann Arbor, MI 48109 USA.
[Fischer, Michael] Univ Illinois, Chicago, IL USA.
[Lustigova, Eva] Tulane Univ, New Orleans, LA 70118 USA.
[Kusek, John] NIDDK, DKUHD, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD MAY
PY 2013
VL 28
SU 1
BP 52
EP 52
PG 1
WC Transplantation; Urology & Nephrology
SC Transplantation; Urology & Nephrology
GA 151ZF
UT WOS:000319498200129
ER
PT J
AU Kruit, MC
Thijs, RD
Ferrari, MD
Launer, LJ
van Buchem, MA
van Dijk, JG
AF Kruit, Mark C.
Thijs, Roland D.
Ferrari, Michel D.
Launer, Lenore J.
van Buchem, Mark A.
van Dijk, J. Gert
TI Syncope and orthostatic intolerance increase risk of brain lesions in
migraineurs and controls
SO NEUROLOGY
LA English
DT Article
ID WHITE-MATTER LESIONS; MULTIPLE SYSTEM ATROPHY; BLOOD-PRESSURE; CEREBRAL
PERFUSION; REFLEX SYNCOPE; HYPOTENSION; ATHEROSCLEROSIS; ABNORMALITIES;
PREVALENCE; DISEASE
AB Objectives: We and others showed that migraineurs are at increased risk of subclinical and clinical ischemic brain lesions. Migraineurs also have a higher prevalence of frequent syncope and orthostatic intolerance, symptoms that are associated with transient reductions in cerebral blood flow. In this study, we assessed whether these autonomic symptoms may contribute to the increased risk of brain lesions in migraine.
Methods: Migraineurs (n = 291) and controls (n = 140) from the population-based, cross-sectional CAMERA (Cerebral Abnormalities in Migraine, an Epidemiologic Risk Analysis) cohort (aged 30-60 years, and free of other neurologic symptoms) underwent 1) brain MRI scan, and 2) structured telephone interview including questions on frequent syncope (>= 5/lifetime) and orthostatic intolerance.
Results: Frequent syncope (odds ratio [OR] = 2.7; 95% confidence interval: 1.3-5.5) and orthostatic intolerance (OR = 2.0 [1.1-3.6]) were independent risk factors for high load of deep white matter lesions. Effects were strongest in women and similar inmigraineurs and controls. Migraine diagnosis did not mediate or moderate these associations. Individuals with orthostatic intolerance had higher prevalence of high periventricular white matter lesion load (OR = 1.9 [1.1-3.5]). Syncope and orthostatic intolerance were not related to subclinical infarcts or infratentorial lesions.
Conclusions: Frequent syncope, orthostatic intolerance, and migraine independently increase the risk of white matter lesions, particularly in females. Neurology (R) 2013;80:1958-1965
C1 [Kruit, Mark C.; van Buchem, Mark A.] Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
[Thijs, Roland D.; Ferrari, Michel D.; van Dijk, J. Gert] Leiden Univ, Med Ctr, Dept Neurol, Leiden, Netherlands.
[Thijs, Roland D.; Ferrari, Michel D.; van Dijk, J. Gert] Leiden Univ, Med Ctr, Dept Clin Neurophysiol, Leiden, Netherlands.
[Launer, Lenore J.] Natl Inst Publ Hlth & Environm, Dept Chron Dis & Environm Epidemiol, NL-3720 BA Bilthoven, Netherlands.
[Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
RP Kruit, MC (reprint author), Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
EM m.c.kruit@lumc.nl
RI Kruit, Mark/K-2431-2012
OI Kruit, Mark/0000-0002-4319-834X
FU Netherlands Heart Foundation [97.108]
FX This study was supported by grant 97.108 from the Netherlands Heart
Foundation.
NR 39
TC 7
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD MAY
PY 2013
VL 80
IS 21
BP 1958
EP 1965
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 149PJ
UT WOS:000319332900013
PM 23616159
ER
PT J
AU Vachon, DD
Lynam, DR
Widiger, TA
Miller, JD
McCrae, RR
Costa, PT
AF Vachon, David D.
Lynam, Donald R.
Widiger, Thomas A.
Miller, Joshua D.
McCrae, Robert R.
Costa, Paul T.
TI Basic Traits Predict the Prevalence of Personality Disorder Across the
Life Span: The Example of Psychopathy
SO PSYCHOLOGICAL SCIENCE
LA English
DT Article
DE personality disorder; personality; prevalence rates; psychopathy;
antisocial behavior; psychopathology
ID 5-FACTOR MODEL; DIMENSIONAL MODEL; GENERAL-MODEL; POPULATIONS;
REPRESENT; SELF; AGE
AB Personality disorders (PDs) may be better understood in terms of dimensions of general personality functioning rather than as discrete categorical conditions. Personality-trait descriptions of PDs are robust across methods and settings, and PD assessments based on trait measures show good construct validity. The study reported here extends research showing that basic traits (e.g., impulsiveness, warmth, straightforwardness, modesty, and deliberation) can re-create the epidemiological characteristics associated with PDs. Specifically, we used normative changes in absolute trait levels to simulate age-related differences in the prevalence of psychopathy in a forensic setting. Results demonstrated that trait information predicts the rate of decline for psychopathy over the life span; discriminates the decline of psychopathy from that of a similar disorder, antisocial PD; and accurately predicts the differential decline of subfactors of psychopathy. These findings suggest that basic traits provide a parsimonious account of PD prevalence across the life span.
C1 [Vachon, David D.; Lynam, Donald R.] Purdue Univ, Dept Psychol Sci, W Lafayette, IN 47907 USA.
[Widiger, Thomas A.] Univ Kentucky, Dept Psychol, Lexington, KY 40506 USA.
[Miller, Joshua D.] Univ Georgia, Dept Psychol, Athens, GA 30602 USA.
[McCrae, Robert R.] NIH, Lab Personal & Cognit, Bethesda, MD 20892 USA.
[Costa, Paul T.] Johns Hopkins Univ, Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD 21218 USA.
RP Lynam, DR (reprint author), Purdue Univ, Dept Psychol Sci, 703 3rd St, W Lafayette, IN 47907 USA.
EM dlynam@purdue.edu
RI Lynam, Donald/J-5755-2014
OI Lynam, Donald/0000-0001-8306-498X
NR 38
TC 15
Z9 15
U1 7
U2 31
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0956-7976
J9 PSYCHOL SCI
JI Psychol. Sci.
PD MAY
PY 2013
VL 24
IS 5
BP 698
EP 705
DI 10.1177/0956797612460249
PG 8
WC Psychology, Multidisciplinary
SC Psychology
GA 143GI
UT WOS:000318854600010
PM 23528790
ER
PT J
AU Kimmel, PL
AF Kimmel, Paul L.
TI The Weather and Quality of Life in ESRD Patients: Everybody Talks About
it, But Does Anybody Do Anything About it?
SO SEMINARS IN DIALYSIS
LA English
DT Editorial Material
ID STAGE RENAL-DISEASE; CHRONIC KIDNEY-DISEASE; HEMODIALYSIS-PATIENTS;
DIALYSIS PATIENTS; PSYCHOSOCIAL FACTORS; DEPRESSION; MORTALITY;
DIAGNOSIS; SYMPTOMS; OUTCOMES
C1 NIDDKD, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
RP Kimmel, PL (reprint author), NIDDKD, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
EM kimmelp@extra.niddk.nih.gov
NR 29
TC 2
Z9 2
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-0959
J9 SEMIN DIALYSIS
JI Semin. Dial.
PD MAY-JUN
PY 2013
VL 26
IS 3
BP 260
EP 262
DI 10.1111/sdi.12063
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 146DL
UT WOS:000319069300004
PM 23406381
ER
PT J
AU Vogel, JL
Kristie, TM
AF Vogel, Jodi L.
Kristie, Thomas M.
TI The Dynamics of HCF-1 Modulation of Herpes Simplex Virus Chromatin
during Initiation of Infection
SO VIRUSES-BASEL
LA English
DT Review
DE herpes simplex virus; chromatin; HCF-1; Setd1A; latency; histone
demethylase
ID HOST-CELL FACTOR; TRANSCRIPTIONAL COACTIVATOR HCF-1; HISTONE DEMETHYLASE
LSD1; EMBRYONIC STEM-CELLS; MECHANISM-BASED INACTIVATOR; IMMEDIATE-EARLY
PROMOTERS; HOX GENE-EXPRESSION; LYTIC INFECTION; DNA-REPLICATION;
FACTOR-I
AB Successful infection of herpes simplex virus is dependent upon chromatin modulation by the cellular coactivator host cell factor-1 (HCF-1). This review focuses on the multiple chromatin modulation components associated with HCF-1 and the chromatin-related dynamics mediated by this coactivator that lead to the initiation of herpes simplex virus (HSV) immediate early gene expression.
C1 [Vogel, Jodi L.; Kristie, Thomas M.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Kristie, TM (reprint author), NIAID, NIH, Bld 33,33 North Dr, Bethesda, MD 20892 USA.
EM jvogel@niaid.nih.gov; tkristie@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, USA
FX The authors acknowledge the members of the Molecular Genetics Section,
Laboratory of Viral Diseases, for their comments on this manuscript.
Funding for this review and studies ascribed to the Kristie Laboratory
were provided to T.M.K. by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, USA.
NR 124
TC 12
Z9 12
U1 2
U2 5
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD MAY
PY 2013
VL 5
IS 5
BP 1272
EP 1291
DI 10.3390/v5051272
PG 20
WC Virology
SC Virology
GA 151CK
UT WOS:000319438000006
PM 23698399
ER
PT J
AU Mehta, S
Waldo, JP
Neuenswander, B
Lushington, GH
Larock, RC
AF Mehta, Saurabh
Waldo, Jesse P.
Neuenswander, Benjamin
Lushington, Gerald H.
Larock, Richard C.
TI Solution-Phase Parallel Synthesis of a Multisubstituted Cyclic Imidate
Library
SO ACS COMBINATORIAL SCIENCE
LA English
DT Article
DE solution-phase; parallel synthesis; iodocyclization; cyclic imidates;
iminolactones; palladium coupling
ID ELECTROPHILIC CYCLIZATION; DEVELOPMENT SETTINGS; GAMMA-IMINOLACTONES;
EFFICIENT SYNTHESIS; ESTIMATE SOLUBILITY; DIVERSE LIBRARY; DRUG
DISCOVERY; ONE-POT; ARYL; 2,3-ALLENAMIDES
AB The solution-phase parallel synthesis of a diverse 71-member library of multisubstituted cyclic imidates is described. The key intermediates, 3-iodomethylene-containing cyclic imidates, are readily prepared in good to excellent yields by the palladium/copper-catalyzed cross-coupling of various o-iodobenzamides and terminal alkynes, followed by electrophilic cyclization with I-2. These cyclic imidates were further functionalized by palladium-catalyzed Suzuki-Miyaura, Sonogashira, carbonylative amidation, and Heck chemistry using sublibraries of commercially available building blocks.
C1 [Mehta, Saurabh; Waldo, Jesse P.; Larock, Richard C.] Iowa State Univ, Dept Chem, Ames, IA 50011 USA.
[Mehta, Saurabh] Delhi Technol Univ, Dept Appl Chem, Delhi 110042, India.
[Neuenswander, Benjamin; Lushington, Gerald H.] Univ Kansas, NIH, Ctr Excellence Chem Methodol, Lawrence, KS 66047 USA.
[Neuenswander, Benjamin; Lushington, Gerald H.] Univ Kansas, Lib Dev, Lawrence, KS 66047 USA.
RP Larock, RC (reprint author), Iowa State Univ, Dept Chem, Ames, IA 50011 USA.
EM larock@iastate.edu
OI Mehta, Saurabh/0000-0002-9174-128X
FU National Institute of General Medical Sciences [GM070620, GM079593];
University of Kansas National Institutes of Health Center of Excellence
in Chemical Methodologies and Library Development [GM069663]
FX We thank the National Institute of General Medical Sciences (GM070620
and GM079593) and the University of Kansas National Institutes of Health
Center of Excellence in Chemical Methodologies and Library Development
(GM069663) for support of this research.
NR 34
TC 6
Z9 6
U1 0
U2 8
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 2156-8952
J9 ACS COMB SCI
JI ACS Comb. Sci.
PD MAY
PY 2013
VL 15
IS 5
BP 247
EP 254
DI 10.1021/co3001605
PG 8
WC Chemistry, Applied; Chemistry, Medicinal; Chemistry, Multidisciplinary
SC Chemistry; Pharmacology & Pharmacy
GA 145RP
UT WOS:000319034800005
PM 23514214
ER
PT J
AU Freedman, DM
Kuncl, RW
Weinstein, SJ
Malila, N
Virtamo, J
Albanes, D
AF Freedman, D. Michal
Kuncl, Ralph W.
Weinstein, Stephanie J.
Malila, Nea
Virtamo, Jarmo
Albanes, Demetrius
TI Vitamin E serum levels and controlled supplementation and risk of
amyotrophic lateral sclerosis
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE Amyotrophic lateral sclerosis; vitamin E; cohort studies; risk factors
in epidemiology
ID INCREASED OXIDATIVE DAMAGE; ALPHA-TOCOPHEROL; BETA-CAROTENE;
NEURODEGENERATIVE DISEASES; DOUBLE-BLIND; STRESS; SMOKING; RILUZOLE;
CANCER; COHORT
AB There are no observational studies or controlled trials of amyotrophic lateral sclerosis (ALS) and circulating alpha-tocopherol (vitamin E) for prevention of ALS. This study addresses that gap. The study population comprised 29,127 Finnish male smokers, aged 50-69 years, who participated in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, which is both a prospective cohort and a randomized, double-blind, placebo-controlled trial of alpha-tocopherol (50 mg/day) and beta-carotene (20 mg/day). Serum alpha-tocopherol and beta-carotene was assayed at baseline (1985 - 1988). Follow-up (median 16.7 years) continued through 2004. ALS cases were identified through the national Hospital Discharge Register with diagnostic verification by hospital records and death certificates. During 407,260 person-years of follow-up, 50 men were identified with ALS. For males with serum alpha-tocopherol concentration above the median (>= 11.6 mg/l), the age-adjusted relative risk (RR) compared to alpha-tocopherol below the median, was 0.56 (95% confidence interval 0.32 - 0.99), p = 0.046. The RR among alpha-tocopherol supplement recipients was 0.75 (95% CI 0.32 - 1.79), p = 0.52. Neither serum beta-carotene level nor beta-carotene supplementation was associated with ALS. In conclusion, the results are consistent with a hypothesized protective effect of alpha-tocopherol on ALS risk. However, pooled analyses of cohorts with serum and controlled trials are needed to clarify the role of alpha-tocopherol in ALS risk.
C1 [Freedman, D. Michal; Weinstein, Stephanie J.; Albanes, Demetrius] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Kuncl, Ralph W.] Univ Redlands, Redlands, CA 92373 USA.
[Malila, Nea] Finnish Canc Registry, FIN-00170 Helsinki, Finland.
[Malila, Nea] Univ Tampere, Sch Hlth Sci, Helsinki, Finland.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Freedman, DM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, EPS Room 7036,6120 Exec Blvd, Bethesda, MD 20892 USA.
EM freedmam@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015
FU National Institutes of Health, National Cancer Institute; U.S. Public
Health Service; United States 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
National Institutes of Health, National Cancer Institute, and the U.S.
Public Health Service, and in part by contracts from the United States
National Cancer Institute, National Institutes of Health, Department of
Health and Human Services.
NR 33
TC 5
Z9 5
U1 0
U2 5
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
IS 4
BP 246
EP 251
DI 10.3109/21678421.2012.745570
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 143QT
UT WOS:000318883000002
ER
PT J
AU Peters, TL
Fang, F
Weibull, CE
Sandler, DP
Kamel, F
Ye, WM
AF Peters, Tracy L.
Fang, Fang
Weibull, Caroline E.
Sandler, Dale P.
Kamel, Freya
Ye, Weimin
TI Severe head injury and amyotrophic lateral sclerosis
SO AMYOTROPHIC LATERAL SCLEROSIS AND FRONTOTEMPORAL DEGENERATION
LA English
DT Article
DE Amyotrophic lateral sclerosis; head injury; risk factors; nested
case-control study; motor neuron disease
ID MOTOR-NEURON DISEASE; TDP-43 PROTEINOPATHY; TRAUMA; COHORT; RISK;
REGISTER; PROVINCE; PLAYERS; SWEDEN; ALS
AB Our objective was to examine whether severe head injury, subtypes of head injury, or repeated head injuries are associated with ALS risk based on the Swedish population and health registers.
We conducted a case-control study, nested within a cohort of 5,764,522 individuals who were born in Sweden during 1901-1970 and followed between 1991 and 2007. The study included 4004 ALS patients identified from the Swedish Patient Register during follow-up and 20,020 randomly selected controls matched by gender and birth year. We evaluated hospitalization for severe head injury that was recorded in the inpatient register before ALS diagnosis. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).
Results showed that there was an association of ALS risk with severe head injury <= 1 year before diagnosis (OR: 3.9, 95% CI 2.6-6.1). No association was observed for severe head injury > 3 years before ALS diagnosis, nor was ALS associated with subtypes of head injury or repeated injuries occurring > 3 years before diagnosis. In conclusion, our findings from the Swedish registers provide no strong support for an etiological relationship between severe head injury in adulthood and ALS risk.
C1 [Peters, Tracy L.; Fang, Fang; Weibull, Caroline E.; Ye, Weimin] Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden.
[Sandler, Dale P.; Kamel, Freya] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Peters, TL (reprint author), Karolinska Inst, Dept Med Epidemiol & Biostat, POB 281, S-17177 Stockholm, Sweden.
EM tracy.peters@ki.se; weimin.ye@ki.se
OI Fang, Fang/0000-0002-3310-6456; Kamel, Freya/0000-0001-5052-6615;
Sandler, Dale/0000-0002-6776-0018
FU Swedish Research Council; FAS; National Institute of Environmental
Health Sciences, National Institutes of Health
FX This study was supported by grants from the Swedish Research Council,
FAS, and the Intramural Research Program of The National Institute of
Environmental Health Sciences, National Institutes of Health.
NR 35
TC 8
Z9 8
U1 0
U2 6
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 2167-8421
J9 AMYOTROPH LAT SCL FR
JI Amyotroph. Lateral Scher. Frontotemp. Degenerat.
PD MAY
PY 2013
VL 14
IS 4
BP 267
EP 272
DI 10.3109/21678421.2012.754043
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 143QT
UT WOS:000318883000005
PM 23286749
ER
PT J
AU Robinson, OJ
AF Robinson, Oliver J.
TI Prediction Error Representation in Major Depression and Anxiety
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE prediction error; ventral striatum; depression; anxiety; emotional
processing
C1 [Robinson, Oliver J.] NIMH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 8
BP 3S
EP 3S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800009
ER
PT J
AU Weinberger, DR
Jose, A
Trampush, J
Berman, K
Bigos, K
Zhang, FY
Dickenson, D
AF Weinberger, Daniel R.
Jose, Apud
Trampush, Joey
Berman, Karen
Bigos, Kristi
Zhang, Fengyu
Dickenson, Dwight
TI Ion Channel Genes as Keys to Cognition and Treatment Response in
Psychosis
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE ion channels; antipsychotic response; GWAS; KCNH2; SCN2a
C1 [Weinberger, Daniel R.; Bigos, Kristi; Zhang, Fengyu] Lieber Inst Brain Dev, Baltimore, MD USA.
[Jose, Apud; Berman, Karen; Dickenson, Dwight] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
[Trampush, Joey] NIMHb, Clin Brain Disorders Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 35
BP 11S
EP 11S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800036
ER
PT J
AU Zalesky, A
McAdams, H
Classen, L
Greenstein, D
Fornito, A
Pantelis, C
Gogtay, N
AF Zalesky, Andrew
McAdams, Harrison
Classen, Liv
Greenstein, Dede
Fornito, Alex
Pantelis, Christos
Gogtay, Nitin
TI Delayed Maturation of Occipito-Temporal Connectivity in Childhood-Onset
Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Schizophrenia; Connectivity; Neurodevelopment; Connectopathy;
Childhood-Onset Schizophrenia
C1 [Zalesky, Andrew; Fornito, Alex; Pantelis, Christos] Univ Melbourne, Dept Psychiat, Melbourne, Vic, Australia.
[McAdams, Harrison; Classen, Liv; Greenstein, Dede; Gogtay, Nitin] NIMH, Child Psychiat Branch, Bethseda, MD USA.
RI Pantelis, Christos/H-7722-2014; Alex, Fornito/N-8214-2013
OI Pantelis, Christos/0000-0002-9565-0238; Alex,
Fornito/0000-0001-9134-480X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 58
BP 19S
EP 19S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800059
ER
PT J
AU Grillon, C
Robinson, OJ
AF Grillon, Christian
Robinson, Oliver J.
TI Amygdala-Prefrontal Coupling During Induced-Anxiety: A Role in Aversive
Amplification and Attention Biases
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Anxiety; attention bias; startle
C1 [Grillon, Christian] NIMH, Bethesda, MD 20892 USA.
[Robinson, Oliver J.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 68
BP 22S
EP 22S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800069
ER
PT J
AU Kleinman, JE
AF Kleinman, Joel E.
TI Genetic Variation and Alternative Transcripts in Human Brain Development
and Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Genetic variation; Alternative transcripts; Human brain development;
Schizophrenia; Epigenetics
C1 [Kleinman, Joel E.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 73
BP 24S
EP 24S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800074
ER
PT J
AU Vytal, K
Overstreet, C
Robinson, O
Grillon, C
AF Vytal, Katye
Overstreet, Cassie
Robinson, Oliver
Grillon, Christian
TI Differential Prefrontal-Amygdala Coupling Supports the Interplay Between
Anxiety and Cognition
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Anxiety; Neuroimaging; Prefrontal Cortex; Amygdala; Working Memory
C1 [Vytal, Katye] NIMH, Bethesda, MD 20892 USA.
[Overstreet, Cassie; Robinson, Oliver; Grillon, Christian] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 78
BP 25S
EP 25S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800079
ER
PT J
AU Kreisl, WC
AF Kreisl, William C.
TI Correcting for a Genetic Polymorphism on the Translocator Protein
Improves Measurement of Neuroinflammation With [11C]PBR28
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Neuroinflammation; PET imaging; schizophrenia; Alzheimer's disease
C1 [Kreisl, William C.] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 85
BP 28S
EP 28S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800086
ER
PT J
AU Gogtay, N
AF Gogtay, Nitin
TI Evidence of the Structural Bases of Memory Impairments in Childhood
Onset Schizophrenia: Mapping Hippocampal Shape Abnormalities
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE childhood schizophrenia; imaging; hippocampus
C1 [Gogtay, Nitin] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 93
BP 30S
EP 30S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800094
ER
PT J
AU Farber, GK
AF Farber, Gregory K.
TI The National Database for Autism Research
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE database; autism; unique identifier; data sharing; data federation
C1 [Farber, Gregory K.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 97
BP 31S
EP 31S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800098
ER
PT J
AU Dickinson, D
Straub, RE
Trampush, J
Gao, Y
Feng, NP
Bigos, K
Kolachana, B
Hashimoto, R
Takeda, M
Rujescu, D
Hyde, TM
Berman, KF
Kleinman, JM
Weinberger, DR
AF Dickinson, Dwight
Straub, Richard E.
Trampush, Joey
Gao, Yuan
Feng, Ningping
Bigos, Kristin
Kolachana, Bhaskar
Hashimoto, Ryota
Takeda, Masatoshi
Rujescu, Dan
Hyde, Thomas M.
Berman, Karen F.
Kleinman, Joel M.
Weinberger, Daniel R.
TI Support for the Association of SCN2A Variants with Cognition in
Schizophrenia from Analyses of Unaffected Siblings, Independent
Schizophrenia Samples, and MRNA Expression in Brain
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE schizophrenia; general cognitive ability; SCN2A; GWAS; genetics
C1 [Dickinson, Dwight; Trampush, Joey; Feng, Ningping; Kolachana, Bhaskar; Hyde, Thomas M.; Berman, Karen F.; Kleinman, Joel M.; Weinberger, Daniel R.] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
[Straub, Richard E.; Gao, Yuan; Bigos, Kristin; Hyde, Thomas M.; Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
[Hashimoto, Ryota; Takeda, Masatoshi] Osaka Univ, Grad Sch Med, Dept Psychiat, Osaka, Japan.
[Rujescu, Dan] Univ Munich, Dept Psychiat, D-80539 Munich, Germany.
RI Hashimoto, Ryota/P-8572-2014
OI Hashimoto, Ryota/0000-0002-5941-4238
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 108
BP 35S
EP 35S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800109
ER
PT J
AU Tsuang, D
Timms, A
Dorschner, M
Wechsler, J
Wechsler, J
Choi, KY
Kirkwood, R
Girirajan, S
Baker, C
Eichler, E
Korvatska, O
Roche, KW
Horwitz, M
AF Tsuang, Debby
Timms, Andrew
Dorschner, Michael
Wechsler, Jeremy
Wechsler, Jeremy
Choi, Kyu Yeong
Kirkwood, Robert
Girirajan, Santhosh
Baker, Carl
Eichler, Evan
Korvatska, Olena
Roche, Katherine W.
Horwitz, Marshall
TI Support for the NMDA Receptor Hypofunction Hypothesis of Schizophrenia
from Exome Sequencing in Multiplex Families
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE schizophrenia; genetics; NMDA; exome; families
C1 [Tsuang, Debby] Puget Sound VA Med Ctr, Seattle, WA USA.
[Timms, Andrew; Dorschner, Michael; Wechsler, Jeremy; Wechsler, Jeremy; Kirkwood, Robert; Baker, Carl; Eichler, Evan; Horwitz, Marshall] Univ Washington, Seattle, WA 98195 USA.
[Choi, Kyu Yeong; Roche, Katherine W.] NINDS, NIH, Bethesda, MD 20892 USA.
[Girirajan, Santhosh] Penn State Univ, University Pk, PA 16802 USA.
[Korvatska, Olena] Univ Washington, Div Med Genet, Seattle, WA 98195 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 110
BP 36S
EP 36S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800111
ER
PT J
AU Jimenez, DV
Schloesser, RJ
Greene, JS
Hardy, NF
Lu, B
Martinowich, K
AF Jimenez, Dennisse V.
Schloesser, Robert J.
Greene, Joshua S.
Hardy, Nicholas F.
Lu, Bai
Martinowich, Keri
TI Epigenetic Brain Modifications Associated with Early-Life Adversity in a
Rodent Model
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE epigenetic; DNA methylation; bdnf; maltreatment
C1 [Jimenez, Dennisse V.; Schloesser, Robert J.; Hardy, Nicholas F.; Martinowich, Keri] Lieber Inst Brain Dev, Baltimore, MD USA.
[Jimenez, Dennisse V.; Schloesser, Robert J.; Martinowich, Keri] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Schloesser, Robert J.] Univ Maryland, Dept Psychiat, Baltimore, MD 21201 USA.
[Greene, Joshua S.; Hardy, Nicholas F.; Lu, Bai; Martinowich, Keri] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA.
[Lu, Bai] GlaxoSmithKline, Res & Dev, Shanghai, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 121
BP 39S
EP 40S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800122
ER
PT J
AU Jimenez, DV
Schloesser, RJ
Greene, JS
Hardy, NF
Lu, B
Martinowich, K
AF Jimenez, Dennisse V.
Schloesser, Robert J.
Greene, Joshua S.
Hardy, Nicholas F.
Lu, Bai
Martinowich, Keri
TI Interaction Between BDNF and Social Environment in Brain Physiology and
Behavior
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE BDNF; slow-wave activity; environment; social; development
C1 [Jimenez, Dennisse V.; Schloesser, Robert J.; Hardy, Nicholas F.; Martinowich, Keri] Lieber Inst Brain Dev, Baltimore, MD USA.
[Jimenez, Dennisse V.; Schloesser, Robert J.; Martinowich, Keri] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Schloesser, Robert J.] Univ Maryland, Dept Psychiat, Baltimore, MD 21201 USA.
[Greene, Joshua S.; Hardy, Nicholas F.; Lu, Bai; Martinowich, Keri] Univ Maryland, Genes Cognit & Psychosis Program, Baltimore, MD 21201 USA.
[Lu, Bai] GlaxoSmithKline, Res & Dev, Shanghai, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 120
BP 39S
EP 39S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800121
ER
PT J
AU Furey, M
AF Furey, Maura
TI Rapid Antidepressant Effects And Biomarkers Associated with the
Antimuscarinic Agent Scopolamine
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE mood disorders; scopolamine; biomarker
C1 [Furey, Maura] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 147
BP 48S
EP 48S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800148
ER
PT J
AU Schmitz, A
Grillon, C
Merikangas, KR
AF Schmitz, Anja
Grillon, Christain
Merikangas, Kathleen R.
TI Anxiety-Potentiated Startle as Potential Endophenotype for Anxiety
Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Anxiety; Fear; Startle; Endophenotype; Heritability
C1 [Schmitz, Anja; Grillon, Christain; Merikangas, Kathleen R.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 157
BP 51S
EP 51S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800158
ER
PT J
AU Chauret, M
Maheu, FS
Nassim, M
Nelson, EE
Pine, DS
Ernst, M
AF Chauret, Melissa
Maheu, Francoise S.
Nassim, Marouane
Nelson, Eric E.
Pine, Daniel S.
Ernst, Monique
TI Impaired Default Mode Network During the Processing of Negative Cues in
Youths at Parental Risk for Anxiety Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Default mode network; At risk population; Youth; Anxiety
C1 [Chauret, Melissa] Univ Quebec, Dept Psychol, Montreal, PQ H3C 3P8, Canada.
[Chauret, Melissa; Maheu, Francoise S.; Nassim, Marouane] St Justine Univ Hosp, Res Ctr, Montreal, PQ, Canada.
[Maheu, Francoise S.] Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada.
[Nelson, Eric E.; Pine, Daniel S.; Ernst, Monique] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 162
BP 52S
EP 53S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800163
ER
PT J
AU Cruz, JR
Wong, LM
Angkustsiri, K
Fox, N
Fox, N
Pine, D
Perez-Edgar, K
Simon, TJ
AF Cruz, Joshua R.
Wong, Ling M.
Angkustsiri, Kathleen
Fox, Nathan
Fox, Nathan
Pine, Daniel
Perez-Edgar, Koraly
Simon, Tony J.
TI Children with Chromosome 22Q11.2 Deletion Syndrome Exhibit High Levels
of Anxiety and a Threat Bias in a Dot Probe Experiment
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE 22q11.2 Deletion Syndrome; Anxiety; Threat Bias; Attention;
Schizophrenia
C1 [Cruz, Joshua R.; Wong, Ling M.; Angkustsiri, Kathleen; Simon, Tony J.] Univ Calif Davis, Sacramento, CA 95817 USA.
[Fox, Nathan; Fox, Nathan] Univ Maryland, College Pk, MD 20742 USA.
[Pine, Daniel] NIMH, Div Intramural Res Programs, Bethesday, MD USA.
[Perez-Edgar, Koraly] Penn State Univ, Child Study Ctr, University Pk, PA 16802 USA.
NR 0
TC 0
Z9 0
U1 3
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 160
BP 52S
EP 52S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800161
ER
PT J
AU Chauret, M
La Buissonniere-Ariza, V
Saint-Amour, D
Pine, DS
Maheu, FS
AF Chauret, Melissa
La Buissonniere-Ariza, Valerie
Saint-Amour, Dave
Pine, Daniel S.
Maheu, Francoise S.
TI Pubertal Modulation of Emotion Regulation During the Conditioning and
Extinction of Fear in Healthy Youths
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Maturation; Emotion regulation; Conditioning; Extinction; Threat
processing
C1 [Chauret, Melissa; Saint-Amour, Dave] Univ Quebec, Dept Psychol, Montreal, PQ H3C 3P8, Canada.
[Chauret, Melissa; La Buissonniere-Ariza, Valerie; Saint-Amour, Dave; Maheu, Francoise S.] St Justine Univ Hosp, Res Ctr, Montreal, PQ, Canada.
[La Buissonniere-Ariza, Valerie] Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada.
[Pine, Daniel S.] NIMH, NIH, Bethesda, MD 20892 USA.
[Maheu, Francoise S.] Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 169
BP 55S
EP 55S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800170
ER
PT J
AU Watson, B
Malek, M
Wharton, A
Aitken, W
Sharp, W
Shaw, WP
AF Watson, Bethany
Malek, Meaghan
Wharton, Amy
Aitken, William
Sharp, Wendy
Shaw, W. Philip
TI Motor Control Dysfunction and Attention Deficit Hyperactivity Disorder
(ADHD)
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Attention Deficit Hyperactivity Disorder (ADHD); Motor Dysfunction;
Movement Assessment Battery For Children
C1 [Watson, Bethany; Malek, Meaghan; Wharton, Amy; Aitken, William; Sharp, Wendy; Shaw, W. Philip] NHGRI, Neurobehav Clin Res Sect, NIH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 172
BP 56S
EP 56S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800173
ER
PT J
AU Driver, DI
Greenstein, D
Farmer, M
Rapoport, JL
Gogtay, N
AF Driver, David I.
Greenstein, Dede
Farmer, Madison
Rapoport, Judith L.
Gogtay, Nitin
TI Premorbid Speech/Language, Motor, Academic and Social Impairments in
Childhood-Onset Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Childhood Onset Schizophrenia; Motor Impairment; Speech/Language
Impairment; Social Impairment; Academic Impairment
C1 [Driver, David I.; Greenstein, Dede; Farmer, Madison; Rapoport, Judith L.; Gogtay, Nitin] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 199
BP 64S
EP 65S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800200
ER
PT J
AU Hwang, S
White, SF
Meffert, H
Nolan, ZT
Sinclair, S
Blair, J
AF Hwang, Soonjo
White, Stuart F.
Meffert, Harma
Nolan, Zachary T.
Sinclair, Stephen
Blair, James
TI The Development of the Interaction of Top Down Attention Control and
Emotional Responding
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE anxiety disorder; functional magnetic resonance imaging;
neuropsychological testing; developmental neuroscience
C1 [Hwang, Soonjo; White, Stuart F.; Meffert, Harma; Nolan, Zachary T.; Sinclair, Stephen; Blair, James] NIMH, Sect Affect Cognit Neurosci, Bethesda, MD 20892 USA.
OI Meffert, Harma/0000-0002-7298-7276
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 234
BP 76S
EP 76S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800234
ER
PT J
AU Jarcho, JM
Romer, A
Guyer, AE
Shechner, T
Pine, DS
Nelson, EE
AF Jarcho, Johanna M.
Romer, Adrienne
Guyer, Amanda E.
Shechner, Tomer
Pine, Daniel S.
Nelson, Eric E.
TI The Role of Development in the Neural Response to Social Threat in
Patients with Anxiety Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE social threat; development; fMRI; anxiety; amygdala
C1 [Jarcho, Johanna M.; Romer, Adrienne; Shechner, Tomer; Pine, Daniel S.; Nelson, Eric E.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
[Guyer, Amanda E.] Univ Calif Davis, Ctr Mind & Brain, Davis, CA 95616 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 235
BP 76S
EP 76S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800235
ER
PT J
AU Britton, J
Clementi, MA
Suway, J
Bar-Haim, Y
Fox, NA
Pine, DS
AF Britton, Jennifer
Clementi, Michelle A.
Suway, Jenna
Bar-Haim, Yair
Fox, Nathan A.
Pine, Daniel S.
TI Attention Bias Modification (ABM): Understanding the Neural Changes
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE fMRI; attention; training; amygdala; anterior cingulate
C1 [Britton, Jennifer] Univ Miami, Coral Gables, FL 33124 USA.
[Britton, Jennifer; Clementi, Michelle A.; Pine, Daniel S.] NIMH, Intramural Res Program, Bethesda, MD 20892 USA.
[Clementi, Michelle A.] Univ Houston, Houston, FL USA.
[Suway, Jenna; Fox, Nathan A.] Univ Maryland, Dept Human Dev & Quantitat Methodol, College Pk, MD 20742 USA.
[Bar-Haim, Yair] Tel Aviv Univ, Sch Psychol Sci, IL-69978 Tel Aviv, Israel.
NR 0
TC 0
Z9 0
U1 2
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 238
BP 77S
EP 77S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800238
ER
PT J
AU Kaplan, CM
Molina, JL
Chen, Q
Apud, JA
Weinberger, DR
Tan, HY
AF Kaplan, Claire M.
Molina, Juan L.
Chen, Qiang
Apud, Jose A.
Weinberger, Daniel R.
Tan, Hao Yang
TI Adult Development of Prefrontal Connectivity and Deficits in
Schizophrenia in Context Evaluation and Updating
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Connectivity; Prefrontal; Schizophrenia; Development; Reasoning
C1 [Kaplan, Claire M.; Molina, Juan L.; Chen, Qiang; Apud, Jose A.; Weinberger, Daniel R.; Tan, Hao Yang] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
[Chen, Qiang; Weinberger, Daniel R.; Tan, Hao Yang] Johns Hopkins, Lieber Inst Brain Dev, Baltimore, MD 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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 257
BP 83S
EP 84S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800257
ER
PT J
AU Hulvershorn, L
Hummer, T
Leibenluft, E
Dir, A
Finn, P
Anand, A
AF Hulvershorn, Leslie
Hummer, Tom
Leibenluft, Ellen
Dir, Allison
Finn, Peter
Anand, Amit
TI Medial Prefrontal Hyperactivation During Facial Emotion Processing in
Youth at High Risk for the Development of Substance Use Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE substance use disorders; adolescent; prefrontal cortex; affective
regulation; addiction risk
C1 [Hulvershorn, Leslie; Hummer, Tom; Dir, Allison] Indiana Univ Sch Med, Dept Psychiat, Indianapolis, IN USA.
[Leibenluft, Ellen] NIMH, Intramural Program, Bethesda, MD 20892 USA.
[Finn, Peter] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN USA.
[Anand, Amit] Cleveland Clin, Dept Psychiat, Cleveland, OH 44106 USA.
RI Hulvershorn, Leslie/J-3421-2013; Anand, Amit/D-4232-2013
OI Hulvershorn, Leslie/0000-0001-5827-4889;
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 264
BP 86S
EP 86S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800264
ER
PT J
AU Wharton, A
Chakravarty, M
Aitken, W
Malek, M
de Rossi, P
Sharp, W
Shaw, P
AF Wharton, Amy
Chakravarty, Mallar
Aitken, William
Malek, Meaghan
de Rossi, Pietro
Sharp, Wendy
Shaw, Philip
TI Mapping the Development of the Striatum in Children with Attention
Deficit Hyperactivity Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE ADHD; Striatal development; Longitudinal MRI research; Abnormal reward
processing
C1 [Wharton, Amy; Aitken, William; Malek, Meaghan; Sharp, Wendy; Shaw, Philip] NHGRI, Neurobehav Clin Res Sect, Social & Behav Res Branch, Bethesda, MD 20892 USA.
[Chakravarty, Mallar] Baycrest Hosp, Rotman Res Inst, Toronto, ON, Canada.
[de Rossi, Pietro] Univ Roma La Sapienza, St Andrea Hosp, NESMOS Dept Neurosci Mental Hlth & Sensory Funct, Sch Med & Psychol, Rome, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 266
BP 87S
EP 87S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800266
ER
PT J
AU Niciu, MJ
Luckenbuagh, DA
Ionescu, DF
Mathews, DC
Ibrahim, L
DiazGranados, N
Brutsche, NE
Zarate, CA
AF Niciu, Mark J.
Luckenbuagh, David A.
Ionescu, Dawn F.
Mathews, Daniel C.
Ibrahim, Lobna
DiazGranados, Nancy
Brutsche, Nancy E.
Zarate, Carlos A.
TI Personal and Family History of Alcohol Dependence Alters Antidepresant
Response to Oral Riluzole Post-Ketamine Infusion
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE depression; alcoholism; ketamine; riluzole; glutamate
C1 [Niciu, Mark J.; Luckenbuagh, David A.; Ionescu, Dawn F.; Mathews, Daniel C.; Ibrahim, Lobna; DiazGranados, Nancy; Brutsche, Nancy E.; Zarate, Carlos A.] NIMH, Expt Therapeut & Pathophysiol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 326
BP 105S
EP 105S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800325
ER
PT J
AU Chauret, M
La Buissonniere-Ariza, V
Tremblay, VL
Servonnet, A
Pine, DS
Maheu, FS
AF Chauret, Melissa
La Buissonniere-Ariza, Valerie
Tremblay, Vickie Lamoureux
Servonnet, Alice
Pine, Daniel S.
Maheu, Francoise S.
TI Are Fearful Faces of Women and Men Conditioned and Extinguished the Same
in Adolescent Girls and Boys?
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Fear conditionning; Fear extinction; Gender
C1 [Chauret, Melissa] Univ Quebec, Dept Psychol, Montreal, PQ H3C 3P8, Canada.
[Chauret, Melissa; La Buissonniere-Ariza, Valerie; Tremblay, Vickie Lamoureux; Servonnet, Alice; Maheu, Francoise S.] St Justine Univ Hosp, Res Ctr, Montreal, PQ, Canada.
[La Buissonniere-Ariza, Valerie] Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada.
[Pine, Daniel S.] NIMH, NIH, Bethesda, MD 20892 USA.
[Maheu, Francoise S.] Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 339
BP 109S
EP 109S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800338
ER
PT J
AU Weinberger, DR
Shin, JH
Hyde, T
Kleinman, J
Gao, Y
AF Weinberger, Daniel R.
Shin, Joo Heon
Hyde, Tom
Kleinman, Joel
Gao, Yuan
TI DNA Methylation Signatures in Post Mortem Brain of Patients with
Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Schizophrenia; genes; environment; RNA seq; DNA methylation
C1 [Weinberger, Daniel R.] Johns Hopkins Univ, Lieber Inst Brain Dev, Baltimore, MD USA.
[Shin, Joo Heon; Hyde, Tom; Gao, Yuan] Lieber Inst Brain Dev, Baltimore, MD USA.
[Kleinman, Joel] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 377
BP 121S
EP 121S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800373
ER
PT J
AU Holmes, A
AF Holmes, Andrew
TI Basolateral Amygdala Volume in Mouse is Associated with Stress
Reactivity and Fear Learning
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE amygdala; PTSD; gene; mouse; fear
C1 [Holmes, Andrew] NIH, Rockville, MD USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 388
BP 125S
EP 125S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800384
ER
PT J
AU Lohoff, FW
Hodge, R
Narasimhan, S
Nall, A
Ferraro, T
Mickey, BJ
Heitzeg, MM
Langenecker, SA
Zubieta, JK
Bogdan, R
Nikolova, Y
Drabant, E
Hariri, AR
Bevilacua, L
Goldman, D
Doyle, G
AF Lohoff, Falk W.
Hodge, Rachel
Narasimhan, Sneha
Nall, Aleksandra
Ferraro, Thomas
Mickey, Brian J.
Heitzeg, Mary M.
Langenecker, Scott A.
Zubieta, Jon-Kar
Bogdan, Ryan
Nikolova, Yuliya
Drabant, Emily
Hariri, Ahmad R.
Bevilacua, Laura
Goldman, David
Doyle, Glenn
TI Functional Genetic Variants in the Vesicular Monoamine Transporter 1
(VMAT1) Modulate Emotion Processing
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE slc18a1; emotion regulation; dopamine; translational; presynaptic
C1 [Lohoff, Falk W.; Hodge, Rachel; Narasimhan, Sneha; Nall, Aleksandra; Ferraro, Thomas; Doyle, Glenn] Univ Penn, Philadelphia, PA 19104 USA.
[Mickey, Brian J.; Heitzeg, Mary M.; Zubieta, Jon-Kar] Univ Michigan, Ann Arbor, MI 48109 USA.
[Langenecker, Scott A.] Univ Michigan, Philadelphia, MI USA.
[Bogdan, Ryan; Nikolova, Yuliya; Hariri, Ahmad R.] Duke Univ, Durham, NC USA.
[Drabant, Emily] 23 & Me, Psychiat, Mountain View, CA USA.
[Bevilacua, Laura; Goldman, David] NIAAA, Rockville, MD 20852 USA.
RI Lohoff, Falk/M-7951-2016
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 390
BP 125S
EP 125S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800386
ER
PT J
AU Hou, LP
Akula, N
Wendland, J
Chen, DTW
Jiang, XY
Choi, K
Lipska, BK
Kleinman, JE
McMahon, FJ
AF Hou, Liping
Akula, Nirmala
Wendland, Jens
Chen, David T. W.
Jiang, Xueying
Choi, Kwang
Lipska, Barbara K.
Kleinman, Joel E.
McMahon, Francis J.
TI Widespread Novel RNA Editing in Human Brain Tissue Identified By RNA-Seq
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE RNA editing; RNA-Seq; Bipolar disorder
C1 [Hou, Liping; Akula, Nirmala; Wendland, Jens; Chen, David T. W.; Jiang, Xueying; McMahon, Francis J.] NIMH, Human Genet Branch, Bethesda, MD 20892 USA.
[Hou, Liping; Akula, Nirmala; Wendland, Jens; Chen, David T. W.; Jiang, Xueying; McMahon, Francis J.] NIMH, Genet Basis Mood & Anxiety Disorders Sect, Bethesda, MD 20892 USA.
[Choi, Kwang] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA.
[Lipska, Barbara K.; Kleinman, Joel E.] NIMH, Sect Neuropathol, Clin Brain Disorders Branch, IRP,NIH,US Dept HHS, Bethesda, MD 20892 USA.
RI Hou, Liping/G-1648-2011; Lipska, Barbara/E-4569-2017
OI Hou, Liping/0000-0003-3972-245X;
NR 0
TC 0
Z9 0
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 393
BP 126S
EP 126S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800389
ER
PT J
AU Fujita, M
Hines, C
Zoghbi, S
Niciu, M
Ionescu, D
Mallinger, A
Zhang, Y
Pike, V
Drevets, W
Innis, R
Zarate, CA
AF Fujita, Masahiro
Hines, Christina
Zoghbi, Sami
Niciu, Mark
Ionescu, Dawn
Mallinger, Alan
Zhang, Yi
Pike, Victor
Drevets, Wayne
Innis, Robert
Zarate, Carlos Alberto
TI Changes of Brain Phosphodiesterase Type 4 Measured with 11C-(R)-Rolipram
Pet in Major Depressive Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Imaging; Major Depression; PDE4; Treatment
C1 [Fujita, Masahiro; Hines, Christina; Zoghbi, Sami; Zhang, Yi; Pike, Victor; Innis, Robert] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Niciu, Mark; Ionescu, Dawn; Mallinger, Alan; Zarate, Carlos Alberto] NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Program, Bethesda, MD 20892 USA.
[Drevets, Wayne] Univ Oklahoma, Dept Psychiat, Tulsa, OK USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 397
BP 128S
EP 128S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800393
ER
PT J
AU Kravitz, AV
Kreitzer, AC
AF Kravitz, Alexxai V.
Kreitzer, A. C.
TI Dissecting the Striatal Contributions to Reinforcement and Punishment
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE accumbens; cocaine; optogenetics; plasticity; reinforcement
C1 [Kravitz, Alexxai V.] NIDDKD, Baltimore, MD USA.
[Kreitzer, A. C.] Gladstone Inst Neurol Dis, San Francisco, CA 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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 436
BP 140S
EP 140S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800432
ER
PT J
AU Gregory, MD
Kippenhan, JS
Xiao, E
Tong, YX
Kolachana, BS
Weinberger, DR
Mattay, VS
Berman, KF
AF Gregory, Michael D.
Kippenhan, J. Shane
Xiao, Ena
Tong, Yunxia
Kolachana, Bhaskar S.
Weinberger, Daniel R.
Mattay, Venkata S.
Berman, Karen F.
TI Genetic Variation in the Williams Syndrome Gene LIMK1 Affects Resting
Functional Connectivity Between Dorsal and Ventral Visual Processing
Streams
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE fmri; IPS; intraparietal; LIMK1; Williams
C1 [Gregory, Michael D.; Kippenhan, J. Shane; Berman, Karen F.] NIMH, Sect Integrat Neuroimaging, Intramural Res Program, Bethesda, MD 20892 USA.
[Gregory, Michael D.; Kippenhan, J. Shane; Xiao, Ena; Tong, Yunxia; Kolachana, Bhaskar S.; Weinberger, Daniel R.; Mattay, Venkata S.; Berman, Karen F.] NIMH, Clin Brain Disorders Branch, Intramural Res Program, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 456
BP 147S
EP 147S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800452
ER
PT J
AU Nguyen, TV
Schmidt, PJ
Li, C
Lipska, BK
Kleinman, J
Berman, KF
AF Nguyen, Tuong-Vi
Schmidt, Peter J.
Li, Chao
Lipska, Barbara K.
Kleinman, Joel
Berman, Karen F.
TI Expression of Sex Steroid Receptor Genes in the Human Cortex and
Interaction with Genes Involved in Neuronal Migration
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Sex Steroid Receptors; Neuronal migration; Human Cortex; Gene
expression; Prenatal period
C1 [Nguyen, Tuong-Vi; Schmidt, Peter J.; Lipska, Barbara K.; Kleinman, Joel; Berman, Karen F.] NIMH, NIH, Bethesda, MD 20892 USA.
[Li, Chao] Lieber Inst Brain Dev, Maltz Res Labs, Baltimore, MD USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 457
BP 148S
EP 148S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800453
ER
PT J
AU Schloesser, R
Jimenez, DV
Hardy, NF
Paredes, D
Catlow, BJ
Manji, HK
McKay, RD
Martinowich, K
AF Schloesser, Robert
Jimenez, Dennisse V.
Hardy, Nicholas F.
Paredes, Daniel
Catlow, Briony J.
Manji, Husseini K.
McKay, Ron D.
Martinowich, Keri
TI Atrophy of Pyramidal Neurons and Increased Stress-Induced Glutamate
Levels in CA3 Following Suppression of Adult Neurogenesis
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE hippocampus; neurogenesis; glutamate; atrophy; dendrite
C1 [Schloesser, Robert] Univ Maryland, Dept Psychiat, Baltimore, MD 21201 USA.
[Schloesser, Robert; Jimenez, Dennisse V.; Hardy, Nicholas F.; Paredes, Daniel; Catlow, Briony J.; McKay, Ron D.; Martinowich, Keri] Johns Hopkins Med Campus, Lieber Inst Brain Dev, Baltimore, MD USA.
[Schloesser, Robert; Jimenez, Dennisse V.; Martinowich, Keri] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Hardy, Nicholas F.; Martinowich, Keri] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA.
[Manji, Husseini K.] Janssen, Res & Dev, Titusville, NJ USA.
RI Paredes , Daniel/L-6610-2013
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 470
BP 150S
EP 150S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800458
ER
PT J
AU Brockmeyer, JS
Zarate, CA
Luckenbaugh, DA
Rasimas, JJ
Mathews, DC
Ionescu, DF
Niciu, MJ
Richards, EM
Furey, ML
AF Brockmeyer, Jessica S.
Zarate, Carlos A.
Luckenbaugh, David A.
Rasimas, Joseph J.
Mathews, Daniel C.
Ionescu, Dawn F.
Niciu, Mark J.
Richards, Erica M.
Furey, Maura L.
TI Anti-Depressant Treatment History as a Predictor of Response to
Scopolamine
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Depression; Treatment; Scopolamine
C1 [Brockmeyer, Jessica S.; Zarate, Carlos A.; Luckenbaugh, David A.; Rasimas, Joseph J.; Mathews, Daniel C.; Ionescu, Dawn F.; Niciu, Mark J.; Richards, Erica M.; Furey, Maura L.] NIMH, Expt Therapeut & Pathophysiol Branch, Bethesda, MD 20892 USA.
RI Furey, Maura/H-5273-2013
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 498
BP 158S
EP 158S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800486
ER
PT J
AU Szczepanik, J
Furey, M
Nugent, A
Brutsche, N
Luckenbaugh, D
Nolan, N
Zarate, C
AF Szczepanik, Joanna
Furey, Maura
Nugent, Allison
Brutsche, Nancy
Luckenbaugh, David
Nolan, Neal
Zarate, Carlos
TI Baseline Neural Response During the Processing of Emotional Faces
Predicts Antidepressant Response to Ketamine
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE depression; pharmacology; emotion; fMRI; prediction
C1 [Szczepanik, Joanna; Furey, Maura; Nugent, Allison; Brutsche, Nancy; Luckenbaugh, David; Nolan, Neal; Zarate, Carlos] NIMH, Expt Therapeut & Pathophysiolgy Branch, Bethesda, MD 20892 USA.
[Szczepanik, Joanna] Univ Maryland, Neurosci & Cognit Sci Program, College Pk, MD 20742 USA.
RI Furey, Maura/H-5273-2013
NR 0
TC 0
Z9 0
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 516
BP 163S
EP 164S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800504
ER
PT J
AU Spencer, BE
Callicott, JH
Zheutlin, AB
Mattay, VS
Chen, Q
Wang, KH
Weinberger, DR
AF Spencer, Barbara E.
Callicott, Joseph H.
Zheutlin, Amanda B.
Mattay, Venkata S.
Chen, Qiang
Wang, Kuan H.
Weinberger, Daniel R.
TI ARC Risk Predicts DLPFC, Hippocampal, and Parahippocampal Gyrus Function
in Memory Tasks
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Schizophrenia; Genetics; fMRI; Memory
C1 [Spencer, Barbara E.; Callicott, Joseph H.; Zheutlin, Amanda B.; Weinberger, Daniel R.] NIMH, Unit Dynam Imaging Genet, CBDB, GCAP,DIRP,NIH, Bethesda, MD 20892 USA.
[Mattay, Venkata S.; Chen, Qiang; Wang, Kuan H.; Weinberger, Daniel R.] NIMH, Genes Cognit & Psychosis Program, DIRP, NIH, Bethesda, MD 20892 USA.
[Mattay, Venkata S.; Chen, Qiang; Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, Dept Neurosci, Baltimore, MD USA.
[Weinberger, Daniel R.] Johns Hopkins Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 531
BP 168S
EP 168S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800519
ER
PT J
AU Vega, NR
Trampush, J
Berman, K
Weinberger, D
Dickinson, D
AF Vega, Nattali Rodriguez
Trampush, Joey
Berman, Karen
Weinberger, Daniel
Dickinson, Dwight
TI Higher Order Factor Analysis of Personality Dimensions Does not Support
a Simple Extension of the "Five-Factor Model" of Typical Personality to
Pathological Personality
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE personality pathology; typical personality; personality dimensions;
Five-Factor Model; factor analysis
C1 [Vega, Nattali Rodriguez; Trampush, Joey; Berman, Karen; Dickinson, Dwight] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
[Weinberger, Daniel] Johns Hopkins Med Ctr, Lieber Inst Brain Dev, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 530
BP 168S
EP 168S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800518
ER
PT J
AU Warner, V
Wickramaratne, P
Grillon, C
Weissman, M
AF Warner, Virginia
Wickramaratne, Priya
Grillon, Christian
Weissman, Myrna
TI Startle Response, Family Environment, Serotonin Transporter and the Risk
for Depression: Three Generations
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE startle; multigenerational; depression; fear; serotonin
C1 [Warner, Virginia; Wickramaratne, Priya] New York State Psychiat Inst & Hosp, Div Epidemiol, New York, NY 10032 USA.
[Grillon, Christian] NIMH, Bethesda, MD 20892 USA.
[Weissman, Myrna] New York State Psychiat Inst & Hosp, Div Epidemiol, New York, NY 10032 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 547
BP 174S
EP 174S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800535
ER
PT J
AU Roy, A
Gorodetsky, E
Hodgkinson, CA
Goldman, D
Enoch, MA
AF Roy, Alec
Gorodetsky, Elena
Hodgkinson, Colin A.
Goldman, David
Enoch, Mary-Anne
TI Independent Effects of 5 ' and 3 ' Functional Variants in the Serotonin
Transporter Gene on Suicidal Behavior in the Context of Childhood Trauma
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE 5-HTTLR; rs3813034-rs1042173; suicide attempt; childhood trauma;
gene-environment interaction
C1 [Roy, Alec] New Jersey VA Hlth Care Syst, Dept Vet Affairs, E Orange, NJ USA.
[Gorodetsky, Elena; Hodgkinson, Colin A.; Goldman, David; Enoch, Mary-Anne] NIAAA, LNG, NIH, Bethesda, MD USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 554
BP 176S
EP 176S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800542
ER
PT J
AU Brotman, MA
Deveney, CM
Hinton, KE
Thomas, LA
Pine, DS
Leibenluft, E
AF Brotman, Melissa A.
Deveney, Christen M.
Hinton, Kendra E.
Thomas, Laura A.
Pine, Daniel S.
Leibenluft, Ellen
TI Parametric Modulation of Neural Activity During Face Emotion Processing
in Youth at Familial Risk for Bipolar Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE face emotion processing; fMRI; bipolar disorder; at risk youth;
parametric modulation
C1 [Brotman, Melissa A.; Deveney, Christen M.; Hinton, Kendra E.; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, Bethesda, MD 20892 USA.
[Thomas, Laura A.] NIDA, Off Director, Rockville, MD USA.
RI Brotman, Melissa/H-7409-2013
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 589
BP 187S
EP 187S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800577
ER
PT J
AU Perez-Rodriguez, MM
New, AS
Yuan, QP
Zhou, ZF
Hodgkinson, C
Goodman, M
Koenigsberg, HW
Goldstein, KE
Goldman, D
Siever, LJ
Hazlett, EA
AF Perez-Rodriguez, M. Mercedes
New, Antonia S.
Yuan, Qiaoping
Zhou, Zhifeng
Hodgkinson, Colin
Goodman, Manrianne
Koenigsberg, Harold W.
Goldstein, Kim E.
Goldman, David
Siever, Larry J.
Hazlett, Erin A.
TI Impaired Extinction of Amygdala Response to Unpleasant Pictures in
Borderline Personality Disorder Associated with BDNF genotype
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE BDNF; habituation; emotional processing; amygdala; borderline
personality disorder
C1 [Perez-Rodriguez, M. Mercedes; New, Antonia S.; Goodman, Manrianne; Koenigsberg, Harold W.; Goldstein, Kim E.; Siever, Larry J.; Hazlett, Erin A.] Mt Sinai Sch Med, New York, NY USA.
[Perez-Rodriguez, M. Mercedes; New, Antonia S.; Goodman, Manrianne; Siever, Larry J.; Hazlett, Erin A.] James J Peters VAMC, Mirecc, Bronx, NY USA.
[Yuan, Qiaoping; Zhou, Zhifeng; Hodgkinson, Colin; Goldman, David] NIAAA, Rockville, MD 20852 USA.
[Koenigsberg, Harold W.] James J Peters VAMC, Mhcc, Bronx, NY USA.
RI Perez Rodriguez, Maria/B-9410-2013
OI Perez Rodriguez, Maria/0000-0001-5137-1993
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 629
BP 200S
EP 200S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800617
ER
PT J
AU Nakazawa, K
Zsiros, V
AF Nakazawa, Kazu
Zsiros, Veronika
TI Cellular Insights into the Mechanism of Synchrony Impairment in
Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE schizophrenia; NMDA receptor hypofunction; interneuron; fast-spiking
cell; synchronous oscillation
C1 [Nakazawa, Kazu; Zsiros, Veronika] NIMH, NIH, Bethesda, MD 20892 USA.
[Zsiros, Veronika] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 673
BP 213S
EP 214S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800660
ER
PT J
AU Sacchet, MD
Hamilton, JP
Glover, GH
Bagarinao, E
Chang, C
Mackey, S
Gotlib, IH
AF Sacchet, Matthew D.
Hamilton, J. Paul
Glover, Gary H.
Bagarinao, Epifanio
Chang, Catie
Mackey, Sean
Gotlib, Ian H.
TI The Effects of Neurofeedback Training of Salience Network Nodes on
Affective Biases in Major Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Neurofeedback; Major Depressive Disorder (MDD); Salience Network;
Affective biases; Functional Magnetic Resonance Imaging (fMRI)
C1 [Sacchet, Matthew D.; Gotlib, Ian H.] Stanford Univ, Sch Med, Neurosci Program, Stanford, CA 94305 USA.
[Sacchet, Matthew D.; Hamilton, J. Paul; Gotlib, Ian H.] Stanford Univ, Dept Psychol, Stanford, CA 94305 USA.
[Glover, Gary H.] Stanford Univ, Sch Med, Dept Radiol, Stanford, CA 94305 USA.
[Bagarinao, Epifanio; Mackey, Sean] Stanford Univ, Sch Med, Dept Anesthesiol, Stanford, CA 94305 USA.
[Chang, Catie] NIH, Adv MRI Sect, Bethesda, MD 20892 USA.
RI Bagarinao, Epifanio/A-5002-2012
NR 0
TC 0
Z9 0
U1 2
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 690
BP 220S
EP 220S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671800677
ER
PT J
AU Insel, TR
AF Insel, Thomas R.
TI The Next Generation of Therapeutics: Where? When? How?
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
C1 [Insel, Thomas R.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 2
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 691
BP 221S
EP 221S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801001
ER
PT J
AU Jaffe, AE
Fertig, E
Ochs, M
Marchionni, L
Lipska, BK
Weinberger, DR
Kleinman, JE
Hyde, TM
Colantuoni, C
AF Jaffe, Andrew Ellis
Fertig, Elana
Ochs, Michael
Marchionni, Luigi
Lipska, Barbara K.
Weinberger, Daniel R.
Kleinman, Joel E.
Hyde, Thomas M.
Colantuoni, Carlo
TI Transcriptional Patterns of Brain Development
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE genomics; post-mortem human brain; gene expression; development; data
processing
C1 [Jaffe, Andrew Ellis; Weinberger, Daniel R.; Hyde, Thomas M.; Colantuoni, Carlo] Lieber Inst Brain Dev, Baltimore, MD USA.
[Fertig, Elana; Ochs, Michael; Marchionni, Luigi] Johns Hopkins Univ, Div Biostat & Bioinformat, Baltimore, MD USA.
[Lipska, Barbara K.; Kleinman, Joel E.] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
RI Jaffe, Andrew/L-3089-2016; Lipska, Barbara/E-4569-2017
OI Jaffe, Andrew/0000-0001-6886-1454;
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 695
BP 222S
EP 222S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801005
ER
PT J
AU Karlsen, AS
Trampush, JW
Dickinson, D
Weinberger, DR
Ye, TZ
Kleinman, JE
Plath, N
Hyde, TM
AF Karlsen, Anna S.
Trampush, Joey W.
Dickinson, Dwight
Weinberger, Daniel R.
Ye, Tianzhang
Kleinman, Joel E.
Plath, Niels
Hyde, Thomas M.
TI Temporal Expression of Genes in the WNT Pathway Associated with
Cognition
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE schizophrenia; Wnt pathway; cognition; BrainCloud; gene expression
C1 [Karlsen, Anna S.] Bispebjerg Hosp, Res Lab Stereol & Neurosci, Copenhagen, Denmark.
[Trampush, Joey W.; Dickinson, Dwight; Weinberger, Daniel R.; Kleinman, Joel E.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, IRP,NIH, Bethesda, MD 20892 USA.
[Weinberger, Daniel R.; Ye, Tianzhang; Hyde, Thomas M.] Johns Hopkins Univ, Lieber Inst Brain Dev, Baltimore, MD USA.
[Plath, Niels] H Lundbeck & Co AS, Synapt Transmiss 1, Valby, Denmark.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 696
BP 222S
EP 223S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801006
ER
PT J
AU Hyde, TM
Davis, K
Tao, R
Lipska, BK
Ye, TZ
Herman, MM
Weinberger, DR
Kleinman, JE
AF Hyde, Thomas M.
Davis, Kasey
Tao, Ran
Lipska, Barbara K.
Ye, Tianzhang
Herman, Mary M.
Weinberger, Daniel R.
Kleinman, Joel E.
TI Understanding the Complex Dynamic Expression of Risk-Associated Genes
and Developmental Neuropsychiatric Disorders: GABA Signaling and Risk
for Illness
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Neuropsychiatric Disorders; GABA Signaling; Schizophrenia; Gene
expression; Alternative transcription
C1 [Hyde, Thomas M.; Davis, Kasey; Ye, Tianzhang; Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
[Davis, Kasey; Tao, Ran; Lipska, Barbara K.; Herman, Mary M.; Weinberger, Daniel R.; Kleinman, Joel E.] NIMH, Clin Brains Disorders Branch, Bethesda, MD 20892 USA.
[Davis, Kasey] Howard Univ, Washington, DC 20059 USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 697
BP 223S
EP 223S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801007
ER
PT J
AU Goldman, D
AF Goldman, David
TI Discovery of Functional Loci in Old Animal Models by Exome Sequencing: A
Grm2 Stop Codon in the Alcohol-Preferring Rat
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE alcoholism; exome sequencing; linkage; metabotropic glutamate receptor
C1 [Goldman, David] NIAAA, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 700
BP 224S
EP 224S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801010
ER
PT J
AU Geerlings, MI
Sigurdsson, S
Eiriksdottir, G
Garcia, ME
Yu, BB
Harris, TB
Gudnason, V
Launer, LJ
AF Geerlings, Mirjam I.
Sigurdsson, Sigurdur
Eiriksdottir, Gudny
Garcia, Melissa E.
Yu, Binbing
Harris, Tamara B.
Gudnason, Vilmundur
Launer, Lenore J.
TI Hypothalamic-Pituitary-Adrenal Axis Activity and Regional Brain Volumes
in Community-Dwelling Older Persons: The Ages-Reykjavik Study
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE cortisol; brain; MRI; cohort; HPA-axis
C1 [Geerlings, Mirjam I.] NIA, NIH, Bethesda, MD 20892 USA.
[Geerlings, Mirjam I.] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Sigurdsson, Sigurdur; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Garcia, Melissa E.; Yu, Binbing; Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 728
BP 232S
EP 233S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801038
ER
PT J
AU Wei, SM
Schmidt, PJ
Baller, EB
Kohn, PD
Kippenhan, JS
Kolachana, B
Rubinow, DR
Weinberger, DR
Berman, KF
AF Wei, Shau-Ming
Schmidt, Peter J.
Baller, Erica B.
Kohn, Philip D.
Kippenhan, Jonathan S.
Kolachana, Bhaskar
Rubinow, David R.
Weinberger, Daniel R.
Berman, Karen F.
TI Interaction Between Catechol-O-Methyl Transferase (COMT) and Gonadal
Steroid Hormones Affects Dorsolateral Prefrontal (DLPFC)-Dependent
Working Memory Function -- A Positron Emission Tomography (PET) Study
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE catechol-O-methyl transferase (COMT); estradiol and progesterone;
working memory; dorsolateral prefrontal cortex (DLPFC); Positron
Emission Tomography (PET)
C1 [Wei, Shau-Ming; Schmidt, Peter J.; Baller, Erica B.; Kohn, Philip D.; Kippenhan, Jonathan S.; Kolachana, Bhaskar; Berman, Karen F.] NIMH, NIH, Bethesda, MD 20892 USA.
[Rubinow, David R.] Univ N Carolina, Bethesda, MD USA.
[Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 745
BP 238S
EP 239S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801055
ER
PT J
AU Lipska, BK
AF Lipska, Barbara K.
TI Epigenetic Signatures of Developing Human Prefrontal Cortex
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE development; prefrontal cortex; DNA methylation; epigenetics; human
brain
C1 [Lipska, Barbara K.] NIMH, Bethesda, MD 20892 USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 751
BP 240S
EP 241S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801061
ER
PT J
AU Cornwell, BR
Overstreet, C
Lieberman, L
Grillon, C
AF Cornwell, Brian R.
Overstreet, Cassie
Lieberman, Lynne
Grillon, Christian
TI Contextual and Pharmacological Modulation of Human Hippocampal Theta
Oscillations
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE anxiety; hippocampus; theta oscillations; magnetoencephalography;
benzodiazepine
C1 [Cornwell, Brian R.] NIMH, Bethesda, MD 20892 USA.
[Overstreet, Cassie; Lieberman, Lynne; Grillon, Christian] NIMH, Sect Neurobiol Fear & Anxiety, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 780
BP 249S
EP 249S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801090
ER
PT J
AU Robinson, OJ
AF Robinson, Oliver J.
TI The Role of Serotonin In Inhibition of the Neural Circuitry of Anxiety
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE serotonin; anxiety circuitry; bed nucleus of the stria terminalis;
dorsal prefrontal; amygdala
C1 [Robinson, Oliver J.] NIMH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 781
BP 249S
EP 249S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801091
ER
PT J
AU Maheu, FS
La Buissonniere-Ariza, V
Seguin, JR
Boivin, M
Pine, DS
Tremblay, RE
AF Maheu, Francoise S.
La Buissonniere-Ariza, Valerie
Seguin, Jean R.
Boivin, Michel
Pine, Daniel S.
Tremblay, Richard E.
TI Harsh Parenting and Neural Fear Circuitry Function in High and Low
Anxious Youths
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Development; harsh parenting; anxiety; fear circuitry; fMRI
C1 [Maheu, Francoise S.; La Buissonniere-Ariza, Valerie; Seguin, Jean R.] Univ Montreal, Montreal, PQ, Canada.
[Boivin, Michel] Univ Laval, Quebec City, PQ, Canada.
[Pine, Daniel S.] NIMH, Emot Dev Branch, Bethesda, MD 20892 USA.
[Tremblay, Richard E.] Univ Coll Dublin, Sch Publ Hlth, Dublin 2, Ireland.
RI Seguin, Jean/B-5349-2008; Boivin, Michel/J-3652-2013; Tremblay,
Richard/O-1360-2014
OI Seguin, Jean/0000-0003-3359-6202;
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 796
BP 254S
EP 255S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801106
ER
PT J
AU Rapoport, SI
Blanchard, H
Cheon, Y
Fox, MA
Basselin, M
Ramadan, E
AF Rapoport, Stanley I.
Blanchard, Helene
Cheon, Yewon
Fox, Meredith A.
Basselin, Mireille
Ramadan, Epolia
TI Transient Postnatal Fluoxetine Administration to Mice Decreases Brain
Arachidonic Acid Metabolism in Adulthood: Long Term Metabolic Effects of
Early SSRI
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE fluoxetine; arachidonic; neonatal; brain; imaging
C1 [Rapoport, Stanley I.; Blanchard, Helene; Cheon, Yewon; Basselin, Mireille; Ramadan, Epolia] NIA, Brain Physiol & Metab Sect, Bethesda, MD 20892 USA.
[Fox, Meredith A.] NIMH, Clin Sci Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 798
BP 255S
EP 255S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801108
ER
PT J
AU Akula, N
Barb, J
Jiang, XY
Wendland, J
Choi, K
Sen, SK
Hou, LP
Chen, DTW
Laje, G
Lipska, BK
Kleinman, JE
Corrada-Bravo, H
Detera-Wadleigh, S
Munson, PJ
McMahon, FJ
AF Akula, Nirmala
Barb, Jennifer
Jiang, Xueying
Wendland, Jens
Choi, Kwang
Sen, Shurjo K.
Hou, Liping
Chen, David T. W.
Laje, Gonzalo
Lipska, Barbara K.
Kleinman, Joel E.
Corrada-Bravo, Hector
Detera-Wadleigh, Sevilla
Munson, Peter J.
McMahon, Francis J.
TI Brain Transcriptome in Bipolar Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE RNA-sequencing; functional annotation; microarrays; gene ontology;
genome-wide association studies
C1 [Akula, Nirmala; Jiang, Xueying; Wendland, Jens; Hou, Liping; Chen, David T. W.; Laje, Gonzalo; Detera-Wadleigh, Sevilla; McMahon, Francis J.] NIMH, Human Genet Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Barb, Jennifer; Munson, Peter J.] NIH, Math & Stat Comp Lab, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Choi, Kwang] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA.
[Sen, Shurjo K.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Lipska, Barbara K.; Kleinman, Joel E.] NIMH, Neuropathol Sect, Clin Brain Disorders Branch, IRP,NIH, Bethesda, MD 20892 USA.
[Corrada-Bravo, Hector] Univ Maryland, Dept Comp Sci, Bethesda, MD USA.
RI Hou, Liping/G-1648-2011; Lipska, Barbara/E-4569-2017
OI Hou, Liping/0000-0003-3972-245X;
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 803
BP 257S
EP 257S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801113
ER
PT J
AU Cadet, JL
Jayanthi, S
AF Cadet, Jean Lud
Jayanthi, Subramaniam
TI Chronic, but Not Acute, Methamphetamine Exposure Decreases the
Expression of Glutamate AMPA Receptors by Causing Hypoacetylation of
Histone H4 in the Dorsal Striatum
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Epigenetics; Methamphetamine; dorsal striatum; glutamate receptors;
Valproic acid
C1 [Cadet, Jean Lud; Jayanthi, Subramaniam] NIDA, Mol Neuropsychiat Res Branch, NIH, DHHS, Baltimore, MD USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 826
BP 264S
EP 264S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801136
ER
PT J
AU Hibbeln, JR
Umhau, JC
Majchrzak-Hong, S
Salem, N
AF Hibbeln, Joseph R.
Umhau, John C.
Majchrzak-Hong, Sharon
Salem, Norman
TI Restoration of Omega-3 Status Among Aggressive Alcoholics: Effects on
Neurotransmitter Metabolites, Affective Symptoms and Drinking Behaviors
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Omega-3; Alcohol; Aggression; Serotonin; Relapse
C1 [Hibbeln, Joseph R.; Majchrzak-Hong, Sharon; Salem, Norman] NIAAA, Sect Nur Neurosci, Rockville, MD 20852 USA.
[Umhau, John C.] NIAAA, Lab Clin & Translat Studies, Rockville, MD 20852 USA.
RI Majchrzak, Sharon/F-1830-2013
OI Majchrzak, Sharon/0000-0001-8934-7294
NR 0
TC 0
Z9 0
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 837
BP 267S
EP 268S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801147
ER
PT J
AU Koola, MM
McMahon, RP
Liu, F
Gorelick, DA
Buchanan, RW
Huestis, MA
Linthicum, J
Feldman, S
Kelly, DL
AF Koola, Maju Mathew
McMahon, Robert P.
Liu, Fang
Gorelick, David A.
Buchanan, Robert W.
Huestis, Marilyn A.
Linthicum, Jared
Feldman, Stephanie
Kelly, Deanna L.
TI Clinical Characteristics in People with Schizophrenia Enrolling in a
Clinical Trial with or without Lifetime Alcohol and Cannabis Use
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Schizophrenia; Substance use; Clinical symptoms
C1 [Koola, Maju Mathew; McMahon, Robert P.; Liu, Fang; Buchanan, Robert W.; Linthicum, Jared; Feldman, Stephanie; Kelly, Deanna L.] Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA.
[Gorelick, David A.; Huestis, Marilyn A.] NIDA, Baltimore, MD USA.
RI McMahon, Robert/C-5462-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 835
BP 267S
EP 267S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801145
ER
PT J
AU Baum, GL
Callicott, JH
Dickinson, D
Weinberger, DR
AF Baum, Graham L.
Callicott, Joseph H.
Dickinson, Dwight
Weinberger, Daniel R.
TI SCN2A (RS10174400) Differentially Modulates Prefrontal Efficiency in
N-Back Task in Healthy Adults and Schizophrenia Patients
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Schizophrenia; fMRI; Working memory; Genetics; SCN2A
C1 [Baum, Graham L.; Callicott, Joseph H.; Dickinson, Dwight] NIMH, DIRP, Clin Brain Disorders Branch, Bethesda, MD 20892 USA.
[Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
[Weinberger, Daniel R.] Dept Psychiat, Baltimore, MD USA.
[Weinberger, Daniel R.] McKusick Nathans Inst Genet Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 847
BP 271S
EP 271S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801157
ER
PT J
AU Perez-Rodriguez, MM
Shen, PH
Bevilacqua, L
Yuang, QP
Zhou, ZF
Hodgkinson, C
Ripoll, L
Goodman, M
Koenigsberg, H
Goldman, D
Siever, LJ
New, AS
AF Perez-Rodriguez, M. Mercedes
Shen, Pei-Hong
Bevilacqua, Laura
Yuang, Qiaoping
Zhou, Zhifeng
Hodgkinson, Colin
Ripoll, Luis
Goodman, Marianne
Koenigsberg, Harold
Goldman, David
Siever, Larry J.
New, Antonia S.
TI Oxytocin Gene Variants Modulate Core Dimensions of Borderline
Personality Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Oxytocin; Single Nucleotide Polymorphism; Empathy; Impulsivity;
Aggression
C1 [Perez-Rodriguez, M. Mercedes; Ripoll, Luis; Goodman, Marianne; Koenigsberg, Harold; Siever, Larry J.; New, Antonia S.] James J Peters VAMC, Mt Sinai Sch Med, New York, NY USA.
[Perez-Rodriguez, M. Mercedes; Ripoll, Luis; Goodman, Marianne; Koenigsberg, Harold; Siever, Larry J.; New, Antonia S.] James J Peters VAMC, MIRECC, New York, NY USA.
[Shen, Pei-Hong; Bevilacqua, Laura; Yuang, Qiaoping; Zhou, Zhifeng; Hodgkinson, Colin; Goldman, David] NIAAA, Lab Neurogenet, NIH, Rockville, MD 20852 USA.
RI Perez Rodriguez, Maria/B-9410-2013
OI Perez Rodriguez, Maria/0000-0001-5137-1993
NR 0
TC 0
Z9 0
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 891
BP 285S
EP 285S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801201
ER
PT J
AU McFadden, WC
Ye, TZ
Weinberger, D
Kleinman, J
Lipska, B
AF McFadden, Whitney C.
Ye Tianzhang
Weinberger, Daniel
Kleinman, Joel
Lipska, Barbara
TI CNVS in CHRFAM7A and Their Associations with Expression of CHRNA7 and
CHRFAM7A
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
C1 [McFadden, Whitney C.; Kleinman, Joel; Lipska, Barbara] NIMH, NIH, Bethesda, MD 20892 USA.
[Ye Tianzhang; Weinberger, Daniel] Johns Hopkins Univ, Lieber Inst Brain Dev, Baltimore, MD USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 895
BP 286S
EP 286S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801204
ER
PT J
AU Amador, FJ
Cadilla, CL
Holmes, A
Quirk, GJ
Martinez, KG
AF Amador, Francisco J.
Cadilla, Carmen L.
Holmes, Andrew
Quirk, Gregory J.
Martinez, Karen G.
TI The Role of FAAHC385A in Human Threat Anticipation
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE FAAHC385A; endocannabinoids; threat; neuroticism; Emotional Stroop Task
C1 [Amador, Francisco J.; Cadilla, Carmen L.; Quirk, Gregory J.; Martinez, Karen G.] UPR Sch Med, San Juan, PR USA.
[Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 908
BP 290S
EP 290S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801216
ER
PT J
AU McAdams, H
Moran, ME
Johnson, S
Weisinger, B
Stidd, R
Greenstein, D
Miller, R
Clasen, L
Mattai, A
Rapoport, JL
Gogtay, N
AF McAdams, Harrison
Moran, Marcel E.
Johnson, Sarah
Weisinger, Brian
Stidd, Reva
Greenstein, Deanna
Miller, Rachel
Clasen, Liv
Mattai, Andy
Rapoport, Judith L.
Gogtay, Nitin
TI Structural Abnormalities of the Fusiform Gyrus in Patients with
Childhood-Onset Schizophrenia, Their Nonpsychotic Siblings, and Healthy
Volunteers
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE fusiform; schizophrenia; childhood; mri; structural
C1 [McAdams, Harrison; Moran, Marcel E.; Johnson, Sarah; Weisinger, Brian; Stidd, Reva; Greenstein, Deanna; Miller, Rachel; Clasen, Liv; Mattai, Andy; Rapoport, Judith L.; Gogtay, Nitin] NIMH, Childhood Psychiat Branch, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 926
BP 296S
EP 296S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801234
ER
PT J
AU Moran, ME
Weisinger, B
Greenstein, D
Gochman, P
Miller, R
Rapoport, J
Gogtay, N
AF Moran, Marcel E.
Weisinger, Brian
Greenstein, Deanna
Gochman, Pete
Miller, Rachel
Rapoport, Judith
Gogtay, Nitin
TI At the Boundary of the Self: Abnormalitites in the Insular Cortex in
Patients with Childhood-Onset Schizophrenia, their Healthy Sibling and
Normal Volunteers
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Schizophrenia; Imaging; MRI; Endophenotype; Psychosis
C1 [Moran, Marcel E.; Weisinger, Brian; Greenstein, Deanna; Gochman, Pete; Miller, Rachel; Rapoport, Judith; Gogtay, Nitin] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 927
BP 296S
EP 296S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801235
ER
PT J
AU Vyas, NS
Rubinstein, DY
Chen, G
Carver, FW
Greenstein, D
Holroyd, T
Weisinger, B
David, CN
Turner, C
Clasen, L
Miller, R
Coppola, R
Rapoport, JL
Gogtay, N
AF Vyas, Nora S.
Rubinstein, Daniel Y.
Chen, Gang
Carver, Frederick W.
Greenstein, Deanne
Holroyd, Tom
Weisinger, Brian
David, Christopher N.
Turner, Cheryl
Clasen, Liv
Miller, Rachel
Coppola, Richard
Rapoport, Judith L.
Gogtay, Nitin
TI Resting State Oscillatory Brain Dynamics During Adolescence in
Childhood-Onset Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE schizophrenia; adolescence; resting state; default-mode network; MEG
C1 [Vyas, Nora S.; Greenstein, Deanne; Weisinger, Brian; David, Christopher N.; Turner, Cheryl; Clasen, Liv; Miller, Rachel; Rapoport, Judith L.; Gogtay, Nitin] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Rubinstein, Daniel Y.; Carver, Frederick W.; Holroyd, Tom; Coppola, Richard] NIH, MEG Core Facil, Bethesda, MD 20892 USA.
[Chen, Gang] NIH, Sci & Stat Comp Core, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 928
BP 296S
EP 296S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801236
ER
PT J
AU Ludovici, K
Weisinger, B
Greenstein, D
Clasen, L
Lalonde, F
Miller, R
Gochman, P
Rapoport, J
Gogtay, N
AF Ludovici, Katharine
Weisinger, Brian
Greenstein, Deanna
Clasen, Liv
Lalonde, Francois
Miller, Rachel
Gochman, Peter
Rapoport, Judith
Gogtay, Nitin
TI Psychosis as a Dimensional Construct: Cortical Development in
Schizophrenia Spectrum Diagnosed Siblings of Patients with
Childhood-Onset Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE schizophrenia; psychiatry; imaging; childhood; psychosis
C1 [Ludovici, Katharine; Weisinger, Brian; Greenstein, Deanna; Clasen, Liv; Lalonde, Francois; Miller, Rachel; Gochman, Peter; Rapoport, Judith; Gogtay, Nitin] NIMH, Bethesda, MD 20892 USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 930
BP 297S
EP 297S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801238
ER
PT J
AU Salmeron, BJ
AF Salmeron, Betty Jo
TI Frontal Lobe Structure-Function Alterations in Adolescents Prenatally
Exposed to Drugs of Abuse
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Prenatal drug exposure; adolescents; brain structure; frontal lobe;
structure function relationship
C1 [Salmeron, Betty Jo] NIDA, Neuroimaging Res Branch, 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 ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 963
BP 308S
EP 308S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801271
ER
PT J
AU Love, T
Enoch, MA
Goldman, D
Hodgkinson, C
Zubieta, JK
AF Love, Tiffany
Enoch, Mary-Anne
Goldman, David
Hodgkinson, Colin
Zubieta, Jon-Kar
TI OXT Genotype Predicts Anticipatory Responses to Reward
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Oxytocin; Genetics; fMRI; Reward; Nucleus Accumbens
C1 [Love, Tiffany; Zubieta, Jon-Kar] Univ Michigan, Ann Arbor, MI 48109 USA.
[Enoch, Mary-Anne; Goldman, David; Hodgkinson, Colin] NIAAA, NIH, Bethesda, MD USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 974
BP 311S
EP 312S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801282
ER
PT J
AU Guerrieri, GM
Martinez, PE
Klug, SP
Haq, NA
Vanderhoof, V
Koziol, DE
Popat, V
Rubinow, DR
Schmidt, PJ
Nelson, LM
AF Guerrieri, Gioia M.
Martinez, Pedro E.
Klug, Summer P.
Haq, Nazli A.
Vanderhoof, Vien
Koziol, Deloris E.
Popat, Vaishali
Rubinow, David R.
Schmidt, Peter J.
Nelson, Lawrence M.
TI Lack of Effects of Testosterone Augmentation of Combined Estradiol and
Progesterone Replacement on Mood in Women with Primary Ovarian
Insufficiency
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE Primary Ovarian Insufficiency; Testosterone; Mood; Depression;
Hypoandrogenism
C1 [Guerrieri, Gioia M.; Martinez, Pedro E.; Klug, Summer P.; Haq, Nazli A.; Schmidt, Peter J.] NIMH, Behav Endocrinol Branch, Bethesda, MD 20892 USA.
[Vanderhoof, Vien; Popat, Vaishali; Nelson, Lawrence M.] NICHHD, Integrat Reprod Med Unit, Bethesda, MD 20892 USA.
[Koziol, Deloris E.] NIH, Bethesda, MD 20892 USA.
[Rubinow, David R.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 981
BP 314S
EP 314S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801289
ER
PT J
AU Lee, MR
Glassman, M
Kelly, DL
Schroeder, J
Salmeron, BJ
AF Lee, Mary R.
Glassman, Matthew
Kelly, Deanne L.
Schroeder, Jennifer
Salmeron, Betty Jo
TI Dissociation of Oxytocin's Effects in Cocaine Dependence: Enhancement of
Small, Short-Term Reward not Social Salience
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE oxytocin; addiction; reward; social cognition; craving
C1 [Lee, Mary R.] Natl Inst Drug Abuse & Alcoholism, Lab Clin & Translat Studies, Bethesda, MD USA.
[Glassman, Matthew; Kelly, Deanne L.] Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Baltimore, MD 21201 USA.
[Schroeder, Jennifer; Salmeron, Betty Jo] NIDA, Intramural Res Program, Neuroimaging Branch, 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 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 1004
BP 321S
EP 321S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801312
ER
PT J
AU Li, X
Stoker, A
Xi, ZX
Gardner, E
Markou, A
AF Li, Xia
Stoker, Astrid
Xi, Zheng-Xiong
Gardner, Eliot
Markou, Athina
TI Activation of Metabotropic Glutamate Receptor 7 by AMN082 Attenuates the
Rewarding Effects of Cocaine and Nicotine in Rats
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE mGluR7; cocaine; nicotine; reward
C1 [Li, Xia; Stoker, Astrid; Markou, Athina] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Xi, Zheng-Xiong; Gardner, Eliot] NIDA, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 1012
BP 324S
EP 324S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801320
ER
PT J
AU Silverman, M
Cassab, R
Muniz, R
Shavitt, RG
Toledo, MC
Cappi, C
Thayer, J
de Mathis, MA
Diniz, JB
Hoexter, MQ
D'Alcante, CC
Borcato, S
Hounie, AG
Whitfield, J
Belyavskaya, E
Sternberg, E
Miguel, E
Marques, AH
AF Silverman, Marni
Cassab, Raony
Muniz, Renan
Shavitt, Roseli G.
Toledo, Maria Cecilia
Cappi, Carolina
Thayer, Julian
de Mathis, Maria Alice
Diniz, Juliana B.
Hoexter, Marcelo Q.
D'Alcante, Carina C.
Borcato, Sonia
Hounie, Ana G.
Whitfield, Jessie
Belyavskaya, Elena
Sternberg, Esther
Miguel, Euripedes
Marques, Andrea H.
TI Does Inflammation Play a Role in Obsessive-Compulsive Disorder?
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE obsessive-compulsive disorder; inflammation; immunology; treatment
C1 [Silverman, Marni; Belyavskaya, Elena; Sternberg, Esther] NIMH, Bethesda, MD 20892 USA.
[Cassab, Raony; Muniz, Renan; Shavitt, Roseli G.; Toledo, Maria Cecilia; Cappi, Carolina; de Mathis, Maria Alice; Diniz, Juliana B.; Hoexter, Marcelo Q.; D'Alcante, Carina C.; Borcato, Sonia; Hounie, Ana G.; Miguel, Euripedes] Univ Sao Paulo, Sao Paulo, Brazil.
[Thayer, Julian] Ohio State Univ, Columbus, OH 43210 USA.
[Whitfield, Jessie; Marques, Andrea H.] Columbia Univ, Mallman Sch Publ Hlth, New York, NY USA.
NR 0
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 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 1013
BP 324S
EP 324S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801321
ER
PT J
AU Gorelick, DA
Holcomb, HH
Boggs, DL
West, JT
Wittenberg, GF
Lee, MR
Huestis, MA
AF Gorelick, David A.
Holcomb, Henry H.
Boggs, Douglas L.
West, Jeffrey T.
Wittenberg, George F.
Lee, Mary R.
Huestis, Marilyn A.
TI Individual Differences in FMRI Cortical Bold Responses to Nicotine
Visual Cues in Dependent Cigarette Smokers
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
CY MAY 16-18, 2013
CL San Francisco, CA
SP Soc Biol Psychiat
DE craving; cue-induced; fMRI; nicotine; individual differences
C1 [Gorelick, David A.; Lee, Mary R.; Huestis, Marilyn A.] NIDA, Intramural Res Program, Baltimore, MD USA.
[Holcomb, Henry H.; Boggs, Douglas L.; West, Jeffrey T.] Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Baltimore, MD 21201 USA.
[Boggs, Douglas L.] VA CT Healthcare Syst, Dept Psychiat, West Haven, CT USA.
[Boggs, Douglas L.] Yale Univ, Sch Med, West Haven, CT 06516 USA.
[Wittenberg, George F.] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
NR 0
TC 1
Z9 1
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2013
VL 73
IS 9
SU S
MA 1018
BP 326S
EP 326S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 140RE
UT WOS:000318671801326
ER
PT J
AU Lewis, SS
Hutchinson, MR
Zhang, YN
Hund, DK
Maier, SF
Rice, KC
Watkins, LR
AF Lewis, Susannah S.
Hutchinson, Mark R.
Zhang, Yingning
Hund, Dana K.
Maier, Steven F.
Rice, Kenner C.
Watkins, Linda R.
TI Glucuronic acid and the ethanol metabolite ethyl-glucuronide cause
toll-like receptor 4 activation and enhanced pain
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE Glucuronic acid; Ethanol; Ethyl glucuronide; TLR4; (+)-Naloxone;
Glucoronidation; Metabolite; Dextro-naloxone
ID SPINAL-CORD; NEUROPATHIC PAIN; RAT MODEL; LIPOPOLYSACCHARIDE; ALCOHOL;
HYALURONAN; EXPRESSION; MECHANISM; MORPHINE-3-GLUCURONIDE;
NEUROINFLAMMATION
AB We have previously observed that the non-opioid morphine metabolite, morphine-3-glucuronide, enhances pain via a toll-like receptor 4 (TLR4) dependent mechanism. The present studies were undertaken to determine whether TLR4-dependent pain enhancement generalizes to other classes of glucuronide metabolites. In silico modeling predicted that glucuronic acid alone and ethyl glucuronide, a minor but long-lasting ethanol metabolite, would dock to the same MD-2 portion of the TLR4 receptor complex previously characterized as the docking site for morphine-3-glucuronide. Glucuronic acid, ethyl glucuronide and ethanol all caused an increase in TLR4-dependent reporter protein expression in a cell line transfected with TLR4 and associated co-signaling molecules. Glucuronic acid-, ethyl glucuronide-, and ethanol-induced increases in TLR4 signaling were blocked by the TLR4 antagonists LPS-RS and (+)-naloxone. Glucuronic acid and ethyl glucuronide both caused allodynia following intrathecal injection in rats, which was blocked by intrathecal co-administration of the TLR4 antagonist LPS-RS. The finding that ethyl glucuronide can cause TLR4-dependent pain could have implications for human conditions such as hangover headache and alcohol withdrawal hyperalgesia, as well as suggesting that other classes of glucuronide metabolites could have similar effects. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Lewis, Susannah S.; Zhang, Yingning; Hund, Dana K.; Maier, Steven F.; Watkins, Linda R.] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA.
[Hutchinson, Mark R.] Univ Adelaide, Sch Med Sci, Discipline Pharmacol, Adelaide, SA, Australia.
[Hutchinson, Mark R.] Univ Adelaide, Sch Med Sci, Discipline Physiol, Adelaide, SA, Australia.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, NIH, Rockville, MD USA.
[Rice, Kenner C.] NIAAA, NIH, Rockville, MD 20852 USA.
RP Watkins, LR (reprint author), Univ Colorado, Dept Psychol, Campus Box 345, Boulder, CO 80309 USA.
EM linda.watkins@colorado.edu
RI Hutchinson, Mark/G-4147-2014
OI Hutchinson, Mark/0000-0003-2154-5950
FU NIH [DA023132, DA024044, DE017782]; NIDA; NIAAA
FX This work was supported in part by NIH Grants DA023132, DA024044, and
DE017782. This work was also supported in part by the NIH Intramural
Research Programs of NIDA and NIAAA. Mark R. Hutchinson is a NHMRC CJ
Martin Fellow (ID 465423; 2007-2010) and an Australian Research Council
Research Fellow (DPI 10100297). We thank Dr. Kirk Johnson from Avigen
for the gift of the HEK-TLR4 cell line.
NR 54
TC 16
Z9 17
U1 2
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD MAY
PY 2013
VL 30
BP 24
EP 32
DI 10.1016/j.bbi.2013.01.005
PG 9
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 142YT
UT WOS:000318834200005
PM 23348028
ER
PT J
AU Phillips, SM
McAuley, E
AF Phillips, Siobhan M.
McAuley, Edward
TI Physical Activity and Fatigue in Breast Cancer Survivors: A Panel Model
Examining the Role of Self-efficacy and Depression
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID MAXIMUM-LIKELIHOOD-ESTIMATION; STRUCTURAL EQUATION MODELS; SYMPTOM
INVENTORY; MISSING DATA; EXERCISE; PREVALENCE; WOMEN; METAANALYSIS;
ASSOCIATION; PERFORMANCE
AB Background: Physical activity is associated with reductions in fatigue in breast cancer survivors. However, mechanisms underlying this relationship are not well-understood. The purpose of this study was to longitudinally test a model examining the role of self-efficacy and depression as potential mediators of the relationship between physical activity and fatigue in a sample of breast cancer survivors using both self-report and objective measures of physical activity.
Methods: All participants (N = 1,527) completed self-report measures of physical activity, self-efficacy, depression, and fatigue at baseline and 6 months. A subsample was randomly selected to wear an accelerometer at both time points. It was hypothesized that physical activity indirectly influences fatigue via self-efficacy and depression. Relationships among model constructs were examined over the 6-month period using panel analysis within a covariance modeling framework.
Results: The hypothesized model provided a good model-data fit (chi(2) = 599.66, df = 105, P <= 0.001; CFI = 0.96; SRMR = 0.02) in the full sample when controlling for covariates. At baseline, physical activity indirectly influenced fatigue via self-efficacy and depression. These relationships were also supported across time. In addition, the majority of the hypothesized relationships were supported in the subsample with accelerometer data (chi(2) = 387.48, df = 147, P <= 0.001, CFI = 0.94, SRMR = 0.04).
Conclusions: This study provides evidence to suggest the relationship between physical activity and fatigue in breast cancer survivors may be mediated by more proximal, modifiable outcomes of physical activity participation.
Impact: Recommendations are made relative to future applications and research concerning these relationships. (c) 2013 AACR.
C1 [Phillips, Siobhan M.; McAuley, Edward] Univ Illinois, Dept Kinesiol & Community Hlth, Urbana, IL USA.
RP Phillips, SM (reprint author), NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, 6116 Execut Blvd,Suite 404, Bethesda, MD 20892 USA.
EM siobhan.phillips@nih.gov
FU National Institute on Aging [F31AG034025, AG020118]; Shahid and Ann
Carlson Khan endowed professorship
FX This work was supported by award #F31AG034025 from the National
Institute on Aging awarded to S.M. Phillips and a Shahid and Ann Carlson
Khan endowed professorship awarded to E. McAuley, who is also supported
by grant #AG020118 from the National Institute on Aging. All work was
conducted at the University of Illinois.
NR 51
TC 16
Z9 18
U1 0
U2 19
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 773
EP 781
DI 10.1158/1055-9965.EPI-12-0983
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200004
PM 23456557
ER
PT J
AU Troisi, R
Doody, DR
Mueller, BA
AF Troisi, Rebecca
Doody, David R.
Mueller, Beth A.
TI A Linked-Registry Study of Gestational Factors and Subsequent Breast
Cancer Risk in the Mother
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BIRTH CERTIFICATE DATA; HOSPITAL DISCHARGE DATA; MATERNAL RISK; MULTIPLE
BIRTHS; WASHINGTON-STATE; PREGNANCY CHARACTERISTICS; 1ST PREGNANCY;
UNITED-STATES; WOMEN; RECORDS
AB Background: Women who were younger at their first live birth have a reduced breast cancer risk. Other pregnancy characteristics, including complications, also may affect risk but because they are rare, require large datasets to study.
Methods: The association of pregnancy history and breast cancer risk was assessed in a population-based study including 22,646 cases diagnosed in Washington State 1974 to 2009, and 224,721 controls, frequency matched on parity, age, calendar year of delivery, and race/ethnicity. Information on prediagnosis pregnancies derived from linked birth certificate and hospital discharge databases. Adjusted odd ratios (ORs) and 95% confidence intervals (CI) were calculated.
Results: Multiple gestation pregnancies were associated with decreased breast cancer risk (OR, 0.65; 95% CI, 0.57-0.74) as was prepregnancy obesity (OR, 0.76; 95% CI, 0.65-0.90). Infant birth weight was positively associated (6% per 1,000 g; 95% CI, 3%-9%). The ORs for first trimester bleeding (OR, 3.35; 95% CI, 1.48-7.55) and placental abnormality/insufficiency (OR, 2.24; 95% CI, 1.08-4.67) were increased in women diagnosed at age 50+ years and 15+ years after the index pregnancy. Results were similar in analyses restricted to first pregnancies, those closest to diagnosis, and when excluding in situ disease.
Conclusion: These data suggest that multiple gestation pregnancies are protective, whereas delivering larger infants increases risk for later development of maternal breast cancer. Placental abnormalities that result in bleeding in pregnancy also may reverse the long-term protection in postmenopausal women associated with parity.
Impact: Certain pregnancy characteristics seem to be associated with later maternal breast cancer risk. (C) 2013 AACR.
C1 [Troisi, Rebecca] NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA.
[Doody, David R.; Mueller, Beth A.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Mueller, Beth A.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
RP Troisi, R (reprint author), NIH, 6120 Execut Blvd,EPS 8096, Rockville, MD 20892 USA.
EM troisir@mail.nih.gov
FU National Cancer Institute [HHSN261201000725P]
FX This research was funded by National Cancer Institute Contract
#HHSN261201000725P (to R. Troisi, D.R. Doody, B.A. Mueller).
NR 47
TC 5
Z9 5
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 835
EP 847
DI 10.1158/1055-9965.EPI-12-1375
PG 13
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200011
PM 23592822
ER
PT J
AU Kabat, GC
Wu, JW
Moore, SC
Morton, LM
Park, Y
Hollenbeck, AR
Rohan, TE
AF Kabat, Geoffrey C.
Wu, Jennifer W.
Moore, Steven C.
Morton, Lindsay M.
Park, Yikyung
Hollenbeck, Albert R.
Rohan, Thomas E.
TI Lifestyle and Dietary Factors in Relation to Risk of Chronic Myeloid
Leukemia in the NIH-AARP Diet and Health Study
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID UNITED-STATES VETERANS; BODY-MASS INDEX; OBESITY; COHORT; MALIGNANCIES;
METAANALYSIS; ASSOCIATION; OVERWEIGHT; SMOKING
AB Background: Aside from exposure to ionizing radiation and benzene, little is known about lifestyle risk factors for chronic myeloid leukemia (CML) in the general population.
Methods: We examined the relation between lifestyle and dietary risk factors for CML in 493,188 participants (294,271 males and 198,917 females) aged 50 to 71 years who completed a baseline questionnaire in the National Institutes of Health-AARP Diet and Health Study in 1995 to 1996. Over a median of 10.5 years of follow-up, 178 incident cases of CML (139 males and 39 females) were ascertained from state registries. We used Cox proportional hazards models to estimate hazard ratios and 95% confidence intervals for exposures of interest, adjusting for potential confounding variables.
Results: In multivariable analysis of all participants combined, female sex, years of education, and vigorous physical activity (HR for >= 3 times/week vs. <1 time/week 0.70; 95% CI, 0.49-0.99) were inversely associated with risk of CML, whereas smoking intensity (HR for smokers of >= 20 cigarettes per day vs. never smokers: 1.53; 95% CI, 1.03-2.27) and body mass (HR for BMI >= 30 vs. <25 kg/m(2) 1.46; 95% CI, 0.95-2.23) were associated with increased risk. A range of dietary factors was not associated with disease.
Conclusions: This study adds to the sparse information about lifestyle factors, which affect the risk of CML in the general population.
Impact: If these findings are confirmed, it would suggest that CML may be amenable to preventive strategies. (C) 2013 AACR.
C1 [Kabat, Geoffrey C.; Rohan, Thomas E.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA.
[Wu, Jennifer W.; Moore, Steven C.; Morton, Lindsay M.; Park, Yikyung] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Wu, Jennifer W.; Moore, Steven C.; Morton, Lindsay M.; Park, Yikyung] NIH, Rockville, MD USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Kabat, GC (reprint author), Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA.
EM Geoffrey.kabat@einstein.yu.edu
RI Morton, Lindsay/B-5234-2015; Moore, Steven/D-8760-2016;
OI Morton, Lindsay/0000-0001-9767-2310; Moore, Steven/0000-0002-8169-1661;
Park, Yikyung/0000-0002-6281-489X
FU Intramural NIH HHS [Z99 CA999999, ZIA CP010170-12]
NR 19
TC 7
Z9 8
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 848
EP 854
DI 10.1158/1055-9965.EPI-13-0093
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200012
PM 23625904
ER
PT J
AU Sigurdardottir, LG
Valdimarsdottir, UA
Mucci, LA
Fall, K
Rider, JR
Schernhammer, E
Czeisler, CA
Launer, L
Harris, T
Stampfer, MJ
Gudnason, V
Lockley, SW
AF Sigurdardottir, Lara G.
Valdimarsdottir, Unnur A.
Mucci, Lorelei A.
Fall, Katja
Rider, Jennifer R.
Schernhammer, Eva
Czeisler, Charles A.
Launer, Lenore
Harris, Tamara
Stampfer, Meir J.
Gudnason, Vilmundur
Lockley, Steven W.
TI Sleep Disruption Among Older Men and Risk of Prostate Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID ROTATING-SHIFT WORKERS; ANTIPROLIFERATIVE ACTION; OXIDATIVE STRESS;
LEAD-TIME; IN-VIVO; MELATONIN; COHORT; CELLS; NIGHT; PROGRESSION
AB Background: Although positive associations have consistently been reported between sleep disruption and breast cancer, less is known about its potential role in prostate cancer.
Methods: Within the prospective AGES-Reykjavik cohort study, we followed 2,102 men recruited in 20022006 until the end of 2009. Participants answered questions on sleep disruption. Information on the occurrence of prostate cancer was obtained through record linkages across the Icelandic Cancer Registry. We used Cox regression models with 95% confidence intervals (CI) to estimate HRs of prostate cancer by symptoms of sleep disruption.
Results: During follow-up, 135 men (6.4%) were diagnosed with prostate cancer. Compared with men without sleep disruption, those with problems falling and staying asleep were at significantly increased risk of prostate cancer [HR, 1.7 (95% CI, 1.0-2.9) and 2.1 (95% CI, 1.2-3.7)], respectively, with increasing sleep disruption severity. When restricted to advanced prostate cancer (>= stage T3 or lethal disease), these associations became even stronger [HR 2.1 (95% CI, 0.7-6.2) and 3.2 (95% CI, 1.1-9.7)]. The results did not change after excluding from the analyses men who woke up during the night, indicative of nocturia, suggesting limited risk of reverse association.
Conclusions: Our data suggest that certain aspects of sleep disruption may confer an increased risk of prostate cancer and call for additional, larger studies with longer follow-up times.
Impact: Prostate cancer is one of the leading public health concerns in men; if confirmed in future studies, the association between sleep disruption and prostate cancer risk may open new avenues for prevention. (C) 2013 AACR.
C1 [Sigurdardottir, Lara G.; Valdimarsdottir, Unnur A.; Mucci, Lorelei A.; Fall, Katja] Univ Iceland, Ctr Publ Hlth Sci, IS-101 Reykjavik, Iceland.
[Sigurdardottir, Lara G.; Valdimarsdottir, Unnur A.; Gudnason, Vilmundur] Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.
[Sigurdardottir, Lara G.] Iceland Canc Soc, Reykjavik, Iceland.
[Valdimarsdottir, Unnur A.; Fall, Katja] Orebro Univ Hosp, Clin Epidemiol Unit, Orebro, Sweden.
[Valdimarsdottir, Unnur A.; Fall, Katja] Univ Orebro, Orebro, Sweden.
[Valdimarsdottir, Unnur A.; Mucci, Lorelei A.; Fall, Katja; Rider, Jennifer R.; Schernhammer, Eva; Stampfer, Meir J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Mucci, Lorelei A.; Rider, Jennifer R.; Schernhammer, Eva; Stampfer, Meir J.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab, Boston, MA 02115 USA.
[Czeisler, Charles A.; Lockley, Steven W.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Sleep Med,Dept Med, Boston, MA 02115 USA.
[Launer, Lenore; Harris, Tamara] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
[Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
RP Sigurdardottir, LG (reprint author), Univ Iceland, Ctr Publ Hlth Sci, Stapi V Hringbraut, IS-101 Reykjavik, Iceland.
EM lara@sessionimpossible.com
RI Gudnason, Vilmundur/K-6885-2015;
OI Gudnason, Vilmundur/0000-0001-5696-0084; Rider,
Jennifer/0000-0002-2637-6036; Fall, Katja/0000-0002-3649-2639
FU RANNIS (the Icelandic Research Fund); Harvard Catalyst Award (CTSA) from
the National Center for Research Resources, a part of the NIH [UL1 RR
025758, KL2 RR 025757]; U.S. National Institute on Aging
[N01-AG-1-2100]; Icelandic Parliament; Icelandic Cancer Society;
Icelandic Heart Association
FX This study was supported by RANNIS (the Icelandic Research Fund) and the
Harvard Catalyst Award (CTSA; awards UL1 RR 025758 and KL2 RR 025757)
from the National Center for Research Resources, a part of the NIH. This
study was also funded in part by the U.S. National Institute on Aging
contract N01-AG-1-2100, the Intramural Research Program of the National
Institute on Aging, the Icelandic Parliament, the Icelandic Cancer
Society, and the Icelandic Heart Association.
NR 37
TC 23
Z9 24
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 872
EP 879
DI 10.1158/1055-9965.EPI-12-1227-T
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200015
PM 23652374
ER
PT J
AU Pearce, CL
Rossing, MA
Lee, AW
Ness, RB
Webb, PM
Chenevix-Trench, G
Jordan, SM
Stram, DA
Chang-Claude, J
Hein, R
Nickels, S
Lurie, G
Thompson, PJ
Carney, ME
Goodman, MT
Moysich, K
Hogdall, E
Jensen, A
Goode, EL
Fridley, BL
Cunningham, JM
Vierkant, RA
Weber, RP
Ziogas, A
Anton-Culver, H
Gayther, SA
Gentry-Maharaj, A
Menon, U
Ramus, SJ
Brinton, L
Wentzensen, N
Lissowska, J
Garcia-Closas, M
Massuger, LFAG
Kiemeney, LALM
Van Altena, AM
Aben, KKH
Berchuck, A
Doherty, JA
Iversen, E
McGuire, V
Moorman, PG
Pharoah, P
Pike, MC
Risch, H
Sieh, W
Stram, DO
Terry, KL
Whittemore, A
Wu, AH
Schildkraut, JM
Kjaer, SK
AF Pearce, Celeste Leigh
Rossing, Mary Anne
Lee, Alice W.
Ness, Roberta B.
Webb, Penelope M.
Chenevix-Trench, Georgia
Jordan, Susan M.
Stram, Douglas A.
Chang-Claude, Jenny
Hein, Rebecca
Nickels, Stefan
Lurie, Galina
Thompson, Pamela J.
Carney, Michael E.
Goodman, Marc T.
Moysich, Kirsten
Hogdall, Estrid
Jensen, Allan
Goode, Ellen L.
Fridley, Brooke L.
Cunningham, Julie M.
Vierkant, Robert A.
Weber, Rachel Palmieri
Ziogas, Argyrios
Anton-Culver, Hoda
Gayther, Simon A.
Gentry-Maharaj, Aleksandra
Menon, Usha
Ramus, Susan J.
Brinton, Louise
Wentzensen, Nicolas
Lissowska, Jolanta
Garcia-Closas, Montserrat
Massuger, Leon F. A. G.
Kiemeney, Lambertus A. L. M.
Van Altena, Anne M.
Aben, Katja K. H.
Berchuck, Andrew
Doherty, Jennifer A.
Iversen, Edwin
McGuire, Valerie
Moorman, Patricia G.
Pharoah, Paul
Pike, Malcolm C.
Risch, Harvey
Sieh, Weiva
Stram, Daniel O.
Terry, Kathryn L.
Whittemore, Alice
Wu, Anna H.
Schildkraut, Joellen M.
Kjaer, Susanne K.
CA Australian Canc Study
Australian Ovarian Canc Study Grp
Ovarian Canc Assoc Consortium
TI Combined and Interactive Effects of Environmental and GWAS-Identified
Risk Factors in Ovarian Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ORAL-CONTRACEPTIVES; HISTOLOGIC TYPE;
SUSCEPTIBILITY; INFLAMMATION; WOMEN
AB Background: There are several well-established environmental risk factors for ovarian cancer, and recent genome-wide association studies have also identified six variants that influence disease risk. However, the interplay between such risk factors and susceptibility loci has not been studied.
Methods: Data from 14 ovarian cancer case-control studies were pooled, and stratified analyses by each environmental risk factor with tests for heterogeneity were conducted to determine the presence of interactions for all histologic subtypes. A genetic "risk score" was created to consider the effects of all six variants simultaneously. A multivariate model was fit to examine the association between all environmental risk factors and genetic risk score on ovarian cancer risk.
Results: Among 7,374 controls and 5,566 cases, there was no statistical evidence of interaction between the six SNPs or genetic risk score and the environmental risk factors on ovarian cancer risk. In a main effects model, women in the highest genetic risk score quartile had a 65% increased risk of ovarian cancer compared with women in the lowest [95% confidence interval (CI), 1.48-1.84]. Analyses by histologic subtype yielded risk differences across subtype for endometriosis (P-het < 0.001), parity (P-het < 0.01), and tubal ligation (P-het = 0.041).
Conclusions: The lack of interactions suggests that a multiplicative model is the best fit for these data. Under such a model, we provide a robust estimate of the effect of each risk factor that sets the stage for absolute risk prediction modeling that considers both environmental and genetic risk factors. Further research into the observed differences in risk across histologic subtype is warranted. (C) 2013 AACR.
C1 [Pearce, Celeste Leigh; Lee, Alice W.; Stram, Douglas A.; Gayther, Simon A.; Ramus, Susan J.; Pike, Malcolm C.; Stram, Daniel O.; Wu, Anna H.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Rossing, Mary Anne] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
[Ness, Roberta B.] Univ Texas Sch Publ Hlth, Houston, TX USA.
[Chenevix-Trench, Georgia; Jordan, Susan M.; Australian Canc Study] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Australian Ovarian Canc Study Grp] Peter MacCallum Canc Ctr, Melbourne, Australia.
[Chang-Claude, Jenny; Hein, Rebecca; Nickels, Stefan] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Lurie, Galina; Thompson, Pamela J.; Carney, Michael E.; Goodman, Marc T.] Univ Hawaii, Canc Res Ctr Hawaii, Honolulu, HI 96822 USA.
[Moysich, Kirsten] Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY 14263 USA.
[Hogdall, Estrid; Jensen, Allan; Kjaer, Susanne K.] Danish Canc Soc Res Ctr, Copenhagen, Denmark.
[Kjaer, Susanne K.] Univ Copenhagen, Rigshosp, Juliane Marie Ctr, Gynecol Clin, DK-2100 Copenhagen, Denmark.
[Goode, Ellen L.; Fridley, Brooke L.; Vierkant, Robert A.] Mayo Clin, Coll Med, Dept Hlth Sci Res, Rochester, MN USA.
[Cunningham, Julie M.] Mayo Clin, Coll Med, Dept Lab Med & Pathol, Rochester, MN USA.
[Weber, Rachel Palmieri; Moorman, Patricia G.; Schildkraut, Joellen M.] Duke Univ, Dept Community & Family Med, Durham, NC USA.
[Berchuck, Andrew; Iversen, Edwin] Duke Univ, Durham, NC USA.
[Schildkraut, Joellen M.] Duke Canc Inst, Canc Prevent Detect & Control Res Program, Durham, NC USA.
[Ziogas, Argyrios; Anton-Culver, Hoda] Univ Calif Irvine, Sch Med, Dept Epidemiol, Irvine, CA 92717 USA.
[Gayther, Simon A.; Gentry-Maharaj, Aleksandra; Menon, Usha; Ramus, Susan J.] UCL, Inst Womens Hlth, Gynaecol Ctr Res Ctr, London, England.
[Garcia-Closas, Montserrat] Inst Canc Res, Epidemiol Sect, London SW3 6JB, England.
[Garcia-Closas, Montserrat] Inst Canc Res, Genet Sect, London SW3 6JB, England.
[Garcia-Closas, Montserrat] Breakthrough Breast Canc Res Ctr, London, England.
[Brinton, Louise; Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lissowska, Jolanta] M Sklodowska Curie Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Massuger, Leon F. A. G.; Van Altena, Anne M.] Radboud Univ Nijmegen, Dept Gynecol, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Kiemeney, Lambertus A. L. M.; Aben, Katja K. H.] Radboud Univ Nijmegen, Dept Epidemiol Biostat & HTA, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Kiemeney, Lambertus A. L. M.; Aben, Katja K. H.] Comprehens Canc Ctr Netherlands, Utrecht, Netherlands.
[McGuire, Valerie; Sieh, Weiva; Whittemore, Alice] Stanford Univ, Sch Med, Div Epidemiol & Biostat, Dept Hlth Res & Policy, Stanford, CA 94305 USA.
[Pharoah, Paul] Univ Cambridge, Strangeways Res Lab, Canc Res UK Dept Oncol, Cambridge, England.
[Pike, Malcolm C.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Risch, Harvey] Yale Univ, Dept Epidemiol & Publ Hlth, Sch Publ Hlth, New Haven, CT 06520 USA.
[Terry, Kathryn L.] Brigham & Womens Hosp, Obstetr & Gynecol Epidemiol Ctr, Boston, MA 02115 USA.
[Doherty, Jennifer A.] Geisel Sch Med Dartmouth, Dept Community & Family Med, Lebanon, NH USA.
[Fridley, Brooke L.] Univ Kansas, Med Ctr, Dept Biostat, Kansas City, KS 66103 USA.
RP Pearce, CL (reprint author), 1441 Eastlake Ave,Norris Topping Tower,Room 4417, Los Angeles, CA 90089 USA.
EM cpearce@usc.edu
RI Kiemeney, Lambertus/D-3357-2009; Whittemore, Alice/F-9925-2014;
Massuger, Leon/H-8072-2014; Fridley, Brooke/D-8315-2015; Garcia-Closas,
Montserrat /F-3871-2015; Aben, Katja/G-9686-2016; Bowtell,
David/H-1007-2016; Brinton, Louise/G-7486-2015; van Altena,
Anne/B-9824-2016;
OI Kiemeney, Lambertus/0000-0002-2368-1326; Fridley,
Brooke/0000-0001-7739-7956; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Aben, Katja/0000-0002-0214-2147; Bowtell,
David/0000-0001-9089-7525; Kjaer, Susanne/0000-0002-8347-1398; Ramus,
Susan/0000-0003-0005-7798; Webb, Penelope/0000-0003-0733-5930; Brinton,
Louise/0000-0003-3853-8562; Lissowska, Jolanta/0000-0003-2695-5799
FU NIH [CA14089, CA17054, CA61132, CA136891, CA141154, N01 PC67010, R01
CA112523, R01 CA87538, R01 CA58598, N01 PC67001, N01 CN55424, R01
CA76016, CA58860, CA92044, PSA 042205, R01 CA61107, U01 CA71966, R01
CA16056]; California Cancer Research Program [2II0200, 00-01389V-20170,
R03 CA113148, R03 CA115195, N01 CN25403]; National Cancer Institute; Lon
V. Smith Foundation [LVS 39420]; European Community
[HEALTH-F2-2009-223175]; UK NIHR University College London Hospitals
Biomedical Research Centre; German Federal Ministry of Education and
Research Programme of Clinical Biomedical Research [01GB9401]; German
Cancer Research Center; Eve Appeal; OAK Foundation; Medical Research
Council [MRC28209]; Cancer Research UK [C8804/A7058]; National Health
and Medical Research Council of Australia [199600, 400281, 400413];
Department of Defense [DAMD17-02-1-0669, DAMD17-02-1-0666]; U.S. Army
Medical Research and Materiel Command [DAMD17-01-1-0729]; Cancer Council
of New South Wales; Cancer Council of Victoria; Cancer Council of
Queensland; Cancer Council of South Australia; Cancer Council of
Tasmania; Cancer Foundation of Western Australia; Mermaid 1; Danish
Cancer Society; Radboud University Nijmegen Medical Centre; Genetic
Associations and Mechanisms in Oncology (GAME-ON): a NCI Cancer
Post-GWAS Initiative [U19CA148112]; N.I.H [K07 CA143047, U01 CA69417,
R01 CA122443, P50-CA136393, R01 CA95023]
FX This work was supported by the family and friends of Kathryn Sladek
Smith through their donations to the Ovarian Cancer Research Fund. This
work was also supported by the NIH [CA14089, CA17054, CA61132, CA136891,
CA141154, N01 PC67010 (for USC), R01 CA112523, R01 CA87538 (for DOV),
R01 CA58598, N01 PC67001, N01 CN55424 (for HAW), R01 CA76016 (for NCO),
CA58860, CA92044, PSA 042205 (for UCI), R01 CA61107 (for MAL), U01
CA71966, R01 CA16056, K07 CA143047, U01 CA69417 (for STA)], R01
CA122443, P50-CA136393 (for MAY), R01 CA95023 (for HOP); the California
Cancer Research Program [2II0200, 00-01389V-20170, R03 CA113148, R03
CA115195, N01 CN25403 (for USC)]; Intramural Research Program of the
National Cancer Institute (for POL); the Lon V. Smith Foundation [LVS
39420 (for UCI)]; European Community's Seventh Framework Programme
[HEALTH-F2-2009-223175 (for GER and UKO)]; UK NIHR University College
London Hospitals Biomedical Research Centre (for UKO); the German
Federal Ministry of Education and Research Programme of Clinical
Biomedical Research (01GB9401; for GER); the German Cancer Research
Center (for GER); the Eve Appeal (for UKO); the OAK Foundation (for
UKO); Medical Research Council Grant (MRC28209; for UKO); Cancer
Research UK (C8804/A7058; for UKO); the National Health and Medical
Research Council of Australia (199600, 400281, 400413; for AUS);
Department of Defense [DAMD17-02-1-0669 (for HOP), DAMD17-02-1-0666 (for
NCO)]; the U.S. Army Medical Research and Materiel Command
[DAMD17-01-1-0729 (for AUS)]; Cancer Councils of New South Wales,
Victoria, Queensland, South Australia and Tasmania (for AUS); Cancer
Foundation of Western Australia (for AUS); Mermaid 1 (for MAL); the
Danish Cancer Society (for MAL); and Radboud University Nijmegen Medical
Centre (for NTH). The scientific development and funding of this project
were in part supported by the Genetic Associations and Mechanisms in
Oncology (GAME-ON): a NCI Cancer Post-GWAS Initiative (U19CA148112).
NR 34
TC 11
Z9 11
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 880
EP 890
DI 10.1158/1055-9965.EPI-12-1030-T
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200016
PM 23462924
ER
PT J
AU Hendrickson, SJ
Lindstrom, S
Eliassen, AH
Rosner, BA
Chen, C
Barrdahl, M
Brinton, L
Buring, J
Canzian, F
Chanock, S
Clavel-Chapelon, F
Figueroa, JD
Gapstur, SM
Garcia-Closas, M
Gaudet, MM
Haiman, CA
Hazra, A
Henderson, B
Hoover, R
Husing, A
Johansson, M
Kaaks, R
Khaw, KT
Kolonel, LN
Le Marchand, L
Lissowska, J
Lund, E
McCullough, ML
Peplonska, B
Riboli, E
Sacerdote, C
Sanchez, MJ
Tjonneland, A
Trichopoulos, D
van Gils, CH
Yeager, M
Kraft, P
Hunter, DJ
Ziegler, RG
Willett, WC
AF Hendrickson, Sara J.
Lindstroem, Sara
Eliassen, A. Heather
Rosner, Bernard A.
Chen, Constance
Barrdahl, Myrto
Brinton, Louise
Buring, Julie
Canzian, Federico
Chanock, Stephen
Clavel-Chapelon, Francoise
Figueroa, Jonine D.
Gapstur, Susan M.
Garcia-Closas, Montserrat
Gaudet, Mia M.
Haiman, Christopher A.
Hazra, Aditi
Henderson, Brian
Hoover, Robert
Husing, Anika
Johansson, Mattias
Kaaks, Rudolf
Khaw, Kay-Tee
Kolonel, Laurence N.
Le Marchand, Loic
Lissowska, Jolanta
Lund, Eiliv
McCullough, Marjorie L.
Peplonska, Beata
Riboli, Elio
Sacerdote, Carlotta
Sanchez, Maria-Jose
Tjonneland, Anne
Trichopoulos, Dimitrios
van Gils, Carla H.
Yeager, Meredith
Kraft, Peter
Hunter, David J.
Ziegler, Regina G.
Willett, Walter C.
TI Plasma Carotenoid- and Retinol-Weighted Multi-SNP Scores and Risk of
Breast Cancer in the National Cancer Institute Breast and Prostate
Cancer Cohort Consortium
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SINGLE NUCLEOTIDE POLYMORPHISMS; BETA-CAROTENE; MENDELIAN RANDOMIZATION;
VITAMIN-A; POOLED ANALYSIS; LUNG-CANCER; DISEASE; ENZYMES;
15,15-MONOOXYGENASE; CLEAVAGE
AB Background: Dietary and circulating carotenoids have been inversely associated with breast cancer risk, but observed associations may be due to confounding. Single-nucleotide polymorphisms (SNPs) in beta-carotene 15,15'-monooxygenase 1 (BCMO1), a gene encoding the enzyme involved in the first step of synthesizing vitamin A from dietary carotenoids, have been associated with circulating carotenoid concentrations and may serve as unconfounded surrogates for those biomarkers. We determined associations between variants in BCMO1 and breast cancer risk in a large cohort consortium.
Methods: We used unconditional logistic regression to test four SNPs in BCMO1 for associations with breast cancer risk in 9,226 cases and 10,420 controls from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3). We also tested weighted multi-SNP scores composed of the two SNPs with strong, confirmed associations with circulating carotenoid concentrations.
Results: Neither the individual SNPs nor the weighted multi-SNP scores were associated with breast cancer risk [OR (95% confidence interval) comparing extreme quintiles of weighted multi-SNP scores = 1.04 (0.94-1.16) for beta-carotene, 1.08 (0.98-1.20) for alpha-carotene, 1.04 (0.94-1.16) for beta-cryptoxanthin, 0.95 (0.87-1.05) for lutein/zeaxanthin, and 0.92 (0.83-1.02) for retinol]. Furthermore, no associations were observed when stratifying by estrogen receptor status, but power was limited.
Conclusions: Our results do not support an association between SNPs associated with circulating carotenoid concentrations and breast cancer risk.
Impact: Future studies will need additional genetic surrogates and/or sample sizes at least three times larger to contribute evidence of a causal link between carotenoids and breast cancer. (C) 2013 AACR.
C1 [Hendrickson, Sara J.; Hunter, David J.; Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hendrickson, Sara J.; Lindstroem, Sara; Eliassen, A. Heather; Chen, Constance; Hazra, Aditi; Trichopoulos, Dimitrios; Kraft, Peter; Hunter, David J.; Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Eliassen, A. Heather; Rosner, Bernard A.; Hazra, Aditi; Hunter, David J.; Willett, Walter C.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Buring, Julie] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.
[Buring, Julie] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Buring, Julie] Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA 02115 USA.
[Barrdahl, Myrto; Husing, Anika; Kaaks, Rudolf] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Canzian, Federico] German Canc Res Ctr, Genom Epidemiol Grp, Heidelberg, Germany.
[Brinton, Louise; Figueroa, Jonine D.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Chanock, Stephen; Hoover, Robert; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA.
[Yeager, Meredith] Frederick Natl Lab Canc Res, Core Genotyping Facil, Gaithersburg, MD USA.
[Clavel-Chapelon, Francoise] Inst Gustave Roussy, INSERM, Ctr Res Epidemiol & Populat Hlth, Lyon, France.
[Clavel-Chapelon, Francoise] Paris South Univ, Villejuif, France.
[Johansson, Mattias] Int Agcy Res Canc, F-69372 Lyon, France.
[Gapstur, Susan M.; Gaudet, Mia M.; McCullough, Marjorie L.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Garcia-Closas, Montserrat] Univ London Imperial Coll Sci Technol & Med, Inst Canc Res & Breakthrough Breast Canc Res, Div Genet & Epidemiol, London, England.
[Riboli, Elio] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England.
[Khaw, Kay-Tee] Univ Cambridge, Clin Gerontol Unit, Cambridge, England.
[Haiman, Christopher A.; Henderson, Brian] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Johansson, Mattias] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
[Kolonel, Laurence N.; Le Marchand, Loic] Univ Hawaii, Ctr Canc, Epidemiol Program, Honolulu, HI 96822 USA.
[Lissowska, Jolanta] Ctr Canc, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] M Sklodowska Curie Inst Oncol, Warsaw, Poland.
[Peplonska, Beata] Nofer Inst Occupat Med, Lodz, Poland.
[Lund, Eiliv] Univ Tromso, Dept Community Med, Tromso, Norway.
[Sacerdote, Carlotta] Ctr Canc Prevent CPO Piemonte, Turin, Italy.
[Sacerdote, Carlotta] Human Genet Fdn HuGeF, Turin, Italy.
[Sanchez, Maria-Jose] Escuela Andaluza Salud Publ, Granada, Spain.
[Sanchez, Maria-Jose] CIBERESP, CIBER Epidemiol Salud Publ, Madrid, Spain.
[Tjonneland, Anne] Diet Genest & Environm Danish Canc Soc Res Ctr, Copenhagen, Denmark.
[Trichopoulos, Dimitrios] Acad Athens, Bereau Epidemiol Res, Athens, Greece.
[Trichopoulos, Dimitrios] Hellen Hlth Fdn, Athens, Greece.
[van Gils, Carla H.] Univ Med Ctr Utrecht, Julius Ctr, Utrecht, Netherlands.
RP Hendrickson, SJ (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave, Boston, MA 02115 USA.
EM slindstr@hsph.harvard.edu
RI Clavel-Chapelon, Francoise/G-6733-2014; SANCHEZ-PEREZ, MARIA
JOSE/D-1087-2011; Garcia-Closas, Montserrat /F-3871-2015; Brinton,
Louise/G-7486-2015;
OI SANCHEZ-PEREZ, MARIA JOSE/0000-0003-4817-0757; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562; Lissowska,
Jolanta/0000-0003-2695-5799; Sacerdote, Carlotta/0000-0002-8008-5096
FU U.S. NIH, NCI [U01-CA98233-07, U01-CA98710-06, U01-CA98216-06,
U01-CA98758-07]; NIH; NCI, Division of Cancer Epidemiology and Genetics;
NCI's Cancer Genetic Markers of Susceptibility Study (CGEMS); [P01
CA87969]; [R01 CA131218]; [R01 CA49449]; [U01 CA098233]; [R03
CA133937]; [NIH 5 T32 CA09001]; [R25 CA098566]
FX This project was supported in part by the U.S. NIH, NCI (cooperative
agreements U01-CA98233-07 to D.J. Hunter; U01-CA98710-06 to Michael J.
Thun; U01-CA98216-06 to E. Riboli and R. Kaaks; and U01-CA98758-07 to B.
Henderson) and Intramural Research Program of NIH and NCI, Division of
Cancer Epidemiology and Genetics. This project was additionally
supported in part by P01 CA87969, R01 CA131218, R01 CA49449, U01
CA098233, and R03 CA133937. The GWAS of breast cancer in NHS was
supported by the NCI's Cancer Genetic Markers of Susceptibility Study
(CGEMS). S.J. Hendrickson was supported in part by training grants NIH 5
T32 CA09001 and R25 CA098566.
NR 29
TC 4
Z9 4
U1 0
U2 17
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 927
EP 936
DI 10.1158/1055-9965.EPI-13-0017
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200021
PM 23515144
ER
PT J
AU White, KL
Vierkant, RA
Fogarty, ZC
Charbonneau, B
Block, MS
Pharoah, PDP
Chenevix-Trench, G
Rossing, MA
Cramer, DW
Pearce, CL
Schildkraut, JM
Menon, U
Kjaer, SK
Levine, DA
Gronwald, J
Culver, HA
Whittemore, AS
Karlan, BY
Lambrechts, D
Wentzensen, N
Kupryjanczyk, J
Chang-Claude, J
Bandera, EV
Hogdall, E
Heitz, F
Kaye, SB
Fasching, PA
Campbell, I
Goodman, MT
Pejovic, T
Bean, Y
Lurie, G
Eccles, D
Hein, A
Beckmann, MW
Ekici, AB
Paul, J
Brown, R
Flanagan, JM
Harter, P
Du Bois, A
Schwaab, I
Hogdall, CK
Lundvall, L
Olson, SH
Orlow, I
Paddock, LE
Rudolph, A
Eilber, U
Dansonka-Mieszkowska, A
Rzepecka, IK
Ziolkowska-Seta, I
Brinton, L
Yang, H
Garcia-Closas, M
Despierre, E
Lambrechts, S
Vergote, I
Walsh, C
Lester, J
Sieh, W
McGuire, V
Rothstein, JH
Ziogas, A
Lubinski, J
Cybulski, C
Menkiszak, J
Jensen, A
Gayther, SA
Ramus, SJ
Gentry-Maharaj, A
Berchuck, A
Wu, AH
Pike, MC
Van denBerg, D
Terry, KL
Vitonis, AF
Doherty, JA
Johnatty, SE
Defazio, A
Song, HL
Tyrer, J
Sellers, TA
Phelan, CM
Kalli, KR
Cunningham, JM
Fridley, BL
Goode, EL
AF White, Kristin L.
Vierkant, Robert A.
Fogarty, Zachary C.
Charbonneau, Bridget
Block, Matthew S.
Pharoah, Paul D. P.
Chenevix-Trench, Georgia
Rossing, Mary Anne
Cramer, Daniel W.
Pearce, Celeste Leigh
Schildkraut, Joellen M.
Menon, Usha
Kjaer, Susanne Kruger
Levine, Douglas A.
Gronwald, Jacek
Culver, Hoda Anton
Whittemore, Alice S.
Karlan, Beth Y.
Lambrechts, Diether
Wentzensen, Nicolas
Kupryjanczyk, Jolanta
Chang-Claude, Jenny
Bandera, Elisa V.
Hogdall, Estrid
Heitz, Florian
Kaye, Stanley B.
Fasching, Peter A.
Campbell, Ian
Goodman, Marc T.
Pejovic, Tanja
Bean, Yukie
Lurie, Galina
Eccles, Diana
Hein, Alexander
Beckmann, Matthias W.
Ekici, Arif B.
Paul, James
Brown, Robert
Flanagan, James M.
Harter, Philipp
Du Bois, Andreas
Schwaab, Ira
Hogdall, Claus K.
Lundvall, Lene
Olson, Sara H.
Orlow, Irene
Paddock, Lisa E.
Rudolph, Anja
Eilber, Ursula
Dansonka-Mieszkowska, Agnieszka
Rzepecka, Iwona K.
Ziolkowska-Seta, Izabela
Brinton, Louise
Yang, Hannah
Garcia-Closas, Montserrat
Despierre, Evelyn
Lambrechts, Sandrina
Vergote, Ignace
Walsh, Christine
Lester, Jenny
Sieh, Weiva
McGuire, Valerie
Rothstein, Joseph H.
Ziogas, Argyrios
Lubinski, Jan
Cybulski, Cezary
Menkiszak, Janusz
Jensen, Allan
Gayther, Simon A.
Ramus, Susan J.
Gentry-Maharaj, Aleksandra
Berchuck, Andrew
Wu, Anna H.
Pike, Malcolm C.
Van denBerg, David
Terry, Kathryn L.
Vitonis, Allison F.
Doherty, Jennifer A.
Johnatty, Sharon E.
Defazio, Anna
Song, Honglin
Tyrer, Jonathan
Sellers, Thomas A.
Phelan, Catherine M.
Kalli, Kimberly R.
Cunningham, Julie M.
Fridley, Brooke L.
Goode, Ellen L.
CA AOCS ACS Grp
TI Analysis of Over 10,000 Cases Finds No Association between Previously
Reported Candidate Polymorphisms and Ovarian Cancer Outcome
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SUSCEPTIBILITY
AB Background: Ovarian cancer is a leading cause of cancer-related death among women. In an effort to understand contributors to disease outcome, we evaluated single-nucleotide polymorphisms (SNP) previously associated with ovarian cancer recurrence or survival, specifically in angiogenesis, inflammation, mitosis, and drug disposition genes.
Methods: Twenty-seven SNPs in VHL, HGF, IL18, PRKACB, ABCB1, CYP2C8, ERCC2, and ERCC1 previously associated with ovarian cancer outcome were genotyped in 10,084 invasive cases from 28 studies from the Ovarian Cancer Association Consortium with over 37,000-observed person-years and 4,478 deaths. Cox proportional hazards models were used to examine the association between candidate SNPs and ovarian cancer recurrence or survival with and without adjustment for key covariates.
Results: We observed no association between genotype and ovarian cancer recurrence or survival for any of the SNPs examined.
Conclusions: These results refute prior associations between these SNPs and ovarian cancer outcome and underscore the importance of maximally powered genetic association studies.
Impact: These variants should not be used in prognostic models. Alternate approaches to uncovering inherited prognostic factors, if they exist, are needed. (C) 2013 AACR.
C1 [White, Kristin L.] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
[Vierkant, Robert A.; Fogarty, Zachary C.] Mayo Clin, Div Biomed Stat & Informat, Dept Hlth Sci Res, Rochester, MN 55905 USA.
[Charbonneau, Bridget; Goode, Ellen L.] Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN 55905 USA.
[Block, Matthew S.; Kalli, Kimberly R.] Mayo Clin, Dept Med Oncol, Rochester, MN 55905 USA.
[Pharoah, Paul D. P.; Song, Honglin; Tyrer, Jonathan] Univ Cambridge, Dept Oncol, Cambridge, England.
[Pharoah, Paul D. P.] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Chenevix-Trench, Georgia; Johnatty, Sharon E.] Queensland Inst Med Res, Canc Div, Herston, Qld 4006, Australia.
[Rossing, Mary Anne] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA 98104 USA.
[Cramer, Daniel W.; Terry, Kathryn L.; Vitonis, Allison F.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Cramer, Daniel W.; Terry, Kathryn L.; Vitonis, Allison F.] Brigham & Womens Hosp, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA.
[Cramer, Daniel W.; Terry, Kathryn L.; Vitonis, Allison F.] Harvard Univ, Sch Med, Boston, MA USA.
[Cramer, Daniel W.; Terry, Kathryn L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Pearce, Celeste Leigh; Gayther, Simon A.; Ramus, Susan J.; Wu, Anna H.; Pike, Malcolm C.; Van denBerg, David] Univ So Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Schildkraut, Joellen M.] Duke Canc Inst, Cancer Prevent Detect & Control Res Program, Durham, NC USA.
[Schildkraut, Joellen M.] Duke Univ, Med Ctr, Dept Community & Family Med, Durham, NC 27710 USA.
[Menon, Usha; Gentry-Maharaj, Aleksandra] UCL EGA Inst Womens Hlth, Gynaecol Canc Res Ctr, London, England.
[Kjaer, Susanne Kruger; Hogdall, Claus K.; Lundvall, Lene] Rigshosp, Juliane Marie Ctr, Dept Obstet & Gynecol, DK-2100 Copenhagen, Denmark.
[Kjaer, Susanne Kruger; Hogdall, Estrid; Jensen, Allan] Danish Canc Soc Res Ctr, Copenhagen, Denmark.
[Levine, Douglas A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Gronwald, Jacek; Lubinski, Jan; Cybulski, Cezary] Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
[Culver, Hoda Anton; Ziogas, Argyrios] Univ Calif Irvine, Sch Med, Dept Epidemiol, Ctr Canc Genet Res & Prevent, Irvine, CA 92717 USA.
[Whittemore, Alice S.; Sieh, Weiva; McGuire, Valerie; Rothstein, Joseph H.] Stanford Univ, Sch Med, Dept Hlth Res & Policy Epidemiol, Palo Alto, CA 94304 USA.
[Karlan, Beth Y.; Walsh, Christine; Lester, Jenny] Cedars Sinai Med Ctr, Womens Canc Program, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Lambrechts, Diether] Univ Louvain, Vesalius Res Ctr, Louvain, Belgium.
[Lambrechts, Diether] Univ Louvain, Lab Translat Genet, Dept Oncol, Louvain, Belgium.
[Wentzensen, Nicolas; Brinton, Louise; Yang, Hannah] NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA.
[Dansonka-Mieszkowska, Agnieszka; Rzepecka, Iwona K.] Maria Sklodowska Curie Mem Canc Ctr, Dept Mol Pathol, Warsaw, Poland.
[Dansonka-Mieszkowska, Agnieszka; Rzepecka, Iwona K.] Inst Oncol, Warsaw, Poland.
[Chang-Claude, Jenny; Rudolph, Anja; Eilber, Ursula] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Kupryjanczyk, Jolanta; Bandera, Elisa V.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, New Brunswick, NJ USA.
[Hogdall, Estrid] Univ Copenhagen, Mol Unit, Dept Pathol, Herlev Hosp, Copenhagen, Denmark.
[Heitz, Florian; Harter, Philipp; Du Bois, Andreas] Dr Horst Schmidt Kliniken Wiesbaden, Dept Gynecol & Gynecol Oncol, Wiesbaden, Germany.
[Heitz, Florian; Harter, Philipp; Du Bois, Andreas] Evang Huyssens Stiftung Knappschaft GmbH, Kliniken Essen Mitte, Dept Gynecol & Gynecol Oncol, Essen, Germany.
[Kaye, Stanley B.] Inst Canc Res, Sect Med, Sutton, Surrey, England.
[Kaye, Stanley B.] Royal Marsden Hosp, Sutton, Surrey, England.
[Fasching, Peter A.; Hein, Alexander; Beckmann, Matthias W.] Univ Erlangen Nurnberg, Univ Hosp Erlangen, Dept Gynecol & Obstet, Ctr Comprehens Canc, D-91054 Erlangen, Germany.
[Fasching, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA.
[Campbell, Ian] Peter MacCallum Canc Ctr, Div Res, Canc Genet Lab, Melbourne, Vic, Australia.
[Campbell, Ian] Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia.
[Goodman, Marc T.] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Pejovic, Tanja; Bean, Yukie] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Pejovic, Tanja; Bean, Yukie] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Lurie, Galina] Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA.
[Eccles, Diana] Univ Southampton, Southampton Univ Hosp, Fac Med, Southampton SO9 5NH, Hants, England.
[Ekici, Arif B.] Univ Erlangen Nurnberg, Inst Human Genet, Erlangen, Germany.
[Paul, James] Beatson West Scotland Canc Ctr, Glasgow, Lanark, Scotland.
[Brown, Robert; Flanagan, James M.] Univ London Imperial Coll Sci Technol & Med, Dept Surg & Canc, London, England.
[Schwaab, Ira] Inst Human Genet Wiesbaden, Wiesbaden, Germany.
[Olson, Sara H.; Orlow, Irene; Pike, Malcolm C.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Paddock, Lisa E.] New Jersey Dept Hlth, Trenton, NJ USA.
[Ziolkowska-Seta, Izabela] Maria Sklodowska Curie Memorial Canc Ctr, Warsaw, Poland.
[Garcia-Closas, Montserrat] Inst Canc Res, Div Genet & Epidemiol, Sutton, Surrey, England.
[Garcia-Closas, Montserrat] Breakthrough Breast Canc Res Ctr, London, England.
[Despierre, Evelyn; Lambrechts, Sandrina; Vergote, Ignace] Univ Hosp Leuven, Louvain, Belgium.
[Despierre, Evelyn; Lambrechts, Sandrina; Vergote, Ignace] Katholieke Univ Leuven, Dept Oncol, Louvain, Belgium.
[Menkiszak, Janusz] Pomeranian Med Univ, Clin Gynaecol Surg & Oncol, Szczecin, Poland.
[Berchuck, Andrew] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
[Doherty, Jennifer A.] Geisel Sch Med Dartmouth, Epidemiol & Biostat Sect, Lebanon, NH USA.
[Defazio, Anna] Univ Sydney, Westmead Hosp, Dept Gynaecol Oncol, Westmead, NSW 2145, Australia.
[Defazio, Anna] Univ Sydney, Westmead Millennium Inst, Westmead Inst Canc Res, Westmead, NSW 2145, Australia.
[Sellers, Thomas A.; Phelan, Catherine M.] Univ S Florida, H Lee Moffitt Canc Ctr, Div Populat Sci, Dept Canc Epidemiol, Tampa, FL 33682 USA.
[Cunningham, Julie M.] Mayo Clin, Dept Lab Med & Pathol, Div Expt Pathol, Rochester, MN USA.
[Fridley, Brooke L.] Univ Kansas, Med Ctr, Dept Biostat, Kansas City, KS 66103 USA.
RP Goode, EL (reprint author), Mayo Clin, Coll Med, Dept Hlth Sci Res, 200 1st St SW, Rochester, MN 55905 USA.
EM egoode@mayo.edu
RI Johnatty, Sharon/R-8890-2016; Hein, Alexander/F-6999-2010; Whittemore,
Alice/F-9925-2014; Gronwald, Jacek/A-4576-2017; Bandera,
Elisa/M-4169-2014; deFazio, Anna/D-3939-2013; campbell, Ian/F-6006-2011;
Fridley, Brooke/D-8315-2015; Garcia-Closas, Montserrat /F-3871-2015;
Brinton, Louise/G-7486-2015; Bowtell, David/H-1007-2016; Menkiszak,
Janusz/I-4036-2014
OI Ramus, Susan/0000-0003-0005-7798; Kjaer, Susanne/0000-0002-8347-1398;
Orlow, Irene/0000-0001-6234-6961; Johnatty, Sharon/0000-0002-7888-1966;
Hein, Alexander/0000-0003-2601-3398; Gronwald,
Jacek/0000-0002-3643-2871; Rudolph, Anja/0000-0001-7520-2035; Bandera,
Elisa/0000-0002-8789-2755; deFazio, Anna/0000-0003-0057-4744; Fridley,
Brooke/0000-0001-7739-7956; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562; Bowtell,
David/0000-0001-9089-7525;
FU Novartis; Amgen; American Cancer Society [CRTG-00-196-01-CCE,
SIOP-06-258-01-COUN]; California Cancer Research Program
[00-01389V-20170, N01-CN25403, 2II0200]; Canadian Institutes for Health
Research; Cancer Council Victoria; Cancer Council Queensland; Cancer
Council New South Wales; Cancer Council South Australia; Cancer Council
Tasmania; Cancer Foundation of Western Australia; Cancer Institute of
New Jersey; Cancer Research UK [C490/A6187, C490/A10119, C490/A10124,
C536/A13086, C536/A6689]; Celma Mastry Ovarian Cancer Foundation; Danish
Cancer Society [94-222-52]; ELAN Program of the University of
Erlangen-Nuremberg; Eve Appeal; Helsinki University Central Hospital
Research Fund; Helse Vest; Imperial Experimental Cancer Research Centre
[C1312/A15589]; Norwegian Cancer Society; Norwegian Research Council;
Ovarian Cancer Research Fund [PPD/RPCI.07]; Nationaal Kankerplan of
Belgium; L & S Milken Foundation; Polish Ministry of Science and Higher
Education; US National Cancer Institute [K07-CA095666, K07-CA143047,
K22-CA138563, N01-CN55424, N01-PC067010, N01-PC035137, P01-CA017054,
P01-CA087696, P30-CA072720, P30-CA15083, P50-CA105009, P50-CA136393,
R01-CA014089, R01-CA016056, R01-CA017054, R01-CA049449, R01-CA050385,
R01-CA054419, R01-CA058598]; US Army Medical Research and Material
Command [DAMD17-98-1-8659, DAMD17-01-1-0729, DAMD17-02-1-0666,
DAMD17-02-1-0669, W81XWH-10-1-0280]; National Health and Medical
Research Council of Australia [199600, 400281]; German Federal Ministry
of Education and Research of Germany Programme of Clinical Biomedical
Research [01 GB 9401]; state of Baden-Wurttemberg through Medical
Faculty of the University of Ulm [P.685]; Minnesota Ovarian Cancer
Alliance; Mayo Foundation; Fred C. and Katherine B. Andersen Foundation;
Lon V. Smith Foundation [LVS-39420]; Polish Committee for Scientific
Research [4P05C 028 14, 2P05A 068 27]; Oak Foundation; OHSU Foundation;
Mermaid I project; Rudolf-Bartling Foundation; UK National Institute for
Health Research Biomedical Research Centres at the University of
Cambridge; Imperial College London; University College Hospital "Womens
Health Theme"; Royal Marsden Hospital; WorkSafeBC; European Commission
[223175-HEALTH-F2-2009-223175]; Genetic Associations and Mechanisms in
Oncology (GAME-ON): a NCI Cancer Post-GWAS Initiative [U19-CA148112];
National Health and Medical Research Council; U.S. Natl Canc Inst
[R01-095023, R01-CA106414, R01-CA122443, R01-CA61107, R01-CA112523,
R01-CA114343, R01-CA126841, R01-CA136924, R01-CA149429, R03-CA113148,
R03-CA115195, R37-CA070867, R37-CA70867, U01-CA069417, U01-CA071966]; US
Natl Canc Inst [R01-CA058860, R01-CA061107, R01-CA061132, R01-CA063682,
R01-CA064277, R01-CA067262, R01-CA071766, R01-CA074850, R01-CA076016,
R01-CA080742, R01-CA080978, R01-CA083918, R01-CA087538, R01-CA092044]
FX P.A. Fasching has a commercial research grant from Novartis and Amgen;
honoraria from speakers' bureau from Novartis, Roche; and is a
consultant/advisory board member of Novartis. A. DeFazio has honoraria
from speakers' bureau from Roche. No potential conflicts of interest
were disclosed by the other authors.; Funding of the constituent studies
was provided by the American Cancer Society (CRTG-00-196-01-CCE); the
California Cancer Research Program (00-01389V-20170, N01-CN25403,
2II0200); the Canadian Institutes for Health Research; Cancer Council
Victoria; Cancer Council Queensland; Cancer Council New South Wales;
Cancer Council South Australia; Cancer Council Tasmania; Cancer
Foundation of Western Australia; the Cancer Institute of New Jersey;
Cancer Research UK (C490/A6187, C490/A10119, C490/A10124, C536/A13086,
C536/A6689); the Celma Mastry Ovarian Cancer Foundation; the Danish
Cancer Society (94-222-52); the ELAN Program of the University of
Erlangen-Nuremberg; the Eve Appeal; the Helsinki University Central
Hospital Research Fund; Helse Vest; Imperial Experimental Cancer
Research Centre (C1312/A15589); the Norwegian Cancer Society; the
Norwegian Research Council; the Ovarian Cancer Research Fund; Nationaal
Kankerplan of Belgium; the L & S Milken Foundation; the Polish Ministry
of Science and Higher Education; the US National Cancer Institute
(K07-CA095666, K07-CA143047, K22-CA138563, N01-CN55424, N01-PC067010,
N01-PC035137, P01-CA017054, P01-CA087696, P30-CA072720, P30-CA15083,
P50-CA105009, P50-CA136393, R01-CA014089, R01-CA016056, R01-CA017054,
R01-CA049449, R01-CA050385, R01-CA054419, R01-CA058598, R01-CA058860,
R01-CA061107, R01-CA061132, R01-CA063682, R01-CA064277, R01-CA067262,
R01-CA071766, R01-CA074850, R01-CA076016, R01-CA080742, R01-CA080978,
R01-CA083918, R01-CA087538, R01-CA092044, R01-095023, R01-CA106414,
R01-CA122443, R01-CA61107, R01-CA112523, R01-CA114343, R01-CA126841,
R01-CA136924, R01-CA149429, R03-CA113148, R03-CA115195, R37-CA070867,
R37-CA70867, U01-CA069417, U01-CA071966, and Intramural research funds);
the US Army Medical Research and Material Command (DAMD17-98-1-8659,
DAMD17-01-1-0729, DAMD17-02-1-0666, DAMD17-02-1-0669, and
W81XWH-10-1-0280); the National Health and Medical Research Council of
Australia (199600 and 400281); the German Federal Ministry of Education
and Research of Germany Programme of Clinical Biomedical Research (01 GB
9401); the state of Baden-Wurttemberg through Medical Faculty of the
University of Ulm (P.685); the Minnesota Ovarian Cancer Alliance; the
Mayo Foundation; the Fred C. and Katherine B. Andersen Foundation; the
Lon V. Smith Foundation (LVS-39420); the Polish Committee for Scientific
Research (4P05C 028 14 and 2P05A 068 27); the Oak Foundation; the OHSU
Foundation; the Mermaid I project; the Rudolf-Bartling Foundation; the
UK National Institute for Health Research Biomedical Research Centres at
the University of Cambridge, Imperial College London, University College
Hospital "Womens Health Theme" and the Royal Marsden Hospital; and
WorkSafeBC. The COGS project is funded through a European Commission's
Seventh Framework Programme grant (agreement number
223175-HEALTH-F2-2009-223175). The Ovarian Cancer Association Consortium
is supported by a grant from the Ovarian Cancer Research Fund thanks to
donations by the family and friends of Kathryn Sladek Smith
(PPD/RPCI.07). The scientific development and funding for this project
were in part supported by the Genetic Associations and Mechanisms in
Oncology (GAME-ON): a NCI Cancer Post-GWAS Initiative (U19-CA148112).
G.C. Trench and P.M.W. are supported by the National Health and Medical
Research Council. B.K. holds an American Cancer Society Early Detection
Professorship (SIOP-06-258-01-COUN).
NR 8
TC 12
Z9 14
U1 0
U2 20
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 987
EP 992
DI 10.1158/1055-9965.EPI-13-0028
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200027
PM 23513043
ER
PT J
AU Hofmann, JN
Lan, Q
Cawthon, R
Hosgood, HD
Shuch, B
Moore, LE
Rothman, N
Chow, WH
Purdue, MP
AF Hofmann, Jonathan N.
Lan, Qing
Cawthon, Richard
Hosgood, H. Dean, III
Shuch, Brian
Moore, Lee E.
Rothman, Nathaniel
Chow, Wong-Ho
Purdue, Mark P.
TI A Prospective Study of Leukocyte Telomere Length and Risk of Renal Cell
Carcinoma
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID MULTIPLEX QUANTITATIVE PCR; PREDISPOSITION FACTOR; CANCER; DYSFUNCTION;
LUNG
AB Background: It has been hypothesized that genomic instability related to telomere dysfunction may contribute to carcinogenesis. There is some evidence from case-control studies suggesting that short leukocyte telomere length may be associated with an increased risk of renal cell carcinoma (RCC); however, this association has not been investigated prospectively.
Methods: We conducted a nested case-control study (209 cases, 410 controls) of RCC risk in relation to prediagnostic leukocyte telomere length in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. ORs and 95% confidence intervals (CI) were estimated using conditional logistic regression.
Results: Leukocyte telomere length was not significantly associated with future risk of RCC(highest quartile vs. lowest: OR, 0.8; 95% CI, 0.5-1.5; P-trend = 0.6). Analyses stratified by sex, age, and time from blood collection to RCC diagnosis were similarly null.
Conclusions: The results of this study, to our knowledge the first prospective investigation of its kind, do not support an association between prediagnostic leukocyte telomere length and risk of RCC.
Impact: In contrast to some earlier reports, our findings add to the evidence that leukocyte telomere length is not a biomarker of risk related to the etiology of RCC. (C) 2013 AACR.
C1 [Hofmann, Jonathan N.; Lan, Qing; Moore, Lee E.; Rothman, Nathaniel; Purdue, Mark P.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Cawthon, Richard] Univ Utah, Dept Human Genet, Salt Lake City, UT USA.
[Hosgood, H. Dean, III] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Shuch, Brian] NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chow, Wong-Ho] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
RP Hofmann, JN (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 8113, Bethesda, MD 20892 USA.
EM hofmannjn@mail.nih.gov
RI Purdue, Mark/C-9228-2016
OI Purdue, Mark/0000-0003-1177-3108
FU Division of Cancer Epidemiology and Genetics; Division of Cancer
Prevention, National Cancer Institute, NIH, Department of Health and
Human Services (DHHS)
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, NIH,
Department of Health and Human Services (DHHS).
NR 8
TC 4
Z9 4
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2013
VL 22
IS 5
BP 997
EP 1000
DI 10.1158/1055-9965.EPI-13-0142
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 143UR
UT WOS:000318894200029
PM 23513041
ER
PT J
AU Ghabril, M
Bonkovsky, HL
Kum, C
Davern, T
Hayashi, PH
Kleiner, DE
Serrano, J
Rochon, J
Fontana, RJ
Bonacini, M
AF Ghabril, Marwan
Bonkovsky, Herbert L.
Kum, Clarissa
Davern, Tim
Hayashi, Paul H.
Kleiner, David E.
Serrano, Jose
Rochon, Jim
Fontana, Robert J.
Bonacini, Maurizio
CA US Drug-Induced Liver Injury Netwo
TI Liver Injury From Tumor Necrosis Factor-alpha Antagonists: Analysis of
Thirty-four Cases
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Drug-Induced Liver Injury; Tumor Necrosis Factor; TNF-alpha Antagonists;
Hepatotoxicity; Autoimmunity
ID INDUCED AUTOIMMUNE HEPATITIS; INFLIXIMAB-INDUCED HEPATITIS;
RHEUMATOID-ARTHRITIS; CROHNS-DISEASE; ANKYLOSING-SPONDYLITIS;
PSORIATIC-ARTHRITIS; ALCOHOLIC HEPATITIS; SUCCESSFUL SWITCH; NO RELAPSE;
ETANERCEPT
AB BACKGROUND & AIMS: Tumor necrosis factor (TNF)-alpha antagonists have been associated with drug-induced liver injury (DILI). We reviewed cases of DILI in the United States to identify those associated with use of TNF-alpha antagonists.
METHODS: We searched the U.S. DILI Network (DILIN) database, from 2003 to 2011, for cases associated with TNF-alpha antagonists. Mean Roussel-Uclaf Causality Assessment Method scores were calculated. A DILIN severity score was assigned according to a previously published scale, and we identified 6 subjects likely to have DILI associated with use of TNF-alpha antagonists. We also searched PubMed for articles that reported hepatotoxicity from TNF-alpha antagonists, identifying 28 additional cases suitable for analysis.
RESULTS: The drugs presumed to have caused DILI were infliximab (n = 26), etanercept (n = 4), and adalimumab (n = 4). The anti-TNF-alpha agent was the probable cause of 12 cases of DILI (35%), a very likely cause for 21 (62%), and a definite cause for 1 (3%). Median latency was 13 weeks (range, 2-104); however, 7 cases (20%) had latency periods longer than 24 weeks. Twenty-two of 33 subjects who underwent serologic analysis (67%) tested positive for anti-nuclear and/or smooth muscle antibodies. Of these 22, 17 underwent liver biopsy; 15 subjects had clear features of autoimmunity. The 22 subjects with autoimmune features had longer median latency (16 vs 10 weeks) and higher peak levels of alanine aminotransferase (784 vs 528 U/L) than the 12 without such features. There was 1 case of severe cholestasis. All but one subject improved after discontinuation of the implicated drug; 12 subjects received corticosteroid therapy. No deaths were attributed to liver injury, although one patient with preexistent cirrhosis required liver transplantation.
CONCLUSIONS: Acute liver injury caused by TNF-alpha antagonists may be a class effect because multiple agents in this category have been implicated. The most common presentation is an autoimmune phenotype with marked hepatocellular injury, but a mixed non-autoimmune pattern or predominant cholestasis also occurs. The prognosis is usually good after drug discontinuation, although some patients may benefit from a course of corticosteroids. ClinicalTrials.gov: Number, NCT00345930
C1 [Ghabril, Marwan] Indiana Univ Sch Med, Dept Med, Indianapolis, IN USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Dept Internal Med, Cannon Res Ctr, Charlotte, NC 28203 USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Liver Biliary Pancreat Ctr, Charlotte, NC 28203 USA.
[Kum, Clarissa; Davern, Tim; Bonacini, Maurizio] Calif Pacific Med Ctr, Dept Transplantat, San Francisco, CA 94110 USA.
[Hayashi, Paul H.] Univ N Carolina, Dept Internal Med, Chapel Hill, NC USA.
[Kleiner, David E.; Serrano, Jose] NIDDKD, Liver Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Rochon, Jim] Duke Clin Res Inst, Durham, NC USA.
[Fontana, Robert J.] Univ Michigan, Med Ctr, Dept Internal Med, Ann Arbor, MI 48109 USA.
RP Bonacini, M (reprint author), Calif Pacific Med Ctr, Dept Med, 1580 Valencia St,Suite 804, San Francisco, CA 94110 USA.
EM bonacim@sutterhealth.org
OI Ghabril, Marwan/0000-0002-4784-3246
FU National Institute of Diabetes and Digestive and Kidney Diseases
[1U01DK065021, U01DK065193, 1U01DK065201, 1U01DK065193, 1U01DK065184,
1U01DK065211, 1U01DK065238, 1U01DK065176]
FX The U.S. Drug Induced Liver Injury Network (DILIN) is supported by the
National Institute of Diabetes and Digestive and Kidney Diseases under
the following cooperative agreements: 1U01DK065021, U01DK065193,
1U01DK065201, 1U01DK065193, 1U01DK065184, 1U01DK065211, 1U01DK065238,
and 1U01DK065176.
NR 45
TC 48
Z9 51
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD MAY
PY 2013
VL 11
IS 5
BP 558
EP +
DI 10.1016/j.cgh.2012.12.025
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 140UX
UT WOS:000318682600025
PM 23333219
ER
PT J
AU Spagnolo, PA
Badiani, A
Nencini, P
AF Spagnolo, Primavera A.
Badiani, Aldo
Nencini, Paolo
TI Polydrug Abuse by Intravenous Use of Heroin and Tropicamide-Containing
Eyedrops
SO CLINICAL NEUROPHARMACOLOGY
LA English
DT Review
DE tropicamide; opiates; polydrug use; antimuscarinc drugs
ID MORPHINE-WITHDRAWAL; MUSCARINIC RECEPTORS; CHOLINERGIC SYSTEMS;
EXPRESSION; SYMPTOMS; PREVENTION; ACCUMBENS; DOPAMINE; DRUGS
AB Background: Drug abuse is rarely limited to a single substance; polydrug use is the norm rather than the exception. In many cases, the misuse of potentially psychoactive substances can lead to serious intoxications and results in addictive behavior.
Case Description: A 22-year-old heroin-addicted woman presented in our clinic reporting a 2-year history of intravenous injection of an eyedrop solution containing 1% tropicamide, an antimuscarinic agent. She reported injecting tropicamide because it attenuated symptoms and signs of opiate withdrawal and it also has hallucinogenic and euphorigenic effects. Despite the large amounts (up to 1.5 g), the rapidity of injection, and the long-term use, tropicamide was relatively well tolerated, without life-threatening consequences.
An outpatient detoxification program was performed without any sign or symptom caused by discontinuing tropicamide.
Conclusions: The present case claims a role for pharmacological interactions, in addition to rewarding effects, in influencing drug association in polyabuse pattern.
Moreover, this case underlines the need for physicians to be aware of the potential emergence of tropicamide as a drug of misuse, to prevent further harm.
C1 [Spagnolo, Primavera A.] NIAAA, NIH, Bethesda, MD 20892 USA.
[Spagnolo, Primavera A.; Badiani, Aldo; Nencini, Paolo] Univ Roma La Sapienza, Dept Physiol & Pharmacol Vittorio Erspamer, Rome, Italy.
[Spagnolo, Primavera A.] Fdn Villa Maraini, Rome, Italy.
[Badiani, Aldo; Nencini, Paolo] Univ Roma La Sapienza, Univ Hosp Policlin Umberto 1, Drug Addict & Clin Pharmacol Unit, Rome, Italy.
RP Spagnolo, PA (reprint author), NIAAA, NIH, LCTS, 10 Ctr Dr 10CRC I3449, Bethesda, MD 20892 USA.
EM vera.spagnolo@nih.gov
NR 23
TC 4
Z9 4
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0362-5664
EI 1537-162X
J9 CLIN NEUROPHARMACOL
JI Clin. Neuropharmacol.
PD MAY-JUN
PY 2013
VL 36
IS 3
BP 100
EP 101
DI 10.1097/WNF.0b013e31828da20e
PG 2
WC Clinical Neurology; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 146UM
UT WOS:000319118500008
PM 23673915
ER
PT J
AU Seymour, LK
Calvert, AH
Lobbezoo, MW
Eisenhauer, EA
Giaccone, G
AF Seymour, Lesley K.
Calvert, A. Hilary
Lobbezoo, Marinus W.
Eisenhauer, Elizabeth A.
Giaccone, Giuseppe
TI Design and conduct of early clinical studies of two or more targeted
anticancer therapies: Recommendations from the task force on Methodology
for the Development of Innovative Cancer Therapies
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Combination studies; Phase I trials; Targeted therapy; Novel therapy;
Recommendations
ID RATIONAL DRUG-COMBINATIONS; RENAL-CELL CARCINOMA; PHASE-I;
ACQUIRED-RESISTANCE; AGENTS; TRIALS; BEVACIZUMAB; TUMORS
AB The Methodology for the Development of Innovative Cancer Therapies (MDICT) task force considered aspects of the design and conduct of early (phase I and II) studies of combinations of molecular targeted agents during their 2012 meeting. The task force defined necessary non-clinical data, such as evidence of additive or synergistic effects in multiple molecularly credentialed and validated models, and appropriate pharmacodynamic marker development. A robust hypothesis was considered critical while non-clinical pharmacokinetic studies were also considered valuable.
Clinical trials should include clear objectives that will prove or disprove the hypothesis. Predictive biomarkers/classifiers should be explored in phase I studies, rather than used to select patients. Trial design should be efficient and flexible rather than based on a strict progression from phase I to II to III; researchers could consider phase I studies with an expansion cohort, Phase I/II designs or phase II studies with a safety run in. Pharmacokinetics are recommended when interactions or overlapping toxicity is expected. Pharmacodynamic evaluations should be considered especially in a subset of patients closest to the recommended dose; an attempt should be made to validate surrogate tissues to enable inclusion for all patients. Schedule and or dose should be formally explored for e. g. with a randomised or an adaptive design.
Data and knowledge sharing was strongly recommended, including the creation of formal or informal consortia of laboratories with individual expertise in pathway or target based models, collaboration between companies to ensure that agents which are 'best inclass' are combined, and the development of databases which will be able to inform the development of future recommendations/guidelines. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Seymour, Lesley K.; Eisenhauer, Elizabeth A.] NCIC Clin Trials Grp, Kingston, ON K7L 3N6, Canada.
[Calvert, A. Hilary] UCL, Inst Canc, London, England.
[Giaccone, Giuseppe] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Lobbezoo, Marinus W.] NDDO Educ Fdn, Amsterdam, Netherlands.
RP Seymour, LK (reprint author), NCIC Clin Trials Grp, 10 Stuart St, Kingston, ON K7L 3N6, Canada.
EM lseymour@ctg.queensu.ca
RI Giaccone, Giuseppe/E-8297-2017
OI Giaccone, Giuseppe/0000-0002-5023-7562
FU NDDO Research Foundation (Amsterdam, The Netherlands)
FX The NDDO Research Foundation (Amsterdam, The Netherlands) is
acknowledged for its administrative and financial support to the MDICT
task force.
NR 29
TC 4
Z9 4
U1 0
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
J9 EUR J CANCER
JI Eur. J. Cancer
PD MAY
PY 2013
VL 49
IS 8
BP 1808
EP 1814
DI 10.1016/j.ejca.2013.01.014
PG 7
WC Oncology
SC Oncology
GA 139UN
UT WOS:000318610500002
PM 23428669
ER
PT J
AU Brooks, GA
Li, L
Sharma, DB
Weeks, JC
Hassett, MJ
Yabroff, KR
Schrag, D
AF Brooks, Gabriel A.
Li, Ling
Sharma, Dhruv B.
Weeks, Jane C.
Hassett, Michael J.
Yabroff, K. Robin
Schrag, Deborah
TI Regional Variation in Spending and Survival for Older Adults With
Advanced Cancer
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID OF-LIFE TREATMENT; CELL LUNG-CANCER; PALLIATIVE CARE; COMORBIDITY INDEX;
COSTS; END; INTENSITY; OUTCOMES; SATISFACTION; PREFERENCES
AB Background Medicare spending varies substantially across the United States. We evaluated the association between mean regional spending and survival in advanced cancer.
Methods We identified 116 523 subjects with advanced cancer from 2002 to 2007, using Surveillance, Epidemiology and End Results (SEER)-Medicare linked data. Subjects were aged 65 years and older with non-small cell lung, colon, breast, prostate, or pancreas cancer. Of these subjects, 61 083 had incident advanced-stage cancer (incident cohort) and 98 935 had death from cancer (decedent cohort); 37% of subjects were included in both cohorts. Subjects were linked to one of 80 hospital referral regions within SEER areas. We estimated mean regional spending in both cohorts. We assessed the primary outcome, survival, in the incident cohort; the exposure measure was the quintile of regional spending in the decedent cohort. Survival in quintiles 2 through 5 was compared with that in quintile 1 (lowest spending quintile) using Cox regression models.
Results From quintile 1 to 5, mean regional spending increased by 32% and 41% in the incident and decedent cohorts (incident cohort: $28 854 to $37 971; decedent cohort: $27 446 to $38 630). The association between spending and survival varied by cancer site and quintile; hazard ratios ranged from 0.92 (95% confidence interval [CI] = 0.82 to 1.04, pancreas cancer quintile 5) to 1.24 (95% CI = 1.11 to 1.39, breast cancer quintile 3). In most cases, differences in survival between quintile 1 and quintiles 2 through 5 were not statistically significant.
Conclusion There is substantial regional variation in Medicare spending for advanced cancer, yet no consistent association between mean regional spending and survival.
C1 [Brooks, Gabriel A.; Li, Ling; Sharma, Dhruv B.; Weeks, Jane C.; Hassett, Michael J.; Schrag, Deborah] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Yabroff, K. Robin] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Brooks, GA (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM gabrooks@partners.org
OI Brooks, Gabriel/0000-0003-3984-9995; Yabroff, K.
Robin/0000-0003-0644-5572
FU National Cancer Institute of the National Institutes of Health
[5R01CA131847, T32CA009172]
FX This work was supported by grants from the National Cancer Institute of
the National Institutes of Health (5R01CA131847 to DS, and T32CA009172,
an institutional training grant supporting GAB). Contents of this
publication are solely the responsibility of the authors and do not
necessarily represent the official views of the National Cancer
Institute or the National Institutes of Health.
NR 39
TC 33
Z9 33
U1 5
U2 13
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-J. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 9
BP 634
EP 642
DI 10.1093/jnci/djt025
PG 9
WC Oncology
SC Oncology
GA 140UK
UT WOS:000318681200010
PM 23482657
ER
PT J
AU Sahasrabuddhe, VV
Sherman, ME
AF Sahasrabuddhe, Vikrant V.
Sherman, Mark E.
TI RE: Population-Level Impact of the Bivalent, Quadrivalent, and Candidate
Nonavalent Human Papillomavirus Vaccines: A Comparative Model-Based
Analysis Response
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
C1 [Sahasrabuddhe, Vikrant V.; Sherman, Mark E.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Vanderbilt Inst Global Hlth, Nashville, TN 37212 USA.
[Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
RP Sahasrabuddhe, VV (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 5032, Rockville, MD 20852 USA.
EM vikrant.sahasrabuddhe@nih.gov
NR 7
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 9
BP 665
EP 666
DI 10.1093/jnci/djt057
PG 3
WC Oncology
SC Oncology
GA 140UK
UT WOS:000318681200015
ER
PT J
AU Sahasrabuddhe, VV
Gunja, MZ
Graubard, BI
Trabert, B
Schwartz, LM
Park, Y
Hollenbeck, AR
Freedman, ND
McGlynn, KA
AF Sahasrabuddhe, Vikrant V.
Gunja, Munira Z.
Graubard, Barry I.
Trabert, Britton
Schwartz, Lauren M.
Park, Yikyung
Hollenbeck, Albert R.
Freedman, Neal D.
McGlynn, Katherine A.
TI Re: Nonsteroidal Antiinflammatory Drug Use, Chronic Liver Disease, and
Hepatocellular Carcinoma Response
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
ID CANCER; CHEMOPREVENTION; STATINS; RISK; ASPIRIN
C1 [Sahasrabuddhe, Vikrant V.; Gunja, Munira Z.; Graubard, Barry I.; Trabert, Britton; Schwartz, Lauren M.; Park, Yikyung; Freedman, Neal D.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Vanderbilt Inst Global Hlth, Nashville, TN 37212 USA.
[Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Sahasrabuddhe, VV (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS Ste 550 Rm 5032,MSC 7234, Rockville, MD 20852 USA.
EM vikrant.sahasrabuddhe@nih.gov
RI Freedman, Neal/B-9741-2015; Trabert, Britton/F-8051-2015
OI Freedman, Neal/0000-0003-0074-1098;
FU Intramural NIH HHS [Z99 CA999999]
NR 14
TC 0
Z9 0
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD MAY
PY 2013
VL 105
IS 9
BP 668
EP 671
DI 10.1093/jnci/djt063
PG 4
WC Oncology
SC Oncology
GA 140UK
UT WOS:000318681200019
PM 23767058
ER
PT J
AU Mishra, A
AF Mishra, Amarjit
TI New insights of P2X7 receptor signaling pathway in alveolar functions
SO JOURNAL OF BIOMEDICAL SCIENCE
LA English
DT Review
ID ACUTE LUNG INJURY; T-CELL-ACTIVATION; EXTRACELLULAR ATP; P2X(7)
RECEPTOR; EPITHELIAL-CELLS; SURFACTANT SECRETION; ESCHERICHIA-COLI;
NEUTROPHIL SEQUESTRATION; NUCLEOTIDE RECEPTORS; PURINERGIC RECEPTORS
AB Purinergic P2X7 receptor (P2X7R), an ATP-gated cation channel, is unique among all other family members because of its ability to respond to various stimuli and to modulate pro-inflammatory signaling. The activation of P2X7R in immune cells is absolutely required for mature interleukin -1beta (IL-1beta) and IL-18 production and release. Lung alveoli are lined by the structural alveolar epithelial type I (AEC I) and alveolar epithelial type II cells (AEC II). AEC I plays important roles in alveolar barrier protection and fluid homeostasis whereas AEC II synthesizes and secrete surfactant and prevents alveoli from collapse. Earlier studies indicated that purinergic P2X7 receptors were specifically expressed in AEC I. However, their implication in alveolar functions has not been explored. This paper reviews two important signaling pathways of P2X7 receptors in surfactant homeostatsis and Acute Lung Injury (ALI). Thus, P2X7R resides at the critical nexus of alveolar pathophysiology.
C1 NIH, Bethesda, MD 20892 USA.
RP Mishra, A (reprint author), NIH, 10 Ctr Dr,Bldg 10, Bethesda, MD 20892 USA.
EM amarjitmisra@gmail.com
FU Center for Veterinary Health Sciences, Oklahoma State University,
Stillwater, USA
FX This work was partly supported by Center for Veterinary Health Sciences,
Oklahoma State University, Stillwater, USA.
NR 70
TC 4
Z9 4
U1 0
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1021-7770
EI 1423-0127
J9 J BIOMED SCI
JI J. Biomed. Sci.
PD MAY 1
PY 2013
VL 20
AR 26
DI 10.1186/1423-0127-20-26
PG 6
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 143NY
UT WOS:000318875500001
PM 23634990
ER
PT J
AU Yamashita, T
Wang, XW
AF Yamashita, Taro
Wang, Xin Wei
TI Cancer stem cells in the development of liver cancer
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Review
ID HUMAN HEPATOCELLULAR-CARCINOMA; HEPATIC PROGENITOR CELLS;
TUMOR-INITIATING CELLS; GROWTH-FACTOR-BETA; EPITHELIAL-MESENCHYMAL
TRANSITION; ACUTE MYELOID-LEUKEMIA; VIRUS CORE PROTEIN; ADULT-MOUSE
LIVER; SELF-RENEWAL; STEM/PROGENITOR CELLS
AB Liver cancer is an aggressive disease with a poor outcome. Several hepatic stem/progenitor markers are useful for isolating a subset of liver cells with stem cell features, known as cancer stem cells (CSCs). These cells are responsible for tumor relapse, metastasis, and chemoresistance. Liver CSCs dictate a hierarchical organization that is shared in both organogenesis and tumorigenesis. An increased understanding of the molecular signaling events that regulate cellular hierarchy and sternness, and success in defining key CSC-specific genes, have opened up new avenues to accelerate the development of novel diagnostic and treatment strategies. This Review highlights recent advances in understanding the pathogenesis of liver CSCs and discusses unanswered questions about the concept of liver CSCs.
C1 [Yamashita, Taro] Kanazawa Univ Hosp, Dept Gen Med, Kanazawa, Ishikawa 9208641, Japan.
[Wang, Xin Wei] NCI, Lab Human Carcinogenesis, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Yamashita, T (reprint author), Kanazawa Univ Hosp, Dept Gen Med, Kanazawa, Ishikawa 9208641, Japan.
EM taroy@m-kanazawa.jp; xw3u@nih.gov
RI Wang, Xin/B-6162-2009
FU Ministry of Education, Culture, Sports, Science and Technology; National
Cancer Center Research and Development Fund of Japan; Intramural
Research Program of the Center for Cancer Research, US National Cancer
Institute [Z01 BC010876]
FX We apologize to those investigators whose original works were not cited
due to space limitations. T. Yamashita is supported by a grant from the
Ministry of Education, Culture, Sports, Science and Technology and the
National Cancer Center Research and Development Fund of Japan. X.W. Wang
is supported by the Intramural Research Program of the Center for Cancer
Research, US National Cancer Institute (grant Z01 BC010876).
NR 150
TC 130
Z9 139
U1 7
U2 57
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 MAY
PY 2013
VL 123
IS 5
BP 1911
EP 1918
DI 10.1172/JCI66024
PG 8
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 145OA
UT WOS:000319025100010
PM 23635789
ER
PT J
AU Winkler, T
Hong, SG
Decker, JE
Morgan, MJ
Wu, CF
Hughes, WM
Yang, YQ
Wangsa, D
Padilla-Nash, HM
Ried, T
Young, NS
Dunbar, CE
Calado, RT
AF Winkler, Thomas
Hong, So Gun
Decker, Jake E.
Morgan, Mary J.
Wu, Chuanfeng
Hughes, William M.
Yang, Yanqin
Wangsa, Danny
Padilla-Nash, Hesed M.
Ried, Thomas
Young, Neal S.
Dunbar, Cynthia E.
Calado, Rodrigo T.
TI Defective telomere elongation and hematopoiesis from telomerase-mutant
aplastic anemia iPSCs
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; DYSKERATOSIS-CONGENITA; PULMONARY-FIBROSIS;
REVERSE-TRANSCRIPTASE; HUMAN FIBROBLASTS; DEFINED FACTORS; MUTATIONS;
DIFFERENTIATION; GENERATION; DISEASE
AB Critically short telomeres activate p53-mediated apoptosis, resulting in organ failure and leading to malignant transformation. Mutations in genes responsible for telomere maintenance are linked to a number of human diseases. We derived induced pluripotent stem cells (iPSCs) from 4 patients with aplastic anemia or hypocellular bone marrow carrying heterozygous mutations in the telomerase reverse transcriptase (TERT) or the telomerase RNA component (TERC) telomerase genes. Both mutant and control iPSCs upregulatecl TERT and TERC expression compared with parental fibroblasts, but mutant iPSCs elongated telomeres at a lower rate compared with healthy iPSCs, and the deficit correlated with the mutations' impact on telomerase activity. There was no evidence for alternative lengthening of telomere (ALT) pathway activation. Elongation varied among iPSC clones derived from the same patient and among clones from siblings harboring identical mutations. Clonal heterogeneity was linked to genetic and environmental factors, but was not influenced by residual expression of reprogramming transgenes. Hypoxia increased telomere extension in both mutant and normal iPSCs. Additionally, telomerase-mutant iPSCs showed defective hematopoietic differentiation in vitro, mirroring the clinical phenotype observed in patients and demonstrating that human telomere diseases can be modeled utilizing iPSCs. Our data support the necessity of studying multiple clones when using iPSCs to model disease.
C1 [Winkler, Thomas; Hong, So Gun; Decker, Jake E.; Morgan, Mary J.; Wu, Chuanfeng; Hughes, William M.; Young, Neal S.; Dunbar, Cynthia E.; Calado, Rodrigo T.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Decker, Jake E.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Yang, Yanqin] NHLBI, DNA Sequencing & Genom Core Facil, Bethesda, MD 20892 USA.
[Wangsa, Danny; Padilla-Nash, Hesed M.; Ried, Thomas] NCI, Sect Canc Genom, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Calado, Rodrigo T.] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Internal Med, Sao Paulo, Brazil.
RP Dunbar, CE (reprint author), NHLBI, Hematol Branch, NIH, 10 Ctr Dr,Bldg 10 CRC,Rm 4E-5132, Bethesda, MD 20892 USA.
EM dunbarc@nhlbi.nih.gov
RI Terapia celular, Cepid/I-4398-2013; Calado, Rodrigo/G-2619-2011; Wu,
Chuanfeng/A-1109-2016
FU Divisions of Intramural Research at the NHLBI; National Human Genome
Research Institute; National Cancer Institute; National Center for
Regenerative Medicine at the NIH; FAPESP [98/14247-6]
FX This research was supported by the Divisions of Intramural Research at
the NHLBI, the National Human Genome Research Institute, the National
Cancer Institute, and the National Center for Regenerative Medicine at
the NIH. R.T. Calado was supported by a FAPESP (grant 98/14247-6). The
authors have no conflicts of interest to declare. We would like to thank
Jichun Chen, Marie Desierto, and Zu Xi Yu from the NHLBI pathology core
facility for their support during the teratoma assays. We thank Dara
Wangsa for providing the probes for SKY analysis and Vicky Guo for
assisting with the iPSC culture. We are also grateful to Sachiko
Kajigaya for her excellent technical support.
NR 51
TC 30
Z9 34
U1 2
U2 11
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD MAY
PY 2013
VL 123
IS 5
BP 1952
EP 1963
DI 10.1172/JCI67146
PG 12
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 145OA
UT WOS:000319025100019
PM 23585473
ER
PT J
AU Gilchuk, P
Spencer, CT
Conant, SB
Hill, T
Gray, JJ
Niu, XN
Zheng, M
Erickson, JJ
Boyd, KL
McAfee, KJ
Oseroff, C
Hadrup, SR
Bennink, JR
Hildebrand, W
Edwards, KM
Crowe, JE
Williams, JV
Buus, S
Sette, A
Schumacher, TNM
Link, AJ
Joyce, S
AF Gilchuk, Pavlo
Spencer, Charles T.
Conant, Stephanie B.
Hill, Timothy
Gray, Jennifer J.
Niu, Xinnan
Zheng, Mu
Erickson, John J.
Boyd, Kelli L.
McAfee, K. Jill
Oseroff, Carla
Hadrup, Sine R.
Bennink, Jack R.
Hildebrand, William
Edwards, Kathryn M.
Crowe, James E., Jr.
Williams, John V.
Buus, Soren
Sette, Alessandro
Schumacher, Ton N. M.
Link, Andrew J.
Joyce, Sebastian
TI Discovering naturally processed antigenic determinants that confer
protective T cell immunity
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID HLA-B-ASTERISK-0702 TRANSGENIC MICE; VACCINIA VIRUS; MALARIA VACCINE;
IN-VIVO; MEDIATED PROTECTION; RESPONSE MAGNITUDE; SMALLPOX VACCINES;
MASS-SPECTROMETRY; MEMORY; PROTEIN
AB CD8(+) T cells (TCD8) confer protective immunity against many infectious diseases, suggesting that microbial TCD8 determinants are promising vaccine targets. Nevertheless, current T cell antigen identification approaches do not discern which epitopes drive protective immunity during active infection information that is critical for the rational design of TCD8-targeted vaccines. We employed a proteomics-based approach for large-scale discovery of naturally processed determinants derived from a complex pathogen, vaccinia virus (VACV), that are presented by the most frequent representatives of four major HLA class I supertypes. Immunologic characterization revealed that many previously unidentified VACV determinants were recognized by smallpox-vaccinated human peripheral blood cells in a variegated manner. Many such determinants were recognized by HLA class I-transgenic mouse immune TCD8 too and elicited protective TCD8 immunity against lethal intranasal VACV infection. Notably, efficient processing and stable presentation of immune determinants as well as the availability of naive TCD8 precursors were sufficient to drive a multifunctional, protective TCD8 response. Our approach uses fundamental insights into T cell epitope processing and presentation to define targets of protective TCD8 immunity within human pathogens that have complex proteomes, suggesting that this approach has general applicability in vaccine sciences.
C1 [Gilchuk, Pavlo; Spencer, Charles T.; Conant, Stephanie B.; Hill, Timothy; Gray, Jennifer J.; Niu, Xinnan; Zheng, Mu; Erickson, John J.; Boyd, Kelli L.; McAfee, K. Jill; Crowe, James E., Jr.; Williams, John V.; Link, Andrew J.; Joyce, Sebastian] Vanderbilt Univ, Sch Med, Dept Pathol Microbiol & Immunol, Nashville, TN 37232 USA.
[Oseroff, Carla; Sette, Alessandro] La Jolla Inst Allergy & Immunol, Ctr Infect Dis Allergy & Asthma Res, La Jolla, CA USA.
[Hadrup, Sine R.] Herlev Hosp, Dept Hematol, Ctr Canc Immunotherapy, DK-2730 Herlev, Denmark.
[Bennink, Jack R.] NIAID, Cellular Biol & Viral Immunol Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Hildebrand, William] Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Oklahoma City, OK 73190 USA.
[Edwards, Kathryn M.; Crowe, James E., Jr.; Williams, John V.] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37232 USA.
[Buus, Soren] Univ Copenhagen, Lab Expt Immunol, Copenhagen, Denmark.
[Schumacher, Ton N. M.] Netherlands Canc Inst, Div Immunol, NL-1066 CX Amsterdam, Netherlands.
[Link, Andrew J.] Vanderbilt Univ, Sch Med, Dept Biochem, Nashville, TN 37232 USA.
RP Joyce, S (reprint author), Vanderbilt Univ, Sch Med, Dept Pathol Microbiol & Immunol, A4223 Med Ctr North,1161 21st Ave South, Nashville, TN 37232 USA.
EM sebastian.joyce@vanderbilt.edu
RI Spencer, Charles/J-6489-2012; spencer, charles/B-9411-2014; Crowe,
James/B-5549-2009; Hadrup, Sine Reker/P-3388-2014; Buus,
Soren/F-5446-2010; Williams, John/F-6962-2010;
OI Crowe, James/0000-0002-0049-1079; Hadrup, Sine
Reker/0000-0002-5937-4344; Williams, John/0000-0001-8377-5175; Buus,
Soren/0000-0001-8363-1999
FU NIH [NO1 AI040079, AI0400024, AI025462, HL054977, AI042284, AI061721,
CA068485, DK058404, RR024975]; NIAID Intramural Program
FX We dedicate this work to the memory of late Professor Stanley G.
Nathenson whose numerous pioneering works laid foundation to this line
of research. We thank J.S. Bezbradica and Luc Van Kaer for critical
reading and advice on the manuscript as well as J.W. Yewdell for helpful
discussions on the project. This work was supported by contracts (NO1
AI040079, AI0400024, AI025462), research grants (HL054977, AI042284,
AI061721), and core grants (CA068485, DK058404, RR024975) from the NIH
and the NIAID Intramural Program.
NR 68
TC 23
Z9 23
U1 0
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
J9 J CLIN INVEST
JI J. Clin. Invest.
PD MAY
PY 2013
VL 123
IS 5
BP 1976
EP 1987
DI 10.1172/JCI67388
PG 12
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 145OA
UT WOS:000319025100021
PM 23543059
ER
PT J
AU Moreno-Smith, M
Halder, JB
Meltzer, PS
Gonda, TA
Mangala, LS
Rupaimoole, R
Lu, CH
Nagaraja, AS
Gharpure, KM
Kang, Y
Rodriguez-Aguayo, C
Vivas-Mejia, PE
Zand, B
Schmandt, R
Wang, H
Langley, RR
Jennings, NB
Ivan, C
Coffin, JE
Armaiz, GN
Bottsford-Miller, J
Kim, SB
Halleck, MS
Hendrix, MJC
Bornman, W
Bar-Eli, M
Lee, JS
Siddik, ZH
Lopez-Berestein, G
Sood, AK
AF Moreno-Smith, Myrthala
Halder, J. B.
Meltzer, Paul S.
Gonda, Tamas A.
Mangala, Lingegowda S.
Rupaimoole, Rajesha
Lu, Chunhua
Nagaraja, Archana S.
Gharpure, Kshipra M.
Kang, Yu
Rodriguez-Aguayo, Cristian
Vivas-Mejia, Pablo E.
Zand, Behrouz
Schmandt, Rosemarie
Wang, Hua
Langley, Robert R.
Jennings, Nicholas B.
Ivan, Cristina
Coffin, Jeremy E.
Armaiz, Guillermo N.
Bottsford-Miller, Justin
Kim, Sang Bae
Halleck, Margaret S.
Hendrix, Mary J. C.
Bornman, William
Bar-Eli, Menashe
Lee, Ju-Seog
Siddik, Zahid H.
Lopez-Berestein, Gabriel
Sood, Anil K.
TI ATP11B mediates platinum resistance in ovarian cancer
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID P-TYPE ATPASES; TRANS-GOLGI NETWORK; ADENOCARCINOMA CELL-LINES;
CARCINOMA CELLS; AMINOPHOSPHOLIPID TRANSLOCASE; CISPLATIN RESISTANCE;
BIOLOGICAL FUNCTIONS; VESICLE TRAFFICKING; TRANSPORTER ATP7B;
DRUG-RESISTANCE
AB Platinum compounds display clinical activity against a wide variety of solid tumors; however, resistance to these agents is a major limitation in cancer therapy. Reduced platinum uptake and increased platinum export are examples of resistance mechanisms that limit the extent of DNA damage. Here, we report the discovery and characterization of the role of ATP11B, a P-type ATPase membrane protein, in cisplatin resistance. We found that ATP11B expression was correlated with higher tumor grade in human ovarian cancer samples and with cisplatin resistance in human ovarian cancer cell lines. ATP11B gene silencing restored the sensitivity of ovarian cancer cell lines to cisplatin in vitro. Combined therapy of cisplatin and ATP11B-targeted siRNA significantly decreased cancer growth in mice bearing ovarian tumors derived from cisplatin-sensitive and -resistant cells. In vitro mechanistic studies on cellular platinum content and cisplatin efflux kinetics indicated that ATP11B enhances the export of cisplatin from cells. The colocalization of ATP11B with fluorescent cisplatin and with vesicular trafficking proteins, such as syntaxin-6 (STX6) and vesicular-associated membrane protein 4 (VAMP4), strongly suggests that ATP11B contributes to secretory vesicular transport of cisplatin from Golgi to plasma membrane. In conclusion, inhibition of ATP11B expression could serve as a therapeutic strategy to overcome cisplatin resistance.
C1 [Moreno-Smith, Myrthala; Halder, J. B.; Rupaimoole, Rajesha; Lu, Chunhua; Nagaraja, Archana S.; Gharpure, Kshipra M.; Kang, Yu; Zand, Behrouz; Schmandt, Rosemarie; Jennings, Nicholas B.; Armaiz, Guillermo N.; Bottsford-Miller, Justin; Sood, Anil K.] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA.
[Meltzer, Paul S.] NCI, Ctr Canc Res, Genet Branch, Bethesda, MD 20892 USA.
[Gonda, Tamas A.] Columbia Univ, Dept Med, New York, NY USA.
[Mangala, Lingegowda S.; Ivan, Cristina; Lopez-Berestein, Gabriel; Sood, Anil K.] Univ Texas MD Anderson Canc Ctr, Ctr RNA Interference & Noncoding RNA, Houston, TX 77030 USA.
[Rodriguez-Aguayo, Cristian; Bornman, William; Siddik, Zahid H.; Lopez-Berestein, Gabriel] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA.
[Vivas-Mejia, Pablo E.] Univ Puerto Rico, Dept Biochem, San Juan, PR 00936 USA.
[Vivas-Mejia, Pablo E.] Univ Puerto Rico, Ctr Canc, San Juan, PR 00936 USA.
[Wang, Hua; Langley, Robert R.; Bar-Eli, Menashe; Sood, Anil K.] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA.
[Coffin, Jeremy E.] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA.
[Kim, Sang Bae; Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
[Halleck, Margaret S.] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
[Hendrix, Mary J. C.] Northwestern Univ, Feinberg Sch Med, Childrens Mem Res Ctr, Chicago, IL 60611 USA.
RP Sood, AK (reprint author), Univ Texas MD Anderson Canc Ctr, 1155 Herman Pressler,Unit 1362, Houston, TX 77030 USA.
EM asood@mdanderson.org
RI rupaimoole, rajesha/K-3272-2016;
OI rupaimoole, rajesha/0000-0002-4795-7921; Armaiz-Pena, Guillermo
N/0000-0002-9081-5339; Nagaraja, Archana/0000-0002-2851-9272; Gharpure,
Kshipra/0000-0003-4954-5696
FU CPRIT [RP110595-P2]; Gynecologic Cancer Foundation; National Institutes
of Health [CA109298, P50 CA083639, P50 CA098258, CA128797, RC2GM092599,
U54 CA151668]; Program Project Development Grant from the Ovarian Cancer
Research Fund; Department of Defense [00073399, W81XWH-10-1-0158,
BC085265]; Baylor College of Medicine; MD Anderson Cancer Center
Multidisciplinary Research Program; Zarrow Foundation; Marcus
Foundation; Estate of C.G. Johnson Jr.; Blanton-Davis Ovarian Cancer
Research Program; Gilder Foundation; RGK Foundation; Bettyann Asche
Murray Distinguished Professorship; National Cancer Institute [T32
CA101642]
FX The authors thank Svetlana Lutsenko for helpful discussions and
guidance. We also thank Michael White (UT Southwestern Medical Center)
for providing the patient cell lines and Donna Reynolds for assistance
with immunohistochemistry. This work was supported in part by grants
from the CPRIT (RP110595-P2), Gynecologic Cancer Foundation; grants
(CA109298, P50 CA083639, P50 CA098258, CA128797, RC2GM092599, U54
CA151668) from the National Institutes of Health; a Program Project
Development Grant from the Ovarian Cancer Research Fund; grants
(00073399, W81XWH-10-1-0158, and BC085265) from the Department of
Defense; the Baylor College of Medicine and MD Anderson Cancer Center
Multidisciplinary Research Program; the Zarrow Foundation; the Marcus
Foundation; the Estate of C.G. Johnson Jr.; the Blanton-Davis Ovarian
Cancer Research Program; the Gilder Foundation; the RGK Foundation; the
Bettyann Asche Murray Distinguished Professorship; and a training grant
(T32 CA101642 supported J. Bottsford-Miller) from the National Cancer
Institute.
NR 49
TC 24
Z9 25
U1 0
U2 23
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD MAY
PY 2013
VL 123
IS 5
BP 2119
EP 2130
DI 10.1172/JCI65425
PG 12
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 145OA
UT WOS:000319025100032
PM 23585472
ER
PT J
AU Ramirez, AS
Freres, D
Martinez, LS
Lewis, N
Bourgoin, A
Kelly, BJ
Lee, CJ
Nagler, R
Schwartz, JS
Hornik, RC
AF Ramirez, A. Susana
Freres, Derek
Martinez, Lourdes S.
Lewis, Nehama
Bourgoin, Angel
Kelly, Bridget J.
Lee, Chul-Joo
Nagler, Rebekah
Schwartz, J. Sanford
Hornik, Robert C.
TI Information Seeking From Media and Family/Friends Increases the
Likelihood of Engaging in Healthy Lifestyle Behaviors
SO JOURNAL OF HEALTH COMMUNICATION
LA English
DT Article
ID CANCER NEWS COVERAGE; PLANNED BEHAVIOR; PHYSICAL-ACTIVITY;
UNITED-STATES; PREVENTION; INTENTION; SERVICE; RISK; VARIABLES
AB The amount of cancer-related information available to the general population continues to grow; yet, its effects are unclear. This study extends previous cross-sectional research establishing that cancer information seeking across a variety of sources is extensive and positively associated with engaging in health-related behaviors. The authors studied how active information seeking about cancer prevention influenced three healthy lifestyle behaviors using a 2-round nationally representative sample of adults ages 4070 years (n=1,795), using propensity scoring to control for potential confounders including baseline behavior. The adjusted odds of dieting at follow-up were 1.51 (95% CI: 1.05, 2.19) times higher for those who reported baseline seeking from media and interpersonal sources relative to nonseekers. Baseline seekers ate 0.59 (95% CI: 0.28, 0.91) more fruits and vegetable servings per day and exercised 0.36 (95% CI: 0.12, 0.60) more days per week at 1-year follow-up compared with nonseekers. The effects of seeking from media and friends/family on eating fruits and vegetables and exercising were independent of seeking from physicians. The authors offer several explanations for why information seeking predicts healthy lifestyle behaviors: information obtained motivates these behaviors; information sought teaches specific techniques; and the act of information seeking may reinforce a psychological commitment to dieting, eating fruits and vegetables, and exercising.
C1 [Ramirez, A. Susana] NCI, Canc Prevent Fellowship Program, Bethesda, MD 20892 USA.
[Freres, Derek; Bourgoin, Angel; Hornik, Robert C.] Univ Penn, Annenberg Sch Commun, Ctr Excellence Canc Commun Res, Philadelphia, PA 19104 USA.
[Martinez, Lourdes S.] Michigan State Univ, E Lansing, MI 48824 USA.
[Lewis, Nehama] Florida Int Univ, Miami, FL 33199 USA.
[Kelly, Bridget J.] RTI Int, Washington, DC USA.
[Lee, Chul-Joo] Ohio State Univ, Sch Commun, Columbus, OH 43210 USA.
[Nagler, Rebekah] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schwartz, J. Sanford] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Schwartz, J. Sanford] Univ Penn, Wharton Sch, Philadelphia, PA 19104 USA.
RP Ramirez, AS (reprint author), NCI, Canc Prevent Fellowship Program, 6130 Execut Blvd,Room 4051A, Bethesda, MD 20892 USA.
EM a.susana.ramirez@gmail.com
OI Hornik, Robert/0000-0002-2148-8805
FU NCI NIH HHS [P20 CA095856, P50 CA095856, P50-CA095856-05]
NR 42
TC 18
Z9 19
U1 3
U2 27
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 CHESTNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1081-0730
EI 1087-0415
J9 J HEALTH COMMUN
JI J. Health Commun.
PD MAY 1
PY 2013
VL 18
IS 5
BP 527
EP 542
DI 10.1080/10810730.2012.743632
PG 16
WC Communication; Information Science & Library Science
SC Communication; Information Science & Library Science
GA 136HO
UT WOS:000318353200004
PM 23472825
ER
PT J
AU Marcus, AC
Diefenbach, MA
Stanton, AL
Miller, SM
Fleisher, L
Raich, PC
Morra, ME
Perocchia, RS
Tran, ZV
Bright, MA
AF Marcus, Alfred C.
Diefenbach, Michael A.
Stanton, Annette L.
Miller, Suzanne M.
Fleisher, Linda
Raich, Peter C.
Morra, Marion E.
Perocchia, Rosemarie Slevin
Zung Vu Tran
Bright, Mary Anne
TI Cancer Patient and Survivor Research From the Cancer Information Service
Research Consortium: A Preview of Three Large Randomized Trials and
Initial Lessons Learned
SO JOURNAL OF HEALTH COMMUNICATION
LA English
DT Article
ID QUALITY-OF-LIFE; STAGE BREAST-CANCER; CONSERVING SURGICAL-PROCEDURES;
TREATMENT DECISION-MAKING; PROSTATE-CANCER; FUNCTIONAL ASSESSMENT;
HEALTH-CARE; PSYCHOMETRIC PROPERTIES; EDUCATION MATERIALS; BEHAVIORAL
CHANGE
AB The authors describe 3 large randomized trials from the Cancer Information Service Research Consortium. Three web-based multimedia programs are being tested to help newly diagnosed prostate (Project 1) and breast cancer patients (Project 2) make informed treatment decisions and breast cancer patients prepare for life after treatment (Project 3). Project 3 also tests a telephone callback intervention delivered by a cancer information specialist. All participants receive standard print material specific to each project. Preliminary results from the 2-month follow-up interviews are reported for the initial wave of enrolled participants, most of whom were recruited from the Cancer Information Service (1-800-4-CANCER) telephone information program (Project 1: n =208; Project 2: n =340; Project 3: n =792). Self-reported use of the multimedia program was 51%, 52%, and 67% for Projects 1, 2, and 3, respectively. Self-reported use of the print materials (read all, most, or some) was 90%, 85%, and 83% for Projects 1, 2, and 3, respectively. The callback intervention was completed by 92% of Project 3 participants. Among those using the Cancer Information Service Research Consortium interventions, perceived usefulness and benefit was high, and more than 90% reported that they would recommend them to other cancer patients. The authors present 5 initial lessons learned that may help inform future cancer communications research.
C1 [Marcus, Alfred C.; Zung Vu Tran] Univ Colorado, Ctr Canc, Denver, CO 80262 USA.
[Diefenbach, Michael A.] Mt Sinai Sch Med, New York, NY USA.
[Stanton, Annette L.] Univ Calif Los Angeles, Dept Psychol, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
[Stanton, Annette L.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Dept Psychiat Biobehav Sci, Los Angeles, CA 90024 USA.
[Miller, Suzanne M.; Fleisher, Linda] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Raich, Peter C.] Denver Hlth & Hosp Author, Denver, CO USA.
[Morra, Marion E.] Yale Univ, Sch Nursing, New Haven, CT 06536 USA.
[Perocchia, Rosemarie Slevin] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Bright, Mary Anne] NCI, Canc Informat Serv, Bethesda, MD 20892 USA.
RP Marcus, AC (reprint author), Univ Colorado, Ctr Canc, 12474 E 19th Ave,Mail Stop F427,Room 141, Aurora, CO 80045 USA.
EM al.marcus@ucdenver.edu
OI Tran, Zung/0000-0002-9322-9562
FU NCI NIH HHS [5P01CA057586, P01 CA057586, P30 CA006927, P30 CA046934,
P30CA06927]
NR 94
TC 10
Z9 10
U1 1
U2 11
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 1081-0730
J9 J HEALTH COMMUN
JI J. Health Commun.
PD MAY 1
PY 2013
VL 18
IS 5
BP 543
EP 562
DI 10.1080/10810730.2012.743629
PG 20
WC Communication; Information Science & Library Science
SC Communication; Information Science & Library Science
GA 136HO
UT WOS:000318353200005
PM 23448232
ER
PT J
AU Vogel, KR
Pearl, PL
Theodore, WH
McCarter, RC
Jakobs, C
Gibson, KM
AF Vogel, Kara R.
Pearl, Phillip L.
Theodore, William H.
McCarter, Robert C.
Jakobs, Cornelis
Gibson, K. Michael
TI Thirty years beyond discovery-Clinical trials in succinic semialdehyde
dehydrogenase deficiency, a disorder of GABA metabolism
SO JOURNAL OF INHERITED METABOLIC DISEASE
LA English
DT Article; Proceedings Paper
CT Farewell Symposium Cornelis Jakobs
CY NOV 25, 2011
CL Amsterdam, NETHERLANDS
SP Pediat Neurotransmitter Dis Assoc
ID GAMMA-HYDROXYBUTYRIC ACID; CENTRAL-NERVOUS-SYSTEM; VISUAL-FIELD DEFECTS;
4-HYDROXYBUTYRIC ACIDURIA; VIGABATRIN THERAPY; MICE DEFICIENT; SSADH
DEFICIENCY; INBORN ERROR; ORNITHINE AMINOTRANSFERASE;
GLUTAMATE-DECARBOXYLASE
AB This review summarizes a presentation made at the retirement Symposium of Prof. Dr. Cornelis Jakobs in November of 2011, highlighting the progress toward clinical trials in succinic semialdehyde dehydrogenase (SSADH) deficiency, a disorder first recognized in 1981. Active and potential clinical interventions, including vigabatrin, L-cycloserine, the GHB receptor antagonist NCS-382, and the ketogenic diet, are discussed. Several biomarkers to gauge clinical efficacy have been identified, including cerebrospinal fluid metabolites, neuropsychiatric testing, MRI, EEG, and measures of GABAergic function including (11 C)flumazenil positron emission tomography (PET) and transcranial magnetic stimulation (TMS). Thirty years after its discovery, encompassing extensive studies in both patients and the corresponding murine model, we are now running an open-label trial of taurine intervention, and are poised to undertake a phase II trial of the GABA(B) receptor antagonist SGS742.
C1 [Vogel, Kara R.; Gibson, K. Michael] Washington State Univ, Coll Pharm, Clin Pharmacol Sect, Spokane, WA 99202 USA.
[Pearl, Phillip L.] Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
[Pearl, Phillip L.; McCarter, Robert C.] George Washington Univ, Sch Med, Washington, DC USA.
[Theodore, William H.] NINDS, Sect Clin Epilepsy, NIH, Bethesda, MD 20892 USA.
[McCarter, Robert C.] Childrens Natl Med Ctr, Dept Epidemiol & Biostat, Childrens Res Inst, Washington, DC 20010 USA.
[Jakobs, Cornelis] Vrije Univ Amsterdam, Med Ctr, Dept Clin Chem, Amsterdam, Netherlands.
RP Vogel, KR (reprint author), Washington State Univ, Coll Pharm, Clin Pharmacol Sect, SAC 520,412 E Spokane Falls Blvd, Spokane, WA 99202 USA.
EM k.vogel@wsu.edu; mike.gibson@wsu.edu
FU NCRR NIH HHS [UL1 RR031988, UL1RR031988]; NICHD NIH HHS [P30 HD040677,
HD 58553, P30HD40677, R01 HD058553]
NR 83
TC 16
Z9 16
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0141-8955
EI 1573-2665
J9 J INHERIT METAB DIS
JI J. Inherit. Metab. Dis.
PD MAY
PY 2013
VL 36
IS 3
BP 401
EP 410
DI 10.1007/s10545-012-9499-5
PG 10
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 143OV
UT WOS:000318877900001
PM 22739941
ER
PT J
AU Brady, RO
Yang, CZ
Zhuang, ZP
AF Brady, Roscoe O.
Yang, Chunzhang
Zhuang, Zhengping
TI An innovative approach to the treatment of Gaucher disease and possibly
other metabolic disorders of the brain
SO JOURNAL OF INHERITED METABOLIC DISEASE
LA English
DT Article; Proceedings Paper
CT Brains for Brain Meeting
CY MAR 09-11, 2012
CL Frankfurt, GERMANY
ID MACROPHAGE-TARGETED GLUCOCEREBROSIDASE; HISTONE DEACETYLASE INHIBITORS;
REPLACEMENT-THERAPY; BARRIER; CHOLESTEROL; DEFICIENCY; RESTORE; VII
AB The extraordinary benefit of enzyme replacement therapy (ERT) on the systemic manifestations of Gaucher disease was demonstrated in 1991. Since that time, investigators have devoted substantial effort to improve the delivery of enzymes to the brain because many hereditary metabolic disorders are characterized by extensive central nervous system involvement. Because the required supplemental enzyme is too large to cross the blood-brain barrier (BBB), ERT for central nervous system involvement was out of the question at that time. Several innovative strategies that have been reported to overcome this impediment are discussed. Recent investigations have provided additional insight concerning the pathogenesis of enzyme deficiency disorders. For many years it was presumed that alterations of the amino acid sequence of enzymes such as glucocerebrosidase reduced the catalytic activity of the enzyme. It has recently been shown that the decrease of glucocerebrosidase activity was the result of a quantitative loss of the amount of this enzyme. Significant increases of its activity were obtained with small molecule inhibitors of histone deacetylase that cross the BBB. The effect of such materials on neuronopathic Gaucher disease and other CNS metabolic disorders is discussed.
C1 [Brady, Roscoe O.] NIH, Bethesda, MD 20892 USA.
[Yang, Chunzhang; Zhuang, Zhengping] NIH, Surg Neurol Branch, Bethesda, MD 20892 USA.
RP Brady, RO (reprint author), NIH, Bldg 10 Room 3D03, Bethesda, MD 20892 USA.
EM bradyr@ninds.nih.gov; yangc2@ninds.nih.gov; ZhuangP@ninds.nih.gov
FU Intramural NIH HHS [Z99 NS999999]
NR 20
TC 7
Z9 7
U1 1
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0141-8955
EI 1573-2665
J9 J INHERIT METAB DIS
JI J. Inherit. Metab. Dis.
PD MAY
PY 2013
VL 36
IS 3
BP 451
EP 454
DI 10.1007/s10545-012-9515-9
PG 4
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 143OV
UT WOS:000318877900006
PM 22814681
ER
PT J
AU Butail, S
Manoukis, NC
Diallo, M
Ribeiro, JMC
Paley, DA
AF Butail, Sachit
Manoukis, Nicholas C.
Diallo, Moussa
Ribeiro, Jose M. C.
Paley, Derek A.
TI The Dance of Male Anopheles gambiae in Wild Mating Swarms
SO JOURNAL OF MEDICAL ENTOMOLOGY
LA English
DT Article
DE swarming; Anopheles gambiae; autocorrelation
ID REPRODUCTIVE ISOLATION; BEHAVIOR; MOSQUITOS; FORMS; MODEL
AB An important element of mating in the malaria vector Anopheles gambiae Giles in nature is the crepuscular mating aggregation (swarm) composed almost entirely of males, where most coupling and insemination is generally believed to occur. In this study, we mathematically characterize the oscillatory movement of male An. gambiae in terms of an established individual-based mechanistic model that parameterizes the attraction of a mosquito toward the center of the swarm using the natural frequency of oscillation and the resistance to its motion, characterized by the damping ratio. Using three-dimensional trajectory data of ten wild mosquito swarms filmed in Mali, Africa, we show two new results for low and moderate wind conditions, and indicate how these results may vary in high wind. First, we show that in low and moderate wind the vertical component of the mosquito motion has a lower frequency of oscillation and higher damping ratio than horizontal motion. In high wind, the vertical and horizontal motions are similar to one another and the natural frequencies are higher than in low and moderate wind. Second, we show that the predicted average disagreement in the direction of motion of swarming mosquitoes moving randomly is greater than the average disagreement we observed between each mosquito and its three closest neighbors, with the smallest level of disagreement occurring for the nearest neighbor in seven out of 10 swarms. The alignment of the direction of motion between nearest neighbors is the highest in high wind. This result provides evidence for flight-path coordination between swarming male mosquitoes.
C1 [Butail, Sachit] NYU, Polytech Inst, Brooklyn, NY 11201 USA.
[Manoukis, Nicholas C.] USDA, US Pacific Basin Agr Res Ctr, Agr Res Serv, Hilo, HI 96720 USA.
[Diallo, Moussa] Univ Bamako, Malaria Res & Training Ctr, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Ribeiro, Jose M. C.] NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA.
[Paley, Derek A.] Univ Maryland, Dept Aerosp Engn, College Pk, MD 20742 USA.
[Paley, Derek A.] Univ Maryland, Syst Res Inst, College Pk, MD 20742 USA.
RP Paley, DA (reprint author), Univ Maryland, Dept Aerosp Engn, College Pk, MD 20742 USA.
EM dpaley@umd.edu
RI Paley, Derek/B-4437-2013; Butail, Sachit/O-2928-2013;
OI Paley, Derek/0000-0002-3086-2395; Butail, Sachit/0000-0001-9785-7374;
Ribeiro, Jose/0000-0002-9107-0818
FU Intramural NIH HHS [Z01 AI000810-11]
NR 26
TC 12
Z9 12
U1 4
U2 20
PU ENTOMOLOGICAL SOC AMER
PI LANHAM
PA 10001 DEREKWOOD LANE, STE 100, LANHAM, MD 20706-4876 USA
SN 0022-2585
J9 J MED ENTOMOL
JI J. Med. Entomol.
PD MAY
PY 2013
VL 50
IS 3
BP 552
EP 559
DI 10.1603/ME12251
PG 8
WC Entomology; Veterinary Sciences
SC Entomology; Veterinary Sciences
GA 146VT
UT WOS:000319123600010
PM 23802449
ER
PT J
AU Conde, V
Vollmann, H
Taubert, M
Sehm, B
Cohen, LG
Villringer, A
Ragert, P
AF Conde, Virginia
Vollmann, Henning
Taubert, Marco
Sehm, Bernhard
Cohen, Leonardo G.
Villringer, Arno
Ragert, Patrick
TI Reversed timing-dependent associative plasticity in the human brain
through interhemispheric interactions
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE paired-associative stimulation; spike timing-dependent plasticity;
primary somatosensory cortex; primary motor cortex; interhemispheric
inhibition
ID HUMAN MOTOR CORTEX; PRIMARY SOMATOSENSORY CORTEX; BOLD SIGNAL CHANGES;
CORTICAL PLASTICITY; MAGNETIC STIMULATION; NEURONAL INHIBITION;
SENSORIMOTOR CORTEX; GABA(B) RECEPTORS; SENSORY SIGNALS; HAND MOVEMENTS
AB Spike timing-dependent plasticity (STDP) has been proposed as one of the key mechanisms underlying learning and memory. Repetitive median nerve stimulation, followed by transcranial magnetic stimulation (TMS) of the contralateral primary motor cortex (M1), defined as paired-associative stimulation (PAS), has been used as an in vivo model of STDP in humans. PAS-induced excitability changes in M1 have been repeatedly shown to be time-dependent in a STDP-like fashion, since synchronous arrival of inputs within M1 induces long-term potentiation-like effects, whereas an asynchronous arrival induces long-term depression (LTD)-like effects. Here, we show that interhemispheric inhibition of the sensorimotor network during PAS, with the peripheral stimulation over the hand ipsilateral to the motor cortex receiving TMS, results in a LTD-like effect, as opposed to the standard STDP-like effect seen for contralateral PAS. Furthermore, we could show that this reversed-associative plasticity critically depends on the timing interval between afferent and cortical stimulation. These results indicate that the outcome of associative stimulation in the human brain depends on functional network interactions (inhibition or facilitation) at a systems level and can either follow standard or reversed STDP-like mechanisms.
C1 [Conde, Virginia; Vollmann, Henning; Taubert, Marco; Sehm, Bernhard; Villringer, Arno; Ragert, Patrick] Univ Hosp Leipzig, Max Planck Inst Human Cognit & Brain Sci, Leipzig, Germany.
[Conde, Virginia; Vollmann, Henning; Taubert, Marco; Sehm, Bernhard; Villringer, Arno; Ragert, Patrick] Univ Hosp Leipzig, Dept Neurol, Leipzig, Germany.
[Conde, Virginia; Vollmann, Henning; Taubert, Marco; Sehm, Bernhard; Villringer, Arno; Ragert, Patrick] Univ Hosp Leipzig, Clin Cognit Neurol, Leipzig, Germany.
[Villringer, Arno] Charite, Mind Brain Inst, Berlin, Germany.
[Villringer, Arno] Humboldt Univ, D-10099 Berlin, Germany.
[Cohen, Leonardo G.] NINDS, Human Cort Physiol & Stroke Neurorehabil Sect, NIH, Bethesda, MD 20892 USA.
RP Conde, V (reprint author), Max Planck Inst Human Cognit & Brain Sci, Dept Neurol, Stephanstr 1A, D-04103 Leipzig, Germany.
EM conde@cbs.mpg.de
NR 62
TC 8
Z9 8
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD MAY
PY 2013
VL 109
IS 9
BP 2260
EP 2271
DI 10.1152/jn.01004.2012
PG 12
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 138YU
UT WOS:000318549100003
PM 23407353
ER
PT J
AU Charron, CS
Clevidence, BA
Albaugh, GA
Kramer, MH
Vinyard, BT
Milner, JA
Novotny, JA
AF Charron, Craig S.
Clevidence, Beverly A.
Albaugh, George A.
Kramer, Matthew H.
Vinyard, Bryan T.
Milner, John A.
Novotny, Janet A.
TI Assessment of DNA damage and repair in adults consuming allyl
isothiocyanate or Brassica vegetables
SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY
LA English
DT Article
DE Sinigrin; Glucosinolate; COMET; SCGE
ID LUNG-CANCER RISK; ELECTROPHORESIS (SCGE)/HEPG2 ASSAY; HUMAN GLUTATHIONE
TRANSFERASES; CELL-CYCLE ARREST; PHASE-II ENZYMES; PROSTATE-CANCER;
CRUCIFEROUS VEGETABLES; DIETARY ISOTHIOCYANATES; PHENETHYL
ISOTHIOCYANATE; CHEMOPREVENTIVE AGENT
AB Allyl isothiocyanate (AITC) is a dietary component with possible anticancer effects, though much information about AITC and cancer has been obtained from cell studies. To investigate the effect of AITC on DNA integrity in vivo, a crossover study was conducted. Adults (n=46) consumed AITC, AITC-rich vegetables [mustard and cabbage (M/C)] or a control treatment with a controlled diet for 10 days each. On day 11, volunteers provided blood and urine before and after consuming treatments. Volunteers were characterized for genotype for GSTM1 and GSTT1 (glutathione S-transferases) and XPD (DNA repair). DNA integrity in peripheral blood mononuclear cells was assessed by single-cell gel electrophoresis. Urine was analyzed for 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and creatinine. Ten-day intake of neither AITC nor M/C resulted in statistically significant differences in DNA strand breaks [least squares mean (LSmean) % DNA in tail +/- S.E.M.: 4.8 +/- 0.6 for control, 5.7 +/- 0.7 for AITC, 5.3 +/- 0.6 for M/C] or urinary 8-oxodG (LSmean mu g 8-oxodG/g creatinine S.E.M.: 2.95 +/- 0.09 for control, 2.88 +/- 0.09 for AITC, 3.06+0.09 for M/C). Both AITC and M/C increased DNA strand breaks 3 h postconsumption (LSmean % DNA in tail +/- S.E.M.: 3.2 +/- 0.7 for control, 8.3 +/- 1.7 for AITC, 8.0 +/- 1.7 for M/C), and this difference disappeared at 6 h (4.2 +/- 0.9 for control, 5.7 +/- 1.2 for AITC, 5.5 +/- 1.2 for M/C). Genotypes for GSTM1, GSTF1 and XPD were not associated with treatment effects. In summary, DNA damage appeared to be induced in the short term by AITC and AITC-rich products, but that damage disappeared quickly, and neither AITC nor AITC-rich products affected DNA base excision repair. (C) Published by Elsevier Inc.
C1 [Charron, Craig S.; Clevidence, Beverly A.; Albaugh, George A.; Novotny, Janet A.] ARS, USDA, Beltsville Human Nutr Res Ctr, Beltsville, MD 20705 USA.
[Kramer, Matthew H.; Vinyard, Bryan T.] ARS, USDA, Biometr Consulting Serv, Beltsville, MD 20705 USA.
[Milner, John A.] NCI, NIH, Canc Prevent Div, Nutr Sci Res Grp, Rockville, MD 20892 USA.
RP Novotny, JA (reprint author), USDA, Human Nutr Res Ctr, Beltsville, MD 20705 USA.
EM Janet.Novotny@ars.usda.gov
FU US Department of Agriculture; National Cancer Institute Division for
Cancer Prevention
FX This work was supported by the US Department of Agriculture and the
National Cancer Institute Division for Cancer Prevention.
NR 84
TC 3
Z9 3
U1 1
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0955-2863
J9 J NUTR BIOCHEM
JI J. Nutr. Biochem.
PD MAY
PY 2013
VL 24
IS 5
BP 894
EP 902
DI 10.1016/j.jnutbio.2012.06.004
PG 9
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 142VL
UT WOS:000318825600022
PM 22902324
ER
PT J
AU Hensler, MA
Katz, ER
Wiener, L
Berkow, R
Madan-Swain, A
AF Hensler, Molly A.
Katz, Ernest R.
Wiener, Lori
Berkow, Roger
Madan-Swain, Avi
TI Benefit Finding in Fathers of Childhood Cancer Survivors: A
Retrospective Pilot Study
SO JOURNAL OF PEDIATRIC ONCOLOGY NURSING
LA English
DT Article
DE childhood cancer; fathers; benefit finding
ID POSTTRAUMATIC STRESS SYMPTOMS; BREAST-CANCER; ADOLESCENT SURVIVORS;
FAMILY RESILIENCY; CHILDREN; GROWTH; MOTHERS; POPULATION; ADJUSTMENT;
PARENTS
AB There is a growing literature examining positive outcomes following traumatic experiences. Although the diagnosis of a child with cancer poses extraordinary challenges for the family, awareness is growing that such a life-changing event can be a catalyst for positive growth. The current mixed methods study investigated benefit finding in fathers (N = 25) of childhood cancer survivors. Benefit finding included positive changes resulting from adversity. Participants completed a benefit finding measure and an interview describing their experience and benefits from the challenges faced during their child's cancer journey. Findings indicated that fathers endorsed high levels of benefit finding (mean = 4.1 out of 5) specifically in personal growth, spiritual change, and relationships with others. Our study extends the literature by examining how their child's cancer journey contributed to specific domains of paternal benefit finding. These results support the use of a positive psychology framework for understanding effects of a child's cancer diagnosis on caregivers.
C1 [Hensler, Molly A.] Univ Alabama Birmingham, Dept Psychol, Birmingham, AL 35294 USA.
[Berkow, Roger; Madan-Swain, Avi] Univ Alabama Birmingham, Div Pediat Hematol Oncol, Birmingham, AL 35294 USA.
[Katz, Ernest R.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Katz, Ernest R.] Univ So Calif, Dornsife Coll Letters Arts & Sci, Los Angeles, CA USA.
[Wiener, Lori] NCI, Psychosocial Support & Res Program, Ctr Canc Res, Bethesda, MD 20892 USA.
[Wiener, Lori] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Hensler, MA (reprint author), Univ Alabama Birmingham, Dept Psychol, 1530 3rd Ave South,CH 415, Birmingham, AL 35294 USA.
EM hensler@uab.edu
FU National Cancer Institute [5R25CA047888-22]; Intramural program of the
National Cancer Institute
FX This research was funded in part by a training grant from the National
Cancer Institute (grant number 5R25CA047888-22). Ms. Hensler receives
financial support from this grant. This work is also supported in part
by the Intramural program of the National Cancer Institute. No other
authors have any financial disclosures.
NR 24
TC 3
Z9 3
U1 0
U2 13
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1043-4542
J9 J PEDIATR ONCOL NURS
JI J. Pediatr. Oncol. Nurs.
PD MAY-JUN
PY 2013
VL 30
IS 3
BP 161
EP 168
DI 10.1177/1043454213487435
PG 8
WC Oncology; Nursing
SC Oncology; Nursing
GA 144PJ
UT WOS:000318951600005
PM 23674549
ER
PT J
AU Willey, JZ
Khatri, P
Khoury, JC
Merino, JG
Ford, AL
Rost, NS
Gonzales, NR
Ali, LK
Meyer, BC
Broderick, JP
AF Willey, Joshua Z.
Khatri, Pooja
Khoury, Jane C.
Merino, Jose G.
Ford, Andria L.
Rost, Natalia S.
Gonzales, Nicole R.
Ali, Latisha K.
Meyer, Brett C.
Broderick, Joseph P.
TI Variability in the Use of Intravenous Thrombolysis for Mild Stroke:
Experience Across the SPOTRIAS Network
SO JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
LA English
DT Article
DE Mild stroke; stenosis
ID TISSUE-PLASMINOGEN ACTIVATOR; ACUTE ISCHEMIC-STROKE;
NEUROLOGICAL-DISORDERS; SCIENTIFIC STATEMENT; NATIONAL-INSTITUTE; EARLY
MANAGEMENT; ASSOCIATION; ELIGIBILITY; GUIDELINES; SYMPTOMS
AB Background: Current guidelines do not define the lower severity threshold for thrombolysis. In this study, we describe the variability of treatment of mild stroke patients across a network of academic stroke centers. Methods: Stroke centers within the Specialized Program of Translational Research in Acute Stroke (SPOTRIAS) prospectively collect data on patients treated with intravenous recombinant tissue plasminogen activator (IV rt-PA), including demographics, pretreatment National Institutes of Health Stroke Scale (NIHSS) scores, and in-hospital mortality. We examined the variability in proportion of total tissue plasminogen activator-treated patients in the NIHSS categories (0-3, 4-5, or >= 6) and associated outcomes. Results: A total of 2514 patients with reported NIHSS scores were treated with IV rt-PA between January 1, 2005 and December 31, 2009. The proportion of patients with mild stroke (NIHSS scores of 0-3) who were treated with IV rt-PA varied substantially across the centers (2.7-18.0%; P < .001). There were 5 deaths in the 256 treated with an NIHSS score of 0-3 (2.0%). The proportion of treated patients across the network with an NIHSS score of 0 to 3 increased from 4.8% in 2005 to 10.7% in 2009 (P = .001). Conclusions: There is substantial variability in the proportion of treated patients who have mild stroke across the SPOTRIAS centers, reflecting a paucity of data on how to best treat patients with mild stroke. Randomized trial data for this group of patients are needed to clarify the use of rt-PA in patients with the mildest strokes.
C1 [Willey, Joshua Z.] Columbia Univ, Dept Neurol, New York, NY USA.
[Khatri, Pooja; Broderick, Joseph P.] Univ Cincinnati, Cincinnati, OH 45221 USA.
[Ford, Andria L.] Washington Univ, St Louis, MO USA.
[Gonzales, Nicole R.] Univ Texas Houston, Houston, TX USA.
[Ali, Latisha K.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Meyer, Brett C.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Khoury, Jane C.] Cincinnati Childrens Hosp Med Ctr, Div Biostat & Epidemiol, Cincinnati, OH USA.
[Merino, Jose G.] NINDS, Sect Stroke Diagnost & Therapeut, Div Intramural Res, Bethesda, MD 20892 USA.
[Rost, Natalia S.] Massachusetts Gen Hosp, Dept Neurol, Stroke Div, Boston, MA 02114 USA.
RP Willey, JZ (reprint author), Dept Neurol, 710 West 168th St,Box 30, New York, NY 10032 USA.
EM jzw2@columbia.edu
RI Khoury, Jane/O-2068-2015;
OI Merino, Jose/0000-0002-6676-0008
FU Intramural Division of the National Institute of Neurological Disorders
and Stroke/National Institutes of Health; National Institutes of
Neurological Diseases and Stroke [NINDS P50 NS049060]; NINDS
[1K23NS073104-01A1]
FX Supported in part by the Intramural Division of the National Institute
of Neurological Disorders and Stroke/National Institutes of Health.
SPOTRIAS is funded by the National Institutes of Neurological Diseases
and Stroke (NINDS P50 NS049060). JZW was funded by NINDS
1K23NS073104-01A1.
NR 19
TC 8
Z9 8
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1052-3057
J9 J STROKE CEREBROVASC
JI J. Stroke Cerebrovasc. Dis.
PD MAY
PY 2013
VL 22
IS 4
BP 318
EP 322
DI 10.1016/j.jstrokecerebrovasdis.2011.09.005
PG 5
WC Neurosciences; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 144BX
UT WOS:000318915500006
PM 22177935
ER
PT J
AU Kalyani, RR
Tra, Y
Yeh, HC
Egan, JM
Ferrucci, L
Brancati, FL
AF Kalyani, Rita Rastogi
Tra, Yolande
Yeh, Hsin-Chieh
Egan, Josephine M.
Ferrucci, Luigi
Brancati, Frederick L.
TI Quadriceps Strength, Quadriceps Power, and Gait Speed in Older US Adults
with Diabetes Mellitus: Results from the National Health and Nutrition
Examination Survey, 19992002
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE type 2 diabetes mellitus; muscle loss; physical function; gait
ID EXAMINATION SURVEY NHANES; SKELETAL-MUSCLE STRENGTH; BODY-COMPOSITION;
PERIPHERAL NEUROPATHY; MASS; INFLAMMATION; ASSOCIATION; DISABILITY;
QUALITY; RISK
AB Objectives To examine the independent association between diabetes mellitus (and its duration and severity) and quadriceps strength, quadriceps power, and gait speed in a national population of older adults. Design Cross-sectional nationally representative survey. Setting United States. Participants Two thousand five hundred seventy-three adults aged 50 and older in the National Health and Nutrition Examination Survey 19992002 who had assessment of quadriceps strength. Methods Diabetes mellitus was ascertained according to questionnaire. Measurement of isokinetic knee extensor (quadriceps) strength was performed at 60o/s. Gait speed was assessed using a 20-foot walk test. Multiple linear regression analyses were used to assess the association between diabetes mellitus status and outcomes, adjusting for potential confounders or mediators. Results Older U.S. adults with diabetes mellitus had significantly slower gait speed (0.96 +/- 0.02m/s) than those without (1.08 +/- 0.01m/s; P<.001). After adjusting for demographic characteristics, weight, and height, diabetes mellitus was also associated with significantly lower quadriceps strength (4.6 +/- 1.9 Nm; P=.02) and power (4.9 +/- 2.0W; P=.02) and slower gait speed (0.05 +/- 0.02m/s; P=.002). Associations remained significant after adjusting for physical activity and C-reactive protein. After accounting for comorbidities (cardiovascular disease, peripheral neuropathy, amputation, cancer, arthritis, fracture, chronic obstructive pulmonary disease), diabetes mellitus was independently associated only with gait speed (0.04 +/- 0.02m/s; P=.02). Diabetes mellitus duration in men and women was negatively associated with age-adjusted quadriceps strength (5.7 and 3.5 Nm/decade of diabetes mellitus, respectively) and power (6.1 and 3.8W/decade of diabetes mellitus, respectively) (all P.001, no significant interactions according to sex). Glycosylated hemoglobin was not associated with outcomes after accounting for body weight. Conclusion Older U.S. adults with diabetes mellitus have lower quadriceps strength and quadriceps power that is related to the presence of comorbidities and walk slower than those without diabetes mellitus. Future studies should investigate the relationship between hyperglycemia and subsequent declines in leg muscle function.
C1 [Kalyani, Rita Rastogi; Brancati, Frederick L.] Johns Hopkins Univ, Div Endocrinol & Metab, Baltimore, MD 21287 USA.
[Tra, Yolande] Univ Maryland, Sch Pharm, Maryland Poison Ctr, Baltimore, MD 21201 USA.
[Yeh, Hsin-Chieh; Brancati, Frederick L.] Johns Hopkins Univ, Sch Med, Dept Med, Div Gen Internal Med, Baltimore, MD 21287 USA.
[Yeh, Hsin-Chieh; Brancati, Frederick L.] Johns Hopkins Univ, Div Dept Epidemiol, Baltimore, MD 21287 USA.
[Yeh, Hsin-Chieh; Brancati, Frederick L.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Div Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21287 USA.
[Egan, Josephine M.; Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
RP Kalyani, RR (reprint author), Johns Hopkins Univ, Sch Med, Dept Med, Div Endocrinol & Metab, 1830 East Monument St,Suite 333, Baltimore, MD 21287 USA.
EM rrastogi@jhmi.edu
FU Johns Hopkins Older Americans Independence Center [P30-AG021334];
Intramural Research Program of the National Institute on Aging; National
Institute of Diabetes and Digestive and Kidney Diseases [K23-DK093583,
K24-DK062222, P60-DK079637]
FX This work was supported by the Johns Hopkins Older Americans
Independence Center (P30-AG021334), the Intramural Research Program of
the National Institute on Aging, and the National Institute of Diabetes
and Digestive and Kidney Diseases (K23-DK093583, K24-DK062222 and
P60-DK079637).
NR 29
TC 32
Z9 32
U1 4
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD MAY
PY 2013
VL 61
IS 5
BP 769
EP 775
DI 10.1111/jgs.12204
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 145GB
UT WOS:000319002100012
PM 23617584
ER
PT J
AU Frommelt, PC
Gerstenberger, E
Baffa, J
Border, WL
Bradley, TJ
Colan, S
Gorentz, J
Heydarian, H
John, JB
Lai, WW
Levine, J
Lu, JC
McCandless, RT
Miller, S
Nutting, A
Ohye, RG
Pearson, GD
Wong, PC
Cohen, MS
AF Frommelt, Peter C.
Gerstenberger, Eric
Baffa, Jeanne
Border, William L.
Bradley, Tim J.
Colan, Steven
Gorentz, Jessica
Heydarian, Haleh
John, J. Blaine
Lai, Wyman W.
Levine, Jami
Lu, Jimmy C.
McCandless, Rachel T.
Miller, Stephen
Nutting, Arni
Ohye, Richard G.
Pearson, Gail D.
Wong, Pierre C.
Cohen, Meryl S.
CA Pediat Heart Network Investigators
TI Doppler Flow Patterns in the Right Ventricle-to-Pulmonary Artery Shunt
and Neo-Aorta in Infants with Single Right Ventricle Anomalies: Impact
on Outcome after Initial Staged Palliations
SO JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY
LA English
DT Article
DE Hypoplastic left heart syndrome; Norwood; Echocardiography; Single
ventricle
ID LEFT-HEART SYNDROME; DIASTOLIC DURATION RATIO; NORWOOD PROCEDURE;
RECONSTRUCTION TRIAL; 1ST-STAGE PALLIATION; FAILURE SECONDARY; CHILDREN;
ECHOCARDIOGRAPHY; CARDIOMYOPATHY; MULTICENTER
AB Background: A Pediatric Heart Network trial compared outcomes in infants with single right ventricle anomalies undergoing Norwood procedures randomized to modified Blalock-Taussig shunt (MBTS) or right ventricle-to-pulmonary artery shunt (RVPAS). Doppler patterns in the neo-aorta and RVPAS may characterize physiologic changes after staged palliations that affect outcomes and right ventricular (RV) function.
Methods: Neo-aortic cardiac index (CI), retrograde fraction (RF) in the descending aorta and RVPAS conduit, RVPAS/neo-aortic systolic ejection time ratio, and systolic/diastolic (S/D) ratio were measured early after Norwood, before stage II palliation, and at 14 months. These parameters were compared with transplantation-free survival, length of hospital stay, and RV functional indices.
Results: In 529 subjects (mean follow-up period, 3.0 +/- 2.1 years), neo-aortic CI and descending aortic RF were significantly higher in the MBTS cohort after Norwood. The RVPAS RF averaged <25% at both interstage intervals. Higher pre-stage II descending aortic RF was correlated with lower RV ejection fraction (R = -0.24; P = .032) at 14 months for the MBTS cohort. Higher post-Norwood CI (5.6 vs 4.4 L/min/m(2), P = .04) and lower S/D ratio (1.40 vs 1.68, P = .01) were correlated with better interstage transplantation-free survival for the RVPAS cohort. No other Doppler flow patterns were correlated with outcomes.
Conclusions: After the Norwood procedure, infants tolerated significant descending aortic RF (MBTS) and conduit RF (RVPAS), with little correlation with clinical outcomes or RV function. Neo-aortic CI, ejection time, and S/D ratios also had limited correlations with outcomes or RV function, but higher post-Norwood neo-aortic CI and lower S/D ratio were correlated with better interstage survival in those with RVPAS.
C1 [Frommelt, Peter C.; Gorentz, Jessica] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Gerstenberger, Eric] New England Res Inst, Watertown, MA 02172 USA.
[Baffa, Jeanne] Alfred I DuPont Hosp Children, Wilmington, DE USA.
[Border, William L.] Emory Univ, Sch Med, Atlanta, GA USA.
[Bradley, Tim J.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Colan, Steven; Levine, Jami] Boston Childrens Hosp, Boston, MA USA.
[Heydarian, Haleh] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[John, J. Blaine] Congenital Heart Inst Florida, Tampa, FL USA.
[Lai, Wyman W.] Columbia Univ, Med Ctr, New York, NY USA.
[Lu, Jimmy C.; Ohye, Richard G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[McCandless, Rachel T.] Univ Utah, Salt Lake City, UT USA.
[Miller, Stephen] Duke Univ, Durham, NC USA.
[Nutting, Arni] Med Univ S Carolina, Charleston, SC 29425 USA.
[Pearson, Gail D.] NHLBI, Bethesda, MD 20892 USA.
[Wong, Pierre C.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Cohen, Meryl S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
RP Frommelt, PC (reprint author), Med Coll Wisconsin, Childrens Hosp Wisconsin, 9000 W Wisconsin Ave,MS 713, Milwaukee, WI 53226 USA.
EM pfrommelt@chw.org
OI Lu, Jimmy/0000-0002-2544-7402
FU National Heart, Lung, and Blood Institute [HL068269, HL068270, HL068279,
HL068281, HL068285, HL068292, HL068290, HL068288, HL085057, HL109781,
HL109737]
FX This study was supported by U01 grants from the National Heart, Lung,
and Blood Institute (HL068269, HL068270, HL068279, HL068281, HL068285,
HL068292, HL068290, HL068288, HL085057, HL109781, and HL109737). The
contents of this work are solely the responsibility of the authors and
do not necessarily represent the official views of the National Heart,
Lung, and Blood Institute.
NR 19
TC 1
Z9 1
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0894-7317
J9 J AM SOC ECHOCARDIOG
JI J. Am. Soc. Echocardiogr.
PD MAY
PY 2013
VL 26
IS 5
BP 521
EP 529
DI 10.1016/j.echo.2013.02.012
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 143YV
UT WOS:000318906400011
PM 23540728
ER
PT J
AU Arora, M
Pidala, J
Cutler, CS
Chai, X
Kurland, B
Jacobsohn, DA
Pavletic, SZ
Palmer, J
Vogelsang, G
Jagasia, M
Schultz, K
Lee, SJ
AF Arora, M.
Pidala, J.
Cutler, C. S.
Chai, X.
Kurland, B.
Jacobsohn, D. A.
Pavletic, S. Z.
Palmer, J.
Vogelsang, G.
Jagasia, M.
Schultz, K.
Lee, S. J.
TI Impact of prior acute GVHD on chronic GVHD outcomes: a chronic graft
versus host disease consortium study
SO LEUKEMIA
LA English
DT Letter
ID CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT;
MARROW-TRANSPLANTATION; CLINICAL-TRIALS; CRITERIA; SEVERITY; COHORT
C1 [Arora, M.] Univ Minnesota, Div Hematol Oncol & Transplant, Minneapolis, MN 55455 USA.
[Pidala, J.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Cutler, C. S.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
[Chai, X.; Kurland, B.; Lee, S. J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Chai, X.; Kurland, B.; Lee, S. J.] Univ Washington, Seattle, WA 98195 USA.
[Jacobsohn, D. A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Pavletic, S. Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Palmer, J.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Vogelsang, G.] Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Jagasia, M.] Vanderbilt Univ, Nashville, TN USA.
[Schultz, K.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
RP Arora, M (reprint author), Univ Minnesota, Div Hematol Oncol & Transplant, Minneapolis, MN 55455 USA.
EM arora005@umn.edu
OI Kurland, Brenda/0000-0002-5669-0595
FU NCI NIH HHS [CA 118953, R01 CA118953, U54 CA163438]
NR 15
TC 5
Z9 5
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD MAY
PY 2013
VL 27
IS 5
BP 1196
EP 1201
DI 10.1038/leu.2012.292
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 141AS
UT WOS:000318698300030
PM 23047477
ER
PT J
AU Zhang, XX
Wang, Z
Yue, XY
Ma, Y
Kiesewetter, DO
Chen, XY
AF Zhang, Xiao-Xiang
Wang, Zhe
Yue, Xuyi
Ma, Ying
Kiesewetter, Dale O.
Chen, Xiaoyuan
TI pH-Sensitive Fluorescent Dyes: Are They Really pH-Sensitive in Cells?
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE aza-BODIPY; pH-sensitive; pK(a) change in membrane; fluorescent imaging
ID INTRACELLULAR PH; CYSTIC-FIBROSIS; APOPTOSIS; ACIDIFICATION; AGENTS;
CHEMOSENSOR; PROBE
AB Chemically synthesized near-infrared aza-BODIPY dyes displayed off-on fluorescence at acidic pH (pK(a) = 6.2-6.6) through the suppression of the photoinduced electron transfer and/or internal charge transfer process. The apparent pK(a)s of the dyes were shifted well above physiological pH in a hydrophobic microenvironment, which led to "turned-on" fluorescence in micelles and liposomes at neutral and basic pH. Bovine serum albumin also activated the fluorescence, though to a much lesser extent. When these small molecular dyes entered cells, instead of being fluorescent only in acidic organelles, the whole cytoplasm exhibited fluorescence, with a signal/background ratio as high as similar to 10 in no-wash live-cell imaging. The dye 1-labeled cells remained highly fluorescent even after 3 days. Moreover, slight variations of the dye structure resulted in significantly different intracellular fluorescence behaviors, possibly because of their different cellular uptake and intracellular activation capabilities. After the separation of cellular components, the fraction of plasma membrane and endoplasmic reticulum showed the highest fluorescence, further confirming the fluorescence activation by membrane structures. The fluorescence intensity of these dyes at different intracellular pHs (6.80 and 8.00) did not differ significantly, indicating that intracellular pH did not play a critical role. Altogether, we showed here for the first time that the fluorescence of pH-sensitive aza-BODIPY dyes was switched intracellularly not by acidic pH, but by intracellular membranes (and proteins as well). The excellent membrane permeability, ultrahigh fluorescence contrast ratio, persistent fluorescent signal, and minimal biological interference of dye 1 make it an ideal choice for live-cell imaging and in vivo cell tracking. These findings also imply that the intracellular fluorescence properties of pH-sensitive dyes should be carefully examined before they are used as pH indicators.
C1 [Zhang, Xiao-Xiang; Wang, Zhe; Yue, Xuyi; Ma, Ying; Kiesewetter, Dale O.; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Wang, Zhe; Yue, Xuyi] Xiamen Univ, Sch Publ Hlth, Ctr Mol Imaging & Translat Med, Xiamen 361005, Peoples R China.
RP Chen, XY (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
EM shawn.chen@nih.gov
FU National Institute of Biomedical Imaging and Bioengineering (NIBIB),
National Institutes of Health; NIBIB; National Institute of Standards
and Technology
FX This work is supported by the Intramural Research Program (IRP) of the
National Institute of Biomedical Imaging and Bioengineering (NIBIB),
National Institutes of Health. This work was performed while X.-X.Z.
held a National Research Council Research Associateship Award from NIBIB
and the National Institute of Standards and Technology.
NR 30
TC 21
Z9 21
U1 8
U2 94
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 MAY
PY 2013
VL 10
IS 5
BP 1910
EP 1917
DI 10.1021/mp3006903
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 140QI
UT WOS:000318669600039
PM 23464828
ER
PT J
AU Zou, P
Helson, L
Maitra, A
Stern, ST
McNeil, SE
AF Zou, Peng
Helson, Lawrence
Maitra, Anirban
Stern, Stephan T.
McNeil, Scott E.
TI Polymeric Curcumin Nanoparticle Pharmacokinetics and Metabolism in Bile
Duct Cannulated Rats
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE curcumin; nanoformulation; metabolite profile; biliary excretion;
urinary excretion
ID IN-VITRO STABILITY; DRUG-DELIVERY; TISSUE DISTRIBUTION; COPOLYMER
MICELLES; VIVO EVALUATION; FORMULATION; CANCER; GLUCURONIDATION;
NANOMEDICINE; EXCRETION
AB The objective of this study was to compare the pharmacokinetics and metabolism of polymeric nanoparticle-encapsulated (nanocurcumin) and solvent-solubilized curcumin formulations in Sprague-Dawley (SD) rats. Nanocurcumin is currently under development for cancer therapy. Since free, unencapsulated curcumin is rapidly metabolized and excreted in rats, upon intravenous (i.v.) administration of nanocurcumin only nanoparticle-encapsulated curcumin can be detected in plasma samples. Hence, the second objective of this study was to utilize the metabolic instability of curcumin to assess in vivo drug release from nanocurcumin. Nanocurcumin and solvent-solubilized curcumin were administered at 10 mg curcurmin/kg by jugular vein to bile duct-cannulated male SD rats (n = 5). Nanocurcumin increased the plasma C-max of curcumin 1749 fold relative to the solvent-solubilized curcumin. Nanocurcumin also increased the relative abundance of curcumin and glucuronides in bile but did not dramatically alter urine and tissue metabolite profiles. The observed increase in biliary and urinary excretion of both curcumin and metabolites for the nanocurcumin formulation suggested a rapid "burst" release of curcumin. Although the burst release observed in this study is a limitation for targeted tumor delivery, nanocurcumin still exhibits major advantages over solvent-solubilized curcumin, as the nanoformulation does not result in the lung accumulation observed for the solvent-solubilized curcumin and increases overall systemic curcumin exposure. Additionally, the remaining encapsulated curcumin fraction following burst release is available for tumor delivery via the enhanced permeation and retention effect commonly observed for nanoparticle formulations.
C1 [Zou, Peng; Stern, Stephan T.; McNeil, Scott E.] NCI, Nanotechnol Characterizat Lab, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Helson, Lawrence] Sign Path Pharma Inc, Quakertown, PA 18951 USA.
[Maitra, Anirban] Johns Hopkins Univ, Sch Med, Baltimore, MD 21231 USA.
RP Stern, ST (reprint author), NCI, Nanotechnol Characterizat Lab, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
EM sternstephan@mail.nih.gov
RI Nanotechnology Characterization Lab, NCL/K-8454-2012; Zou,
Peng/J-9300-2015
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; SignPath Pharma
FX The authors thank Dr. Rachael M. Crist for assistance in revising the
manuscript, Ms. Sarah Skoczen for assistance with bioanalysis, and Dr.
Jeffrey D. Clogston for assistance with particle size measurement. 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 authors declare the following competing financial interest(s):
NanoCurc is a registered trademark of SignPath Pharmaceuticals,
Quakertown, PA, USA. A.M. is a member of the scientific advisory board,
and L.H. is CEO of SignPath Pharma, and any conflicts of interest under
this arrangement are handled in accordance with the Johns Hopkins
University Office of Policy Coordination guidelines. SignPath Pharma has
provided partial support for these studies through offsetting the costs
of polymer synthesis. A.M. has filed a patent application (US
2008/0107749) that is relevant to the formulation described in this
article. A report of invention to this effect has been filed with Johns
Hopkins Technology Transfer and licensed by SignPath Pharma.
NR 48
TC 23
Z9 23
U1 2
U2 48
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 MAY
PY 2013
VL 10
IS 5
BP 1977
EP 1987
DI 10.1021/mp4000019
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 140QI
UT WOS:000318669600046
PM 23534919
ER
PT J
AU Eddy, M
AF Eddy, Mitch
TI Norman B. Hecht (December 14, 1940-February 28, 2013)
SO MOLECULAR REPRODUCTION AND DEVELOPMENT
LA English
DT Biographical-Item
C1 NIEHS, Lab Reprod & Dev Toxicol, NIH, Bethesda, MD USA.
RP Eddy, M (reprint author), NIEHS, Lab Reprod & Dev Toxicol, NIH, Bethesda, MD USA.
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 1040-452X
J9 MOL REPROD DEV
JI Mol. Reprod. Dev.
PD MAY
PY 2013
VL 80
IS 5
BP I
EP III
DI 10.1002/mrd.22186
PG 3
WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology;
Reproductive Biology
SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology;
Reproductive Biology
GA 145KN
UT WOS:000319014700001
ER
PT J
AU Ilinskaya, AN
Dobrovolskaia, MA
AF Ilinskaya, Anna N.
Dobrovolskaia, Marina A.
TI Nanoparticles and the blood coagulation system. Part I: benefits of
nanotechnology
SO NANOMEDICINE
LA English
DT Review
DE coagulopathy; disseminated intravascular coagulation; endothelial cell;
leukocyte; nanoparticle; platelet; procoagulant activity; thrombosis
ID LOADED POLYMERIC NANOPARTICLES; RECOMBINANT FACTOR VIIA; HEMOPHILIA-A
PATIENTS; DRUG-DELIVERY SYSTEM; ACCELERATED THROMBOLYSIS; PLASMINOGEN
ACTIVATORS; MYOCARDIAL-INFARCTION; PLATELET-AGGREGATION; PEGYLATED
LIPOSOMES; THROMBIN ACTIVITY
AB Nanotechnology is proven to provide certain benefits in drug delivery by improving solubility, increasing uptake to target sites and changing pharmacokinetics profiles of traditional drugs. Since properties of many materials change tremendously at the nanoscale levels, nanotechnology is also being explored in various industrial applications. As such, nanoparticles are rapidly entering various areas of industry, biology and medicine. The benefits of using nanotechnology for industrial and biomedical applications are often tempered by concerns about the safety of these new materials. One such area of concern includes their effect on the immune system. While nanoparticle interactions with various constituents of the immune system have been reviewed before, little attention was given to nanoparticle effects on the blood coagulation system. Nanoparticle interface with the blood coagulation system may lead to either benefits to the host or adverse reactions. This article reviews recent advances in our understanding of nanoparticle interactions with plasma coagulation factors, platelets, endothelial cells and leukocytes. Part I is focused on desirable interactions between nanoparticles and the coagulation system, and discusses benefits of using nanotechnology to intervene in coagulation disorders. Undesirable interactions posing safety concerns are covered in part II, which will be published in the June issue of Nanomedicine.
C1 [Ilinskaya, Anna N.; Dobrovolskaia, Marina A.] SAIC Frederick Inc, NCI Frederick, Adv Technol Program, Nanotechnol Characterizat Lab, Frederick, MD 21702 USA.
RP Dobrovolskaia, MA (reprint author), SAIC Frederick Inc, NCI Frederick, Adv Technol Program, Nanotechnol Characterizat Lab, 1050 Boyles St,Bldg 469, Frederick, MD 21702 USA.
EM marina@mail.nih.gov
RI Nanotechnology Characterization Lab, NCL/K-8454-2012
FU National Cancer Institute, NIH [HHSN261200800001E]
FX This project has been funded in whole with federal funds from the
National Cancer Institute, NIH, under contract HHSN261200800001E. The
authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or
financial conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed.
NR 91
TC 23
Z9 23
U1 5
U2 67
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1743-5889
J9 NANOMEDICINE-UK
JI Nanomedicine
PD MAY
PY 2013
VL 8
IS 5
BP 773
EP 784
DI 10.2217/NNM.13.48
PG 12
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
SC Biotechnology & Applied Microbiology; Science & Technology - Other
Topics
GA 143FL
UT WOS:000318852100014
PM 23656264
ER
PT J
AU Cannas, A
Borghero, G
Floris, GL
Solla, P
Chio, A
Traynor, BJ
Calvo, A
Restagno, G
Majounie, E
Costantino, E
Piras, V
Lavra, L
Pani, C
Orofino, G
Di Stefano, F
Tacconi, P
Mascia, MM
Muroni, A
Murru, MR
Tranquilli, S
Corongiu, D
Rolesu, M
Cuccu, S
Marrosu, F
Marrosu, MG
AF Cannas, Antonino
Borghero, Giuseppe
Floris, Gian Luca
Solla, Paolo
Chio, Adriano
Traynor, Bryan J.
Calvo, Andrea
Restagno, Gabriella
Majounie, Elisa
Costantino, Emanuela
Piras, Valeria
Lavra, Loredana
Pani, Carla
Orofino, Gianni
Di Stefano, Francesca
Tacconi, Paolo
Mascia, Marcello Mario
Muroni, Antonella
Murru, Maria Rita
Tranquilli, Stefania
Corongiu, Daniela
Rolesu, Marcella
Cuccu, Stefania
Marrosu, Francesco
Marrosu, Maria Giovanna
TI The p.A382T TARDBP gene mutation in Sardinian patients affected by
Parkinson's disease and other degenerative parkinsonisms
SO NEUROGENETICS
LA English
DT Article
DE TARDBP gene mutation; Degenerative parkinsonism; TDP-43 proteinopathies;
Sardinia
ID FRONTOTEMPORAL LOBAR DEGENERATION; AMYOTROPHIC-LATERAL-SCLEROSIS;
MOTOR-NEURON DISEASE; TDP-43 PROTEINOPATHIES; LEWY BODIES; DNA-BINDING;
INCLUSIONS; DIAGNOSIS; PATHOLOGY; DEMENTIA
AB Based on our previous finding of the p.A382T founder mutation in ALS patients with concomitant parkinsonism in the Sardinian population, we hypothesized that the same variant may underlie Parkinson's disease (PD) and/or other forms of degenerative parkinsonism on this Mediterranean island. We screened a cohort of 611 patients with PD (544 cases) and other forms of degenerative parkinsonism (67 cases) and 604 unrelated controls for the c.1144G > A (p.A382T) missense mutation of the TARDBP gene. The p.A382T mutation was identified in nine patients with parkinsonism. Of these, five (0.9 % of PD patients) presented a typical PD (two with familiar forms), while four patients (6.0 % of all other forms of parkinsonism) presented a peculiar clinical presentation quite different from classical atypical parkinsonism with an overlap of extrapyramidal-pyramidal-cognitive clinical signs. The mutation was found in eight Sardinian controls (1.3 %) consistent with a founder mutation in the island population. Our findings suggest that the clinical presentation of the p.A382T TARDBP gene mutation may include forms of parkinsonism in which the extrapyramidal signs are the crucial core of the disease at onset. These forms can present PSP or CBD-like clinical signs, with bulbar and/or extrabulbar pyramidal signs and cognitive impairment. No evidence of association has been found between TARDBP gene mutation and typical PD.
C1 [Cannas, Antonino; Solla, Paolo; Costantino, Emanuela; Mascia, Marcello Mario; Muroni, Antonella] Univ Cagliari, Policlin Univ, Ctr Disordini Movimento, Dipartimento Sci Cardiovasc & Neurol,Sez Neurol, I-09042 Cagliari, Italy.
[Borghero, Giuseppe; Floris, Gian Luca; Piras, Valeria; Lavra, Loredana; Pani, Carla; Orofino, Gianni; Di Stefano, Francesca; Tacconi, Paolo; Marrosu, Francesco; Marrosu, Maria Giovanna] Univ Cagliari, Policlin Univ, Dipartimento Sci Cardiovasc & Neurol, I-09042 Cagliari, Italy.
[Chio, Adriano; Calvo, Andrea] Univ Turin, Dipartimento Neurosci, CRESLA, Turin, Italy.
[Traynor, Bryan J.; Majounie, Elisa] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Restagno, Gabriella] ASO OIRM St Anna, Lab Genet Mol, Turin, Italy.
[Murru, Maria Rita; Tranquilli, Stefania; Corongiu, Daniela; Rolesu, Marcella; Cuccu, Stefania] Univ Cagliari, Osped Binaghi, Lab Ctr Sclerosi Multipla, I-09042 Cagliari, Italy.
RP Cannas, A (reprint author), Univ Cagliari, Policlin Univ, Ctr Disordini Movimento, Dipartimento Sci Cardiovasc & Neurol,Sez Neurol, SS 554 Bivio Sestu, I-09042 Cagliari, Italy.
EM antonino.cannas@tiscali.it
RI Traynor, Bryan/G-5690-2010; Calvo, Andrea/K-4141-2016;
OI Calvo, Andrea/0000-0002-5122-7243; Chio, Adriano/0000-0001-9579-5341;
Solla, Paolo/0000-0002-2982-0665; Marrosu, Maria
Giovanna/0000-0003-2334-2081; Di Stefano, Francesca/0000-0001-5921-2778
FU European Community's Health Seventh Framework Programme [259867];
Intramural Research Programs of the NIH, National Institute on Aging
[Z01-AG000949-02]; Italian Ministry of Health; Regione Piemonte; Italian
Ministry of University and Research; University of Torino; Federazione
Italiana Giuoco Calcio; European Commission; ALS Association; Packard
Center for ALS Research; Microsoft Research; Myasthenia Gravis
Foundation; Italiana Giuoco Calcio (FIGC); Compagnia di San Paolo
FX 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. This work was supported in part by the
Intramural Research Programs of the NIH, National Institute on Aging
(Z01-AG000949-02).; Dr. Chio serves on the editorial advisory board of
Amyotrophic Lateral Sclerosis and has received research support from the
Italian Ministry of Health (Ricerca Finalizzata), Regione Piemonte
(Ricerca Finalizzata), Italian Ministry of University and Research,
University of Torino, Federazione Italiana Giuoco Calcio, and European
Commission (Health Seventh Framework Programme); he serves on a
scientific advisory board for Biogen Idec. Dr. Bryan J. Traynor is on
the editorial board for the journal Neurology and has received research
support from the ALS Association, the Packard Center for ALS Research,
Microsoft Research, the Myasthenia Gravis Foundation, and Italiana
Giuoco Calcio (FIGC). Dr. Calvo has received research support from
Regione Piemonte (Ricerca Finalizzata) and Compagnia di San Paolo. All
other authors report no disclosures.
NR 24
TC 17
Z9 19
U1 1
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1364-6745
J9 NEUROGENETICS
JI Neurogenetics
PD MAY
PY 2013
VL 14
IS 2
BP 161
EP 166
DI 10.1007/s10048-013-0360-2
PG 6
WC Genetics & Heredity; Clinical Neurology
SC Genetics & Heredity; Neurosciences & Neurology
GA 143QA
UT WOS:000318881100008
PM 23546887
ER
PT J
AU Johnson, J
Clifton, RG
Roberts, JM
Myatt, L
Hauth, JC
Spong, CY
Varner, MW
Wapner, RJ
Thorp, JM
Mercer, BM
Peaceman, AM
Ramin, SM
Samuels, P
Sciscione, A
Harper, M
Tolosa, JE
Saade, G
Sorokin, Y
AF Johnson, Julie
Clifton, Rebecca G.
Roberts, James M.
Myatt, Leslie
Hauth, John C.
Spong, Catherine Y.
Varner, Michael W.
Wapner, Ronald J.
Thorp, John M., Jr.
Mercer, Brian M.
Peaceman, Alan M.
Ramin, Susan M.
Samuels, Philip
Sciscione, Anthony
Harper, Margaret
Tolosa, Jorge E.
Saade, George
Sorokin, Yoram
CA Eunice Kennedy Shriver Natl Inst C
TI Pregnancy Outcomes With Weight Gain Above or Below the 2009 Institute of
Medicine Guidelines
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID WOMEN
AB OBJECTIVE: To evaluate pregnancy outcomes according to 2009 Institute of Medicine (IOM) gestational weight gain guidelines.
METHODS: This study is a secondary analysis of a preeclampsia prevention trial among nulliparas carrying singletons. Odds ratios and 95% confidence intervals (adjusted for maternal age, race, smoking, and treatment group) were calculated based on total weight gain below or above the IOM guidelines stratified by prepregnancy body mass index (BMI). The referent group was weight gain within the guidelines.
RESULTS: Of 8,293 pregnancies, 9.5% had weight gain below, 17.5% within, and 73% above IOM guidelines. With excess weight gain, all BMI categories had an increased risk of hypertensive disorders; normal weight and overweight women also had increased risk of cesarean delivery and neonatal birth weight at or above the 90th centile but a decreased risk of weight below the 10th centile. There were no consistent associations with insufficient weight gain and adverse outcomes.
CONCLUSION: Excess weight gain was prevalent and associated with an increased risk of hypertensive disorders, cesarean delivery, and large-for-gestational-age neonates.
C1 Brown Univ, Dept Obstet & Gynecol, Providence, RI 02905 USA.
Univ Pittsburgh, Dept Obstet & Gynecol, Pittsburgh, PA USA.
Univ Cincinnati, Dept Obstet & Gynecol, Cincinnati, OH USA.
Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
Univ Utah, Dept Obstet & Gynecol, Salt Lake City, UT USA.
Columbia Univ, Dept Obstet & Gynecol, New York, NY USA.
Univ N Carolina, Dept Obstet & Gynecol, Chapel Hill, NC USA.
Case Western Reserve Univ, Dept Obstet & Gynecol, MetroHlth Med Ctr, Cleveland, OH 44106 USA.
Northwestern Univ, Dept Obstet & Gynecol, Chicago, IL 60611 USA.
Univ Texas Hlth Sci Ctr Houston, Dept Obstet & Gynecol, Houston, TX USA.
Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
Drexel Univ, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
Wake Forest Univ Hlth Sci, Dept Obstet & Gynecol, Winston Salem, NC USA.
Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
Univ Texas Med Branch, Dept Obstet & Gynecol, Galveston, TX 77555 USA.
Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
George Washington Univ, Ctr Biostat, Washington, DC USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Johnson, J (reprint author), Brown Univ, Women & Infants Hosp, 101 Dudley St, Providence, RI 02905 USA.
EM Juliejohnson14@me.com
RI Samuels, Philip/E-4011-2011; Varner, Michael/K-9890-2013
OI Peaceman, Alan/0000-0002-4515-4850; Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) [HD34208, HD27869, HD40485, HD40560, HD40544,
HD34116, HD40512, HD21410, HD40545, HD40500, HD27915, HD34136, HD27860,
HD53118, HD53097, HD27917, HD36801]; National Heart, Lung, and Blood
Institute (NHLBI); National Center for Research Resources (NCRR) [M01
RR00080, UL1 RR024153, UL1 RR024989]
FX The project described was supported by grants from the Eunice Kennedy
Shriver National Institute of Child Health and Human Development (NICHD)
(HD34208, HD27869, HD40485, HD40560, HD40544, HD34116, HD40512, HD21410,
HD40545, HD40500, HD27915, HD34136, HD27860, HD53118, HD53097, HD27917,
and HD36801); the National Heart, Lung, and Blood Institute (NHLBI); and
the National Center for Research Resources (NCRR) (M01 RR00080, UL1
RR024153, UL1 RR024989) and its contents do not necessarily represent
the official view of NICHD, NHLBI, NCRR, or National Institutes of
Health.
NR 11
TC 67
Z9 75
U1 1
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD MAY
PY 2013
VL 121
IS 5
BP 969
EP 975
DI 10.1097/AOG.0b013e31828aea03
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 139SU
UT WOS:000318605400009
PM 23635732
ER
PT J
AU Berger, JT
Carcillo, JA
Shanley, TP
Wessel, DL
Clark, A
Holubkov, R
Meert, KL
Newth, CJL
Berg, RA
Heidemann, S
Harrison, R
Pollack, M
Dalton, H
Harvill, E
Karanikas, A
Liu, T
Burr, JS
Doctor, A
Dean, JM
Jenkins, TL
Nicholson, CE
AF Berger, John T.
Carcillo, Joseph A.
Shanley, Thomas P.
Wessel, David L.
Clark, Amy
Holubkov, Richard
Meert, Kathleen L.
Newth, Christopher J. L.
Berg, Robert A.
Heidemann, Sabrina
Harrison, Rick
Pollack, Murray
Dalton, Heidi
Harvill, Eric
Karanikas, Alexia
Liu, Teresa
Burr, Jeri S.
Doctor, Allan
Dean, J. Michael
Jenkins, Tammara L.
Nicholson, Carol E.
CA Eunice Kennedy Shriver NICHD CPCCR
TI Critical Pertussis Illness in Children: A Multicenter Prospective Cohort
Study
SO PEDIATRIC CRITICAL CARE MEDICINE
LA English
DT Article
DE intensive care; leukocyte reduction procedures; outcome; pertussis;
pulmonary hypertension; respiratory failure
ID ADENYLATE-CYCLASE TOXIN; REGULATORY T-CELLS; BORDETELLA-PERTUSSIS;
INTERLEUKIN-10 PRODUCTION; IL-12 PRODUCTION; DENDRITIC CELLS;
INTENSIVE-CARE; UNITED-STATES; INFECTION; INFANTS
AB Objective: Pertussis persists in the United States despite high immunization rates. This report characterizes the presentation and acute course of critical pertussis by quantifying demographic data, laboratory findings, clinical complications, and critical care therapies among children requiring admission to the PICU.
Design: Prospective cohort study.
Setting: Eight PICUs comprising the Eunice Kennedy Shriver National Institute for Child Health and Human Development Collaborative Pediatric Critical Care Research Network and 17 additional PICUs across the United States.
Patients: Eligible patients had laboratory confirmation of pertussis infection, were younger than 18 years old, and died in the PICU or were admitted to the PICU for at least 24 hours between June 2008 and August 2011.
Interventions: None.
Measurements and Main Results: A total of 127 patients were identified. Median age was 49 days, and 105 (83%) patients were less than 3 months old. Fifty-five (43%) patients required mechanical ventilation and 12 patients (9.4%) died during initial hospitalization. Pulmonary hypertension was found in 16 patients (12.5%) and was present in 75% of patients who died, compared with 6% of survivors (p < 0.001). Median WBC was significantly higher in those requiring mechanical ventilation (p < 0.001), those with pulmonary hypertension (p < 0.001), and nonsurvivors (p < 0.001). Age, sex, and immunization status did not differ between survivors and nonsurvivors. Fourteen patients received leukoreduction therapy (exchange transfusion [12], leukopheresis [1], or both [1]). Survival benefit was not apparent.
Conclusions: Pulmonary hypertension may be associated with mortality in pertussis critical illness. Elevated WBC is associated with the need for mechanical ventilation, pulmonary hypertension, and mortality risk. Research is indicated to elucidate how pulmonary hypertension, immune responsiveness, and elevated WBC contribute to morbidity and mortality and whether leukoreduction might be efficacious.
C1 [Berger, John T.; Wessel, David L.] Childrens Natl Med Ctr, Dept Pediat, Washington, DC 20010 USA.
[Carcillo, Joseph A.] Childrens Hosp Pittsburgh, Dept Crit Care Med, Pittsburgh, PA 15213 USA.
[Shanley, Thomas P.] Univ Michigan, CS Mott Childrens Hosp, Dept Pediat, Ann Arbor, MI 48109 USA.
[Clark, Amy; Holubkov, Richard; Liu, Teresa; Burr, Jeri S.; Dean, J. Michael] Univ Utah, Dept Pediat, Salt Lake City, UT USA.
[Meert, Kathleen L.; Heidemann, Sabrina] Childrens Hosp Michigan, Dept Pediat, Detroit, MI 48201 USA.
[Newth, Christopher J. L.] Childrens Hosp Los Angeles, Dept Anesthesiol & Crit Care Med, Los Angeles, CA 90027 USA.
[Berg, Robert A.] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA.
[Harrison, Rick] Mattel Childrens Hosp UCLA, Dept Pediat, Los Angeles, CA USA.
[Pollack, Murray; Dalton, Heidi] Phoenix Childrens Hosp, Dept Child Hlth, Phoenix, AZ USA.
[Harvill, Eric; Karanikas, Alexia] Penn State Univ, University Pk, PA 16802 USA.
[Doctor, Allan] St Louis Childrens Hosp, Dept Pediat, St Louis, MO 63110 USA.
[Doctor, Allan] St Louis Childrens Hosp, Dept Biochem, St Louis, MO 63110 USA.
[Jenkins, Tammara L.; Nicholson, Carol E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Dept Pediat, Bethesda, MD USA.
RP Berger, JT (reprint author), Childrens Natl Med Ctr, Dept Pediat, Washington, DC 20010 USA.
EM jberger@cnmc.org
RI Weber, Michael/L-9836-2016;
OI Weber, Michael/0000-0002-8507-2219; Doctor, Allan/0000-0002-6096-6400
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, Department of Health and Human Services [U10HD050096,
U10HD049981, U10HD049983, U10HD050012, U10HD063108, U10HD063106,
U10HD063114, U10HD049945, U10HD050009, U01HD049934]; National Vaccine
Program Office at the United States Department of Health and Human
Services
FX Supported, in part, by cooperative agreements from the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
Department of Health and Human Services (U10HD050096, U10HD049981,
U10HD049983, U10HD050012, U10HD063108, U10HD063106, U10HD063114,
U10HD049945, U10HD050009, and U01HD049934), and the National Vaccine
Program Office at the United States Department of Health and Human
Services.
NR 41
TC 28
Z9 33
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1529-7535
J9 PEDIATR CRIT CARE ME
JI Pediatr. Crit. Care Med.
PD MAY
PY 2013
VL 14
IS 4
BP 356
EP 365
DI 10.1097/PCC.0b013e31828a70fe
PG 10
WC Critical Care Medicine; Pediatrics
SC General & Internal Medicine; Pediatrics
GA 140UA
UT WOS:000318680000009
PM 23548960
ER
PT J
AU Holubkov, R
Casper, TC
Dean, JM
Anand, KJS
Zimmerman, J
Meert, KL
Newth, CJL
Berger, J
Harrison, R
Willson, DF
Nicholson, C
AF Holubkov, Richard
Casper, T. Charles
Dean, J. Michael
Anand, K. J. S.
Zimmerman, Jerry
Meert, Kathleen L.
Newth, Christopher J. L.
Berger, John
Harrison, Rick
Willson, Douglas F.
Nicholson, Carol
CA Eunice Kennedy Shriver Natl Inst C
TI The Role of the Data and Safety Monitoring Board in a Clinical Trial:
The CRISIS Study
SO PEDIATRIC CRITICAL CARE MEDICINE
LA English
DT Review
DE clinical trials; interim analysis; nosocomial infection; randomized;
safety; sepsis
ID FUTILITY
AB Objectives: Randomized clinical trials are commonly overseen by a Data and Safety Monitoring Board comprised of experts in medicine, ethics, and biostatistics. Data and Safety Monitoring Board responsibilities include protocol approval, interim review of study enrollment, protocol compliance, safety, and efficacy data. Data and Safety Monitoring Board decisions can affect study design and conduct, as well as reported findings. Researchers must incorporate Data and Safety Monitoring Board oversight into the design, monitoring, and reporting of randomized trials.
Design: Case study, narrative review.
Methods: The Data and Safety Monitoring Board's role during the comparative pediatric Critical Illness Stress-Induced Immune Suppression (CRISIS) Prevention Trial is described.
Findings: The National Institutes of Health-appointed CRISIS Data and Safety Monitoring Board was charged with monitoring sample size adequacy and feasibility, safety with respect to adverse events and 28-day mortality, and efficacy with respect to the primary nosocomial infection/sepsis outcome. The Federal Drug Administration also requested Data and Safety Monitoring Board interim review before opening CRISIS to children below 1 yr of age. The first interim analysis found higher 28-day mortality in one treatment arm. The Data and Safety Monitoring Board maintained trial closure to younger children and requested a second interim data review 6 months later. At this second meeting, mortality was no longer of concern, whereas a weak efficacy trend of lower infection/sepsis rates in one study arm emerged. As over 40% of total patients had been enrolled, the Data and Safety Monitoring Board elected to examine conditional power and unmask treatment arm identities. On finding somewhat greater efficacy in the placebo arm, the Data and Safety Monitoring Board recommended stopping CRISIS due to futility.
Conclusions: The design and operating procedures of a multicenter randomized trial must consider a pivotal Data and Safety Monitoring Board role. Maximum study design flexibility must be allowed, and investigators must be prepared for protocol modifications due to interim findings. The Data and Safety Monitoring Board must have sufficient clinical and statistical expertise to assess potential importance of interim treatment differences in the setting of multiple looks at accumulating data with numerous outcomes and subgroups.
C1 [Holubkov, Richard; Casper, T. Charles; Dean, J. Michael] Univ Utah, Sch Med, Dept Pediat, Div Crit Care, Salt Lake City, UT 84112 USA.
[Anand, K. J. S.] Univ Tennessee, Ctr Hlth Sci, Dept Pediat, Le Bonheur Childrens Hosp, Memphis, TN 38163 USA.
[Anand, K. J. S.] Univ Tennessee, Ctr Hlth Sci, Le Bonheur Childrens Hosp, Dept Anesthesiol, Memphis, TN 38163 USA.
[Anand, K. J. S.] Univ Tennessee, Ctr Hlth Sci, Le Bonheur Childrens Hosp, Dept Neurobiol, Memphis, TN 38163 USA.
[Zimmerman, Jerry] Univ Washington, Sch Med, Dept Pediat, Seattle Childrens Hosp, Seattle, WA 98195 USA.
[Meert, Kathleen L.] Childrens Hosp Michigan, Dept Pediat, Detroit, MI 48201 USA.
[Newth, Christopher J. L.] Childrens Hosp Los Angeles, Dept Anesthesiol & Crit Care Med, Los Angeles, CA 90027 USA.
[Berger, John] Childrens Natl Med Ctr, Dept Pediat, Washington, DC 20010 USA.
[Harrison, Rick] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[Willson, Douglas F.] Univ Virginia, Dept Pediat, Childrens Hosp, Charlottesville, VA USA.
[Nicholson, Carol] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Holubkov, R (reprint author), Univ Utah, Sch Med, Dept Pediat, Div Crit Care, Salt Lake City, UT 84112 USA.
EM rich.holubkov@hsc.utah.edu
OI Anand, Kanwaljeet/0000-0001-6498-1483
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD); National Institutes of Health (NIH); Department of
Health and Human Services (DHHS) [U10HD050096, U10HD049981, U10HD500009,
U10HD049945, U10HD049983, U10HD050012, U01HD049934]
FX Supported, in part, by cooperative agreements from the Eunice Kennedy
Shriver National Institute of Child Health and Human Development
(NICHD), National Institutes of Health (NIH), Department of Health and
Human Services (DHHS) (U10HD050096, U10HD049981, U10HD500009,
U10HD049945, U10HD049983, U10HD050012 and U01HD049934).
NR 20
TC 2
Z9 2
U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1529-7535
J9 PEDIATR CRIT CARE ME
JI Pediatr. Crit. Care Med.
PD MAY
PY 2013
VL 14
IS 4
BP 374
EP 383
DI 10.1097/PCC.0b013e318274568c
PG 10
WC Critical Care Medicine; Pediatrics
SC General & Internal Medicine; Pediatrics
GA 140UA
UT WOS:000318680000011
PM 23392377
ER
PT J
AU Heidemann, SM
Holubkov, R
Meert, KL
Dean, JM
Berger, J
Bell, M
Anand, KJS
Zimmerman, J
Newth, CJL
Harrison, R
Willson, DF
Nicholson, C
Carcillo, J
AF Heidemann, Sabrina M.
Holubkov, Richard
Meert, Kathleen L.
Dean, J. Michael
Berger, John
Bell, Michael
Anand, K. J. S.
Zimmerman, Jerry
Newth, Christopher J. L.
Harrison, Rick
Willson, Douglas F.
Nicholson, Carol
Carcillo, Joseph
CA Eunice Kennedy Shriver NICHD CPCCR
TI Baseline Serum Concentrations of Zinc, Selenium, and Prolactin in
Critically III Children
SO PEDIATRIC CRITICAL CARE MEDICINE
LA English
DT Article
DE children; intensive care; lymphocytes; prolactin; selenium; zinc
ID PEDIATRIC CRITICAL ILLNESS; MULTIPLE ORGAN FAILURE; HOMEOSTASIS; CELLS;
SCORE
AB Objectives: To describe serum concentrations of zinc, selenium, and prolactin in critically ill children within 72 hours of PICU admission, and to investigate relationships between these immunomodulators and lymphopenia.
Design: An analysis of baseline data collected as part of the multi-center Critical Illness Stress Induced Immune Suppression (CRISIS) Prevention Trial.
Setting: PICUs affiliated with the Collaborative Pediatric Critical Care Research Network.
Patients: All children enrolled in the CRISIS Prevention Trial that had baseline serum samples available for analysis.
Interventions: None.
Measurements and Main Results: Of 293 critically ill children enrolled in the CRISIS Prevention Trial, 284 had baseline serum samples analyzed for prolactin concentration, 280 for zinc concentration, and 278 for selenium concentration within 72 hours of PICU admission. Lymphocyte counts were available for 235 children. Zinc levels ranged from nondetectable (< 0.1 mu g/mL) to 2.87 mu g/mL (mean 0.46 mu g/mL and median 0.44 mu g/mL) and were below the normal reference range for 235 (83.9%) children. Selenium levels ranged from 26 to 145 ng/mL (mean 75.4 ng/mL and median 74.5 ng/mL) and were below the normal range for 156 (56.1%) children. Prolactin levels ranged from nondetectable (< 1 ng/mL) to 88 ng/mL (mean 12.2 ng/mL and median 10 ng/mL). Hypoprolactinemia was present in 68 (23.9%) children. Lymphopenia was more likely in children with zinc levels below normal than those with zinc levels within or above the normal range (82 of 193 [42.5%] vs. 10 of 39 [25.6%], p = 0.0498). Neither selenium nor prolactin concentrations were associated with lymphopenia (p = 1.0 and p = 0.72, respectively).
Conclusions: Serum concentrations of zinc, selenium, and prolactin are often low in critically ill children early after PICU admission. Low serum zinc levels are associated with lymphopenia, whereas low selenium and prolactin levels are not. The implications of these findings and the mechanisms by which they occur merit further study.
C1 [Heidemann, Sabrina M.; Meert, Kathleen L.] Childrens Hosp Michigan, Dept Pediat, Detroit, MI 48201 USA.
[Holubkov, Richard; Dean, J. Michael] Univ Utah, Dept Pediat, State Lake City, UT USA.
[Berger, John] Childrens Natl Med Ctr, Dept Pediat, Washington, DC 20010 USA.
[Bell, Michael; Carcillo, Joseph] Childrens Hosp Pittsburgh, Dept Crit Care Med, Pittsburgh, PA 15213 USA.
[Anand, K. J. S.] Arkansas Childrens Hosp, Dept Pediat, Little Rock, AR 72202 USA.
[Zimmerman, Jerry] Seattle Childrens Hosp, Dept Pediat, Seattle, WA USA.
[Newth, Christopher J. L.] Childrens Hosp Los Angeles, Dept Pediat, Los Angeles, CA 90027 USA.
[Harrison, Rick] Univ Calif Los Angeles, Dept Pediat, Mattel Childrens Hosp, Los Angeles, CA 90024 USA.
[Willson, Douglas F.] Univ Virginia, Childrens Hosp, Dept Pediat, Charlottesville, VA USA.
[Nicholson, Carol] Natl Inst Child Hlth & Human Dev, Rockville, MD USA.
RP Meert, KL (reprint author), Childrens Hosp Michigan, Dept Pediat, Detroit, MI 48201 USA.
EM kmeert@med.wayne.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD), National Institutes of Health (NIH), Department of
Health and Human Services (DHHS) [U10HD050096, U10HD049981, U10HD500009,
U10HD049945, U10HD049983, U10HD050012, U01HD049934]
FX Supported, in part, by the following cooperative agreements from the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD), National Institutes of Health (NIH), Department of
Health and Human Services (DHHS): U10HD050096, U10HD049981, U10HD500009,
U10HD049945, U10HD049983, U10HD050012, and U01HD049934.
NR 16
TC 10
Z9 11
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1529-7535
J9 PEDIATR CRIT CARE ME
JI Pediatr. Crit. Care Med.
PD MAY
PY 2013
VL 14
IS 4
BP E202
EP E206
DI 10.1097/PCC.0b013e31827200f5
PG 5
WC Critical Care Medicine; Pediatrics
SC General & Internal Medicine; Pediatrics
GA 140UA
UT WOS:000318680000006
PM 23392368
ER
PT J
AU Levran, O
Peles, E
Randesi, M
Shu, X
Ott, J
Shen, PH
Adelson, M
Kreek, MJ
AF Levran, Orna
Peles, Einat
Randesi, Matthew
Shu, Xu
Ott, Jurg
Shen, Pei-Hong
Adelson, Miriam
Kreek, Mary Jeanne
TI Association of genetic variation in pharmacodynamic factors with
methadone dose required for effective treatment of opioid addiction
SO PHARMACOGENOMICS
LA English
DT Article
DE ANKK1; BDNF; DRD2; methadone maintenance; NTRK2; OPRM1; pharmacogenetics
ID NEUROTROPHIC FACTOR GENE; FAMILY-BASED ASSOCIATION; RECEPTOR GENE;
BIPOLAR DISORDER; ALCOHOL DEPENDENCE; HEROIN-ADDICTION; ANTIDEPRESSANT
TREATMENT; CONFERS SUSCEPTIBILITY; MAINTENANCE TREATMENT; FUNCTIONAL
VARIANTS
AB Aim: The interindividual variability in the dose required for effective methadone maintenance treatment (MMT) for opioid addiction may be influenced in part by genetic variations in genes encoding pharmacodynamic factors of methadone. This study was conducted to identify some of these variants. Materials & methods: This study focused on 11 genes encoding components of the opioidergic (OPRM1, POMC and ARRB2), the dopaminergic (ANKK1 and DRD2) and the glutamatergic pathways (GRIN1 and GRIN2A), as well as the neurotrophin system (NGFB, BDNF, NTRK1 and NTRK2). The study includes 227 Israeli patients undergoing stable MMT. Results: Out of the 110 variants analyzed, 12 SNPs (in BDNF, NTRK2, OPRM1, DRD2 and ANKK1) were associated with methadone dose (nominal p < 0.05). Of these SNPs, ANKK1 rs7118900 and DRD2 rs2283265 are known to affect gene expression. Logistic regression of five representative SNPs discriminated between individuals requiring a methadone dose of >120 mg/day and <120 mg/day (p = 0.019), and showed moderate sensitivity and specificity (AUC of 0.63 in receiver operating characteristic analysis). Conclusion: This data should stimulate further research on the potential influence and clinical significance of these variants on MMT. Original submitted 14 November 2012; Revision submitted 12 March 2013.
C1 [Levran, Orna; Randesi, Matthew; Kreek, Mary Jeanne] Rockefeller Univ, Lab Biol Addicit Dis, New York, NY 10021 USA.
[Peles, Einat; Adelson, Miriam] Ellas Sourasky Med Ctr, Dr Miriam & Sheidom G Adelison Clin Drug Abuse Tr, Tel Aviv, Israel.
[Shu, Xu] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Ott, Jurg] Inst Psychol CAS, Beijing, Peoples R China.
[Ott, Jurg] Rockefeller Univ, Lab Stat Genet, New York, NY USA.
[Shen, Pei-Hong] NIAAA, Neurogenet Lab, Bethesda, MD USA.
RP Levran, O (reprint author), Rockefeller Univ, Lab Biol Addicit Dis, New York, NY 10021 USA.
EM levrano@rockefeller.edu
FU NIDA [P60-05130]; National Center fir Research Resources [8 UL1
TR000043]; National Center for Advancing Translational Sciences, NIH;
Adelson Medical Research Foundation
FX Funding was provided by P60-05130 from NIDA (MJ Kreek), grant # 8 UL1
TR000043 from the National Center fir Research Resources and the
National Center for Advancing Translational Sciences, NIH (pilot award,
O Levran) and the Adelson Medical Research Foundation. 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 watt or materials discussed in the manuscript
apart from those disclosed.
NR 98
TC 10
Z9 12
U1 2
U2 14
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1462-2416
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PD MAY
PY 2013
VL 14
IS 7
BP 755
EP 768
DI 10.2217/PGS.13.58
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 143DH
UT WOS:000318846100016
PM 23651024
ER
PT J
AU Fernandez-Vina, MA
Wang, T
Lee, SJ
Haagenson, M
Aljurf, M
Askar, M
Battiwalla, M
Baxter-Lowe, LA
Gajewski, J
Jakubowski, A
Marino, S
Oudshoorn, M
Marsh, SGE
Petersdorf, EW
Schultz, K
Turner, V
Waller, E
Woolfrey, A
Umejiego, J
Spellman, SR
Setterholm, M
AF Fernandez-Vina, Marcelo A.
Wang, Tao
Lee, Stephanie J.
Haagenson, Michael
Aljurf, Mahmoud
Askar, Medhat
Battiwalla, Minoo
Baxter-Lowe, Lee-Ann
Gajewski, James
Jakubowski, Ann
Marino, Susana
Oudshoorn, Machteld
Marsh, Steven G. E.
Petersdorf, Effie W.
Schultz, Kirk
Turner, Victoria
Waller, Edmund
Woolfrey, Ann
Umejiego, John
Spellman, Stephen R.
Setterholm, Michelle
TI MISMATCHES FOR HLA-C*03:03/03:04 MAY BE BETTER TOLERATED THAN OTHER
MISMATCHES IN UNRELATED DONOR HEMATOPOIETIC STEM CELL TRANSPLANTATION
SO TISSUE ANTIGENS
LA English
DT Meeting Abstract
CT 27th Annual EFI European Immunogenetics and Histocompatibility
Conference
CY MAY 11-14, 2013
CL Maastricht, NETHERLANDS
SP EFI
C1 [Fernandez-Vina, Marcelo A.] Stanford Sch Med, Palo Alto, CA USA.
[Wang, Tao] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Lee, Stephanie J.; Petersdorf, Effie W.; Woolfrey, Ann] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Haagenson, Michael; Umejiego, John; Spellman, Stephen R.] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
[Aljurf, Mahmoud] King Faisal Specialist Hosp & Res Ctr, Riyadh 11211, Saudi Arabia.
[Askar, Medhat] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
[Battiwalla, Minoo] NHLBI, NIH, Bethesda, MD 20892 USA.
[Baxter-Lowe, Lee-Ann] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Gajewski, James] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Jakubowski, Ann] Mem Sloan Kettering, New York, NY USA.
[Marino, Susana] Univ Chicago, Chicago, IL 60637 USA.
[Oudshoorn, Machteld] Leiden Univ, Med Ctr, Europdonor Fdn, Leiden, Netherlands.
[Marsh, Steven G. E.] Anthony Nolan Res Trust, London, England.
[Schultz, Kirk] British Columbia Childrens Hosp, Vancouver, BC V6H 3V4, Canada.
[Turner, Victoria] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Waller, Edmund] Emory Univ Hosp, Atlanta, GA 30322 USA.
[Setterholm, Michelle] Natl Marrow Donor Program, Minneapolis, MN USA.
EM marcelof@stanford.edu
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 0001-2815
J9 TISSUE ANTIGENS
JI Tissue Antigens
PD MAY
PY 2013
VL 81
IS 5
BP 292
EP 293
PG 2
WC Cell Biology; Immunology; Pathology
SC Cell Biology; Immunology; Pathology
GA 138QN
UT WOS:000318523600070
ER
PT J
AU Saenz-Lopez, P
Reinboth, J
Rodriguez, AI
Bedognetti, D
Carretero, R
Marincola, F
Garrido, F
Wang, E
Cabrera, T
AF Saenz-Lopez, Pablo
Reinboth, Jennifer
Rodriguez, Ana I.
Bedognetti, Davide
Carretero, Rafael
Marincola, Francesco
Garrido, Federico
Wang, Ena
Cabrera, Teresa
TI COMPARATIVE GENE EXPRESSION ANALYSIS OF GENES ASSOCIATED WITH T CELLS
SUBSETS IN BLADDER TUMORS TREATED WITH BCG: ASSOCIATION WITH CANCER
RECURRENCE
SO TISSUE ANTIGENS
LA English
DT Meeting Abstract
CT 27th Annual EFI European Immunogenetics and Histocompatibility
Conference
CY MAY 11-14, 2013
CL Maastricht, NETHERLANDS
SP EFI
C1 [Saenz-Lopez, Pablo; Rodriguez, Ana I.; Garrido, Federico] Hosp Univ de las Virgen Nieves, Granada, Spain.
[Reinboth, Jennifer; Bedognetti, Davide; Marincola, Francesco; Wang, Ena] NIH, Bethesda, MD 20892 USA.
[Carretero, Rafael] Deutsch Krebsforschungszentrum DKFZ, Heidelberg, Germany.
[Cabrera, Teresa] Univ Granada, Granada, Spain.
EM tcabrera@ugr.es
RI Cabrera, Teresa/L-5332-2015
OI Cabrera, Teresa/0000-0002-9871-1374
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 0001-2815
J9 TISSUE ANTIGENS
JI Tissue Antigens
PD MAY
PY 2013
VL 81
IS 5
BP 353
EP 353
PG 1
WC Cell Biology; Immunology; Pathology
SC Cell Biology; Immunology; Pathology
GA 138QN
UT WOS:000318523600218
ER
PT J
AU Panch, SR
Riordan, MM
Miranda, SJ
Leitman, SF
AF Panch, Sandhya R.
Riordan, Monica M.
Miranda, Susan J.
Leitman, Susan F.
TI Intermittent leukocytosis in an asymptomatic platelet donor
SO TRANSFUSION
LA English
DT Letter
ID EXERCISE; NEUTROPHILIA; CELLS
C1 [Panch, Sandhya R.; Riordan, Monica M.; Miranda, Susan J.; Leitman, Susan F.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Panch, SR (reprint author), NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
EM Sandhya.Panch@nih.gov
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 0041-1132
J9 TRANSFUSION
JI Transfusion
PD MAY
PY 2013
VL 53
IS 5
BP 1144
EP 1146
DI 10.1111/trf.12155
PG 3
WC Hematology
SC Hematology
GA 140MC
UT WOS:000318657200032
PM 23659533
ER
PT J
AU Tholpady, A
Chiosea, I
Lyons, JJ
Baird, K
Leitman, SF
AF Tholpady, Ashok
Chiosea, Ion
Lyons, Jonathan J.
Baird, Kristin
Leitman, Susan F.
TI Systemic hypersensitivity reaction mimicking anaphylaxis after first
filgrastim administration in a healthy donor
SO TRANSFUSION
LA English
DT Letter
ID COLONY-STIMULATING FACTOR
C1 [Tholpady, Ashok; Chiosea, Ion; Lyons, Jonathan J.] NIAID, Bethesda, MD 20892 USA.
[Baird, Kristin] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Leitman, Susan F.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
RP Tholpady, A (reprint author), NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM tholpady.ashok@nih.gov
OI Tholpady, Ashok/0000-0003-3978-9574; Lyons, Jonathan/0000-0002-2346-8189
FU Intramural NIH HHS [Z99 AI999999]
NR 6
TC 5
Z9 5
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0041-1132
J9 TRANSFUSION
JI Transfusion
PD MAY
PY 2013
VL 53
IS 5
BP 1146
EP 1147
DI 10.1111/trf.12149
PG 2
WC Hematology
SC Hematology
GA 140MC
UT WOS:000318657200033
PM 23659534
ER
PT J
AU Cimms, TA
DeBusk, K
Howard, K
Siuciak, JA
Llorens, L
Crawley, J
Halling, K
Powers, JH
AF Cimms, T. A.
DeBusk, K.
Howard, K.
Siuciak, J. A.
Llorens, L.
Crawley, J.
Halling, K.
Powers, J. H.
CA FNIH Biomarkers Consortium CABP AB
TI ACUTE BACTERIAL SKIN AND SKIN STRUCTURE INFECTIONS (ABSSSI)
SIGNS/SYMPTOMS AND PROS: A COMPREHENSIVE LITERATURE REVIEW
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Cimms, T. A.; DeBusk, K.; Howard, K.] Oxford Outcomes Ltd, San Francisco, CA USA.
[Siuciak, J. A.; FNIH Biomarkers Consortium CABP AB] Fdn Natl Inst Hlth, Bethesda, MD USA.
[Llorens, L.] Cerexa Inc, Oakland, CA USA.
[Crawley, J.] AstraZeneca Pharmaceut LP, Wilmington, DE USA.
[Howard, K.] AstraZeneca, Molndal, Sweden.
[Powers, J. H.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD MAY
PY 2013
VL 16
IS 3
BP A32
EP A32
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 144CE
UT WOS:000318916400166
ER
PT J
AU Cimms, TA
DeBusk, K
Howard, K
Siuciak, JA
Llorens, L
Crawley, J
Halling, K
Powers, JH
AF Cimms, T. A.
DeBusk, K.
Howard, K.
Siuciak, J. A.
Llorens, L.
Crawley, J.
Halling, K.
Powers, J. H.
CA FNIH Biomarkers Consortium CABP AB
TI CLINICAL MEASUREMENT CONCEPTS IN ACUTE SKIN AND SKIN STRUCTURE
INFECTIONS AND OTHER SKIN ABNORMALITIES: A COMPREHENSIVE LITERATURE
REVIEW
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Cimms, T. A.; DeBusk, K.; Howard, K.] Oxford Outcomes Ltd, San Francisco, CA USA.
[Siuciak, J. A.; FNIH Biomarkers Consortium CABP AB] Fdn Natl Inst Hlth, Bethesda, MD USA.
[Llorens, L.] Cerexa Inc, Oakland, CA USA.
[Crawley, J.] AstraZeneca Pharmaceut LP, Wilmington, DE USA.
[Halling, K.] AstraZeneca, Molndal, Sweden.
[Powers, J. H.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD MAY
PY 2013
VL 16
IS 3
BP A31
EP A31
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 144CE
UT WOS:000318916400160
ER
PT J
AU Guy, GP
Ekwueme, DU
Yabroff, KR
Dowling, EC
Li, C
Rodriguez, J
de Moor, JS
Virgo, KS
AF Guy, G. P., Jr.
Ekwueme, D. U.
Yabroff, K. R.
Dowling, E. C.
Li, C.
Rodriguez, J.
de Moor, J. S.
Virgo, K. S.
TI THE ECONOMIC BURDEN OF CANCER SURVIVORSHIP AMONG ADULTS IN THE UNITED
STATES
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Guy, G. P., Jr.; Ekwueme, D. U.; Li, C.; Rodriguez, J.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Yabroff, K. R.; de Moor, J. S.] NCI, Bethesda, MD 20892 USA.
[Dowling, E. C.] Inst Technol Assessment, Boston, MA USA.
[Virgo, K. S.] Emory Univ, Atlanta, GA 30322 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD MAY
PY 2013
VL 16
IS 3
BP A136
EP A137
PG 3
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 144CE
UT WOS:000318916401207
ER
PT J
AU Powers, JH
Siuciak, JA
Llorens, L
Talbot, GH
Crawley, J
Halling, K
Cimms, TA
DeBusk, K
Howard, K
AF Powers, J. H.
Siuciak, J. A.
Llorens, L.
Talbot, G. H.
Crawley, J.
Halling, K.
Cimms, T. A.
DeBusk, K.
Howard, K.
CA FNIH Biomarkers Consortium CABP AB
TI DEVELOPMENT OF A NEW PATIENT REPORTED OUTCOME (PRO) MEASURE FOR ACUTE
BACTERIAL SKIN AND SKIN STRUCTURE INFECTIONS (ABSSSI)
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Powers, J. H.] NIAID, NIH, Bethesda, MD 20892 USA.
[Siuciak, J. A.; FNIH Biomarkers Consortium CABP AB] Fdn Natl Inst Hlth, Bethesda, MD USA.
[Llorens, L.] Cerexa Inc, Oakland, CA USA.
[Talbot, G. H.] Talbot Advisors LLC, Anna Maria, FL USA.
[Crawley, J.] AstraZeneca Pharmaceut LP, Wilmington, DE USA.
[Halling, K.] AstraZeneca, Molndal, Sweden.
[Cimms, T. A.; DeBusk, K.; Howard, K.] Oxford Outcomes Ltd, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD MAY
PY 2013
VL 16
IS 3
BP A46
EP A46
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 144CE
UT WOS:000318916400236
ER
PT J
AU Gustafson, C
Roizen, MF
AF Gustafson, Craig
Roizen, Michael F.
TI Michael Roizen, MD: Motivating Patients to Live Younger and the Fatal
Flaw of Wellness Programs
SO ALTERNATIVE THERAPIES IN HEALTH AND MEDICINE
LA English
DT Editorial Material
C1 [Roizen, Michael F.] NIH, Bethesda, MD USA.
[Roizen, Michael F.] US FDA, Advisory Comm, Rockville, MD 20857 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU INNOVISION COMMUNICATIONS
PI ALISO VIEJO
PA 101 COLUMBIA, ALISO VIEJO, CA 92656 USA
SN 1078-6791
J9 ALTERN THER HEALTH M
JI Altern. Ther. Health Med.
PD MAY-JUN
PY 2013
VL 19
IS 3
BP 48
EP 54
PG 7
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 142TZ
UT WOS:000318821800007
ER
PT J
AU Lacro, RV
Guey, LT
Dietz, HC
Pearson, GD
Yetman, AT
Gelb, BD
Loeys, BL
Benson, DW
Bradley, TJ
De Backer, J
Forbus, GA
Klein, GL
Lai, WW
Levine, JC
Lewin, MB
Markham, LW
Paridon, SM
Pierpont, ME
Radojewski, E
Tierney, ESS
Sharkey, AM
Wechsler, SB
Mahony, L
AF Lacro, Ronald V.
Guey, Lin T.
Dietz, Harry C.
Pearson, Gail D.
Yetman, Anji T.
Gelb, Bruce D.
Loeys, Bart L.
Benson, D. Woodrow
Bradley, Timothy J.
De Backer, Julie
Forbus, Geoffrey A.
Klein, Gloria L.
Lai, Wyman W.
Levine, Jami C.
Lewin, Mark B.
Markham, Larry W.
Paridon, Stephen M.
Pierpont, Mary Ella
Radojewski, Elizabeth
Tierney, Elif Seda Selamet
Sharkey, Angela M.
Wechsler, Stephanie Burns
Mahony, Lynn
TI Characteristics of children and young adults with Marfan syndrome and
aortic root dilation in a randomized trial comparing atenolol and
losartan therapy
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID BETA-BLOCKER THERAPY; FBN1 MUTATIONS; MOUSE MODEL; PATHOGENESIS;
PROBANDS
AB Background The Pediatric Heart Network designed a clinical trial to compare aortic root growth and other short-term cardiovascular outcomes in children and young adults with Marfan syndrome randomized to receive atenolol or losartan. We report here the characteristics of the screened population and enrolled subjects.
Methods and results Between 2007 and 2011, 21 clinical sites randomized 608 subjects, aged 6 months to 25 years who met the original Ghent criteria and had a body surface area-adjusted aortic root diameter z-score >3.0. The mean age at study entry was 11.2 years, 60% were male, and 25% were older teenagers and young adults. The median aortic root diameter z-score was 4.0. Aortic root diameter z-score did not vary with age. Mitral valve prolapse and mitral regurgitation were more common in females. Among those with a positive family history, 56% had a family member with aortic surgery, and 32% had a family member with a history of aortic dissection.
Conclusions Baseline demographic, clinical, and anthropometric characteristics of the randomized cohort are representative of patients in this population with moderate to severe aortic root dilation. The high percentage of young subjects with relatives who have had aortic dissection or surgery illustrates the need for more definitive therapy; we expect that the results of the study and the wealth of systematic data collected will make an important contribution to the management of individuals with Marfan syndrome.
C1 [Lacro, Ronald V.; Levine, Jami C.; Tierney, Elif Seda Selamet] Childrens Hosp Boston, Boston, MA 02115 USA.
[Guey, Lin T.; Klein, Gloria L.] New England Res Inst, Watertown, MA 02172 USA.
[Dietz, Harry C.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Pearson, Gail D.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Yetman, Anji T.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Yetman, Anji T.] Univ Utah, Salt Lake City, UT USA.
[Gelb, Bruce D.] Mt Sinai Sch Med, New York, NY USA.
[Loeys, Bart L.] Univ Antwerp Hosp, Antwerp, Belgium.
[Loeys, Bart L.] Univ Antwerp, B-2020 Antwerp, Belgium.
[Benson, D. Woodrow] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Bradley, Timothy J.; Radojewski, Elizabeth] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[De Backer, Julie] Ghent Univ Hosp, Ghent, Belgium.
[Forbus, Geoffrey A.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Lai, Wyman W.] Childrens Hosp New York, New York, NY USA.
[Lewin, Mark B.] Seattle Childrens Hosp, Seattle, WA USA.
[Markham, Larry W.] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
[Paridon, Stephen M.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Pierpont, Mary Ella] Childrens Hosp & Clin Minnesota, St Paul, MN USA.
[Sharkey, Angela M.] St Louis Univ, Sch Med, St Louis, MO USA.
[Wechsler, Stephanie Burns] Duke Univ, Med Ctr, Durham, NC USA.
[Mahony, Lynn] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
RP Lacro, RV (reprint author), Childrens Hosp Boston, Dept Cardiol, 300 Longwood Ave, Boston, MA 02115 USA.
EM ron.lacro@cardio.chboston.org
RI De Backer, Julie/B-2897-2014;
OI De Backer, Julie/0000-0001-8878-1507; Loeys, Bart/0000-0003-3703-9518
FU NCATS NIH HHS [UL1 TR000077]; NHLBI NIH HHS [U01 HL068288, U01 HL068269,
U01 HL068270, U01 HL068279, U01 HL068281, U01 HL068285, U01 HL068290,
U01 HL068292, U01 HL085057, U10 HL068270, U10 HL109741, U10 HL109816]
NR 21
TC 23
Z9 24
U1 1
U2 17
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD MAY
PY 2013
VL 165
IS 5
BP 828
EP +
DI 10.1016/j.ahj.2013.02.019
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 141KL
UT WOS:000318724000026
PM 23622922
ER
PT J
AU Kim, NH
Mason, CC
Nelson, RG
Afton, SE
Essader, AS
Medlin, JE
Levine, KE
Hoppin, JA
Lin, C
Knowler, WC
Sandler, DP
AF Kim, Nan Hee
Mason, Clinton C.
Nelson, Robert G.
Afton, Scott E.
Essader, Amal S.
Medlin, James E.
Levine, Keith E.
Hoppin, Jane A.
Lin, Cynthia
Knowler, William C.
Sandler, Dale P.
TI Arsenic Exposure and Incidence of Type 2 Diabetes in Southwestern
American Indians
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE arsenic; diabetes mellitus; type 2; incidence; Indians; North American;
nested case-control studies
ID PANCREATIC BETA-CELLS; INSULIN-SECRETION; DRINKING-WATER; MELLITUS;
POPULATION; PREVALENCE; TAIWAN; ASSOCIATION; INHIBITION; BANGLADESH
AB Association of urinary arsenic concentration with incident diabetes was examined in American Indians from Arizona who have a high prevalence of type 2 diabetes and were screened for diabetes between 1982 and 2007. The population resides where drinking water contains arsenic at concentrations above federally recommended limits. A total of 150 nondiabetic subjects aged >= 25 years who subsequently developed type 2 diabetes were matched by year of examination and sex to 150 controls who remained nondiabetic for >= 10 years. Total urinary arsenic concentration, adjusted for urinary creatinine level, ranged from 6.6 mu g/L to 123.1 mu g/L, and inorganic arsenic concentration ranged from 0.1 mu g/L to 36.0 mu g/L. In logistic regression models adjusted for age, sex, body mass index, and urinary creatinine level, the odds ratios for incident diabetes were 1.11 ( 95% confidence interval ( CI): 0.79, 1.57) and 1.16 ( 95% CI: 0.89, 1.53) for a 2-fold increase in total arsenic and inorganic arsenic, respectively. Categorical analyses suggested a positive relationship between quartiles of inorganic arsenic and incident diabetes ( P = 0.056); post-hoc comparison of quartiles 2-4 with quartile 1 revealed 2-fold higher odds of diabetes in the upper quartiles ( OR = 2.14, 95% CI: 1.19, 3.85). Modestly elevated exposure to inorganic arsenic may predict type 2 diabetes in American Indians. Larger studies that include measures of speciated arsenic are required for confirmation.
C1 [Kim, Nan Hee; Mason, Clinton C.; Nelson, Robert G.; Knowler, William C.] NIDDKD, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ USA.
[Afton, Scott E.; Essader, Amal S.; Medlin, James E.; Levine, Keith E.] Res Triangle Inst, Res Triangle Pk, NC 27709 USA.
[Hoppin, Jane A.; Lin, Cynthia; Sandler, Dale P.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Nelson, RG (reprint author), NIH, 1550 East Indian Sch Rd, Phoenix, AZ 85014 USA.
EM rnelson@nih.gov
OI Sandler, Dale/0000-0002-6776-0018
FU Intramural Research Programs of the National Institute of Environmental
Health Sciences; National Institute of Diabetes and Digestive and Kidney
Diseases
FX This research was supported by the Intramural Research Programs of the
National Institute of Environmental Health Sciences and the National
Institute of Diabetes and Digestive and Kidney Diseases.
NR 29
TC 15
Z9 16
U1 2
U2 53
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD MAY 1
PY 2013
VL 177
IS 9
BP 962
EP 969
DI 10.1093/aje/kws329
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 139IR
UT WOS:000318576300014
PM 23504692
ER
PT J
AU Oppermann, M
Carota, I
Schiessl, I
Eisner, C
Castrop, H
Schnermann, J
AF Oppermann, Mona
Carota, Isabel
Schiessl, Ina
Eisner, Christoph
Castrop, Hayo
Schnermann, Jurgen
TI Direct assessment of tubuloglomerular feedback responsiveness in
connexin 40-deficient mice
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE micropuncture; stop-flow pressure; genetic background; vascular
resistance
ID RECEPTOR-DEFICIENT MICE; NITRIC-OXIDE SYNTHASE; RAT MESANGIAL CELLS;
ADENOSINE RECEPTORS; FILTRATION-RATE; ANGIOTENSIN-II; HENLE FLOW;
PRESSURE; EXPRESSION; RENIN
AB Participation of connexin 40 (Cx40) in the regulation of renin secretion and in the tubuloglomerular feedback (TGF) component of renal autoregulation suggests that gap junctional coupling through Cx40 contributes to the function of the juxtaglomerular apparatus. In the present experiments, we determined the effect of targeted Cx40 deletion in C57BL/6 and FVB mice on TGF responsiveness. In C57BL/6 mice, stop-flow pressure (P-SF) fell from 40.3 +/- 2 to 34.5 +/- 2 mmHg in wild-type (WT) and from 31 +/- 1.06 to 26.6 +/- 0.98 mmHg in Cx40-/- mice. PSF changes of 5.85 +/- 0.67 mmHg in WT and of 4.3 +/- 0.55 mmHg in Cx40-/- mice were not significantly different (P = 0.08). In FVB mice, P-SF fell from 37.4 +/- 1.5 to 31.6 +/- 1.5 mmHg in WT and from 28.1 +/- 1.6 to 25.4 +/- 1.7 mmHg in Cx40-/-, with mean TGF responses being significantly greater in WT than Cx40-/- (5.5 +/- 0.55 vs. 2.7 +/- 0.84 mmHg; P = 0.002). In both genetic backgrounds, PSF values were significantly lower in Cx40-/- than WT mice at all flow rates. Arterial blood pressure in the animals prepared for micropuncture was not different between WT and Cx40-/- mice. We conclude that the TGF response magnitude in superficial cortical nephrons is reduced by 30-50% in mice without Cx40, but that with the exception of a small number of nephrons, residual TGF activity is maintained. Thus gap junctional coupling appears to modulate TGF, perhaps by determining the kinetics of signal transmission.
C1 [Oppermann, Mona; Carota, Isabel; Schiessl, Ina; Castrop, Hayo] Univ Regensburg, Inst Physiol, D-93053 Regensburg, Germany.
[Oppermann, Mona] Univ Regensburg, Univ Med Ctr, Childrens Hosp, D-93053 Regensburg, Germany.
[Eisner, Christoph] Med Fac Mannheim, Dept Anesthesiol, Mannheim, Germany.
[Schnermann, Jurgen] NIDDKD, Kidney Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Schnermann, J (reprint author), NIDDKD, NIH, Bldg 10,Rm 4D51 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jurgens@intra.niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health, Bethesda, MD; Deutsche
Forschungsgemeinschaft [SFB699/B7]; Alexander-von-Humboldt Foundation
FX This work was supported by the intramural research program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health, Bethesda, MD, and by a grant from the
Deutsche Forschungsgemeinschaft (SFB699/B7). J. Schnermann was the
recipient of a Humboldt Research Award from the Alexander-von-Humboldt
Foundation.
NR 32
TC 4
Z9 4
U1 1
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD MAY
PY 2013
VL 304
IS 9
BP F1181
EP F1186
DI 10.1152/ajprenal.00721.2012
PG 6
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 137YE
UT WOS:000318473600006
PM 23445620
ER
PT J
AU Messier, EM
Day, BJ
Kleeberger, SR
Tuder, RM
Bowler, RP
Chu, HW
Mason, RJ
Kosmider, B
AF Messier, Elise M.
Day, Brian J.
Kleeberger, Steven R.
Tuder, Rubin M.
Bowler, Russell P.
Chu, Hong Wei
Mason, Robert J.
Kosmider, Beata
TI N-Acetylcysteine Protects Murine Alveolar Type II Cells from Cigarette
Smoke Injury in a Nuclear Erythroid 2-Related Factor-2-Independent
Manner
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE murine alveolar type II cells; lung; Nrf2; NAC; cigarette smoke
ID OBSTRUCTIVE PULMONARY-DISEASE; INDUCED EMPHYSEMA; LUNG INJURY; OXIDATIVE
STRESS; NRF2; MICE; EXPRESSION; APOPTOSIS; COPD; PROLIFERATION
AB Emphysema is caused by the cigarette smoke (CS)-induced destruction of alveolar wall septa, and CS is the main risk factor for chronic obstructive pulmonary disease (COPD). To study the mechanisms of response to this insult, we focused on oxidant-induced lung injury and the potential role of nuclear erythroid 2-related factor-2 (Nrf2), which is a key regulator of the antioxidant defense system. We studied the protective role of N-acetylcysteine (NAC) against the injury of alveolar type II (ATII) cells induced by CS in vivo and in vitro. ATII cells were isolated and purified using magnetic MicroBeads (Miltenyi Biotec, Auburn, CA) from Nrf2(-/-) mice and wild-type mice. We analyzed pulmonary injury, inflammation, glutathione (GSH) concentrations, the expression of glutathione cysteine ligase catalytic subunit mRNA, glutathione cysteine ligase modifier subunit mRNA, and glutathione reductase mRNA, and Nrf2, heme oxygenase-1, and nicotinamide adenine dinucleotide phosphate-reduced:quinone oxireductase levels by Western blotting, TUNEL assay, and immunocytofluorescence for 4-hydroxynonenal as a marker of oxidative stress. We found that CS induced greater injury in ATII cells obtained from Nrf2(-/-) mice than from wild-type mice. Furthermore, NAC attenuated the injuries by CS in ATII cells obtained from wild-type mice both in vivo and in vitro. Moreover, NAC decreased the injury of ATII cells obtained from Nrf2(-/-) mice. Our results suggest that Nrf2-GSH signaling is important for the protective activity of NAC. In addition, in ATII cells deficient in Nrf2, this compound can provide partial protection through its reactive oxygen species-scavenging activities. Targeting the antioxidant system regulated by Nrf2 may provide an effective strategy against lung injury in COPD.
C1 [Messier, Elise M.; Day, Brian J.; Bowler, Russell P.; Chu, Hong Wei; Mason, Robert J.; Kosmider, Beata] Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA.
[Kleeberger, Steven R.] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
[Tuder, Rubin M.] Univ Colorado, Sch Med, Dept Med, Denver, CO USA.
RP Kosmider, B (reprint author), Natl Jewish Hlth, Dept Med, 1400 Jackson St, Denver, CO 80206 USA.
EM KosmiderB@NJHealth.org
FU Young Clinical Scientist Award from the Flight Attendant Medical
Research Institute; Intramural Program of the National Institutes of
Health
FX This work was supported by a Young Clinical Scientist Award from the
Flight Attendant Medical Research Institute (B.K.). S.R.K. was supported
by the Intramural Program of the National Institutes of Health.
NR 46
TC 10
Z9 12
U1 1
U2 10
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1044-1549
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD MAY
PY 2013
VL 48
IS 5
BP 559
EP 567
DI 10.1165/rcmb.2012-0295OC
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA 137YU
UT WOS:000318475300004
PM 23492188
ER
PT J
AU Moosmann, B
Kneisel, S
Wohlfarth, A
Brecht, V
Auwarter, V
AF Moosmann, Bjoern
Kneisel, Stefan
Wohlfarth, Ariane
Brecht, Volker
Auwaerter, Volker
TI A fast and inexpensive procedure for the isolation of synthetic
cannabinoids from 'Spice' products using a flash chromatography system
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Flash chromatography; Spice; Synthetic cannabinoids; Reference compounds
ID TANDEM MASS-SPECTROMETRY; STRUCTURAL-CHARACTERIZATION; HERBAL PRODUCT;
GERMAN MARKET; DESIGNER DRUG; WHOLE-BLOOD; IDENTIFICATION; JWH-018;
QUANTIFICATION; SERUM
AB In the age of the Internet, the variety of drugs offered online is constantly increasing, and new drugs emerge every month. One group of drugs showing such an enormous increase is that of synthetic cannabinoids. Since their first identification in 'herbal mixtures', new structural modifications continue to appear on the market. In order to keep up with this process, toxicological screening methods need to be up to date. This can become extremely difficult if no reference material is available. In this article, a fast and effective way to extract and purify synthetic cannabinoids from 'herbal mixtures' is presented. This method opens a new opportunity for a timely reaction by obtaining reference material straight out of the 'herbal mixtures' ordered via the Internet. Isolation was carried out on a flash chromatography system with gradient elution on a C18 column using methanol and 0.55 % formic acid as mobile phases. The obtained purity of all compounds exceeded 99 %. In addition to the isolation of single compounds, the method proved to be suitable for the separation of various synthetic cannabinoids in one mixture, including the diastereomers cis- and trans-CP-47,497-C8. This approach for obtaining pure standards of new drugs proved to be effective, inexpensive and much quicker than waiting for the substances to be commercially available as reference material.
C1 [Moosmann, Bjoern; Kneisel, Stefan; Wohlfarth, Ariane; Auwaerter, Volker] Univ Med Ctr Freiburg, Dept Forens Toxicol, Inst Forens Med, D-79104 Freiburg, Germany.
[Moosmann, Bjoern; Kneisel, Stefan] Univ Freiburg, Hermann Staudinger Grad Sch, D-79104 Freiburg, Germany.
[Wohlfarth, Ariane] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Brecht, Volker] Univ Freiburg, Inst Pharmaceut Sci, D-79104 Freiburg, Germany.
RP Auwarter, V (reprint author), Univ Med Ctr Freiburg, Dept Forens Toxicol, Inst Forens Med, Albertstr 9, D-79104 Freiburg, Germany.
EM volker.auwaerter@uniklinik-freiburg.de
NR 35
TC 8
Z9 8
U1 2
U2 32
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD MAY
PY 2013
VL 405
IS 12
BP 3929
EP 3935
DI 10.1007/s00216-012-6462-0
PG 7
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 126TK
UT WOS:000317643900005
PM 23064708
ER
PT J
AU Desrosiers, NA
Barnes, AJ
Hartman, RL
Scheidweiler, KB
Kolbrich-Spargo, EA
Gorelick, DA
Goodwin, RS
Huestis, MA
AF Desrosiers, Nathalie A.
Barnes, Allan J.
Hartman, Rebecca L.
Scheidweiler, Karl B.
Kolbrich-Spargo, Erin A.
Gorelick, David A.
Goodwin, Robert S.
Huestis, Marilyn A.
TI Oral fluid and plasma 3,4-methylenedioxymethamphetamine (MDMA) and
metabolite correlation after controlled oral MDMA administration
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Toxicology; 3,4-Methylenedioxymethamphetamine; MDMA; Oral fluid
ID MASS-SPECTROMETRY; AMPHETAMINES; GUIDELINES; ECSTASY; SALIVA; DRUGS;
SWEAT
AB Oral fluid (OF) offers a noninvasive sample collection for drug testing. However, 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) in OF has not been adequately characterized in comparison to plasma. We administered oral low-dose (1.0 mg/kg) and high-dose (1.6 mg/kg) MDMA to 26 participants and collected simultaneous OF and plasma specimens for up to 143 h after dosing. We compared OF/plasma (OF/P) ratios, time of initial detection (t (first)), maximal concentrations (C (max)), time of peak concentrations (t (max)), time of last detection (t (last)), clearance, and 3,4-methylenedioxyamphetamine (MDA)-to-MDMA ratios over time. For OF MDMA and MDA, C (max) was higher, t (last) was later, and clearance was slower compared to plasma. For OF MDA only, t (first) was later compared to plasma. Median (range) OF/P ratios were 5.6 (0.1-52.3) for MDMA and 3.7 (0.7-24.3) for MDA. OF and plasma concentrations were weakly but significantly correlated (MDMA: R (2) = 0.438, MDA: R (2) = 0.197, p < 0.0001). Median OF/P ratios were significantly higher following high dose administration: MDMA low = 5.2 (0.1-40.4), high = 6.0 (0.4-52.3, p < 0.05); MDA low = 3.3 (0.7-17.1), high = 4.1 (0.9-24.3, p < 0.001). There was a large inter-subject variation in OF/P ratios. The MDA/MDMA ratios in plasma were higher than those in OF (p < 0.001), and the MDA/MDMA ratios significantly increased over time in OF and plasma. The MDMA and MDA concentrations were higher in OF than in plasma. OF and plasma concentrations were correlated, but large inter-subject variability precludes the estimation of plasma concentrations from OF.
C1 [Desrosiers, Nathalie A.; Barnes, Allan J.; Hartman, Rebecca L.; Scheidweiler, Karl B.; Gorelick, David A.; Huestis, Marilyn A.] NIDA IRP, Chem & Drug Metab Sect, Clin Pharmacol & Therapeut Res Branch, Baltimore, MD 21224 USA.
[Desrosiers, Nathalie A.; Hartman, Rebecca L.] Univ Maryland, Toxicol Program, Baltimore, MD 21201 USA.
[Kolbrich-Spargo, Erin A.] Southwestern Inst Forens Sci, Dallas, TX 75207 USA.
RP Huestis, MA (reprint author), NIDA IRP, Chem & Drug Metab Sect, Clin Pharmacol & Therapeut Res Branch, 251 Bayview Blvd,Suite 200 Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU Intramural Research Program, National Institute on Drug Abuse, NIH
FX We acknowledge the contributions of the clinical staffs of the National
Institute on Drug Abuse, Intramural Research Program, and Behavioral
Pharmacology Research Unit, Johns Hopkins Bayview Medical Center, as
well as the Graduate Partnership Program, NIH and the Fondation Baxter
et Alma Ricard. This research was funded by the Intramural Research
Program, National Institute on Drug Abuse, NIH.
NR 17
TC 6
Z9 6
U1 2
U2 16
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD MAY
PY 2013
VL 405
IS 12
BP 4067
EP 4076
DI 10.1007/s00216-013-6848-7
PG 10
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 126TK
UT WOS:000317643900020
PM 23471370
ER
PT J
AU de Castro, A
Diaz, A
Pineiro, B
Lendoiro, E
Cruz, A
Lopez-Rivadulla, M
Concheiro, M
AF de Castro, Ana
Diaz, Ariana
Pineiro, Beatriz
Lendoiro, Elena
Cruz, Angelines
Lopez-Rivadulla, Manuel
Concheiro, Marta
TI Simultaneous determination of opiates, methadone, amphetamines, cocaine,
and metabolites in human placenta and umbilical cord by LC-MS/MS
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Placenta; Umbilical cord; Cocaine; Methadone; Opioids; Amphetamines
ID UTERO DRUG EXPOSURE; CHROMATOGRAPHY-MASS SPECTROMETRY; NEONATAL
OUTCOMES; AMNIOTIC-FLUID; SIMULTANEOUS QUANTIFICATION; MECONIUM; ABUSE;
BUPRENORPHINE; PREGNANCY; TISSUE
AB LC-MS/MS methods for the quantification of morphine, morphine-3-glucuronide, morphine-6-glucuronide, codeine, 6-acetylmorphine, cocaine, benzoylecgonine, ecgonine methyl ester, hydroxybenzoylecgonine, cocaethylene, amphetamine, methamphetamine, 3,4-methylenedioxyamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), methadone, and 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine in human placenta and umbilical cord were developed and validated. Specimens (1 +/- 0.02 g) were homogenized with the Ultra-Turrax T8 disperser and centrifuged, and the supernatant was submitted to solid-phase extraction with Oasis MCX cartridges. Chromatographic separation was performed using an Atlantis T3 analytical column (100 x 2.1 mm, 3 mu m) and a gradient of 0.1 % formic acid and acetonitrile. Selectivity was verified in 10 different blank specimens. The method was linear from 1-5 to 100-500 ng/g, depending on the analyte. Limits of detection and quantification ranged from 0.5 to 2.5 ng/g and 1 to 5 ng/g, respectively. Method imprecision was a parts per thousand currency sign15.3 %, except for MDMA at low quality control (18.1 %); accuracy, 87.1 to 114 %; extraction efficiency, 16.3 to 154.0 % (%CV = 1.8-39.4 %); matrix effect, -75.7 to 449.9 % (%CV = 3.5-50 %); and process efficiency, 8.7 to 316.0 %. The method was applied to authentic placenta and umbilical cord specimens from drug-user pregnant women.
C1 [de Castro, Ana; Diaz, Ariana; Pineiro, Beatriz; Lendoiro, Elena; Cruz, Angelines; Lopez-Rivadulla, Manuel; Concheiro, Marta] Univ Santiago de Compostela, Toxicol Serv, Inst Forens Sci, Santiago De Compostela 15782, Spain.
[de Castro, Ana] Cienytech SL, Res Dept, Santiago De Compostela 15705, Spain.
[Concheiro, Marta] NIDA, Chem & Drug Metab Sect, NIH, Baltimore, MD 21224 USA.
RP de Castro, A (reprint author), Cienytech SL, Res Dept, C Xose Chao Rego,10 Bajo, Santiago De Compostela 15705, Spain.
EM ana.decastro@usc.es
RI RIVADULLA, MANUEL/H-4316-2015; DE CASTRO, ANA/M-5159-2015;
OI DE CASTRO, ANA/0000-0002-9832-012X; CRUZ LANDEIRA,
ANGELINES/0000-0003-1382-4546
FU Ministerio de Sanidad, Plan Nacional Sobre Drogas, Gobierno de Espana
[2011/097]; Conselleria de Cultura, Educacion e Ordenacion
Universitaria, Xunta de Galicia [PRE/2011/072]; Ministerio de Ciencia e
Innovacion, Gobierno de Espana [PTQ-10-03936]
FX This study was supported by the Ministerio de Sanidad, Plan Nacional
Sobre Drogas, Gobierno de Espana (2011/097 Project). E. Lendoiro thanks
Conselleria de Cultura, Educacion e Ordenacion Universitaria, Xunta de
Galicia, for her predoctoral contract (PRE/2011/072), and A. de Castro
thanks the Ministerio de Ciencia e Innovacion, Gobierno de Espana, for
her "Torres Quevedo" contract (PTQ-10-03936).
NR 31
TC 8
Z9 8
U1 3
U2 43
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD MAY
PY 2013
VL 405
IS 12
BP 4295
EP 4305
DI 10.1007/s00216-013-6784-6
PG 11
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 126TK
UT WOS:000317643900041
PM 23397092
ER
PT J
AU Saldana, TM
Moshesh, M
Baird, DD
AF Saldana, Tina Marie
Moshesh, Malana
Baird, Donna Day
TI Self-reported family history of leiomyoma: not a reliable marker of high
risk
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Uterine leiomyoma; Fibroids; Family history; Epidemiology; Genetics;
Epidemiology
ID UTERINE LEIOMYOMAS; WHITE WOMEN; FIBROIDS; PREDISPOSITION; HYSTERECTOMY;
ASSOCIATION; PREVALENCE; TWIN; DIAGNOSIS; INSIGHTS
AB Purpose: To examine the importance of self-reported family history of uterine leiomyoma (fibroids) as a marker of risk.
Methods: Women, aged 35 to 49, were randomly selected from the membership of a large, urban health plan. Participants completed a self-administered questionnaire about family history of fibroids. Ultrasound screening for fibroids followed, regardless of whether participants had been previously diagnosed (660 black, 412 white). Data for each ethnic group were analyzed separately using Poisson regression.
Results: In both ethnic groups, women who reported a family history of fibroids had an elevated risk of fibroids compared with those without family history. However, no elevated risk was apparent for cases who did not know they had fibroids when they reported the family history information.
Conclusions: Many women may first learn about their family history of fibroids when discussing their own clinical diagnosis with family members. Such bias would invalidate self-reported family history as a predictor of fibroid risk. As new pharmacologic treatments for fibroids are developed, women at high risk of fibroids would benefit from early screening and pharmacologic treatment to delay development of large fibroids and reduce the need for invasive treatments. Self-reported family history is not useful for identifying high-risk women. Published by Elsevier Inc.
C1 [Saldana, Tina Marie] Social & Sci Syst Inc, Durham, NC USA.
[Moshesh, Malana; Baird, Donna Day] NIEHS, NIH, Durham, NC USA.
RP Baird, DD (reprint author), NIEHS, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM baird@niehs.nih.gov
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU Intramural NIH HHS [Z01 ES049013-13]
NR 33
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 1047-2797
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD MAY
PY 2013
VL 23
IS 5
BP 286
EP 290
DI 10.1016/j.annepidem.2013.03.003
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 140OL
UT WOS:000318664700009
PM 23621994
ER
PT J
AU Drahos, J
Vanwormer, JJ
Greenlee, RT
Landgren, O
Koshiol, J
AF Drahos, Jennifer
Vanwormer, Jeffrey J.
Greenlee, Robert T.
Landgren, Ola
Koshiol, Jill
TI Accuracy of ICD-9-CM codes in identifying infections of pneumonia and
herpes simplex virus in administrative data
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Administrative data; Electronic medical records; ICD-9-CM; HSV;
Pneumonia
ID VALIDITY
AB Purpose: Clinical epidemiology studies increasingly rely on electronic medical records data. The validity of International Classification of Disease, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis codes is crucial as they are often used to identify conditions of interest. We evaluated the use of archived ICD-9-CM codes to identify two representative infection-related conditions, pneumonia and herpes simplex virus (HSV), in a defined health system.
Methods: Records were obtained for a sample of 175 and 179 patients with ICD-9-CM codes for pneumonia and HSV, respectively. An adjudicated case status was assigned for each subject.
Results: The presence of a single ICD-9-CM code had a positive predictive value of 88% for pneumonia and 86% for HSV. False positives (noncases) accounted for less than 10% of records evaluated for each condition.
Conclusions: Our study demonstrates that ICD-9-CM codes for pneumonia and HSV were valid markers of a true history of these conditions, suggesting that ICD-9-CM codes can be used to successfully identify infection-related conditions in epidemiologic studies. However, validation studies for individual conditions may help identify condition-specific strategies to improve the performance of diagnostic codes. Published by Elsevier Inc.
C1 [Drahos, Jennifer; Koshiol, Jill] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20852 USA.
[Drahos, Jennifer] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, NIH,Dept Hlth & Human Serv, Bethesda, MD 20852 USA.
[Vanwormer, Jeffrey J.; Greenlee, Robert T.] Marshfield Clin Res Fdn, Marshfield, WI USA.
[Landgren, Ola] NCI, Multiple Myeloma Sect, Metab Branch, Ctr Canc Res,NIH, Bethesda, MD 20852 USA.
RP Drahos, J (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,EPS Suite 550 Room 5034, Bethesda, MD 20852 USA.
EM jennifer.drahos@nih.gov
FU Intramural NIH HHS [Z99 CA999999]; NCATS NIH HHS [UL1 TR000427]
NR 12
TC 14
Z9 14
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD MAY
PY 2013
VL 23
IS 5
BP 291
EP 293
DI 10.1016/j.annepidem.2013.02.005
PG 3
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 140OL
UT WOS:000318664700010
PM 23522903
ER
PT J
AU Morrison, S
Shenassa, ED
Mendola, P
Wu, TT
Schoendorf, K
AF Morrison, Stephanie
Shenassa, Edmond D.
Mendola, Pauline
Wu, Tongtong
Schoendorf, Kenneth
TI Allostatic load may not be associated with chronic stress in pregnant
women, NHANES 1999-2006
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Allostasis; Stress; Psychological; Pregnancy complications
ID CUMULATIVE BIOLOGICAL RISK; NUTRITION EXAMINATION SURVEY;
NATIONAL-HEALTH; UNITED-STATES; AGE; MACARTHUR; PATTERNS; BIRTH
AB Purpose: Pregnant women are generally excluded from studies that measure allostatic load (AL) because there is concern that the changing levels of AL-related biomarkers during pregnancy do not reflect a woman's true AL The goal of this study was to determine whether AL can be measured in a meaningful way during pregnancy.
Methods: The National Health and Nutrition Examination Survey (NHANES) is a nationally representative, cross-sectional survey of the U.S. civilian population. AL was based on the distributions of 10 biomarkers in pregnant (n = 1138) and nonpregnant (n = 4993) women aged 15 to 44 from NHANES (1999-2006).
Results: The distribution of each AL-related biomarker differed significantly between pregnant and nonpregnant women (P < .01). Among nonpregnant women, high AL findings were consistent with previous studies (e.g., higher AL in women who are black, are older, and who have lower incomes). However, these associations were not seen in pregnant women.
Conclusions: Our results suggest that the various biomarkers that comprise AL may reflect proximal factors in pregnancy more strongly than they represent exposure to chronic stress over a woman's lifetime. Therefore, our approach to measuring AL may not provide meaningful information about chronic stress in pregnant women without further consideration of pregnancy-related factors. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Morrison, Stephanie; Shenassa, Edmond D.; Wu, Tongtong] Univ Maryland, Sch Publ Hlth, Dept Epidemiol & Biostat, College Pk, MD 20742 USA.
[Shenassa, Edmond D.] Univ Maryland, Sch Publ Hlth, Maternal & Child Hlth Program, College Pk, MD 20742 USA.
[Mendola, Pauline] Eunice Kennedy Shriver Natl Inst Hlth & Human Dev, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Rockville, MD USA.
[Schoendorf, Kenneth] Ctr Dis Control & Prevent, Infant Child & Womens Hlth Stat Branch, Off Anal & Epidemiol, Natl Ctr Hlth Stat, Hyattsville, MD USA.
RP Shenassa, ED (reprint author), 1142GG Sch Publ Hlth, Maternal & Child Hlth Program, College Pk, MD USA.
EM Shenassa@UMD.edu
OI Mendola, Pauline/0000-0001-5330-2844
FU Flight Attendants Medical Research Institute; Intramural Research
Program of the NIH Eunice Kennedy Shriver National Institute of Child
Health and Human Development
FX E. Shenassa was supported by Flight Attendants Medical Research
Institute. P. Mendola: This research was supported in part by the
Intramural Research Program of the NIH Eunice Kennedy Shriver National
Institute of Child Health and Human Development. The findings and
conclusions in this paper are those of the authors and do not
necessarily represent the official position of the National Center for
Health Statistics, Centers for Disease Control and Prevention.
NR 20
TC 9
Z9 9
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
EI 1873-2585
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD MAY
PY 2013
VL 23
IS 5
BP 294
EP 297
DI 10.1016/j.annepidem.2013.03.006
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 140OL
UT WOS:000318664700011
PM 23621995
ER
PT J
AU Dean, M
Lou, H
AF Dean, Michael
Lou, Hong
TI Genetics and genomics of prostate cancer
SO ASIAN JOURNAL OF ANDROLOGY
LA English
DT Review
DE androgen receptor; cancer progression; chromatin remodeling; metastasis;
prostate cancer (PCa); risk factor; somatic mutation; tumor
heterogeneity
ID WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; FUNCTIONAL-ANALYSIS; ERG
ONCOPROTEIN; BRCA MUTATIONS; RISK LOCUS; MSMB; 8Q24; VARIANT; GENES
AB Prostate cancer (PCa) is one of the most common malignancies in the world with over 890 000 cases and over 258 000 deaths worldwide each year. Nearly all mortalities from PCa are due to metastatic disease, typically through tumors that evolve to be hormone-refractory or castrate-resistant. Despite intensive epidemiological study, there are few known environmental risk factors, and age and family history are the major determinants. However, there is extreme heterogeneity in PCa incidence worldwide, suggesting that major determining factors have not been described. Genome-wide association studies have been performed and a considerable number of significant, but low-risk loci have been identified. In addition, several groups have analyzed PCa by determination of genomic copy number, fusion gene generation and targeted resequencing of candidate genes, as well as exome and whole genome sequencing. These initial studies have examined both primary and metastatic tumors as well as murine xenografts and identified somatic alterations in TP53 and other potential driver genes, and the disturbance of androgen response and cell cycle pathways. It is hoped that continued characterization of risk factors as well as gene mutation and misregulation in tumors will aid in understanding, diagnosing and better treating PCa.
C1 [Dean, Michael] NCI, NIH, Canc & Inflammat Program, Ft Detrick, MD 21702 USA.
[Lou, Hong] NCI, NIH, SAIC Frederick, Basic Sci Program, Ft Detrick, MD 21702 USA.
RP Dean, M (reprint author), NCI, NIH, Canc & Inflammat Program, Ft Detrick, MD 21702 USA.
EM deanm@mail.nih.gov
RI Dean, Michael/G-8172-2012
OI Dean, Michael/0000-0003-2234-0631
FU Intramural Research Program of the NIH, the National Cancer Institute
Center for Cancer Research
FX This work was supported by the Intramural Research Program of the NIH,
the National Cancer Institute Center for Cancer Research.
NR 58
TC 13
Z9 13
U1 1
U2 9
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
INDIA
SN 1008-682X
EI 1745-7262
J9 ASIAN J ANDROL
JI Asian J. Androl.
PD MAY
PY 2013
VL 15
IS 3
SI SI
BP 309
EP 313
DI 10.1038/aja.2013.29
PG 5
WC Andrology; Urology & Nephrology
SC Endocrinology & Metabolism; Urology & Nephrology
GA 140YD
UT WOS:000318691500003
PM 23564043
ER
PT J
AU Liang, S
Steffen, LM
Steffen, BT
Guan, WH
Weir, NL
Rich, SS
Manichaikul, A
Vargas, JD
Tsai, MY
AF Liang, Shuang
Steffen, Lyn M.
Steffen, Brian T.
Guan, Weihua
Weir, Natalie L.
Rich, Stephen S.
Manichaikul, Ani
Vargas, Jose D.
Tsai, Michael Y.
TI APOE genotype modifies the association between plasma omega-3 fatty
acids and plasma lipids in the Multi-Ethnic Study of Atherosclerosis
(MESA)
SO ATHEROSCLEROSIS
LA English
DT Article
DE APOE genotype; Eicosapentaenoic acid (EPA); Docosahexaenoic acid (DHA);
Plasma lipids; Lipoproteins
ID N-3 FATTY-ACIDS; LONG-CHAIN OMEGA-3-FATTY-ACIDS; DISEASE RISK-FACTORS;
REVERSE CHOLESTEROL TRANSPORT; APOLIPOPROTEIN-E POLYMORPHISM; FISH-OIL
SUPPLEMENTATION; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION;
LIPOPROTEIN PHENOTYPE; ATRIAL-FIBRILLATION
AB Objective: The benefits of fish oil fatty acids eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) on plasma lipid profiles have been inconsistent but may partially depend on individual Apolipoprotein E (APOE) genotypes. We aimed to determine whether APOE genotype modifies the association of lipid profile characteristics with plasma EPA and DHA levels.
Methods: APOE genotype was determined in this cross-sectional analysis of 2340 Multi-Ethnic Study of Atherosclerosis (MESA) participants. Relative plasma phospholipid EPA and DHA levels, plasma lipids, and lipoprotein subclass particle sizes and concentrations were measured.
Results: Significant gene-EPA interactions were found with HDL-C, and particle concentrations of large and total HDL (p(interaction) = 0.0002, 0.006, and 0.007, respectively). The above lipid targets were positively associated with EPA in the E2 groups, whereas negative trends were observed among the E4 participants. Gene-DHA interactions were noted for small LDL particle concentrations alone (p(interaction) = 0.01), where a positive trend was found among E4 but not E2 or E3 participants.
Conclusions: These results indicate a significant contribution of the APOE genotype to the EPA-lipid profile relationship; however, the results do not explain the differences in previous findings regarding LDL-C, triglycerides or total cholesterol. Future investigators examining the effects of EPA on HDL-C or lipoprotein characteristics may consider including APOE genotype in their analyses. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Liang, Shuang; Steffen, Brian T.; Weir, Natalie L.; Tsai, Michael Y.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Steffen, Lyn M.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
[Guan, Weihua] Univ Minnesota, Sch Publ Hlth, Div Biostat, Minneapolis, MN 55455 USA.
[Rich, Stephen S.; Manichaikul, Ani] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA 22908 USA.
[Vargas, Jose D.] Johns Hopkins Sch Med, Baltimore, MD 21287 USA.
[Vargas, Jose D.] NIH, Bethesda, MD 20892 USA.
RP Tsai, MY (reprint author), 420 Delaware St SE,Mayo Mail Code 609, Minneapolis, MN 55455 USA.
EM tsaix001@umn.edu
OI Manichaikul, Ani/0000-0002-5998-795X
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95169]
FX Research was supported by the following contracts, N01-HC-95159 through
N01-HC-95169 from the National Heart, Lung, and Blood Institute.
NR 55
TC 12
Z9 12
U1 0
U2 11
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD MAY
PY 2013
VL 228
IS 1
BP 181
EP 187
DI 10.1016/j.atherosclerosis.2013.02.004
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 139FJ
UT WOS:000318567000027
PM 23466070
ER
PT J
AU Nussinov, R
Ma, BY
Tsai, CJ
AF Nussinov, Ruth
Ma, Buyong
Tsai, Chung-Jung
TI A broad view of scaffolding suggests that scaffolding proteins can
actively control regulation and signaling of multienzyme complexes
through allostery
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Review
DE Multi-enzyme complex; Allosteric; Multiprotein; Multi-protein;
Population shift; Conformational selection
ID UBIQUITIN-CONJUGATING ENZYME; CONFORMATIONAL CONTROL; METABOLIC
PATHWAYS; ENERGY LANDSCAPES; SUMO CONJUGATION; BINDING CASCADES;
STRUCTURAL BASIS; LIGASE ACTIVITY; MAP KINASE; FATTY-ACID
AB Enzymes often work sequentially in pathways; and consecutive reaction steps are typically carried out by molecules associated in the same multienzyme complex. Localization confines the enzymes; anchors them; increases the effective concentration of substrates and products; and shortens pathway timescales; however, it does not explain enzyme coordination or pathway branching. Here, we distinguish between metabolic and signaling multienzyme complexes. We argue for a central role of scaffolding proteins in regulating multienzyme complexes signaling and suggest that metabolic multienzyme complexes are less dependent on scaffolding because they undergo conformational control through direct subunit-subunit contacts. In particular, we propose that scaffolding proteins have an essential function in controlling branching in signaling pathways. This new broadened definition of scaffolding proteins goes beyond cases such as the classic yeast mitogen-activated protein kinase Ste5 and encompasses proteins such as E3 ligases which lack active sites and work via allostery. With this definition, we classify the mechanisms of multienzyme complexes based on whether the substrates are transferred through the involvement of scaffolding proteins, and outline the functional merits to metabolic or signaling pathways. Overall, while co-localization topography helps multistep pathways non-specifically, allosteric regulation requires precise multienzyme organization and interactions and works via population shift, either through direct enzyme subunit-subunit interactions or through active involvement of scaffolding proteins. This article is part of a Special Issue entitled: The emerging dynamic view of proteins: Protein plasticity in allostery, evolution and self-assembly. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Nussinov, Ruth; Ma, Buyong; Tsai, Chung-Jung] SAIC Frederick Inc, Basic Res Program, Ctr Canc Res, Nanobiol Program,Frederick Natl Lab Canc Res,NCI, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Dept Human Genet & Mol Med, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), SAIC Frederick Inc, Basic Res Program, Ctr Canc Res, Nanobiol Program,Frederick Natl Lab Canc Res,NCI, Frederick, MD 21702 USA.
EM NussinoR@helix.nih.gov
RI Ma, Buyong/F-9491-2011
OI Ma, Buyong/0000-0002-7383-719X
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; 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 number HHSN261200800001E. The content of this publication does
not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government This
research was supported (in part) by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research.
NR 89
TC 25
Z9 25
U1 2
U2 39
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-9639
J9 BBA-PROTEINS PROTEOM
JI BBA-Proteins Proteomics
PD MAY
PY 2013
VL 1834
IS 5
BP 820
EP 829
DI 10.1016/j.bbapap.2012.12.014
PG 10
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 136UG
UT WOS:000318388300002
PM 23291467
ER
PT J
AU Zhang, FK
Angermann, BR
Meier-Schellersheim, M
AF Zhang, Fengkai
Angermann, Bastian R.
Meier-Schellersheim, Martin
TI The Simmune Modeler visual interface for creating signaling networks
based on bi-molecular interactions
SO BIOINFORMATICS
LA English
DT Article
AB Motivation: Biochemical modeling efforts now frequently take advantage of the possibility to automatically create reaction networks based on the specification of pairwise molecular interactions. Even though a variety of tools exist to visualize the resulting networks, defining the rules for the molecular interactions typically requires writing scripts, which impacts the non-specialist accessibility of those approaches. We introduce the Simmune Modeler that allows users to specify molecular complexes and their interactions as well as the reaction-induced modifications of the molecules through a flexible visual interface. It can take into account the positions of the components of transmembrane complexes relative to the embedding membranes as well as symmetry aspects affecting the reactions of multimeric molecular structures. Models created with this tool can be simulated using the Simmune Simulator or be exported as SBML code or as files describing the reaction networks as systems of ODEs for import into Matlab.
C1 [Zhang, Fengkai; Angermann, Bastian R.; Meier-Schellersheim, Martin] NIAID, Computat Biol Unit, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
RP Zhang, FK (reprint author), NIAID, Computat Biol Unit, Lab Syst Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM zhangfen@niaid.nih.gov; mms@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, NIAID
FX This work was supported by the intramural program of the National
Institute of Allergy and Infectious Diseases, NIAID.
NR 8
TC 11
Z9 11
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD MAY 1
PY 2013
VL 29
IS 9
BP 1229
EP 1230
DI 10.1093/bioinformatics/btt134
PG 2
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 139HW
UT WOS:000318573900023
PM 23508970
ER
PT J
AU Ma, CX
Suman, VJ
Goetz, M
Haluska, P
Moynihan, T
Nanda, R
Olopade, O
Pluard, T
Guo, ZF
Chen, HX
Erlichman, C
Ellis, MJ
Fleming, GF
AF Ma, Cynthia X.
Suman, Vera J.
Goetz, Matthew
Haluska, Paul
Moynihan, Timothy
Nanda, Rita
Olopade, Olufunmilayo
Pluard, Timothy
Guo, Zhanfang
Chen, Helen X.
Erlichman, Charles
Ellis, Matthew J.
Fleming, Gini F.
TI A phase I trial of the IGF-1R antibody Cixutumumab in combination with
temsirolimus in patients with metastatic breast cancer
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Cixutumumab; Temsirolimus; Metastatic breast cancer; IGF-1R; mTOR
ID SIGNALING PATHWAYS; MAMMALIAN TARGET; PIK3CA GENE; MTOR INHIBITORS;
HIGH-FREQUENCY; MESSENGER-RNA; SOLID TUMORS; GROWTH; RECEPTOR; CELLS
AB The mammalian target of rapamycin (mTOR) plays a critical role in promoting tumor cell growth and is frequently activated in breast cancer. In preclinical studies, the antitumor activity of mTOR inhibitors is attenuated by feedback up-regulation of AKT mediated in part by Insulin-like growth factor type 1 receptor (IGF-1R). We designed a phase I trial to determine the maximum-tolerated dose (MTD) and pharmacodynamic effects of the IGF-1R antibody Cixutumumab in combination with temsirolimus in patients with metastatic breast cancer refractory to standard therapies. A 3 + 3 Phase I design was chosen. Temsirolimus and Cixutumumab were administered intravenously on days 1, 8, 15, and 22 of a 4-week cycle. Of the 26 patients enrolled, four did not complete cycle 1 because of disease progression (n = 3) or comorbid condition (n = 1) and were replaced. The MTD was determined from the remaining 22 patients, aged 34-72 (median 48) years. Most patients (86 %) had estrogen receptor positive cancer. The median number of prior chemotherapy regimens for metastatic disease was 3. The MTD was determined to be Cixutumumab 4 mg/kg and temsirolimus 15 mg weekly. Dose-limiting toxicities (DLTs) included mucositis, neutropenia, and thrombocytopenia. Other adverse events included grade 1/2 fatigue, anemia, and hyperglycemia. No objective responses were observed, but four patients experienced stable disease that lasted for at least 4 months. Compared with baseline, there was a significant increase in the serum levels of IGF-1 (p < 0.001) and IGFBP-3 (p = 0.019) on day 2. Compared with day 2, there were significant increases in the serum levels of IGF-1 (p < 0.001), IGF-2 (p = 0.001), and IGFBP-3 (p = 0.019) on day 8. A phase II study in women with metastatic breast cancer is ongoing.
C1 [Ma, Cynthia X.; Pluard, Timothy; Guo, Zhanfang; Ellis, Matthew J.] Washington Univ, Sch Med, Dept Internal Med, Sect Breast Oncol,Div Oncol, St Louis, MO 63110 USA.
[Ma, Cynthia X.; Pluard, Timothy; Ellis, Matthew J.] Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO 63110 USA.
[Suman, Vera J.] Mayo Clin, Div Biomed Stat & Informat, Rochester, MO USA.
[Goetz, Matthew; Haluska, Paul; Moynihan, Timothy; Erlichman, Charles] Mayo Clin, Dept Oncol, Rochester, MO USA.
[Nanda, Rita; Olopade, Olufunmilayo; Fleming, Gini F.] Univ Chicago, Med Ctr, Dept Med, Div Hematol & Oncol, Chicago, IL 60637 USA.
[Chen, Helen X.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Ma, CX (reprint author), Washington Univ, Sch Med, Dept Internal Med, Sect Breast Oncol,Div Oncol, 660 South Euclid Ave,POB 8056, St Louis, MO 63110 USA.
EM cma@dom.wustl.edu
FU American Society of Clinical Oncology; St. Louis Komen Foundation;
[N01-CM62205]; [N01-CM-2011-00071]
FX We wish to thank the patients and their families for participation in
this study. We also thank the nurses, clinical research, and regulatory
coordinators at Washington University Siteman Cancer Center, Mayo Clinic
Rochester and University of Chicago. This trial was partly supported by
a Career Development Award from the American Society of Clinical
Oncology (C.X.M.), St. Louis Komen Foundation (C.X.M.), N01-CM62205, and
N01-CM-2011-00071.
NR 51
TC 27
Z9 31
U1 0
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD MAY
PY 2013
VL 139
IS 1
BP 145
EP 153
DI 10.1007/s10549-013-2528-8
PG 9
WC Oncology
SC Oncology
GA 138QX
UT WOS:000318524600015
PM 23605083
ER
PT J
AU Hyland, PL
Freedman, ND
Hu, N
Tang, ZZ
Wang, LM
Wang, CY
Ding, T
Fan, JH
Qiao, YL
Golozar, A
Wheeler, W
Yu, K
Yuenger, J
Burdett, L
Chanock, SJ
Dawsey, SM
Tucker, MA
Goldstein, AM
Abnet, CC
Taylor, PR
AF Hyland, Paula L.
Freedman, Neal D.
Hu, Nan
Tang, Ze-Zhong
Wang, Lemin
Wang, Chaoyu
Ding, Ti
Fan, Jin-Hu
Qiao, You-Lin
Golozar, Asieh
Wheeler, William
Yu, Kai
Yuenger, Jeff
Burdett, Laurie
Chanock, Stephen J.
Dawsey, Sanford M.
Tucker, Margaret A.
Goldstein, Alisa M.
Abnet, Christian C.
Taylor, Philip R.
TI Genetic variants in sex hormone metabolic pathway genes and risk of
esophageal squamous cell carcinoma
SO CARCINOGENESIS
LA English
DT Article
ID CANCER-RISK; STEROIDOGENIC ENZYMES; POSTMENOPAUSAL WOMEN; SEGREGATION
ANALYSIS; GASTRIC CANCERS; SHANXI PROVINCE; SERUM ESTROGEN; ELDERLY-MEN;
CHINA; POLYMORPHISMS
AB In China, esophageal cancer is the fourth leading cause of cancer death where essentially all cases are histologically esophageal squamous cell carcinoma (ESCC), in contrast to esophageal adenocarcinoma in the West. Globally, ESCC is 2.4 times more common among men than women and recently it has been suggested that sex hormones may be associated with the risk of ESCC. We examined the association between genetic variants in sex hormone metabolic genes and ESCC risk in a population from north central China with high-incidence rates. A total of 1026 ESCC cases and 1452 controls were genotyped for 797 unique tag single-nucleotide polymorphisms (SNPs) in 51 sex hormone metabolic genes. SNP-, gene- and pathway-based associations with ESCC risk were evaluated using unconditional logistic regression adjusted for age, sex and geographical location and the adaptive rank truncated product (ARTP) method. Statistical significance was determined through use of permutation for pathway- and gene-based associations. No associations were observed for the overall sex hormone metabolic pathway (P 0.14) or subpathways (androgen synthesis: P 0.30, estrogen synthesis: P 0.15 and estrogen removal: P 0.19) with risk of ESCC. However, six individual genes (including SULT2B1, CYP1B1, CYP3A7, CYP3A5, SHBG and CYP11A1) were significantly associated with ESCC risk (P < 0.05). Our examination of genetic variation in the sex hormone metabolic pathway is consistent with a potential association with risk of ESCC. These positive findings warrant further evaluation in relation to ESCC risk and replication in other populations.
C1 [Hyland, Paula L.; Hu, Nan; Wang, Lemin; Wang, Chaoyu; Golozar, Asieh; Goldstein, Alisa M.; Taylor, Philip R.] NCI, Genet Epidemiol Branch, DCEG, NIH, Bethesda, MD 20892 USA.
[Hyland, Paula L.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Freedman, Neal D.; Dawsey, Sanford M.; Abnet, Christian C.] NCI, Nutr Epidemiol Branch, DCEG, NIH, Bethesda, MD 20892 USA.
[Tang, Ze-Zhong; Ding, Ti] Shanxi Canc Hosp, Taiyuan, Peoples R China.
[Fan, Jin-Hu; Qiao, You-Lin] Chinese Acad Med Sci, Canc Inst Hosp, Dept Epidemiol, Beijing 100730, Peoples R China.
[Wheeler, William] Informat Management Serv Inc, Silver Spring, MD USA.
[Yu, Kai] NCI, Biostat Branch, DCEG, NIH, Bethesda, MD 20892 USA.
[Yuenger, Jeff; Burdett, Laurie; Chanock, Stephen J.] NCI Frederick, Core Genotyping Facil, SAIC Frederick Inc, Bethesda, MD USA.
[Yuenger, Jeff; Burdett, Laurie; Chanock, Stephen J.] DCEG, Bethesda, MD USA.
[Tucker, Margaret A.] NCI, Human Genet Program, DCEG, NIH, Bethesda, MD 20892 USA.
RP Hyland, PL (reprint author), NIH, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
EM hylandpl@mail.nih.gov
RI Qiao, You-Lin/B-4139-2012; Tucker, Margaret/B-4297-2015; Abnet,
Christian/C-4111-2015; Freedman, Neal/B-9741-2015
OI Qiao, You-Lin/0000-0001-6380-0871; Abnet, Christian/0000-0002-3008-7843;
Freedman, Neal/0000-0003-0074-1098
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Division of Cancer Epidemiology and Genetics;
Cancer Prevention Fellowship Program, Division of Cancer Prevention,
National Cancer Institute, Bethesda, USA; Health and Social Care,
Northern Ireland, UK
FX Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Division of Cancer Epidemiology and Genetics;
Cancer Prevention Fellowship Program, Division of Cancer Prevention,
National Cancer Institute, Bethesda, USA (to P.L.H.); Health and Social
Care, Northern Ireland, UK (to P.L.H.).
NR 50
TC 11
Z9 14
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD MAY
PY 2013
VL 34
IS 5
BP 1062
EP 1068
DI 10.1093/carcin/bgt030
PG 7
WC Oncology
SC Oncology
GA 140HV
UT WOS:000318646000015
PM 23358850
ER
PT J
AU Kasaikina, MV
Turanov, AA
Avanesov, A
Schweizer, U
Seeher, S
Bronson, RT
Novoselov, SN
Carlson, BA
Hatfield, DL
Gladyshev, VN
AF Kasaikina, Marina V.
Turanov, Anton A.
Avanesov, Andrei
Schweizer, Ulrich
Seeher, Sandra
Bronson, Roderick T.
Novoselov, Sergey N.
Carlson, Bradley A.
Hatfield, Dolph L.
Gladyshev, Vadim N.
TI Contrasting roles of dietary selenium and selenoproteins in chemically
induced hepatocarcinogenesis
SO CARCINOGENESIS
LA English
DT Article
ID SELENOCYSTEINE TRANSFER-RNA; TRANSGENIC MICE; NUTRITIONAL PREVENTION;
CANCER TRIAL; DEFICIENCY; EXPRESSION; SUPPLEMENTATION; GROWTH; CELLS
AB Selenium (Se) has long been known for its cancer prevention properties, but the molecular basis remains unclear. The principal questions in assessing the effect of dietary Se in cancer are whether selenoproteins, small molecule selenocompounds, or both, are involved, and under which conditions and genotypes Se may be protective. In this study, we examined diethylnitrosamine-induced hepatocarcinogenesis in mice lacking a subset of selenoproteins due to expression of a mutant selenocysteine tRNA gene (Trsp(A37G) mice). To uncouple the effects of selenocompounds and selenoproteins, these animals were examined at several levels of dietary Se. Our analysis revealed that tumorigenesis in Trsp(A37G) mice maintained on the adequate Se diet was increased. However, in the control, wild-type mice, both Se deficiency and high Se levels protected against tumorigenesis. We further found that the Se-deficient diet induced severe neurological phenotypes in TrspA37G mice. Surprisingly, a similar phenotype could be induced in these mice at high dietary Se intake. Overall, our results show a complex role of Se in chemically induced hepatocarcinogenesis, which involves interaction among selenoproteins, selenocompounds and toxins, and depends on genotype and background of the animals.
C1 [Kasaikina, Marina V.; Turanov, Anton A.; Avanesov, Andrei; Gladyshev, Vadim N.] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA.
[Kasaikina, Marina V.; Turanov, Anton A.; Avanesov, Andrei; Gladyshev, Vadim N.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Schweizer, Ulrich; Seeher, Sandra] Charite, Inst Expt Endokrinol, D-13353 Berlin, Germany.
[Bronson, Roderick T.] Harvard Univ, Sch Med, Rodent Histopathol Lab, Boston, MA 02115 USA.
[Novoselov, Sergey N.] Univ Nebraska, Dept Biochem, Lincoln, NE 68588 USA.
[Carlson, Bradley A.; Hatfield, Dolph L.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Gladyshev, VN (reprint author), Brigham & Womens Hosp, Dept Med, Div Genet, 75 Francis St, Boston, MA 02115 USA.
EM vgladyshev@rics.bwh.harvard.edu
OI Schweizer, Ulrich/0000-0003-1380-4780
FU National Institute of Health [CA080946]; Intramural Research Program of
the Center for Cancer Research, National Cancer Institute, National
Institute of Health
FX National Institute of Health (CA080946 to V.N.G.); Intramural Research
Program of the Center for Cancer Research, National Cancer Institute,
National Institute of Health (to D.L.H.).
NR 26
TC 9
Z9 9
U1 0
U2 13
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 MAY
PY 2013
VL 34
IS 5
BP 1089
EP 1095
DI 10.1093/carcin/bgt011
PG 7
WC Oncology
SC Oncology
GA 140HV
UT WOS:000318646000018
PM 23389288
ER
PT J
AU Roecklein, KA
Scher, AI
Smith, A
Harris, T
Eiriksdottir, G
Garcia, M
Gudnason, V
Launer, LJ
AF Roecklein, Kathryn A.
Scher, Ann I.
Smith, Albert
Harris, Tamara
Eiriksdottir, Gudny
Garcia, Melissa
Gudnason, Villi
Launer, Lenore J.
TI Haplotype analysis of the folate-related genes MTHFR, MTRR, and MTR and
migraine with aura
SO CEPHALALGIA
LA English
DT Article
DE Migraine; folate; haplotype; genetics
ID METHYLENETETRAHYDROFOLATE REDUCTASE GENE; GENOME-WIDE ASSOCIATION;
CORONARY-ARTERY-DISEASE; CARDIOVASCULAR-DISEASE; METHIONINE SYNTHASE;
RISK; SUSCEPTIBILITY; POLYMORPHISMS; METAANALYSIS; MORTALITY
AB Aims: The C677T variant in the methylenetetrahydrofolate reductase (MTHFR; EC 1.5.1.20) enzyme, a key player in the folate metabolic pathway, has been associated with increased risk of migraine with aura. Other genes encoding molecular components of this pathway include methionine synthase (MTR; EC 2.1.1.13) and methionine synthase reductase (MTRR; EC 2.1.1.135) among others. We performed a haplotype analysis of migraine risk and MTHFR, MTR, and MTRR.
Methods: Study participants are from a random sub-sample participating in the population-based AGES-Reykjavik Study, including subjects with non-migraine headache (n = 367), migraine without aura (n = 85), migraine with aura (n = 167), and no headache (n = 1347). Haplotypes spanning each gene were constructed using Haploview. Association testing was performed on single SNP and haplotypes using logistic regression, controlling for demographic and cardiovascular risk factors and correcting for multiple testing.
Results: Haplotype analysis suggested an association between MTRR haplotypes and reduced risk of migraine with aura. All other associations were not significant after correcting for multiple testing.
Conclusions: These results suggest that MTRR variants may protect against migraine with aura in an older population.
C1 [Roecklein, Kathryn A.] Univ Pittsburgh, Dept Psychol, Ctr Neural Basis Cognit, Pittsburgh, PA 15260 USA.
[Scher, Ann I.] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD 20814 USA.
[Scher, Ann I.; Harris, Tamara; Garcia, Melissa; Launer, Lenore J.] NIA, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
[Gudnason, Villi] Univ Iceland, Iceland Heart Assoc Res Inst, IS-101 Reykjavik, Iceland.
RP Roecklein, KA (reprint author), Univ Pittsburgh, Dept Psychol, Ctr Neural Basis Cognit, 210 S Bouquet St, Pittsburgh, PA 15260 USA.
EM kroecklein@gmail.com
RI Gudnason, Vilmundur/K-6885-2015; Smith, Albert/K-5150-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084; Smith,
Albert/0000-0003-1942-5845
FU National Institutes of Health [N01-AG-1-2100]; National Institute on
Aging Intramural Research Program; Hjartavernd (the Icelandic Heart
Association); Althingi (the Icelandic Parliament)
FX This study was supported by a grant from the National Institutes of
Health (N01-AG-1-2100), the National Institute on Aging Intramural
Research Program, the Hjartavernd (the Icelandic Heart Association) and
the Althingi (the Icelandic Parliament).
NR 27
TC 3
Z9 3
U1 0
U2 13
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0333-1024
J9 CEPHALALGIA
JI Cephalalgia
PD MAY
PY 2013
VL 33
IS 7
BP 469
EP 482
DI 10.1177/0333102413477738
PG 14
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 142NL
UT WOS:000318804000005
PM 23430981
ER
PT J
AU Schafer, MKH
Hartwig, NR
Kalmbach, N
Klietz, M
Anlauf, M
Eiden, LE
Weihe, E
AF Schaefer, M. K. -H.
Hartwig, N. R.
Kalmbach, N.
Klietz, M.
Anlauf, M.
Eiden, L. E.
Weihe, E.
TI Species-specific vesicular monoamine transporter 2 (VMAT2) expression in
mammalian pancreatic beta cells: implications for optimising
radioligand-based human beta cell mass (BCM) imaging in animal models
SO DIABETOLOGIA
LA English
DT Article
DE Beta cell mass; Imaging; Pancreas; Tetrabenazine; Vesicular monoamine
transporter
ID POSITRON-EMISSION-TOMOGRAPHY; ENDOCRINE PANCREAS; GENE-EXPRESSION; RAT
PANCREAS; 2 ISOFORMS; DISEASE; BINDING; PET; DIHYDROTETRABENAZINE;
TETRABENAZINE
AB Aims/hypothesis Imaging of beta cell mass (BCM) is a major challenge in diabetes research. The vesicular monoamine transporter 2 (VMAT2) is abundantly expressed in human beta cells. Radiolabelled analogues of tetrabenazine (TBZ; a low-molecular-weight, cell-permeant VMAT2-selective ligand) have been employed for pancreatic islet imaging in humans. Since reports on TBZ-based VMAT2 imaging in rodent pancreas have been fraught with confusion, we compared VMAT2 gene expression patterns in the mouse, rat, pig and human pancreas, to identify appropriate animal models with which to further validate and optimise TBZ imaging in humans.
Methods We used a panel of highly sensitive VMAT2 antibodies developed against equivalently antigenic regions of the transporter from each species in combination with immunostaining for insulin and species-specific in situ hybridisation probes. Individual pancreatic islets were obtained by laser-capture microdissection and subjected to analysis of mRNA expression of VMAT2.
Results The VMAT2 protein was not expressed in beta cells in the adult pancreas of common mouse or rat laboratory strains, in contrast to its expression in beta cells (but not other pancreatic endocrine cell types) in the pancreas of pigs and humans. VMAT2- and tyrosine hydroxylase co-positive (catecholaminergic) innervation was less abundant in humans than in rodents. VMAT2-positive mast cells were identified in the pancreas of all species.
Conclusions/interpretation Primates and pigs are suitable models for TBZ imaging of beta cells. Rodents, because of a complete lack of VMAT2 expression in the endocrine pancreas, are a 'null' model for assessing interference with BCM measurements by VMAT2-positive mast cells and sympathetic innervation in the pancreas.
C1 [Schaefer, M. K. -H.; Hartwig, N. R.; Kalmbach, N.; Klietz, M.; Weihe, E.] Univ Marburg, Dept Mol Neurosci, Inst Anat & Cell Biol, D-35037 Marburg, Germany.
[Anlauf, M.] Univ Dusseldorf, Sect Neuroendocrine Neoplasms, Dept Pathol & Biomat Bank, Univ Canc Ctr, D-40225 Dusseldorf, Germany.
[Eiden, L. E.] NIMH, Sect Mol Neurosci, Bethesda, MD 20892 USA.
RP Schafer, MKH (reprint author), Univ Marburg, Dept Mol Neurosci, Inst Anat & Cell Biol, Robert Koch Str 8, D-35037 Marburg, Germany.
EM mkh.schafer@staff.uni-marburg.de
OI Eiden, Lee/0000-0001-7524-944X
FU BetaImage Consortium; EU [222980]; University of Marburg Medical
Faculty; NIMH [1Z01MH002386]
FX Support by the BetaImage Consortium and EU grant EU FP7/-2013 No.
222980, and the University of Marburg Medical Faculty is gratefully
acknowledged. L. E. Eiden acknowledges the NIMH Intramural Research
program (under Project 1Z01MH002386) for research support.
NR 36
TC 14
Z9 14
U1 1
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD MAY
PY 2013
VL 56
IS 5
BP 1047
EP 1056
DI 10.1007/s00125-013-2847-7
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 142HD
UT WOS:000318787100012
PM 23404442
ER
PT J
AU Nacif, MS
Barranhas, AD
Turkbey, E
Marchiori, E
Kawel, N
Mello, RAF
Falcao, RO
Oliveira, AC
Rochitte, CE
AF Nacif, Marcelo Souto
Barranhas, Adriana Dias
Tuerkbey, Evrim
Marchiori, Edson
Kawel, Nadine
Mello, Ricardo A. F.
Falcao, Ricardo Oliveira
Oliveira, Amarino C., Jr.
Rochitte, Carlos Eduardo
TI Left atrial volume quantification using cardiac MRI in atrial
fibrillation: comparison of the Simpson's method with biplane
area-length, ellipse, and three-dimensional methods
SO DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID MAGNETIC-RESONANCE; RADIOFREQUENCY ABLATION; PULMONARY VEINS;
ECHOCARDIOGRAPHY; DIMENSIONS; INITIATION
AB PURPOSE
Left atrial volume is an important predictor of future arrhythmias, and it can be assessed by several different methods. Simpson's method is well accepted as a reference standard, although no standardization exists for cardiac magnetic resonance (CMR). We aimed to compare the estimations of left atrial volumes obtained by the Simpson's method with three other methods.
MATERIALS AND METHODS
Eighty-one consecutive patients referred for CMR imaging between February 2007 and May 2010 were included in the study (47 males; mean age, 59.4 +/- 11.5 years; body mass index, 26.3 +/- 3.7 kg/m(2)). Left atrial volume measurements were performed using the Simpson's, biplane area-length, ellipse, and three-dimensional methods. Results were correlated using a Bland-Altman plot and linear regression models and compared by two-tailed paired-sample t tests. Reader variability was also calculated.
RESULTS
Left atrial volume measurements using the biplane area-length technique showed the best correlation with Simpson's method (r=0.92; P < 0.001). Quantification values using the ellipse and three-dimensional methods were significantly different than values obtained using the Simpson's method (P < 0.05, for both). All methods showed excellent observer reliability (intra-class correlation coefficient >0.99).
CONCLUSION
The biplane area-length method can be used for left atrial volume measurement when the Simpson's method cannot be performed. If these two methods are not feasible, then all methods are highly reproducible and can be used, but should not be used interchangeably for follow-up studies.
C1 [Nacif, Marcelo Souto; Barranhas, Adriana Dias; Marchiori, Edson] Univ Fed Fluminense, Dept Radiol, Niteroi, RJ, Brazil.
[Barranhas, Adriana Dias; Marchiori, Edson; Mello, Ricardo A. F.; Falcao, Ricardo Oliveira] Univ Fed Rio de Janeiro, Dept Radiol, Rio De Janeiro, Brazil.
[Tuerkbey, Evrim; Kawel, Nadine] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Oliveira, Amarino C., Jr.; Rochitte, Carlos Eduardo] Hosp Procardiaco, Dept Radiol, Rio De Janeiro, Brazil.
RP Nacif, MS (reprint author), Univ Fed Fluminense, Dept Radiol, Niteroi, RJ, Brazil.
EM msnacif@gmail.com
NR 19
TC 11
Z9 11
U1 0
U2 4
PU TURKISH SOC RADIOLOGY
PI ANKARA
PA HOSDERE CAD, GUZELKENT SOK, CANKAYA EVLERI, F-2, ANKARA, 06540, TURKEY
SN 1305-3825
J9 DIAGN INTERV RADIOL
JI Diagn. Interv. Radiol.
PD MAY-JUN
PY 2013
VL 19
IS 3
BP 213
EP 220
DI 10.5152/dir.2012.002
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 136ZV
UT WOS:000318404500007
PM 23233400
ER
PT J
AU Spampanato, C
Feeney, E
Li, LS
Cardone, M
Lim, JA
Annunziata, F
Zare, H
Polishchuk, R
Puertollano, R
Parenti, G
Ballabio, A
Raben, N
AF Spampanato, Carmine
Feeney, Erin
Li, Lishu
Cardone, Monica
Lim, Jeong-A
Annunziata, Fabio
Zare, Hossein
Polishchuk, Roman
Puertollano, Rosa
Parenti, Giancarlo
Ballabio, Andrea
Raben, Nina
TI Transcription factor EB (TFEB) is a new therapeutic target for Pompe
disease
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE acid alpha-glucosidase; autophagy; lysosomal storage; Pompe disease;
TFEB
ID LYSOSOMAL STORAGE DISORDERS; ENZYME REPLACEMENT THERAPY; ACID
ALPHA-GLUCOSIDASE; CHOLESTEROL ACCUMULATION; SKELETAL-MUSCLE; SATELLITE
CELLS; MOUSE MODEL; AUTOPHAGY; EXOCYTOSIS; BIOGENESIS
AB A recently proposed therapeutic approach for lysosomal storage disorders (LSDs) relies upon the ability of transcription factor EB (TFEB) to stimulate autophagy and induce lysosomal exocytosis leading to cellular clearance. This approach is particularly attractive in glycogen storage disease type II [a severe metabolic myopathy, Pompe disease (PD)] as the currently available therapy, replacement of the missing enzyme acid alpha-glucosidase, fails to reverse skeletal muscle pathology. PD, a paradigm for LSDs, is characterized by both lysosomal abnormality and dysfunctional autophagy. Here, we show that TFEB is a viable therapeutic target in PD: overexpression of TFEB in a new muscle cell culture system and in mouse models of the disease reduced glycogen load and lysosomal size, improved autophagosome processing, and alleviated excessive accumulation of autophagic vacuoles. Unexpectedly, the exocytosed vesicles were labelled with lysosomal and autophagosomal membrane markers, suggesting that TFEB induces exocytosis of autophagolysosomes. Furthermore, the effects of TFEB were almost abrogated in the setting of genetically suppressed autophagy, supporting the role of autophagy in TFEB-mediated cellular clearance.
C1 [Spampanato, Carmine; Cardone, Monica; Annunziata, Fabio; Polishchuk, Roman; Parenti, Giancarlo; Ballabio, Andrea] Telethon Inst Genet & Med TIGEM, Naples, Italy.
[Spampanato, Carmine; Ballabio, Andrea] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Spampanato, Carmine; Ballabio, Andrea] Texas Children Hosp, Jan & Dan Duncan Neurol Res Inst, Houston, TX USA.
[Feeney, Erin; Li, Lishu; Lim, Jeong-A; Zare, Hossein; Raben, Nina] NIAMSD, Lab Muscle Stem Cells & Gene Regulat, NIH, Bethesda, MD 20892 USA.
[Puertollano, Rosa] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Parenti, Giancarlo; Ballabio, Andrea] Univ Naples Federico II, Dept Pediat, Naples, Italy.
RP Ballabio, A (reprint author), Telethon Inst Genet & Med TIGEM, Naples, Italy.
EM ballabio@tigem.it; rabenn@mail.nih.gov
RI Li, Lishu /J-3191-2015; Annunziata, Fabio/D-5074-2016; di Ronza,
Alberto/H-7674-2016;
OI Annunziata, Fabio/0000-0001-8598-5459; di Ronza,
Alberto/0000-0002-9813-5143; BALLABIO, Andrea/0000-0003-1381-4604
FU Intramural Research Program of the National Institute of Arthritis and
Musculoskeletal and Skin diseases of the National Institutes of Health;
CRADA; Italian Telethon Foundation [TGPMT4TELD, TGM11CB6]; European
Research Council [250154]; Beyond Batten Disease Foundation; March of
Dimes [6-FY11-306]; US National Institute of Health [R01-NS078072]
FX We would like to thank Drs. Kristein Zaal and Evelyn Ralston (NIAMS,
NIH) for their useful comments and help with the imaging. We would also
like to thank Dr. Hoi Ming Li for his contribution to our tissue culture
and electroporation experiments. We are also grateful to G. Diez-Roux
for critical reading of the manuscript and helpful discussions. This
research was supported in part by the Intramural Research Program of the
National Institute of Arthritis and Musculoskeletal and Skin diseases of
the National Institutes of Health. Drs. Li and Lim are supported in part
by a CRADA between NIH and Genzyme Corporation. We acknowledge the
support of the Italian Telethon Foundation (grant # TGPMT4TELD to G. P;
grant # TGM11CB6 to A. B, C. S and F. A.), the European Research Council
Advanced Investigator grant no. 250154 (A. B.), the Beyond Batten
Disease Foundation (A. B.), March of Dimes # 6-FY11-306 (A. B.), and US
National Institute of Health R01-NS078072 (A.B.).
NR 66
TC 80
Z9 82
U1 2
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD MAY
PY 2013
VL 5
IS 5
BP 691
EP 706
DI 10.1002/emmm.201202176
PG 16
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 139EZ
UT WOS:000318565900005
PM 23606558
ER
PT J
AU Wang, HH
Xi, SH
Liu, ZG
Yang, Y
Zheng, QM
Wang, F
Xu, YY
Wang, Y
Zheng, Y
Sun, GG
AF Wang, Huihui
Xi, Shuhua
Liu, Zhuogang
Yang, Ying
Zheng, Quanmei
Wang, Fei
Xu, Yuanyuan
Wang, Yi
Zheng, Yi
Sun, Guifan
TI Arsenic Methylation Metabolism and Liver Injury of Acute Promyelocytic
Leukemia Patients Undergoing Arsenic Trioxide Treatment
SO ENVIRONMENTAL TOXICOLOGY
LA English
DT Article
DE arsenic trioxide; arsenic methylation; liver injury; acute promyelocytic
leukemia; urinary arsenic species
ID DRINKING-WATER; SKIN-LESIONS; ENZYMATIC METHYLATION; HYPERENDEMIC
VILLAGES; BLADDER-CANCER; TOXICITY; ADULTS; EXPOSURE; CHILDREN; TAIWAN
AB Although arsenic is effective in the treatment of acute promyelocytic leukemia (APL), as a well-known environmental toxicant, the side effects of arsenic treatment and arsenic methylation metabolism of the patients are rarely reported. In this manuscript, we investigated 23 APL patients treated with 10 mg arsenic trioxide daily, detected the arsenic metabolites in urine samples collected on the 0, 10th, and 20th day of arsenic treatment. At the same time, liver function and blood routine examination were also investigated in these APL patients. We found that, urinary monomethylated arsenic proportion (MMA%) increased, but dimethylated arsenic proportion (DMA%), the first methylation ratio (FMR) and the secondary methylation ratio (SMR) decreased with consecutive administration of arsenic trioxide. After adjustment for age impact, no statistical difference was observed in urinary arsenic concentrations and arsenic methylation capacity between male and female at the same treatment time point. During arsenic trioxide treatment of APL, transient elevation of serum aminotransferases was found in the blood samples, which indicated that liver injury occurred and probably reversible. Leukocytosis developed in 5 of the 23 patients with the administration of arsenic trioxide. No statistical difference was observed in the other blood routine examination parameters. These results demonstrated that the capacity of arsenic methylation decreased and transient liver injury occurred during arsenic trioxide treatment of APL, which indicated that the side effects of clinical arsenic treatment can not be ignored. (C) 2011 Wiley Periodicals, Inc. Environ Toxicol 28: 267-275, 2013.
C1 [Wang, Huihui; Xi, Shuhua; Zheng, Quanmei; Wang, Fei; Wang, Yi; Zheng, Yi; Sun, Guifan] China Med Univ, Dept Occupat & Environm Hlth, Sch Publ Hlth, Shenyang, Liaoning, Peoples R China.
[Liu, Zhuogang; Yang, Ying] China Med Univ, Shengjing Hosp, Hematol Dis Treatment Ctr, Shenyang, Liaoning, Peoples R China.
[Xu, Yuanyuan] NIEHS, Natl Toxicol Program Labs, Res Triangle Pk, NC 27709 USA.
RP Sun, GG (reprint author), China Med Univ, Dept Occupat & Environm Hlth, Sch Publ Hlth, Shenyang, Liaoning, Peoples R China.
EM sungf@mail.cmu.edu.cn
FU National Natural Science Foundation of China (NSFC) [30771865]; National
Science and Technology Pillar Program of China during the 11th Five-Year
Plan Period [2006BAI06B04]; Department of Education of Liaoning
Province, China [2009A756]
FX Contract grant sponsor: National Natural Science Foundation of China
(NSFC).; Contract grant number: 30771865.; Contract grant sponsor:
National Science and Technology Pillar Program of China during the 11th
Five-Year Plan Period.; Contract grant number: 2006BAI06B04.; Contract
grant sponsor: Department of Education of Liaoning Province, China.;
Contract grant number: 2009A756.
NR 63
TC 5
Z9 5
U1 1
U2 28
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1520-4081
J9 ENVIRON TOXICOL
JI Environ. Toxicol.
PD MAY
PY 2013
VL 28
IS 5
BP 267
EP 275
DI 10.1002/tox.20717
PG 9
WC Environmental Sciences; Toxicology; Water Resources
SC Environmental Sciences & Ecology; Toxicology; Water Resources
GA 139IQ
UT WOS:000318576200003
PM 23589229
ER
PT J
AU Psota, T
Chen, KY
AF Psota, T.
Chen, K. Y.
TI Measuring energy expenditure in clinical populations: rewards and
challenges
SO EUROPEAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Review
DE basal metabolic rate; indirect calorimetry; oxygen consumption; obesity;
children; elderly
ID RESTING METABOLIC-RATE; BODY-MASS INDEX; BIRTH-WEIGHT INFANTS;
GAS-ANALYSIS SYSTEMS; PREDICTIVE EQUATIONS; CALORIC REQUIREMENTS;
ENTERAL NUTRITION; LIVER-CIRRHOSIS; CRITICALLY-ILL; KIDNEY-DISEASE
AB The measurement of energy expenditure (EE) is recommended as an important component of comprehensive clinical nutrition assessments in patients with altered metabolic states, who failed to respond to nutrition support and with critical illness that require individualized nutrition support. There is evidence that EE is variable in patients with metabolic diseases, such as chronic renal disease, cirrhosis, HIV, cancer cachexia, cystic fibrosis and patients under intensive care. By using appropriate techniques and interpretations of basal or resting EE, clinicians can facilitate the adequate nutrition support with minimum negative impacts from under- or overfeeding in these patients. This review is based on our current understanding of the different components of EE and the techniques to measure them, and to re-examine advances and challenges to determine energy needs in clinical populations with more focuses on the obese, pediatric and elderly patients. In addition, technological advances have expanded the choices of market-available equipments for assessing EE, which also bring specific challenges and rewards in selecting the right equipment with specific performance criteria. Lastly, analytical considerations of interpreting the results of EE in the context of changing body composition are presented and discussed.
C1 [Psota, T.] NIH, Dept Nutr, Ctr Clin, Bethesda, MD 20892 USA.
[Chen, K. Y.] NIDDKD, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
RP Chen, KY (reprint author), NIH, CRC, 10 Ctr Dr MSC 1613,Bldg 10,RM 6-3940, Bethesda, MD 20892 USA.
EM chenkong@niddk.nih.gov
RI Andrade, Hugo/M-6631-2013;
OI Andrade, Hugo/0000-0001-6781-6125; Chen, Kong/0000-0002-0306-1904
FU NIH Intramural research funding resources [NIDDK Z01 DK071013, Z01
DK071014]
FX We thank Ms Rachel Perron and Dr Lilian de Jonge for their help in this
review. This work was funded by NIH Intramural research funding
resources (NIDDK Z01 DK071013, Z01 DK071014 and Clinical Center).
NR 93
TC 9
Z9 11
U1 0
U2 39
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0954-3007
J9 EUR J CLIN NUTR
JI Eur. J. Clin. Nutr.
PD MAY
PY 2013
VL 67
IS 5
BP 436
EP 442
DI 10.1038/ejcn.2013.38
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 139AW
UT WOS:000318554800004
PM 23443826
ER
PT J
AU Levy, G
Hill, MJ
Ramirez, C
Plowden, T
Pilgrim, J
Howard, RS
Segars, JH
Csokmay, J
AF Levy, Gary
Hill, Micah J.
Ramirez, Christina
Plowden, Torrie
Pilgrim, Justin
Howard, Robin S.
Segars, James H.
Csokmay, John
TI Serum human chorionic gonadotropin levels on the day before oocyte
retrieval do not correlate with oocyte maturity
SO FERTILITY AND STERILITY
LA English
DT Article
DE Assisted reproductive technologies; infertility; in vitro fertilization
ID IN-VITRO FERTILIZATION; OVARIAN STIMULATION; INJECTION; MATURATION;
OVULATION; CYCLES; WOMEN; HCG
AB Objective: To evaluate the correlation of preretrieval quantitative serum hCG level with oocyte maturity.
Design: Retrospective cohort study.
Setting: Military assisted reproductive technology (ART) program.
Patient(s): Fresh autologous ART cycles.
Intervention(s): Serum hCG level the day before oocyte retrieval.
Main Outcome Measure(s): Linear regression was used to correlate serum hCG levels and oocyte maturity rates. Normal oocyte maturity was defined as >= 75% and the Wilcoxon rank sum test was used to compare serum hCG levels in patients with normal and low oocyte maturity. Threshold analysis was performed to determine hCG levels that could predict oocyte maturity.
Result(s): A total of 468 ART cycles were analyzed. Serum hCG level was not correlated with hCG dose; however, it was negatively correlated with body mass index (BMI). Serum hCG levels did not differ between patients with oocyte maturity of <75% and >= 75%. Serum hCG levels did not correlate with oocyte maturity rates. Receiver operator characteristic and less than efficiency curves failed to demonstrate thresholds at which hCG could predict oocyte maturity.
Conclusion(s): Serum hCG levels were not correlated with oocyte maturity. Although a positive hCG was reassuring that mature oocytes would be retrieved for most patients, the specific value was not helpful. (C) 2013 by American Society for Reproductive Medicine.
C1 [Levy, Gary; Ramirez, Christina; Segars, James H.; Csokmay, John] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Plowden, Torrie; Pilgrim, Justin] Bayne Jones Army Community Hosp, Dept OB GYN, Ft Polk, LA USA.
[Howard, Robin S.] Walter Reed Natl Mil Med Ctr Bethesda, Dept Biostat, Bethesda, MD USA.
[Hill, Micah J.; Csokmay, John] Walter Reed Natl Mil Med Ctr Bethesda, Dept Reprod Endocrinol & Infertil, Bethesda, MD USA.
RP Levy, G (reprint author), NIH, 10 Ctr Dr,Room 1-3140,MSC 1109, Bethesda, MD 20892 USA.
EM gary.levy@nih.gov
FU intramural research program of the Program in Reproductive and Adult
Endocrinology, National Institute of Child Health and Human Development,
National Institutes of Health
FX Supported, in part, by intramural research program of the Program in
Reproductive and Adult Endocrinology, National Institute of Child Health
and Human Development, National Institutes of Health.
NR 16
TC 1
Z9 2
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD MAY
PY 2013
VL 99
IS 6
BP 1610
EP 1614
DI 10.1016/j.fertnstert.2012.12.053
PG 5
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 139VF
UT WOS:000318612400025
PM 23375205
ER
PT J
AU Hill, MJ
Richter, KS
Heitmann, RJ
Lewis, TD
DeCherney, AH
Graham, JR
Widra, E
Levy, MJ
AF Hill, Micah J.
Richter, Kevin S.
Heitmann, Ryan J.
Lewis, Terrance D.
DeCherney, Alan H.
Graham, James R.
Widra, Eric
Levy, Michael J.
TI Number of supernumerary vitrified blastocysts is positively correlated
with implantation and live birth in single-blastocyst embryo transfers
SO FERTILITY AND STERILITY
LA English
DT Article
DE Blastocyst; implantation; live birth; supernumerary embryos; vitrified
ID REPRODUCTIVE TECHNOLOGY DATABASE; WOMEN 38 YEARS; TROPHECTODERM
MORPHOLOGY; STAGE EMBRYOS; AGE; CRYOPRESERVATION; PROFESSIONALS;
PREGNANCY; SOCIETY; OLDER
AB Objective: To estimate whether live birth in single-blastocyst transfers is correlated with the number of sibling supernumerary vitrified blastocysts (embryos not transferred) generated from that same cycle.
Design: Retrospective cohort study.
Setting: A large academic assisted reproduction clinic.
Patient(s): All single-blastocyst transfers in 2010 graded as "good" embryos by Society for Assisted Reproductive Technologies (SART) criteria.
Intervention(s): None.
Main Outcome Measure(s): Implantation and live birth.
Result(s): Of the 655 single-blastocyst transfers that met inclusion criteria, implantation occurred in 65% and live birth in 54% of cycles. In chi-square analysis, patients with supernumerary vitrified blastocysts had a statistically higher implantation rate (65% versus 50%) and live-birth rate (56% versus 41%) when compared with patients without supernumerary blastocysts. Univariate logistic regression demonstrated an increase in implantation (OR 1.09; 95% CI, 1.03-1.15) and live birth (OR 1.06; 95% CI, 1.02-1.09) with increasing number of supernumerary blastocysts. Multivariate logistic regression analysis demonstrated that patient age and the number of supernumerary blastocysts were statistically significantly associated with implantation and live birth.
Conclusion(s): The number of supernumerary vitrified blastocysts correlated positively with the odds of implantation and live birth in good quality single-blastocyst transfers. Patients with supernumerary blastocysts are good candidates for single-embryo transfer. (C) 2013 by American Society for Reproductive Medicine.
C1 [Hill, Micah J.; Heitmann, Ryan J.; Lewis, Terrance D.; DeCherney, Alan H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
[Hill, Micah J.; Richter, Kevin S.; Heitmann, Ryan J.; Graham, James R.; Widra, Eric; Levy, Michael J.] Shady Grove Fertil Reprod Sci Ctr, Rockville, MD USA.
RP Levy, MJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, CRC, 10 Ctr Dr,Bldg 10,Room E1-3140, Bethesda, MD 20892 USA.
EM michael.levy@integremed.com
FU Intramural Research Program of the Program in Reproductive and Adult
Endocrinology, National Institute of Child Health and Human Development,
National Institutes of Health
FX Supported in part by the Intramural Research Program of the Program in
Reproductive and Adult Endocrinology, National Institute of Child Health
and Human Development, National Institutes of Health.
NR 21
TC 7
Z9 7
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD MAY
PY 2013
VL 99
IS 6
BP 1631
EP 1636
DI 10.1016/j.fertnstert.2013.01.130
PG 6
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 139VF
UT WOS:000318612400028
PM 23433518
ER
PT J
AU Klein, WMP
Rothman, AJ
Cameron, LD
AF Klein, William M. P.
Rothman, Alexander J.
Cameron, Linda D.
TI Theoretical Innovations in Social and Personality Psychology and
Implications for Health: Introduction to Special Issue
SO HEALTH PSYCHOLOGY
LA English
DT Editorial Material
C1 [Klein, William M. P.] NCI, Behav Res Program, Bethesda, MD 20892 USA.
[Rothman, Alexander J.] Univ Minnesota, Dept Psychol, Minneapolis, MN 55455 USA.
[Cameron, Linda D.] Univ Calif Merced, Merced, CA USA.
[Cameron, Linda D.] Univ Calif Merced, Sch Psychol Sci Humanities & Arts, Merced, CA USA.
RP Klein, WMP (reprint author), NCI, Behav Res Program, Execut Blvd Room 4060, Bethesda, MD 20892 USA.
EM kleinwm@mail.nih.gov
NR 18
TC 3
Z9 4
U1 0
U2 6
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0278-6133
J9 HEALTH PSYCHOL
JI Health Psychol.
PD MAY
PY 2013
VL 32
IS 5
SI SI
BP 457
EP 459
DI 10.1037/a0032386
PG 3
WC Psychology, Clinical; Psychology
SC Psychology
GA 138QL
UT WOS:000318523400001
PM 23646830
ER
PT J
AU Rothman, AJ
Klein, WMP
Cameron, LD
AF Rothman, Alexander J.
Klein, William M. P.
Cameron, Linda D.
TI Advancing Innovations in Social/Personality Psychology and Health:
Opportunities and Challenges
SO HEALTH PSYCHOLOGY
LA English
DT Editorial Material
DE theory; practice; Pasteur's quadrant; social psychology; personality
psychology
ID SMOKING-CESSATION; BEHAVIOR-CHANGE; SATISFACTION; SCIENCE; MAINTENANCE;
INITIATION; MODEL
AB Social, personality, and health psychologists have a long tradition of active and productive collaborations that have advanced the development of intervention strategies that promote health and well-being and the specification of the theoretical principles that underlie those strategies. This special issue is designed to continue this tradition of collaboration and to highlight areas of research and investigative strategies that offer opportunities for innovation. This concluding paper examines how investigators construe the interface between theory and practice and, with that lens, considers several themes that have emerged across the papers that comprise this special issue. As evidenced by the papers in this special issue, investigators are well-positioned to leverage advances in understanding of human health and well-being. However, to capitalize on this opportunity, investigators need to commit to cultivating a culture of scientific activity that prioritizes the engagement of theory and practice-the pursuit of both understanding and use.
C1 [Rothman, Alexander J.] Univ Minnesota, Dept Psychol, Minneapolis, MN 55455 USA.
[Klein, William M. P.] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Cameron, Linda D.] Univ Calif Merced, Sch Social Sci Humanities & Arts, Merced, CA USA.
RP Rothman, AJ (reprint author), Univ Minnesota, Dept Psychol, 75 E River Rd, Minneapolis, MN 55455 USA.
EM rothm001@umn.edu
NR 44
TC 6
Z9 6
U1 5
U2 25
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0278-6133
J9 HEALTH PSYCHOL
JI Health Psychol.
PD MAY
PY 2013
VL 32
IS 5
SI SI
BP 602
EP 608
DI 10.1037/a0032116
PG 7
WC Psychology, Clinical; Psychology
SC Psychology
GA 138QL
UT WOS:000318523400017
PM 23646845
ER
PT J
AU Everhart, JE
Wright, EC
AF Everhart, James E.
Wright, Elizabeth C.
TI Association of gamma-Glutamyl Transferase (GGT) Activity With Treatment
and Clinical Outcomes in Chronic Hepatitis C (HCV)
SO HEPATOLOGY
LA English
DT Article
ID SUSTAINED VIROLOGICAL RESPONSE; STANDARD LABORATORY TESTS; COFFEE
CONSUMPTION; ALANINE AMINOTRANSFERASE; INTERFERON-ALPHA; PREDICTIVE
MODEL; LIVER FIBROSIS; TRANSPEPTIDASE; MORTALITY; ALCOHOL
AB Increased gamma-glutamyl transferase (GGT) activity is associated with liver injury and with mortality in the general population. Less is known about its association with chronic hepatitis C (HCV) outcomes. We examined GGT as a predictor of both virological response to treatment and long-term clinical outcomes in the Hepatitis C Anti-viral Treatment Against Cirrhosis Trial (HALT-C). HALT-C enrolled patients with advanced liver disease (Ishak fibrosis score >= 3) in two phases: a lead-in to establish lack of sustained viral response with full dose pegylated interferon (IFN) and ribavirin followed by a 3.5-year randomized trial with low-dose IFN. Low-dose IFN did not prevent liver disease progression, and patients were then followed for up to an additional 5 years off therapy. Analyses were performed for 1,319 patients who had GGT measured prior to initiation of treatment. Increases in risk with each increase in quintile of GGT (10-57, 58-89, 90-139, 140-230, 231-2,000 IU/L) were determined by logistic regression for treatment response or Cox regression for clinical outcomes. Baseline GGT was associated with male sex, nonwhite ethnicity, diabetes and insulin resistance, interleukin (IL)28B rs12979860 CT and TT genotypes, and numerous markers of liver disease injury and severity. In the lead-in phase, increasing GGT was strongly associated with diminished week 20 response, end of treatment response, and sustained virological response in both univariate and multivariate analyses controlling for factors known to be associated with treatment response (P < 0.0001). GGT was also associated with all clinical outcomes in univariate and multivariate analysis (P < 0.05) except for hepatocellular carcinoma (P = 0.46 in multivariate analysis). Conclusion: GGT is an independent predictor of both virological response and clinical outcomes among patients with advanced liver disease due to HCV. (HEPATOLOGY 2013;57:1725-1733)
C1 [Everhart, James E.; Wright, Elizabeth C.] NIDDKD, Bethesda, MD 20892 USA.
RP Everhart, JE (reprint author), NIDDKD, Epidemiol & Clin Trials Branch, Div Digest Dis & Nutr, 2 Democracy Plaza,Room 655,6707 Democracy Blvd,MS, Bethesda, MD 20892 USA.
EM JE17G@NIH.GOV
FU National Institute of Diabetes & Digestive & Kidney Diseases
[N01-DK-9-2326, N01-DK-9-2324, N01-DK-9-2319, N01-DK-9-2327,
N01-DK-9-2320, N01-DK-9-2321, N01-DK-9-2325, N01-DK-9-2323,
N01-DK-9-2322, N01-DK-9-2318, N01-DK-9-2328]; Hoffmann-La Roche;
National Institutes of Health
FX Supported by National Institute of Diabetes & Digestive & Kidney
Diseases contracts N01-DK-9-2326, N01-DK-9-2324, Contract N01-DK-9-2319,
N01-DK-9-2327, N01-DK-9-2320, N01-DK-9-2321, N01-DK-9-2325,
N01-DK-9-2323, N01-DK-9-2322, N01-DK-9-2318, and N01-DK-9-2328.
Additional financial support was provided by Hoffmann-La Roche, through
a Cooperative Research and Development Agreement (CRADA) with the
National Institutes of Health.
NR 49
TC 22
Z9 24
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2013
VL 57
IS 5
BP 1725
EP 1733
DI 10.1002/hep.26203
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 133TC
UT WOS:000318162200009
PM 23258530
ER
PT J
AU Everson, GT
Terrault, NA
Lok, AS
Rodrigo, DR
Brown, RS
Saab, S
Shiffman, ML
Al-Osaimi, AMS
Kulik, LM
Gillespie, BW
Everhart, JE
AF Everson, Gregory T.
Terrault, Norah A.
Lok, Anna S.
Rodrigo, Del R.
Brown, Robert S., Jr.
Saab, Sammy
Shiffman, Mitchell L.
Al-Osaimi, Abdullah M. S.
Kulik, Laura M.
Gillespie, Brenda W.
Everhart, James E.
CA Adult-to-Adult Living Donor Liver
TI A Randomized Controlled Trial of Pretransplant Antiviral Therapy to
Prevent Recurrence of Hepatitis C After Liver Transplantation
SO HEPATOLOGY
LA English
DT Article
ID PEGINTERFERON ALPHA-2A; PLUS RIBAVIRIN; VIRUS; INFECTION; IMPACT
AB Hepatitis C virus (HCV) infection recurs in liver recipients who are viremic at transplantation. We conducted a randomized, controlled trial to test the efficacy and safety of pretransplant pegylated interferon alpha-2b plus ribavirin (Peg-IFN-alpha 2b/RBV) for prevention of post-transplant HCV recurrence. Enrollees had HCV and were listed for liver transplantation, with either potential living donors or Model for End-Stage Liver Disease upgrade for hepatocellular carcinoma. Patients with HCV genotypes (G) 1/4/6 (n = 44/2/1) were randomized 2: 1 to treatment (n = 31) or untreated control (n = 16); HCV G2/3 (n=32) were assigned to treatment. Overall, 59 were treated and 20 were not. Peg-IFN-alpha 2b, starting at 0.75 mu g/kg/week, and RBV, starting at 600 mg/day, were escalated as tolerated. Patients assigned to treatment versus control had similar baseline characteristics. Combined virologic response (CVR) included pretransplant sustained virologic response and post-transplant virologic response (pTVR), defined as undetectable HCV RNA 12 weeks after end of treatment or transplant, respectively. In intent-to-treat analyses, 12 (19%) assigned to treatment and 1 (6%) assigned to control achieved CVR (P = 0.29); per-protocol values were 13 (22%) and 0 (0%) (P = 0.03). Among treated G1/4/6 patients, 23 of 30 received transplant, of whom 22% had pTVR; among treated G2/3 patients 21 of 29 received transplant, of whom 29% had pTVR. pTVR was 0%, 18%, and 50% in patients treated for <8, 8-16, and >16 weeks, respectively (P = 0.01). Serious adverse events (SAEs) occurred with similar frequency in treated versus untreated patients (68% versus 55%; P = 0.30), but the number of SAEs per patient was higher in the treated group (2.7 versus 1.3; P = 0.003). Conclusion: Pretransplant treatment with Peg-IFN-alpha 2b/RBV prevents post-transplant recurrence of HCV in selected patients. Efficacy is higher with >16 weeks of treatment, but treatment is associated with increased risk of potentially serious complications. (HEPATOLOGY 2013;57:1752-1762)
C1 [Everson, Gregory T.] Univ Colorado Denver, Sect Hepatol, Aurora, CO 80045 USA.
[Terrault, Norah A.] Univ Calif San Francisco, Div Gastroenterol, San Francisco, CA 94143 USA.
[Lok, Anna S.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Rodrigo, Del R.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
[Brown, Robert S., Jr.] Columbia Univ Coll Phys & Surg, Dept Med & Surg, New York, NY 10032 USA.
[Saab, Sammy] Univ Calif Los Angeles, Dept Med & Surg, Los Angeles, CA USA.
[Shiffman, Mitchell L.] Virginia Commonwealth Univ, Dept Med, Richmond, VA 23298 USA.
[Al-Osaimi, Abdullah M. S.] Univ Virginia, Dept Med, Charlottesville, VA USA.
[Kulik, Laura M.] Northwestern Univ, Dept Med & Surg, Chicago, IL 60611 USA.
[Gillespie, Brenda W.] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Everhart, James E.] NIDDKD, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
RP Everson, GT (reprint author), Univ Colorado Denver, Sect Hepatol, 1635 North Aurora Court,B-154, Aurora, CO 80045 USA.
EM greg.everson@UCDenver.edu
OI Yang, Shuman/0000-0002-9638-0890
FU National Institutes of Health (NIH); National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK) [U01-DK62536, U01-DK62444,
U01-DK62467, U01-DK62483, U01-DK62484, U01-DK62494, U01-DK62496,
U01-DK62498, U01-DK62505, U01-DK62531]; Schering-Plough; NIH-NIDDK;
Ortho-Biotech; NIDDKD; Health Resources and Services Administration;
American Society of Transplant Surgeons; Merck; Roche; Genentech;
Vertex; Idenix; Novartis; Gilead; Valeant; Intermune; Pharmasset;
HemoLife Medical; Genzyme; Ortho Biotech; GalxoSMithKline;
Sanofi-Aventis; Bayer Healthcare; Hyperion; Bristol-Myers Squibb; Vital;
Octapharma; Achillion; Boehringer-Ingelheim; Globeimmune; Inhibitex;
Zymogenetics; Conatus; Anandys
FX The patients participating in this trial were enrolled in the National
Institutes of Health (NIH)-sponsored Adult-to-Adult Living Donor Liver
Transplantation Cohort Study. This study was supported by the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) through
cooperative agreements (NIDDK grant nos.: U01-DK62536, U01-DK62444,
U01-DK62467, U01-DK62483, U01-DK62484, U01-DK62494, U01-DK62496,
U01-DK62498, U01-DK62505, and U01-DK62531). The trial was also funded by
research grants from Schering-Plough, through a cooperative research and
development agreement with NIH-NIDDK, and through a clinical trial
agreement between Ortho-Biotech and NIH-NIDDK. This study was supported
by the NIDDKD through cooperative agreements (listed in parentheses).
Additional support was provided by the Health Resources and Services
Administration and the American Society of Transplant Surgeons.; Dr.
Everson advises, consults for, and received grants from Merck and
Schering-Plough. Dr. Terrault consults for, and received grants from
Roche and Genentech. Dr. Lok consults for and received grants from
Schering-Plough, Merck, Roche, and Genentech. Dr. Brown consults for
Merck. Dr. Saab owns stock in, consults for, advises, and is in the
speakers' bureau of Bristol-Myers Squibb. He consults for, advises, and
is on the speakers' bureau of Genentech and Merck. Dr. Al-Osaimi
consults for, advises, is on the speakers' bureau of, and received
grants from Merck and Vertex. He is on the speakers' bureau of and
received grants from Idenix, Novartis, and Gilead. He also consults for
Amgen and received grants from Genentech, Valeant, Intermune,
Pharmasset, HemoLife Medical, Genzyme, Ortho Biotech, GalxoSMithKline,
Sanofi-Aventis, Bayer Healthcare, Hyperion, Bristol-Myers Squibb, Vital,
and Octapharma. Dr. Shiffman advises and received grants from Achillion,
Boehringer-Ingelheim, Globeimmune, Inhibitex, Novartis, Vertex, and
Zymogenetics. He consults for Biolex, Human Genome Sciences, Romark. He
advises Pfizer and Janssen. He received grants from Idenix. He advises,
is on the speakers' bureau of, and received grants from Schering-Plough,
Gilead, and Bristol-Myers Squibb. He consults for, advises, and received
grants from Conatus. He consults for, advises, is on the speakers bureau
of, and received grants from Roche and Anandys. He is on the speakers'
bureau of and advises Bayer.
NR 19
TC 62
Z9 64
U1 0
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2013
VL 57
IS 5
BP 1752
EP 1762
DI 10.1002/hep.25976
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 133TC
UT WOS:000318162200012
PM 22821361
ER
PT J
AU Proctor, WR
Chakraborty, M
Chea, LS
Morrison, JC
Berkson, JD
Semple, K
Bourdi, M
Pohl, LR
AF Proctor, William R.
Chakraborty, Mala
Chea, Lynette S.
Morrison, Jeffrey C.
Berkson, Julia D.
Semple, Kenrick
Bourdi, Mohammed
Pohl, Lance R.
TI Eosinophils Mediate the Pathogenesis of Halothane-Induced Liver Injury
in Mice
SO HEPATOLOGY
LA English
DT Article
ID INDUCED HEPATITIS; MURINE MODEL; MOUSE MODEL; HEPATOTOXICITY; CELLS;
EXPRESSION; DISEASE; ASTHMA; POLYMORPHISMS; NEUTROPHILS
AB Drug-induced liver injury (DILI) is a major health issue, as it remains difficult to predict which new drugs will cause injury and who will be susceptible to this disease. This is due in part to the lack of animal models and knowledge of susceptibility factors that predispose individuals to DILI. In this regard, liver eosinophilia has often been associated with DILI, although its role remains unclear. We decided to investigate this problem in a murine model of halothane-induced liver injury (HILI). When female Balb/cJ mice were administered halothane, eosinophils were detected by flow cytometry in the liver within 12 hours and increased thereafter proportionally to liver damage. Chemokines, eotaxin-1 (CCL11) and eotaxin-2 (CCL24), which are known to attract eosinophils, increased in response to halothane treatment. The severity of HILI was decreased significantly when the study was repeated in wildtype mice made deficient in eosinophils with a depleting antibody and in eosinophil lineage-ablated Delta dblGata -/- mice. Moreover, depletion of neutrophils by pretreating animals with Gr-1 antibody prior to halothane administration failed to reduce the severity of HILI at antibody concentrations that did not affect hepatic eosinophils. Immunohistochemical staining for the granule protein, major basic protein, revealed that eosinophils accumulated exclusively around areas of hepatocellular necrosis. Conclusion: Our findings indicate that eosinophils have a pathologic role in HILI in mice and suggest that they may contribute similarly in many clinical cases of DILI. (HEPATOLOGY 2013;57:2026-2036)
C1 [Proctor, William R.; Chakraborty, Mala; Chea, Lynette S.; Morrison, Jeffrey C.; Berkson, Julia D.; Semple, Kenrick; Bourdi, Mohammed; Pohl, Lance R.] NHLBI, Mol & Cellular Toxicol Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Proctor, WR (reprint author), NHLBI, Mol & Cellular Toxicol Sect, Lab Mol Immunol, NIH, Bldg 10,Room 8N110,10 Ctr Dr, Bethesda, MD 20892 USA.
EM william.proctor@nih.gov
FU National Institutes of Health; National Heart, Lung and Blood Institute
FX Supported by the Intramural Research Program of the National Institutes
of Health and the National Heart, Lung and Blood Institute.
NR 40
TC 14
Z9 14
U1 1
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD MAY
PY 2013
VL 57
IS 5
BP 2026
EP 2036
DI 10.1002/hep.26196
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 133TC
UT WOS:000318162200037
PM 23238640
ER
PT J
AU He, JP
Burstein, M
Schmitz, A
Merikangas, KR
AF He, Jian-Ping
Burstein, Marcy
Schmitz, Anja
Merikangas, Kathleen R.
TI The Strengths and Difficulties Questionnaire (SDQ): the Factor Structure
and Scale Validation in U.S. Adolescents
SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY
LA English
DT Article
DE Strengths and difficulties questionnaire (SDQ); Confirmatory factor
analysis (CFA); Construct validity; National comorbidity
survey-adolescent supplement (NCS-A)
ID SUPPLEMENT NCS-A; PRIMARY-SCHOOL CHILDREN; MENTAL-HEALTH-CARE; OF-FIT
INDEXES; PSYCHOMETRIC PROPERTIES; MEASUREMENT INVARIANCE; COMMUNITY
SAMPLE; PSYCHIATRIC-DISORDERS; VERSION; VALIDITY
AB The Strengths and Difficulties Questionnaire (SDQ) is one of the most commonly used instruments for screening psychopathology in children and adolescents. This study evaluated the hypothesized five-factor structure of the SDQ and examined its convergent validity against comprehensive clinical diagnostic assessments. Data were derived from the National Comorbidity Survey - Adolescent Supplement (NCS-A), a nationally representative sample of U.S. adolescents aged 13 to 18 years. Parents/parent surrogates (n=6,483) was asked to complete a self-administered questionnaire including the SDQ and DSM-IV comprehensive diagnostic information on the participating adolescents. Confirmatory factor analysis (CFA) was conducted to assess the factor structure of the SDQ. The five-factor solution of the SDQ (including emotional, conduct, hyperactivity-inattention, peer relationship, and prosocial) provided a satisfactory fit to the data, and was invariant across sex, age, race/ethnicity and income subgroups. SDQ scores predicted a significantly increased probability of meeting criteria for a DSM-IV disorder, with better prediction for behavior disorders than for mood disorders. Decreasing the SDQ cutoffs to the 80th percentile significantly increased the sensitivity from 39% to 63% for the SDQ Total Difficulties Score, with an expected decrease in specificity from 93% to 87%. This work confirms the five-factor structure of the SDQ in an ethnically and sociodemogrpahically diverse community sample of adolescents. Our findings strengthen empirical evidence for the use of the parent-reported SDQ as a screening tool for DSM-IV behavioral and emotional disorders in adolescents identified in the general population.
C1 [He, Jian-Ping; Burstein, Marcy; Schmitz, Anja; Merikangas, Kathleen R.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
RP Merikangas, KR (reprint author), NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bldg 35,Room 1A201,35 Convent Dr,MSC 3720, Bethesda, MD 20892 USA.
EM hejian@mail.nih.gov; bursteinme@mail.nih.gov; Schmitza2@mail.nih.gov;
kathleen.merikangas@nih.gov
FU NIMH NIH HHS [U01-MH60220, Z01 MH002808-08]
NR 66
TC 22
Z9 23
U1 3
U2 46
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0091-0627
J9 J ABNORM CHILD PSYCH
JI J. Abnorm. Child Psychol.
PD MAY
PY 2013
VL 41
IS 4
BP 583
EP 595
DI 10.1007/s10802-012-9696-6
PG 13
WC Psychology, Clinical; Psychology, Developmental
SC Psychology
GA 136NP
UT WOS:000318368900007
PM 23183936
ER
PT J
AU Mahabir, S
AF Mahabir, Somdat
TI Association Between Diet During Preadolescence and Adolescence and Risk
for Breast Cancer During Adulthood
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Review
ID CORONARY-HEART-DISEASE; ASIAN-AMERICAN WOMEN; BOYD-ORR COHORT;
WORLD-WAR-II; BIRTH-WEIGHT; YOUNG-WOMEN; PREMENOPAUSAL WOMEN;
ALCOHOL-CONSUMPTION; BODY-SIZE; FOLLOW-UP
AB It is increasingly evident that diet during preadolescence and adolescence has important consequences for breast cancer during adulthood. However, only a few epidemiologic studies have been conducted on the relationship between diet during preadolescence and adolescence, and cancer during adulthood. This situation is partly because of methodological challenges such as the long latency period, the complexity of breast cancer, the lack of validated diet assessment tools, and the large number of subjects that must be followed, all of which increase costs. In addition, funding opportunities are few for such studies. Results from the small number of epidemiologic studies are inconsistent, but evidence is emerging that specific aspects of the diet during preadolescence and adolescence are important. For example, during preadolescence and adolescence, severe calorie restriction with poor food quality, high total fat intake, and alcohol intake tend to increase risk, whereas high soy intake decreases risk. Research on preadolescent and adolescent diet is a paradigm shift in breast cancer investigations. This research paradigm has the potential to produce transformative knowledge to inform breast cancer prevention strategies through dietary intervention during preadolescence and adolescence, rather than later in life, as is current practice, when it is perhaps less effective. Methodological challenges that have plagued the field might now be overcome by leveraging several existing large-scale cohort studies in the U.S. and around the world to investigate the role of diet during preadolescence and adolescence in risk for adult breast cancer. Published by Elsevier Inc on behalf of Society for Adolescent Health and Medicine.
C1 NCI, Modifiable Risk Factors Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Mahabir, S (reprint author), NCI, Modifiable Risk Factors Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci, Execut Plaza North,Room 5138, Bethesda, MD 20892 USA.
EM mahabir@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 67
TC 9
Z9 9
U1 1
U2 29
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD MAY
PY 2013
VL 52
IS 5
SU S
BP S30
EP S35
DI 10.1016/j.jadohealth.2012.08.008
PG 6
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA 140UQ
UT WOS:000318681800005
PM 23298994
ER
PT J
AU Nadarajah, S
Berger, AM
Thomas, SA
AF Nadarajah, Sheeba
Berger, Ann M.
Thomas, Sue Ann
TI Current Status of Spirituality in Cardiac Rehabilitation Programs A
REVIEW OF LITERATURE
SO JOURNAL OF CARDIOPULMONARY REHABILITATION AND PREVENTION
LA English
DT Review
DE cardiac; rehabilitation; relaxation response; spiritual
ID CORONARY-HEART-DISEASE; 2007 PERFORMANCE-MEASURES;
MYOCARDIAL-INFARCTION; PREVENTION PROGRAMS; RISK-FACTORS; METAANALYSIS;
ASSOCIATION; DEPRESSION; ADHERENCE; DISTRESS
AB PURPOSE: Strong spiritual experiences in life are a protective, positive, prognostic factor in cardiovascular diseases. However, spirituality is often neglected in cardiac rehabilitation (CR) programs. The purpose of this article was to review studies that investigated spirituality in CR programs.
METHODS: The electronic databases PubMed, CINHAL, PsycINFO, and Cochrane Library of Systematic Reviews were searched for studies that measured spirituality in a CR population. The search included studies with and without spiritual interventions in CR settings.
RESULTS: Five quantitative studies and 1 qualitative study that enrolled a total of 1636 patients in phase 2 CR programs were reviewed. The spiritual interventions found were relaxation responses and spiritual classes. Two studies showed preliminary evidence that supports the further exploration of spiritual interventions in CR programs.
CONCLUSIONS: Evidence supporting the use of spiritual interventions for medical and psychological outcomes in CR programs is very limited because of a lack of controlled clinical trials. However, the descriptive and observational studies provide some empirical support to further explore spiritual interventions in CR programs, with the goal of enhancing the psychosocial and emotional status of CR participants. Further rigorous research design and procedures are needed to establish the contribution of spirituality in CR programs for cardiac patients.
C1 [Nadarajah, Sheeba; Berger, Ann M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Thomas, Sue Ann] Univ Maryland, Sch Nursing, Baltimore, MD 21201 USA.
RP Nadarajah, S (reprint author), NIH, Ctr Clin, 10 Ctr Dr,MSC 1517 2-1733, Bethesda, MD 20892 USA.
EM nadarajahs@mail.nih.gov
NR 48
TC 5
Z9 5
U1 0
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1932-7501
J9 J CARDIOPULM REHABIL
JI J. Cardiopulm. Rehabil. Prev.
PD MAY-JUN
PY 2013
VL 33
IS 3
BP 135
EP 143
DI 10.1097/HCR.0b013e318291381e
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 138WT
UT WOS:000318542700001
PM 23635834
ER
PT J
AU Neary, NM
Booker, OJ
Abel, BS
Matta, JR
Muldoon, N
Sinaii, N
Pettigrew, RI
Nieman, LK
Gharib, AM
AF Neary, Nicola M.
Booker, O. Julian
Abel, Brent S.
Matta, Jatin R.
Muldoon, Nancy
Sinaii, Ninet
Pettigrew, Roderic I.
Nieman, Lynnette K.
Gharib, Ahmed M.
TI Hypercortisolism Is Associated With Increased Coronary Arterial
Atherosclerosis: Analysis of Noninvasive Coronary Angiography Using
Multidetector Computerized Tomography
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID BONE-MINERAL DENSITY; KOREAN SARCOPENIC OBESITY; FREE MASS INDEX;
BODY-COMPOSITION; POSTMENOPAUSAL WOMEN; SERUM OSTEOCALCIN; FAT MASS;
MUSCULOSKELETAL SYSTEM; CLINICAL-PRACTICE; CHINESE MEN
AB Background: Observational studies show that glucocorticoid therapy and the endogenous hypercortisolism of Cushing's syndrome (CS) are associated with increased rates of cardiovascular morbidity and mortality. However, the causes of these findings remain largely unknown.
Objective: To determine whether CS patients have increased coronary atherosclerosis.
Design: A prospective case-control study was performed.
Setting: Subjects were evaulated in a clinical research center.
Subjects: Fifteen consecutive patients with ACTH-dependent CS, 14 due to an ectopic source and 1 due to pituitary Cushing's disease were recruited. Eleven patients were studied when hypercortisolemic; 4 patients were eucortisolemic due to medication (3) or cyclic hypercortisolism (1). Fifteen control subjects with at least one risk factor for cardiac disease were matched 1:1 for age, sex, and body mass index.
Primary outcome variables: Agatston score a measure of calcified plaque and non-calcified coronary plaque volume were quantified using a multidetector CT (MDCT) coronary angiogram scan. Additional variables included fasting lipids, blood pressure, history of hypertension or diabetes, and 24-hour urine free cortisol excretion.
Results: CS patients had significantly greater noncalcified plaque volume and Agatston score (noncalcified plaque volume [mm(3)] median [interquartile ranges]: CS 49.5 [31.4, 102.5], controls 17.9 [2.6, 25.3], P < .001; Agatston score: CS 70.6 [0, 253.1], controls 0 [0, 7.6]; P < .05). CS patients had higher systolic and diastolic blood pressures than controls (systolic: CS 143 mm Hg [135, 173]; controls, 134 [123, 136], P < .02; diastolic CS: 86 [80, 99], controls, 76 [72, 84], P < .05).
Conclusions: Increased coronary calcifications and noncalcified coronary plaque volumes are present in patients with active or previous hypercortisolism. Increased atherosclerosis may contribute to the increased rates of cardiovascular morbidity and mortality in patients with glucocorticoid excess.
C1 [Neary, Nicola M.; Abel, Brent S.; Nieman, Lynnette K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
[Booker, O. Julian] NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA.
[Matta, Jatin R.; Pettigrew, Roderic I.; Gharib, Ahmed M.] NIDDKD, Integrat Cardiovasc Imaging Lab, NIH, Bethesda, MD 20892 USA.
[Muldoon, Nancy] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Sinaii, Ninet] NIH, Ctr Clin, Biostat & Clin Epidemiol Serv, Bethesda, MD 20892 USA.
RP Neary, NM (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RI Gharib, Ahmed/O-2629-2016
OI Gharib, Ahmed/0000-0002-2476-481X
FU National Nature Science Foundation of China [81070693, 30725037,
81170804]; Shanghai Education Committee Key Project [11ZZ101]; Shanghai
Municipal Heath Bureau Project, China [2012-235]
FX This work was supported by National Nature Science Foundation of China
(Nos. 81070693, 30725037, 81170804), Shanghai Education Committee Key
Project (11ZZ101), and Shanghai Municipal Heath Bureau Project
(2012-235), China.
NR 40
TC 23
Z9 25
U1 0
U2 2
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD MAY
PY 2013
VL 98
IS 5
BP 2045
EP 2152
DI 10.1210/jc.2012-3754
PG 108
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 140WX
UT WOS:000318688200066
PM 23559084
ER
PT J
AU Turcu, AF
Kumar, S
Neumann, S
Coenen, M
Iyer, S
Chiriboga, P
Gershengorn, MC
Bahn, RS
AF Turcu, Adina F.
Kumar, Seema
Neumann, Susanne
Coenen, Michael
Iyer, Seethalakshmi
Chiriboga, Pamela
Gershengorn, Marvin C.
Bahn, Rebecca S.
TI A Small Molecule Antagonist Inhibits Thyrotropin Receptor
Antibody-Induced Orbital Fibroblast Functions Involved in the
Pathogenesis of Graves Ophthalmopathy
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID STIMULATING HORMONE-RECEPTOR; PREADIPOCYTE FIBROBLASTS; CAMP PRODUCTION;
DISEASE; AGONIST; AUTOIMMUNITY; UPDATE
AB Context: Graves ophthalmopathy (GO) is an autoimmune disorder characterized by increased adipogenesis and hyaluronan (HA) production by orbital fibroblasts. Circulating autoantibodies (thyroid-stimulating antibodies [TSAbs]) directed at the thyrotropin receptor (TSHR) on these cells stimulate or augment these cellular processes. A recently developed drug-like small molecule inverse agonist of TSHR, NCGC00229600, termed 1, binds to TSHR and blocks basal and stimulated signal transduction.
Objective: The purpose of this article was to determine whether 1 might inhibit HA production and relevant signaling pathways in orbital fibroblasts cultured in the presence of monoclonal TSAbs or bovine TSH (bTSH).
Design: Primary cultures of undifferentiated GO orbital fibroblasts (n = 13) were untreated or treated with a TSAb (M22 or MS-1) or bTSH in serum-free medium, with or without 1 or a TSHR neutral antagonist, NCGC00242595, termed 2, which does not inhibit basal signaling but does inhibit stimulated signaling.
Main Outcome Measures: cAMP production, Akt phosphorylation (Ser473pAkt in media and immunoblotting for pAkt/total Akt), and HA production were analyzed.
Results: Compound 1 inhibited basal cAMP, pAkt, and HA production and that stimulated by M22 in undifferentiated orbital fibroblasts. Inhibition of HA production was dose-dependent, with a half-maximal inhibitory dose of 830 nM. This compound also inhibited MS-1- and bTSH-stimulated cAMP, pAkt, and HA production. Compound 2 did not inhibit basal HA production but did inhibit M22-stimulated HA production.
Conclusions: Because cAMP, pAkt, and HA production are fibroblast functions that are activated via TSHR signaling and are important in the pathogenesis of GO, small molecule TSHR antagonists may prove to be effective in the treatment or prevention of the disease in the future.
C1 [Turcu, Adina F.; Coenen, Michael; Iyer, Seethalakshmi; Chiriboga, Pamela; Bahn, Rebecca S.] Mayo Clin, Div Endocrinol Diabet Metab & Nutr, Rochester, MN 55905 USA.
[Kumar, Seema] Mayo Clin, Div Pediat Endocrinol & Metab, Rochester, MN 55905 USA.
[Neumann, Susanne; Gershengorn, Marvin C.] NIDDKD, Lab Endocrinol & Receptor Biol, NIH, Bethesda, MD 20892 USA.
RP Bahn, RS (reprint author), Mayo Clin, Div Endocrinol Diabet Metab & Nutr, 200 1st St Southwest, Rochester, MN 55902 USA.
EM bahn.rebecca@mayo.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases
[DK77814]
FX This work was supported in part by the National Institute of Diabetes
and Digestive and Kidney Diseases (Grant DK77814).
NR 23
TC 25
Z9 28
U1 0
U2 6
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD MAY
PY 2013
VL 98
IS 5
BP 2153
EP 2159
DI 10.1210/jc.2013-1149
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 140WX
UT WOS:000318688200067
PM 23482611
ER
PT J
AU Taieb, D
Yang, CZ
Delenne, B
Zhuang, ZP
Barlier, A
Sebag, F
Pacak, K
AF Taieb, David
Yang, Chunzhang
Delenne, Blandine
Zhuang, Zhengping
Barlier, Anne
Sebag, Frederic
Pacak, Karel
TI First Report of Bilateral Pheochromocytoma in the Clinical Spectrum of
HIF2A-Related Polycythemia-Paraganglioma Syndrome
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID HIPPEL-LINDAU DISEASE; NECK PARAGANGLIOMAS; GERMLINE MUTATIONS; OXYGEN
HOMEOSTASIS; MOLECULAR-BASIS; HIF2A GENE; ERYTHROCYTOSIS; HEREDITARY;
HYPOXIA; HEAD
AB Context: Molecular genetic research has so far resulted in the identification of 10 well-characterized susceptibility genes for hereditary pheochromocytoma (PHEO) or paraganglioma (PGL). Recently, a new syndrome characterized by multiple PGLs and somatostatinomas associated with congenital polycythemia due to somatic mutations in HIF2A has been reported.
Objective: The aim of the study was to define the genetic defect in a new case of bilateral PHEO and multiple PGLs associated with congenital polycythemia.
Patient: A female patient presented with neonatal polycythemia (treated by phlebotomies, 1 session approximately every 4 mo), mildly enlarged cerebral ventricles, and bilateral PHEO and multiple PGLs. There was no family history of any neuroendocrine tumor or polycythemia. Surgical removal of the tumors only temporarily normalized plasma erythropoietin (Epo) levels and discontinued phlebotomies. No germline mutations were initially detected in the SDHB, SDHC, SDHD, VHL, and PHD2 genes, known to be associated with polycythemia. The PHEOs presented with a typical noradrenergic biochemical phenotype.
Results: A heterozygous missense mutation (c.1589C>T) was identified in exon 12 of HIF2A, resulting in an alanine 530 substitution in the HIF-2 alpha protein with valine (A530V). This somatic mutation was detected in the tissue from 1 PHEO and 1 PGL, with no HIF2A germline mutation found. This mutation led to stabilization of HIF-2 alpha and hence a gain-of-function phenotype, as in previously published studies.
Conclusion: This case represents the first association of a somatic HIF2A gain-of-function mutation with PHEO and congenital polycythemia, and it alerts physicians to perform proper genetic screening in patients presenting with multiple norepinephrine-producing PHEOs and polycythemia. This report also extends the previous findings of a new syndrome of only multiple PGLs, somatostatinomas, and polycythemia to multiple PHEOs.
C1 [Taieb, David] Aix Marseille Univ, Ctr Europeen Rech Imagerie Med, La Timone Univ Hosp, Dept Nucl Med, F-13005 Marseille, France.
[Yang, Chunzhang; Zhuang, Zhengping] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Delenne, Blandine] Aix Provence Gen Hosp, Dept Endocrinol, F-13616 Aix En Provence, France.
[Barlier, Anne] Aix Marseille Univ, Concept Hosp, Lab Biochem & Mol Biol, F-13005 Marseille, France.
[Sebag, Frederic] Aix Marseille Univ, La Timone Univ Hosp, Dept Endocrine Surg, F-13005 Marseille, France.
[Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Pacak, K (reprint author), NIH, Sect Med Neuroendocrinol, Clin Res Ctr, Bldg 10,Room 1E-3140,10 Ctr Dr MSC-1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
OI Barlier, Anne/0000-0002-3740-6173
FU Centre Europeen de Recherche en Imagerie Medicale; Intramural Research
Program of the Eunice Kennedy Shriver Institutes of Health and Child
Development; National Institute of Neurological Disorders and Stroke at
the National Institutes of Health
FX This research was supported by Centre Europeen de Recherche en Imagerie
Medicale and the Intramural Research Program of the Eunice Kennedy
Shriver Institutes of Health and Child Development and the National
Institute of Neurological Disorders and Stroke at the National
Institutes of Health.
NR 24
TC 26
Z9 26
U1 1
U2 6
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD MAY
PY 2013
VL 98
IS 5
BP E908
EP E913
DI 10.1210/jc.2013-1217
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 140WX
UT WOS:000318688200016
PM 23539726
ER
PT J
AU Yavuz, S
Linderman, JD
Smith, S
Zhao, XC
Pucino, F
Celi, FS
AF Yavuz, Sahzene
Linderman, Joyce D.
Smith, Sheila
Zhao, Xiongce
Pucino, Frank
Celi, Francesco S.
TI The Dynamic Pituitary Response to Escalating-Dose TRH Stimulation Test
in Hypothyroid Patients Treated With Liothyronine or Levothyroxine
Replacement Therapy
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID THYROTROPIN-RELEASING-HORMONE; YOUNG-ADULT MEN; THYROID-HORMONES; TSH
RESPONSE; DOUBLE-BLIND; TRIIODOTHYRONINE; T-3
AB Context: A recent trial showed that 1:3 mu g:mu g liothyronine (L-T3) substitution for levothyroxine (L-T4) achieving near-identical TSH levels resulted in a significant decrease in weight and cholesterol levels with no appreciable changes in cardiovascular parameters, suggesting a differential peripheral response to the therapy.
Objective: We characterized the pituitary-thyroid axis in hypothyroid patients receiving equivalent doses of L-T3 or L-T4 by escalating-dose TRH stimulation test.
Design: A secondary analysis of a L-T3 vs L-T4 therapy trial was performed.
Setting: The study was conducted at the National Institutes of Health.
Patients: Thirteen patients were studied.
Interventions: Escalating-dose (5, 15, and 200 mu g) TRH stimulation test on both treatment arms.
Main Outcome Measures: Study outcomes were peak serum TSH concentration (Cmax), time to peak TSH concentration (Tmax), area under the curve from 0 to 60 minutes (AUC(0-60)) after TRH injection.
Results: Thirteen patients aged 51.2 +/- 8.29 years completed escalating-dose TRH stimulation test. No significant difference between L-T3 and L-T4 treatments was observed in TSH Cmax or area under the curve. L-T4 resulted in a small but significantly shorter Tmax compared to L-T3 (3.5 +/- 0.73 min on 200 mu g TRH dose, P < .03). In addition, 5 mu g TRH dose compared to 200 mu g resulted in a shorter Tmax on both treatment arms (6.9 +/- 0.59 min L-T3, 4 +/- 0.3 min L-T4; P = .0002).
Conclusions: The assessment of the dynamic pituitary response to escalating doses of TRH confirms that substitution of L-T3 for L-T4 on a 1:3 ratio achieves a near-identical degree of pituitary euthyroidism. Furthermore, the data suggest that lower doses of TRH might provide clinically relevant information of thyrotroph function, particularly when investigating partial pituitary insufficiency states.
C1 [Yavuz, Sahzene; Linderman, Joyce D.; Smith, Sheila; Pucino, Frank; Celi, Francesco S.] NIDDKD, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Zhao, Xiongce] NIDDKD, NIH, Bethesda, MD 20892 USA.
RP Celi, FS (reprint author), NIDDKD, Diabet Endocrinol & Obes Branch, NIH, Clin Res Ctr, Bldg 10,Room 6-3940,10 Ctr Dr, Bethesda, MD 20892 USA.
EM fc93a@nih.gov
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases program [Z01-DK047057-02]; Clinical
Center, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases program
Z01-DK047057-02, and the Clinical Center, National Institutes of Health.
NR 18
TC 4
Z9 4
U1 0
U2 3
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD MAY
PY 2013
VL 98
IS 5
BP E862
EP E866
DI 10.1210/jc.2012-4196
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 140WX
UT WOS:000318688200007
PM 23585666
ER
PT J
AU Wan, WX
Guo, N
Pan, DH
Yu, CJ
Weng, Y
Luo, SN
Ding, H
Xu, YP
Wang, LZ
Lang, LX
Xie, QG
Yang, M
Chen, XY
AF Wan, Weixing
Guo, Ning
Pan, Donghui
Yu, Chunjing
Weng, Yuan
Luo, Shineng
Ding, Hong
Xu, Yuping
Wang, Lizhen
Lang, Lixin
Xie, Qingguo
Yang, Min
Chen, Xiaoyuan
TI First Experience of F-18-Alfatide in Lung Cancer Patients Using a New
Lyophilized Kit for Rapid Radiofluorination
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE RGD peptide; alfatide; aluminum fluoride; PET; lung cancer
ID INTEGRIN ALPHA(V)BETA(3) EXPRESSION; CYCLIC RGD PEPTIDES; TUMOR
ANGIOGENESIS; GRAPHICAL ANALYSIS; BLOOD-VESSELS; PET; MICE; KINETICS;
THERAPY; AGENT
AB F-18-FPPRGD2, which was approved for clinical study recently, has favorable properties for integrin targeting and showed potential for antiangiogenic therapy and early response monitoring. However, the time-consuming multiple-step synthesis may limit its widespread applications in the clinic. In this study, we developed a simple lyophilized kit for labeling PRGD2 peptide (F-18-AlF-NOTA-PRGD2, denoted as F-18-alfatide) using a fluoride-aluminum complex that significantly simplified the labeling procedure. Methods: Nine patients with a primary diagnosis of lung cancer were examined by both static and dynamic PET imaging with F-18-alfatide, and 1 tuberculosis patient was investigated using both F-18-alfatide and F-18-FDG imaging. Standardized uptake values were measured in tumors and other main organs at 30 min and 1 h after injection. Kinetic parameters were calculated by Logan graphical analysis. Immunohistochemistry and staining intensity quantification were performed to confirm the expression of integrin alpha(v)beta(3). Results: Under the optimal conditions, the whole radiosynthesis including purification was accomplished within 20 min with a decay-corrected yield of 42.1% +/- 2.0% and radiochemical purity of more than 95%. F-18-alfatide PET imaging identified all tumors, with mean standardized uptake values of 2.90 +/- 0.10. Tumor-to-muscle and tumor-to-blood ratios were 5.87 +/- 2.02 and 2.71 +/- 0.92, respectively. Conclusion: F-18-alfatide can be produced with excellent radiochemical yield and purity via a simple, 1-step, lyophilized kit. PET scanning with F-18-alfatide allows specific imaging of alpha(v)beta(3) expression with good contrast in lung cancer patients. This technique might be used for the assessment of angiogenesis and for planning and response evaluation of cancer therapies that would affect angiogenesis status and integrin expression levels.
C1 [Wan, Weixing; Pan, Donghui; Luo, Shineng; Ding, Hong; Xu, Yuping; Wang, Lizhen; Yang, Min] Jiangsu Inst Nucl Med, Minist Hlth, Key Lab Nucl Med, Jiangsu Key Lab Mol Nucl Med, Wuxi 214063, Peoples R China.
[Wan, Weixing; Yu, Chunjing; Weng, Yuan] Wuxi 4 Peoples Hosp, Dept Nucl Med, Wuxi, Peoples R China.
[Guo, Ning; Lang, Lixin; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Guo, Ning; Xie, Qingguo] Huazhong Univ Sci & Technol, Dept Biomed Engn, Wuhan 430074, Hubei, Peoples R China.
[Guo, Ning] Xiamen Univ, Ctr Mol Imaging & Translat Med, Xiamen, Fujian, Peoples R China.
RP Chen, XY (reprint author), NIBIB, Lab Mol Imaging & Nanomed, NIH, 31 Ctr Dr,1C22, Bethesda, MD 20892 USA.
EM ymzfk@yahoo.com.hk; shawn.chen@nih.gov
FU National Basic Research Program of China (973 program) [2013CB733802];
National Science Foundation of China (NSFC) [81028009, 81171399,
81101077, 60972099]; Jiangsu Province Social Development Program
[BE2012622]; Health Ministry in Jiangsu Province [RC2011095]; National
Institute of Biomedical Imaging and Bioengineering (NIBIB), National
Institutes of Health (NIH); China Scholarship Council (CSC)
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This work was supported by the National Basic Research
Program of China (973 program, 2013CB733802); the National Science
Foundation of China (NSFC) (81028009, 81171399, 81101077, and 60972099);
Jiangsu Province Social Development Program (BE2012622); Outstanding
Professional Fund of Health Ministry in Jiangsu Province (RC2011095);
Intramural Research Program of the National Institute of Biomedical
Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH);
and China Scholarship Council (CSC). No other potential conflict of
interest relevant to this article was reported.
NR 33
TC 65
Z9 69
U1 2
U2 37
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY 1
PY 2013
VL 54
IS 5
BP 691
EP 698
DI 10.2967/jnumed.112.113563
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 137CS
UT WOS:000318413200030
PM 23554506
ER
PT J
AU Sano, K
Mitsunaga, M
Nakajima, T
Choyke, PL
Kobayashi, H
AF Sano, Kohei
Mitsunaga, Makoto
Nakajima, Takahito
Choyke, Peter L.
Kobayashi, Hisataka
TI Acute Cytotoxic Effects of Photoimmunotherapy Assessed by F-18-FDG PET
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE F-18-FDG; PET; monitoring therapy; photoimmunotherapy; acute
cytotoxicity
ID GASTROINTESTINAL STROMAL TUMORS; NEAR-INFRARED PHOTOIMMUNOTHERAPY;
IN-VIVO; IMATINIB MESYLATE; CANCER-CELLS; THERAPY; IMMUNOTHERAPY;
PREDICTION; EFFICACY; GROWTH
AB We have recently developed a cancer-specific therapy, photoimmunotherapy, which uses an antibody-IR700 (phototoxic phthalocyanine dye) conjugate to bind to the cell membrane and near-infrared light to induce immediate and highly specific tumor killing in vivo. For monitoring the acute cytotoxic effects of photoimmunotherapy before the tumor begins to shrink, we used F-18-FDG PET before and after this intervention in mice. Methods: Photoimmunotherapy was performed by binding panitumumab (anti-HER1)-IR700 to HER1-positive tumor cells (A431), followed by near-infrared light irradiation in vitro and in vivo. The uptake of F-18-FDG in the tumor after photoimmunotherapy was evaluated in cellular uptake studies and PET imaging studies. Serial histologic analyses were conducted after photoimmunotherapy. Results: The in vitro cellular uptake of F-18-FDG was reduced as the dose of light increased, and at high light dose (2 J/cm(2)) the uptake was reduced by more than 99% within 1 h after photoimmunotherapy. In vivo F-18-FDG PET imaging showed that the accumulation of radioactivity in the treated tumors decreased 76% at 75 min after photoimmunotherapy and did not change for 24 h. In contrast, no significant changes were demonstrated in nontreated tumors. None of tumors changed size within 24 h after photoimmunotherapy, although diffuse necrosis was observed in photoimmunotherapy-treated tumors. Conclusion: Immediate cytotoxic effects induced by photoimmunotherapy were clearly detected by decreased glucose uptake using F-18-FDG PET even before changes in tumor size became evident. F-18-FDG allows the clinical assessment of the therapeutic effects of photoimmunotherapy earlier than anatomic methods that rely on tumor size.
C1 [Sano, Kohei; Mitsunaga, Makoto; Nakajima, Takahito; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bldg 10,Rm B3B69,MSC1088, Bethesda, MD 20892 USA.
EM kobayash@mail.nih.gov
FU U.S. NIH, National Cancer Institute, Center for Cancer Research
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This research was supported by the Intramural Research
Program of the U.S. NIH, National Cancer Institute, Center for Cancer
Research. No other potential conflict of interest relevant to this
article was reported.
NR 24
TC 7
Z9 7
U1 1
U2 6
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY 1
PY 2013
VL 54
IS 5
BP 770
EP 775
DI 10.2967/jnumed.112.112110
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 137CS
UT WOS:000318413200040
PM 23536226
ER
PT J
AU Manna, SK
Krausz, KW
Bonzo, JA
Idle, JR
Gonzalez, FJ
AF Manna, Soumen K.
Krausz, Kristopher W.
Bonzo, Jessica A.
Idle, Jeffrey R.
Gonzalez, Frank J.
TI Metabolomics Reveals Aging-associated Attenuation of Noninvasive
Radiation Biomarkers in Mice: Potential Role of Polyamine Catabolism and
Incoherent DNA Damage-repair
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE ionizing radiation; age; exposure history; biomarker; metabolomics;
UPLC-ESI-QTOFMS; DNA damage-repair; polyamine metabolism
ID GAMMA-IRRADIATED RATS; BASE EXCISION-REPAIR; IONIZING-RADIATION;
MASS-SPECTROMETRY; OXIDATIVE STRESS; MAMMALIAN-CELLS; EXPOSURE;
IDENTIFICATION; MECHANISMS; DISEASE
AB Development of methods for rapid screening and stratification of subjects after exposure is an integral part of countermeasures against radiation. The potential demographic and exposure history-related heterogeneity of exposed populations warrants robust biomarkers that withstand and reflect such differences. In this study, the effect of aging and repeated exposure on the metabolic response to sublethal irradiation was examined in mice using UPLC-ESI-QTOF mass spectrometry. Aging attenuated postexposure elevation in excretions of DNA damage biomarkers as well as N-1-acetylspermidine. Although N-1-acetylspermidine and 2'-deoxyuridine elevation was highly correlated in all age groups, xanthine and N-1-acetylspermidine elevation was poorly correlated in older mice. These results may reflect the established decline in DNA damage-repair efficiency associated with aging and indicate a novel role for polyamine metabolism in the process. Although repeated irradiation at long intervals did not affect the elevation of N-1-acetylspermidine, 2'-deoxyuridine, and xanthine, it did significantly attenuate the elevation of 2'-deoxycytidine and thymidine compared to a single exposure. However, these biomarkers were found to identify exposed subjects with accuracy ranging from 82% (xanthosine) to 98% (2'-deoxyuridine), irrespective of their age and exposure history. This indicates that metabolic biomarkers can act as robust noninvasive signatures of sublethal radiation exposure.
C1 [Manna, Soumen K.; Krausz, Kristopher W.; Bonzo, Jessica A.; Idle, Jeffrey R.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Idle, Jeffrey R.] Univ Bern, Dept Clin Res, Hepatol Res Unit, Bern, Switzerland.
RP Gonzalez, FJ (reprint author), NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA.
EM gonzalef@mail.nih.gov
OI Idle, Jeff/0000-0002-6143-1520
FU National Cancer Institute Intramural Research Program; Columbia
University Center for Medical Countermeasures against Radiation; NIH
(NIAID) [U19 AI067773-05/06]; NIAID Radiation/Nuclear Medical
Countermeasures Program, NIH Intramural Laboratory Collaboration Funding
FX This work was supported by the National Cancer Institute Intramural
Research Program, the Columbia University Center for Medical
Countermeasures against Radiation (P.I. David Brenner) funded by NIH
(NIAID) grant U19 AI067773-05/06 to J.R.I., and the NIAID
Radiation/Nuclear Medical Countermeasures Program, NIH Intramural
Laboratory Collaboration Funding to F.J.G.
NR 40
TC 12
Z9 13
U1 0
U2 20
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
J9 J PROTEOME RES
JI J. Proteome Res.
PD MAY
PY 2013
VL 12
IS 5
BP 2269
EP 2281
DI 10.1021/pr400161k
PG 13
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 139NI
UT WOS:000318589000025
PM 23586774
ER
PT J
AU Zanuy, D
Kotla, R
Nussinov, R
Teesalu, T
Sugahara, KN
Aleman, C
Haspel, N
AF Zanuy, David
Kotla, Rohith
Nussinov, Ruth
Teesalu, Tambet
Sugahara, Kazuki N.
Aleman, Carlos
Haspel, Nurit
TI Sequence dependence of C-end rule peptides in binding and activation of
neuropilin-1 receptor
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE CendR peptide; Binding affinity; Neuropilin-1; Molecular dynamics
ID ENDOTHELIAL GROWTH-FACTOR; MOLECULAR-DYNAMICS; TUMOR-CELLS; FORCE-FIELD;
ANGIOGENESIS; PROTEINS; CANCER
AB Neuropilin-1 (NRP-1) is a hub receptor that plays an essential role in angiogenesis and vascular permeability. It is over-expressed in the new blood vessels grown by tumor cells and is a target for anti-tumor treatments. Peptides that expose the consensus sequence R/K/XXR/K at the C-terminus (C-end rule or CendR peptides) bind to NRP-1 and are internalized into the cell. We used peptide phage display binding assays and molecular dynamics (MD) simulations to study the potential role of the central residues of CendR peptides in binding and activation of the NRP-1 receptor. The high stability of RPAR-receptor domain complex stems from the formation of a characteristic pattern of three hydrogen bonds between the peptide C-terminus and the residues in the NRP-1 loop III. Any changes in the peptide structure that fail to preserve this triad result in a less-stable complex. We performed a systematic study of RXXR mutants, where X = A/D/S/R/P, in order to test the effect of replacement of A or P on the binding capabilities. Our results, both experimental and computational, show that RRAR, RDAR, RPDR, RPRR and RPPR are capable of binding NRP-1. However, only RPPR and RPRR segments form an optimal organization around loop III with low potential energy. In other analogs, the absence of these stabilizing interactions always results in higher potential energy of the complexes. The binding of RPAR analogs does not guarantee receptor activation; only stable complexes that are properly stabilized via loop III appear able to trigger NRP-1 activation. (c) 2013 Elsevier Inc. All rights reserved.
C1 [Zanuy, David; Aleman, Carlos] Univ Politecn Cataluna, ETS Engn Ind Barcelona, Dept Engn Quim, E-08028 Barcelona, Spain.
[Kotla, Rohith; Haspel, Nurit] Univ Massachusetts, Dept Comp Sci, Boston, MA 02125 USA.
[Nussinov, Ruth] NCI, Ctr Canc Res Nanobiol Program, SAIC Frederick, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Fac Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
[Teesalu, Tambet; Sugahara, Kazuki N.] Univ Calif Santa Barbara, Ctr Nanomed, Sanford Burnham Med Res Inst UCSB, Santa Barbara, CA 93106 USA.
[Aleman, Carlos] Univ Politecn Cataluna, Ctr Res Nanoengn, E-08028 Barcelona, Spain.
RP Zanuy, D (reprint author), Univ Politecn Cataluna, ETS Engn Ind Barcelona, Dept Engn Quim, Diagonal 647, E-08028 Barcelona, Spain.
EM david.zanuy@upc.edu; nurit.haspel@umb.edu
RI Zanuy, David/G-3930-2014; Teesalu, Tambet/J-1802-2015; Haspel,
Nurit/D-1961-2017
OI Zanuy, David/0000-0001-7704-2178;
FU Generalitat de Catalunya [SGR 925]; National Science Foundation
[TG-MCB100025]; National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Intramural Research Program of the NIH, National
Cancer Institute, Center for Cancer Research
FX Financial support by the provided by the Generalitat de Catalunya
(Research Group 2009 SGR 925; XRQTC; ICREA Academia prize for excellence
in research to C.A.) is gratefully acknowledged. D.Z.and C.A are
indebted for the computational resources provided the "Centre de
Supercomputacio de Catalunya" (CESCA). D.Z. is grateful for the
high-performance computational capabilities of the Biowulf Linux cluster
at the National Institutes of Health, Bethesda, Md.
(http://biowulf.nih.gov). The research was supported in part by the
National Science Foundation through TeraGrid resources provided by the
Texas Advanced Computing Center (TACC) under grant number TG-MCB100025
(N.H.). The computations were carried out in part on the supercomputing
facilities managed by the Research Computing Group at the University of
Massachusetts Boston. This project has been funded in whole or in part
with Federal funds from the National Cancer Institute, National
Institutes of Health, under contract number HHSN261200800001E. The
content of this publication does not necessarily reflect the views or
policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the US Government. This research was supported (in part)
by the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research.
NR 29
TC 12
Z9 13
U1 2
U2 30
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD MAY
PY 2013
VL 182
IS 2
BP 78
EP 86
DI 10.1016/j.jsb.2013.02.006
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 136VI
UT WOS:000318391100003
PM 23462097
ER
PT J
AU Bereszczak, JZ
Rose, RJ
van Duijn, E
Watts, NR
Wingfield, PT
Steven, AC
Heck, AJR
AF Bereszczak, Jessica Z.
Rose, Rebecca J.
van Duijn, Esther
Watts, Norman R.
Wingfield, Paul T.
Steven, Alasdair C.
Heck, Albert J. R.
TI Epitope-distal Effects Accompany the Binding of Two Distinct Antibodies
to Hepatitis B Virus Capsids
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID EXCHANGE MASS-SPECTROMETRY; AMIDE HYDROGEN-EXCHANGE; OF-FLIGHT
INSTRUMENT; CORE ANTIGEN; HYDROGEN/DEUTERIUM EXCHANGE; ELECTRON
CRYOMICROSCOPY; CONFORMATIONAL-CHANGES; MONOCLONAL-ANTIBODIES; DEUTERIUM
EXCHANGE; STRUCTURAL-CHANGES
AB Infection of humans by hepatitis B virus (HBV) induces the copious production of antibodies directed against the capsid protein (Cp). A large variety of anticapsid antibodies have been identified that differ in their epitopes. These data, and the status of the capsid as a major clinical antigen, motivate studies to achieve a more detailed understanding of their interactions. In this study, we focused on the Fab fragments of two monoclonal antibodies, E1 and 3120. E1 has been shown to bind to the side of outward-protruding spikes whereas 3120 binds to the "floor" region of the capsid, between spikes. We used hydrogen-deuterium exchange coupled to mass spectrometry (HDX-MS) to investigate the effects on HBV capsids of binding these antibodies. Conventionally, capsids loaded with saturating amounts of Fabs would be too massive to be readily amenable to HDX-MS. However, by focusing on the Cp protein, we were able to acquire deuterium uptake profiles covering the entire 149-residue sequence and reveal, in localized detail, changes in H/D exchange rates accompanying antibody binding. We find increased protection of the known E1 and 3120 epitopes on the capsid upon binding and show that regions distant from the epitopes are also affected. In particular, the alpha 2a helix (residues 24-34) and the mobile C-terminus (residues 141-149) become substantially less solvent-exposed. Our data indicate that even at substoichiometric antibody binding an overall increase in the rigidity of the capsid is elicited, as well as a general dampening of its breathing motions.
C1 [Bereszczak, Jessica Z.; Rose, Rebecca J.; van Duijn, Esther; Heck, Albert J. R.] Univ Utrecht, Bijvoet Ctr Biomol Res, NL-3584 CH Utrecht, Netherlands.
[Bereszczak, Jessica Z.; Rose, Rebecca J.; van Duijn, Esther; Heck, Albert J. R.] Univ Utrecht, Utrecht Inst Pharmaceut Sci, NL-3584 CH Utrecht, Netherlands.
[Steven, Alasdair C.] NIAMSD, Struct Biol Lab, NIH, Bethesda, MD 20892 USA.
[Watts, Norman R.; Wingfield, Paul T.] NIAMSD, Prot Express Lab, NIH, Bethesda, MD 20892 USA.
RP Heck, AJR (reprint author), Univ Utrecht, Bijvoet Ctr Biomol Res, Padualaan 8, NL-3584 CH Utrecht, Netherlands.
EM a.j.r.heck@uu.nl
RI Heck, Albert/D-7098-2011
OI Heck, Albert/0000-0002-2405-4404
FU Netherlands Organization for Scientific Research (NWO); VENI grant
[700.58.402]; Intramural Research Program of NIAMS; Netherlands
Proteomics Centre; ALW-ECHO [819.02.10]
FX This work was supported in part by The Netherlands Organization for
Scientific Research (NWO) with ALW-ECHO (819.02.10) to A.J.R.H. and a
VENI grant to E.v.D (700.58.402) and in part by the Intramural Research
Program of NIAMS. We thank The Netherlands Proteomics Centre, embedded
in The Netherlands Genomics Initiative, for financial support.
NR 72
TC 17
Z9 18
U1 0
U2 19
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD MAY 1
PY 2013
VL 135
IS 17
BP 6504
EP 6512
DI 10.1021/ja402023x
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 137WO
UT WOS:000318469100025
PM 23597076
ER
PT J
AU Prasad, V
AF Prasad, Vinay
TI Double-Crossed: Why Crossover in Clinical Trials May Be Distorting
Medical Science
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Editorial Material
ID CANCER
C1 NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
RP Prasad, V (reprint author), NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
NR 6
TC 3
Z9 3
U1 0
U2 1
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD MAY
PY 2013
VL 11
IS 5
BP 625
EP 627
PG 3
WC Oncology
SC Oncology
GA 141US
UT WOS:000318752600012
PM 23667211
ER
PT J
AU Shalhub, S
McDonnel, N
Cecchi, AC
Azizzadeh, A
Charlton-Ouw, KM
Black, J
Pyeritz, R
Estrera, AL
Safi, H
Milewicz, D
AF Shalhub, Sherene
McDonnel, Nazli
Cecchi, Alana C.
Azizzadeh, Ali
Charlton-Ouw, Kristofer M.
Black, James
Pyeritz, Reed
Estrera, Anthony L.
Safi, Hazim
Milewicz, Dianna
TI COL3A1 Gene Mutation Predicts Arterial Involvement and Prognosis in
Vascular Ehlers Danlos Syndrome
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Meeting Abstract
CT Vascular Annual Meeting of the Society-for-Vascular-Surgery (SVS)
CY MAY 30-JUN 01, 2013
CL San Francisco, CA
SP Soc Vasc Surg (SVS)
C1 [Shalhub, Sherene; Cecchi, Alana C.; Azizzadeh, Ali; Charlton-Ouw, Kristofer M.; Estrera, Anthony L.; Safi, Hazim; Milewicz, Dianna] Univ Texas Med Sch Houston, Dept Cardiothorac & Vasc Surg, Houston, TX USA.
[McDonnel, Nazli] NIA, NIH, Baltimore, MD 21224 USA.
[Black, James] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Pyeritz, Reed] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD MAY
PY 2013
VL 57
IS 5
SU S
BP 25S
EP 26S
PG 4
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 140VV
UT WOS:000318685300045
ER
PT J
AU Farber, A
Hu, B
Dember, L
Beck, G
Dixon, B
Kusek, J
Feldman, H
AF Farber, Alik
Hu, Bo
Dember, Laura
Beck, Gerald
Dixon, Brad
Kusek, John
Feldman, Harold
TI Patency of Forearm and Upper Arm Hemodialysis Arteriovenous Grafts: Does
Configuration or Location Matter?
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Meeting Abstract
CT Vascular Annual Meeting of the Society-for-Vascular-Surgery (SVS)
CY MAY 30-JUN 01, 2013
CL San Francisco, CA
SP Soc Vasc Surg (SVS)
C1 [Farber, Alik] Boston Univ, Med Ctr, Boston, MA USA.
[Hu, Bo; Beck, Gerald] Cleveland Clin, Cleveland, OH 44106 USA.
[Dember, Laura; Feldman, Harold] Univ Penn, Philadelphia, PA 19104 USA.
[Kusek, John] NIH, Bethesda, MD 20892 USA.
[Dixon, Brad] Univ Iowa, Iowa City, IA USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD MAY
PY 2013
VL 57
IS 5
SU S
BP 31S
EP 32S
PG 4
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 140VV
UT WOS:000318685300057
ER
PT J
AU Ito, T
Igarashi, H
Uehara, H
Berna, MJ
Jensen, RT
AF Ito, Tetsuhide
Igarashi, Hisato
Uehara, Hirotsugu
Berna, Marc J.
Jensen, Robert T.
TI Causes of Death and Prognostic Factors in Multiple Endocrine Neoplasia
Type 1: A Prospective Study Comparison of 106 MEN1/Zollinger-Ellison
Syndrome Patients With 1613 Literature MEN1 Patients With or Without
Pancreatic Endocrine Tumors
SO MEDICINE
LA English
DT Article
ID ZOLLINGER-ELLISON-SYNDROME; ISLET CELL TUMORS; SOMATOSTATIN RECEPTOR
SCINTIGRAPHY; LONG-TERM SURVIVAL; GASTROENTEROPANCREATIC NEUROENDOCRINE
TUMORS; ENETS CONSENSUS GUIDELINES; DES-TUMEURS-ENDOCRINES; PROTON PUMP
INHIBITORS; SELECTIVE INTRAARTERIAL INJECTION; GASTRIC-ACID
HYPERSECRETION
AB Multiple endocrine neoplasia type 1 (MEN1) is classically characterized by the development of functional or nonfunctional hyperplasia or tumors in endocrine tissues (parathyroid, pancreas, pituitary, adrenal). Because effective treatments have been developed for the hormone excess state, which was a major cause of death in these patients in the past, coupled with the recognition that nonendocrine tumors increasingly develop late in the disease course, the natural history of the disease has changed. An understanding of the current causes of death is important to tailor treatment for these patients and to help identify prognostic factors; however, it is generally lacking.
To add to our understanding, we conducted a detailed analysis of the causes of death and prognostic factors from a prospective long-term National Institutes of Health (NIH) study of 106 MEN1 patients with pancreatic endocrine tumors with Zollinger-Ellison syndrome (MEN1/ZES patients) and compared our results to those from the pooled literature data of 227 patients with MEN1 with pancreatic endocrine tumors (MEN1/PET patients) reported in case reports or small series, and to 1386 patients reported in large MEN1 literature series. In the NIH series over a mean follow-up of 24.5 years, 24 (23%) patients died (14 MEN1-related and 10 non-MEN1-related deaths). Comparing the causes of death with the results from the 227 patients in the pooled literature series, we found that no patients died of acute complications due to acid hypersecretion, and 8%-14% died of other hormone excess causes, which is similar to the results in 10 large MEN1 literature series published since 1995. In the 2 series (the NIH and pooled literature series), two-thirds of patients died from an MEN1-related cause and one-third from a non-MEN1-related cause, which agrees with the mean values reported in 10 large MEN1 series in the literature, although in the literature the causes of death varied widely. In the NIH and pooled literature series, the main causes of MEN1-related deaths were due to the malignant nature of the PETs, followed by the malignant nature of thymic carcinoid tumors. These results differ from the results of a number of the literature series, especially those reported before the 1990s. The causes of non-MEN1-related death for the 2 series, in decreasing frequency, were cardiovascular disease, other nonendocrine tumors > lung diseases, cerebrovascular diseases. The most frequent non-MEN1-related tumor deaths were colorectal, renal > lung > breast, oropharyngeal. Although both overall and disease-related survival are better than in the past (30-yr survival of NIH series: 82% overall, 88% disease-related), the mean age at death was 55 years, which is younger than expected for the general population.
Detailed analysis of causes of death correlated with clinical, laboratory, and tumor characteristics of patients in the 2 series allowed identification of a number of prognostic factors. Poor prognostic factors included higher fasting gastrin levels, presence of other functional hormonal syndromes, need for >3 parathyroidectomies, presence of liver metastases or distant metastases, aggressive PET growth, large PETs, or the development of new lesions.
The results of this study have helped define the causes of death of MEN1 patients at present, and have enabled us to identify a number of prognostic factors that should be helpful in tailoring treatment for these patients for both short- and long-term management, as well as in directing research efforts to better define the natural history of the disease and the most important factors determining long-term survival at present.
C1 [Ito, Tetsuhide; Igarashi, Hisato] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Fukuoka 812, Japan.
[Ito, Tetsuhide; Igarashi, Hisato; Uehara, Hirotsugu; Berna, Marc J.; Jensen, Robert T.] NIDDK, NIH, DDB, Bethesda, MD 20892 USA.
[Berna, Marc J.] Hop Kirchberg, Luxembourg, Luxembourg.
RP Jensen, RT (reprint author), NIDDK, NIH, DDB, Bldg 10,Rm 9C-103,10 Ctr Dr,MSC 1804, Bethesda, MD 20892 USA.
EM robertj@bdg10.niddk.nih.gov
FU intramural research program of the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK), National Institutes of Health
FX This research was supported in part by funding from the intramural
research program of the National Institute of Diabetes and Digestive and
Kidney Diseases (NIDDK), National Institutes of Health. The authors have
no conflicts of interest to disclose.
NR 484
TC 25
Z9 27
U1 1
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD MAY
PY 2013
VL 92
IS 3
BP 135
EP 181
DI 10.1097/MD.0b013e3182954af1
PG 47
WC Medicine, General & Internal
SC General & Internal Medicine
GA 142HA
UT WOS:000318786800003
PM 23645327
ER
PT J
AU Avella, MA
Xiong, B
Dean, J
AF Avella, Matteo A.
Xiong, Bo
Dean, Jurrien
TI The molecular basis of gamete recognition in mice and humans
SO MOLECULAR HUMAN REPRODUCTION
LA English
DT Review
DE gamete recognition; zona pellucida; ZP3 glycan-release models; ZP2
cleavage model; sperm surface receptor
ID ZONA-PELLUCIDA GLYCOPROTEINS; SPERM-EGG INTERACTION; GUINEA-PIG SPERM;
O-LINKED OLIGOSACCHARIDES; SITE-DIRECTED MUTAGENESIS; INTACT MOUSE
SPERM; ACROSOME REACTION; BINDING-PROTEIN; HUMAN-SPERMATOZOA;
MEMBRANE-PROTEIN
AB Successful fertilization heralds the onset of development and requires both gamete recognition and a definitive block to polyspermy. Sperm initially bind and penetrate the extracellular zona pellucida (ZP) that surrounds ovulated eggs, but are unable to bind the zona surrounding preimplantation embryos. The ZP of humans is composed of four (ZP14) and that of mouse three (ZP13) glycoproteins. Models for gamete recognition developed in mice had proposed that sperm bind to ZP3 glycans. However, phenotypes observed in genetically engineered mice are not consistent with this widely accepted model. More recently, taking advantage of the observation that human sperm do not bind to mouse eggs, human ZP2 was defined as the zona ligand in transgenic mouse models using gain-of-function assays. The sperm-binding site is an N-terminal domain of ZP2 that is cleaved by ovastacin, a metalloendoprotease released from egg cortical granules following fertilization. Proteolysis of this docking site provides a definitive block to polyspermy as sperm bind to uncleaved, but not cleaved ZP2 even after fertilization and cortical granule exocytosis. While progress has been made in defining the ZP ligand, less headway has been made in identifying the cognate sperm receptor. Although a number of sperm receptor candidates have been documented to interact with specific proteins in the ZP in vitro, continued fertility after genetic ablation of the cognate gene indicates that none are essential for gamete recognition. These on-going investigations inform reproductive medicine and suggest new therapies to improve fertility and/or provide contraception, thus expanding reproductive choices for human couples.
C1 [Avella, Matteo A.; Xiong, Bo; Dean, Jurrien] NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
RP Avella, MA (reprint author), NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
EM matteo.avella@nih.gov
FU National Institutes of Health, NIDDK
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, NIDDK.
NR 150
TC 25
Z9 26
U1 1
U2 52
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1360-9947
J9 MOL HUM REPROD
JI Mol. Hum. Reprod.
PD MAY
PY 2013
VL 19
IS 5
BP 279
EP 289
DI 10.1093/molehr/gat004
PG 11
WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
GA 142PB
UT WOS:000318808400002
PM 23335731
ER
PT J
AU Kalia, J
Swartz, KJ
AF Kalia, Jeet
Swartz, Kenton J.
TI The design principle of paddle motifs in voltage sensors
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Editorial Material
ID DEPENDENT K+ CHANNEL; GATED SODIUM-CHANNEL; CRYSTAL-STRUCTURE; POTASSIUM
CHANNELS; LIPID-BILAYER; CHARGE; PHARMACOLOGY; DYNAMICS; DOMAIN
C1 [Kalia, Jeet; Swartz, Kenton J.] NINDS, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Kalia, J (reprint author), NINDS, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM SwartzK@ninds.nih.gov
NR 28
TC 0
Z9 0
U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD MAY
PY 2013
VL 20
IS 5
BP 534
EP 535
DI 10.1038/nsmb.2578
PG 2
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 139WZ
UT WOS:000318617000002
PM 23649359
ER
PT J
AU Aygun, O
Mehta, S
Grewal, SIS
AF Ayguen, Ozan
Mehta, Sameet
Grewal, Shiv I. S.
TI HDAC-mediated suppression of histone turnover promotes epigenetic
stability of heterochromatin
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID JMJC DOMAIN PROTEIN; RNA-POLYMERASE-II; FISSION YEAST;
SCHIZOSACCHAROMYCES-POMBE; HP1 PROTEINS; LYSINE-9 METHYLATION; H3
EXCHANGE; GENOME; CHROMATIN; TRANSCRIPTION
AB Heterochromatin causes epigenetic repression that can be transmitted through multiple cell divisions. However, the mechanisms underlying silencing and stability of heterochromatin are not fully understood. We show that heterochromatin differs from euchromatin in histone turnover and identify histone deacetylase (HDAC) Clr3 as a factor required for inhibiting histone turnover across heterochromatin domains in Schizosaccharomyces pombe. Loss of RNA-interference factors, Clr4 methyltransferase or HP1 proteins involved in HDAC localization causes increased histone turnover across pericentromeric domains. Clr3 also affects histone turnover at the silent mating-type region, where it can be recruited by alternative mechanisms acting in parallel to H3K9me-HP1. Notably, the JmjC-domain protein Epe1 promotes histone exchange, and loss of Epe1 suppresses both histone turnover and defects in heterochromatic silencing. Our results suggest that heterochromatic-silencing factors preclude histone turnover to promote silencing and inheritance of repressive chromatin.
C1 [Ayguen, Ozan; Mehta, Sameet; Grewal, Shiv I. S.] NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Grewal, SIS (reprint author), NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM grewals@mail.nih.gov
OI Mehta, Sameet/0000-0002-3029-3217
FU US National Institutes of Health, National Cancer Institute; European
Molecular Biology Organization long-term post-doctoral fellowship
FX We are thankful to J. Barrowman for editing the manuscript, K. Zhang, K.
Yamane and E. Luk for discussions, members of the Grewal laboratory for
their help and P. Russell (Scripps Research Institute, La Jolla,
California, USA) for the gift of pINV1 plasmid. This work is supported
by the Intramural Research Program of the US National Institutes of
Health, National Cancer Institute. O.A. was supported by a European
Molecular Biology Organization long-term post-doctoral fellowship.
NR 60
TC 27
Z9 27
U1 0
U2 23
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD MAY
PY 2013
VL 20
IS 5
BP 547
EP +
DI 10.1038/nsmb.2565
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 139WZ
UT WOS:000318617000007
PM 23604080
ER
PT J
AU Arbel-Goren, R
Tal, A
Friedlander, T
Meshner, S
Costantino, N
Court, DL
Stavans, J
AF Arbel-Goren, Rinat
Tal, Asaf
Friedlander, Tamar
Meshner, Shiri
Costantino, Nina
Court, Donald L.
Stavans, Joel
TI Effects of post-transcriptional regulation on phenotypic noise in
Escherichia coli
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID STOCHASTIC GENE-EXPRESSION; RYHB SMALL RNA; PROTEIN EXPRESSION;
DECISION-MAKING; SINGLE-CELL; LEVEL; NETWORK; NUMBER; RECOMBINATION;
SURVIVAL
AB Cell-to-cell variations in protein abundance, called noise, give rise to phenotypic variability between isogenic cells. Studies of noise have focused on stochasticity introduced at transcription, yet the effects of post-transcriptional regulatory processes on noise remain unknown. We study the effects of RyhB, a small-RNA of Escherichia coli produced on iron stress, on the phenotypic variability of two of its downregulated target proteins, using dual chromosomal fusions to fluorescent reporters and measurements in live individual cells. The total noise of each of the target proteins is remarkably constant over a wide range of RyhB production rates despite cells being in stress. In fact, coordinate downregulation of the two target proteins by RyhB reduces the correlation between their levels. Hence, an increase in phenotypic variability under stress is achieved by decoupling the expression of different target proteins in the same cell, rather than by an increase in the total noise of each. Extrinsic noise provides the dominant contribution to the total protein noise over the total range of RyhB production rates. Stochastic simulations reproduce qualitatively key features of our observations and show that a feed-forward loop formed by transcriptional extrinsic noise, an sRNA and its target genes exhibits strong noise filtration capabilities.
C1 [Arbel-Goren, Rinat; Tal, Asaf; Meshner, Shiri; Stavans, Joel] Weizmann Inst Sci, Dept Phys Complex Syst, IL-76100 Rehovot, Israel.
[Friedlander, Tamar] Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel.
[Costantino, Nina; Court, Donald L.] NCI, Gene Regulat & Chromosome Biol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
RP Stavans, J (reprint author), Weizmann Inst Sci, Dept Phys Complex Syst, IL-76100 Rehovot, Israel.
EM joel.stavans@weizmann.ac.il
FU Israel Science Foundation [842/08]; Clore fellowship; Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, Center for Cancer Research; Trans National Institutes of
Health/Food and Drug Administration Intramural Biodefense Program Grant
of National Institutes of Allergy and Infectious Disease
FX Funding for open access charge: Israel Science Foundation (842/08 to
J.S.); Clore fellowship (to T.F.); Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research (in part) and Trans National Institutes of Health/Food
and Drug Administration Intramural Biodefense Program Grant of National
Institutes of Allergy and Infectious Disease (in part) (to D.L.C.).
NR 46
TC 11
Z9 11
U1 1
U2 22
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD MAY
PY 2013
VL 41
IS 9
BP 4825
EP 4834
DI 10.1093/nar/gkt184
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 139GM
UT WOS:000318570000015
PM 23519613
ER
PT J
AU Sztuba-Solinska, J
Teramoto, T
Rausch, JW
Shapiro, BA
Padmanabhan, R
Le Grice, SFJ
AF Sztuba-Solinska, Joanna
Teramoto, Tadahisa
Rausch, Jason W.
Shapiro, Bruce A.
Padmanabhan, Radhakrishnan
Le Grice, Stuart F. J.
TI Structural complexity of Dengue virus untranslated regions: cis-acting
RNA motifs and pseudoknot interactions modulating functionality of the
viral genome
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID TURNIP CRINKLE VIRUS; DE-NOVO SYNTHESIS; WEST-NILE-VIRUS;
3'-UNTRANSLATED REGION; SECONDARY STRUCTURE; CYCLIZATION SEQUENCES;
TERTIARY INTERACTIONS; 3'-NONCODING REGION; PROTEIN-SYNTHESIS;
GENE-EXPRESSION
AB The Dengue virus (DENV) genome contains multiple cis-acting elements required for translation and replication. Previous studies indicated that a 719-nt subgenomic minigenome (DENV-MINI) is an efficient template for translation and (-) strand RNA synthesis in vitro. We performed a detailed structural analysis of DENV-MINI RNA, combining chemical acylation techniques, Pb2+ ion-induced hydrolysis and site-directed mutagenesis. Our results highlight protein-independent 5'-3' terminal interactions involving hybridization between recognized cis-acting motifs. Probing analyses identified tandem dumbbell structures (DBs) within the 3' terminus spaced by single-stranded regions, internal loops and hairpins with embedded GNRA-like motifs. Analysis of conserved motifs and top loops (TLs) of these dumbbells, and their proposed interactions with downstream pseudoknot (PK) regions, predicted an H-type pseudoknot involving TL1 of the 5' DB and the complementary region, PK2. As disrupting the TL1/PK2 interaction, via 'flipping' mutations of PK2, previously attenuated DENV replication, this pseudoknot may participate in regulation of RNA synthesis. Computer modeling implied that this motif might function as autonomous structural/regulatory element. In addition, our studies targeting elements of the 3' DB and its complementary region PK1 indicated that communication between 5'-3' terminal regions strongly depends on structure and sequence composition of the 5' cyclization region.
C1 [Sztuba-Solinska, Joanna; Rausch, Jason W.; Le Grice, Stuart F. J.] Frederick Natl Lab Canc Res, RT Biochem Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Teramoto, Tadahisa; Padmanabhan, Radhakrishnan] Georgetown Univ, Sch Med, Dept Microbiol & Immunol, Washington, DC 20057 USA.
[Shapiro, Bruce A.] Frederick Natl Lab Canc Res, CCR Nanobiol Program, Computat RNA Struct Grp, Frederick, MD 21702 USA.
RP Le Grice, SFJ (reprint author), Frederick Natl Lab Canc Res, RT Biochem Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA.
EM legrices@mail.nih.gov
FU National Cancer Institute, National Institutes of Health, Department of
Health and Human Services; National Institutes of Health
[R01AI070791-03S1, U01-AI082068, R011R01AI 087856]
FX Intramural Research Program (IRP) of the National Cancer Institute,
National Institutes of Health, Department of Health and Human Services
(to J.S.S., J.W.R., B. A. S. and S. L. G.); National Institutes of
Health [R01AI070791-03S1, U01-AI082068 and R011R01AI 087856 to T. T. and
R. P.]. Funding for open access charge: National Cancer Institute,
National Institutes of Health, Department of Health and Human Services.
NR 60
TC 19
Z9 20
U1 2
U2 20
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD MAY
PY 2013
VL 41
IS 9
BP 5075
EP 5089
DI 10.1093/nar/gkt203
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 139GM
UT WOS:000318570000035
PM 23531545
ER
PT J
AU Rodriguez-Blanco, J
Schilling, NS
Tokhunts, R
Giambelli, C
Long, J
Fei, DL
Singh, S
Black, KE
Wang, Z
Galimberti, F
Bejarano, PA
Elliot, S
Glassberg, MK
Nguyen, DM
Lockwood, WW
Lam, WL
Dmitrovsky, E
Capobianco, AJ
Robbins, DJ
AF Rodriguez-Blanco, J.
Schilling, N. S.
Tokhunts, R.
Giambelli, C.
Long, J.
Fei, D. Liang
Singh, S.
Black, K. E.
Wang, Z.
Galimberti, F.
Bejarano, P. A.
Elliot, S.
Glassberg, M. K.
Nguyen, D. M.
Lockwood, W. W.
Lam, W. L.
Dmitrovsky, E.
Capobianco, A. J.
Robbins, D. J.
TI The Hedgehog processing pathway is required for NSCLC growth and
survival
SO ONCOGENE
LA English
DT Article
DE dispatched; lung cancer; hedgehog; hedgehog acyltransferase; skinny
hedgehog
ID BASAL-CELL CARCINOMA; SMALL-MOLECULE MODULATION; HUMAN SONIC HEDGEHOG;
LUNG-CANCER; SIGNALING PATHWAY; LONG-RANGE; CHROMOSOMAL IMBALANCES;
ANIMAL DEVELOPMENT; GENE-EXPRESSION; HUMAN HOMOLOG
AB Considerable interest has been generated from the results of recent clinical trials using smoothened (SMO) antagonists to inhibit the growth of hedgehog (HH) signaling-dependent tumors. This interest is tempered by the discovery of SMO mutations mediating resistance, underscoring the rationale for developing therapeutic strategies that interrupt HH signaling at levels distinct from those inhibiting SMO function. Here, we demonstrate that HH-dependent non-small cell lung carcinoma (NSCLC) growth is sensitive to blockade of the HH pathway upstream of SMO, at the level of HH ligand processing. Individually, the use of different lentivirally delivered shRNA constructs targeting two functionally distinct HH-processing proteins, skinny hedgehog (SKN) or dispatched-1 (DISP-1), in NSCLC cell lines produced similar decreases in cell proliferation and increased cell death. Further, providing either an exogenous source of processed HH or a SMO agonist reverses these effects. The attenuation of HH processing, by knocking down either of these gene products, also abrogated tumor growth in mouse xenografts. Finally, we extended these findings to primary clinical specimens, showing that SKN is frequently overexpressed in NSCLC and that higher DISP-1 expression is associated with an unfavorable clinical outcome. Our results show a critical role for HH processing in HH-dependent tumors, identifies two potential druggable targets in the HH pathway, and suggest that similar therapeutic strategies could be explored to treat patients harboring HH ligand-dependent cancers.
C1 [Rodriguez-Blanco, J.; Schilling, N. S.; Tokhunts, R.; Giambelli, C.; Long, J.; Fei, D. Liang; Singh, S.; Black, K. E.; Wang, Z.; Nguyen, D. M.; Capobianco, A. J.; Robbins, D. J.] Univ Miami, Dept Surg, Mol Oncol Program, Miami, FL 33136 USA.
[Schilling, N. S.; Tokhunts, R.; Fei, D. Liang; Galimberti, F.; Dmitrovsky, E.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Pharmacol & Toxicol, Hanover, NH 03756 USA.
[Bejarano, P. A.] Univ Miami, Dept Pathol, Miami, FL 33136 USA.
[Elliot, S.] Univ Miami, Dept Surg, Lab Sex & Gender Differences Hlth & Dis, Miami, FL 33136 USA.
[Glassberg, M. K.] Univ Miami, Jackson Mem Hosp, Dept Med, Miami, FL 33136 USA.
[Glassberg, M. K.] Univ Miami, Jackson Mem Hosp, Dept Surg, Miami, FL 33136 USA.
[Nguyen, D. M.; Capobianco, A. J.; Robbins, D. J.] Univ Miami, Miller Sch Med, Sylvester Canc Ctr, Miami, FL 33136 USA.
[Lockwood, W. W.] NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA.
[Lam, W. L.] British Columbia Canc Res Ctr, Dept Integrat Biol, Vancouver, BC V5Z 1L3, Canada.
[Dmitrovsky, E.] Dartmouth Med Sch, Norris Cotton Canc Ctr, Lebanon, NH USA.
[Dmitrovsky, E.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
[Robbins, D. J.] Univ Miami, Dept Biochem & Mol Biol, Miami, FL 33136 USA.
RP Robbins, DJ (reprint author), Univ Miami, Miller Sch Med, Sylvester Canc Ctr, 1042 RMSB,1600 NW 10th Ave, Miami, FL 33136 USA.
EM drobbins@med.miami.edu
RI Singh, Samer/H-8468-2013; Wang, Zhiqiang/O-6810-2014; LONG,
JUN/N-7270-2015
FU NIH [GM64011, R03-CA132166, R01-CA087546, R01-CA111422]; Samuel Waxman
Cancer Research Foundation; American Lung Association/LUNGevity
Foundation; [FICYT-POST10-27]
FX This work was supported by the NIH grants GM64011 (DJ Robbins),
R03-CA132166 (E Dmitrovsky), R01-CA087546 (E Dmitrovsky) and
R01-CA111422 (E Dmitrovsky); grants from the Samuel Waxman Cancer
Research Foundation (E Dmitrovsky, A Capobianco); FICYT-POST10-27 (J
Rodriguez-Blanco) and from the American Lung Association/LUNGevity
Foundation (DJ Robbins). E Dmitrovsky is an American Cancer Society
Professor supported by a generous gift from the FM Kirby Foundation.
NR 79
TC 14
Z9 14
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD MAY
PY 2013
VL 32
IS 18
BP 2335
EP 2345
DI 10.1038/onc.2012.243
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 140VF
UT WOS:000318683600010
PM 22733134
ER
PT J
AU Simon, AE
Lukacs, SL
Mendola, P
AF Simon, Alan E.
Lukacs, Susan L.
Mendola, Pauline
TI National Trends in Emergency Department Use of Urinalysis, Complete
Blood Count, and Blood Culture for Fever Without a Source Among Children
Aged 2 to 24 Months in the Pneumococcal Conjugate Vaccine 7 Era
SO PEDIATRIC EMERGENCY CARE
LA English
DT Article
DE fever; PCV-7; testing
ID URINARY-TRACT-INFECTION; PRIMARY-CARE PHYSICIANS; FEBRILE INFANTS;
PRACTICE GUIDELINES; YOUNG-CHILDREN; OCCULT BACTEREMIA; INITIAL UTI;
MANAGEMENT; DISEASE; PEDIATRICIANS
AB Objectives: The epidemiology of serious bacterial infections in children has changed since the introduction of the pneumococcal conjugate vaccine (PCV-7) in 2000. Whether emergency department (ED) physicians have changed diagnostic approaches to fever without a source (FWS) in response is unknown. We examine trends in rates of complete blood count (CBC), urinalysis (UA), and blood cultures among 2- to 24-month-old children with FWS since the introduction of PCV-7.
Methods: The National Hospital Ambulatory Medical Care Survey-Emergency Department, 2001-2009, was used to identify visits to the ED by 2- to 24-month-old children with FWS. Rates of CBC, UA, neither CBC nor UA, and blood culture were tracked across time. Trends were identified using Joinpoint regression and bivariate and multivariate logistic regressions with year as the independent variables and ordering of each test as the dependent variables.
Results: In bivariate and multivariate analyses, CBC orders declined between 2004 and 2009 for visits by all children 2 to 24 months, children 2 to 11 months, and boys 2 to 24 months (adjusted odds ratio [aOR], 0.88 per year [P < 0.01]; aOR, 0.88 [P < 0.05]; and aOR, 0.83 [P < 0.01], respectively). Between 2004 and 2009, ordering neither CBC nor UA increased among all children 2 to 24 months (aOR, 1.10; P < 0.05) and among boys (aOR, 1.16; P < 0.05). Orders for blood cultures declined across the time period in bivariate analysis, but not in multivariate analysis.
Conclusions: The rate of ordering a CBC for children in the 2- to 24-month age group presenting to the ED with FWS declined, a change coincident with the changing epidemiology of serious bacterial infection since the PCV-7 vaccine was introduced.
C1 [Simon, Alan E.; Lukacs, Susan L.] Ctr Dis Control & Prevent, Infant Child & Womens Hlth Stat Branch, Off Anal & Epidemiol, Natl Ctr Hlth Stat, Hyattsville, MD USA.
[Mendola, Pauline] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, Div Epidemiol Stat & Prevent Res, NIH, Rockville, MD USA.
RP Simon, AE (reprint author), Natl Ctr Hlth Stat, 3311 Toledo Rd,Rm 6122, Hyattsville, MD 20782 USA.
EM fpa8@cdc.gov
OI Mendola, Pauline/0000-0001-5330-2844
FU Intramural Research Program of the NIH, Eunice Kennedy Shriver National
Institute of Child Health and Human Development
FX This research was supported in part by the Intramural Research Program
of the NIH, Eunice Kennedy Shriver National Institute of Child Health
and Human Development.
NR 40
TC 2
Z9 2
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0749-5161
J9 PEDIATR EMERG CARE
JI Pediatr. Emerg. Care
PD MAY
PY 2013
VL 29
IS 5
BP 560
EP 567
DI 10.1097/PEC.0b013e31828e56e1
PG 8
WC Emergency Medicine; Pediatrics
SC Emergency Medicine; Pediatrics
GA 138YW
UT WOS:000318549400002
PM 23603643
ER
PT J
AU Purswani, M
Patel, K
Kopp, JB
Seage, GR
Chernoff, MC
Hazra, R
Siberry, GK
Mofenson, LM
Scott, GB
Van Dyke, RB
AF Purswani, Murli
Patel, Kunjal
Kopp, Jeffrey B.
Seage, George R., III
Chernoff, Miriam C.
Hazra, Rohan
Siberry, George K.
Mofenson, Lynne M.
Scott, Gwendolyn B.
Van Dyke, Russell B.
CA Pediat HIV AIDS Cohort Study
TI Tenofovir Treatment Duration Predicts Proteinuria in a Multiethnic
United States Cohort of Children and Adolescents With Perinatal HIV-1
Infection
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE tenofovir; proteinuria; chronic kidney disease; proximal tubules;
nephrotoxicity; urine protein/creatinine ratio
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; TERM RENAL
SAFETY; DISOPROXIL FUMARATE; RISK-FACTORS; KIDNEY-DISEASE; NAIVE
PATIENTS; NEPHROTOXICITY; NEPHROPATHY; DYSFUNCTION
AB Background: Tenofovir is associated with renal proximal tubule injury. Such toxicity has not been extensively studied in HIV-1-infected children, in whom tenofovir is increasingly used.
Methods: History, urine and blood were collected at regular intervals from 448 children and adolescents with perinatal HIV-1 infection followed in the Pediatric HIV/AIDS Cohort study. Relationships between tenofovir use and proteinuria and chronic kidney disease (CKD) outcomes were examined using multivariable logistic regression models. Proteinuria was defined as at least one urine protein/creatinine ratio (uPCR) >= 0.2, and CKD as >= 2 sequential uPCR >= 0.2 or estimated glomerular filtration rates <60 mL/min/1.73 m(2) with no subsequent resolution, or a clinical diagnosis not contradicted by a normal uPCR. Subjects with >= 2 uPCR <0.2, and no abnormal uPCR and eGFR comprised the comparison group.
Results: Subjects were 47% male, 72% black, 24% Hispanic, with entry mean age (+/- standard deviation) of 11.5 +/- 2.5 years. Proteinuria prevalence at entry, and annually during 3 years, ranged from 10.3% to 13.7%. The cumulative prevalence of proteinuria was 22% (94/434, 95% confidence interval: 18%-26%) and CKD 4.5% (20/448, 95% confidence interval: 2.7%-6.8%). Duration of tenofovir use was an independent predictor of proteinuria, with >3 years of exposure having the highest risk compared with no exposure (odds ratio: 2.53, 95% confidence interval: 1.23-5.22, overall P = 0.01). Overall, duration of tenofovir use did not significantly predict the presence of CKD.
Conclusions: Rates of proteinuria and CKD were lower than those seen in the pre-highly active antiretroviral therapy era. However, prolonged exposure to tenofovir increases risk of renal injury.
C1 [Purswani, Murli] Bronx Lebanon Hosp Ctr, Albert Einstein Coll Med, Bronx, NY 10457 USA.
[Patel, Kunjal; Seage, George R., III] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Patel, Kunjal; Seage, George R., III; Chernoff, Miriam C.] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD USA.
[Hazra, Rohan; Siberry, George K.; Mofenson, Lynne M.] Eunice Kennedy Shriver NICHHD, Pediat Adolescent Maternal AIDS Branch, NIH, Bethesda, MD USA.
[Scott, Gwendolyn B.] Univ Miami, Miller Sch Med, Dept Pediat, Miami, FL 33136 USA.
[Van Dyke, Russell B.] Tulane Univ, Hlth Sci Ctr, New Orleans, LA 70118 USA.
RP Purswani, M (reprint author), Bronx Lebanon Hosp Ctr, Albert Einstein Coll Med, 1650 Selwyn Ave, Bronx, NY 10457 USA.
EM mpurswan@bronxleb.org
OI Mofenson, Lynne/0000-0002-2818-9808; Kopp, Jeffrey/0000-0001-9052-186X
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institute on Drug Abuse; National Institute of
Allergy and Infectious Diseases; Office of AIDS Research; National
Institute of Mental Health; National Institute of Neurological Disorders
and Stroke; National Institute on Deafness and Other Communication
Disorders; National Heart Lung and Blood Institute; National Institute
of Dental and Craniofacial Research; National Institute on Alcohol Abuse
and Alcoholism; Harvard University School of Public Health [HD052102,
3U01HD052102-05S1, 3U01HD052102-06S3]; Tulane University School of
Medicine [HD052104, 3U01HD052104-06S1]
FX The Pediatric HIV/AIDS Cohort Study was supported by the Eunice Kennedy
Shriver National Institute of Child Health and Human Development with
cofunding from the National Institute on Drug Abuse, the National
Institute of Allergy and Infectious Diseases, the Office of AIDS
Research, the National Institute of Mental Health, the National
Institute of Neurological Disorders and Stroke, the National Institute
on Deafness and Other Communication Disorders, the National Heart Lung
and Blood Institute, the National Institute of Dental and Craniofacial
Research and the National Institute on Alcohol Abuse and Alcoholism,
through cooperative agreements with the Harvard University School of
Public Health (HD052102, 3U01HD052102-05S1, 3U01HD052102-06S3) and the
Tulane University School of Medicine (HD052104, 3U01HD052104-06S1). The
authors have no other funding or conflicts of interest to disclose.
NR 41
TC 22
Z9 22
U1 0
U2 1
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 MAY
PY 2013
VL 32
IS 5
BP 495
EP 500
DI 10.1097/INF.0b013e31827f4eff
PG 6
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 140VN
UT WOS:000318684400019
PM 23249917
ER
PT J
AU Puthanakit, T
Ananworanich, J
Vonthanak, S
Kosalaraksa, P
Hansudewechakul, R
van der Lugt, J
Kerr, SJ
Kanjanavanit, S
Ngampiyaskul, C
Wongsawat, J
Luesomboon, W
Vibol, U
Pruksakaew, K
Suwarnlerk, T
Apornpong, T
Ratanadilok, K
Paul, R
Mofenson, LM
Fox, L
Valcour, V
Brouwers, P
Ruxrungtham, K
AF Puthanakit, Thanyawee
Ananworanich, Jintanat
Vonthanak, Saphonn
Kosalaraksa, Pope
Hansudewechakul, Rawiwan
van der Lugt, Jasper
Kerr, Stephen J.
Kanjanavanit, Suparat
Ngampiyaskul, Chaiwat
Wongsawat, Jurai
Luesomboon, Wicharn
Vibol, Ung
Pruksakaew, Kanchana
Suwarnlerk, Tulathip
Apornpong, Tanakorn
Ratanadilok, Kattiya
Paul, Robert
Mofenson, Lynne M.
Fox, Lawrence
Valcour, Victor
Brouwers, Pim
Ruxrungtham, Kiat
CA PREDICT Study Grp
TI Cognitive Function and Neurodevelopmental Outcomes in HIV-infected
Children Older Than 1 Year of Age Randomized to Early Versus Deferred
Antiretroviral Therapy: The PREDICT Neurodevelopmental Study
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE HIV; children; antiretroviral therapy; neurodevelopment;
resource-limited settings
ID PERINATALLY ACQUIRED HIV; YOUNG-CHILDREN; INFANTS; MANIFESTATIONS;
TRANSMISSION; PREVENTION; DIAGNOSES; HIV/AIDS; PROGRAM; IMPACT
AB Background: We previously reported similar AIDS-free survival at 3 years in children who were >1 year old initiating antiretroviral therapy (ART) and randomized to early versus deferred ART in the Pediatric Randomized to Early versus Deferred Initiation in Cambodia and Thailand (PREDICT) study. We now report neurodevelopmental outcomes.
Methods: Two hundred eighty-four HIV-infected Thai and Cambodian children aged 1-12 years with CD4 counts between 15% and 24% and no AIDS-defining illness were randomized to initiate ART at enrollment ("early," n = 139) or when CD4 count became <15% or a Centers for Disease Control (CDC) category C event developed ("deferred," n = 145). All underwent age-appropriate neurodevelopment testing including Beery Visual Motor Integration, Purdue Pegboard, Color Trails and Child Behavioral Checklist. Thai children (n = 170) also completed Wechsler Intelligence Scale (intelligence quotient) and Stanford Binet Memory test. We compared week 144 measures by randomized group and to HIV-uninfected children (n = 319).
Results: At week 144, the median age was 9 years and 69 (48%) of the deferred arm children had initiated ART. The early arm had a higher CD4 (33% versus 24%, P < 0.001) and a greater percentage of children with viral suppression (91% versus 40%, P < 0.001). Neurodevelopmental scores did not differ by arm, and there were no differences in changes between arms across repeated assessments in time-varying multivariate models. HIV-infected children performed worse than uninfected children on intelligence quotient, Beery Visual Motor Integration, Binet memory and Child Behavioral Checklist.
Conclusions: In HIV-infected children surviving beyond 1 year of age without ART, neurodevelopmental outcomes were similar with ART initiation at CD4 15%-24% versus <15%, but both groups performed worse than HIV-uninfected children. The window of opportunity for a positive effect of ART initiation on neurodevelopment may remain in infancy.
C1 [Puthanakit, Thanyawee; Ananworanich, Jintanat; van der Lugt, Jasper; Kerr, Stephen J.; Pruksakaew, Kanchana; Suwarnlerk, Tulathip; Apornpong, Tanakorn; Ruxrungtham, Kiat] HIV NAT, Thai Red Cross AIDS Res Ctr, Bangkok 10330, Thailand.
[Puthanakit, Thanyawee] Chulalongkorn Univ, Fac Med, Dept Pediat, Bangkok 10330, Thailand.
[Ananworanich, Jintanat; Ruxrungtham, Kiat] Chulalongkorn Univ, Fac Med, Dept Med, Bangkok 10330, Thailand.
[Ananworanich, Jintanat; Valcour, Victor] SEARCH, Thai Red Cross AIDS Res Ctr, Bangkok, Thailand.
[Vonthanak, Saphonn] Natl Ctr HIV AIDS Dermatol & STDs, Phnom Penh, Cambodia.
[Kosalaraksa, Pope] Khon Kaen Univ, Fac Med, Dept Pediat, Khon Kaen, Thailand.
[Hansudewechakul, Rawiwan] Chiangrai Prachanukroh Hosp, Chiang Rai, Thailand.
[Ananworanich, Jintanat; van der Lugt, Jasper] Amsterdam Inst Global Hlth & Dev, Amsterdam, Netherlands.
[Ananworanich, Jintanat; Kerr, Stephen J.] Univ New S Wales, Kirby Inst Infect & Immun Soc, Sydney, NSW, Australia.
[Kanjanavanit, Suparat] Nakornping Hosp, Chiang Mai, Thailand.
[Ngampiyaskul, Chaiwat] Prapokklao Hosp, Chanthaburi, Thailand.
[Wongsawat, Jurai] Bamrasnaradura Infect Dis Inst, Nonthaburi, Thailand.
[Luesomboon, Wicharn] Queen Savang Vadhana Mem Hosp, Chon Buri, Thailand.
[Vibol, Ung] Natl Pediat Hosp, Phnom Penh, Cambodia.
[Paul, Robert] Univ Missouri, Dept Psychol, St Louis, MO 63121 USA.
[Mofenson, Lynne M.] Eunice Kennedy Shriver NICHHD, NIH, Bethesda, MD USA.
[Fox, Lawrence] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Valcour, Victor] Univ Calif San Francisco, Memory & Aging Ctr, San Francisco, CA 94143 USA.
[Brouwers, Pim] NIMH, NIH, Bethesda, MD 20892 USA.
RP Ananworanich, J (reprint author), HIV NAT, Thai Red Cross AIDS Res Ctr, 104 Rajdumri Rd, Bangkok 10330, Thailand.
EM Jintanat.A@hivnat.org
OI Mofenson, Lynne/0000-0002-2818-9808; Kerr, Stephen/0000-0002-1919-4525
FU National Institute of Allergy and Infectious Diseases of the National
Institutes of Health through the Comprehensive International Program of
Research on AIDS Network [U19 AI53741]; Eunice Kennedy Shriver National
Institute of Child Health and Human Development; National Institute of
Mental Health; ViiV Health Care/GlaxoSmithKline; Boehringer-Ingelheim;
Merck; Abbott; Roche; National Research University Project of CHE
[HR1161A]; Ratchadaphiseksomphot Endowment Fund, Thailand; Professional
Researcher Strengthen Grant from the National Science and Technology
Development Agency, BIOTEC; Senior Researcher Scholar from Thai Research
Fund, Thailand
FX The work was supported by a grant from the National Institute of Allergy
and Infectious Diseases of the National Institutes of Health through the
Comprehensive International Program of Research on AIDS Network (U19
AI53741); cofunded by the Eunice Kennedy Shriver National Institute of
Child Health and Human Development and the National Institute of Mental
Health. The antiretroviral was drug supported by ViiV Health
Care/GlaxoSmithKline, Boehringer-Ingelheim, Merck, Abbott and Roche. The
views in this report do not necessary reflect the views of the National
Institutes of Health or US Department of Health and Human Services. K.R.
has received support through grants HR1161A from the National Research
University Project of CHE and the Ratchadaphiseksomphot Endowment Fund,
Thailand; the Professional Researcher Strengthen Grant from the National
Science and Technology Development Agency, BIOTEC, and the Senior
Researcher Scholar from Thai Research Fund, Thailand.
NR 29
TC 42
Z9 43
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD MAY
PY 2013
VL 32
IS 5
BP 501
EP 508
DI 10.1097/INF.0b013e31827fb19d
PG 8
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 140VN
UT WOS:000318684400020
PM 23263176
ER
PT J
AU Issa, PC
Gillies, MC
Chew, EY
Bird, AC
Heeren, TFC
Peto, T
Holz, FG
Scholl, HPN
AF Issa, Peter Charbel
Gillies, Mark C.
Chew, Emily Y.
Bird, Alan C.
Heeren, Tjebo F. C.
Peto, Tunde
Holz, Frank G.
Scholl, Hendrik P. N.
TI Macular telangiectasia type 2
SO PROGRESS IN RETINAL AND EYE RESEARCH
LA English
DT Article
DE Macular telangiectasia; Macular pigment; Phenotype; Treatment; Muller
cell; Imaging; Vascular endothelial growth factor (VEGF); Optical
coherence tomography (OCT); Neurodegeneration; Retina
ID JUXTAFOVEOLAR RETINAL TELANGIECTASIS; OPTICAL COHERENCE TOMOGRAPHY;
CILIARY NEUROTROPHIC FACTOR; IDIOPATHIC PERIFOVEAL TELANGIECTASIA;
SUBRETINAL NEOVASCULARIZATION SECONDARY; INTRAVITREAL TRIAMCINOLONE
ACETONIDE; ENDOTHELIAL GROWTH-FACTOR; FACIOSCAPULOHUMERAL
MUSCULAR-DYSTROPHY; GRID LASER PHOTOCOAGULATION;
SJOGREN-LARSSON-SYNDROME
AB Macular telangiectasia type 2 is a bilateral disease of unknown cause with characteristic alterations of the macular capillary network and neurosensory atrophy. Its prevalence may be underestimated and has recently been shown to be as high as 0.1% in persons 40 years and older. Biomicroscopy may show reduced retinal transparency, crystalline deposits, mildly ectatic capillaries, blunted venules, retinal pigment plaques, foveal atrophy, and neovascular complexes. Fluorescein angiography shows telangiectatic capillaries predominantly temporal to the foveola in the early phase and a diffuse hyperfluorescence in the late phase. High-resolution optical coherence tomography (OCT) may reveal disruption of the photoreceptor inner segment-outer segment border, hyporeflective cavities at the level of the inner or outer retina, and atrophy of the retina in later stages. Macular telangiectasia type 2 shows a unique depletion of the macular pigment in the central retina and recent therapeutic trials showed that such depleted areas cannot re-accumulate lutein and zeaxanthin after oral supplementation. There have been various therapeutic approaches with limited or no efficacy. Recent clinical trials with compounds that block vascular endothelial growth factor (VEGF) have established the role of VEGF in the pathophysiology of the disease, but have not shown significant efficacy, at least for the non-neovascular disease stages. Recent progress in structure-function correlation may help to develop surrogate outcome measures for future clinical trials.
In this review article, we summarize the current knowledge on macular telangiectasia type 2, including the epidemiology, the genetics, the clinical findings, the staging and the differential diagnosis of the disease. Findings using retinal imaging are discussed, including fluorescein angiography, OCT, adaptive optics imaging, confocal scanning laser ophthalmoscopy, and fundus autofluorescence, as are the findings using visual function testing including visual acuity and fundus-controlled microperimetry. We provide an overview of the therapeutic approaches for both non-neovascular and neovascular disease stages and provide a perspective of future directions including animal models and potential therapeutic approaches. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Issa, Peter Charbel; Heeren, Tjebo F. C.; Holz, Frank G.] Univ Bonn, Dept Ophthalmol, D-53127 Bonn, Germany.
[Gillies, Mark C.] Univ Sydney, Save Sight Inst, Dept Clin Ophthalmol, Sydney, NSW 2006, Australia.
[Chew, Emily Y.] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Bird, Alan C.; Peto, Tunde] Moorfields Eye Hosp NHS Fdn Trust, NIHR Biomed Res Ctr Ophthalmol, London, England.
[Bird, Alan C.; Peto, Tunde] UCL Inst Ophthalmol, London, England.
[Scholl, Hendrik P. N.] Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21287 USA.
RP Scholl, HPN (reprint author), Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, 748 Maumenee Bldg,1800 Orleans St, Baltimore, MD 21287 USA.
EM peter.issa@ukb.uni-bonn.de; hscholl1@jhmi.edu
OI Charbel Issa, Peter/0000-0002-0351-6673; Heeren,
Tjebo/0000-0001-5297-2301
FU Lowy Medical Research Institute; Pro-Retina Deutschland; Wynn-Gund
Translational Research Acceleration Program Enhanced Research and
Clinical Training Award, National Neurovision Research Institute (NNRI)
- Foundation Fighting Blindness (FFB) [NNCD-CL-0310.0049-JHU-WG];
Macular Degeneration Research Award, American Health Assistance
Foundation (AHAF) [M2010042]; Research to Prevent Blindness;
Baylor-Johns Hopkins Center for Mendelian Genetics (National Human
Genome Research Institute, NHGRI/NIH) [1U54HG006542-01]
FX Supported by the Lowy Medical Research Institute (The Macular
Telangiectasia Project, www.mactelresearch.com); Pro-Retina Deutschland
(P.C.I.); Wynn-Gund Translational Research Acceleration Program Enhanced
Research and Clinical Training Award, National Neurovision Research
Institute (NNRI) - Foundation Fighting Blindness (FFB;
NNCD-CL-0310.0049-JHU-WG); Macular Degeneration Research Award, American
Health Assistance Foundation (AHAF; M2010042); Unrestricted grant to the
Wilmer Eye Institute from Research to Prevent Blindness; Baylor-Johns
Hopkins Center for Mendelian Genetics (National Human Genome Research
Institute, NHGRI/NIH; Identification number: 1U54HG006542-01). H.P.N.S.
is the Dr. Frieda Derdeyn Bambas Professor of Ophthalmology. None of the
authors has a conflict of interest.
NR 207
TC 39
Z9 39
U1 1
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1350-9462
J9 PROG RETIN EYE RES
JI Prog. Retin. Eye Res.
PD MAY
PY 2013
VL 34
BP 49
EP 77
DI 10.1016/j.preteyeres.2012.11.002
PG 29
WC Ophthalmology
SC Ophthalmology
GA 141RT
UT WOS:000318744900003
ER
PT J
AU Lehmann, ML
Mustafa, T
Eiden, AM
Herkenham, M
Eiden, LE
AF Lehmann, Michael L.
Mustafa, Tomris
Eiden, Adrian M.
Herkenham, Miles
Eiden, Lee E.
TI PACAP-deficient mice show attenuated corticosterone secretion and fail
to develop depressive behavior during chronic social defeat stress
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE Psychological stress; Social defeat; Depression; Stress resiliency;
Forced swim test; HPA axis; Pituitary adenylate cyclase-activating
polypeptide; Neuropeptide; Hypercortisolemia
ID CYCLASE-ACTIVATING POLYPEPTIDE; MEDIAL PREFRONTAL CORTEX; HYPOTHALAMIC
PARAVENTRICULAR NUCLEUS; CORTICOTROPIN-RELEASING-FACTOR; MIDBRAIN
PERIAQUEDUCTAL GRAY; PITUITARY-ADRENAL RESPONSES; STRIA TERMINALIS BNST;
ANXIETY-LIKE BEHAVIOR; HORMONE CRH GENE; BED NUCLEUS
AB The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) regulates activation of the hypothalamic-pituitary-adrenal (HPA) axis and the adrenal gland in response to various stressors. We previously found that in response to acute psychological stress (restraint), elevated corticotrophin-releasing hormone (CRH) mRNA levels in the hypothalamic paraventricular nucleus (PVN) as well as elevated plasma corticosterone (CORT) were profoundly attenuated in PACAP-deficient mice. To determine whether HPA axis responses and stress-induced depressive-like behaviors in a chronic stress paradigm are affected by PACAP deficiency, we subjected mice to 14 days of social defeat stress. Defeat-exposed PACAP-/- mice showed a marked attenuation of stress-induced increases in serum CORT levels, cellular PVN Delta FosB immunostaining, and depressive-like behaviors (social interaction and forced swim tests) compared to wild-type control mice. The PACAP-/- mice showed reduced PVN FosB-positive cell numbers, but relatively elevated cell counts in several forebrain areas including the medial prefrontal cortex, after social stress. PACAP appears to be specific for mediating HPA activation only in psychological stress because marked elevations in plasma CORT after a systemic stressor (lipopolysaccharide administration) occurred regardless of genotype. We conclude that chronically elevated CORT is a key component of depressive effects of social defeat, and that attenuation of the CORT response at the level of the PVN, as well as extrahypothalamic forebrain regions, in PACAP-deficient mice protects from development of depressive behavior. Published by Elsevier Ltd.
C1 [Lehmann, Michael L.; Eiden, Adrian M.; Herkenham, Miles] NIMH, Funct Neuroanat Sect, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
[Mustafa, Tomris; Eiden, Lee E.] NIMH, Sect Mol Neurosci, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
RP Eiden, LE (reprint author), Sect Mol Neurosci, Bldg 49,Room 5A-38,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM eidenl@mail.nih.gov
OI Lehmann, Michael/0000-0003-4476-8268; Eiden, Lee/0000-0001-7524-944X;
Herkenham, Miles/0000-0003-2228-4238
FU NIMH [Z01-MH001090, Z01-002386]
FX This work was supported as a part of NIMH Projects Z01-MH001090 and
Z01-002386.
NR 72
TC 21
Z9 21
U1 1
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4530
J9 PSYCHONEUROENDOCRINO
JI Psychoneuroendocrinology
PD MAY
PY 2013
VL 38
IS 5
BP 702
EP 715
DI 10.1016/j.psyneuen.2012.09.006
PG 14
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA 137VE
UT WOS:000318465500013
PM 23062748
ER
PT J
AU Mueller, SC
Daniele, T
MacIntyre, J
Korelitz, K
Carlisi, C
Hardin, MG
Van Ryzin, C
Merke, DP
Ernst, M
AF Mueller, Sven C.
Daniele, Teresa
MacIntyre, Jessica
Korelitz, Katherine
Carlisi, Christina
Hardin, Michael G.
Van Ryzin, Carol
Merke, Deborah P.
Ernst, Monique
TI Incentive processing in Congenital Adrenal Hyperplasia (CAH): A
reward-based antisaccade study
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE Inhibitory control; Androgen; Development; Adolescence; Sex steroids;
Testosterone; Cortisol
ID EARLY STEROID ABNORMALITIES; HIPPOCAMPAL-FORMATION; INHIBITORY CONTROL;
DOPAMINE RELEASE; DEPRESSIVE STATE; STRESS; ADOLESCENTS; DISORDER;
SUPPRESSION; PERFORMANCE
AB Little is known about how steroid hormones contribute to the beneficial effect of incentives on cognitive control during adolescent development. In this study, 27 adolescents with Congenital Adrenal Hyperplasia (CAH, mean age 15.6 years, 12 female), a disorder of cortisol deficiency and androgen excess, and 36 healthy participants (mean age 16.3 years, 18 female) completed a reward-based antisaccade task. In this mixed-saccade task, participants performed eye movements towards (prosaccades) or away (antisaccades) from a peripherally occuring stimulus. On incentive trials, monetary reward was provided for correct performance, while no such reward was provided on no-incentive trials. Consistent with the hypothesis, the results showed that healthy, but not CAH adolescents, significantly improved their inhibitory control (antisaccade accuracy) during incentive trials relative to no-incentive trials. These findings were not driven by severity of CAH (salt wasters vs. simple virilizers), individual hormone levels, sex, age-at-diagnosis, or medication type (dexamethasone vs. hydrocortisone). In addition, no significant differences between groups were found on orienting responses (prosaccades). Additional analyses revealed an impact of glucocorticoid (GC) dosage, such that higher GC dose predicted better antisaccade performance. However, this effect did not impact incentive processing. The data are discussed within the context of steroid hormone mediated effects on cognitive control and reward processing.
C1 [Mueller, Sven C.; Daniele, Teresa; MacIntyre, Jessica; Korelitz, Katherine; Carlisi, Christina; Hardin, Michael G.; Ernst, Monique] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
[Mueller, Sven C.] Univ Ghent, Dept Expt Clin & Hlth Psychol, B-9000 Ghent, Belgium.
[Van Ryzin, Carol; Merke, Deborah P.] NIH Clin Ctr, Bethesda, MD 20892 USA.
[Merke, Deborah P.] NICHHD, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
RP Mueller, SC (reprint author), Univ Ghent, Dept Expt Clin & Hlth Psychol, Henri Dunantlaan 2, B-9000 Ghent, Belgium.
EM Sven.Mueller@UGent.be
OI Carlisi, Christina/0000-0002-0942-8586
FU Intramural Research Program of the National Institute of Mental Health;
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development; Intramural Research
Program of the National Institutes of Health Clinical Center; Ghent
University (Multidisciplinary Research Partnership "The integrative
neuroscience of behavioral control"); Phoqus Pharmaceuticals
FX This work was supported (in part) by The Intramural Research Programs of
the National Institute of Mental Health, the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, and the
National Institutes of Health Clinical Center. We also acknowledge the
support of Ghent University (Multidisciplinary Research Partnership "The
integrative neuroscience of behavioral control").; SCM, EWL, BC, CG, SF,
CVR, ME have nothing to declare. DPM received research funds from Phoqus
Pharmaceuticals during 2007-2008.
NR 32
TC 3
Z9 3
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4530
J9 PSYCHONEUROENDOCRINO
JI Psychoneuroendocrinology
PD MAY
PY 2013
VL 38
IS 5
BP 716
EP 721
DI 10.1016/j.psyneuen.2012.08.001
PG 6
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA 137VE
UT WOS:000318465500014
PM 22917623
ER
PT J
AU Yao, YG
Kajigaya, S
Feng, XM
Samsel, L
Mccoy, JP
Torelli, G
Young, NS
AF Yao, Yong-Gang
Kajigaya, Sachiko
Feng, Xingmin
Samsel, Leigh
McCoy, J. Philip, Jr.
Torelli, Giuseppe
Young, Neal S.
TI Accumulation of mtDNA variations in human single CD34(+) cells from
maternally related individuals: Effects of aging and family genetic
background
SO STEM CELL RESEARCH
LA English
DT Article
ID MITOCHONDRIAL-DNA MUTATIONS; CONTROL REGION; SEQUENCE HETEROGENEITY;
POINT MUTATIONS; HUMAN-DISEASE; STEM-CELLS; REPLICATION; LONGEVITY;
POPULATION; SITES
AB Marked sequence variation in the mtDNA control region has been observed in human single CD34(+) cells, which persist in vivo and are present also in differentiated hematopoietic cells. In this study, we analyzed 5071 single CD34(+) cells from 49 individuals (including 31 maternally related members from four families and 18 unrelated donors) in order to determine the mutation spectrum within the mtDNA control region in single cells, as related to aging and family genetic background. Many highly mutated sites among family members were hypervariable sites in the mtDNA control region. Further, CD34(+) cells from members of the same family also shared several unique mtDNA variants, suggesting pedigree-specific occurrence of these variants. Overall age-related accumulation of mtDNA mutations in CD34(+) cells varied in different families, suggesting a specific accumulation pattern, which might be modulated by family genetic background. Our current findings have implications for the occurrence of mtDNA mutations in hematopoietic stem cells and progenitors. (c) 2013 Elsevier B.V. All rights reserved.
C1 [Yao, Yong-Gang; Kajigaya, Sachiko; Feng, Xingmin; Samsel, Leigh; McCoy, J. Philip, Jr.; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Yao, Yong-Gang; Kajigaya, Sachiko; Feng, Xingmin; Samsel, Leigh; McCoy, J. Philip, Jr.; Young, Neal S.] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
[Yao, Yong-Gang] Chinese Acad Sci, Key Lab Anim Models & Human Dis Mech, Kunming Inst Zool, Kunming 650223, Yunnan, Peoples R China.
Univ Modena & Reggio Emilia, Dipartimento Oncol & Ematol, I-41100 Modena, Italy.
RP Yao, YG (reprint author), Chinese Acad Sci, Key Lab Anim Models & Human Dis Mech, Kunming Inst Zool, Kunming 650223, Yunnan, Peoples R China.
EM ygyaozh@gmail.com
FU Intramural Research Program of the NIH, NHLBI; Ministry of Science and
Technology of China [2011CB910900]; Yunnan Province [2009CI119]; Natural
Science Foundation of China [30925021]
FX We thank our blood donors for participating in this study and Thomas M.
Herndon and Carol Boss for their help with sample collection. This
research was supported (in part) by the Intramural Research Program of
the NIH, NHLBI. Y.-G.Y was supported by the Ministry of Science and
Technology of China (2011CB910900), Yunnan Province (2009CI119), and
Natural Science Foundation of China (30925021).
NR 39
TC 13
Z9 14
U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1873-5061
J9 STEM CELL RES
JI Stem Cell Res.
PD MAY
PY 2013
VL 10
IS 3
BP 361
EP 370
DI 10.1016/j.scr.2013.01.006
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA 135ZY
UT WOS:000318330400009
PM 23455392
ER
PT J
AU Zhu, DM
Huang, SH
McClellan, H
Dai, WL
Syed, NR
Gebregeorgis, E
Rausch, KM
Mullen, GED
Long, C
Martin, LB
Narum, D
Duffy, P
Miller, LH
Saul, A
AF Zhu, Daming
Huang, Shuhui
McClellan, Holly
Dai, Weili
Syed, Najam R.
Gebregeorgis, Elizabeth
Rausch, Kelly M.
Mullen, Gregory E. D.
Long, Carole
Martin, Laura B.
Narum, David
Duffy, Patrick
Miller, Louis H.
Saul, Allan
TI Efficient extraction of vaccines formulated in aluminum hydroxide gel by
including surfactants in the extraction buffer (vol 30, pg 189, 2012)
SO VACCINE
LA English
DT Correction
C1 [Zhu, Daming; Huang, Shuhui; McClellan, Holly; Dai, Weili; Syed, Najam R.; Gebregeorgis, Elizabeth; Rausch, Kelly M.; Mullen, Gregory E. D.; Long, Carole; Martin, Laura B.; Narum, David; Duffy, Patrick; Miller, Louis H.; Saul, Allan] NIAID, Lab Malaria Immunol & Vaccinol, NIH, Rockville, MD 20852 USA.
RP Zhu, DM (reprint author), NIAID, Lab Malaria Immunol & Vaccinol, NIH, Rockville, MD 20852 USA.
EM dzhu@niaid.nih.gov
RI Saul, Allan/I-6968-2013; Martin, Laura/N-1789-2013
OI Saul, Allan/0000-0003-0665-4091; Martin, Laura/0000-0002-4431-4381
NR 1
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD MAY 1
PY 2013
VL 31
IS 19
BP 2416
EP 2416
DI 10.1016/j.vaccine.2013.02.069
PG 1
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 136RL
UT WOS:000318381000014
ER
PT J
AU Rylance, J
Gordon, SB
Naeher, LP
Patel, A
Balmes, JR
Adetona, O
Rogalsky, DK
Martin, WJ
AF Rylance, Jamie
Gordon, Stephen B.
Naeher, Luke P.
Patel, Archana
Balmes, John R.
Adetona, Olorunfemi
Rogalsky, Derek K.
Martin, William J., II
TI Household air pollution: a call for studies into biomarkers of exposure
and predictors of respiratory disease
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE air pollution; exposure; global health; biomarkers
ID WOOD SMOKE EXPOSURE; POLYCYCLIC AROMATIC-HYDROCARBONS; CARBON-MONOXIDE;
WOODSMOKE EXPOSURE; URINARY 1-HYDROXYPYRENE; NONINVASIVE MEASUREMENT;
DEVELOPING-WORLD; RURAL GUATEMALA; HEALTHY HUMANS; TERM EXPOSURE
AB Household air pollution (HAP) from indoor burning of biomass or coal is a leading global cause of morbidity and mortality, mostly due to its association with acute respiratory infection in children and chronic respiratory and cardiovascular diseases in adults. Interventions that have significantly reduced exposure to HAP improve health outcomes and may reduce mortality. However, we lack robust, specific, and field-ready biomarkers to identify populations at greatest risk and to monitor the effectiveness of interventions. New scientific approaches are urgently needed to develop biomarkers of human exposure that accurately reflect exposure or effect. In this Perspective, we describe the global need for such biomarkers, the aims of biomarker development, and the state of development of tests that have the potential for rapid transition from laboratory bench to field use.
C1 [Rylance, Jamie; Gordon, Stephen B.] Univ Liverpool, Liverpool Sch Trop Med, Liverpool L3 5QA, Merseyside, England.
[Naeher, Luke P.; Adetona, Olorunfemi] Univ Georgia, Dept Environm Hlth Sci, Coll Publ Hlth, Athens, GA 30602 USA.
[Patel, Archana] Indira Med Coll, Nagpur, Maharashtra, India.
[Balmes, John R.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Balmes, John R.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Rogalsky, Derek K.] Georgetown Univ, Sch Med, Washington, DC USA.
[Martin, William J., II] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Martin, WJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, 31 Ctr Dr,Bldg 31,Rm 2A31, Bethesda, MD 20892 USA.
EM wjmartin@mail.nih.gov
OI Gordon, Stephen/0000-0001-6576-1116; Rylance, Jamie/0000-0002-2323-3611
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development of the National
Institutes of Health
FX This manuscript was supported in part by the Intramural Research Program
of the Eunice Kennedy Shriver National Institute of Child Health and
Human Development of the National Institutes of Health.
NR 53
TC 14
Z9 14
U1 5
U2 31
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1040-0605
J9 AM J PHYSIOL-LUNG C
JI Am. J. Physiol.-Lung Cell. Mol. Physiol.
PD MAY
PY 2013
VL 304
IS 9
BP L571
EP L578
DI 10.1152/ajplung.00416.2012
PG 8
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA 137YH
UT WOS:000318473900001
PM 23457186
ER
PT J
AU Trowbridge, MJ
Huang, TTK
Botchwey, ND
Fisher, TR
Pyke, C
Rodgers, AB
Ballard-Barbash, R
AF Trowbridge, Matthew J.
Huang, Terry T-K
Botchwey, Nisha D.
Fisher, Thomas R.
Pyke, Chris
Rodgers, Anne B.
Ballard-Barbash, Rachel
TI Public Health and the Green Building Industry Partnership Opportunities
for Childhood Obesity Prevention
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID PROMOTE PHYSICAL-ACTIVITY; BUILT ENVIRONMENT; RESEARCH AGENDA; URBAN
SPRAWL; STAIR USE; SCHOOL; CHILDREN; DESIGN; TRAVEL; IMPACT
C1 [Trowbridge, Matthew J.] Univ Virginia, Sch Med, Dept Emergency Med, Charlottesville, VA USA.
[Huang, Terry T-K] Univ Nebraska, Med Ctr, Dept Hlth Promot, Omaha, NE USA.
[Huang, Terry T-K] Univ Nebraska, Med Ctr, Social & Behav Hlth Coll Publ Hlth, Omaha, NE USA.
[Botchwey, Nisha D.] Georgia Inst Technol, Sch Architecture, Sch City & Reg Planning, Atlanta, GA USA.
[Fisher, Thomas R.] Univ Minnesota, Coll Design, Minneapolis, MN USA.
[Pyke, Chris] US Green Bldg Council, Washington, DC USA.
[Rodgers, Anne B.; Ballard-Barbash, Rachel] NIH, Natl Canc Inst, Div Canc Control & Populat Sci, Appl Res Program, Bethesda, MD 20892 USA.
RP Trowbridge, MJ (reprint author), POB 800609, Charlottesville, VA 22908 USA.
EM mtrowbridge@virginia.edu
NR 71
TC 6
Z9 6
U1 1
U2 22
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD MAY
PY 2013
VL 44
IS 5
BP 489
EP 495
DI 10.1016/j.amepre.2013.01.010
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 128XS
UT WOS:000317803600010
PM 23597813
ER
PT J
AU Chubak, J
Rutter, CM
Kamineni, A
Johnson, EA
Stout, NK
Weiss, NS
Doria-Rose, VP
Doubeni, CA
Buist, DSM
AF Chubak, Jessica
Rutter, Carolyn M.
Kamineni, Aruna
Johnson, Eric A.
Stout, Natasha K.
Weiss, Noel S.
Doria-Rose, V. Paul
Doubeni, Chyke A.
Buist, Diana S. M.
TI Measurement in Comparative Effectiveness Research
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID SECONDARY DATA SOURCES; CENTERED OUTCOMES RESEARCH; CLUSTER
RANDOMIZED-TRIALS; CANCER SCREENING-PROGRAM; CERVICAL-CANCER; VISUAL
INSPECTION; FILM MAMMOGRAPHY; ACETIC-ACID; PERFORMANCE; COUNTRIES
AB Comparative effectiveness research (CER) on preventive services can shape policy and help patients, their providers, and public health practitioners select regimens and programs for disease prevention. Patients and providers need information about the relative effectiveness of various regimens they may choose. Decision makers need information about the relative effectiveness of various programs to offer or recommend. The goal of this paper is to define and differentiate measures of relative effectiveness of regimens and programs for disease prevention. Cancer screening is used to demonstrate how these measures differ in an example of two hypothetical screening regimens and programs.
Conceptually and algebraically defined measures of relative regimen and program effectiveness also are presented. The measures evaluate preventive services that range from individual tests through organized, population-wide prevention programs. Examples illustrate how effective screening regimens may not result in effective screening programs and how measures can vary across subgroups and settings. Both regimen and program relative effectiveness measures assess benefits of prevention services in real-world settings, but each addresses different scientific and policy questions. As the body of CER grows, a common lexicon for various measures of relative effectiveness becomes increasingly important to facilitate communication and shared understanding among researchers, healthcare providers, patients, and policymakers. (Am J Prev Med 2013;44(5):513-519) (C) 2013 American Journal of Preventive Medicine
C1 [Chubak, Jessica; Rutter, Carolyn M.; Kamineni, Aruna; Johnson, Eric A.; Buist, Diana S. M.] Grp Hlth Res Inst, Seattle, WA 98101 USA.
[Chubak, Jessica; Weiss, Noel S.; Buist, Diana S. M.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Rutter, Carolyn M.] Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA.
[Rutter, Carolyn M.; Buist, Diana S. M.] Univ Washington, Sch Publ Hlth, Dept Hlth Serv, Seattle, WA 98195 USA.
[Weiss, Noel S.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
[Stout, Natasha K.] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
[Doria-Rose, V. Paul] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Doubeni, Chyke A.] Univ Penn, Perelman Sch Med, Dept Family Med & Community Hlth, Philadelphia, PA 19104 USA.
RP Chubak, J (reprint author), Grp Hlth Res Inst, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
EM chubak.j@ghc.org
OI Doria-Rose, Vincent/0000-0002-8802-5143; Doubeni,
Chyke/0000-0001-7495-0285
FU National Cancer Institute of the NIH [UC2CA148576]
FX Research reported in this publication was supported by the National
Cancer Institute of the NIH under Award Number UC2CA148576 (DSMB and
CAD). The content is solely the responsibility of the authors and does
not necessarily represent the official views of the NIH. The authors
thank Dr. Michael Von Korff, Dr. Rebecca Hubbard, and Dr. Chris
Tachibana for comments on earlier versions of the paper. This work
resulted from a collaboration generated within the HMO Cancer Research
Network (CRN), a collaboration of 14 HMOs that conducts research to
determine the effectiveness of preventive, curative, and supportive
interventions for major cancers that span the natural history of those
cancers among diverse populations and health systems.
NR 38
TC 2
Z9 2
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD MAY
PY 2013
VL 44
IS 5
BP 513
EP 519
DI 10.1016/j.amepre.2013.01.006
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 128XS
UT WOS:000317803600013
PM 23597816
ER
PT J
AU Lamers, F
Hickie, I
Merikangas, KR
AF Lamers, Femke
Hickie, Ian
Merikangas, Kathleen R.
TI Prevalence and Correlates of Prolonged Fatigue in a US Sample of
Adolescents
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID SUPPLEMENT NCS-A; COMMON MENTAL-DISORDERS; CROSS-SECTIONAL SURVEY;
RISK-FACTORS; NEURASTHENIA; COMMUNITY; CHILDREN; CARE; EPIDEMIOLOGY;
IMPAIRMENT
AB Objective: Prolonged fatigue in adolescents has a major impact on social functioning and school attendance. In adults, prolonged fatigue substantially overlaps with mood and anxiety disorders. Extending the data to adolescents, the authors studied the prevalence and correlates of fatigue in a representative U.S. sample.
Method: The participants were 10,123 adolescents ages 13-18 years from the National Comorbidity Survey Adolescent Supplement. They were interviewed about prolonged fatigue, defined as extreme fatigue with at least one associated symptom (pains, dizziness, headache, sleep disturbance, inability to relax, irritability) that does not resolve by resting or relaxing and lasting at least 3 months.
Results: The prevalence of prolonged fatigue was 3.0% (SE=0.3), with 1.4% (SE=0.2) for prolonged fatigue only and 1.6% (SE=0.2) for prolonged fatigue concomitant with a depressive or anxiety disorder. Nearly 60% of the adolescents with prolonged fatigue only had severe or very severe disability, and their rates of poor physical and mental health were comparable to those of adolescents with mood or anxiety disorders only. Adolescents with prolonged fatigue and comorbid mood or anxiety disorders had significantly greater disability, poorer mental health, and more health service use than those with either condition alone.
Conclusions: These findings suggest that prolonged fatigue is associated with disability and is an important clinical entity independent of mood and anxiety disorders in adolescents. Persistent fatigue with a comorbid mood or anxiety state is related to even more functional impairment, suggesting that prolonged fatigue may reflect greater severity of mood and anxiety disorders in adolescents. (Am J Psychiatry 2013; 170:502-510)
C1 [Merikangas, Kathleen R.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
Univ Sydney, Clin Res Unit, Brain & Mind Res Inst, Sydney, NSW 2006, Australia.
RP Merikangas, KR (reprint author), NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
EM merikank@mail.nih.gov
FU Bupa Australia; Servier; Pfizer; AstraZeneca; Pfizer (Wyeth); Eli Lilly;
Broadcast Psychiatry; Janssen Cilag; Merck Sharp; Dohme; Elixir
Healthcare Education; Australian Mental Health Leadership Program;
Australian Independent Schools of New South Wales; Australian Doctor
Education; Intelligence Squared Australia; Drinkwise Australia; Western
Australia (Labor) Government; Australian Department of Health and
Ageing; Sydney Magazine; Sydney City Council; Royal Australian and New
Zealand College of Psychiatry; Wyeth; Heart Foundation; Beyond Blue;
Bupa Foundation; NIMH Intramural Research Program through the National
Comorbidity Survey Adolescent Supplement (NCS-A) [Z01 MH-002808-08];
NIMH [U01 MH-60220]; Rubicon Fellowship from the Netherlands
Organisation for Scientific Research (NWO); Supplemental Intramural
Research Training Award from the NIMH Genetic Epidemiology Research
Branch
FX Dr. Hickie reports that 1) he currently serves on the board of the
Psychosis Australia Trust (unpaid position) and on the Defence Mental
Health Advisory Group (government committee); 2) he currently receives
fees for consulting or reports from Bupa Australia (private health
insurance) as a member of the Medical Advisory Panel; 3) he has received
travel support in the last 5 years from. Servier, AstraZeneca,
PricewaterhouseCoopers, the American Psychiatric Association, Returned
and Services League (RSL) National Congress, the Chinese Society of
Psychiatry and Neurology, Australian General Practice Network, and Focus
Sunshine Coast; 4) he has received research support in the last 5 years
from Servier and Pfizer; 5) he has received payments for educational
seminars or resources in the last 5 years from Servier, AstraZeneca,
Pfizer (Wyeth), Eli Lilly, Broadcast Psychiatry, Janssen Cilag, Merck
Sharp and Dohme, Elixir Healthcare Education, the Australian Mental
Health Leadership Program, Australian Independent Schools of New South
Wales, Australian Doctor Education, and Intelligence Squared Australia;
6) he previously had a business interest in St. George Neuropsychiatry
Pty. Ltd. (director); 7) he previously held positions at the Australian
Department of Health and Ageing (sitting fee for the National Advisory
Council on Mental Health), the Australian National Council on Drugs, and
Headspace: the National Youth Mental Health Foundation (director on
behalf of the University of Sydney, a member of the company); 8) he
previously served on the following government advisory committees:
Mental Health Expert Working Group (member), Access to Allied
Psychological Services (member of expert advisory committee), National
Advisory Council for Mental Health (member), and Common Approach to
Assessment Referral and System Task Force co-convened by the Minister
for Families, Housing, and Community Services (member); 9) he previously
received payments for consulting, reports, or advisory work from
Drinkwise Australia, Western Australia (Labor) Government, the
Australian Department of Health and Ageing, Sydney Magazine, Sydney City
Council, the Royal Australian and New Zealand College of Psychiatry,
Wyeth, and Eli Lilly; 10) his partner Dr. Elizabeth Scott is Clinical
Director of Headspace Camperdown and Cambebelltown and previously had a
business interest in Pearl 100, a partnership (ABN 55 251 484 962)
trading as The Clinical Centre and registered to S. Duncan and St.
George Neuropsychiatry Pty. Ltd.; 11) mental health research conducted
at the Brain & Mind Research Institute has been supported by Servier,
Pfizer, the Heart Foundation, Beyond Blue, and the Bupa Foundation. The
other authors report no financial relationships with commercial
interests.; Supported by NIMH Intramural Research Program grant Z01
MH-002808-08 and, through the National Comorbidity Survey Adolescent
Supplement (NCS-A) and the larger program of related NCS surveys, NIMH
grant U01 MH-60220. Dr. Lamers is supported by a Rubicon Fellowship from
the Netherlands Organisation for Scientific Research (NWO) and by a
Supplemental Intramural Research Training Award from the NIMH Genetic
Epidemiology Research Branch.
NR 32
TC 15
Z9 15
U1 2
U2 13
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD MAY
PY 2013
VL 170
IS 5
BP 502
EP 510
DI 10.1176/appi.ajp.2012.12040454
PG 9
WC Psychiatry
SC Psychiatry
GA 135XO
UT WOS:000318324200011
PM 23632835
ER
PT J
AU Orozco, MM
Enriquez, GF
Alvarado-Otegui, JA
Cardinal, MV
Schijman, AG
Kitron, U
Gurtler, RE
AF Marcela Orozco, M.
Enriquez, Gustavo F.
Alvarado-Otegui, Julian A.
Victoria Cardinal, M.
Schijman, Alejandro G.
Kitron, Uriel
Guertler, Ricardo E.
TI New Sylvatic Hosts of Trypanosoma cruzi and Their Reservoir Competence
in the Humid Chaco of Argentina: A Longitudinal Study
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID RURAL NORTHWESTERN ARGENTINA; WILD TRIATOMA-INFESTANS; CHAGAS-DISEASE
CONTROL; AMERICAN TRYPANOSOMIASIS; MOLECULAR EPIDEMIOLOGY;
DIDELPHIS-MARSUPIALIS; PARAGUAYAN CHACO; GRAN-CHACO; INFECTION; LINEAGES
AB A four-year longitudinal study of the structure of sylvatic transmission cycles of Trypanosoma cruzi, reservoir host competence and parasite discrete typing units was conducted in a disturbed rural area of the humid Chaco in Argentina. Among 190 mammals examined by xenodiagnosis and polymerase chain reaction amplification, the composite prevalence of infection was substantially higher in Dasypus novemcinctus armadillos (57.7%) and Didelphis albiventris opossums (38.1%) than in Euphractus sexcinctus (20.0%), Tolypeutes matacus (12.5%), and Chaetophractus vellerosus (6.3%) armadillos. Trypanosoma cruzi was detected for the first time in Thylamys pusilla small opossums and in two unidentified small rodents. Infection was spatially aggregated only in armadillos. All Didelphis were infected with T. cruzi I and all armadillo species were infected with T. cruzi III, implying two distinct sylvatic cycles with no inputs from the domestic cycle. Dasypus armadillos and Didelphis opossums were much more infectious to vectors than other armadillos, small opossums, or rodents.
C1 [Marcela Orozco, M.; Enriquez, Gustavo F.; Alvarado-Otegui, Julian A.; Victoria Cardinal, M.; Guertler, Ricardo E.] Univ Buenos Aires, Dept Ecol Genet & Evolut, Lab Ecoepidemiol, Buenos Aires, DF, Argentina.
[Schijman, Alejandro G.] Inst Invest Ingn Genet & Biol Mol, Lab Biol Mol Enfermedad Chagas, Buenos Aires, DF, Argentina.
[Kitron, Uriel] Emory Univ, Dept Environm Studies, Atlanta, GA 30322 USA.
NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Gurtler, RE (reprint author), Univ Buenos Aires, Dept Ecol Genet & Evolut, Lab Ecoepidemiol, Buenos Aires, DF, Argentina.
EM marcelaorozco.vet@gmail.com; gustavoenriquez@ege.fcen.uba.ar;
lavizcachasp@hotmail.com; mvcardinal@ege.fcen.uba.ar;
aleschijman@gmail.com; ukitron@emory.edu; gurtler@ege.fcen.uba.ar
FU International Development Research Center (EcoHealth Program), Tropical
Disease Research (UNICEF/PNUD/WB/WHO), University of Buenos Aires;
National Institutes of Health/National Science Foundation Ecology of
Infectious Disease program [R01 TW05836]; Fogarty International Center;
National Institute of Environmental Health Sciences
FX This study was supported by awards from the International Development
Research Center (EcoHealth Program), Tropical Disease Research
(UNICEF/PNUD/WB/WHO), University of Buenos Aires to Ricardo E. Gurtler,
and National Institutes of Health/National Science Foundation Ecology of
Infectious Disease program award R01 TW05836 funded by the Fogarty
International Center and the National Institute of Environmental Health
Sciences to Uriel Kitron, Ricardo E. Gurtler, and Joel Cohen. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript. Ricardo E.
Girder, M. Victoria Cardinal, and Alejandro G. Schijman are members of
Consejo Nacional de Investigaciones Cientificas y Tecnicas Researcher's
Career.
NR 54
TC 16
Z9 17
U1 2
U2 12
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD MAY
PY 2013
VL 88
IS 5
BP 872
EP 882
DI 10.4269/ajtmh.12-0519
PG 11
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 136WR
UT WOS:000318394600011
PM 23530075
ER
PT J
AU Hill, KP
Bennett, HE
Griffin, ML
Fitzmaurice, GM
Subramaniam, G
Woody, GE
Weiss, RD
AF Hill, Kevin P.
Bennett, Heather E.
Griffin, Margaret L.
Fitzmaurice, Garrett M.
Subramaniam, Geetha
Woody, George E.
Weiss, Roger D.
TI Association of Cannabis Use with Opioid Outcomes Among Opioid-Dependent
Youth
SO AMERICAN JOURNAL ON ADDICTIONS
LA English
DT Meeting Abstract
C1 [Hill, Kevin P.; Bennett, Heather E.; Griffin, Margaret L.; Fitzmaurice, Garrett M.; Weiss, Roger D.] McLean Hosp, Mclean, VA USA.
[Griffin, Margaret L.; Fitzmaurice, Garrett M.; Weiss, Roger D.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Subramaniam, Geetha] Natl Inst Drug Abuse, Bethesda, MD USA.
[Woody, George E.] Univ Penn, Philadelphia, PA 19104 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 1055-0496
J9 AM J ADDICTION
JI Am. J. Addict.
PD MAY-JUN
PY 2013
VL 22
IS 3
BP 310
EP 310
PG 1
WC Substance Abuse
SC Substance Abuse
GA 134RO
UT WOS:000318232200037
ER
PT J
AU Hsiao, CP
Wang, D
Kaushal, A
Saligan, L
AF Hsiao, Chao-Pin
Wang, Dan
Kaushal, Aradhana
Saligan, Leorey
TI Mitochondria-Related Gene Expression Changes Are Associated With Fatigue
in Patients With Nonmetastatic Prostate Cancer Receiving External Beam
Radiation Therapy
SO CANCER NURSING
LA English
DT Article
DE Fatigue; Gene expression; Mitochondria; Prostate cancer; Radiation
therapy
ID NORMAL TISSUE-INJURY; OXIDATIVE STRESS; RADIOTHERAPY; APOPTOSIS;
DYSFUNCTION; DEPRESSION; EXPERIENCE; PATHWAYS; SYSTEM; FAMILY
AB Background: Cancer-related fatigue (CRF) is associated with negative health outcomes and decreased health-related quality of life; however, few longitudinal studies have investigated molecular-genetic mechanisms of CRF. Objective: The objective of this study was to describe relationships between mitochondria-related gene expression changes and self-reported fatigue in prostate cancer patients receiving external beam radiation therapy (EBRT). Methods: A prospective, exploratory, and repeated-measures design was used. Self-report questionnaires and peripheral whole-blood samples were collected from 15 patients at 7 time points. Baseline data were compared against 15 healthy controls. The Human Mitochondria RT2 Profiler PCR Array was used to identify differential regulation of genes involved in mitochondrial biogenesis and function. Results: Compared with baseline, there were significant increases in fatigue scores (P = .02-.04) and changes in mitochondria-related gene expression (P = .001-.05) over time. Mean fatigue scores were 1.66 (SD, 1.66) at baseline, 3.06 (SD, 1.95) at EBRT midpoint, 2.98 (SD, 2.20) at EBRT completion, and 2.64 (SD, 2.56) at 30 days after EBRT. Over time, 11 genes related to mitochondrial function and structure were differentially expressed. Of these 11 genes, 3 (BCL2L1, FIS1, SLC25A37) were more than 2.5 fold up-regulated, and 8 (AIFM2, BCL2, IMMP2L, MIPEP, MSTO1, NEFL, SLC25A23, SLC25A4) were greater than 2-fold down-regulated. Furthermore, 8 genes (AIFM2, BCL2, FIS1, IMMP2L, MSTO1, SLC25A23, SLC25A37, SLC25A4) were significantly associated with the changes in fatigue scores. Conclusion: This study provides preliminary evidence that 8 mitochondrial function genes were significantly associated with fatigue in prostate cancer patients during EBRT. Implications for Practice: These findings identify possible pathways and early biomarkers for targeting novel interventions for CRF.
C1 [Hsiao, Chao-Pin; Wang, Dan; Saligan, Leorey] NINR, NIH, Bethesda, MD 20892 USA.
[Kaushal, Aradhana] NCI, NIH, Bethesda, MD 20892 USA.
RP Hsiao, CP (reprint author), Natl Inst Nursing Resources, NIH, 10 Ctr Dr,CRC-2-1339, Bethesda, MD 20892 USA.
EM hsiaoc@mail.nih.gov
FU Intramural Research Program of National Institute of Nursing Research
FX This study was supported by Intramural Research Program of National
Institute of Nursing Research.
NR 45
TC 11
Z9 11
U1 0
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0162-220X
J9 CANCER NURS
JI Cancer Nurs.
PD MAY-JUN
PY 2013
VL 36
IS 3
BP 189
EP 197
DI 10.1097/NCC.0b013e318263f514
PG 9
WC Oncology; Nursing
SC Oncology; Nursing
GA 135DP
UT WOS:000318266700009
PM 23047795
ER
PT J
AU Perloff, M
Steele, VE
AF Perloff, Marjorie
Steele, Vernon E.
TI Early-Phase Development of Cancer Prevention Agents: Challenges and
Opportunities
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID CLINICAL-TRIALS; DRUG
AB Chemoprevention is the administration of agents (drugs, biologics, dietary supplements, or nutrients) to reduce the risk of developing cancer or prevent the recurrence of cancer. The National Cancer Institute, Division of Cancer Prevention (NCI, DCP), is a major sponsor of cancer preventive preclinical and clinical research. As such, it has developed a comprehensive drug development program specifically designed to meet the requirements needed for cancer preventive drugs to achieve initial regulatory approval. Clinical development of cancer prevention agents presents unique challenges that are not encountered with most cancer therapeutic agents. To meet these challenges, NCI, DCP has implemented new approaches and programs, including phase 0 clinical trial designs and microdose studies. In addition, the PREVENT Cancer Program was recently implemented by NCI, DCP to offer a formalized structure for moving drugs forward in the prevention pipeline using a continue/not continue decision process. Likewise, DCP has implemented a Clinical Trials Consortium to further develop these agents. These and other approaches will be discussed in this commentary. (C) 2013 AACR.
C1 [Perloff, Marjorie; Steele, Vernon E.] NCI, Canc Prevent Div, Rockville, MD 20892 USA.
RP Perloff, M (reprint author), NCI, Canc Prevent Div, 6130 Execut Blvd EPN 2112, Rockville, MD 20892 USA.
EM perloffm@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 12
TC 4
Z9 4
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2013
VL 6
IS 5
BP 379
EP 383
DI 10.1158/1940-6207.CAPR-12-0463
PG 5
WC Oncology
SC Oncology
GA 137ZE
UT WOS:000318476600003
PM 23466485
ER
PT J
AU Armstrong, WB
Taylor, TH
Kennedy, AR
Melrose, RJ
Messadi, DV
Gu, M
Le, AD
Perloff, M
Civantos, F
Goodwin, WJ
Wirth, LJ
Kerr, AR
Meyskens, FL
AF Armstrong, William B.
Taylor, Thomas H.
Kennedy, Ann R.
Melrose, Raymond J.
Messadi, Diana V.
Gu, Mai
Le, Anh D.
Perloff, Marjorie
Civantos, Francisco
Goodwin, William Jarrard
Wirth, Lori J.
Kerr, Alexander Ross
Meyskens, Frank L., Jr.
TI Bowman Birk Inhibitor Concentrate and Oral Leukoplakia: A Randomized
Phase IIb Trial
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID PROTEASE ACTIVITY; IN-VITRO; CANCER; C-ERBB-2; CHEMOPREVENTION; SERUM;
SOY; LESIONS; RISK
AB Oral premalignancy serves as an ideal model for study of chemopreventive agents. Although 13-cis-retinoic acid showed reversal of oral premalignancy, toxicity, and reversal of clinical response after cessation of therapy obviated its widespread use. A search for nontoxic agents with cancer preventive activity led us to evaluate Bowman Birk Inhibitor (BBI) formulated as BBI Concentrate (BBIC). We previously reported encouraging results in a phase IIa trial of BBIC in patients with oral leukoplakia with measurable clinical responses and favorable biomarker changes. On the basis of these results, we undertook a randomized, placebo controlled phase IIb trial with patients receiving BBIC or placebo for 6 months, with assessment of clinical response and change in lesion area as primary end point and an intent-to-treat analysis. One hundred and thirty two subjects were randomized; and 89 subjects completed six months on study drug or placebo. Both placebo and BBIC showed a statistically significant decrease in mean lesion area of 17.1% and 20.6%, respectively, and partial or greater clinical responses of 30% and 28% respectively. No significant difference between placebo and study drug arms was observed. Histologic review, review of photographs of lesions, and comparison of serum neu protein and oral mucosal cell protease activity also did not show significant differences between study arms. Probable reasons for these negative results were considered, are discussed, and include a placebo with non-BBIC clinical activity and reduced pharmacokinetic availability of the second batch of BBIC. This experience should be a strong cautionary note to those considering "Green" chemoprevention. (C) 2013 AACR.
C1 [Armstrong, William B.; Taylor, Thomas H.; Meyskens, Frank L., Jr.] UC Irvine, Chao Family Comprehens Canc Ctr, Philadelphia, PA USA.
[Armstrong, William B.] UC Irvine, Dept Otolaryngol Head & Neck Surg, Philadelphia, PA USA.
[Taylor, Thomas H.] Univ Penn, Genet Epidemiol Res Inst, Philadelphia, PA 19104 USA.
[Taylor, Thomas H.] Univ Penn, Dept Epidemiol, Philadelphia, PA 19104 USA.
[Kennedy, Ann R.] Univ Penn, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
[Melrose, Raymond J.] Univ So Calif, Dept Pathol, Los Angeles, CA 90089 USA.
[Messadi, Diana V.] Univ Calif Los Angeles, Sch Dent, Los Angeles, CA 90024 USA.
[Gu, Mai] Univ Calif Irvine, Dept Pathol & Lab Med, Irvine, CA USA.
[Le, Anh D.] Univ Penn, Philadelphia, PA 19104 USA.
[Perloff, Marjorie] NCI, Canc Prevent Div, Rockville, MD USA.
[Civantos, Francisco; Goodwin, William Jarrard] Univ Miami, Dept Otolaryngol Head & Neck Surg, Miami, FL USA.
[Wirth, Lori J.] Harvard Univ, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kerr, Alexander Ross] NYU, Coll Dent, New York, NY USA.
RP Meyskens, FL (reprint author), Univ Calif Irvine, Chao Family Comprehens Canc Ctr, Bldg 56,Route 81,101 City Dr Canc Ctr, Orange, CA 92868 USA.
EM flmeyske@uci.edu
FU NIH [U01-CA72294, P30-CA 62203]
FX This work is supported by the NIH (U01-CA72294, P30-CA 62203; to F.L.
Meyskens).
NR 28
TC 17
Z9 18
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2013
VL 6
IS 5
BP 410
EP 418
DI 10.1158/1940-6207.CAPR-13-0004
PG 9
WC Oncology
SC Oncology
GA 137ZE
UT WOS:000318476600007
PM 23639862
ER
PT J
AU Lubet, RA
Szabo, E
Iwata, KK
Gill, SC
Tucker, C
Bode, A
Steele, VE
Juliana, MM
Nicastro, HL
Grubbs, CJ
AF Lubet, Ronald A.
Szabo, Eva
Iwata, Kenneth K.
Gill, Stanley C.
Tucker, Chris
Bode, Ann
Steele, Vernon E.
Juliana, M. Margaret
Nicastro, Holly L.
Grubbs, Clinton J.
TI Effect of Intermittent Dosing Regimens of Erlotinib on
Methylnitrosourea-Induced Mammary Carcinogenesis
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID METASTATIC BREAST-CANCER; PHASE-II; CELL-PROLIFERATION;
RANDOMIZED-TRIAL; GEFITINIB; ANASTROZOLE; PLACEBO; MODEL; MALIGNANCIES;
INHIBITOR
AB EGF receptor (EGFR) inhibitors are used in the therapy of lung and pancreatic cancers and effectively prevent cancers in multiple animal models. Although daily dosing with erlotinib is effective, weekly dosing may reduce toxicity and have advantages, particularly for prevention. We tested alternative dosing regimens for preventive/therapeutic efficacy in a rat mammary cancer model. For prevention, erlotinib was administered by gavage beginning 5 days after methylnitrosourea (MNU). For therapy and biomarker studies, rats with palpable mammary cancers were treated for six weeks or for six days, respectively. Experiment A, erlotinib (6 mg/kg body weight/day, intragastric): daily (7 times/week); one day on/one day off; and two days on/two days off. All regimens decreased tumor incidence, increased tumor latency, and decreased cancer multiplicity versus controls (P < 0.01). However, intermittent dosing was less effective than daily dosing (P < 0.05). Experiment B, erlotinib (6 mg/kg body weight/day) daily or two days on/two days off or one time per week at 42 mg/kg body weight. All regimens reduced cancer incidence and multiplicity versus controls (P < 0.01). Interestingly, daily and weekly dosing were equally effective (P > 0.5). Experiment C, erlotinib administered at 42 or 21 mg/kg body weight 1 time per week, decreased tumor incidence and multiplicity (P < 0.01). Erlotinib had a serum half-life of <= 8 hours and weekly treatment yielded effective serum levels for <= 48 hours. Daily or weekly treatment of cancer bearing rats reduced mammary tumor size 25% to 35%, whereas control cancers increased > 250%. Levels of phosphorylated extracellular signal-regulated kinase (ERK) were strongly decreased in rats treated daily/weekly with erlotinib. Thus, altering the dose of erlotinib retained most of its preventive and therapeutic efficacy, and based on prior clinical studies, is likely to reduce its toxicity. (C) 2013 AACR.
C1 [Lubet, Ronald A.; Szabo, Eva; Steele, Vernon E.; Nicastro, Holly L.] NCI, Canc Prevent Div, Bethesda, MD 20852 USA.
[Iwata, Kenneth K.] Astellas Pharmaceut LLC, Farmingdale, NY USA.
[Gill, Stanley C.; Tucker, Chris] Astellas Pharmaceut LLC, Deerfield, IL USA.
[Bode, Ann] Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
[Juliana, M. Margaret; Grubbs, Clinton J.] Univ Alabama Birmingham, Dept Surg, Birmingham, AL 35294 USA.
[Juliana, M. Margaret; Grubbs, Clinton J.] Univ Alabama Birmingham, Dept Genet, Birmingham, AL USA.
RP Lubet, RA (reprint author), NCI, Execut Plaza North,Suite 2110,6130 Execut Blvd, Bethesda, MD 20852 USA.
EM lubetr@mail.nih.gov
FU National Cancer Institute [HHSN261200433001C]
FX This study is supported by National Cancer Institute Contract no.
HHSN261200433001C.
NR 29
TC 1
Z9 1
U1 1
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2013
VL 6
IS 5
BP 448
EP 454
DI 10.1158/1940-6207.CAPR-12-0322
PG 7
WC Oncology
SC Oncology
GA 137ZE
UT WOS:000318476600011
PM 23531447
ER
PT J
AU Shakeri, R
Malekzadeh, R
Etemadi, A
Nasrollahzadeh, D
Abedi-Ardekani, B
Khoshnia, M
Islami, F
Pourshams, A
Pawlita, M
Boffetta, P
Dawsey, SM
Kamangar, F
Abnet, CC
AF Shakeri, Ramin
Malekzadeh, Reza
Etemadi, Arash
Nasrollahzadeh, Dariush
Abedi-Ardekani, Behnoush
Khoshnia, Masoud
Islami, Farhad
Pourshams, Akram
Pawlita, Michael
Boffetta, Paolo
Dawsey, Sanford M.
Kamangar, Farin
Abnet, Christian C.
TI Association of Tooth Loss and Oral Hygiene with Risk of Gastric
Adenocarcinoma
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; SQUAMOUS-CELL CARCINOMA; MALE
HEALTH-PROFESSIONALS; ESOPHAGEAL CANCER; PERIODONTAL-DISEASE; GOLESTAN
COHORT; PANCREATIC-CANCER; LIFE-STYLE; EPIDEMIOLOGY; ACETALDEHYDE
AB Poor oral health and tooth loss have been proposed as possible risk factors for some chronic diseases, including gastric cancer. However, a small number of studies have tested these associations. We conducted a case-control study in Golestan Province, Iran, that enrolled 309 cases diagnosed with gastric adenocarcinoma (118 noncardia, 161 cardia, and 30 mixed-locations) and 613 sex, age, and neighborhood matched controls. Data on oral health were obtained through physical examination and questionnaire including tooth loss, the number of decayed, missing, and filled teeth, and frequency of tooth brushing. ORs and 95% confidence intervals (95% CI) were obtained using conditional logistic regression models adjusted for potential confounders. Standard one degree-of-freedom linear trend test and a multiple degree-of-freedom global test of the effect of adding oral hygiene variables to the model were also calculated. Our results showed apparent associations between tooth loss and decayed, missing, filled teeth (DMFT) score with risk of gastric cancer, overall and at each anatomic subsite. However, these associations were not monotonic and were strongly confounded by age. The results also showed that subjects who brushed their teeth less than daily were at significantly higher risk for gastric cardia adenocarcinoma ORs (95% CI) of 5.6 (1.6-19.3). We found evidence for an association between oral health and gastric cancer, but the nonmonotonic association, the relatively strong effect of confounder adjustment, and inconsistent results across studies must temper the strength of any conclusions. (C) 2013 AACR.
C1 [Shakeri, Ramin; Malekzadeh, Reza; Etemadi, Arash; Nasrollahzadeh, Dariush; Abedi-Ardekani, Behnoush; Khoshnia, Masoud; Islami, Farhad; Pourshams, Akram] Univ Tehran Med Sci, Digest Dis Res Ctr, Tehran, Iran.
[Shakeri, Ramin; Etemadi, Arash; Dawsey, Sanford M.; Kamangar, Farin; Abnet, Christian C.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Nasrollahzadeh, Dariush] Karolinska Inst, Stockholm, Sweden.
[Abedi-Ardekani, Behnoush] IARC, Lyon, France.
[Khoshnia, Masoud] Gorgan Univ Med Sci, Golestan Res Ctr Gastroenterol & Hepatol, Gorgan, Iran.
[Islami, Farhad; Boffetta, Paolo] Mt Sinai Sch Med, Inst Translat Epidemiol, New York, NY USA.
[Islami, Farhad; Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Pawlita, Michael] Deutsch Krebsforschungszentrum DKFZ, German Canc Res Ctr, Infect & Canc Program, Genome Modificat & Carcinogenesis Div, Heidelberg, Germany.
[Dawsey, Sanford M.] Morgan State Univ, Sch Community Hlth & Policy, Dept Publ Hlth Anal, Baltimore, MD 21239 USA.
RP Abnet, CC (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM malek@ams.ac.ir; abnetc@mail.nih.gov
RI Pawlita, Labor/C-9720-2011; Abnet, Christian/C-4111-2015; Etemadi,
Arash/C-1386-2016; Abedi-Ardekani, Behnoush/O-7829-2016; Khoshnia,
Masoud/P-5665-2016; Waterboer, Tim/G-1252-2010;
OI Pawlita, Michael/0000-0002-4720-8306; Abnet,
Christian/0000-0002-3008-7843; Etemadi, Arash/0000-0002-3458-1072;
Abedi-Ardekani, Behnoush/0000-0002-0980-0587; Khoshnia,
Masoud/0000-0001-7352-8058; , Ramin/0000-0003-0487-3629; Malekzadeh,
Reza/0000-0003-1043-3814
FU Intramural NIH HHS [Z99 CA999999]
NR 42
TC 10
Z9 10
U1 0
U2 12
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 MAY
PY 2013
VL 6
IS 5
BP 477
EP 482
DI 10.1158/1940-6207.CAPR-12-0491
PG 6
WC Oncology
SC Oncology
GA 137ZE
UT WOS:000318476600014
PM 23503651
ER
PT J
AU Ittmann, M
Huang, J
Radaelli, E
Martin, P
Signoretti, S
Sullivan, R
Simons, BW
Ward, JM
Robinson, BD
Chu, GC
Loda, M
Thomas, G
Borowsky, A
Cardiff, RD
AF Ittmann, Michael
Huang, Jiaoti
Radaelli, Enrico
Martin, Philip
Signoretti, Sabina
Sullivan, Ruth
Simons, Brian W.
Ward, Jerrold M.
Robinson, Brian D.
Chu, Gerald C.
Loda, Massimo
Thomas, George
Borowsky, Alexander
Cardiff, Robert D.
TI Animal Models of Human Prostate Cancer: The Consensus Report of the New
York Meeting of the Mouse Models of Human Cancers Consortium Prostate
Pathology Committee
SO CANCER RESEARCH
LA English
DT Review
ID GENETICALLY-ENGINEERED MICE; TO-MESENCHYMAL TRANSITION; INTRAEPITHELIAL
NEOPLASIA; ANDROGEN RECEPTOR; REACTIVE STROMA; PTEN LOSS; XENOGRAFT
MODELS; IN-VIVO; EXPRESSION; GROWTH
AB Animal models, particularly mouse models, play a central role in the study of the etiology, prevention, and treatment of human prostate cancer. While tissue culture models are extremely useful in understanding the biology of prostate cancer, they cannot recapitulate the complex cellular interactions within the tumor microenvironment that play a key role in cancer initiation and progression. The National Cancer Institute (NCI) Mouse Models of Human Cancers Consortium convened a group of human and veterinary pathologists to review the current animal models of prostate cancer and make recommendations about the pathologic analysis of these models. More than 40 different models with 439 samples were reviewed, including genetically engineered mouse models, xenograft, rat, and canine models. Numerous relevant models have been developed over the past 15 years, and each approach has strengths and weaknesses. Analysis of multiple genetically engineered models has shown that reactive stroma formation is present in all the models developing invasive carcinomas. In addition, numerous models with multiple genetic alterations display aggressive phenotypes characterized by sarcomatoid carcinomas and metastases, which is presumably a histologic manifestation of epithelial-mesenchymal transition. The significant progress in development of improved models of prostate cancer has already accelerated our understanding of the complex biology of prostate cancer and promises to enhance development of new approaches to prevention, detection, and treatment of this common malignancy. (C) 2013 AACR.
C1 [Ittmann, Michael] Baylor Coll Med, Dept Pathol & Immunol, Houston, TX 77030 USA.
[Ittmann, Michael] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Huang, Jiaoti] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
[Borowsky, Alexander; Cardiff, Robert D.] Univ Calif Davis, Dept Pathol & Lab Med, Davis, CA 95616 USA.
[Borowsky, Alexander; Cardiff, Robert D.] Univ Calif Davis, Ctr Comparat Med, Davis, CA 95616 USA.
[Martin, Philip] Ctr Adv Preclin Res, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Simons, Brian W.] Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD USA.
[Ward, Jerrold M.] NIAID, Virol & Cellular Immunol Sect, Immunogenet Lab, NIH, Bethesda, MD USA.
[Signoretti, Sabina] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
Brigham & Womens Hosp, Dept Med Oncol, Boston, MA 02115 USA.
[Loda, Massimo] Harvard Univ, Sch Med, Dept Pathol, Ctr Mol Oncol Pathol, Boston, MA 02115 USA.
[Loda, Massimo] Harvard Univ, Sch Med, Dept Med Oncol, Ctr Mol Oncol Pathol, Boston, MA 02115 USA.
[Chu, Gerald C.; Loda, Massimo] Harvard Univ, Sch Med, Dept Med Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Sullivan, Ruth] Univ Wisconsin, Madison Carbone Canc Ctr, Madison, WI USA.
[Sullivan, Ruth] Res Anim Resources Ctr, Madison, WI USA.
[Sullivan, Ruth] Lab Opt & Computat Instrumentat, Madison, WI USA.
[Robinson, Brian D.] Weill Cornell Med Coll, Dept Pathol & Lab Med, New York, NY USA.
[Thomas, George] Oregon Hlth & Sci Univ, Dept Pathol & Lab Med, Portland, OR 97201 USA.
[Radaelli, Enrico] Univ Milan, Sch Vet Med, Dept Anim Pathol Hyg & Publ Hlth, Milan, Italy.
RP Ittmann, M (reprint author), Baylor Coll Med, Dept Pathol & Immunol, 1 Baylor Plaza, Houston, TX 77030 USA.
EM mittmann@bcm.edu
RI Simons, Brian/G-7352-2015
OI Simons, Brian/0000-0003-0644-211X
FU NCI: U01 Mouse Models of Human Cancers Consortium [U01CA141497, U01
CA141582]; UCLA, Pacific Northwest and DF/HCC SPOREs in Prostate Cancer
[P01 CA89021, RO1 CA131945]; UWCCC Core Grant through the OHSU-Knight
Cancer Institute [P30 CA014520, P30 CA069533 13S5]; Department of
Defense Prostate Cancer Research Program [W81XWH-11-1-0227]; Prostate
Cancer Foundation; [P30CA125123]
FX This study was supported by NCI: U01 Mouse Models of Human Cancers
Consortium (U01CA141497 and U01 CA141582); P30CA125123 (M. Ittmann);
UCLA, Pacific Northwest and DF/HCC SPOREs in Prostate Cancer, P01
CA89021 (M. Loda) and RO1 CA131945 (M. Loda); UWCCC Core Grant P30
CA014520 (R. Sullivan) P30 CA069533 13S5 through the OHSU-Knight Cancer
Institute (G. Thomas); Department of Defense Prostate Cancer Research
Program (W81XWH-11-1-0227; J. Huang); and Prostate Cancer Foundation.
NR 74
TC 64
Z9 68
U1 4
U2 27
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2013
VL 73
IS 9
BP 2718
EP 2736
DI 10.1158/0008-5472.CAN-12-4213
PG 19
WC Oncology
SC Oncology
GA 136KJ
UT WOS:000318360500002
PM 23610450
ER
PT J
AU Shan, JX
DSouza, SP
Bakhru, S
Al-Azwani, EK
Ascierto, ML
Sastry, KS
Bedri, S
Kizhakayil, D
Aigha, II
Malek, J
Al-Bozom, I
Gehani, S
Furtado, S
Mathiowitz, E
Wang, E
Marincola, FM
Chouchane, L
AF Shan, Jingxuan
DSouza, Shoba P.
Bakhru, Sasha
Al-Azwani, Eman K.
Ascierto, Maria L.
Sastry, Konduru S.
Bedri, Shahinaz
Kizhakayil, Dhanya
Aigha, Idil I.
Malek, Joel
Al-Bozom, Issam
Gehani, Salah
Furtado, Stacia
Mathiowitz, Edith
Wang, Ena
Marincola, Francesco M.
Chouchane, Lotfi
TI TNRC9 Downregulates BRCA1 Expression and Promotes Breast Cancer
Aggressiveness
SO CANCER RESEARCH
LA English
DT Article
ID TRANSCRIPTIONAL REGULATION; COPY NUMBER; MESSENGER-RNA; SUSCEPTIBILITY;
METHYLATION; GENES; RISK; POLYMORPHISMS; HETEROGENEITY; LOCALIZATION
AB Although the linkage between germline mutations of BRCA1 and hereditary breast/ovarian cancers is well established, recent evidence suggests that altered expression of wild-type BRCA1 might contribute to the sporadic forms of breast cancer. The breast cancer gene trinucleotide-repeat-containing 9 (TNRC9; TOX3) has been associated with disease susceptibility but its function is undetermined. Here, we report that TNRC9 is often amplified and overexpressed in breast cancer, particularly in advanced breast cancer. Gene amplification was associated with reduced disease-free and metastasis-free survival rates. Ectopic expression of TNRC9 increased breast cancer cell proliferation, migration, and survival after exposure to apoptotic stimuli. These phenotypes were associated with tumor progression in a mouse model of breast cancer. Gene expression profiling, protein analysis, and in silico assays of large datasets of breast and ovarian cancer samples suggested that TNRC9 and BRCA1 expression were inversely correlated. Notably, we found that TNRC9 bound to both the BRCA1 promoter and the cAMP-responsive element-binding protein (CREB) complex, a regulator of BRCA1 transcription. In support of this connection, expression of TNRC9 downregulated expression of BRCA1 by altering the methylation status of its promoter. Our studies unveil a function for TNRC9 in breast cancer that highlights a new paradigm in BRCA1 regulation. (C) 2013 AACR.
C1 [Shan, Jingxuan; DSouza, Shoba P.; Sastry, Konduru S.; Kizhakayil, Dhanya; Aigha, Idil I.; Chouchane, Lotfi] Qatar Fdn, Weill Cornell Med Coll Qatar, Lab Genet Med & Immunol, Doha, Qatar.
[Al-Azwani, Eman K.; Malek, Joel] Qatar Fdn, Weill Cornell Med Coll Qatar, Genom Core, Doha, Qatar.
[Bedri, Shahinaz] Qatar Fdn, Weill Cornell Med Coll Qatar, Biomarkers Unit, Doha, Qatar.
[Al-Bozom, Issam] Hamad Med Corp, Dept Lab Med & Pathol, Doha, Qatar.
[Gehani, Salah] Hamad Med Corp, Dept Surg, Doha, Qatar.
[Bakhru, Sasha; Furtado, Stacia; Mathiowitz, Edith] Brown Univ, Dept Mol Pharmacol Physiol & Biotechnol, Providence, RI 02912 USA.
[Bakhru, Sasha; Furtado, Stacia; Mathiowitz, Edith] Brown Univ, Ctr Biomed Engn, Providence, RI 02912 USA.
[Ascierto, Maria L.; Wang, Ena; Marincola, Francesco M.] NIH, Dept Transfus Med, Infect Dis & Immunogenet Sect, Ctr Clin, Bethesda, MD 20892 USA.
[Ascierto, Maria L.; Wang, Ena; Marincola, Francesco M.] NIH, Transnat Inst Hlth Ctr Human Immunol, Bethesda, MD 20892 USA.
RP Chouchane, L (reprint author), Qatar Fdn, Weill Cornell Med Coll Qatar, Doha, Qatar.
EM loc2008@qatar-med.cornell.edu
FU Weill Cornell Medical College in Qatar; Qatar National Research Fund
[NPRP08-083-3-031]
FX This work was supported by Weill Cornell Medical College in Qatar, and
by a grant from the Qatar National Research Fund (NPRP08-083-3-031).
NR 35
TC 10
Z9 11
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD MAY 1
PY 2013
VL 73
IS 9
BP 2840
EP 2849
DI 10.1158/0008-5472.CAN-12-4313
PG 10
WC Oncology
SC Oncology
GA 136KJ
UT WOS:000318360500013
PM 23447579
ER
PT J
AU Oubrahim, H
Wong, A
Wilson, BA
Chock, PB
AF Oubrahim, Hammou
Wong, Allison
Wilson, Brenda A.
Chock, P. Boon
TI Pasteurella multocida toxin (PMT) upregulates CTGF which leads to mTORC1
activation in Swiss 3T3 cells
SO CELLULAR SIGNALLING
LA English
DT Article
DE mTOR; PMT; CTGF; TGF beta; G alpha(q/11)
ID TISSUE-GROWTH-FACTOR; IMMEDIATE-EARLY GENE; CCN FAMILY; TGF-BETA;
SIGNALING PATHWAYS; INDUCIBLE GENE; POTENT MITOGEN; PROTEIN-KINASE;
EXPRESSION; MECHANISMS
AB Pasteurella multocida toxin (PMT) is a mitogenic protein that hijacks cellular signal transduction pathways via deamidation of heterotrimeric G proteins. We previously showed that rPMT activates mTOR signaling via a G alpha(q/11)/PLC beta/PKC mediated pathway, leading in part to cell proliferation and migration. Herein, we show that mTOR and MAPK, but not membrane-associated tyrosine kinases, are activated in serum-starved 3T3 cells by an autocrine/paracrine substance(s) secreted into the conditioned medium following rPMT treatment. Surprisingly, this diffusible factor(s) is capable of activating mTOR and MAPK pathways even in MEF G alpha(q/11) double knockout cells. Microarray analysis identified connective tissue growth factor (CTGF) mRNA as the most upregulated gene in rPMT-treated serum-starved 3T3 cells relative to untreated cells. These results were further confirmed using RT-PCR and Western blot analyses. In accord with rPMT-induced mTOR activation, upregulation of CTGF protein was observed in WT MEF, but not in G alpha(q/11) double knockout MEF cells. Although CTGF expression is regulated by TGF beta, rPMT did not activate TGF beta pathway. In addition, MEK inhibitors U0126 or PD98059, but not mTOR specific inhibitors, rapamycin and Torin 1, inhibited rPMT-induced upregulation of CTGF. Importantly, CTGF overexpression in serum-starved 3T3 cells using adenovirus led to phosphorylation of ribosomal protein S6, a downstream target of mTOR. However, despite the ability of CTGF to activate the mTOR pathway, upregulation of CTGF alone could not induce morphological changes as those observed in rPMT-treated cells. Our findings reveal that CTGF plays an important role, but there are additional factors involved in the mitogenic action of PMT.
C1 [Oubrahim, Hammou; Wong, Allison; Chock, P. Boon] NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
[Wilson, Brenda A.] Univ Illinois, Dept Microbiol, Urbana, IL 61801 USA.
RP Oubrahim, H (reprint author), NHLBI, Biochem Lab, Biochem & Biophys Ctr, NIH, Bldg 50,Room 2130,50 South Dr,MSC 8012, Bethesda, MD 20892 USA.
EM oubrahih@nhlbi.nih.gov; bchock@nih.gov
FU NIH, NHLBI; NIH/NIAID [A1038396]
FX This research was supported by the Intramural Research Program of the
NIH, NHLBI. (BAW is supported by NIH/NIAID grant #A1038396).
NR 56
TC 8
Z9 9
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0898-6568
J9 CELL SIGNAL
JI Cell. Signal.
PD MAY
PY 2013
VL 25
IS 5
BP 1136
EP 1148
DI 10.1016/j.cellsig.2013.01.026
PG 13
WC Cell Biology
SC Cell Biology
GA 136QA
UT WOS:000318377300011
PM 23415771
ER
PT J
AU Jardin, I
Dionisio, N
Frischauf, I
Berna-Erro, A
Woodard, GE
Lopez, JJ
Salido, GM
Rosado, JA
AF Jardin, Isaac
Dionisio, Natalia
Frischauf, Irene
Berna-Erro, Alejandro
Woodard, Geoffrey E.
Lopez, Jose J.
Salido, Gines M.
Rosado, Juan A.
TI The polybasic lysine-rich domain of plasma membrane-resident STIM1 is
essential for the modulation of store-operated divalent cation entry by
extracellular calcium
SO CELLULAR SIGNALLING
LA English
DT Article
DE Plasma membrane-resident STIM1; Orai1; TRPC1; Cation entry
ID ACTIVATES CRAC CHANNELS; MEDIATED CA2+ ENTRY; HUMAN-PLATELETS; TRPC
CHANNELS; ORAI1; DEPLETION; TERMINUS; SENSOR; PHOSPHORYLATION;
IDENTIFICATION
AB STIM1 acts as an endoplasmic reticulum Ca2+ sensor that communicates the filling state of the intracellular stores to the store-operated channels. In addition, STIM1 is expressed in the plasma membrane, with the Ca2+ binding EF-hand motif facing the extracellular medium; however, its role sensing extracellular Ca2+ concentrations in store-operated Ca2+ entry (SOCE), as well as the underlying mechanism remains unclear. Here we report that divalent cation entry stimulated by thapsigargin (TG) is attenuated by extracellular Ca2+ in a concentration-dependent manner. Expression of the Ca2+-binding defective STIM1(D76A) mutant did not alter the surface expression of STIM1 but abolishes the regulation of divalent cation entry by extracellular Ca2+. Orai1 and TRPC1 have been shown to play a major role in SOCE. Expression of the STIM1(D76A) mutant did not alter Orai1 phosphoserine content. TRPC1 silencing significantly attenuated TG-induced Mn2+ entry. Expression of the STIM1(K684,685E) mutant impaired the association of plasma membrane STIM1 with TRPC1, as well as the regulation of TG-induced divalent cation entry by extracellular Ca2+, which suggests that TRPC1 might be involved in the regulation of divalent cation entry by extracellular Ca2+ mediated by plasma membrane-resident STIM1. Expression of the STIM1(D76A) or STIM1(K684,685E) mutants reduced store-operated divalent cation entry and resulted in loss of dependence on the extracellular Ca2+ concentration, providing evidence for a functional role of plasma membrane-resident STIM1 in the regulation of store-operated divalent cation entry, which at least involves the EF-hand motif and the C-terminal polybasic lysine-rich domain. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Dionisio, Natalia; Berna-Erro, Alejandro; Lopez, Jose J.; Salido, Gines M.; Rosado, Juan A.] Univ Extremadura, Cell Physiol Res Grp, Dept Physiol, Caceres 10003, Spain.
[Jardin, Isaac; Frischauf, Irene] Univ Linz, Inst Biophys, A-4040 Linz, Austria.
[Woodard, Geoffrey E.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Rosado, JA (reprint author), Univ Extremadura, Cell Physiol Res Grp, Dept Physiol, Caceres 10003, Spain.
EM jarosado@unex.es
RI Salido, Gines/A-4292-2009; rosado, juan/H-3488-2015; Jardin,
Isaac/E-8310-2016; LOPEZ, JOSE/F-4602-2016
OI Salido, Gines/0000-0002-8687-2445; rosado, juan/0000-0002-9749-2325;
Jardin, Isaac/0000-0003-4575-8264; LOPEZ, JOSE/0000-0002-5234-1478
FU MICINN [BFU2010-21043-C02-01]; Junta de Extremadura [GR10010, PRE09020];
Austrian Science Fund (FWF) [P21118, M 1506-B21, V286-B21]; University
of Extremadura [D01]
FX This work was supported by MICINN grant BFU2010-21043-C02-01, Junta de
Extremadura (GR10010) and the Austrian Science Fund (FWF - project
P21118). N.D. held a fellowship from Junta de Extremadura (PRE09020).
I.J. is supported by the Austrian Science Fund (FWF - Project M
1506-B21), A. B.-E. is supported by the University of Extremadura (D01),
N.D. held a fellowship from Junta de Extremadura (PRE09020) and I.F. was
supported by the Austrian Science Fund (FWF - project V286-B21).
NR 52
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 0898-6568
J9 CELL SIGNAL
JI Cell. Signal.
PD MAY
PY 2013
VL 25
IS 5
BP 1328
EP 1337
DI 10.1016/j.cellsig.2013.01.025
PG 10
WC Cell Biology
SC Cell Biology
GA 136QA
UT WOS:000318377300032
PM 23395841
ER
PT J
AU Lieske, JC
Bondar, O
Miller, WG
Bachmann, LM
Narva, AS
Itoh, Y
Zegers, I
Schimmel, H
Phinney, K
Bunk, DM
AF Lieske, John C.
Bondar, Olga
Miller, W. Greg
Bachmann, Lorin M.
Narva, Andrew S.
Itoh, Yoshihisa
Zegers, Ingrid
Schimmel, Heinz
Phinney, Karen
Bunk, David M.
CA Natl Kidney Dis Educ Program-IFCC
TI A reference system for urinary albumin: current status
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article
DE chronic kidney disease; microalbumin; reference material; reference
method; urine albumin
ID MASS-SPECTROMETRY; SERUM-ALBUMIN; STANDARDIZATION; QUANTIFICATION
AB Background: Increased urinary excretion of albumin reflects kidney damage and is a recognized risk factor for progression of renal and cardiovascular disease. Considerable inter-method differences have been reported for both albumin and creatinine measurement results, and therefore the albumin-to-creatinine ratio. Measurement accuracy is unknown and there are no independent reference measurement procedures for albumin and no reference materials for either measurand in urine.
Methods: The National Kidney Disease Education Program (NKDEP) Laboratory Working Group and the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) have initiated joint projects to facilitate standardization of urinary albumin and creatinine measurement.
Results: A candidate LC-MS/MS reference measurement procedure for urinary albumin and candidate reference materials for urinary albumin and creatinine has been developed. The status of validations of these reference system components is reported.
Conclusions: The development of certified reference materials and reference measurement procedures for urinary albumin will enable standardization of this important measurand.
C1 [Lieske, John C.; Bondar, Olga] Mayo Clin, Renal Funct Lab, Dept Lab Med & Pathol, Div Nephrol & Hypertens,Dept Internal Med, Rochester, MN 55905 USA.
[Miller, W. Greg; Bachmann, Lorin M.] Virginia Commonwealth Univ, Dept Pathol, Richmond, VA USA.
[Narva, Andrew S.] Natl Inst Diabet & Digest Dis, Natl Kidney Dis Educ Program, NIH, Bethesda, MD USA.
[Itoh, Yoshihisa] Asahikawa Med Coll, Dept Lab Med, Asahikawa, Hokkaido 078, Japan.
[Zegers, Ingrid; Schimmel, Heinz] Commiss European Communities, Joint Res Ctr, IRMM, Geel, Belgium.
[Phinney, Karen; Bunk, David M.] NIST, Div Analyt Chem, Gaithersburg, MD 20899 USA.
RP Lieske, JC (reprint author), Mayo Clin, Renal Funct Lab, Dept Lab Med & Pathol, Div Nephrol & Hypertens,Dept Internal Med, Rochester, MN 55905 USA.
EM Lieske.John@mayo.edu
NR 12
TC 14
Z9 19
U1 1
U2 10
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD MAY
PY 2013
VL 51
IS 5
BP 981
EP 989
DI 10.1515/cclm-2012-0768
PG 9
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 138GB
UT WOS:000318495900020
PM 23241608
ER
PT J
AU Xu, ZH
Voichita, C
Draghici, S
Romero, R
AF Xu, Zhonghui
Voichita, Calin
Draghici, Sorin
Romero, Roberto
TI Z-BAG: A CLASSIFICATION ENSEMBLE SYSTEM WITH POSTERIOR PROBABILISTIC
OUTPUTS
SO COMPUTATIONAL INTELLIGENCE
LA English
DT Article
DE ensemble classifier; posterior probability; bagging; z statistic;
support vector machines
ID VECTOR MACHINE ENSEMBLE; CLASSIFIERS
AB Ensemble systems improve the generalization of single classifiers by aggregating the prediction of a set of base classifiers. Assessing classification reliability (posterior probability) is crucial in a number of applications, such as biomedical and diagnosis applications, where the cost of a misclassified input vector can be unacceptable high. Available methods are limited to either calibrate the posterior probability on an aggregated decision value or obtain a posterior probability for each base classifier and aggregate the result. We propose a method that takes advantage of the distribution of the decision values from the base classifiers to summarize a statistic which is subsequently used to generate the posterior probability. Three approaches are considered to fit the probabilistic output to the statistic: the standard Gaussian CDF, isotonic regression, and linear logistic. Even though this study focuses on a bagged support vector machine ensemble (Z-bag), our approach is not limited by the aggregation method selected, the choice of base classifiers, nor the statistic used. Performance is assessed on one artificial and 12 real-world data sets from the UCI Machine Learning Repository. Our approach achieves comparable or better generalization on accuracy and posterior estimation to existing ensemble calibration methods although lowering computational cost.
C1 [Xu, Zhonghui; Draghici, Sorin; Romero, Roberto] NICHHD, Perinatol Res Branch, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Xu, Zhonghui; Draghici, Sorin; Romero, Roberto] NICHHD, Perinatol Res Branch, Dept Hlth & Human Serv, NIH, Detroit, MI USA.
[Voichita, Calin; Draghici, Sorin] Wayne State Univ, Dept Comp Sci, Detroit, MI 48202 USA.
[Draghici, Sorin] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI 48202 USA.
[Draghici, Sorin] Wayne State Univ, Dept Clin & Translat Sci, Detroit, MI 48202 USA.
[Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI 48202 USA.
RP Draghici, S (reprint author), Wayne State Univ, Dept Comp Sci, 5057 Woodward Ave,Suite 3010, Detroit, MI 48202 USA.
EM sorin@wayne.edu
OI Draghici, Sorin/0000-0002-0786-8377
FU Perinatology Research Branch, Division of Intramural Research, National
Institute of Child Health and Human Development, NIH; [NIH R01
DK089167]; [NIH STTR R42GM087013]; [NSF DBI-0965741]
FX Any opinions, findings, and conclusions or recommendations expressed in
this material are those of the author(s) and do not necessarily reflect
the views of the NSF, NIH, or any other of the funding agencies. This
material is based upon work supported in part by the Perinatology
Research Branch, Division of Intramural Research, National Institute of
Child Health and Human Development, NIH, and the following grants: NIH
R01 DK089167, NIH STTR R42GM087013, and NSF DBI-0965741 (to S.D.)
NR 33
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0824-7935
EI 1467-8640
J9 COMPUT INTELL-US
JI Comput. Intell.
PD MAY
PY 2013
VL 29
IS 2
BP 310
EP 330
DI 10.1111/j.1467-8640.2012.00432.x
PG 21
WC Computer Science, Artificial Intelligence
SC Computer Science
GA 139EO
UT WOS:000318564800005
ER
PT J
AU Liu, MM
Chan, CC
Tuo, JS
AF Liu, Melissa M.
Chan, Chi-Chao
Tuo, Jingsheng
TI Epigenetics in Ocular Diseases
SO CURRENT GENOMICS
LA English
DT Article
DE Age-related macular generation; Cataract; Diabetic retinopathy;
Epigenetics; DNA methylation; microRNA
ID DEVELOPING MOUSE RETINA; MACULAR DEGENERATION; DNA METHYLATION; VASCULAR
INTEGRITY; GENE-EXPRESSION; MICRORNA; AGE; ANGIOGENESIS; DICER;
NEOVASCULARIZATION
AB Epigenetics pertains to heritable alterations in gene expression that do not involve modification of the underlying genomic DNA sequence. Historically, the study of epigenetic mechanisms has focused on DNA methylation and histone modifications, but the concept of epigenetics has been more recently extended to include microRNAs as well. Epigenetic patterning is modified by environmental exposures and may be a mechanistic link between environmental risk factors and the development of disease. Epigenetic dysregulation has been associated with a variety of human diseases, including cancer, neurological disorders, and autoimmune diseases. In this review, we consider the role of epigenetics in common ocular diseases, with a particular focus on DNA methylation and microRNAs. DNA methylation is a critical regulator of gene expression in the eye and is necessary for the proper development and postmitotic survival of retinal neurons. Aberrant methylation patterns have been associated with age-related macular degeneration, susceptibility to oxidative stress, cataract, pterygium, and retinoblastoma. Changes in histone modifications have also been observed in experimental models of diabetic retinopathy and glaucoma. The expression levels of specific microRNAs have also been found to be altered in the context of ocular inflammation, retinal degeneration, pathological angiogenesis, diabetic retinopathy, and ocular neoplasms. Although the complete spectrum of epigenetic modifications remains to be more fully explored, it is clear that epigenetic dysregulation is an important contributor to common ocular diseases and may be a relevant therapeutic target.
C1 [Liu, Melissa M.; Chan, Chi-Chao; Tuo, Jingsheng] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Liu, Melissa M.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Tuo, JS (reprint author), 10-10N103,10 Ctr Dr, Bethesda, MD 20892 USA.
EM tuoj@nei.nih.gov
FU NEI intramural Research Program
FX The work was supported by NEI intramural Research Program.
NR 59
TC 7
Z9 8
U1 2
U2 29
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2029
J9 CURR GENOMICS
JI Curr. Genomics
PD MAY
PY 2013
VL 14
IS 3
BP 166
EP 172
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 136FJ
UT WOS:000318347300002
PM 24179439
ER
PT J
AU Gogineni, E
Marshall, V
Miley, W
Bayat, A
Whitby, D
Kovacs, JA
Burbelo, PD
AF Gogineni, Emile
Marshall, Vickie
Miley, Wendell
Bayat, Ahmad
Whitby, Denise
Kovacs, Joseph A.
Burbelo, Peter D.
TI Quantitative determinations of anti-Kaposi sarcoma-associated
herpesvirus antibody levels in men who have sex with men
SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE
LA English
DT Article
DE Antibodies; Kaposi's Sarcoma-Associated Herpesvirus (KSHV); MSM
ID MULTICENTRIC CASTLEMAN DISEASE; HUMAN-HERPESVIRUS-8 INFECTION;
RISK-FACTORS; PREVALENCE; HIV; TRANSMISSION; ELISA
AB Infection with Kaposi sarcoma-associated herpesvirus (KSHV: also called human herpesvirus-8) is common among men who have sex with men (MSM). Here, quantitative anti-KSHV antibody levels were measured using luciferase immunoprecipitation systems (LIPS) in an MSM cohort with and without HIV from the NIH Clinical Center. Antibodies were detected using a mixture of 4 KSHV antigens in the MSM cohort and in Kaposi sarcoma (KS) patients. Along with HIV status, these results were compared with K8.1 and ORF73 ELISA, PCR virus detection, and additional LIPS testing. LIPS revealed that 25% (76/307) of the MSM cohort were KSHV seropositive, including 59 HIV+ and 17 HIV subjects. The anti-KSHV antibody levels detected by LIPS were not statistically different between the KSHV+/HIV+ and KSHV+/HIV- subgroups but were lower than the KS patients (P < 0.0001). ELISA analysis of the MSM cohort detected a 35.5% frequency of KSHV infection and showed agreement with 81% of the samples evaluated by LIPS. Further LIPS testing with v-cyclin, a second ORF73 fragment and ORF38 reconciled some of the differences observed between LIPS and the ELISA immunoassays, and the revised LIPS seroprevalence in the MSM cohort was increased to 31%. Additional quantitative antibody analysis demonstrated statistically lower KSHV antibody levels in MSM compared to KS patients, but no difference was found between KSHV infected with and without HIV coinfection. These findings also suggest that antibodies against v-cyclin and ORF38 are useful for identifying patients with asymptomatic KSHV infection. Published by Elsevier Inc.
C1 [Gogineni, Emile; Kovacs, Joseph A.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Marshall, Vickie; Miley, Wendell; Whitby, Denise] NCI, NIH, Ft Detrick, MD 21702 USA.
[Marshall, Vickie; Miley, Wendell; Whitby, Denise] NCI, Viral Oncol Sect, AIDS & Canc Virus Program, Sci Applicat Int Corp Frederick, Ft Detrick, MD 21702 USA.
[Bayat, Ahmad; Burbelo, Peter D.] Natl Inst Dent & Craniofacial Res, Neurobiol & Pain Therapeut Sect, Lab Sensory Biol, NIH, Bethesda, MD 20892 USA.
RP Burbelo, PD (reprint author), Natl Inst Dent & Craniofacial Res, Neurobiol & Pain Therapeut Sect, Lab Sensory Biol, NIH, Bethesda, MD 20892 USA.
EM burbelop@nidcr.nih.gov
FU Division of Intramural Research, National Institute of Dental and
Craniofacial Research; NIH Clinical Center; Bench to Bedside award from
the NIH Clinical Center; National Cancer Institute, National Institutes
of Health [N01-CO-12400]
FX Funding: This work was supported by the Division of Intramural Research,
National Institute of Dental and Craniofacial Research and the NIH
Clinical Center and, in part, by a Bench to Bedside award from the NIH
Clinical Center and in part with federal funds from the National Cancer
Institute, National Institutes of Health, under contract N01-CO-12400.
NR 22
TC 1
Z9 2
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0732-8893
J9 DIAGN MICR INFEC DIS
JI Diagn. Microbiol. Infect. Dis.
PD MAY
PY 2013
VL 76
IS 1
BP 56
EP 60
DI 10.1016/j.diagmicrobio.2013.02.026
PG 5
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 135YF
UT WOS:000318325900012
PM 23541691
ER
PT J
AU Tavassoli, S
Chao, JT
Young, BP
Cox, RC
Prinz, WA
de Kroon, AIPM
Loewen, CJR
AF Tavassoli, Shabnam
Chao, Jesse T.
Young, Barry P.
Cox, Ruud C.
Prinz, William A.
de Kroon, Anton I. P. M.
Loewen, Christopher J. R.
TI Plasma membrane-endoplasmic reticulum contact sites regulate
phosphatidylcholine synthesis
SO EMBO REPORTS
LA English
DT Article
DE membrane contact sites; phosphatidylcholine synthesis; Opi3; Osh3; Pah1
ID SACCHAROMYCES-CEREVISIAE; LIPIN HOMOLOG; CORTICAL ER; YEAST; PROTEINS;
METABOLISM; CELL; METHYLTRANSFERASE; HOMEOSTASIS; REVEALS
AB Synthesis of phospholipids, sterols and sphingolipids is thought to occur at contact sites between the endoplasmic reticulum (ER) and other organelles because many lipid-synthesizing enzymes are enriched in these contacts. In only a few cases have the enzymes been localized to contacts in vivo and in no instances have the contacts been demonstrated to be required for enzyme function. Here, we show that plasma membrane (PM)-ER contact sites in yeast are required for phosphatidylcholine synthesis and regulate the activity of the phosphatidylethanolamine N-methyltransferase enzyme, Opi3. Opi3 activity requires Osh3, which localizes to PM-ER contacts where it might facilitate in trans catalysis by Opi3. Thus, membrane contact sites provide a structural mechanism to regulate lipid synthesis.
C1 [Tavassoli, Shabnam; Chao, Jesse T.; Young, Barry P.; Loewen, Christopher J. R.] Univ British Columbia, Inst Life Sci, Dept Cellular & Physiol Sci, Vancouver, BC V6T 1Z3, Canada.
[Cox, Ruud C.; de Kroon, Anton I. P. M.] Univ Utrecht, Bijvoet Ctr, Dept Membrane Biochem & Biophys, NL-3584 CH Utrecht, Netherlands.
[Cox, Ruud C.; de Kroon, Anton I. P. M.] Univ Utrecht, Inst Biomembranes, NL-3584 CH Utrecht, Netherlands.
[Prinz, William A.] NIDDKD, Lab Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Loewen, CJR (reprint author), Univ British Columbia, Inst Life Sci, Dept Cellular & Physiol Sci, 2350 Hlth Sci Mall, Vancouver, BC V6T 1Z3, Canada.
EM cloewen@mail.ubc.ca
RI de Kroon, Anton/O-4119-2016
FU Canadian Institutes of Health Research; Michael Smith Foundation for
Health Research; Canadian Foundation for Innovation
FX We thank W. Vogel and also the UBC Bio-imaging Facility for their
technical expertise with transmission electron microscopy. This work was
supported by the Canadian Institutes of Health Research, the Michael
Smith Foundation for Health Research and the Canadian Foundation for
Innovation.
NR 26
TC 37
Z9 38
U1 0
U2 17
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD MAY
PY 2013
VL 14
IS 5
BP 434
EP 440
DI 10.1038/embor.2013.36
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 138AQ
UT WOS:000318481000009
PM 23519169
ER
PT J
AU Wong, ACY
Birnbaumer, L
Housley, GD
AF Wong, Ann Chi Yan
Birnbaumer, Lutz
Housley, Gary D.
TI Canonical transient receptor potential channel subtype 3-mediated hair
cell Ca2+entry regulates sound transduction and auditory
neurotransmission
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE auditory brainstem response; Ca2+imaging; canonical transient receptor
potential channel subtype3 (TRPC3); cochlear hair cell; distortion
product otoacoustic emission; knockout mouse
ID GUINEA-PIG COCHLEA; METABOTROPIC GLUTAMATE RECEPTORS; INTRACELLULAR
CA2+; SYNAPTIC-TRANSMISSION; TRPC3/6/7 SUBFAMILY; CATION CHANNELS;
PLASMA-MEMBRANE; BINDING DOMAIN; ION CHANNELS; GROUP-I
AB The physiological significance of canonical transient receptor potential (TRPC) ion channels in sensory systems is rapidly emerging. Heterologous expression studies show that TRPC3 is a significant Ca2+ entry pathway, with dual activation via G protein-coupled receptor (GPCR)phospholipase Cdiacylglycerol second messenger signaling, and through negative feedback, whereby a fall in cytosolic Ca2+ releases Ca2+calmodulin channel block. We hypothesised that the latter process contributes to cochlear hair cell cytosolic Ca2+ homeostasis. Confocal microfluorimetry with the Ca2+ indicator Fluo-4 acetoxymethylester showed that, when cytosolic Ca2+ was depleted, Ca2+ re-entry was significantly impaired in mature TRPC3/ inner and outer hair cells. The impact of this disrupted Ca2+ homeostasis on sound transduction was assessed with the use of distortion product otoacoustic emissions (DPOAEs), which constitute a direct measure of the outer hair cell transduction that underlies hearing sensitivity and frequency selectivity. TRPC3/ mice showed significantly stronger DPOAE (2f1f2) growth functions than wild-type (WT) littermates within the frequency range of best hearing acuity. This translated to hyperacusis (decreased threshold) measured by the auditory brainstem response (ABR). TRPC3/ and WT mice did not differ in the levels of temporary and permanent threshold shift arising from noise exposure, indicating that potential GPCR signaling via TRPC3 is not pronounced. Overall, these data suggest that the Ca2+ set-point in the hair cell, and hence membrane conductance, is modulated by TRPC3s through their function as a negative feedback-regulated Ca2+ entry pathway. This TPRC3-regulated Ca2+ homeostasis shapes the sound transduction inputoutput function and auditory neurotransmission.
C1 [Wong, Ann Chi Yan; Housley, Gary D.] Univ New S Wales, Translat Neurosci Facil, Sydney, NSW 2052, Australia.
[Wong, Ann Chi Yan; Housley, Gary D.] Univ New S Wales, Sch Med Sci, Dept Physiol, Sydney, NSW 2052, Australia.
[Birnbaumer, Lutz] NIEHS, Neurobiol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Housley, GD (reprint author), Univ New S Wales, Translat Neurosci Facil, Sydney, NSW 2052, Australia.
EM g.housley@unsw.edu.au
OI Wong, Ann CY/0000-0001-7011-0369
FU Australian Research Council [ARC DP1097202]; NIH [Z01-ES-101684]
FX We acknowledge funding support from the Australian Research Council (ARC
DP1097202) and the Intramural Research Program of the NIH (Z01-ES-101684
to L. Birnbaumer).
NR 42
TC 9
Z9 9
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD MAY
PY 2013
VL 37
IS 9
BP 1478
EP 1486
DI 10.1111/ejn.12158
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 137OG
UT WOS:000318444700012
PM 23442051
ER
PT J
AU Jupp, B
Caprioli, D
Saigal, N
Reverte, I
Shrestha, S
Cumming, P
Everitt, BJ
Robbins, TW
Dalley, JW
AF Jupp, Bianca
Caprioli, Daniele
Saigal, Niel
Reverte, Ingrid
Shrestha, Saurav
Cumming, Paul
Everitt, Barry J.
Robbins, Trevor W.
Dalley, Jeffrey W.
TI Dopaminergic and GABA-ergic markers of impulsivity in rats: evidence for
anatomical localisation in ventral striatum and prefrontal cortex
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE autoradiography; dopamine; GABA; nucleus accumbens; opioid; serotonin
ID NUCLEUS-ACCUMBENS CORE; REACTION-TIME-TASK; DEFICIT HYPERACTIVITY
DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; INHIBITORY RESPONSE
CONTROL; DORSAL ANTERIOR CINGULATE; NMDA RECEPTOR ANTAGONISM;
GAMMA-AMINOBUTYRIC-ACID; ORBITOFRONTAL CORTEX; DOUBLE DISSOCIATION
AB Accumulating evidence indicates that impulsivity, in its multiple forms, involves cortical and subcortical mechanisms and abnormal dopamine (DA) transmission. Although decreased DA D2/D3 receptor availability in the nucleus accumbens (NAcb) predicts trait-like impulsivity in rats it is unclear whether this neurochemical marker extends to both the NAcb core (NAcbC) and shell (NAcbS) and whether markers for other neurotransmitter systems implicated in impulsivity such as serotonin (5-HT), endogenous opioids and -amino-butyric acid (GABA) are likewise altered in impulsive rats. We therefore used autoradiography to investigate DA transporter (DAT), 5-HT transporter (5-HTT) and D1, D2/D3, -opioid and GABA(A) receptor binding in selected regions of the prefrontal cortex and striatum in rats expressing low and high impulsive behaviour on the five-choice serial reaction-time task. High-impulsive (HI) rats exhibited significantly lower binding for DAT and D2/D3 receptors in the NAcbS and for D1 receptors in the NAcbC compared with low-impulsive (LI) rats. HI rats also showed significantly lower GABA(A) receptor binding in the anterior cingulate cortex. For all regions where receptor binding was altered in HI rats, binding was inversely correlated with impulsive responding on task. There were no significant differences in binding for 5-HTT or -opioid receptors in any of the regions investigated. These results indicate that altered D2/D3 receptor binding is localised to the NAcbS of trait-like impulsive rats and is accompanied by reduced binding for DAT. Alterations in binding for D1 receptors in the NAcbC and GABA(A) receptors in the anterior cingulate cortex demonstrate additional markers and putative mechanisms underlying the expression of behavioural impulsivity.
C1 [Jupp, Bianca; Caprioli, Daniele; Saigal, Niel; Everitt, Barry J.; Robbins, Trevor W.; Dalley, Jeffrey W.] Univ Cambridge, Behav & Clin Neurosci Inst, Cambridge CB2 3EB, England.
[Jupp, Bianca; Caprioli, Daniele; Saigal, Niel; Everitt, Barry J.; Robbins, Trevor W.; Dalley, Jeffrey W.] Univ Cambridge, Dept Psychol, Cambridge CB2 3EB, England.
[Jupp, Bianca] Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3052, Australia.
[Reverte, Ingrid] Univ Rovira & Virgili, IISPV, Sch Med, Lab Toxicol & Environm Hlth, E-43201 Reus, Spain.
[Reverte, Ingrid] Univ Rovira & Virgili, Dept Psychol, Terragona, Spain.
[Reverte, Ingrid] Univ Rovira & Virgili, Res Ctr Behav Assessment CRAMC, Terragona, Spain.
[Shrestha, Saurav] NIMH, IRP, Bethesda, MD 20892 USA.
[Cumming, Paul] Univ Munich, Dept Nucl Med, Munich, Germany.
[Dalley, Jeffrey W.] Univ Cambridge, Addenbrookes Hosp, Dept Psychiat, Cambridge CB2 3EB, England.
RP Dalley, JW (reprint author), Univ Cambridge, Dept Psychol, Downing St, Cambridge CB2 3EB, England.
EM jwd20@cam.ac.uk
RI Reverte, Ingrid/A-4164-2014; Reverte, Ingrid/I-1225-2015;
OI Reverte, Ingrid/0000-0002-4120-9324; Everitt, Barry/0000-0003-4431-6536
FU UK Medical Research Council within the MRC [MRC: G0701500, G0802729];
NHMRC, Australia [1016313]; MRC; Wellcome Trust
FX This research was supported by the UK Medical Research Council (MRC:
G0701500, G0802729) within the MRC-funded ICCAM consortium, a research
fellowship to B.J. (NHMRC, Australia: 1016313) and by a joint award from
the MRC and Wellcome Trust in support of the Behavioural and Clinical
Neuroscience Institute at Cambridge University.
NR 74
TC 34
Z9 34
U1 3
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD MAY
PY 2013
VL 37
IS 9
BP 1519
EP 1528
DI 10.1111/ejn.12146
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 137OG
UT WOS:000318444700016
PM 23368520
ER
PT J
AU Oza, NM
Siegenthaler, M
Horvath, K
Rosing, DR
Chen, MY
Arai, AE
Gould, HN
Bakalov, V
Bondy, CA
AF Oza, Nishaki Mehta
Siegenthaler, Michael
Horvath, Keith
Rosing, Douglas R.
Chen, Marcus Y.
Arai, Andrew E.
Gould, Harley N.
Bakalov, Vladimir
Bondy, Carolyn A.
TI Serious aortic complications in a patient with Turner syndrome
SO EUROPEAN JOURNAL OF PEDIATRICS
LA English
DT Article
DE Aortic dissection; X chromosome; Hypoplastic aorta; Congenital heart
defect
AB An asymptomatic young woman was discovered to have life-threatening aneurysms and dissection of the thoracic aorta during routine evaluation in a Turner syndrome (TS) study. The presence of a heart murmur and hypertension had led to diagnosis and surgical repair of an atrial septal defect at age 5 and of aortic coarctation at age 12. The diagnosis of TS was made at 16 years of age due to short stature and delayed pubertal development. She was treated with growth hormone from age 16 to 18 and with atenolol, thyroid hormone, and estrogen. She discontinued her medications and was lost to medical follow-up at age 20. Upon presenting here at age 26, she reported a very active lifestyle, including vigorous exercise and an acting career, with no symptoms of chest or back pain or shortness of breath. Cardiovascular imaging revealed aortic regurgitation, an unsuspected dissection of a severely dilated ascending aorta, and a large descending aortic aneurysm. She required surgical replacement of her aortic valve and ascending aorta, followed by endovascular repair of the descending aortic aneurysm. This patient illustrates the importance of considering the diagnosis of TS in girls with congenital aortic defects and the absolute necessity for close, expert follow-up of these patients who are at high risk for complications after surgical repair due to an underlying aortopathy, hypertension, and metabolic disorders. This patient also emphasizes the need to publicize and follow screening guidelines as there is an increasing number of patients with congenital defects who need transition to adult care.
C1 [Oza, Nishaki Mehta] Ohio State Univ, Columbus, OH 43210 USA.
[Siegenthaler, Michael; Horvath, Keith; Rosing, Douglas R.; Chen, Marcus Y.; Arai, Andrew E.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Gould, Harley N.; Bakalov, Vladimir; Bondy, Carolyn A.] NICHHD, NIH, Bethesda, MD 20892 USA.
RP Bondy, CA (reprint author), NICHHD, NIH, CRC 1-3330,10 Ctr Dr, Bethesda, MD 20892 USA.
EM bondyc@mail.nih.gov
FU NIH [1 Z01 HL004607-08 CE]
FX This work was supported by the intramural research program of the NIH
including 1 Z01 HL004607-08 CE.
NR 6
TC 4
Z9 4
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6199
J9 EUR J PEDIATR
JI Eur. J. Pediatr.
PD MAY
PY 2013
VL 172
IS 5
BP 703
EP 705
DI 10.1007/s00431-012-1808-3
PG 3
WC Pediatrics
SC Pediatrics
GA 131GI
UT WOS:000317980400018
PM 22923005
ER
PT J
AU Pacher, P
Kunos, G
AF Pacher, Pal
Kunos, George
TI Modulating the endocannabinoid system in human health and disease
successes and failures
SO FEBS JOURNAL
LA English
DT Review
DE cannabinoids; clinical trials; disease; endocannabinoid system; human;
pharmacology; therapeutic potential
ID CANNABINOID CB2 RECEPTORS; ACID AMIDE HYDROLASE; HEPATIC
ISCHEMIA/REPERFUSION INJURY; ISCHEMIA-REPERFUSION INJURY;
CORONARY-ARTERY-DISEASE; CEREBRAL ISCHEMIC/REPERFUSION INJURY;
AMYOTROPHIC-LATERAL-SCLEROSIS; ACUTE MYOCARDIAL-INFARCTION; HUMAN
MONOCYTE MIGRATION; FOS PROTEIN EXPRESSION
AB The discovery of the endocannabinoid system, comprising the G-protein coupled cannabinoid 1 and 2 receptors (CB1/2), their endogenous lipid ligands or endocannabinoids, and synthetic and metabolizing enzymes, has triggered an avalanche of experimental studies implicating the endocannabinoid system in a growing number of physiological/pathological functions. These studies have also suggested that modulating the activity of the endocannabinoid system holds therapeutic promise for a broad range of diseases, including neurodegenerative, cardiovascular and inflammatory disorders; obesity/metabolic syndrome; cachexia; chemotherapy-induced nausea and vomiting; and tissue injury and pain, amongst others. However, clinical trials with globally acting CB1 antagonists in obesity/metabolic syndrome, and other studies with peripherally-restricted CB1/2 agonists and inhibitors of the endocannabinoid metabolizing enzyme in pain, have introduced unexpected complexities, suggesting that a better understanding of the pathophysiological role of the endocannabinoid system is required to devise clinically successful treatment strategies.
C1 [Pacher, Pal; Kunos, George] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
RP Pacher, P (reprint author), NIAAA, Lab Physiol Studies, NIH, 5625 Fishers Lane,MSC 9413, Bethesda, MD 20892 USA.
EM pacher@mail.nih.gov
RI Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU NIAAA
FX This study was supported by funds from the Intramural Research Program
of NIAAA to P.P. and G.K. The authors apologize to colleagues whose
important work could not be cited because of space limitations.
NR 281
TC 117
Z9 122
U1 5
U2 70
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1742-464X
J9 FEBS J
JI FEBS J.
PD MAY
PY 2013
VL 280
IS 9
BP 1918
EP 1943
DI 10.1111/febs.12260
PG 26
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 135GQ
UT WOS:000318277000005
PM 23551849
ER
PT J
AU Lieber, SR
Millum, J
AF Lieber, Sarah R.
Millum, Joseph
TI Preventing Sin: The Ethics of Vaccines Against Smoking
SO HASTINGS CENTER REPORT
LA English
DT Article
ID NICOTINE CONJUGATE VACCINE; MANIPULATION; DEPENDENCE; SAFETY;
IMMUNOGENICITY; EFFICACY; AUTONOMY; ALCOHOL; MORTALITY; SMOKERS
AB The alarming rates of smoking, obesity, and substance abuse pose an enormous challenge for parents and public health officials: how do we prevent children and adolescents from adopting unhealthy behaviors? One new option that may soon be available is the use of nicotine vaccines. Immunological therapies to help smokers stop smoking have shown promise in phase I and II trials; similar therapies could combat smoking addiction before it starts. Nicotine vaccines are distinctive because they confer protection not against infectionthe normal target for vaccinesbut against enticing pleasures that lead to unhealthy behaviors. As a result, using them preventively in children would be likely to arouse some novel ethical concerns that should be addressed before the vaccines become commonly available and their off-label use as a preventive measure becomes a real option. In this paper, we consider whether it would be ethical for parents to vaccinate their children against smoking if a nicotine vaccine were to be proven effective as a preventive intervention for children or adolescents. We begin by explaining the current state of nicotine vaccine science and suggesting some likely ethical concerns about allowing parents to have their children receive a vaccine. We then present a preliminary argument for making vaccination permissible, at least if nicotine vaccination substantially reduces the probability that someone subsequently becomes a smoker. We consider a series of possible ethical objections, which are useful for identifying the conditions under which it would be ethical for parents to vaccinate their children against smoking. We conclude that it would be permissible for parents to give their child a nicotine vaccine if the following conditions were met: the vaccine is expected to result in a net benefit to each individual vaccinated, the expected harms from the side effects of the vaccine are lower than the nonvoluntary harms caused by smoking, and there are no other, less manipulative methods available that are as effective at preventing smoking initiation.
C1 [Lieber, Sarah R.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Millum, Joseph] NIH, Ctr Clin, Dept Bioeth, Bethesda, MD USA.
[Millum, Joseph] NIH, Fogarty Int Ctr, Bethesda, MD USA.
RP Lieber, SR (reprint author), Univ Michigan, Ann Arbor, MI 48109 USA.
FU Intramural NIH HHS [Z99 CL999999]
NR 62
TC 4
Z9 4
U1 0
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0093-0334
J9 HASTINGS CENT REP
JI Hastings Cent. Rep.
PD MAY-JUN
PY 2013
VL 43
IS 3
BP 23
EP 33
DI 10.1002/hast.159
PG 11
WC Ethics; Health Care Sciences & Services; Medical Ethics; Social
Sciences, Biomedical
SC Social Sciences - Other Topics; Health Care Sciences & Services; Medical
Ethics; Biomedical Social Sciences
GA 138WJ
UT WOS:000318541100014
PM 23650065
ER
PT J
AU Geeraert, P
Williams, JS
Brownell, I
AF Geeraert, Pieter
Williams, Jonathan S.
Brownell, Isaac
TI Targeting the Hedgehog Pathway to Treat Basal Cell Carcinoma
SO JOURNAL OF DRUGS IN DERMATOLOGY
LA English
DT Article
ID SONIC-HEDGEHOG; NEVUS SYNDROME; SKIN-CANCER; SMOOTHENED ANTAGONISTS;
ACQUIRED-RESISTANCE; HUMAN HOMOLOG; MUTATIONS; IDENTIFICATION;
INHIBITION; DROSOPHILA
AB The discovery of mutations that activate hedgehog (Hh) signaling in basal cell carcinoma (BCC) and other cancers has spurred the development of small molecule inhibitors that target the Hh pathway. High-throughput screens have identified a number of drug candidates that antagonize smoothened (SMO), an essential protein in the Hh signaling pathway. Clinical studies of the oral SMO inhibitor vismodegib (GDC-0449) in patients with inoperable or metastatic BCC have led to its recent approval by the US Food and Drug Administration. This review aims to give the clinician an overview of vismodegib and other Hh pathway inhibitors in the treatment of patients with advanced BCC and basal cell nevus syndrome. Issues of drug mechanism, efficacy, safety, tolerability, and tumor resistance are addressed.
C1 [Geeraert, Pieter] Univ Hosp, Dept Radiol, Brussels, Belgium.
[Geeraert, Pieter] NHLBI, NIH, Bethesda, MD 20892 USA.
[Williams, Jonathan S.; Brownell, Isaac] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
RP Brownell, I (reprint author), NCI, Dermatol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM Isaac.brownell@nih.gov
FU National Institutes of Health (NIH) Intramural Research Program, Center
of Cancer Research, National Cancer Institute
FX Dr. Geeraert is a Belgian American Education Foundation Fellow. This
publication was supported by the National Institutes of Health (NIH)
Intramural Research Program, Center of Cancer Research, National Cancer
Institute. Its contents are solely the responsibility of the authors and
do not necessarily represent the official views of the NIH.
NR 42
TC 9
Z9 10
U1 0
U2 10
PU JOURNAL OF DRUGS IN DERMATOLOGY
PI NEW YORK
PA 377 PARK AVE SOUTH, 6TH FLOOR, NEW YORK, NY 10016 USA
SN 1545-9616
J9 J DRUGS DERMATOL
JI J. Drugs Dermatol.
PD MAY
PY 2013
VL 12
IS 5
BP 519
EP 523
PG 5
WC Dermatology
SC Dermatology
GA 136WV
UT WOS:000318395000005
PM 23652945
ER
PT J
AU Kempadoo, KA
Tourino, C
Cho, SL
Magnani, F
Leinninger, GM
Stuber, GD
Zhang, F
Myers, MG
Deisseroth, K
de Lecea, L
Bonci, A
AF Kempadoo, Kimberly A.
Tourino, Clara
Cho, Saemi L.
Magnani, Francesco
Leinninger, Gina-Marie
Stuber, Garret D.
Zhang, Feng
Myers, Martin G.
Deisseroth, Karl
de Lecea, Luis
Bonci, Antonello
TI Hypothalamic Neurotensin Projections Promote Reward by Enhancing
Glutamate Transmission in the VTA
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID VENTRAL TEGMENTAL AREA; LONG-TERM POTENTIATION; NUCLEUS-ACCUMBENS;
SYNAPTIC PLASTICITY; DOPAMINE NEURONS; BEHAVIORAL SENSITIZATION;
POSITIVE REINFORCEMENT; SEEKING BEHAVIOR; COCAINE-SEEKING;
NMDA-RECEPTORS
AB The lateral hypothalamus (LH) sends a dense glutamatergic and peptidergic projection to dopamine neurons in the ventral tegmental area (VTA), a cell group known to promote reinforcement and aspects of reward. The role of the LH to VTA projection in reward-seeking behavior can be informed by using optogenetic techniques to dissociate the actions of LH neurons from those of other descending forebrain inputs to the VTA. In the present study, we identify the effect of neurotensin (NT), one of the most abundant peptides in the LH to VTA projection, on excitatory synaptic transmission in the VTA and reward-seeking behavior. Mice displayed robust intracranial self-stimulation of LH to VTA fibers, an operant behavior mediated by NT 1 receptors (Nts1) and NMDA receptors. Whole-cell patch-clamp recordings of VTA dopamine neurons demonstrated that NT (10 nM) potentiated NMDA-mediated EPSCs via Nts1. Results suggest that NT release from the LH into the VTA activates Nts1, thereby potentiating NMDA-mediated EPSCs and promoting reward. The striking behavioral and electrophysiological effects of NT and glutamate highlight the LH to VTA pathway as an important component of reward.
C1 [Kempadoo, Kimberly A.; Cho, Saemi L.; Magnani, Francesco; Stuber, Garret D.; Bonci, Antonello] Ernest Gallo Clin & Res Ctr, Emeryville, CA 94608 USA.
[Kempadoo, Kimberly A.] Univ Calif San Francisco, Neurosci Grad Program, San Francisco, CA 94158 USA.
[Tourino, Clara; Zhang, Feng; Deisseroth, Karl; de Lecea, Luis] Stanford Univ, Dept Neurosci, Palo Alto, CA 94305 USA.
[Leinninger, Gina-Marie; Myers, Martin G.] Univ Michigan, Dept Neurosci, Ann Arbor, MI 48105 USA.
[Bonci, Antonello] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA.
[Bonci, Antonello] NIDA, Intramural Program, Baltimore, MD 21224 USA.
[Bonci, Antonello] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
RP Bonci, A (reprint author), NIDA IRP, 251 Bayview Blvd,Room 04A521, Baltimore, MD 21224 USA.
EM antonello.bonci@nih.gov
RI Stuber, Garret/E-1160-2011
FU National Institute on Drug Abuse; National Institute of General Medical
Sciences; National Institute of Mental Health; Klarman Family
Foundation; State of California
FX This work was supported by the National Institute on Drug Abuse
Intramural Research Program, the National Institute of General Medical
Sciences, the National Institute of Mental Health, the Klarman Family
Foundation, and the State of California. We thank Adrianne Kisch-Hancock
for assistance with histology; Howard L. Fields, Stephanie L. Borgland,
Viktor Kharazia, and Steven P. Lieske for intellectual discussions
regarding this work; and Roy A. Wise for comments on the manuscript.
NR 60
TC 56
Z9 58
U1 2
U2 7
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 1
PY 2013
VL 33
IS 18
BP 7618
EP +
DI 10.1523/JNEUROSCI.2588-12.2013
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 137FH
UT WOS:000318420400002
PM 23637156
ER
PT J
AU Calejo, AI
Jorgacevski, J
Kucka, M
Kreft, M
Goncalves, PP
Stojilkovic, SS
Zorec, R
AF Calejo, Ana Isabel
Jorgacevski, Jernej
Kucka, Marek
Kreft, Marko
Goncalves, Paula P.
Stojilkovic, Stanko S.
Zorec, Robert
TI cAMP-Mediated Stabilization of Fusion Pores in Cultured Rat Pituitary
Lactotrophs
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID KISS-AND-RUN; DENSE-CORE VESICLES; PROTEIN-KINASE-A; NEUROENDOCRINE
CELLS; MEMBRANE CAPACITANCE; CHROMAFFIN CELLS; REGULATED EXOCYTOSIS;
PEPTIDERGIC VESICLES; TRANSMITTER RELEASE; BOVINE LACTOTROPHS
AB Regulated exocytosis mediates the release of hormones and transmitters. The last step of this process is represented by the merger between the vesicle and the plasma membranes, and the formation of a fusion pore. Once formed, the initially stable and narrow fusion pore may reversibly widen (transient exocytosis) or fully open (full-fusion exocytosis). Exocytosis is typically triggered by an elevation in cytosolic calcium activity. However, other second messengers, such as cAMP, have been reported to modulate secretion. The way in which cAMP influences the transitions between different fusion pore states remains unclear. Here, hormone release studies show that prolactin release from isolated rat lactotrophs stimulated by forskolin, an activator of adenylyl cyclases, and by membrane-permeable cAMP analog (dbcAMP), exhibit a biphasic concentration dependency. Although at lower concentrations (2-10 mu M forskolin and 2.5-5 mM dbcAMP) these agents stimulate prolactin release, an inhibition is measured at higher concentrations (50 mu M forskolin and 10-15 mM dbcAMP). By using high-resolution capacitance (C-m) measurements, we recorded discrete increases in C-m, which represent elementary exocytic events. An elevation of cAMP leaves the frequency of full-fusion events unchanged while increasing the frequency of transient events. These exhibited a wider fusion pore as measured by increased fusion pore conductance and a prolonged fusion pore dwell time. The probability of observing rhythmic reopening of transient fusion pores was elevated by dbcAMP. In conclusion, cAMP-mediated stabilization of wide fusion pores prevents vesicles from proceeding to the full-fusion stage of exocytosis, which hinders vesicle content discharge at high cAMP concentrations.
C1 [Calejo, Ana Isabel; Goncalves, Paula P.] Univ Aveiro, Dept Biol, Ctr Environm & Marine Studies, P-3810193 Aveiro, Portugal.
[Calejo, Ana Isabel; Jorgacevski, Jernej; Kreft, Marko; Zorec, Robert] Univ Ljubljana, Lab Neuroendocrinol Mol Cell Physiol, Fac Med, Ljubljana 1000, Slovenia.
[Jorgacevski, Jernej; Kreft, Marko; Zorec, Robert] Celica Biomed Ctr, Ljubljana 1000, Slovenia.
[Kucka, Marek; Stojilkovic, Stanko S.] NICHHD, Sect Cellular Signaling, Dev Neurosci Program, NIH, Bethesda, MD 20892 USA.
[Kreft, Marko] Univ Ljubljana, Biotech Fac, Dept Biol, Ljubljana 1000, Slovenia.
RP Zorec, R (reprint author), Univ Ljubljana, Fac Med, Inst Pathophysiol, LN MCP, Zaloska 4, Ljubljana 1000, Slovenia.
EM robert.zorec@mf.uni-lj.si
RI Polonia Goncalves, Maria Paula/B-1056-2011; CESAM, UA/M-3762-2015;
OI Polonia Goncalves, Maria Paula/0000-0001-6891-3963; Jorgacevski,
Jernej/0000-0003-3550-2011
FU Ministry of Higher Education, Sciences, and Technology of the Republic
of Slovenia [P3 310, J3 3654, J3 4051, J3 4146]; Portuguese Foundation
of Science and Technology of the Portuguese Ministry of Sciences,
Technology, and High Education [441.00 SLOVENIA, SFRH/BD/41217/2007];
National Institute of Child Health and Human Development Intramural
FX This work was supported by the Ministry of Higher Education, Sciences,
and Technology of the Republic of Slovenia (P3 310; J3 3654; J3 4051; J3
4146), the Portuguese Foundation of Science and Technology of the
Portuguese Ministry of Sciences, Technology, and High Education
(Bilateral Agreement between Portugal and Slovenia; Project 441.00
SLOVENIA, SFRH/BD/41217/2007 to A. I. C.), and the National Institute of
Child Health and Human Development Intramural.
NR 54
TC 14
Z9 14
U1 0
U2 8
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 1
PY 2013
VL 33
IS 18
BP 8068
EP 8078
DI 10.1523/JNEUROSCI.5351-12.2013
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 137FH
UT WOS:000318420400042
PM 23637196
ER
PT J
AU Bauer, TR
Tuschong, LM
Calvo, KR
Shive, HR
Burkholder, TH
Karlsson, EK
West, RR
Russell, DW
Hickstein, DD
AF Bauer, Thomas R., Jr.
Tuschong, Laura M.
Calvo, Katherine R.
Shive, Heather R.
Burkholder, Tanya H.
Karlsson, Eleanor K.
West, Robert R.
Russell, David W.
Hickstein, Dennis D.
TI Long-Term Follow-up of Foamy Viral Vector-Mediated Gene Therapy for
Canine Leukocyte Adhesion Deficiency
SO MOLECULAR THERAPY
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; STEM-CELL TRANSPLANTATION; VIRUS VECTORS;
LENTIVIRAL VECTORS; BETA-THALASSEMIA; MOUSE MODEL; T-CELLS; IN-VIVO;
ACTIVATION; SCID-X1
AB The development of leukemia following gammaretroviral vector-mediated gene therapy for X-linked severe combined immunodeficiency disease and chronic granulomatous disease (CGD) has emphasized the need for long-term follow-up in animals treated with hematopoietic stem cell gene therapy. In this study, we report the long-term follow-up (4-7 years) of four dogs with canine leukocyte adhesion deficiency (CLAD) treated with foamy viral (FV) vector-mediated gene therapy. All four CLAD dogs previously received nonmyeloablative conditioning with 200 cGy total body irradiation followed by infusion of autologous, CD34(+) hematopoietic stem cells transduced by a FV vector expressing canine CD18 from an internal Murine Stem Cell Virus (MSCV) promoter. CD18(+) leukocyte levels were >2% following infusion of vector-transduced cells leading to ongoing reversal of the CLAD phenotype for >4 years. There was no clinical development of lymphoid or myeloid leukemia in any of the four dogs and integration site analysis did not reveal insertional oncogenesis. These results showing disease correction/amelioration of disease in CLAD without significant adverse events provide support for the use of a FV vector to treat children with leukocyte adhesion deficiency type 1 (LAD-1) in a human gene therapy clinical trial.
C1 [Bauer, Thomas R., Jr.; Tuschong, Laura M.; Shive, Heather R.; West, Robert R.; Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Hematol Sect, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Burkholder, Tanya H.; Karlsson, Eleanor K.] NIH, Div Vet Resources, Off Res Serv, Bethesda, MD 20892 USA.
[Russell, David W.] Univ Washington, Dept Med, Div Hematol, Seattle, WA USA.
[Russell, David W.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
RP Hickstein, DD (reprint author), NCI, ETIB, NIH, 10 Ctr Dr,MSC1203,Bldg 10-CRC,Rm 3-3142, Bethesda, MD 20892 USA.
EM hicksted@mail.nihi.gov
RI Calvo, Katherine/A-8109-2009;
OI Calvo, Katherine/0000-0002-0771-4191
FU Intramural Research Program of the US National Institutes of Health,
National Cancer Institute, Center for Cancer Research; US National
Institutes of Health [HL85107]
FX We thank William Telford and Veena Kapoor (Experimental Transplantation
and Immunology Branch, National Cancer Institute, National Institutes of
Health) for assistance with flow cytometry and sorting. We thank Erika
Wiltrout and Sharon Miller (Division of Veterinary Resources, Office of
Research Services, National Institutes of Health) and the rest of the
DVR staff for excellent veterinary care of dogs. We thank Matthew
Starost (Division of Veterinary Resources, Office of Research Services,
National Institutes of Health) for necropsy of dogs, collection of
tissues, and initial histological analysis. This work was supported by
the Intramural Research Program of the US National Institutes of Health,
National Cancer Institute, Center for Cancer Research, and by US
National Institutes of Health grant HL85107 (to D. W. R.). The authors
declared no conflict of interest.
NR 48
TC 14
Z9 14
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
J9 MOL THER
JI Mol. Ther.
PD MAY
PY 2013
VL 21
IS 5
BP 964
EP 972
DI 10.1038/mt.2013.34
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 136BQ
UT WOS:000318334800008
PM 23531552
ER
PT J
AU Simon, R
Roychowdhury, S
AF Simon, Richard
Roychowdhury, Sameek
TI Implementing personalized cancer genomics in clinical trials
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Article
ID GASTROINTESTINAL STROMAL TUMORS; ACUTE MYELOID-LEUKEMIA; CELL
LUNG-CANCER; INTRATUMOR HETEROGENEITY; BRAF INHIBITION; HIGH-FREQUENCY;
BREAST-CANCER; COLON-CANCER; MUTATIONS; GENE
AB The recent surge in high-throughput sequencing of cancer genomes has supported an expanding molecular classification of cancer. These studies have identified putative predictive biomarkers signifying aberrant oncogene pathway activation and may provide a rationale for matching patients with molecularly targeted therapies in clinical trials. Here, we discuss some of the challenges of adapting these data for rare cancers or molecular subsets of certain cancers, which will require aligning the availability of investigational agents, rapid turnaround of clinical grade sequencing, molecular eligibility and reconsidering clinical trial design and end points.
C1 [Simon, Richard] US Natl Canc Inst, Biometr Res Branch, Bethesda, MD 20892 USA.
[Roychowdhury, Sameek] Ohio State Univ, Div Med Oncol, Dept Internal Med, Columbus, OH 43210 USA.
[Roychowdhury, Sameek] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Roychowdhury, Sameek] Ohio State Univ, Dept Pharmacol, Columbus, OH 43210 USA.
RP Roychowdhury, S (reprint author), Ohio State Univ, Div Med Oncol, Dept Internal Med, Biomed Res Tower,Room 508,460 West 12th Ave, Columbus, OH 43210 USA.
EM Sameek.roychowdhury@osumc.edu
FU Pelotonia, the American Cancer Society [MRSG-12-194-01];
Landon-Foundation AACR Innovator Award for Personalized Cancer Medicine;
Prostate Cancer Foundation
FX S.R. is supported by Pelotonia, the American Cancer Society (grant
MRSG-12-194-01), the Landon-Foundation AACR Innovator Award for
Personalized Cancer Medicine, and a Young Investigator Award from the
Prostate Cancer Foundation. Special thanks to J. Bush for reading the
manuscript and A. Marsell for administrative support.
NR 77
TC 116
Z9 117
U1 3
U2 40
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD MAY
PY 2013
VL 12
IS 5
BP 359
EP 370
DI 10.1038/nrd3979
PG 12
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 136GR
UT WOS:000318350900014
PM 23629504
ER
PT J
AU Chang, HH
Larson, J
Blencowe, H
Spong, CY
Howson, CP
Cairns-Smith, S
Lackritz, EM
Lee, SK
Mason, E
Serazin, AC
Walani, S
Simpson, JL
Lawn, JE
AF Chang, Hannah H.
Larson, Jim
Blencowe, Hannah
Spong, Catherine Y.
Howson, Christopher P.
Cairns-Smith, Sarah
Lackritz, Eve M.
Lee, Shoo K.
Mason, Elizabeth
Serazin, Andrew C.
Walani, Salimah
Simpson, Joe Leigh
Lawn, Joy E.
CA Born Too Soon Preterm Prevention A
TI Preventing Preterm Births: Analysis of Trends and Potential Reductions
With Interventions in 39 Countries With Very High Human Development
Index EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
C1 [Chang, Hannah H.; Larson, Jim; Cairns-Smith, Sarah] Boston Consulting Grp Inc, Boston, MA USA.
[Blencowe, Hannah] Univ London London Sch Hyg & Trop Med, London WC1E 7HT, England.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Howson, Christopher P.; Walani, Salimah; Simpson, Joe Leigh] March Dimes Fdn, White Plains, NY USA.
[Lackritz, Eve M.] Global Alliance Prevent Prematur & Stillbirth, Seattle, WA USA.
[Lee, Shoo K.] Canadian Inst Hlth Res, Inst Human Dev, Toronto, ON, Canada.
[Mason, Elizabeth] WHO, Dept Maternal Newborn Child & Adolescent Hlth, CH-1211 Geneva, Switzerland.
[Serazin, Andrew C.] Bill & Melinda Gates Fdn, Global Hlth Program, Seattle, WA USA.
[Lawn, Joy E.] Save Children, Saving Newborn Lives, London, England.
RP Chang, HH (reprint author), Boston Consulting Grp Inc, Boston, MA USA.
NR 1
TC 0
Z9 0
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD MAY
PY 2013
VL 68
IS 5
BP 339
EP 341
DI 10.1097/01.ogx.0000430376.22369.5c
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 138BD
UT WOS:000318482300006
ER
PT J
AU Wong, JR
Harris, JK
Rodriguez-Galindo, C
Johnson, KJ
AF Wong, Jeannette R.
Harris, Jenine K.
Rodriguez-Galindo, Carlos
Johnson, Kimberly J.
TI Incidence of Childhood and Adolescent Melanoma in the United States:
1973-2009
SO PEDIATRICS
LA English
DT Article
DE melanoma; childhood; adolescence; incidence; SEER; trends; UV; cancer;
epidemiology
ID CUTANEOUS MALIGNANT-MELANOMA; ULTRAVIOLET-LIGHT EXPOSURE; INDOOR TANNING
FACILITIES; LYMPH-NODE BIOPSY; SKIN-CANCER; XERODERMA-PIGMENTOSUM;
POPULAR ATTITUDES; YOUNG-ADULTS; INVASIVE MELANOMA; MELANOCYTIC NEVI
AB OBJECTIVE: Childhood and adolescent melanoma is rare but has been increasing. To gain insight into possible reasons underlying this observation, we analyzed trends in melanoma incidence diagnosed between the ages of 0 and 19 years among US whites by gender, stage, age at diagnosis, and primary site. We also investigated incidence trends by UV-B exposure levels.
METHODS: By using Surveillance, Epidemiology, and End Results (SEER) program data (1973-2009), we calculated age-adjusted incidence rates (IRs), annual percent changes, and 95% confidence intervals for each category of interest. Incidence trends were also evaluated by using joinpoint and local regression models. SEER registries were categorized with respect to low or high UV-B radiation exposure.
RESULTS: From 1973 through 2009, 1230 children of white race were diagnosed with malignant melanoma. Overall, pediatric melanoma increased by an average of 2% per year (95% confidence interval, 1.4%-2.7%). Girls, 15- to 19-year-olds, and individuals with low UV-B exposure had significantly higher IRs than boys, younger children, and those living in SEER registries categorized as high UV-B. Over the study period, boys experienced increased IRs for melanoma on the face and trunk, and females on the lower limbs and hip. The only decreased incidence trend we observed was among 15- to 19-year-olds in the high UV-B exposure group from 1985 through 2009. Local regression curves indicated similar patterns.
CONCLUSIONS: These results may help elucidate possible risk factors for adolescent melanoma, but additional individual-level studies will be necessary to determine the reasons for increasing incidence trends.
C1 [Wong, Jeannette R.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Harris, Jenine K.; Johnson, Kimberly J.] Washington Univ, Brown Sch, St Louis, MO USA.
[Johnson, Kimberly J.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
[Rodriguez-Galindo, Carlos] Harvard Univ, Dana Farber Canc Inst, Cambridge, MA 02138 USA.
RP Johnson, KJ (reprint author), Washington Univ, 237 Goldfarb Hall,Campus Box 1196,1 Brookings Dr, St Louis, MO 63130 USA.
EM kijohnson@brownschool.wustl.edu
FU National Institutes of Health; National Cancer Institute; National
Institutes of Health (NIH)
FX Supported in part by the intramural research program of the National
Institutes of Health and the National Cancer Institute. Funded by the
National Institutes of Health (NIH).
NR 64
TC 49
Z9 53
U1 0
U2 20
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD MAY
PY 2013
VL 131
IS 5
BP 846
EP 854
DI 10.1542/peds.2012-2520
PG 9
WC Pediatrics
SC Pediatrics
GA 135EO
UT WOS:000318270700046
PM 23589817
ER
PT J
AU Canagarajah, BJ
Ren, XF
Bonifacino, JS
Hurley, JH
AF Canagarajah, Bertram J.
Ren, Xuefeng
Bonifacino, Juan S.
Hurley, James H.
TI The clathrin adaptor complexes as a paradigm for membrane-associated
allostery
SO PROTEIN SCIENCE
LA English
DT Review
DE membrane traffic; Arf1; phosphoinositides; membrane biology; protein
structure; protein crystallography
ID ADP-RIBOSYLATION FACTOR; GTP-BINDING PROTEIN; SORTING SIGNALS; ARF
FAMILY; AP2 COMPLEX; HIV-1 NEF; STRUCTURAL EXPLANATION; MEDIATED
ENDOCYTOSIS; GOLGI MEMBRANES; RECRUITMENT
AB The clathrin-associated adaptor protein (AP) complexes AP-1 and AP-2 are two members of a family of heterotetrameric assemblies that connect transmembrane protein cargo to vesicular coats. Cargo binding by AP-1 is activated by the small GTPase Arf1, while AP-2 is activated by the phosphoinositide PI(4,5)P2. The structures of both AP-1 and AP-2 have been determined in their locked and unlocked conformations. The structures show how different activators use different mechanisms to trigger similar large scale conformational rearrangements. The details of these mechanisms show how membrane docking and allosteric activation of AP complexes are intimately connected.
C1 [Canagarajah, Bertram J.; Hurley, James H.] NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Ren, Xuefeng; Bonifacino, Juan S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
RP Bonifacino, JS (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
EM bonifacinoj@helix.nih.gov; james.hurley@nih.gov
OI Bonifacino, Juan S./0000-0002-5673-6370
FU NICHD, NIH; NIDDK, NIH
FX This research was supported by the Intramural Programs of NICHD (J.S.B.)
and NIDDK (J.H.H.), NIH.
NR 51
TC 22
Z9 22
U1 4
U2 28
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0961-8368
EI 1469-896X
J9 PROTEIN SCI
JI Protein Sci.
PD MAY
PY 2013
VL 22
IS 5
BP 517
EP 529
DI 10.1002/pro.2235
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 134TW
UT WOS:000318238700001
PM 23424177
ER
PT J
AU Weinstein, AA
Chin, LMK
Keyser, RE
Kennedy, M
Nathan, SD
Woolstenhulme, JG
Connors, G
Chan, L
AF Weinstein, Ali A.
Chin, Lisa M. K.
Keyser, Randall E.
Kennedy, Michelle
Nathan, Steven D.
Woolstenhulme, Joshua G.
Connors, Gerilynn
Chan, Leighton
TI Effect of aerobic exercise training on fatigue and physical activity in
patients with pulmonary arterial hypertension
SO RESPIRATORY MEDICINE
LA English
DT Article
DE Hypertension; Pulmonary; Fatigue; Motor activity; Exercise
ID QUALITY-OF-LIFE; PRACTICE GUIDELINES; DIAGNOSIS; EFFICACY; SAFETY; SCALE
AB Objective: To investigate the effectiveness of an exercise intervention for decreasing fatigue severity and increasing physical activity in individuals with pulmonary arterial hypertension (PAH). A small, phase 2 randomized clinical trial of the effect of aerobic exercise training on fatigue severity and physical activity in patients with idiopathic or PAH associated with other conditions was conducted.
Methods: Twenty-four patients with PAH (24 female; age: 54.4 +/- 10.4 years; BMI: 30.8 +/- 7.2 kg/m(2)) participated in the study. A convenience sample was recruited in which 9% (28 of 303) of screened patients were enrolled. The project was carried out in a clinical pulmonary rehabilitation clinic during existing pulmonary rehabilitation program sessions.
Patients with PH were randomized into a 10-week program that consisted of patient education only or patient education plus an aerobic exercise-training regimen. Both groups received 20 lectures, two per week over the 10-weeks, on topics related to PAH and its management. The aerobic exercise training consisted of 24-30 sessions of treadmill walking for 30-45 min per session at an intensity of 70-80% of heart rate reserve, three days per week over the 10 weeks.
Results: After 10-weeks of intervention, patients receiving aerobic exercise training plus education reported routinely engaging in higher levels of physical activity (p < 0.05) and a decrease in fatigue severity (p = 0.03). Patients in the education only group did not report changes in fatigue severity or participation in physical activity.
Conclusions: The 10-week aerobic exercise training intervention resulted in increased physical activity and decreased fatigue in individuals with PAH. ClinicalTrials.gov Identifier: NCT00678821. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Weinstein, Ali A.] George Mason Univ, Ctr Study Chron Illness & Disabil, Coll Hlth & Human Serv, Fairfax, VA 22030 USA.
[Chin, Lisa M. K.; Keyser, Randall E.; Woolstenhulme, Joshua G.] George Mason Univ, Dept Rehabil Sci, Fairfax, VA 22030 USA.
[Chin, Lisa M. K.; Keyser, Randall E.; Kennedy, Michelle; Woolstenhulme, Joshua G.; Chan, Leighton] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
[Nathan, Steven D.] Inova Fairfax Hosp, Dept Med, Adv Lung Dis & Transplant Program, Falls Church, VA 22042 USA.
[Connors, Gerilynn] Inova Fairfax Hosp, Resp Care Serv, Falls Church, VA 22042 USA.
RP Weinstein, AA (reprint author), George Mason Univ, Ctr Study Chron Illness & Disabil, Coll Hlth & Human Serv, 4400 Univ Dr,MSN 2G7, Fairfax, VA 22030 USA.
EM aweinst2@gmu.edu
RI Chin, Lisa/O-4706-2014
OI Chin, Lisa/0000-0002-0178-739X
FU National Institutes of Health [1 Z01 CL060068-05]
FX This work was supported by the National Institutes of Health [Intramural
Funds 1 Z01 CL060068-05].
NR 25
TC 32
Z9 34
U1 2
U2 23
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0954-6111
J9 RESP MED
JI Respir. Med.
PD MAY
PY 2013
VL 107
IS 5
BP 778
EP 784
DI 10.1016/j.rmed.2013.02.006
PG 7
WC Cardiac & Cardiovascular Systems; Respiratory System
SC Cardiovascular System & Cardiology; Respiratory System
GA 135YU
UT WOS:000318327400018
PM 23478192
ER
PT J
AU Kuhn, NZ
Nagahara, LA
AF Kuhn, Nastaran Z.
Nagahara, Larry A.
TI Integrating Physical Sciences Perspectives in Cancer Research
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
ID MIGRATION
C1 [Kuhn, Nastaran Z.; Nagahara, Larry A.] NCI, Off Phys Sci Oncol, Ctr Strateg Sci Initiat, Off Director,NIH, Bethesda, MD 20892 USA.
RP Kuhn, NZ (reprint author), NCI, Off Phys Sci Oncol, Ctr Strateg Sci Initiat, Off Director,NIH, Bethesda, MD 20892 USA.
EM nas.kuhn@nih.gov
NR 10
TC 1
Z9 1
U1 0
U2 2
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD MAY 1
PY 2013
VL 5
IS 183
AR 183fs14
DI 10.1126/scitranslmed.3005804
PG 3
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 137FM
UT WOS:000318420900001
PM 23636090
ER
PT J
AU Zhang, JH
Lamers, F
Hickie, IB
He, JP
Feig, E
Merikangas, KR
AF Zhang, Jihui
Lamers, Femke
Hickie, Ian B.
He, Jian-Ping
Feig, Emily
Merikangas, Kathleen R.
TI Differentiating Nonrestorative Sleep from Nocturnal Insomnia Symptoms:
Demographic, Clinical, Inflammatory, and Functional Correlates
SO SLEEP
LA English
DT Article
DE C-reactive protein; functional impairment; medical condition; nocturnal
insomnia symptoms; nonrestorative sleep
ID GENERAL-POPULATION; CHRONIC ILLNESS; PREVALENCE; COMORBIDITY; DISORDERS;
HEALTH; IMPACT; SAMPLE; IMPAIRMENT; DEPRESSION
AB Study Objectives: Recent studies have suggested that nonrestorative sleep (NRS) symptoms may be distinct from nocturnal insomnia symptoms (NIS). However, there is limited information on the demographic, medical, and biologic correlates of NRS independent from NIS in the general population. This report presents the sociodemographic correlates, patterns of comorbidity with other sleep and physical disorders, C-reactive protein (CRP) levels, and general productivity associated with NIS and NRS in a nationally representative sample of US adults.
Design: National Health and Nutrition Examination Survey (NHANES).
Setting: The 2005-2008 surveys of the general population in the United States.
Participants: There were 10,908 individuals (20 years or older)
Interventions: N/A.
Measurements and Results: Respondents were classified by the presence or absence of NIS and NRS. Compared with those without insomnia symptoms, respondents with NIS were older and had lower family income and educational levels than those with NRS. In addition, there was a significant association between NIS and cardiovascular disease, whereas NRS was associated with other primary sleep disorders (including habitual snoring, sleep apnea, and restless legs syndrome), respiratory diseases (emphysema and chronic bronchitis), thyroid disease, and cancer as well as increased CRP levels. In addition, the study participants with NRS only reported poorer scores on the Functional Outcomes of Sleep Questionnaire (FOSQ) than those without insomnia symptoms or those with NIS only.
Conclusions: These findings suggest that there are substantial differences between NIS and NRS in terms of sociodemographic factors, comorbidity with other sleep and physical disorders, increased CRP level, and functional impairment. An inflammatory response might play a unique role in the pathogenesis of NRS.
C1 [Zhang, Jihui; Lamers, Femke; He, Jian-Ping; Feig, Emily; Merikangas, Kathleen R.] NIMH, Genet Epidemiol Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Zhang, Jihui] Chinese Univ Hong Kong, Dept Psychiat, Shatin, Hong Kong, Peoples R China.
[Hickie, Ian B.] Univ Sydney, Clin Res Unit, Brain & Mind Res Inst, Camperdown, NSW, Australia.
RP Merikangas, KR (reprint author), NIMH, Intramural Res Program, Genet Epidemiol Res Branch, 35 Convent Dr,MSC 3720, Bethesda, MD 20892 USA.
EM Kathleen.meri-kangas@nih.gov
FU National Institute of Mental Health [1Z011Z01MH002870]; National Health
and Medical Research Council [511921]; Servier; Pfizer; Astra Zeneca;
Netherlands Organisation for Scientific Research (NWO)
FX This was not an industry supported study. This study was funded by an
intramural grant (1Z011Z01MH002870) from the National Institute of
Mental Health. Dr. Hickie is supported by a National Health and Medical
Research Council Australia Fellowship (No. 511921). He was a director of
Headspace: The National Youth Mental Health Foundation until January
2012. He is a member of the new Australian National Mental Health
commission and was previously the CEO of Beyondblue: The National
Depression Initiative. He has led depression and other mental health
research projects that have been supported by a variety of
pharmaceutical partners. Current investigator-initiated studies are
supported by Servier and Pfizer. Dr. Hickie has served on the board,
advisory council, or consulted for Bupa Australia, Drinkwise Australia,
Western Australia (Labor) Government, DOHA Australian Government, Sydney
Magazine, and Sydney City Council. He has also received travel
compensation from RANZCP 7, Wyeth, Eli Lilly, Servier, Astra Zeneca,
Price Waterhouse Cooper, American Psychiatric Association, RSL National
congress, Chinese Society of Psychiatry and Neurology, Australian
General Practice Network, and Focus-Sunshine Coast Research. He has
received research support or received other support from Servier,
Pfizer, Servier, and Astra Zeneca. Dr. Lamers is supported by a Rubicon
Fellowship from the Netherlands Organisation for Scientific Research
(NWO). The other authors have indicated no financial conflicts of
interest. The views and opinions expressed in the report are those of
the authors and should not be construed to represent the views of any of
the sponsoring organizations, agencies, or US Government.
NR 49
TC 25
Z9 28
U1 1
U2 7
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PD MAY 1
PY 2013
VL 36
IS 5
BP 671
EP 679
DI 10.5665/sleep.2624
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 137AL
UT WOS:000318406600009
PM 23633749
ER
PT J
AU Chami, HA
Fontes, JD
Vasan, RS
Keaney, JF
O'Connor, GT
Larson, MG
Benjamin, EJ
Gottlieb, DJ
AF Chami, Hassan A.
Fontes, Joao D.
Vasan, Ramachandran S.
Keaney, John F., Jr.
O'Connor, George T.
Larson, Martin G.
Benjamin, Emelia J.
Gottlieb, Daniel J.
TI Vascular Inflammation and Sleep Disordered Breathing in a
Community-Based Cohort
SO SLEEP
LA English
DT Article
DE Epidemiology; inflammation; sleep apnea syndromes
ID C-REACTIVE PROTEIN; POSITIVE AIRWAY PRESSURE; CORONARY-HEART-DISEASE;
NECROSIS-FACTOR-ALPHA; APNEA SYNDROME; CARDIOVASCULAR-DISEASE;
INTERLEUKIN-6; ASSOCIATION; HEALTH; ATHEROSCLEROSIS
AB Study Objectives: Sleep disordered breathing is associated with cardiovascular disease. The pathophysiologic mechanisms remain unclear, but enhanced vascular inflammation is implicated. We sought to evaluate the association of sleep disordered breathing with biomarkers of inflammation.
Design: Cross-sectional, observational.
Setting: Community-based.
Participants: There were 900 participants from the Framingham Heart Study site of the Sleep Heart Health Study (52% females, mean age 60 y, 23% ethnic minorities).
Interventions: None.
Measurements: We assessed circulating levels of nine inflammatory biomarkers in relation to polysomnographically-derived apnea-hypopnea index and hypoxemia index (% sleep time with oxyhemoglobin saturation < 90%). Multivariable models were adjusted for demographics, smoking, cardiovascular diseases, diabetes, and other potential confounders, without and with adjustment for body mass index.
Results: With multivariable adjustment not including body mass index, the apnea-hypopnea index was associated with C-reactive protein, interleukin-6, fibrinogen, intercellular adhesion molecule-1, and P-selectin levels and hypoxemia index was associated with C-reactive protein, interleukin-6, and fibrinogen levels. After adjustment for body mass index, only the association of interleukin-6 with sleep disordered breathing remained significant: the adjusted mean serum interleukin-6 level was 2.93, 3.14, 3.34, and 4.62 pg/mL, respectively, in participants with apnea-hypopnea index < 5, 5-14.9, 15-29.9, and >= 30 events/h (P = 0.01 for trend) and 2.97, 3.01, 3.35, and 4.85 pg/mL, respectively, in participants with hypoxemia index < 0.5, 0.5-4.9, 5-9.9, and >= 10% of sleep time (P = 0.02 for trend).
Conclusions: In a community-based sample, sleep disordered breathing is associated with higher levels of interleukin-6, a marker of myocardial infarction risk and mortality. Adiposity may mediate the increased levels of C-reactive protein, fibrinogen, intercellular adhesion molecule-1, and P-selectin observed in sleep disordered breathing.
C1 [Chami, Hassan A.] Amer Univ Beirut, Dept Med, Beirut 11072020, Lebanon.
[Chami, Hassan A.; Fontes, Joao D.; Vasan, Ramachandran S.; O'Connor, George T.; Benjamin, Emelia J.; Gottlieb, Daniel J.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Vasan, Ramachandran S.; Larson, Martin G.; Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Keaney, John F., Jr.] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA USA.
[Larson, Martin G.] Boston Univ, Sch Publ Hlth, Dept Math & Stat, Boston, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Gottlieb, Daniel J.] VA Boston Hlth Care Syst, West Roxbury, MA USA.
RP Chami, HA (reprint author), Amer Univ Beirut, Dept Med, POB 11-0236, Beirut 11072020, Lebanon.
EM hchami@aub.edu.lb
OI Chami, Hassan/0000-0002-9239-2528; O'Connor, George/0000-0002-6476-3926;
Ramachandran, Vasan/0000-0001-7357-5970
FU Sleep Heart Health Study National Heart, Lung, and Blood Institute
[U01HL53940, U01HL53941, U01HL53938, U01HL53916, U01HL53934, U01HL53931,
U01HL53937, U01HL64360, U01HL63463, U01HL63429]; [N01-HC 25195]; [1RO1
HL64753]; [R01 HL076784]; [1 R01 AG028321]
FX This study was supported by: N01-HC 25195; 1RO1 HL64753; R01 HL076784; 1
R01 AG028321; Sleep Heart Health Study National Heart, Lung, and Blood
Institute cooperative agreements U01HL53940 (University of Washington),
U01HL53941 (Boston University), U01HL53938 (University of Arizona),
U01HL53916 (University of California, Davis), U01HL53934 (University of
Minnesota), U01HL53931 (New York University), U01HL53937 and U01HL64360
(Johns Hopkins University), U01HL63463 (Case Western Reserve
University), and U01HL63429 (Missouri Breaks Research); Lp-PLA2 activity
measurements were provided by GlaxoSmithKline and mass measurements by
diaDexus at no cost to the Framingham Heart Study.
NR 44
TC 11
Z9 12
U1 3
U2 7
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PD MAY 1
PY 2013
VL 36
IS 5
BP 763
EP 768
DI 10.5665/sleep.2644
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 137AL
UT WOS:000318406600019
PM 23633759
ER
PT J
AU Zhang, FY
Shan, L
Liu, YY
Neville, D
Woo, JH
Chen, Y
Korotcov, A
Lin, S
Huang, S
Sridhar, R
Liang, W
Wang, PC
AF Zhang, Fayun
Shan, Liang
Liu, Yuanyi
Neville, David
Woo, Jung-Hee
Chen, Yue
Korotcov, Alexandru
Lin, Stephen
Huang, Sophia
Sridhar, Rajagopalan
Liang, Wei
Wang, Paul C.
TI An Anti-PSMA Bivalent Immunotoxin Exhibits Specificity and Efficacy for
Prostate Cancer Imaging and Therapy
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Article
DE diphtheria toxin DT390; immunotoxin; prostate-specific membrane antigen;
targeted drug delivery; tumor imaging
ID SINGLE-CHAIN IMMUNOTOXIN; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
TOXIN-BASED IMMUNOTOXIN; MEMBRANE ANTIGEN; DIPHTHERIA-TOXIN;
MONOCLONAL-ANTIBODY; CELLS; EXPRESSION; PREVENTION; MODELS
AB Prostate specific membrane antigen (PSMA) is overexpressed on prostate tumor cells and the neovascular endothelia various solid tumors. A bivalent immunotoxin generated by fusing a fold-back single-chain diabody derived from the Fv fragments of an anti-PSMA monoclonal antibody with a truncated diphtheria toxin (DT) containing the activity and translocation domains [A-dmDT390-scfbDb(PSMA)] might be suitable for targeted therapy of tumors that overexpress PSMA. In this study, a PSMA-positive and a PSMA-negative prostate cancer cell lines were treated with immunotoxin A-dmDT390-scfbDb(PSMA) in order to study the tumor targeting specificity and therapeutic potential of the immunotoxin. The cellular uptake and selective toxicity of the immunotoxin were evident in monolayer cultures of PSMA-positive LNCaP prostate cancer cells but not in cultures of PSMA-negative PC-3 prostate cancer cells. Cellular accumulation of A-dmDT390-scfbDb(PSMA) increased with increasing incubation times and concentrations in LNCaP cells. The proportion of apoptotic LNCaP cells increased upon incubation with increasing doses of the fold-back immunotoxin. Optical imaging and MRI with the Alexa Fluor 680-labeled A-dmDT390-scfbDb(PSMA) confirmed the specific targeting and therapeutic efficacy of this immunotoxin towards PSMA-positive LNCaP solid tumor xenografts in athymic nude mice.
C1 [Zhang, Fayun; Shan, Liang; Chen, Yue; Korotcov, Alexandru; Lin, Stephen; Huang, Sophia; Sridhar, Rajagopalan; Wang, Paul C.] Howard Univ, Mol Imaging Lab, Dept Radiol, Washington, DC 20060 USA.
[Zhang, Fayun; Liang, Wei] Chinese Acad Sci, Prot & Peptide Pharmaceut Lab, Natl Lab Biomacromol, Inst Biophys, Beijing 100101, Peoples R China.
[Shan, Liang] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Liu, Yuanyi; Neville, David] Angimmune LLC, Bethesda, MD 20852 USA.
[Woo, Jung-Hee] Scott & White Healthcare, Canc Res Inst, Texas A&M Hlth Sci Ctr, Temple, TX 76502 USA.
RP Wang, PC (reprint author), Howard Univ, Mol Imaging Lab, Dept Radiol, Washington, DC 20060 USA.
EM pwang@howard.edu
FU NIH/NCRR [3 G12 RR003048]; NIH/NIMHD [8 G12 MD007597]; USAMRMC
[W81XWH-10-1-0767]
FX This work was supported in part by NIH/NCRR 3 G12 RR003048, NIH/NIMHD 8
G12 MD007597, and USAMRMC W81XWH-10-1-0767 grants.
NR 32
TC 8
Z9 8
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2192-2640
J9 ADV HEALTHC MATER
JI Adv. Healthc. Mater.
PD MAY
PY 2013
VL 2
IS 5
BP 736
EP 744
DI 10.1002/adhm.201200254
PG 9
WC Engineering, Biomedical; Nanoscience & Nanotechnology; Materials
Science, Biomaterials
SC Engineering; Science & Technology - Other Topics; Materials Science
GA 135TU
UT WOS:000318312200013
PM 23184611
ER
PT J
AU Parsons, JT
Kowalczyk, WJ
Botsko, M
Tomassilli, J
Golub, SA
AF Parsons, Jeffrey T.
Kowalczyk, William J.
Botsko, Michael
Tomassilli, Julia
Golub, Sarit A.
TI Aggregate Versus Day Level Association Between Methamphetamine Use and
HIV Medication Non-adherence Among Gay and Bisexual Men
SO AIDS AND BEHAVIOR
LA English
DT Article
DE Adherence; Methamphetamine; Methods; Day-level
ID SEXUAL RISK BEHAVIORS; RANDOMIZED-CONTROLLED-TRIAL; PROTEASE INHIBITOR
THERAPY; MULTICENTER AIDS COHORT; LESS-THAN 95-PERCENT; ANTIRETROVIRAL
THERAPY; DRUG-USE; CONTINGENCY MANAGEMENT; CRYSTAL METHAMPHETAMINE;
SUBSTANCE-ABUSE
AB Methamphetamine use is associated with HIV infection, especially among gay and bisexual men. Methamphetamine use contributes to disease progression both directly, by increasing viral load and damaging the immune system, and indirectly, by decreasing medication adherence. Research examining the association of methamphetamine use and non-adherence has traditionally compared groups of users and nonusers on adherence, compared methamphetamine use between participants above or below some threshold level of adherence (e.g. > 90 % dose adherence), or examined aggregate relationships. Using Timeline Follow-back procedures, the present study examined aggregate, threshold, and day-level associations of methamphetamine use with non-adherence in 210 HIV-positive gay and bisexual methamphetamine-using men. Methamphetamine use was not associated with adherence behavior at the aggregate-level, but methamphetamine use on a given day was associated with 2.3 times the odds of non-adherence on that day. Threshold results were equivocal. These data suggest that the methamphetamine and non-adherence relationship is complicated: non-adherence is more likely to occur on days in which methamphetamine is used, but participants reported more non-adherence days in which methamphetamine was not used. This seeming paradox generates questions about the selection of analytical techniques and has important implications for behavioral interventions targeting substance use and adherence among HIV-positive individuals.
C1 [Parsons, Jeffrey T.; Kowalczyk, William J.; Botsko, Michael; Tomassilli, Julia] Ctr HIV AIDS Educ Studies & Training CHEST, New York, NY USA.
[Parsons, Jeffrey T.; Golub, Sarit A.] CUNY, CUNY Hunter Coll, Dept Psychol, New York, NY 10065 USA.
[Parsons, Jeffrey T.] CUNY Hunter Coll, CUNY Sch Publ Hlth, New York, NY 10065 USA.
[Parsons, Jeffrey T.; Golub, Sarit A.] CUNY, Grad Ctr, Doctoral Program Hlth Psychol, New York, NY 10065 USA.
[Parsons, Jeffrey T.; Golub, Sarit A.] CUNY, Grad Ctr, Doctoral Program Basic & Appl Social Psychol, New York, NY 10065 USA.
[Kowalczyk, William J.] NIDA, Nicotine Pharmacol Sect, Intramural Res Program, Baltimore, MD USA.
RP Parsons, JT (reprint author), Ctr HIV AIDS Educ Studies & Training CHEST, New York, NY USA.
EM jeffrey.parsons@hunter.cuny.edu
OI Kowalczyk, William/0000-0001-8026-285X; Parsons,
Jeffrey/0000-0002-6875-7566
FU NIDA NIH HHS [R01 DA023395]
NR 86
TC 11
Z9 11
U1 1
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1090-7165
J9 AIDS BEHAV
JI AIDS Behav.
PD MAY
PY 2013
VL 17
IS 4
BP 1478
EP 1487
DI 10.1007/s10461-013-0463-7
PG 10
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 133WO
UT WOS:000318171800028
PM 23553345
ER
PT J
AU Daniel, CR
Park, Y
Chow, WH
Graubard, BI
Hollenbeck, AR
Sinha, R
AF Daniel, Carrie R.
Park, Yikyung
Chow, Wong-Ho
Graubard, Barry I.
Hollenbeck, Albert R.
Sinha, Rashmi
TI Intake of fiber and fiber-rich plant foods is associated with a lower
risk of renal cell carcinoma in a large US cohort
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID HEALTH-AMERICAN-ASSOCIATION; RETIRED-PERSONS DIET; C-REACTIVE PROTEIN;
CANCER PREVENTION; FREQUENCY QUESTIONNAIRES; NATIONAL-INSTITUTES;
PHYSICAL-ACTIVITY; KIDNEY CANCER; VEGETABLES; NUTRITION
AB Background: Plant-based and fiber-rich diets high in vegetables, fruit, and whole grains are recommended to prevent cancer and chronic conditions associated with renal cell carcinoma (RCC), such as obesity, hypertension, and diabetes. Diet may play a role in the etiology of RCC directly and/or indirectly.
Objective: In a large prospective cohort of US men and women, we comprehensively investigated dietary intake and food sources of fiber in relation to RCC risk.
Design: Participants of the NIH-AARP Diet and Health Study (n = 491,841) completed a self-administered questionnaire of demographics, diet, lifestyle, and medical history. Over 9 (mean) years of followup we identified 1816 incident cases of RCC. HRs and 95% CIs were estimated within quintiles by using multivariable Cox proportional hazards regression.
Results: Total dietary fiber intake was associated with a significant 15-20% lower risk of RCC in the 2 highest quintiles compared with the lowest (P-trend = 0.005). Intakes of legumes, whole grains, and cruciferous vegetables were also associated with a 16-18% reduced risk of RCC. Conversely, refined grain intake was positively associated with RCC risk in a comparison of quintile 5 with quintile 1 (HR: 1.19; 95% CI: 1.02, 1.39; P-trend = 0.04). The inverse association between fiber intake and RCC was consistent among participants who never smoked, had a body mass index [BMI (in kg/m(2))] <30, and did not report of history of diabetes or hypertension.
Conclusions: Intake of fiber and fiber-rich plant foods was associated with a significantly lower risk of RCC in this large US cohort. This trial was registered at clinicaltrials.gov as NCT00340015. Am J Clin Nutr 2013;97:1036-43.
C1 [Daniel, Carrie R.; Park, Yikyung; Chow, Wong-Ho; Graubard, Barry I.; Sinha, Rashmi] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Daniel, Carrie R.; Chow, Wong-Ho] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Daniel, CR (reprint author), 1515 Holcombe Blvd,Unit 1340, Houston, TX 77030 USA.
EM cdaniel@mdanderson.org
RI Sinha, Rashmi/G-7446-2015;
OI Sinha, Rashmi/0000-0002-2466-7462; Park, Yikyung/0000-0002-6281-489X
FU National Cancer Institute, NIH
FX Supported by the Intramural Research Program of the National Cancer
Institute, NIH.
NR 54
TC 10
Z9 10
U1 0
U2 25
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY
PY 2013
VL 97
IS 5
BP 1036
EP 1043
DI 10.3945/ajcn.112.045351
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 131NP
UT WOS:000318000700019
PM 23515007
ER
PT J
AU Breslow, RA
Chen, CM
Graubard, BI
Jacobovits, T
Kant, AK
AF Breslow, Rosalind A.
Chen, Chiung M.
Graubard, Barry I.
Jacobovits, Tova
Kant, Ashima K.
TI Diets of drinkers on drinking and nondrinking days: NHANES 2003-2008
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID ALCOHOLIC BEVERAGE PREFERENCE; UNITED-STATES; FOOD-INTAKE; NUTRIENT
INTAKE; BODY-WEIGHT; ENERGY; CONSUMPTION; APPETITE; OBESITY; POPULATION
AB Background: Alcohol may affect dietary intake. However, little is known about diets on drinking days in the US population.
Objective: We determined whether the diets of drinkers differ on drinking compared with nondrinking days.
Design: Data were from the 2003-2008 NHANES Mobile Examination Center interview. We identified 1864 current drinkers (1126 men and 738 women) who completed two 24-h dietary recalls, one of which was on a drinking day and the other of which was on a nondrinking day. Sex-specific repeated-measures analyses that were adjusted for dietary recall order and recall day of the week were used to compare within-individual differences in energy, nutrient, and food-group intakes. Analyses were weighted to produce representative estimates.
Results: On their drinking (compared with nondrinking) days, men consumed an excess 168 nonalcohol kcal (P < 0.01), which was reflected in higher intakes of nutrients including total protein (P < 0.001), total fat (P < 0.01), saturated fat (P < 0.01), monounsaturated fat (P < 0.01), potassium (P < 0.001), and sodium (P < 0.05). Men also had higher intakes of food groups including meat (P < 0.001), white potatoes (P < 0.05), and discretionary oil and solid fat (P < 0.05) and lower intakes of total fruit (P < 0.05) and milk (P < 0.05). Women did not consume excess nonalcohol kilocalories but had higher intakes of total fat (P < 0.05), monounsaturated fat (P < 0.05), polyunsaturated fat (P < 0.05), potassium (P < 0.01), and discretionary oil and solid fat (P < 0.05) and lower intakes of milk (P < 0.01) and milk products (P < 0.01).
Conclusions: These mostly moderate drinkers had poorer diets on drinking days. Same-day associations between alcohol and diet could be useful targets for public health efforts to improve dietary intake. Am J Clin Nutr 2013;97:1068-75.
C1 [Breslow, Rosalind A.; Jacobovits, Tova] NIAAA, Div Epidemiol & Prevent Res, Bethesda, MD 20892 USA.
[Graubard, Barry I.] NCI, Div Canc Epidemiol & Genet, Biostat Branch, NIH, Bethesda, MD 20892 USA.
[Chen, Chiung M.] CSR Inc, Arlington, VA USA.
[Kant, Ashima K.] CUNY Queens Coll, Dept Family Nutr & Exercise Sci, Flushing, NY 11367 USA.
[Kant, Ashima K.] CUNY, Flushing, NY USA.
RP Breslow, RA (reprint author), NIAAA, Div Epidemiol & Prevent Res, 5635 Fishers Lane,Room 2071, Bethesda, MD 20892 USA.
EM rbreslow@mail.nih.gov
FU Alcohol Epidemiologic Data System of the National Institute on Alcohol
Abuse and Alcoholism [HHSN267200800023C]
FX Computer programming and data analysis by CSR Inc (CMC) were funded
through Alcohol Epidemiologic Data System contract HHSN267200800023C of
the National Institute on Alcohol Abuse and Alcoholism.
NR 31
TC 8
Z9 8
U1 0
U2 10
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD MAY
PY 2013
VL 97
IS 5
BP 1068
EP 1075
DI 10.3945/ajcn.112.050161
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 131NP
UT WOS:000318000700023
PM 23535109
ER
PT J
AU Venkataraman, G
Uldrick, TS
Aleman, K
O'Mahony, D
Karcher, DS
Steinberg, SM
Raffeld, MA
Marshall, V
Whitby, D
Little, RF
Yarchoan, R
Pittaluga, S
Maric, I
AF Venkataraman, Girish
Uldrick, Thomas S.
Aleman, Karen
O'Mahony, Deirdre
Karcher, Donald S.
Steinberg, Seth M.
Raffeld, Mark A.
Marshall, Vickie
Whitby, Denise
Little, Richard F.
Yarchoan, Robert
Pittaluga, Stefania
Maric, Irina
TI Bone Marrow Findings in HIV-Positive Patients With Kaposi Sarcoma
Herpesvirus-Associated Multicentric Castleman Disease
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Kaposi sarcoma herpesvirus; Human herpesvirus-8; Multicentric Castleman
disease; Human immunodeficiency virus; Bone marrow; Bone marrow
examination; Plasmacytosis
ID DNA-SEQUENCES; MAST-CELLS; VIRAL IL-6; INTERLEUKIN-10; INFECTION; AIDS;
RITUXIMAB; POPULATION; EXPRESSION; LYMPHOMA
AB Kaposi sarcoma herpesvirus (KSHV), also known as human herpesvirus-8, is associated with 1 form of multicentric Castleman disease (MCD) and is the etiologic agent for most MCD in human immunodeficiency virus (HIV)-infected patients. Diagnosis is usually determined by lymph node biopsy. Bone marrow findings in KSHV-MCD are not well characterized. We conducted histomorphologic and immunohistochemical evaluation of bone marrow biopsy specimens in HIV-infected patients with KSHV-MCD, including evaluation for KSHV latency-associated nuclear antigen. Findings were correlated with clinical features and KSHV viral load. Reactive plasmacytosis was the predominant feature. Lymphoid aggregates were less common and not diagnostic of KSHV-MCD. Forty-eight percent of cases contained scattered KSHV-infected mononuclear cells. Although patients were generally cytopenic, bone marrow biopsy specimens were normocellular to hypercellular except in patients receiving hematotoxic therapy. Bone marrow biopsy specimens in KSHV-MCD patients recapitulate findings of interleukin-6 excess. In patients with HIV, unexplained cytopenias, and bone marrow plasmacytosis, evaluation for KSHV-MCD is warranted.
C1 [Venkataraman, Girish; Raffeld, Mark A.; Pittaluga, Stefania] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Uldrick, Thomas S.; Aleman, Karen; O'Mahony, Deirdre; Little, Richard F.; Yarchoan, Robert] NCI, HIV & AIDS Malignancy Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Karcher, Donald S.] George Washington Univ, Dept Pathol, Washington, DC USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Marshall, Vickie; Whitby, Denise] NCI Frederick, Viral Oncol Sect, AIDS & Canc Virus Program, Frederick, MD USA.
[Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Maric, I (reprint author), NIH, Hematol Sect, DLM, CC, Bldg 10,Room 2C390,10 Ctr Dr, Bethesda, MD 20892 USA.
EM uldrickts@mail.nih.gov; marici@mail.nih.gov
OI Venkataraman, Girish/0000-0002-8674-2608
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX Supported by the Intramural Research Program of the National Institutes
of Health. Additional funding comes from the National Cancer Institute,
National Institutes of Health (contract No. HHSN261200800001E).
NR 34
TC 14
Z9 16
U1 0
U2 1
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD MAY
PY 2013
VL 139
IS 5
BP 651
EP 661
DI 10.1309/AJCPKGF7U8AWQBVG
PG 11
WC Pathology
SC Pathology
GA 131MA
UT WOS:000317996600011
PM 23596117
ER
PT J
AU Evans, JD
AF Evans, Jovier D.
TI Biological Mechanisms of Age-Related Disease and Geriatric Clinical
Research: A Commentary from the NIMH
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Editorial Material
ID DISORDERS; DEPRESSION
C1 NIMH, Rockville, MD 20852 USA.
RP Evans, JD (reprint author), NIMH, Rockville, MD 20852 USA.
EM Jevans1@mail.nih.gov
NR 10
TC 2
Z9 2
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1064-7481
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD MAY
PY 2013
VL 21
IS 5
BP 415
EP 417
DI 10.1016/j.jagp.2012.09.007
PG 3
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA 132HB
UT WOS:000318057400002
PM 23570885
ER
PT J
AU Buchanan, S
Noinaj, N
Easley, N
Oke, M
Mizuno, N
Gumbart, J
Boura, E
Steele, A
Zak, O
Aisen, P
Tajkhorshid, E
Evans, R
Gorringe, A
Mason, A
Steven, A
AF Buchanan, Susan
Noinaj, Nicholas
Easley, Nicole
Oke, Muse
Mizuno, Naoko
Gumbart, James
Boura, Evzen
Steele, Ashley
Zak, Olga
Aisen, Philip
Tajkhorshid, Emad
Evans, Robert
Gorringe, Andrew
Mason, Anne
Steven, Alasdair
TI STRUCTURAL BASIS FOR IRON PIRACY BY PATHOGENIC NEISSERIA
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Meeting Abstract
C1 [Buchanan, Susan; Noinaj, Nicholas; Easley, Nicole; Oke, Muse; Boura, Evzen] NIDDK, NIH, Bethesda, MD 20892 USA.
[Mizuno, Naoko; Steven, Alasdair] NIS, NIH, Bethesda, MD 20892 USA.
[Gumbart, James; Tajkhorshid, Emad] U IL Urbana, Urbana, IL USA.
[Steele, Ashley; Mason, Anne] U Vermont, Burlington, VT USA.
[Zak, Olga; Aisen, Philip] Albert Einstein Coll Med, New York, NY USA.
[Evans, Robert] Brunel U, Uxbridge, Middx, England.
[Gorringe, Andrew] Hlth Protect Agcy, Porton Down, England.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD MAY
PY 2013
VL 88
IS 5
BP E14
EP E14
PG 1
WC Hematology
SC Hematology
GA 132BT
UT WOS:000318043500015
ER
EF