FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Wilson, SH
AF Wilson, Samuel H.
TI Reflections on the Superfund Research Program: A tribute to its Founding
Director, William A. Suk
SO DNA REPAIR
LA English
DT Editorial Material
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
EM swilson18@nc.rr.com
NR 5
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD OCT
PY 2014
VL 22
BP V
EP VIII
DI 10.1016/S1568-7864(14)00232-8
PG 4
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA AR1OR
UT WOS:000343355000001
PM 25246422
ER
PT J
AU Bienstock, RJ
Beard, WA
Wilson, SH
AF Bienstock, Rachelle J.
Beard, William A.
Wilson, Samuel H.
TI Phylogenetic analysis and evolutionary origins of DNA polymerase
X-family members
SO DNA REPAIR
LA English
DT Article
DE DNA polymerase; Evolution; Genomics; Phylogenetic; Structure-function;
X-family
ID SITE-DIRECTED MUTAGENESIS; MULTIPLE SEQUENCE ALIGNMENT;
THERMUS-THERMOPHILUS HB8; AMINO-ACID SUBSTITUTION; STATE KINETIC
ANALYSES; ACTIVE-SITE; DEINOCOCCUS-RADIODURANS; SUBSTRATE-SPECIFICITY;
NUCLEOTIDYL TRANSFER; EXONUCLEASE ACTIVITY
AB Mammalian DNA polymerase (pol) beta is the founding member of a large group of DNA polymerases now termed the X-family. DNA polymerase beta has been kinetically, structurally, and biologically well characterized and can serve as a phylogenetic reference. Accordingly, we have performed a phylogenetic analysis to understand the relationship between pol beta and other members of the X-family of DNA polymerases. The bacterial X-family DNA polymerases, Saccharomyces cerevisiae pol IV, and four mammalian X-family polymerases appear to be directly related. These enzymes originated from an ancient common ancestor characterized in two Bacillus species. Understanding distinct functions for each of the X-family polymerases, evolving from a common bacterial ancestor is of significant interest in light of the specialized roles of these enzymes in DNA metabolism. Published by Elsevier B.V.
C1 [Bienstock, Rachelle J.; Beard, William A.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU National Institutes of Health, National Institute of Environmental
Health Sciences [Z01-ES050158, Z01-ES050159]; National Institutes of
Health [1U19CA105010]
FX This research was supported by Research Project Numbers Z01-ES050158 and
Z01-ES050159 in the Intramural Research Program of the National
Institutes of Health, National Institute of Environmental Health
Sciences and was in association with the National Institutes of Health
Grant 1U19CA105010.
NR 76
TC 4
Z9 4
U1 0
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD OCT
PY 2014
VL 22
BP 77
EP 88
DI 10.1016/j.dnarep.2014.07.003
PG 12
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA AR1OR
UT WOS:000343355000009
PM 25112931
ER
PT J
AU Resnick, MA
AF Resnick, Michael A.
TI A Holliday in science: Robin Holliday, Ph.D., FRS and FAA (1932-2014)
SO DNA REPAIR
LA English
DT Editorial Material
C1 NIEHS, NIH, Genet Mol Lab, Res Triangle Pk, NC 27709 USA.
RP Resnick, MA (reprint author), NIEHS, NIH, Genet Mol Lab, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD OCT
PY 2014
VL 22
BP 175
EP 175
DI 10.1016/j.dnarep.2014.04.007
PG 1
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA AR1OR
UT WOS:000343355000019
ER
PT J
AU Chongwatpol, J
Phurithititanapong, T
AF Chongwatpol, Jongsawas
Phurithititanapong, Thanrawee
TI Applying analytics in the energy industry: A case study of heat rate and
opacity prediction in a coal-fired power plant
SO ENERGY
LA English
DT Article
DE Analytics; Coal-fired; Power plant; Data mining; Heat rate; Opacity
ID DATA-MINING APPROACH; OPTIMIZATION; BOILER; EFFICIENCY; IMPACT
AB Power producers are looking for ways not only to improve the efficiency of power plant assets but also to alleviate concerns about the environmental impact of power generation without compromising their market competitiveness. To meet this challenge, advanced analytics through data mining approaches has been applied to predict and explain the leading causes of variation in heat rates and the opacity of the flue gas exhaust emissions, which are key factors in measuring the overall efficiency of the power plant. The results from a case study from a coal-fired power plant in Thailand demonstrate the practical validity of our approaches. The key finding contributes to identifying parameters that are the key determinants of excessive heat rates and opacity levels. Thus, corrective and preventive actions related to those parameters can be regularly evaluated and monitored. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Chongwatpol, Jongsawas; Phurithititanapong, Thanrawee] NIDA, Sch Business, Natl Inst Dev Adm, Bangkok 10240, Thailand.
RP Chongwatpol, J (reprint author), NIDA, Sch Business, Natl Inst Dev Adm, 118 Seri Thai Rd, Bangkok 10240, Thailand.
EM jong_tn@hotmail.com
NR 28
TC 1
Z9 1
U1 5
U2 15
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0360-5442
EI 1873-6785
J9 ENERGY
JI Energy
PD OCT 1
PY 2014
VL 75
SI SI
BP 463
EP 473
DI 10.1016/j.energy.2014.08.002
PG 11
WC Thermodynamics; Energy & Fuels
SC Thermodynamics; Energy & Fuels
GA AR1IW
UT WOS:000343339900047
ER
PT J
AU Nayak, RK
Pearson, SD
AF Nayak, Rahul K.
Pearson, Steven D.
TI The Ethics Of 'Fail First': Guidelines And Practical Scenarios For Step
Therapy Coverage Policies
SO HEALTH AFFAIRS
LA English
DT Article
ID ANTIPSYCHOTIC-DRUGS; MEDICAL UTILIZATION; SCHIZOPHRENIA; EXPENDITURES;
PROTOCOLS
AB In an effort to control health costs, payers are increasingly turning to step therapy (or "fail first") policies in pharmacy benefit design. These policies restrict coverage of expensive therapies unless patients have already failed treatment with a lower-cost alternative. More than other utilization management tools such as formulary tiering, step therapy raises important ethical concerns regarding the proper balance between cost control and the ability of patients and clinicians to tailor care to the needs of the individual patient. This article provides eight design criteria to guide the ethical development and evaluation of step therapy policies and describes six clinical scenarios in which step therapy may be appropriate. The ethical criteria and scenarios are intended to provide guidance and transparency for insurers, patients, clinicians, and policy makers in choosing and paying for the appropriate therapies.
C1 [Nayak, Rahul K.] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Pearson, Steven D.] Inst Clin & Econ Review, Boston, MA USA.
RP Nayak, RK (reprint author), NIH, Dept Bioeth, Bldg 10, Bethesda, MD 20892 USA.
EM pearsonsd@cc.nih.gov
OI Nayak, Rahul/0000-0001-6725-7634
NR 23
TC 3
Z9 3
U1 1
U2 2
PU PROJECT HOPE
PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD OCT
PY 2014
VL 33
IS 10
BP 1779
EP 1785
DI 10.1377/hlthaff.2014.0516
PG 7
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA AR2IE
UT WOS:000343406500011
PM 25288422
ER
PT J
AU Bartels, K
Ma, Q
Venkatraman, TN
Campos, CR
Smith, L
Cannon, RE
Podgoreanu, MV
Lascola, CD
Miller, DS
Mathew, JP
AF Bartels, Karsten
Ma, Qing
Venkatraman, Talaignair N.
Campos, Christopher R.
Smith, Lindsay
Cannon, Ronald E.
Podgoreanu, Mihai V.
Lascola, Christopher D.
Miller, David S.
Mathew, Joseph P.
TI Effects of Deep Hypothermic Circulatory Arrest on the Blood Brain
Barrier in a Cardiopulmonary Bypass Model - A Pilot Study
SO HEART LUNG AND CIRCULATION
LA English
DT Article
DE Blood brain barrier; Deep hypothermic circulatory arrest;
Cardiopulmonary bypass; Cardiac surgery; Neurologic injury
ID CARDIAC-SURGERY; P-GLYCOPROTEIN; PERMEABILITY; MODULATION
AB Background Neurologic injury is common after cardiac surgery and disruption of the blood brain barrier (BBB) has been proposed as a contributing factor. We sought to study BBB characteristics in a rodent model of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA).
Methods Adult rats were subjected to CPB/DHCA or to sham surgery. Analysis included Western blotting of relevant BBB proteins in addition to in vivo brain magnetic resonance imaging (MRI) with a clinically used low-molecular contrast agent.
Results While quantitative analysis of BBB proteins revealed similar expression levels, MRI showed evidence of BBB disruption after CPB/DHCA compared to sham surgery.
Conclusions Combining molecular BBB analysis and MRI technology in a rodent model is a highly translatable approach to study adverse neurologic outcomes following CPB/DHCA.
C1 [Bartels, Karsten; Ma, Qing; Podgoreanu, Mihai V.; Mathew, Joseph P.] Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA.
[Venkatraman, Talaignair N.; Lascola, Christopher D.] Duke Univ, Med Ctr, Dept Radiol, Durham, NC 27710 USA.
[Campos, Christopher R.; Smith, Lindsay; Cannon, Ronald E.; Miller, David S.] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
RP Mathew, JP (reprint author), UMC, Box 3094 Mail 41,2301 Erwin Rd,5688 HAFS, Durham, NC 27710 USA.
EM joseph.mathew@duke.edu
RI Lascola, Christopher/B-9126-2017;
OI Lascola, Christopher/0000-0002-8031-782X; Podgoreanu,
Mihai/0000-0001-5539-4674
FU NHLBI NIH HHS [R01 HL096978, R21 HL108280, R21 HL109971]
NR 11
TC 5
Z9 5
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1443-9506
EI 1444-2892
J9 HEART LUNG CIRC
JI Heart Lung Circ.
PD OCT
PY 2014
VL 23
IS 10
BP 981
EP 984
DI 10.1016/j.hlc.2014.04.131
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AR1PA
UT WOS:000343355900014
PM 24931068
ER
PT J
AU Kendrick, SL
Redd, L
Muranyi, A
Henricksen, LA
Stanislaw, S
Smith, LM
Perry, AM
Fu, K
Weisenburger, DD
Rosenwald, A
Ott, G
Gascoyne, RD
Jaffe, ES
Campo, E
Delabie, J
Braziel, RM
Cook, JR
Tubbs, RR
Staudt, LM
Chan, WC
Steidl, C
Grogan, TM
Rimsza, LM
AF Kendrick, Samantha L.
Redd, Lucas
Muranyi, Andrea
Henricksen, Leigh A.
Stanislaw, Stacey
Smith, Lynette M.
Perry, Anamarija M.
Fu, Kai
Weisenburger, Dennis D.
Rosenwald, Andreas
Ott, German
Gascoyne, Randy D.
Jaffe, Elaine S.
Campo, Elias
Delabie, Jan
Braziel, Rita M.
Cook, James R.
Tubbs, Raymond R.
Staudt, Louis M.
Chan, Wing Chung
Steidl, Christian
Grogan, Thomas M.
Rimsza, Lisa M.
TI BCL2 antibodies targeted at different epitopes detect varying levels of
protein expression and correlate with frequent gene amplification in
diffuse large B-cell lymphoma
SO HUMAN PATHOLOGY
LA English
DT Article
DE Diffuse large B-cell lymphoma; E17 and SP66 BCL2 antibodies; Dual in
situ hybridization (dual ISH); BCL2 phosphorylation; BCL2 amplification
and translocation
ID MESSENGER-RNA; COPY NUMBER; SURVIVAL; MYC; RITUXIMAB; MUTATIONS;
SUBGROUPS; DEFINES; SUBSET
AB Patients with aggressive, BCL2 protein-positive (+) diffuse large B-cell lymphoma (DLBCL) often experience rapid disease progression that is refractory to standard therapy. However, there is potential for false-negative staining of BCL2 using the standard monoclonal mouse 124 antibody that hinders the identification of these high-risk DLBCL patients. Herein, we compare 2 alternative rabbit monoclonal antibodies (E17 and SP66) to the 124 clone in staining for BCL2 in formalin-fixed, paraffin-embedded DLBCL tissues. Overall, in 2 independent DLBCL cohorts, E17 and SP66 detected BCL2 expression more frequently than 124. In the context of MYC expression, cases identified as BCL2 (+) with SP66 demonstrated the strongest correlation with worse overall survival. The 124 clone failed to detect BCL2 expression in the majority of translocation (+), amplification (+), and activated B-cell DLBCL cases in which high levels of BCL2 protein are expected. Using dual in situ hybridization as a new tool to detect BCL2 translocation and amplification, we observed similar results as previously reported for fluorescence in situ hybridization for translocation but a higher amplification frequency, indicating that BCL2 amplification may be underreported in DLBCL. Among the discrepant cases, phosphorylation of BCL2 at T69 and/or S70 was more common than in the concordant cases and may contribute to the 124 false negatives, in addition to previously associated mutations within the epitope region. The accurate detection of BCL2 expression is important in the prognosis and treatment of DLBCL particularly with new anti-BCL2 therapies. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Kendrick, Samantha L.; Redd, Lucas; Grogan, Thomas M.; Rimsza, Lisa M.] Univ Arizona, Dept Pathol, Tucson, AZ 85724 USA.
[Muranyi, Andrea; Henricksen, Leigh A.; Stanislaw, Stacey; Grogan, Thomas M.] Ventana Med Syst Inc, Tucson, AZ 85755 USA.
[Smith, Lynette M.] Univ Nebraska Med Ctr, Dept Biostat, Omaha, NE 68198 USA.
[Perry, Anamarija M.] Univ Manitoba, Dept Pathol, Winnipeg, MB R3A 1R9, Canada.
[Fu, Kai] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA.
[Weisenburger, Dennis D.] City Hope Natl Med Ctr, Dept Pathol, Duarte, CA 91010 USA.
[Rosenwald, Andreas] Univ Wurzburg, Dept Pathol, D-97070 Wurzburg, Germany.
[Ott, German] Robert Bosch Krankenhaus, Dept Clin Pathol, D-70376 Stuttgart, Germany.
[Ott, German] Dr Margarete Fischer Bosch Inst Klin Pharmakol IK, D-70376 Stuttgart, Germany.
[Gascoyne, Randy D.; Chan, Wing Chung; Steidl, Christian] British Columbia Canc Agcy, Dept Pathol & Lab Med, Vancouver, BC V5Z 4E6, Canada.
[Jaffe, Elaine S.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Campo, Elias] Hosp Clin Barcelona, Dept Pathol, Barcelona 08028, Spain.
[Delabie, Jan] Univ Oslo, Dept Pathol, Norwegian Radium Hosp, N-0310 Oslo, Norway.
[Braziel, Rita M.] Oregon Hlth & Sci Univ, Dept Clin Pathol, Portland, OR 97239 USA.
[Cook, James R.; Tubbs, Raymond R.] Cleveland Clin, Dept Mol Pathol & Lab Med, Cleveland, OH 44195 USA.
[Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Rimsza, LM (reprint author), Univ Arizona, Dept Pathol, 1501 N Campbell Ave,Room 5208A,POB 245043, Tucson, AZ 85724 USA.
EM lrimsza@pathology.arizona.edu
RI Campo, elias/O-7192-2016;
OI Campo, elias/0000-0001-9850-9793; Delabie, Jan/0000-0001-5023-0689
FU National Cancer Institute Bethesda, MD; National Institutes of Health
(Bethesda, MD); Lymphoma Research Foundation (New York, NY); Lymphoma
Research Foundation; [CA009213]
FX This work was supported by grants from the National Cancer Institute
(CA157581) Bethesda, MD, the National Institutes of Health (Bethesda,
MD), and the Lymphoma Research Foundation (New York, NY). Samantha
Kendrick was fully supported by CA009213 and the Lymphoma Research
Foundation.
NR 27
TC 12
Z9 12
U1 2
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD OCT
PY 2014
VL 45
IS 10
BP 2144
EP 2153
DI 10.1016/j.humpath.2014.06.005
PG 10
WC Pathology
SC Pathology
GA AR3ZQ
UT WOS:000343528200021
PM 25090918
ER
PT J
AU Zein, WM
Jeffrey, BG
Wiley, HE
Turriff, AE
Tumminia, SJ
Tao, W
Bush, RA
Marangoni, D
Wen, R
Wei, LL
Sieving, PA
AF Zein, Wadih M.
Jeffrey, Brett G.
Wiley, Henry E.
Turriff, Amy E.
Tumminia, Santa J.
Tao, Weng
Bush, Ronald A.
Marangoni, Dario
Wen, Rong
Wei, Lisa L.
Sieving, Paul A.
TI CNGB3-Achromatopsia Clinical Trial With CNTF: Diminished Rod Pathway
Responses With No Evidence of Improvement in Cone Function
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE CNTF; human clinical trial; CNGB3; achromatopsia; cone photoreceptor;
rod photoreceptor; ECT implant; CNTF-releasing implant
ID CILIARY NEUROTROPHIC FACTOR; CELL INTRAOCULAR IMPLANTS; NUCLEOTIDE-GATED
CHANNELS; RETINITIS-PIGMENTOSA; GENE-THERAPY; CONGENITAL ACHROMATOPSIA;
RETINAL DEGENERATION; ANIMAL-MODELS; MICE LACKING; LONG-TERM
AB PURPOSE. Ciliary neurotrophic factor (CNTF) protects rod photoreceptors from retinal degenerative disease in multiple nonhuman models. Thus far, CNTF has failed to demonstrate rod protection in trials for human retinitis pigmentosa. Recently, CNTF was found to improve cone photoreceptor function in a canine CNGB3 achromatopsia model. This study explores whether this finding translates to humans with CNGB3 achromatopsia.
METHODS. A five-subject, open-label Phase I/II study was initiated by implanting intraocular microcapsules releasing CNTF (nominally 20 ng/d) into one eye each of CNGB3 achromat participants. Fellow eyes served as untreated controls. Subjects were followed for 1 year.
RESULTS. Pupil constriction in treated eyes gave evidence of intraocular CNTF release. Additionally, scotopic ERG responses were reduced, and dark-adapted psychophysical absolute thresholds were increased, attributable to diminished rod or rod pathway activity. Optical coherence tomography revealed that the cone-rich fovea underwent structural changes as the foveal hyporeflective zone (HRZ) became diminished in CNTF-treated eyes. No objectively measurable enhancement of cone function was found by assessments of visual acuity, mesopic increment sensitivity threshold, or the photopic ERG. Careful measurements of color hue discrimination showed no change. Nonetheless, subjects reported beneficial changes of visual function in the treated eyes, including reduced light sensitivity and aversion to bright light, which may trace to decreased effective ambient light from the pupillary constriction; further they noted slowed adaptation to darkness, consistent with CNTF action on rod photoreceptors.
CONCLUSIONS. Ciliary neurotrophic factor did not measurably enhance cone function, which reveals a species difference between human and canine CNGB3 cones in response to CNTF. (ClinicalTrials.gov number, NCT01648452.)
C1 [Zein, Wadih M.; Jeffrey, Brett G.; Wiley, Henry E.; Turriff, Amy E.; Tumminia, Santa J.; Wei, Lisa L.; Sieving, Paul A.] NEI, NIH, Bethesda, MD 20892 USA.
[Tao, Weng] Neurotech Pharmaceut Inc, Cumberland, RI USA.
[Bush, Ronald A.; Marangoni, Dario; Sieving, Paul A.] NIDCD, NIH, Bethesda, MD USA.
[Marangoni, Dario] Univ Aquila, Dept Biotechnol & Appl Clin Sci, I-67100 Laquila, Italy.
[Wen, Rong] Univ Miami, Miller Sch Med, Bascom Palmer Eye Inst, Dept Ophthalmol, Miami, FL 33136 USA.
RP Sieving, PA (reprint author), NIH, Bldg 31,Room 6A03,31 Ctr Dr,MSC 2510, Bethesda, MD 20892 USA.
EM paulsieving@nei.nih.gov
FU National Institutes of Health Intramural Research Programs of the
National Eye Institute; National Institute on Deafness and Other
Communication Disorders; National Institutes of Health [12-EI-0167,
N01-EY-12113]
FX Supported by the National Institutes of Health Intramural Research
Programs of the National Eye Institute and the National Institute on
Deafness and Other Communication Disorders. This work also was supported
by the National Institutes of Health Intramural Program Funding for
Human Protocol 12-EI-0167 and by Contract N01-EY-12113.
NR 48
TC 10
Z9 10
U1 1
U2 2
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 2014
VL 55
IS 10
BP 6301
EP 6308
DI 10.1167/iovs.14-14860
PG 8
WC Ophthalmology
SC Ophthalmology
GA AQ9DY
UT WOS:000343147100025
PM 25205868
ER
PT J
AU Doney, B
Hnizdo, E
Syamlal, G
Kullman, G
Burchfiel, C
Martin, CJ
Mujuru, P
AF Doney, Brent
Hnizdo, Eva
Syamlal, Girija
Kullman, Greg
Burchfiel, Cecil
Martin, Christopher J.
Mujuru, Priscah
TI Prevalence of Chronic Obstructive Pulmonary Disease Among US Working
Adults Aged 40 to 70 Years National Health Interview Survey Data 2004 to
2011
SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID HEALTH INTERVIEW SURVEY; NATIONAL-HEALTH; UNITED-STATES; OCCUPATIONAL
EXPOSURES; COPD; BURDEN; ASSOCIATION; POPULATION; SYMPTOMS; GENDER
AB Objective: To estimate the prevalence and prevalence odds ratios of chronic obstructive pulmonary disease (COPD) among US workers by major occupational groups. Methods: The 2004 to 2011 National Health Interview Survey data for working adults 40 to 70 years old was analyzed to estimate the prevalence of COPD by major occupational groups. Logistic regression models were used to evaluate the associations between COPD (chronic bronchitis or emphysema) and occupations. Results: The estimated overall COPD prevalence was 4.2% (95% CI, 4.0 to 4.3). The odds of COPD were highest among workers in health care support occupations (prevalence odds ratio, 1.64; 95% CI, 1.25 to 2.14) followed by food preparation and serving-related occupations (prevalence odds ratio, 1.57; 95% CI, 1.20 to 2.06). Conclusions: Prevalence varied by occupations, suggesting workplace exposures may contribute to COPD. Preventive measures such as interventions to reduce smoking may reduce the prevalence of COPD.
C1 [Doney, Brent; Hnizdo, Eva; Syamlal, Girija; Kullman, Greg; Burchfiel, Cecil] NIOSH, Morgantown, WV 26505 USA.
[Martin, Christopher J.] W Virginia Univ, Morgantown, WV 26506 USA.
[Mujuru, Priscah] NIH, Bethesda, MD 20892 USA.
RP Doney, B (reprint author), NIOSH, Div Resp Dis Studies, Surveillance Branch, Mailstop HG 900-2,1095 Willowdale Rd, Morgantown, WV 26505 USA.
EM bdoney@cdc.gov
FU Intramural CDC HHS [CC999999]
NR 36
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1076-2752
EI 1536-5948
J9 J OCCUP ENVIRON MED
JI J. Occup. Environ. Med.
PD OCT
PY 2014
VL 56
IS 10
BP 1088
EP 1093
DI 10.1097/JOM.0000000000000232
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AR4YE
UT WOS:000343591300018
PM 25285832
ER
PT J
AU Alter, H
AF Alter, H.
TI Keeping blood safe - a global challenge
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Meeting Abstract
CT Viral Hepatitis Congress
CY OCT 09-11, 2014
CL Frankfurt, GERMANY
C1 [Alter, H.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1352-0504
EI 1365-2893
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD OCT
PY 2014
VL 21
SU 2
SI SI
MA OL1
BP 1
EP 1
DI 10.1111/jvh.12331
PG 1
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA AR7DA
UT WOS:000343738800002
ER
PT J
AU Ouaguia, L
Morales, O
Wychowski, C
Carpentier, A
Aoudjehane, L
Dubuisson, J
Calmus, Y
de Launoit, Y
Conti, F
Delhem, N
AF Ouaguia, L.
Morales, O.
Wychowski, C.
Carpentier, A.
Aoudjehane, L.
Dubuisson, J.
Calmus, Y.
de Launoit, Y.
Conti, F.
Delhem, N.
TI HCV contributes to the aggravation suppressive activity of natural
regulatory T cells and induces the emergence of type 1 regulatory T
cells
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Meeting Abstract
CT Viral Hepatitis Congress
CY OCT 09-11, 2014
CL Frankfurt, GERMANY
C1 [Ouaguia, L.; Morales, O.; de Launoit, Y.; Delhem, N.] CNRS UMR 8161 Biol Inst Lille, Lille, France.
[Wychowski, C.; Dubuisson, J.] Inserm U1019 CNRS UMR8204 Ctr Infect & Immunite L, Lille, France.
[Carpentier, A.] NIH, Bethesda, MD 20892 USA.
[Aoudjehane, L.] Univ Paris 06, Paris, France.
[Aoudjehane, L.] INSERM, UMR S 938, Paris, France.
[Calmus, Y.; Conti, F.] Hop St Antoine, AP HP, Ctr Transplantat Hepat, F-75571 Paris, France.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1352-0504
EI 1365-2893
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD OCT
PY 2014
VL 21
SU 2
SI SI
MA O314
BP 18
EP 18
DI 10.1111/jvh.12332_21
PG 1
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA AR7DA
UT WOS:000343738800026
ER
PT J
AU Clayton, JA
Kornstein, SG
AF Clayton, Janine A.
Kornstein, Susan G.
TI Toward More Individualized Medicine: Introducing the Women of Color
Health Data Book, Fourth Edition
SO JOURNAL OF WOMENS HEALTH
LA English
DT Editorial Material
C1 [Clayton, Janine A.] NIH, Off Res Womens Health, Bethesda, MD 20892 USA.
[Kornstein, Susan G.] Virginia Commonwealth Univ, Sch Med, Inst Womens Hlth, Richmond, VA USA.
RP Clayton, JA (reprint author), NIH, Off Res Womens Health, Bethesda, MD 20892 USA.
EM ORWHinfo@mail.nih.gov
NR 7
TC 1
Z9 1
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
EI 1931-843X
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT 1
PY 2014
VL 23
IS 10
BP 781
EP 782
DI 10.1089/jwh.2014.1508
PG 2
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA AR0DT
UT WOS:000343237900001
PM 25259717
ER
PT J
AU Nagel, JD
AF Nagel, Joan Davis
TI Eleventh Annual NIH Interdisciplinary Women's Health Research Symposium
November 6, 2014 Introduction
SO JOURNAL OF WOMENS HEALTH
LA English
DT Editorial Material
C1 [Nagel, Joan Davis] NIH, Off Res Womens Hlth, Bethesda, MD USA.
EM ORWHINFO@mail.nih.gov
NR 4
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
EI 1931-843X
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT 1
PY 2014
VL 23
IS 10
BP 850
EP 851
PG 2
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA AR0DT
UT WOS:000343237900013
ER
PT J
AU Perera, S
Studenski, S
Newman, A
Simonsick, E
Harris, T
Schwartz, A
Visser, M
AF Perera, Subashan
Studenski, Stephanie
Newman, Anne
Simonsick, Eleanor
Harris, Tamara
Schwartz, Ann
Visser, Marjolein
CA Hlth ABC Study
TI Are Estimates of Meaningful Decline in Mobility Performance Consistent
Among Clinically Important Subgroups? (Health ABC Study)
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Balance; Epidemiology; Functional performance; Gait
ID LOWER-EXTREMITY FUNCTION; OLDER-ADULTS; PHYSICAL PERFORMANCE;
DISABILITY; ASSOCIATION; PREDICTOR; MORTALITY; AGE
AB Background. Meaningful change criteria help determine if function has improved or declined, but their magnitudes may vary across clinically relevant subgroups. We estimate meaningful decline in four common measures of physical performance in subgroups of older adults based on initial performance, demographics, chronic conditions, and health status.
Methods. We used baseline (Year 1) and Year 4 data from the Health, Aging and Body Composition (Health ABC) study, a well-functioning cohort at baseline of white and black men and women (age 70-79), to evaluate the magnitude of meaningful decline in performance (6 m gait speed, 400-m walk time (400MWT), Short Physical Performance Battery, and Health ABC Physical Performance Battery (PPB), based on self-reported perceived mobility anchors (climbing 10 steps and walking 1/4 mile). Estimates were stratified by initial performance, demographics, health status, chronic conditions, and body mass index, and compared across strata.
Results. For all four measures, small and substantial decline estimates were generally consistent among subgroups based on initial performance, demographics, health status, and chronic conditions. The only exception was for 400MWT, where men had greater estimates than women. For PPB, small change was 0.12 points, and substantial change was 0.22 points.
Conclusions. Estimates of small and substantial meaningful decline resemble those previously reported for gait speed, 400MWT, and SPPB. Magnitudes of meaningful performance decline appear to be generally consistent across strata of initial performance, demographics, health status, body mass index, and chronic conditions.
C1 [Perera, Subashan; Studenski, Stephanie] Univ Pittsburgh, Div Geriatr Med, Pittsburgh, PA 15213 USA.
[Newman, Anne] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Simonsick, Eleanor; Harris, Tamara] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
[Schwartz, Ann] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
[Visser, Marjolein] Vrije Univ Amsterdam, Dept Epidemiol & Biostat, Amsterdam, Netherlands.
RP Perera, S (reprint author), Univ Pittsburgh, Div Geriatr Med, 3471 Fifth Ave,Suite 500, Pittsburgh, PA 15213 USA.
EM ksp9@pitt.edu
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
FU National Institute on Aging [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, R01-AG028050, P30-AG024827]; NINR [R01-NR012459]; NIH,
National Institute on Aging
FX This research was supported by National Institute on Aging contracts and
grants (N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106, R01-AG028050,
P30-AG024827), NINR grant (R01-NR012459), and Intramural Research
Program of the NIH, National Institute on Aging.
NR 24
TC 13
Z9 13
U1 3
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD OCT
PY 2014
VL 69
IS 10
BP 1260
EP 1268
DI 10.1093/gerona/glu033
PG 9
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AR2JJ
UT WOS:000343410000009
PM 24615070
ER
PT J
AU Tian, Q
Erickson, KI
Simonsick, EM
Aizenstein, HJ
Glynn, NW
Boudreau, RM
Newman, AB
Kritchevsky, SB
Yaffe, K
Harris, TB
Rosano, C
AF Tian, Qu
Erickson, Kirk I.
Simonsick, Eleanor M.
Aizenstein, Howard J.
Glynn, Nancy W.
Boudreau, Robert M.
Newman, Anne B.
Kritchevsky, Stephen B.
Yaffe, Kristine
Harris, Tamara B.
Rosano, Caterina
TI Physical Activity Predicts Microstructural Integrity in Memory-Related
Networks in Very Old Adults
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Brain aging; Physical activity; Neuroimaging; Epidemiology
ID WHITE-MATTER INTEGRITY; AGING BRAIN; COGNITIVE FUNCTION;
BODY-COMPOSITION; AEROBIC FITNESS; GAIT SPEED; EXERCISE; HEALTH;
ANGIOGENESIS; VOLUME
AB Background. Although the beneficial effects of physical activity (PA) on memory and executive function are well established in older adults, little is known about the relationship between PA and brain microstructure and the contributions of physical functional limitations and chronic diseases. This study examined whether higher PA would be longitudinally associated with greater microstructural integrity in memory-and executive function-related networks and whether these associations would be independent of physical function and chronic diseases.
Methods. Diffusion tensor imaging was obtained in 2006-2008 in 276 participants (mean age = 83.0 years, 58.7% female, 41.3% black) with PA (sedentary, lifestyle active, and exercise active) measured in 1997-1998. Gait speed, cognition, depressive symptoms, cardiovascular and pulmonary diseases, hypertension, stroke, and diabetes were measured at both time points. Mean diffusivity and fractional anisotropy were computed from normal-appearing gray and white matter in frontoparietal and subcortical networks. Moderating effects of physical function and chronic diseases were tested using hierarchical regression models.
Results. Compared with the sedentary, the exercise active group had lower mean diffusivity in the medial temporal lobe and the cingulate cortex (beta, p values: -.405,.023 and -.497,.006, respectively), independent of age, sex, and race. Associations remained independent of other variables, although they were attenuated after adjustment for diabetes. Associations between PA and other neuroimaging markers were not significant.
Conclusions. Being exercise active predicts greater memory-related microstructural integrity in older adults. Future studies in older adults with diabetes are warranted to examine the neuroprotective effect of PA in these networks.
C1 [Tian, Qu; Newman, Anne B.; Rosano, Caterina] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Erickson, Kirk I.] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
[Simonsick, Eleanor M.] NIA, Translat Gerontol Branch, Intramural Res Program, Baltimore, MD 21224 USA.
[Aizenstein, Howard J.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Glynn, Nancy W.; Kritchevsky, Stephen B.] Wake Forest Sch Med, Sect Gerontol & Geriatr Med, Dept Internal Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Boudreau, Robert M.; Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat Neurol & Epidemiol, San Francisco, CA 94143 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
RP Tian, Q (reprint author), Grad Sch Publ Hlth, Dept Epidemiol, 251 Bayview Blvd,Suite 100,Rm 04B316, Baltimore, MD 21224 USA.
EM qu.tian@nih.gov
RI Newman, Anne/C-6408-2013;
OI Newman, Anne/0000-0002-0106-1150; Rosano, Caterina/0000-0002-0909-1506;
Rosano, Caterina/0000-0002-4271-6010; Boudreau,
Robert/0000-0003-0162-5187; Glynn, Nancy/0000-0003-2265-0162
FU National Institute on Aging (NIA) [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, K23-AG028966-01]; NIA [R01-AG028050, R01-AG029232,
P30-AG024827]; National Institute of Nursing Research (NINR)
[R01-NR012459]; National Institutes of Health (NIH), National Institute
on Aging
FX This research was supported by National Institute on Aging (NIA)
Contracts N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106, K23-AG028966-01;
NIA grants R01-AG028050, R01-AG029232, P30-AG024827; and National
Institute of Nursing Research (NINR) grant R01-NR012459. This research
was supported in part by the Intramural Research Program of the National
Institutes of Health (NIH), National Institute on Aging.
NR 36
TC 16
Z9 16
U1 3
U2 17
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD OCT
PY 2014
VL 69
IS 10
BP 1284
EP 1290
DI 10.1093/gerona/glt287
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AR2JJ
UT WOS:000343410000012
PM 24474004
ER
PT J
AU Carpenter, RD
Saeed, I
Bonaretti, S
Schreck, C
Keyak, JH
Streeper, T
Harris, TB
Lang, TF
AF Carpenter, R. Dana
Saeed, Isra
Bonaretti, Serena
Schreck, Carole
Keyak, Joyce H.
Streeper, Timothy
Harris, Tamara B.
Lang, Thomas F.
TI Inter-scanner differences in in vivo QCT measurements of the density and
strength of the proximal femur remain after correction with
anthropomorphic standardization phantoms
SO MEDICAL ENGINEERING & PHYSICS
LA English
DT Article
DE Quantitative computed tomography; Hip; Bone mineral density;
Biomechanics
ID LONG-DURATION SPACEFLIGHT; QUANTITATIVE COMPUTED-TOMOGRAPHY;
FINITE-ELEMENT-ANALYSIS; FEMORAL STRENGTH; BONE STRENGTH; HIP FRACTURE;
TRABECULAR BONE; CT; CALIBRATION; PRECISION
AB In multicenter studies and longitudinal studies that use two or more different quantitative computed tomography (QCT) imaging systems, anthropomorphic standardization phantoms (ASPs) are used to correct inter-scanner differences and allow pooling of data. In this study, in vivo imaging of 20 women on two imaging systems was used to evaluate inter-scanner differences in hip integral BMD (iBMD), trabecular BMD (tBMD), cortical BMD (cBMD), femoral neck yield moment (M-y) and yield force (F-y), and finite-element derived strength of the femur under stance (FEstance) and fall (FEfall) loading. Six different ASPs were used to derive inter-scanner correction equations. Significant (p < 0.05) inter-scanner differences were detected in all measurements except M-y and FEfall, and no ASP-based correction was able to reduce inter-scanner variability to corresponding levels of intra-scanner precision. Inter-scanner variability was considerably higher than intra-scanner precision, even in cases where the mean inter-scanner difference was statistically insignificant. A significant (p < 0.01) effect of body size on inter-scanner differences in BMD was detected, demonstrating a need to address the effects of body size on QCT measurements. The results of this study show that significant inter-scanner differences in QCT-based measurements of BMD and bone strength can remain even when using an ASP. (C) 2014 IPEM. Published by Elsevier Ltd. All rights reserved.
C1 [Carpenter, R. Dana] Univ Colorado, Dept Mech Engn, Denver, CO 80217 USA.
[Saeed, Isra; Bonaretti, Serena; Schreck, Carole; Streeper, Timothy; Lang, Thomas F.] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
[Keyak, Joyce H.] Univ Calif Irvine, Dept Radiol Sci, Irvine, CA 92717 USA.
[Harris, Tamara B.] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
RP Carpenter, RD (reprint author), Univ Colorado, Dept Mech Engn, Mail Stop 112,POB 173364, Denver, CO 80217 USA.
EM dana.carpenter@ucdenver.edu
OI Lang, Thomas/0000-0002-3720-8038
FU National Institute on Aging [HHSN311200800243P]; Intramural Research
Program of the National Institute on Aging
FX This study was funded by the National Institute on Aging contract
HHSN311200800243P and was supported in part by the Intramural Research
Program of the National Institute on Aging. All procedures were
authorized by the UCSF Committee on Human Research, Authorization Number
10-04697.
NR 28
TC 3
Z9 3
U1 0
U2 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1350-4533
EI 1873-4030
J9 MED ENG PHYS
JI Med. Eng. Phys.
PD OCT
PY 2014
VL 36
IS 10
BP 1225
EP 1232
DI 10.1016/j.medengphy.2014.06.010
PG 8
WC Engineering, Biomedical
SC Engineering
GA AR5ML
UT WOS:000343628600001
PM 25001172
ER
PT J
AU Sati, P
Thomasson, DM
Li, N
Pham, DL
Biassou, NM
Reich, DS
Butman, JA
AF Sati, P.
Thomasson, D. M.
Li, N.
Pham, D. L.
Biassou, N. M.
Reich, D. S.
Butman, J. A.
TI Rapid, high-resolution, whole-brain, susceptibility-based MRI of
multiple sclerosis
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Article
DE Multiple sclerosis; brain imaging; MRI; contrast agent; lesion; veins;
iron
ID WHITE-MATTER LESIONS; IN-VIVO; MS LESIONS; PARENCHYMAL VEINS; 7 T; IRON;
DEMYELINATION; VENOGRAPHY; TESLA
AB Background: Susceptibility-based MRI offers a unique opportunity to study neurological diseases such as multiple sclerosis (MS). In this work, we assessed a three-dimensional segmented echo-planar-imaging (3D-EPI) sequence to rapidly acquire high-resolution T-2*-weighted and phase contrast images of the whole brain. We also assessed if these images could depict important features of MS at clinical field strength, and we tested the effect of a gadolinium-based contrast agent (GBCA) on these images.
Materials and methods: The 3D-EPI acquisition was performed on four healthy volunteers and 15 MS cases on a 3T scanner. The 3D sagittal images of the whole brain were acquired with a voxel size of 0.55 x 0.55 x 0.55 mm(3) in less than 4 minutes. For the MS cases, the 3D-EPI acquisition was performed before, during, and after intravenous GBCA injection.
Results: Both T-2*-weighted and phase-contrast images from the 3D-EPI acquisition were sensitive to the presence of lesions, parenchymal veins, and tissue iron. Conspicuity of the veins was enhanced when images were obtained during injection of GBCA.
Conclusions: We propose this rapid imaging sequence for investigating, in a clinical setting, the spatiotemporal relationship between small parenchymal veins, iron deposition, and lesions in MS patient brains.
C1 [Sati, P.; Reich, D. S.] NINDS, Translat Neuroradiol Unit, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Thomasson, D. M.] NIAID, Integrated Res Facil, NIH, Bethesda, MD 20892 USA.
[Li, N.; Pham, D. L.; Butman, J. A.] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
[Li, N.; Pham, D. L.; Butman, J. A.] NIH, Bethesda, MD 20892 USA.
[Biassou, N. M.; Reich, D. S.; Butman, J. A.] NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA.
RP Sati, P (reprint author), NINDS, Translat Neuroradiol Unit, NIH, 9000 Rockville Pike,Bldg 10-5C101A, Bethesda, MD 20892 USA.
EM satip@ninds.nih.gov
RI Reich, Daniel/E-5701-2010; Butman, John/J-2780-2013
OI Reich, Daniel/0000-0002-2628-4334; Butman, John/0000-0002-1547-9195
FU NIH, National Institute of Neurological Disorders and Stroke; Clinical
Center at the NIH; Department of Defense in the Center for Neuroscience
and Regenerative Medicine
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Neurological Disorders and Stroke and the
Clinical Center at the NIH. Support for this work also included funding
from the Department of Defense in the Center for Neuroscience and
Regenerative Medicine.
NR 32
TC 13
Z9 13
U1 0
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
EI 1477-0970
J9 MULT SCLER J
JI Mult. Scler. J.
PD OCT
PY 2014
VL 20
IS 11
BP 1464
EP 1470
DI 10.1177/1352458514525868
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AR5KO
UT WOS:000343623900009
PM 24639479
ER
PT J
AU Kaufman, AR
Mays, D
Koblitz, AR
Portnoy, DB
AF Kaufman, Annette R.
Mays, Darren
Koblitz, Amber R.
Portnoy, David B.
TI Judgments, Awareness, and the Use of Snus Among Adults in the United
States
SO NICOTINE & TOBACCO RESEARCH
LA English
DT Article
ID TOBACCO PRODUCT USE; SMOKING-CESSATION; SMOKELESS TOBACCO; HARM
REDUCTION; RELATIVE RISK; CIGARETTES; PERCEPTIONS
AB Introduction: Alternative tobacco products, such as snus, are emerging in the U. S. market. Understanding correlates of awareness and use, particularly judgments about harm and addictiveness, can inform public health communications about these products.
Methods: Data were collected from a web panel representative of the U. S. population in March 2013 (N = 2,067). The survey assessed awareness and use of snus among adults. Absolute and comparative snus judgments, intentions, smoking status, and sociodemographic variables were measured. Bivariate and multivariable logistic regression analyses were conducted to examine associations between these variables and snus awareness and use.
Results: Nearly 36% of the population was aware of snus, and 5.2% reported ever using snus. Current cigarette smokers were about 4 times more likely as nonsmokers to report snus awareness and use. Sociodemographic correlates of snus awareness and use included being male, employed full time, and younger. Compared with respondents who perceived snus to be as harmful and as addictive as cigarettes, those who perceived snus to be less harmful and less addictive than cigarettes were more likely to have used snus.
Conclusions: Current smokers are more likely to be aware of and have used snus. Multiple tobacco product use poses a significant challenge for public health efforts to reduce tobacco-associated morbidity and mortality. Perceptions that snus is less harmful and less addictive compared with cigarettes are associated with snus use. These judgments can inform public health communications about emerging tobacco products and multiple product use.
C1 [Kaufman, Annette R.] NCI, Tobacco Control Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20850 USA.
[Mays, Darren] US FDA, Tobacco Regulatory Sci Fellowship Program, Silver Spring, MD USA.
[Mays, Darren] Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20007 USA.
[Koblitz, Amber R.; Portnoy, David B.] US FDA, Ctr Tobacco Prod, Silver Spring, MD USA.
RP Kaufman, AR (reprint author), NCI, Tobacco Control Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, 9609 Med Ctr Dr,3-E-546, Rockville, MD 20850 USA.
EM kaufmana@mail.nih.gov
OI Portnoy, David/0000-0003-2175-9457
FU National Cancer Institute; Center for Tobacco Products, U.S. Food and
Drug Administration; RTI International
FX This work was supported by the National Cancer Institute and the Center
for Tobacco Products, U.S. Food and Drug Administration. Data collection
was funded by RTI International.
NR 12
TC 10
Z9 10
U1 2
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1462-2203
EI 1469-994X
J9 NICOTINE TOB RES
JI Nicotine Tob. Res.
PD OCT
PY 2014
VL 16
IS 10
BP 1404
EP 1408
DI 10.1093/ntr/ntu116
PG 5
WC Substance Abuse; Public, Environmental & Occupational Health
SC Substance Abuse; Public, Environmental & Occupational Health
GA AR6CS
UT WOS:000343671300016
PM 25098672
ER
PT J
AU Sakakibara, Y
Kasahara, Y
Hall, FS
Lesch, KP
Murphy, DL
Uhl, GR
Sora, I
AF Sakakibara, Yasufumi
Kasahara, Yoshiyuki
Hall, F. Scott
Lesch, Klaus-Peter
Murphy, Dennis L.
Uhl, George R.
Sora, Ichiro
TI Developmental alterations in anxiety and cognitive behavior in serotonin
transporter mutant mice
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Anxiety; Spontaneous alternation; Social behavior; Dendritic spines;
Medial prefrontal cortex; Orbitofrontal cortex; Basolateral amygdala;
Adolescence
ID DENDRITIC SPINE PATHOLOGY; EARLY-LIFE BLOCKADE; KNOCK-OUT MICE;
BRAIN-DEVELOPMENT; PREFRONTAL CORTEX; 5-HT TRANSPORTER; SOCIAL APPROACH;
RAT-BRAIN; AMYGDALA; DEPRESSION
AB A promoter variant of the serotonin transporter (SERT) gene is known to affect emotional and cognitive regulation. In particular, the "short" allelic variant is implicated in the etiology of multiple neuropsychiatric disorders. Heterozygous (SERT+/-) and homozygous (SERT-/-) SERT mutant mice are valuable tools for understanding the mechanisms of altered SERT levels. Although these genetic effects are well investigated in adulthood, the developmental trajectory of altered SERT levels for behavior has not been investigated.
We assessed anxiety-like and cognitive behaviors in SERT mutant mice in early adolescence and adulthood to examine the developmental consequences of reduced SERT levels. Spine density of pyramidal neurons was also measured in corticolimbic brain regions.
Adult SERT-/- mice exhibited increased anxiety-like behavior, but these differences were not observed in early adolescent SERT-/- mice. Conversely, SERT+/- and SERT-/- mice did display higher spontaneous alternation during early adolescence and adulthood. SERT+/- and SERT-/- also exhibited greater neuronal spine densities in the orbitofrontal but not the medial prefrontal cortices. Adult SERT-/- mice also showed an increased spine density in the basolateral amygdala.
Developmental alterations of the serotonergic system caused by genetic inactivation of SERT can have different influences on anxiety-like and cognitive behaviors through early adolescence into adulthood, which may be associated with changes of spine density in the prefrontal cortex and amygdala. The altered maturation of serotonergic systems may lead to specific age-related vulnerabilities to psychopathologies that develop during adolescence.
C1 [Sakakibara, Yasufumi; Kasahara, Yoshiyuki; Sora, Ichiro] Tohoku Univ, Grad Sch Med, Dept Biol Psychiat, Aoba Ku, Sendai, Miyagi 9808574, Japan.
[Hall, F. Scott; Uhl, George R.] NIDA, Mol Neurobiol Branch, Intramural Res Program, NIH, Baltimore, MD USA.
[Lesch, Klaus-Peter] Univ Wurzburg, Div Mol Psychiat, Lab Translat Neurosci, Dept Psychiat Psychosomat & Psychotherapy, D-97070 Wurzburg, Germany.
[Murphy, Dennis L.] NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA.
RP Sora, I (reprint author), Kobe Univ, Grad Sch Med, Dept Psychiat, Kobe, Hyogo 657, Japan.
EM sora@med.tohoku.ac.jp
RI Lesch, Klaus-Peter/J-4906-2013; Hall, Frank/C-3036-2013
OI Lesch, Klaus-Peter/0000-0001-8348-153X; Hall, Frank/0000-0002-0822-4063
FU MHLW of Japan; MEXT of Japan; Intramural Research Program of the
National Institute on Drug Abuse, NIH/DHHS, USA; Ishidsu Shun Memorial
Scholarship
FX The authors gratefully thank Drs. Daisuke Suzuki and Yosefu Arime for
statistical consultation. This study was supported by a Grant-in-Aid for
Health and Labour Science Research (Research on Pharmaceutical and
Medical Safety) from MHLW of Japan; by Grants-in-Aid for Core Research
for Evolutional Science and Technology (CREST), Global COE Program
(Basic and Translational Research Center for Global Brain Science) from
MEXT of Japan and through funding from the Intramural Research Program
of the National Institute on Drug Abuse, NIH/DHHS, USA (GRU and FSH). YS
was supported by an Ishidsu Shun Memorial Scholarship. All animal
handling and experimental procedures were performed in accordance with
the Guidelines for the Care of Laboratory Animals of Tohoku University
Graduate School of Medicine (Sendai, Japan).
NR 95
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U1 3
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2014
VL 231
IS 21
BP 4119
EP 4133
DI 10.1007/s00213-014-3554-x
PG 15
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AR6WO
UT WOS:000343721600004
PM 24728652
ER
PT J
AU Blough, BE
Landavazo, A
Decker, AM
Partilla, JS
Baumann, MH
Rothman, RB
AF Blough, Bruce E.
Landavazo, Antonio
Decker, Ann M.
Partilla, John S.
Baumann, Michael H.
Rothman, Richard B.
TI Interaction of psychoactive tryptamines with biogenic amine transporters
and serotonin receptor subtypes
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Tryptamines; Shulgin; Psychedelic; Serotonin; Serotonin transporter;
Serotonin releaser; Serotonin 2A receptor; Serotonin 1A receptor;
beta-Arrestin recruitment; Psilocybin
ID LYSERGIC-ACID DIETHYLAMIDE; RAT-BRAIN; SALVINORIN-A; HALLUCINOGENS;
DOPAMINE; RELEASE; DRUGS; LSD; 3,4-METHYLENEDIOXYMETHAMPHETAMINE;
5-METHOXY-N,N-DIMETHYLTRYPTAMINE
AB Synthetic hallucinogenic tryptamines, especially those originally described by Alexander Shulgin, continue to be abused in the USA. The range of subjective experiences produced by different tryptamines suggests that multiple neurochemical mechanisms are involved in their actions, in addition to the established role of agonist activity at serotonin 2A (5-HT2A) receptors.
This study evaluated the interaction of a series of synthetic tryptamines with biogenic amine neurotransmitter transporters and with serotonin (5-HT) receptor subtypes implicated in psychedelic effects.
Neurotransmitter transporter activity was determined in rat brain synaptosomes. Receptor activity was determined using calcium mobilization and DiscoveRx PathHunterA (R) assays in HEK293, G alpha 16-CHO, and CHOk1 cells transfected with human receptors.
Twenty-one tryptamines were analyzed in transporter uptake and release assays, and 5-HT2A, serotonin 1A (5-HT1A), and 5-HT2A beta-arrestin functional assays. Eight of the compounds were found to have 5-HT-releasing activity. Thirteen compounds were found to be 5-HT uptake inhibitors or were inactive. All tryptamines were 5-HT2A agonists with a range of potencies and efficacies, but only a few compounds were 5-HT1A agonists. Most tryptamines recruited beta-arrestin through 5-HT2A activation.
All psychoactive tryptamines are 5-HT2A agonists, but 5-HT transporter (SERT) activity may contribute significantly to the pharmacology of certain compounds. The in vitro transporter data confirm structure-activity trends for releasers and uptake inhibitors whereby releasers tend to be structurally smaller compounds. Interestingly, two tertiary amines were found to be selective substrates at SERT, which dispels the notion that 5-HT-releasing activity is limited only to primary or secondary amines.
C1 [Blough, Bruce E.; Landavazo, Antonio; Decker, Ann M.] RTI Int, Ctr Drug Discovery, Durham, NC 27709 USA.
[Partilla, John S.; Baumann, Michael H.; Rothman, Richard B.] NIDA, Med Chem Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Blough, BE (reprint author), RTI Int, Ctr Drug Discovery, 3040 Cornwallis Rd, Durham, NC 27709 USA.
EM beb@rti.org
FU NIDA [DA12970]; Intramural Research Program, National Institute on Drug
Abuse, NIH, DHHS
FX We would like to thank NIDA for their financial support (DA12970).
Portions of this work were supported by the Intramural Research Program,
National Institute on Drug Abuse, NIH, DHHS.
NR 49
TC 7
Z9 7
U1 4
U2 28
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2014
VL 231
IS 21
BP 4135
EP 4144
DI 10.1007/s00213-014-3557-7
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AR6WO
UT WOS:000343721600005
PM 24800892
ER
PT J
AU Bubser, M
Bridges, TM
Dencker, D
Gould, RW
Grannan, M
Noetzel, MJ
Lamsal, A
Niswender, CM
Daniels, JS
Poslusney, MS
Melancon, BJ
Tarr, JC
Byers, FW
Wess, J
Duggan, ME
Dunlop, J
Wood, MW
Brandon, NJ
Wood, MR
Lindsley, CW
Conn, PJ
Jones, CK
AF Bubser, Michael
Bridges, Thomas M.
Dencker, Ditte
Gould, Robert W.
Grannan, Michael
Noetzel, Meredith J.
Lamsal, Atin
Niswender, Colleen M.
Daniels, J. Scott
Poslusney, Michael S.
Melancon, Bruce J.
Tarr, James C.
Byers, Frank W.
Wess, Juergen
Duggan, Mark E.
Dunlop, John
Wood, Michael W.
Brandon, Nicholas J.
Wood, Michael R.
Lindsley, Craig W.
Conn, P. Jeffrey
Jones, Carrie K.
TI Selective Activation of M-4 Muscarinic Acetylcholine Receptors Reverses
MK-801-Induced Behavioral Impairments and Enhances Associative Learning
in Rodents
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE Allosteric modulator; antipsychotic; cognitive enhancement; M4
muscarinic; MK-801; VU0467154
ID METHYL-D-ASPARTATE; ANTIPSYCHOTIC-LIKE ACTIVITY; NUCLEUS ACCUMBENS
SEPTI; NMDA RECEPTOR; ALLOSTERIC MODULATOR; AGONIST XANOMELINE;
PREFRONTAL CORTEX; MEMORY CONSOLIDATION; MOLECULAR-MECHANISMS;
DIZOCILPINE MK-801
AB Positive allosteric modulators (PAMs) of the M-4 muscarinic acetylcholine receptor (mAChR) represent a novel approach for the treatment of psychotic symptoms associated with schizophrenia and other neuropsychiatric disorders. We recently reported that the selective M-4 PAM VU0152100 produced an antipsychotic drug-like profile in rodents after amphetamine challenge. Previous studies suggest that enhanced cholinergic activity may also improve cognitive function and reverse deficits observed with reduced signaling through the N-methyl-D-aspartate subtype of the glutamate receptor (NMDAR) in the central nervous system. Prior to this study, the M-1 mAChR subtype was viewed as the primary candidate for these actions relative to the other mAChR subtypes. Here we describe the discovery of a novel M-4 PAM, VU0467154, with enhanced in vitro potency and improved pharmacokinetic properties relative to other M-4 PAMs, enabling a more extensive characterization of M-4 actions in rodent models. We used VU0467154 to test the hypothesis that selective potentiation of M-4 receptor signaling could ameliorate the behavioral, cognitive, and neurochemical impairments induced by the noncompetitive NMDAR antagonist MK-801. VU0467154 produced a robust dose-dependent reversal of MK-801-induced hyperlocomotion and deficits in preclinical models of associative learning and memory functions, including the touchscreen pairwise visual discrimination task in wild-type mice, but failed to reverse these stimulant-induced deficits in M-4 KO mice. VU0467154 also enhanced the acquisition of both contextual and cue-mediated fear conditioning when administered alone in wild-type mice. These novel findings suggest that M-4 PAMs may provide a strategy for addressing the more complex affective and cognitive disruptions associated with schizophrenia and other neuropsychiatric disorders.
C1 [Bubser, Michael; Bridges, Thomas M.; Gould, Robert W.; Grannan, Michael; Noetzel, Meredith J.; Lamsal, Atin; Niswender, Colleen M.; Daniels, J. Scott; Melancon, Bruce J.; Byers, Frank W.; Wood, Michael R.; Lindsley, Craig W.; Conn, P. Jeffrey; Jones, Carrie K.] Vanderbilt Univ, Dept Pharmacol, Med Ctr, Nashville, TN 37232 USA.
[Bubser, Michael; Bridges, Thomas M.; Gould, Robert W.; Grannan, Michael; Noetzel, Meredith J.; Lamsal, Atin; Niswender, Colleen M.; Daniels, J. Scott; Poslusney, Michael S.; Melancon, Bruce J.; Tarr, James C.; Byers, Frank W.; Wood, Michael R.; Lindsley, Craig W.; Conn, P. Jeffrey; Jones, Carrie K.] Vanderbilt Univ, Vanderbilt Ctr Neurosci Drug Discovery, Med Ctr, Nashville, TN 37232 USA.
[Bridges, Thomas M.; Noetzel, Meredith J.; Lamsal, Atin; Niswender, Colleen M.; Daniels, J. Scott; Poslusney, Michael S.; Melancon, Bruce J.; Tarr, James C.; Byers, Frank W.; Wood, Michael R.; Lindsley, Craig W.; Conn, P. Jeffrey; Jones, Carrie K.] Vanderbilt Specialized Chem Ctr Probe Dev MLPCN, Nashville, TN 37232 USA.
[Wood, Michael R.; Lindsley, Craig W.] Vanderbilt Univ, Dept Chem, Nashville, TN 37232 USA.
[Dencker, Ditte] Copenhagen Univ Hosp, Psychiat Ctr Copenhagen, Lab Neuropsychiat, DK-2100 Copenhagen, Denmark.
[Wess, Juergen] Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD 20814 USA.
[Duggan, Mark E.; Dunlop, John; Wood, Michael W.; Brandon, Nicholas J.] AstraZeneca, Neurosci Innovat Med, Cambridge, MA 02139 USA.
RP Jones, CK (reprint author), Vanderbilt Univ, Dept Pharmacol, Med Ctr, 418A PRB,2220 Pierce Ave, Nashville, TN 37232 USA.
EM carrie.jones@vanderbilt.edu
OI Bubser, Michael/0000-0002-0583-5248
FU National Institute of Mental Health [MH86601, MH87965]; Psychiatric
Center Copenhagen Research Foundation; Carlsberg Foundation; AstraZeneca
FX This work was supported by grants from the National Institute of Mental
Health to C.K.J. (Grant MH86601) and P.J.C. (Grant MH87965), the
Psychiatric Center Copenhagen Research Foundation (D.D.), the Carlsberg
Foundation (D.D.), and by AstraZeneca.
NR 71
TC 18
Z9 18
U1 2
U2 20
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 OCT
PY 2014
VL 5
IS 10
BP 920
EP 942
DI 10.1021/cn500128b
PG 23
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA AR0QO
UT WOS:000343276600009
PM 25137629
ER
PT J
AU Zanotti-Fregonara, P
Zhang, Y
Jenko, KJ
Gladding, RL
Zoghbi, SS
Fujita, M
Sbardella, G
Castellano, S
Taliani, S
Martini, C
Innis, RB
Da Settimo, F
Pike, VW
AF Zanotti-Fregonara, Paolo
Zhang, Yi
Jenko, Kimberly J.
Gladding, Robert L.
Zoghbi, Sami S.
Fujita, Masahiro
Sbardella, Gianluca
Castellano, Sabrina
Taliani, Sabrina
Martini, Claudia
Innis, Robert B.
Da Settimo, Federico
Pike, Victor W.
TI Synthesis and Evaluation of Trans locator 18 kDa Protein (TSPO) Positron
Emission Tomography (PET) Radioligands with Low Binding Sensitivity to
Human Single Nucleotide Polymorphism rs6971
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE TSPO; PET; radioligand; carbon-11; imaging; brain
ID PERIPHERAL BENZODIAZEPINE-RECEPTORS; TRANSLOCATOR PROTEIN; IN-VIVO;
HUMAN-BRAIN; GENETIC-POLYMORPHISM; ACTIVATED MICROGLIA; HEALTHY HUMANS;
FREE-FRACTION; SITES; LIGANDS
AB The imaging of translocator 18 kDa protein (TSPO) in living human brain with radioligands by positron emission tomography (PET) has become an important means for the study of neuroinflammatory conditions occurring in several neuropsychiatric disorders. The widely used prototypical PET radioligand [(11)C](R)-PK 11195 ([(11)C](R)-1; [N-methyl-(11)C](R)-N-sec-butyl-1-(2-chlorophenyl)-N-methylisoquinoline-3-carboxamide) gives a low PET signal and is difficult to quantify, whereas later generation radioligands have binding sensitivity to a human single nucleotide polymorphism (SNP) rs6971, which imposes limitations on their utility for comparative quantitative PET studies of normal and diseased subjects. Recently, azaisosteres of 1 have been developed with improved drug-like properties, including enhanced TSPO affinity accompanied by moderated lipophilicity. Here we selected three of these new ligands (7-9) for labeling with carbon-11 and for evaluation in monkey as candidate PET radioligands for imaging brain TSPO. Each radioligand was readily prepared by (11)C-methylation of an N-desmethyl precursor and was found to give a high proportion of TSPO-specific binding in monkey brain. One of these radioligands, [(11)C]7, the direct 4-azaisostere of 1, presents many radioligand properties that are superior to those reported for [(11)C]1, including higher affinity, lower lipophilicity, and stable quantifiable PET signal. Importantly, 7 was also found to show very low sensitivity to the human SNP rs6971 in vitro. Therefore, [(11)C]7 now warrants evaluation in human subjects with PET to assess its utility for imaging TSPO in human brain, irrespective of subject genotype.
C1 [Zanotti-Fregonara, Paolo; Zhang, Yi; Jenko, Kimberly J.; Gladding, Robert L.; Zoghbi, Sami S.; Fujita, Masahiro; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Sbardella, Gianluca; Castellano, Sabrina] Univ Salerno, Dept Pharm, I-84084 Fisciano, SA, Italy.
[Taliani, Sabrina; Martini, Claudia; Da Settimo, Federico] Univ Pisa, Dept Pharm, I-56126 Pisa, Italy.
RP Pike, VW (reprint author), NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
EM pikev@mail.nih.gov
RI Sbardella, Gianluca/E-2823-2010; Castellano, Sabrina/B-7635-2011; Da
Settimo, Federico/M-1451-2015;
OI Sbardella, Gianluca/0000-0003-0748-1145; Da Settimo,
Federico/0000-0002-7897-7917; TALIANI, SABRINA/0000-0001-8675-939X;
Castellano, Sabrina/0000-0002-7449-3704; Martini,
Claudia/0000-0001-9379-3027
FU Intramural Research Program of the National Institutes of Health (NIH);
National Institute of Mental Health (NIMH); MIUR
FX This study was supported by the Intramural Research Program of the
National Institutes of Health (NIH), specifically the National Institute
of Mental Health (NIMH), and MIUR (PRIN 2009, Futuro in Ricerca 2010,
PRIN 2011).
NR 51
TC 10
Z9 10
U1 4
U2 16
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 OCT
PY 2014
VL 5
IS 10
BP 963
EP 971
DI 10.1021/cn500138n
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA AR0QO
UT WOS:000343276600012
PM 25123416
ER
PT J
AU Wlodawer, A
AF Wlodawer, Alexander
TI On the prompt update of literature references in the Protein Data Bank
SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY
LA English
DT Letter
C1 NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA.
RP Wlodawer, A (reprint author), NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA.
EM wlodawer@nih.gov
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0907-4449
EI 1399-0047
J9 ACTA CRYSTALLOGR D
JI Acta Crystallogr. Sect. D-Biol. Crystallogr.
PD OCT
PY 2014
VL 70
BP 2779
EP 2779
DI 10.1107/S1399004714009973
PN 10
PG 1
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Crystallography
SC Biochemistry & Molecular Biology; Biophysics; Crystallography
GA AQ8FY
UT WOS:000343060900028
PM 25286862
ER
PT J
AU Coghill, AE
Hildesheim, A
AF Coghill, Anna E.
Hildesheim, Allan
TI Epstein-Barr Virus Antibodies and the Risk of Associated Malignancies:
Review of the Literature
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Review
DE Burkitt lymphoma; EBV antibodies; EBV immune response; EBV serology;
gastric carcinoma; Hodgkin lymphoma; nasopharyngeal carcinoma;
non-Hodgkin lymphoma
ID NON-HODGKIN-LYMPHOMA; HUMAN-IMMUNODEFICIENCY-VIRUS; NERVOUS-SYSTEM
LYMPHOMA; NASOPHARYNGEAL CARCINOMA; BURKITTS-LYMPHOMA; SERUM ANTIBODIES;
POSITIVE PERSONS; EBV PERSISTENCE; WUZHOU-CITY; B-CELLS
AB Epstein-Barr virus (EBV), a ubiquitous herpes virus that infects 90% of humans by adulthood, is linked to the development of various cancers, including nasopharyngeal carcinoma, gastric cancer, Burkitt lymphoma, non-Hodgkin lymphoma (NHL), and Hodgkin lymphoma. We reviewed the literature published since 1980 regarding an association between antibodies against EBV proteins and the risk of EBV-associated malignancies. Immunoglobulin A antibody levels that are elevated before diagnosis have consistently been associated with the risk of nasopharyngeal carcinoma, and patients with Hodgkin lymphoma have significantly higher immunoglobulin G antibody levels than disease-free controls. However, the link between the immune response to EBV and other EBV-associated malignancies was less clear. Although evidence of an association between the risk of Burkitt lymphoma and immunoglobulin G antibodies was consistent for available studies, the sample sizes were limited. Evidence for a link between antibodies against EBV and risk of either gastric cancer or NHL was inconsistent. Future investigations should account for tumor EBV status because only 7%-10% of gastric tumors and select NHL subtypes are related to EBV infection. Comparing differences in the associations between the humoral immune response to EBV and disease risk across cancers may help elucidate how this ubiquitous virus contributes to distinct tumors globally.
C1 [Coghill, Anna E.; Hildesheim, Allan] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Coghill, AE (reprint author), NCI, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM anna.coghill@nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU National Cancer Institute
FX This research was funded by the intramural program at the National
Cancer Institute.
NR 75
TC 16
Z9 17
U1 1
U2 11
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 1
PY 2014
VL 180
IS 7
BP 687
EP 695
DI 10.1093/aje/kwu176
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AQ8DU
UT WOS:000343054500004
PM 25167864
ER
PT J
AU Falk, RT
Maas, P
Schairer, C
Chatterjee, N
Mabie, JE
Cunningham, C
Buys, SS
Isaacs, C
Ziegler, RG
AF Falk, Roni T.
Maas, Paige
Schairer, Catherine
Chatterjee, Nilanjan
Mabie, Jerome E.
Cunningham, Christopher
Buys, Saundra S.
Isaacs, Claudine
Ziegler, Regina G.
TI Alcohol and Risk of Breast Cancer in Postmenopausal Women: An Analysis
of Etiological Heterogeneity by Multiple Tumor Characteristics
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE alcohol; breast cancer; ductal carcinoma; estrogen receptor; lobular
carcinoma; progesterone receptor
ID PROGESTERONE-RECEPTOR STATUS; PROSPECTIVE COHORT; SCREENING TRIAL;
POOLED ANALYSIS; CONSUMPTION; ESTROGEN; METAANALYSIS; TAMOXIFEN;
PROSTATE; THERAPY
AB Alcohol consumption is an established risk factor for breast cancer. Whether associations vary by specific tumor characteristics independent of other characteristics is unclear. We evaluated the association between alcohol consumption and breast cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial cohort (54,562 women aged 55-74 years recruited at 10 US screening centers between 1993 and 2001; median follow-up, 8.9 years; 1,905 invasive breast cancer cases). Hazard ratios and 95% confidence intervals for subtypes defined by histological type and estrogen receptor (ER)/progesterone receptor (PR) status were calculated with standard Cox models. A novel 2-stage Cox model assessed heterogeneity in risk for individual tumor characteristics while adjusting for others. Significant trends across categories of alcohol consumption were observed, with hazard ratios for those consuming 7 or more drinks per week versus never drinkers as follows: for estrogen receptor-positive (ER+) cancer, 1.48 (95% confidence interval (CI): 1.19, 1.83); for progesterone receptor-positive (PR+) cancer, 1.64 (95% CI: 1.31, 2.06); for ER+/PR+ cancer, 1.63 (95% CI: 1.30, 2.05); and for mixed ductal/lobular cancer, 2.51 (95% CI: 1.20, 5.24). For ER+ and PR+ cancers, trends were significant for ductal and mixed ductal/lobular types. PR status explained the positive association with ER status (for ER status, P-heterogeneity = 0.70 after adjustment for PR status). Alcohol consumption was not associated with all breast cancer subtypes. Future work should emphasize large collaborative studies, precise definition of subtypes, and adjustment for correlated tumor characteristics.
C1 [Falk, Roni T.; Maas, Paige; Schairer, Catherine; Chatterjee, Nilanjan; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Mabie, Jerome E.; Cunningham, Christopher] Informat Management Serv Inc, Rockville, MD USA.
[Buys, Saundra S.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
[Isaacs, Claudine] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC USA.
RP Falk, RT (reprint author), NCI, 9609 Med Ctr Dr,Room 7-E224, Bethesda, MD 20892 USA.
EM falkr@mail.nih.gov
FU Division of Cancer Epidemiology and Genetics, National Cancer Institute
FX This work was supported by the intramural research program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute.
NR 28
TC 2
Z9 2
U1 2
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 1
PY 2014
VL 180
IS 7
BP 705
EP 717
DI 10.1093/aje/kwu189
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AQ8DU
UT WOS:000343054500006
PM 25150269
ER
PT J
AU Eurlings, IMJ
Dentener, MA
Mercken, EM
de Cabo, R
Bracke, KR
Vernooy, JHJ
Wouters, EFM
Reynaert, NL
AF Eurlings, Irene M. J.
Dentener, Mieke A.
Mercken, Evi M.
de Cabo, Rafael
Bracke, Ken R.
Vernooy, Juanita H. J.
Wouters, Emiel F. M.
Reynaert, Niki L.
TI A comparative study of matrix remodeling in chronic models for COPD;
mechanistic insights into the role of TNF-alpha
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE chronic obstructive pulmonary disease; elastin; mice model; tumor
necrosis factor-alpha
ID NECROSIS-FACTOR-ALPHA; OBSTRUCTIVE PULMONARY-DISEASE; SMOKE-EXPOSED
MICE; CIGARETTE-SMOKE; INDUCED SPUTUM; MOUSE MODEL; LUNG; EMPHYSEMA;
INFLAMMATION; EXPRESSION
AB Remodeling in chronic obstructive pulmonary disease (COPD) has at least two dimensions: small airway wall thickening and destruction of alveolar walls. Recently we showed comparable alterations of the extracellular matrix (ECM) compounds collagen, hyaluoran, and elastin in alveolar and small airway walls of COPD patients. The aim of this study was to characterize and assess similarities in alveolar and small airway wall matrix remodeling in chronic COPD models. From this comparative characterization of matrix remodeling we derived and elaborated underlying mechanisms to the matrix changes reported in COPD. Lung tissue sections of chronic models for COPD, either induced by exposure to cigarette smoke, chronic intratracheal lipopolysaccharide instillation, or local tumor necrosis factor (TNF) expression [surfactant protein C (SPC)-TNF alpha mice], were stained for elastin, collagen, and hyaluronan. Furthermore TNF-alpha matrix metalloproteinase (MMP)-2, -9, and -12 mRNA expression was analyzed using qPCR and localized using immunohistochemistry. Both collagen and hyaluronan were increased in alveolar and small airway walls of all three models. Interestingly, elastin contents were differentially affected, with a decrease in both alveolar and airway walls in SPC-TNF alpha mice. Furthermore TNF-alpha and MMP-2 and -9 mRNA and protein levels were found to be increased in alveolar walls and around airway walls only in SPC-TNF alpha mice. We show that only SPC-TNF alpha mice show changes in elastin remodeling that are comparable to what has been observed in COPD patients. This reveals that the SPC-TNF alpha model is a suitable model to study processes underlying matrix remodeling and in particular elastin breakdown as seen in COPD. Furthermore we indicate a possible role for MMP-2 and MMP-9 in the breakdown of elastin in airways and alveoli of SPC-TNF alpha mice.
C1 [Eurlings, Irene M. J.; Dentener, Mieke A.; Vernooy, Juanita H. J.; Wouters, Emiel F. M.; Reynaert, Niki L.] Maastricht Univ, Med Ctr, NUTRIM Sch Nutr Toxicol & Metab, Dept Resp Med, Maastricht, Netherlands.
[Mercken, Evi M.; de Cabo, Rafael] NIA, Expt Gerontol Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Bracke, Ken R.] Ghent Univ Hosp, Dept Resp Med, Lab Translat Res Obstruct Pulm Dis, Ghent, Belgium.
RP Eurlings, IMJ (reprint author), Univ Hosp Maastricht, Dept Resp Med, POB 5800, NL-6202 AZ Maastricht, Netherlands.
EM irene.eurlings@maastrichtuniversity.nl
RI Reynaert, Niki/C-5491-2014; de Cabo, Rafael/J-5230-2016
OI de Cabo, Rafael/0000-0002-3354-2442
FU Intramural Research Program of the National Institute on Aging
FX For the SPC-TNF alpha study, funding was provided by the Intramural
Research Program of the National Institute on Aging.
NR 39
TC 15
Z9 15
U1 0
U2 11
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1040-0605
EI 1522-1504
J9 AM J PHYSIOL-LUNG C
JI Am. J. Physiol.-Lung Cell. Mol. Physiol.
PD OCT 1
PY 2014
VL 307
IS 7
BP L557
EP L565
DI 10.1152/ajplung.00116.2014
PG 9
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA AR0FV
UT WOS:000343245600006
PM 25106431
ER
PT J
AU Kiley, JP
Gibbons, GH
AF Kiley, James P.
Gibbons, Gary H.
TI Primary and Secondary Prevention of Chronic Obstructive Pulmonary
Disease: Where to Next? Reply
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Letter
ID CHRONIC LUNG-DISEASES; NHLBI WORKSHOP
C1 [Kiley, James P.; Gibbons, Gary H.] Natl Heart Lung & Blood Inst, NIH, Bethesda, MD 20892 USA.
RP Kiley, JP (reprint author), Natl Heart Lung & Blood Inst, NIH, Bethesda, MD 20892 USA.
NR 8
TC 0
Z9 0
U1 0
U2 1
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD OCT 1
PY 2014
VL 190
IS 7
BP 840
EP 841
PG 2
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA AQ7TS
UT WOS:000343022700023
PM 25271752
ER
PT J
AU Sieber, BA
Landis, S
Koroshetz, W
Bateman, R
Siderowf, A
Galpern, WR
Dunlop, J
Finkbeiner, S
Sutherland, M
Wang, H
Lee, VMY
Orr, HT
Gwinn, K
Ludwig, K
Taylor, A
Torborg, C
Montine, TJ
AF Sieber, Beth-Anne
Landis, Story
Koroshetz, Walter
Bateman, Randall
Siderowf, Andrew
Galpern, Wendy R.
Dunlop, John
Finkbeiner, Steven
Sutherland, Margaret
Wang, Hao
Lee, Virginia M. -Y.
Orr, Harry T.
Gwinn, Katrina
Ludwig, Kip
Taylor, Anna
Torborg, Christine
Montine, Thomas J.
CA Parkinson's Dis 2014 Advancing Res
TI Prioritized Research Recommendations from the National Institute of
Neurological Disorders and Stroke Parkinson's Disease 2014 Conference
SO ANNALS OF NEUROLOGY
LA English
DT Editorial Material
ID BURDEN
C1 [Sieber, Beth-Anne; Landis, Story; Koroshetz, Walter; Galpern, Wendy R.; Sutherland, Margaret; Wang, Hao; Gwinn, Katrina; Ludwig, Kip; Taylor, Anna; Torborg, Christine] NINDS, Bethesda, MD 20892 USA.
[Bateman, Randall] Washington Univ, Dept Neurol, St Louis, MO USA.
[Siderowf, Andrew] Avid Radiopharmaceut, Philadelphia, PA USA.
[Dunlop, John] AstraZeneca, Cambridge, MA USA.
[Finkbeiner, Steven] Gladstone Inst Neurol Dis, San Francisco, CA USA.
[Lee, Virginia M. -Y.] Univ Penn, Inst Aging, Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA.
[Lee, Virginia M. -Y.] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA USA.
[Orr, Harry T.] Univ Minnesota, Dept Lab Med & Pathol, Inst Translat Neurosci, Minneapolis, MN 55455 USA.
[Montine, Thomas J.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
RP Sieber, BA (reprint author), NINDS, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
OI Taylor, Anna/0000-0002-6501-3393; Gwinn, Katrina/0000-0002-8277-651X
FU NINDS NIH HHS [P50 NS053488]
NR 10
TC 12
Z9 12
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2014
VL 76
IS 4
BP 469
EP 472
DI 10.1002/ana.24261
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ8FB
UT WOS:000343058400002
PM 25164235
ER
PT J
AU Maggi, P
Macri, SMC
Gaitan, MI
Leibovitch, E
Wholer, JE
Knight, HL
Ellis, M
Wu, TX
Silva, AC
Massacesi, L
Jacobson, S
Westmoreland, S
Reich, DS
AF Maggi, Pietro
Macri, Sheila M. Cummings
Gaitan, Maria I.
Leibovitch, Emily
Wholer, Jillian E.
Knight, Heather L.
Ellis, Mary
Wu, Tianxia
Silva, Afonso C.
Massacesi, Luca
Jacobson, Steven
Westmoreland, Susan
Reich, Daniel S.
TI The Formation of Inflammatory Demyelinated Lesions in Cerebral White
Matter
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID MULTIPLE-SCLEROSIS LESIONS; CENTRAL-NERVOUS-SYSTEM; BLOOD-BRAIN-BARRIER;
MACROPHAGE DIFFERENTIATION; ACTIVATION; MRI; CELLS; MODEL; CNS;
PATHOGENESIS
AB Objective: Vascular permeability and inflammatory demyelination are intimately linked in the brain, but what is their temporal relationship? We aimed to determine the radiological correlates of the earliest tissue changes accompanying demyelination in a primate model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE) in the common marmoset.
Methods: By 7T magnetic resonance imaging (MRI), T1 maps, proton density, and T2-weighted images were acquired before and after EAE induction in 5 marmosets (every other week before lesions appeared, weekly thereafter). From scans before and after intravenous injection of contrast material, we measured the evolution of lesional blood-brain barrier (BBB) permeability, comparing in vivo MRI to postmortem tissue examination.
Results: On average, BBB permeability increased 3.5-fold (p<0.0001) over the 4 weeks prior to lesion appearance. Permeability gradually decreased after lesion appearance, with attendant changes in the distribution of inflammatory cells (predominantly macrophages and microglia) and demyelination. On tissue analysis, we also identified small perivascular foci of microglia and T cells without blood-derived macrophages or demyelination. These foci had no visible MRI correlates, although permeability within the foci, but not outside, increased in the weeks before the animals died (p<0.0001).
Interpretation: This study provides compelling evidence that in marmoset EAE, which forms lesions strongly resembling those of MS, early changes in vascular permeability are associated with perivascular inflammatory cuffing and parenchymal microglial activation but precede the arrival of blood-derived monocytes that accompany demyelination. Prospective detection of transient permeability changes could afford an opportunity for early intervention to forestall tissue damage in newly forming lesions.
C1 [Maggi, Pietro; Gaitan, Maria I.; Leibovitch, Emily; Wholer, Jillian E.; Wu, Tianxia; Silva, Afonso C.; Massacesi, Luca; Jacobson, Steven; Reich, Daniel S.] NINDS, NIH, Bethesda, MD 20892 USA.
[Maggi, Pietro; Massacesi, Luca] Univ Florence, Dept Neurosci Drug Res & Childs Hlth, Florence, Italy.
[Macri, Sheila M. Cummings; Knight, Heather L.; Ellis, Mary; Westmoreland, Susan] Harvard Univ, Sch Med, New England Primate Res Ctr, Southborough, MA 01772 USA.
[Leibovitch, Emily] George Washington Univ, Inst Biomed Sci, Washington, DC USA.
RP Reich, DS (reprint author), NINDS, Translat Neuroradiol Unit, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM daniel.reich@nih.gov
RI Reich, Daniel/E-5701-2010;
OI Reich, Daniel/0000-0002-2628-4334; Massacesi, Luca/0000-0001-5083-372X
FU NIH National Institute of Neurological Disorders and Stroke
FX This research was supported by the Intramural Research Program of the
NIH National Institute of Neurological Disorders and Stroke.
NR 46
TC 22
Z9 22
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2014
VL 76
IS 4
BP 594
EP 608
DI 10.1002/ana.24242
PG 15
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ8FB
UT WOS:000343058400015
PM 25088017
ER
PT J
AU Greig, NH
Sambamurti, K
Lahiri, DK
Becker, RE
AF Greig, Nigel H.
Sambamurti, Kumar
Lahiri, Debomoy K.
Becker, Robert E.
TI Amyloid-beta Precursor Protein Synthesis Inhibitors for Alzheimer's
Disease Treatment
SO ANNALS OF NEUROLOGY
LA English
DT Letter
ID DRUG; POSIPHEN; PEPTIDE
C1 [Greig, Nigel H.; Becker, Robert E.] NIA, Drug Design & Dev Sect, Translat Gerontol Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
[Sambamurti, Kumar] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
[Lahiri, Debomoy K.] Indiana Univ Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA.
[Lahiri, Debomoy K.] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Becker, Robert E.] Aristea Translat Med Corp, Carrabassett Valley, ME USA.
RP Greig, NH (reprint author), NIA, Drug Design & Dev Sect, Translat Gerontol Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
FU Intramural NIH HHS [ZIA AG000311-14]
NR 7
TC 0
Z9 0
U1 3
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2014
VL 76
IS 4
BP 629
EP 630
DI 10.1002/ana.24254
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ8FB
UT WOS:000343058400019
PM 25146731
ER
PT J
AU Bosetti, C
Rosato, V
Li, D
Silverman, D
Petersen, GM
Bracci, PM
Neale, RE
Muscat, J
Anderson, K
Gallinger, S
Olson, SH
Miller, AB
Bueno-de-Mesquita, HB
Scelo, G
Janout, V
Holcatova, I
Lagiou, P
Serraino, D
Lucenteforte, E
Fabianova, E
Ghadirian, P
Baghurst, PA
Zatonski, W
Foretova, L
Fontham, E
Bamlet, WR
Holly, EA
Negri, E
Hassan, M
Prizment, A
Cotterchio, M
Cleary, S
Kurtz, RC
Maisonneuve, P
Trichopoulos, D
Polesel, J
Duell, EJ
Boffetta, P
La Vecchia, C
AF Bosetti, C.
Rosato, V.
Li, D.
Silverman, D.
Petersen, G. M.
Bracci, P. M.
Neale, R. E.
Muscat, J.
Anderson, K.
Gallinger, S.
Olson, S. H.
Miller, A. B.
Bueno-de-Mesquita, H. Bas
Scelo, G.
Janout, V.
Holcatova, I.
Lagiou, P.
Serraino, D.
Lucenteforte, E.
Fabianova, E.
Ghadirian, P.
Baghurst, P. A.
Zatonski, W.
Foretova, L.
Fontham, E.
Bamlet, W. R.
Holly, E. A.
Negri, E.
Hassan, M.
Prizment, A.
Cotterchio, M.
Cleary, S.
Kurtz, R. C.
Maisonneuve, P.
Trichopoulos, D.
Polesel, J.
Duell, E. J.
Boffetta, P.
La Vecchia, C.
TI Diabetes, antidiabetic medications, and pancreatic cancer risk: an
analysis from the International Pancreatic Cancer Case-Control
Consortium
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE oral antidiabetics; case-control study; diabetes; insulin; pancreatic
cancer; pooled analysis
ID BODY-MASS INDEX; TEMPORAL ASSOCIATION; GLUCOSE-METABOLISM; MELLITUS;
METAANALYSIS; INSULIN; HISTORY; PREVALENCE; DIAGNOSIS; METFORMIN
AB Background: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time-risk relationship are unclear, and there is limited information on the role of antidiabetic medications.
Patients and methods: We analyzed individual-level data from 15 case-control studies within the Pancreatic Cancer Case-Control Consortium, including 8305 cases and 13 987 controls. Pooled odds ratios (ORs) were estimated from multiple logistic regression models, adjusted for relevant covariates.
Results: Overall, 1155 (15%) cases and 1087 (8%) controls reported a diagnosis of diabetes 2 or more years before cancer diagnosis (or interview, for controls), corresponding to an OR of 1.90 (95% confidence interval, CI, 1.72-2.09). Consistent risk estimates were observed across strata of selected covariates, including body mass index and tobacco smoking. Pancreatic cancer risk decreased with duration of diabetes, but a significant excess risk was still evident 20 or more years after diabetes diagnosis (OR 1.30, 95% CI 1.03-1.63). Among diabetics, long duration of oral antidiabetic use was associated with a decreased pancreatic cancer risk (OR 0.31, 95% CI 0.14-0.69, for >= 15 years). Conversely, insulin use was associated with a pancreatic cancer risk in the short term (OR 5.60, 95% CI 3.75-8.35, for <5 years), but not for longer duration of use (OR 0.95, 95% CI 0.53-1.70, for >= 15 years).
Conclusion: This study provides the most definitive quantification to date of an excess risk of pancreatic cancer among diabetics. It also shows that a 30% excess risk persists for more than two decades after diabetes diagnosis, thus supporting a causal role of diabetes in pancreatic cancer. Oral antidiabetics may decrease the risk of pancreatic cancer, whereas insulin showed an inconsistent duration-risk relationship.
C1 [Bosetti, C.; Rosato, V.; Negri, E.] IRCCS Ist Ric Farmacol Mario Negri, Dept Epidemiol, I-2056 Milan, Italy.
[Li, D.; Hassan, M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Silverman, D.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Petersen, G. M.; Bamlet, W. R.] Mayo Clin, Dept Hlth Sci Res Med & Med Genet, Rochester, MN USA.
[Bracci, P. M.; Holly, E. A.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Neale, R. E.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Muscat, J.] Penn State Univ, Dept Publ Hlth Sci, University Pk, PA 16802 USA.
[Anderson, K.; Prizment, A.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Gallinger, S.; Cleary, S.] Univ Toronto, Dept Surg, Univ Hlth Network, Toronto, ON, Canada.
[Olson, S. H.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Miller, A. B.; Cotterchio, M.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Bueno-de-Mesquita, H. Bas] Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.
[Bueno-de-Mesquita, H. Bas] Univ Med Ctr Utrecht UMCU, Dept Gastroenterol & Hepatol, Utrecht, Netherlands.
[Bueno-de-Mesquita, H. Bas] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
[Scelo, G.] Int Agcy Res Canc, F-69372 Lyon, France.
[Janout, V.] Palacky Univ, Fac Med, Dept Prevent Med, CR-77147 Olomouc, Czech Republic.
[Holcatova, I.] Charles Univ Prague, Fac Med 1, Inst Hyg & Epidemiol, Prague, Czech Republic.
[Lagiou, P.; Trichopoulos, D.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Lagiou, P.] Univ Athens, Sch Med, Dept Hyg Epidemiol & Med Stat, GR-11527 Athens, Greece.
[Serraino, D.; Polesel, J.] IRCCS, CRO Aviano Natl Canc Inst, Unit Epidemiol & Biostat, Aviano, Italy.
[Lucenteforte, E.] Univ Florence, Dept Preclin & Clin Pharmacol Mario Aiazz, Florence, Italy.
[Fabianova, E.] Reg Author Publ Hlth Banska Bystrica, Banska Bystrica, Slovakia.
[Baghurst, P. A.] Womens & Childrens Hosp, Adelaide, SA, Australia.
[Zatonski, W.] Canc Ctr & Inst Oncol, Warsaw, Poland.
[Foretova, L.] Inst & MF MU, Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
[Fontham, E.] Louisiana State Univ, Sch Publ Hlth, New Orleans, LA USA.
[Cotterchio, M.] Canc Care Ontario, Toronto, ON, Canada.
[Kurtz, R. C.] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
[Maisonneuve, P.] European Inst Oncol, Div Epidemiol & Biostat, Milan, Italy.
[Duell, E. J.] Catalan Inst Oncol ICO IDIBELL, Unit Nutr Environm & Canc, Barcelona, Spain.
[Boffetta, P.] Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA.
[Boffetta, P.] Icahn Sch Med Mt Sinai, Inst Translat Epidemiol, New York, NY 10029 USA.
[La Vecchia, C.] Univ Milan, Dept Clin Sci & Community Hlth, Milan, Italy.
RP Bosetti, C (reprint author), IRCCS Ist Ric Farmacol Mario Negri, Dept Epidemiol, Via La Masa 19, I-2056 Milan, Italy.
EM cristina.bosetti@marionegri.it
RI Gallinger, Steven/E-4575-2013; Janout, Vladimir/M-5133-2014; Rosato,
Valentina/K-6482-2016;
OI Rosato, Valentina/0000-0003-3123-4072; Duell, Eric
J/0000-0001-5256-0163; Serraino, Diego/0000-0003-0565-8920; La Vecchia,
Carlo/0000-0003-1441-897X; Lucenteforte, Ersilia/0000-0001-5608-5902;
Neale, Rachel/0000-0001-7162-0854; Maisonneuve,
Patrick/0000-0002-5309-4704
FU Italian Association for Cancer Research (AIRC) [13203]; Grant Agency of
Ministry of Health of the Czech Republic [IGA MZ CR 8090-3, 9422-3]; MH
CZ-DRO (MMCI) [00209805]; RECAMO [CZ.1.05/2.1.00/03.0101]; Italian
Association for Cancer Research; Louisiana Board of Regents Millennium
Trust Health Excellence Fund [5: HEF 2000-05]; National Institutes of
Health (NIH) US [P50 CA102701, P01CA068384]; NIH Research Project Grant
Program [RO1 CA98380]; Prevention, Control, and Population Research
Goldstein Award; Society of MSKCC; Geoffrey Beene Cancer Research Fund;
Intramural Research Program of the National Institute of Health,
National Cancer Institute, Division of Cancer Epidemiology and Genetics
[N01-CP-51090, N01-CP-51089, N01-CP-51092, N01-CP-05225, N01-CP-31022,
N01-CP-05227]; National Health and Medical Research Council (Australia)
[442302]; Cancer Research Society; National Institutes of Health (as
part of the PACGENE consortium) [R01 CA97075]; National Institutes of
Health [U01-CA74783]; Lustgarten Foundation for Pancreatic Cancer
Research; Ontario Cancer Research Network; National Cancer Institute
[CA59706, CA108370, CA109767, CA89726, CA098889]; Rombauer Pancreatic
Cancer Research Fund; California Department of Public Health, the
National Cancer Institute's Surveillance, Epidemiology and End Results
Program [N01-PC-35136]; Red Tematica de Investigacion Cooperativa en
Cancer (RTICC) [Rd06/0020/0091, Rd12/0036/0018]; Generalitat de
Catalunya; National Health and Medical Research Council (Australia)
Senior Research Fellowship
FX This work was conducted with the contribution of the Italian Association
for Cancer Research (AIRC, project N. 13203, PI CB) and within the COST
Action (BM1214) EU-Pancreas. The Central Europe study was supported by
the Grant Agency of Ministry of Health of the Czech Republic (IGA MZ CR
8090-3 and 9422-3). The center of Brno, Czech Republic-within the
Central Europe study-was supported by MH CZ-DRO (MMCI, 00209805) and
RECAMO CZ.1.05/2.1.00/03.0101. The Italy and Milan studies were
supported by the Italian Association for Cancer Research. The Louisiana
State University study was supported by the Louisiana Board of Regents
Millennium Trust Health Excellence Fund (Project 5: HEF 2000-05,
Genetics Studies in the Acadian Population). The Mayo Clinic Biospecimen
Resource for Pancreas Research is partially supported by The National
Institutes of Health (NIH) US (P50 CA102701). The MD Anderson Cancer
Center study was supported by the NIH Research Project Grant Program
(RO1 CA98380). The Pancreatic Cancer Family Registry at the Memorial
Sloan Kettering Cancer Center (MSKCC) was supported by the Prevention,
Control, and Population Research Goldstein Award; the Society of MSKCC;
and the Geoffrey Beene Cancer Research Fund. The NCI study was supported
by the Intramural Research Program of the National Institute of Health,
National Cancer Institute, Division of Cancer Epidemiology and Genetics
(contract numbers: N01-CP-51090, N01-CP-51089, N01-CP-51092,
N01-CP-05225, N01-CP-31022, and N01-CP-05227). The Penn State study was
supported by the National Institutes of Health (NIH) US (P01CA068384).
The Queensland Pancreatic Cancer study was funded by the National Health
and Medical Research Council (Australia) (grant 442302). The Montreal
investigation in the Surveillance of Environmental Aspects Related to
Cancer in Humans study was supported by the Cancer Research Society, the
Toronto contribution was supported by the National Cancer Institute of
Canada, and the Netherlands contribution was supported by the Dutch
Ministry of Public Health, Welfare and Sports (formerly Welfare, Health
and Culture). The Ontario Pancreas Cancer Study was supported by grants
from the National Institutes of Health (R01 CA97075, as part of the
PACGENE consortium and U01-CA74783), the Lustgarten Foundation for
Pancreatic Cancer Research, and the Ontario Cancer Research Network. The
University of California, San Francisco (UCSF) study work was supported
in part by National Cancer Institute grants (CA59706, CA108370,
CA109767, CA89726, and CA098889), and by the Rombauer Pancreatic Cancer
Research Fund. Cancer incidence data collection in the UCSF study was
supported by the California Department of Public Health, the National
Cancer Institute's Surveillance, Epidemiology and End Results Program
(contract N01-PC-35136) awarded to the Northern California Cancer
Center. EJD was supported by the Red Tematica de Investigacion
Cooperativa en Cancer (RTICC; Rd06/0020/0091 and Rd12/0036/0018) and by
the Generalitat de Catalunya. REN was funded by a National Health and
Medical Research Council (Australia) Senior Research Fellowship.
NR 49
TC 34
Z9 35
U1 1
U2 23
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD OCT
PY 2014
VL 25
IS 10
BP 2065
EP 2072
DI 10.1093/annonc/mdu276
PG 9
WC Oncology
SC Oncology
GA AQ8BG
UT WOS:000343045500029
PM 25057164
ER
PT J
AU Dores, GM
Curtis, RE
van Leeuwen, FE
Stovall, M
Hall, P
Lynch, CF
Smith, SA
Weathers, RE
Storm, HH
Hodgson, DC
Kleinerman, RA
Joensuu, H
Johannesen, TB
Andersson, M
Holowaty, EJ
Kaijser, M
Pukkala, E
Vaalavirta, L
Fossa, SD
Langmark, F
Travis, LB
Fraumeni, JF
Aleman, BM
Morton, LM
Gilbert, ES
AF Dores, G. M.
Curtis, R. E.
van Leeuwen, F. E.
Stovall, M.
Hall, P.
Lynch, C. F.
Smith, S. A.
Weathers, R. E.
Storm, H. H.
Hodgson, D. C.
Kleinerman, R. A.
Joensuu, H.
Johannesen, T. B.
Andersson, M.
Holowaty, E. J.
Kaijser, M.
Pukkala, E.
Vaalavirta, L.
Fossa, S. D.
Langmark, F.
Travis, L. B.
Fraumeni, J. F., Jr.
Aleman, B. M.
Morton, L. M.
Gilbert, E. S.
TI Pancreatic cancer risk after treatment of Hodgkin lymphoma
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE Hodgkin lymphoma; pancreatic cancer; radiotherapy; chemotherapy; second
cancer
ID LONG-TERM SURVIVORS; CHILDHOOD-CANCER; GASTROINTESTINAL CANCER;
STOMACH-CANCER; DISEASE; CHEMOTHERAPY; RADIOTHERAPY
AB Background: Although elevated risks of pancreatic cancer have been observed in long-term survivors of Hodgkin lymphoma (HL), no prior study has assessed the risk of second pancreatic cancer in relation to radiation dose and specific chemotherapeutic agents.
Patients and methods: We conducted an international case-control study within a cohort of 19 882 HL survivors diagnosed from 1953 to 2003 including 36 cases and 70 matched controls.
Results: Median ages at HL and pancreatic cancer diagnoses were 47 and 60.5 years, respectively; median time to pancreatic cancer was 19 years. Pancreatic cancer risk increased with increasing radiation dose to the pancreatic tumor location (P-trend = 0.005) and increasing number of alkylating agent (AA)-containing cycles of chemotherapy (P-trend = 0.008). The odds ratio (OR) for patients treated with both subdiaphragmatic radiation (>= 10 Gy) and >= 6 AA-containing chemotherapy cycles (13 cases, 6 controls) compared with patients with neither treatment was 17.9 (95% confidence interval 3.5-158). The joint effect of these two treatments was significantly greater than additive (P = 0.041) and nonsignificantly greater than multiplicative (P = 0.29). Especially high risks were observed among patients receiving >= 8400 mg/m(2) of procarbazine with nitrogen mustard or >= 3900 mg/m(2) of cyclophosphamide.
Conclusion: Our study demonstrates for the first time that both radiotherapy and chemotherapy substantially increase pancreatic cancer risks among HL survivors treated in the past. These findings extend the range of nonhematologic cancers associated with chemotherapy and add to the evidence that the combination of radiotherapy and chemotherapy can lead to especially large risks.
C1 [Dores, G. M.; Curtis, R. E.; Kleinerman, R. A.; Fraumeni, J. F., Jr.; Morton, L. M.; Gilbert, E. S.] NCI, Div Canc Epidemiol & Genet, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Dores, G. M.] Dept Vet Affairs Med Ctr, Oklahoma City, OK USA.
[van Leeuwen, F. E.] Netherlands Canc Inst, Dept Epidemiol & Biostat, Amsterdam, Netherlands.
[Stovall, M.; Smith, S. A.; Weathers, R. E.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
[Hall, P.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Lynch, C. F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Storm, H. H.] Danish Canc Soc, Copenhagen, Denmark.
[Hodgson, D. C.] Univ Toronto, Dept Radiat Oncol, Toronto, ON, Canada.
[Joensuu, H.; Vaalavirta, L.] Univ Helsinki, Cent Hosp, Dept Oncol, Helsinki, Finland.
[Johannesen, T. B.; Langmark, F.] Canc Registry Norway, Oslo, Norway.
[Andersson, M.] Copenhagen Univ Hosp, Dept Oncol, Copenhagen, Denmark.
[Holowaty, E. J.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Kaijser, M.] Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.
[Pukkala, E.] Finnish Canc Registry, Inst Stat & Epidemiol Canc Res, FIN-00170 Helsinki, Finland.
[Pukkala, E.] Univ Tampere, Sch Hlth Sci, FIN-33101 Tampere, Finland.
[Fossa, S. D.] Oslo Univ Hosp, Dept Oncol, Oslo, Norway.
[Fossa, S. D.] Univ Oslo, Oslo, Norway.
[Travis, L. B.] Univ Rochester, Med Ctr, Dept Radiat Oncol, Rochester, NY 14627 USA.
[Aleman, B. M.] Netherlands Canc Inst, Dept Radiat Oncol, Amsterdam, Netherlands.
RP Dores, GM (reprint author), Vet Affairs Med Ctr, 921 NE 13th St, Oklahoma City, OK 73104 USA.
EM doresg@mail.nih.gov
RI Morton, Lindsay/B-5234-2015;
OI Morton, Lindsay/0000-0001-9767-2310; Storm, Hans/0000-0001-7223-8198;
Kleinerman, Ruth/0000-0001-7415-2478; Joensuu,
Heikki/0000-0003-0281-2507
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health, Department of Health and Human Services; National
Cancer Institute [N01-CP-31157]; Danish Cancer Society, Copenhagen,
Denmark [N01-CP-31019]; Finnish Cancer Registry, Helsinki, Finland
[N01-CP-31154]; Information Management Services, Inc., Silver Spring,
USA [N01-CP-31003]; Karolinska Institute, Stockholm, Sweden
[N01-CP-31156]; University of Iowa, Iowa City, USA [N01-CP-31155];
University of Texas MD Anderson Cancer Center, Houston, USA
[N02-CP-55503]; Westat, Inc., Rockville, USA [N02-CP-31136]; Lance
Armstrong Foundation; Dutch Cancer Society [NKI 04-3068]
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health, Department of
Health and Human Services, and National Cancer Institute contracts to
Cancer Care Ontario, Toronto, Canada (N01-CP-31157); Danish Cancer
Society, Copenhagen, Denmark (N01-CP-31019); Finnish Cancer Registry,
Helsinki, Finland (N01-CP-31154); Information Management Services, Inc.,
Silver Spring, USA (N01-CP-31003); Karolinska Institute, Stockholm,
Sweden (N01-CP-31156); University of Iowa, Iowa City, USA
(N01-CP-31155); The University of Texas MD Anderson Cancer Center,
Houston, USA (N02-CP-55503); and Westat, Inc., Rockville, USA
(N02-CP-31136). The Dutch study also was supported by the Lance
Armstrong Foundation and the Dutch Cancer Society (grant no. NKI
04-3068).
NR 27
TC 11
Z9 11
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD OCT
PY 2014
VL 25
IS 10
BP 2073
EP 2079
DI 10.1093/annonc/mdu287
PG 7
WC Oncology
SC Oncology
GA AQ8BG
UT WOS:000343045500030
PM 25185241
ER
PT J
AU Iribarne, A
Chang, H
Alexander, JH
Gillinov, AM
Moquete, E
Puskas, JD
Bagiella, E
Acker, MA
Mayer, ML
Ferguson, TB
Burks, S
Perrault, LP
Welsh, S
Johnston, KC
Murphy, M
DeRose, JJ
Neill, A
Dobrev, E
Baio, KT
Taddei-Peters, W
Moskowitz, AJ
O'Gara, PT
AF Iribarne, Alexander
Chang, Helena
Alexander, John H.
Gillinov, A. Marc
Moquete, Ellen
Puskas, John D.
Bagiella, Emilia
Acker, Michael A.
Mayer, Mary Lou
Ferguson, T. Bruce
Burks, Sandra
Perrault, Louis P.
Welsh, Stacey
Johnston, Karen C.
Murphy, Mandy
DeRose, Joseph J.
Neill, Alexis
Dobrev, Edlira
Baio, Kim T.
Taddei-Peters, Wendy
Moskowitz, Alan J.
O'Gara, Patrick T.
TI Readmissions After Cardiac Surgery: Experience of the National
Institutes of Health/Canadian Institutes of Health Research
Cardiothoracic Surgical Trials Network
SO ANNALS OF THORACIC SURGERY
LA English
DT Article; Proceedings Paper
CT 49th Annual Meeting of the Society-of-Thoracic-Surgeons
CY JAN 26-30, 2013
CL Los Angeles, CA
SP Soc Thorac Surg
ID CORONARY-ARTERY-BYPASS; 30-DAY READMISSIONS; HOSPITAL READMISSION;
GRAFT-SURGERY; PREDICTORS; QUALITY; CARE; ASSOCIATION; INFECTIONS;
PREVENTION
AB Background. Readmissions are a common problem in cardiac surgery. The goal of this study was to examine the frequency, timing, and associated risk factors for readmission after cardiac operations.
Methods. A 10-center cohort study prospectively enrolled 5,158 adult cardiac surgical patients (5,059 included in analysis) to assess risk factors for infection after cardiac operations. Data were also collected on all-cause readmissions occurring within 65 days after the operation. Major outcomes included the readmission rate stratified by procedure type, cause of readmission, length of readmission stay, and discharge disposition after readmission. Multivariable Cox regression was used to determine risk factors for time to first readmission.
Results. The overall rate of readmission was 18.7% (number of readmissions, 945). When stratified by the most common procedure type, readmission rates were isolated coronary artery bypass grafting, 14.9% (n = 248); isolated valve, 18.3% (n = 337); and coronary artery bypass grafting plus valve, 25.0% (n = 169). The three most common causes of first readmission within 30 days were infection (17.1% [n = 115]), arrhythmia (17.1% [n = 115]), and volume overload (13.5% [n = 91]). More first readmissions occurred within 30 days (80.6% [n = 672]) than after 30 days (19.4% [n = 162]), and 50% of patients were readmitted within 22 days from the index operation. The median length of stay during the first readmission was 5 days. Discharge in 15.8% of readmitted patients (n = 128) was to a location other than home. Baseline patient characteristics associated with readmission included female gender, diabetes mellitus on medication, chronic obstructive pulmonary disease, elevated creatinine, lower hemoglobin, and longer operation time. More complex surgical procedures were associated with an increased risk of readmission compared with the coronary artery bypass grafting group.
Conclusions. Nearly 1 of 5 patients who undergo cardiac operations require readmission, an outcome with significant health and economic implications. Management practices to avert in-hospital infections, reduce postoperative arrhythmias, and avoid volume overload offer important targets for quality improvement. (C) 2014 by The Society of Thoracic Surgeons
C1 Duke Univ Med Ctr, Div Cardiovasc & Thorac Surg, Durham, NC USA.
Icahn Sch Med Mt Sinai, Int Ctr Hlth Outcomes & Innovat Res InCHOIR, Dept Hlth Evidence & Policy, New York, NY 10029 USA.
Duke Univ Med Ctr, Duke Clin Res Inst, Durham, NC USA.
Cleveland Clin, Div Thorac & Cardiovasc Surg, Cleveland, OH 44106 USA.
Mt Sinai Beth Israel, Icahn Sch Med Mt Sinai, Dept Cardiothorac Surg, New York, NY USA.
Univ Penn, Div Cardiothorac Surg, Philadelphia, PA 19104 USA.
E Carolina Univ, East Carolina Heart Inst, Dept Cardiovasc Sci, Greenville, NC USA.
Univ Virginia Hlth Syst, Div Thorac & Cardiovasc Surg, Dept Surg, Charlottesville, VA USA.
Univ Montreal, Montreal Heart Inst, Dept Surg, Div Cardiothorac Surg, Montreal, PQ, Canada.
Univ Virginia Hlth Syst, Dept Neurol, Charlottesville, VA USA.
Suburban Hosp, Natl Inst Hlth Heart Ctr, Bethesda, MD USA.
Montefiore Einstein Heart Ctr, Dept Cardiovasc & Thorac Surg, New York, NY USA.
Emory Univ Sch Med, Div Cardiothorac Surg, Atlanta, GA USA.
NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
Hosp Univ Penn, Dept Surg, Div Cardiothorac Surg, Philadelphia, PA 19104 USA.
RP Chang, H (reprint author), Icahn Sch Med Mt Sinai, One Gustave L Levy Pl,Box 1077, New York, NY 10029 USA.
EM helena.l.chang@mountsinai.org
OI Moskowitz, Alan/0000-0002-4412-9450
FU Canadian Institutes of Health Research; NHLBI NIH HHS [5 U01 HL088942,
U01 HL088942, UM1 HL088925]
NR 24
TC 9
Z9 9
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
EI 1552-6259
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD OCT
PY 2014
VL 98
IS 4
BP 1274
EP 1280
DI 10.1016/j.athoracsur.2014.06.059
PG 7
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA AQ9DM
UT WOS:000343143400026
PM 25173721
ER
PT J
AU Cook, K
Warri, A
Soto-Pantoja, D
Clarke, P
Cruz, I
Zwart, A
Clarke, R
AF Cook, Katherine
Waerri, Anni
Soto-Pantoja, David
Clarke, Pamela
Cruz, Idalia
Zwart, Alan
Clarke, Robert
TI INHIBITING AUTOPHAGY AS A STRATEGY TO IMPROVE ANTIESTROGEN RESPONSES IN
BREAST CANCER
SO ANTICANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Cook, Katherine; Waerri, Anni; Clarke, Pamela; Cruz, Idalia; Zwart, Alan; Clarke, Robert] Georgetown Univ, Med Ctr, Georgetown Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Soto-Pantoja, David] NCI, Bethesda, MD 20894 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD OCT
PY 2014
VL 34
IS 10
MA 124
BP 5868
EP 5869
PG 2
WC Oncology
SC Oncology
GA AQ9CO
UT WOS:000343139500196
ER
PT J
AU Boggs, AE
Charpentier, MS
Vitolo, MI
Whipple, RA
Thompson, K
Bhandary, L
Chakrabarti, K
Ioffe, OB
Goloubeva, OG
Lu, YL
Mills, GB
Martin, SS
AF Boggs, Amanda E.
Charpentier, Monica S.
Vitolo, Michele I.
Whipple, Rebecca A.
Thompson, Keyata
Bhandary, Lekhana
Chakrabarti, Kristi
Ioffe, Olga B.
Goloubeva, Olga G.
Lu, Yiling
Mills, Gordon B.
Martin, Stuart S.
TI TARGETING MICROTENTACLES ON CIRCULATING BREAST TUMOR CELLS TO REDUCE
METASTASIS
SO ANTICANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Boggs, Amanda E.; Charpentier, Monica S.; Vitolo, Michele I.; Whipple, Rebecca A.; Thompson, Keyata; Bhandary, Lekhana; Chakrabarti, Kristi; Ioffe, Olga B.; Goloubeva, Olga G.; Martin, Stuart S.] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum NCI Canc Ctr, Baltimore, MD 21201 USA.
[Lu, Yiling; Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
EM smartin@som.umaryland.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD OCT
PY 2014
VL 34
IS 10
MA 403
BP 6049
EP 6050
PG 2
WC Oncology
SC Oncology
GA AQ9CO
UT WOS:000343139500475
ER
PT J
AU Zarbl, H
Takizawa, N
Graham, JC
Estrella, B
Gong, Z
Ren, X
AF Zarbl, H.
Takizawa, N.
Graham, J. C.
Estrella, B.
Gong, Z.
Ren, X.
TI DECREASED EXPRESSION AND/OR MUTATION OF FRY, A PROMOTER OF EPITHELIAL
CELL DIFFERENTIATION, IS ASSOCIATED WITH EPITHELIAL MESENCHYMAL
TRANSITION AND CLINICAL PROGRESSION OF BREAST CANCER
SO ANTICANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Zarbl, H.; Takizawa, N.; Graham, J. C.; Estrella, B.] Environm & Occupat Hlth Sci Inst, Piscataway, NJ USA.
[Zarbl, H.; Graham, J. C.; Estrella, B.] RWJMS, Dept Environm & Occupat Med, New Brunswick, NJ USA.
[Zarbl, H.] NIEHS Ctr Environm Exposures & Dis, Piscataway, NJ USA.
[Zarbl, H.] Rutgers State Univ, Canc Inst New Jersey, Piscataway, NJ 08855 USA.
[Zarbl, H.; Takizawa, N.] GeneAssess Inc, North Brunswick, NJ USA.
[Gong, Z.] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Ren, X.] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
EM zarbl@eohsi.rutgers.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD OCT
PY 2014
VL 34
IS 10
MA 729
BP 6252
EP 6253
PG 2
WC Oncology
SC Oncology
GA AQ9CO
UT WOS:000343139500801
ER
PT J
AU Zhou, Y
Kim, YS
Milenic, DE
Baidoo, KE
Brechbiel, MW
AF Zhou, Yang
Kim, Young-Seung
Milenic, Diane E.
Baidoo, Kwamena E.
Brechbiel, Martin W.
TI In Vitro and In Vivo Analysis of Indocyanine Green-Labeled Panitumumab
for Optical Imaging-A Cautionary Tale
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID QUANTUM DOTS; ANTIBODY; CANCER; THERAPY; SURGERY; LIGHT; PET
AB Indocyanine green (IC-Green), the only FDA approved near-infrared (NIR) fluorophore for clinical use, is attractive to researchers for the development of targeted optical imaging agents by modification of its structure and conjugation to monoclonal antibodies (mAbs) or their fragments. IC-Green derivative, ICG-sulfo-OSu (ICG-sOSu), is frequently used for antibody conjugation. However, ICG-sOSu is amphiphilic and readily facilitates aggregation of mAbs that is not easily separable from the desired immunoconjugates. Complications originating from this behavior are frequently overlooked by researchers. This study examined detailed chemical and biological characteristics of an ICG-sOSu-labeled mAb, panitumumab, and provided a clinically applicable strategy to deliver a pure conjugation product. Size-exclusion high-performance liquid chromatography (SE-HPLC) analysis of conjugation reactions, performed at molar reaction ratios of ICG-sOSu: mAb of 5, 10, or 20, resulted in isolable desired ICG-sOSu-panitumumab conjugation product in 72%, 53%, and 19% yields, respectively, with the remainder consisting of high molecular weight aggregates (>150 kDa) 14%, 30%, and 51%, respectively. The HPLC-purified ICG-sOSu-panitumumab products were analyzed by native and SDS polyacrylamide gel electrophoresis (PAGE) followed by optical imaging. Results indicated that the interaction between ICG-sOSu and panitumumab was due to both covalent and noncovalent binding of the ICG-sOSu to the protein. Noncovalently bound dye in the ICG-sOSu-panitumumab conjugate products was removed by extraction with ethyl acetate to further purify the HPLC-isolated conjugation products. With conserved immunoreactivity, excellent target-specific uptake of the doubly purified bioconjugates was observed with minimal liver retention in athymic nude mice bearing HER1-expressing tumor xenografts. In summary, the preparation of well-defined bioconjugate products labeled with commercial ICG-sOSu dye is not a simple process and control of the conjugation reaction ratio and conditions is crucial. Furthermore, absolute purification and characterization of the products is necessitated prior to in vivo optical imaging. Use of validated and characterized dye conjugate products should facilitate the development of clinically viable and reproducible IC-Green derivative and other NIR dye mAb conjugates for optical imaging applications.
C1 [Zhou, Yang; Kim, Young-Seung; Milenic, Diane E.; Baidoo, Kwamena E.; Brechbiel, Martin W.] NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, Bethesda, MD 20892 USA.
RP Brechbiel, MW (reprint author), NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM martinwb@mail.nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. We would
like to thank the EIB Microscopy and Digital Imaging Facility and Dr.
Michael Kruhlak for the technical assistance in fluorescence microscopy.
NR 27
TC 8
Z9 8
U1 1
U2 14
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 OCT
PY 2014
VL 25
IS 10
BP 1801
EP 1810
DI 10.1021/bc500312w
PG 10
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA AR0QM
UT WOS:000343276400009
PM 25243604
ER
PT J
AU Bahamonde, MI
Taura, J
Paoletta, S
Gakh, AA
Chakraborty, S
Hernando, J
Fernandez-Duenas, V
Jacobson, KA
Gorostiza, P
Ciruela, F
AF Isabel Bahamonde, Maria
Taura, Jaume
Paoletta, Silvia
Gakh, Andrei A.
Chakraborty, Saibal
Hernando, Jordi
Fernandez-Duenas, Victor
Jacobson, Kenneth A.
Gorostiza, Pau
Ciruela, Francisco
TI Photomodulation of G Protein-Coupled Adenosine Receptors by a Novel
Light-Switchable Ligand
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID CIS-TRANS ISOMERIZATION; A(2A); ACTIVATION; AGONIST; RAT; AZOBENZENE;
CHANNELS; DOCKING; REMOTE
AB The adenosinergic system operates through G protein-coupled adenosine receptors, which have become promising therapeutic targets for a wide range of pathological conditions. However, the ubiquity of adenosine receptors and the eventual lack of selectivity of adenosine-based drugs have frequently diminished their therapeutic potential. Accordingly, here we aimed to develop a new generation of light-switchable adenosine receptor ligands that change their intrinsic activity upon irradiation, thus allowing the spatiotemporal control of receptor functioning (i.e., receptor activation/inactivation dependent on location and timing). Therefore, we synthesized an orthosteric, photoisomerizable, and nonselective adenosine receptor agonist, nucleoside derivative MRS5543 containing an aryl diazo linkage on the N6 substituent, which in the dark (relaxed isomer) behaved as a full adenosine A(3) receptor (A(3)R) and partial adenosine A(2A) receptor (A(2A)R) agonist. Conversely, upon photoisomerization with blue light (460 nm), it remained a full A3R agonist but became an A(2A)R antagonist. Interestingly, molecular modeling suggested that structural differences encountered within the third extracellular loop of each receptor could modulate the intrinsic, receptor subtype-dependent, activity. Overall, the development of adenosine receptor ligands with photoswitchable activity expands the pharmacological toolbox in support of research and possibly opens new pharmacotherapeutic opportunities.
C1 [Isabel Bahamonde, Maria; Gorostiza, Pau] Inst Bioengn Catalonia IBEC, Barcelona 08028, Spain.
[Taura, Jaume; Fernandez-Duenas, Victor; Ciruela, Francisco] Univ Barcelona, Fac Med, IDIBELL, Unitat Farmacol,Dept Patol & Terapeut Expt, Barcelona 08907, Spain.
[Paoletta, Silvia; Gakh, Andrei A.; Chakraborty, Saibal; Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Hernando, Jordi] Univ Autonoma Barcelona, Dept Quim, E-08193 Barcelona, Spain.
[Gorostiza, Pau] ICREA, Barcelona 08010, Spain.
[Gorostiza, Pau] Ctr Invest Biomed Red Bioingn Biomat & Nanomed CI, Zaragoza 50118, Spain.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM kennethj@helix.nih.gov; pau@icrea.cat; fciruela@ub.edu
RI Jacobson, Kenneth/A-1530-2009; Hernando, Jordi/G-8661-2015; Gorostiza,
Pau/Q-2544-2015
OI Jacobson, Kenneth/0000-0001-8104-1493; Hernando,
Jordi/0000-0002-1126-4138; Gorostiza, Pau/0000-0002-7268-5577
FU "Ministerio de Economia y Competitividad" (MINECO) [SAF2011-24779,
CTQ2012-30853, PCIN-2013-019-C03-03, Consolider-Ingenio CSD2008-00005];
Catalan Institution for Research and Advanced Studies (ICREA); U.S.
Department of Energy in collaboration with the National Cancer
Institute; Beatriu de Pinos (Generalitat de Catalunya); Marie Curie
(European Union); European Union [270483, 210355, 335011]; RecerCaixa
foundation [2010ACUP00378]; Marato de TV3 foundation [111531]
FX This work was supported by grants SAF2011-24779, CTQ2012-30853,
PCIN-2013-019-C03-03 and Consolider-Ingenio CSD2008-00005 from
"Ministerio de Economia y Competitividad" (MINECO) and ICREA
Academia-2010 from the Catalan Institution for Research and Advanced
Studies (ICREA) to PC. Also, V.F.-D., J.T., and F.C. belong to the
"Neuropharmacology and Pain" accredited research group (Generalitat de
Catalunya, 2014 SGR 1054) and P.G. belongs to the "Bioelectrochemistry
and nanotechnology" accredited research group (Generalitat de Catalunya,
2014 SGR 1251). Support to K.A.J., S.P, A.A.G., and S.C. from the NIDDK
Intramural Research Program of the National Institutes of Health,
Bethesda, MD, USA is acknowledged. Also, support to AAG from the
Discovery Chemistry Project funded in part by the U.S. Department of
Energy in collaboration with the National Cancer Institute is
acknowledged. MIB acknowledges postdoctoral fellowships from the Beatriu
de Pinos (Generalitat de Catalunya) and Marie Curie (European Union)
programs. This project has received funding from the European Union's
Seventh Framework Programme for research, technological development and
demonstration under grant agreement numbers 270483 (Focus), 210355
(Opticalbullet), and 335011 (Theralight). We are also grateful to the
RecerCaixa foundation (2010ACUP00378) and the Marato de TV3 foundation
(111531).
NR 36
TC 1
Z9 1
U1 0
U2 18
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 OCT
PY 2014
VL 25
IS 10
BP 1847
EP 1854
DI 10.1021/bc5003373
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA AR0QM
UT WOS:000343276400014
PM 25248077
ER
PT J
AU Ding, JL
Zhou, HB
Liu, YY
Cai, JW
Longnecker, MP
AF Ding, Jieli
Zhou, Haibo
Liu, Yanyan
Cai, Jianwen
Longnecker, Matthew P.
TI Estimating effect of environmental contaminants on women's subfecundity
for the MoBa study data with an outcome-dependent sampling scheme
SO BIOSTATISTICS
LA English
DT Article
DE Biased-sampling; Empirical likelihood; Proportional hazards model;
Survival analysis
ID CASE-COHORT DESIGN; REGRESSION-MODELS; LIKELIHOOD METHOD; COX
REGRESSION; HAZARDS MODEL; BIAS
AB Motivated by the need from our on-going environmental study in the Norwegian Mother and Child Cohort (MoBa) study, we consider an outcome-dependent sampling (ODS) scheme for failure-time data with censoring. Like the case-cohort design, the ODS design enriches the observed sample by selectively including certain failure subjects. We present an estimated maximum semiparametric empirical likelihood estimation (EMSELE) under the proportional hazards model framework. The asymptotic properties of the proposed estimator were derived. Simulation studies were conducted to evaluate the small-sample performance of our proposed method. Our analyses show that the proposed estimator and design is more efficient than the current default approach and other competing approaches. Applying the proposed approach with the data set from the MoBa study, we found a significant effect of an environmental contaminant on fecundability.
C1 [Ding, Jieli; Liu, Yanyan] Wuhan Univ, Sch Math & Stat, Wuhan 430072, Hubei, Peoples R China.
[Zhou, Haibo; Cai, Jianwen] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
[Longnecker, Matthew P.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Zhou, HB (reprint author), Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
EM zhou@bios.unc.edu
OI Longnecker, Matthew/0000-0001-6073-5322
FU U.S. National Institute of Health [R01 ES021900, UL1 RR025747, P01
CA142538]; Intramural Research Program of the National Institutes of
Health, National Institute of Environmental Health Sciences; Norwegian
Ministry of Health and the Ministry of Education and Research, NIH/NIEHS
[N01-ES-75558]; Norwegian Ministry of Health and the Ministry of
Education and Research, NIH/NINDS [UO1 NS 047537-01, UO1 NS
047537-06A1]; Norwegian Research Council/FUGE [151918/S10]; National
Science Foundation of China [11101314, 11171263, 11371299]
FX This research was supported in part by U.S. National Institute of Health
grants (R01 ES021900, UL1 RR025747, P01 CA142538), and the Intramural
Research Program of the National Institutes of Health, National
Institute of Environmental Health Sciences. The Norwegian Mother and
Child Cohort Study is supported by the Norwegian Ministry of Health and
the Ministry of Education and Research, NIH/NIEHS (N01-ES-75558),
NIH/NINDS (UO1 NS 047537-01, UO1 NS 047537-06A1), and the Norwegian
Research Council/FUGE (151918/S10). This research is also funded in part
by National Science Foundation of China (11101314 to J.D. and 11171263,
11371299 to Y.L.).
NR 28
TC 5
Z9 5
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1465-4644
EI 1468-4357
J9 BIOSTATISTICS
JI Biostatistics
PD OCT
PY 2014
VL 15
IS 4
BP 636
EP 650
DI 10.1093/biostatistics/kxu016
PG 15
WC Mathematical & Computational Biology; Statistics & Probability
SC Mathematical & Computational Biology; Mathematics
GA AQ8OA
UT WOS:000343085100004
PM 24812419
ER
PT J
AU Liu, DP
Albert, PS
AF Liu, Danping
Albert, Paul S.
TI Combination of longitudinal biomarkers in predicting binary events
SO BIOSTATISTICS
LA English
DT Article
DE Area under ROC curve; Fetal growth; Longitudinal biomarker combination;
Macrosomia; Pattern mixture model; Risk estimation
ID IMPROVE DIAGNOSTIC-ACCURACY; LINEAR-COMBINATIONS; CLASSIFICATION; ROC;
MARKERS; MODEL
AB In disease screening, the combination of multiple biomarkers often substantially improves the diagnostic accuracy over a single marker. This is particularly true for longitudinal biomarkers where individual trajectory may improve the diagnosis. We propose a pattern mixture model (PMM) framework to predict a binary disease status from a longitudinal sequence of biomarkers. The marker distribution given the disease status is estimated from a linear mixed effects model. A likelihood ratio statistic is computed as the combination rule, which is optimal in the sense of the maximum receiver operating characteristic (ROC) curve under the correctly specified mixed effects model. The individual disease risk score is then estimated by Bayes' theorem, and we derive the analytical form of the 95% confidence interval. We show that this PMM is an approximation to the shared random effects (SRE) model proposed by Albert (2012. A linear mixed model for predicting a binary event from longitudinal data under random effects mis-specification. Statistics in Medicine 31(2), 143-154). Further, with extensive simulation studies, we found that the PMM is more robust than the SRE model under wide classes of models. This new PPM approach for combining biomarkers is motivated by and applied to a fetal growth study, where the interest is in predicting macrosomia using longitudinal ultrasound measurements.
C1 [Liu, Danping; Albert, Paul S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, NIH, Rockville, MD 20852 USA.
RP Liu, DP (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, NIH, Rockville, MD 20852 USA.
EM danping.liu@nih.gov
FU Intramural Research Program of the National Institute of Health (NIH);
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD)
FX This research is supported by the Intramural Research Program of the
National Institute of Health (NIH), Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD).
NR 17
TC 4
Z9 4
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1465-4644
EI 1468-4357
J9 BIOSTATISTICS
JI Biostatistics
PD OCT
PY 2014
VL 15
IS 4
BP 706
EP 718
DI 10.1093/biostatistics/kxu020
PG 13
WC Mathematical & Computational Biology; Statistics & Probability
SC Mathematical & Computational Biology; Mathematics
GA AQ8OA
UT WOS:000343085100009
PM 24831103
ER
PT J
AU Schuessler, TK
Chan, XY
Chen, HJ
Ji, KM
Park, KM
Roshan-Ghias, A
Sethi, P
Thakur, A
Tian, X
Villasante, A
Zervantonakis, IK
Moore, NM
Nagahara, LA
Kuhn, NZ
AF Schuessler, Teresa K.
Chan, Xin Yi
Chen, Huanhuan Joyce
Ji, Kyungmin
Park, Kyung Min
Roshan-Ghias, Alireza
Sethi, Pallavi
Thakur, Archana
Tian, Xi
Villasante, Aranzazu
Zervantonakis, Ioannis K.
Moore, Nicole M.
Nagahara, Larry A.
Kuhn, Nastaran Z.
TI Biomimetic Tissue-Engineered Systems for Advancing Cancer Research: NCI
Strategic Workshop Report
SO CANCER RESEARCH
LA English
DT Editorial Material
ID EXTRACELLULAR-MATRIX; IN-VITRO; MICROPHYSIOLOGICAL SYSTEMS; TUMOR;
MICROENVIRONMENT; CULTURE; MODEL; MICROFLUIDICS; SCAFFOLDS; MIGRATION
AB Advanced technologies and biomaterials developed for tissue engineering and regenerative medicine present tractable biomimetic systems with potential applications for cancer research. Recently, the National Cancer Institute convened a Strategic Workshop to explore the use of tissue biomanufacturing for development of dynamic, physiologically relevant in vitro and ex vivo biomimetic systems to study cancer biology and drug efficacy. The workshop provided a forum to identify current progress, research gaps, and necessary steps to advance the field. Opportunities discussed included development of tumor biomimetic systems with an emphasis on reproducibility and validation of new biomimetic tumor models, as described in this report. (C)2014 AACR.
C1 [Schuessler, Teresa K.; Moore, Nicole M.; Nagahara, Larry A.; Kuhn, Nastaran Z.] NCI, Div Canc Biol, Rockville, MD 20850 USA.
[Chan, Xin Yi; Park, Kyung Min] Johns Hopkins Univ, Phys Sci Oncol Ctr, Inst NanoBioTechnol, Dept Chem & Biomol Engn, Baltimore, MD USA.
[Chen, Huanhuan Joyce] Cornell Univ, Dept Biomed Engn, Ithaca, NY USA.
[Ji, Kyungmin] Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.
[Roshan-Ghias, Alireza; Villasante, Aranzazu] Columbia Univ, Dept Biomed Engn, Lab Stem Cells & Tissue Engn, New York, NY USA.
[Sethi, Pallavi] Univ Kentucky, Coll Pharm, Canc Nanotechnol Training Ctr, Dept Pharmaceut Sci, Lexington, KY USA.
[Thakur, Archana] Wayne State Univ, Karmanos Canc Inst, Dept Oncol, Detroit, MI USA.
[Tian, Xi] Univ N Carolina, Lineberger Canc Res Ctr, Dept Radiat Oncol, Chapel Hill, NC 27599 USA.
[Zervantonakis, Ioannis K.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA USA.
RP Kuhn, NZ (reprint author), NCI, Div Canc Biol, 9609 Med Ctr Dr,Room 6W556, Rockville, MD 20850 USA.
EM nas.kuhn@nih.gov
RI Tian, Xi/H-4192-2016; Villasante, Aranzazu/A-9100-2017
OI Villasante, Aranzazu/0000-0001-7919-9670
FU Intramural NIH HHS [Z99 CA999999]
NR 33
TC 10
Z9 10
U1 0
U2 17
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT 1
PY 2014
VL 74
IS 19
BP 5359
EP 5363
DI 10.1158/0008-5472.CAN-14-1706
PG 5
WC Oncology
SC Oncology
GA AQ8WP
UT WOS:000343118900002
PM 25095784
ER
PT J
AU Chang, CM
Stapleton, JT
Klinzman, D
McLinden, JH
Purdue, MP
Katki, HA
Engels, EA
AF Chang, Cindy M.
Stapleton, Jack T.
Klinzman, Donna
McLinden, James H.
Purdue, Mark P.
Katki, Hormuzd A.
Engels, Eric A.
TI GBV-C Infection and Risk of NHL among US Adults
SO CANCER RESEARCH
LA English
DT Article
ID HEPATITIS-G VIRUS; C/HEPATITIS-G VIRUS; NON-HODGKINS-LYMPHOMA; B-CELL;
ENVELOPE PROTEIN; BLOOD-DONORS; HIGH PREVALENCE; ASSOCIATION;
ACTIVATION; HIV
AB Some retrospective studies suggest an association between infection with GB virus-C (GBV-C) and non-Hodgkin lymphoma (NHL). We evaluated this association prospectively in a nested case-control study within the U.S. Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. Cases (N = 658) and controls (N = 1,316) were individually matched by age, sex, race/ethnicity, timing of study entry, and sample selection. Prediagnostic PLCO serum samples were tested for GBV-C RNA (as a measure of active infection) and E2 antibody (active or resolved infection). Logistic regression was used to estimate odds ratios (OR) for the association between GBV-C and NHL overall and NHL subtypes. Twelve cases (1.8%) and seven controls (0.5%) were GBV-C RNA-positive. GBV-C RNA positivity was associated with NHL overall [OR, 3.43; 95% confidence interval (CI), 1.35-8.71] and, based on small numbers, diffuse large B-cell lymphoma (OR, 5.31; 95% CI, 1.54-18.36). The association with NHL persisted when the interval between testing and selection was greater than 4 years (OR, 6.00; 95% CI, 1.21-29.73). In contrast, E2 antibody positivity was not associated with NHL risk (OR, 1.08; 95% CI, 0.74-1.58). Our study demonstrates that GBV-C infection precedes development of NHL. GBV-C infection may play an etiologic role in a small proportion of NHL cases, perhaps by causing chronic immune stimulation or impaired immunosurveillance. (C) 2014 AACR.
C1 [Chang, Cindy M.; Purdue, Mark P.; Katki, Hormuzd A.; Engels, Eric A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Stapleton, Jack T.; Klinzman, Donna; McLinden, James H.] Univ Iowa, Dept Internal Med, Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA.
RP Chang, CM (reprint author), Food & Drug Adm, Ctr Tobacco Prod, Dept Hlth & Human Serv, Off Sci, Bldg 71,Room G335,10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM cindy.chang@fda.hhs.gov
RI Katki, Hormuzd/B-4003-2015; Purdue, Mark/C-9228-2016
OI Purdue, Mark/0000-0003-1177-3108
FU Intramural Research Program of the National Cancer Institute at the NIH;
Department of Veterans Affairs Merit Review Grant [CX000821]
FX This work was supported by the Intramural Research Program of the
National Cancer Institute at the NIH and by the Department of Veterans
Affairs Merit Review Grant (CX000821; J.T. Stapleton).
NR 47
TC 5
Z9 5
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT 1
PY 2014
VL 74
IS 19
BP 5553
EP 5560
DI 10.1158/0008-5472.CAN-14-0209
PG 8
WC Oncology
SC Oncology
GA AQ8WP
UT WOS:000343118900020
PM 25115299
ER
PT J
AU Tuttle, KR
Bakris, GL
Bilous, RW
Chiang, JL
de Boer, IH
Goldstein-Fuchs, J
Hirsch, IB
Kalantar-Zadeh, K
Narva, AS
Navaneethan, SD
Neumiller, JJ
Patel, UD
Ratner, RE
Whaley-Connell, AT
Molitch, ME
AF Tuttle, Katherine R.
Bakris, George L.
Bilous, Rudolf W.
Chiang, Jane L.
de Boer, Ian H.
Goldstein-Fuchs, Jordi
Hirsch, Irl B.
Kalantar-Zadeh, Kamyar
Narva, Andrew S.
Navaneethan, Sankar D.
Neumiller, Joshua J.
Patel, Uptal D.
Ratner, Robert E.
Whaley-Connell, Adam T.
Molitch, Mark E.
TI Diabetic Kidney Disease: A Report From an ADA Consensus Conference
SO DIABETES CARE
LA English
DT Article
ID DIETARY-PROTEIN RESTRICTION; CLINICAL-PRACTICE GUIDELINE;
GLOMERULAR-FILTRATION-RATE; STAGE RENAL-DISEASE; PERITONEAL-DIALYSIS
PATIENTS; HEMOGLOBIN A(1C) LEVELS; GLYCEMIC CONTROL; LONG-TERM; REVERSE
EPIDEMIOLOGY; BLOOD-PRESSURE
AB The incidence and prevalence of diabetes mellitus have grown significantly throughout the world, due primarily to the increase in type 2 diabetes. This overall increase in the number of people with diabetes has had a major impact on development of diabetic kidney disease (DKD), one of the most frequent complications of both types of diabetes. DKD is the leading cause of end-stage renal disease (ESRD), accounting for approximately 50% of cases in the developed world. Although incidence rates for ESRD attributable to DKD have recently stabilized, these rates continue to rise in high-risk groups such as middle-aged African Americans, Native Americans, and Hispanics. The costs of care for people with DKD are extraordinarily high. In the Medicare population alone, DKD-related expenditures among this mostly older group were nearly $25 billion in 2011. Due to the high human and societal costs, the Consensus Conference on Chronic Kidney Disease and Diabetes was convened by the American Diabetes Association in collaboration with the American Society of Nephrology and the National Kidney Foundation to appraise issues regarding patient management, highlighting current practices and new directions. Major topic areas in DKD included 1) identification and monitoring, 2) cardiovascular disease and management of dyslipidemia, 3) hypertension and use of renin-angiotensin-aldosterone system blockade and mineralocorticoid receptor blockade, 4) glycemia measurement, hypoglycemia, and drug therapies, 5) nutrition and general care in advanced-stage chronic kidney disease, 6) children and adolescents, and 7) multidisciplinary approaches and medical home models for health care delivery. This current state summary and research recommendations are designed to guide advances in care and the generation of new knowledge that will meaningfully improve life for people with DKD.
C1 [Tuttle, Katherine R.] Univ Washington, Sch Med, Seattle, WA USA.
[Tuttle, Katherine R.] Providence Hlth Care, Spokane, WA USA.
[Bakris, George L.] Univ Chicago Med, Comprehens Hypertens Ctr, Chicago, IL USA.
[Bilous, Rudolf W.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Chiang, Jane L.; Ratner, Robert E.] Amer Diabet Assoc, Alexandria, VA 22311 USA.
[de Boer, Ian H.] Univ Washington, Div Nephrol, Seattle, WA 98195 USA.
[Goldstein-Fuchs, Jordi] Sierra Nevada Nephrol Consultants, Reno, NV USA.
[Hirsch, Irl B.] Univ Washington, Sch Med, Div Metab Endocrinol & Nutr, Seattle, WA USA.
[Kalantar-Zadeh, Kamyar] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
[Narva, Andrew S.] NIDDK, NIH, Bethesda, MD USA.
[Navaneethan, Sankar D.] Cleveland Clin, Dept Nephrol & Hypertens, Novick Ctr Clin & Translat Res, Glickman Urol & Kidney Inst, Cleveland, OH 44106 USA.
[Neumiller, Joshua J.] Washington State Univ, Coll Pharm, Dept Pharmacotherapy, Spokane, WA USA.
[Patel, Uptal D.] Duke Univ, Sch Med, Duke Clin Res Inst, Div Nephrol, Durham, NC USA.
[Patel, Uptal D.] Duke Univ, Sch Med, Duke Clin Res Inst, Div Pediat Nephrol, Durham, NC USA.
[Whaley-Connell, Adam T.] Harry S Truman Mem Vet Hosp, Columbia, MO 65201 USA.
[Whaley-Connell, Adam T.] Univ Missouri, Sch Med, Dept Internal Med, Div Nephrol & Hypertens, Columbia, MO USA.
[Ratner, Robert E.; Molitch, Mark E.] Northwestern Univ, Feinberg Sch Med, Div Endocrinol Metab & Mol Med, Chicago, IL 60611 USA.
RP Chiang, JL (reprint author), Amer Diabet Assoc, Alexandria, VA 22311 USA.
EM jchiang@diabetes.org
OI Whaley-Connell, Adam/0000-0001-8955-5560; Kalantar-Zadeh,
Kamyar/0000-0002-8666-0725
FU Eli Lilly; Takeda; AbbVie; Medtronic; Relypsa; Daiichi Sankyo; Janssen;
Novartis; Bayer; Roche Pharma; Mitsubishi; Boehringer Ingelheim; Sanofi;
Halozyme; Abbott; Roche; Amgen; Fresnius; DaVita; Keryx; Otsuka; Shire;
National Institutes of Health/NIDDK; Genzyme; AstraZeneca; Johnson
Johnson; Merck; Novo Nordisk; Eli Lilly and Co.; Luitpold
Pharmaceuticals; Angion Biomedica Corp.; CSL Limited; Ablative Solutions
Inc.; Kia Pharmaceuticals; Reata Pharmaceuticals; Gilead Sciences;
Bristol-Myers Squibb
FX All authors have completed the Unified Competing Interest form at
www.icmje.org/conflicts-of-interest (available upon request from J.L.C.)
and declare the following conflicts of interest. K. R. T. has received
personal fees from Eli Lilly and Co. G. L. B. has received grants from
Takeda and consultancy fees for his institution from AbbVie, Takeda,
Medtronic, Relypsa, Daiichi Sankyo, Janssen, Novartis, and Bayer. R. W.
B. has received personal fees from Roche Pharma, AbbVie, Mitsubishi, and
Boehringer Ingelheim. I.H.d.B. has received grants from AbbVie. I. B. H.
has received grants from Sanofi and Halozyme and personal fees from
Abbott and Roche. K.K.-Z. has received honoraria from Abbott, AbbVie,
Amgen, Fresnius, DaVita, Keryx, Otsuka, and Shire. S.D.N. received
grants from the National Institutes of Health/NIDDK and Genzyme. J.J.N.
has received grants from AstraZeneca, Johnson & Johnson, Merck, and Novo
Nordisk. U. D. P. has received personal fees from Amgen and grants from
Amgen, Daiichi Sankyo, Eli Lilly and Co., Luitpold Pharmaceuticals,
Angion Biomedica Corp., CSL Limited, Ablative Solutions Inc., Kia
Pharmaceuticals, Reata Pharmaceuticals, Keryx, and Gilead Sciences. M.
E. M. has received grants from Sanofi, Bayer, Eli Lilly and Co., Novo
Nordisk, and Novartis and consultant fees from AbbVie, Merck, Janssen,
AstraZeneca, and Bristol-Myers Squibb. No other potential conflicts of
interest relevant to this article were reported.
NR 178
TC 78
Z9 81
U1 5
U2 15
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2014
VL 37
IS 10
BP 2864
EP 2883
DI 10.2337/dc14-1296
PG 20
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AR4UM
UT WOS:000343582400041
PM 25249672
ER
PT J
AU Sarkar, G
Alattar, M
Brown, RJ
Quon, MJ
Harlan, DM
Rother, KI
AF Sarkar, Gayatri
Alattar, May
Brown, Rebecca J.
Quon, Michael J.
Harlan, David M.
Rother, Kristina I.
TI Exenatide Treatment for 6 Months Improves Insulin Sensitivity in Adults
With Type 1 Diabetes. Diabetes Care 2014;37:666-670 RESPONSE
SO DIABETES CARE
LA English
DT Letter
C1 [Sarkar, Gayatri; Alattar, May; Brown, Rebecca J.; Rother, Kristina I.] NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Quon, Michael J.] Univ Maryland Sch Med, Div Endocrinol Diabet & Nutr, Baltimore, MD USA.
[Harlan, David M.] Univ Massachusetts Sch Med, Dept Internal Med, Diabet Div, Worcester, MA USA.
[Harlan, David M.] UMass Mem Hlth Care, Worcester, MA USA.
RP Rother, KI (reprint author), NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
EM kristina.rother@nih.gov
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2014
VL 37
IS 10
BP E219
EP E220
DI 10.2337/dc14-1482
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AR4UM
UT WOS:000343582400007
PM 25249681
ER
PT J
AU Ward, MH
Colt, JS
Deziel, NC
Whitehead, TP
Reynolds, P
Gunier, RB
Nishioka, M
Dahl, GV
Rappaport, SM
Buffler, PA
Metayer, C
AF Ward, Mary H.
Colt, Joanne S.
Deziel, Nicole C.
Whitehead, Todd P.
Reynolds, Peggy
Gunier, Robert B.
Nishioka, Marcia
Dahl, Gary V.
Rappaport, Stephen M.
Buffler, Patricia A.
Metayer, Catherine
TI Residential Levels of Polybrominated Diphenyl Ethers and Risk of
Childhood Acute Lymphoblastic Leukemia in California
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID BROMINATED FLAME RETARDANTS; IN-HOUSE DUST; POLYCHLORINATED-BIPHENYLS;
UNITED-STATES; INDOOR DUST; BREAST-MILK; B6C3F1 MICE; NEW-ZEALAND;
PBDES; EXPOSURE
AB BACKGROUND: House dust is a major source of exposure to polybrominated diphenyl ethers (PBDEs), which are found at high levels in U.S. homes.
METHODS: We studied 167 acute lymphoblastic leukemia (ALL) cases 0-7 years of age and 214 birth certificate controls matched on date of birth, sex, and race/ethnicity from the Northern California Childhood Leukemia Study. In 2001-2007, we sampled carpets in the room where the child spent the most time while awake; we used a high-volume small-surface sampler or we took dust from the home vacuum. We measured concentrations of 14 PBDE congeners including penta (28, 47, 99, 100, 153, 154), octa (183, 196, 197, 203), and decaBDEs (206-209). Odds ratios (ORs) were calculated using logistic regression, adjusting for demographics, income, year of dust collection, and sampling method.
RESULTS: BDE-47, BDE-99, and BDE-209 were found at the highest concentrations (medians, 1,173, 1,579, and 938 ng/g, respectively). Comparing the highest to lowest quartile, we found no association with ALL for summed pentaBDEs (OR = 0.7; 95% CI: 0.4, 1.3), octaBDEs (OR = 1.3; 95% CI: 0.7, 2.3), or decaBDEs (OR = 1.0; 95% CI: 0.6, 1.8). Comparing homes in the highest concentration (nanograms per gram) tertile to those with no detections, we observed significantly increased ALL risk for BDE-196 (OR = 2.1; 95% CI: 1.1, 3.8), BDE-203 (OR = 2.0; 95% CI: 1.1, 3.6), BDE-206 (OR = 2.1; 95% CI: 1.1, 3.9), and BDE-207 (OR = 2.0; 95% CI: 1.03, 3.8).
CONCLUSION: We found no association with ALL for common PBDEs, but we observed positive associations for specific octa and nonaBDEs. Additional studies with repeated sampling and biological measures would be informative.
C1 [Ward, Mary H.; Colt, Joanne S.; Deziel, Nicole C.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv,NIH, Rockville, MD 20850 USA.
[Whitehead, Todd P.; Gunier, Robert B.; Rappaport, Stephen M.; Buffler, Patricia A.; Metayer, Catherine] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Reynolds, Peggy] Canc Prevent Inst Calif, Berkeley, CA USA.
[Nishioka, Marcia] Battelle Mem Inst, Columbus, OH 43201 USA.
[Dahl, Gary V.] Stanford Univ, Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA.
RP Ward, MH (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E138, Rockville, MD 20850 USA.
EM wardm@mail.nih.gov
FU Intramural Research Program of the National Cancer Institute (NCI),
National Institutes of Health; University of California, Berkeley
[7590-S-04]; Battelle Memorial Institute [7590-S-01]; National Institute
of Environmental Health Sciences grants [R01ES009137, P-42-ES-04705-18,
5R01CA092683-03]
FX This research was partially supported by the Intramural Research Program
of the National Cancer Institute (NCI), National Institutes of Health
and through NCI subcontracts 7590-S-04 (University of California,
Berkeley) and 7590-S-01 (Battelle Memorial Institute) under NCI contract
N02-CP-11015 (Westat). This research was also financially supported by
National Institute of Environmental Health Sciences grants R01ES009137
and P-42-ES-04705-18 (University of California, Berkeley) and NCI grant
5R01CA092683-03 (Colorado State University).
NR 52
TC 15
Z9 15
U1 7
U2 33
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
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2014
VL 122
IS 10
BP 1110
EP 1116
DI 10.1289/ehp.1307602
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA AQ9BO
UT WOS:000343136200024
PM 24911217
ER
PT J
AU Markunas, CA
Xu, ZL
Harlid, S
Wade, PA
Lie, RT
Taylor, JA
Wilcox, AJ
AF Markunas, Christina A.
Xu, Zongli
Harlid, Sophia
Wade, Paul A.
Lie, Rolv T.
Taylor, Jack A.
Wilcox, Allen J.
TI Identification of DNA Methylation Changes in Newborns Related to
Maternal Smoking during Pregnancy
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; NICOTINE DEPENDENCE; DEVELOPMENTAL ORIGINS;
PARENTAL SMOKING; EXPRESSION; DISEASE; GALNT2; ACTIVATION; SMOKERS;
FRMD4A
AB BACKGROUND: Maternal smoking during pregnancy is associated with significant infant morbidity and mortality, and may influence later disease risk. One mechanism by which smoking (and other environmental factors) might have long-lasting effects is through epigenetic modifications such as DNA methylation.
OBJECTIVES: We conducted an epigenome-wide association study (EWAS) investigating alterations in DNA methylation in infants exposed in utero to maternal tobacco smoke, using the Norway Facial Clefts Study.
METHODS: The Illumina HumanMethylation450 BeadChip was used to assess DNA methylation in whole blood from 889 infants shortly after delivery. Of 889 mothers, 287 reported smoking-twice as many smokers as in any previous EWAS of maternal smoking. CpG sites related to maternal smoking during the first trimester were identified using robust linear regression.
RESULTS: We identified 185 CpGs with altered methylation in infants of smokers at genome-wide significance (q-value < 0.05; mean Delta beta = +/- 2%). These correspond to 110 gene regions, of which 7 have been previously reported and 10 are newly confirmed using publicly available results. Among these 10, the most noteworthy are FRMD4A, ATP9A, GALNT2, and MEG3, implicated in processes related to nicotine dependence, smoking cessation, and placental and embryonic development.
CONCLUSIONS: Our study identified 10 genes with newly established links to maternal smoking. Further, we note differences between smoking-related methylation changes in newborns and adults, suggesting possible distinct effects of direct versus indirect tobacco smoke exposure as well as potential differences due to age. Further work would be needed to determine whether these small changes in DNA methylation are biologically or clinically relevant. The methylation changes identified in newborns may mediate the association between in utero maternal smoking exposure and later health outcomes.
C1 [Markunas, Christina A.; Xu, Zongli; Taylor, Jack A.; Wilcox, Allen J.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Harlid, Sophia; Wade, Paul A.; Taylor, Jack A.] Natl Inst Environm Hlth Sci, Lab Mol Carcinogenesis, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Lie, Rolv T.] Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway.
[Lie, Rolv T.] Norwegian Inst Publ Hlth, Med Birth Registry Norway, Bergen, Norway.
RP Wilcox, AJ (reprint author), Natl Inst Environm Hlth Sci, POB 12233,Mail Drop A3-05, Res Triangle Pk, NC 27709 USA.
EM wilcox1@niehs.nih.gov
OI Harlid, Sophia/0000-0001-8540-6891; xu, zongli/0000-0002-9034-8902;
Wilcox, Allen/0000-0002-3376-1311; taylor, jack/0000-0001-5303-6398
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences.
NR 47
TC 48
Z9 49
U1 4
U2 25
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
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2014
VL 122
IS 10
BP 1147
EP 1153
DI 10.1289/ehp.1307892
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA AQ9BO
UT WOS:000343136200030
PM 24906187
ER
PT J
AU Birnbaum, LS
Tart, KT
AF Birnbaum, Linda S.
Tart, Kimberly Thigpen
TI Protecting Our Children from Climate Change
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Editorial Material
C1 [Birnbaum, Linda S.; Tart, Kimberly Thigpen] Natl Inst Environm Hlth Sci, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA.
RP Birnbaum, LS (reprint author), Natl Inst Environm Hlth Sci, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA.
EM birnbaumls@niehs.nih.gov
NR 5
TC 1
Z9 1
U1 0
U2 9
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
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2014
VL 122
IS 10
BP A260
EP A261
DI 10.1289/ehp.1409165
PG 2
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA AQ9BO
UT WOS:000343136200001
PM 25271472
ER
PT J
AU Sinner, MF
Stepas, KA
Moser, CB
Krijthe, BP
Aspelund, T
Sotoodehnia, N
Fontes, JD
Janssens, ACJW
Kronmal, RA
Magnani, JW
Witteman, JC
Chamberlain, AM
Lubitz, SA
Schnabel, RB
Vasan, RS
Wang, TJ
Agarwal, SK
McManus, DD
Franco, OH
Yin, XY
Larson, MG
Burke, GL
Launer, LJ
Hofman, A
Levy, D
Gottdiener, JS
Kaab, S
Couper, D
Harris, TB
Astor, BC
Ballantyne, CM
Hoogeveen, RC
Arai, AE
Soliman, EZ
Ellinor, PT
Stricker, BHC
Gudnason, V
Heckbert, SR
Pencina, MJ
Benjamin, EJ
Alonso, A
AF Sinner, Moritz F.
Stepas, Katherine A.
Moser, Carlee B.
Krijthe, Bouwe P.
Aspelund, Thor
Sotoodehnia, Nona
Fontes, Joao D.
Janssens, A. Cecile J. W.
Kronmal, Richard A.
Magnani, Jared W.
Witteman, Jacqueline C.
Chamberlain, Alanna M.
Lubitz, Steven A.
Schnabel, Renate B.
Vasan, Ramachandran S.
Wang, Thomas J.
Agarwal, Sunil K.
McManus, David D.
Franco, Oscar H.
Yin, Xiaoyan
Larson, Martin G.
Burke, Gregory L.
Launer, Lenore J.
Hofman, Albert
Levy, Daniel
Gottdiener, John S.
Kaeaeb, Stefan
Couper, David
Harris, Tamara B.
Astor, Brad C.
Ballantyne, Christie M.
Hoogeveen, Ron C.
Arai, Andrew E.
Soliman, Elsayed Z.
Ellinor, Patrick T.
Stricker, Bruno H. C.
Gudnason, Vilmundur
Heckbert, Susan R.
Pencina, Michael J.
Benjamin, Emelia J.
Alonso, Alvaro
TI B-type natriuretic peptide and C-reactive protein in the prediction of
atrial fibrillation risk: the CHARGE-AF Consortium of community-based
cohort studies
SO EUROPACE
LA English
DT Article
DE Atrial fibrillation; Risk prediction; Epidemiology; Biomarker; B-type
natriuretic peptide; C-reactive protein
ID ASSOCIATION CONSENSUS CONFERENCE; NT-PROBNP; INFLAMMATION; MANAGEMENT;
BNP; RECLASSIFICATION; DISCRIMINATION; BIOMARKERS; REDUCTION; DYSPNEA
AB Aims B-type natriuretic peptide (BNP) and C-reactive protein (CRP) predict atrial fibrillation (AF) risk. However, their risk stratification abilities in the broad community remain uncertain. We sought to improve risk stratification for AF using biomarker information.
Methods and results We ascertained AF incidence in 18 556 Whites and African Americans from the Atherosclerosis Risk in Communities Study (ARIC, n=10 675), Cardiovascular Health Study (CHS, n=5043), and Framingham Heart Study (FHS, n = 2838), followed for 5 years (prediction horizon). We added BNP (ARIC/CHS: N-terminal pro-B-type natriuretic peptide; FHS: BNP), CRP, or both to a previously reported AF risk score, and assessed model calibration and predictive ability [C-statistic, integrated discrimination improvement (IDI), and net reclassification improvement (NRI)]. We replicated models in two independent European cohorts: Age, Gene/Environment Susceptibility Reykjavik Study (AGES), n=4467; Rotterdam Study (RS), n=3203. B-type natriuretic peptide and CRP were significantly associated with AF incidence (n=1186): hazard ratio per 1-SD ln-transformed biomarker 1.66 [95% confidence interval (CI), 1.56-1.76], P < 0.0001 and 1.18 (95% CI, 1.11-1.25), P < 0.0001, respectively. Model calibration was sufficient (BNP, chi(2)=17.0; CRP, chi(2)=10.5; BNP and CRP, chi(2)=13.1). B-type natriuretic peptide improved the C-statistic from 0.765 to 0.790, yielded an IDI of 0.027 (95% CI, 0.022-0.032), a relative IDI of 41.5%, and a continuous NRI of 0.389 (95% CI, 0.322-0.455). The predictive ability of CRP was limited (C-statistic increment 0.003). B-type natriuretic peptide consistently improved prediction in AGES and RS.
Conclusion B-type natriuretic peptide, not CRP, substantially improved AF risk prediction beyond clinical factors in an independently replicated, heterogeneous population. B-type natriuretic peptide may serve as a benchmark to evaluate novel putative AF risk biomarkers.
C1 [Sinner, Moritz F.; Kaeaeb, Stefan] Univ Munich, Univ Hosp Munich, Dept Med 1, D-81377 Munich, Germany.
[Stepas, Katherine A.; Moser, Carlee B.; Yin, Xiaoyan; Pencina, Michael J.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA.
[Krijthe, Bouwe P.; Janssens, A. Cecile J. W.; Witteman, Jacqueline C.; Franco, Oscar H.; Hofman, Albert; Arai, Andrew E.; Stricker, Bruno H. C.] Erasmus MC, Dept Epidemiol, NL-3000 CA Rotterdam, Netherlands.
[Krijthe, Bouwe P.; Janssens, A. Cecile J. W.; Witteman, Jacqueline C.; Hofman, Albert; Stricker, Bruno H. C.] NCHA, NL-2300 RC Leiden, Netherlands.
[Aspelund, Thor; Gudnason, Vilmundur] Iceland Heart Assoc, Res Inst, IS-201 Kopavogur, Iceland.
[Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, IS-101 Reykjavik, Iceland.
[Sotoodehnia, Nona] Univ Washington, Dept Med, Div Cardiol, Seattle, WA 98195 USA.
[Sotoodehnia, Nona] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98101 USA.
[Fontes, Joao D.; Magnani, Jared W.; Vasan, Ramachandran S.; Wang, Thomas J.; McManus, David D.; Yin, Xiaoyan; Larson, Martin G.; Levy, Daniel; Benjamin, Emelia J.] NHLBI, Framingham, MA 01702 USA.
[Fontes, Joao D.; Magnani, Jared W.; Vasan, Ramachandran S.; Wang, Thomas J.; McManus, David D.; Yin, Xiaoyan; Larson, Martin G.; Levy, Daniel; Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA 01702 USA.
[Kronmal, Richard A.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Magnani, Jared W.; Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Chamberlain, Alanna M.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN 55905 USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Schnabel, Renate B.] Univ Heart Ctr, Dept Gen & Intervent Cardiol, D-20246 Hamburg, Germany.
[Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA.
[Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Agarwal, Sunil K.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[McManus, David D.] Univ Massachusetts, Dept Med, Worcester, MA 01605 USA.
[McManus, David D.] Univ Massachusetts, Dept Quantitat Hlth Sci, Worcester, MA 01605 USA.
[McManus, David D.] Worcester Polytech Inst, Dept Biomed Engn, Worcester, MA 01609 USA.
[Burke, Gregory L.] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
[Launer, Lenore J.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Framingham, MA 01702 USA.
[Gottdiener, John S.] Univ Maryland, Med Ctr, Div Cardiol, Baltimore, MD 21201 USA.
[Kaeaeb, Stefan] Deutsch Zentrum Herz Kreislauferkrankungen DZHK, Munich Heart Alliance, D-80802 Munich, Germany.
[Couper, David] Univ N Carolina, Dept Biostat, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27599 USA.
[Astor, Brad C.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53705 USA.
[Ballantyne, Christie M.; Hoogeveen, Ron C.] Baylor Coll Med, Houston, TX 77030 USA.
[Ballantyne, Christie M.] Methodist DeBakey Heart & Vasc Ctr, Houston, TX 77030 USA.
[Arai, Andrew E.] NHLBI, Cardiovasc & Pulm Branch, Bethesda, MD 20892 USA.
[Soliman, Elsayed Z.] Wake Forest Univ, Bowman Gray Sch Med, Epidemiol Cardiol Res Ctr EPICARE, Winston Salem, NC 27157 USA.
[Stricker, Bruno H. C.] Erasmus MC, Dept Internal Med, NL-3000 CA Rotterdam, Netherlands.
[Stricker, Bruno H. C.] Inspectorate Hlth Care, NL-3500 GR The Hague, Netherlands.
[Stricker, Bruno H. C.] Erasmus MC, Dept Med Informat, Rotterdam, Netherlands.
[Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
RP Benjamin, EJ (reprint author), NHLBI, Framingham, MA 01702 USA.
EM emelia@bu.edu; alonso@umn.edu
RI Gudnason, Vilmundur/K-6885-2015; Aspelund, Thor/C-5983-2008; Alonso,
Alvaro/A-4917-2010;
OI Gudnason, Vilmundur/0000-0001-5696-0084; Aspelund,
Thor/0000-0002-7998-5433; Alonso, Alvaro/0000-0002-2225-8323;
Ramachandran, Vasan/0000-0001-7357-5970; Benjamin,
Emelia/0000-0003-4076-2336
FU US National Institutes of Health, Bethesda, MD [1RC1HL101056]
FX This work was supported by the US National Institutes of Health,
Bethesda, MD [1RC1HL101056]. Details on additional funding are available
in the supplemental material.
NR 37
TC 30
Z9 31
U1 1
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1099-5129
EI 1532-2092
J9 EUROPACE
JI Europace
PD OCT
PY 2014
VL 16
IS 10
BP 1426
EP 1433
DI 10.1093/europace/euu175
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AR1EL
UT WOS:000343326200003
PM 25037055
ER
PT J
AU Barrett, AJ
AF Barrett, Austin John
TI Stem cell transplants for myelodysplastic syndromes: refining the
outcome predictions
SO HAEMATOLOGICA
LA English
DT Letter
ID HYPOMETHYLATING AGENTS; SCORING SYSTEM; LEUKEMIA; TOOL
C1 NHLBI, Stem Cell Allotransplantat Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Barrett, AJ (reprint author), NHLBI, Stem Cell Allotransplantat Sect, Hematol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM barrettj@nhlbi.nih.gov
FU Intramural NIH HHS
NR 12
TC 0
Z9 0
U1 0
U2 1
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOLOGICA
JI Haematologica
PD OCT 1
PY 2014
VL 99
IS 10
BP 1536
EP 1537
DI 10.3324/haematol.2014.113555
PG 3
WC Hematology
SC Hematology
GA AQ7ZC
UT WOS:000343038500015
PM 25271312
ER
PT J
AU Inamoto, Y
Martin, PJ
Storer, BE
Palmer, J
Weisdorf, DJ
Pidala, J
Flowers, MED
Arora, M
Jagasia, M
Arai, S
Chai, XY
Pavletic, SZ
Vogelsang, GB
Lee, SJ
AF Inamoto, Yoshihiro
Martin, Paul J.
Storer, Barry E.
Palmer, Jeanne
Weisdorf, Daniel J.
Pidala, Joseph
Flowers, Mary E. D.
Arora, Mukta
Jagasia, Madan
Arai, Sally
Chai, Xiaoyu
Pavletic, Steven Z.
Vogelsang, Georgia B.
Lee, Stephanie J.
CA Chronic GVHD Consortium
TI Association of severity of organ involvement with mortality and
recurrent malignancy in patients with chronic graft-versus-host disease
SO HAEMATOLOGICA
LA English
DT Article
ID NIH CONSENSUS CRITERIA; STEM-CELL TRANSPLANTATION; ALLOGENEIC MARROW
TRANSPLANTATION; CHRONIC GVHD; LEUKEMIA REACTIONS; RISK-FACTORS;
SURVIVAL; OUTCOMES; CONSORTIUM; DIAGNOSIS
AB The National Institutes of Health global score for chronic graft-versus-host disease was devised by experts but was not based on empirical data. We hypothesized that analysis of prospectively collected data would enable derivation of a more accurate model for estimating mortality risk. We analyzed 574 adult patients with chronic graft-versus-host disease enrolled in a multicenter, observational study, using multivariate time-varying analysis accounting for serial changes in severity of involvement of eight individual organ sites over time. In the training set, severity of skin, mouth, gastrointestinal tract, liver and lung involvement were independently associated with the risk of non-relapse mortality. Weighted mortality points were assigned to individual organs based on the hazard ratios and were summed. The population was divided into three risk groups based on the total mortality points. The three new risk groups were validated in an independent validation set, but did not show better discriminative performance than the National Institutes of Health global score. As compared to a moderate or mild global score, a severe global score was associated with increased risks of non-relapse and overall mortality across time but not with a decreased risk of recurrent malignancy. The National Institutes of Health global score predicts patients' mortality risk throughout the course of their chronic graft-versus-host disease. Further research is required in order to improve outcomes in patients with severe chronic graft-versus-host disease, since their risk of mortality remains elevated.
C1 [Inamoto, Yoshihiro; Martin, Paul J.; Storer, Barry E.; Flowers, Mary E. D.; Chai, Xiaoyu; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Palmer, Jeanne] Mayo Clin Arizona, Div Hematol & Oncol, Scottsdale, AZ USA.
[Weisdorf, Daniel J.; Arora, Mukta] Univ Minnesota, Blood & Marrow Transplant Program, Minneapolis, MN USA.
[Pidala, Joseph] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Jagasia, Madan] Vanderbilt Univ, Med Ctr, Hematol & Stem Cell Transplant Program, Nashville, TN USA.
[Arai, Sally] Stanford Univ, Med Ctr, Div Blood & Marrow Transplantat, Stanford, CA 94305 USA.
[Pavletic, Steven Z.] NCI, Bethesda, MD 20892 USA.
[Vogelsang, Georgia B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
RP Inamoto, Y (reprint author), Fred Hutchinson Canc Res Ctr, Div Clin Res, 1124 Columbia St, Seattle, WA 98104 USA.
EM yinamoto@fhcrc.org
FU National Institutes of Health [CA118953, CA163438]; Chronic GVHD
Consortium, National Institutes of Health Rare Diseases Clinical
Research Network [U54 CA163438]; National Institutes of Health Office of
Rare Diseases Research at the National Center for Advancing
Translational Science; National Cancer Institute; Fred Hutchinson Cancer
Research Center
FX This work was supported by grants CA118953 and CA163438 from the
National Institutes of Health. The Chronic GVHD Consortium (U54
CA163438) is a part of the National Institutes of Health Rare Diseases
Clinical Research Network, supported through collaboration between the
National Institutes of Health Office of Rare Diseases Research at the
National Center for Advancing Translational Science, the National Cancer
Institute, and the Fred Hutchinson Cancer Research Center. The content
of this paper is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institutes of
Health. The authors thank Drs. Corey Cutler, Jenna Goldberg and Iskra
Pusic for contributing patients.
NR 25
TC 5
Z9 5
U1 0
U2 2
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOLOGICA
JI Haematologica
PD OCT 1
PY 2014
VL 99
IS 10
BP 1618
EP 1623
DI 10.3324/haematol.2014.109611
PG 6
WC Hematology
SC Hematology
GA AQ7ZC
UT WOS:000343038500026
PM 24997150
ER
PT J
AU Morton, LM
Gilbert, ES
Stovall, M
van Leeuwen, FE
Dores, GM
Lynch, CF
Hall, P
Smith, SA
Weathers, RE
Storm, HH
Hodgson, DC
Kleinerman, RA
Joensuu, H
Johannesen, TB
Andersson, M
Holowaty, EJ
Kaijser, M
Pukkala, E
Vaalavirta, L
Fossa, SD
Langmark, F
Travis, LB
Lamart, S
Simon, SL
Fraumeni, JF
Aleman, BM
Curtis, RE
AF Morton, Lindsay M.
Gilbert, Ethel S.
Stovall, Marilyn
van Leeuwen, Flora E.
Dores, Graa M.
Lynch, Charles F.
Hall, Per
Smith, Susan A.
Weathers, Rita E.
Storm, Hans H.
Hodgson, David C.
Kleinerman, Ruth A.
Joensuu, Heikki
Johannesen, Tom Borge
Andersson, Michael
Holowaty, Eric J.
Kaijser, Magnus
Pukkala, Eero
Vaalavirta, Leila
Fossa, Sophie D.
Langmark, Froydis
Travis, Lois B.
Lamart, Stephanie
Simon, Steven L.
Fraumeni, Joseph F., Jr.
Aleman, Berthe M.
Curtis, Rochelle E.
TI Risk of esophageal cancer following radiotherapy for Hodgkin lymphoma
SO HAEMATOLOGICA
LA English
DT Letter
DE radiotherapy; Hodgkin lymphoma; esophageal cancer; late effects
ID LONG-TERM SURVIVORS; MALIGNANT NEOPLASMS; LUNG-CANCER; DISEASE;
CHEMOTHERAPY; ADOLESCENCE; CHILDHOOD; COHORT
C1 [Morton, Lindsay M.; Gilbert, Ethel S.; Dores, Graa M.; Kleinerman, Ruth A.; Simon, Steven L.; Fraumeni, Joseph F., Jr.; Curtis, Rochelle E.] Natl Canc Inst, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Stovall, Marilyn; Smith, Susan A.; Weathers, Rita E.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
[van Leeuwen, Flora E.] Netherlands Canc Inst, Dept Epidemiol & Biostat, Amsterdam, Netherlands.
[Dores, Graa M.] Med Ctr, Dept Vet Affairs, Oklahoma City, OK USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Hall, Per] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Storm, Hans H.] Danish Canc Soc, Copenhagen, Denmark.
[Hodgson, David C.] Univ Toronto, Dept Radiat Oncol, Toronto, ON, Canada.
[Joensuu, Heikki; Vaalavirta, Leila] Univ Helsinki, Cent Hosp, Dept Oncol, Helsinki, Finland.
[Johannesen, Tom Borge; Langmark, Froydis] Canc Registry Norway, Oslo, Norway.
[Andersson, Michael] Univ Copenhagen Hosp, Dept Oncol, DK-2100 Copenhagen, Denmark.
[Holowaty, Eric J.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Kaijser, Magnus] Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.
[Pukkala, Eero] Inst Stat & Epidemiol Canc Res, Finnish Canc Registry, Helsinki, Finland.
[Fossa, Sophie D.] Univ Tampere, Sch Hlth Sci, FIN-33101 Tampere, Finland.
[Fossa, Sophie D.] Oslo Univ Hosp, Dept Oncol, Oslo, Norway.
[Fossa, Sophie D.] Univ Oslo, N-0316 Oslo, Norway.
[Travis, Lois B.] Univ Rochester, Med Ctr, Dept Radiat Oncol, Rochester, NY 14627 USA.
[Aleman, Berthe M.] Netherlands Canc Inst, Dept Radiat Oncol, Amsterdam, Netherlands.
RP Morton, LM (reprint author), Natl Canc Inst, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
EM mortonli@mail.nih.gov
RI Morton, Lindsay/B-5234-2015;
OI Kleinerman, Ruth/0000-0001-7415-2478; Joensuu,
Heikki/0000-0003-0281-2507; Morton, Lindsay/0000-0001-9767-2310; Storm,
Hans/0000-0001-7223-8198
FU NCI NIH HHS [N01CP31154, N01-CP-31003, N01-CP-31155, N01-CP-31156,
N01-CP-31157, N01CP31019, N02CP31003, N02CP31136, N02CP55503, P30
CA086862]; NIAID NIH HHS [N01CP31156]
NR 15
TC 5
Z9 5
U1 0
U2 2
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOLOGICA
JI Haematologica
PD OCT 1
PY 2014
VL 99
IS 10
BP E193
EP E196
DI 10.3324/haematol.2014.108258
PG 4
WC Hematology
SC Hematology
GA AQ7ZC
UT WOS:000343038500006
PM 25271315
ER
PT J
AU Narayanan, S
Townsend, K
Macharia, T
Majid, A
Nelson, A
Redfield, RR
Kottilil, S
Talwani, R
Osinusi, A
AF Narayanan, Shivakumar
Townsend, Kerry
Macharia, Thomas
Majid, Adrian
Nelson, Amy
Redfield, Robert R.
Kottilil, Shyam
Talwani, Rohit
Osinusi, Anu
TI Favorable adverse event profile of sofosbuvir/ribavirin compared to
boceprevir/interferon/ribavirin for treatment of hepatitis C
SO HEPATOLOGY INTERNATIONAL
LA English
DT Article
DE Sofosbuvir; Ribavirin; HCV monoinfection; Adverse events
ID GENOTYPE 1 INFECTION; VIRUS-INFECTION; PLUS RIBAVIRIN; UNITED-STATES;
BOCEPREVIR; TELAPREVIR; PEGINTERFERON; BURDEN; TRIAL
AB Background Triple therapy for the treatment of hepatitis C virus (HCV) with first-generation directly acting antiviral agents, the non-structural serine protease inhibitors boceprevir (BOC) and telaprevir have resulted in improved sustained virologic response (SVR) rates. However, a high incidence of adverse events (AEs), high pill burdens and drug interactions remain significant barriers to successful completion of therapy. The aim of this study was to evaluate the AEs observed with BOC triple therapy in comparison to IFN-free sofosbuvir/ribavirin (SOF/RBV) therapy in HCV monoinfected, genotype-1 (GT-1) individuals.
Methods We retrospectively evaluated HCV monoinfected, treatment-naive or -experienced, GT-1 individuals treated with either BOC/IFN/RBV at the Veterans Affairs Medical Center, Baltimore (n = 97) or SOF/RBV in the NIAID SPARE clinical trial (n = 60). AEs, namely hematologic (hemoglobin, neutrophil and platelet counts), hepatic (alanine transaminase or bilirubin) and renal (eGFR), were measured according to the DAIDS toxicity table (version 1.0).
Results BOC/IFN/RBV was associated with significantly more AEs, most commonly neutropenia, anemia and thrombocytopenia. In the SOF/RBV cohort, five (8 %) patients discontinued treatment early, but none (0 %) were because of AEs, while 60 (62 %) patients on triple therapy discontinued treatment early, 34 (57 %) because of AEs. SVR24 rates were 68 versus 34 % with SOF/RBV versus BOC/IFN/RBV.
Conclusions SOF/RBV treatment was associated with fewer side effects than BOC-based triple therapy, appearing to be a safer and more tolerable alternative for HCV GT-1 subjects. These results show that emerging IFN-free therapies may enhance patient adherence, allowing treatment of larger number of patients with improved efficacy.
C1 [Narayanan, Shivakumar; Macharia, Thomas; Majid, Adrian; Redfield, Robert R.; Talwani, Rohit; Osinusi, Anu] Univ Maryland, Sch Med, Inst Human Virol, Div Infect Dis, Baltimore, MD 21201 USA.
[Townsend, Kerry; Nelson, Amy; Kottilil, Shyam; Osinusi, Anu] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Kottilil, S (reprint author), NIAID, Immunoregulat Lab, NIH, 10-11N204,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM skottilil@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases
FX We would like to acknowledge the contributions of the following
individuals: Laura Heytens, who was the study coordinator on the SPARE
study. This research was supported in part by the intramural program of
the National Institute of Allergy and Infectious Diseases. The data from
this study have been partially presented at The Conference for
Retroviruses and Opportunistic Infections (CROI) 2014 in Boston, MA,
USA.
NR 23
TC 4
Z9 4
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1936-0533
EI 1936-0541
J9 HEPATOL INT
JI Hepatol. Int.
PD OCT
PY 2014
VL 8
IS 4
BP 560
EP 566
DI 10.1007/s12072-014-9574-0
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ9DQ
UT WOS:000343144200012
PM 26202761
ER
PT J
AU Myers, RA
Scott, NM
Gauderman, WJ
Qiu, WL
Mathias, RA
Romieu, I
Levin, AM
Pino-Yanes, M
Graves, PE
Villarreal, AB
Beaty, TH
Carey, VJ
Croteau-Chonka, DC
Navarro, BD
Edlund, C
Hernandez-Cadena, L
Navarro-Olivos, E
Padhukasahasram, B
Salam, MT
Torgerson, DG
Van den Berg, DJ
Vora, H
Bleecker, ER
Meyers, DA
Williams, LK
Martinez, FD
Burchard, EG
Barnes, KC
Gilliland, FD
Weiss, ST
London, SJ
Raby, BA
Ober, C
Nicolae, DL
AF Myers, Rachel A.
Scott, Nicole M.
Gauderman, W. James
Qiu, Weiliang
Mathias, Rasika A.
Romieu, Isabelle
Levin, Albert M.
Pino-Yanes, Maria
Graves, Penelope E.
Barraza Villarreal, Albino
Beaty, Terri H.
Carey, Vincent J.
Croteau-Chonka, Damien C.
del Rio Navarro, Blanca
Edlund, Christopher
Hernandez-Cadena, Leticia
Navarro-Olivos, Efrain
Padhukasahasram, Badri
Salam, Muhammad T.
Torgerson, Dara G.
Van den Berg, David J.
Vora, Hita
Bleecker, Eugene R.
Meyers, Deborah A.
Williams, L. Keoki
Martinez, Fernando D.
Burchard, Esteban G.
Barnes, Kathleen C.
Gilliland, Frank D.
Weiss, Scott T.
London, Stephanie J.
Raby, Benjamin A.
Ober, Carole
Nicolae, Dan L.
CA GRAAD
TI Genome-wide interaction studies reveal sex-specific asthma risk alleles
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID REGULATORY FACTOR-1 POLYMORPHISMS; GTPASE-ACTIVATING PROTEIN;
GENE-EXPRESSION; AUTOIMMUNE-DISEASE; ASSOCIATION; METAANALYSIS;
DIMORPHISM; CHILDHOOD; PLATELETS; LOCI
AB Asthma is a complex disease with sex-specific differences in prevalence. Candidate gene studies have suggested that genotype-by-sex interaction effects on asthma risk exist, but this has not yet been explored at a genome-wide level. We aimed to identify sex-specific asthma risk alleles by performing a genome-wide scan for genotype-by-sex interactions in the ethnically diverse participants in the EVE Asthma Genetics Consortium. We performed male- and female-specific genome-wide association studies in 2653 male asthma cases, 2566 female asthma cases and 3830 non-asthma controls from European American, African American, African Caribbean and Latino populations. Association tests were conducted in each study sample, and the results were combined in ancestry-specific and cross-ancestry meta-analyses. Six sex-specific asthma risk loci had P-values < 1 x 10(-6), of which two were male specific and four were female specific; all were ancestry specific. The most significant sex-specific association in European Americans was at the interferon regulatory factor 1 (IRF1) locus on 5q31.1. We also identify a Latino female-specific association in RAP1GAP2. Both of these loci included single-nucleotide polymorphisms that are known expression quantitative trait loci and have been associated with asthma in independent studies. The IRF1 locus is a strong candidate region for male-specific asthma susceptibility due to the association and validation we demonstrate here, the known role of IRF1 in asthma-relevant immune pathways and prior reports of sex-specific differences in interferon responses.
C1 [Myers, Rachel A.; Scott, Nicole M.; Ober, Carole; Nicolae, Dan L.] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
[Nicolae, Dan L.] Univ Chicago, Dept Stat & Med, Chicago, IL 60637 USA.
[Gauderman, W. James; Edlund, Christopher; Salam, Muhammad T.; Van den Berg, David J.; Vora, Hita; Gilliland, Frank D.] Univ So Calif, Dept Prevent Med, Los Angeles, CA 90032 USA.
[Qiu, Weiliang; Carey, Vincent J.; Croteau-Chonka, Damien C.; Weiss, Scott T.; Raby, Benjamin A.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Mathias, Rasika A.; Beaty, Terri H.; Barnes, Kathleen C.] Johns Hopkins Univ, Dept Med & Epidemiol, Baltimore, MD 21205 USA.
[Romieu, Isabelle] Int Agcy Res Canc, F-69372 Lyon, France.
[Levin, Albert M.] Henry Ford Hlth Syst, Dept Publ Hlth Sci, Detroit, MI 48202 USA.
[Padhukasahasram, Badri; Williams, L. Keoki] Henry Ford Hlth Syst, Ctr Hlth Policy & Hlth Serv Res, Detroit, MI 48202 USA.
[Williams, L. Keoki] Henry Ford Hlth Syst, Dept Internal Med, Detroit, MI 48202 USA.
[Pino-Yanes, Maria; Torgerson, Dara G.; Burchard, Esteban G.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Pino-Yanes, Maria; Torgerson, Dara G.; Burchard, Esteban G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Pino-Yanes, Maria] Inst Salud Carlos III, CIBER Enfermedades Resp, Madrid, Spain.
[Graves, Penelope E.; Martinez, Fernando D.] Univ Arizona, Arizona Resp Care Ctr, Inst BIO5, Tucson, AZ 85721 USA.
[Barraza Villarreal, Albino; Hernandez-Cadena, Leticia; Navarro-Olivos, Efrain] Natl Inst Publ Hlth Mexico, Cuernavaca, Morelos, Mexico.
[del Rio Navarro, Blanca] Hosp Infantil Mexico Dr Federico Gomez, Mexico City, DF, Mexico.
[Bleecker, Eugene R.; Meyers, Deborah A.] Wake Forest Sch Med, Ctr Genom & Personalized Med, Winston Salem, NC 27157 USA.
[London, Stephanie J.] NIEHS, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
RP Myers, RA (reprint author), Univ Chicago, Dept Human Genet, 920 East 58th St,CLSC 431F, Chicago, IL 60637 USA.
EM ram330@gmail.com; nicolae@galton.uchicago.edu
RI Pino-Yanes, Maria/C-8498-2017;
OI Pino-Yanes, Maria/0000-0003-0332-437X; London,
Stephanie/0000-0003-4911-5290
FU Office of the Director, National Institutes of Health; National Heart,
Lung and Blood Institute [HL101651, HL085197, HL087699, HL075419,
HL65899, HL083069, HL066289, HL101543, HL115606, HL087680, HL61768,
HL76647, HL079055, HL118267, HL088133, HL078885, HL004464, HL104608];
National Institute of Allergy and Infection Diseases [AI079139,
AI061774, AI095230, AI077439]; National Institute of Environmental
Health Sciences [ES022719, ES011627, ES007048, ES009581, ES015794];
National Institute on Minority Health and Health Disparities [MD006902];
National Institute of General Medical Sciences [GM007546]; Fundacion
Ramon Areces; American Asthma Foundation; Fund for Henry Ford Hospital;
Hastings Foundation; RWJF Amos Medical Faculty Development Award;
Sandler Foundation; Mary Beryl Patch Turnbull Scholar Program; National
Institutes of Health, National Institute of Environmental Health
Sciences
FX This work was supported by grants from the Office of the Director,
National Institutes of Health to C.O. and D.L.N.; the National Heart,
Lung and Blood Institute (HL101651 to C.O. and D.L.N., HL085197 to C.O.,
HL087699 to K.C.B.,HL075419,HL65899, HL083069 and HL066289 to S.T.W.,
HL101543 to B.A.R. and S.T.W., HL115606 and HL087680 to W.J.G., HL61768
and HL76647 to F.D.G., HL079055 and HL118267 to L.K.W., HL088133,
HL078885, HL004464 and HL104608 to E.G.B.); the National Institute of
Allergy and Infection Diseases (AI079139, AI061774 to L.K.W., AI095230
to C.O., AI077439 to E.G.B.); the National Institute of Environmental
Health Sciences (ES022719 to W.J.G., ES011627 to F.D.G., ES007048 and
ES009581 to F.D.G. and W.J.G., ES015794 to E.G.B.); the National
Institute on Minority Health and Health Disparities (MD006902 to E.G.B.)
the National Institute of General Medical Sciences (GM007546 to E.G.B.);
Fundacion Ramon Areces (M.P.Y.); American Asthma Foundation (L.K.W. and
E.G.B.); the Fund for Henry Ford Hospital (L.K.W.); Hastings Foundation
(F.D.G.); RWJF Amos Medical Faculty Development Award (E.G.B.); the
Sandler Foundation (E.G.B.) and the Mary Beryl Patch Turnbull Scholar
Program (K.C.B.). This research was supported in part by the Intramural
Research Program of the National Institutes of Health, National
Institute of Environmental Health Sciences.
NR 51
TC 15
Z9 15
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 1
PY 2014
VL 23
IS 19
BP 5251
EP 5259
DI 10.1093/hmg/ddu222
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AQ9OM
UT WOS:000343185200019
PM 24824216
ER
PT J
AU Barrdahl, M
Canzian, F
Joshi, AD
Travis, RC
Chang-Claude, J
Auer, PL
Gapstur, SM
Gaudet, M
Diver, WR
Henderson, BE
Haiman, CA
Schumacher, FR
Le Marchand, L
Berg, CD
Chanock, SJ
Hoover, RN
Rudolph, A
Ziegler, RG
Giles, GG
Baglietto, L
Severi, G
Hankinson, SE
Lindstrom, S
Willet, W
Hunter, DJ
Buring, JE
Lee, IM
Zhang, SM
Dossus, L
Cox, DG
Khaw, KT
Lund, E
Naccarati, A
Peeters, PH
Quiros, JR
Riboli, E
Sund, M
Trichopoulos, D
Prentice, RL
Kraft, P
Kaaks, R
Campa, D
AF Barrdahl, Myrto
Canzian, Federico
Joshi, Amit D.
Travis, Ruth C.
Chang-Claude, Jenny
Auer, Paul L.
Gapstur, Susan M.
Gaudet, Mia
Diver, W. Ryan
Henderson, Brian E.
Haiman, Christopher A.
Schumacher, Fredrick R.
Le Marchand, Loic
Berg, Christine D.
Chanock, Stephen J.
Hoover, Robert N.
Rudolph, Anja
Ziegler, Regina G.
Giles, Graham G.
Baglietto, Laura
Severi, Gianluca
Hankinson, Susan E.
Lindstroem, Sara
Willet, Walter
Hunter, David J.
Buring, Julie E.
Lee, I-Min
Zhang, Shumin
Dossus, Laure
Cox, David G.
Khaw, Kay-Tee
Lund, Eiliv
Naccarati, Alessio
Peeters, Petra H.
Ramon Quiros, J.
Riboli, Elio
Sund, Malin
Trichopoulos, Dimitrios
Prentice, Ross L.
Kraft, Peter
Kaaks, Rudolf
Campa, Daniele
TI Post-G WAS gene-environment interplay in breast cancer: results from the
Breast and Prostate Cancer Cohort Consortium and a meta-analysis on 79
000 women
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; BASE-LINE CHARACTERISTICS; BRCA2 MUTATION
CARRIERS; LOW-PENETRANCE BREAST; SUSCEPTIBILITY LOCI; COMMON VARIANTS;
CONFER SUSCEPTIBILITY; LEAD CONCENTRATION; TOBACCO-SMOKE; RISK VARIANT
AB We studied the interplay between 39 breast cancer (BC) risk SNPs and established BC risk (body mass index, height, age at menarche, parity, age at menopause, smoking, alcohol and family history of BC) and prognostic factors (TNM stage, tumor grade, tumor size, age at diagnosis, estrogen receptor status and progesterone receptor status) as joint determinants of BC risk. We used a nested case-control design within the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium (BPC3), with 16 285 BC cases and 19 376 controls. We performed stratified analyses for both the risk and prognostic factors, testing for heterogeneity for the risk factors, and case-case comparisons for differential associations of polymorphisms by subgroups of the prognostic factors. We analyzed multiplicative interactions between the SNPs and the risk factors. Finally, we also performed a meta-analysis of the interaction ORs from BPC3 and the Breast Cancer Association Consortium. After correction for multiple testing, no significant interaction between the SNPs and the established risk factors in the BPC3 study was found. The meta-analysis showed a suggestive interaction between smoking status and SLC4A7-rs4973768 (P-interaction = 8.84 x 10(-4)) which, although not significant after considering multiple comparison, has a plausible biological explanation. In conclusion, in this study of up to almost 79 000 women we can conclusively exclude any novel major interactions between genome-wide association studies hits and the epidemiologic risk factors taken into consideration, but we propose a suggestive interaction between smoking status and SLC4A7-rs4973768 that if further replicated could help our understanding in the etiology of BC.
C1 [Barrdahl, Myrto; Chang-Claude, Jenny; Rudolph, Anja; Kaaks, Rudolf; Campa, Daniele] German Canc Res Ctr, Div Canc Epidemiol, D-69120 Heidelberg, Germany.
[Canzian, Federico] German Canc Res Ctr, Genom Epidemiol Grp, D-69120 Heidelberg, Germany.
[Joshi, Amit D.; Hankinson, Susan E.; Lindstroem, Sara; Willet, Walter; Hunter, David J.; Buring, Julie E.; Lee, I-Min; Zhang, Shumin; Trichopoulos, Dimitrios; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Travis, Ruth C.] Univ Oxford, Canc Epidemiol Unit, Oxford OX3 7LF, England.
[Auer, Paul L.; Prentice, Ross L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Auer, Paul L.] Univ Wisconsin, Sch Publ Hlth, Milwaukee, WI USA.
[Gapstur, Susan M.; Gaudet, Mia; Diver, W. Ryan] Amer Canc Soc, Dept Epidemiol, Atlanta, GA 30303 USA.
[Henderson, Brian E.; Haiman, Christopher A.; Schumacher, Fredrick R.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Le Marchand, Loic] Univ Hawaii, Ctr Canc, Honolulu, HI 96813 USA.
[Berg, Christine D.; Chanock, Stephen J.; Hoover, Robert N.; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Giles, Graham G.; Baglietto, Laura; Severi, Gianluca] Canc Council Victoria, Canc Epidemiol Ctr Melbourne, Carlton, Vic 3004, Australia.
[Giles, Graham G.; Baglietto, Laura; Severi, Gianluca] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Sch Populat Hlth, Melbourne, Vic 3010, Australia.
[Giles, Graham G.] Monash Univ, Fac Med, Melbourne, Vic 3800, Australia.
[Hankinson, Susan E.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Hankinson, Susan E.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Hankinson, Susan E.] Univ Massachusetts, Div Biostat & Epidemiol, Amherst, MA 01003 USA.
[Dossus, Laure] Inst Gustave Roussy, INSERM, Ctr Res Epidemiol & Populat Hlth, F-94805 Villejuif, France.
[Dossus, Laure] Paris South Univ, F-94807 Villejuif, France.
[Cox, David G.; Peeters, Petra H.; Riboli, Elio] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London SW7 2AZ, England.
[Cox, David G.] Univ Lyon 1, ISPB, F-69007 Lyon, France.
[Cox, David G.] Ctr Rech Cancerol Lyon, INSERM, U1052, F-69008 Lyon, France.
[Cox, David G.] Ctr Rech Cancerol Lyon, CNRS, UMR5286, F-69008 Lyon, France.
[Cox, David G.] Ctr Leon Berard, F-69008 Lyon, France.
[Khaw, Kay-Tee] Univ Cambridge, Dept Publ Hlth & Primary Care, Sch Clin Med, Cambridge CB2 0SP, England.
[Lund, Eiliv] Univ Tromso, Inst Community Med, N-9037 Tromso, Norway.
[Naccarati, Alessio] Human Genet Fdn Torino, Mol & Genet Epidemiol Unit, I-10126 Turin, Italy.
[Peeters, Petra H.] Univ Med Ctr, Dept Epidemiol, Julius Ctr Hlth Sci & Primary Care, NL-3584 CS Utrecht, Netherlands.
[Ramon Quiros, J.] Publ Hlth Directorate, Asturias, Spain.
[Sund, Malin] Umea Univ, Dept Surg & Perioperat Sci, S-90185 Umea, Sweden.
[Trichopoulos, Dimitrios] Acad Athens, Bur Epidemiol Res, Athens 10679, Greece.
[Trichopoulos, Dimitrios] Hellen Hlth Fdn, Athens 11527, Greece.
RP Campa, D (reprint author), German Canc Res Ctr, Div Canc Epidemiol, Neuenheimer Feld 280, D-69120 Heidelberg, Germany.
EM d.campa@dkfz.de
RI Campa, Daniele/K-1617-2016; Cox, David/A-2023-2009;
OI Campa, Daniele/0000-0003-3220-9944; Cox, David/0000-0002-2152-9259;
Naccarati, Alessio/0000-0001-5774-0905; Giles,
Graham/0000-0003-4946-9099
FU U.S. National Institutes of Health, National Cancer Institute
[U19-CA148065, U01-CA98233-07, U01-CA98710-06, U01-CA98216-06,
U01-CA98758-07]; Intramural Research Program of National Institutes of
Health; National Cancer Institute, Division of Cancer Epidemiology and
Genetics; National Heart, Lung, and Blood Institute, National Institutes
of Health, U.S. Department of Health and Human Services
[HHSN268201100046C, HHSN268201100001C, HHS N268201100002C,
HHSN268201100003C, HHSN2682011000 04C, HHSN271201100004C]
FX This work was supported by U.S. National Institutes of Health, National
Cancer Institute (U19-CA148065, cooperative agreements U01-CA98233-07 to
D. J.H., U01-CA98710-06 to M.J.T., U01-CA98216-06 to E.R. and R.K., and
U01-CA98758-07 to B.E.H.) and Intramural Research Program of National
Institutes of Health and National Cancer Institute, Division of Cancer
Epidemiology and Genetics. The WHI program is funded by the National
Heart, Lung, and Blood Institute, National Institutes of Health, U.S.
Department of Health and Human Services through contracts
HHSN268201100046C, HHSN268201100001C, HHS N268201100002C,
HHSN268201100003C, HHSN2682011000 04C, and HHSN271201100004C. A full
listing of WHI investigators can be found at:
https://cleo.whi.org/researchers/Documents%20%20Write%20a%20Paper/WHI%20
Investigator%20Short%20List.pdf. The Founding Sources had no role in the
study design; in the collection, analysis and interpretation of data and
in the decision to submit the paper for publication.
NR 60
TC 10
Z9 10
U1 3
U2 15
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 1
PY 2014
VL 23
IS 19
BP 5260
EP 5270
DI 10.1093/hmg/ddu223
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AQ9OM
UT WOS:000343185200020
PM 24895409
ER
PT J
AU Yousif, AS
Stanlie, A
Begum, NA
Honjo, T
AF Yousif, Ashraf S.
Stanlie, Andre
Begum, Nasim A.
Honjo, Tasuku
TI Opinion: uracil DNA glycosylase (UNG) plays distinct and non-canonical
roles in somatic hypermutation and class switch recombination
SO INTERNATIONAL IMMUNOLOGY
LA English
DT Article
DE AID; Brd4; CSR; NHEJ; SHM; UNG
ID CRYSTAL-STRUCTURE; DEFICIENT MICE; AID; POLYMERASE; MUTATIONS; REGIONS;
REPAIR; REQUIREMENT; SPECIFICITY; DEAMINATION
AB Activation-induced cytidine deaminase (AID) is essential to class switch recombination (CSR) and somatic hypermutation (SHM). Uracil DNA glycosylase (UNG), a member of the base excision repair complex, is required for CSR. The role of UNG in CSR and SHM is extremely controversial. AID deficiency in mice abolishes both CSR and SHM, while UNG-deficient mice have drastically reduced CSR but augmented SHM raising a possibility of differential functions of UNG in CSR and SHM. Interestingly, UNG has been associated with a CSR-specific repair adapter protein Brd4, which interacts with acetyl histone 4, gamma H2AX and 53BP1 to promote non-homologous end joining during CSR. A non-canonical scaffold function of UNG, but not the catalytic activity, can be attributed to the recruitment of essential repair proteins associated with the error-free repair during SHM, and the end joining during CSR.
C1 [Yousif, Ashraf S.; Begum, Nasim A.; Honjo, Tasuku] Kyoto Univ, Grad Sch Med, Dept Immunol & Genom Med, Sakyo Ku, Kyoto 6068501, Japan.
[Stanlie, Andre] NCI, Lab Genome Integr, NIH, Bethesda, MD 20892 USA.
RP Honjo, T (reprint author), Kyoto Univ, Grad Sch Med, Dept Immunol & Genom Med, Sakyo Ku, Kyoto 6068501, Japan.
EM honjo@mfour.med.kyoto-u.ac.jp
RI Honjo, Tasuku/N-4470-2016
FU [17002015]; [24590352]
FX Grant-in-Aid for Specially Promoted Research (17002015 to T.H.);
Grant-in-Aid for Scientific Research (C) (24590352 to N.A.B.)
NR 33
TC 1
Z9 2
U1 3
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0953-8178
EI 1460-2377
J9 INT IMMUNOL
JI Int. Immunol.
PD OCT
PY 2014
VL 26
IS 10
BP 575
EP 578
DI 10.1093/intimm/dxu071
PG 4
WC Immunology
SC Immunology
GA AR1DG
UT WOS:000343321400005
PM 24994819
ER
PT J
AU Quinn, GE
Ying, GS
Daniel, E
Hildebrand, PL
Ells, A
Baumritter, A
Kemper, AR
Schron, EB
Wade, K
AF Quinn, Graham E.
Ying, Gui-Shuang
Daniel, Ebenezer
Hildebrand, P. Lloyd
Ells, Anna
Baumritter, Agnieshka
Kemper, Alex R.
Schron, Eleanor B.
Wade, Kelly
CA e-ROP Cooperative Grp
TI Validity of a Telemedicine System for the Evaluation of Acute-Phase
Retinopathy of Prematurity
SO JAMA OPHTHALMOLOGY
LA English
DT Article
ID DIGITAL FUNDUS CAMERA; DIABETIC-RETINOPATHY; PLUS DISEASE; DIAGNOSIS;
ROP; AGREEMENT; CARE; RELIABILITY; ACCURACY; QUALITY
AB IMPORTANCE The present strategy to identify infants needing treatment for retinopathy of prematurity (ROP) requires repeated examinations of at-risk infants by physicians. However, less than 10% ultimately require treatment. Retinal imaging by nonphysicians with remote image interpretation by nonphysicians may provide a more efficient strategy.
OBJECTIVE To evaluate the validity of a telemedicine system to identify infants who have sufficiently severe ROP to require evaluation by an ophthalmologist.
DESIGN, SETTING, AND PARTICIPANTS An observational study of premature infants starting at 32 weeks' postmenstrual age was conducted. This study involved 1257 infants with birth weight less than 1251 g in neonatal intensive care units in 13 North American centers enrolled from May 25, 2011, through October 31, 2013.
INTERVENTIONS Infants underwent regularly scheduled diagnostic examinations by an ophthalmologist and digital imaging by nonphysician staff using a wide-field digital camera. Ophthalmologists documented findings consistent with referral-warranted (RW) ROP (ie, zone I ROP, stage 3 ROP or worse, or plus disease). A standard 6-image set per eye was sent to a central server and graded by 2 trained, masked, nonphysician readers. A reading supervisor adjudicated disagreements.
MAIN OUTCOMES AND MEASURES The validity of grading retinal image sets was based on the sensitivity and specificity for detecting RW-ROP compared with the criterion standard diagnostic examination.
RESULTS A total of 1257 infants (mean birth weight, 864 g; mean gestational age, 27 weeks) underwent a median of 3 sessions of examinations and imaging. Diagnostic examination identified characteristics of RW-ROP in 18.2% of eyes (19.4% of infants). Remote grading of images of an eye at a single session had sensitivity of 81.9% (95% CI, 77.4-85.6) and specificity of 90.1% (95% CI, 87.9-91.8). When both eyes were considered for the presence of RW-ROP, as would routinely be done in a screening, the sensitivity was 90.0%(95% CI, 85.4-93.5), with specificity of 87.0% (95% CI, 84.0-89.5), negative predictive value of 97.3%, and positive predictive value of 62.5% at the observed RW-ROP rate of 19.4%.
CONCLUSIONS AND RELEVANCE When compared with the criterion standard diagnostic examination, these results provide strong support for the validity of remote evaluation by trained nonphysician readers of digital retinal images taken by trained nonphysician imagers from infants at risk for RW-ROP.
C1 [Quinn, Graham E.; Baumritter, Agnieshka] Univ Penn, Childrens Hosp Philadelphia, Perelman Sch Med, Div Pediat Ophthalmol, Philadelphia, PA 19104 USA.
[Ying, Gui-Shuang; Daniel, Ebenezer] Univ Penn, Perelman Sch Med, Scheie Eye Inst, Dept Ophthalmol, Philadelphia, PA 19104 USA.
[Hildebrand, P. Lloyd] Univ Oklahoma, Hlth Sci Ctr, Dept Ophthalmol, Oklahoma City, OK USA.
[Ells, Anna] Univ Calgary, Calgary, AB, Canada.
[Kemper, Alex R.] Duke Univ, Duke Clin Res Inst, Program Pediat Hlth Serv Res, Durham, NC USA.
[Schron, Eleanor B.] NIH, Div Extramural Res, Bethesda, MD 20892 USA.
[Wade, Kelly] Univ Penn, Childrens Hosp Philadelphia, Perelman Sch Med, Dept Pediat,Div Neonatol, Philadelphia, PA 19104 USA.
RP Quinn, GE (reprint author), Childrens Hosp Philadelphia, Wood Ctr, Div Ophthalmol, 1st Floor, Philadelphia, PA 19104 USA.
EM quinn@email.chop.edu
OI Freedman, Sharon/0000-0003-3615-3511
FU National Eye Institute of the National Institutes of Health, Department
of Health and Human Services [U10 EY017014]
FX This study was funded by a cooperative agreement grant (U10 EY017014)
from the National Eye Institute of the National Institutes of Health,
Department of Health and Human Services. Dr Daniel has received grants
from the National Institutes of Health and Dr Hildebrand has received
grants from the National Eye Institute; this funding was not related to
the current research.
NR 35
TC 32
Z9 32
U1 0
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6165
EI 2168-6173
J9 JAMA OPHTHALMOL
JI JAMA Ophthalmol.
PD OCT
PY 2014
VL 132
IS 10
BP 1178
EP 1184
DI 10.1001/jamaophthalmol.2014.1604
PG 7
WC Ophthalmology
SC Ophthalmology
GA AQ8FZ
UT WOS:000343061000005
PM 24970095
ER
PT J
AU Sherrod, CE
Vitale, S
Frick, KD
Ramulu, PY
AF Sherrod, Cheryl E.
Vitale, Susan
Frick, Kevin D.
Ramulu, Pradeep Y.
TI Association of Vision Loss and Work Status in the United States
SO JAMA OPHTHALMOLOGY
LA English
DT Article
ID EMPLOYMENT; IMPACT; IMPAIRMENT
AB IMPORTANCE Working is critical to personal health and well-being. We examine the association of vision measured objectively with work status using a nationally representative sample of working-age Americans.
OBSERVATION A total of 19 849 participants from the 1999-2008 National Health and Nutrition Examination Survey completed a vision examination and employment/demographic questionnaires. Employment rates for men with visual impairment, uncorrected refractive error, and normal vision were 58.7%, 66.5%, and 76.2%, respectively; employment rates for women with visual impairment, uncorrected refractive error, and normal vision were 24.5%, 56.0%, and 62.9%, respectively. In multivariable models adjusting for age, sex, race/ethnicity, and chronic disease status, both uncorrected refractive error (odds ratio [OR], 1.36; 95% CI, 1.15-1.60) and visual impairment (OR, 3.04; 95% CI, 1.93-4.79) were associated with a higher likelihood of not working. Subgroups in which visual impairment was associated with even higher odds of not working included women (OR, 4.9; 95% CI, 2.5-9.6), participants younger than 55 years (OR, 4.3; 95% CI, 2.9-6.5), and diabetic individuals (OR, 14.8; 95% CI, 5.8-37.3).
CONCLUSIONS AND RELEVANCE Decreased vision is associated with a significantly higher likelihood of not working. Visually impaired diabetic individuals, women, and those younger than 55 years have a particularly high risk of not working. Further investigation is warranted to understand barriers for employment in individuals with decreased vision.
C1 [Sherrod, Cheryl E.; Ramulu, Pradeep Y.] Johns Hopkins Univ Hosp, Wilmer Eye Inst, Baltimore, MD 21287 USA.
[Sherrod, Cheryl E.] Johns Hopkins Univ Hosp, Bloomberg Sch Publ Hlth, Baltimore, MD 21287 USA.
[Vitale, Susan] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD USA.
[Frick, Kevin D.] Johns Hopkins Univ Hosp, Carey Business Sch, Baltimore, MD 21287 USA.
RP Ramulu, PY (reprint author), Johns Hopkins Univ Hosp, Wilmer Eye Inst, 600 N Wolf St, Baltimore, MD 21287 USA.
EM pramulu1@jhmi.edu
FU National Institutes of Health and Research to Prevent Blindness
[EY018595]
FX This work was supported by grant EY018595 from the National Institutes
of Health and Research to Prevent Blindness.
NR 10
TC 3
Z9 3
U1 3
U2 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6165
EI 2168-6173
J9 JAMA OPHTHALMOL
JI JAMA Ophthalmol.
PD OCT
PY 2014
VL 132
IS 10
BP 1239
EP 1242
DI 10.1001/jamaophthalmol.2014.2213
PG 4
WC Ophthalmology
SC Ophthalmology
GA AQ8FZ
UT WOS:000343061000016
PM 25032668
ER
PT J
AU Bodelon, C
Pfeiffer, RM
Buys, SS
Black, A
Sherman, ME
AF Bodelon, Clara
Pfeiffer, Ruth M.
Buys, Saundra S.
Black, Amanda
Sherman, Mark E.
TI Analysis of Serial Ovarian Volume Measurements and Incidence of Ovarian
Cancer: Implications for Pathogenesis
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID TRANSVAGINAL SONOGRAPHY; POSTMENOPAUSAL WOMEN; SCREENING TRIAL;
EARLY-DIAGNOSIS; ALGORITHM ROCA; RISK; PROSTATE; LUNG; MORTALITY;
CARCINOMA
AB Background Accumulating evidence suggests that many ovarian cancers represent metastases from occult fallopian tube carcinomas or tumors arising within ovarian endometriosis. We hypothesized that small ovarian volumes, as reflected in nonvisualization by transvaginal ultrasound (TVU), would be a marker of lower ovarian cancer risk, whereas enlargement on serial examinations would indicate higher risk.
Methods To address these hypotheses, we analyzed serial ovarian volume measurements determined by TVU for 29 321 women (102 787 scans) performed in the ovarian cancer screening arm of the Prostate, Lung, Colorectal, and Ovarian (PLCO) trial. Cox models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) as measures of association between TVU results and ovarian cancer. We assessed whether increasing ovarian volume preceded diagnosis of ovarian cancer in a nested case-control analysis comparing case patients and control patients matched on age, center, and screening year (1: 4 ratio). All statistical tests were two-sided.
Results Visualization of normal-appearing ovaries at the last TVU scan was associated with marginally higher ovarian cancer risk compared with nonvisualization of the ovaries (HR = 1.42, 95% CI = 1.00 to 2.01). Ovarian volume increased statistically significantly in ovarian cancer case patients one to two years before diagnosis (P < .001), but not in matched control patients.
Conclusion Our analysis of TVU data suggests that increasing ovarian volume is associated with greater ovarian cancer risk, but it is only detectable one to two years before diagnosis.
C1 [Bodelon, Clara; Pfeiffer, Ruth M.; Black, Amanda; Sherman, Mark E.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Sherman, Mark E.] NCI, Canc Prevent Div, Rockville, MD USA.
[Buys, Saundra S.] Univ Utah, Hlth Sci Ctr, Huntsman Canc Inst, Salt Lake City, UT USA.
RP Bodelon, C (reprint author), Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Rm 7-E220, Bethesda, MD 20892 USA.
EM clara.bodelon@nih.gov
FU National Cancer Institute; Division of Cancer Prevention, National
Cancer Institute, National Institutes of Health, Department of Health
and Human Services
FX This research was supported by the Intramural Research Program of the
National Cancer Institute and by contracts from the Division of Cancer
Prevention, National Cancer Institute, National Institutes of Health,
Department of Health and Human Services.
NR 35
TC 2
Z9 2
U1 1
U2 4
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 OCT
PY 2014
VL 106
IS 10
AR dju262
DI 10.1093/jnci/dju262
PG 7
WC Oncology
SC Oncology
GA AQ7ZA
UT WOS:000343038200011
ER
PT J
AU Figueroa, JD
Pfeiffer, RM
Patel, DA
Linville, L
Brinton, LA
Gierach, GL
Yang, XHR
Papathomas, D
Visscher, D
Mies, C
Degnim, AC
Anderson, WF
Hewitt, S
Khodr, ZG
Clare, SE
Storniolo, AM
Sherman, ME
AF Figueroa, Jonine D.
Pfeiffer, Ruth M.
Patel, Deesha A.
Linville, Laura
Brinton, Louise A.
Gierach, Gretchen L.
Yang, Xiaohong R.
Papathomas, Daphne
Visscher, Daniel
Mies, Carolyn
Degnim, Amy C.
Anderson, William F.
Hewitt, Stephen
Khodr, Zeina G.
Clare, Susan E.
Storniolo, Anna Maria
Sherman, Mark E.
TI Terminal Duct Lobular Unit Involution of the Normal Breast: Implications
for Breast Cancer Etiology
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID MAMMARY-GLAND INVOLUTION; RISK-FACTORS; CIGARETTE-SMOKING; REPRODUCTIVE
FACTORS; TISSUE-BANK; WOMEN; ESTROGEN; AGE; PREGNANCY; METAANALYSIS
AB Background Greater degrees of terminal duct lobular unit (TDLU) involution have been linked to lower breast cancer risk; however, factors that influence this process are poorly characterized.
Methods To study this question, we developed three reproducible measures that are inversely associated with TDLU involution: TDLU counts, median TDLU span, and median acini counts/TDLU. We determined factors associated with TDLU involution using normal breast tissues from 1938 participants (1369 premenopausal and 569 postmenopausal) ages 18 to 75 years in the Susan G. Komen Tissue Bank at the Indiana University Simon Cancer Center. Multivariable zero-inflated Poisson models were used to estimate relative risks (RRs) and 95% confidence intervals (95% CIs) for factors associated with TDLU counts, and multivariable ordinal logistic regression models were used to estimate odds ratios (ORs) and 95% CIs for factors associated with categories of median TDLU span and acini counts/TDLU.
Results All TDLU measures started declining in the third age decade (all measures, two-sided P-trend <= .001); and all metrics were statistically significantly lower among postmenopausal women. Nulliparous women demonstrated lower TDLU counts compared with uniparous women (among premenopausal women, RR = 0.79, 95% CI = 0.73 to 0.85; among postmenopausal, RR = 0.67, 95% CI = 0.56 to 0.79); however, rates of age-related TDLU decline were faster among parous women. Other factors were related to specific measures of TDLU involution.
Conclusion Morphometric analysis of TDLU involution warrants further evaluation to understand the pathogenesis of breast cancer and assessing its role as a progression marker for women with benign biopsies or as an intermediate endpoint in prevention studies.
C1 [Figueroa, Jonine D.; Pfeiffer, Ruth M.; Patel, Deesha A.; Linville, Laura; Brinton, Louise A.; Gierach, Gretchen L.; Yang, Xiaohong R.; Papathomas, Daphne; Anderson, William F.; Khodr, Zeina G.; Sherman, Mark E.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Hewitt, Stephen] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Sherman, Mark E.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Visscher, Daniel; Degnim, Amy C.] Mayo Clin, Ctr Canc, Rochester, MN USA.
[Mies, Carolyn] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA USA.
[Clare, Susan E.] Northwestern Univ, Dept Surg, Feinberg Sch Med, Chicago, IL 60611 USA.
[Storniolo, Anna Maria] Indiana Univ, Simon Canc Ctr, Susan G Komen Tissue Bank, Indianapolis, IN 46204 USA.
RP Figueroa, JD (reprint author), NCI, NIH, Div Canc Epidemiol & Genet, Hormonal & Reprod Epidemiol Branch, 9609 Med Ctr Dr Rm 7-E122,MSC 9774, Bethesda, MD 20892 USA.
EM figueroaj@mail.nih.gov
RI Brinton, Louise/G-7486-2015; Gierach, Gretchen/E-1817-2016
OI Brinton, Louise/0000-0003-3853-8562; Gierach,
Gretchen/0000-0002-0165-5522
FU Susan G. Komen; Breast Cancer Research Foundation; Oracle Giving;
Catherine Peachey Fund, Inc.; National Cancer Institute, Intramural
Research Program
FX The KTB is supported by the Susan G. Komen, the Breast Cancer Research
Foundation, Oracle Giving, and the Catherine Peachey Fund, Inc. This
study was supported through funds from the National Cancer Institute,
Intramural Research Program.
NR 49
TC 12
Z9 12
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD OCT
PY 2014
VL 106
IS 10
AR dju286
DI 10.1093/jnci/dju286
PG 11
WC Oncology
SC Oncology
GA AQ7ZA
UT WOS:000343038200022
ER
PT J
AU Iles, MM
Bishop, DT
Taylor, JC
Hayward, NK
Brossard, M
Cust, AE
Dunning, AM
Lee, JE
Moses, EK
Akslen, LA
Andresen, PA
Avril, MF
Azizi, E
Scarra, GB
Brown, KM
Debniak, T
Elder, DE
Friedman, E
Ghiorzo, P
Gillanders, EM
Goldstein, AM
Gruis, NA
Hansson, J
Harland, M
Helsing, P
Hocevar, M
Hoiom, V
Ingvar, C
Kanetsky, PA
Landi, MT
Lang, J
Lathrop, GM
Lubinski, J
Mackie, RM
Martin, NG
Molven, A
Montgomery, GW
Novakovic, S
Olsson, H
Puig, S
Puig-Butille, JA
Radford-Smith, GL
Randerson-Moor, J
van der Stoep, N
van Doorn, R
Whiteman, DC
MacGregor, S
Pooley, KA
Ward, SV
Mann, GJ
Amos, CI
Pharoah, PDP
Demenais, F
Law, MH
Bishop, JAN
Barrett, JH
AF Iles, Mark M.
Bishop, D. Timothy
Taylor, John C.
Hayward, Nicholas K.
Brossard, Myriam
Cust, Anne E.
Dunning, Alison M.
Lee, Jeffrey E.
Moses, Eric K.
Akslen, Lars A.
Andresen, Per A.
Avril, Marie-Francoise
Azizi, Esther
Scarra, Giovanna Bianchi
Brown, Kevin M.
Debniak, Tadeusz
Elder, David E.
Friedman, Eitan
Ghiorzo, Paola
Gillanders, Elizabeth M.
Goldstein, Alisa M.
Gruis, Nelleke A.
Hansson, Johan
Harland, Mark
Helsing, Per
Hocevar, Marko
Hoiom, Veronica
Ingvar, Christian
Kanetsky, Peter A.
Landi, Maria Teresa
Lang, Julie
Lathrop, G. Mark
Lubinski, Jan
Mackie, Rona M.
Martin, Nicholas G.
Molven, Anders
Montgomery, Grant W.
Novakovic, Srdjan
Olsson, Hakan
Puig, Susana
Anton Puig-Butille, Joan
Radford-Smith, Graham L.
Randerson-Moor, Juliette
van der Stoep, Nienke
van Doorn, Remco
Whiteman, David C.
MacGregor, Stuart
Pooley, Karen A.
Ward, Sarah V.
Mann, Graham J.
Amos, Christopher I.
Pharoah, Paul D. P.
Demenais, Florence
Law, Matthew H.
Bishop, Julia A. Newton
Barrett, Jennifer H.
CA AMFS Investigators
IBD Investigators
QMEGA Investigator
QTWIN Investigator
SDH Study Grp
GenoMEL Consortium
TI The Effect on Melanoma Risk of Genes Previously Associated With Telomere
Length
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CANCER-RISK; VARIANTS; LOCI; SUSCEPTIBILITY;
METAANALYSIS; INDIVIDUALS; SURVIVAL; DISEASE
AB Telomere length has been associated with risk of many cancers, but results are inconsistent. Seven single nucleotide polymorphisms (SNPs) previously associated with mean leukocyte telomere length were either genotyped or well-imputed in 11 108 case patients and 13 933 control patients from Europe, Israel, the United States and Australia, four of the seven SNPs reached a P value under .05 (two-sided). A genetic score that predicts telomere length, derived from these seven SNPs, is strongly associated (P = 8.92x10(-9), two-sided) with melanoma risk. This demonstrates that the previously observed association between longer telomere length and increased melanoma risk is not attributable to confounding via shared environmental effects (such as ultraviolet exposure) or reverse causality. We provide the first proof that multiple germline genetic determinants of telomere length influence cancer risk.
C1 [Iles, Mark M.; Bishop, D. Timothy; Taylor, John C.; Harland, Mark; Randerson-Moor, Juliette; Bishop, Julia A. Newton; Barrett, Jennifer H.] Univ Leeds, Leeds Inst Canc & Pathol, Leeds Canc Res UK Ctr, Epidemiol & Biostat Sect, Leeds, W Yorkshire, England.
[Hayward, Nicholas K.; Martin, Nicholas G.; Montgomery, Grant W.; MacGregor, Stuart; Law, Matthew H.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
[Radford-Smith, Graham L.] QIMR Berghofer Med Res Inst, Inflammatory Bowel Dis Lab, Brisbane, Qld, Australia.
[Whiteman, David C.] QIMR Berghofer Med Res Inst, Canc Control Grp, Brisbane, Qld, Australia.
[Brossard, Myriam; Demenais, Florence] INSERM, UMR 946, Genet Variat & Human Dis Unit, Paris, France.
[Brossard, Myriam; Demenais, Florence] Univ Paris Diderot, Sorbonne Paris Cite, Inst Univ Hematol, Paris, France.
[Cust, Anne E.] Univ Sydney, Sydney Sch Publ Hlth, Sydney, NSW 2006, Australia.
[Dunning, Alison M.; Pharoah, Paul D. P.] Univ Cambridge, Dept Oncol, Cambridge, England.
[Lee, Jeffrey E.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
[Moses, Eric K.; Ward, Sarah V.] Univ Western Australia, Fac Med Dent & Hlth Sci, Ctr Genet Origins Hlth & Dis, Crawley, Australia.
[Akslen, Lars A.] Univ Bergen, Ctr Canc Biomarkers CCBIO, Bergen, Norway.
[Molven, Anders] Univ Bergen, Gade Lab Pathol, Dept Clin Med, Bergen, Norway.
[Akslen, Lars A.] Haukeland Hosp, Dept Pathol, N-5021 Bergen, Norway.
[Andresen, Per A.] Univ Oslo, Rikshosp, Dept Pathol, Oslo Univ Hosp, N-0027 Oslo, Norway.
[Helsing, Per] Univ Oslo, Rikshosp, Dept Dermatol, Oslo Univ Hosp, N-0027 Oslo, Norway.
[Avril, Marie-Francoise] Univ Paris 05, Hop Cochin, Assistance Publ Hop Paris, Serv Dermatol, Paris, France.
[Azizi, Esther] Chaim Sheba Med Ctr, Dept Dermatol, IL-52621 Tel Hashomer, Israel.
[Azizi, Esther; Friedman, Eitan] Chaim Sheba Med Ctr, Oncogen Unit, IL-52621 Tel Hashomer, Israel.
[Azizi, Esther] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
[Scarra, Giovanna Bianchi; Friedman, Eitan] Univ Genoa, Dept Internal Med & Med Specialties, Genoa, Italy.
[Scarra, Giovanna Bianchi; Friedman, Eitan; Ghiorzo, Paola] San Martino IST Res Hosp, Lab Genet Rare Hereditary Canc, Genoa, Italy.
[Brown, Kevin M.; Goldstein, Alisa M.; Landi, Maria Teresa] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Debniak, Tadeusz; Lang, Julie] Pomeranian Med Univ, Int Hereditary Canc Ctr, Szczecin, Poland.
[Elder, David E.] Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA USA.
[Kanetsky, Peter A.] Univ Penn, Ctr Clin Epidemiol & Biostat, Perelman Sch Med, Philadelphia, PA USA.
[Kanetsky, Peter A.] Univ Penn, Dept Biostat & Epidemiol, Perelman Sch Med, Philadelphia, PA USA.
[Gillanders, Elizabeth M.] NHGRI, Inherited Dis Res Branch, NIH, Baltimore, MD USA.
[Gruis, Nelleke A.; van Doorn, Remco] Leiden Univ, Med Ctr, Dept Dermatol, Leiden, Netherlands.
[van der Stoep, Nienke] Leiden Univ, Dept Clin Genet, Ctr Human & Clin Genet, Med Ctr, Leiden, Netherlands.
[Hansson, Johan; Hoiom, Veronica] Karolinska Inst, Karolinska Univ Hosp, Dept Oncol Pathol, Stockholm, Sweden.
[Hocevar, Marko] Inst Oncol Ljubljana, Dept Surg Oncol, Ljubljana, Slovenia.
[Novakovic, Srdjan] Inst Oncol Ljubljana, Dept Mol Diagnost, Ljubljana, Slovenia.
[Ingvar, Christian] Lund Univ, Dept Surg, Lund, Sweden.
[Olsson, Hakan] Lund Univ, Dept Oncol, Lund, Sweden.
[Olsson, Hakan] Lund Univ, Dept Canc Epidemiol, Lund, Sweden.
[Mackie, Rona M.] Univ Glasgow, Dept Publ Hlth, Glasgow, Lanark, Scotland.
[Lang, Julie; Mackie, Rona M.] Univ Glasgow, Dept Med Genet, Glasgow, Lanark, Scotland.
[Lathrop, G. Mark] McGill Univ, Montreal, PQ, Canada.
[Lathrop, G. Mark] Genome Quebec Innovat Ctr, Montreal, PQ, Canada.
[Lathrop, G. Mark] Commissariat Energie Atom, Inst Genom, Ctr Natl Genotypage, Evry, France.
[Puig, Susana; Anton Puig-Butille, Joan] Univ Barcelona, Melanoma Unit, Dept Dermatol, Hosp Clin,Inst Invest Biomed August Pi Sune, Barcelona, Spain.
[Puig, Susana; Anton Puig-Butille, Joan] Inst Salud Carlos III, CIBER Enfermedades Raras, Barcelona, Spain.
[Radford-Smith, Graham L.] Royal Brisbane & Womens Hosp, Dept Gastroenterol & Hepatol, Herston, Qld, Australia.
[Radford-Smith, Graham L.] Univ Queensland, Sch Med, Herston, Qld, Australia.
[Pooley, Karen A.; Pharoah, Paul D. P.] Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge CB1 4RN, England.
[Mann, Graham J.] Univ Sydney Westmead, Millennium Inst, Westmead Inst Canc Res, Sydney, NSW, Australia.
[Mann, Graham J.] Melanoma Inst Australia, Sydney, NSW, Australia.
[Amos, Christopher I.] Dartmouth Coll, Dept Community & Family Med, Geisel Sch Med, Hanover, NH 03755 USA.
RP Iles, MM (reprint author), St James Univ Hosp, Canc Genet Bldg,Beckett St, Leeds LS9 7TF, W Yorkshire, England.
EM m.m.iles@leeds.ac.uk
RI Macgregor, Stuart/C-6442-2009; hayward, nicholas/C-1367-2015;
Montgomery, Grant/B-7148-2008; Whiteman, David/P-2728-2014; Hoiom,
Veronica/F-4153-2012; Akslen, Lars /C-1202-2017;
OI Martin, Nicholas/0000-0003-4069-8020; Barrett,
Jenny/0000-0002-1720-7724; Dunning, Alison Margaret/0000-0001-6651-7166;
Bishop, Tim/0000-0002-8752-8785; Newton Bishop,
Julia/0000-0001-9147-6802; Puig, Susana/0000-0003-1337-9745; Macgregor,
Stuart/0000-0001-6731-8142; hayward, nicholas/0000-0003-4760-1033;
Montgomery, Grant/0000-0002-4140-8139; Whiteman,
David/0000-0003-2563-9559; Akslen, Lars /0000-0003-2710-9543; Gruis,
Nelleke/0000-0002-5210-9150
FU European Commission [LSHC-CT-2006-018702]; Cancer Research UK Programme
[C588/A4994, C588/A10589]; Cancer Research UK [C8216/A6129]; US National
Institutes of Health (NIH) [CA83115]; NIH, National Cancer Institute
(NCI), Division of Cancer Epidemiology and Genetics; Wellcome Trust
[076113, WT084766/Z/08/Z]; Stockholm: Swedish Cancer Society, Karolinska
Institutet's research funds; Lund: Swedish Cancer Society; Lund: Gunnar
Nilsson Foundation; Lund: European Research Council [ERC-2011-294576];
Genoa: Italian Ministry of Education, University and Research; Genoa:
IMI; Genoa: Mara Naum foundation; University of Genoa [D31J13000000005];
Intergruppo Melanoma Italiano and Mara Naum foundation; National
Institutes of Health, National Cancer Institute, Division of Cancer
Epidemiology and Genetics; Institut National du Cancer [INCa-PL016];
Ligue Nationale Contre Le Cancer [PRE05/FD, PRE 09/FD]; Programme
Hospitalier de Recherche Clinique [AOM-07-195]; Ligue Nationale Contre
Le Cancer doctoral fellowship; European Biobanking and Biomolecular
Resources Research Infrastructure (BBMRI)-Netherlands hub [CO18]; Fondo
de Investigaciones Sanitarias, Spain [09/01393]; CIBER de Enfermedades
Raras of the Instituto de Salud Carlos III, Spain; Catalan Government,
Spain [AGAUR 2009 SGR 1337]; Comprehensive Cancer Center, Oslo
University Hospital [SE0728]; Norwegian Cancer Society
[71512-PR-2006-0356]; National Institutes of Health/National Cancer
Institute [2P50CA093459, P30CA023108]; Marit Peterson Fund for Melanoma
Research; National Health and Medical Research Council of Australia
(NHMRC) [566946, 107359, 211172, 402761, 200071, 241944, 339462, 380385,
389927, 389875, 389891, 389892, 389938, 443036, 442915, 442981, 496610,
496675, 496739, 552485, 552498]; Cancer Council New South Wales [77/00,
06/10]; Cancer Council Victoria; Cancer Council Queensland [371]; US
National Institutes of Health (via NIH RO1) [CA-83115-01A2]; Victorian
Cancer Agency Early Career Seed Grant [ECSG07_010]; Cancer Institute NSW
[10/ECF/2-06]; NHMRC [496610, 520018, 339446, 619667]; Australian
National Health and Medical Research Council; Australian Research
Council; Cancer Australia [1011143]; Scott Kirkbride Melanoma Research
Centre; Melanoma Research Alliance; NIH NCI [CA83115, CA88363, CA122838,
CA87969, CA055075, CA100264, CA133996, CA49449]; Cancer Council New
South Wales; Cancer Council Queensland; Cancer Institute New South
Wales; Cooperative Research Centre for Discovery of Genes for Common
Human Diseases (CRC); Cerylid Biosciences (Melbourne); Australian Cancer
Research Foundation; National Health and Medical Research Council
(NHMRC) of Australia [496610]; National Cancer Institute [5 RO1 CA
001833-02]; United States National Cancer Institute [CA 001833-03];
National Health and Medical Research Council of Australia
FX The GenoMEL study (http://www.genomel.org/) was funded by the European
Commission under the 6th Framework Programme (contract no.
LSHC-CT-2006-018702), by Cancer Research UK Programme Awards (C588/A4994
and C588/A10589), by a Cancer Research UK Project Grant (C8216/A6129),
and by a grant from the US National Institutes of Health (NIH; CA83115).
This research was also supported by the intramural Research Program of
the NIH, National Cancer Institute (NCI), Division of Cancer
Epidemiology and Genetics. Funding for the Wellcome Trust Case Control
Consortium project was provided by the Wellcome Trust under award
076113.; Stockholm: Swedish Cancer Society, Karolinska Institutet's
research funds.; Lund: Swedish Cancer Society, Gunnar Nilsson Foundation
and European Research Council Advanced Grant (ERC-2011-294576). Genoa:
Italian Ministry of Education, University and Research PRIN 2008, IMI
and Mara Naum foundation. University of Genoa (PRA 2012 D31J13000000005
to PG). Intergruppo Melanoma Italiano and Mara Naum foundation to GBS;
Emilia Romagna: Intramural Research Program of National Institutes of
Health, National Cancer Institute, Division of Cancer Epidemiology and
Genetics.; Paris: Grants from Institut National du Cancer (INCa-PL016)
and Ligue Nationale Contre Le Cancer (PRE05/FD and PRE 09/FD) to FD,
Programme Hospitalier de Recherche Clinique (AOM-07-195) to MFA and FD.
Ligue Nationale Contre Le Cancer doctoral fellowship to MB.; Leiden:
Grant provided by European Biobanking and Biomolecular Resources
Research Infrastructure (BBMRI)-Netherlands hub (CO18).; Spain: The
research at the Melanoma Unit in Barcelona is partially funded by Grants
from Fondo de Investigaciones Sanitarias PI, 09/01393, Spain; by the
CIBER de Enfermedades Raras of the Instituto de Salud Carlos III, Spain;
by the AGAUR 2009 SGR 1337 of the Catalan Government, Spain.; Norway:
Grants from the Comprehensive Cancer Center, Oslo University Hospital
(SE0728), and the Norwegian Cancer Society (71512-PR-2006-0356).;
Houston (MD Anderson): Support by the National Institutes of
Health/National Cancer Institute (2P50CA093459 and P30CA023108), and by
the Marit Peterson Fund for Melanoma Research.; Australian Melanoma
Family Study (AMFS): AMFS is supported by the National Health and
Medical Research Council of Australia (NHMRC) (project grants 566946,
107359, 211172 and program grant number 402761 to GJM and RFK); the
Cancer Council New South Wales (project grant 77/00, 06/10), the Cancer
Council Victoria and the Cancer Council Queensland (project grant 371);
the US National Institutes of Health (via NIH RO1 grant CA-83115-01A2 to
the International Melanoma Genetics Consortium - GenoMEL) and a
Victorian Cancer Agency Early Career Seed Grant (ECSG07_010). AEC is
supported by fellowships from the Cancer Institute NSW (10/ECF/2-06) and
NHMRC (520018).; Brisbane: SM is supported by fellowships from the
Australian National Health and Medical Research Council and the
Australian Research Council. MHL is supported by Cancer Australia grant
1011143.; Western Australian Melanoma Health Study (WAMHS): The WAMHS
gratefully acknowledges all study participants for their time and
contributions, and the Western Australian DNA Bank and the Ark at the
University of Western Australia for biospecimen and bioinformatics
related support. The Western Australian Cancer Registry, the WAMHS study
team and the WAMHS Management Committee are also gratefully acknowledged
for their assistance, as well as the Scott Kirkbride Melanoma Research
Centre for funding the establishment of the WAMHS resource and related
salaries and PhD stipends.; Q-MEGA and QTWIN: The Q-MEGA/QTWIN studies
were supported by the Melanoma Research Alliance, the NIH NCI (CA88363,
CA83115, CA122838, CA87969, CA055075, CA100264, CA133996, and CA49449),
the National Health and Medical Research Council of Australia (NHMRC)
(200071, 241944, 339462, 380385, 389927, 389875, 389891, 389892, 389938,
443036, 442915, 442981, 496610, 496675, 496739, 552485, 552498), the
Cancer Councils New South Wales, Victoria and Queensland, the Cancer
Institute New South Wales, the Cooperative Research Centre for Discovery
of Genes for Common Human Diseases (CRC), Cerylid Biosciences
(Melbourne), the Australian Cancer Research Foundation, the Wellcome
Trust (WT084766/Z/08/Z), and donations from Neville and Shirley
Hawkins.; QIMR Endometriosis study: The QIMR Study was supported by
grants from the National Health and Medical Research Council (NHMRC) of
Australia (496610), the Cooperative Research Centre for Discovery of
Genes for Common Human Diseases (CRC) and Cerylid Biosciences
(Melbourne). Endometriosis sample genotyping was funded by grants from
the NHMRC (496610) and Wellcome Trust (WT084766/Z/08/Z). GWM was
supported by an NHMRC Fellowship (339446, 619667).; Study of Digestive
Health (SDH): The SDH was supported by the National Cancer Institute (5
RO1 CA 001833-02).; Inflammatory Bowel Disease study (IBD): This
research was supported by the United States National Cancer Institute
(grant number CA 001833-03). DCW is a Senior Research Fellow of the
National Health and Medical Research Council of Australia. NP was
supported by a PhD scholarship from the National Health and Medical
Research Council of Australia.
NR 24
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U2 11
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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 OCT
PY 2014
VL 106
IS 10
AR dju267
DI 10.1093/jnci/dju267
PG 5
WC Oncology
SC Oncology
GA AQ7ZA
UT WOS:000343038200014
ER
PT J
AU Kehl, KL
Arora, NK
Schrag, D
Ayanian, JZ
Clauser, SB
Klabunde, CN
Kahn, KL
Fletcher, RH
Keating, NL
AF Kehl, Kenneth L.
Arora, Neeraj K.
Schrag, Deborah
Ayanian, John Z.
Clauser, Steven B.
Klabunde, Carrie N.
Kahn, Katherine L.
Fletcher, Robert H.
Keating, Nancy L.
TI Discussions About Clinical Trials Among Patients With Newly Diagnosed
Lung and Colorectal Cancer
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID CARE OUTCOMES RESEARCH; AGE-BASED DISPARITIES; DECISION-MAKING;
BREAST-CANCER; PARTICIPATION; ENROLLMENT; OLDER; COMMUNICATION;
PREFERENCES; EXPERIENCE
AB Background Clinical trials are essential to establish the effectiveness of new cancer therapies, but less than 5% of adults with cancer enroll in trials. In addition to ineligibility or lack of available trials, barriers to enrollment may include limited patient awareness about the option of participation.
Methods We surveyed a multiregional cohort of patients with lung or colorectal cancer (or their surrogates) three to six months after diagnosis. We assessed whether respondents reported learning that clinical trial participation might be an option, and, if so, with whom they discussed trials. We used logistic regression to assess the association of patient characteristics with discussing trial participation and enrolling in trials. All statistical tests were two-sided.
Results Of 7887 respondents, 1114 (14.1%) reported discussing the possibility of clinical trial participation; most learned about trials from their physicians, and 287 patients (3.6% of all patients, 25.8% of trial discussants) enrolled. Among 2173 patients who received chemotherapy for advanced (stage III/IV lung or stage IV colorectal) cancer, 25.7% discussed trials, and 7.6% (29.5% of trial discussants) enrolled. Discussions were less frequent among older patients, African American or Asian vs white patients, and those with lower incomes and more comorbidity. Enrollment was higher among patients reporting shared vs physician-driven decisions (all P < .05).
Conclusions In this population-based cohort, only 14% of patients discussed participation in clinical trials. Discussions were more frequent among advanced cancer patients but were still reported by a minority of patients. Strategies to expand access to trials and facilitate patient-provider communication about participation may accelerate development of better cancer therapeutics.
C1 [Keating, Nancy L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA.
[Arora, Neeraj K.; Clauser, Steven B.; Klabunde, Carrie N.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Schrag, Deborah] Dana Farber Canc Inst, Div Populat Sci, Boston, MA 02115 USA.
[Ayanian, John Z.] Univ Michigan, Inst Healthcare Policy & Innovat, Ann Arbor, MI 48109 USA.
Univ Calif Los Angeles, Los Angeles, CA USA.
RAND Corp, Santa Monica, CA USA.
[Fletcher, Robert H.] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA 02115 USA.
[Ayanian, John Z.; Keating, Nancy L.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
RP Keating, NL (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM keating@hcp.med.harvard.edu
FU National Cancer Institute (NCI) (Dana Farber Cancer Institute) [U01
CA093344]; NCI (Dana Farber Cancer Institute/Cancer Research Network)
[U01 CA093332]; NCI (Harvard Medical School/Northern California Cancer
Center) [U01 CA093324]; NCI (RAND/UCLA) [U01 CA093348]; NCI (University
of Alabama at Birmingham) [U01 CA093329]; NCI (University of Iowa) [U01
CA093339]; NCI (University of North Carolina) [U01 CA093326]; Department
of Veterans Affairs [CRS 02-164]; [1R01CA164021-01A1]
FX This work of the Cancer Care Outcomes Research and Surveillance
(CanCORS) Consortium was supported by grants from the National Cancer
Institute (NCI) to the Statistical Coordinating Center (Dana Farber
Cancer Institute U01 CA093344) and the NCI-supported Primary Data
Collection and Research Centers (Dana Farber Cancer Institute/Cancer
Research Network U01 CA093332, Harvard Medical School/Northern
California Cancer Center U01 CA093324, RAND/UCLA U01 CA093348,
University of Alabama at Birmingham U01 CA093329, University of Iowa U01
CA093339, University of North Carolina U01 CA093326) and by a Department
of Veterans Affairs grant to the Durham VA Medical Center CRS 02-164.
Drs. Keating and Schrag were also supported by 1R01CA164021-01A1.
NR 34
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U1 5
U2 9
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 OCT
PY 2014
VL 106
IS 10
AR dju216
DI 10.1093/jnci/dju216
PG 9
WC Oncology
SC Oncology
GA AQ7ZA
UT WOS:000343038200001
ER
PT J
AU Pinsky, PF
AF Pinsky, Paul F.
TI RE: Prostate Cancer Mortality in Areas With High and Low Prostate Cancer
Incidence
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
C1 NCI, Canc Prevent Div, Bethesda, MD 20824 USA.
RP Pinsky, PF (reprint author), NCI, Canc Prevent Div, Bethesda, MD 20824 USA.
EM pp4f@nih.gov
NR 3
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
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD OCT
PY 2014
VL 106
IS 10
AR dju292
DI 10.1093/jnci/dju292
PG 1
WC Oncology
SC Oncology
GA AQ7ZA
UT WOS:000343038200023
ER
PT J
AU Xi, LF
Schiffman, M
Koutsky, LA
Hughes, JP
Winer, RL
Mao, C
Hulbert, A
Lee, SK
Shen, ZP
Kiviat, NB
AF Xi, Long Fu
Schiffman, Mark
Koutsky, Laura A.
Hughes, James P.
Winer, Rachel L.
Mao, Constance
Hulbert, Ayaka
Lee, Shu-Kuang
Shen, Zhenping
Kiviat, Nancy B.
TI Lineages of Oncogenic Human Papillomavirus Types Other Than Type 16 and
18 and Risk for Cervical Intraepithelial Neoplasia
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID UTERINE CERVIX; JAPANESE WOMEN; E6 VARIANTS; COSTA-RICA; CANCER;
INFECTION; ASSOCIATION; LESIONS; POLYMORPHISM; POPULATION
AB Background Data on clinical outcomes of infection with variants of oncogenic human papillomavirus (HPV) types other than HPV16 and HPV18 are rare. We investigated intratypic variations in non-HPV16/18 oncogenic types and their corresponding relationships with cervical intraepithelial neoplasia grades 2-3 (CIN2/3).
Methods Study subjects were women who were positive for one or more of 11 non-HPV16/18 oncogenic types. Subjects were followed every six months for two years for detection of HPV and cervical lesions. Variant lineages were defined by sequencing the 3' part of the long control region and the entire E6/E7 region of HPV genome. Lineage-associated risk of CIN2/3 was assessed using logistic regression with generalized estimating equations.
Results A total of 4591 type-specific HPV infections among 2667 women were included in the analysis. The increase in risk of CIN2/3 was statistically significant for women with HPV31 A or B compared with C variants, HPV33 A1 compared with B variants, HPV45 A3 or B2 compared with B1 variants, HPV56 B compared with A2 variants, and HPV58 A1 or A3 compared with C variants. For these five types, the adjusted odds ratio associated with CIN2/3 was 2.0 (95% confidence interval [CI] = 1.5 to 2.6) for infections with single-type high-risk (HR) variants, 1.7 (95% CI = 1.0 to 2.7) for infections with two or more types but only one HR variant, and 5.3 (95% CI = 3.1 to 8.4) for infections with HR variants of two or more types as compared with those with single-type non-HR variants. The likelihood of CIN2/3 was similar for women with HPV16 infection and for those with HPV58 A1 variant infection.
Conclusions These findings suggest that for a given HPV type, intratypic nucleotide changes may alter phenotypic traits that affect the probability of neoplasia.
C1 [Xi, Long Fu; Hulbert, Ayaka; Shen, Zhenping; Kiviat, Nancy B.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98104 USA.
[Mao, Constance] Univ Washington, Sch Med, Dept Obstet & Gynecol, Seattle, WA 98104 USA.
[Xi, Long Fu; Koutsky, Laura A.; Winer, Rachel L.; Lee, Shu-Kuang] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98104 USA.
[Hughes, James P.] Univ Washington, Sch Publ Hlth & Community Med, Dept Biostat, Seattle, WA 98104 USA.
[Schiffman, Mark] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Xi, LF (reprint author), Univ Washington, Dept Pathol, Harborview Med Ctr, NJB Ste 1187,325 9th Ave, Seattle, WA 98104 USA.
EM longfu@u.washington.edu
FU National Cancer Institute of the National Institutes of Health
[CA133569]
FX The research reported in this publication was supported by National
Cancer Institute of the National Institutes of Health under award number
CA133569.
NR 54
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U1 0
U2 11
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 OCT
PY 2014
VL 106
IS 10
AR dju270
DI 10.1093/jnci/dju270
PG 10
WC Oncology
SC Oncology
GA AQ7ZA
UT WOS:000343038200015
ER
PT J
AU Badalyan, V
Thompson, R
Addo, K
Borthwick, LA
Fisher, AJ
Ort, T
Myers, TG
Wynn, TA
Ramalingam, TR
AF Badalyan, Vahe
Thompson, Robert
Addo, Kezia
Borthwick, Lee A.
Fisher, Andrew J.
Ort, Tatiana
Myers, Timothy G.
Wynn, Thomas A.
Ramalingam, Thirumalai R.
TI TNF-alpha/IL-17 synergy inhibits IL-13 bioactivity via IL-13R alpha 2
induction
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Letter
ID RECEPTOR ALPHA-2; FIBROBLASTS; REVEALS; ASTHMA
C1 [Badalyan, Vahe; Thompson, Robert; Addo, Kezia; Wynn, Thomas A.; Ramalingam, Thirumalai R.] NIAID, Immunopathogenesis Sect, Bethesda, MD 20892 USA.
[Badalyan, Vahe] Childrens Natl Med Ctr, Div Gastroenterol Hepatol & Nutr, Washington, DC 20010 USA.
[Borthwick, Lee A.; Fisher, Andrew J.] Newcastle Univ, Inst Cellular Med, Tissue Fibrosis & Repair Grp, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Ort, Tatiana] Janssen R&D Companies Johnson & Johnson, Spring House, PA USA.
[Myers, Timothy G.] NIAID, Genom Technol Sect, Bethesda, MD 20892 USA.
RP Badalyan, V (reprint author), NIAID, Immunopathogenesis Sect, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ramalingamt@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 11
TC 4
Z9 4
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2014
VL 134
IS 4
BP 975
EP 978
DI 10.1016/j.jaci.2014.05.019
PG 5
WC Allergy; Immunology
SC Allergy; Immunology
GA AQ9GC
UT WOS:000343155700033
PM 24954262
ER
PT J
AU Smith, ML
Nichols, DC
Underwood, P
Fuller, Z
Moser, MA
Flegel, R
Gorelick, DA
Newmeyer, MN
Concheiro, M
Huestis, MA
AF Smith, Michael L.
Nichols, Daniel C.
Underwood, Paula
Fuller, Zachary
Moser, Matthew A.
Flegel, Ron
Gorelick, David A.
Newmeyer, Matthew N.
Concheiro, Marta
Huestis, Marilyn A.
TI Methamphetamine and Amphetamine Isomer Concentrations in Human Urine
Following Controlled Vicks VapoInhaler Administration
SO JOURNAL OF ANALYTICAL TOXICOLOGY
LA English
DT Article
AB Legitimate use of legal intranasal decongestants containing L-methamphetamine may complicate interpretation of urine drug tests positive for amphetamines. Our study hypotheses were that commonly used immunoassays would produce no false-positive results and a recently developed enantiomer-specific gas chromatography-mass spectrometry (GC-MS) procedure would find no D-amphetamine or D-methamphetamine in urine following controlled Vicks VapoInhaler administration at manufacturer's recommended doses. To evaluate these hypotheses, 22 healthy adults were each administered one dose (two inhalations in each nostril) of a Vicks VapoInhaler every 2 h for 10 h on Day 1 (six doses), followed by a single dose on Day 2. Every urine specimen was collected as an individual void for 32 h after the first dose and assayed for D-and L-amphetamines specific isomers with a GC-MS method with > 99% purity of R-(2)-alpha-methoxy-alpha-(trifluoromethyl) phenylacetyl derivatives and 10 mu g/L lower limits of quantification. No D-methamphetamine or D-amphetamine was detected in any urine specimen by GC-MS. The median L-methamphetamine maximum concentration was 62.8 mu g/L (range: 11.0-1,440). Only two subjects had detectable L-amphetamine, with maximum concentrations coinciding with L-methamphetamine peak levels, and always <= 4% of the parent's maximum. Three commercial immunoassays for amphetamines EMIT (R) II Plus, KIMS (R) II and DRI (R) had sensitivities, specificities and efficiencies of 100, 97.8, 97.8; 100, 99.6, 99.6 and 100, 100, 100%, respectively. The immunoassays had high efficiencies, but our first hypothesis was not affirmed. The EMIT w II Plus assay produced 2.2% false-positive results, requiring an enantiomer-specific confirmation.
C1 [Smith, Michael L.; Nichols, Daniel C.; Underwood, Paula; Fuller, Zachary; Moser, Matthew A.] US Army Forens Toxicol Drug Testing Lab, Ft George G Meade, MD USA.
[Flegel, Ron] US Dept HHS, Div Workplace Programs, Subst Abuse Mental Hlth Serv Adm, Rockville, MD USA.
[Gorelick, David A.; Newmeyer, Matthew N.; Concheiro, Marta; Huestis, Marilyn A.] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Gorelick, David A.] Univ Maryland, Sch Med, Dept Psychiat, Baltimore, MD 21201 USA.
[Newmeyer, Matthew N.] Univ Maryland, Toxicol Program, Baltimore, MD 21201 USA.
RP Huestis, MA (reprint author), NIDA, Intramural Res Program, NIH, 251 Bayview Blvd,Suite 200 Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
OI Newmeyer, Matthew/0000-0002-0653-1553
FU National Institutes of Health, National Institute on Drug Abuse;
Division of Workplace Programs, Substance Abuse Mental Health Services
Administration
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Drug Abuse and the
Division of Workplace Programs, Substance Abuse Mental Health Services
Administration.
NR 6
TC 2
Z9 2
U1 0
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0146-4760
EI 1945-2403
J9 J ANAL TOXICOL
JI J. Anal. Toxicol.
PD OCT
PY 2014
VL 38
IS 8
SI SI
BP 524
EP 527
DI 10.1093/jat/bku077
PG 4
WC Chemistry, Analytical; Toxicology
SC Chemistry; Toxicology
GA AR1DY
UT WOS:000343324100009
PM 25217541
ER
PT J
AU Huang, IH
Hsiao, CT
Wu, JC
Shen, RF
Liu, CY
Wang, YK
Chen, YC
Huang, CM
del Alamo, JC
Chang, ZF
Tang, MJ
Khoo, KH
Kuo, JC
AF Huang, I-Husan
Hsiao, Cheng-Te
Wu, Jui-Chung
Shen, Rong-Fong
Liu, Ching-Yi
Wang, Yang-Kao
Chen, Yu-Chen
Huang, Chi-Ming
del Alamo, Juan C.
Chang, Zee-Fen
Tang, Ming-Jer
Khoo, Kay-Hooi
Kuo, Jean-Cheng
TI GEF-H1 controls focal adhesion signaling that regulates mesenchymal stem
cell lineage commitment
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Focal adhesions; Mesenchymal stem cell; Osteogenesis; Stress fiber
ID NUCLEOTIDE EXCHANGE FACTOR; ACTIN STRESS FIBERS; RHO-GTPASES;
CYTOSKELETAL ORGANIZATION; EXTRACELLULAR-MATRIX; ENDOTHELIAL-CELLS;
INTEGRIN ADHESOME; STROMAL CELLS; HEAVY-CHAIN; II-B
AB Focal adhesions (FAs) undergo maturation that culminates in size and composition changes that modulate adhesion, cytoskeleton remodeling and differentiation. Although it is well recognized that stimuli for osteogenesis of mesenchymal stem cells (MSCs) drive FA maturation, actin organization and stress fiber polarization, the extent to which FA-mediated signals regulated by the FA protein composition specifies MSC commitment remains largely unknown. Here, we demonstrate that, upon dexamethasone (osteogenic induction) treatment, guanine nucleotide exchange factor H1 (GEF-H1, also known as Rho guanine nucleotide exchange factor 2, encoded by ARHGEF2) is significantly enriched in FAs. Perturbation of GEF-H1 inhibits FA formation, anisotropic stress fiber orientation and MSC osteogenesis in an actomyosin-contractility-independent manner. To determine the role of GEF-H1 in MSC osteogenesis, we explore the GEF-H1-modulated FA proteome that reveals non-muscle myosin-II heavy chain-B (NMIIB, also known as myosin-10, encoded by MYH10) as a target of GEF-H1 in FAs. Inhibition of targeting NMIIB into FAs suppresses FA formation, stress fiber polarization, cell stiffness and osteogenic commitments in MSCs. Our data demonstrate a role for FA signaling in specifying MSC commitment.
C1 [Huang, I-Husan; Wu, Jui-Chung; Chen, Yu-Chen; Huang, Chi-Ming; Chang, Zee-Fen; Kuo, Jean-Cheng] Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 11221, Taiwan.
[Hsiao, Cheng-Te; Khoo, Kay-Hooi] Natl Taiwan Univ, Inst Biochem Sci, Taipei 10617, Taiwan.
[Hsiao, Cheng-Te; Khoo, Kay-Hooi] Acad Sinica, Inst Biol Chem, Taipei 11529, Taiwan.
[Shen, Rong-Fong] NIA, Res Resources Branch, Prote & Analyt Biochem Unit, NIH, Baltimore, MD 21224 USA.
[Liu, Ching-Yi; Tang, Ming-Jer] Natl Cheng Kung Univ, Inst Basic Med Sci, Tainan 70101, Taiwan.
[Liu, Ching-Yi; Tang, Ming-Jer] Natl Cheng Kung Univ, Dept Physiol, Tainan 70101, Taiwan.
[Wang, Yang-Kao] Natl Cheng Kung Univ, Dept Cell Biol & Anat, Tainan 70101, Taiwan.
[Wang, Yang-Kao] Taipei Med Univ, Ctr Neurotrauma & Neuroregenerat, Taipei 11031, Taiwan.
[del Alamo, Juan C.] Univ Calif San Diego, Inst Engn Med, La Jolla, CA 92093 USA.
[del Alamo, Juan C.] Univ Calif San Diego, Dept Mech & Aerosp Engn, La Jolla, CA 92093 USA.
RP Kuo, JC (reprint author), Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 11221, Taiwan.
EM jckuo@ym.edu.tw
OI Liu, Ching-Yi/0000-0002-8997-5941; del Alamo, Juan
Carlos/0000-0001-5683-0239
FU Taiwan Ministry of Science and Technology [MOST 101-2628-B-010-003-MY3,
MOST 103-2628-B-010-003-MY4]; UST-UCSD International Center of
Excellence in Advanced Bio-engineering, Taiwan Ministry of Science and
Technology IRICE Program [MOST 100-2911-I-009-101]; Yen Tjing Ling
Medical Foundation; Ministry of Education's 'Aim for the Top University
Plan'
FX J.C.K. is supported by research grants from the Taiwan Ministry of
Science and Technology [grant numbers MOST 101-2628-B-010-003-MY3, MOST
103-2628-B-010-003-MY4]; the UST-UCSD International Center of Excellence
in Advanced Bio-engineering sponsored by the Taiwan Ministry of Science
and Technology IRICE Program [grant number MOST 100-2911-I-009-101]; the
Yen Tjing Ling Medical Foundation; and the Ministry of Education's 'Aim
for the Top University Plan'. Deposited in PMC for immediate release.
NR 62
TC 9
Z9 9
U1 0
U2 6
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
EI 1477-9137
J9 J CELL SCI
JI J. Cell Sci.
PD OCT 1
PY 2014
VL 127
IS 19
BP 4186
EP 4200
DI 10.1242/jcs.150227
PG 15
WC Cell Biology
SC Cell Biology
GA AQ8XT
UT WOS:000343123500009
PM 25107365
ER
PT J
AU Tao, P
Sodt, AJ
Shao, YH
Konig, G
Brooks, BR
AF Tao, Peng
Sodt, Alexander J.
Shao, Yihan
Koenig, Gerhard
Brooks, Bernard R.
TI Computing the Free Energy along a Reaction Coordinate Using Rigid Body
Dynamics
SO JOURNAL OF CHEMICAL THEORY AND COMPUTATION
LA English
DT Article
ID CONSTRAINED MOLECULAR-DYNAMICS; AQUEOUS-SOLUTION; GRADIENT-METHOD;
REACTION-PATH; RARE EVENTS; SIMULATIONS; OPTIMIZATION; MECHANICS;
ALGORITHMS; PROGRAM
AB The calculations of potential of mean force along complex chemical reactions or rare events pathways are of great interest because of their importance for many areas in chemistry, molecular biology, and material science. The major difficulty for free energy calculations comes from the great computational cost for adequate sampling of the system in high-energy regions, especially close to the reaction transition state. Here, we present a method, called PEG-RED, in which the free energy gradients were obtained from rigid body dynamics simulations. Then the free energy gradients were integrated along a reference reaction pathway to calculate free energy profiles. In a given system, the reaction coordinates defining a subset of atoms (e.g., a solute, or the quantum mechanics (QM) region of a quantum mechanics/molecular mechanics simulation) are selected to form a rigid body during the simulation. The first-order derivatives (gradients) of the free energy with respect to the reaction coordinates are obtained through the integration of constraint forces within the rigid body. Each structure along the reference reaction path is separately subjected to such a rigid body simulation. The individual free energy gradients are integrated along the reference pathway to obtain the free energy profile. Test cases provided demonstrate both the strengths and weaknesses of the FEG-RBD method. The most significant benefit of this method comes from the fast convergence rate of the free energy gradient using rigid-body constraints instead of restraints. A correction to the free energy due to approximate relaxation of the rigid-body constraint is estimated and discussed. A comparison with umbrella sampling using a simple test case revealed the improved sampling efficiency of FEG-RBD by a factor of 4 on average. The enhanced efficiency makes this method effective for calculating the free energy of complex chemical reactions when the reaction coordinate can be unambiguously defined by a small subset of atoms within the system.
C1 [Tao, Peng] So Methodist Univ, Dept Chem, Dallas, TX 75275 USA.
[Sodt, Alexander J.; Shao, Yihan; Koenig, Gerhard; Brooks, Bernard R.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Shao, Yihan] Q Chem Inc, Pleasanton, CA 94588 USA.
RP Tao, P (reprint author), So Methodist Univ, Dept Chem, 3215 Daniel Ave, Dallas, TX 75275 USA.
EM ptao@smu.edu
OI Tao, Peng/0000-0002-2488-0239
FU U.S. National Institutes of Health (NIH); U.S. National Heart, Lung, and
Blood Institute; Southern Methodist University (SMU)
FX This research was supported by the Intramural Research Program of the
U.S. National Institutes of Health (NIH), U.S. National Heart, Lung, and
Blood Institute, and startup research fund at Southern Methodist
University (SMU). Computational resources and services used in this work
were provided by the LoBoS cluster of the NIH and High-Performance
Computing Facilities at SMU. We thank Dr. D. Smith for helpful
discussions and Dr. W. Horsthemke for critical reading of the
manuscript.
NR 44
TC 6
Z9 6
U1 4
U2 23
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9618
EI 1549-9626
J9 J CHEM THEORY COMPUT
JI J. Chem. Theory Comput.
PD OCT
PY 2014
VL 10
IS 10
BP 4198
EP 4207
DI 10.1021/ct500342h
PG 10
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA AQ9SO
UT WOS:000343196300004
ER
PT J
AU Stratakis, CA
AF Stratakis, Constantine A.
TI E Pluribus Unum? The Main Protein Kinase A Catalytic Subunit (PRKACA), a
Likely Oncogene, and Cortisol-Producing Tumors
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Editorial Material
ID MACRONODULAR ADRENAL-HYPERPLASIA; PHOSPHODIESTERASE 11A PDE11A;
MCCUNE-ALBRIGHT SYNDROME; CARNEY COMPLEX; CUSHINGS-SYNDROME; PRKAR1A
MUTATION; ADRENOCORTICAL TUMORS; HORMONE RESISTANCE;
HEPATOCELLULAR-CARCINOMA; GENETIC-HETEROGENEITY
C1 [Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
[Stratakis, Constantine A.] NICHD, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
[Stratakis, Constantine A.] NIH, Interinst Pediat Endocrinol Training Program, Bethesda, MD 20892 USA.
RP Stratakis, CA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet, NIH, CRC Room 1-3330,East Labs,Bldg 10-CRC,10 Ctr Dr, Bethesda, MD 20892 USA.
EM stratakc@mail.nih.gov
FU Intramural NIH HHS
NR 52
TC 9
Z9 9
U1 0
U2 1
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2014
VL 99
IS 10
BP 3629
EP 3633
DI 10.1210/jc.2014-3295
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AR2NC
UT WOS:000343423300062
PM 25279575
ER
PT J
AU Richter, S
Peitzsch, M
Rapizzi, E
Lenders, JW
Qin, N
de Cubas, AA
Schiavi, F
Rao, JU
Beuschlein, F
Quinkler, M
Timmers, HJ
Opocher, G
Mannelli, M
Pacak, K
Robledo, M
Eisenhofer, G
AF Richter, Susan
Peitzsch, Mirko
Rapizzi, Elena
Lenders, Jacques W.
Qin, Nan
de Cubas, Aguirre A.
Schiavi, Francesca
Rao, Jyotsna U.
Beuschlein, Felix
Quinkler, Marcus
Timmers, Henri J.
Opocher, Giuseppe
Mannelli, Massimo
Pacak, Karel
Robledo, Mercedes
Eisenhofer, Graeme
TI Krebs Cycle Metabolite Profiling for Identification and Stratification
of Pheochromocytomas/Paragangliomas due to Succinate Dehydrogenase
Deficiency
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID MITOCHONDRIAL-FUNCTION; NECK PARAGANGLIOMAS; SDH MUTATIONS;
2-HYDROXYGLUTARATE; ACCUMULATION; ONCOGENESIS; DIAGNOSIS; DELETIONS;
GENETICS; GLIOMAS
AB Context: Mutations of succinate dehydrogenase A/B/C/D genes (SDHx) increase susceptibility to development of pheochromocytomas and paragangliomas (PPGLs), with particularly high rates of malignancy associated with SDHB mutations.
Objective: We assessed whether altered succinate dehydrogenase product-precursor relationships, manifested by differences in tumor ratios of succinate to fumarate or other metabolites, might aid in identifying and stratifying patients with SDHx mutations.
Design, Setting, and Patients: PPGL tumor specimens from 233 patients, including 45 with SDHx mutations, were provided from eight tertiary referral centers for mass spectrometric analyses of Krebs cycle metabolites.
Main Outcome Measure: Diagnostic performance of the succinate: fumarate ratio for identification of pathogenic SDHx mutations.
Results: SDH-deficient PPGLs were characterized by 25-fold higher succinate and 80% lower fumarate, cis-aconitate, and isocitrate tissue levels than PPGLs without SDHx mutations. Receiver-operating characteristic curves for use of ratios of succinate to fumarate or to cis-aconitate and isocitrate to identify SDHx mutations indicated areas under curves of 0.94 to 0.96; an optimal cut-off of 97.7 for the succinate: fumarate ratio provided a diagnostic sensitivity of 93% at a specificity of 97% to identify SDHX-mutated PPGLs. Succinate: fumarate ratios were higher in both SDHB-mutated and metastatic tumors than in those due to SDHD/C mutations or without metastases.
Conclusions: Mass spectrometric-based measurements of ratios of succinate: fumarate and other metabolites in PPGLs offer a useful method to identify patients for testing of SDHx mutations, with additional utility to quantitatively assess functionality of mutations and metabolic factors responsible for malignant risk.
C1 [Richter, Susan; Peitzsch, Mirko; Qin, Nan; Eisenhofer, Graeme] Tech Univ Dresden, Med Fac Carl Gustav Carus, Univ Hosp Carl Gustav Carus, Inst Clin Chem & Lab Med, D-01307 Dresden, Germany.
[Rapizzi, Elena; Mannelli, Massimo] Univ Florence, Dept Expt & Clin Biomed Sci Mario Serio, I-50139 Florence, Italy.
Ist Toscano Tumori, I-50139 Florence, Italy.
[Lenders, Jacques W.; Rao, Jyotsna U.; Timmers, Henri J.] Radboud Univ Nijmegen, Med Ctr, Dept Med, NL-6525 GA Nijmegen, Netherlands.
[Lenders, Jacques W.; Eisenhofer, Graeme] Univ Hosp Dresden, Dept Med 3, D-01307 Dresden, Germany.
[de Cubas, Aguirre A.; Robledo, Mercedes] CNIO, Hereditary Endocrine Canc Grp, Madrid, Spain.
[de Cubas, Aguirre A.; Robledo, Mercedes] Ctr Invest Biomed Red Enfermedades Raras CIBERER, Madrid 28029, Spain.
[Schiavi, Francesca; Opocher, Giuseppe] Veneto Inst Oncol IRCCS, I-35128 Padua, Italy.
[Beuschlein, Felix] Univ Munich, Med Klin & Poliklin 4, D-80336 Munich, Germany.
[Quinkler, Marcus] Univ Hosp Charite, D-10117 Berlin, Germany.
[Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Richter, S (reprint author), Tech Univ Dresden, Div Clin Neurochem, Inst Clin Chem & Lab Med, Fetscherstr 74, D-01307 Dresden, Germany.
EM Susan.Richter2@uniklinikum-dresden.de
RI Robledo, Mercedes/O-2230-2013;
OI Robledo, Mercedes/0000-0001-6256-5902; schiavi,
francesca/0000-0001-8529-4455; Mannelli, Massimo/0000-0002-8001-9857;
Opocher, Giuseppe/0000-0002-9845-9623
FU European Union [259735]; Deutsche Forschungsgesellschaft [EI855/1-1];
Fondo de Investigaciones Sanitarias [PI11/01359]; Eunice Kennedy Shriver
National Institute of Child Health and Human Development
FX This work was funded by the European Union Seventh Framework Programme
(FP7/2007-2013) under Grant Agreement No. 259735 (project ENS@T-Cancer)
(S.R., M.P., N.Q., G.E., A.A.dC., M.R., E.R., M.M., J.U.R., H.J.T.,
F.B.), the Deutsche Forschungsgesellschaft (EI855/1-1) (S.R., M.P.,
N.Q., G.E., J.W.L.), the Fondo de Investigaciones Sanitarias (Project
PI11/01359)(A.A.dC, M.R.), and the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (K.P.).
NR 35
TC 17
Z9 17
U1 0
U2 19
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2014
VL 99
IS 10
BP 3903
EP 3911
DI 10.1210/jc.2014-2151
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AR2NC
UT WOS:000343423300094
PM 25014000
ER
PT J
AU Dey, R
Natarajan, G
Bhattacharya, P
Cummings, H
Dagur, PK
Terrazas, C
Selvapandiyan, A
Mccoy, JP
Duncan, R
Satoskar, AR
Nakhasi, HL
AF Dey, Ranadhir
Natarajan, Gayathri
Bhattacharya, Parna
Cummings, Hannah
Dagur, Pradeep K.
Terrazas, Cesar
Selvapandiyan, Angamuthu
Mccoy, John P., Jr.
Duncan, Robert
Satoskar, Abhay R.
Nakhasi, Hira L.
TI Characterization of Cross-Protection by Genetically Modified
Live-Attenuated Leishmania donovani Parasites against Leishmania
mexicana
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID PROTEINASE-DEFICIENT MUTANTS; AZAR DERMAL LEISHMANIASIS; CD8(+) T-CELLS;
DENDRITIC CELLS; CUTANEOUS LEISHMANIASIS; MURINE LEISHMANIASIS; BALB/C
MICE; L. MAJOR; VISCERAL LEISHMANIASIS; AMAZONENSIS INFECTION
AB Previously, we showed that genetically modified live-attenuated Leishmania donovani parasite cell lines (LdCen(-/-) and Ldp27(-/-)) induce a strong cellular immunity and provide protection against visceral leishmaniasis in mice. In this study, we explored the mechanism of cross-protection against cutaneous lesion-causing Leishmania mexicana. Upon challenge with wild-type L. mexicana, mice immunized either for short or long periods showed significant protection. Immunohistochemical analysis of ears from immunized/challenged mice exhibited significant influx of macrophages, as well as cells expressing MHC class II and inducible NO synthase, suggesting an induction of potent host-protective proinflammatory responses. In contrast, substantial inhibition of IL-10, IL-4, and IL-13 expression and the absence of degranulated mast cells and less influx of eosinophils within the ears of immunized/challenged mice suggested a controlled anti-inflammatory response. L. mexicana Ag-stimulated lymph node cell culture from the immunized/challenged mice revealed induction of IFN-gamma secretion by the CD4 and CD8 T cells compared with non-immunized/challenged mice. We also observed suppression of Th2 cytokines in the culture supernatants of immunized/challenged lymph nodes compared with non-immunized/challenged mice. Adoptively transferred total T cells from immunized mice conferred strong protection in recipient mice against L. mexicana infection, suggesting that attenuated L. donovani can provide protection against heterologous L. mexicana parasites by induction of a strong T cell response. Furthermore, bone marrow-derived dendritic cells infected with LdCen(-/-) and Ldp27(-/-) parasites were capable of inducing a strong proinflammatory response leading to the proliferation of Th1 cells. These studies demonstrate the potential of live-attenuated L. donovani parasites as pan-Leishmania species vaccines.
C1 [Dey, Ranadhir; Bhattacharya, Parna; Duncan, Robert; Nakhasi, Hira L.] US FDA, Div Emerging & Transfus Transmitted Dis, Ctr Biol Evaluat & Res, Silver Spring, MD 20993 USA.
[Natarajan, Gayathri; Cummings, Hannah; Terrazas, Cesar; Satoskar, Abhay R.] Ohio State Univ, Wexner Med Ctr, Dept Pathol, Columbus, OH 43210 USA.
[Dagur, Pradeep K.; Mccoy, John P., Jr.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Selvapandiyan, Angamuthu] Inst Mol Med, New Delhi 110020, India.
RP Nakhasi, HL (reprint author), US FDA, Div Emerging & Transfus Transmitted Dis, Ctr Biol Evaluat & Res, Bldg 71,Room 4266,10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM Abhay.Satoskar@osumc.edu; Hira.Nakhasi@fda.hhs.gov
FU Center for Biologics Evaluation and Research, U.S. Food and Drug
Administration
FX This work was supported by intramural funds and a critical path
initiative of the Center for Biologics Evaluation and Research, U.S.
Food and Drug Administration. Findings of this study are an informal
communication and represent the best judgment of the authors. These
comments do not bind or obligate the U.S. Food and Drug Administration.
NR 73
TC 8
Z9 8
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2014
VL 193
IS 7
BP 3513
EP 3527
DI 10.4049/jimmunol.1303145
PG 15
WC Immunology
SC Immunology
GA AR0XQ
UT WOS:000343298700032
PM 25156362
ER
PT J
AU Kaushal, N
Kudva, AK
Patterson, AD
Chiaro, C
Kennett, MJ
Desai, D
Amin, S
Carlson, BA
Cantorna, MT
Prabhu, KS
AF Kaushal, Naveen
Kudva, Avinash K.
Patterson, Andrew D.
Chiaro, Christopher
Kennett, Mary J.
Desai, Dhimant
Amin, Shantu
Carlson, Bradley A.
Cantorna, Margherita T.
Prabhu, K. Sandeep
TI Crucial Role of Macrophage Selenoproteins in Experimental Colitis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; PROSTAGLANDIN D-2 SYNTHASE;
ULCERATIVE-COLITIS; 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE;
ARACHIDONIC-ACID; GENE-EXPRESSION; COLONIC INJURY; CROHNS-DISEASE;
TNF-ALPHA; RECEPTOR
AB Inflammation is a hallmark of inflammatory bowel disease (IBD) that involves macrophages. Given the inverse link between selenium (Se) status and IBD-induced inflammation, our objective was to demonstrate that selenoproteins in macrophages were essential to suppress proinflammatory mediators, in part, by the modulation of arachidonic acid metabolism. Acute colitis was induced using 4% dextran sodium sulfate in wild-type mice maintained on Se-deficient (<0.01 ppm Se), Se-adequate (0.08 ppm; sodium selenite), and two supraphysiological levels in the form of Se-supplemented (0.4 ppm; sodium selenite) and high Se (1.0 ppm; sodium selenite) diets. Selenocysteinyl transfer RNA knockout mice (Trsp(fl/fl)LysM(Cre)) were used to examine the role of selenoproteins in macrophages on disease progression and severity using histopathological evaluation, expression of proinflammatory and anti-inflammatory genes, and modulation of PG metabolites in urine and plasma. Whereas Se-deficient and Se-adequate mice showed increased colitis and exhibited poor survival, Se supplementation at 0.4 and 1.0 ppm increased survival of mice and decreased colitis-associated inflammation with an upregulation of expression of proinflammatory and anti-inflammatory genes. Metabolomic profiling of urine suggested increased oxidation of PGE(2) at supraphysiological levels of Se that also correlated well with Se-dependent upregulation of 15-hydroxy-PG dehydrogenase (15-PGDH) in macrophages. Pharmacological inhibition of 15-PGDH, lack of selenoprotein expression in macrophages, and depletion of infiltrating macrophages indicated that macrophage-specific selenoproteins and upregulation of 15-PGDH expression were key for Se-dependent anti-inflammatory and proresolving effects. Selenoproteins in macrophages protect mice from dextran sodium sulfate-colitis by enhancing 15-PGDH-dependent oxidation of PGE2 to alleviate inflammation, suggesting a therapeutic role for Se in IBD.
C1 [Kaushal, Naveen; Kudva, Avinash K.; Patterson, Andrew D.; Chiaro, Christopher; Kennett, Mary J.; Cantorna, Margherita T.; Prabhu, K. Sandeep] Penn State Univ, Ctr Mol Immunol & Infect Dis, University Pk, PA 16802 USA.
[Kaushal, Naveen; Kudva, Avinash K.; Patterson, Andrew D.; Chiaro, Christopher; Kennett, Mary J.; Cantorna, Margherita T.; Prabhu, K. Sandeep] Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, Dept Vet & Biomed Sci, University Pk, PA 16802 USA.
[Desai, Dhimant; Amin, Shantu] Penn State Coll Med, Dept Pharmacol, Hershey, PA 17033 USA.
[Carlson, Bradley A.] NCI, Mol Biol Selenium Sect, Mouse Canc Genet Program, NIH, Bethesda, MD 20892 USA.
RP Prabhu, KS (reprint author), Penn State Univ, 115 Henning Bldg, University Pk, PA 16802 USA.
EM ksprabhu@psu.edu
RI Patterson, Andrew/G-3852-2012
OI Patterson, Andrew/0000-0003-2073-0070
FU National Institutes of Health Public Health Service Grants [DK077152,
ES022186]
FX This work was supported by National Institutes of Health Public Health
Service Grants DK077152 (to K.S.P.) and ES022186 (to A.D.P.).
NR 51
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Z9 9
U1 1
U2 12
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2014
VL 193
IS 7
BP 3683
EP 3692
DI 10.4049/jimmunol.1400347
PG 10
WC Immunology
SC Immunology
GA AR0XQ
UT WOS:000343298700048
PM 25187657
ER
PT J
AU McMahon, DBT
Bondar, IV
Afuwape, OAT
Ide, DC
Leopold, DA
AF McMahon, David B. T.
Bondar, Igor V.
Afuwape, Olusoji A. T.
Ide, David C.
Leopold, David A.
TI One month in the life of a neuron: longitudinal single-unit
electrophysiology in the monkey visual system
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE fMRI; macaque; object recognition; physiology; vision
ID INFERIOR TEMPORAL CORTEX; PRIMARY MOTOR CORTEX; MACAQUE INFEROTEMPORAL
CORTEX; LONG-TERM STABILITY; SHAPE SELECTIVITY; REPRESENTATION; OBJECT;
EXPERIENCE; RESPONSES; PATTERNS
AB Conventional recording methods generally preclude following the activity of the same neurons in awake animals across days. This limits our ability to systematically investigate the principles of neuronal specialization, or to study phenomena that evolve over multiple days such as experience-dependent plasticity. To redress this shortcoming, we developed a drivable, chronically implanted microwire recording preparation that allowed us to follow visual responses in inferotemporal (IT) cortex in awake behaving monkeys across multiple days, and in many cases across months. The microwire bundle and other implanted components were MRI compatible and thus permitted in the same animals both functional imaging and long-term recording from multiple neurons in deep structures within a region the approximate size of one voxel (< 1 mm). The distinct patterns of stimulus selectivity observed in IT neurons, together with stable features in spike waveforms and interspike interval distributions, allowed us to track individual neurons across weeks and sometimes months. The long-term consistency of visual responses shown here permits large-scale mappings of neuronal properties using massive image libraries presented over the course of days. We demonstrate this possibility by screening the visual responses of single neurons to a set of 10,000 stimuli.
C1 [McMahon, David B. T.; Afuwape, Olusoji A. T.; Leopold, David A.] NIMH, Sect Cognit Neurophysiol & Imaging, NIH, Bethesda, MD 20892 USA.
[Bondar, Igor V.] Russian Acad Sci, Inst Higher Nervous Act & Neurophysiol, Moscow, Russia.
[Ide, David C.] NIMH, Sect Instrumentat, NIH, Bethesda, MD 20892 USA.
[Leopold, David A.] NEI, Neurophysiol Imaging Facil, NIMH, Bethesda, MD 20982 USA.
[Leopold, David A.] NINDS, NIH, Bethesda, MD 20892 USA.
RP McMahon, DBT (reprint author), NEI, Sensorimotor Res Lab, Bldg 49,Rm 2A5049,49 Convent Dr, Bethesda, MD 20982 USA.
EM mcmahond@mail.nih.gov
OI Leopold, David/0000-0002-1345-6360
FU National Institute of Mental Health; National Institute of Neurological
Disorders and Stroke; National Eye Institute Intramural Research
Programs; National Institutes of Health Fellowship [EY-018028]
FX This work was supported by National Institute of Mental Health, National
Institute of Neurological Disorders and Stroke, and National Eye
Institute Intramural Research Programs and by National Institutes of
Health Fellowship EY-018028 to D. B. T. McMahon.
NR 65
TC 7
Z9 7
U1 0
U2 13
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
EI 1522-1598
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD OCT 1
PY 2014
VL 112
IS 7
BP 1748
EP 1762
DI 10.1152/jn.00052.2014
PG 15
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA AR0BA
UT WOS:000343226600015
PM 24966298
ER
PT J
AU Dahut, WL
Madan, RA
AF Dahut, William L.
Madan, Ravi A.
TI Real-world experience with abiraterone
SO LANCET ONCOLOGY
LA English
DT Editorial Material
ID METASTATIC PROSTATE-CANCER; INCREASED SURVIVAL; CLINICAL ACTIVITY;
ENZALUTAMIDE; CHEMOTHERAPY; RESISTANCE; DOCETAXEL
C1 [Dahut, William L.; Madan, Ravi A.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Dahut, WL (reprint author), NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
EM dahutw@mail.nih.gov
NR 10
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD OCT
PY 2014
VL 15
IS 11
BP 1188
EP 1190
DI 10.1016/S1470-2045(14)70463-2
PG 4
WC Oncology
SC Oncology
GA AQ8QY
UT WOS:000343096800041
PM 25242047
ER
PT J
AU Liu, JF
Barry, WT
Birrer, M
Lee, JM
Buckanovich, RJ
Fleming, GF
Rimel, BJ
Buss, MK
Nattam, S
Hurteau, J
Luo, WX
Quy, P
Whalen, C
Obermayer, L
Lee, H
Winer, EP
Kohn, EC
Ivy, SP
Matulonis, UA
AF Liu, Joyce F.
Barry, William T.
Birrer, Michael
Lee, Jung-Min
Buckanovich, Ronald J.
Fleming, Gini F.
Rimel, B. J.
Buss, Mary K.
Nattam, Sreenivasa
Hurteau, Jean
Luo, Weixiu
Quy, Philippa
Whalen, Christin
Obermayer, Lisa
Lee, Hang
Winer, Eric P.
Kohn, Elise C.
Ivy, S. Percy
Matulonis, Ursula A.
TI Combination cediranib and olaparib versus olaparib alone for women with
recurrent platinum-sensitive ovarian cancer: a randomised phase 2 study
SO LANCET ONCOLOGY
LA English
DT Article
ID NEGATIVE BREAST-CANCER; POLY(ADP-RIBOSE) POLYMERASE; EPITHELIAL OVARIAN;
DOWN-REGULATION; MAINTENANCE THERAPY; PRIMARY PERITONEAL;
FALLOPIAN-TUBE; OPEN-LABEL; TRIAL; BEVACIZUMAB
AB Background Olaparib is a poly(ADP-ribose) polymerase inhibitor and cediranib is an anti-angiogenic agent with activity against VEGF receptor (VEGFR) 1, VEGFR2, and VEGFR3. Both oral agents have antitumour activity in women with recurrent ovarian cancer, and their combination was active and had manageable toxicities in a phase 1 trial. We investigated whether this combination could improve progression-free survival (PFS) compared with olaparib monotherapy in women with recurrent platinum-sensitive ovarian cancer.
Methods In our randomised, open-label, phase 2 study, we recruited women (aged >= 18 years) who had measurable platinum-sensitive, relapsed, high-grade serous or endometrioid ovarian, fallopian tube, or primary peritoneal cancer, or those with deleterious germline BRCA1/2 mutations from nine participating US academic medical centres. We randomly allocated participants (1:1) according to permuted blocks, stratified by germline BRCA status and previous anti-angiogenic therapy, to receive olaparib capsules 400 mg twice daily or the combination at the recommended phase 2 dose of cediranib 30 mg daily and olaparib capsules 200 mg twice daily. The primary endpoint was progression-free survival analysed in the intention-to-treat population. The phase 2 trial is no longer accruing patients. An interim analysis was conducted in November, 2013, after 50% of expected events had occurred and efficacy results were unmasked. The primary analysis was performed on March 31, 2014, after 47 events (66% of those expected). The trial is registered with ClinicalTrials. gov, number NCT01116648.
Findings Between Oct 26, 2011, and June 3, 2013, we randomly allocated 46 women to receive olaparib alone and 44 to receive the combination of olaparib and cediranib. Median PFS was 17.7 months (95% CI 14.7-not reached) for the women treated with cediranib plus olaparib compared with 9.0 months (95% CI 5.7-16.5) for those treated with olaparib monotherapy (hazard ratio 0.42, 95% CI 0.23-0.76; p=0.005). Grade 3 and 4 adverse events were more common with combination therapy than with monotherapy, including fatigue (12 patients in the cediranib plus olaparib group vs five patients in the olaparib monotherapy group), diarrhoea (ten vs none), and hypertension (18 vs none).
Interpretation Cediranib plus olaparib seems to improve PFS in women with recurrent platinum-sensitive high-grade serous or endometrioid ovarian cancer, and warrants study in a phase 3 trial. The side-effect profile suggests such investigations should include assessments of quality of life and patient-reported outcomes to understand the effects of a continuing oral regimen with that of intermittent chemotherapy.
C1 [Liu, Joyce F.; Quy, Philippa; Whalen, Christin; Obermayer, Lisa; Winer, Eric P.; Matulonis, Ursula A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Barry, William T.; Luo, Weixiu] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Birrer, Michael] Massachusetts Gen Hosp, Dept Med Oncol, Boston, MA 02114 USA.
[Lee, Hang] Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA.
[Lee, Jung-Min; Kohn, Elise C.] NCI, Ctr Canc Res, Womens Malignancies Branch, Bethesda, MD 20892 USA.
[Kohn, Elise C.; Ivy, S. Percy] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Buckanovich, Ronald J.] Univ Michigan, Dept Med Oncol, Ann Arbor, MI 48109 USA.
[Fleming, Gini F.] Univ Chicago, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Rimel, B. J.] Cedars Sinai Med Ctr, Dept Obstet & Gynecol, Los Angeles, CA 90048 USA.
[Buss, Mary K.] Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA.
[Nattam, Sreenivasa] Ft Wayne Med Oncol & Hematol, Dept Oncol, Ft Wayne, IN USA.
[Hurteau, Jean] North Shore Univ Hlth Syst, Evanston Hosp, Div Gynecol Oncol, Evanston, IL 60201 USA.
RP Liu, JF (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM joyce_liu@dfci.harvard.edu
FU Cancer Therapy Evaluation Program of the National Cancer Institute
-American Recovery and Reinvestment Act (ARRA) through US National
Institutes of Health [3 U01 CA062490-16S2]; CJL Charitable Foundation;
Intramural Program of the Center for Cancer Research (CCR); CCR;
Division of Cancer Treatment and Diagnosis, National Cancer Institute,
US National Institutes of Health, Bethesda, MD, USA
FX This study was funded by the Cancer Therapy Evaluation Program of the
National Cancer Institute and supported by an American Recovery and
Reinvestment Act (ARRA) grant through the US National Institutes of
Health (3 U01 CA062490-16S2). WTB was supported by the CJL Charitable
Foundation. J-ML was supported by the Intramural Program of the Center
for Cancer Research (CCR), and ECK by the CCR and Division of Cancer
Treatment and Diagnosis, National Cancer Institute, US National
Institutes of Health, Bethesda, MD, USA. The funding source had no role
in the conduct, data collection, or analysis of the study.
NR 31
TC 115
Z9 117
U1 3
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD OCT
PY 2014
VL 15
IS 11
BP 1207
EP 1214
DI 10.1016/S1470-2045(14)70391-2
PG 8
WC Oncology
SC Oncology
GA AQ8QY
UT WOS:000343096800046
PM 25218906
ER
PT J
AU Cuzick, J
Thorat, MA
Andriole, G
Brawley, OW
Brown, PH
Culig, Z
Eeles, RA
Ford, LG
Hamdy, FC
Holmberg, L
Ilic, D
Key, TJ
La Vecchia, C
Lilja, H
Marberger, M
Meyskens, FL
Minasian, LM
Parker, C
Parnes, HL
Perner, S
Rittenhouse, H
Schalken, J
Schmid, HP
Schmitz-Drager, BJ
Schroder, FH
Stenzl, A
Tombal, B
Wilt, TJ
Wolk, A
AF Cuzick, Jack
Thorat, Mangesh A.
Andriole, Gerald
Brawley, Otis W.
Brown, Powel H.
Culig, Zoran
Eeles, Rosalind A.
Ford, Leslie G.
Hamdy, Freddie C.
Holmberg, Lars
Ilic, Dragan
Key, Timothy J.
La Vecchia, Carlo
Lilja, Hans
Marberger, Michael
Meyskens, Frank L.
Minasian, Lori M.
Parker, Chris
Parnes, Howard L.
Perner, Sven
Rittenhouse, Harry
Schalken, Jack
Schmid, Hans-Peter
Schmitz-Draeger, Bernd J.
Schroder, Fritz H.
Stenzl, Arnulf
Tombal, Bertrand
Wilt, Timothy J.
Wolk, Alicja
TI Prevention and early detection of prostate cancer
SO LANCET ONCOLOGY
LA English
DT Review
ID RANDOMIZED CONTROLLED-TRIALS; RADICAL PROSTATECTOMY; SCREENING TRIAL;
FOLLOW-UP; PROSPECTIVE COHORT; PHYSICAL-ACTIVITY; UNITED-STATES;
DOUBLE-BLIND; COPY NUMBER; HIGH-RISK
AB Prostate cancer is a common malignancy in men and the worldwide burden of this disease is rising. Lifestyle modifications such as smoking cessation, exercise, and weight control off er opportunities to reduce the risk of developing prostate cancer. Early detection of prostate cancer by prostate-specific antigen (PSA) screening is controversial, but changes in the PSA threshold, frequency of screening, and the use of other biomarkers have the potential to minimise the overdiagnosis associated with PSA screening. Several new biomarkers for individuals with raised PSA concentrations or those diagnosed with prostate cancer are likely to identify individuals who can be spared aggressive treatment. Several pharmacological agents such as 5 alpha-reductase inhibitors and aspirin could prevent development of prostate cancer. In this Review, we discuss the present evidence and research questions regarding prevention, early detection of prostate cancer, and management of men either at high risk of prostate cancer or diagnosed with low-grade prostate cancer.
C1 [Cuzick, Jack; Thorat, Mangesh A.] Queen Mary Univ London, Ctr Canc Prevent, Wolfson Inst Prevent Med, London EC1M 6BQ, England.
[Andriole, Gerald] Washington Univ, Barnes Jewish Hosp, Sch Med, Div Urol Surg, St Louis, MO USA.
[Brawley, Otis W.] Amer Canc Soc, Off Chief Med Officer, Atlanta, GA 30329 USA.
[Brawley, Otis W.] Emory Univ, Dept Hematol & Oncol, Atlanta, GA 30322 USA.
[Brown, Powel H.] Univ Texas MD Anderson Canc Ctr, Dept Clin Canc Prevent Canc Prevent & Populat Sci, Houston, TX 77030 USA.
[Culig, Zoran] Med Univ Innsbruck, Dept Urol, A-6020 Innsbruck, Austria.
[Eeles, Rosalind A.] Inst Canc Res, Div Canc Genet & Epidemiol, London SW3 6JB, England.
[Eeles, Rosalind A.; Parker, Chris] Royal Marsden NHS Fdn Trust, Acad Urol Unit, London, England.
[Ford, Leslie G.; Minasian, Lori M.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Hamdy, Freddie C.] Univ Oxford, Oxford, England.
[Lilja, Hans] Univ Oxford, Nuffield Dept Surg Sci, Oxford, England.
[Key, Timothy J.] Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England.
[Holmberg, Lars] Kings Coll London, Sch Med, London, England.
[Holmberg, Lars] Uppsala Univ, Reg Canc Ctr Uppsala Orebro, Uppsala, Sweden.
[Holmberg, Lars] Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
[Ilic, Dragan] Monash Univ, Sch Publ Hlth & Prevent Med, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[La Vecchia, Carlo] Univ Milan, Dept Clin Sci & Community Hlth, Milan, Italy.
[Lilja, Hans] Mem Sloan Kettering Canc Ctr, Dept Surg Urol, Lab Med & Med GU Oncol, New York, NY 10021 USA.
[Lilja, Hans] Lund Univ, Univ Hosp UMAS, Dept Lab Med, Malmo, Sweden.
[Marberger, Michael] Univ Vienna, Sch Med, Dept Urol, Vienna, Austria.
[Meyskens, Frank L.] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
[Parnes, Howard L.] NCI, Prostate & Urol Canc Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
[Perner, Sven] Univ Hosp Bonn, Inst Pathol, Dept Prostate Canc Res, Bonn, Germany.
[Rittenhouse, Harry] IR2Dx Inc, Director Assay Dev, Moraga, CA USA.
[Schalken, Jack] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Schmid, Hans-Peter] Kantonsspital St Gallen, Dept Urol, St Gallen, Switzerland.
[Schmitz-Draeger, Bernd J.] Schon Klin Nurnberg Furth & Urol 24, Furth, Germany.
[Schroder, Fritz H.] Erasmus Univ, Rotterdam, Netherlands.
[Schroder, Fritz H.] Erasmus MC, Rotterdam, Netherlands.
[Stenzl, Arnulf] Univ Tubingen Hosp, Dept Urol, Tubingen, Germany.
[Tombal, Bertrand] Catholic Univ Louvain, Dept Urol, B-1200 Brussels, Belgium.
[Wilt, Timothy J.] Univ Minnesota, Sch Med, Minneapolis Vet Aff airs Hlth Care Syst, Ctr Chron Dis Outcomes Res, Minneapolis, MN 55455 USA.
[Wilt, Timothy J.] Univ Minnesota, Sch Med, Sect Gen Med, Minneapolis, MN 55455 USA.
[Wolk, Alicja] Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, S-10401 Stockholm, Sweden.
RP Cuzick, J (reprint author), Queen Mary Univ London, Ctr Canc Prevent, Wolfson Inst Prevent Med, London EC1M 6BQ, England.
EM j.cuzick@qmul.ac.uk
RI Schalken, Jack/B-1277-2014; Thorat, Mangesh/A-9787-2008
OI Schalken, Jack/0000-0001-8274-7797; Thorat, Mangesh/0000-0001-8673-5320
FU International Society of Cancer Prevention (ISCaP); European Association
of Urology (EAU); National Cancer Institute; USA (NCI)
[1R13CA171707-01]; Prostate Cancer UK; Cancer Research UK (CRUK)
[C569/A16477]; Association for International Cancer Research (AICR)
FX We thank Vesna Florijancic, Liz Pinney, and Ellie Stewart for
administrative assistance. This Review was sponsored and funded by the
International Society of Cancer Prevention (ISCaP), the European
Association of Urology (EAU), the National Cancer Institute, USA (NCI)
(grant number 1R13CA171707-01), Prostate Cancer UK, Cancer Research UK
(CRUK) (grant number C569/A16477), and the Association for International
Cancer Research (AICR). Sponsors and funding sources had no role in the
discussion or writing of this manuscript. The findings and conclusions
in this report are those of the authors and do not represent the
official position of the authors' respective institutions.
NR 85
TC 70
Z9 72
U1 6
U2 44
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD OCT
PY 2014
VL 15
IS 11
BP E484
EP E492
PG 9
WC Oncology
SC Oncology
GA AQ8QY
UT WOS:000343096800029
PM 25281467
ER
PT J
AU Bera, TK
Onda, M
Kreitman, RJ
Pastan, I
AF Bera, Tapan K.
Onda, Masanori
Kreitman, Robert J.
Pastan, Ira
TI An improved recombinant Fab-immunotoxin targeting CD22 expressing
malignancies
SO LEUKEMIA RESEARCH
LA English
DT Article
DE B-cell malignancies; Moxetumomab pasudotox; Less immunogenic PE38
ID HAIRY-CELL LEUKEMIA; HEMATOLOGIC MALIGNANCIES; RFB4(DSFV)-PE38 BL22; LOW
IMMUNOGENICITY; ANTITUMOR-ACTIVITY; ANIMAL TOXICITY; TRIAL; MICE;
EPITOPES; CANCER
AB Moxetumomab pasudotox (HA22) is a recombinant immunotoxin, now in clinical trials, that combines an anti-CD22-Fv with a 38-kDa fragment of Pseudomonas exotoxin A. To produce a less immunogenic molecule without reducing the half-life in circulation, we constructed LMB11 combining an anti-CD22 Fab with a less immunogenic version of PE38. We found that LMB11 retains full activity toward CD22 expressing cells. In mice, the half-life of LMB11 is 29 min and the antitumor activity of LMB11 is better than that of HA22. Because it can be safely given at much higher doses, LMB11 produced complete tumor remissions in 7/7 mice. Published by Elsevier Ltd.
C1 [Bera, Tapan K.; Onda, Masanori; Kreitman, Robert J.; Pastan, Ira] NCI, Lab Mol Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pastan, I (reprint author), NCI, Lab Mol Biol, Ctr Canc Res, NIH, 37 Convent Dr,Room 5106, Bethesda, MD 20892 USA.
EM pastani@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 17
TC 11
Z9 11
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
J9 LEUKEMIA RES
JI Leuk. Res.
PD OCT
PY 2014
VL 38
IS 10
BP 1224
EP 1229
DI 10.1016/j.leukres.2014.06.014
PG 6
WC Oncology; Hematology
SC Oncology; Hematology
GA AQ8TL
UT WOS:000343105300017
PM 25127689
ER
PT J
AU Kvale, PA
Johnson, CC
Tammemagi, M
Marcus, PM
Zylak, CJ
Spizarny, DL
Hocking, W
Oken, M
Commins, J
Ragard, L
Hu, P
Berg, C
Prorok, P
AF Kvale, Paul A.
Johnson, Christine Cole
Tammemagi, Martin
Marcus, Pamela M.
Zylak, Carl J.
Spizarny, David L.
Hocking, William
Oken, Martin
Commins, John
Ragard, Lawrence
Hu, Ping
Berg, Christine
Prorok, Philip
TI Interval lung cancers not detected on screening chest X-rays: How are
they different?
SO LUNG CANCER
LA English
DT Article
DE Lung cancer; PLCO Cancer Screening Trial; Screening interval lung
cancers; Chest X-ray screen-detected lung cancers; Chest radiograph;
Pulmonary tumour
ID STATISTICS; RADIOGRAPH; MORTALITY; TRIAL
AB Background: The Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial provides us an opportunity to describe interval lung cancers not detected by screening chest X-ray (OCR) compared to screen-detected cancers.
Methods: Participants were screened for lung cancer with CXR at baseline and annually for two (never smokers) or three (ever smokers) more years. Screen-detected cancers were those with a positive CXR and diagnosed within 12 months. Putative interval cancers were those with a negative CXR screen but with a diagnosis of lung cancer within 12 months. Potential interval cancers were re-reviewed to determine whether lung cancer was missed and probably present during the initial interpretation or whether the lesion was a "true interval" cancer.
Results: 77,445 participants were randomized to the intervention arm with 70,633 screened. Of 5227 positive screens from any screening round, 299 resulted in screen-detected lung cancers; 151 had potential interval cancers with 127 CXR available for re-review. Cancer was probably present in 45/127 (35.4%) at time of screening; 82 (64.6%) were "true interval" cancers. Compared to screen-detected cancers, true interval cancers were more common among males, persons with <12 years education and those with a history of smoking. True interval lung cancers were more often small cell, 28.1% vs. 7.4%, and less often adenocarcinoma, 25.6% vs. 56.2% (p < 0.001), more advanced stage IV (30.5% vs. 16.6%, p < 0.02), and less likely to be in the right upper lobe, 17.1% vs. 36.1% (p < 0.02).
Conclusion: True interval lung cancers differ from CXR-screen-detected cancers with regard to demographic variables, stage, cell type and location. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Kvale, Paul A.] Henry Ford Hlth Syst, Div Pulm & Crit Care Med, Detroit, MI 48202 USA.
[Johnson, Christine Cole] Henry Ford Hlth Syst, Dept Publ Hlth Sci, Detroit, MI 48202 USA.
[Tammemagi, Martin] Brock Univ, Dept Community Hlth Sci, St Catharines, ON L2S 3A1, Canada.
[Marcus, Pamela M.; Hu, Ping; Berg, Christine; Prorok, Philip] NCI, Bethesda, MD 20892 USA.
[Zylak, Carl J.; Spizarny, David L.] Henry Ford Hlth Syst, Dept Radiol, Detroit, MI 48202 USA.
[Hocking, William] Marshfield Clin Fdn Med Res & Educ, Dept Clin Oncol, Marshfield, WI USA.
[Oken, Martin] Univ Minnesota, Sch Publ Hlth, Div Environm Hlth Sci, Minneapolis, MN USA.
[Commins, John] Informat Management Serv Inc, Rockville, MD USA.
[Ragard, Lawrence] Westat Corp, Rockville, MD USA.
RP Kvale, PA (reprint author), Henry Ford Hlth Syst, Div Pulm & Crit Care Med, 2799 W Grand Blvd, Detroit, MI 48202 USA.
EM pkvale1@hfhs.org; cjohnso1@hfhs.org; martin.tammemagi@brocku.ca;
marcusp@mail.nih.gov; zylak@rad.hfh.edu; davidl@rad.hfh.edu;
hocking.william@marshfieldclinic.org; travelermmo@yahoo.com;
comminsj@imsweb.com; lawrenceragard@westat.com; pingh@mail.nih.gov;
bergc@mail.nih.gov; prorokp@mail.nih.gov
FU Division of Cancer Prevention, National Cancer Institute [N01-CN-25476,
N01-CN-25512, N01-CN-25518, N01-CN-25513, N01-CN-25511, N01-CN-25514,
N01-CN-25515, N01-CN-25516, N01-CN-25522, N01-CN-25524, N01-CN-75022]
FX This work was supported by contracts from the Division of Cancer
Prevention, National Cancer Institute, to the 10 screening centers and
to the coordinating center (N01-CN-25476, to Westat; N01-CN-25512, to
Henry Ford Health System; N01-CN-25518, to Marshfield Clinic Research
Foundation; N01-CN-25513, to the University of Minnesota School of
Public Health; N01-CN-25511, to the University of Pittsburgh Cancer
Institute; N01-CN-25514, to the University of Colorado; N01-CN-25515, to
Pacific Health Research and Education Institute; N01-CN-25516, to
Washington University; N01-CN-25522, to Georgetown University Medical
Center; N01-CN-25524, to the University of Utah; and N01-CN-75022, to
the University of Alabama at Birmingham).
NR 16
TC 0
Z9 0
U1 0
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
EI 1872-8332
J9 LUNG CANCER
JI Lung Cancer
PD OCT
PY 2014
VL 86
IS 1
BP 41
EP 46
DI 10.1016/j.lungcan.2014.07.013
PG 6
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AR2CK
UT WOS:000343391000007
PM 25123333
ER
PT J
AU Duan, Q
Duyn, JH
Gudino, N
de Zwart, JA
van Gelderen, P
Sodickson, DK
Brown, R
AF Duan, Qi
Duyn, Jeff H.
Gudino, Natalia
de Zwart, Jacco A.
van Gelderen, Peter
Sodickson, Daniel K.
Brown, Ryan
TI Characterization of a dielectric phantom for high-field magnetic
resonance imaging applications
SO MEDICAL PHYSICS
LA English
DT Article
DE high-field MRI; wavelength effects
ID TISSUE-MIMICKING PHANTOM; BIOLOGICAL TISSUES; RANGE; TRANSMIT; DESIGN;
GHZ
AB Purpose: In this work, a generic recipe for an inexpensive and nontoxic phantom was developed within a range of biologically relevant dielectric properties from 150 MHz to 4.5 GHz.
Methods: The recipe includes deionized water as the solvent, NaCl to primarily control conductivity, sucrose to primarily control permittivity, agar-agar to gel the solution and reduce heat diffusivity, and benzoic acid to preserve the gel. Two hundred and seventeen samples were prepared to cover the feasible range of NaCl and sucrose concentrations. Their dielectric properties were measured using a commercial dielectric probe and were fitted to a 3D polynomial to generate a recipe describing the properties as a function of NaCl concentration, sucrose concentration, and frequency.
Results: Results indicated that the intuitive linear and independent relationships between NaCl and conductivity and between sucrose and permittivity are not valid. A generic polynomial recipe was developed to characterize the complex relationship between the solutes and the resulting dielectric values and has been made publicly available as a web application. In representative mixtures developed to mimic brain and muscle tissue, less than 2% difference was observed between the predicted and measured conductivity and permittivity values.
Conclusions: It is expected that the recipe will be useful for generating dielectric phantoms for general magnetic resonance imaging (MRI) coil development at high magnetic field strength, including coil safety evaluation as well as pulse sequence evaluation (including B-1(+) mapping, B-1(+) shimming, and selective excitation pulse design), and other non-MRI applications which require biologically equivalent dielectric properties. (C) 2014 American Association of Physicists in Medicine.
C1 [Duan, Qi; Duyn, Jeff H.; Gudino, Natalia; de Zwart, Jacco A.; van Gelderen, Peter] NINDS, Adv MRI Sect, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
[Sodickson, Daniel K.; Brown, Ryan] NYU, Sch Med, Bernard & Irene Schwartz Ctr Biomed Imaging, Dept Radiol, New York, NY 10016 USA.
RP Duan, Q (reprint author), NINDS, Adv MRI Sect, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
EM Qi.Duan@nih.gov
RI Duan, Qi/J-7916-2016;
OI Duan, Qi/0000-0002-2407-6611; Sodickson, Daniel/0000-0002-2436-4664;
Brown, Ryan/0000-0002-2683-712X
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke; NIH [R01 EB002568]
FX This research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke and NIH R01
EB002568.
NR 28
TC 8
Z9 8
U1 1
U2 8
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
EI 2473-4209
J9 MED PHYS
JI Med. Phys.
PD OCT
PY 2014
VL 41
IS 10
AR 102303
DI 10.1118/1.4895823
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AQ7XF
UT WOS:000343032400037
PM 25281973
ER
PT J
AU Lee, YL
Sante, J
Comerci, CJ
Cyge, B
Menezes, LF
Li, FQ
Germino, GG
Moerner, WE
Takemaru, KI
Stearns, T
AF Lee, Yin Loon
Sante, Joshua
Comerci, Colin J.
Cyge, Benjamin
Menezes, Luis F.
Li, Feng-Qian
Germino, Gregory G.
Moerner, W. E.
Takemaru, Ken-Ichi
Stearns, Tim
TI Cby1 promotes Ahi1 recruitment to a ring-shaped domain at the
centriole-cilium interface and facilitates proper cilium formation and
function
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID CILIARY TRANSITION ZONE; JOUBERT-SYNDROME; FLUORESCENCE MICROSCOPY;
PERICENTRIOLAR MATERIAL; EPITHELIAL-CELLS; STED MICROSCOPY; CYSTIC
KIDNEY; DISEASE GENE; I SYNDROME; PROTEIN
AB Defects in centrosome and cilium function are associated with phenotypically related syndromes called ciliopathies. Cby1, the mammalian orthologue of the Drosophila Chibby protein, localizes to mature centrioles, is important for ciliogenesis in multiciliated airway epithelia in mice, and antagonizes canonical Wnt signaling via direct regulation of beta-catenin. We report that deletion of the mouse Cby1 gene results in cystic kidneys, a phenotype common to ciliopathies, and that Cby1 facilitates the formation of primary cilia and ciliary recruitment of the Joubert syndrome protein Arl13b. Localization of Cby1 to the distal end of mature centrioles depends on the centriole protein Ofd1. Superresolution microscopy using both three-dimensional SIM and STED reveals that Cby1 localizes to an similar to 250-nm ring at the distal end of the mature centriole, in close proximity to Ofd1 and Ahi1, a component of the transition zone between centriole and cilium. The amount of centriole-localized Ahi1, but not Ofd1, is reduced in Cby1(-/-) cells. This suggests that Cby1 is required for efficient recruitment of Ahi1, providing a possible molecular mechanism for the ciliogenesis defect in Cby1(-/-) cells.
C1 [Lee, Yin Loon; Sante, Joshua; Stearns, Tim] Stanford Univ, Stanford Sch Med, Dept Biol, Stanford, CA 94305 USA.
[Comerci, Colin J.; Moerner, W. E.] Stanford Univ, Stanford Sch Med, Dept Chem, Stanford, CA 94305 USA.
[Stearns, Tim] Stanford Univ, Stanford Sch Med, Dept Genet, Stanford, CA 94305 USA.
[Cyge, Benjamin; Li, Feng-Qian; Takemaru, Ken-Ichi] SUNY Stony Brook, Dept Pharmacol Sci, Stony Brook, NY 11794 USA.
[Menezes, Luis F.; Germino, Gregory G.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Stearns, T (reprint author), Stanford Univ, Stanford Sch Med, Dept Biol, Stanford, CA 94305 USA.
EM stearns@stanford.edu
RI Menezes, Luis Fernando/C-7286-2015; Lee, Yin Loon/F-9616-2012
OI Lee, Yin Loon/0000-0003-0681-2993
FU National Institutes of Health Grants [R01GM52022, R01HL107493,
R01GM086196]; Intramural Program of the National Institute of Diabetes
and Digestive and Kidney Diseases [ZIA DK075042]; Singapore Agency for
Science, Technology and Research; National Science Foundation Graduate
Fellowship; National Center for Research Resources [1S10OD01227601]
FX We thank Daniel Van de Mark and Christian Hoerner for critical reading
of the manuscript, Christian Hoerner for generating pTS3517, Johanna
Schaub for recombinant LIF, Jeremy Reiter (University of California, San
Francisco, San Francisco, CA) for the gift of Ofd1+/+ and
Ofd1-/- ES cells, and Cheryl M. Craft (Mary D. Allen
Laboratory for Vision Research, Doheny Eye Institute, University of
Southern California, Los Angeles, CA), Brian Dynlacht (New York
University, New York, NY), and Jeremy Reiter (University of California,
San Francisco) for gifts of antibodies. This work was supported in part
by National Institutes of Health Grants R01GM52022 (T.S.), R01HL107493
(K.T.), and R01GM086196 (W.E.M.), the Intramural Program of the National
Institute of Diabetes and Digestive and Kidney Diseases (ZIA DK075042;
G.G.G.), a graduate fellowship from the Singapore Agency for Science,
Technology and Research (Y.L.L.), and a National Science Foundation
Graduate Fellowship (C.J.C.). The 3D-SIM superresolution experiments
were supported, in part, by Award 1S10OD01227601 from the National
Center for Research Resources.
NR 74
TC 13
Z9 13
U1 0
U2 6
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD OCT 1
PY 2014
VL 25
IS 19
BP 2919
EP 2933
DI 10.1091/mbc.E14-02-0735
PG 15
WC Cell Biology
SC Cell Biology
GA AQ8XV
UT WOS:000343124100004
PM 25103236
ER
PT J
AU Kannan, R
Kuzina, I
Wincovitch, S
Nowotarski, SH
Giniger, E
AF Kannan, Ramakrishnan
Kuzina, Irina
Wincovitch, Stephen
Nowotarski, Stephanie H.
Giniger, Edward
TI The Abl/Enabled signaling pathway regulates Golgi architecture in
Drosophila photoreceptor neurons
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID ABELSON TYROSINE KINASE; MOTOR AXON GUIDANCE; ACTIN CYTOSKELETON;
SECRETORY PATHWAY; EPITHELIAL MORPHOGENESIS; CISTERNAL MATURATION;
MEMBRANE SYSTEM; ABL; RECEPTOR; DYNAMICS
AB The Golgi apparatus is optimized separately in different tissues for efficient protein trafficking, but we know little of how cell signaling shapes this organelle. We now find that the Abl tyrosine kinase signaling pathway controls the architecture of the Golgi complex in Drosophila photoreceptor (PR) neurons. The Abl effector, Enabled (Ena), selectively labels the cis-Golgi in developing PRs. Overexpression or loss of function of Ena increases the number of cis- and trans-Golgi cisternae per cell, and Ena overexpression also redistributes Golgi to the most basal portion of the cell soma. Loss of Abl or its upstream regulator, the adaptor protein Disabled, lead to the same alterations of Golgi as does overexpression of Ena. The increase in Golgi number in Abl mutants arises in part from increased frequency of Golgi fission events and a decrease in fusions, as revealed by live imaging. Finally, we demonstrate that the effects of Abl signaling on Golgi are mediated via regulation of the actin cytoskeleton. Together, these data reveal a direct link between cell signaling and Golgi architecture. Moreover, they raise the possibility that some of the effects of Abl signaling may arise, in part, from alterations of protein trafficking and secretion.
C1 [Kannan, Ramakrishnan; Kuzina, Irina; Giniger, Edward] NINDS, Basic Neurosci Program, Axon Guidance & Neural Connect Unit, Bethesda, MD 20892 USA.
[Wincovitch, Stephen] NHGRI, Cytogenet & Microscopy Core, NIH, Bethesda, MD 20892 USA.
[Nowotarski, Stephanie H.] Univ N Carolina, Dept Biol, Chapel Hill, NC 27599 USA.
RP Giniger, E (reprint author), NINDS, Basic Neurosci Program, Axon Guidance & Neural Connect Unit, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM ginigere@ninds.nih.gov
RI Giniger, Edward/C-1764-2015
OI Giniger, Edward/0000-0002-8340-6158
FU Basic Neuroscience Program of the National Institute of Neurological
Disorders and Stroke Intramural Research Program, National Institutes of
Health [Z01-NS003013]; National Institutes of Health [GM47857];
intramural program of the National Human Genome Research Institute
FX We thank all the members of our lab for many helpful discussions during
the course of this work. We are also grateful to Chi-Hon Lee and
Chun-Yuan Ting for their help with analysis of photoreceptor
development. For comments on the manuscript, we are grateful to Craig
Blackstone, Frank Gertler, and Mark Peifer. Antibodies and fly stocks
were generously provided by Donald Ready for anti-Rab11, Bing Ye
(University of Michigan, Ann Arbor, MI) for Golgi markers, and William
Trimble for anti-dSyx-16. We gratefully acknowledge the excellent
technical assistance of Joy Gu in preparing samples for immuno-electron
microscopy and also of Carolyn Smith (National Institute of Neurological
Disorders and Stroke Light Imaging Facility) and Susan Cheng and
Virginia Crocker (National Institute of Neurological Disorders and
Stroke Electron Microscopy Facility). These experiments were supported
by the Basic Neuroscience Program of the National Institute of
Neurological Disorders and Stroke Intramural Research Program, National
Institutes of Health, Grant Z01-NS003013 to E.G. S.H.N. was supported by
National Institutes of Health Grant GM47857 to Mark Peifer. S.W. was
supported by the intramural program of the National Human Genome
Research Institute.
NR 71
TC 4
Z9 4
U1 1
U2 6
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD OCT 1
PY 2014
VL 25
IS 19
BP 2993
EP 3005
DI 10.1091/mbc.E14-02-0729
PG 13
WC Cell Biology
SC Cell Biology
GA AQ8XV
UT WOS:000343124100010
PM 25103244
ER
PT J
AU An, E
Narayanan, M
Manes, NP
Nita-Lazar, A
AF An, Eunkyung
Narayanan, Manikandan
Manes, Nathan P.
Nita-Lazar, Aleksandra
TI Characterization of Functional Reprogramming during Osteoclast
Development Using Quantitative Proteomics and mRNA Profiling
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID DEPENDENT ANION CHANNEL; GENE-EXPRESSION DATA; TANDEM MASS-SPECTRA;
CELL-DEATH; BONE-RESORPTION; C-JUN; DIFFERENTIATION FACTOR; MACROPHAGE
ACTIVATION; PROTON PUMP; PROTEIN
AB In addition to forming macrophages and dendritic cells, monocytes in adult peripheral blood retain the ability to develop into osteoclasts, mature bone-resorbing cells. The extensive morphological and functional transformations that occur during osteoclast differentiation require substantial reprogramming of gene and protein expression. Here we employ -omic-scale technologies to examine in detail the molecular changes at discrete developmental stages in this process (precursor cells, intermediate osteoclasts, and multinuclear osteoclasts), quantitatively comparing their transcriptomes and proteomes. The data have been deposited to the ProteomeXchange with identifier PXD000471. Our analysis identified mitochondrial changes, along with several alterations in signaling pathways, as central to the development of mature osteoclasts, while also confirming changes in pathways previously implicated in osteoclast biology. In particular, changes in the expression of proteins involved in metabolism and redirection of energy flow from basic cellular function toward bone resorption appeared to play a key role in the switch from monocytic immune system function to specialized bone-turnover function. These findings provide new insight into the differentiation program involved in the generation of functional osteoclasts.
C1 [An, Eunkyung; Narayanan, Manikandan; Manes, Nathan P.; Nita-Lazar, Aleksandra] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
RP Nita-Lazar, A (reprint author), NIAID, Cellular Networks Prote Unit, Lab Syst Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM nitalazarau@niaid.nih.gov
RI Manes, Nathan/E-2817-2012
OI Manes, Nathan/0000-0001-6701-3314
FU NIAID, National Institutes of Health
FX This research was supported by the Intramural Research Program of NIAID,
National Institutes of Health.
NR 94
TC 5
Z9 5
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD OCT
PY 2014
VL 13
IS 10
BP 2687
EP 2704
DI 10.1074/mcp.M113.034371
PG 18
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA AR0BK
UT WOS:000343228300013
PM 25044017
ER
PT J
AU Schwarz, A
Tenzer, S
Hackenberg, M
Erhart, J
Gerhold-Ay, A
Mazur, J
Kuharev, J
Ribeiro, JMC
Kotsyfakis, M
AF Schwarz, Alexandra
Tenzer, Stefan
Hackenberg, Michael
Erhart, Jan
Gerhold-Ay, Aslihan
Mazur, Johanna
Kuharev, Joerg
Ribeiro, Jose M. C.
Kotsyfakis, Michail
TI A Systems Level Analysis Reveals Transcriptomic and Proteomic Complexity
in Ixodes Ricinus Midgut and Salivary Glands During Early Attachment and
Feeding
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID NEXT-GENERATION; TICKS; TRANSMISSION; PROTEINS; EUROPE; ABYSS
AB Although pathogens are usually transmitted within the first 24-48 h of attachment of the castor bean tick Ixodes ricinus, little is known about the tick's biological responses at these earliest phases of attachment. Tick midgut and salivary glands are the main tissues involved in tick blood feeding and pathogen transmission but the limited genomic information for I. ricinus delays the application of high-throughput methods to study their physiology. We took advantage of the latest advances in the fields of Next Generation RNA-Sequencing and Label-free Quantitative Proteomics to deliver an unprecedented, quantitative description of the gene expression dynamics in the midgut and salivary glands of this disease vector upon attachment to the vertebrate host. A total of 373 of 1510 identified proteins had higher expression in the salivary glands, but only 110 had correspondingly high transcript levels in the same tissue. Furthermore, there was midgut-specific expression of 217 genes at both the transcriptome and proteome level. Tissue-dependent transcript, but not protein, accumulation was revealed for 552 of 885 genes. Moreover, we discovered the enrichment of tick salivary glands in proteins involved in gene transcription and translation, which agrees with the secretory role of this tissue; this finding also agrees with our finding of lower tick t-RNA representation in the salivary glands when compared with the midgut. The midgut, in turn, is enriched in metabolic components and proteins that support its mechanical integrity in order to accommodate and metabolize the ingested blood. Beyond understanding the physiological events that support hematophagy by arthropod ectoparasites, we discovered more than 1500 proteins located at the interface between ticks, the vertebrate host, and the tick-borne pathogens. Thus, our work significantly improves the knowledge of the genetics underlying the transmission lifecycle of this tick species, which is an essential step for developing alternative methods to better control tick-borne diseases.
C1 [Schwarz, Alexandra; Erhart, Jan; Kotsyfakis, Michail] Acad Sci Czech Republic, Ctr Biol, Budweis 37005, Czech Republic.
[Tenzer, Stefan; Kuharev, Joerg] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Immunol, D-55131 Mainz, Germany.
[Hackenberg, Michael] Univ Granada, Computat Genom & Bioinformat Grp, Dept Genet, E-18071 Granada, Spain.
[Gerhold-Ay, Aslihan; Mazur, Johanna] Johannes Gutenberg Univ Mainz, Univ Med Ctr, IMBEI, D-55131 Mainz, Germany.
[Ribeiro, Jose M. C.] NIAID, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
RP Kotsyfakis, M (reprint author), Acad Sci Czech Republic, Ctr Biol, Budweis 37005, Czech Republic.
EM mich_kotsyfakis@yahoo.com
RI Hackenberg, Michael/A-2503-2009; Kotsyfakis, Michail/G-9525-2014;
OI Hackenberg, Michael/0000-0003-2248-3114; Kotsyfakis,
Michail/0000-0002-7526-1876; Tenzer, Stefan/0000-0003-3034-0017;
Ribeiro, Jose/0000-0002-9107-0818
FU Grant Agency of the Czech Republic (GACR) [P502/12/2409]; Academy of
Sciences of the Czech Republic [Z60220518]; European Union (EU)
[PIRG07-GA-2010-268177]; European Union
[FP7-INFRASTRUCTURES-2008-228403]; Alexander von Humboldt Foundation;
Forschungszentrum Immunologie (FZI); Naturwissenschaftlich-Medizinische
Forschungszentrum (NMFZ) of the Johannes Gutenberg University Mainz;
Academy of Sciences of the Czech Republic; European Molecular Biology
Organization (EMBO, ASTF) [482-2012]; Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This work was supported by the Grant Agency of the Czech Republic (GACR
grant P502/12/2409 to MK), by the Academy of Sciences of the Czech
Republic (grant no. Z60220518 to Biology Center), and by the 7th
Framework Program of the European Union (EU FP7; Marie Curie
Reintegration grant PIRG07-GA-2010-268177 to MK). Library constructions
and Illumina sequencing of all the samples were supported by the
European Union, 7th Framework Programm, project TRANSVAC
(FP7-INFRASTRUCTURES-2008-228403 to MK). This publication reflects only
the authors' views and the European Union is not liable for any use that
maybe made of the information contained herein. This works was supported
by the Alexander von Humboldt Foundation (Feodor Lynen Research
Fellowship to AS) and by the Forschungszentrum Immunologie (FZI) and the
Naturwissenschaftlich-Medizinische Forschungszentrum (NMFZ) of the
Johannes Gutenberg University Mainz (support to ST). This work was
supported by the Academy of Sciences of the Czech Republic (Jan
Evangelista Purkyne Fellowship to MK) and from the European Molecular
Biology Organization (EMBO Short Term Fellowship, ASTF number 482-2012
to MK). This work was supported by the Intramural Research Program of
the Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health where JMCR is an
employee. Because JMCR is a government employee and this is a government
work, the work is in the public domain in the United States.
Notwithstanding any other agreements, the National Institutes of Health
reserves the right to provide the work to PubMedCentral for display and
use by the public, and PubMedCentral may tag or modify the work
consistent with its customary practices. Rights can be established
outside the United States subject to a government use license.
NR 29
TC 23
Z9 23
U1 5
U2 17
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD OCT
PY 2014
VL 13
IS 10
BP 2725
EP 2735
DI 10.1074/mcp.M114.039289
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA AR0BK
UT WOS:000343228300015
PM 25048707
ER
PT J
AU Afonin, KA
Viard, M
Koyfman, AY
Martins, AN
Kasprzak, WK
Panigaj, M
Desai, R
Santhanam, A
Grabow, WW
Jaeger, L
Heldman, E
Reiser, J
Chiu, W
Freed, EO
Shapiro, BA
AF Afonin, Kirill A.
Viard, Mathias
Koyfman, Alexey Y.
Martins, Angelica N.
Kasprzak, Wojciech K.
Panigaj, Martin
Desai, Ravi
Santhanam, Arti
Grabow, Wade W.
Jaeger, Luc
Heldman, Eliahu
Reiser, Jakob
Chiu, Wah
Freed, Eric O.
Shapiro, Bruce A.
TI Multifunctional RNA Nanoparticles
SO NANO LETTERS
LA English
DT Article
DE RNA nanotechnology; RNA nanoparticles; RNA interference; aptamers;
RNA-DNA hybrid reassociation
ID MALACHITE GREEN APTAMER; IN-SILICO; THERAPEUTIC APPLICATIONS; SPLIT
FUNCTIONALITIES; EMERGING FIELD; DNA HYBRIDS; DESIGN; NANOTECHNOLOGY;
DELIVERY; INTERFERENCE
AB Our recent advancements in RNA nanotechnology introduced novel nanoscaffolds (nanorings); however, the potential of their use for biomedical applications was never fully revealed. As presented here, besides functionalization with multiple different short interfering RNAs for combinatorial RNA interference (e.g., against multiple HIV-1 genes), nanorings also allow simultaneous embedment of assorted RNA aptamers, fluorescent dyes, proteins, as well as recently developed RNADNA hybrids aimed to conditionally activate multiple split functionalities inside cells.
C1 [Afonin, Kirill A.; Viard, Mathias; Desai, Ravi; Santhanam, Arti; Shapiro, Bruce A.] NCI, Basic Res Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Viard, Mathias; Kasprzak, Wojciech K.; Heldman, Eliahu] NCI, Basic Sci Program, Leidos Biomed Res Inc, Ctr Canc Res,Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Koyfman, Alexey Y.; Chiu, Wah] Baylor Coll Med, Natl Ctr Macromol Imaging, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA.
[Martins, Angelica N.; Freed, Eric O.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Panigaj, Martin; Reiser, Jakob] US FDA, Ctr Biol Evaluat & Res, Off Cellular Tissue & Gene Therapies, Silver Spring, MD 20993 USA.
[Grabow, Wade W.] Seattle Pacific Univ, Dept Chem, Seattle, WA 98119 USA.
[Jaeger, Luc] Univ Calif Santa Barbara, Dept Chem & Biochem, Biomol Sci & Engn Program, Santa Barbara, CA 93106 USA.
RP Shapiro, BA (reprint author), NCI, Basic Res Lab, Ctr Canc Res, Frederick, MD 21702 USA.
EM shapirbr@mail.nih.gov
RI Panigaj, Martin/G-6492-2013
FU NIH, Center for Cancer Research, NCI-Frederick; Frederick National
Laboratory for Cancer Research, National Institutes of Health
[HHSN261200800001E]; National Institutes of Health [P41GM103832, P50
GM1003297]; Postdoctoral Training Fellowship from the Keck Center
Computational Cancer Biology Training Program of the Gulf Coast
Consortia (CPRIT) [RP101489]; NIH [R01GM-079604]; U.S. Department of
Energy; U.S. Food and Drug Administration
FX We thank Faye M. Walker for her assistance at early stages of this
project. We thank the Pathology Histology Lab of Leidos Biomedical
Research, Inc. at the Frederick National Laboratory for Cancer Research
for help with ex vivo imaging. We thank Patricia S. Steeg at the
National Cancer Institute for providing GFP expressing cells for the in
vivo experiments. We thank Andrew Anderson for technical assistance
during electron microscopy reconstruction. This research was supported
[in part] by the Intramural Research Program of the NIH, Center for
Cancer Research, NCI-Frederick. This work has been funded in whole or in
part with Federal funds from the Frederick National Laboratory for
Cancer Research, National Institutes of Health, under contract no.
HHSN261200800001E. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U.S. Government. This research
was supported in part by the National Institutes of Health P41GM103832
and P50 GM1003297 (to W.C.) and the Postdoctoral Training Fellowship
from the Keck Center Computational Cancer Biology Training Program of
the Gulf Coast Consortia to A.Y.K. (CPRIT grant no. RP101489). This
research was also supported by NIH grant no. R01GM-079604 (to L.J.).
M.P. is supported in part by an appointment to the Research
Participation Program at the Center for Biologics Evaluation and
Research administered by the Oak Ridge Institute for Science and
Education through an inter agency agreement between the U.S. Department
of Energy and the U.S. Food and Drug Administration.
NR 64
TC 31
Z9 31
U1 5
U2 51
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1530-6984
EI 1530-6992
J9 NANO LETT
JI Nano Lett.
PD OCT
PY 2014
VL 14
IS 10
BP 5662
EP 5671
DI 10.1021/nl502385k
PG 10
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
Physics, Condensed Matter
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA AQ7RH
UT WOS:000343016400029
PM 25267559
ER
PT J
AU Dobrovolskaia, MA
Neun, BW
Man, S
Ye, XY
Hansen, M
Patri, AK
Crist, RM
McNeil, SE
AF Dobrovolskaia, Marina A.
Neun, Barry W.
Man, Sonny
Ye, Xiaoying
Hansen, Matthew
Patri, Anil K.
Crist, Rachael M.
McNeil, Scott E.
TI Protein corona composition does not accurately predict
hematocompatibility of colloidal gold nanoparticles
SO NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE
LA English
DT Article
DE Nanoparticles; Protein corona; Complement; Coagulation;
Hematocompatibility
ID SOLID LIPID NANOPARTICLES; PLASMA-PROTEINS; ADSORPTION-KINETICS; CARBON
NANOTUBES; DRUG-DELIVERY; FIBRINOGEN; BINDING; BIODISTRIBUTION;
ACTIVATION; RECEPTOR
AB Proteins bound to nanoparticle surfaces are known to affect particle clearance by influencing immune cell uptake and distribution to the organs of the mononuclear phagocytic system. The composition of the protein corona has been described for several types of nanomaterials, but the role of the corona in nanoparticle biocompatibility is not well established. In this study we investigate the role of nanoparticle surface properties (PEGylation) and incubation times on the protein coronas of colloidal gold nanoparticles. While neither incubation time nor PEG molecular weight affected the specific proteins in the protein corona, the total amount of protein binding was governed by the molecular weight of PEG coating. Furthermore, the composition of the protein corona did not correlate with nanoparticle hematocompatibility. Specialized hematological tests should be used to deduce nanoparticle hematotoxicity.
From the Clinical Editor: It is overall unclear how the protein corona associated with colloidal gold nanoparticles may influence hematotoxicity. This study warns that PEGylation itself may be insufficient, because composition of the protein corona does not directly correlate with nanoparticle hematocompatibility. The authors suggest that specialized hematological tests must be used to deduce nanoparticle hematotoxicity. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Dobrovolskaia, Marina A.; Neun, Barry W.; Man, Sonny; Hansen, Matthew; Patri, Anil K.; Crist, Rachael M.; McNeil, Scott E.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Nanotechnol Characterizat Lab, Frederick, MD USA.
[Ye, Xiaoying] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Lab Prote & Analyt Technol, Canc Res Technol Program, Frederick, MD USA.
RP Dobrovolskaia, MA (reprint author), Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Nanotechnol Characterizat Lab, Frederick, MD USA.
EM marina@mail.nih.gov
RI Nanotechnology Characterization Lab, NCL/K-8454-2012; Crist,
Rachael/K-7603-2012
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX The study was supported in whole or in part by federal funds from the
National Cancer Institute, National Institutes of Health, under contract
HHSN261200800001E. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U.S. Government.
NR 40
TC 35
Z9 36
U1 8
U2 56
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1549-9634
EI 1549-9642
J9 NANOMED-NANOTECHNOL
JI Nanomed.-Nanotechnol. Biol. Med.
PD OCT
PY 2014
VL 10
IS 7
BP 1453
EP 1463
DI 10.1016/j.nano.2014.01.009
PG 11
WC Nanoscience & Nanotechnology; Medicine, Research & Experimental
SC Science & Technology - Other Topics; Research & Experimental Medicine
GA AR1AU
UT WOS:000343312100010
PM 24512761
ER
PT J
AU Jardine, D
Emond, M
Meert, KL
Harrison, R
Carcillo, JA
Anand, KJS
Berger, J
Newth, CJL
Willson, DF
Nicholson, C
Dean, JM
Zimmerman, JJ
AF Jardine, David
Emond, Mary
Meert, Kathleen L.
Harrison, Rick
Carcillo, Joseph A.
Anand, Kanwaljeet J. S.
Berger, John
Newth, Christopher J. L.
Willson, Douglas F.
Nicholson, Carol
Dean, J. Michael
Zimmerman, Jerry J.
CA Eunice Kennedy Shriver Natl Inst
TI A Single Nucleotide Polymorphism in the Corticotropin Receptor Gene Is
Associated With a Blunted Cortisol Response During Pediatric Critical
Illness
SO PEDIATRIC CRITICAL CARE MEDICINE
LA English
DT Article
DE adrenocorticotropin hormone (corticotropin, ACTH) receptor; critical
illness; Pediatric Risk of Mortality III; serum free cortisol; single
nucleotide polymorphism; single nucleotide variant; stress response
ID 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; PITUITARY-ADRENAL AXIS;
SEPTIC SHOCK; ACTH RECEPTOR; PROMOTER POLYMORPHISM; CORTICOSTEROID
TREATMENT; INFANTILE SPASMS; STRESS-RESPONSE; SEVERE SEPSIS; ILL
PATIENTS
AB Objectives: The cortisol response during critical illness varies widely among patients. Our objective was to examine single nucleotide polymorphisms in candidate genes regulating cortisol synthesis, metabolism, and activity to determine if genetic differences were associated with variability in the cortisol response among critically ill children.
Design: This was a prospective observational study employing tag single nucleotide polymorphism methodology to examine genetic contributions to the variability of the cortisol response in critical illness. Thirty-one candidate genes and 31 ancestry markers were examined.
Setting: Patients were enrolled from seven pediatric critical care units that constitute the Eunice Kennedy Shriver Collaborative Pediatric Critical Care Research Network.
Subjects: Critically ill children (n = 92), age 40 weeks gestation to 18 years old, were enrolled.
Interventions: Blood samples were obtained from all patients for serum cortisol measurements and DNA isolation. Demographic and illness severity data were collected.
Measurements and Main Results: Single nucleotide polymorphisms were tested for association with serum free cortisol concentrations in context of higher illness severity as quantified by Pediatric Risk of Mortality III score greater than 7. A single nucleotide polymorphism (rs1941088) in the MC2R gene was strongly associated (p = 0.0005) with a low free cortisol response to critical illness. Patients with the AA genotype were over seven times more likely to have a low free cortisol response to critical illness than those with a GG genotype. Patients with the GA genotype exhibited an intermediate free cortisol response to critical illness.
Conclusions: The A allele at rs1941088 in the MC2R gene, which encodes the adrenocorticotropic hormone (corticotropin, ACTH) receptor, is associated with a low cortisol response in critically ill children. These data provide evidence for a genetic basis for a portion of the variability in cortisol production during critical illness. Independent replication of these findings will be important and could facilitate development of personalized treatment for patients with a low cortisol response to severe illness.
C1 [Jardine, David] Univ Washington, Sch Med, Dept Anesthesiol, Seattle, WA 98195 USA.
[Emond, Mary] Univ Washington, Dept Biostat, Sch Med, Seattle, WA 98195 USA.
[Meert, Kathleen L.] Childrens Hosp Michigan, Dept Pediat, Detroit, MI 48201 USA.
[Harrison, Rick] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[Carcillo, Joseph A.] Childrens Hosp Pittsburgh, Dept Crit Care Med, Pittsburgh, PA 15213 USA.
[Anand, Kanwaljeet J. S.] Le Bonheur Childrens Hosp, Dept Pediat, Memphis, TN USA.
[Anand, Kanwaljeet J. S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Berger, John] Childrens Natl Med Ctr, Dept Pediat, Washington, DC 20010 USA.
[Newth, Christopher J. L.] Childrens Hosp Los Angeles, Dept Anesthesiol & Crit Care Med, Los Angeles, CA 90027 USA.
[Willson, Douglas F.] Univ Virginia, Dept Pediat, Childrens Hosp, Charlottesville, VA USA.
[Nicholson, Carol] NICHHD, Eunice Kennedy Shriver, Washington, DC USA.
[Dean, J. Michael] Univ Utah, Sch Med, Dept Pediat, Salt Lake City, UT USA.
[Zimmerman, Jerry J.] Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 USA.
RP Jardine, D (reprint author), Univ Washington, Sch Med, Dept Anesthesiol, Seattle, WA 98195 USA.
EM dsj@u.washington.edu
OI Jardine, David/0000-0001-9000-271X; Anand,
Kanwaljeet/0000-0001-6498-1483
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, Department of Health and Human Services [U10HD050096,
U10HD049981, U10HD500009, U10HD049945, U10HD049983, U10HD050012,
U01HD049934]; National Institutes of Health (NIH); NIH
[3U10HD049945-05S1, 1R01HD073362-01A1]; NIH; NICHD; NIH (CPCCRN); NICHD
- CPCCRN; Association of Pediatric Pulmonary Hypertension; NIH / NICHD
(Collaborative Pediatric Critical Care Research Network (CPCCRN);
Nellcor
FX This work was supported, in part, by cooperative agreements
(U10HD050096, U10HD049981, U10HD500009, U10HD049945, U10HD049983,
U10HD050012, and U01HD049934) from the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, Department of Health
and Human Services, as well as a Recovery Act Administrative Supplement
3U10HD049945-05S1.; Dr. Zimmerman served as board member for the Council
of the Society of Critical Care Money (reimbursement for travel); is
employed by the Seattle Children's Hospital, Children's University
Medical Group, and the University of Washington; received royalties from
Elsevier Publishing (Co-editor royalties for Pediatric Critical Care);
and received support for article research from the National Institutes
of Health (NIH). His institution received grant support from the NIH
3U10HD049945-05S1 and the NIH 1R01HD073362-01A1. Dr. Jardine received
support for article research from the NIH. His institution received
grant support, support for travel, and support for participation in
review activities. Dr. Emond received support for article research from
the NIH. Her institution received grant support. Dr. Meert received
support for article research from the NIH. Her institution received
grant support from the NICHD. Dr. Harrison received support for article
research from the NIH. His institution received grant support from the
NIH (CPCCRN grant). Dr. Carcillo received support for article research
from the NIH and disclosed other support from the NICHD - CPCCRN. His
institution received grant support and support for travel from the
NICHD. Dr. Anand consulted for AstraZeneca, received royalties from
Up-To-Date Website, received support for article research from the NIH,
and disclosed government work. His institution received grant support
and support for travel from the NICHD. Dr. Berger received support for
article research from the NIH. His institution received grant support
from the NIH and the Association of Pediatric Pulmonary Hypertension.
Dr. Newth consulted for Philips Medical and received support for article
research from the NIH. His institution received grant support from the
NIH / NICHD (Collaborative Pediatric Critical Care Research Network
(CPCCRN) and Nellcor. Dr. Nicholson disclosed government work and
received support for article research from the NIH (He was the Project
Scientist for the CPCCRN during the study, assisted in its design, and
implemented funding for the project). Dr. Dean received support for
article research from the NIH. His institution received grant support
from the NIH. Dr. Willson disclosed that he does not have any potential
conflicts of interest.
NR 39
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1529-7535
EI 1947-3893
J9 PEDIATR CRIT CARE ME
JI Pediatr. Crit. Care Med.
PD OCT
PY 2014
VL 15
IS 8
BP 698
EP 705
DI 10.1097/PCC.0000000000000193
PG 8
WC Critical Care Medicine; Pediatrics
SC General & Internal Medicine; Pediatrics
GA AQ8CD
UT WOS:000343049200006
PM 25055195
ER
PT J
AU Lederman, HM
Connolly, MA
Kalpatthi, R
Ware, RE
Wang, WC
Luchtman-Jones, L
Waclawiw, M
Goldsmith, JC
Swift, A
Casella, JF
AF Lederman, Howard M.
Connolly, Margaret A.
Kalpatthi, Ram
Ware, Russell E.
Wang, Winfred C.
Luchtman-Jones, Lori
Waclawiw, Myron
Goldsmith, Jonathan C.
Swift, Andrea
Casella, James F.
CA BABY HUG Investigators
TI Immunologic Effects of Hydroxyurea in Sickle Cell Anemia
SO PEDIATRICS
LA English
DT Article
DE sickle cell disease; hydroxyurea; immunology; vaccines
ID LYMPHOCYTE SUBSETS; BABY HUG; CHILDREN; VACCINATION; POLYSACCHARIDE;
ANTIBODIES; LEUKEMIA; DISEASE; TRIAL; INFECTIONS
AB BACKGROUND AND OBJECTIVE: Susceptibility to encapsulated bacteria is well known in sickle cell disease (SCD). Hydroxyurea use is common in adults and children with SCD, but little is known about hydroxyurea's effects on immune function in SCD. Because hydroxyurea inhibits ribonucleotide reductase, causing cell cycle arrest at the G1-S interface, we postulated that hydroxyurea might delay transition from naive to memory T cells, with inhibition of immunologic maturation and vaccine responses.
METHODS: T-cell subsets, naive and memory T cells, and antibody responses to pneumococcal and measles, mumps, and rubella vaccines were measured among participants in a multicenter, randomized, doubleblind, placebo-controlled trial of hydroxyurea in infants and young children with SCD (BABY HUG).
RESULTS: Compared with placebo, hydroxyurea treatment resulted in significantly lower total lymphocyte, CD4, and memory T-cell counts; however, these numbers were still within the range of historical healthy controls. Antibody responses to pneumococcal vaccination were not affected, but a delay in achieving protective measles antibody levels occurred in the hydroxyurea group. Antibody levels to measles, mumps, and rubella showed no differences between groups at exit, indicating that effective immunization can be achieved despite hydroxyurea use.
CONCLUSIONS: Hydroxyurea does not appear to have significant deleterious effects on the immune function of infants and children with SCD. Additional assessments of lymphocyte parameters of hydroxyurea-treated children may be warranted. No changes in current immunization schedules are recommended; however, for endemic disease or epidemics, adherence to accelerated immunization schedules for the measles, mumps, and rubella vaccine should be reinforced. Pediatrics 2014; 134: 686-695
C1 [Lederman, Howard M.; Swift, Andrea] Johns Hopkins Univ, Sch Med, Dept Pediat, Eudowood Div Allergy & Immunol, Baltimore, MD 21205 USA.
[Casella, James F.] Johns Hopkins Univ, Sch Med, Dept Pediat, Div Hematol, Baltimore, MD 21205 USA.
[Connolly, Margaret A.] Clin Trials & Surveys Corp, Owings Mills, MD USA.
[Kalpatthi, Ram] Childrens Mercy Hosp, Kansas City, MO 64108 USA.
[Ware, Russell E.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Wang, Winfred C.] St Jude Childrens Res Hosp, Dept Hematol, Memphis, TN 38105 USA.
[Luchtman-Jones, Lori] Childrens Natl Med Ctr, Dept Pediat, Div Hematol, Washington, DC 20010 USA.
[Waclawiw, Myron; Goldsmith, Jonathan C.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Casella, JF (reprint author), Dept Pediat, Div Hematol, Ross Res Bldg,Room 1125,720 Rutland Ave, Baltimore, MD 21205 USA.
EM jcasella@jhmi.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [P01-HD31921]; federal agencies and foundations
FX This research used data from Add Health, a program project directed by
Kathleen Mullan Harris and designed by J.Richard Udry, Peter S. Bearman,
and Kathleen Mullan Harris at the University of North Carolina at Chapel
Hill and funded by grant P01-HD31921 from the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, with
cooperative funding from 23 other federal agencies and foundations.
Special acknowledgment is due Ronald R. Rindfuss and Barbara Entwisle
for assistance in the original design. Information on how to obtain the
Add Health data files is available on the Add Health Web site
(http://www.cpc.unc.edu/addhealth). No direct support was received from
grant P01-HD31921 for the present analysis. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health. Dr Clark had full
access to all of the data in the study and takes responsibility for the
integrity of the data and the accuracy of the data analysis.
NR 26
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U1 1
U2 7
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2014
VL 134
IS 4
BP 686
EP 695
PG 10
WC Pediatrics
SC Pediatrics
GA AQ9CV
UT WOS:000343140500051
PM 25180279
ER
PT J
AU Muller, M
Sigurdsson, S
Kjartansson, O
Jonsson, PV
Garcia, M
von Bonsdorff, MB
Gunnarsdottir, I
Thorsdottir, I
Harris, TB
van Buchem, M
Gudnason, V
Launer, LJ
AF Muller, Majon
Sigurdsson, Sigurdur
Kjartansson, Olafur
Jonsson, Palmi V.
Garcia, Melissa
von Bonsdorff, Mikaela B.
Gunnarsdottir, Ingibjorg
Thorsdottir, Inga
Harris, Tamara B.
van Buchem, Mark
Gudnason, Vilmundur
Launer, Lenore J.
TI Birth Size and Brain Function 75 Years Later
SO PEDIATRICS
LA English
DT Article
DE birth size; education; brain atrophy; cognition; aging
ID WHITE-MATTER LESIONS; COGNITIVE FUNCTION; EARLY-LIFE;
GENERAL-POPULATION; HEAD CIRCUMFERENCE; COMMON VARIANTS; DISEASE; FETAL;
RISK; MATURATION
AB BACKGROUND: There are several lines of evidence pointing to fetal and other early origins of diseases of the aging brain, but there are no data directly addressing the hypotheses in an older population. We investigated the association of fetal size to late-age measures of brain structure and function in a large cohort of older men and women and explored the modifying effect of education on these associations.
METHODS: Within the AGES (Age Gene/Environment Susceptibility)Reykjavik population-based cohort (born between 1907 and 1935), archived birth records were abstracted for 1254 men and women who similar to 75 years later underwent an examination that included brain MRI and extensive cognitive assessment.
RESULTS: Adjustment for intracranial volume, demographic and medical history characteristics, and lower Ponderal index at birth (per kg/m(3)), an indicator of third-trimester fetal wasting, was significantly associated with smaller volumes of total brain and white matter; beta s (95% confidence intervals) were -1.0 (-1.9 to -0.0) and -0.5 (-1.0 to -0.0) mL. Furthermore, lower Ponderal index was associated with slower processing speed and reduced executive functioning but only in those with low education (beta [95% confidence interval]: -0.136 [-0.235 to -0.036] and -0.077 [-0.153 to -0.001]).
CONCLUSIONS: This first study of its kind provides clinical measures suggesting that smaller birth size, as an indicator of a suboptimal intrauterine environment, is associated with late-life alterations in brain tissue volume and function. In addition, it shows that the effects of a suboptimal intrauterine environment on late-life cognitive function were present only in those with lower educational levels.
C1 [Muller, Majon; Garcia, Melissa; von Bonsdorff, Mikaela B.; Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, Bethesda, MD 20892 USA.
[Muller, Majon] Leiden Univ, Med Ctr, Dept Gerontol & Geriatr, Leiden, Netherlands.
[van Buchem, Mark] Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
[Sigurdsson, Sigurdur; Kjartansson, Olafur; Jonsson, Palmi V.; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Kjartansson, Olafur] Landspitali Univ Hosp, Dept Neurol & Radiol, Reykjavik, Iceland.
[Jonsson, Palmi V.] Landspitali Univ Hosp, Dept Geriatr, Reykjavik, Iceland.
[Gunnarsdottir, Ingibjorg; Thorsdottir, Inga] Landspitali Univ Hosp, Unit Nutr Res, Reykjavik, Iceland.
[von Bonsdorff, Mikaela B.] Univ Jyvaskyla, Gerontol Res Ctr, Dept Hlth Sci, Jyvaskyla, Finland.
RP Launer, LJ (reprint author), NIA, Lab Epidemiol & Populat Sci, Suite 3C309,Gateway Bldg,7201 Wisconsin Ave, Bethesda, MD 20892 USA.
EM launerl@nia.nih.gov
RI Krammel, Vera/N-4826-2014; von Bonsdorff, Mikaela/A-5218-2015; Gudnason,
Vilmundur/K-6885-2015; Gunnarsdottir, Ingibjorg/L-9371-2015;
OI Krammel, Vera/0000-0002-8273-8396; von Bonsdorff,
Mikaela/0000-0001-8530-5230; Gudnason, Vilmundur/0000-0001-5696-0084;
Gunnarsdottir, Ingibjorg/0000-0001-9447-8627
FU National Institutes of Health [N01-AG-1-2100]; National Institutes of
Health (NIH)
FX This work was supported by a grant from the National Institutes of
Health (N01-AG-1-2100), with contributions from NINDS, NEI, NIDCD,
NHLBI, NIA Intramural Research Program, the Icelandic Heart Association
(Hjartavernd), and the Icelandic Parliament (the Althingi). Funded by
the National Institutes of Health (NIH).
NR 37
TC 10
Z9 10
U1 2
U2 6
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2014
VL 134
IS 4
BP 761
EP 770
DI 10.1542/peds.2014-1108
PG 10
WC Pediatrics
SC Pediatrics
GA AQ9CV
UT WOS:000343140500060
PM 25180277
ER
PT J
AU Farah, J
Sayah, R
Martinetti, F
Donadille, L
Lacoste, V
Herault, J
Delacroix, S
Nauraye, C
Vabre, I
Lee, C
Bolch, WE
Clairand, I
AF Farah, J.
Sayah, R.
Martinetti, F.
Donadille, L.
Lacoste, V.
Herault, J.
Delacroix, S.
Nauraye, C.
Vabre, I.
Lee, C.
Bolch, W. E.
Clairand, I.
TI SECONDARY NEUTRON DOSES IN PROTON THERAPY TREATMENTS OF OCULAR MELANOMA
AND CRANIOPHARYNGIOMA
SO RADIATION PROTECTION DOSIMETRY
LA English
DT Article
ID STRAY RADIATION; PROSTATE-CANCER; 2ND CANCER; RADIOTHERAPY; EQUIVALENT;
PHANTOMS; IRRADIATION; PATIENT; RISK
AB Monte Carlo simulations were used to assess secondary neutron doses received by patients treated with proton therapy for ocular melanoma and craniopharyngioma. MCNPX calculations of out-of-field doses were done for similar to 20 different organs considering realistic treatment plans and using computational phantoms representative of an adult male individual. Simulations showed higher secondary neutron doses for intracranial treatments, similar to 14 mGy to the salivary glands, when compared with ocular treatments, similar to 0.6 mGy to the non-treated eye. This secondary dose increase is mainly due to the higher proton beam energy (178 vs. 75 MeV) as well as to the impact of the different beam parameters (modulation, collimation, field size etc.). Moreover, when compared with published data, the assessed secondary neutron doses showed similar trends, but sometimes with sensitive differences. This confirms secondary neutrons to be directly dependent on beam energy, modulation technique, treatment configuration and methodology.
C1 [Farah, J.; Sayah, R.; Martinetti, F.; Donadille, L.; Lacoste, V.; Clairand, I.] IRSN, PRP HOM SDE, F-92262 Fontenay Aux Roses, France.
[Herault, J.] Ctr Antoine Lacassagne CAL Cyclotron Biomed, F-06200 Nice, France.
[Delacroix, S.; Nauraye, C.] Ctr Protontherapie Orsay ICPO, Inst Curie, F-91898 Orsay, France.
[Vabre, I.] Inst Phys Nucl, F-91406 Orsay, France.
[Lee, C.] NIH, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Bolch, W. E.] Univ Florida, Dept Nucl & Radiol Engn, Gainesville, FL 32611 USA.
[Bolch, W. E.] Univ Florida, Dept Biomed Engn, Gainesville, FL 32611 USA.
RP Farah, J (reprint author), IRSN, PRP HOM SDE, BP17, F-92262 Fontenay Aux Roses, France.
EM jad.farah@irsn.fr
RI Lee, Choonsik/C-9023-2015
OI Lee, Choonsik/0000-0003-4289-9870
NR 20
TC 2
Z9 2
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0144-8420
EI 1742-3406
J9 RADIAT PROT DOSIM
JI Radiat. Prot. Dosim.
PD OCT
PY 2014
VL 161
IS 1-4
BP 363
EP 367
DI 10.1093/rpd/nct283
PG 5
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA AQ8EV
UT WOS:000343057600078
PM 24222710
ER
PT J
AU Muallem, S
AF Muallem, Shmuel
TI CFTR does it again: control of insulin secretion
SO SCIENCE CHINA-LIFE SCIENCES
LA English
DT Editorial Material
C1 NIDCR, Epithelial Signaling & Transport Sect, NIH, Bethesda, MD 20892 USA.
RP Muallem, S (reprint author), NIDCR, Epithelial Signaling & Transport Sect, NIH, Bethesda, MD 20892 USA.
EM shmuel.muallem@nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SCIENCE PRESS
PI BEIJING
PA 16 DONGHUANGCHENGGEN NORTH ST, BEIJING 100717, PEOPLES R CHINA
SN 1674-7305
EI 1869-1889
J9 SCI CHINA LIFE SCI
JI Sci. China-Life Sci.
PD OCT
PY 2014
VL 57
IS 10
BP 1046
EP 1046
DI 10.1007/s11427-014-4741-z
PG 1
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AR1MC
UT WOS:000343348300016
PM 25216710
ER
PT J
AU Arnardottir, ES
Nikonova, EV
Shockley, KR
Podtelezhnikov, AA
Anafi, RC
Tanis, KQ
Maislin, G
Stone, DJ
Renger, JJ
Winrow, CJ
Pack, AI
AF Arnardottir, Erna S.
Nikonova, Elena V.
Shockley, Keith R.
Podtelezhnikov, Alexei A.
Anafi, Ron C.
Tanis, Keith Q.
Maislin, Greg
Stone, David J.
Renger, John J.
Winrow, Christopher J.
Pack, Allan I.
TI Blood-Gene Expression Reveals Reduced Circadian Rhythmicity in
Individuals Resistant to Sleep Deprivation
SO SLEEP
LA English
DT Article
DE sleep deprivation; gene expression; microarray analysis; circadian
rhythm; psychomotor vigilance test
ID SALIVARY ALPHA-AMYLASE; HUMAN PERIPHERAL-BLOOD; TRANSCRIPTIONAL
REPRESSOR; CLOCK GENES; PERFORMANCE; COMPONENTS; BIOMARKER; TISSUES;
VULNERABILITY; PREVALENCE
AB Study Objectives: To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation.
Design: Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake.
Setting: Sleep laboratory.
Participants: Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT.
Intervention: Thirty-eight hours of continuous wakefulness.
Measurements and Results: We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes.
Conclusion: Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity.
C1 [Arnardottir, Erna S.; Maislin, Greg; Pack, Allan I.] Univ Penn, Perelman Sch Med, Ctr Sleep & Circadian Neurobiol, Philadelphia, PA 19104 USA.
[Arnardottir, Erna S.; Maislin, Greg; Pack, Allan I.] Univ Penn, Perelman Sch Med, Dept Med, Div Sleep Med, Philadelphia, PA 19104 USA.
[Arnardottir, Erna S.] Landspitali Natl Univ Hosp, Dept Resp Med & Sleep, IS-108 Reykjavik, Iceland.
[Arnardottir, Erna S.; Anafi, Ron C.] Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.
[Nikonova, Elena V.; Podtelezhnikov, Alexei A.; Tanis, Keith Q.; Stone, David J.] Merck Res Labs, Dept Exploratory & Translat Sci, West Point, PA USA.
[Shockley, Keith R.] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Renger, John J.; Winrow, Christopher J.] Merck Res Labs, Dept Neurosci, West Point, PA USA.
RP Arnardottir, ES (reprint author), Landspitali Natl Univ Hosp, Dept Resp Med & Sleep E7, IS-108 Reykjavik, Iceland.
EM ernasif@landspitali.is
RI Winrow, Christopher/K-1864-2014
FU NIH [HL94307]; Eimskip Fund of the University of Iceland; Merck Research
Laboratories (Merck Co., Inc.); National Center for Research Resources
[UL1RR024134]; Intramural Research Program of the NIH, National
Institute of Environmental Health Sciences [ZIA ES103166-01]; ResMed
foundation
FX This work was supported by the NIH grant HL94307 and the Eimskip Fund of
the University of Iceland, Merck Research Laboratories (Merck & Co.,
Inc.) as well as by the National Center for Research Resources grant
UL1RR024134. This research was supported in part by the Intramural
Research Program of the NIH, National Institute of Environmental Health
Sciences (ZIA ES103166-01). The content is solely the responsibility of
the authors and does not necessarily represent the official views of the
National Center for Research Resources or the National Institutes of
Health. Dr. Arnardottir is a part-time consultant for Nox Medical
(Reykjavik, Iceland) and has received grant support from the ResMed
foundation as well as paid speaking engagement from ResMed, Sweden and
Pfizer, Iceland. Dr. Nikonova was employed by Merck & Co during the
study period. Drs. Podtelezhnikov, Tanis, Stone, Renger, and Winrow are
employees of Merck & Co. Drs. Tanis, Stone, Renger, and Winrow are also
shareholders of Merck & Co. Mr. Maislin is Principal Biostatistician of
Biomedical Statistical Consulting (BSC). The other authors have
indicated no financial conflicts of interest. The study was performed at
University of Pennsylvania Perelman School of Medicine, Philadelphia,
PA.
NR 62
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Z9 7
U1 2
U2 7
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
EI 1550-9109
J9 SLEEP
JI Sleep
PD OCT 1
PY 2014
VL 37
IS 10
BP 1589
EP U172
DI 10.5665/sleep.4064
PG 20
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ9EA
UT WOS:000343147400005
PM 25197809
ER
PT J
AU Muthusubramaniam, L
Zaitseva, T
Paukshto, M
Martin, G
Desai, T
AF Muthusubramaniam, Lalitha
Zaitseva, Tatiana
Paukshto, Michael
Martin, George
Desai, Tejal
TI Effect of Collagen Nanotopography on Keloid Fibroblast Proliferation and
Matrix Synthesis: Implications for Dermal Wound Healing
SO TISSUE ENGINEERING PART A
LA English
DT Article
ID HYPERTROPHIC SCAR; IN-VITRO; CELL-SHAPE; PHENOTYPE; TISSUE;
METALLOPROTEINASE; EXPRESSION; DEPOSITION; APOPTOSIS; TARGET
AB Keloids are locally exuberant dermal scars characterized by excessive fibroblast proliferation and matrix accumulation. Although treatment strategies include surgical removal and intralesional steroid injections, an effective regimen is yet to be established due to a high rate of recurrence. The regressing center and growing margin of the keloid have different collagen architecture and also differ in the rate of proliferation. To investigate whether proliferation is responsive to collagen topography, keloid, scar, and dermal fibroblasts were cultured on nanopatterned scaffolds varying in collagen fibril diameter and alignment-small and large diameter, aligned and random fibrils, and compared to cells grown on flat collagen-coated substrates, respectively. Cell morphology, proliferation, and expression of six genes related to proliferation (cyclin D1), phenotype (alpha-smooth muscle actin), and matrix synthesis (collagens I and III, and matrix metalloproteinase-1 and -2) were measured to evaluate cell response. Fibril alignment was shown to reduce proliferation and matrix synthesis in all three types of fibroblasts. Further, keloid cells were found to be most responsive to nanotopography.
C1 [Muthusubramaniam, Lalitha; Desai, Tejal] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, San Francisco, CA 94158 USA.
[Muthusubramaniam, Lalitha; Desai, Tejal] Univ Calif San Francisco, Joint Grad Grp Bioengn, Berkeley, CA USA.
[Zaitseva, Tatiana; Paukshto, Michael] Fibralign Corp, Sunnyvale, CA USA.
[Martin, George] NIH, Bethesda, MD 20892 USA.
RP Desai, T (reprint author), Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, Box 2520,Byers Hall Rm 203C, San Francisco, CA 94158 USA.
EM tejal.desai@ucsf.edu
FU NIH [5T32GM008155-26]
FX We would like to thank Dr. Russell for the kind gift of KF and SF used
in the study. We also thank Dr. Yuri Bobrov for AFM measurements, Dr.
Vuk Uskokovic for help with scanning electron microscopy measurements,
Dr. Kurt Thorn at the UCSF Nikon Imaging Center for assistance with
confocal microscopy, and Laura Walsh and Kristina Krebs for help with
qPCR. Funding for this work was provided by the NIH Training Grant
5T32GM008155-26.
NR 35
TC 8
Z9 8
U1 0
U2 9
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1937-3341
EI 1937-335X
J9 TISSUE ENG PT A
JI Tissue Eng. Part A
PD OCT 1
PY 2014
VL 20
IS 19-20
BP 2728
EP 2736
DI 10.1089/ten.tea.2013.0539
PG 9
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA AR0AS
UT WOS:000343225400019
PM 24724556
ER
PT J
AU Valent, P
Escribano, L
Broesby-Olsen, S
Hartmann, K
Grattan, C
Brockow, K
Niedoszytko, M
Nedoszytko, B
Elberink, JNGO
Kristensen, T
Butterfield, JH
Triggiani, M
Alvarez-Twose, I
Reiter, A
Sperr, WR
Sotlar, K
Yavuz, S
Kluin-Nelemans, HC
Hermine, O
Radia, D
van Doormaal, JJ
Gotlib, J
Orfao, A
Siebenhaar, F
Schwartz, LB
Castells, M
Maurer, M
Horny, HP
Akin, C
Metcalfe, DD
Arock, M
AF Valent, P.
Escribano, L.
Broesby-Olsen, S.
Hartmann, K.
Grattan, C.
Brockow, K.
Niedoszytko, M.
Nedoszytko, B.
Elberink, J. N. G. Oude
Kristensen, T.
Butterfield, J. H.
Triggiani, M.
Alvarez-Twose, I.
Reiter, A.
Sperr, W. R.
Sotlar, K.
Yavuz, S.
Kluin-Nelemans, H. C.
Hermine, O.
Radia, D.
van Doormaal, J. J.
Gotlib, J.
Orfao, A.
Siebenhaar, F.
Schwartz, L. B.
Castells, M.
Maurer, M.
Horny, H. -P.
Akin, C.
Metcalfe, D. D.
Arock, M.
TI Proposed diagnostic algorithm for patients with suspected mastocytosis:
a proposal of the European Competence Network on Mastocytosis
SO ALLERGY
LA English
DT Review
DE diagnostic algorithm; KIT D816V; mast cells; mastocytosis; tryptase
ID MAST-CELL ACTIVATION; OF-THE-ART; INDOLENT SYSTEMIC MASTOCYTOSIS; KIT
D816V MUTATION; TRYPTASE LEVELS; SERUM TRYPTASE; PROLIFERATIVE
DISORDERS; FUTURE PERSPECTIVES; CONSENSUS PROPOSAL; CONSECUTIVE ADULTS
AB Mastocytosis is an emerging differential diagnosis in patients with more or less specific mediator-related symptoms. In some of these patients, typical skin lesions are found and the diagnosis of mastocytosis can be established. In other cases, however, skin lesions are absent, which represents a diagnostic challenge. In the light of this unmet need, we developed a diagnostic algorithm for patients with suspected mastocytosis. In adult patients with typical lesions of mastocytosis in the skin, a bone marrow (BM) biopsy should be considered, regardless of the basal serum tryptase concentration. In adults without skin lesions who suffer from mediator-related or other typical symptoms, the basal tryptase level is an important parameter. In those with a slightly increased tryptase level, additional investigations, including a sensitive KIT mutation analysis of blood leucocytes or measurement of urinary histamine metabolites, may be helpful. In adult patients in whom (i) KIT D816V is detected and/or (ii) the basal serum tryptase level is clearly increased (>25-30ng/ml) and/or (iii) other clinical or laboratory features suggest the presence of occult' mastocytosis or another haematologic neoplasm, a BM investigation is recommended. In the absence of KIT D816V and other signs or symptoms of mastocytosis or another haematopoietic disease, no BM investigation is required, but the clinical course and tryptase levels are monitored in the follow-up. In paediatric patients, a BM investigation is usually not required, even if the tryptase level is increased. Although validation is required, it can be expected that the algorithm proposed herein will facilitate the management of patients with suspected mastocytosis and help avoid unnecessary referrals and investigations.
C1 [Valent, P.; Sperr, W. R.] Med Univ Vienna, Div Haematol, Dept Internal Med, Vienna, Austria.
[Escribano, L.; Orfao, A.] Univ Salamanca, IBSAL & Dept Med, Serv Cent Citometria, Ctr Invest Canc IBMCC CSIC USAL, Salamanca, Spain.
[Broesby-Olsen, S.] Odense Univ Hosp, Dept Dermatol, DK-5000 Odense, Denmark.
[Hartmann, K.] Univ Cologne, Dept Dermatol, Cologne, Germany.
[Grattan, C.] Norfolk & Norwich Univ Hosp, Norwich, Norfolk, England.
[Brockow, K.] Tech Univ Munich, Dept Dermatol & Allergy Biederstein, D-80290 Munich, Germany.
[Niedoszytko, M.] Med Univ Gdansk, Dept Allergol, Gdansk, Poland.
[Nedoszytko, B.] Med Univ Gdansk, Dept Dermatol, Gdansk, Poland.
[Elberink, J. N. G. Oude; van Doormaal, J. J.] Univ Groningen, Univ Med Ctr Groningen, Dept Allergol, Groningen, Netherlands.
[Kristensen, T.] Odense Univ Hosp, Dept Pathol, DK-5000 Odense, Denmark.
[Butterfield, J. H.] Mayo Clin, Div Allerg Dis, Rochester, MN USA.
[Triggiani, M.] Univ Salerno, Div Allergy & Clin Immunol, I-84100 Salerno, Italy.
[Alvarez-Twose, I.] Hosp Virgen de Valle, Inst Estudios Mastocitosis Castilla La Mancha CLM, Toledo, Spain.
[Reiter, A.] Heidelberg Univ, Univ Med Mannheim, Med Klin 3, Mannheim, Germany.
[Sotlar, K.; Horny, H. -P.] Univ Munich, Inst Pathol, D-80539 Munich, Germany.
[Yavuz, S.] Istanbul Univ, Dept Internal Med, Div Haematol, Istanbul, Turkey.
[Kluin-Nelemans, H. C.] Univ Groningen, Univ Med Ctr Groningen, Dept Haematol, Groningen, Netherlands.
[Hermine, O.] Univ Paris 05, Imagine Inst, Sorbonne Paris Cite, Ctr Natl Reference Mastocytoses, Paris, France.
[Radia, D.] Guys Hosp, Guys & St Thomas NHS Fdn Trust, Dept Haematol, London SE1 9RT, England.
[Gotlib, J.] Stanford Univ, Sch Med, Stanford Canc Inst, Stanford, CA 94305 USA.
[Siebenhaar, F.; Maurer, M.] Charite, Dept Dermatol & Allergy, D-13353 Berlin, Germany.
[Schwartz, L. B.] Virginia Commonwealth Univ, Dept Internal Med, Div Rheumatol Allergy & Immunol, Richmond, VA USA.
[Castells, M.; Akin, C.] Harvard Univ, Brigham & Womens Hosp, Dept Med, Div Allergy & Immunol,Med Sch, Boston, MA 02115 USA.
[Metcalfe, D. D.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Arock, M.] Ecole Normale Super, LBPA CNRS UMR8113, Cachan, France.
[Broesby-Olsen, S.] Odense Univ Hosp, Allergy Ctr, DK-5000 Odense, Denmark.
RP Valent, P (reprint author), Med Univ Vienna, Div Haematol & Hemostaseol, Dept Med 1, Wahringer Gurtel 18-20, Vienna, Austria.
EM peter.valent@meduniwien.ac.at
RI Hartmann, Karin/N-4865-2015;
OI Hartmann, Karin/0000-0002-4595-8226; Akin, Cem/0000-0001-6301-4520
FU Austrian Science Funds (FWF) Project [SFB F4611, SFB F4704-B20];
Division of Intramural Research, NIAID
FX This work was supported in part by the Austrian Science Funds (FWF)
Project SFB F4611 and SFB F4704-B20 and the Division of Intramural
Research, NIAID.
NR 51
TC 37
Z9 37
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-4538
EI 1398-9995
J9 ALLERGY
JI Allergy
PD OCT
PY 2014
VL 69
IS 10
BP 1267
EP 1274
DI 10.1111/all.12436
PG 8
WC Allergy; Immunology
SC Allergy; Immunology
GA AQ4IT
UT WOS:000342759700003
PM 24836395
ER
PT J
AU Tuttle, KR
Bakris, GL
Bilous, RW
Chiang, JL
de Boer, IH
Goldstein-Fuchs, J
Hirsch, IB
Kalantar-Zadeh, K
Narva, AS
Navaneethan, SD
Neumiller, JJ
Patel, UD
Ratner, RE
Whaley-Connell, AT
Molitch, ME
AF Tuttle, Katherine R.
Bakris, George L.
Bilous, Rudolf W.
Chiang, Jane L.
de Boer, Ian H.
Goldstein-Fuchs, Jordi
Hirsch, Irl B.
Kalantar-Zadeh, Kamyar
Narva, Andrew S.
Navaneethan, Sankar D.
Neumiller, Joshua J.
Patel, Uptal D.
Ratner, Robert E.
Whaley-Connell, Adam T.
Molitch, Mark E.
TI Diabetic Kidney Disease: A Report From an ADA Consensus Conference
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE diabetic kidney disease (DKD); end-stage renal disease (ESRD); chronic
kidney disease (CKD); diabetes mellitus; cardiovascular disease;
hypertension; glycemia; nutrition; medical home
ID DIETARY-PROTEIN RESTRICTION; STAGE RENAL-DISEASE; CLINICAL-PRACTICE
GUIDELINE; GLOMERULAR-FILTRATION-RATE; PERITONEAL-DIALYSIS PATIENTS;
NUTRITION EXAMINATION SURVEY; HEMOGLOBIN A(1C) LEVELS; GLYCEMIC CONTROL;
BLOOD-PRESSURE; LONG-TERM
AB The incidence and prevalence of diabetes mellitus have grown significantly throughout the world, due primarily to the increase in type 2 diabetes. This overall increase in the number of people with diabetes has had a major impact on development of diabetic kidney disease (DKD), one of the most frequent complications of both types of diabetes. DKD is the leading cause of end-stage renal disease (ESRD), accounting for approximately 50% of cases in the developed world. Although incidence rates for ESRD attributable to DKD have recently stabilized, these rates continue to rise in high-risk groups such as middle-aged African Americans, Native Americans, and Hispanics. The costs of care for people with DKD are extraordinarily high. In the Medicare population alone, DKD-related expenditures among this mostly older group were nearly $25 billion in 2011. Due to the high human and societal costs, the Consensus Conference on Chronic Kidney Disease and Diabetes was convened by the American Diabetes Association in collaboration with the American Society of Nephrology and the National Kidney Foundation to appraise issues regarding patient management, highlighting current practices and new directions. Major topic areas in DKD included (1) identification and monitoring, (2) cardiovascular disease and management of dyslipidemia, (3) hypertension and use of renin-angiotensin-aldosterone system blockade and mineralocorticoid receptor blockade, (4) glycemia measurement, hypoglycemia, and drug therapies, (5) nutrition and general care in advanced-stage chronic kidney disease, (6) children and adolescents, and (7) multidisciplinary approaches and medical home models for health care delivery. This current state summary and research recommendations are designed to guide advances in care and the generation of new knowledge that will meaningfully improve life for people with DKD. (C) 2014 by the American Diabetes Association and the National Kidney Foundation. Published by Elsevier Inc. All rights reserved.
C1 [Tuttle, Katherine R.] Univ Washington, Sch Med, Seattle, WA USA.
[Tuttle, Katherine R.] Providence Hlth Care, Spokane, WA USA.
[Bakris, George L.] Univ Chicago Med, Comprehens Hypertens Ctr, Chicago, IL USA.
[Bilous, Rudolf W.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Chiang, Jane L.; Ratner, Robert E.] Amer Diabet Assoc, Alexandria, VA 22311 USA.
[de Boer, Ian H.] Univ Washington, Div Nephrol, Seattle, WA USA.
[Goldstein-Fuchs, Jordi] Sierra Nevada Nephrol Consultants, Reno, NV USA.
[Hirsch, Irl B.] Univ Washington, Sch Med, Div Metab Endocrinol & Nutr, Seattle, WA USA.
[Kalantar-Zadeh, Kamyar] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
[Narva, Andrew S.] NIDDK, NIH, Bethesda, MD USA.
[Navaneethan, Sankar D.] Cleveland Clin, Glickman Urol & Kidney Inst, Novick Ctr Clin & Translat Res, Dept Hypertens & Nephrol, Cleveland, OH 44106 USA.
[Neumiller, Joshua J.] Washington State Univ, Coll Pharm, Dept Pharmacotherapy, Spokane, WA USA.
[Patel, Uptal D.] Duke Univ, Sch Med, Duke Clin Res Inst, Div Nephrol, Durham, NC USA.
[Patel, Uptal D.] Duke Univ, Sch Med, Duke Clin Res Inst, Div Pediat Nephrol, Durham, NC USA.
[Whaley-Connell, Adam T.] Harry S Truman Mem Vet Hosp, Columbia, MO 65201 USA.
[Whaley-Connell, Adam T.] Univ Missouri, Sch Med, Div Nephrol & Hypertens, Dept Internal Med, Columbia, MO USA.
[Molitch, Mark E.] Northwestern Univ Feinberg, Sch Med, Div Endocrinol Metab & Mol Med, Chicago, IL USA.
RP Chiang, JL (reprint author), Amer Diabet Assoc, Alexandria, VA 22311 USA.
EM jchiang@diabetes.org
OI Whaley-Connell, Adam/0000-0001-8955-5560; Kalantar-Zadeh,
Kamyar/0000-0002-8666-0725
FU ADA
FX Support: The conference was supported by ADA; no industry support was
used.
NR 188
TC 42
Z9 47
U1 1
U2 16
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD OCT
PY 2014
VL 64
IS 4
BP 510
EP 533
DI 10.1053/j.ajkd.2014.08.001
PG 24
WC Urology & Nephrology
SC Urology & Nephrology
GA AQ4CN
UT WOS:000342739900011
PM 25257325
ER
PT J
AU Goldenstein, L
Driver, TH
Fried, LF
Rifkin, DE
Patel, KV
Yenchek, RH
Harris, TB
Kritchevsky, SB
Newman, AB
Sarnak, MJ
Shlipak, MG
Ix, JH
AF Goldenstein, Leonard
Driver, Todd H.
Fried, Linda F.
Rifkin, Dena E.
Patel, Kushang V.
Yenchek, Robert H.
Harris, Tamara B.
Kritchevsky, Stephen B.
Newman, Anne B.
Sarnak, Mark J.
Shlipak, Michael G.
Ix, Joachim H.
CA Hlth ABC Study Investigators
TI Serum Bicarbonate Concentrations and Kidney Disease Progression in
Community-Living Elders: The Health, Aging, and Body Composition (Health
ABC) Study
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; INJURY MOLECULE-1 KIM-1; METABOLIC-ACIDOSIS;
SODIUM-BICARBONATE; FUNCTION DECLINE; LIPOCALIN NGAL; RENAL BIOPSY;
OLDER-ADULTS; CKD; RISK
AB Background: In populations with prevalent chronic kidney disease (CKD), lower serum bicarbonate levels are associated with more rapid CKD progression, but whether lower bicarbonate levels also are associated with risk of incident estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m 2 and CKD progression among community-living persons with predominantly preserved kidney function is unknown.
Study Design: Longitudinal observational cohort study.
Setting & Participants: Well-functioning community-living elders aged 70-79 years at inception.
Predictor: Serum bicarbonate level measured at the time of collection by arterialized venous blood sample using an arterial blood gas analyzer.
Outcomes: Change in eGFR over 7 years, and new eGFR, 60 mL/min/1.73 m(2) with a rate of loss of at least 1 mL/min/1.73 m(2) per year.
Measurements: Linear and logistic regressions were used to evaluate associations of baseline serum bicarbonate level with change in eGFR and incident eGFR < 60 mL/min/1.73 m(2).
Results: At baseline, mean eGFR was 84 +/- 16 (SD) mL/min/1.73 m(2), and serum bicarbonate level was 25.2 +/- 1.9 mmol/L. Compared with participants with higher bicarbonate concentrations (23.0-28.0 mmol/L), those with bicarbonate concentrations < 23 mmol/L (n = 85 [8%]) lost eGFR 0.55 (95% CI, 0.13-0.97) mL/min/1.73 m(2) per year faster inmodels adjusted for demographics, CKDrisk factors, baseline eGFR, and urinealbumin-creatinine ratio. Among the 989 (92%) participantswith baseline eGFRs > 60 mL/min/1.73 m(2), 252 (25%) developed incident eGFRs < 60 mL/min/1.73 m(2) at follow-up. Adjusting for the same covariates, participants with bicarbonate concentrations, 23 mmol/L had nearly 2-fold greater odds of incident eGFRs < 60 mL/min/1.73 m(2) (OR, 1.72; 95% CI, 0.97-3.07) compared with those with higher bicarbonate concentrations.
Limitations: Only 2 measurements of kidney function separated by 7 years and loss to follow-up due to intervening mortality in this elderly population.
Conclusions: Lower serum bicarbonate concentrations are associated independently with decline in eGFR and incident eGFR < 60 mL/min/1.73 m(2) in community-living older persons. If confirmed, serum bicarbonate levels may give insight into kidney tubule health in persons with preserved eGFRs and suggest a possible new target for intervention to prevent CKD development. Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc.
C1 [Goldenstein, Leonard; Rifkin, Dena E.; Ix, Joachim H.] Univ Calif San Diego, Dept Med, Div Nephrol & Hypertens, San Diego, CA 92161 USA.
[Goldenstein, Leonard; Rifkin, Dena E.; Ix, Joachim H.] Vet Affairs San Diego Healthcare Syst, Nephrol Sect, San Diego, CA USA.
[Driver, Todd H.; Shlipak, Michael G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Fried, Linda F.] Vet Affairs Hosp, Nephrol Sect, Pittsburgh, PA USA.
[Fried, Linda F.] Univ Pittsburgh, Dept Med, Div Nephrol, Pittsburgh, PA USA.
[Fried, Linda F.; Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Rifkin, Dena E.; Ix, Joachim H.] Univ Calif San Diego, Dept Family & Prevent Med, Div Prevent Med, San Diego, CA 92161 USA.
[Patel, Kushang V.] Univ Washington, Dept Anesthesiol & Pain Med, Seattle, WA 98195 USA.
[Yenchek, Robert H.] Univ Utah, Dept Med, Div Nephrol, Salt Lake City, UT 84112 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Sarnak, Mark J.] Tufts Med Ctr, Dept Med, Div Nephrol, Boston, MA USA.
[Shlipak, Michael G.] San Francisco VA Med Ctr, Gen Internal Med Sect, San Francisco, CA USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
RP Ix, JH (reprint author), Univ Calif San Diego, Dept Med, Div Nephrol & Hypertens, 3350 La Jolla Village Dr,Mail Code 111-H, San Diego, CA 92161 USA.
EM joeix@ucsd.edu
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
FU National Institute of Diabetes and Digestive and Kidney Diseases
[R01DK098234, T32DK069263]; National Institute on Aging [R01AG 027002,
R01-AG028050, N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106]; National
Institute of Nursing Research [R01-NR012459]; National Institutes of
Health, NIA
FX This research was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases by grants R01DK098234 (Drs Ix and Shlipak)
and T32DK069263 (Dr Goldenstein); the National Institute on Aging by
grants R01AG 027002 (Dr Sarnak) and R01-AG028050 (Dr Strotmeyer) and
contracts N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106; the National
Institute of Nursing Research by grant R01-NR012459 (Dr Albert); and the
Intramural Research Program of the National Institutes of Health, NIA.
The funders of this study had no role in study design; collection,
analysis, and interpretation of data; writing the report; or the
decision to submit the report for publication.
NR 33
TC 15
Z9 16
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD OCT
PY 2014
VL 64
IS 4
BP 542
EP 549
DI 10.1053/j.ajkd.2014.05.009
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA AQ4CN
UT WOS:000342739900013
PM 24953890
ER
PT J
AU Hanley, KA
Guerbois, M
Kautz, TF
Brown, M
Whitehead, SS
Weaver, SC
Vasilakis, N
Marx, PA
AF Hanley, Kathryn A.
Guerbois, Mathilde
Kautz, Tiffany F.
Brown, Meredith
Whitehead, Stephen S.
Weaver, Scott C.
Vasilakis, Nikos
Marx, Preston A.
TI Short Report: Infection Dynamics of Sylvatic Dengue Virus in a Natural
Primate Host, the African Green Monkey
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID TYPE-4 VACCINE CANDIDATE; YELLOW-FEVER VIRUS; RHESUS-MONKEYS; SENEGAL;
STRAINS; POPULATION; PROSPECTS; MOSQUITOS; RESPONSES; FEATURES
AB The four serotypes of mosquito-borne dengue virus (DENV-1, -2, -3, and -4) that circulate in humans each emerged from an enzootic, sylvatic cycle in non-human primates. Herein, we present the first study of sylvatic DENV infection dynamics in a primate. Three African green monkeys were inoculated with 10(5) plaque-forming units (pfu) DENV-2 strain PM33974 from the sylvatic cycle, and one African green monkey was inoculated with 10(5) pfu DENV-2 strain New Guinea C from the human cycle. All four monkeys seroconverted (more than fourfold rise in 80% plaque reduction neutralization titer [PRNT80]) against the strain of DENV with which they were inoculated; only one (33%) of three monkeys infected with sylvatic DENV showed a neutralizing antibody response against human-endemic DENV. Virus was detected in two of three monkeys inoculated with sylvatic DENV at low titer (<= 1.3 log(10)pfu/mL) and brief duration (<= 2 days). Clinical signs included rash and elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels.
C1 [Hanley, Kathryn A.] New Mexico State Univ, Dept Biol, Las Cruces, NM 88003 USA.
[Weaver, Scott C.; Vasilakis, Nikos] Univ Texas Med Branch, Ctr Trop Dis, Dept Pathol, Galveston, TX 77555 USA.
[Guerbois, Mathilde; Weaver, Scott C.; Vasilakis, Nikos] Univ Texas Med Branch, Ctr Biodefense & Emerging Infect Dis, Galveston, TX 77555 USA.
[Guerbois, Mathilde; Weaver, Scott C.; Vasilakis, Nikos] Univ Texas Med Branch, Ctr Trop Dis, Inst Human Infect & Immun, Galveston, TX 77555 USA.
[Kautz, Tiffany F.] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA.
[Brown, Meredith] Banfield Pet Hosp, Las Cruces, NM USA.
[Whitehead, Stephen S.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Marx, Preston A.] Tulane Natl Primate Res Ctr, Div Microbiol, Covington, LA USA.
RP Hanley, KA (reprint author), New Mexico State Univ, Dept Biol, Foster Hall, Las Cruces, NM 88003 USA.
EM khanley@nmsu.edu; mathildeguerbois@yahoo.fr; tfkautz@utmb.edu;
Meredith.Brown@banfield.net; swhitehead@niaid.nih.gov; sweaver@utmb.edu;
nivasila@utmb.edu; pmarx@tulane.edu
RI Weaver, Scott/D-6490-2011
FU National Center for Research Resources and Office of Research
Infrastructure Programs, National Institutes of Health (NIH) [P51
RR00164-50]; National Center for Research Resources Grant
[5P20RR016480-12]; National Institute of General Medical Sciences, NIH
Grant [8 P20 GM103451-12]; National Institute of Allergy and Infectious
Diseases Intramural Research Program, NIH
FX This project was supported by National Center for Research Resources and
Office of Research Infrastructure Programs, National Institutes of
Health (NIH) Grant P51 RR00164-50, National Center for Research
Resources Grant 5P20RR016480-12, and National Institute of General
Medical Sciences, NIH Grant 8 P20 GM103451-12. Support was also
provided, in part, by the National Institute of Allergy and Infectious
Diseases Intramural Research Program, NIH.
NR 36
TC 3
Z9 3
U1 0
U2 12
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
EI 1476-1645
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD OCT
PY 2014
VL 91
IS 4
BP 672
EP 676
DI 10.4269/ajtmh.13-0492
PG 5
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA AQ6XQ
UT WOS:000342957600005
PM 25092823
ER
PT J
AU Venkatesan, M
Gadalla, NB
Stepniewska, K
Dahal, P
Nsanzabana, C
Moriera, C
Price, RN
Martensson, A
Rosenthal, PJ
Dorsey, G
Sutherland, CJ
Guerin, P
Davis, TME
Menard, D
Adam, I
Ademowo, G
Arze, C
Baliraine, FN
Berens-Riha, N
Bjorkman, A
Borrmann, S
Checchi, F
Desai, M
Dhorda, M
Djimde, AA
El-Sayed, BB
Eshetu, T
Eyase, F
Falade, C
Faucher, JF
Froberg, G
Grivoyannis, A
Hamour, S
Houze, S
Johnson, J
Kamugisha, E
Kariuki, S
Kiechel, JR
Kironde, F
Kofoed, PE
LeBras, J
Malmberg, M
Mwai, L
Ngasala, B
Nosten, F
Nsobya, SL
Nzila, A
Oguike, M
Otienoburu, SD
Ogutu, B
Ouedraogo, JB
Piola, P
Rombo, L
Schramm, B
Some, AF
Thwing, J
Ursing, J
Wong, RPM
Zeynudin, A
Zongo, I
Plowe, CV
Sibley, CH
AF Venkatesan, Meera
Gadalla, Nahla B.
Stepniewska, Kasia
Dahal, Prabin
Nsanzabana, Christian
Moriera, Clarissa
Price, Ric N.
Martensson, Andreas
Rosenthal, Philip J.
Dorsey, Grant
Sutherland, Colin J.
Guerin, Philippe
Davis, Timothy M. E.
Menard, Didier
Adam, Ishag
Ademowo, George
Arze, Cesar
Baliraine, Frederick N.
Berens-Riha, Nicole
Bjorkman, Anders
Borrmann, Steffen
Checchi, Francesco
Desai, Meghna
Dhorda, Mehul
Djimde, Abdoulaye A.
El-Sayed, Badria B.
Eshetu, Teferi
Eyase, Frederick
Falade, Catherine
Faucher, Jean-Francois
Froberg, Gabrielle
Grivoyannis, Anastasia
Hamour, Sally
Houze, Sandrine
Johnson, Jacob
Kamugisha, Erasmus
Kariuki, Simon
Kiechel, Jean-Rene
Kironde, Fred
Kofoed, Poul-Erik
LeBras, Jacques
Malmberg, Maja
Mwai, Leah
Ngasala, Billy
Nosten, Francois
Nsobya, Samuel L.
Nzila, Alexis
Oguike, Mary
Otienoburu, Sabina Dahlstrom
Ogutu, Bernhards
Ouedraogo, Jean-Bosco
Piola, Patrice
Rombo, Lars
Schramm, Birgit
Some, A. Fabrice
Thwing, Julie
Ursing, Johan
Wong, Rina P. M.
Zeynudin, Ahmed
Zongo, Issaka
Plowe, Christopher V.
Sibley, Carol Hopkins
CA WWARN AL & ASAQ Mol Marker Study
TI Polymorphisms in Plasmodium falciparum Chloroquine Resistance
Transporter and Multidrug Resistance 1 Genes: Parasite Risk Factors that
Affect Treatment Outcomes for P-falciparum Malaria after
Artemether-Lumefantrine and Artesunate-Amodiaquine
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID PLUS SULFADOXINE-PYRIMETHAMINE; PFMDR1 COPY NUMBER; UNCOMPLICATED
MALARIA; IN-VIVO; DRUG-RESISTANCE; PLASMODIUM-FALCIPARUM-PFMDR1 ALLELES;
DIHYDROARTEMISININ-PIPERAQUINE; COMBINATION THERAPIES; TYROSINE-86
ALLELE; TANZANIAN CHILDREN
AB Adequate clinical and parasitologic cure by artemisinin combination therapies relies on the artemisinin component and the partner drug. Polymorphisms in the Plasmodium falciparum chloroquine resistance transporter (pfcrt) and P. falciparum multidrug resistance 1 (pfmdr1) genes are associated with decreased sensitivity to amodiaquine and lumefantrine, but effects of these polymorphisms on therapeutic responses to artesunate-amodiaquine (ASAQ) and artemether-lumefantrine (AL) have not been clearly defined. Individual patient data from 31 clinical trials were harmonized and pooled by using standardized methods from the WorldWide Antimalarial Resistance Network. Data for more than 7,000 patients were analyzed to assess relationships between parasite polymorphisms in pfcrt and pfmdr1 and clinically relevant outcomes after treatment with AL or ASAQ. Presence of the pfmdr1 gene N86 (adjusted hazards ratio = 4.74, 95% confidence interval = 2.29 - 9.78, P < 0.001) and increased pfmdr1 copy number (adjusted hazards ratio = 6.52, 95% confidence interval = 2.36-17.97, P < 0.001) were significant independent risk factors for recrudescence in patients treated with AL. AL and ASAQ exerted opposing selective effects on single-nucleotide polymorphisms in pfcrt and pfmdr1. Monitoring selection and responding to emerging signs of drug resistance are critical tools for preserving efficacy of artemisinin combination therapies; determination of the prevalence of at least pfcrt K76T and pfmdr1 N86Y should now be routine.
C1 [Venkatesan, Meera; Plowe, Christopher V.] Univ Maryland, Sch Med, WorldWide Antimalarial Resistance Network Mol Mod, Baltimore, MD 21201 USA.
[Venkatesan, Meera; Plowe, Christopher V.] Univ Maryland, Sch Med, Howard Hughes Med Inst, Ctr Vaccine Dev, Baltimore, MD 21201 USA.
[Gadalla, Nahla B.] NIAID, NIH, Bethesda, MD 20892 USA.
[Gadalla, Nahla B.] Res Inst Trop Med, Dept Epidemiol, Khartoum, Sudan.
[Stepniewska, Kasia; Dahal, Prabin; Nsanzabana, Christian; Moriera, Clarissa; Price, Ric N.; Guerin, Philippe; Piola, Patrice; Sibley, Carol Hopkins] Univ Oxford, Nuffield Dept Clin Med, Ctr Trop Med, World Wide Antimalarial Resistance Network, Oxford, England.
[Price, Ric N.] Menzies Sch Hlth Res, Global Hlth Div, Darwin, NT, Australia.
[Price, Ric N.] Charles Darwin Univ, Darwin, NT 0909, Australia.
[Martensson, Andreas; Bjorkman, Anders; Froberg, Gabrielle; Malmberg, Maja; Rombo, Lars; Ursing, Johan] Dept Med Solna, Infect Dis Unit, Stockholm, Sweden.
[Martensson, Andreas] Karolinska Inst, Global Hlth, Dept Publ Hlth Sci, Stockholm, Sweden.
[Rosenthal, Philip J.; Dorsey, Grant] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Sutherland, Colin J.; Oguike, Mary] London Sch Hyg & Trop Med, Fac Infect & Trop Dis, Dept Immunol & Infect, London WC1, England.
[Davis, Timothy M. E.; Wong, Rina P. M.] Univ Western Australia, Fremantle Hosp, Sch Med & Pharmacol, Nedlands, WA 6009, Australia.
[Menard, Didier] Inst Pasteur Cambodge, Malaria Mol Epidemiol Unit, Phnom Penh, Cambodia.
[Adam, Ishag] Univ Khartoum, Fac Med, Khartoum, Sudan.
[Ademowo, George] Univ Ibadan, Coll Med, Inst Adv Med Res & Training, Ibadan, Nigeria.
[Arze, Cesar] Univ Maryland, Sch Med, Module & Inst Genome Sci, WorldWide Antimalarial Resistance Network Mol, Baltimore, MD 21201 USA.
[Baliraine, Frederick N.] LeTourneau Univ, Dept Biol, Longview, TX USA.
[Berens-Riha, Nicole] Univ Munich, Dept Infect Dis & Trop Med, Munich, Germany.
[Borrmann, Steffen; Mwai, Leah; Nzila, Alexis] Wellcome Trust Res Programme, Kenya Med Res Inst, Kilifi, Kenya.
[Borrmann, Steffen] Univ Magdeburg, Sch Med, Dept Microbiol, D-39106 Magdeburg, Germany.
[Checchi, Francesco] Save Children, Paris, France.
[Desai, Meghna; Thwing, Julie] Ctr Dis Control & Prevent, Ctr Global Hlth, Div Parasit Dis & Malaria, Malaria Branch, Atlanta, GA USA.
[Dhorda, Mehul] Univ Maryland, Sch Med, WorldWide Antimalarial Resistance Network Mol Mod, Baltimore, MD 21201 USA.
[Dhorda, Mehul] Epictr Uganda Res Base, Mbarara, Uganda.
[Djimde, Abdoulaye A.] Univ Sci Techn & Technol Bamako, Fac Pharm, Malaria Res & Training Ctr, Bamako, Mali.
[El-Sayed, Badria B.] Res Inst Trop Med, Dept Epidemiol, Khartoum, Sudan.
[Eshetu, Teferi; Zeynudin, Ahmed] Jimma Univ, Med Parasitol Unit, Dept Med, Lab Sci & Pathol, Jimma, Ethiopia.
[Eyase, Frederick; Ogutu, Bernhards] US Army, Res Unit Kenya Walter Reed, Kenya Med Res Inst Project, Kisumu, Kenya.
[Falade, Catherine] Univ Ibadan, Dept Pharmacol & Therapeut, Ibadan, Nigeria.
[Faucher, Jean-Francois] Univ Med Ctr, Dept Infect Dis, Besancon, France.
[Faucher, Jean-Francois] Inst Rech Dev, Paris, France.
[Grivoyannis, Anastasia] Univ Washington, Dept Med, Div Emergency Med, Seattle, WA USA.
[Hamour, Sally] UCL, Ctr Nephrol, Royal Free Hosp, London, England.
[Houze, Sandrine; LeBras, Jacques] Hop Xavier Bichat, AP HP, Malaria Natl Reference Ctr, Parasitol Lab, Paris, France.
[Houze, Sandrine; LeBras, Jacques] Mere & Enfant Face Infect Trop, Inst Rech Dev, Paris, France.
[Houze, Sandrine; LeBras, Jacques] Univ Paris 05, Sorbonne Paris Cite, PRES, Fac Pharm, Paris, France.
[Johnson, Jacob] US Army, Med Res Unit Kenya, Nairobi, Kenya.
[Kamugisha, Erasmus] Catholic Univ Hlth & Allied Sci Bugando, Mwanza, Tanzania.
[Kariuki, Simon] Ctrs Dis Control & Prevent, Kenya Med Res Inst, Malaria Branch, Kisumu, Kenya.
[Kiechel, Jean-Rene] Drugs Neglected Dis Initiat, Geneva, Switzerland.
[Kironde, Fred] Makerere Univ, Coll Hlth Sci, Kampala, Uganda.
[Kironde, Fred] St Augustine Int Univ, Kampala, Uganda.
[Kofoed, Poul-Erik] INDEPTH Network, Projecto Saude Bandim, Bissau, Guinea Bissau.
[Kofoed, Poul-Erik] Kolding Cty Hosp, Dept Pediat, Kolding, Denmark.
[Ngasala, Billy] Muhimbili Univ Hlth & Allied Sci, Dept Parasitol, Dar Es Salaam, Tanzania.
[Nosten, Francois] Univ Oxford, Nuffield Dept Med, Ctr Trop Med, Oxford, England.
[Nosten, Francois] Mahidol Univ, Fac Trop Med, Mahidol Oxford Trop Med Res Unit, Shoklo Malaria Res Unit, Bangkok, Thailand.
[Nsobya, Samuel L.] Makerere Univ, Coll Hlth Sci, Sch Biomed Sci, Dept Pathol, Kampala, Uganda.
[Otienoburu, Sabina Dahlstrom] Hop Bichat Claude Bernard, Inst Med & Epidemiol Appliquee, Worldwide Antimalarial Resistance Network, F-75877 Paris 18, France.
[Ouedraogo, Jean-Bosco; Some, A. Fabrice; Zongo, Issaka] Ctr Muraz, Inst Rech Sci Sante, Bobo Dioulasso, Burkina Faso.
[Schramm, Birgit] Epictr, Paris, France.
[Sibley, Carol Hopkins] Univ Washington, Dept Genome Sci, Seattle, WA USA.
RP Sibley, CH (reprint author), Univ Washington, Dept Genome Sci, Box 355065, Seattle, WA 98195 USA.
EM carol.sibley@wwarn.org
RI Malmberg, Maja/H-1890-2014; guo, hong/N-7392-2014;
OI Malmberg, Maja/0000-0002-4506-0408; Guerin,
Philippe/0000-0002-6008-2963; SOME, Anyirekun
Fabrice/0000-0002-1530-1493; Price, Richard/0000-0003-2000-2874; Dahal,
Prabin/0000-0002-2158-846X; Borrmann, Steffen/0000-0001-9189-4393;
Ursing, Johan/0000-0002-5508-9327; GADALLA, NAHLA/0000-0002-6177-6705;
Nosten, Francois/0000-0002-7951-0745
FU Bill and Melinda Gates Foundation
FX The WorldWide Antimalarial Resistance Network is supported by the Bill
and Melinda Gates Foundation.Disclaimer: The opinions and assertions
contained herein are the personal opinions of authors and are not to be
construed as reflecting the views of the U.S. Army Medical Research
Unit-Kenya or the U.S. Department of Defense.
NR 68
TC 37
Z9 37
U1 1
U2 16
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
EI 1476-1645
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD OCT
PY 2014
VL 91
IS 4
BP 833
EP 843
DI 10.4269/ajtmh.14-0031
PG 11
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA AQ6XQ
UT WOS:000342957600033
PM 25048375
ER
PT J
AU Deodhar, A
Reveille, JD
van den Bosch, F
Braun, J
Burgos-Vargas, R
Caplan, L
Clegg, DO
Colbert, RA
Gensler, LS
van der Heijde, D
van der Horst-Bruinsma, IE
Inman, RD
Maksymowych, WP
Mease, PJ
Raychaudhuri, S
Reimold, A
Rudwaleit, M
Sieper, J
Weisman, MH
Landewe, RBM
AF Deodhar, Atul
Reveille, John D.
van den Bosch, Filip
Braun, Juergen
Burgos-Vargas, Ruben
Caplan, Liron
Clegg, Daniel O.
Colbert, Robert A.
Gensler, Lianne S.
van der Heijde, Desiree
van der Horst-Bruinsma, Irene E.
Inman, Robert D.
Maksymowych, Walter P.
Mease, Philip J.
Raychaudhuri, Siba
Reimold, Andreas
Rudwaleit, Martin
Sieper, Joachim
Weisman, Michael H.
Landewe, Robert B. M.
TI The Concept of Axial Spondyloarthritis
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID SOCIETY CLASSIFICATION CRITERIA; PLACEBO-CONTROLLED TRIAL;
ANKYLOSING-SPONDYLITIS; DIAGNOSTIC-CRITERIA; DOUBLE-BLIND;
SPONDYLARTHRITIS; EFFICACY; SAFETY; PREVALENCE
C1 [Deodhar, Atul] Oregon Hlth & Sci Univ, Portland, OR 97239 USA.
[Reveille, John D.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[van den Bosch, Filip] Ghent Univ Hosp, Ghent, Belgium.
[Braun, Juergen] Rheumazentrum Ruhrgebiet, Herne, Germany.
[Burgos-Vargas, Ruben] Hosp Gen Mexico City, Mexico City, DF, Mexico.
[Burgos-Vargas, Ruben] Univ Nacl Autonoma Mexico, Mexico City 04510, DF, Mexico.
[Caplan, Liron] Univ Colorado, Denver, CO 80202 USA.
[Caplan, Liron] Denver VA Med Ctr, Denver, CO USA.
[Clegg, Daniel O.] Univ Utah, Med Ctr, Salt Lake City, UT USA.
[Colbert, Robert A.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Gensler, Lianne S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[van der Heijde, Desiree] Leiden Univ, Med Ctr, Leiden, Netherlands.
[van der Horst-Bruinsma, Irene E.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Inman, Robert D.] Toronto Western Hosp, Toronto, ON M5T 2S8, Canada.
[Inman, Robert D.] Univ Toronto, Toronto, ON, Canada.
[Maksymowych, Walter P.] Alberta Heritage Fdn Med Res, Edmonton, AB, Canada.
[Maksymowych, Walter P.] Univ Alberta, Edmonton, AB, Canada.
[Mease, Philip J.] Seattle Rheumatol Associates, Seattle, WA USA.
[Raychaudhuri, Siba] Univ Calif Davis, Sacramento, CA 95817 USA.
[Reimold, Andreas] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Rudwaleit, Martin; Sieper, Joachim] Charite, Campus Benjamin Franklin, D-13353 Berlin, Germany.
[Weisman, Michael H.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Landewe, Robert B. M.] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
[Landewe, Robert B. M.] Univ Amsterdam, Amsterdam, Netherlands.
RP Deodhar, A (reprint author), Oregon Hlth & Sci Univ, Div Arthrit & Rheumat Dis, OP09,3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM deodhara@ohsu.edu
FU UCB; Novartis; AbbVie; Pfizer; MSD; Amgen; Celgene; AbbVie (Abbott);
Bristol-Myers Squibb; Boehringer; Celltrion; Centocor; Chugai; EBEWE
Pharma; Medac; MSD (Schering-Plough); Mundipharma; Pfizer (Wyeth);
Roche; Sanofi-Aventis; Janssen; AstraZeneca; Augunex; Covagen; Daiichi;
Eli Lilly; Galapagos NV; GlaxoSmithKline; Janssen Biologics; Merck; Novo
Nordisk; Otsuka; Vertex; Quest; Biogen Idec; Crescendo; Genentech;
Lilly; Abbott; Wyeth
FX Dr. Deodhar has received consulting fees, speaking fees, and/or
honoraria from UCB, Novartis, AbbVie, Pfizer, and MSD (less than $10,000
each), has served as an expert witness on behalf of UCB and AbbVie, and
has received research grants from UCB, AbbVie, Novartis, Pfizer, and
Amgen. Dr. van den Bosch has received consulting fees, speaking fees,
and/or honoraria from AbbVie, Celgene, MSD, Pfizer, and UCB (less than
$10,000 each). Dr. Braun has received consulting fees, speaking fees,
and/or honoraria from AbbVie (Abbott), Amgen, Bristol-Myers Squibb,
Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Medac,
MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche,
Sanofi-Aventis, and UCB (less than $10,000 each). Dr. Burgos-Vargas has
received consulting fees, speaking fees, and/or honoraria from AbbVie,
Bristol-Myers Squibb, Janssen, Pfizer, Roche, and UCB (less than $10,000
each). Dr. Clegg has received consulting fees, speaking fees, and/or
honoraria from Abbott (less than $10,000). Dr. Gensler has received
consulting fees from UCB and AbbVie (less than $10,000 each). Dr. van
der Heijde has received consulting fees, speaking fees, and/or honoraria
from AbbVie, Amgen, AstraZeneca, Augunex, Bristol-Myers Squibb, Celgene,
Chugai, Covagen, Daiichi, Eli Lilly, Galapagos NV, GlaxoSmithKline,
Janssen Biologics, Merck, Novartis, Novo Nordisk, Otsuka, Pfizer, Roche,
Sanofi-Aventis, Schering-Plough, UCB, and Vertex (less than $10,000
each) and is the director of Imaging Rheumatology BV. Dr. Inman has
received consulting fees from AbbVie, Amgen, Janssen, Pfizer, and UCB
(less than $10,000 each). Dr. Maksymowych has received consulting fees,
speaking fees, and/or honoraria from Pfizer, Eli Lilly, Merck, Janssen,
and Quest (less than $10,000 each) and from AbbVie and UCB (more than
$10,000 each). Dr. Mease has received consulting fees, speaking fees,
and/or honoraria from Biogen Idec, Celgene, Covagen, Crescendo,
Genentech, Janssen, Lilly, Merck, Novartis, and Vertex (less than
$10,000 each) and from AbbVie, Amgen, Bristol-Myers Squibb, Pfizer, and
UCB (more than $10,000 each). Dr. Raychaudhuri has received speaking
fees or honoraria from Abbott, Amgen, and UCB (less than $10,000 each).
Dr. Reimold has received consulting fees, speaking fees, and/or
honoraria from UCB (less than $10,000). Dr. Rudwaleit has received
consulting fees, speaking fees, and/or honoraria from AbbVie,
Bristol-Myers Squibb, MSD, Pfizer, Roche, UCB, and Janssen (less than
$10,000 each) and has served as an expert witness on behalf of UCB. Dr.
Sieper has received consulting fees, speaking fees, and/or honoraria
from AbbVie, Pfizer, Merck, UCB, and Novartis (less than $10,000 each).
Dr. Weisman has received consulting fees from UCB (less than $10,000).
Dr. Landewe has received consulting fees, speaking fees, and/or
honoraria from AbbVie, Pfizer, UCB, Amgen, Wyeth, Merck, Novartis, and
Janssen (less than $10,000 each) and is director of Rheumatology
Consultancy BV.
NR 23
TC 28
Z9 30
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD OCT
PY 2014
VL 66
IS 10
BP 2649
EP 2656
DI 10.1002/art.38776
PG 8
WC Rheumatology
SC Rheumatology
GA AQ4DZ
UT WOS:000342744300001
PM 25154344
ER
PT J
AU Yazdany, J
Marafino, BJ
Dean, ML
Bardach, NS
Duseja, R
Ward, MM
Dudley, RA
AF Yazdany, Jinoos
Marafino, Ben J.
Dean, Mitzi L.
Bardach, Naomi S.
Duseja, Reena
Ward, Michael M.
Dudley, R. Adams
TI Thirty-Day Hospital Readmissions in Systemic Lupus Erythematosus
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID QUALITY-OF-CARE; 3 ETHNIC-GROUPS; MYOCARDIAL-INFARCTION; HEART-FAILURE;
UNITED-STATES; HEALTH-CARE; CLAIMS DATA; MORTALITY; COHORT; DISEASE
AB ObjectiveSystemic lupus erythematosus (SLE) has one of the highest hospital readmission rates among chronic conditions. This study was undertaken to identify patient-level, hospital-level, and geographic predictors of 30-day hospital readmissions associated with SLE.
MethodsUsing hospital discharge databases from 5 geographically dispersed states, we studied all-cause readmission of SLE patients between 2008 and 2009. We evaluated each hospitalization as a possible index event leading up to a readmission, our primary outcome. We accounted for clustering of hospitalizations within patients and within hospitals and adjusted for hospital case mix. Using multilevel mixed-effects logistic regression, we examined factors associated with 30-day readmission and calculated risk-standardized hospital-level and state-level readmission rates.
ResultsWe examined 55,936 hospitalizations among 31,903 patients with SLE. Of these hospitalizations, 9,244 (16.5%) resulted in readmission within 30 days. In adjusted analyses, age was inversely related to risk of readmission. African American and Hispanic patients were more likely to be readmitted than white patients, as were those with Medicare or Medicaid insurance (versus private insurance). Several clinical characteristics of lupus, including nephritis, serositis, and thrombocytopenia, were associated with readmission. Readmission rates varied significantly between hospitals after accounting for patient-level clustering and hospital case mix. We also found geographic variation, with risk-adjusted readmission rates lower in New York and higher in Florida as compared to California.
ConclusionWe found that approximate to 1 in 6 hospitalized patients with SLE were readmitted within 30 days of discharge, with higher rates among historically underserved populations. Significant geographic and hospital-level variation in risk-adjusted readmission rates suggests potential for quality improvement.
C1 [Yazdany, Jinoos] San Francisco Gen Hosp, San Francisco, CA 94110 USA.
[Marafino, Ben J.; Dean, Mitzi L.; Bardach, Naomi S.; Duseja, Reena; Dudley, R. Adams] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Ward, Michael M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Yazdany, J (reprint author), Univ Calif San Francisco, Div Rheumatol, Box 0920, San Francisco, CA 94143 USA.
EM jinoos.yazdany@ucsf.edu
FU NIH (National Institute of Arthritis and Musculoskeletal and Skin
Diseases) [K23-AR-060259, P60-AR-053308]; University of California, San
Francisco Comparative Effectiveness Large Dataset Analysis Core;
Rosalind Russell Medical Research Center for Arthritis
FX Supported by the NIH (National Institute of Arthritis and
Musculoskeletal and Skin Diseases grants K23-AR-060259 and
P60-AR-053308), the University of California, San Francisco Comparative
Effectiveness Large Dataset Analysis Core, and the Rosalind Russell
Medical Research Center for Arthritis. Dr. Ward's work was supported by
the National Institute of Arthritis and Musculoskeletal and Skin
Diseases, NIH.
NR 29
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD OCT
PY 2014
VL 66
IS 10
BP 2828
EP 2836
DI 10.1002/art.38768
PG 9
WC Rheumatology
SC Rheumatology
GA AQ4DZ
UT WOS:000342744300020
PM 25110993
ER
PT J
AU Artz, AS
Xue, QL
Wickrema, A
Hesdorffer, C
Ferrucci, L
Langdon, JM
Walston, JD
Roy, CN
AF Artz, Andrew S.
Xue, Qian-Li
Wickrema, Amittha
Hesdorffer, Charles
Ferrucci, Luigi
Langdon, Jacqueline M.
Walston, Jeremy D.
Roy, Cindy N.
TI Unexplained anaemia in the elderly is characterised by features of low
grade inflammation
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Letter
DE anaemia; elderly; inflammation; neopterin
C1 [Artz, Andrew S.; Wickrema, Amittha] Univ Chicago, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Xue, Qian-Li] Johns Hopkins Bloomberg Sch Publ Hlth, Div Biostat & Epidemiol, Baltimore, MD USA.
[Xue, Qian-Li; Langdon, Jacqueline M.; Walston, Jeremy D.; Roy, Cindy N.] Johns Hopkins Univ, Div Geriatr Med & Gerontol, Baltimore, MD USA.
[Hesdorffer, Charles; Ferrucci, Luigi] Natl Inst Aging, Baltimore Longitudinal Study Aging, Baltimore, MD USA.
[Roy, Cindy N.] Johns Hopkins Univ, Div Hematol, Baltimore, MD USA.
RP Artz, AS (reprint author), Univ Chicago, Hematol Oncol Sect, Chicago, IL 60637 USA.
EM croy6@jhmi.edu
FU NCATS NIH HHS [UL1 TR001079, UL1 TR000430]; NCRR NIH HHS [UL1 RR025005,
UL1 RR 025005]; NIA NIH HHS [U01AG034661, U01 AG034661]; NIDDK NIH HHS
[R01 DK082722, R01DK082722]
NR 10
TC 5
Z9 5
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD OCT
PY 2014
VL 167
IS 2
BP 286
EP 289
DI 10.1111/bjh.12984
PG 4
WC Hematology
SC Hematology
GA AQ4TP
UT WOS:000342792900022
PM 24935746
ER
PT J
AU Bukalo, O
Pinard, CR
Holmes, A
AF Bukalo, Olena
Pinard, Courtney R.
Holmes, Andrew
TI Mechanisms to medicines: elucidating neural and molecular substrates of
fear extinction to identify novel treatments for anxiety disorders
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Review
ID MEDIAL PREFRONTAL CORTEX; RAT BASOLATERAL AMYGDALA; LONG-TERM
EXTINCTION; BETWEEN-SESSION EXTINCTION; SINGLE PROLONGED STRESS;
CYCLOSERINE FACILITATES EXTINCTION; CONDITIONED EMOTIONAL RESPONSE;
HISTONE DEACETYLASE INHIBITORS; COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED
CONTROLLED-TRIAL
AB The burden of anxiety disorders is growing, but the efficacy of available anxiolytic treatments remains inadequate. Cognitive behavioural therapy for anxiety disorders focuses on identifying and modifying maladaptive patterns of thinking and behaving, and has a testable analogue in rodents in the form of fear extinction. A large preclinical literature has amassed in recent years describing the neural and molecular basis of fear extinction in rodents. In this review, we discuss how this work is being harnessed to foster translational research on anxiety disorders and facilitate the search for new anxiolytic treatments. We begin by summarizing the anatomical and functional connectivity of a medial prefrontal cortex (mPFC)-amygdala circuit that subserves fear extinction, including new insights from optogenetics. We then cover some of the approaches that have been taken to model impaired fear extinction and associated impairments with mPFC-amygdala dysfunction. The principal goal of the review is to evaluate evidence that various neurotransmitter and neuromodulator systems mediate fear extinction by modulating the mPFC-amygdala circuitry. To that end, we describe studies that have tested how fear extinction is impaired or facilitated by pharmacological manipulations of dopamine, noradrenaline, 5-HT, GABA, glutamate, neuropeptides, endocannabinoids and various other systems, which either directly target the mPFC-amygdala circuit, or produce behavioural effects that are coincident with functional changes in the circuit. We conclude that there are good grounds to be optimistic that the progress in defining the molecular substrates of mPFC-amygdala circuit function can be effectively leveraged to identify plausible candidates for extinction-promoting therapies for anxiety disorders.
C1 [Bukalo, Olena; Pinard, Courtney R.; Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, Bethesda, MD USA.
RP Bukalo, O (reprint author), 5625 Fishers Ln,Room 2N-09, Rockville, MD 20852 USA.
EM bukalool@mail.nih.gov
FU NIAAA
FX We thank A.J. McDonald for critical reading of manuscript and NIAAA
intramural funding for support.
NR 428
TC 19
Z9 19
U1 2
U2 25
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1188
EI 1476-5381
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD OCT
PY 2014
VL 171
IS 20
SI SI
BP 4690
EP 4718
DI 10.1111/bph.12779
PG 29
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AQ5AK
UT WOS:000342814300010
PM 24835117
ER
PT J
AU Seow, WJ
Hu, W
Vermeulen, R
Hosgood, HD
Downward, GS
Chapman, RS
He, XZ
Bassig, BA
Kim, C
Wen, CJ
Rothman, N
Lan, Q
AF Seow, Wei Jie
Hu, Wei
Vermeulen, Roel
Hosgood, H. Dean, III
Downward, George S.
Chapman, Robert S.
He, Xingzhou
Bassig, Bryan A.
Kim, Christopher
Wen, Cuiju
Rothman, Nathaniel
Lan, Qing
TI Household air pollution and lung cancer in China: a review of studies in
Xuanwei
SO CHINESE JOURNAL OF CANCER
LA English
DT Review
DE Coal; household air pollution; lung cancer
ID COMPARATIVE RISK-ASSESSMENT; STOVE IMPROVEMENT; SMOKY COAL;
RETROSPECTIVE COHORT; MORTALITY; WEI; HEALTH; SUSCEPTIBILITY;
METAANALYSIS; EXPOSURES
AB Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity.
C1 [Seow, Wei Jie; Hu, Wei; Bassig, Bryan A.; Kim, Christopher; Wen, Cuiju; Rothman, Nathaniel; Lan, Qing] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Vermeulen, Roel; Downward, George S.] Univ Utrecht, Div Environm Epidemiol, Inst Risk Assessment Sci, NL-3508 Utrecht, Netherlands.
[Hosgood, H. Dean, III] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA.
[Chapman, Robert S.] Chulalongkorn Univ, Coll Publ Hlth Sci, Bangkok 10330, Thailand.
[He, Xingzhou] Chinese Ctr Dis Control & Prevent, Beijing 102206, Peoples R China.
RP Seow, WJ (reprint author), 9609 Med Ctr Dr Room 6E128, Rockville, MD 20850 USA.
EM weijie.seow2@nih.gov
RI Vermeulen, Roel/F-8037-2011
OI Vermeulen, Roel/0000-0003-4082-8163
NR 30
TC 9
Z9 11
U1 4
U2 43
PU SUN YAT SEN UNIV MED SCI WHO
PI GUANGZHOU
PA 651 DONGFENG RD E, GUANGZHOU, GUANGDONG 510060, PEOPLES R CHINA
SN 1000-467X
EI 1944-446X
J9 CHIN J CANCER
JI Chin. J. Cancer
PD OCT
PY 2014
VL 33
IS 10
BP 471
EP 475
DI 10.5732/cjc.014.10132
PG 5
WC Oncology
SC Oncology
GA AQ5ZJ
UT WOS:000342886800002
PM 25223911
ER
PT J
AU Guay-Woodford, LM
Henske, E
Igarashi, P
Perrone, RD
Reed-Gitomer, B
Somlo, S
Torres, VE
Ketchum, CJ
Star, RA
Flessner, MF
Rasooly, RS
AF Guay-Woodford, Lisa M.
Henske, Elizabeth
Igarashi, Peter
Perrone, Ronald D.
Reed-Gitomer, Berenice
Somlo, Stefan
Torres, Vicente E.
Ketchum, Christian J.
Star, Robert A.
Flessner, Michael F.
Rasooly, Rebekah S.
TI Filling the Holes in Cystic Kidney Disease Research
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
AB Kidney disease is a significant medical and public health problem. The National Institute of Diabetes and Digestive and Kidney Diseases recently asked the community to identify research objectives, which, if addressed, could improve understanding of basic kidney function and aid in prevention, treatment, and reversal of kidney disease. The Kidney Research National Dialogue invited interested parties to submit, discuss, and prioritize ideas using an interactive website; 1600 participants posted more than 300 ideas covering all areas of kidney disease, including the cystic kidney diseases. Although much is known about the genetics and pathogenesis of cystic diseases, there remain challenges to our understanding of the fundamental mechanisms of cyst formation, what genes act as modifiers to cause variable responses in different people, and how to detect and monitor disease progression. This article summarizes key research questions for cystic kidney diseases.
C1 [Rasooly, Rebekah S.] NIDDK, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
RP Rasooly, RS (reprint author), NIDDK, Div Kidney Urol & Hematol Dis, NIH, Two Democracy Plaza,6707 Democracy Blvd,MSC 5458, Bethesda, MD 20892 USA.
EM rr185i@nih.gov
OI Rasooly, Rebekah/0000-0002-6357-5528; Igarashi,
Peter/0000-0001-8698-1185
FU NIDDK NIH HHS [P30 DK074038]
NR 2
TC 4
Z9 4
U1 0
U2 2
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD OCT
PY 2014
VL 9
IS 10
BP 1799
EP 1801
DI 10.2215/CJN.03410414
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA AQ3SF
UT WOS:000342713100018
PM 24903391
ER
PT J
AU Tuot, DS
Diamantidis, CJ
Corbett, CF
Boulware, LE
Fox, CH
Harwood, DH
Star, RA
Rys-Sikora, KE
Narva, A
AF Tuot, Delphine S.
Diamantidis, Clarissa Jonas
Corbett, Cynthia F.
Boulware, L. Ebony
Fox, Chester H.
Harwood, Donna H.
Star, Robert A.
Rys-Sikora, Krystyna E.
Narva, Andrew
TI The Last Mile: Translational Research to Improve CKD Outcomes
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
AB The National Institute of Diabetes and Digestive and Kidney Diseases supported Kidney Research National Dialogue asked the scientific community to formulate and prioritize research objectives that would enhance understanding of kidney function and disease and improve clinical outcomes. An engaged and growing group of investigators working in type 2 translation (from clinical evidence to implementation in the community) identified barriers to improving patient care in CKD and suggested research priorities to test translational strategies that have been effective for other chronic diseases.
C1 [Narva, Andrew] NIDDK, Div Kidney & Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
RP Narva, A (reprint author), NIDDK, Div Kidney & Urol & Hematol Dis, NIH, 6707 Democracy Blvd,MSC 5458, Bethesda, MD 20892 USA.
EM narvaa@niddk.nih.gov
FU National Institutes of Health (NIDDK, National Institute on Aging);
Patient-Centered Outcomes Research Institute
FX C.F.C currently receives funding from the National Institutes of Health
(NIDDK, National Institute on Aging), and current funding from the
Patient-Centered Outcomes Research Institute.
NR 3
TC 4
Z9 4
U1 0
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD OCT
PY 2014
VL 9
IS 10
BP 1802
EP 1805
DI 10.2215/CJN.04310514
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA AQ3SF
UT WOS:000342713100019
PM 24970870
ER
PT J
AU Bonventre, JV
Boulware, LE
Dember, LM
Freedman, BI
Furth, SL
Holzman, LB
Ketchum, CJ
Little, MH
Mehrotra, R
Moe, SM
Sands, JM
Sedor, JR
Somlo, S
Star, RA
Rys-Sikora, KE
AF Bonventre, Joseph V.
Boulware, L. Ebony
Dember, Laura M.
Freedman, Barry I.
Furth, Susan L.
Holzman, Lawrence B.
Ketchum, Christian J.
Little, Melissa H.
Mehrotra, Rajnish
Moe, Sharon M.
Sands, Jeff M.
Sedor, John R.
Somlo, Stefan
Star, Robert A.
Rys-Sikora, Krystyna E.
CA KRND
TI The Kidney Research National Dialogue: Gearing Up to Move Forward
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID DISEASE; THERAPIES
AB The National Institute of Diabetes and Digestive and Kidney Diseases supported Kidney Research National Dialogue asked the scientific community to formulate and prioritize research objectives that would improve our understanding of kidney function and disease; >1600 participants from >30 countries posted >300 ideas and >500 comments covering all areas of kidney research. Smaller groups of investigators interrogated the postings and published a series of commentaries in CJASN. Additional review of the entire series identified six cross-cutting themes: (1) increase training and team science opportunities to maintain/expand the nephrology workforce, (2) develop novel technologies to assess kidney function, (3) promote human discovery research to better understand normal and diseased kidney function, (4) establish integrative models of kidney function to inform diagnostic and treatment strategies, (5) promote interventional studies that incorporate more responsive outcomes and improved trial designs, and (6) foster translation from clinical investigation to community implementation. Together, these cross-cutting themes provide a research plan to better understand normal kidney biology and improve the prevention, diagnosis, and treatment of kidney disease, and as such, they will inform future research efforts supported by the National Institute of Diabetes and Digestive and Kidney Diseases through workshops and initiatives.
C1 [Rys-Sikora, Krystyna E.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Rys-Sikora, KE (reprint author), NIDDK, NIH, 6707 Democracy Blvd, Bethesda, MD 20892 USA.
EM Ryssikok@niddk.nih.gov
RI Little, Melissa/A-6170-2010
OI Little, Melissa/0000-0003-0380-2263
FU Novo Nordisk; National Institutes of Health; Baxter HealthCare; DaVita
FX J.V.B. is a coinventor on KIM-1 patents, which have been licensed by
Partners Healthcare to Sekisui, Ortho, Novartis, and Astute; received
grant funding from Novo Nordisk; received income for patient safety,
biomarkers, and kidney therapeutic consulting from Astellas, Sanofi, and
Keryx; and owns equity in Thrasos, Sentien, and Medibeacon. L.B.H.
received a consulting agreement with GlaxoSmithKline and grants from the
National Institutes of Health. M.H.L. is a scientific advisor to
Organovo Inc. R.M. received grant support and/or honoraria and/or data
for research from Baxter HealthCare and DaVita.
NR 12
TC 6
Z9 6
U1 0
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD OCT
PY 2014
VL 9
IS 10
BP 1806
EP 1811
DI 10.2215/CJN.07310714
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA AQ3SF
UT WOS:000342713100020
PM 25225184
ER
PT J
AU Suffredini, AF
Noveck, RJ
AF Suffredini, A. F.
Noveck, R. J.
TI Human Endotoxin Administration as an Experimental Model in Drug
Development
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Editorial Material
ID RESPONSES
AB Linking human physiology to inflammatory mechanisms discovered in vitro or in animal models is essential to determine their importance. Innate immunity underlies many of these inflammatory responses in health and disease. Bacterial endotoxin is the quintessential trigger of innate immune responses. When administered to humans, endotoxin has been an important means of demonstrating key inflammatory mechanisms in vivo. Furthermore, endotoxin challenges have provided opportunities to test the effects of novel inflammation-modifying agents in humans.
C1 [Suffredini, A. F.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Noveck, R. J.] Duke Univ, Sch Med, Dept Med, Div Clin Pharmacol,Duke Clin Res Unit, Durham, NC 27706 USA.
RP Noveck, RJ (reprint author), Duke Univ, Sch Med, Dept Med, Div Clin Pharmacol,Duke Clin Res Unit, Durham, NC 27706 USA.
EM robert.noveck@duke.edu
FU Intramural NIH HHS; NCATS NIH HHS [UL1TR001117]
NR 10
TC 6
Z9 6
U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
EI 1532-6535
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD OCT
PY 2014
VL 96
IS 4
BP 418
EP 422
DI 10.1038/clpt.2014.146
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AQ3FN
UT WOS:000342675400018
PM 25236665
ER
PT J
AU Rasmussen-Torvik, LJ
Stallings, SC
Gordon, AS
Almoguera, B
Basford, MA
Bielinski, SJ
Brautbar, A
Brilliant, MH
Carrell, DS
Connolly, JJ
Crosslin, DR
Doheny, KF
Gallego, CJ
Gottesman, O
Kim, DS
Leppig, KA
Li, R
Lin, S
Manzi, S
Mejia, AR
Pacheco, JA
Pan, V
Pathak, J
Perry, CL
Peterson, JF
Prows, CA
Ralston, J
Rasmussen, LV
Ritchie, MD
Sadhasivam, S
Scott, SA
Smith, M
Vega, A
Vinks, AA
Volpi, S
Wolf, WA
Bottinger, E
Chisholm, RL
Chute, CG
Haines, JL
Harley, JB
Keating, B
Holm, IA
Kullo, IJ
Jarvik, GP
Larson, EB
Manolio, T
McCarty, CA
Nickerson, DA
Scherer, SE
Williams, MS
Roden, DM
Denny, JC
AF Rasmussen-Torvik, L. J.
Stallings, S. C.
Gordon, A. S.
Almoguera, B.
Basford, M. A.
Bielinski, S. J.
Brautbar, A.
Brilliant, M. H.
Carrell, D. S.
Connolly, J. J.
Crosslin, D. R.
Doheny, K. F.
Gallego, C. J.
Gottesman, O.
Kim, D. S.
Leppig, K. A.
Li, R.
Lin, S.
Manzi, S.
Mejia, A. R.
Pacheco, J. A.
Pan, V.
Pathak, J.
Perry, C. L.
Peterson, J. F.
Prows, C. A.
Ralston, J.
Rasmussen, L. V.
Ritchie, M. D.
Sadhasivam, S.
Scott, S. A.
Smith, M.
Vega, A.
Vinks, A. A.
Volpi, S.
Wolf, W. A.
Bottinger, E.
Chisholm, R. L.
Chute, C. G.
Haines, J. L.
Harley, J. B.
Keating, B.
Holm, I. A.
Kullo, I. J.
Jarvik, G. P.
Larson, E. B.
Manolio, T.
McCarty, C. A.
Nickerson, D. A.
Scherer, S. E.
Williams, M. S.
Roden, D. M.
Denny, J. C.
TI Design and Anticipated Outcomes of the eMERGE-PGx Project: A Multicenter
Pilot for Preemptive Pharmacogenomics in Electronic Health Record
Systems
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; MEDICAL-RECORDS; PERSONALIZED MEDICINE;
GENETIC-VARIANTS; RESEARCH NETWORK; AFRICAN-AMERICANS; EXTRACTION
SYSTEM; PHENOME-WIDE; IMPLEMENTATION; CONSORTIUM
AB We describe here the design and initial implementation of the eMERGE-PGx project. eMERGE-PGx, a partnership of the Electronic Medical Records and Genomics Network and the Pharmacogenomics Research Network, has three objectives: (i) to deploy PGRNseq, a next-generation sequencing platform assessing sequence variation in 84 proposed pharmacogenes, in nearly 9,000 patients likely to be prescribed drugs of interest in a 1- to 3-year time frame across several clinical sites; (ii) to integrate well-established clinically validated pharmacogenetic genotypes into the electronic health record with associated clinical decision support and to assess process and clinical outcomes of implementation; and (iii) to develop a repository of pharmacogenetic variants of unknown significance linked to a repository of electronic health record-based clinical phenotype data for ongoing pharmacogenomics discovery. We describe site-specific project implementation and anticipated products, including genetic variant and phenotype data repositories, novel variant association studies, clinical decision support modules, clinical and process outcomes, approaches to managing incidental findings, and patient and clinician education methods.
C1 [Rasmussen-Torvik, L. J.; Rasmussen, L. V.] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Stallings, S. C.] Vanderbilt Inst Clin & Translat Res, Nashville, TN USA.
[Gordon, A. S.; Crosslin, D. R.; Kim, D. S.; Nickerson, D. A.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Almoguera, B.; Connolly, J. J.; Keating, B.] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
[Bielinski, S. J.] Mayo Clin, Dept Hlth Sci Res, Div Epidemiol, Rochester, MN USA.
[Brautbar, A.; Brilliant, M. H.] Marshfield Clin Res Fdn, Ctr Human Genet, Marshfield, WI USA.
[Carrell, D. S.; Leppig, K. A.; Ralston, J.; Larson, E. B.] Grp Hlth Res Inst, Seattle, WA USA.
[Doheny, K. F.] Johns Hopkins Univ, Sch Med, Inst Med Genet, Ctr Inherited Dis Res, Baltimore, MD USA.
[Gallego, C. J.; Jarvik, G. P.] Univ Washington, Div Med Genet, Seattle, WA 98195 USA.
[Gottesman, O.; Mejia, A. R.; Bottinger, E.] Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.
[Li, R.; Volpi, S.; Manolio, T.] NHGRI, Div Genom Med, Bethesda, MD 20892 USA.
[Lin, S.] Marshfield Clin Res Fdn, Biomed Informat Res Ctr, Marshfield, WI USA.
[Manzi, S.; Perry, C. L.; Wolf, W. A.] Boston Childrens Hosp, Div Genet & Genom, Boston, MA USA.
[Pacheco, J. A.; Pan, V.; Smith, M.; Chisholm, R. L.] Northwestern Univ, Feinberg Sch Med, Ctr Genet Med, Chicago, IL 60611 USA.
[Pathak, J.] Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN USA.
[Peterson, J. F.; Denny, J. C.] Vanderbilt Univ, Med Ctr, Dept Biomed Informat & Med, Nashville, TN USA.
[Prows, C. A.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat, Div Human Genet, Cincinnati, OH 45229 USA.
[Ritchie, M. D.] Penn State Univ, Dept Biochem & Mol Biol, State Coll, PA USA.
[Sadhasivam, S.] Cincinnati Childrens Hosp Med Ctr, Dept Anesthesia, Cincinnati, OH 45229 USA.
[Sadhasivam, S.; Vinks, A. A.; Harley, J. B.] Univ Cincinnati, Coll Med, Dept Pediat, Cincinnati, OH USA.
[Scott, S. A.] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
Icahn Sch Med Mt Sinai, Mt Sinai Fac Practice Associates Primary Care Pro, New York, NY 10029 USA.
[Prows, C. A.; Vinks, A. A.] Cincinnati Childrens Hosp Med Ctr, Div Clin Pharmacol, Cincinnati, OH 45229 USA.
[Wolf, W. A.; Holm, I. A.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Chute, C. G.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Haines, J. L.] Vanderbilt Univ, Med Ctr, Ctr Human Genet Res, Nashville, TN USA.
[Harley, J. B.] Univ Cincinnati, Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Harley, J. B.] US Dept Vet Affairs, Med Ctr, Cincinnati, OH USA.
[Holm, I. A.] Boston Childrens Hosp, Manton Ctr Orphan Dis Res, Boston, MA USA.
[Kullo, I. J.] Mayo Clin, Div Cardiovasc Dis, Rochester, MN USA.
[McCarty, C. A.] Essentia Inst Rural Hlth, Duluth, MN USA.
[Scherer, S. E.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Williams, M. S.] Geisinger Hlth Syst, Genom Med Inst, Danville, PA USA.
[Roden, D. M.] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37212 USA.
[Roden, D. M.; Denny, J. C.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
RP Rasmussen-Torvik, LJ (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
EM ljrtorvik@northwestern.edu
RI Bielinski, Suzette/A-2238-2009;
OI Bielinski, Suzette/0000-0002-2905-5430; Pan, Vivian/0000-0002-1666-9273;
Rasmussen, Luke/0000-0002-4497-8049
FU Cincinnati Children's Hospital Medical Center/Harvard [U01HG006828];
Children's Hospital of Philadelphia [U01HG006830]; Essentia Institute of
Rural Health [U01HG006389]; Geisinger Clinic [U01HG006382]; Group Health
Cooperative [U01HG006375]; University of Washington [U01HG006375]; Mayo
Clinic [U01HG006379]; Icahn School of Medicine at Mount Sinai
[U01HG006380]; Northwestern University [U01HG006388]; Vanderbilt
University [U01HG006378]; Vanderbilt serving as the coordinating center
[U01HG006385]; Deep Resequencing Resources of the Pharmacogenomic
Research Network [U01 HL069757, U19 GM61388, U01 GM097119]; National
Human Genome Research Institute [5U01HG006507]; Mayo Clinic Center for
Individualized Medicine; National Institutes of Health (Pharmacogenomics
Research Network) [U19 GM61388]; Rochester Epidemiology Project [R01
GM28157, U01 HG005137, R01 CA138461, R01 AG034676]; Pharmacogenomics of
Arrhythmia Therapy PGRN site grant from the National Institute of
General Medical Sciences; National Heart, Lung, and Blood Institute [U19
HL65262]; [U01HG004438]; [HL069757]
FX The eMERGE Network was funded through the following grants: U01HG006828
(Cincinnati Children's Hospital Medical Center/Harvard); U01HG006830
(Children's Hospital of Philadelphia); U01HG006389 (Essentia Institute
of Rural Health); U01HG006382 (Geisinger Clinic); U01HG006375 (Group
Health Cooperative and the University of Washington); U01HG006379 (Mayo
Clinic)); U01HG006380 (Icahn School of Medicine at Mount Sinai);
U01HG006388 (Northwestern University); U01HG006378 (Vanderbilt
University); and U01HG006385 (Vanderbilt serving as the coordinating
center). The development of the PGRN-Seq platform was supported by the
Deep Resequencing Resources of the Pharmacogenomic Research Network: U01
HL069757, U19 GM61388, and U01 GM097119. The activities being performed
at Johns Hopkins Center for Inherited Disease Research and Johns Hopkins
DNA Diagnostic Lab are funded by grant U01HG004438. This work is also
supported by grant (HL069757). One list of actionable genes was
generated with funding from the National Human Genome Research
Institute, 5U01HG006507. At Mayo Clinic this work was also supported in
part by Mayo Clinic Center for Individualized Medicine and National
Institutes of Health grants U19 GM61388 (the Pharmacogenomics Research
Network), R01 GM28157, U01 HG005137, R01 CA138461, and R01 AG034676 (the
Rochester Epidemiology Project). At Vanderbilt University, the work was
also supported by the Pharmacogenomics of Arrhythmia Therapy PGRN site
grant from the National Institute of General Medical Sciences and the
National Heart, Lung, and Blood Institute (U19 HL65262), which also
supports the site's participation in the Translational Pharmacogenetics
Program and the Clinical Pharmacogenetics Implementation Consortium.
NR 47
TC 53
Z9 54
U1 3
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9236
EI 1532-6535
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD OCT
PY 2014
VL 96
IS 4
BP 482
EP 489
DI 10.1038/clpt.2014.137
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AQ3FN
UT WOS:000342675400027
PM 24960519
ER
PT J
AU Baumlova, A
Chalupska, D
Rozycki, B
Jovic, M
Wisniewski, E
Klima, M
Dubankova, A
Kloer, DP
Nencka, R
Balla, T
Boura, E
AF Baumlova, Adriana
Chalupska, Dominika
Rozycki, Bartosz
Jovic, Marko
Wisniewski, Eva
Klima, Martin
Dubankova, Anna
Kloer, Daniel P.
Nencka, Radim
Balla, Tamas
Boura, Evzen
TI The crystal structure of the phosphatidylinositol 4-kinase II alpha
SO EMBO REPORTS
LA English
DT Article
DE crystal structure; kinase; membrane; Monte Carlo simulations;
phosphatidyl inositol
ID KINASE; GOLGI; COMPLEXES; REVEALS; BINDING; PROTEIN; DOMAIN;
PHOSPHOINOSITIDES; DETERMINANTS; RECRUITMENT
AB Phosphoinositides are a class of phospholipids generated by the action of phosphoinositide kinases with key regulatory functions in eukaryotic cells. Here, we present the atomic structure of phosphatidylinositol 4-kinase type II alpha (PI4K II alpha), in complex with ATP solved by X-ray crystallography at 2.8 angstrom resolution. The structure revealed a non-typical kinase fold that could be divided into Nand C-lobes with the ATP binding groove located in between. Surprisingly, a second ATP was found in a lateral hydrophobic pocket of the C-lobe. Molecular simulations and mutagenesis analysis revealed the membrane binding mode and the putative function of the hydrophobic pocket. Taken together, our results suggest a mechanism of PI4K II alpha recruitment, regulation, and function at the membrane.
C1 [Baumlova, Adriana; Chalupska, Dominika; Klima, Martin; Dubankova, Anna; Nencka, Radim; Boura, Evzen] Inst Organ Chem & Biochem AS CR, Prague, Czech Republic.
[Rozycki, Bartosz] Polish Acad Sci, Inst Phys, Warsaw, Poland.
[Jovic, Marko; Wisniewski, Eva; Balla, Tamas] NICHD, Sect Mol Signal Transduct, Program Dev Neurosci, NIH, Bethesda, MD USA.
[Kloer, Daniel P.] Syngenta, Jealotts Hill Int Res Ctr, Bracknell, Berks, England.
RP Boura, E (reprint author), Inst Organ Chem & Biochem AS CR, Prague, Czech Republic.
EM boura@uochb.cas.cz
RI Klima, Martin/G-5265-2014; Rozycki, Bartosz/B-7005-2009; Wisniewski,
Eva/O-9233-2015; Boura, Evzen/G-5275-2014; Nencka, Radim/G-5296-2014;
OI Rozycki, Bartosz/0000-0001-5938-7308; Wisniewski,
Eva/0000-0001-8698-6867; Balla, Tamas/0000-0002-9077-3335
FU MarieCurie FP7-PEOPLE-CIG [333916]; Ministry of Education of the Czech
Republic [LO1302]; Academy of Sciences Czech Republic [RVO: 61388963];
Polish National Science Centre [2012/05/B/NZ1/00631]; Eunice Kennedy
Shriver National Institute of Child Health and Human Development of the
NIH, Bethesda, MD, USA
FX Crystallographic data were collected at ESRF beamlines ID 14-4 and
ID-23-1 and at beamlines 14-1 and 14-2 operated by the Helmholtz-Zentrum
Berlin (HZB) at the BESSY II electron storage ring. This project was
supported by MarieCurie FP7-PEOPLE-2012-CIG, project number 333916 ( to
E.B.), by Project InterBioMed LO1302 from Ministry of Education of the
Czech Republic, and by the Academy of Sciences Czech Republic (RVO:
61388963). The work of B.R. was supported by the Polish National Science
Centre Grant No. 2012/05/B/NZ1/00631. The work of M.J., E.W., and T.B.
is supported by the intramural research program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development of the
NIH, Bethesda, MD, USA.
NR 35
TC 15
Z9 16
U1 2
U2 22
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1469-221X
EI 1469-3178
J9 EMBO REP
JI EMBO Rep.
PD OCT
PY 2014
VL 15
IS 10
BP 1085
EP 1092
DI 10.15252/embr.201438841
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AQ6AW
UT WOS:000342890700012
PM 25168678
ER
PT J
AU Berg, BA
Schoenbaum, G
McDannald, MA
AF Berg, Benjamin A.
Schoenbaum, Geoffrey
McDannald, Michael A.
TI The dorsal raphe nucleus is integral to negative prediction errors in
Pavlovian fear
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE conditioned suppression; learning; omission; rat
ID CONDITIONED SUPPRESSION; BASOLATERAL AMYGDALA; PERIAQUEDUCTAL GRAY;
OPIOID RECEPTORS; DOPAMINE NEURONS; RATS; PROJECTIONS; EXTINCTION;
UNCERTAINTY; MODULATION
AB Prediction errors are central to modern learning theories. While brain regions contributing to reward prediction errors have been uncovered, the sources of aversive prediction errors remain largely unknown. Here we used probabilistic and deterministic reinforcement procedures, followed by extinction, to examine the contribution of the dorsal raphe nucleus to negative, aversive prediction errors in Pavlovian fear. Rats with dorsal raphe lesions were able to acquire fear and reduce fear to a non-reinforced deterministic cue. However, dorsal raphe lesions impaired the reduction of fear to a probabilistic cue and fear extinction to a deterministic cue, both of which involve the use of negative prediction errors. The results point to an integral role for the dorsal raphe nucleus in negative prediction error signaling in Pavlovian fear.
C1 [Berg, Benjamin A.; Schoenbaum, Geoffrey; McDannald, Michael A.] NIDA, Intramural Res Program, Baltimore, MD USA.
[Schoenbaum, Geoffrey] Johns Hopkins Univ, Solomon H Snyder Dept Neurosci, Baltimore, MD USA.
[Schoenbaum, Geoffrey] Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA.
[McDannald, Michael A.] Boston Coll, Dept Psychol, Chestnut Hill, MA 02467 USA.
RP McDannald, MA (reprint author), Boston Coll, Dept Psychol, 514 McGuinn Hall,140 Commonwealth Ave, Chestnut Hill, MA 02467 USA.
EM michael.mcdannald@bc.edu
FU Intramural Research Program at the National Institute on Drug Abuse;
[DA034010]
FX We thank Dr Antonello Bonci for NIDA-IRP support, Dr Yavin Shaham and Dr
Donna Calu for laboratory space, Dr Peter Holland for discussion of the
results, Dr Thomas Stalnaker for extensive comments on early drafts, Dr
Bruce Hope and Klil Babin for microphotograph assistance, Dr Charles
Pickens for programming assistance and Aaron Mirenzi for histological
assistance. This work was supported by the Intramural Research Program
at the National Institute on Drug Abuse and DA034010 (M.A.M).
NR 35
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PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
EI 1460-9568
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD OCT
PY 2014
VL 40
IS 7
BP 3096
EP 3101
DI 10.1111/ejn.12676
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA AQ4VV
UT WOS:000342799400010
PM 25041165
ER
PT J
AU Yeboah, J
Carr, JJ
Terry, JG
Ding, JZ
Zeb, I
Liu, ST
Nasir, K
Post, W
Blumenthal, RS
Budoff, MJ
AF Yeboah, Joseph
Carr, J. Jeffery
Terry, James G.
Ding, Jingzhong
Zeb, Irfan
Liu, Songtao
Nasir, Khurram
Post, Wendy
Blumenthal, Roger S.
Budoff, Matthew J.
TI Computed tomography-derived cardiovascular risk markers, incident
cardiovascular events, and all-cause mortality in nondiabetics: the
Multi-Ethnic Study of Atherosclerosis
SO EUROPEAN JOURNAL OF PREVENTIVE CARDIOLOGY
LA English
DT Article
DE Cardiac CT-derived risk factors; cardiovascular events; coronary heart
disease; risk prediction
ID CORONARY-HEART-DISEASE; FATTY LIVER-DISEASE; ARTERY CALCIUM SCORE;
CALCIFICATION; CLASSIFICATION; PREDICTION; COHORT; MODEL; MESA; CT
AB Aim We assess the improvement in discrimination afforded by the addition of the computed tomography risk markers thoracic aorta calcium (TAC), aortic valve calcification (AVC), mitral annular calcification (MAC), pericardial adipose tissue volume (PAT), and liver attenuation (LA) to the Framingham risk score (FRS)+coronary artery calcium (CAC) for incident coronary heart disease (CHD) and incident cerebrovascular disease (CVD) in a multiethnic cohort.
Methods and results A total of 5745 participants were enrolled, with 2710 at intermediate Framingham risk, 210 CVD events, and 155 CHD events). Over 9 years of follow up, 251 had adjudicated CHD, 346 had CVD events, and 321 died. The data were analysed using Cox proportional hazard, receiver operator curve (ROC), and net reclassification improvement (NRI) analyses. In the whole cohort and also when the analysis was restricted to only the intermediate-risk participants, CAC, TAC, AVC, and MAC were all significantly associated with incident CVD, incident CHD, and mortality, and CAC had the strongest association. When added to the FRS, CAC had the highest area under the curve (AUC) for the prediction of incident CVD and incident CHD; LA had the least. The addition of TAC, AVC, MAC, PAT, and LA to FRS+CAC all resulted in a significant reduction in AUC for incident CHD (0.712 vs. 0.646, 0.655, 0.652, 0.648, and 0.569; all p<0.01, respectively) in participants with intermediate FRS. The addition of CAC to FRS resulted in an NRI of 0.547 for incident CHD in the intermediate-risk group. The NRI when TAC, AVC, MAC, PAT, and LA were added to FRS+CAC were 0.024, 0.026, 0.019, 0.012, and 0.012, respectively, for incident CHD in the intermediate-risk group. Similar results were obtained for incident CVD in the intermediate-risk group and also when the whole cohort was used instead of the intermediate FRS group.
Conclusions The addition of CAC to the FRS provides superior discrimination especially in intermediate-risk individuals compared with the addition of TAC, AVC, MAC, PAT, or LA for incident CVD and incident CHD. Compared with FRS+CAC, the addition of TAC, AVC, MAC, PAT, or LA individually to FRS+CAC worsens the discrimination for incident CVD and incident CHD. These risk markers are unlikely to be useful for improving cardiovascular risk prediction.
C1 [Yeboah, Joseph; Carr, J. Jeffery; Terry, James G.; Ding, Jingzhong] Wake Forest Sch Med, Winston Salem, NC 27157 USA.
[Zeb, Irfan] Bronx Lebanon Hosp Ctr, Bronx, NY 10456 USA.
[Liu, Songtao] NIH, Bethesda, MD 20892 USA.
[Nasir, Khurram; Post, Wendy; Blumenthal, Roger S.] Johns Hopkins Univ, Baltimore, MD USA.
[Budoff, Matthew J.] Harbor UCLA Med Ctr, Torrance, CA 90509 USA.
RP Yeboah, J (reprint author), Wake Forest Sch Med, Dept Internal Med Cardiol, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM jyeboah@wakehealth.edu
OI Carr, John/0000-0002-4398-8237
FU [N01-HC-95159]; [N01-HC-95167]; [R01 HL098445-02S1]; [R01 HL071739]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95167 and Diversity Supplement project (R01 HL098445-02S1; Carr
PI of parent grant; Yeboah PI of project) and R01 HL071739 (PI: Matthew
Budoff).
NR 24
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U1 0
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 2047-4873
EI 2047-4881
J9 EUR J PREV CARDIOL
JI Eur. J. Prev. Cardiol.
PD OCT
PY 2014
VL 21
IS 10
BP 1233
EP 1241
DI 10.1177/2047487313492065
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AQ5BP
UT WOS:000342818000005
PM 23689526
ER
PT J
AU Xiao, Y
Williams, JS
Brownell, I
AF Xiao, Ying
Williams, Jonathan S.
Brownell, Isaac
TI Merkel cells and touch domes: more than mechanosensory functions?
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Article
DE endocrine; immune; mechanosensation; Merkel cell; touch dome
ID HUMAN-FETAL SKIN; HAIR-FOLLICLES; CHROMOGRANIN-A;
SUBCELLULAR-DISTRIBUTION; LANGERHANS CELLS; DENDRITIC CELLS; MOUSE SKIN;
CD200; IMMUNOREACTIVITY; PROLIFERATION
AB The touch dome (TD) is an innervated structure in the epidermis of mammalian skin. Composed of specialized keratinocytes and neuroendocrine Merkel cells, the TD has distinct molecular characteristics compared to the surrounding epidermal keratinocytes. Much of the research on Merkel cell function has focused on their role in mechanosensation, specifically light touch. Recently, more has been discovered about Merkel cell molecular characteristics and their cells of origin. Here we review Merkel cell and TD biology, and discuss potential functions beyond mechanosensation.
C1 [Xiao, Ying; Williams, Jonathan S.; Brownell, Isaac] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Brownell, I (reprint author), 10 Ctr Dr,12N238, Bethesda, MD 20892 USA.
EM isaac.brownell@nih.gov
FU National Institutes of Health Intramural Research Program, Center for
Cancer Research, National Cancer Institute
FX We thank Dr. Amy Coxon for critical reading of the manuscript. This
manuscript was supported by the National Institutes of Health Intramural
Research Program, Center for 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 58
TC 3
Z9 3
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0906-6705
EI 1600-0625
J9 EXP DERMATOL
JI Exp. Dermatol.
PD OCT
PY 2014
VL 23
IS 10
BP 692
EP 695
DI 10.1111/exd.12456
PG 4
WC Dermatology
SC Dermatology
GA AQ4FY
UT WOS:000342749900002
PM 24862916
ER
PT J
AU Yin, LL
Coelho, SG
Ebsen, D
Smuda, C
Mahns, A
Miller, SA
Beer, JZ
Kolbe, L
Hearing, VJ
AF Yin, Lanlan
Coelho, Sergio G.
Ebsen, Dominik
Smuda, Christoph
Mahns, Andre
Miller, Sharon A.
Beer, Janusz Z.
Kolbe, Ludger
Hearing, Vincent J.
TI Epidermal gene expression and ethnic pigmentation variations among
individuals of Asian, European and African ancestry
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Article
DE microarray; pigmentation; racial; ethnic; skin
ID HUMAN SKIN PIGMENTATION; ULTRAVIOLET-RADIATION; MELANOCYTE DEVELOPMENT;
MELANIN CONTENT; UV-RADIATION; DNA-DAMAGE; RESPONSES; COLOR; PROTEIN;
PHOTOPROTECTION
AB Differences in visible skin pigmentation give rise to the wide variation of skin colours seen in racial/ethnic populations. Skin pigmentation is important not only from cosmetic and psychological points of view, but more importantly because of its implications for the risk of all types of skin cancers, on photoaging, etc. Despite differences in those parameters in Caucasian and Asian skin types, they are remarkably similar in their production and distribution of melanins, and the mechanism(s) underlying their different characteristics have remained obscure. In this study, we used microarray analysis of skin suction blisters to investigate molecular differences underlying the determination of pigmentation in various skin types, and we used immunohistochemistry to validate the expression patterns of several interesting targets that were identified. Intriguingly, Caucasian and Asian skins had highly similar gene expression patterns that differed significantly from the pattern of African skin. The results of this study suggest the dynamic interactions of different types of cells in human skin that regulate its pigmentation, reveal that the known pigmentation genes have a limited contribution and uncover a new array of genes, including NINL and S100A4, that might be involved in that regulation.
C1 [Yin, Lanlan; Coelho, Sergio G.; Ebsen, Dominik; Hearing, Vincent J.] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Smuda, Christoph; Mahns, Andre; Kolbe, Ludger] Beiersdorf AG, R&D Skin Res, Hamburg, Germany.
[Miller, Sharon A.; Beer, Janusz Z.] US FDA, Ctr Devices & Radiol Hlth, Silver Spring, MD USA.
RP Hearing, VJ (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37,Room 2132,MSC 4256, Bethesda, MD 20892 USA.
EM hearingv@nih.gov
FU Intramural Research Program of the National Cancer Institute; Office of
Science; Center for Devices and Radiological Health, Food and Drug
Administration
FX This work was supported in part by the Intramural Research Program of
the National Cancer Institute and in part by the Office of Science and
the Center for Devices and Radiological Health, Food and Drug
Administration.
NR 41
TC 4
Z9 4
U1 1
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0906-6705
EI 1600-0625
J9 EXP DERMATOL
JI Exp. Dermatol.
PD OCT
PY 2014
VL 23
IS 10
BP 731
EP 735
DI 10.1111/exd.12518
PG 5
WC Dermatology
SC Dermatology
GA AQ4FY
UT WOS:000342749900012
PM 25055985
ER
PT J
AU Guo, L
Gao, R
Xu, J
Jin, L
Cotrim, AP
Yan, X
Zheng, C
Goldsmith, CM
Shan, Z
Hai, B
Zhou, J
Zhang, C
Baum, BJ
Wang, S
AF Guo, L.
Gao, R.
Xu, J.
Jin, L.
Cotrim, A. P.
Yan, X.
Zheng, C.
Goldsmith, C. M.
Shan, Z.
Hai, B.
Zhou, J.
Zhang, C.
Baum, B. J.
Wang, S.
TI AdLTR(2)EF1 alpha-FGF2-mediated prevention of fractionated
irradiation-induced salivary hypofunction in swine
SO GENE THERAPY
LA English
DT Article
ID ADENOVIRAL-MEDIATED TRANSFER; RADIATION-INDUCED XEROSTOMIA; INCREASED
FLUID SECRETION; HUMAN AQUAPORIN-1 CDNA; PIG PAROTID-GLANDS;
QUALITY-OF-LIFE; NECK-CANCER; MINIATURE PIG; INDUCED APOPTOSIS;
GASTROINTESTINAL SYNDROME
AB Patients frequently experience a loss of salivary function following irradiation (IR) for the treatment of an oral cavity and oropharyngeal cancer. Herein, we tested if transfer of fibroblast growth factor-2 (FGF2) cDNA could limit salivary dysfunction after fractionated IR (7.5 or 9 Gy for 5 consecutive days to one parotid gland) in the miniature pig (minipig). Parotid salivary flow rates steadily decreased by 16 weeks post-IR, whereas blood flow in the targeted parotid gland began to decrease 3 days after beginning IR. By 2 weeks, post-IR salivary blood flow was reduced by 50%, at which point it remained stable for the remainder of the study. The single preadministration of a hybrid serotype 5 adenoviral vector encoding FGF2 (AdLTR(2)EF1a-FGF2) resulted in the protection of parotid microvascular endothelial cells from IR damage and significantly limited the decline of parotid salivary flow. Our results suggest that a local treatment directed at protecting salivary gland endothelial cells may be beneficial for patients undergoing IR for oral cavity and oropharyngeal cancer.
C1 [Guo, L.; Gao, R.; Xu, J.; Jin, L.; Yan, X.; Shan, Z.; Hai, B.; Zhou, J.; Zhang, C.; Wang, S.] Capital Med Univ, Salivary Gland Dis Ctr, Sch Stomatol, Beijing 100050, Peoples R China.
[Guo, L.; Gao, R.; Xu, J.; Jin, L.; Yan, X.; Shan, Z.; Hai, B.; Zhou, J.; Zhang, C.; Wang, S.] Capital Med Univ, Beijing Key Lab Tooth Regenerat & Funct Reconstru, Sch Stomatol, Beijing 100050, Peoples R China.
[Cotrim, A. P.; Zheng, C.; Goldsmith, C. M.; Baum, B. J.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, DHHS, Bethesda, MD USA.
[Wang, S.] Capital Med Univ, Sch Basic Med Sci, Sch Stomatol, Dept Biochem & Mol Biol, Beijing 100050, Peoples R China.
RP Wang, S (reprint author), Capital Med Univ, Sch Basic Med Sci, Sch Stomatol, Dept Biochem & Mol Biol, Tian Tan Xi Li 4, Beijing 100050, Peoples R China.
EM slwang@ccmu.edu.cn
FU National Natural Science Foundation of China [30430690, 81271164,
81070843]; National Special Foundation for Excellent PhD Paper [200778];
Division of Intramural Research of the National Institute of Dental and
Craniofacial Research
FX This study was supported by the National Natural Science Foundation of
China (Grant nos. 30430690,81271164 and 81070843) and the National
Special Foundation for Excellent PhD Paper No. 200778, and by the
Division of Intramural Research of the National Institute of Dental and
Craniofacial Research.
NR 38
TC 8
Z9 8
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0969-7128
EI 1476-5462
J9 GENE THER
JI Gene Ther.
PD OCT
PY 2014
VL 21
IS 10
BP 866
EP 873
DI 10.1038/gt.2014.63
PG 8
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 AQ7UD
UT WOS:000343023800002
PM 25030610
ER
PT J
AU Kocak, H
Ballew, BJ
Bisht, K
Eggebeen, R
Hicks, BD
Suman, S
O'Neil, A
Giri, N
Maillard, I
Alter, BP
Keegan, CE
Nandakumar, J
Savage, SA
AF Kocak, Hande
Ballew, Ban J.
Bisht, Kamlesh
Eggebeen, Rebecca
Hicks, Belynda D.
Suman, Shalabh
O'Neil, Adri
Giri, Neelam
Maillard, Ivan
Alter, Blanche P.
Keegan, Catherine E.
Nandakumar, Jayakrishnan
Savage, Sharon A.
CA NCI DCEG Canc Genomics Res Lab
NCI DCEG Canc Sequencing Working G
TI Hoyeraal-Hreidarsson syndrome caused by a germline mutation in the TEL
patch of the telomere protein TPP1
SO GENES & DEVELOPMENT
LA English
DT Article
DE dyskeratosis congenita; Hoyeraal-Hreidarsson syndrome; telomere; TPP1;
ACD; telomerase
ID BONE-MARROW FAILURE; DYSKERATOSIS-CONGENITA; BIOLOGY DISORDERS; LENGTH
REGULATOR; RECRUITMENT; COMPLEX; POT1; PROCESSIVITY; PROTECTION; RTEL1
AB Germline mutations in telomere biology genes cause dyskeratosis congenita (DC), an inherited bone marrow failure and cancer predisposition syndrome. DC is a clinically heterogeneous disorder diagnosed by the triad of dysplastic nails, abnormal skin pigmentation, and oral leukoplakia; Hoyeraal-Hreidarsson syndrome (HH), a clinically severe variant of DC, also includes cerebellar hypoplasia, immunodeficiency, and intrauterine growth retardation. Approximately 70% of DC cases are associated with a germline mutation in one of nine genes, the products of which are all involved in telomere biology. Using exome sequencing, we identified mutations in Adrenocortical Dysplasia Homo log (ACD) (encoding TPP1), a component of the telomeric shelterin complex, in one family affected by HH. The proband inherited a deletion from his father and a missense mutation from his mother, resulting in extremely short telomeres and a severe clinical phenotype. Characterization of the mutations revealed that the single-amino-acid deletion affecting the TEL patch surface of the TPP1 protein significantly compromises both telomerase recruitment and processivity, while the missense mutation in the TIN2-binding region of TPP1 is not as clearly deleterious to TPP1 function. Our results emphasize the critical roles of the TEL patch in proper stem cell function and demonstrate that TPP1 is the second shelterin component (in addition to TIN 2) to be implicated in DC.
C1 [Kocak, Hande; Keegan, Catherine E.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Ballew, Ban J.; Giri, Neelam; Alter, Blanche P.; Savage, Sharon A.; NCI DCEG Canc Genomics Res Lab; NCI DCEG Canc Sequencing Working G] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
[Bisht, Kamlesh] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA.
[Eggebeen, Rebecca; Hicks, Belynda D.; Suman, Shalabh; O'Neil, Adri] NCI Frederick, Canc Genom Res Lab, Leidos Biomed Res, Rockville, MD 20850 USA.
[Maillard, Ivan] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
[Maillard, Ivan] Univ Michigan, Div Hematol Oncol, Dept Internal Med, Aim Arbor, MI 48109 USA.
[Maillard, Ivan] Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA.
[Keegan, Catherine E.] Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA.
RP Savage, SA (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
EM jknanda@umich.edu; savagesh@mail.nih.gov
RI Tucker, Margaret/B-4297-2015; Hildesheim, Allan/B-9760-2015; Savage,
Sharon/B-9747-2015; Tobias, Geoffrey/M-4135-2016;
OI Hildesheim, Allan/0000-0003-0257-2363; Savage,
Sharon/0000-0001-6006-0740; Tobias, Geoffrey/0000-0002-2878-8253;
Dagnall, Casey/0000-0001-7334-4718
FU NIH [R00-CA-167644-03]; University of Michigan Nathan Shock Center
[P30-AG-013283, R01-HD-058606]; University of Michigan Rackham Graduate
School Barbour Scholarship; D. Dan and Betty Kahn Foundation; Division
of Cancer Epidemiology and Genetics, National Cancer Institute; Westat
[HHSN2612006550018C]
FX We thank Valerie Tesmer (J.N. laboratory) for expressing and purifying
human POT1 protein from insect cells, Jooho Chung (I.M. laboratory) and
Dr. David Ginsburg (University of Michigan) for access to and help with
the use of the cytocentrifuge, Gregg Sobocinski (University of Michigan)
for help with microscopy, Titia de Lange (Rockefeller University) for
the rabbit polyclonal TIN2 and TPP1 antibodies and the HeLa1.2.11 cell
line, Joachim Lingner (EPFL, Lausanne, Switzerland) for the
TERT-cDNA6/myc-HisC plasmid and phTR-Bluescript II SK(+) plasmids, Tom
Cech (University of Colorado) for the p3X-Flag-TPP1-CMV plasmid, and
Lisa Leathwood, RN, Ann Carr, MS, and Maureen Risch, RN, Westat
(Rockville, MD) for their excellent study support. We are grateful to
the study participants for their valuable contributions. This work was
supported in part by NIH R00-CA-167644-03 (to J.N.), University of
Michigan Nathan Shock Center P30-AG-013283 (pilot grant to J.N.),
R01-HD-058606 (to C.E.K.), a University of Michigan Rackham Graduate
School Barbour Scholarship (to H.K.), the D. Dan and Betty Kahn
Foundation (to I.M.), the intramural research program of the Division of
Cancer Epidemiology and Genetics, National Cancer Institute, and
contract HHSN2612006550018C with Westat.
NR 57
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U1 0
U2 14
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
EI 1549-5477
J9 GENE DEV
JI Genes Dev.
PD OCT 1
PY 2014
VL 28
IS 19
BP 2090
EP 2102
DI 10.1101/gad.248567.114
PG 13
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA AQ5ZX
UT WOS:000342888200003
PM 25233904
ER
PT J
AU Gray, SW
Martins, Y
Feuerman, LZ
Bernhardt, BA
Biesecker, BB
Christensen, KD
Joffe, S
Rini, C
Veenstra, D
McGuire, AL
AF Gray, Stacy W.
Martins, Yolanda
Feuerman, Lindsay Z.
Bernhardt, Barbara A.
Biesecker, Barbara B.
Christensen, Kurt D.
Joffe, Steven
Rini, Christine
Veenstra, David
McGuire, Amy L.
CA CSER Consortium Outcomes Measures
TI Social and behavioral research in genomic sequencing: approaches from
the Clinical Sequencing Exploratory Research Consortium Outcomes and
Measures Working Group
SO GENETICS IN MEDICINE
LA English
DT Review
DE behavior; genome sequencing; measures; outcomes; psychosocial
ID SMOKING-CESSATION; PSYCHOMETRIC EVALUATION; CANCER SUSCEPTIBILITY;
HUNTINGTONS-DISEASE; INFORMED-CONSENT; SCALE; RISK; VALIDATION; IMPACT;
QUESTIONNAIRE
AB The routine use of genomic sequencing in clinical medicine has the potential to dramatically alter patient care and medical outcomes. To fully understand the psychosocial and behavioral impact of sequencing integration into clinical practice, it is imperative that we identify the factors that influence sequencing-related decision making and patient outcomes. In an effort to develop a collaborative and conceptually grounded approach to studying sequencing adoption, members of the National Human Genome Research Institute's Clinical Sequencing Exploratory Research Consortium formed the Outcomes and Measures Working Group. Here we highlight the priority areas of investigation and psychosocial and behavioral outcomes identified by the Working Group. We also review some of the anticipated challenges to measurement in social and behavioral research related to genomic sequencing; opportunities for Instrument development; and the importance of qualitative, quantitative, and mixed-method approaches. This work represents the early, shared efforts of multiple research teams as we strive to understand individuals' experiences with genomic sequencing. The resulting body of knowledge will guide recommendations for the optimal use of sequencing in clinical practice.
C1 [Gray, Stacy W.; Martins, Yolanda] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Gray, Stacy W.; Christensen, Kurt D.] Harvard Univ, Sch Med, Boston, MA USA.
[Gray, Stacy W.; Christensen, Kurt D.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Feuerman, Lindsay Z.; McGuire, Amy L.] Baylor Coll Med, Ctr Med Eth & Hlth Policy, Houston, TX 77030 USA.
[Bernhardt, Barbara A.] Univ Penn, Sch Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Bernhardt, Barbara A.] Univ Penn, Penn Ctr Integrat Genet Healthcare Technol, Philadelphia, PA 19104 USA.
[Biesecker, Barbara B.] NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA.
[Joffe, Steven] Univ Penn, Dept Med Eth & Hlth Policy, Philadelphia, PA 19104 USA.
[Rini, Christine] Univ N Carolina, Chapel Hill, NC USA.
[Rini, Christine] UNC Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
[Veenstra, David] Univ Washington, Pharmaceut Outcomes Res & Policy Program, Dept Pharm, Seattle, WA 98195 USA.
RP Gray, SW (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM stacyw_gray@dfci.harvard.edu
OI Martins, Yolanda/0000-0002-3983-3531
FU National Human Genome Research Institute [1U01HG006485, 1U01HG006487,
1U01HG006492, 1U01HG006500, 1U01HG006507, 1U01HG005211, 1U01HG006546,
1U01HG007307, U01HG007303, 5R01HG006618, 5R01HG006615, 5R01HG006600,
5R21HG006596, 5R21HG006612, 5R21HG006613, 5R21HG006594, 1F32HG006993,
R01 GM109743]; National Human Research Institute, National Institutes of
Health; American Cancer Society [120529-MRSG-11-006-01-CPPB]
FX This work was funded by the National Human Genome Research Institute
grants 1U01HG006485, 1U01HG006487, 1U01HG006492, 1U01HG006500,
1U01HG006507, 1U01HG005211, 1U01HG006546, 1U01HG007307, U01HG007303,
5R01HG006618, 5R01HG006615, 5R01HG006600, 5R21HG006596, 5R21HG006612,
5R21HG006613, 5R21HG006594, 1F32HG006993, and R01 GM109743, Rettie AE;
the Intramural Research Program of the National Human Research
Institute, National Institutes of Health; and the American Cancer
Society (120529-MRSG-11-006-01-CPPB).
NR 75
TC 14
Z9 14
U1 4
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2014
VL 16
IS 10
BP 727
EP 735
DI 10.1038/gim.2014.26
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA AQ5YM
UT WOS:000342884500001
PM 24625446
ER
PT J
AU Lawrence, L
Sincan, M
Markel, T
Adams, DR
Gill, F
Godfrey, R
Golas, G
Groden, C
Landis, D
Nehrebecky, M
Park, G
Soldatos, A
Tifft, C
Toro, C
Wahl, C
Wolfe, L
Gahl, WA
Boerkoel, CF
AF Lawrence, Lauren
Sincan, Murat
Markel, Thomas
Adams, David R.
Gill, Fred
Godfrey, Rena
Golas, Gretchen
Groden, Catherine
Landis, Dennis
Nehrebecky, Michele
Park, Grace
Soldatos, Ariane
Tifft, Cynthia
Toro, Camilo
Wahl, Colleen
Wolfe, Lynne
Gahl, William A.
Boerkoel, Cornelius F.
TI The implications of familial incidental findings from exome sequencing:
the NIH Undiagnosed Diseases Program experience
SO GENETICS IN MEDICINE
LA English
DT Article
DE exome sequencing; familial; incidental findings; NIH Undiagnosed
Diseases Program; secondary variants
ID CARDIAC SODIUM-CHANNEL; LONG-QT SYNDROME; DEFECTIVE APOLIPOPROTEIN
B-100; HYPERTROPHIC CARDIOMYOPATHY; ATRIAL-FIBRILLATION;
GENETIC-VARIANTS; ADRENOCORTICAL TUMORS; ACMG RECOMMENDATIONS; HIGH
PREVALENCE; SCN5A VARIANTS
AB Purpose: Using exome sequence data from 159 families participating in the National Institutes of Health Undiagnosed Diseases Program, we evaluated the number and inheritance mode of reportable incidental sequence variants.
Methods: Following the American College of Medical Genetics and Genomics recommendations for reporting of incidental findings from next-generation sequencing, we extracted variants in 56 genes from the exome sequence data of 543 subjects and determined the reportable incidental findings for each participant. We also defined variant status as inherited or de novo for those with available parental sequence data.
Results: We identified 14 independent reportable variants in 159 (8.8%) families. For nine families with parental sequence data in our cohort, a parent transmitted the variant to one or more children (nine minor children and four adult children). The remaining five variants occurred in adults for whom parental sequences Were unavailable.
Conclusion: Our results are consistent with the expectation that a small percentage of exomes will result in identification of an incidental finding under the American College of Medical Genetics and Genomics recommendations. Additionally, our analysis of family sequence data highlights that genome and exome sequencing of families has unavoidable implications for immediate family members and therefore requires appropriate counseling for the family.
C1 [Lawrence, Lauren; Sincan, Murat; Markel, Thomas; Adams, David R.; Godfrey, Rena; Golas, Gretchen; Groden, Catherine; Landis, Dennis; Nehrebecky, Michele; Soldatos, Ariane; Tifft, Cynthia; Toro, Camilo; Wahl, Colleen; Wolfe, Lynne; Gahl, William A.; Boerkoel, Cornelius F.] NIH, Undiagnosed Dis Program, Common Fund, NIH Off Director, Bethesda, MD 20892 USA.
[Lawrence, Lauren; Sincan, Murat; Markel, Thomas; Adams, David R.; Godfrey, Rena; Golas, Gretchen; Groden, Catherine; Landis, Dennis; Nehrebecky, Michele; Soldatos, Ariane; Tifft, Cynthia; Toro, Camilo; Wahl, Colleen; Wolfe, Lynne; Gahl, William A.; Boerkoel, Cornelius F.] NHGRI, Bethesda, MD 20892 USA.
[Lawrence, Lauren] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Gill, Fred; Park, Grace] NIH, Internal Med Consult Serv, Ctr Clin, Bethesda, MD 20892 USA.
RP Sincan, M (reprint author), NIH, Undiagnosed Dis Program, Common Fund, NIH Off Director, Bldg 10, Bethesda, MD 20892 USA.
EM murat.sincan@nih.gov
FU Office of the Director; NHGRI (National Institutes of Health, Bethesda,
MD)
FX We thank Patricia Birch and Shelin Adam for critical review of the
manuscript. We thank the staff at the National Human Genome Research
Institute (NHGRI) Intramural Sequencing Center for their sequencing,
alignment, genotyping, and annotation services. This work was supported
in part by the Common Fund, Office of the Director, and the Intramural
Research Program of the NHGRI (National Institutes of Health, Bethesda,
MD).
NR 52
TC 16
Z9 16
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2014
VL 16
IS 10
BP 741
EP 750
DI 10.1038/gim.2014.29
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA AQ5YM
UT WOS:000342884500004
PM 24784157
ER
PT J
AU Ruhl, CE
Menke, A
Cowie, CC
Everhart, JE
AF Ruhl, Constance E.
Menke, Andy
Cowie, Catherine C.
Everhart, James E.
TI Relationship of Hepatitis C Virus Infection With Diabetes in the US
Population
SO HEPATOLOGY
LA English
DT Article
ID BETA-CELL FUNCTION; INSULIN-RESISTANCE; LIVER-CIRRHOSIS; PREVALENCE;
MELLITUS; METAANALYSIS; IMPACT; RISK; ASSOCIATION; GLUCOSE
AB An association of hepatitis C virus (HCV) infection with diabetes has been reported in many studies, but few have been population based and applied standard criteria for diabetes diagnosis. We examined this relationship using recent population-based data from the U.S. National Health and Nutrition Examination Survey. Adult participants (15,128) in the 1999-2010 surveys had data on diabetes status and serum HCV antibody (anti-HCV) or HCV RNA. Using American Diabetes Association criteria, diabetes was defined as a health care provider diagnosis, serum hemoglobin A(1C) (A1C) 6.5%, or fasting plasma glucose (FPG) 126 mg/dL, prediabetes as A1C 5.7%-<6.5% or FPG 100-<126 mg/dL, and normal glucose as A1C <5.7% and FPG <100 mg/dL. Odds ratios (ORs) for diabetes and prediabetes, comparing persons with HCV infection to those without, were adjusted for demographics, BMI, C-reactive protein, smoking, drinking, and blood transfusion before 1992. Among participants without diabetes, we compared mean insulin resistance (IR), estimated using homeostasis model assessment (HOMA-IR), by HCV status. The overall prevalence of anti-HCV+ was 1.7%, of HCV RNA(+) 1.1%, of diabetes 10.5%, and of prediabetes 32.8%. The prevalence of diabetes and prediabetes did not differ by HCV status. In multivariate-adjusted analysis, diabetes remained unassociated with anti-HCV (OR, 1.0; 95% confidence interval [CI]: 0.6-1.7) or with HCV RNA (OR, 1.1; 95% CI: 0.6-1.9). In contrast, elevated alanine aminotransferase and gamma glutamyltransferase activities were associated with diabetes regardless of HCV status. HOMA-IR was not associated with HCV markers in unadjusted or multivariate-adjusted analyses (P > 0.05). Conclusion: In the U.S. population, HCV was not associated with diabetes or with IR among persons with normal glucose. Previously reported relationships of HCV with diabetes were possibly attributable to the effect of elevated liver enzymes. (Hepatology 2014;60:1139-1149)
C1 [Ruhl, Constance E.; Menke, Andy] Social & Sci Syst Inc, Silver Spring, MD 20910 USA.
[Cowie, Catherine C.; Everhart, James E.] NIDDK, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Ruhl, CE (reprint author), Social & Sci Syst Inc, 8757 Georgia Ave,12th Floor, Silver Spring, MD 20910 USA.
EM cruhl@s-3.com
FU National Institute of Diabetes and Digestive and Kidney Diseases
[HHSN276201200161U]
FX This work was supported by a contract from the National Institute of
Diabetes and Digestive and Kidney Diseases (HHSN276201200161U).
NR 34
TC 30
Z9 32
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2014
VL 60
IS 4
BP 1139
EP 1149
DI 10.1002/hep.27047
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ3AW
UT WOS:000342662100007
PM 24500979
ER
PT J
AU Werner, JM
Serti, E
Chepa-Lotrea, X
Stoltzfus, J
Ahlenstiel, G
Noureddin, M
Feld, JJ
Liang, TJ
Rotman, Y
Rehermann, B
AF Werner, Jens M.
Serti, Elisavet
Chepa-Lotrea, Xenia
Stoltzfus, Jonathan
Ahlenstiel, Golo
Noureddin, Mazen
Feld, Jordan J.
Liang, T. Jake
Rotman, Yaron
Rehermann, Barbara
TI Ribavirin Improves the IFN-gamma Response of Natural Killer Cells to
IFN-Based Therapy of Hepatitis C Virus Infection
SO HEPATOLOGY
LA English
DT Article
ID INTERFERON-ALPHA; GENE-EXPRESSION; PEGINTERFERON; COMBINATION;
INDUCTION; DYNAMICS; STAT4
AB Ribavirin (RBV) is an important component of interferon (IFN)-based and direct antiviral treatment regimens for hepatitis C virus (HCV) infection. Immunomodulation, in particular improvement of the host IFN response, has been proposed as RBV's mechanism of action. Natural killer (NK) cells are sensitive biomarkers for IFN-/ receptor signaling, as NK cell cytotoxicity and IFN- production are regulated by signal transducer and activator of transcription (STAT)1- and STAT4-phosphorylation, respectively. Specifically, pSTAT1-dependent NK cell cytotoxicity increases and pSTAT4-dependent IFN- production decreases in response to endogenous, virus-induced IFN- and during IFN--based therapy. To assess whether RBV has a direct effect on NK cells and/or improves the IFN- response of NK cells in the presence of IFN-, we prospectively studied 22 HCV patients with and 32 patients without 4 weeks of RBV pretreatment, who all received subsequent pegylated (Peg)IFN/ribavirin combination therapy. During RBV pretreatment, both the frequency of CD56(dim) NK cells with cytotoxic effector functions and the frequency of CD56(bright) NK cells with the capacity to produce IFN- decreased (P=0.049 and P=0.001, respectively). In vitro or in vivo exposure of NK cells to RBV improved the pSTAT4 (P<0.01) but not pSTAT1 response of NK cells to subsequent stimulation with IFN-. This was associated with an increase in IFN- production but not cytotoxicity of NK cells during subsequent IFN--based therapy. The frequency of IFN--producing NK cells was greater in fast second-phase virological responders than in slow responders. Conclusion: RBV enhances the pSTAT4 and IFN- response of NK cells to IFN--stimulation.
C1 [Werner, Jens M.; Serti, Elisavet; Chepa-Lotrea, Xenia; Stoltzfus, Jonathan; Ahlenstiel, Golo; Rehermann, Barbara] NIDDK, Immunol Sect, NIH, DHHS, Bethesda, MD 20892 USA.
[Werner, Jens M.; Serti, Elisavet; Chepa-Lotrea, Xenia; Stoltzfus, Jonathan; Ahlenstiel, Golo; Noureddin, Mazen; Feld, Jordan J.; Liang, T. Jake; Rotman, Yaron; Rehermann, Barbara] NIDDK, Liver Dis Branch, NIH, DHHS, Bethesda, MD 20892 USA.
RP Rehermann, B (reprint author), NIDDK, Immunol Sect, Liver Dis Branch, NIH,DHHS, 10 Ctr Dr,Bldg 10,Rm 9B16, Bethesda, MD 20892 USA.
EM Rehermann@nih.gov
OI Ahlenstiel, Golo/0000-0003-0026-1457
FU NIDDK, NIH intramural research program; Deutsche Forschungsgemeinschaft
(DFG), Bonn, Germany [We-4675/1-1]
FX Supported by the NIDDK, NIH intramural research program. J.M.W. was
supported by grant We-4675/1-1 from the Deutsche Forschungsgemeinschaft
(DFG), Bonn, Germany.
NR 32
TC 12
Z9 12
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2014
VL 60
IS 4
BP 1160
EP 1169
DI 10.1002/hep.27092
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ3AW
UT WOS:000342662100009
PM 24700342
ER
PT J
AU Yin, S
Wang, H
Bertola, A
Feng, DC
Xu, MJ
Wang, Y
Gao, B
AF Yin, Shi
Wang, Hua
Bertola, Adeline
Feng, Dechun
Xu, Ming-jiang
Wang, Yan
Gao, Bin
TI Activation of Invariant Natural Killer T Cells Impedes Liver
Regeneration by Way of Both IFN-gamma- and IL-4-Dependent Mechanisms
SO HEPATOLOGY
LA English
DT Article
ID HEPATIC NKT CELLS; PARTIAL-HEPATECTOMY; INNATE IMMUNITY; IN-VIVO; SIGNAL
TRANSDUCER; MICE; RESPONSES; SYSTEM; INJURY; ROLES
AB Invariant natural killer T (iNKT) cells are a major subset of lymphocytes found in the liver. These cells mediate various functions, including hepatic injury, fibrogenesis, and carcinogenesis. However, the function of iNKT cells in liver regeneration remains unclear. In the present study, partial hepatectomy (PHx) was used to study liver regeneration. -Galactosylceramide (-GalCer), a specific ligand for iNKT cells, was used to induce iNKT cell activation. After PHx, two strains of iNKT cell-deficient mice, CD1d(-/-) and J281(-/-) mice, showed normal liver regeneration. Injection of -GalCer before or after PHx, which rapidly stimulated interferon-gamma (IFN-) and interleukin (IL)-4 production by iNKT cells, markedly inhibited liver regeneration. In vitro treatment with IFN- inhibited hepatocyte proliferation. In agreement with this in vitro finding, genetic disruption of IFN- or its downstream signaling molecule signal transducer and activator of transcription (STAT)1 significantly abolished the -GalCer-mediated inhibition of liver regeneration. In vitro exposure to IL-4 did not affect hepatocyte proliferation, but surprisingly, genetic ablation of IL-4 or its downstream signaling molecule STAT6 partially eliminated the inhibitory effect of -GalCer on liver regeneration. Further studies revealed that IL-4 contributed to -GalCer-induced iNKT cell expansion and IFN- production, thereby inhibiting liver regeneration. Conclusion: iNKT cells play a minor role in controlling liver regeneration after PHx under healthy conditions. Activation of iNKT cells by -GalCer induces the production of IFN-, which directly inhibits liver regeneration, and IL-4, which indirectly attenuates liver regeneration by stimulating iNKT cell expansion and IFN- production. (Hepatology 2014;60:1356-1366)
C1 [Yin, Shi; Wang, Hua; Bertola, Adeline; Feng, Dechun; Xu, Ming-jiang; Wang, Yan; Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD 20892 USA.
[Yin, Shi] Anhui Med Univ, Dept Geriatr, Affiliated Prov Hosp, Hefei, Peoples R China.
[Wang, Hua] Anhui Med Univ, Inst Liver Dis, Hefei, Peoples R China.
RP Gao, B (reprint author), NIAAA, Lab Liver Dis, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA.
EM bgao@mail.nih.gov
RI Feng, Dechun/Q-5962-2016
FU NIAAA, NIH; Natural Science Foundation of China [81100311/H0318]; New
Century Excellent Talents in University, Ministry of Education of China
[NCET-13-0644]
FX Supported in part through funding from the intramural program of NIAAA,
NIH (B Gao), the Natural Science Foundation of China (to S. Yin, No.
81100311/H0318), and the New Century Excellent Talents in University,
Ministry of Education of China (to H. Wang, No. NCET-13-0644).
NR 31
TC 9
Z9 9
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2014
VL 60
IS 4
BP 1356
EP 1366
DI 10.1002/hep.27128
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ3AW
UT WOS:000342662100027
PM 24623351
ER
PT J
AU Navarro, VJ
Barnhart, H
Bonkovsky, HL
Davern, T
Fontana, RJ
Grant, L
Reddy, KR
Seeff, LB
Serrano, J
Sherker, AH
Stolz, A
Talwalkar, J
Vega, M
Vuppalanchi, R
AF Navarro, Victor J.
Barnhart, Huiman
Bonkovsky, Herbert L.
Davern, Timothy
Fontana, Robert J.
Grant, Lafaine
Reddy, K. Rajender
Seeff, Leonard B.
Serrano, Jose
Sherker, Averell H.
Stolz, Andrew
Talwalkar, Jayant
Vega, Maricruz
Vuppalanchi, Raj
TI Liver Injury From Herbals and Dietary Supplements in the US Drug-Induced
Liver Injury Network
SO HEPATOLOGY
LA English
DT Article
ID UNITED-STATES; HEAVY-METALS; MEDICINES; ADULTS; PATTERNS; OUTCOMES;
HEALTH
AB The Drug-Induced Liver Injury Network (DILIN) studies hepatotoxicity caused by conventional medications as well as herbals and dietary supplements (HDS). To characterize hepatotoxicity and its outcomes from HDS versus medications, patients with hepatotoxicity attributed to medications or HDS were enrolled prospectively between 2004 and 2013. The study took place among eight U.S. referral centers that are part of the DILIN. Consecutive patients with liver injury referred to a DILIN center were eligible. The final sample comprised 130 (15.5%) of all subjects enrolled (839) who were judged to have experienced liver injury caused by HDS. Hepatotoxicity caused by HDS was evaluated by expert opinion. Demographic and clinical characteristics and outcome assessments, including death and liver transplantation (LT), were ascertained. Cases were stratified and compared according to the type of agent implicated in liver injury; 45 had injury caused by bodybuilding HDS, 85 by nonbodybuilding HDS, and 709 by medications. Liver injury caused by HDS increased from 7% to 20% (P<0.001) during the study period. Bodybuilding HDS caused prolonged jaundice (median, 91 days) in young men, but did not result in any fatalities or LT. The remaining HDS cases presented as hepatocellular injury, predominantly in middle-aged women, and, more frequently, led to death or transplantation, compared to injury from medications (13% vs. 3%; P<0.05). Conclusions: The proportion of liver injury cases attributed to HDS in DILIN has increased significantly. Liver injury from nonbodybuilding HDS is more severe than from bodybuilding HDS or medications, as evidenced by differences in unfavorable outcomes (death and transplantation). (Hepatology 2014;60:1399-1408)
C1 [Navarro, Victor J.; Seeff, Leonard B.; Vega, Maricruz] Einstein Med Ctr, Hepatol Div, Dept Med, Philadelphia, PA 19141 USA.
[Barnhart, Huiman] Duke Univ Med Ctr, Duke Sch Med, Dept Biostat & Bioinformat, Duke Clin Res Inst, Durham, NC USA.
[Bonkovsky, Herbert L.] Carolinas HealthCare Syst, Dept Med, Charlotte, NC USA.
[Bonkovsky, Herbert L.] Carolinas HealthCare Syst, Dept Res, Charlotte, NC USA.
[Davern, Timothy] Calif Pacific Med Ctr, Dept Transplantat, San Francisco, CA USA.
[Fontana, Robert J.] Univ Michigan, Dept Internal Med, Univ Michigan Med Sch, Ann Arbor, MI 48109 USA.
[Grant, Lafaine] Univ Texas Southwestern, Div Digest & Liver Dis, Dept Internal Med, Dallas, TX USA.
[Reddy, K. Rajender] Univ Penn, Div Gastroenterol & Hepatol, Philadelphia, PA 19104 USA.
[Serrano, Jose] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
[Sherker, Averell H.] NIDDK, Liver Dis Res Branch, NIH, Bethesda, MD USA.
[Stolz, Andrew] Univ So Calif, Keck Sch Med, Dept Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA.
[Talwalkar, Jayant] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Vuppalanchi, Raj] Indiana Univ, Dept Med, Div Gastroenterol, Indianapolis, IN USA.
RP Navarro, VJ (reprint author), Einstein Med Ctr, Div Hepatol, 5401 Old York Rd,Suite 505, Philadelphia, PA 19141 USA.
EM NavarroV@einstein.edu
OI Vuppalanchi, Raj/0000-0003-0637-1577
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
FX The Drug Induced Liver Injury Network (DILIN) is a cooperative network
funded by the National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK). See the DILIN website
(https://dilin.dcri.duke.edu/publications-1) for a complete listing of
funding sources, sites, investigators, coinvestigators, coordinators,
and staff.
NR 39
TC 57
Z9 61
U1 4
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2014
VL 60
IS 4
BP 1399
EP 1408
DI 10.1002/hep.27317
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ3AW
UT WOS:000342662100031
PM 25043597
ER
PT J
AU Landis, WG
Rohr, JR
Moe, SJ
Balbus, JM
Clements, W
Fritz, A
Helm, R
Hickey, C
Hooper, M
Stahl, RG
Stauber, J
AF Landis, Wayne G.
Rohr, Jason R.
Moe, S. Jannicke
Balbus, John M.
Clements, William
Fritz, Alyce
Helm, Roger
Hickey, Christopher
Hooper, Michael
Stahl, Ralph G.
Stauber, Jenny
TI Global Climate Change and Contaminants, a Call to Arms Not Yet Heard?
SO INTEGRATED ENVIRONMENTAL ASSESSMENT AND MANAGEMENT
LA English
DT Editorial Material
C1 [Landis, Wayne G.] Western Washington Univ, Huxley Coll, Bellingham, WA 98225 USA.
[Rohr, Jason R.] Univ S Florida, Tampa, FL USA.
[Moe, S. Jannicke] Norwegian Inst Water Res, Oslo, Norway.
[Balbus, John M.] NIH, Bethesda, MD 20892 USA.
[Clements, William] Colorado State Univ, Ft Collins, CO 80523 USA.
[Fritz, Alyce] NOAA, Seattle, WA USA.
[Helm, Roger] US Fish & Wildlife Serv, Arlington, VA USA.
[Hickey, Christopher] Natl Inst Water & Atmospher Res, Hamilton, New Zealand.
[Hooper, Michael] US Geol Survey, Columbia, MO USA.
[Stahl, Ralph G.] DuPont Co Inc, Wilmington, DC USA.
RP Landis, WG (reprint author), Western Washington Univ, Huxley Coll, Bellingham, WA 98225 USA.
EM wayne.landis@wwu.edu
RI Stauber, Jenny/G-8418-2011;
OI Moe, Jannicke/0000-0002-3681-3551; Hooper, Michael/0000-0002-4161-8961
NR 10
TC 4
Z9 4
U1 3
U2 22
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1551-3777
EI 1551-3793
J9 INTEGR ENVIRON ASSES
JI Integr. Environ. Assess. Manag.
PD OCT
PY 2014
VL 10
IS 4
BP 483
EP 484
DI 10.1002/ieam.1568
PG 2
WC Environmental Sciences; Toxicology
SC Environmental Sciences & Ecology; Toxicology
GA AQ2KZ
UT WOS:000342616200001
PM 25069904
ER
PT J
AU Sun, Y
Desierto, MJ
Ueda, Y
Kajigaya, S
Chen, JC
Young, NS
AF Sun, Yu
Desierto, Marie J.
Ueda, Yasutaka
Kajigaya, Sachiko
Chen, Jichun
Young, Neal S.
TI Peromyscus leucopus mice: a potential animal model for haematological
studies
SO INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE haematological measurements; monocytes; Mus musculus mice; Peromyscus
leucopus mice; platelets; reactive oxygen species; megakaryocytes;
spleen; disease modeling
ID WHITE-FOOTED MOUSE; DISEASE-ENZOOTIC SITE; BORRELIA-BURGDORFERI; BRAIN
SITE; MELATONIN; AGE; HANTAVIRUSES; INHIBITION; INFECTION; RESPONSES
AB Peromyscus leucopus mice share physical similarities with laboratory mice Mus musculus (MM) but have higher agility and longer lifespan. We compared domesticated P. leucopus linville (PLL) and M. musculus C57BL/6 (MMB6) mice for cellular composition of peripheral blood (PB), bone marrow (BM) and spleen. PLL mice had significantly fewer platelets and significantly more monocytes in the blood, and notably fewer megakaryocytes in the BM. Spleens of PLL mice were significantly smaller, with 50% fewer cells and reduced 'red pulp'. There was no obvious haematological change in PLL mice between 2-8 and 16-26 months of age, except for a significant increase in blood monocytes. Cellular reactive oxygen species (ROS) content showed no change with age but differed significantly between different cell types. Treating two to eight month-old PLL mice with antioxidant N-acetylcysteine in drinking water for three months did not affect cellular ROS content, but increased blood leucocytes especially the concentration of monocytes. The low platelets, low megakaryocytes, high monocytes and low splenic erythropoiesis in PLL mice resemble human measurements better than the values seen in MMB6.
C1 [Sun, Yu] Soochow Univ, Affiliated Hosp 2, Dept Hematol, Suzhou, Jiangsu, Peoples R China.
[Sun, Yu; Desierto, Marie J.; Ueda, Yasutaka; Kajigaya, Sachiko; Chen, Jichun; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Chen, JC (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10 Clin Res Ctr,Room 3-5132,10 Ctr Dr, Bethesda, MD 20892 USA.
EM chenji@nhlbi.nih.gov
FU National Heart, Lung and Blood Institute; Soochow University
FX This work was supported by National Heart, Lung and Blood Institute
Intramural Research Program and by a scholarship from Soochow University
to Dr. Yu Sun.
NR 32
TC 3
Z9 3
U1 2
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0959-9673
EI 1365-2613
J9 INT J EXP PATHOL
JI Int. J. Exp. Pathol.
PD OCT
PY 2014
VL 95
IS 5
BP 342
EP 350
DI 10.1111/iep.12091
PG 9
WC Pathology
SC Pathology
GA AQ4MY
UT WOS:000342773500004
PM 25116892
ER
PT J
AU Golding, J
Gregory, S
Iles-Caven, Y
Lingam, R
Davis, JM
Emmett, P
Steer, CD
Hibbeln, JR
AF Golding, Jean
Gregory, Steven
Iles-Caven, Yasmin
Lingam, Raghu
Davis, John M.
Emmett, Pauline
Steer, Colin D.
Hibbeln, Joseph R.
TI Parental, Prenatal, and Neonatal Associations With Ball Skills at Age 8
Using an Exposome Approach
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article
DE ALSPAC; ball skills; motor coordination; maternal environmental
background; exposome
ID MOTOR DEVELOPMENT; CHILDREN ALSPAC; FULL-TERM; COHORT; COORDINATION
AB There is little consistency in the literature concerning factors that influence motor coordination in children. A hypothesis-free exposome approach was used with 7359 children using longitudinal information covering 3 generations in regard to throwing a ball accurately at age 7 years. The analyses showed an independent robust negative association with mother's unhappiness in her midchildhood (6-11 years). No such association was present for study fathers. The offspring of parents who described themselves as having poor eyesight had poorer ability. This hypothesis-free approach has identified a strong negative association with an unhappy childhood. Future studies of this cohort will be used to determine whether the mechanism is manifest through differing parenting skills, or a biological mechanism reflecting epigenetic effects.
C1 [Golding, Jean; Gregory, Steven; Iles-Caven, Yasmin; Emmett, Pauline; Steer, Colin D.] Univ Bristol, Sch Social & Community Med, Ctr Child & Adolescent Hlth, Bristol BS8 2BN, Avon, England.
[Lingam, Raghu] Univ London London Sch Hyg & Trop Med, Dept Populat Hlth, London WC1E 7HT, England.
[Davis, John M.] Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA.
[Hibbeln, Joseph R.] NIAAA, Sect Nutr Neurosci, NIH, Bethesda, MD USA.
RP Golding, J (reprint author), Univ Bristol, Sch Social & Community Med, Ctr Child & Adolescent Hlth, Barley House, Bristol BS8 2BN, Avon, England.
EM jean.golding@bristol.ac.uk
OI Emmett, Pauline/0000-0003-1076-4779; Golding, Jean/0000-0003-2826-3307
FU The UK Medical Research Council (MRC); Wellcome Trust; University of
Bristol; Waterloo Foundation [130/1478]; National Institute on Alcohol
Abuse and Alcoholism, National Institutes of Health (NIH); Medical
Research Council [G1100226]
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: The UK Medical
Research Council (MRC), the Wellcome Trust and the University of Bristol
currently provide core support for the Avon Longitudinal Study of
Parents and Children. The statistical analyses for this project were
undertaken with funding from the Waterloo Foundation (grant no.
130/1478), the support from the Intramural Research Program of the
National Institute on Alcohol Abuse and Alcoholism, National Institutes
of Health (NIH) and the Medical Research Council (grant no. G1100226).
NR 21
TC 0
Z9 0
U1 0
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0883-0738
EI 1708-8283
J9 J CHILD NEUROL
JI J. Child Neurol.
PD OCT
PY 2014
VL 29
IS 10
BP 1390
EP 1398
DI 10.1177/0883073814530501
PG 9
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA AQ5CZ
UT WOS:000342823700029
PM 24828115
ER
PT J
AU Baskin, DG
Hewitt, SM
AF Baskin, Denis G.
Hewitt, Stephen M.
TI Improving the State of the Science of Immunohistochemistry: The
Histochemical Society's Standards of Practice
SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
LA English
DT Editorial Material
C1 [Baskin, Denis G.] Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, R&D Serv, Seattle, WA USA.
[Baskin, Denis G.] Univ Washington, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA 98195 USA.
[Hewitt, Stephen M.] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Hewitt, SM (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM genejock@helix.nih.gov
OI Hewitt, Stephen/0000-0001-8283-1788
FU Intramural NIH HHS; NIDDK NIH HHS [P30DK017047, P30 DK017047]
NR 2
TC 2
Z9 2
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0022-1554
EI 1551-5044
J9 J HISTOCHEM CYTOCHEM
JI J. Histochem. Cytochem.
PD OCT
PY 2014
VL 62
IS 10
BP 691
EP 692
DI 10.1369/0022155414538453
PG 2
WC Cell Biology
SC Cell Biology
GA AQ5GU
UT WOS:000342836200001
PM 25085896
ER
PT J
AU Hewitt, SM
Baskin, DG
Frevert, CW
Stahl, WL
Rosa-Molinar, E
AF Hewitt, Stephen M.
Baskin, Denis G.
Frevert, Charles W.
Stahl, William L.
Rosa-Molinar, Eduardo
TI Controls for Immunohistochemistry: The Histochemical Society's Standards
of Practice for Validation of Immunohistochemical Assays
SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
LA English
DT Article
DE Immunohistochemistry; immunocytochemistry; antibodies; controls;
validation; assay; standards
ID ANTIBODY SPECIFICITY; IMMUNOCYTOCHEMISTRY
AB Immunohistochemistry is widely used in biomedical research to localize specific epitopes of molecules in cells and tissues. The validity of interpretations based on immunohistochemistry requires appropriate positive and negative controls that are often not reported in publications. This omission may lead to incorrect interpretations and irreproducible results in the literature and contribute to wasted time, effort, and resources as well as erosion of confidence in scientific investigation by the general public, legislative bodies and funding agencies. The present article summarizes essential controls required for validation of immunohistochemical findings and represents a standard of practice for the use of immunohistochemistry in research and diagnostic investigations. Adherence to the guidelines described in the present article can be cited by authors as support for the validity of interpretations of the immunohistochemistry reported in their publications.
C1 [Hewitt, Stephen M.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Baskin, Denis G.; Stahl, William L.] Univ Washington, Dept Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Baskin, Denis G.; Stahl, William L.] Univ Washington, Dept Med, Seattle, WA USA.
[Frevert, Charles W.] Univ Washington, Dept Comparat Med, Seattle, WA USA.
[Stahl, William L.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
[Stahl, William L.] Univ Washington, Dept Physiol & Biophys, Seattle, WA 98195 USA.
[Rosa-Molinar, Eduardo] Univ Puerto Rico Med Sci, Inst Neurobiol, San Juan, PR USA.
RP Hewitt, SM (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, MSC 4605, Bethesda, MD 20892 USA.
EM genejock@helix.nih.gov
OI Hewitt, Stephen/0000-0001-8283-1788
FU NIH, National Cancer Institute, Center for Cancer Research; Research and
Development Service of the Department of Veterans Health Administration,
Department of Veterans Affairs; Cellular and Molecular Imaging Core of
the Diabetes Research Center at the University of Washington (NIH)
[P30DK017047]; Department of Veterans Affairs Senior Research Career
Scientist award; NIH [GM108470]; NSF [NSF-1002410, NSF-1137725]; Puerto
Rico Science Technology and Research Trust [2013-000034]
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: Partial
funding for SMH's research was provided by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research. DGB acknowledges the Research and Development Service of the
Department of Veterans Health Administration, Department of Veterans
Affairs, and the Cellular and Molecular Imaging Core of the Diabetes
Research Center at the University of Washington (NIH grant P30DK017047),
for providing partial funding for this research.". DGB is the recipient
of a Department of Veterans Affairs Senior Research Career Scientist
award. ERM acknowledges NIH (GM108470), NSF (NSF-1002410 and
NSF-1137725), and the Puerto Rico Science Technology and Research Trust
(Agreement No: 2013-000034) for providing partial funding for this
research. CWF acknowledges NIH (P30 DK089507).
NR 12
TC 20
Z9 20
U1 0
U2 10
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0022-1554
EI 1551-5044
J9 J HISTOCHEM CYTOCHEM
JI J. Histochem. Cytochem.
PD OCT
PY 2014
VL 62
IS 10
BP 693
EP 697
DI 10.1369/0022155414545224
PG 5
WC Cell Biology
SC Cell Biology
GA AQ5GU
UT WOS:000342836200002
PM 25023613
ER
PT J
AU Veech, RL
AF Veech, Richard L.
TI Ketone ester effects on metabolism and transcription
SO JOURNAL OF LIPID RESEARCH
LA English
DT Review
DE D-beta-hydroxybutyrate - R-1,3 butanediol monoester; elevated blood
ketones; Alzheimer's disease; antioxidants; diabetes; fatty acid;
deacetylase; ketosis
ID KETOGENIC DIET; (R)-3-HYDROXYBUTYL (R)-3-HYDROXYBUTYRATE;
PYRUVATE-DEHYDROGENASE; BETA-HYDROXYBUTYRATE; BODIES; INSULIN; RAT
AB Ketosis induced by starvation or feeding a ketogenic diet has widespread and often contradictory effects due to the simultaneous elevation of both ketone bodies and free fatty acids. The elevation of ketone bodies increases the energy of ATP hydrolysis by reducing the mitochondrial NAD couple and oxidizing the coenzyme Q couple, thus increasing the redox span between site I and site II. In contrast, metabolism of fatty acids leads to a reduction of both mitochondrial NAD and mitochondrial coenzyme Q causing a decrease in the Delta G of ATP hydrolysis. In contrast, feeding ketone body esters leads to pure ketosis, unaccompanied by elevation of free fatty acids, producing a physiological state not previously seen in nature. The effects of pure ketosis on transcription and upon certain neurodegenerative diseases make approach not only interesting, but of potential therapeutic value.
C1 NIAAA, Lab Metab Control, NIH, Bethesda, MD 20892 USA.
RP Veech, RL (reprint author), NIAAA, Lab Metab Control, NIH, Bethesda, MD 20892 USA.
EM rveech@mail.nih.gov
NR 29
TC 5
Z9 5
U1 2
U2 14
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
EI 1539-7262
J9 J LIPID RES
JI J. Lipid Res.
PD OCT
PY 2014
VL 55
IS 10
BP 2004
EP 2006
DI 10.1194/jlr.R046292
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AQ6MA
UT WOS:000342925400004
PM 24714648
ER
PT J
AU Zha, WB
Edin, ML
Vendrov, KC
Schuck, RN
Lih, FB
Jat, JL
Bradbury, JA
DeGraff, LM
Hua, KJ
Tomer, KB
Falck, JR
Zeldin, DC
Lee, CR
AF Zha, Weibin
Edin, Matthew L.
Vendrov, Kimberly C.
Schuck, Robert N.
Lih, Fred B.
Jat, Jawahar Lal
Bradbury, J. Alyce
DeGraff, Laura M.
Hua, Kunjie
Tomer, Kenneth B.
Falck, John R.
Zeldin, Darryl C.
Lee, Craig R.
TI Functional characterization of cytochrome P450-derived
epoxyeicosatrienoic acids in adipogenesis and obesity
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE adipose tissue; arachidonic acid; eicosanoids; high-fat diet;
metabolomics; soluble epoxide hydrolase
ID SOLUBLE EPOXIDE HYDROLASE; HIGH-FAT DIET; CELL-DERIVED ADIPOCYTES;
INSULIN-RESISTANCE; ADIPOSE-TISSUE; 3T3-L1 PREADIPOCYTES;
TRANSCRIPTIONAL REGULATION; EICOSANOID METABOLISM; INFLAMMATORY
RESPONSE; GLUCOSE-HOMEOSTASIS
AB Adipogenesis plays a critical role in the initiation and progression of obesity. Although cytochrome P450 (CYP)-derived epoxyeicosatrienoic acids (EETs) have emerged as a potential therapeutic target for cardiometabolic disease, the functional contribution of EETs to adipogenesis and the pathogenesis of obesity remain poorly understood. Our studies demonstrated that induction of adipogenesis in differentiated 3T3-L1 cells (in vitro) and obesity-associated adipose expansion in high-fat diet (HFD)-fed mice (in vivo) significantly dysregulate the CYP epoxygenase pathway and evoke a marked suppression of adipose-derived EET levels. Subsequent in vitro experiments demonstrated that exogenous EET analog administration elicits potent anti-adipogenic effects via inhibition of the early phase of adipogenesis. Furthermore, EET analog administration to mice significantly mitigated HFD-induced weight gain, adipose tissue expansion, pro-adipogenic gene expression, and glucose intolerance. Collectively, these findings suggest that suppression of EET bioavailability in adipose tissue is a key pathological consequence of obesity, and strategies that promote the protective effects of EETs in adipose tissue offer enormous therapeutic potential for obesity and its downstream pathological consequences.
C1 [Zha, Weibin; Vendrov, Kimberly C.; Schuck, Robert N.; Lee, Craig R.] Univ N Carolina, Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC 27514 USA.
[Hua, Kunjie] Univ N Carolina, UNC Nutr Obes Res Ctr, Chapel Hill, NC USA.
[Edin, Matthew L.; Lih, Fred B.; Bradbury, J. Alyce; DeGraff, Laura M.; Tomer, Kenneth B.; Zeldin, Darryl C.] NIEHS, Lab Resp Biol, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
[Jat, Jawahar Lal; Falck, John R.] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA.
RP Lee, CR (reprint author), Univ N Carolina, Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC 27514 USA.
EM craig_lee@unc.edu
OI Edin, Matthew/0000-0002-7042-500X; Lee, Craig/0000-0003-3595-5301
FU American Heart Association; Robert A. Welch Foundation [GM31278];
Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01 ES050167, Z01
ES025034]; [R01 GM088199]; [P30 DK34987]; [P30 DK056350]
FX This work was supported by grant R01 GM088199 to C. R. L.; a predoctoral
fellowship from the American Heart Association to R.N.S.; grant GM31278
and support from the Robert A. Welch Foundation to J.R.F.; grant P30
DK34987 to the UNC Center for Gastrointestinal Biology and Disease;
grant P30 DK056350 to the UNC Nutrition Obesity Research Center; and
funds from the Intramural Research Program of the National Institutes of
Health, National Institute of Environmental Health Sciences to K. B. T.
(Z01 ES050167) and D.C.Z. (Z01 ES025034).
NR 49
TC 12
Z9 12
U1 0
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
EI 1539-7262
J9 J LIPID RES
JI J. Lipid Res.
PD OCT
PY 2014
VL 55
IS 10
BP 2124
EP 2136
DI 10.1194/jlr.M053199
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AQ6MA
UT WOS:000342925400016
PM 25114171
ER
PT J
AU Seaborn, T
Ravni, A
Au, R
Chow, BKC
Fournier, A
Wurtz, O
Vaudry, H
Eiden, LE
Vaudry, D
AF Seaborn, Tommy
Ravni, Aurelia
Au, Ruby
Chow, Bill K. C.
Fournier, Alain
Wurtz, Olivier
Vaudry, Hubert
Eiden, Lee E.
Vaudry, David
TI Induction of serpinb1a by PACAP or NGF is required for PC12 cells
survival after serum withdrawal
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE caspase; cell death; cell survival; nerve growth factor;
neuroprotection; pituitary adenylate cyclase-activating polypeptide
ID NERVE GROWTH-FACTOR; CYCLASE-ACTIVATING POLYPEPTIDE; PROTEIN-KINASE-C;
CEREBELLAR GRANULE CELLS; ELEMENT-BINDING PROTEIN; ADENYLATE-CYCLASE;
NEURITE OUTGROWTH; GENE-EXPRESSION; INDUCED APOPTOSIS; CYCLIC-AMP
AB PC12 cells are used to study the signaling mechanisms underlying the neurotrophic and neuroprotective activities of pituitary adenylate cyclase-activating polypeptide (PACAP) and nerve growth factor (NGF). Previous microarray experiments indicated that serpinb1a was the most induced gene after 6h of treatment with PACAP or NGF. This study confirmed that serpinb1a is strongly activated by PACAP and NGF in a time-dependent manner with a maximum induction (similar to 50-fold over control) observed after 6h of treatment. Co-incubation with PACAP and NGF resulted in a synergistic up-regulation of serpinb1a expression (200-fold over control), suggesting that PACAP and NGF act through complementary mechanisms. Consistently, PACAP-induced serpinb1a expression was not blocked by TrkA receptor inhibition. Nevertheless, the stimulation of serpinb1a expression by PACAP and NGF was significantly reduced in the presence of extracellular signal-regulated kinase, calcineurin, protein kinase A, p38, and PI3K inhibitors, indicating that the two trophic factors share some common pathways in the regulation of serpinb1a. Finally, functional investigations conducted with siRNA revealed that serpinb1a is not involved in the effects of PACAP and NGF on PC12 cell neuritogenesis, proliferation or body cell volume but mediates their ability to block caspases 3/7 activity and to promote PC12 cell survival.
C1 [Seaborn, Tommy; Ravni, Aurelia; Au, Ruby; Wurtz, Olivier; Vaudry, Hubert; Vaudry, David] INSERM, Neurotroph Factor & Neuronal Differentiat Team, DC2N, U982, Mont St Aignan, France.
[Seaborn, Tommy; Ravni, Aurelia; Au, Ruby; Fournier, Alain; Wurtz, Olivier; Vaudry, Hubert; Vaudry, David] Int Associated Lab Samuel de Champlain, Mont St Aignan, France.
[Seaborn, Tommy] Univ Laval, CRCHUQ, Hop St Francois Assise, Dept Pediat, Quebec City, PQ, Canada.
[Ravni, Aurelia; Wurtz, Olivier; Vaudry, Hubert; Vaudry, David] Univ Rouen, PRIMACEN, IRIB, F-76821 Mont St Aignan, France.
[Au, Ruby; Chow, Bill K. C.] Univ Hong Kong, Dept Zool, Hong Kong, Hong Kong, Peoples R China.
[Fournier, Alain] Univ Quebec, Inst Natl Rech Sci, Inst Armand Frappier, Pointe Claire, PQ, Canada.
[Eiden, Lee E.] NIMH, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
RP Vaudry, D (reprint author), Univ Rouen, INSERM, Neurotroph Factor & Neuronal Differentiat Team, U982, F-76821 Mont St Aignan, France.
EM david.vaudry@univ-rouen.fr
RI Wurtz, Olivier/H-5494-2015;
OI Wurtz, Olivier/0000-0003-2628-4745; Eiden, Lee/0000-0001-7524-944X;
Vaudry, David/0000-0003-3567-7452
FU Ministry of Education; INSERM postdoctoral fellowship; INSERM (U982);
National Institute of Mental Health (NIMH) Intramural Research Program;
INSERM-FRSQ program; Interreg TC2N project; Region Haute-Normandie
FX The authors wish to thank Mr Colas Calbrix and Mrs Milene Tetsi for
skillful technical assistance. A. R. was the recipient of a doctoral
fellowship from the Ministry of Education. T. S. was the recipient of an
INSERM postdoctoral fellowship. D. V. and H. V. are Affiliated
Professors at the INRS - Institut Armand-Frappier. This study was
supported by INSERM (U982), the National Institute of Mental Health
(NIMH) Intramural Research Program, an INSERM-FRSQ program (to A. F. and
D. V.), the Interreg TC2N project, and the Region Haute-Normandie.
Authors declare that they have no conflict of interest. Part of this
work was presented on a poster during the 11th International Symposium
on VIP. PACAP and related Peptides that took place in Pies, Hungary from
August 23 to 31, 2013.
NR 81
TC 2
Z9 2
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD OCT
PY 2014
VL 131
IS 1
BP 21
EP 32
DI 10.1111/jnc.12780
PG 12
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AQ5KZ
UT WOS:000342849000004
PM 24899316
ER
PT J
AU Yong, RL
Wu, TX
Mihatov, N
Shen, MJ
Brown, MA
Zaghloul, KA
Park, GE
Park, JK
AF Yong, Raymund L.
Wu, Tianxia
Mihatov, Nino
Shen, Michael J.
Brown, M. Anthony
Zaghloul, Kareem A.
Park, Grace E.
Park, John K.
TI Residual tumor volume and patient survival following reoperation for
recurrent glioblastoma
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE reoperation; recurrent tumor; glioblastoma; survival; oncology
ID TEMOZOLOMIDE; MULTIFORME; SURGERY; TRIALS
AB Object. Maximal safe tumor resection is part of the standard of care for patients with newly diagnosed glioblastoma. The role of reoperation in the care of patients with recurrent glioblastoma is less clear, and less than a quarter of patients undergo a second surgery. Previous studies have identified preoperative variables associated with the improved survival of patients following reoperation, and guidelines for the selection of patients for reoperation have been devised and validated. In this study, the authors analyzed the relative survival benefit of maximal safe tumor removal in a series of patients with recurrent glioblastoma who all underwent reoperation.
Methods. In this longitudinal study, the clinical and radiological data of 97 consecutive patients who underwent reoperation for recurrent glioblastoma were prospectively collected. Multiple regression analyses and Kaplan-Meier plotting were performed to identify pre- and postoperative clinical and radiological variables associated with increased survival following reoperation.
Results. The median postoperative survival of all patients following reoperation was 12.4 months (95% confidence interval [CI] 9.0-15.6 months). Multiple Cox regression analysis revealed that patients with large (>3 cm(3)) residual tumors following reoperation had significantly decreased survival relative to those with residual tumors that were small (>0-3 cm(3); hazard ratio [HR] = 3.10,95% CI 1.69-5.70; p < 0.001) or radiologically absent (0 cm(3); HR = 5.82, 95% CI 2.98-11.37; p < 0.001). Large residual tumors had faster rates of subsequent regrowth than small (odds ratio [OR] = 4.22,95% CI 1.19-14.97; p = 0.026) or radiologically absent (OR = 11.00,95% CI 2.79-43.43; p = 0.001) residual tumors, and a faster regrowth rate was significantly associated with decreased survival (BR = 4.01, 95% CI 2.26-7.14; p < 0.001).
Conclusions. The overall survival of patients with recurrent glioblastoma who underwent reoperations increased with decreasing postoperative residual tumor volumes. For patients meeting prognostic criteria for reoperation, the surgical goal should be to minimize residual tumor volume to maximize overall survival.
C1 [Yong, Raymund L.; Wu, Tianxia; Mihatov, Nino; Shen, Michael J.; Brown, M. Anthony; Zaghloul, Kareem A.] NINDS, NIH, Bethesda, MD 20892 USA.
[Park, Grace E.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Park, John K.] Santa Barbara Neurosci Inst Cottage Hlth Syst, Santa Barbara, CA 93105 USA.
RP Park, JK (reprint author), Santa Barbara Neurosci Inst Cottage Hlth Syst, 400 W Pueblo St, Santa Barbara, CA 93105 USA.
EM jparkmd@outlook.com
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke, NIH
FX This work was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, NIH. The
authors report no conflict of interest concerning the materials or
methods used in this study or the findings specified in this paper.
NR 13
TC 8
Z9 8
U1 0
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
EI 1933-0693
J9 J NEUROSURG
JI J. Neurosurg.
PD OCT
PY 2014
VL 121
IS 4
BP 802
EP 809
DI 10.3171/2014.6.JNS132038
PG 8
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA AQ7DR
UT WOS:000342973300008
PM 25061868
ER
PT J
AU Linge, SO
Mardal, KA
Helgeland, A
Heiss, JD
Haughton, V
AF Linge, Svein O.
Mardal, Kent-A.
Helgeland, Anders
Heiss, John D.
Haughton, Victor
TI Effect of craniovertebral decompression on CSF dynamics in Chiari
malformation Type I studied with computational fluid dynamics
SO JOURNAL OF NEUROSURGERY-SPINE
LA English
DT Article
DE Chiari malformation; decompression surgery; cervical; computer
simulation
ID CEREBROSPINAL-FLUID; CRANIOCERVICAL DECOMPRESSION; INTRACRANIAL
COMPLIANCE; FORAMEN MAGNUM; FLOW-ANALYSIS
AB Object. The effect of craniovertebral decompression surgery on CSF flow dynamics in patients with Chiari malformation Type I (CM-I) has been incompletely characterized. The authors used computational fluid dynamics to calculate the effect of decompression surgery on CSF flow dynamics in the posterior fossa and upper cervical spinal canal.
Methods. Oscillatory flow was simulated in idealized 3D models of the normal adult and the CM-I subarachnoid spaces (both previously described) and in 3 models of CM-I post craniovertebral decompressions. The 3 postoperative models were created from the CM model by virtually modifying the CM model subarachnoid space to simulate surgical decompressions of different magnitudes. Velocities and pressures were computed with the Navier-Stokes equations in Star-CD for multiple cycles of CSF flow oscillating at 80 cycles/min. Pressure gradients and velocities were compared for 8 levels extending from the posterior fossa to the C3-4 level. Relative pressures and peak velocities were plotted by level from the posterior fossa to C3-4. The heterogeneity of flow velocity distribution around the spinal cord was compared between models.
Results. Peak systolic velocities were generally lower in the postoperative models than in the preoperative CM model. With the 2 larger surgical defects, peak systolic velocities were brought closer to normal model velocities (equal values at C-3 and C-4) than with the smallest surgical defect. For the smallest defect, peak velocities were decreased, but not to levels in the normal model. In the postoperative models, heterogeneity in flow velocity distribution around the spinal cord increased from normal model levels as the degree of decompression increased.
Pressures in the 5 models differed in magnitude and in pattern. Pressure gradients along the spinal canal in the normal and CM models were nonlinear, with steeper gradients below C3-4 than above. The CM model had a steeper pressure gradient than the normal model above C3-4 and the same gradient below. The postoperative models had lower pressure gradients than the CM model above C2-3. The most conservative decompression had lower pressure gradients than the normal model above C2-3. The two larger decompression defects had CSF pressure gradients below those in the normal model above C2-3. These 2 models had a less steep gradient above C-3 and a steeper gradient below.
Conclusions. In computer simulations, craniovertebral surgical defects generally diminished CSF velocities and CSF pressures.
C1 [Linge, Svein O.] Telemark Univ Coll, N-3901 Porsgrunn, Norway.
[Linge, Svein O.; Mardal, Kent-A.; Helgeland, Anders; Haughton, Victor] Simula Res Lab, Ctr Biomed Comp, Lysake, Norway.
[Helgeland, Anders] Norwegian Def Res Estab FFI, Kjeller, Norway.
[Heiss, John D.] NIH, Surg Neurol Branch, Bethesda, MD 20892 USA.
[Haughton, Victor] Univ Wisconsin Hosp & Clin, Dept Radiol, Madison, WI 53792 USA.
RP Linge, SO (reprint author), Telemark Univ Coll, POB 203, N-3901 Porsgrunn, Norway.
EM sveinlin@simula.no
FU Norwegian Research Council to the Center for Biomedical Computing at
Simula Research Laboratory
FX This study was supported by a Center of Excellence grant from the
Norwegian Research Council to the Center for Biomedical Computing at
Simula Research Laboratory.
NR 22
TC 2
Z9 4
U1 0
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 1547-5654
EI 1547-5646
J9 J NEUROSURG-SPINE
JI J. Neurosurg.-Spine
PD OCT
PY 2014
VL 21
IS 4
BP 559
EP 564
DI 10.3171/2014.6.SPINE13950
PG 6
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA AQ7CO
UT WOS:000342970400008
PM 25084032
ER
PT J
AU Atkinson, EC
Thiara, D
Tamura, D
DiGiovanna, JJ
Kraemer, KH
Hadigan, C
AF Atkinson, Emily C.
Thiara, Diana
Tamura, Deborah
DiGiovanna, John J.
Kraemer, Kenneth H.
Hadigan, Colleen
TI Growth and Nutrition in Children With Trichothiodystrophy
SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION
LA English
DT Article
DE DNA repair defects; failure to thrive; growth; nutrition; transcription
defects; trichothiodystrophy
ID DNA-REPAIR DEFICIENCY; XERODERMA-PIGMENTOSUM; COCKAYNE-SYNDROME; BRITTLE
HAIR; FACTOR TFIIH; TRANSCRIPTION; MITOCHONDRIA; INDIVIDUALS; MICE
AB Objectives: Trichothiodystrophy (TTD) is a rare autosomal recessive disorder of DNA repair and transcription. Patients have multisystem abnormalities, including alterations in growth and development. This report characterizes the growth and nutritional status of a cohort of children with TTD.
Methods: Twenty-five patients with TTD were evaluated through a natural history study of patients with DNA repair diseases at the National Institutes of Health. Mean length of follow-up was 2.7 years. Retrospective and prospective data on nutritional status and height/weight were collected.
Results: In general, patients with TTD had considerable abnormalities in growth, with a mean height-for-age z score of -2.75 and a mean weight-for-age z score of -2.60 at baseline clinical evaluation. The median weight-for-length at baseline was, however, 50th percentile and indicators of adequate nutrition such as serum albumin, hemoglobin, and vitamins D and B-12 were largely within normal limits. Changes in growth parameters as children aged were characterized by further separation from standard growth curves (change height-for-age z score/year [-0.18 +/- 0.42] and weight-for-age z score/year [-0.36 +/- 0.51]). Patients who died during follow-up (n = 5) had significantly lower standardized height (P = 0.03) and weight (P = 0.006), weight-for-length (<0.0001), and higher heart rates (P = 0.02) compared with the remainder of the cohort.
Conclusions: Children with TTD have markedly diminished weight-for-age and height-for-age relative to reference populations. The cause for this stunted growth remains unclear but does not appear to be related to poor nutrient absorption or malnutrition.
C1 [Atkinson, Emily C.; Thiara, Diana; Hadigan, Colleen] NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA.
[Tamura, Deborah; DiGiovanna, John J.; Kraemer, Kenneth H.] NCI, DNA Repair Sect, Dermatol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Hadigan, C (reprint author), NIAID, 10 Ctr Dr,Bldg 10,11C103, Bethesda, MD 20892 USA.
EM hadiganc@niaid.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute of Allergy and Infectious Diseases; National Cancer
Institute, Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases, and the National Cancer Institute, Center for
Cancer Research.
NR 22
TC 1
Z9 1
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-2116
EI 1536-4801
J9 J PEDIATR GASTR NUTR
JI J. Pediatr. Gastroenterol. Nutr.
PD OCT
PY 2014
VL 59
IS 4
BP 458
EP 464
DI 10.1097/MPG.0000000000000458
PG 7
WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
GA AQ2YG
UT WOS:000342655300009
PM 24918982
ER
PT J
AU Levine, ZA
Venable, RM
Watson, MC
Lerner, MG
Shea, JE
Pastor, RW
Brown, FLH
AF Levine, Zachary A.
Venable, Richard M.
Watson, Max C.
Lerner, Michael G.
Shea, Joan-Emma
Pastor, Richard W.
Brown, Frank L. H.
TI Determination of Biomembrane Bending Moduli in Fully Atomistic
Simulations
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID LIPID-BILAYERS; FORCE-FIELD; CHAIN-LENGTH; MEMBRANES; ELASTICITY;
CURVATURE; CHARMM; FLUCTUATIONS; UNDULATIONS; ENERGY
AB The bilayer bending modulus (K-c) is one of the most important physical constants characterizing lipid membranes, but precisely measuring it is a challenge, both experimentally and computationally. Experimental measurements on chemically identical bilayers often differ depending upon the techniques employed, and robust simulation results have previously been limited to coarse-grained models (at varying levels of resolution). This Communication demonstrates the extraction of K-c from fully atomistic molecular dynamics simulations for three different single-component lipid bilayers (DPPC, DOPC, and DOPE). The results agree quantitatively with experiments that measure thermal shape fluctuations in giant unilamellar vesicles. Lipid tilt, twist, and compression moduli are also reported.
C1 [Levine, Zachary A.; Shea, Joan-Emma; Brown, Frank L. H.] Univ Calif Santa Barbara, Dept Phys, Santa Barbara, CA 93106 USA.
[Levine, Zachary A.; Shea, Joan-Emma; Brown, Frank L. H.] Univ Calif Santa Barbara, Dept Chem & Biochem, Santa Barbara, CA 93106 USA.
[Venable, Richard M.; Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Watson, Max C.] NIST, Ctr Neutron Res, Gaithersburg, MD 20899 USA.
[Lerner, Michael G.] Earlham Coll, Dept Phys & Astron, Richmond, IN 47374 USA.
RP Brown, FLH (reprint author), Univ Calif Santa Barbara, Dept Phys, Santa Barbara, CA 93106 USA.
EM flbrown@chem.ucsb.edu
FU NSF [CHE-1153096, MCB-1158577]; NIH, National Heart, Lung and Blood
Institute; Center for Scientific Computing at the CNSI; MRL (an NSF
MRSEC) [DMR-11210S3, NSF CNS-0960316]
FX We thank John Nagle and Evan Evans for helpful discussions regarding
this work. Partial financial support was provided by NSF grants
CHE-1153096 and MCB-1158577, and the intramural research program at the
NIH, National Heart, Lung and Blood Institute. We also acknowledge
support from the Center for Scientific Computing at the CNSI and MRL (an
NSF MRSEC) under grants DMR-11210S3 and NSF CNS-0960316, in addition to
the computational capabilities of the National Institutes of Health,
Bethesda, MD (NHLBI LoBoS cluster) and Texas Advanced Computing Center
(TACC) at the University of Texas at Austin.
NR 28
TC 14
Z9 14
U1 7
U2 55
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 OCT 1
PY 2014
VL 136
IS 39
BP 13582
EP 13585
DI 10.1021/ja507910r
PG 4
WC Chemistry, Multidisciplinary
SC Chemistry
GA AQ2IK
UT WOS:000342608800029
PM 25202918
ER
PT J
AU Inglese, J
AF Inglese, J.
TI Designing innovative therapies for neuropathic pain: pros and cons of
target-based drug discovery
SO JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM
LA English
DT Article
ID IN-VITRO SELECTION; THROUGHPUT
C1 [Inglese, J.] NIH, Natl Ctr Adv Translat Sci, Rockville, MD 20892 USA.
[Inglese, J.] NHGRI, NIH, Rockville, MD USA.
RP Inglese, J (reprint author), NIH, Natl Ctr Adv Translat Sci, Rockville, MD 20892 USA.
NR 15
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1085-9489
EI 1529-8027
J9 J PERIPHER NERV SYST
JI J. Peripher. Nerv. Syst.
PD OCT
PY 2014
VL 19
SU 2
BP S6
EP S9
DI 10.1111/jns.12079_3
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ4LG
UT WOS:000342767900004
PM 25269741
ER
PT J
AU Trepiccione, F
Pisitkun, T
Hoffert, JD
Poulsen, SB
Capasso, G
Nielsen, S
Knepper, MA
Fenton, RA
Christensen, BM
AF Trepiccione, Francesco
Pisitkun, Trairak
Hoffert, Jason D.
Poulsen, Soren B.
Capasso, Giovambattista
Nielsen, Soren
Knepper, Mark A.
Fenton, Robert A.
Christensen, Birgitte M.
TI Early targets of lithium in rat kidney inner medullary collecting duct
include p38 and ERK1/2
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE cell and transport physiology; cell signaling; diabetes insipidus; mass
spectrometry; renal cell biology
ID NEPHROGENIC DIABETES-INSIPIDUS; MASS-SPECTROMETRY; DOWN-REGULATION;
PHOSPHORYLATION; AQUAPORIN-2; VASOPRESSIN; CELLS; IDENTIFICATION;
PROTEINS; AQP2
AB Almost half of patients receiving lithium salts have nephrogenic diabetes insipidus. Chronic lithium exposure induces AQP2 downregulation and changes in the cellular composition of the collecting duct. In order to understand these pathophysiological events, we determined the earliest lithium targets in rat inner medullary collecting duct (IMCD) by examining changes in the IMCD phosphoproteome after acute lithium administration. IMCDs were isolated 9 h after lithium exposure, a time when urinary concentrating impairment was evident. We found 1093 unique phosphopeptides corresponding to 492 phosphoproteins identified and quantified by mass spectrometry. Label-free quantification identified 152 upregulated and 56 downregulated phosphopeptides in response to lithium. Bioinformatic analysis highlighted several signaling proteins including MAP kinases and cell-junction proteins. The majority of the upregulated phosphopeptides contained a proline-directed motif, a known target of MAPK. Four hours after lithium exposure, phosphorylation sites in the activation loops of ERK1/2 and p38 were upregulated. Increased expression of phospho-Ser261-AQP2 (proline-directed motif) was concomitant with the increase in urine output. Pretreatment with MAPK inhibitors reversed the increased Ser261-AQP2 phosphorylation. Thus, in IMCD, ERK1/2 and p38 are early targets of lithium and may play a role in the onset of lithium-induced polyuria.
C1 [Trepiccione, Francesco; Poulsen, Soren B.; Nielsen, Soren; Fenton, Robert A.; Christensen, Birgitte M.] Aarhus Univ, Dept Biomed, Water & Salt Res Ctr, DK-8000 Aarhus C, Denmark.
[Trepiccione, Francesco; Capasso, Giovambattista] Univ Naples 2, Dept Cardiothorac & Resp Sci, Div Nephrol, Naples, Italy.
[Pisitkun, Trairak; Hoffert, Jason D.; Knepper, Mark A.] NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
[Pisitkun, Trairak] Chulalongkorn Univ, Fac Med, Bangkok 10330, Thailand.
RP Christensen, BM (reprint author), Aarhus Univ, Dept Biomed, Water & Salt Res Ctr, DK-8000 Aarhus C, Denmark.
EM bmc@ana.au.dk
RI Trepiccione, Francesco/H-7255-2015;
OI Trepiccione, Francesco/0000-0002-0622-6612; Capasso,
Giovambattista/0000-0003-3469-8614; Christensen, Birgitte
Monster/0000-0002-6140-4629
FU Danish National Research Foundation (Grundforskningsfonden); Marie Curie
Research Program (EU's Sixth Framework Programme); Lundbeck Foundation;
The Danish Council for Independent Research-Medical Sciences; Division
of Intramural Research, NHLBI [ZO1-HL001285]; National Research
University Project, Office of Higher Education Commission
[WCU-006-HR-57]
FX Financial support for this study was provided by the Danish National
Research Foundation (Grundforskningsfonden), the Marie Curie Research
Program (EU's Sixth Framework Programme), the Lundbeck Foundation and
The Danish Council for Independent Research-Medical Sciences. MAK was
supported by the operating budget of the Division of Intramural
Research, NHLBI (project ZO1-HL001285, MAK). TP was supported by the
National Research University Project, Office of Higher Education
Commission (WCU-006-HR-57). Mass spectrometry was conducted in the NHLBI
Proteomics Core Facility (director, Marjan Gucek). We thank Helle Hoyer,
Inger Merete S Paulsen, and Tina Drejer for expert technical assistance.
NR 46
TC 6
Z9 6
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD OCT
PY 2014
VL 86
IS 4
BP 757
EP 767
DI 10.1038/ki.2014.107
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA AQ5XD
UT WOS:000342881000015
PM 24786704
ER
PT J
AU Kelemen, LE
Terry, KL
Goodman, MT
Webb, PM
Bandera, EV
McGuire, V
Rossing, MA
Wang, Q
Dicks, E
Tyrer, JP
Song, H
Kupryjanczyk, J
Dansonka-Mieszkowska, A
Plisiecka-Halasa, J
Timorek, A
Menon, U
Gentry-Maharaj, A
Gayther, SA
Ramus, SJ
Narod, SA
Risch, HA
McLaughlin, JR
Siddiqui, N
Glasspool, R
Paul, J
Carty, K
Gronwald, J
Lubinski, J
Jakubowska, A
Cybulski, C
Kiemeney, LA
Massuger, LFAG
Van Altena, AM
Aben, KKH
Olson, SH
Orlow, I
Cramer, DW
Levine, DA
Bisogna, M
Giles, GG
Southey, MC
Bruinsma, F
Kjaer, SK
Hogdall, E
Jensen, A
Hogdall, CK
Lundvall, L
Engelholm, SA
Heitz, F
Du Bois, A
Harter, P
Schwaab, I
Butzow, R
Nevanlinna, H
Pelttari, LM
Leminen, A
Thompson, PJ
Lurie, G
Wilkens, LR
Lambrechts, D
Van Nieuwenhuysen, E
Lambrechts, S
Vergote, I
Beesley, J
Investigators, ASGA
Fasching, PA
Beckmann, MW
Hein, A
Ekici, AB
Doherty, JA
Wu, AH
Pearce, CL
Pike, MC
Stram, D
Chang-Claude, J
Rudolph, A
Doerk, T
Duerst, M
Hillemanns, P
Runnebaum, IB
Bogdanova, N
Antonenkova, N
Odunsi, K
Edwards, RP
Kelley, JL
Modugno, F
Ness, RB
Karlan, BY
Walsh, C
Lester, J
Orsulic, S
Fridley, BL
Vierkant, RA
Cunningham, JM
Wu, X
Lu, K
Liang, D
Hildebrandt, MAT
Weber, RP
Iversen, ES
Tworoger, SS
Poole, EM
Salvesen, HB
Krakstad, C
Bjorge, L
Tangen, IL
Pejovic, T
Bean, Y
Kellar, M
Wentzensen, N
Brinton, LA
Lissowska, J
Garcia-Closas, M
Campbell, IG
Eccles, D
Whittemore, AS
Sieh, W
Rothstein, JH
Anton-Culver, H
Ziogas, A
Phelan, CM
Moysich, KB
Goode, EL
Schildkraut, JM
Berchuck, A
Pharoah, PDP
Sellers, TA
Brooks-Wilson, A
Cook, LS
Le, ND
AF Kelemen, Linda E.
Terry, Kathryn L.
Goodman, Marc T.
Webb, Penelope M.
Bandera, Elisa V.
McGuire, Valerie
Rossing, Mary Anne
Wang, Qinggang
Dicks, Ed
Tyrer, Jonathan P.
Song, Honglin
Kupryjanczyk, Jolanta
Dansonka-Mieszkowska, Agnieszka
Plisiecka-Halasa, Joanna
Timorek, Agnieszka
Menon, Usha
Gentry-Maharaj, Aleksandra
Gayther, Simon A.
Ramus, Susan J.
Narod, Steven A.
Risch, Harvey A.
McLaughlin, John R.
Siddiqui, Nadeem
Glasspool, Rosalind
Paul, James
Carty, Karen
Gronwald, Jacek
Lubinski, Jan
Jakubowska, Anna
Cybulski, Cezary
Kiemeney, Lambertus A.
Massuger, Leon F. A. G.
Van Altena, Anne M.
Aben, Katja K. H.
Olson, Sara H.
Orlow, Irene
Cramer, Daniel W.
Levine, Douglas A.
Bisogna, Maria
Giles, Graham G.
Southey, Melissa C.
Bruinsma, Fiona
Kjaer, Susanne K.
Hogdall, Estrid
Jensen, Allan
Hogdall, Claus K.
Lundvall, Lene
Engelholm, Svend-Aage
Heitz, Florian
Du Bois, Andreas
Harter, Philipp
Schwaab, Ira
Butzow, Ralf
Nevanlinna, Heli
Pelttari, Liisa M.
Leminen, Arto
Thompson, Pamela J.
Lurie, Galina
Wilkens, Lynne R.
Lambrechts, Diether
Van Nieuwenhuysen, Els
Lambrechts, Sandrina
Vergote, Ignace
Beesley, Jonathan
Investigators, Aocs Study Grp Acs
Fasching, Peter A.
Beckmann, Matthias W.
Hein, Alexander
Ekici, Arif B.
Doherty, Jennifer A.
Wu, Anna H.
Pearce, Celeste L.
Pike, Malcolm C.
Stram, Daniel
Chang-Claude, Jenny
Rudolph, Anja
Doerk, Thilo
Duerst, Matthias
Hillemanns, Peter
Runnebaum, Ingo B.
Bogdanova, Natalia
Antonenkova, Natalia
Odunsi, Kunle
Edwards, Robert P.
Kelley, Joseph L.
Modugno, Francesmary
Ness, Roberta B.
Karlan, Beth Y.
Walsh, Christine
Lester, Jenny
Orsulic, Sandra
Fridley, Brooke L.
Vierkant, Robert A.
Cunningham, Julie M.
Wu, Xifeng
Lu, Karen
Liang, Dong
Hildebrandt, Michelle A. T.
Weber, Rachel Palmieri
Iversen, Edwin S.
Tworoger, Shelley S.
Poole, Elizabeth M.
Salvesen, Helga B.
Krakstad, Camilla
Bjorge, Line
Tangen, Ingvild L.
Pejovic, Tanja
Bean, Yukie
Kellar, Melissa
Wentzensen, Nicolas
Brinton, Louise A.
Lissowska, Jolanta
Garcia-Closas, Montserrat
Campbell, Ian G.
Eccles, Diana
Whittemore, Alice S.
Sieh, Weiva
Rothstein, Joseph H.
Anton-Culver, Hoda
Ziogas, Argyrios
Phelan, Catherine M.
Moysich, Kirsten B.
Goode, Ellen L.
Schildkraut, Joellen M.
Berchuck, Andrew
Pharoah, Paul D. P.
Sellers, Thomas A.
Brooks-Wilson, Angela
Cook, Linda S.
Le, Nhu D.
TI Consortium analysis of gene and gene-folate interactions in purine and
pyrimidine metabolism pathways with ovarian carcinoma risk
SO MOLECULAR NUTRITION & FOOD RESEARCH
LA English
DT Article
DE Case-control; Dihydropyrimidine dehydrogenase; Folate; Polymorphism;
Serine hydroxymethyltransferase 1 (soluble)
ID FOOD FREQUENCY QUESTIONNAIRE; GENOME-WIDE ASSOCIATION; SQUAMOUS-CELL
CARCINOMA; CARBON TRANSFER PATHWAY; CANCER RISK; SERINE
HYDROXYMETHYLTRANSFERASE; DIHYDROPYRIMIDINE DEHYDROGENASE;
SUSCEPTIBILITY LOCI; POOLED ANALYSIS; BREAST-CANCER
AB Scope: We reevaluated previously reported associations between variants in pathways of one-carbon (1-C) (folate) transfer genes and ovarian carcinoma (OC) risk, and in related pathways of purine and pyrimidine metabolism, and assessed interactions with folate intake.
Methods and results: Odds ratios (OR) for 446 genetic variants were estimated among 13 410 OC cases and 22 635 controls, and among 2281 cases and 3444 controls with folate information. Following multiple testing correction, the most significant main effect associations were for dihydropyrimidine dehydrogenase (DPYD) variants rs11587873 (OR = 0.92; p = 6 x 10(-5)) and rs828054 (OR = 1.06; p = 1 x 10(-4)). Thirteen variants in the pyrimidine metabolism genes, DPYD, DPYS, PPAT, and TYMS, also interacted significantly with folate in a multivariant analysis (corrected p = 9.9 x 10(-6)) but collectively explained only 0.2% of OC risk. Although no other associations were significant after multiple testing correction, variants in SHMT1 in 1-C transfer, previously reported with OC, suggested lower risk at higher folate (p(interaction) = 0.03-0.006).
Conclusion: Variation in pyrimidine metabolism genes, particularly DPYD, which was previously reported to be associated with OC, may influence risk; however, stratification by folate intake is unlikely to modify disease risk appreciably in these women. SHMT1 SNP-by-folate interactions are plausible but require further validation. Polymorphisms in selected genes in purine metabolism were not associated with OC.
C1 [Kelemen, Linda E.] Univ Calgary, Dept Med Genet, Calgary, AB, Canada.
[Kelemen, Linda E.] Univ Calgary, Dept Oncol, Calgary, AB, Canada.
[Terry, Kathryn L.; Cramer, Daniel W.] Brigham & Womens Hosp, Obstet & Gynecol Epidemol Ctr, Boston, MA 02115 USA.
[Terry, Kathryn L.; Cramer, Daniel W.; Tworoger, Shelley S.; Poole, Elizabeth M.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Goodman, Marc T.; Thompson, Pamela J.] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Goodman, Marc T.; Thompson, Pamela J.] Cedars Sinai Med Ctr, Dept Biomed Sci, Community & Populat Hlth Res Inst, Los Angeles, CA 90048 USA.
[Webb, Penelope M.; Investigators, Aocs Study Grp Acs] QIMR Berghofer Med Res Inst, Populat Hlth Dept, Herston, Qld, Australia.
[Bandera, Elisa V.] Rutgers State Univ, Rutgers Canc Inst New Jersey, Canc Prevent & Control Program, New Brunswick, NJ 08903 USA.
[McGuire, Valerie; Whittemore, Alice S.; Sieh, Weiva; Rothstein, Joseph H.] Stanford Univ Sch Med, Dept Hlth Res & Policy Epidemiol, Stanford, CA USA.
[Rossing, Mary Anne; Doherty, Jennifer A.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA USA.
[Rossing, Mary Anne] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Wang, Qinggang; Cook, Linda S.] Alberta Hlth Serv Canc Care, Dept Populat Hlth Res, Calgary, AB, Canada.
[Dicks, Ed; Tyrer, Jonathan P.; Song, Honglin; Pharoah, Paul D. P.] Univ Cambridge, Dept Oncol, Cambridge, England.
[Kupryjanczyk, Jolanta; Dansonka-Mieszkowska, Agnieszka; Plisiecka-Halasa, Joanna] Maria Sklodowska Curie Mem Canc Ctr & Inst Oncol, Dept Pathol, Warsaw, Poland.
[Timorek, Agnieszka] Med Univ Warsaw, Fac Med 2, Dept Obstet Gynecol & Oncol, Warsaw, Poland.
[Timorek, Agnieszka] Brodnowski Hosp, Warsaw, Poland.
[Menon, Usha; Gentry-Maharaj, Aleksandra] UCL, Gynaecol Canc Res Ctr, Inst Womens Hlth, Dept Womens Canc, London, England.
[Gayther, Simon A.; Ramus, Susan J.; Wu, Anna H.; Pearce, Celeste L.; Pike, Malcolm C.; Stram, Daniel] Univ So Calif, Keck Sch Med, USC Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Narod, Steven A.] Univ Toronto, Womens Coll Res Inst, Toronto, ON, Canada.
[Risch, Harvey A.] Yale Univ, Sch Publ Hlth, Dept Chron Dis Epidemiol, New Haven, CT USA.
[McLaughlin, John R.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Prosserman Ctr Hlth Res, Toronto, ON M5G 1X5, Canada.
[Siddiqui, Nadeem] Glasgow Royal Infirm, Dept Gynaecol Oncol, Glasgow G4 0SF, Lanark, Scotland.
[Glasspool, Rosalind; Paul, James; Carty, Karen] Beatson West Scotland Canc Ctr, Glasgow, Lanark, Scotland.
[Gronwald, Jacek; Lubinski, Jan; Jakubowska, Anna; Cybulski, Cezary] Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
[Kiemeney, Lambertus A.; Aben, Katja K. H.] Radboud Univ Nijmegen Med Ctr, Dept Hlth Evidence, Nijmegen, Netherlands.
[Kiemeney, Lambertus A.] Radboud Univ Nijmegen Med Ctr, Dept Urol, Nijmegen, Netherlands.
[Kiemeney, Lambertus A.; Aben, Katja K. H.] Ctr Comprehens Canc, Utrecht, Netherlands.
[Massuger, Leon F. A. G.; Van Altena, Anne M.] Radboud Univ Nijmegen Med Ctr, Dept Gynaecol, Nijmegen, Netherlands.
[Olson, Sara H.; Orlow, Irene; Pike, Malcolm C.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Levine, Douglas A.; Bisogna, Maria] Mem Sloan Kettering Canc Ctr, Dept Surg, Gynecol Serv, New York, NY 10021 USA.
[Giles, Graham G.; Bruinsma, Fiona] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[Giles, Graham G.] Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne, Vic 3010, Australia.
[Giles, Graham G.] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[Southey, Melissa C.; Campbell, Ian G.] Univ Melbourne, Dept Pathol, Melbourne, Vic, Australia.
[Kjaer, Susanne K.; Hogdall, Estrid; Jensen, Allan] Danish Canc Soc Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark.
[Kjaer, Susanne K.; Hogdall, Claus K.; Lundvall, Lene] Univ Copenhagen, Rigshosp, Juliane Marie Ctr, Dept Gynecol, DK-2100 Copenhagen, Denmark.
[Hogdall, Estrid] Univ Copenhagen, Herlev Hosp, Dept Pathol, Copenhagen, Denmark.
[Engelholm, Svend-Aage] Univ Copenhagen, Rigshosp, Dept Radiat Oncol, DK-2100 Copenhagen, Denmark.
[Heitz, Florian; Du Bois, Andreas; Harter, Philipp] Knappschaft GmbH, Evang Huyssens Stiftung, Kliniken Essen Mitte, Dept Gynecol & Gynecol Oncol, Essen, Germany.
[Heitz, Florian; Du Bois, Andreas; Harter, Philipp] Dr Horst Schmidt Kliniken Wiesbaden, Dept Gynecol & Gynecol Oncol, Wiesbaden, Germany.
[Butzow, Ralf] Helsinki Univ Cent Hosp, Dept Pathol, Helsinki, Finland.
[Butzow, Ralf; Nevanlinna, Heli; Pelttari, Liisa M.; Leminen, Arto] Univ Helsinki, Dept Obstet & Gynecol, Helsinki, Finland.
[Butzow, Ralf; Nevanlinna, Heli; Pelttari, Liisa M.; Leminen, Arto] Helsinki Univ Cent Hosp, Helsinki, Finland.
[Lurie, Galina; Wilkens, Lynne R.] Univ Hawaii Canc Ctr, Canc Epidemiol Program, Honolulu, HI USA.
[Lambrechts, Diether] VIB, Vesalius Res Ctr, Leuven, Belgium.
[Lambrechts, Diether] Univ Leuven, Dept Oncol, Lab Translat Genet, Leuven, Belgium.
[Van Nieuwenhuysen, Els; Lambrechts, Sandrina; Vergote, Ignace] Univ Hosp Leuven, Dept Obstet & Gynaecol, Div Gynecol Oncol, Leuven, Belgium.
[Van Nieuwenhuysen, Els; Lambrechts, Sandrina; Vergote, Ignace] Univ Hosp Leuven, Leuven Canc Inst, Leuven, Belgium.
[Beesley, Jonathan; Investigators, Aocs Study Grp Acs] QIMR Berghofer Med Res Inst, Genet & Computat Biol Dept, Herston, Qld, Australia.
[Investigators, Aocs Study Grp Acs] Peter MacCallum Canc Ctr, East Melbourne, Vic, Australia.
[Fasching, Peter A.; Beckmann, Matthias W.; Hein, Alexander] Univ Erlangen Nurnberg, Univ Hosp Erlangen, Dept Gynecol & Obstet, Comprehens Canc Ctr Erlangen EMN, D-91054 Erlangen, Germany.
[Fasching, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, Div Hematol & Oncol, Dept Med, Los Angeles, CA 90095 USA.
[Ekici, Arif B.] Univ Erlangen Nurnberg, Comprehens Canc Ctr Erlangen EMN, Univ Hosp Erlangen, Inst Human Genet, D-91054 Erlangen, Germany.
[Doherty, Jennifer A.] Geisel Sch Med Dartmouth, Dept Community & Family Med, Lebanon, NH USA.
[Chang-Claude, Jenny; Rudolph, Anja] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Doerk, Thilo; Bogdanova, Natalia] Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
[Duerst, Matthias; Runnebaum, Ingo B.] Univ Jena, Jena Univ Hosp, Dept Gynecol, Jena, Germany.
[Hillemanns, Peter] Hannover Med Sch, Clin Obstet, Hannover, Germany.
[Hillemanns, Peter] Hannover Med Sch, Clin Gynaecol, Hannover, Germany.
[Antonenkova, Natalia] Byelorussian Inst Oncol & Med Radiol Aleksandrov, Minsk, Byelarus.
[Odunsi, Kunle] Roswell Pk Canc Inst, Dept Gynecol Oncol, Buffalo, NY 14263 USA.
[Edwards, Robert P.; Kelley, Joseph L.; Modugno, Francesmary] Univ Pittsburgh, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA USA.
[Edwards, Robert P.; Kelley, Joseph L.; Modugno, Francesmary] Univ Pittsburgh, Ovarian Canc Ctr Excellence, Pittsburgh, PA USA.
[Modugno, Francesmary] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Modugno, Francesmary] Univ Pittsburgh, Womens Canc Res Program, Magee Womens Res Inst, Pittsburgh, PA USA.
[Modugno, Francesmary] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[Ness, Roberta B.] Univ Texas Sch Publ Hlth, Houston, TX USA.
[Karlan, Beth Y.; Walsh, Christine; Lester, Jenny; Orsulic, Sandra] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Womens Canc Program, Los Angeles, CA 90048 USA.
[Fridley, Brooke L.] Univ Kansas Med Ctr, Dept Biostat, Kansas City, KS USA.
[Vierkant, Robert A.] Mayo Clin, Div Biomed Stat & Informat, Dept Hlth Sci Res, Rochester, MN USA.
[Cunningham, Julie M.] Mayo Clin, Div Expt Pathol, Dept Lab Med & Pathol, Rochester, MN USA.
[Wu, Xifeng; Hildebrandt, Michelle A. T.] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Lu, Karen] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA.
[Liang, Dong] Texas So Univ, Coll Pharm & Hlth Sci, Houston, TX 77004 USA.
[Weber, Rachel Palmieri; Schildkraut, Joellen M.] Duke Univ Med Ctr, Dept Community & Family Med, Durham, NC USA.
[Iversen, Edwin S.; Schildkraut, Joellen M.] Duke Canc Inst, Durham, NC USA.
[Iversen, Edwin S.] Duke Univ, Dept Stat Sci, Durham, NC USA.
[Tworoger, Shelley S.; Poole, Elizabeth M.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Tworoger, Shelley S.; Poole, Elizabeth M.] Harvard Univ, Sch Med, Boston, MA USA.
[Salvesen, Helga B.; Krakstad, Camilla; Bjorge, Line; Tangen, Ingvild L.] Haukeland Univ Horpital, Dept Gynecol & Obstet, Bergen, Norway.
[Salvesen, Helga B.; Krakstad, Camilla; Bjorge, Line; Tangen, Ingvild L.] Univ Bergen, Ctr Canc Biomarkers, Dept Clin Sci, Bergen, Norway.
[Pejovic, Tanja; Bean, Yukie; Kellar, Melissa] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Pejovic, Tanja; Bean, Yukie; Kellar, Melissa] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Wentzensen, Nicolas; Brinton, Louise A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Garcia-Closas, Montserrat] Inst Canc Res, Div Genet & Epidemiol, Sutton, Surrey, England.
[Garcia-Closas, Montserrat] Breakthrough Breast Canc Res Ctr, London, England.
[Campbell, Ian G.] Peter MacCallum Canc Ctr, Div Res, Canc Genet Lab, East Melbourne, Vic, Australia.
[Eccles, Diana] Univ Southampton, Fac Med, Southampton SO9 5NH, Hants, England.
[Anton-Culver, Hoda; Ziogas, Argyrios] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
[Anton-Culver, Hoda] Univ Calif Irvine, Sch Med, UCI Ctr Canc Genet Res & Prevent, Genet Epidemiol Res Inst, Irvine, CA 92717 USA.
[Phelan, Catherine M.; Sellers, Thomas A.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL 33612 USA.
[Moysich, Kirsten B.] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Goode, Ellen L.] Mayo Clin, Dept Hlth Sci Res, Div Epidemiol, Rochester, MN USA.
[Berchuck, Andrew] Duke Univ Med Ctr, Dept Obstet & Gynecol, Durham, NC USA.
[Pharoah, Paul D. P.] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Brooks-Wilson, Angela] BC Canc Agcy, Canadas Michael Smith Genome Sci Ctr, Vancouver, BC, Canada.
[Brooks-Wilson, Angela] Simon Fraser Univ, Dept Biomed Physiol & Kinesiol, Burnaby, BC V5A 1S6, Canada.
[Cook, Linda S.] Univ New Mexico, Dept Internal Med, Div Epidemiol & Biostat, Albuquerque, NM 87131 USA.
[Le, Nhu D.] BC Canc Agcy, Vancouver, BC, Canada.
RP Kelemen, LE (reprint author), Univ Calgary, Dept Med Genet, Calgary, AB, Canada.
EM LKelemen@post.harvard.edu
RI Dork, Thilo/J-8620-2012; Aben, Katja/G-9686-2016; Bowtell,
David/H-1007-2016; Gronwald, Jacek/A-4576-2017; Bjorge,
Line/C-1307-2017; salvesen, Helga/C-1187-2017; Massuger,
Leon/H-8072-2014; Hein, Alexander/F-6999-2010; Jakubowska,
Anna/O-8050-2014; Bandera, Elisa/M-4169-2014; Kiemeney,
Lambertus/D-3357-2009; Fridley, Brooke/D-8315-2015; Garcia-Closas,
Montserrat /F-3871-2015; Brinton, Louise/G-7486-2015; Brooks-Wilson,
Angela/E-9399-2012; campbell, Ian/F-6006-2011; van Altena,
Anne/B-9824-2016
OI Aben, Katja/0000-0002-0214-2147; Bowtell, David/0000-0001-9089-7525;
Gronwald, Jacek/0000-0002-3643-2871; Bjorge, Line/0000-0002-0240-2770;
salvesen, Helga/0000-0002-4438-8831; Glasspool,
Rosalind/0000-0002-5000-1680; Ramus, Susan/0000-0003-0005-7798;
Nevanlinna, Heli/0000-0002-0916-2976; Kjaer,
Susanne/0000-0002-8347-1398; Orlow, Irene/0000-0001-6234-6961; Hein,
Alexander/0000-0003-2601-3398; Bandera, Elisa/0000-0002-8789-2755;
Kiemeney, Lambertus/0000-0002-2368-1326; Fridley,
Brooke/0000-0001-7739-7956; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562;
Brooks-Wilson, Angela/0000-0003-1009-6408;
FU European Commission [223175-HEALTH-F2-2009-223175]; Ovarian Cancer
Research Fund; Canadian Institutes of Health Research [MOP-86727,
MOP-84340, MSH-87734]; US National Cancer Institute GAME-ON Post-GWAS
Initiative [U19-CA148112]; American Cancer Society [CRTG-00-196-01-CCE,
SIOP-06-258-01- COUN]; California Cancer Research Program
[00-01389V-20170, N01-CN25403, 2II0200]; Cancer Council Victoria; Cancer
Council Queensland; Cancer Council New South Wales; Cancer Council South
Australia; Cancer Council Tasmania; Cancer Foundation of Western
Australia; Cancer Institute of New Jersey; Cancer Research UK
[C490/A6187, C490/A10119, C490/A10124, C536/A13086, C536/A6689]; Celma
Mastry Ovarian Cancer Foundation; Danish Cancer Society [94-222-52];
ELAN Program of University of Erlangen-Nuremberg; Eve Appeal (Oak
Foundation); Fred C. and Katherine B. Andersen Foundation; German Cancer
Research Center; German Federal Ministry of Education and Research of
Germany [01GB 9401]; Helsinki University Central Hospital Research Fund;
Helse Vest; Imperial Experimental Cancer Research Centre [C1312/A15589];
L & S Milken Foundation; Lon V. Smith Foundation [LVS-39420]; Mayo
Foundation; Mermaid I project; Minnesota Ovarian Cancer Alliance;
National Health and Medical Research Council (NHMRC) of Australia
[199600, 209057, 251533, 396414, 400281, 504715]; Nationaal Kankerplan
of Belgium; Norwegian Cancer Society; Norwegian Research Council; OHSU
Foundation; Polish Ministry of Science and Higher Education [4 PO5C 028
14, 2 PO5A 068 27]; Pomeranian Medical University; Radboud University
Medical Center; Roswell Park Cancer Institute Alliance Foundation; Royal
Marsden Hospital; Rudolf-Bartling Foundation; Sigrid Juselius
Foundation; state of Baden-Wurttemberg through Medical Faculty of the
University of Ulm [P.685]; UK National Institute for Health Research
Biomedical Research Centres at the University of Cambridge Hospital; UK
National Institute for Health Research Biomedical Research Centres at
University College London Hospital; 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, W81XWH-07-0449]; US National Cancer
Institute [K07-CA095666, K07-CA143047, K22-CA138563, N01-CN55424,
N01-PC067010, N01-PC035137, P01-CA017054, P01-CA087696, P30-CA15083,
P50-CA105009, P50-CA136393, R01-CA014089, R01-CA016056, R01-CA017054,
R01-CA049449, R01-CA050385, R01-CA054419]; US National Institutes of
Health/National Center for Research Resources/General Clinical Research
Center [MO1-RR000056]; US Public Health Service [PSA-042205]; NHMRC of
Australia; National Cancer Institute [K07-CA080668]; US National Cancer
Institute. [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]; The US National
Cancer Institute [R01-CA087538, R01-CA092044, R01-095023, R01-CA106414,
R01-CA122443, R01-CA112523, R01-CA114343, R01-CA126841, R01-CA136924,
R01-CA149429, R03-CA113148, R03-CA115195, R37-CA070867, R37-CA70867,
U01-CA069417, U01-CA071966]
FX The COGS project is funded through a European Commission's Seventh
Framework Programme grant (agreement number
223175-HEALTH-F2-2009-223175). The OCAC 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 supported by the Canadian
Institutes of Health Research (MOP-86727) and the US National Cancer
Institute GAME-ON Post-GWAS Initiative (U19-CA148112). Funding of the
constituent studies was provided by the Canadian Institutes of Health
Research (MOP-84340), WorkSafeBC 14, and OvCaRe: BC's Ovarian Cancer
Research Team; the American Cancer Society (CRTG-00-196-01-CCE); the
California Cancer Research Program (00-01389V-20170, N01-CN25403,
2II0200); Cancer Council Victoria; Cancer Council Queensland; Cancer
Council New South Wales; Cancer Council South Australia; Cancer Council
Tasmania; Cancer Foundation of Western Australia; the Cancer Institute
of New Jersey; Cancer Research UK (C490/A6187, C490/A10119, C490/A10124,
C536/A13086, C536/A6689); the Celma Mastry Ovarian Cancer Foundation;
the Danish Cancer Society (94-222-52); the ELAN Program of the
University of Erlangen-Nuremberg; the Eve Appeal (Oak Foundation); the
Fred C. and Katherine B. Andersen Foundation; the German Cancer Research
Center; the German Federal Ministry of Education and Research of
Germany, Program of Clinical Biomedical Research (01GB 9401); the
Helsinki University Central Hospital Research Fund; Helse Vest; Imperial
Experimental Cancer Research Centre (C1312/A15589); the L & S Milken
Foundation; the Lon V. Smith Foundation (LVS-39420); the Mayo
Foundation; the Mermaid I project; the Minnesota Ovarian Cancer
Alliance; the National Health and Medical Research Council (NHMRC) of
Australia (199600, 209057, 251533, 396414, 400281, and 504715);
Nationaal Kankerplan of Belgium; the Norwegian Cancer Society; the
Norwegian Research Council; the OHSU Foundation; the Polish Ministry of
Science and Higher Education (4 PO5C 028 14, 2 PO5A 068 27); Pomeranian
Medical University; Radboud University Medical Center; the Roswell Park
Cancer Institute Alliance Foundation; the Royal Marsden Hospital; the
Rudolf-Bartling Foundation; the Sigrid Juselius Foundation; the state of
Baden-Wurttemberg through Medical Faculty of the University of Ulm
(P.685); the UK National Institute for Health Research Biomedical
Research Centres at the University of Cambridge and the University
College London Hospitals; the US Army Medical Research and Material
Command (DAMD17-98-1-8659, DAMD17-01-1-0729, DAMD17-02-1-0666,
DAMD17-02-1-0669, W81XWH-10-1-0280, W81XWH-07-0449); the US National
Cancer Institute (K07-CA095666, K07-CA143047, K22-CA138563, N01-CN55424,
N01-PC067010, N01-PC035137, P01-CA017054, P01-CA087696, P30-CA15083,
P50-CA105009, P50-CA136393, R01-CA014089, R01-CA016056, R01-CA017054,
R01-CA049449, R01-CA050385, R01-CA054419, R01-CA058598, R01-CA058860,
R01-CA061107, R01-CA061132, R01-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-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
National Institutes of Health/National Center for Research
Resources/General Clinical Research Center (MO1-RR000056); and the US
Public Health Service (PSA-042205).; L. E. K. was supported by a
Canadian Institutes of Health Research Investigator award (MSH-87734).
P. M. W. is supported by the NHMRC of Australia. B. Y. K. holds an
American Cancer Society Early Detection Professorship (SIOP-06-258-01-
COUN). F. M. is supported by a K-award from the National Cancer
Institute (K07-CA080668).
NR 58
TC 1
Z9 1
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1613-4125
EI 1613-4133
J9 MOL NUTR FOOD RES
JI Mol. Nutr. Food Res.
PD OCT
PY 2014
VL 58
IS 10
BP 2023
EP 2035
DI 10.1002/mnfr.201400068
PG 13
WC Food Science & Technology
SC Food Science & Technology
GA AQ6DN
UT WOS:000342898900010
PM 25066213
ER
PT J
AU Keniya, MV
Holmes, AR
Niimi, M
Lamping, E
Gillet, JP
Gottesman, MM
Cannon, RD
AF Keniya, Mikhail V.
Holmes, Ann R.
Niimi, Masakazu
Lamping, Erwin
Gillet, Jean-Pierre
Gottesman, Michael M.
Cannon, Richard D.
TI Drug Resistance Is Conferred on the Model Yeast Saccharomyces cerevisiae
by Expression of Full-Length Melanoma-Associated Human ATP-Binding
Cassette Transporter ABCB5
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE human ABC transporters; ABCB5; P-glycoprotein; ABCB1; drug resistance;
melanoma
ID MULTIDRUG-RESISTANCE; CANDIDA-ALBICANS; P-GLYCOPROTEIN; MEMBRANE
TRANSPORTERS; MALIGNANT-MELANOMA; PROTEIN EXPRESSION; AZOLE RESISTANCE;
PICHIA-PASTORIS; CELLS; CANCER
AB ABCB5, an ATP-binding cassette (ABC) transporter, is highly expressed in melanoma cells, and may contribute to the extreme resistance of melanomas to chemotherapy by efflux of anti-cancer drugs. Our goal was to determine whether we could functionally express human ABCB5 in the model yeast Saccharomyces cerevisiae, in order to demonstrate an efflux function for ABCB5 in the absence of background pump activity from other human transporters. Heterologous expression would also facilitate drug discovery for this important target. DNAs encoding ABCB5 sequences were cloned into the chromosomal PDR5 locus of a S. cerevisiae strain in which seven endogenous ABC transporters have been deleted. Protein expression in the yeast cells was monitored by immunodetection using both a specific anti-ABCB5 antibody and a cross-reactive anti-ABCB1 antibody. ABCB5 function in recombinant yeast cells was measured by determining whether the cells possessed increased resistance to known pump substrates, compared to the host yeast strain, in assays of yeast growth. Three ABCB5 constructs were made in yeast. One was derived from the ABCB5-beta mRNA, which is highly expressed in human tissues but is a truncation of a canonical full-size ABC transporter. Two constructs contained full-length ABCB5 sequences: either a native sequence from cDNA or a synthetic sequence codon-harmonized for S. cerevisiae. Expression of all three constructs in yeast was confirmed by immunodetection. Expression of the codon-harmonized full-length ABCB5 DNA conferred increased resistance, relative to the host yeast strain, to the putative substrates rhodamine 123, daunorubicin, tetramethylrhodamine, FK506, or clorgyline. We conclude that full-length ABCB5 can be functionally expressed in S. cerevisiae and confers drug resistance.
C1 [Keniya, Mikhail V.; Holmes, Ann R.; Niimi, Masakazu; Lamping, Erwin; Cannon, Richard D.] Univ Otago, Sir John Walsh Res Inst, Dunedin 9054, New Zealand.
[Keniya, Mikhail V.; Holmes, Ann R.; Niimi, Masakazu; Lamping, Erwin; Cannon, Richard D.] Univ Otago, Dept Oral Sci, Dunedin 9054, New Zealand.
[Gillet, Jean-Pierre] Univ Namur, Lab Mol Canc Biol, URPhyM NARILIS, Dept Biomed Sci, B-5000 Namur, Belgium.
[Gottesman, Michael M.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Cannon, RD (reprint author), Univ Otago, Sir John Walsh Res Inst, POB 647, Dunedin 9054, New Zealand.
EM richard.cannon@otago.ac.nz
OI Cannon, Richard/0000-0002-5398-2066; Lamping, Erwin/0000-0002-4942-4782
FU National Institutes of Health [NIH DE016885]; Foundation for Science
Research and Technology [UOOX0607]; Health Research Council of New
Zealand [09/671]; Royal Society of New Zealand [UOO1004]; NIH, National
Cancer Institute, Center for Cancer Research
FX The authors gratefully acknowledge funding from the National Institutes
of Health (NIH DE016885 to R.D.C.), the Foundation for Science Research
and Technology (UOOX0607 to R.D.C.), and the Health Research Council of
New Zealand (09/671 to R.D.C.). M.V.K. was also supported by the Marsden
Fund of the Royal Society of New Zealand (UOO1004 to Dr. Brian C. Monk).
J.-P.G. and M.M.G. were supported by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research.
NR 53
TC 5
Z9 5
U1 2
U2 10
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 OCT
PY 2014
VL 11
IS 10
BP 3452
EP 3462
DI 10.1021/mp500230b
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA AQ5NX
UT WOS:000342857000024
PM 25115303
ER
PT J
AU Wang, Y
Yue, XY
Kiesewetter, DO
Wang, Z
Lu, J
Niu, G
Teng, GJ
Chen, XY
AF Wang, Yu
Yue, Xuyi
Kiesewetter, Dale O.
Wang, Zhe
Lu, Jie
Niu, Gang
Teng, Gaojun
Chen, Xiaoyuan
TI [F-18]DPA-714 PET Imaging of AMD3100 Treatment in a Mouse Model of
Stroke
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE stroke; AMD3100; translocator protein (TSPO); DPA-714; PET
ID CENTRAL-NERVOUS-SYSTEM; PROTEIN 18 KDA; FOCAL ISCHEMIA; BRAIN-INJURY;
IN-VIVO; BENZODIAZEPINE-RECEPTORS; FUNCTIONAL RECOVERY; FOREBRAIN
ISCHEMIA; DUAL ROLE; NEUROINFLAMMATION
AB Chemokine receptor 4 and stromal-cell-derived factor 1 have been found to be related to the initiation of neuroinflammation in ischemic brain. Herein, we aimed to monitor the changes of neuorinflammation after AMD3100 treatment using a translocator protein (TSPO) specific PET tracer in a mouse model of stroke. The transient MCAO model was established with Balb/C mice. The success of the model was confirmed by magnetic resonance imaging and FDG PET. The treatment started the same day after surgery via daily intraperitoneal injection of 1 mg of AMD3100/kg for three consecutive days. [F-18]DPA-714 was used as the TSPO imaging tracer. In vivo PET was performed at different time points after surgery in both control and treated mice. Ex vivo histological and immunofluorescence staining of brain slices was performed to confirm the lesion site and inflammatory cell activation. The TSPO level was also evaluated using Western blotting. Longitudinal PET scans revealed that the level of [F-18]DPA-714 uptake was significantly increased in the ischemic brain area with a peak accumulation at around day 10 after surgery, and the level of uptake remained high until day 16. The in vivo PET data were consistent with those from ex vivo immunofluorescence staining. After AMD3100 treatment, the signal intensity was significantly decreased compared with that of normal saline-treated control group. In conclusion, TSPO-targeted PET imaging using [F-18]DPA-714 can be used to monitor inflammatory response after stroke and provide a useful method for evaluating the efficacy of anti-inflammation treatment.
C1 [Wang, Yu; Teng, Gaojun] Southeast Univ, Jiangsu Key Lab Mol Imaging & Funct Imaging, Dept Radiol, Sch Med,Zhongda Hosp, Nanjing 210009, Peoples R China.
[Wang, Yu; Yue, Xuyi; Kiesewetter, Dale O.; Wang, Zhe; Lu, Jie; Niu, Gang; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
RP Niu, G (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
EM niug@mail.nih.gov; gjteng@vip.sina.com; shawn.chen@nih.gov
FU National Basic Research Program of China (973 program) [2013CB733803,
2013CB733802]; National Institute of Biomedical Imaging and
Bioengineering, National Institutes of Health
FX This work was supported by the National Basic Research Program of China
(973 program, 2013CB733803, and 2013CB733802) and the Intramural
Research Program (IRP) of the National Institute of Biomedical Imaging
and Bioengineering, National Institutes of Health. We thank the
Microscopy Imaging Core of the The Eunice Kennedy Shriver National
Institute of Child Health and Human Development for their help with
immunofluorescence staining.
NR 44
TC 6
Z9 7
U1 0
U2 12
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 OCT
PY 2014
VL 11
IS 10
BP 3463
EP 3470
DI 10.1021/mp500234d
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA AQ5NX
UT WOS:000342857000025
PM 25157648
ER
PT J
AU Miadlikowska, J
Kauff, F
Hognabba, F
Oliver, JC
Molnar, K
Fraker, E
Gaya, E
Hafellner, J
Hofstetter, V
Gueidan, C
Otalora, MAG
Hodkinson, B
Kukwa, M
Lucking, R
Bjork, C
Sipman, HJM
Burgaz, AR
Thell, A
Passo, A
Myllys, L
Goward, T
Fernandez-Brime, S
Hestmark, G
Lendemer, J
Lumbsch, HT
Schmull, M
Schoch, CL
Serusiaux, E
Maddison, DR
Arnold, AE
Lutzoni, F
Stenroos, S
AF Miadlikowska, Jolanta
Kauff, Frank
Hognabba, Filip
Oliver, Jeffrey C.
Molnar, Katalin
Fraker, Emily
Gaya, Ester
Hafellner, Josef
Hofstetter, Valerie
Gueidan, Cecile
Otalora, Monica A. G.
Hodkinson, Brendan
Kukwa, Martin
Luecking, Robert
Bjoerk, Curtis
Sipman, Harrie J. M.
Rosa Burgaz, Ana
Thell, Arne
Passo, Alfredo
Myllys, Leena
Goward, Trevor
Fernandez-Brime, Samantha
Hestmark, Geir
Lendemer, James
Lumbsch, H. Thorsten
Schmull, Michaela
Schoch, Conrad L.
Serusiaux, Emmanuel
Maddison, David R.
Arnold, A. Elizabeth
Lutzoni, Francois
Stenroos, Soili
TI A multigene phylogenetic synthesis for the class Lecanoromycetes
(Ascomycota): 1307 fungi representing 1139 infrageneric taxa, 317 genera
and 66 families
SO MOLECULAR PHYLOGENETICS AND EVOLUTION
LA English
DT Article
DE Classification; Cumulative supermatrix; Lecanoromycetes; Lichenized
fungi; Multi-gene phylogeny; Systematics
ID LICHEN-FORMING ASCOMYCOTA; RIBOSOMAL-RNA SMALL; SSU RDNA SEQUENCES;
MOLECULAR PHYLOGENY; MITOCHONDRIAL SEQUENCES; CYANOBACTERIAL LICHENS;
OSTROPALES GRAPHIDACEAE; PHOTOBIONT DIVERSITY; POPULATION-STRUCTURE;
SECONDARY CHEMISTRY
AB The Lecanoromycetes is the largest class of lichenized Fungi, and one of the most species-rich classes in the kingdom. Here we provide a multigene phylogenetic synthesis (using three ribosomal RNA-coding and two protein-coding genes) of the Lecanoromycetes based on 642 newly generated and 3329 publicly available sequences representing 1139 taxa, 317 genera, 66 families, 17 orders and five subclasses (four currently recognized: Acarosporomycetidae, Lecanoromycetidae, Ostropomycetidae, Umbilicariomycetidae; and one provisionarily recognized, 'Candelariomycetidae'). Maximum likelihood phylogenetic analyses on four multigene datasets assembled using a cumulative supermatrix approach with a progressively higher number of species and missing data (5-gene, 5 + 4-gene, 5 + 4 + 3-gene and 5 + 4 + 3 + 2-gene datasets) show that the current classification includes non-monophyletic taxa at various ranks, which need to be recircumscribed and require revisionary treatments based on denser taxon sampling and more loci. Two newly circumscribed orders (Arctomiales and Hymeneliales in the Ostropomycetidae) and three families (Ramboldiaceae and Psilolechiaceae in the Lecanorales, and Strangosporaceae in the Lecanoromycetes inc. sed.) are introduced. The potential resurrection of the families Eigleraceae and Lopadiaceae is considered here to alleviate phylogenetic and classification disparities. An overview of the photobionts associated with the main fungal lineages in the Lecanoromycetes based on available published records is provided. A revised schematic classification at the family level in the phylogenetic context of widely accepted and newly revealed relationships across Lecanoromycetes is included. The cumulative addition of taxa with an increasing amount of missing data (i.e., a cumulative supermatrix approach, starting with taxa for which sequences were available for all five targeted genes and ending with the addition of taxa for which only two genes have been sequenced) revealed relatively stable relationships for many families and orders. However, the increasing number of taxa without the addition of more loci also resulted in an expected substantial loss of phylogenetic resolving power and support (especially for deep phylogenetic relationships), potentially including the misplacements of several taxa. Future phylogenetic analyses should include additional single copy protein-coding markers in order to improve the tree of the Lecanoromycetes. As part of this study, a new module ("Hypha") of the freely available Mesquite software was developed to compare and display the internodal support values derived from this cumulative supermatrix approach. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Miadlikowska, Jolanta; Molnar, Katalin; Fraker, Emily; Gaya, Ester; Hofstetter, Valerie; Gueidan, Cecile; Otalora, Monica A. G.; Hodkinson, Brendan; Lutzoni, Francois] Duke Univ, Dept Biol, Durham, NC 27708 USA.
[Kauff, Frank] TU Kaiserslautern, FB Biol, D-67653 Kaiserslautern, Germany.
[Hognabba, Filip; Myllys, Leena; Stenroos, Soili] Univ Helsinki, Finnish Museum Nat Hist, Bot Museum, FI-00014 Helsinki, Finland.
[Oliver, Jeffrey C.] Yale Univ, Dept Ecol & Evolutionary Biol, New Haven, CT 06511 USA.
[Hafellner, Josef] Karl Franzens Univ Graz, Inst Bot, A-8010 Graz, Austria.
[Kukwa, Martin] Univ Gdansk, Dept Plant Taxon & Nat Conservat, PL-80308 Gdansk, Poland.
[Luecking, Robert; Lumbsch, H. Thorsten] Field Museum, Chicago, IL 60605 USA.
[Bjoerk, Curtis; Goward, Trevor] Univ British Columbia, Beaty Museum, UBC Herbarium, Vancouver, BC V6T 1Z4, Canada.
[Sipman, Harrie J. M.] Bot Garten, D-14195 Berlin, Germany.
[Sipman, Harrie J. M.] Bot Museum Berlin Dahlem, D-14195 Berlin, Germany.
[Rosa Burgaz, Ana] Univ Complutense Madrid, Fac CC Biol, Dept Biol Vegetal 1, E-28040 Madrid, Spain.
[Thell, Arne] Lund Univ, Bot Museum, SE-22100 Lund, Sweden.
[Passo, Alfredo] Univ Nacl Comahue, INIBIOMA, Ctr Reg Univ Barilothe, BioLiq Lab Bioindicadores & Liquenol, RA-8400 San Carlos De Bariloche, Rio Negro, Argentina.
[Fernandez-Brime, Samantha] Univ Barcelona, Fac Biol, Bot Unit, Dept Plant Biol, E-08028 Barcelona, Spain.
[Hestmark, Geir] Univ Oslo, Dept Biosci, CEES, N-0315 Oslo, Norway.
[Lendemer, James] New York Bot Garden, Inst Systemat Bot, Bronx, NY 10458 USA.
[Schmull, Michaela] Harvard Univ, Harvard Univ Herbaria Organism & Evolutionary Bio, Cambridge, MA 02138 USA.
[Schoch, Conrad L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Serusiaux, Emmanuel] Univ Liege, B-4000 Liege, Belgium.
[Maddison, David R.] Oregon State Univ, Ctr Genome Res & Biocomput, Corvallis, OR 97331 USA.
[Arnold, A. Elizabeth] Univ Arizona, Sch Plant Sci, Tucson, AZ 85721 USA.
RP Miadlikowska, J (reprint author), Duke Univ, Dept Biol, Box 90338, Durham, NC 27708 USA.
EM jolantam@duke.edu
FU NSF [DEB-0228668, DEB-0640956, DEB-0919455, DEB-0732984, DEB-0640996,
DEB-1025930, DEB-11455511]; Academy of Finland [211171]; NIH, National
Library of Medicine
FX We thank T. Milledge and J. Pormann for their assistance with the Duke
DSCR computer cluster, L. Bukovnik (Duke IGSP) for assistance with DNA
sequencing, members of the Lutzoni lab for helpful comments and
suggestions, M. McMullen (Duke University Herbarium) for curating lichen
specimens and proofreading the manuscript, W. R. Buck and collaborators
in the Assembling the Fungal Tree of Life (AFToL) project for providing
lichen specimens, R. Harris and T. Ahti for verifying identifications of
selected specimens, and reviewers for helpful comments on the
manuscript. This publication was supported by NSF Awards DEB-0228668,
DEB-0640956 and DEB-0919455 to FL, DEB-0732984 to FL and JM, DEB-0640996
to AEA and the Academy of Finland (Grant 211171) to SS. Additional
financial support comes from NSF Award DEB-1025930 to JM and FL,
DEB-11455511 to JL, and the Intramural Research Program of the NIH,
National Library of Medicine to CLS.
NR 189
TC 58
Z9 63
U1 3
U2 42
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1055-7903
EI 1095-9513
J9 MOL PHYLOGENET EVOL
JI Mol. Phylogenet. Evol.
PD OCT
PY 2014
VL 79
BP 132
EP 168
DI 10.1016/j.ympev.2014.04.003
PG 37
WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics &
Heredity
GA AQ5YP
UT WOS:000342884800011
PM 24747130
ER
PT J
AU Stanley, DA
Honko, AN
Asiedu, C
Trefry, JC
Lau-Kilby, AW
Johnson, JC
Hensley, L
Ammendola, V
Abbate, A
Grazioli, F
Foulds, KE
Cheng, C
Wang, LS
Donaldson, MM
Colloca, S
Folgori, A
Roederer, M
Nabel, GJ
Mascola, J
Nicosia, A
Cortese, R
Koup, RA
Sullivan, NJ
AF Stanley, Daphne A.
Honko, Anna N.
Asiedu, Clement
Trefry, John C.
Lau-Kilby, Annie W.
Johnson, Joshua C.
Hensley, Lisa
Ammendola, Virginia
Abbate, Adele
Grazioli, Fabiana
Foulds, Kathryn E.
Cheng, Cheng
Wang, Lingshu
Donaldson, Mitzi M.
Colloca, Stefano
Folgori, Antonella
Roederer, Mario
Nabel, Gary J.
Mascola, John
Nicosia, Alfredo
Cortese, Riccardo
Koup, Richard A.
Sullivan, Nancy J.
TI Chimpanzee adenovirus vaccine generates acute and durable protective
immunity against ebolavirus challenge
SO NATURE MEDICINE
LA English
DT Article
ID NONHUMAN-PRIMATES; VIRUS INFECTION; VECTOR; IMMUNOGENICITY; QUALITY
AB Ebolavirus disease causes high mortality, and the current outbreak has spread unabated through West Africa. Human adenovirus type 5 vectors (rAd5) encoding ebolavirus glycoprotein (GP) generate protective immunity against acute lethal Zaire ebolavirus (EBOV) challenge in macaques, but fail to protect animals immune to Ad5, suggesting natural Ad5 exposure may limit vaccine efficacy in humans. Here we show that a chimpanzee-derived replication-defective adenovirus (ChAd) vaccine also rapidly induced uniform protection against acute lethal EBOV challenge in macaques. Because protection waned over several months, we boosted ChAd3 With modified vaccinia Ankara (MVA) and generated, for the first time, durable protection against lethal EBOV Challenge.
C1 [Stanley, Daphne A.; Asiedu, Clement; Lau-Kilby, Annie W.; Foulds, Kathryn E.; Cheng, Cheng; Wang, Lingshu; Donaldson, Mitzi M.; Roederer, Mario; Nabel, Gary J.; Mascola, John; Koup, Richard A.; Sullivan, Nancy J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Honko, Anna N.; Trefry, John C.; Johnson, Joshua C.; Hensley, Lisa] US Army Med Res Inst Infect Dis, Ft Detrick, MD USA.
[Ammendola, Virginia; Abbate, Adele; Grazioli, Fabiana; Colloca, Stefano; Folgori, Antonella; Nicosia, Alfredo] Okairos, Rome, Italy.
[Nicosia, Alfredo] Ctr Ingn Genet CEINGE, Naples, Italy.
[Nicosia, Alfredo] Univ Naples Federico II, Dept Mol Med & Med Biotechnol, Naples, Italy.
[Cortese, Riccardo] Keires AG, Basel, Switzerland.
RP Sullivan, NJ (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM njsull@mail.nih.gov
OI Lau-Kilby, Annie/0000-0002-2666-1347; Johnson,
Joshua/0000-0002-5677-3841; Honko, Anna/0000-0001-9165-148X
FU US NIH NIAID Vaccine Research Center
FX We thank M. Cichanowski for graphics, A. Tislerics and B. Hartman for
assistance with the manuscript and R. Seder for review and helpful
suggestions. S. Perfetto and S. Norris and D. Follmann for technical
discussions, and the Vaccine Research Center's Nonhuman Primate
Immunogenicity Core for NHP sample processing. We thank the Vaccine
Research Center Laboratory Animal Medicine, S. Rao, A. Taylor, J.P. Todd
and H. Bao for protocol support and the NIH Division of Veterinary
Resources for animal care. We also thank H. Esham for technical
assistance and data management and D. Alves for pathology assistance.
TPG shuttle vector was provided by A. Siccardi (Istituto San Raffaele).
This work was supported by the Intramural Research Program of the US NIH
NIAID Vaccine Research Center. Opinions, interpretations, conclusions
and recommendations are those of the authors and are not necessarily
endorsed by the US Army or the US Department of Defense.
NR 22
TC 97
Z9 100
U1 3
U2 44
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2014
VL 20
IS 10
BP 1126
EP 1129
DI 10.1038/nm.3702
PG 4
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA AQ9RV
UT WOS:000343194100022
PM 25194571
ER
PT J
AU Cheng, XP
Zhang, XL
Gao, Q
Samie, MA
Azar, M
Tsang, WL
Dong, LB
Sahoo, N
Li, XR
Zhuo, Y
Garrity, AG
Wang, X
Ferrer, M
Dowling, J
Xu, L
Han, RZ
Xu, HX
AF Cheng, Xiping
Zhang, Xiaoli
Gao, Qiong
Samie, Mohammad Ali
Azar, Marlene
Tsang, Wai Lok
Dong, Libing
Sahoo, Nirakar
Li, Xinran
Zhuo, Yue
Garrity, Abigail G.
Wang, Xiang
Ferrer, Marc
Dowling, James
Xu, Li
Han, Renzhi
Xu, Haoxing
TI The intracellular Ca2+ channel MCOLN1 is required for sarcolemma repair
to prevent muscular dystrophy
SO NATURE MEDICINE
LA English
DT Article
ID MUCOLIPIDOSIS TYPE-IV; PLASMA-MEMBRANE REPAIR; MOLECULAR-MECHANISMS;
GROWTH-FACTOR; TRP CHANNEL; MUSCLE; DYSFERLIN; MG53; EXOCYTOSIS; DEFECTS
AB The integrity of the plasma membrane is maintained through an active repair process, especially in skeletal and cardiac muscle cells, in which contraction-induced mechanical damage frequently occurs in vivo(1,2). Muscular dystrophies (MDs) are a group of muscle diseases characterized by skeletal muscle wasting and weakness(3,4). An important cause of these group of diseases is defective repair of sarcolemmal injuries, which normally requires Ca2+ sensor proteins5-8 and Ca2+-dependent delivery of intracellular vesicles to the sites of injury(8,9). MCOLN1 (also known as TRPML1, ML1) is an endosomal and lysosomal Ca2+ channel whose human mutations cause mucolipidosis IV (ML4), a neurodegenerative disease with motor disabilities(10,11). Here we report that ML1-null mice develop a primary, early-onset MD independent of neural degeneration. Although the dystrophin-glycoprotein complex and the known membrane repair proteins are expressed normally, membrane resealing was defective in ML1-null muscle fibers and also upon acute and pharmacological inhibition of ML1 channel activity or vesicular Ca2+ release. Injury facilitated the trafficking and exocytosis of vesicles by upmodulating ML1 channel activity. In the dystrophic mdx mouse model, overexpression of ML1 decreased muscle, pathology. Collectively, our data have identified an intracellular Ca2+ channel that regulates membrane repair in skeletal muscle via Ca2+-dependent vesicle exocytosis.
C1 [Cheng, Xiping; Zhang, Xiaoli; Gao, Qiong; Samie, Mohammad Ali; Azar, Marlene; Tsang, Wai Lok; Dong, Libing; Sahoo, Nirakar; Li, Xinran; Zhuo, Yue; Garrity, Abigail G.; Wang, Xiang; Xu, Haoxing] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA.
[Garrity, Abigail G.; Xu, Haoxing] Univ Michigan, Neurosci Grad Program, Ann Arbor, MI 48109 USA.
[Ferrer, Marc] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD USA.
[Dowling, James] Univ Michigan, Med Ctr, Dept Pediat, Ann Arbor, MI 48109 USA.
[Dowling, James] Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada.
[Dowling, James] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1X8, Canada.
[Dowling, James] Univ Toronto, Dept Pediat, Toronto, ON, Canada.
[Dowling, James] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
[Xu, Li; Han, Renzhi] Loyola Univ, Dept Cell & Mol Physiol, Div Hlth Sci, Chicago, IL 60611 USA.
RP Xu, HX (reprint author), Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA.
EM xpcheng@umich.edu; haoxingx@umich.edu
FU National Institutes of Health (NIH) [NS062792, MH096595, AR060837,
HL116546, AR064241]
FX This work was supported by National Institutes of Health (NIH) grants
(NS062792, MH096595 and AR060837 to H.X.; HL116546 and AR064241 to
R.H.). We are grateful to S. Slaugenhaupt for the ML1 KO mice, L. Looger
for the GCaMP3 construct, R. Edwards for the Vamp7-pHluorin construct,
the Center for Live-Cell Imaging at the University of Michigan for the
help on TIRE Imaging, and R. Hume and M. Akaaboune for comments on the
manuscript. We appreciate the encouragement and helpful comments of
other members of the Xu laboratory.
NR 30
TC 27
Z9 27
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2014
VL 20
IS 10
BP 1187
EP 1192
DI 10.1038/nm.3611
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA AQ9RV
UT WOS:000343194100030
PM 25216637
ER
PT J
AU Roukos, V
Burgess, RC
Misteli, T
AF Roukos, Vassilis
Burgess, Rebecca C.
Misteli, Tom
TI Generation of cell-based systems to visualize chromosome damage and
translocations in living cells
SO NATURE PROTOCOLS
LA English
DT Article
ID DOUBLE-STRAND BREAKS; INDUCED DNA-DAMAGE; HOMOLOGOUS RECOMBINATION;
CHROMATIN-STRUCTURE; MAMMALIAN-CELLS; IN-VIVO; NUCLEAR ARCHITECTURE;
PROTEIN INTERACTIONS; UBIQUITIN LIGASE; GENOMIC LOCI
AB Traditional methods for the generation of DNA damage are not well suited for the observation of spatiotemporal aspects of damaged chromosomal loci. We describe a protocol for the derivation of a cellular system to induce and to visualize chromosome damage at specific sites of the mammalian genome in living cells. The system is based on the stable integration of endonuclease I-SceI recognition sites flanked by bacterial LacO/TetO operator arrays, coupled with retroviral-mediated integration of their fluorescent repressors (LacR/TetR) to visualize the LacO/TetO sites. Expression of the I-SceI endonuclease induces double-strand breaks (DSBs) specifically at the sites of integration, and it permits the dynamics of damaged chromatin to be followed by time-lapse microscopy. Sequential LacO-I-SceI/TetO-I-SceI integrations in multiple chromosomes permit the generation of a system to visualize the formation of chromosome translocations in living cells. This protocol requires intermediate cell culture and molecular biology skills, and it is adaptable to the efficient derivation of any integrated clonal reporter system of interest in similar to 3-5 months.
C1 [Roukos, Vassilis; Burgess, Rebecca C.; Misteli, Tom] NCI, NIH, Bethesda, MD 20892 USA.
RP Misteli, T (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM roukosv@mail.nih.gov; mistelit@mail.nih.gov
RI Roukos, Vassilis/K-6248-2012
FU US National Institutes of Health (NIH), National Cancer Insitute (NCI),
Center for Cancer Research
FX Work in the Misteli laboratory is supported by the Intramural Research
Program of the US National Institutes of Health (NIH), National Cancer
Insitute (NCI), Center for Cancer Research. We thank E. Soutoglou and C.
Schmidt for the optimization of specific steps of this protocol, and we
thank T. Karpova (NCI Fluorescence Imaging Microscopy Facility) for help
with microscopy.
NR 69
TC 1
Z9 1
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1754-2189
EI 1750-2799
J9 NAT PROTOC
JI Nat. Protoc.
PD OCT
PY 2014
VL 9
IS 10
BP 2476
EP 2492
DI 10.1038/nprot.2014.167
PG 17
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA AR0BH
UT WOS:000343227800015
PM 25255091
ER
PT J
AU Kastenmuller, W
Kastenmuller, K
Kurts, C
Seder, RA
AF Kastenmueller, Wolfgang
Kastenmueller, Kathrin
Kurts, Christian
Seder, Robert A.
TI Dendritic cell-targeted vaccines - hope or hype?
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Article
ID EFFICIENT ANTIGEN PRESENTATION; NON HUMAN PRIMATES; CROSS-PRESENTATION;
IMMUNOSTIMULATORY DNA; CANCER-IMMUNOTHERAPY; IN-VIVO; NEUTRALIZING
ANTIBODIES; PROTECTIVE IMMUNITY; HUMORAL RESPONSES; NONHUMAN-PRIMATES
AB The development of an effective vaccine that elicits a strong and durable T cell response against intracellular pathogens and cancer is a challenge. One strategy to enhance the effectiveness of vaccination is by targeting dendritic cells (DCs). In this Opinion article, we discuss existing DC-targeting approaches that induce adaptive immunity. We highlight the crucial issues that need to be addressed to move the field forward and discuss whether targeting DCs could be better than current vaccine approaches.
C1 [Kastenmueller, Wolfgang] Univ Bonn, Inst Mol Med, D-53105 Bonn, Germany.
[Kastenmueller, Kathrin; Kurts, Christian] Univ Bonn, Inst Expt Immunol, D-53105 Bonn, Germany.
[Kastenmueller, Kathrin] Univ Bonn, Dept Gen Practice & Family Med, D-53105 Bonn, Germany.
[Seder, Robert A.] NIAID, Cellular Immunol Sect, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP Seder, RA (reprint author), NIAID, Cellular Immunol Sect, Vaccine Res Ctr, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM wkastenm@uni-bonn.de; rseder@mail.nih.gov
FU Deutsche Forschungsgemeinschaft Excellence Cluster ImmunoSensation in
Bonn, Germany [SFB704]; German state of Northrhine-Westfalia
FX W.K. and C.K. are members of the Deutsche Forschungsgemeinschaft
Excellence Cluster ImmunoSensation in Bonn, Germany, and are supported
by grant SFB704. W.K is supported by the NRW-Ruckkehrerprogramm of the
German state of Northrhine-Westfalia. The authors thank G. Gasteiger, N.
Garbi and their laboratory members for critically reading this
manuscript.
NR 69
TC 39
Z9 40
U1 1
U2 30
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD OCT
PY 2014
VL 14
IS 10
BP 705
EP 711
DI 10.1038/nri3727
PG 7
WC Immunology
SC Immunology
GA AQ5PD
UT WOS:000342860200012
PM 25190285
ER
PT J
AU Patwardhan, A
Ashton, A
Brandt, R
Butcher, S
Carzaniga, R
Chiu, W
Collinson, L
Doux, P
Duke, E
Ellisman, MH
Franken, E
Grunewald, K
Heriche, JK
Koster, A
Kuhlbrandt, W
Lagerstedt, I
Larabell, C
Lawson, CL
Saibil, HR
Sanz-Garcia, E
Subramaniam, S
Verkade, P
Swedlow, JR
Kleywegt, GJ
AF Patwardhan, Ardan
Ashton, Alun
Brandt, Robert
Butcher, Sarah
Carzaniga, Raffaella
Chiu, Wah
Collinson, Lucy
Doux, Pascal
Duke, Elizabeth
Ellisman, Mark H.
Franken, Erik
Gruenewald, Kay
Heriche, Jean-Karim
Koster, Abraham
Kuehlbrandt, Werner
Lagerstedt, Ingvar
Larabell, Carolyn
Lawson, Catherine L.
Saibil, Helen R.
Sanz-Garcia, Eduardo
Subramaniam, Sriram
Verkade, Paul
Swedlow, Jason R.
Kleywegt, Gerard J.
TI A 3D cellular context for the macromolecular world
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Editorial Material
ID PROTEIN DATA-BANK; MICROSCOPY DATA; DATA-MANAGEMENT; RESOURCE; DATABASE;
BIOLOGY; TOMOGRAPHY; UNIPROT; GP120
AB We report the outcomes of the discussion initiated at the workshop entitled A 3D Cellular Context for the Macromolecular World and propose how data from emerging three-dimensional (3D) cellular imaging techniques-such as electron tomography, 3D scanning electron microscopy and soft X-ray tomography-should be archived, curated, validated and disseminated, to enable their interpretation and reuse by the biomedical community.
C1 [Patwardhan, Ardan; Lagerstedt, Ingvar; Sanz-Garcia, Eduardo; Kleywegt, Gerard J.] European Bioinformat Inst, European Mol Biol Lab, Prot Data Bank Europe, Hinxton, England.
[Ashton, Alun; Duke, Elizabeth] Diamond Light Source, Didcot, Oxon, England.
[Brandt, Robert; Doux, Pascal] FEI Visualizat Sci Grp, Merignac, France.
[Butcher, Sarah] Univ Helsinki, Inst Biotechnol, Helsinki, Finland.
[Carzaniga, Raffaella; Collinson, Lucy] Canc Res UK London Res Inst, Electron Microscopy Unit, London WC2A 3PX, England.
[Chiu, Wah] Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Natl Ctr Macromol Imaging, Houston, TX 77030 USA.
[Ellisman, Mark H.] Univ Calif San Diego, Natl Ctr Microscopy & Imaging Res, Ctr Res Biol Syst, San Diego, CA 92103 USA.
[Franken, Erik] FEI Electron Opt BV, Eindhoven, Netherlands.
[Gruenewald, Kay] Wellcome Trust Ctr Human Genet, Div Struct Biol, Oxford, England.
[Heriche, Jean-Karim] European Mol Biol Lab, Cell Biol & Biophys Unit, D-69012 Heidelberg, Germany.
[Koster, Abraham] Leiden Univ, Med Ctr, Dept Mol Cell Biol, Leiden, Netherlands.
[Kuehlbrandt, Werner] Max Planck Inst Biophys, Dept Biol Struct, Frankfurt, Germany.
[Larabell, Carolyn] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA.
[Lawson, Catherine L.] Rutgers State Univ, Res Collaboratory Struct Bioinformat, Piscataway, NJ USA.
[Saibil, Helen R.] Birkbeck Coll, Dept Crystallog, Inst Struct & Mol Biol, London, England.
[Subramaniam, Sriram] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Verkade, Paul] Univ Bristol, Sch Biochem, Wolfson Bioimaging Facil, Bristol, Avon, England.
[Swedlow, Jason R.] Univ Dundee, Ctr Gene Regulat & Express, Dundee, Scotland.
RP Kleywegt, GJ (reprint author), European Bioinformat Inst, European Mol Biol Lab, Prot Data Bank Europe, Hinxton, England.
EM j.swedlow@dundee.ac.uk; gerard@ebi.ac.uk
RI Verkade, Paul/N-7240-2014
FU Biotechnology and Biological Sciences Research Council [BB/G022577/1,
BB/G022585, BB/G022585/1]; Medical Research Council [MR/L007835]; NIGMS
NIH HHS [P41 GM103445, R01 GM079429]; Wellcome Trust [088944, 090895,
095931, 097945]
NR 32
TC 15
Z9 15
U1 2
U2 19
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
EI 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD OCT
PY 2014
VL 21
IS 10
BP 841
EP 845
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA AQ5PV
UT WOS:000342862000001
PM 25289590
ER
PT J
AU Bunch, H
Zheng, XF
Burkholder, A
Dillon, ST
Motola, S
Birrane, G
Ebmeier, CC
Levine, S
Fargo, D
Hu, G
Taatjes, DJ
Calderwood, SK
AF Bunch, Heeyoun
Zheng, Xiaofeng
Burkholder, Adam
Dillon, Simon T.
Motola, Shmulik
Birrane, Gabriel
Ebmeier, Christopher C.
Levine, Stuart
Fargo, David
Hu, Guang
Taatjes, Dylan J.
Calderwood, Stuart K.
TI TRIM28 regulates RNA polymerase II promoter-proximal pausing and pause
release
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID POL-II; DROSOPHILA-EMBRYO; IN-VIVO; TRANSCRIPTION; GENOME; GENES;
EXPRESSION; REVEALS; NELF; ATM
AB Promoter-proximal pausing of RNA polymerase II (Pol II) is a major checkpoint in transcription. An unbiased search for new human proteins that could regulate paused Pol II at the HSPA1B gene identified TRIM28. In vitro analyses indicated HSF1-dependent attenuation of Pol II pausing upon TRIM28 depletion, whereas in vivo data revealed de novo expression of HSPA1B and other known genes regulated by paused Pol II upon TRIM28 knockdown. These results were supported by genome-wide ChIP-sequencing analyses of Pol II occupancy that revealed a global role for TRIM28 in regulating Pol II pausing and pause release. Furthermore, in vivo and in vitro mechanistic studies suggest that transcription-coupled phosphorylation regulates Pol II pause release by TRIM28. Collectively, our findings identify TRIM28 as a new factor that modulates Pol II pausing and transcriptional elongation at a large number of mammalian genes.
C1 [Bunch, Heeyoun; Dillon, Simon T.; Birrane, Gabriel; Calderwood, Stuart K.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Radiat Oncol, Boston, MA 02215 USA.
[Zheng, Xiaofeng; Hu, Guang] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Burkholder, Adam; Fargo, David] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
[Dillon, Simon T.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Genom & Prote Ctr, Boston, MA 02215 USA.
[Motola, Shmulik; Levine, Stuart] MIT, BioMicro Ctr, Cambridge, MA 02139 USA.
[Birrane, Gabriel] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med, Boston, MA 02215 USA.
[Ebmeier, Christopher C.; Taatjes, Dylan J.] Univ Colorado, Dept Chem & Biochem, Boulder, CO 80309 USA.
RP Calderwood, SK (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Radiat Oncol, Boston, MA 02215 USA.
EM scalderw@bidmc.harvard.edu
RI Hu, Guang/E-7474-2016;
OI Hu, Guang/0000-0003-0437-4723; Bunch, Heeyoun/0000-0003-0038-1985
FU US National Institutes of Health (NIH) [RO-1CA047407]; Harvard Joint
Center for Radiation Therapy; Koch Institute for Integrative Cancer
Research at MIT [P30-CA14051]; MIT Center for Environmental Health
Sciences [P30-ES002109]; NCI [R01CA127364]; American Cancer Society
(RSG) [0927401DMC]; Intramural Research Program of the NIH NIEHS
[1ZIAES102745-02]
FX We appreciate S. Elledge at the Harvard Medical School for mediating
collaborations and R. Young and D. Orlando at Massachusetts Institute of
Technology (MIT) for providing with helpful comments and perspectives
for the manuscript. We thank A. York, A. Schubert, M. Knuesel, T.
Westerling and J. Stinchfield for technical support and thank C. Wu (US
National Cancer Institute (NCI)) for the HSF1 vector, R. Kelm Jr.
(University of Vermont) for the PURb antibody and E Zhu (Florida State
University) for the GST-TRIM28 vectors. We thank the laboratories of S.
Alper, M. Pollak and M. Brown at Beth Israel Deaconess Medical Center
(BIDMC) for technical assistance, equipment and discussions. H.B. thanks
M. Cross and M.A. Stevenson at BIDMC for administrative support and J.
Park and D. Bunch for loving encouragement throughout the work. This
study was supported by grants from the US National Institutes of Health
(NIH) (RO-1CA047407) and the Harvard Joint Center for Radiation Therapy
to S.K.C. and H.B., from the Koch Institute for Integrative Cancer
Research at MIT (P30-CA14051) and the MIT Center for Environmental
Health Sciences (P30-ES002109) to S.M. and S.L. and also from the NCI
(R01CA127364) and the American Cancer Society (RSG 0927401DMC) to D.J.T.
This research was supported in part by the Intramural Research Program
of the NIH NIEHS (1ZIAES102745-02) to G.H. and X.Z. and to A.B. and D.F.
NR 39
TC 20
Z9 20
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
EI 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD OCT
PY 2014
VL 21
IS 10
BP 876
EP 883
DI 10.1038/nsmb.2878
PG 8
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA AQ5PV
UT WOS:000342862000007
PM 25173174
ER
PT J
AU Kim, KK
Yang, YQ
Zhu, J
Adelstein, RS
Kawamoto, S
AF Kim, Kee K.
Yang, Yanqin
Zhu, Jun
Adelstein, Robert S.
Kawamoto, Sachiyo
TI Rbfox3 controls the biogenesis of a subset of microRNAs
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID HITS-CLIP; MICROPROCESSOR COMPLEX; REGULATORY NETWORK; RNA RECOGNITION;
IN-VIVO; PROTEIN; FOX-1; DROSHA; INCLUSION; SEQUENCE
AB RNA-binding proteins (RBPs) regulate numerous aspects of gene expression; thus, identification of their endogenous targets is important for understanding their cellular functions. Here we identified transcriptome-wide targets of Rbfox3 in neuronally differentiated P19 cells and mouse brain by using photoactivatable ribonucleoside-enhanced cross-linking and immunoprecipitation (PAR-CUP). Although Rbfox3 is known to regulate pre-mRNA splicing through binding the UGCAUG motif, PAR-CLIP analysis revealed diverse Rbfox3 targets including primary microRNAs (pri-miRNAs) that lack the UGCAUG motif. Induced expression and depletion of Rbfox3 led to changes in the expression levels of a subset of PAR-CLIP-detected miRNAs. In vitro analyses revealed that Rbfox3 functions as a positive and a negative regulator at the stage of pri-miRNA processing to precursor miRNA (pre-miRNA). Rbfox3 binds directly to pri-miRNAs and regulates the recruitment of the microprocessor complex to pri-miRNAs. Our study proposes a new function for Rbfox3 in miRNA biogenesis.
C1 [Kim, Kee K.; Adelstein, Robert S.; Kawamoto, Sachiyo] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
[Yang, Yanqin; Zhu, Jun] NHLBI, DNA Sequencing & Genom Core, NIH, Bethesda, MD 20892 USA.
RP Kim, KK (reprint author), NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
EM kimkk@mail.mh.gov; kawamots@mail.nih.gov
RI Kim, Kee/F-8784-2011;
OI Adelstein, Robert/0000-0002-8683-2144
FU Division of Intramural Research, NHLBI, US National Institutes of Health
FX We thank U. Ohler, D.L. Corcoran and N. Mukherjee (Duke University) for
help in PARalyzer analysis, H. Wu (Lawrence Berkeley National
Laboratory) for advice on preparation of a sequence library for
PAR-CLIP, D.-Y. Lee (Biochemistry Core Facility, US National Heart,
Lung, and Blood Institute (NHLBI)) for HPLC analysis of ribonucleosides
and C.A. Combs (Light Microscope Core Facility, NHLBI) for advice on
confocal microscopy. We also thank D.E. Saunders and A.F. Smith for
technical assistance, S. Nakahata for reagents and M.A. Conti for
critical reading of the manuscript. This work was supported by the
Division of Intramural Research, NHLBI, US National Institutes of
Health.
NR 50
TC 14
Z9 14
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
EI 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD OCT
PY 2014
VL 21
IS 10
BP 901
EP 910
DI 10.1038/nsmb.2892
PG 10
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA AQ5PV
UT WOS:000342862000010
PM 25240799
ER
PT J
AU Neto, OA
Martins, CA
Reed, UC
Biancalana, V
Bonnemann, C
Laporte, J
Zanoteli, E
AF Abath Neto, O.
Martins, C. A.
Reed, U. C.
Biancalana, V.
Boennemann, C.
Laporte, J.
Zanoteli, E.
TI Molecular analysis of a Brazilian cohort of myotubular and centronuclear
myopathy patients
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Abath Neto, O.; Martins, C. A.; Reed, U. C.; Zanoteli, E.] Univ Sao Paulo, Sch Med, Sao Paulo, Brazil.
[Biancalana, V.] Nouvel Hop Civil, Fac Med, Lab Diagnost Genet, Strasbourg, France.
[Boennemann, C.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
[Laporte, J.] Univ Strasbourg, Dept Translat Med & Neurogenet, CNRS UMR7104, IGBMC,INSERM U964,Coll France, Illkirch Graffenstaden, France.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.33
BP 804
EP 804
DI 10.1016/j.nmd.2014.06.047
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200044
ER
PT J
AU Chauveau, C
Bonnemann, CG
Julien, C
Kho, AL
Marks, H
Talim, B
Maury, P
Uro-Coste, E
Alexandrovich, A
Vihola, A
Foley, AR
Santi, M
Udd, B
Topaloglu, H
Moore, SA
Gotthardt, M
Samuels, ME
Gautel, M
Ferreiro, A
AF Chauveau, C.
Boennemann, C. G.
Julien, C.
Kho, A. L.
Marks, H.
Talim, B.
Maury, P.
Uro-Coste, E.
Alexandrovich, A.
Vihola, A.
Foley, A. R.
Santi, M.
Udd, B.
Topaloglu, H.
Moore, S. A.
Gotthardt, M.
Samuels, M. E.
Gautel, M.
Ferreiro, A.
TI The expanding spectrum of congenital titinopathies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Chauveau, C.; Julien, C.] UPMC, Inst Myol, INSERM, UMR,U787, Paris, France.
[Boennemann, C. G.] NIH, Bethesda, MD 20892 USA.
[Boennemann, C. G.; Foley, A. R.] Childrens Hosp Philadelphia, Div Neurol, Philadelphia, PA 19104 USA.
[Kho, A. L.; Alexandrovich, A.; Gautel, M.] Kings Coll London, Cardiovasc Div, London WC2R 2LS, England.
[Kho, A. L.; Alexandrovich, A.; Gautel, M.] Kings Coll London, Randall Div Cell & Mol Biophys, London WC2R 2LS, England.
[Marks, H.] St Christophers Hosp Children, Dept Pediat, Philadelphia, PA 19133 USA.
[Talim, B.; Topaloglu, H.] Hacettepe Univ, Fac Med, Dept Pediat, TR-06100 Ankara, Turkey.
[Maury, P.] CHU Rangueil, F-31054 Toulouse, France.
[Uro-Coste, E.] CHU Rangueil, Dept Pathol, F-31054 Toulouse, France.
[Uro-Coste, E.] CHU Rangueil, INSERM, UMR 1037, F-31054 Toulouse, France.
[Vihola, A.; Udd, B.] Folkhalsan Inst Genet, Helsinki, Finland.
[Vihola, A.; Udd, B.] Haartman Inst, Dept Med Genet, Helsinki, Finland.
[Santi, M.] Childrens Hosp Philadelphia, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Moore, S. A.] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA.
[Gotthardt, M.] Max Delbruck Ctr Mol Med, Berlin, Germany.
[Chauveau, C.; Samuels, M. E.] Hop St Justine, Ctr Rech, Montreal, PQ H3T 1C5, Canada.
[Ferreiro, A.] Neuromuscular Disorders Consultat, Paris, France.
RI Kho, Ay Lin/M-4214-2013; Ferreiro, Ana/F-5371-2011
OI Kho, Ay Lin/0000-0002-9753-2091;
NR 0
TC 1
Z9 1
U1 1
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.34
BP 804
EP 805
DI 10.1016/j.nmd.2014.06.048
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200045
ER
PT J
AU Annoussamy, M
Landy, H
Ramsdell, D
Nelken, M
Muntoni, F
Bonnemann, C
Bharucha, D
Dowling, JJ
Amburgey, K
Lilien, C
Ollivier, G
Laporte, J
Biancalana, V
Schara, U
Cuisset, JM
D'Amico, A
Deconinck, N
Jeannet, PY
Klein, A
Fluss, J
Mayer, M
Seferian, AM
Le Moing, AG
Gidaro, T
Hogrel, JY
Mingozzi, F
Buj-Bello, A
Voit, T
Servais, L
AF Annoussamy, M.
Landy, H.
Ramsdell, D.
Nelken, M.
Muntoni, F.
Boennemann, C.
Bharucha, D.
Dowling, J. J.
Amburgey, K.
Lilien, C.
Ollivier, G.
Laporte, J.
Biancalana, V.
Schara, U.
Cuisset, J. M.
D'Amico, A.
Deconinck, N.
Jeannet, P. Y.
Klein, A.
Fluss, J.
Mayer, M.
Seferian, A. M.
Le Moing, A. G.
Gidaro, T.
Hogrel, J. Y.
Mingozzi, F.
Buj-Bello, A.
Voit, T.
Servais, L.
TI An international prospective, longitudinal study of the natural history
and functional status of patients with myotubular myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Annoussamy, M.; Lilien, C.; Ollivier, G.; Seferian, A. M.; Le Moing, A. G.; Gidaro, T.; Hogrel, J. Y.; Voit, T.; Servais, L.] Inst Myol, Paris, France.
[Landy, H.; Ramsdell, D.; Nelken, M.] Valer Therapeut, Concord, MA USA.
[Muntoni, F.] UCL, Inst Child Hlth, London, England.
[Boennemann, C.; Bharucha, D.] NINDS, NIH, Bethesda, MD 20892 USA.
[Dowling, J. J.; Amburgey, K.] Hosp Sick Children, Peter Gilgan Ctr Res & Learning, Toronto, ON M5G 1X8, Canada.
[Laporte, J.] Univ Strasbourg, IGMBC, CNRS, Inserm,U964,UMR7104, Illkirch Graffenstaden, France.
[Biancalana, V.] Nouvel Hop Civil, Strasbourg, France.
[Schara, U.] Univ Essen Gesamthsch, Essen, Germany.
[Cuisset, J. M.] Hop Roger Salengro, Lille, France.
[D'Amico, A.] Bambino Gesu Childrens Res Hosp IRCCS, Rome, Italy.
[Deconinck, N.] Hop Univ Enfants Reine Fabiola, Brussels, Belgium.
[Jeannet, P. Y.] CHU Vaudois, CH-1011 Lausanne, Switzerland.
[Klein, A.] Univ Childrens Hosp Zurich, Zurich, Switzerland.
[Fluss, J.] Hop Cantonal Univ Geneva, Hop Enfants, Geneva, Switzerland.
[Mayer, M.] Hop Armand Trousseau, Paris, France.
[Mingozzi, F.; Buj-Bello, A.] Genethon, Evry, France.
RI d'amico, adele/J-9203-2016; BUJ-BELLO, Anna/J-7556-2013
OI d'amico, adele/0000-0003-2438-2624;
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.39
BP 806
EP 806
DI 10.1016/j.nmd.2014.06.053
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200050
ER
PT J
AU Amburgey, K
Bailey, A
Hwang, JH
Tamopolsky, MA
Bonnemann, CG
Medne, L
Mathews, KD
Collins, J
Daube, JR
Wellman, GP
Callaghan, B
Vajsar, J
Yoon, G
Cohn, R
Clarke, NF
Dowling, JJ
AF Amburgey, K.
Bailey, A.
Hwang, J. H.
Tamopolsky, M. A.
Boennemann, C. G.
Medne, L.
Mathews, K. D.
Collins, J.
Daube, J. R.
Wellman, G. P.
Callaghan, B.
Vajsar, J.
Yoon, G.
Cohn, R.
Clarke, N. F.
Dowling, J. J.
TI Genotype-phenotype correlations in recessive RYR1-related myopathies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Amburgey, K.; Vajsar, J.; Yoon, G.; Cohn, R.; Dowling, J. J.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Bailey, A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Hwang, J. H.] Childrens Hosp Westmead, Sydney, NSW, Australia.
[Tamopolsky, M. A.] McMaster Univ, Med Ctr, Hamilton, ON, Canada.
[Boennemann, C. G.] NIH, Bethesda, MD 20892 USA.
[Medne, L.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Mathews, K. D.] Univ Iowa, Carver Coll Med, Iowa City, IA USA.
[Collins, J.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Daube, J. R.] Mayo Fdn Med Educ & Res, Rochester, MN USA.
[Wellman, G. P.] Delta Pathol Grp, Shreveport, LA USA.
[Callaghan, B.] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
[Clarke, N. F.] Univ Sydney, Sydney, NSW 2006, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.48
BP 809
EP 809
DI 10.1016/j.nmd.2014.06.062
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200059
ER
PT J
AU Malicdan, MC
Mian, L
Leoyklang, P
Celeste, F
Despres, D
Zerfas, P
Carrillo-Carrasco, N
Gahl, WA
AF Malicdan, M. C.
Mian, L.
Leoyklang, P.
Celeste, F.
Despres, D.
Zerfas, P.
Carrillo-Carrasco, N.
Gahl, W. A.
TI Cardiac impairment in GNE myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Malicdan, M. C.; Mian, L.; Leoyklang, P.; Gahl, W. A.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Celeste, F.; Carrillo-Carrasco, N.] NIH, NCATS, Bethesda, MD 20892 USA.
[Despres, D.] NIH, Mouse Imaging Facil, Bethesda, MD 20892 USA.
[Despres, D.] NINDS, NIH, Bethesda, MD 20892 USA.
[Zerfas, P.] NIH, Div Vet Resources, ORS, Bethesda, MD 20892 USA.
RI Carrillo-Carrasco, Nuria/B-9034-2009
OI Carrillo-Carrasco, Nuria/0000-0003-0374-0808
NR 0
TC 0
Z9 0
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.52
BP 810
EP 810
DI 10.1016/j.nmd.2014.06.066
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200063
ER
PT J
AU Maerkens, A
Olive, M
Tasca, G
Claeys, K
Barresi, R
Sarkozy, A
Pfeffer, G
Evangelista, T
Feldkirchner, S
Reimann, J
Hanisch, F
Stenzel, W
Schessl, J
Schoser, B
Goldfarb, L
Udd, B
Chinnery, P
Lochmuller, H
Schroder, R
Marcus, K
Vorgerd, M
Kley, RA
AF Maerkens, A.
Olive, M.
Tasca, G.
Claeys, K.
Barresi, R.
Sarkozy, A.
Pfeffer, G.
Evangelista, T.
Feldkirchner, S.
Reimann, J.
Hanisch, F.
Stenzel, W.
Schessl, J.
Schoser, B.
Goldfarb, L.
Udd, B.
Chinnery, P.
Lochmueller, H.
Schroeder, R.
Marcus, K.
Vorgerd, M.
Kley, R. A.
TI Proteomic analysis in 72 myofibrillar myopathy (MFM) patients identifies
new disease-relevant proteins accumulating in aggregates and reveals
subtype-specific proteomic profiles
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Maerkens, A.; Vorgerd, M.; Kley, R. A.] Ruhr Univ Bochum, Univ Hosp Bergmannsheil, Bochum, Germany.
[Olive, M.] IDIBELL Hosp Univ Bellvitge, Barcelona, Spain.
[Olive, M.] CIBERNED, Barcelona, Spain.
[Tasca, G.] Don Carlo Gnocchi ONLUS Fdn, Milan, Italy.
[Claeys, K.] Univ Hosp RWTH, Aachen, Germany.
[Barresi, R.] NCG Diagnost & Advisory Serv Rare Neuromuscular D, Newcastle Upon Tyne, Tyne & Wear, England.
[Sarkozy, A.; Pfeffer, G.; Evangelista, T.; Chinnery, P.; Lochmueller, H.] Newcastle Univ, Int Ctr Life, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Feldkirchner, S.; Schessl, J.; Schoser, B.] Univ Munich, Friedrich Baur Inst, Munich, Germany.
[Reimann, J.] Univ Hosp Bonn, Bonn, Germany.
[Hanisch, F.] Univ Halle Wittenberg, D-06108 Halle, Saale, Germany.
[Stenzel, W.] Charite, D-13353 Berlin, Germany.
[Goldfarb, L.] NIH, Bethesda, MD 20892 USA.
[Udd, B.] Univ Tampere, Neuromuscular Res Ctr, FIN-33101 Tampere, Finland.
[Schroeder, R.] Univ Hosp Erlangen, Erlangen, Germany.
[Marcus, K.] Ruhr Univ Bochum, Med Proteom Ctr, Bochum, Germany.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA A.P.1
BP 830
EP 830
DI 10.1016/j.nmd.2014.06.131
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200128
ER
PT J
AU Guglieri, M
Sambuughin, N
Sarkozy, A
Barresi, R
Lochmuller, H
Bushby, K
Goldfarb, LG
Straub, V
AF Guglieri, M.
Sambuughin, N.
Sarkozy, A.
Barresi, R.
Lochmueller, H.
Bushby, K.
Goldfarb, L. G.
Straub, V.
TI Autosomal recessive myofibrillar myopathy caused by ACTA1 mutations
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Guglieri, M.; Barresi, R.; Lochmueller, H.; Bushby, K.; Straub, V.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Sambuughin, N.; Goldfarb, L. G.] NINDS, Bethesda, MD 20892 USA.
[Sarkozy, A.] ICH Inst Child Hlth & Great Ormond St Hosp, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA A.P.6
BP 832
EP 832
DI 10.1016/j.nmd.2014.06.136
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200133
ER
PT J
AU Leach, ME
Donkervoort, S
Simpson, K
Tesi-Rocha, AC
Avery, R
Dastgir, J
Reyes, C
Hu, Y
Winder, TL
Bonnemann, CG
AF Leach, M. E.
Donkervoort, S.
Simpson, K.
Tesi-Rocha, A. C.
Avery, R.
Dastgir, J.
Reyes, C.
Hu, Y.
Winder, T. L.
Boennemann, C. G.
TI Novel recessive mutations in MYH2 presenting with congenital facial
weakness, ophthalmoparesis, severe progressive scoliosis, and mild
muscle weakness
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Leach, M. E.; Simpson, K.; Avery, R.; Reyes, C.] Childrens Natl Hlth Syst, Washington, DC USA.
[Donkervoort, S.; Dastgir, J.; Hu, Y.] NIH, Bethesda, MD 20892 USA.
[Tesi-Rocha, A. C.] Lucile Packard Childrens Hosp Stanford, Palo Alto, CA USA.
[Winder, T. L.] PreventionGenetics, Marshfield, WI USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.152
BP 847
EP 847
DI 10.1016/j.nmd.2014.06.182
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200179
ER
PT J
AU Mankodi, A
Janiczek, R
Froeling, M
Azzabou, N
Gaur, L
Stock, D
Evers, R
Bishop, C
Yao, L
Grunseich, C
Arai, A
Carlier, P
Fischbeck, K
AF Mankodi, A.
Janiczek, R.
Froeling, M.
Azzabou, N.
Gaur, L.
Stock, D.
Evers, R.
Bishop, C.
Yao, L.
Grunseich, C.
Arai, A.
Carlier, P.
Fischbeck, K.
TI Skeletal muscle, cardiac, and pulmonary imaging biomarkers of disease
activity in boys with Duchenne muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Mankodi, A.; Stock, D.; Grunseich, C.; Fischbeck, K.] NINDS, NIH, Neurogenet Branch, Bethesda, MD 20892 USA.
[Janiczek, R.] GlaxoSmithKline, Global Imaging Unit, London, England.
[Froeling, M.] Univ Utrecht, Utrecht, Netherlands.
[Azzabou, N.; Carlier, P.] Inst Myol, NMR Lab, Spect Lab, Paris, France.
[Gaur, L.; Arai, A.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Evers, R.; Yao, L.] NIH, CC Radiol, Bethesda, MD 20892 USA.
[Bishop, C.] Imanova Ctr Imaging Sci, London, England.
RI Froeling, Martijn/E-7865-2012
OI Froeling, Martijn/0000-0003-3841-0497
NR 0
TC 0
Z9 0
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.O.10
BP 852
EP 852
DI 10.1016/j.nmd.2014.06.198
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200195
ER
PT J
AU Thurberg, BL
van der Ploeg, A
Kissel, JT
Schoser, B
Pestronk, A
Barohn, RJ
Goker-Alpan, O
Mozaffar, T
Pena, LDM
Simmons, Z
Straub, V
Young, P
Bjartmar, C
AF Thurberg, B. L.
van der Ploeg, A.
Kissel, J. T.
Schoser, B.
Pestronk, A.
Barohn, R. J.
Goker-Alpan, O.
Mozaffar, T.
Pena, L. D. M.
Simmons, Z.
Straub, V.
Young, P.
Bjartmar, C.
TI Alglucosidase alfa reduces lysosomal glycogen in skeletal muscle
biopsies of patients with late-onset Pompe disease (LOPD)
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Thurberg, B. L.; Bjartmar, C.] Genzyme, Cambridge, MA USA.
[van der Ploeg, A.] Erasmus MC Univ Med Ctr, Rotterdam, Netherlands.
[Kissel, J. T.] Ohio State Univ, Columbus, OH 43210 USA.
[Schoser, B.] Klinikum Univ Munchen, Munich, Germany.
[Pestronk, A.] Ctr Adv Med, St Louis, OH USA.
[Barohn, R. J.] Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
[Goker-Alpan, O.] NIH, Bethesda, MD 20892 USA.
[Mozaffar, T.] Univ Calif Irvine, Irvine, CA USA.
[Pena, L. D. M.] Duke Univ, Med Ctr, Durham, NC USA.
[Simmons, Z.] Penn State Hershey Neurol, Hershey, PA USA.
[Straub, V.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Young, P.] Univ Hosp Munster, Munster, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA T.P.24
BP 871
EP 872
DI 10.1016/j.nmd.2014.06.260
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200257
ER
PT J
AU Guadagnin, E
Dastgir, J
Yang, L
Johnson, K
Wang, Q
Hu, Y
Dillmann, A
Cookson, M
Bonnemann, C
AF Guadagnin, E.
Dastgir, J.
Yang, L.
Johnson, K.
Wang, Q.
Hu, Y.
Dillmann, A.
Cookson, M.
Boennemann, C.
TI Investigating the molecular mechanisms underlying the progression of
collagen VI-related muscular dystrophies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Guadagnin, E.; Dastgir, J.; Johnson, K.; Wang, Q.; Hu, Y.; Boennemann, C.] NINDS, NIH, Bethesda, MD 20892 USA.
[Yang, L.] Univ Kentucky, Lexington, KY 40506 USA.
[Dillmann, A.; Cookson, M.] NIA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.213
BP 880
EP 881
DI 10.1016/j.nmd.2014.06.289
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200286
ER
PT J
AU Bolduc, V
Zou, Y
Lindow, M
Obad, S
Bonneman, CG
AF Bolduc, V.
Zou, Y.
Lindow, M.
Obad, S.
Boenneman, C. G.
TI Allele-specific silencing of a dominant-negative mutation using siRNA or
LNA antisense oligonucleotides alleviates the phenotype of a cellular
model of Ullrich congenital muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Bolduc, V.; Zou, Y.; Boenneman, C. G.] NINDS, NIH, Bethesda, MD 20892 USA.
[Lindow, M.; Obad, S.] Santaris Pharma AS, Horsholm, Denmark.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.216
BP 881
EP 882
DI 10.1016/j.nmd.2014.06.292
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200289
ER
PT J
AU Hu, Y
Donkervoot, S
Stojkovic, T
Voermans, N
Foley, AR
Leach, M
Dastgir, J
Bolduc, V
Cullup, T
Becdelievre, A
Yang, L
Su, H
Meilleur, K
Schindler, A
Kamsteeg, E
Richard, P
Butterfield, R
Winder, T
Crawford, T
Weiss, R
Muntoni, F
Allamand, V
Bonnemann, C
AF Hu, Y.
Donkervoot, S.
Stojkovic, T.
Voermans, N.
Foley, A. R.
Leach, M.
Dastgir, J.
Bolduc, V.
Cullup, T.
Becdelievre, A.
Yang, L.
Su, H.
Meilleur, K.
Schindler, A.
Kamsteeg, E.
Richard, P.
Butterfield, R.
Winder, T.
Crawford, T.
Weiss, R.
Muntoni, F.
Allamand, V.
Boennemann, C.
TI Mosaicism for dominant COLVI mutations as a cause for intra-familial
phenotypic variability
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Hu, Y.; Donkervoot, S.; Leach, M.; Dastgir, J.; Bolduc, V.; Schindler, A.; Boennemann, C.] NIH, Bethesda, MD 20892 USA.
[Stojkovic, T.] Grp Hosp Pitie Salpetriere, F-75634 Paris, France.
[Voermans, N.; Kamsteeg, E.] Radboud Univ Nijmegen Med Ctr, Nijmegen, Netherlands.
[Foley, A. R.; Muntoni, F.] Univ Coll London Inst Child Hlth, London, England.
[Foley, A. R.; Muntoni, F.] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Cullup, T.] Guys Hosp, London SE1 9RT, England.
[Becdelievre, A.] Hop Univ La Pitie Salpetriere, Paris, France.
[Yang, L.; Su, H.] Univ Kentucky, Lexington, KY 40506 USA.
[Meilleur, K.] NINR, Bethesda, MD 20892 USA.
[Richard, P.] UPMC, UMR S 1166, Hop Univ La Pitie Salpetriere, Paris, France.
[Butterfield, R.; Weiss, R.] Univ Utah, Salt Lake City, UT USA.
[Winder, T.] Prevent Genet, Marshfield, WI USA.
[Crawford, T.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Allamand, V.] Univ Paris 04, INSERM, Inst Myol, CNRS, Paris, France.
RI Voermans, N.C./L-4724-2015
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.214
BP 881
EP 881
DI 10.1016/j.nmd.2014.06.290
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200287
ER
PT J
AU Medne, L
Bonnemann, C
Scherer, S
Finkel, RS
Ortiz-Gonzalez, X
Glanzman, A
Estilow, T
Moll, A
Leshner, R
Wang, Y
Winder, T
Yum, S
AF Medne, L.
Boennemann, C.
Scherer, S.
Finkel, R. S.
Ortiz-Gonzalez, X.
Glanzman, A.
Estilow, T.
Moll, A.
Leshner, R.
Wang, Y.
Winder, T.
Yum, S.
TI Expanding phenotype of TRPV4 related neuropathies with notable
intrafamilial variability
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Medne, L.; Ortiz-Gonzalez, X.; Glanzman, A.; Estilow, T.; Moll, A.; Yum, S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Boennemann, C.] NIH, Bethesda, MD 20892 USA.
[Scherer, S.] Univ Penn, Philadelphia, PA 19104 USA.
[Finkel, R. S.] Nemours Childrens Hosp, Orlando, FL USA.
[Leshner, R.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Wang, Y.; Winder, T.] Prevent Genet, Marshfield, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.239
BP 888
EP 889
DI 10.1016/j.nmd.2014.06.315
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200312
ER
PT J
AU Donkervoort, S
Neu, M
Kirschner, J
Yang, ML
Marston, SB
Gibbons, MA
Hu, Y
de Winter, JM
Ottenheijm, CAC
Rutkowski, A
Kruger, M
McNamara, E
Ong, R
Nowak, K
Clarke, NF
Bonnemann, CG
AF Donkervoort, S.
Neu, M.
Kirschner, J.
Yang, M. L.
Marston, S. B.
Gibbons, M. A.
Hu, Y.
de Winter, J. M.
Ottenheijm, C. A. C.
Rutkowski, A.
Krueger, M.
McNamara, E.
Ong, R.
Nowak, K.
Clarke, N. F.
Boennemann, C. G.
TI Novel deletions in TPM3 define a hypercontractile phenotype with marked
congenital muscle stiffness: Expanding the spectrum of TPM3 related
disease
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Donkervoort, S.; Neu, M.; Hu, Y.; Boennemann, C. G.] NIH, Bethesda, MD 20892 USA.
[Kirschner, J.; Krueger, M.] Univ Med Ctr Freiburg, Freiburg, Germany.
[Yang, M. L.] Univ Colorado, Sch Med, Aurora, CO USA.
[Marston, S. B.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Gibbons, M. A.] Univ Colorado, Denver Sch Med, Aurora, CO USA.
[de Winter, J. M.; Ottenheijm, C. A. C.] Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands.
[Rutkowski, A.] Kaiser SCPMG, Cure CMD, Olathe, KS USA.
[McNamara, E.; Ong, R.; Nowak, K.] Univ Western Australia, Crawley, Australia.
[Clarke, N. F.] Univ Sydney, Childrens Hosp Westmead, Sydney, NSW 2006, Australia.
RI Kirschner, Janbernd/H-7418-2016
OI Kirschner, Janbernd/0000-0003-1618-7386
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.272
BP 898
EP 899
DI 10.1016/j.nmd.2014.06.348
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200345
ER
PT J
AU Meilleur, KM
Jain, MS
Hynan, LS
Shieh, CY
Kim, E
Waite, M
McGuire, M
Fiorini, C
Glanzman, A
Main, M
Rose, K
Duong, T
Linton, MM
Arveson, IC
Nichols, C
Yang, K
Smith, M
Donkervoort, S
Leach, ME
Foley, AR
Collins, J
Muntoni, F
Rutkowski, A
Bonnemann, CG
AF Meilleur, K. M.
Jain, M. S.
Hynan, L. S.
Shieh, C. Y.
Kim, E.
Waite, M.
McGuire, M.
Fiorini, C.
Glanzman, A.
Main, M.
Rose, K.
Duong, T.
Linton, M. M.
Arveson, I. C.
Nichols, C.
Yang, K.
Smith, M.
Donkervoort, S.
Leach, M. E.
Foley, A. R.
Collins, J.
Muntoni, F.
Rutkowski, A.
Boennemann, C. G.
TI Comparison of three scales of motor function in two subtypes of patients
with congenital muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Meilleur, K. M.; Linton, M. M.; Arveson, I. C.] NINR, Bethesda, MD 20892 USA.
[Jain, M. S.; Waite, M.; Nichols, C.; Smith, M.] Mark O Hatfield Clin Res Ctr, Bethesda, MD USA.
[Hynan, L. S.] Dept Clin Sci Biostat, Dallas, TX USA.
[Hynan, L. S.] Univ Texas Dallas, SW Med Ctr, Dept Psychiat, Dallas, TX USA.
[Shieh, C. Y.] NIH, Bethesda, MD 20892 USA.
[Kim, E.] CureCMD, Los Angeles, CA USA.
[Fiorini, C.] Kennedy Krieger Inst, Baltimore, MD USA.
[Fiorini, C.] Dept Neurol, Baltimore, MD USA.
[Fiorini, C.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
[Glanzman, A.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Main, M.; Foley, A. R.; Muntoni, F.] MRC Ctr Neuromuscular Dis, Dubowitz Neuromuscular Ctr, London, England.
[Rose, K.] Inst Neurosci & Muscle Res, Sydney, NSW, Australia.
[Duong, T.; Leach, M. E.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Yang, K.; Donkervoort, S.; Boennemann, C. G.] NINDS, Bethesda, MD 20892 USA.
[Rutkowski, A.] Kaiser Permanente, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA T.P.42
BP 906
EP 907
DI 10.1016/j.nmd.2014.06.373
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200370
ER
PT J
AU Dastgir, J
Vuillerot, C
Nguyen, D
Yang, K
Auh, S
DonkerVoort, S
Meilleur, K
Leach, M
Jain, M
Rutkowski, A
Bonnemann, C
AF Dastgir, J.
Vuillerot, C.
Nguyen, D.
Yang, K.
Auh, S.
DonkerVoort, S.
Meilleur, K.
Leach, M.
Jain, M.
Rutkowski, A.
Boennemann, C.
TI Acoustic radiation force impulse imaging for the longitudinal assessment
of muscle tissue stiffness in collagen 6 myopathy and LAMA2 related
muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Dastgir, J.; Vuillerot, C.; Nguyen, D.; Yang, K.; Auh, S.; DonkerVoort, S.; Meilleur, K.; Leach, M.; Jain, M.; Boennemann, C.] NIH, Bethesda, MD 20892 USA.
[Rutkowski, A.] Cure Congenital Muscular Dystrophy, Olathe, KS USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA T.P.48
BP 908
EP 908
DI 10.1016/j.nmd.2014.06.379
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200376
ER
PT J
AU Yum, SW
Medne, L
Estilow, T
Glanzman, A
DiVito, D
Bonnemann, CG
AF Yum, S. W.
Medne, L.
Estilow, T.
Glanzman, A.
DiVito, D.
Boennemann, C. G.
TI Severe, early onset Charcot-Marie-Tooth disease with rare presentations
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Yum, S. W.; Medne, L.; Estilow, T.; Glanzman, A.; DiVito, D.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Yum, S. W.] Perelman Sch Med, Philadelphia, PA USA.
[Boennemann, C. G.] NINDS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.296
BP 910
EP 911
DI 10.1016/j.nmd.2014.06.386
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200383
ER
PT J
AU Peay, HL
Scharff, H
Biesecker, BB
Wilfond, BS
Johnson, J
Escolar, DM
Nagaraju, K
Piacentino, J
Bowie, J
Tibben, A
AF Peay, H. L.
Scharff, H.
Biesecker, B. B.
Wilfond, B. S.
Johnson, J.
Escolar, D. M.
Nagaraju, K.
Piacentino, J.
Bowie, J.
Tibben, A.
TI Influences on parental decision making about participation in Duchenne
and Becker muscular dystrophy clinical trials
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Peay, H. L.; Scharff, H.] Parent Project Muscular Dystrophy, Richmond, VA USA.
[Biesecker, B. B.] NHGRI, Bethesda, MD 20892 USA.
[Wilfond, B. S.] Seattle Childrens Res Inst, Seattle, WA USA.
[Escolar, D. M.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Nagaraju, K.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Bowie, J.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Tibben, A.] Leiden Univ, Med Ctr, Leiden, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.303
BP 912
EP 913
DI 10.1016/j.nmd.2014.06.393
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200390
ER
PT J
AU Peay, HL
Scharff, H
Biesecker, BB
Wilfond, BS
Johnson, J
Escolar, DM
Bowie, J
Nagaraju, K
Piacentino, J
Tibben, A
AF Peay, H. L.
Scharff, H.
Biesecker, B. B.
Wilfond, B. S.
Johnson, J.
Escolar, D. M.
Bowie, J.
Nagaraju, K.
Piacentino, J.
Tibben, A.
TI Perceived barriers and facilitators of participation in clinical trials
for Duchenne and Becker muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Peay, H. L.; Scharff, H.] Parent Project Muscular Dystrophy, Richmond, VA USA.
[Biesecker, B. B.] NHGRI, Bethesda, MD 20892 USA.
[Wilfond, B. S.] Seattle Childrens Res Inst, Seattle, WA USA.
[Escolar, D. M.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Bowie, J.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Nagaraju, K.] Childrens Natl Med Ctr, Washington, DC USA.
[Tibben, A.] Leiden Univ, Med Ctr, Leiden, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.302
BP 912
EP 912
DI 10.1016/j.nmd.2014.06.392
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200389
ER
PT J
AU Bharucha-Goebel, DX
Neil, E
Donkervoort, S
Moore, S
Winder, T
Dastgir, J
Iannaccone, S
Bonnemann, CG
AF Bharucha-Goebel, D. X.
Neil, E.
Donkervoort, S.
Moore, S.
Winder, T.
Dastgir, J.
Iannaccone, S.
Boennemann, C. G.
TI Intrafamilial variability in GMPPB associated alpha-dystroglycanopathy
and broadening of the clinical phenotype
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 19th International Congress of the World-Muscle-Society
CY OCT 07-11, 2014
CL Berlin, GERMANY
SP World Muscle Soc
C1 [Bharucha-Goebel, D. X.; Donkervoort, S.; Dastgir, J.; Boennemann, C. G.] NIH, Bethesda, MD 20892 USA.
[Bharucha-Goebel, D. X.] Childrens Natl Med Ctr, Bethesda, MD USA.
[Neil, E.; Iannaccone, S.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Moore, S.] Univ Iowa, Iowa City, IA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2014
VL 24
IS 9-10
MA G.P.312
BP 915
EP 915
DI 10.1016/j.nmd.2014.06.402
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ5SZ
UT WOS:000342870200399
ER
PT J
AU Weinrich, M
Stuart, M
Benvenuti, F
AF Weinrich, Michael
Stuart, Mary
Benvenuti, Francesco
TI Community-Based Exercise for Chronic Disease Management: An Italian
Design for the United States?
SO NEUROREHABILITATION AND NEURAL REPAIR
LA English
DT Article
DE stroke; exercise; chronic disease
ID ADAPTIVE PHYSICAL-ACTIVITY; OLDER-ADULTS; BACK-PAIN; PROGRAM;
INTERVENTIONS; FITNESS; DISABILITIES; STROKE; TRIAL
AB Although only a small proportion of older adults in the United States engage in recommended amounts of physical exercise, the health benefits of exercise for this population and the potential for lowering health care costs are substantial. However, access to regular exercise programs for the frail elderly and individuals with disabilities remains limited. In the context of health reform and emerging opportunities in developing integrated systems of care, the experience in Tuscany in implementing a community-based program of exercise for the elderly should be of interest.
C1 [Weinrich, Michael] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Rockville, MD 20852 USA.
[Stuart, Mary] Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA.
[Benvenuti, Francesco] Azienda Unita Sanit Locale 11, Empoli, Italy.
RP Weinrich, M (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, 31 Ctr Dr,Room 2A-25D, Rockville, MD 20852 USA.
EM weinricm@mail.nih.gov
NR 20
TC 2
Z9 2
U1 1
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1545-9683
EI 1552-6844
J9 NEUROREHAB NEURAL RE
JI Neurorehabil. Neural Repair
PD OCT
PY 2014
VL 28
IS 8
BP 729
EP 732
DI 10.1177/1545968314531073
PG 4
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA AQ5CK
UT WOS:000342820800002
PM 24743228
ER
PT J
AU Gobel, B
Sanghvi, A
Hall, KD
AF Goebel, Britta
Sanghvi, Arjun
Hall, Kevin D.
TI Quantifying Energy Intake Changes During Obesity Pharmacotherapy
SO OBESITY
LA English
DT Article
ID CONTROLLED-RELEASE PHENTERMINE/TOPIRAMATE; SUSTAINED WEIGHT-LOSS;
BODY-WEIGHT; CALORIE RESTRICTION; CONTROLLED-TRIAL; OVERWEIGHT; PLACEBO;
ADULTS; MULTICENTER; SIBUTRAMINE
AB ObjectiveDespite the fact that most obesity drugs primarily work by reducing metabolizable energy intake, elucidation of the time course of energy intake changes during long-term obesity pharmacotherapy has been prevented by the limitations of self-report methods of measuring energy intake.
MethodsA validated mathematical model of human metabolism was used to provide the first quantification of metabolizable energy intake changes during long-term obesity pharmacotherapy using body weight data from randomized, placebo-controlled trials that evaluated 14 different drugs or drug combinations.
ResultsChanges in metabolizable energy intake during obesity pharmacotherapy were reasonably well-described by an exponential pattern comprising three simple parameters, with early large changes in metabolizable energy intake followed by a slow transition to a smaller persistent drug effect.
ConclusionsRepeated body weight measurements along with a mathematical model of human metabolism can be used to quantify changes in metabolizable energy intake during obesity pharmacotherapy. The calculated metabolizable energy intake changes followed an exponential time course, and therefore different drugs can be evaluated and compared using a common mathematical framework.
C1 [Goebel, Britta] Sanofi Aventis Deutschland GmbH, Frankfurt, Germany.
[Sanghvi, Arjun; Hall, Kevin D.] NIDDK, Bethesda, MD 20892 USA.
RP Hall, KD (reprint author), NIDDK, Bethesda, MD 20892 USA.
EM kevinh@niddk.nih.gov
FU Intramural Research Program of the NIH, National Institute of Diabetes
and Digestive and Kidney Diseases; Sanofi
FX Funding agencies: This research was supported by the Intramural Research
Program of the NIH, National Institute of Diabetes and Digestive and
Kidney Diseases (AS, KDH). BG is supported by Sanofi.
NR 26
TC 4
Z9 4
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
EI 1930-739X
J9 OBESITY
JI Obesity
PD OCT
PY 2014
VL 22
IS 10
BP 2105
EP 2108
DI 10.1002/oby.20813
PG 4
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA AQ4ET
UT WOS:000342746800001
PM 24961931
ER
PT J
AU Reddy, U
Abuhamad, A
Levine, D
Saade, G
AF Reddy, Uma
Abuhamad, Alfred
Levine, Deborah
Saade, George
TI Fetal Imaging: Executive Summary of a Joint Eunice Kennedy Shriver
National Institute of Child Health and Human Development, Society for
Maternal-Fetal Medicine, American Institute of Ultrasound in Medicine,
American College of Obstetricians and Gynecologists, American College of
Radiology, Society for Pediatric Radiology, and Society of Radiologists
in Ultrasound Fetal Imaging Workshop Reply
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Letter
C1 [Reddy, Uma] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Abuhamad, Alfred] EVMS Med Grp, Norfolk, VA USA.
[Levine, Deborah] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Saade, George] Univ Texas Med Branch, Galveston, TX 77555 USA.
RP Reddy, U (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
EI 1873-233X
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD OCT
PY 2014
VL 124
IS 4
BP 836
EP 837
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AQ4GZ
UT WOS:000342753000027
PM 25244445
ER
PT J
AU Sturdevant, GL
Caldwell, HD
AF Sturdevant, Gail L.
Caldwell, Harlan D.
TI Innate immunity is sufficient for the clearance of Chlamydia trachomatis
from the female mouse genital tract
SO PATHOGENS AND DISEASE
LA English
DT Article
DE Chlamydiae; human and mouse strains; Rag; mice; female genital tract;
innate immunity; adaptive immunity
ID GAMMA-INTERFERON; IFN-GAMMA; KNOCKOUT MICE; INFECTION; SALPINGITIS;
REQUIRES; DISEASE; VACCINE; STRAIN; CELLS
AB Chlamydia muridarum and Chlamydia trachomatis, mouse and human strains, respectively, have been used to study immunity in a murine model of female genital tract infection. Despite evidence that unique genes of these otherwise genomically similar strains could play a role in innate immune evasion in their respective mouse and human hosts, there have been no animal model findings to directly support this conclusion. Here, we infected C57BL/6 and adaptive immune-deficient Rag1(-/-) female mice with these strains and evaluated their ability to spontaneously resolve genital infection. Predictably, C57BL/6 mice spontaneously cleared infection caused by both chlamydial strains. In contrast, Rag1(-/-) mice which lack mature T and B cell immunity but maintain functional innate immune effectors were incapable of resolving C.muridarum infection but spontaneously cleared C.trachomatis infection. This distinct dichotomy in adaptive and innate immune-mediated clearance between mouse and human strains has important cautionary implications for the study of natural immunity and vaccine development in the mouse model.
C1 [Sturdevant, Gail L.; Caldwell, Harlan D.] NIAID, Intracellular Parasites Lab, NIH, Hamilton, MT 59840 USA.
RP Caldwell, HD (reprint author), NIAID, NIH, Rocky Mt Labs, 903 S 4th St, Hamilton, MT 59840 USA.
EM hcaldwell@niaid.nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX We thank Kelly Matteson for editorial assistance and Dan Sturdevant for
performing statistical analyses. This work was supported by the
Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health.
NR 25
TC 10
Z9 10
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2049-632X
J9 PATHOG DIS
JI Pathog. Dis.
PD OCT
PY 2014
VL 72
IS 1
BP 70
EP 73
DI 10.1111/2049-632X.12164
PG 4
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA AQ4MC
UT WOS:000342770300012
PM 24585717
ER
PT J
AU Xie, B
Li, D
London, SJ
Palmer, PH
Johnshon, CA
Li, Y
Shih, J
Bergen, AW
Nishita, D
Swan, GE
Ahn, R
Conti, DV
AF Xie, B.
Li, D.
London, S. J.
Palmer, P. H.
Johnshon, C. A.
Li, Y.
Shih, J.
Bergen, A. W.
Nishita, D.
Swan, G. E.
Ahn, R.
Conti, D. V.
TI Gender difference in interactions between MAOA promoter uVNTR
polymorphism and negative familial stressors on body mass index among
Chinese adolescents
SO PEDIATRIC OBESITY
LA English
DT Article
DE BMI; familial stressors; gene-environment interaction; MAOA polymorphism
ID MONOAMINE-OXIDASE-A; MAJOR DEPRESSIVE DISORDER; GENE PROMOTER; LIFE
EVENTS; FUNCTIONAL POLYMORPHISM; EUROPEAN ADOLESCENTS; OBESITY;
ASSOCIATION; CHILDREN; SMOKING
AB What is already known about this subject Initial evidence from recent studies indicated a relationship between the high-activity MAOA uVNTR polymorphism and lower risk of obesity even though findings were varied across populations, and hence replication studies with population-based samples are clearly warranted.
What this study addsOur findings confirmed the genetic effects of MAOA uVNTR polymorphism on body mass index in a Chinese adolescent population. This study demonstrated a significant gene-environment interaction with negative familial stressors in girls only, which provides a new insight on the causes of obesity, and thus, potential avenues of prevention.
Summary Objectives Monoamine oxidase A (MAOA) modulates metabolism of serotonin and dopamine metabolism, neurotransmitters involved in regulation of appetite and food intake. The gene coding for MAOA contains a 30-bp tandem repeat (uVNTR) polymorphism in its promoter region that has been previously identified to be associated with obesity with mixed findings in the literature. Our goals were to replicate the population effects of this functional polymorphism on obesity risk, and to further explore gender differences and interaction effects with negative stressors.
Methods Analyses were conducted with data on genotypes, measured weight and height, and self-reported behavioural characteristics among 1101 Chinese adolescents 11-15 years old living in Wuhan, China.
Results Girls with the high-activity allele had significantly lower body mass index (BMI; =-0.250.98, P=0.011) compared to those with the low activity allele. Experience of negative familial stressors (e.g., death or illness of family members, hit or scolded by parents and increased quarrelling with parents, parents argued frequently) significantly weakened this protective genetic effect on BMI (P for interaction=0.043). Stratified analyses showed a significant protective genetic effect on BMI only within the stratum of low stress level (=-0.44 +/- 0.14, P=0.002). No similar effect was observed among boys.
Conclusions Our findings confirm the genetic effects of MAOA uVNTR polymorphism on BMI in a Chinese adolescent population and suggest potential genetic interactions with negative familial stressors.
C1 [Xie, B.; Palmer, P. H.; Johnshon, C. A.] Claremont Grad Univ, Sch Community & Global Hlth, Claremont, CA 91711 USA.
[Li, D.] Univ Calif Los Angeles, Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[London, S. J.] NIEHS, Div Intramural Res, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA.
[Li, Y.] Wuhan City Food & Drug Adm, Wuhan, Peoples R China.
[Shih, J.] Univ So Calif, Sch Pharm, Los Angeles, CA USA.
[Bergen, A. W.; Nishita, D.; Swan, G. E.] SRI Int, Ctr Hlth Sci, Menlo Pk, CA 94025 USA.
[Ahn, R.] Scripps Coll, Joint Sci Program, Claremont, CA 91711 USA.
[Conti, D. V.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
RP Xie, B (reprint author), Claremont Grad Univ, Sch Community & Global Hlth, 675 West Foothill BLVD,Suite 310, Claremont, CA 91711 USA.
EM bin.xie@cgu.edu
OI Bergen, Andrew/0000-0002-1237-7644; London,
Stephanie/0000-0003-4911-5290
FU National Institute of Diabetes and Digestive and Kidney Diseases
[R21DK088313]; Division of Intramural Research, National Institute of
Environmental Health Sciences, National Institutes of Health [ZO1
ES49019]; Claremont Graduate University/University of Southern
California Transdisciplinary Tobacco Use Research Center (TTURC) -
National Institutes of Health [2 P50 CA084735-06]
FX This research was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases (Grant # R21DK088313, PI of Xie) and was
also partially supported by the Division of Intramural Research,
National Institute of Environmental Health Sciences, National Institutes
of Health (ZO1 ES49019), and the Claremont Graduate
University/University of Southern California Transdisciplinary Tobacco
Use Research Center (TTURC) funded by the National Institutes of Health
(Grant # 2 P50 CA084735-06, PI of Johnson). The authors thank the
director and project staff at the Centers for Disease Control and
Prevention in Wuhan City, People's Republic of China, for assistance
with project coordination and data collection. We also thank the
principals, physicians and teachers in the participating schools for
their cooperation.
NR 60
TC 1
Z9 2
U1 2
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-6310
EI 2047-6302
J9 PEDIATR OBES
JI Pediatr. Obes.
PD OCT
PY 2014
VL 9
IS 5
BP E80
EP E90
DI 10.1111/j.2047-6310.2013.00181.x
PG 11
WC Pediatrics
SC Pediatrics
GA AQ7KA
UT WOS:000342991900003
PM 23761378
ER
PT J
AU Oni-Orisan, A
Theken, KN
Schuck, RN
Edin, ML
Hinderliter, AL
Stouffer, GA
Zeldin, DC
Lee, CR
AF Oni-Orisan, Akinyemi
Theken, Katherine N.
Schuck, Robert N.
Edin, Matthew L.
Hinderliter, Alan L.
Stouffer, George A.
Zeldin, Darryl C.
Lee, Craig R.
TI Initial characterization of cytochrome P450-derived eicosanoids as a
predictive biomarker in coronary artery disease.
SO PHARMACOTHERAPY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-College-of-Clinical-Pharmacy (ACCP)
CY OCT 12-15, 2014
CL Austin, TX
SP Amer Coll Clin Pharm
C1 [Oni-Orisan, Akinyemi; Theken, Katherine N.; Schuck, Robert N.; Lee, Craig R.] UNC Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC USA.
[Edin, Matthew L.; Zeldin, Darryl C.] NIEHS, Environm Cardiopulm Dis Grp, Res Triangle Pk, NC 27709 USA.
[Hinderliter, Alan L.; Stouffer, George A.] UNC Sch Med, Div Cardiol, Chapel Hill, NC 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 0277-0008
EI 1875-9114
J9 PHARMACOTHERAPY
JI Pharmacotherapy
PD OCT
PY 2014
VL 34
IS 10
MA 32
BP E187
EP E187
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AQ6JF
UT WOS:000342916800026
ER
PT J
AU Suzuki, K
Hori, A
Kawamoto, K
Thangudu, RR
Ishida, T
Igarashi, K
Samejima, M
Yamada, C
Arakawa, T
Wakagi, T
Koseki, T
Fushinobu, S
AF Suzuki, Kentaro
Hori, Akane
Kawamoto, Kazusa
Thangudu, Ratna Rajesh
Ishida, Takuya
Igarashi, Kiyohiko
Samejima, Masahiro
Yamada, Chihaya
Arakawa, Takatoshi
Wakagi, Takayoshi
Koseki, Takuya
Fushinobu, Shinya
TI Crystal structure of a feruloyl esterase belonging to the tannase
family: A disulfide bond near a catalytic triad
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE carboxylesterase; disulfide; enzyme structure; X-ray crystallography;
lipase; alpha/beta-hydrolase fold; catalytic triad; ESTHER database;
Aspergillus oryzae
ID ASPERGILLUS-ORYZAE; LACTOBACILLUS-PLANTARUM; TALAROMYCES-STIPITATUS;
LIPOLYTIC ENZYME; CLASSIFICATION; DIVERSITY; DATABASE; SERINE; NIGER;
REFINEMENT
AB Feruloyl esterase (FAE) catalyzes the hydrolysis of the ferulic and diferulic acids present in plant cell wall polysaccharides, and tannase catalyzes the hydrolysis of tannins to release gallic acid. The fungal tannase family in the ESTHER database contains various enzymes, including FAEs and tannases. Despite the importance of FAEs and tannases in bioindustrial applications, three-dimensional structures of the fungal tannase family members have been unknown. Here, we determined the crystal structure of FAE B from Aspergillus oryzae (AoFaeB), which belongs to the fungal tannase family, at 1.5 angstrom resolution. AoFaeB consists of a catalytic a/b-hydrolase fold domain and a large lid domain, and the latter has a novel fold. To estimate probable binding models of substrates in AoFaeB, an automated docking analysis was performed. In the active site pocket of AoFaeB, residues responsible for the substrate specificity of the FAE activity were identified. The catalytic triad of AoFaeB comprises Ser203, Asp417, and His457, and the serine and histidine residues are directly connected by a disulfide bond of the neighboring cysteine residues, Cys202 and Cys458. This structural feature, the "CS-D-HC motif," is unprecedented in serine hydrolases. A mutational analysis indicated that the novel structural motif plays essential roles in the function of the active site. (C) 2014 Wiley Periodicals, Inc.
C1 [Suzuki, Kentaro; Yamada, Chihaya; Arakawa, Takatoshi; Wakagi, Takayoshi; Fushinobu, Shinya] Univ Tokyo, Dept Biotechnol, Tokyo 1138657, Japan.
[Hori, Akane; Kawamoto, Kazusa; Koseki, Takuya] Yamagata Univ, Fac Agr, Tsuruoka, Yamagata, Japan.
[Thangudu, Ratna Rajesh] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Ishida, Takuya; Igarashi, Kiyohiko; Samejima, Masahiro] Univ Tokyo, Dept Biomat Sci, Tokyo 1138657, Japan.
RP Fushinobu, S (reprint author), Univ Tokyo, Dept Biotechnol, Bunkyo Ku, 1-1-1 Yayoi, Tokyo 1138657, Japan.
EM asfushi@mail.ecc.u-tokyo.ac.jp
RI Fushinobu, Shinya/E-4987-2011; Igarashi, Kiyohiko/E-6799-2016
OI Fushinobu, Shinya/0000-0003-1346-6435; Igarashi,
Kiyohiko/0000-0001-5152-7177
FU New Energy and Industrial Technology Development Organization (JSPS
KAKENHI) [24380053, 20580071]; Japanese Ministry of Education, Culture,
Sports, and Technology (MEXT) [24114008]
FX Grant sponsor: The New Energy and Industrial Technology Development
Organization (JSPS KAKENHI to S. F. and T. K.); Grant number(s):
24380053 and 20580071; Grant sponsor: Japanese Ministry of Education,
Culture, Sports, and Technology (MEXT; Grant-in-Aid for Innovative Areas
to K. I.); Grant number: 24114008.
NR 48
TC 8
Z9 9
U1 6
U2 42
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0887-3585
EI 1097-0134
J9 PROTEINS
JI Proteins
PD OCT
PY 2014
VL 82
IS 10
BP 2857
EP 2867
DI 10.1002/prot.24649
PG 11
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA AQ5LC
UT WOS:000342849400047
PM 25066066
ER
PT J
AU Gibbons, SW
Ross, A
Bevans, M
AF Gibbons, Susanne W.
Ross, Alyson
Bevans, Margaret
TI Liminality as a Conceptual Frame for Understanding the Family Caregiving
Rite of Passage: An Integrative Review
SO RESEARCH IN NURSING & HEALTH
LA English
DT Article
DE integrative review; family caregiving; chronic illness; liminality; rite
of passage; qualitative
ID QUALITATIVE-ANALYSIS; ALZHEIMERS-DISEASE; CARERS EXPERIENCE;
CANCER-PATIENTS; PARTNERS; LIFE; UNCERTAINTY; TRANSITION; PEOPLE; STROKE
AB Family caregiving is a significant rite of passage experienced by family caregivers of individuals with protracted illness or injury. In an integrative review of 26 studies, we characterized family caregiving from the sociocultural perspective of liminality and explored associated psychosocial implications. Analysis of published evidence on this dynamic and formative transition produced a range of themes. While role ambiguity resolved for most, for others, uncertainty and suffering continued. The process of becoming a caregiver was transformative and can be viewed as a rebirth that is largely socially and culturally driven. The transition to family caregiving model produced by this review provides a holistic perspective on this phenomenon and draws attention to aspects of the experience previously underappreciated. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Gibbons, Susanne W.] Uniformed Serv Univ Hlth Sci, Daniel K Inouye Grad Sch Nursing, Bethesda, MD 20814 USA.
[Ross, Alyson; Bevans, Margaret] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Bevans, M (reprint author), NIH, Ctr Clin, 10 Ctr Dr MSC 1151, Bethesda, MD 20892 USA.
EM mbevans@cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 65
TC 2
Z9 2
U1 3
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0160-6891
EI 1098-240X
J9 RES NURS HEALTH
JI Res. Nurs. Health
PD OCT
PY 2014
VL 37
IS 5
BP 423
EP 436
DI 10.1002/nur.21622
PG 14
WC Nursing
SC Nursing
GA AQ7FB
UT WOS:000342976900011
PM 25176315
ER
PT J
AU DiFonzo, N
Suls, J
Beckstead, JW
Bourgeois, MJ
Homan, CM
Brougher, S
Younge, AJ
Terpstra-Schwab, N
AF DiFonzo, Nicholas
Suls, Jerry
Beckstead, Jason W.
Bourgeois, Martin J.
Homan, Christopher M.
Brougher, Samuel
Younge, Andrew J.
Terpstra-Schwab, Nicholas
TI NETWORK STRUCTURE MODERATES INTERGROUP DIFFERENTIATION OF STEREOTYPED
RUMORS
SO SOCIAL COGNITION
LA English
DT Article
ID DYNAMIC SOCIAL IMPACT; GROUP POLARIZATION; MEDIATED COMMUNICATION;
SELF-ORGANIZATION; ELECTRONIC GROUPS; CONSISTENCY BIAS; DECISION-MAKING;
ATTITUDES; INFORMATION; PSYCHOLOGY
AB The role of network structure in intergroup differentiation-the bipolarization of stereotypes that are defensive (ingroup-positive/outgroup-negative) and non-defensive (outgroup-positive/ingroup-negative)-was investigated using a Dynamic Social Impact Theory (DSIT) framework. Three computermediated laboratory social network experiments were pooled to test the interaction of network clustering (cliquish structure) and segregation (personal network homogeneity) on intergroup differentiation. Democrats and Republicans during the five months preceding the 2008 U.S. Presidential election, deaf and hearing persons, and women and men participated. Twenty-six 16-person groups (e.g., 8 Democrats, 8 Republicans) serially discussed nine controversial stereotyped rumors in lattice (unclustered) or "family" (clustered) network structures. Support was found for an Ingroup Echo Chamber Effect: segregation led to intergroup differentiation (stronger defensive belief, weaker non-defensive belief) in clustered, but not unclustered, structures. At the individual level, network clustering amplified ingroup neighbor social influence, leading participants to think more positively of their ingroup and more negatively of their outgroup.
C1 [DiFonzo, Nicholas; Homan, Christopher M.; Brougher, Samuel; Younge, Andrew J.] Rochester Inst Technol, Rochester, NY 14623 USA.
[Suls, Jerry] NCI, Bethesda, MD 20892 USA.
[Beckstead, Jason W.] Univ S Florida, Tampa, FL 33620 USA.
[Bourgeois, Martin J.] Florida Gulf Coast Univ, Ft Myers, FL USA.
[Terpstra-Schwab, Nicholas] Univ Wyoming, Laramie, WY 82071 USA.
RP DiFonzo, N (reprint author), Rochester Inst Technol, Dept Psychol, 18 Lomb Mem Dr, Rochester, NY 14623 USA.
EM Nicholas.DiFonzo@rit.edu
NR 119
TC 1
Z9 1
U1 4
U2 22
PU GUILFORD PUBLICATIONS INC
PI NEW YORK
PA 72 SPRING STREET, NEW YORK, NY 10012 USA
SN 0278-016X
J9 SOC COGNITION
JI Soc. Cogn.
PD OCT
PY 2014
VL 32
IS 5
BP 409
EP 448
PG 40
WC Psychology, Social
SC Psychology
GA AQ5OR
UT WOS:000342859000001
ER
PT J
AU Wu, HT
Coble, V
Vasalatiy, O
Swenson, RE
Krishna, MC
Mitchell, JB
AF Wu, Haitao
Coble, Vincent
Vasalatiy, Olga
Swenson, Rolf E.
Krishna, Murali C.
Mitchell, James B.
TI An efficient synthesis of
3-(N-piperidinemethyl)-2,2,5,5-tetramethyl-1-oxy-3-pyrroline, a
promising radioprotector for cancer radiotherapy
SO TETRAHEDRON LETTERS
LA English
DT Article
DE Nitroxide; Redox; Radioprotector; MRI; EPRI
ID RADIATION; TEMPOL; NITROXIDE; DAMAGE; TUMOR; MODEL
AB Nitroxides can ameliorate the toxic effects of radiation during cancer therapy. Nitroxides are paramagnetic and can be used in magnetic resonance imaging (MRI) and electron paramagnetic resonance imaging (EPRI) to monitor in vivo oxidative stress status. Compound 5 (3-(N-piperidinemethyl)-2,2,5,5-tetramethyl-1-oxy-3-pyrroline) was found to be the most effective nitroxide radioprotector. An efficient synthesis for this promising radioprotector was developed. Published by Elsevier Ltd.
C1 [Wu, Haitao; Coble, Vincent; Vasalatiy, Olga; Swenson, Rolf E.] NHLBI, Imaging Probe Dev Ctr, NIH, Rockville, MD 20850 USA.
[Krishna, Murali C.; Mitchell, James B.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Wu, HT (reprint author), NHLBI, Imaging Probe Dev Ctr, NIH, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
EM wuh3@mail.nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX This work was supported [in part] by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research and
through intramural research funds for the Imaging Probe Development
Center as administered by the National Heart, Lung, and Blood Institute.
NR 13
TC 0
Z9 0
U1 1
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0040-4039
J9 TETRAHEDRON LETT
JI Tetrahedron Lett.
PD OCT 1
PY 2014
VL 55
IS 40
BP 5570
EP 5571
DI 10.1016/j.tetlet.2014.08.028
PG 2
WC Chemistry, Organic
SC Chemistry
GA AQ5TP
UT WOS:000342871800039
PM 25309004
ER
PT J
AU Beverly, BEJ
Lambright, CS
Furr, JR
Sampson, H
Wilson, VS
McIntyre, BS
Foster, PMD
Travlos, G
Gray, LE
AF Beverly, Brandiese E. J.
Lambright, Christy S.
Furr, Johnathan R.
Sampson, Hunter
Wilson, Vickie S.
McIntyre, Barry S.
Foster, Paul M. D.
Travlos, Gregory
Gray, L. Earl, Jr.
TI Simvastatin and Dipentyl Phthalate Lower Ex Vivo Testicular Testosterone
Production and Exhibit Additive Effects on Testicular Testosterone and
Gene Expression Via Distinct Mechanistic Pathways in the Fetal Rat
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE simvastatin; phthalates; steroidogenesis; cholesterol; sexual
differentiation
ID N-BUTYL PHTHALATE; COA REDUCTASE INHIBITOR; COENZYME-A REDUCTASE;
IN-UTERO EXPOSURE; SEXUAL-DIFFERENTIATION; REPRODUCTIVE DEVELOPMENT;
DI(N-BUTYL) PHTHALATE; LEYDIG-CELLS; DEVELOPMENTAL TOXICITY;
STEROIDOGENIC ENZYMES
AB Sex differentiation of the male reproductive tract in mammals is driven, in part, by fetal androgen production. In utero, some phthalate esters (PEs) alter fetal Leydig cell differentiation, reducing the expression of several genes associated with steroid synthesis/transport, and consequently, lowering fetal androgen and Insl3 hormone levels. Simvastatin (SMV) is a cholesterol-lowering drug that directly inhibits HMG-CoA reductase. SMV may also disrupt steroid biosynthesis, but through a different mode of action (MOA) than the PEs. As cholesterol is a precursor of steroid hormone biosynthesis, we hypothesized that in utero exposure to SMV during the critical period of sex differentiation would lower fetal testicular testosterone (T) production without affecting genes involved in cholesterol and androgen synthesis and transport. Secondly, we hypothesized that a mixture of SMV and a PE, which may have different MOAs, would reduce testosterone levels in an additive manner. Pregnant Sprague Dawley rats were dosed orally with SMV, dipentyl phthalate (DPeP), or SMV plus DPeP from gestational days 14-18, and fetuses were evaluated on GD18. On GD18, SMV lowered fetal T production and serum triglycerides, low density lipoprotein, high density lipoprotein, and total cholesterol levels, and downregulated two genes in the fetal testis that were different from those altered by PEs. When SMV and DPeP were administered as a mixture, fetal T production was significantly reduced in an additive manner, thus demonstrating that a mixture of chemicals can induce additive effects on fetal T production even though they display different MOAs.
C1 [Beverly, Brandiese E. J.; Lambright, Christy S.; Furr, Johnathan R.; Sampson, Hunter; Wilson, Vickie S.; Gray, L. Earl, Jr.] US EPA, Reprod Toxicol Branch, Toxic Assessment Div, Natl Hlth & Environm Effects Res Lab,Off Res & De, Res Triangle Pk, NC 27711 USA.
[Beverly, Brandiese E. J.] Oak Ridge Inst Sci & Educ, Oak Ridge, TN 37831 USA.
[McIntyre, Barry S.; Foster, Paul M. D.; Travlos, Gregory] NIEHS, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
RP Gray, LE (reprint author), MD 72,TW Alexander Dr, Res Triangle Pk, NC 27711 USA.
EM emgray@mindspring.com
OI Wilson, Vickie/0000-0003-1661-8481
FU US Environmental Protection Agency; National Institute of Environmental
Health Sciences at the National Institutes of Health [IA]
[RW-75-92285501]; Oak Ridge Institute for Science and Education
fellowship
FX This work was supported in part by an interagency agreement with the US
Environmental Protection Agency and the National Institute of
Environmental Health Sciences at the National Institutes of Health [IA
no. RW-75-92285501]. B.E.J.B. was funded through an Oak Ridge Institute
for Science and Education fellowship.
NR 44
TC 3
Z9 3
U1 3
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD OCT
PY 2014
VL 141
IS 2
BP 524
EP 537
DI 10.1093/toxsci/kfu149
PG 14
WC Toxicology
SC Toxicology
GA AQ8BD
UT WOS:000343045100022
PM 25055962
ER
PT J
AU Eldridge, S
Guo, L
Mussio, J
Furniss, M
Hamre, J
Davis, M
AF Eldridge, Sandy
Guo, Liang
Mussio, Jodie
Furniss, Mike
Hamre, John, III
Davis, Myrtle
TI Examining the Protective Role of ErbB2 Modulation in Human-Induced
Pluripotent Stem Cell-Derived Cardiomyocytes
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs);
protein expression; ErbB signaling; nanofluidic proteomic immunoassay
(NIA); real-time impedance-based cell assay (RTCA) cardio system
ID IN-VITRO; VENTRICULAR MYOCYTES; HEART-FAILURE; CARDIOTOXICITY;
DIFFERENTIATION; ACTIVATION; ENDOTHELIN; RECEPTORS; TOXICITY; THERAPY
AB Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are being used as an in vitro model system in cardiac biology and in drug discovery (e. g., cardiotoxicity testing). Qualification of these cells for use in mechanistic investigations will require detailed evaluations of cardiomyocyte signaling pathways and cellular responses. ErbB signaling and the ligand neuregulin play critical roles in survival and functional integrity of cardiac myocytes. As such, we sought to characterize the expression and activity of the ErbB family of receptors. Antibody microarray analysis performed on cell lysates derived from maturing hiPSC-CMs detected expression of similar to 570 signaling proteins. EGFR/ErbB1, HER2/ErbB2, and ErbB4, but not ErbB3 receptors, of the epidermal growth factor receptor family were confirmed by Western blot. Activation of ErbB signaling by neuregulin-1 beta (NRG, a natural ligand for ErbB4) and its modulation by trastuzumab (a monoclonal anti-ErbB2 antibody) and lapatinib (a small molecule ErbB2 tyrosine kinase inhibitor) were evaluated through assessing phosphorylation of AKT and Erk1/2, two major downstream kinases of ErbB signaling, using nanofluidic proteomic immunoassay. Downregulation of ErbB2 expression by siRNA silencing attenuated NRG-induced AKT and Erk1/2 phosphorylation. Activation of ErbB signaling with NRG, or inhibition with trastuzumab, alleviated or aggravated doxorubicin-induced cardiomyocyte damage, respectively, as assessed by a real-time cellular impedance analysis and ATP measurement. Collectively, these results support the expanded use of hiPSC-CMs to examine mechanisms of cardiotoxicity and support the value of using these cells in early assessments of cardiotoxicity or efficacy.
C1 [Eldridge, Sandy; Davis, Myrtle] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Guo, Liang; Mussio, Jodie; Furniss, Mike; Hamre, John, III] Leidos Biomed Res Inc, Lab Invest Toxicol, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
RP Eldridge, S (reprint author), NCI, Dev Therapeut Program, Div Canc Treatment & Diag, NIH, 9609 Med Ctr Dr,Room 4-W116,MSC 9734, Bethesda, MD 20892 USA.
EM sandy.eldridge@nih.gov
FU Developmental Therapeutics Program, Division of Cancer Treatment and
Diagnosis of the National Cancer Institute, National Cancer Institute,
National Institutes of Health [HHSN261200800001E]
FX Developmental Therapeutics Program, Division of Cancer Treatment and
Diagnosis of the National Cancer Institute, National Cancer Institute,
National Institutes of Health (HHSN261200800001E).
NR 41
TC 10
Z9 11
U1 2
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD OCT
PY 2014
VL 141
IS 2
BP 547
EP 559
DI 10.1093/toxsci/kfu150
PG 13
WC Toxicology
SC Toxicology
GA AQ8BD
UT WOS:000343045100024
PM 25055963
ER
PT J
AU Calkins, ME
Moore, TM
Merikangas, KR
Burstein, M
Satterthwaite, TD
Bilker, WB
Ruparel, K
Chiavacci, R
Wolf, DH
Mentch, F
Qiu, HJ
Connolly, JJ
Sleiman, PA
Hakonarson, H
Gur, RC
Gur, RE
AF Calkins, Monica E.
Moore, Tyler M.
Merikangas, Kathleen R.
Burstein, Marcy
Satterthwaite, Theodore D.
Bilker, Warren B.
Ruparel, Kosha
Chiavacci, Rosetta
Wolf, Daniel H.
Mentch, Frank
Qiu, Haijun
Connolly, John J.
Sleiman, Patrick A.
Hakonarson, Hakon
Gur, Ruben C.
Gur, Raquel E.
TI The psychosis spectrum in a young US community sample: findings from the
Philadelphia Neurodevelopmental Cohort
SO WORLD PSYCHIATRY
LA English
DT Article
DE Psychosis spectrum; US youths; sub-psychotic positive symptoms;
neurocognition; functional impairment
ID SUPPLEMENT NCS-A; HIGH-RISK STATE; ULTRA-HIGH RISK; GENERAL-POPULATION;
MENTAL-DISORDERS; SUBSTANCE USE; SYMPTOMS; EXPERIENCES; CHILDREN;
PSYCHOPATHOLOGY
AB Little is known about the occurrence and predictors of the psychosis spectrum in large non-clinical community samples of U. S. youths. We aimed to bridge this gap through assessment of psychosis spectrum symptoms in the Philadelphia Neurodevelopmental Cohort, a collaborative investigation of clinical and neurobehavioral phenotypes in a prospectively accrued cohort of youths, funded by the National Institute of Mental Health. Youths (age 11-21; N=7,054) and collateral informants (caregiver/legal guardian) were recruited through the Children's Hospital of Philadelphia and administered structured screens of psychosis spectrum symptoms, other major psychopathology domains, and substance use. Youths were also administered a computerized neurocognitive battery assessing five neurobehavioral domains. Predictors of psychosis spectrum status in physically healthy participants (N=4,848) were examined using logistic regression. Among medically healthy youths, 3.7% reported threshold psychotic symptoms (delusions and/or hallucinations). An additional 12.3% reported significant sub-psychotic positive symptoms, with odd/unusual thoughts and auditory perceptions, followed by reality confusion, being the most discriminating and widely endorsed attenuated symptoms. A minority of youths (2.3%) endorsed subclinical negative/disorganized symptoms in the absence of positive symptoms. Caregivers reported lower symptom levels than their children. Male gender, younger age, and non-European American ethnicity were significant predictors of spectrum status. Youths with spectrum symptoms had reduced accuracy across neurocognitive domains, reduced global functioning, and increased odds of depression, anxiety, behavioral disorders, substance use and suicidal ideation. These findings have public health relevance for prevention and early intervention.
C1 [Calkins, Monica E.; Moore, Tyler M.; Satterthwaite, Theodore D.; Bilker, Warren B.; Ruparel, Kosha; Wolf, Daniel H.; Gur, Ruben C.; Gur, Raquel E.] Univ Penn, Dept Psychiat, Neuropsychiat Sect, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Merikangas, Kathleen R.; Burstein, Marcy] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
[Chiavacci, Rosetta; Mentch, Frank; Qiu, Haijun; Connolly, John J.; Sleiman, Patrick A.; Hakonarson, Hakon] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
[Sleiman, Patrick A.; Hakonarson, Hakon] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Calkins, ME (reprint author), Univ Penn, Dept Psychiat, Neuropsychiat Sect, Perelman Sch Med, 9 Maloney,3600 Spruce St, Philadelphia, PA 19104 USA.
FU National Institute of Mental Health [MH089983, MH089924, K08MH079364]
FX The authors thank the participants of this study, and all the members of
the recruitment, assessment, and data teams whose individual
contributions collectively made this work possible. The study was
supported by RC2 grants from the National Institute of Mental Health:
MH089983 and MH089924 (Gur and Hakonarson) and K08MH079364 (Calkins).
NR 38
TC 27
Z9 27
U1 3
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1723-8617
EI 2051-5545
J9 WORLD PSYCHIATRY
JI World Psychiatry
PD OCT
PY 2014
VL 13
IS 3
BP 296
EP 305
DI 10.1002/wps.20152
PG 10
WC Psychiatry
SC Psychiatry
GA AQ5LR
UT WOS:000342851200020
PM 25273303
ER
PT J
AU Mercken, EM
Mitchell, SJ
Martin-Montalvo, A
Minor, RK
Almeida, M
Gomes, AP
Scheibye-Knudsen, M
Palacios, HH
Licata, JJ
Zhang, YQ
Becker, KG
Khraiwesh, H
Gonzalez-Reyes, JA
Villalba, JM
Baur, JA
Elliott, P
Westphal, C
Vlasuk, GP
Ellis, JL
Sinclair, DA
Bernier, M
de Cabo, R
AF Mercken, Evi M.
Mitchell, Sarah J.
Martin-Montalvo, Alejandro
Minor, Robin K.
Almeida, Maria
Gomes, Ana P.
Scheibye-Knudsen, Morten
Palacios, Hector H.
Licata, Jordan J.
Zhang, Yongqing
Becker, Kevin G.
Khraiwesh, Husam
Gonzalez-Reyes, Jose A.
Villalba, Jose M.
Baur, Joseph A.
Elliott, Peter
Westphal, Christoph
Vlasuk, George P.
Ellis, James L.
Sinclair, David A.
Bernier, Michel
de Cabo, Rafael
TI SRT2104 extends survival of male mice on a standard diet and preserves
bone and muscle mass
SO AGING CELL
LA English
DT Article
DE healthspan; inflammation; lifespan; muscle wasting; osteoporosis;
sirtuins
ID LIFE-SPAN; SKELETAL-MUSCLE; CALORIE RESTRICTION; OXIDATIVE STRESS;
UBIQUITIN LIGASE; STEM-CELLS; SIRT1; RESVERATROL; TRANSCRIPTION;
ACTIVATORS
AB Increased expression of SIRT1 extends the lifespan of lower organisms and delays the onset of age-related diseases in mammals. Here, we show that SRT2104, a synthetic small molecule activator of SIRT1, extends both mean and maximal lifespan of mice fed a standard diet. This is accompanied by improvements in health, including enhanced motor coordination, performance, bone mineral density, and insulin sensitivity associated with higher mitochondrial content and decreased inflammation. Short-term SRT2104 treatment preserves bone and muscle mass in an experimental model of atrophy. These results demonstrate it is possible to design a small molecule that can slow aging and delay multiple age-related diseases in mammals, supporting the therapeutic potential of SIRT1 activators in humans.
C1 [Mercken, Evi M.; Mitchell, Sarah J.; Martin-Montalvo, Alejandro; Minor, Robin K.; Palacios, Hector H.; Licata, Jordan J.; Bernier, Michel; de Cabo, Rafael] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Mitchell, Sarah J.] Royal N Shore Hosp, Kolling Inst Med Res, St Leonards, NSW 2065, Australia.
[Mitchell, Sarah J.] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia.
[Almeida, Maria] Univ Arkansas Med Sci, Div Endocrinol & Metab, Ctr Osteoporosis & Metab Bone Dis, Little Rock, AR 72205 USA.
[Almeida, Maria] Cent Arkansas Vet Hlth Care Syst, Little Rock, AR 72205 USA.
[Gomes, Ana P.; Sinclair, David A.] Harvard Univ, Sch Med, Glenn Labs Biol Mech Aging, Boston, MA 02115 USA.
[Scheibye-Knudsen, Morten] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Zhang, Yongqing; Becker, Kevin G.] NIA, Gene Express & Genom Unit, NIH, Baltimore, MD 21224 USA.
[Khraiwesh, Husam; Gonzalez-Reyes, Jose A.; Villalba, Jose M.] Univ Cordoba, Dept Biol Celular Fisiol & Inmunol, Cordoba 14014, Spain.
[Baur, Joseph A.] Univ Penn, Inst Diabet Obes & Metab, Dept Physiol, Philadelphia, PA 19104 USA.
[Baur, Joseph A.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Elliott, Peter; Westphal, Christoph; Vlasuk, George P.; Ellis, James L.] Sirtris, Cambridge, MA 02139 USA.
RP de Cabo, R (reprint author), NIA, Translat Gerontol Branch, NIH, Suite 100,Room 9C218,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM decabora@grc.nia.nih.gov
RI de Cabo, Rafael/J-5230-2016; Martin-Montalvo, Alejandro/C-2031-2017;
OI de Cabo, Rafael/0000-0002-3354-2442; Martin-Montalvo,
Alejandro/0000-0002-3886-5355; Sinclair, David/0000-0002-9936-436X;
Bernier, Michel/0000-0002-5948-368X; Scheibye-Knudsen,
Morten/0000-0002-6637-1280; Gonzalez-Reyes, Jose A./0000-0003-1918-5490;
, rafael/0000-0003-2830-5693
FU National Medical Health and Research Council of Australia [RGMS ID
2010-01671]; NIH [RO1 AR56679]; Intramural Research Program of the
NIA/NIH; Glenn Foundation for Medical Research; JDRF UMDF, R01
[AG028730]
FX SJM was supported by a National Medical Health and Research Council of
Australia CJ Martin Early Career Fellowship (RGMS ID 2010-01671). MS was
supported by a NIH grant (RO1 AR56679). Funding was provided by the
Intramural Research Program of the NIA/NIH and The Glenn Foundation for
Medical Research. DS was supported by the JDRF UMDF, R01 (AG028730) and
the Glenn Foundation for Medical Research.
NR 46
TC 40
Z9 40
U1 1
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD OCT
PY 2014
VL 13
IS 5
BP 787
EP 796
DI 10.1111/acel.12220
PG 10
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA AQ2PY
UT WOS:000342631100003
PM 24931715
ER
PT J
AU Farrar, JE
Quarello, P
Fisher, R
O'Brien, KA
Aspesi, A
Parrella, S
Henson, AL
Seidel, NE
Atsidaftos, E
Prakash, S
Bari, S
Garelli, E
Arceci, RJ
Dianzani, I
Ramenghi, U
Vlachos, A
Lipton, JM
Bodine, DM
Ellis, SR
AF Farrar, Jason E.
Quarello, Paola
Fisher, Ross
O'Brien, Kelly A.
Aspesi, Anna
Parrella, Sara
Henson, Adrianna L.
Seidel, Nancy E.
Atsidaftos, Eva
Prakash, Supraja
Bari, Shahla
Garelli, Emanuela
Arceci, Robert J.
Dianzani, Irma
Ramenghi, Ugo
Vlachos, Adrianna
Lipton, Jeffrey M.
Bodine, David M.
Ellis, Steven R.
TI Exploiting pre-rRNA processing in Diamond Blackfan anemia gene discovery
and diagnosis
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID PROTEIN; DELETIONS; MUTATION; ABNORMALITIES; TRANSLATION; MATURATION;
SUBUNITS; DATABASE; LIBRARY; UPDATE
AB Diamond Blackfan anemia (DBA), a syndrome primarily characterized by anemia and physical abnormalities, is one among a group of related inherited bone marrow failure syndromes (IBMFS) which share overlapping clinical features. Heterozygous mutations or single-copy deletions have been identified in 12 ribosomal protein genes in approximately 60% of DBA cases, with the genetic etiology unexplained in most remaining patients. Unlike many IBMFS, for which functional screening assays complement clinical and genetic findings, suspected DBA in the absence of typical alterations of the known genes must frequently be diagnosed after exclusion of other IBMFS. We report here a novel deletion in a child that presented such a diagnostic challenge and prompted development of a novel functional assay that can assist in the diagnosis of a significant fraction of patients with DBA. The ribosomal proteins affected in DBA are required for pre-rRNA processing, a process which can be interrogated to monitor steps in the maturation of 40S and 60S ribosomal subunits. In contrast to prior methods used to assess pre-rRNA processing, the assay reported here, based on capillary electrophoresis measurement of the maturation of rRNA in pre-60S ribosomal subunits, would be readily amenable to use in diagnostic laboratories. In addition to utility as a diagnostic tool, we applied this technique to gene discovery in DBA, resulting in the identification of RPL31 as a novel DBA gene. Am. J. Hematol. 89:985-991, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Farrar, Jason E.; Prakash, Supraja; Bari, Shahla] Univ Arkansas Med Sci, Pediat Hematol Oncol Sect, Dept Pediat, Little Rock, AR 72205 USA.
[Quarello, Paola] Regina Margherita Childrens Hosp, Oncohematol Ctr, Turin, Italy.
[Fisher, Ross] Loma Linda Univ, Dept Pediat, Med Ctr, San Bernardino, CA USA.
[O'Brien, Kelly A.; Seidel, Nancy E.; Bodine, David M.] NHGRI, Hematopoiesis Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Aspesi, Anna; Parrella, Sara; Dianzani, Irma] Univ Piemonte Orientale, Dept Hlth Sci, Novara, Italy.
[Henson, Adrianna L.; Ellis, Steven R.] Univ Louisville, Dept Biochem & Mol Biol, Louisville, KY 40292 USA.
[Atsidaftos, Eva; Vlachos, Adrianna; Lipton, Jeffrey M.] Hofstra North Shore LIJ Sch Med, Dept Pediat, Hempstead, NY USA.
[Atsidaftos, Eva; Vlachos, Adrianna; Lipton, Jeffrey M.] Hofstra North Shore LIJ Sch Med, Dept Mol Med, Hempstead, NY USA.
[Atsidaftos, Eva; Vlachos, Adrianna; Lipton, Jeffrey M.] Feinstein Inst Med Res, Manhasset, NY USA.
[Atsidaftos, Eva; Vlachos, Adrianna; Lipton, Jeffrey M.] Steven & Alexandra Cohen Childrens Med Ctr New Yo, Div Hematol Oncol, New Hyde Pk, NY USA.
[Garelli, Emanuela; Ramenghi, Ugo] Univ Turin, Dept Pediat & Publ Hlth, Turin, Italy.
[Arceci, Robert J.] Univ Arizona, Ronald A Matricaria Inst Mol Med, Phoenix Childrens Hosp, Dept Child Hlth,Coll Med, Phoenix, AZ USA.
RP Farrar, JE (reprint author), 1 Childrens Way,MS 512-10, Little Rock, AR 72202 USA.
EM jefarrar@uams.edu; srellis@louisville.edu
OI Farrar, Jason/0000-0003-2148-5839
FU Diamond Blackfan Anemia Foundation; Arkansas Biosciences Institute;
Cariplo [2011-0554]; Feinstein Institute for Medical Research General
Research Center [M01 RR018535]; Istituto Piemontese per la ricerca sulla
Anemia di Diamond-Blackfan; National Institutes of Health [K08 HL092224,
R109 MOHLKE, R01 HL07957]; National Human Genome Research Institute
Intramural Funds; Pediatric Cancer Foundation; PRIN; Telethon [GGP13177]
FX Contract grant sponsor: The Diamond Blackfan Anemia Foundation.;
Contract grant sponsor: The Arkansas Biosciences Institute.; Contract
grant sponsor: Cariplo; Contract grant number: grant 2011-0554.;
Contract grant sponsor: The Feinstein Institute for Medical Research
General Research Center; Contract grant number: grant M01 RR018535.;
Contract grant sponsor: Istituto Piemontese per la ricerca sulla Anemia
di Diamond-Blackfan.; Contract grant sponsor: The National Institutes of
Health; Contract grant number: grants K08 HL092224, R109 MOHLKE, R01
HL07957.; Contract grant sponsor: National Human Genome Research
Institute Intramural Funds.; Contract grant sponsor: The Pediatric
Cancer Foundation.; Contract grant sponsor: PRIN.; Contract grant
sponsor: Telethon; Contract grant number: grant number GGP13177.
NR 41
TC 8
Z9 9
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD OCT
PY 2014
VL 89
IS 10
BP 985
EP 991
DI 10.1002/ajh.23807
PG 7
WC Hematology
SC Hematology
GA AQ3JR
UT WOS:000342689200014
PM 25042156
ER
PT J
AU King, AA
Rodeghier, MJ
Panepinto, JA
Strouse, JJ
Casella, JF
Quinn, CT
Dowling, MM
Sarnaik, SA
Thompson, AA
Woods, GM
Minniti, CP
Redding-Lallinger, RC
Kirby-Allen, M
Kirkham, FJ
McKinstry, R
Noetzel, MJ
White, DA
Kwiatkowski, JK
Howard, TH
Kalinyak, KA
Inusa, B
Rhodes, MM
Heiny, ME
Fuh, B
Fixler, JM
Gordon, MO
DeBaun, MR
AF King, Allison A.
Rodeghier, Mark J.
Panepinto, Julie Ann
Strouse, John J.
Casella, James F.
Quinn, Charles T.
Dowling, Michael M.
Sarnaik, Sharada A.
Thompson, Alexis A.
Woods, Gerald M.
Minniti, Caterina P.
Redding-Lallinger, Rupa C.
Kirby-Allen, Melanie
Kirkham, Fenella J.
McKinstry, Robert
Noetzel, Michael J.
White, Desiree A.
Kwiatkowski, Janet K.
Howard, Thomas H.
Kalinyak, Karen A.
Inusa, Baba
Rhodes, Melissa M.
Heiny, Mark E.
Fuh, Ben
Fixler, Jason M.
Gordon, Mae O.
DeBaun, Michael R.
TI Silent cerebral infarction, income, and grade retention among students
with sickle cell anemia
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID EDUCATIONAL-ATTAINMENT; ACADEMIC-ACHIEVEMENT; CHILDHOOD-CANCER; IMAGING
FINDINGS; RISK-FACTORS; DISEASE; CHILDREN; HEALTH; SCHOOL; CARE
AB Children with sickle cell anemia have a higher-than-expected prevalence of poor educational attainment. We test two key hypotheses about educational attainment among students with sickle cell anemia, as measured by grade retention and use of special education services: (1) lower household per capita income is associated with lower educational attainment; (2) the presence of a silent cerebral infarct is associated with lower educational attainment. We conducted a multicenter, cross-sectional study of cases from 22 U.S. sites included in the Silent Infarct Transfusion Trial. During screening, parents completed a questionnaire that included sociodemographic information and details of their child's academic status. Of 835 students, 670 were evaluable; 536 had data on all covariates and were used for analysis. The students' mean age was 9.4 years (range: 5-15) with 52.2% male; 17.5% of students were retained one grade level and 18.3% received special education services. A multiple variable logistic regression model identified that lower household per capita income (odds ratio [OR] of quartile 1 = 6.36, OR of quartile 2 = 4.7, OR of quartile 3 = 3.87; P = 0.001 for linear trend), age (OR = 1.3; P < 0.001), and male gender (OR, 2.2; P = 0.001) were associated with grade retention; silent cerebral infarct (P = 0.31) and painful episodes (P = 0.60) were not. Among students with sickle cell anemia, household per capita income is associated with grade retention, whereas the presence of a silent cerebral infarct is not. Future educational interventions will need to address both the medical and socioeconomic issues that affect students with sickle cell anemia. Am. J. Hematol. 89:E188-E192, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [King, Allison A.] Washington Univ, Sch Med, Program Occupat Therapy, St Louis, MO 63110 USA.
[King, Allison A.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
[Rodeghier, Mark J.] Rodeghier Consultants, Chicago, IL USA.
[Panepinto, Julie Ann] Med Coll Wisconsin, Dept Pediat, Div Hematol Oncol, Milwaukee, WI 53226 USA.
[Strouse, John J.; Casella, James F.] Johns Hopkins Univ, Sch Med, Dept Pediat, Div Hematol Oncol, Baltimore, MD 21205 USA.
[Quinn, Charles T.; Kalinyak, Karen A.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat, Div Hematol Oncol, Cincinnati, OH 45229 USA.
[Quinn, Charles T.; Kalinyak, Karen A.] Univ Cincinnati, Cincinnati, OH USA.
[Dowling, Michael M.] Univ Texas Southwestern Med Sch, Dept Pediat, Dallas, TX USA.
[Dowling, Michael M.] Univ Texas Southwestern Med Sch, Dept Neurol, Dallas, TX USA.
[Dowling, Michael M.] Univ Texas Southwestern Med Sch, Dept Neurotherapeut, Dallas, TX USA.
[Sarnaik, Sharada A.] Wayne State Univ, Dept Pediat, Div Hematol Oncol, Detroit, MI 48202 USA.
[Thompson, Alexis A.] Northwestern Univ, Dept Pediat, Div Hematol Oncol, Chicago, IL 60611 USA.
[Woods, Gerald M.] Univ Missouri, Dept Pediat, Div Hematol Oncol, Kansas City, MO 64110 USA.
[Minniti, Caterina P.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Redding-Lallinger, Rupa C.] Univ N Carolina, Dept Pediat, Div Hematol Oncol, Chapel Hill, NC USA.
[Kirby-Allen, Melanie] Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Kirkham, Fenella J.] UCL, Inst Child Hlth, Neurosci Unit, London, England.
[McKinstry, Robert] Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA.
[Noetzel, Michael J.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Noetzel, Michael J.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
[White, Desiree A.] Washington Univ, Dept Psychol, St Louis, MO 63130 USA.
[Kwiatkowski, Janet K.] Univ Penn, Childrens Hosp Philadelphia, Dept Pediat, Div Hematol Oncol, Philadelphia, PA 19104 USA.
[Howard, Thomas H.] Univ Alabama Birmingham, Dept Pediat, Div Hematol Oncol, Birmingham, AL USA.
[Inusa, Baba] St Thomas Hosp Natl Hlth Serv Trust, Evelina Childrens Hosp, Dept Paediat, London, England.
[Rhodes, Melissa M.] Ohio State Univ, Dept Pediat, Div Hematol Oncol, Columbus, OH 43210 USA.
[Heiny, Mark E.] Indiana Univ Purdue Univ Indiana, Div Hematol Oncol, Dept Pediat, Indianapolis, IN USA.
[Fuh, Ben] Brody Sch Med, Dept Pediat, Div Hematol Oncol, Greenville, NC USA.
[Fixler, Jason M.] Sinai Hosp, Dept Pediat, Div Hematol Oncol, Baltimore, MD 21215 USA.
[Gordon, Mae O.] Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, St Louis, MO 63110 USA.
[DeBaun, Michael R.] Vanderbilt Univ, Dept Pediat, Vanderbilt Meharry Ctr Excellence Sickle Cell Dis, Div Hematol Oncol, Nashville, TN USA.
RP King, AA (reprint author), Washington Univ, Sch Med, 660 South Euclid,Box 8505, St Louis, MO 63110 USA.
EM king_a@wustl.edu
RI Quinn, Charles/J-6842-2012; Kirkham, Fenella/C-2442-2009;
OI Quinn, Charles/0000-0002-2372-2175; Kirkham,
Fenella/0000-0002-2443-7958; King, Allison/0000-0002-1951-6176
FU National Institute of Neurological Disorders and Stroke (NINDS)
[U01NS042804, K23HL079073, 1 UL1 TR000448]; National Heart, Lung and
Blood Institute (NHLBI); National Center for Advancing Translational
Sciences (NCATS) of the National Institutes of Health (NIH)
FX Contract grant sponsor: National Institute of Neurological Disorders and
Stroke (NINDS); Contract grant numbers: U01NS042804, K23HL079073, 1 UL1
TR000448.; Contract grant sponsors: the National Heart, Lung and Blood
Institute (NHLBI); and the National Center for Advancing Translational
Sciences (NCATS) of the National Institutes of Health (NIH).
NR 47
TC 10
Z9 10
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD OCT
PY 2014
VL 89
IS 10
BP E188
EP E192
DI 10.1002/ajh.23805
PG 5
WC Hematology
SC Hematology
GA AQ3JR
UT WOS:000342689200005
PM 25042018
ER
PT J
AU Schrager, MA
Schrack, JA
Simonsick, EM
Ferrucci, L
AF Schrager, Matthew A.
Schrack, Jennifer A.
Simonsick, Eleanor M.
Ferrucci, Luigi
TI Association Between Energy Availability and Physical Activity in Older
Adults
SO AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION
LA English
DT Article
DE Physical Activity; Energy; Aging; Aerobic Fitness
ID SKELETAL-MUSCLE MASS; VIGOROUS EXERCISE; HEART-DISEASE; GAIT SPEED;
WOMEN; PERFORMANCE; LIFE; AGE; INDEPENDENCE; FITNESS
AB Objective: Age-related declines in physical activity are commonly observed in human and animal populations, but their physiologic bases are not fully understood. The authors hypothesize that a lack of available energy contributes to low levels of activity in older persons.
Design: Cross-sectional analyses of relationships between physical activity level and energy availability were performed in 602 community-dwelling volunteers aged 45Y91 yrs from the Baltimore Longitudinal Study of Aging. Energy expenditure was measured at rest and during a maximal 400-m walk for calculation of "available energy." Overall and vigorous physical activity levels were assessed using standardized questionnaires. General linear regression models were used to assess the relationships between available energy and general and vigorous physical activity, and stratified analyses were used to analyze the possible differential association between available energy and physical activity across high and low (peak sustained walking oxygen consumption per unit time, <18.3 ml of oxygen per kilogram per minute) levels of aerobic fitness.
Results: Low available energy was associated with low levels of total physical activity (beta = 64.678, P = 0.015) and vigorous activity (beta = 9.123, P < 0.0001). The direct relationship between available energy and physical activity was particularly strong in persons categorized as having low aerobic fitness between available energy and physical activity with both total (beta = 119.783, P = 0.022) and vigorous activity (beta = 10.246, P = 0.015) and was independent of body composition and age.
Conclusions: The findings from this study support the hypothesis that available energy promotes the maintenance of physical activity in older persons. The findings also run counter to the perception that age-related declines in physical activity are primarily societally or behaviorally driven.
C1 [Schrager, Matthew A.] Stetson Univ, Dept Integrat Hlth Sci, Deland, FL 32723 USA.
[Schrack, Jennifer A.] Johns Hopkins Sch Med, Div Geriatr Med & Gerontol, Baltimore, MD USA.
[Simonsick, Eleanor M.; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
RP Schrager, MA (reprint author), Stetson Univ, Dept Integrat Hlth Sci, 421 N Woodland Blvd,Unit 8317, Deland, FL 32723 USA.
FU Intramural Research Program of the NIH, National Institute on Aging
FX Supported by the Intramural Research Program of the NIH, National
Institute on Aging. Data for these analyses were obtained from the
Baltimore Longitudinal Study of Aging, a study performed by the National
Institute on Aging. Financial disclosure statements have been obtained,
and no conflicts of interest have been reported by the authors or by any
individuals in control of the content of this article.
NR 40
TC 3
Z9 3
U1 3
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0894-9115
EI 1537-7385
J9 AM J PHYS MED REHAB
JI Am. J. Phys. Med. Rehabil.
PD OCT
PY 2014
VL 93
IS 10
BP 876
EP 883
DI 10.1097/PHM.0000000000000108
PG 8
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA AQ2LE
UT WOS:000342616800005
PM 24800719
ER
PT J
AU Judd, LL
Schettler, PJ
Brown, ES
Wolkowitz, OM
Sternberg, EM
Bender, BG
Bulloch, K
Cidlowski, JA
de Kloet, ER
Fardet, L
Joels, M
Leung, DYM
McEwen, BS
Roozendaal, B
Van Rossum, EFC
Ahn, J
Brown, DW
Plitt, A
Singh, G
AF Judd, Lewis L.
Schettler, Pamela J.
Brown, E. Sherwood
Wolkowitz, Owen M.
Sternberg, Esther M.
Bender, Bruce G.
Bulloch, Karen
Cidlowski, John A.
de Kloet, E. Ronald
Fardet, Laurence
Joels, Marian
Leung, Donald Y. M.
McEwen, Bruce S.
Roozendaal, Benno
Van Rossum, Elisabeth F. C.
Ahn, Junyoung
Brown, David W.
Plitt, Aaron
Singh, Gagandeep
TI Adverse Consequences of Glucocorticoid Medication: Psychological,
Cognitive, and Behavioral Effects
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID RECEIVING CORTICOSTEROID-THERAPY; BDNF MESSENGER-RNA; DECLARATIVE
MEMORY; PSYCHOSOCIAL STRESS; MULTIPLE-SCLEROSIS; INDUCED IMPAIRMENT;
STEROID DEMENTIA; CORTISOL-LEVELS; WORKING-MEMORY; BRAIN ACTIVITY
AB Glucocorticoids are the most commonly prescribed anti-inflammatory/immunosuppressant medications worldwide. This article highlights the risk of clinically significant and sometimes severe psychological, cognitive, and behavioral disturbances that may be associated with glucocorticoid use, as well as ways to prevent and treat these disturbances. An illustrative case vignette is presented describing a patient's experience of cycles of manic-like behavior and depression while on high-dosage prednisone, with long-term cognitive disorganization, vulnerability to stress, and personality changes. Severe neuropsychiatric consequences (including suicide, suicide attempt, psychosis, mania, depression, panic disorder, and delirium, confusion, or disorientation) have been reported to occur in 15.7 per 100 person-years at risk for all glucocorticoid courses, and 22.2 per 100 person-years at risk for first courses. The majority of patients experience less severe but distressing and possibly persistent changes in mood, cognition, memory, or behavior during glucocorticoid treatment or withdrawal. Although prediction of such effects is difficult, risks vary with age, gender, dosage, prior psychiatric history, and several biological markers. Key mechanisms thought to underlie these risk factors are briefly described. Recommendations are given for identifying individual risk factors and for monitoring and managing adverse neuropsychiatric effects of glucocorticoids.
C1 [Judd, Lewis L.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
Univ Arizona, Coll Med, Arizona Ctr Integrat Med, Tucson, AZ USA.
Natl Jewish Med & Res Ctr, Dept Pediat, Denver, CO USA.
Rockefeller Univ, Harold & Margaret Milliken Hatch Lab Neuroendocri, New York, NY 10021 USA.
Rockefeller Univ, Lab Cell Physiol & Immunol, New York, NY 10021 USA.
Natl Inst Environm Hlth Sci, Lab Signal Transduct, Res Triangle Pk, NC USA.
Leiden Univ, Leiden Amsterdam Ctr Drug Res, Leiden, Netherlands.
Univ Paris 06, Hop St Antoine, AP HP, Dept Internal Med, Paris, France.
Univ Med Ctr, Dept Neurosci & Pharmacol, Rudolf Magnus Inst Neurosci, Utrecht, Netherlands.
Natl Jewish Med & Res Ctr, Div Pediat Allergy & Immunol, Denver, CO USA.
Univ Groningen, Univ Med Ctr Groningen, Dept Neurosci, Anat Sect, Groningen, Netherlands.
Erasmus Univ, Med Ctr, Dept Internal Med, Rotterdam, Netherlands.
RP Judd, LL (reprint author), Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
EM ljudd@ucsd.edu
RI Roozendaal, Benno/B-8403-2013; de Kloet, Edo Ronald/H-3278-2011; Joels,
Marian/P-6415-2016
FU Diana Padelford Binkley Foundation; Sunovion; Forest; Corcept
Pharmaceuticals; Netherlands Organization for Scientific Research;
Netherlands Brain Foundation
FX All but the last four authors are members of the Workgroup on
Neuropsychiatric Sequelae of Glucocorticoid Treatment, which is funded
by the Diana Padelford Binkley Foundation. Dr. Schettler received
payment from the Diana Padelford Binkley Foundation for work related to
the Workgroup and to this study. Dr. Brown has received research grants
from Sunovion and Forest. Dr. de Kloet has served as a scientific
adviser for Corcept Therapeutics and DynaCorts Therapeutics and owns
stock in Corcept Therapeutics. Dr. Joels has received a research grant
from Corcept Pharmaceuticals and research support from the Netherlands
Organization for Scientific Research. Dr. van Rossum is supported by the
Netherlands Brain Foundation. The other authors report no financial
relationships with commercial interests.
NR 79
TC 26
Z9 26
U1 4
U2 26
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
EI 1535-7228
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2014
VL 171
IS 10
BP 1045
EP 1051
DI 10.1176/appi.ajp.2014.13091264
PG 7
WC Psychiatry
SC Psychiatry
GA AQ3SM
UT WOS:000342713800007
PM 25272344
ER
PT J
AU Ameri, P
Canepa, M
Fabbi, P
Leoncini, G
Milaneschi, Y
Mussap, M
AlGhatrif, M
Balbi, M
Viazzi, F
Murialdo, G
Pontremoli, R
Brunelli, C
Ferrucci, L
AF Ameri, Pietro
Canepa, Marco
Fabbi, Patrizia
Leoncini, Giovanna
Milaneschi, Yuri
Mussap, Michele
AlGhatrif, Majd
Balbi, Manrico
Viazzi, Francesca
Murialdo, Giovanni
Pontremoli, Roberto
Brunelli, Claudio
Ferrucci, Luigi
TI Vitamin D modulates the association of circulating insulin-like growth
factor-1 with carotid artery intima-media thickness
SO ATHEROSCLEROSIS
LA English
DT Article
DE IGF-1; Vitamin D; Intima-media thickness; Aging; Atherosclerosis;
Endothelial
ID 25-HYDROXYVITAMIN D CONCENTRATION; CARDIOVASCULAR RISK-FACTORS; FACTOR
BINDING PROTEIN-3; HUMAN ENDOTHELIAL-CELLS; VASCULAR SMOOTH-MUSCLE;
TUMOR-NECROSIS-FACTOR; APOE-DEFICIENT MICE; IGF-I; OXIDATIVE STRESS;
PARATHYROID-HORMONE
AB Objective: Experimental evidence indicates that circulating insulin-like growth factor-1 (IGF-1) counteracts vascular aging and atherosclerosis, for which increased carotid artery intima-media thickness (IMT) is a marker. Yet, IGF-1 concentrations have been inconsistently associated with carotid IMT in epidemiological studies. Since vitamin D is also implicated in vascular protection and affects IGF-1 biology, we hypothesized that it would influence the effect of IGF-1 on IMT.
Methods: The relationship between carotid IMT and fasting serum IGF-1 was examined across strata of 25-hydroxyvitamin D [25(OH)D] in 472 participants in the Baltimore Longitudinal Study of Aging (BLSA) with well-controlled blood pressure and in 165 treatment-naive patients with essential hypertension from the Microalbuminuria: A Genoa Investigation on Complications (MAGIC) study. Moreover, the interplay between vitamin D and IGF-1 was preliminarily explored in EA.hy926 endothelial cells.
Results: After adjusting for age, sex, BMI, renal function, smoking, systolic blood pressure, LDL-cholesterol, glycemia, antihypertensive or lipid-lowering therapy, season, parathyroid hormone, and vitamin D supplementation, IGF-1 was significantly and negatively associated with carotid IMT only within the lowest 25(OH)D quartile (range 6.8-26 ng/mL) of the BLSA (beta -0.095, p = 0.03). Similarly, a significant negative correlation between IGF-1 and carotid IMT was found after full adjustment only in MAGIC patients with 25(OH)D concentrations below either the deficiency cut-off of 20 ng/mL (beta -0.214, p = 0.02) or 26 ng/mL (beta -0.174, p = 0.03). Vitamin D dose-dependently decreased hydrogen peroxide-induced endothelial cell oxidative stress and apoptosis, which were further inhibited by IGF in the presence of low, but not high vitamin D concentration.
Conclusions: Circulating IGF-1 is vasoprotective primarily when vitamin D levels are low. Future studies should address the mechanisms of vitamin D/IGF-1 interaction. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Ameri, Pietro; Canepa, Marco; Fabbi, Patrizia; Leoncini, Giovanna; Balbi, Manrico; Viazzi, Francesca; Murialdo, Giovanni; Pontremoli, Roberto; Brunelli, Claudio] Univ Genoa, AOU IRCCS San Martino IST, Dept Internal Med, Genoa, Italy.
[Canepa, Marco; Milaneschi, Yuri; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Milaneschi, Yuri] Vrije Univ Amsterdam, Med Ctr GGZ inGeest, Dept Psychiat, Amsterdam, Netherlands.
[Milaneschi, Yuri] Vrije Univ Amsterdam, Med Ctr GGZ inGeest, EMGO Inst Hlth & Care Res, Amsterdam, Netherlands.
[Mussap, Michele] AOU IRCCS San Martino IST, Dept Lab Med, Genoa, Italy.
[AlGhatrif, Majd] Natl Inst Aging, Human Cardiovasc Studies Unit, Lab Cardiovasc Sci, NIH, Baltimore, MD USA.
RP Ameri, P (reprint author), Res Ctr Cardiovasc Biol, Dept Internal Med, Room 327 Viale Benedetto XV 6, I-16132 Genoa, Italy.
EM pietroameri@unige.it
FU National Institute on Aging (BLSA); Progetto di Ricerca d'Ateneo -
University of Genova, Italy (MAGIC)
FX This study was supported by the Intramural Research Program of the
National Institute on Aging (BLSA) and by the Progetto di Ricerca
d'Ateneo 2011 research grant funded by the University of Genova, Italy
(MAGIC).
NR 55
TC 3
Z9 3
U1 1
U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
EI 1879-1484
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD OCT
PY 2014
VL 236
IS 2
BP 418
EP 425
DI 10.1016/j.atherosclerosis.2014.08.022
PG 8
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9QP
UT WOS:000342414700048
PM 25150940
ER
PT J
AU Johnson, RA
Danis, M
Hafner-Eaton, C
AF Johnson, Rebecca A.
Danis, Marion
Hafner-Eaton, Chris
TI US state variation in autism insurance mandates: Balancing access and
fairness
SO AUTISM
LA English
DT Article
DE autism; distributive justice; ethics; health policy; private insurance
mandates
ID SPECTRUM DISORDER; PRIVATE INSURANCE; SERVICE USE; PREVALENCE; IMPACT;
IDENTIFICATION; EXPENDITURES; CHILDREN; TRENDS; COSTS
AB This article examines how nations split decision-making about health services between federal and sub-federal levels, creating variation between states or provinces. When is this variation ethically acceptable? We identify three sources of ethical acceptability-procedural fairness, value pluralism, and substantive fairness-and examine these sources with respect to a case study: the fact that only 30 out of 51 US states or territories passed mandates requiring private insurers to offer extensive coverage of autism behavioral therapies, creating variation for privately insured children living in different US states. Is this variation ethically acceptable? To address this question, we need to analyze whether mandates go to more or less needy states and whether the mandates reflect value pluralism between states regarding government's role in health care. Using time-series logistic regressions and data from National Survey of Children with Special Health Care Needs, Individual with Disabilities Education Act, legislature political composition, and American Board of Pediatrics workforce data, we find that the states in which mandates are passed are less needy than states in which mandates have not been passed, what we call a cumulative advantage outcome that increases between-state disparities rather than a compensatory outcome that decreases between-state disparities. Concluding, we discuss the implications of our analysis for broader discussions of variation in health services provision.
C1 [Johnson, Rebecca A.; Danis, Marion] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Hafner-Eaton, Chris] NIH, Div Sci Policy & Sci Liaison, Bethesda, MD 20892 USA.
RP Johnson, RA (reprint author), NIH, Dept Bioeth, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM BJohnson88@gmail.com
FU Intramural NIH HHS [Z99 CL999999]
NR 45
TC 2
Z9 2
U1 0
U2 9
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD OCT
PY 2014
VL 18
IS 7
SI SI
BP 803
EP 814
DI 10.1177/1362361314529191
PG 12
WC Psychology, Developmental
SC Psychology
GA AQ2SH
UT WOS:000342638200006
PM 24789870
ER
PT J
AU Costa, VD
Tran, VL
Turchi, J
Averbeck, BB
AF Costa, Vincent D.
Tran, Valery L.
Turchi, Janita
Averbeck, Bruno B.
TI Dopamine Modulates Novelty Seeking Behavior During Decision Making
SO BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE curiosity; dopamine; exploitation; exploration; foraging; impulsivity;
novelty seeking; reinforcement learning; reuptake; uncertainty
ID PARKINSONS-DISEASE; VENTRAL STRIATUM; TRANSPORTER; COCAINE; REWARD;
CORTEX; IMPULSIVITY; ADDICTION; MONKEYS; BRAIN
AB Novelty seeking refers to the tendency of humans and animals to explore novel and unfamiliar stimuli and environments. The idea that dopamine modulates novelty seeking is supported by evidence that novel stimuli excite dopamine neurons and activate brain regions receiving dopaminergic input. In addition, dopamine is shown to drive exploratory behavior in novel environments. It is not clear whether dopamine promotes novelty seeking when it is framed as the decision to explore novel options versus the exploitation of familiar options. To test this hypothesis, we administered systemic injections of saline or GBR-12909, a selective dopamine transporter (DAT) inhibitor, to monkeys and assessed their novelty seeking behavior during a probabilistic decision making task. The task involved pseudorandom introductions of novel choice options. This allowed monkeys the opportunity to explore novel options or to exploit familiar options that they had already sampled. We found that DAT blockade increased the monkeys' preference for novel options. A reinforcement learning (RL) model fit to the monkeys' choice data showed that increased novelty seeking after DAT blockade was driven by an increase in the initial value the monkeys assigned to novel options. However, blocking DAT did not modulate the rate at which the monkeys learned which cues were most predictive of reward or their tendency to exploit that knowledge. These data demonstrate that dopamine enhances novelty-driven value and imply that excessive novelty seeking-characteristic of impulsivity and behavioral addictions-might be caused by increases in dopamine, stemming from less reuptake.
C1 [Costa, Vincent D.; Tran, Valery L.; Turchi, Janita; Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
RP Costa, VD (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49 Room 1B80,49 Convent Dr MSC 4415, Bethesda, MD 20892 USA.
EM vincent.costa@nih.gov; bruno.averbeck@nih.gov
RI Costa, Vincent/A-2086-2015
OI Costa, Vincent/0000-0002-5412-8945
FU Intramural Research Program of the National Institutes of Health,
National Institute of Mental Health (NIMH)
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Mental Health
(NIMH). We thank O. Dal Monte, A. Mitz, and S. Gallagher for technical
assistance.
NR 53
TC 19
Z9 19
U1 11
U2 46
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0735-7044
EI 1939-0084
J9 BEHAV NEUROSCI
JI Behav. Neurosci.
PD OCT
PY 2014
VL 128
IS 5
BP 556
EP 566
DI 10.1037/a0037128
PG 11
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA AQ0UV
UT WOS:000342499100003
PM 24911320
ER
PT J
AU Blough, BE
Landavazo, A
Partilla, JS
Decker, AM
Page, KM
Baumann, MH
Rothman, RB
AF Blough, Bruce E.
Landavazo, Antonio
Partilla, John S.
Decker, Ann M.
Page, Kevin M.
Baumann, Michael H.
Rothman, Richard B.
TI Alpha-ethyltryptamines as dual dopamine-serotonin releasers
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Tryptamines; DA releasers; 5-HT releasers; 5-HT 2A receptor
ID BIOGENIC-AMINE TRANSPORTERS; DISCRIMINATIVE STIMULUS; MEDICATION
DEVELOPMENT; MONOAMINE RELEASERS; COCAINE ADDICTION; RHESUS-MONKEYS;
FOOD; PHENTERMINE; TRYPTAMINES; DEPENDENCE
AB The dopamine (DA), serotonin (5-HT), and norepinephrine (NE) transporter releasing activity and serotonin-2A (5-HT2A) receptor agonist activity of a series of substituted tryptamines are reported. Three compounds, 7b, (+)-7d and 7f, were found to be potent dual DA/5-HT releasers and were > 10-fold less potent as NE releasers. Additionally, these compounds had different activity profiles at the 5-HT2A receptor. The unique combination of dual DA/5-HT releasing activity and 5-HT2A receptor activity suggests that these compounds could represent a new class of neurotransmitter releasers with therapeutic potential. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Blough, Bruce E.; Landavazo, Antonio; Decker, Ann M.; Page, Kevin M.] Res Triangle Inst, Ctr Drug Discovery, Res Triangle Pk, NC 27709 USA.
[Partilla, John S.; Baumann, Michael H.; Rothman, Richard B.] NIDA, Med Chem Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Blough, BE (reprint author), Res Triangle Inst, Ctr Drug Discovery, 3040 Cornwallis Rd, Res Triangle Pk, NC 27709 USA.
EM beb@rti.org
OI Landavazo, Antonio/0000-0003-2946-1057
FU National Institute on Drug Abuse [DA12970]; National Institute on Drug
Abuse, NIH
FX This research was supported by the National Institute on Drug Abuse
Project DA12970 and the Intramural Research Program, National Institute
on Drug Abuse, NIH.
NR 39
TC 6
Z9 7
U1 1
U2 13
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
EI 1464-3405
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD OCT 1
PY 2014
VL 24
IS 19
BP 4754
EP 4758
DI 10.1016/j.bmcl.2014.07.062
PG 5
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA AQ1WL
UT WOS:000342574600026
PM 25193229
ER
PT J
AU Enewold, LR
McGlynn, KA
Zahm, SH
Poudrier, J
Anderson, WF
Shriver, CD
Zhu, KM
AF Enewold, Lindsey R.
McGlynn, Katherine A.
Zahm, Shelia H.
Poudrier, Jill
Anderson, William F.
Shriver, Craig D.
Zhu, Kangmin
TI Breast Reconstruction After Mastectomy Among Department of Defense
Beneficiaries by Race
SO CANCER
LA English
DT Article
DE breast cancer; mastectomy; reconstruction; racial disparities;
epidemiology; health care access
ID HEALTH-INSURANCE; CANCER; IMMEDIATE; IMPACT
AB BACKGROUND: Postmastectomy breast reconstruction increased approximately 20% between 1998 and 2008 in the United States and has been found to improve body image, self-esteem, and quality of life. These procedures, however, tend to be less common among minority women, which may be due to variations in health care access. The Department of Defense provides equal health care access, thereby affording an exceptional environment in which to assess whether racial variations persist when access to care is equal. METHODS: Linked Department of Defense cancer registry and medical claims data were used. The receipt of reconstruction was compared between white women (n=2974) and black women (n=708) who underwent mastectomies to treat incident histologically confirmed breast cancer diagnosed from 1998 through 2007. RESULTS: During the study period, postmastectomy reconstruction increased among both black (27.3% to 40.0%) and white (21.8% to 40.6%) female patients with breast cancer. Receipt of reconstruction did not vary significantly by race (odds ratio, 0.93; 95% confidence interval, 0.76-1.15). Reconstruction decreased significantly with increasing age, tumor stage, and receipt of radiotherapy and was significantly more common in more recent years and among active service-women, TRICARE Prime (health maintenance organization) beneficiaries, and women whose sponsor was an officer. CONCLUSIONS: The receipt of breast reconstruction did not vary by race within this equal-access health system, indicating that the racial disparities reported in previous studies may have been due in part to variations in access to health care. Additional research to determine why a large percentage of patients with breast cancer do not undergo reconstruction might be beneficial, particularly because these procedures have been associated with noncosmetic benefits. Published 2014. This article is a U. S. Government work and is in the public domain in the USA.
C1 [Enewold, Lindsey R.] NCI, Hlth Serv Branch, Appl Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
[McGlynn, Katherine A.; Zahm, Shelia H.; Anderson, William F.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Poudrier, Jill; Shriver, Craig D.; Zhu, Kangmin] Walter Reed Natl Mil Med Ctr, John P Murtha Canc Ctr, Program Epidemiol, Rockville, MD USA.
[Shriver, Craig D.; Zhu, Kangmin] Uniformed Serv Univ Hlth Sci, Dept Preventat Med & Biometr, Bethesda, MD 20814 USA.
RP Enewold, LR (reprint author), NCI, NIH, 9609 Med Ctr Dr,Room 3E506, Bethesda, MD 20892 USA.
EM enewoldlr@mail.nih.gov
RI Zahm, Shelia/B-5025-2015
FU John P. Murtha Cancer Center of Walter Reed National Military Cancer
Center via the Uniformed Services University of the Health Sciences
under Henry M. Jackson Foundation for the Advancement of Military
Medicine
FX Supported by the John P. Murtha Cancer Center of Walter Reed National
Military Cancer Center via the Uniformed Services University of the
Health Sciences under the auspices of the Henry M. Jackson Foundation
for the Advancement of Military Medicine.
NR 20
TC 5
Z9 5
U1 2
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD OCT 1
PY 2014
VL 120
IS 19
BP 3033
EP 3039
DI 10.1002/cncr.28806
PG 7
WC Oncology
SC Oncology
GA AQ2PP
UT WOS:000342630000016
PM 24965236
ER
PT J
AU Cross, AJ
Moore, SC
Boca, S
Huang, WY
Xiong, XQ
Stolzenberg-Solomon, R
Sinha, R
Sampson, JN
AF Cross, Amanda J.
Moore, Steven C.
Boca, Simina
Huang, Wen-Yi
Xiong, Xiaoqin
Stolzenberg-Solomon, Rachael
Sinha, Rashmi
Sampson, Joshua N.
TI A Prospective Study of Serum Metabolites and Colorectal Cancer Risk
SO CANCER
LA English
DT Article
DE colorectal cancer; metabolites; biomarkers; metabolomics; mass
spectrometry; epidemiology
ID COLON-CANCER; SCREENING TRIAL; BILE-ACIDS; EPIDEMIOLOGY; PROFILES;
PROSTATE; PREDICT; LUNG
AB BACKGROUND: Colorectal cancer is highly prevalent, and the vast majority of cases are thought to be sporadic, although few risk factors have been identified. Using metabolomics technology, our aim was to identify biomarkers prospectively associated with colorectal cancer. METHODS: This study included 254 incident colorectal cancers and 254 matched controls nested in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Serum samples were collected at baseline, and the mean length of follow-up was 8 years. Serum metabolites were analyzed by ultra-high performance liquid-phase chromatography with tandem mass spectrometry, and gas chromatography coupled with mass spectrometry. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) for metabolites above the limit of detection and present in at least 80% of participants. RESULTS: A total of 676 serum metabolites were measured; of these, 447 were of known identity and 278 of these were present in >80% of individuals. Overall, there was no association between serum metabolites and colorectal cancer; however, some suggestive associations were observed between individual metabolites and colorectal cancer but none reached statistical significance after Bonferroni correction for multiple comparisons. For example, leucyl-leucine was inversely associated (OR comparing the 90th to the 10th percentile = 0.50; 95% CI50.32-0.80; P = .003). In sex-stratified analyses, serum glycochenodeoxycholate was positively associated with colorectal cancer among women (OR90th (vs. 10th percentile) = 5.34; 95% CI52.09-13.68; P = .0001). CONCLUSIONS: No overall associations were observed between serum metabolites and colorectal cancer, but serum glycochenodeoxycholate, a bile acid metabolite, was positively associated with colorectal cancer among women. (C)2014 American Cancer Society.
C1 [Cross, Amanda J.] Univ London Imperial Coll Sci Technol & Med, Fac Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London W2 1PG, England.
[Moore, Steven C.; Boca, Simina; Huang, Wen-Yi; Stolzenberg-Solomon, Rachael; Sinha, Rashmi; Sampson, Joshua N.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
[Xiong, Xiaoqin] Informat Management Serv Inc, Calverton, MD USA.
RP Cross, AJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Fac Med, Sch Publ Hlth, Dept Epidemiol & Biostat, St Marys Campus,Norfolk Pl, London W2 1PG, England.
EM amanda.cross1@imperial.ac.uk
RI Moore, Steven/D-8760-2016
OI Moore, Steven/0000-0002-8169-1661
FU National Cancer Institute, National Institutes of Health, Department of
Health and Human Services
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health, Department of
Health and Human Services.
NR 38
TC 22
Z9 22
U1 7
U2 29
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD OCT 1
PY 2014
VL 120
IS 19
BP 3049
EP 3057
DI 10.1002/cncr.28799
PG 9
WC Oncology
SC Oncology
GA AQ2PP
UT WOS:000342630000018
PM 24894841
ER
PT J
AU Nagasawa, S
Ogura, K
Tsutsuki, H
Saitoh, H
Moss, J
Iwase, H
Noda, M
Yahiro, K
AF Nagasawa, Sayaka
Ogura, Kohei
Tsutsuki, Hiroyasu
Saitoh, Hisako
Moss, Joel
Iwase, Hirotaro
Noda, Masatoshi
Yahiro, Kinnosuke
TI Uptake of Shiga-toxigenic Escherichia coli SubAB by HeLa cells requires
an actin-and lipid raft-dependent pathway
SO CELLULAR MICROBIOLOGY
LA English
DT Article
ID INTESTINAL EPITHELIAL-CELLS; RETICULUM CHAPERONE BIP; SUBTILASE
CYTOTOXIN; ENDOPLASMIC-RETICULUM; INDEPENDENT ENDOCYTOSIS; MEDIATED
ENDOCYTOSIS; DYNAMIN INHIBITORS; CHOLERA-TOXIN; PRION PROTEIN; AB(5)
TOXIN
AB The novel cytotoxic factor subtilase cytotoxin (SubAB) is produced mainly by non-O157 Shiga-toxigenic Escherichia coli (STEC). SubAB cleaves the molecular chaperone BiP/GRP78 in the endoplasmic reticulum (ER), leading to activation of RNA-dependent protein kinase (PKR)-like ER kinase (PERK), followed by caspase-dependent cell death. However, the SubAB uptake mechanism in HeLa cells is unknown. In this study, a variety of inhibitors and siRNAs were employed to characterize the SubAB uptake process. SubAB-induced BiP cleavage was inhibited by high concentrations of Dynasore, and methyl--cyclodextrin (mCD) and Filipin III, but not suppressed in clathrin-, dynamin I/II-, caveolin1- and caveolin2-knockdown cells. We observed that SubAB treatment led to dramatic actin rearrangements, e.g. formation of plasma membrane blebs, with a significant increase in fluid uptake. Confocal microscopy analysis showed that SubAB uptake required actin cytoskeleton remodelling and lipid raft cholesterol. Furthermore, internalized SubAB in cells was found in the detergent-resistant domain (DRM) structure. Interestingly, IPA-3, an inhibitor of serine/threonine kinase p21-activated kinase (PAK1), an important protein of macropinocytosis, directly inhibited SubAB-mediated BiP cleavage and SubAB internalization. Thus, our findings suggest that SubAB uses lipid raft- and actin-dependent, but not clathrin-, caveolin- and dynamin-dependent pathways as its major endocytic translocation route.
C1 [Nagasawa, Sayaka; Saitoh, Hisako; Iwase, Hirotaro] Chiba Univ, Grad Sch Med, Dept Legal Med, Chiba 2608670, Japan.
[Ogura, Kohei; Tsutsuki, Hiroyasu; Noda, Masatoshi; Yahiro, Kinnosuke] Chiba Univ, Grad Sch Med, Dept Mol Infectiol, Chiba 2608670, Japan.
[Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Yahiro, K (reprint author), Chiba Univ, Grad Sch Med, Dept Mol Infectiol, Chiba 2608670, Japan.
EM yahirok@faculty.chiba-u.jp
FU Ministry of Education, Science and Culture of Japan [B-24390104];
Improvement of Research Environment for Young Researchers from Japan
Science and Technology Agency; Ministry of Health, Labour and Welfare of
Japan [H24-Shinkou-Ippan-012]; Intramural Research Program, National
Institutes of Health and National Heart, Lung, and Blood Institute
FX This work was supported by grants-in-aid for Scientific Research from
the Ministry of Education, Science and Culture of Japan (B-24390104),
Improvement of Research Environment for Young Researchers from Japan
Science and Technology Agency and grant-in-aids from the Ministry of
Health, Labour and Welfare of Japan (H24-Shinkou-Ippan-012). Joel Moss
was supported by the Intramural Research Program, National Institutes of
Health and National Heart, Lung, and Blood Institute. We acknowledge the
expert technical assistance of K. Hirano and A. Kiuchi.
NR 61
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Z9 4
U1 2
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-5814
EI 1462-5822
J9 CELL MICROBIOL
JI Cell Microbiol.
PD OCT
PY 2014
VL 16
IS 10
BP 1582
EP 1601
DI 10.1111/cmi.12315
PG 20
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA AQ3VB
UT WOS:000342720500010
PM 24844382
ER
PT J
AU Ponti, A
Lynge, E
James, T
Majek, O
von Euler-Chelpin, M
Anttila, A
Fitzpatrick, P
Mano, MP
Kawai, M
Scharpantgen, A
Fracheboud, J
Hofvind, S
Vidal, C
Ascunce, N
Salas, D
Bulliard, JL
Segnan, N
Kerlikowske, K
Taplin, S
AF Ponti, Antonio
Lynge, Elsebeth
James, Ted
Majek, Ondrej
von Euler-Chelpin, My
Anttila, Ahti
Fitzpatrick, Patricia
Mano, Maria Piera
Kawai, Masaaki
Scharpantgen, Astrid
Fracheboud, Jacques
Hofvind, Solveig
Vidal, Carmen
Ascunce, Nieves
Salas, Dolores
Bulliard, Jean-Luc
Segnan, Nereo
Kerlikowske, Karla
Taplin, Stephen
CA ICSN DCIS Working Grp
TI International variation in management of screen-detected ductal
carcinoma in situ of the breast
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Breast cancer; Ductal carcinoma in situ (DCIS); Screening mammography;
Overtreatment; Axillary staging; Cancer registration
ID SENTINEL NODE BIOPSY; CONSERVING SURGERY; CANCER; WOMEN; RADIOTHERAPY;
NETHERLANDS; MAMMOGRAPHY; MASTECTOMY; INDICATORS; DIAGNOSIS
AB Background: Ductal carcinoma in situ (DCIS) incidence has grown with the implementation of screening and its detection varies across International Cancer Screening Network (ICSN) countries. The aim of this survey is to describe the management of screen-detected DCIS in ICSN countries and to evaluate the potential for treatment related morbidity.
Methods: We sought screen-detected DCIS data from the ICSN countries identified during 2004-2008. We adopted standardised data collection forms and analysis and explored DCIS diagnosis and treatment processes ranging from pre-operative diagnosis to type of surgery and radiotherapy.
Results: Twelve countries contributed data from a total of 15 screening programmes, all from Europe except the United States of America and Japan. Among women aged 50-69 years, 7,176,050 screening tests and 5324 screen-detected DCIS were reported. From 21% to 93% of DCIS had a pre-operative diagnosis (PO); 67-90% of DCIS received breast conservation surgery (BCS), and in 41-100% of the cases this was followed by radiotherapy; 6.4-59% received sentinel lymph node biopsy (SLNB) only and 0.8-49% axillary dissection (ALND) with 0.6% (range by programmes 0-8.1%) being node positive. Among BCS patients 35% received SLNB only and 4.8% received ALND. Starting in 2006, PO and SLNB use increased while ALND remained stable. SLNB and ALND were associated with larger size and higher grade DCIS lesions.
Conclusions: Variation in DCIS management among screened women is wide and includes lymph node surgery beyond what is currently recommended. This indicates the presence of varying levels of overtreatment and the potential for its reduction. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Ponti, Antonio; Mano, Maria Piera; Segnan, Nereo] AOU Citta Salute & Sci, CPO Piemonte, I-10123 Turin, Italy.
[Lynge, Elsebeth; von Euler-Chelpin, My] Univ Copenhagen, Dept Publ Hlth, Copenhagen, Denmark.
[James, Ted] Univ Vermont, Dept Surg, Burlington, VT 05405 USA.
[Majek, Ondrej] Masaryk Univ, Inst Biostat & Anal, Brno, Czech Republic.
[Anttila, Ahti] Finnish Canc Registry, Mass Screening Registry, FIN-00170 Helsinki, Finland.
[Fitzpatrick, Patricia] Natl Canc Screening Serv, Dublin, Ireland.
[Kawai, Masaaki] Tohoku Univ Grad Sch Med, Dept Surg Oncol, Sendai, Miyagi, Japan.
[Scharpantgen, Astrid] Direct Sante, Programme Mammog, Luxembourg, Luxembourg.
[Fracheboud, Jacques] Erasmus MC, Rotterdam, Netherlands.
[Hofvind, Solveig] Canc Registry Norway, Oslo, Norway.
[Vidal, Carmen] Catalan Inst Oncol, Canc Detect & Control Programme, Barcelona, Spain.
[Ascunce, Nieves] Inst Salud Publ, Breast Canc Screening Programme, Navarra, Spain.
[Salas, Dolores] Gen Directorate Res & Publ Hlth, Valencia, Spain.
[Salas, Dolores] Ctr Publ Hlth Res, Valencia, Spain.
[Bulliard, Jean-Luc] Univ Lausanne Hosp, Lausanne, Switzerland.
[Kerlikowske, Karla] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Kerlikowske, Karla] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Taplin, Stephen] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Ponti, A (reprint author), AOU Citta Salute & Sci, CPO Piemonte, Canc Epidemiol Unit, Via San Francesco Paola 31, I-10123 Turin, Italy.
EM antonio.ponti@cpo.it
RI Garcia, Montse/B-8832-2014;
OI Garcia, Montse/0000-0002-3437-3185; Fitzpatrick,
Patricia/0000-0003-2524-3677; Lynge, Elsebeth/0000-0003-4785-5236; MARIA
PIERA, MANO/0000-0002-0987-9299; Segnan, Nereo/0000-0002-4730-5384;
Vidal, Carmen/0000-0003-2768-2710
FU US National Cancer Institute, Bethesda, Maryland; National Cancer
Institute [U01CA63740, U01CA86076, U01CA86082, U01CA63736, U01CA70013,
U01CA69976, U01CA 63731, U01CA70040]
FX The ICSN is an activity funded by the US National Cancer Institute,
Bethesda, Maryland. Nospecific funding was made available for this
study, but the National Cancer Institute provided co-ordination of the
project and secretarial support. Data management and analysis, for which
the authors acknowledge Mariano Tomatis and Denise Casella, were
provided by CPO Piemonte, Torino, Italy.; The collection of US data was
supported by the National Cancer Institute-funded Breast Cancer
Surveillance Consortium (BCSC) co-operative agreement (U01CA63740,
U01CA86076, U01CA86082, U01CA63736, U01CA70013, U01CA69976, U01CA 63731,
U01CA70040). A list of the BCSC investigators and procedures for
requesting BCSC data for research purposes are provided at:
http://breastscreening.cancer.gov. The collection of cancer data used in
this study was supported in part by several state public health
departments and cancer registries throughout the US. For a full
description of these sources, please see:
http://breastscreening.cancer.gov/work/acknowledgement.html.
NR 35
TC 8
Z9 8
U1 0
U2 8
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD OCT
PY 2014
VL 50
IS 15
BP 2695
EP 2704
DI 10.1016/j.ejca.2014.07.019
PG 10
WC Oncology
SC Oncology
GA AQ3MY
UT WOS:000342699300018
PM 25149183
ER
PT J
AU Smolonska, J
Koppelman, GH
Wijmenga, C
Vonk, JM
Zanen, P
Bruinenberg, M
Curjuric, I
Imboden, M
Thun, GA
Franke, L
Probst-Hensch, NM
Nurnberg, P
Riemersma, RA
van Schayck, CP
Loth, DW
Brusselle, GG
Stricker, BH
Hofman, A
Uitterlinden, AG
Lahousse, L
London, SJ
Loehr, LR
Manichaikul, A
Barr, RG
Donohue, KM
Rich, SS
Pare, P
Bosse, Y
Hao, K
van den Berge, M
Groen, HJM
Lammers, JWJ
Mali, W
Boezen, HM
Postma, DS
AF Smolonska, Joanna
Koppelman, Gerard H.
Wijmenga, Cisca
Vonk, Judith M.
Zanen, Pieter
Bruinenberg, Marcel
Curjuric, Ivan
Imboden, Medea
Thun, Gian-Andri
Franke, Lude
Probst-Hensch, Nicole M.
Nuernberg, Peter
Riemersma, Roland A.
van Schayck, Constant P.
Loth, Daan W.
Brusselle, Guy G.
Stricker, Bruno H.
Hofman, Albert
Uitterlinden, Andre G.
Lahousse, Lies
London, Stephanie J.
Loehr, Laura R.
Manichaikul, Ani
Barr, R. Graham
Donohue, Kathleen M.
Rich, Stephen S.
Pare, Peter
Bosse, Yohan
Hao, Ke
van den Berge, Maarten
Groen, Harry J. M.
Lammers, Jan-Willem J.
Mali, Willem
Boezen, H. Marike
Postma, Dirkje S.
TI Common genes underlying asthma and COPD? Genome-wide analysis on the
Dutch hypothesis
SO EUROPEAN RESPIRATORY JOURNAL
LA English
DT Article
ID OBSTRUCTIVE PULMONARY-DISEASE; LUNG-FUNCTION DECLINE; SPIROMETRIC
PHENOTYPES; SUSCEPTIBILITY GENE; LINKAGE ANALYSIS; CANDIDATE GENE;
ADAM33 GENE; FOLLOW-UP; ASSOCIATION; HYPERRESPONSIVENESS
AB Asthma and chronic obstructive pulmonary disease (COPD) are thought to share a genetic background ("Dutch hypothesis").
We investigated whether asthma and COPD have common underlying genetic factors, performing genome-wide association studies for both asthma and COPD and combining the results in meta-analyses.
Three loci showed potential involvement in both diseases: chr2p24.3, chr5q23.1 and chrl3q14.2, containing DDX1, COMMD10 (both participating in the nuclear factor (NF) kappa beta pathway) and GNG5P5, respectively. Single nucleotide polymorphisms (SNPs) rs9534578 in GNG5P5 reached genome-wide significance after first replication phase (p=9.96 x 10(-9)). The second replication phase, in seven independent cohorts, provided no significant replication. Expression quantitative trait loci (eQTL) analysis in blood cells and lung tissue on the top 20 associated SNPs identified two SNPs in COMMD10 that influenced gene expression.
Inflammatory processes differ in asthma and COPD and are mediated by NF-kappa beta, which could be driven by the same underlying genes, COMMD10 and DDX1. None of the SNPs reached genome-wide significance. Our eQTL studies support a functional role for two COMMD10 SNPs, since they influence gene expression in both blood cells and lung tissue. Our findings suggest that there is either no common genetic component in asthma and COPD or, alternatively, different environmental factors, e.g. lifestyle and occupation in different countries and continents, which may have obscured the genetic common contribution.
C1 [Smolonska, Joanna; Wijmenga, Cisca; Bruinenberg, Marcel; Franke, Lude] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
[Smolonska, Joanna; Vonk, Judith M.; Boezen, H. Marike] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
[Smolonska, Joanna; Koppelman, Gerard H.; Vonk, Judith M.; Riemersma, Roland A.; van den Berge, Maarten; Boezen, H. Marike; Postma, Dirkje S.] Univ Groningen, Univ Med Ctr Groningen, GRIAC Res Inst, Groningen, Netherlands.
[Koppelman, Gerard H.] Univ Groningen, Univ Med Ctr Groningen, Beatrix Childrens Hosp, Dept Paediat Pulmonol & Paediat Allergol, Groningen, Netherlands.
[Zanen, Pieter; Lammers, Jan-Willem J.] Univ Med Ctr Utrecht, Dept Pulmonol, Utrecht, Netherlands.
[Curjuric, Ivan; Imboden, Medea; Thun, Gian-Andri; Probst-Hensch, Nicole M.] Swiss Trop & Publ Hlth Inst, Dept Epidemiol & Publ Hlth, Basel, Switzerland.
[Curjuric, Ivan; Imboden, Medea; Thun, Gian-Andri; Probst-Hensch, Nicole M.] Univ Basel, Basel, Switzerland.
[Nuernberg, Peter] Univ Cologne, Cologne Ctr Genom, D-50931 Cologne, Germany.
[Riemersma, Roland A.; van den Berge, Maarten; Groen, Harry J. M.; Postma, Dirkje S.] Univ Groningen, Univ Med Ctr Groningen, Dept Pulmonol, Groningen, Netherlands.
[van Schayck, Constant P.] Univ Maastricht, Dept Gen Practice, Maastricht, Netherlands.
[Loth, Daan W.; Brusselle, Guy G.; Stricker, Bruno H.; Hofman, Albert; Lahousse, Lies] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Loth, Daan W.; Stricker, Bruno H.] Netherlands Healthcare Inspectorate, The Hague, Netherlands.
[Brusselle, Guy G.; Lahousse, Lies] Ghent Univ Hosp, Dept Resp Med, Ghent, Belgium.
[Brusselle, Guy G.] Erasmus MC, Dept Resp Med, Rotterdam, Netherlands.
[Stricker, Bruno H.; Hofman, Albert; Uitterlinden, Andre G.] NCHA, Rotterdam, Netherlands.
[Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[London, Stephanie J.] NIEHS, Div Intramural Res, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
[Loehr, Laura R.] Univ N Carolina, Chapel Hill, NC USA.
[Manichaikul, Ani; Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Manichaikul, Ani] Univ Virginia, Div Biostat & Epidemiol, Dept Publ Hlth Sci, Charlottesville, VA USA.
[Barr, R. Graham; Donohue, Kathleen M.] Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA.
[Pare, Peter] Univ British Columbia, James Hogg Res Ctr, St Pauls Hosp, Resp Div,Dept Med, Vancouver, BC V5Z 1M9, Canada.
[Bosse, Yohan] Univ Laval, Dept Mol Med, Inst Univ Cardiol & Pneumol Quebec, Quebec City, PQ, Canada.
[Hao, Ke] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
[Mali, Willem] Univ Med Ctr Utrecht, Dept Radiol, Utrecht, Netherlands.
RP Postma, DS (reprint author), Univ Med Ctr Groningen, Groningen Res Inst Asthma & COPD GRIAC, Hanzepl 1, Groningen, Netherlands.
EM d.s.postma@umcg.nl
RI Franke, Lude/P-7036-2016; Wijmenga, Cisca/D-2173-2009;
OI Franke, Lude/0000-0002-5159-8802; Thun, Gian Andri/0000-0003-4436-3455;
Wijmenga, Cisca/0000-0002-5635-1614; Lahousse, Lies/0000-0002-3494-4363;
London, Stephanie/0000-0003-4911-5290
FU Intramural NIH HHS [ZIA ES043012-15]
NR 49
TC 19
Z9 20
U1 1
U2 15
PU EUROPEAN RESPIRATORY SOC JOURNALS LTD
PI SHEFFIELD
PA 442 GLOSSOP RD, SHEFFIELD S10 2PX, ENGLAND
SN 0903-1936
EI 1399-3003
J9 EUR RESPIR J
JI Eur. Resp. J.
PD OCT
PY 2014
VL 44
IS 4
BP 860
EP 872
DI 10.1183/09031936.00001914
PG 13
WC Respiratory System
SC Respiratory System
GA AQ1LU
UT WOS:000342543700010
PM 24993907
ER
PT J
AU de Sousa, RT
Machado-Vieira, R
Zarate, CA
Manji, HK
AF de Sousa, Rafael T.
Machado-Vieira, Rodrigo
Zarate, Carlos A., Jr.
Manji, Husseini K.
TI Targeting mitochondrially mediated plasticity to develop improved
therapeutics for bipolar disorder
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE apoptosis; bipolar disorder; calcium; mitochondria; mood stabilizer;
oxidative stress
ID MAGNETIC-RESONANCE-SPECTROSCOPY; DORSOLATERAL PREFRONTAL CORTEX;
EXTRACELLULAR-SUPEROXIDE DISMUTASE; BRAIN PHOSPHORUS-METABOLISM;
OXIDATIVE STRESS PARAMETERS; POSTMORTEM FRONTAL-CORTEX; LONG-TERM
POTENTIATION; HIPPOCAMPAL H-1 MRS; N-ACETYL-ASPARTATE; DNA COPY NUMBER
AB Introduction: Bipolar disorder (BPD) is a severe illness with few treatments available. Understanding BPD pathophysiology and identifying potential relevant targets could prove useful for developing new treatments. Remarkably, subtle impairments of mitochondrial function may play an important role in BPD pathophysiology.
Areas covered: This article focuses on human studies and reviews evidence of mitochondrial dysfunction in BPD as a promising target for the development of new, improved treatments. Mitochondria are crucial for energy production, generated mainly through the electron transport chain (ETC) and play an important role in regulating apoptosis and calcium (Ca2+) signaling as well as synaptic plasticity. Mitochondria move throughout the neurons to provide energy for intracellular signaling. Studies showed polymorphisms of mitochondria-related genes as risk factors for BPD. Postmortem studies in BPD also show decreased ETC activity/expression and increased nitrosative and oxidative stress (OxS) in patient brains. BPD has been also associated with increased OxS, Ca2+ dysregulation and increased proapoptotic signaling in peripheral blood. Neuroimaging studies consistently show decreased energy levels and pH in brains of BPD patients.
Expert opinion: Targeting mitochondrial function, and their role in energy metabolism, synaptic plasticity and cell survival, may be an important avenue for development of new mood-stabilizing agents.
C1 [de Sousa, Rafael T.] Univ Sao Paulo, Fac Med, Inst & Dept Psychiat, Lab Neurosci, Sao Paulo, Brazil.
[Machado-Vieira, Rodrigo] NIMH, Translat Res Clin Mood Disorders, Hatfield Clin Res Ctr, ETPB, Bethesda, MD 20814 USA.
[Zarate, Carlos A., Jr.] NIMH, NIH, Sect Neurobiol & Treatment Mood Disorders, Bethesda, MD 20814 USA.
[Zarate, Carlos A., Jr.] NIMH, ETPB, Hatfield Clin Res Ctr, Bethesda, MD 20814 USA.
[Zarate, Carlos A., Jr.] George Washington Univ, Washington, DC USA.
RP Manji, HK (reprint author), 1125 Trenton Harbourton Rd, Titusville, NJ 08560 USA.
EM hmanji@its.jnj.com
RI MACHADO-VIEIRA, RODRIGO/D-8293-2012
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190
FU Fapesp [14891-9]; ABADHS
FX Machado-Vieira was supported by Fapesp (14891-9) and ABADHS. Zarate is
listed as a co-inventor on the use of ketamine in depression, he
assigned patent rights to the US government and may receive royalities
from this patent. Writing assistance was utilized in the production of
this manuscript from Wendy P Battisti, PhD, CMPP (Janssen Research &
Development) which included formatting for journal, and ensuring author
comments were appropriately incorporated or addressed. 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 163
TC 18
Z9 18
U1 1
U2 10
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD OCT
PY 2014
VL 18
IS 10
BP 1131
EP 1147
DI 10.1517/14728222.2014.940893
PG 17
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AQ2GX
UT WOS:000342604900004
PM 25056514
ER
PT J
AU Bae, J
Kim, S
Chen, Z
Eisenberg, ML
Louis, GMB
AF Bae, J.
Kim, S.
Chen, Z.
Eisenberg, M. L.
Louis, G. M. Buck
TI SEMEN QUALITY AND THE SECONDARY SEX RATIO
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Bae, J.; Kim, S.; Chen, Z.; Louis, G. M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD USA.
[Bae, J.] Catholic Univ Daegu Sch Med, Dept Prevent Med, Taegu, South Korea.
[Eisenberg, M. L.] Stanford Univ Sch Med, Dept Urol Obstet & Gynecol, Stanford, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-645
BP E350
EP E350
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201398
ER
PT J
AU Baig-Ward, KM
Chu, TJ
Keil, M
Mumford, S
Polk, C
Segars, JH
AF Baig-Ward, K. M.
Chu, T. J.
Keil, M.
Mumford, S.
Polk, C.
Segars, J. H.
TI ANXIETY RELATED PHENOTYPES IN A-KINASE ANCHORING PROTEIN 13 (AKAP13)
MICE: A POTENTIAL MODEL FOR OBSESSIVE-COMPULSIVE DISORDER
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Baig-Ward, K. M.; Chu, T. J.; Polk, C.; Segars, J. H.] NICHD, PRAE, NIH, Bethesda, MD USA.
[Baig-Ward, K. M.] VCU Sch Med, Richmond, VA USA.
[Keil, M.] NICHD, PDEGEN, NIH, Bethesda, MD USA.
[Mumford, S.] NICHD, Epidemiol Branch, NIH, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-131
BP E45
EP E45
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200132
ER
PT J
AU Banks, NK
Kruszka, PS
Cheng, C
Elkahloun, A
Bondy, CA
Muenke, M
AF Banks, N. K.
Kruszka, P. S.
Cheng, C.
Elkahloun, A.
Bondy, C. A.
Muenke, M.
TI VARIABLE GENE EXPRESSION IN TURNER SYNDROME PATIENTS WITH BICUSPID
AORTIC VALVE
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Banks, N. K.; Kruszka, P. S.; Elkahloun, A.; Muenke, M.] NH GRI, Bethesda, MD USA.
[Cheng, C.; Bondy, C. A.] NICHD, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-346
BP E253
EP E254
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201102
ER
PT J
AU Banks, NK
Kruszka, PS
Cheng, C
Elkahloun, A
Bondy, CA
Muenke, M
AF Banks, N. K.
Kruszka, P. S.
Cheng, C.
Elkahloun, A.
Bondy, C. A.
Muenke, M.
TI PARENTAL X CHROMOSOME INHERITANCE AND VARIABLE GENE EXPRESSION IN TURNER
SYNDROME.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Banks, N. K.; Kruszka, P. S.; Elkahloun, A.; Muenke, M.] NHGRI, Bethesda, MD 20892 USA.
[Cheng, C.; Bondy, C. A.] NICHD, Bethesda, MD 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-274
BP E94
EP E94
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200275
ER
PT J
AU Bishop, LA
Devine, K
Richter, KS
Moon, K
AF Bishop, L. A.
Devine, K.
Richter, K. S.
Moon, K.
TI DIMINISHED OVARIAN RESERVE PREDICTS PREGNANCY LOSS IN OLDER BUT NOT
YOUNGER PATIENTS UNDERGOING ART.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Bishop, L. A.] Georgetown Univ, Washington Hosp Ctr, Washington, DC USA.
[Devine, K.] NICHD, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Richter, K. S.] Shady Grove Fertil, Rockville, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-605
BP E336
EP E337
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201359
ER
PT J
AU Boots, CE
Hill, MJ
Feinberg, EC
Lathi, RB
Jungheim, ES
AF Boots, C. E.
Hill, M. J.
Feinberg, E. C.
Lathi, R. B.
Jungheim, E. S.
TI PROBABILITY OF CLINICAL PREGNANCYAND LIVE-BIRTH IN ART FOR WOMEN
PREVIOUSLY TREATED FOR ART-RELATED ECTOPIC PREGNANCY.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Boots, C. E.; Jungheim, E. S.] Washington Univ, Div REI, St Louis, MO USA.
[Hill, M. J.] NICHD, Bethesda, MD USA.
[Hill, M. J.] NIH, Bethesda, MD 20892 USA.
[Feinberg, E. C.] Fertil Ctr Illinois, Highland Pk, IL USA.
[Lathi, R. B.] Stanford Univ, Div REI, Stanford, CA 94305 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-602
BP E335
EP E335
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201356
ER
PT J
AU Boots, CE
Desai, S
Hill, M
Feinberg, EC
Fowler, SA
Jungheim, ES
AF Boots, C. E.
Desai, S.
Hill, M.
Feinberg, E. C.
Fowler, S. A.
Jungheim, E. S.
TI IMPACT OF METHOTREXATE ON OVARIAN RESERVE.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Boots, C. E.; Fowler, S. A.; Jungheim, E. S.] Washington Univ, Div Reprod Endocrinol & Infertil, St Louis, MO USA.
[Hill, M.] Eunice Kennedy Shriver NICHD, Program Reprod & Adult Endocrinol, Bethesda, MD USA.
[Hill, M.] NIH, Bethesda, MD 20892 USA.
[Feinberg, E. C.] Fertil Ctr Illinois, Highland Pk, IL 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-337
BP E116
EP E116
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200343
ER
PT J
AU Britten, JL
Malik, M
Cox, J
Patel, A
Deng, J
Catherino, WH
AF Britten, J. L.
Malik, M.
Cox, J.
Patel, A.
Deng, J.
Catherino, W. H.
TI GNRH ANALOGS INHIBIT THE REGULATORY EFFECTS OF 17-beta-ESTRADIOL
TREATMENT ON EXTRACELLULAR MATRIX PRODUCTION IN LEIOMYOMA 2D AND 3D
CULTURES.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Britten, J. L.; Malik, M.; Cox, J.; Patel, A.; Deng, J.; Catherino, W. H.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Cox, J.; Catherino, W. H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-340
BP E251
EP E252
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201096
ER
PT J
AU Connell, MT
Szatkowski, JM
Terry, N
DeCherney, AH
Propst, AM
Hill, MJ
AF Connell, M. T.
Szatkowski, J. M.
Terry, N.
DeCherney, A. H.
Propst, A. M.
Hill, M. J.
TI STARTING TIME OF PROGESTERONE LUTEAL PHASE SUPPORT IN IVF: A SYSTEMATIC
REVIEW AND META-ANALYSIS.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Connell, M. T.; Szatkowski, J. M.; Terry, N.; DeCherney, A. H.; Hill, M. J.] Eunice Kennedy Shriver NICHD, PRAE, NIH, Bethesda, MD USA.
[Propst, A. M.] Texas Fertil Ctr, Austin, TX 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-294
BP E237
EP E237
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201050
ER
PT J
AU Cox, JM
Hill, MJ
Devine, K
Richter, KS
DeCherney, A
Levy, M
AF Cox, J. M.
Hill, M. J.
Devine, K.
Richter, K. S.
DeCherney, A.
Levy, M.
TI EXOGENOUS GONADOTROPINS FOR POOR ENDOMETRIAL RESPONDERS.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Cox, J. M.; Hill, M. J.; Devine, K.; DeCherney, A.] NICHD, PRAE, NIH, Bethesda, MD USA.
[Richter, K. S.; Levy, M.] Shady Grove Fertil, Rockville, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-478
BP E296
EP E296
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201233
ER
PT J
AU Cox, JM
Fru, K
Purcell, M
Whitcomb, B
Segars, J
Levens, E
Chang, F
AF Cox, J. M.
Fru, K.
Purcell, M.
Whitcomb, B.
Segars, J.
Levens, E.
Chang, F.
TI HCG VERUS AGONIST TRIGGER IN DONOR OOCYTE CYCLES: DOES HCG HAVE A PLACE
IN CURRENT PRACTICE?
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Cox, J. M.; Fru, K.; Segars, J.] NICHD, PRAE, NIH, Bethesda, MD USA.
[Purcell, M.; Levens, E.; Chang, F.] Shady Grove Fertil, Rockville, MD USA.
[Whitcomb, B.] Univ Massachusetts, Amherst, MA 01003 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-352
BP E121
EP E121
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200357
ER
PT J
AU Cox, JM
Fru, K
Lim, J
Earl, T
Hayes, H
Richter, KS
Kaplan, B
Frattarelli, J
DeCherney, A
Levy, M
AF Cox, J. M.
Fru, K.
Lim, J.
Earl, T.
Hayes, H.
Richter, K. S.
Kaplan, B.
Frattarelli, J.
DeCherney, A.
Levy, M.
TI IMPORT AND EXPORT OF FROZEN DONOR OOCYTE BANK: DOES TRANSPORTATION
AFFECT SURVIVAL AND PREGNANCY RATES?
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Cox, J. M.; Fru, K.; DeCherney, A.] NICHD, PRAE, NIH, Bethesda, MD USA.
[Lim, J.; Richter, K. S.; Levy, M.] Shady Grove Fertil, Rockville, MD USA.
[Earl, T.; Hayes, H.] Donor Egg Bank USA, Rockville, MD USA.
[Kaplan, B.] Fertil Ctr Illinois, Chicago, IL USA.
[Frattarelli, J.] Fertil Inst Hawaii, Honolulu, HI 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-122
BP E42
EP E42
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200123
ER
PT J
AU Devine, K
Driggers, PH
Szu, SC
Zarek, S
Cox, J
Segars, JH
AF Devine, K.
Driggers, P. H.
Szu, S. -C.
Zarek, S.
Cox, J.
Segars, J. H.
TI FOLLICLE STIMULATING HORMONE (FSH) INDUCTION OF AROMATASE AND
LUTEINIZING HORMONE RECEPTOR (LHR) IS DEPENDENT, IN PART, ON THE PROTEIN
KINASE A REGULATORY-RHO-GUANINE NUCLEOTIDE EXCHANGE FACTOR AKAP13.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Devine, K.; Driggers, P. H.; Zarek, S.; Cox, J.; Segars, J. H.] NICHD, NIH, Bethesda, MD USA.
[Szu, S. -C.] Georgetown Univ, Washington, DC 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-403
BP E271
EP E272
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201159
ER
PT J
AU Devine, K
Mumford, S
Hill, MJ
Wu, M
DeCherney, AH
Propst, A
AF Devine, K.
Mumford, S.
Hill, M. J.
Wu, M.
DeCherney, A. H.
Propst, A.
TI DIMINISHED OVARIAN RESERVE (DOR) IN THE US ART POPULATION: DIAGNOSTIC
TRENDS AMONG 183,555 CYCLES FROM THE SOCIETY FOR ASSISTED REPRODUCTIVE
TECHNOLOGY - CLINICAL OUTCOMES REPORTING SYSTEM (SART-CORS).
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Devine, K.; Mumford, S.; DeCherney, A. H.] NICHD, NIH, Bethesda, MD USA.
[Hill, M. J.; Wu, M.] Walter Reed, Bethesda, MD USA.
[Propst, A.] TX Fertil Ctr, Austin, TX 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-14
BP E6
EP E6
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200015
ER
PT J
AU Doyle, N
Richter, KS
Bromer, JG
Hill, MJ
Graham, JR
Tucker, MJ
Stillman, RJ
AF Doyle, N.
Richter, K. S.
Bromer, J. G.
Hill, M. J.
Graham, J. R.
Tucker, M. J.
Stillman, R. J.
TI BLASTOCYST QUALITY CAN SELECT OLDER PATIENTS UP TO AND INCLUDING 40
YEARS OF AGE FOR SUCCESSFUL ELECTIVE SINGLE EMBRYO TRANSFER (ESET).
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Richter, K. S.; Bromer, J. G.; Graham, J. R.; Tucker, M. J.; Stillman, R. J.] Shady Grove Fertil, Rockville, MD USA.
[Doyle, N.] MedStar Washington Hosp Ctr, Washington, DC USA.
[Hill, M. J.] Kennedy Shriver Natl Inst Child Hlth & Human Dev, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-524
BP E311
EP E311
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201279
ER
PT J
AU Fritz, R
Bolnick, J
Bolnick, A
Modi, M
Kilburn, B
Diamond, MP
Armant, DR
AF Fritz, R.
Bolnick, J.
Bolnick, A.
Modi, M.
Kilburn, B.
Diamond, M. P.
Armant, D. R.
TI TROPHOBLAST RETRIEVAL AND ISOLATION FROM THE CERVIX (TRIC) TO PREDICT
RISK FOR SPONTANEOUS ABORTION.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Fritz, R.; Bolnick, J.; Bolnick, A.; Modi, M.; Kilburn, B.] Wayne State Univ, Detroit, MI USA.
[Diamond, M. P.] Georgia Regents Univ, Augusta, GA USA.
[Armant, D. R.] NICHHD, Bethesda, MD 20892 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-160
BP E55
EP E56
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200161
ER
PT J
AU Fru, K
Cox, J
Lim, J
Berger, BM
Hayes, H
Segars, JH
Hoffman, DI
AF Fru, K.
Cox, J.
Lim, J.
Berger, B. M.
Hayes, H.
Segars, J. H.
Hoffman, D. I.
TI BANKED FROZEN DONOR OOCYTES DEMONSTRATE HIGH EFFICIENCY IN CONVERSION TO
LIVE BORN INFANTS; A COLLABORATIVE MULTI-SITE EXPERIENCE.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Fru, K.; Cox, J.; Segars, J. H.] NICHD, NIH, Bethesda, MD USA.
[Lim, J.] Shady Grove Fertil, Rockville, MD USA.
[Berger, B. M.; Hayes, H.; Hoffman, D. I.] DEBUSA, Rockville, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-358
BP E123
EP E123
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200362
ER
PT J
AU Fru, KN
Segal, T
Cox, JM
Mumford, SL
Sharara, FI
Segars, JH
AF Fru, K. N.
Segal, T.
Cox, J. M.
Mumford, S. L.
Sharara, F. I.
Segars, J. H.
TI REPLETE VITAMIN D LEVELS ARE ASSOCIATED WITH HIGHER PREGNANCY RATES AND
INCREASED NUMBER OF LIVE BIRTHS IN AUTOLOGOUS IVF CYCLES.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Fru, K. N.; Cox, J. M.; Mumford, S. L.; Segars, J. H.] NICHD, NIH, Bethesda, MD USA.
[Segal, T.] NS LIJ HS, Manhasset, NY USA.
[Sharara, F. I.] VCRM, Reston, VA 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-419
BP E277
EP E277
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201175
ER
PT J
AU Gharwan, H
Wilkerson, J
Fojo, AT
AF Gharwan, H.
Wilkerson, J.
Fojo, A. T.
TI GNRH-AGONIST CO-TREATMENT DURING CHEMOTHERAPY FOR THE PRESERVATION OF
OVARIAN FUNCTION: A META-ANALYSIS.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Gharwan, H.; Wilkerson, J.; Fojo, A. T.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-59
BP E159
EP E159
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200472
ER
PT J
AU Heitmann, RJ
Weitzel, RP
Tisdale, JF
Wolff, EF
AF Heitmann, R. J.
Weitzel, R. P.
Tisdale, J. F.
Wolff, E. F.
TI ADOPTIVE TRANSFER OF TREGS AFTER NATIVE TREG KNOCKDOWN IMPROVES LITTER
SIZES BACK TO BASELINE LEVELS IN A MURINE MODEL.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Heitmann, R. J.; Wolff, E. F.] NICHD, NIH, Bethesda, MD USA.
[Weitzel, R. P.; Tisdale, J. F.; Wolff, E. F.] NHLBI, NIH, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-288
BP E235
EP E235
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201044
ER
PT J
AU Louis, GMB
Chen, Z
Kim, S
Sapra, K
Bae, J
Kannan, K
AF Louis, G. M. Buck
Chen, Z.
Kim, S.
Sapra, K.
Bae, J.
Kannan, K.
TI URINARY CONCENTRATIONS OF BENZOPHENONE-TYPE UV FILTERS AND SEMEN
QUALITY.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Louis, G. M. Buck; Chen, Z.; Kim, S.; Sapra, K.; Bae, J.] NICHD, Div Intramural Populat Hlth, Rockville, MD USA.
[Kannan, K.] Wadsworth Ctr, Dept Environm Hlth, Albany, NY USA.
NR 0
TC 1
Z9 1
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-266
BP E91
EP E92
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200267
ER
PT J
AU Louis, GMB
Sundaram, R
Sapra, K
Maisog, J
Kannan, K
AF Louis, G. M. Buck
Sundaram, R.
Sapra, K.
Maisog, J.
Kannan, K.
TI URINARY CONCENTRATIONS OF BENZOPHENONE-TYPE UV FILTERS AND COUPLE
FECUNDITY.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Louis, G. M. Buck; Sundaram, R.; Sapra, K.] NICHD, Div Intramural Populat Hlth, Rockville, MD USA.
[Maisog, J.] Glotech Inc, Div Intramural Populat Hlth, Rockville, MD USA.
[Kannan, K.] NYS Dept Hlth, Wadsworth Ctr, Albany, NY USA.
NR 0
TC 0
Z9 0
U1 2
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-261
BP E90
EP E90
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200262
ER
PT J
AU Malik, M
Cox, J
Britten, J
Patel, A
Malik, S
Nieman, LK
Catherino, WH
AF Malik, M.
Cox, J.
Britten, J.
Patel, A.
Malik, S.
Nieman, L. K.
Catherino, W. H.
TI ULIPRISTAL ACETATE DECREASES EXTRACELLULAR MATRIX PROTEINS IN PATIENT
LEIOMYOMA SPECIMENS AND IN 3-DIMENSIONAL CULTURES.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Malik, M.; Cox, J.; Britten, J.; Patel, A.; Malik, S.; Catherino, W. H.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Cox, J.; Nieman, L. K.; Catherino, W. H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-448
BP E286
EP E286
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201203
ER
PT J
AU Malik, M
Britten, JL
Catherino, WH
AF Malik, M.
Britten, J. L.
Catherino, W. H.
TI VALIDATION OF EXTRACELLULAR MATRIX COMPOSITION THAT ALTERS THE
MORPHOLOGY OF LEIOMYOMA CELLS IN 3-DIMENSIONAL CULTURE TO CLOSELY
RESEMBLE SURGICAL TISSUE.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Malik, M.; Britten, J. L.; Catherino, W. H.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Catherino, W. H.] Eunice Kennedy Shriver NICHD, Program Reprod & Adult Endocrinol, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-449
BP E286
EP E287
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201204
ER
PT J
AU Marsh, EE
Bernardi, L
de Chavez, P
Ghant, MS
Robins, JC
Baird, DD
Carnethon, M
AF Marsh, E. E.
Bernardi, L.
de Chavez, P.
Ghant, M. S.
Robins, J. C.
Baird, D. D.
Carnethon, M.
TI NORMATIVE ANTIMULLERIAN HORMONE (AMH) LEVELS AMONGST YOUNG
AFRICAN-AMERICAN WOMEN (AGES 23-35 YEARS OLD)
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Marsh, E. E.; Bernardi, L.; Ghant, M. S.; Robins, J. C.] Northwestern Univ, Feinberg Sch Med, Obstet & Gynecol REI Div, Chicago, IL 60611 USA.
[de Chavez, P.; Carnethon, M.] Northwestern Univ, Chicago, IL 60611 USA.
[Baird, D. D.] NIEHS, Res Triangle Pk, NC 27709 USA.
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-35
BP E151
EP E152
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200450
ER
PT J
AU McWilliams, MM
Koohestani, F
Williams, C
Gunewardena, S
Kumar, TR
Chennathukuzhi, V
AF McWilliams, M. M.
Koohestani, F.
Williams, C.
Gunewardena, S.
Kumar, T. R.
Chennathukuzhi, V.
TI PRICKLE-1 (PK-1) LINKS ENVIRONMENTAL ESTROGEN EXPOSURE TO THE LOSS OF
REST IN UTERINE LEIOMYOMA
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [McWilliams, M. M.; Koohestani, F.; Gunewardena, S.; Kumar, T. R.; Chennathukuzhi, V.] Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
[Williams, C.] NIEHS, Res Triangle Pk, NC 27709 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-443
BP E285
EP E285
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201199
ER
PT J
AU Mendola, P
Wallace, M
Hwang, BS
Liu, D
Grantz, K
AF Mendola, P.
Wallace, M.
Hwang, B. S.
Liu, D.
Grantz, K.
TI PEAK AIR POLLUTION IN THE FIRST WEEKS OF PREGNANCY AND PRETERM DELIVERY
RISK.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Mendola, P.; Wallace, M.; Hwang, B. S.; Liu, D.; Grantz, K.] NICHD, Div Intramural Populat Hlth Res, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-265
BP E91
EP E91
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200266
ER
PT J
AU Mumford, SL
Zarek, SM
Mitchell, EM
Stanford, JB
Wactawski-Wende, J
Schisterman, EF
AF Mumford, S. L.
Zarek, S. M.
Mitchell, E. M.
Stanford, J. B.
Wactawski-Wende, J.
Schisterman, E. F.
TI ASSOCIATION BETWEEN ANTI-MULLERIAN HORMONE (AMH) AND TIME-TO-PREGNANCY
(TTP) AMONG WOMEN IN THE EFFECTS OF ASPIRIN ON GESTATION AND
REPRODUCTION (EAGER) TRIAL.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Mumford, S. L.; Zarek, S. M.; Mitchell, E. M.; Schisterman, E. F.] NIH, Rockville, MD USA.
[Stanford, J. B.] Univ Utah, Salt Lake City, UT USA.
[Wactawski-Wende, J.] SUNY Buffalo, Buffalo, NY 14260 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-332
BP E114
EP E114
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200338
ER
PT J
AU Mumford, SL
Lesher, LL
White, MV
Perkins, NJ
Schisterman, EF
Silver, RM
AF Mumford, S. L.
Lesher, L. L.
White, M. V.
Perkins, N. J.
Schisterman, E. F.
Silver, R. M.
TI RANDOMIZED CLINICAL TRIAL OF PRECONCEPTION LOW DOSE ASPIRIN USE AND
PREGNANCY LOSS: RESULTS FROM THE EAGER TRIAL.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Mumford, S. L.; Perkins, N. J.; Schisterman, E. F.] NIH, Rockville, MD USA.
[Lesher, L. L.; Silver, R. M.] Univ Utah, Salt Lake City, UT USA.
[White, M. V.] Commonwealth Med Coll, Scranton, PA 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-156
BP E54
EP E54
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200157
ER
PT J
AU Muneyyirci-Delale, O
Charles, C
Sinaii, N
Dalloul, M
Stratton, P
AF Muneyyirci-Delale, O.
Charles, C.
Sinaii, N.
Dalloul, M.
Stratton, P.
TI HEALTH-RELATED QUALITY OF LIFE IMPROVEMENT IN WOMEN WITH
ENDOMETRIOSIS-ASSOCIATED PAIN DURING TREATMENT.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Muneyyirci-Delale, O.; Charles, C.; Dalloul, M.] Suny Downstate Med Ctr, Brooklyn, NY 11203 USA.
[Muneyyirci-Delale, O.] Kings Cty Hosp Ctr, Brooklyn, NY USA.
[Sinaii, N.] NIH, Biostat & Clin Epidemiol Serv, Ctr Clin, Bethesda, MD 20892 USA.
[Stratton, P.] NICHD, Program Reprod & Adult Endocrinol, NIH, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-38
BP E14
EP E14
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200039
ER
PT J
AU Park, S
Vahidi, N
DeCherney, AH
Wolff, EE
AF Park, S.
Vahidi, N.
DeCherney, A. H.
Wolff, E. E.
TI PRELIMINARY EVALUATION OF PGC DIFFERENTIATION PROTOCOL IN RHESUS MODEL.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Park, S.; Vahidi, N.; DeCherney, A. H.; Wolff, E. E.] NICHD, NIH, Bethesda, MD 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-303
BP E103
EP E103
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200304
ER
PT J
AU Patel, A
Malik, M
Webb, JB
Cox, J
Catherino, W
AF Patel, A.
Malik, M.
Webb, J. Britten
Cox, J.
Catherino, W.
TI DISSECTING THE MOLECULAR MECHANISM OF MIFEPRISTONE FUNCTION IN
LEIOMYOMAS USING 2-AND 3-DIMENSIONAL MODELS.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Patel, A.; Malik, M.; Webb, J. Britten; Cox, J.; Catherino, W.] Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bethesda, MD 20814 USA.
[Cox, J.; Catherino, W.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinolgy, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-446
BP E285
EP E286
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201201
ER
PT J
AU Patounakis, G
Chason, RJ
Norian, JM
Payson, M
DeCherney, AH
Yauger, BJ
AF Patounakis, G.
Chason, R. J.
Norian, J. M.
Payson, M.
DeCherney, A. H.
Yauger, B. J.
TI EMBRYO TRANSFER IN PATIENTS WITH PRIOR CESAREAN DELIVERY ARE MORE
DIFFICULT THAN THOSE WITH ONLY VAGINAL DELIVERIES BUT PREGNANCY RATES
ARE NOT AFFECTED: A PROSPECTIVE STUDY.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Patounakis, G.; DeCherney, A. H.] NICHD, NIH, Bethesda, MD USA.
[Chason, R. J.; Yauger, B. J.] Walter Reed Natl Mil Med Ctr, Bethesda, MD USA.
[Norian, J. M.] Loma Linda Univ Hosp, Loma Linda, CA USA.
[Payson, M.] Dominion Fertil, Arlington, VA USA.
[Payson, M.] Inova Fairfax Hosp Womens Ctr, Falls Church, VA 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-275
BP E230
EP E231
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201031
ER
PT J
AU Patounakis, G
Sundheimer, LW
DeCherney, AH
Hill, MJ
AF Patounakis, G.
Sundheimer, L. W.
DeCherney, A. H.
Hill, M. J.
TI TO FREEZE OR NOT TO FREEZE: THE COST-EFFECTIVENESS OF A FREEZE-ALL
POLICY WHEN PROGESTERONE ON THE DAY OF HCG TRIGGER IS ELEVATED.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Patounakis, G.; DeCherney, A. H.; Hill, M. J.] NICHD, NIH, Bethesda, MD USA.
[Sundheimer, L. W.] Univ Calif Los Angeles, Los Angeles, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-87
BP E168
EP E168
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200496
ER
PT J
AU Patounakis, G
Sundheimer, LW
DeCherney, AH
Hill, MJ
AF Patounakis, G.
Sundheimer, L. W.
DeCherney, A. H.
Hill, M. J.
TI PREIMPLANTATION GENETIC SCREENING (PGS) OF EMBRYOS PRIOR TO TRANSFER: A
COST ANALYSIS OF SINGLE EMBRYO TRANSFERS (SET) AND DOUBLE EMBRYO
TRANSFERS (DET).
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Patounakis, G.; DeCherney, A. H.; Hill, M. J.] NICHD, NIH, Bethesda, MD USA.
[Sundheimer, L. W.] Univ Calif Los Angeles, Los Angeles, CA 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-10
BP E5
EP E5
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200011
ER
PT J
AU Plowden, TC
Napoli, A
DeCherney, AH
Wolff, AB
Wolff, EF
AF Plowden, T. C.
Napoli, A.
DeCherney, A. H.
Wolff, A. B.
Wolff, E. F.
TI WOMEN WITH MALE-ASSOCIATED HIP ABNORMALITIES (CAM FEMOROACETABULAR
IMPINGEMENT) HAVE HIGHER ANTRAL FOLLICLE COUNTS
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Plowden, T. C.; DeCherney, A. H.; Wolff, E. F.] NICHD, PRAE, NIH, Bethesda, MD USA.
[Napoli, A.; Wolff, A. B.] Washington Orthopaed & Sports Med, Washington, DC 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-367
BP E260
EP E260
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201123
ER
PT J
AU Plowden, TC
Chason, RJ
Miles, SM
Yauger, BJ
Segars, JH
Hill, MJ
Csokmay, JM
AF Plowden, T. C.
Chason, R. J.
Miles, S. M.
Yauger, B. J.
Segars, J. H.
Hill, M. J.
Csokmay, J. M.
TI DOES THE PRESENCE OF BLOOD IN THE CATHETER OR THE DEGREE OF DIFFICULTY
OF EMBRYO TRANSFER AFFECT PREGNANCY?
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Plowden, T. C.; Segars, J. H.; Hill, M. J.; Csokmay, J. M.] Eunice Kennedy Shriver NICHD, PRAE, NIH, Bethesda, MD USA.
[Plowden, T. C.; Chason, R. J.; Miles, S. M.; Yauger, B. J.; Hill, M. J.; Csokmay, J. M.] Walter Reed Natl Mil Med Ctr, REI Div, Dept Ob GYN, Bethesda, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-397
BP E136
EP E136
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200401
ER
PT J
AU Royster, GD
Hill, MJ
Zarek, SM
DeCherney, AH
Levens, E
Widra, E
Levy, MJ
AF Royster, G. D.
Hill, M. J.
Zarek, S. M.
DeCherney, A. H.
Levens, E.
Widra, E.
Levy, M. J.
TI THREE DAY PROGESTERONE AREA UNDER THE CURVE: A BETTER TEST THAN
PROGESTERONE ON THE DAY OF HCG?
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Royster, G. D.; Zarek, S. M.; DeCherney, A. H.] NIH, Program Reprod & Adult Endocrinol, Bethesda, MD 20892 USA.
[Hill, M. J.] Walter Reed Natl Mil Med Ctr, Bethesda, MD USA.
[Levens, E.; Widra, E.; Levy, M. J.] Shady Grove Fertil, Rockville, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-248
BP E85
EP E86
PG 2
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200249
ER
PT J
AU Sapra, KJ
Bae, J
Kim, S
Louis, GMB
AF Sapra, K. J.
Bae, J.
Kim, S.
Louis, G. M. Buck
TI TIME-TO-PREGNANCY AND SECONDARY SEX RATIO IN A PRECONCEPTION COHORT.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Sapra, K. J.; Bae, J.; Kim, S.; Louis, G. M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD USA.
OI Sapra, Katherine/0000-0001-5659-6489
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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-116
BP E40
EP E40
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200118
ER
PT J
AU Schisterman, EF
Zarek, SM
Mitchell, EM
Galai, N
Townsend, JM
Mumford, SL
AF Schisterman, E. F.
Zarek, S. M.
Mitchell, E. M.
Galai, N.
Townsend, J. M.
Mumford, S. L.
TI ASSOCIATION OF ANTI-MULLERIAN HORMONE (AMH) AND LIVE BIRTH: RESULTS FROM
THE EFFECTS OF ASPIRIN ON GESTATION AND REPRODUCTION (EAGER) TRIAL.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Schisterman, E. F.; Zarek, S. M.; Mitchell, E. M.; Mumford, S. L.] NIH, Rockville, MD USA.
[Galai, N.] Univ Haifa, IL-31999 Haifa, Israel.
[Townsend, J. M.] Commonwealth Med Coll, Buffalo, NY 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-158
BP E55
EP E55
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200159
ER
PT J
AU Segal, TR
Zarek, SM
Mumford, SL
Plowden, TC
Nieman, LK
Segars, JH
Armstrong, AY
AF Segal, T. R.
Zarek, S. M.
Mumford, S. L.
Plowden, T. C.
Nieman, L. K.
Segars, J. H.
Armstrong, A. Y.
TI RADIOGRAPHIC AND HISTOPATHOLOGIC ENDOMETRIAL CHARACTERISTICS OF WOMEN
UNDERGOING TREATMENT WITH ULIPRISTAL ACETATE (UPA).
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Segal, T. R.] North Shore LIJ Hlth Syst, OB Gyn, Manhasset, NY USA.
[Zarek, S. M.; Plowden, T. C.; Nieman, L. K.; Segars, J. H.; Armstrong, A. Y.] NICHD, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Mumford, S. L.] NICHD, Div Intramural Populat Hlth Res, NIH, Bethesda, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-447
BP E286
EP E286
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201202
ER
PT J
AU Skora, DA
Beall, SA
Mumford, SL
Segars, JH
AF Skora, D. A.
Beall, S. A.
Mumford, S. L.
Segars, J. H.
TI OOCYTE MATURATION FAILURE: DEFINING A CLINICAL SYNDROME.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Skora, D. A.] George Washington Univ, Washington, DC USA.
[Beall, S. A.; Mumford, S. L.; Segars, J. H.] NICHD, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-180
BP E199
EP E199
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200584
ER
PT J
AU Vahidi, N
Plowden, T
Weitzel, P
Tisdale, J
Decherney, A
Heitmann, R
Wolff, E
AF Vahidi, N.
Plowden, T.
Weitzel, P.
Tisdale, J.
Decherney, A.
Heitmann, R.
Wolff, E.
TI CHARACTERIZATION OF T-REGULATORY CELLS DURING THE MENSTRUAL CYCLE IN THE
BLOOD AND ENDOMETRIUM OF REPRODUCTIVE AGE WOMEN
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Vahidi, N.; Plowden, T.; Decherney, A.; Heitmann, R.; Wolff, E.] NICHD, NIH, Bethesda, MD USA.
[Weitzel, P.; Tisdale, J.] NHLBI, NIH, Bethesda, MD 20892 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-428
BP E280
EP E280
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201184
ER
PT J
AU Vahidi, N
Park, S
Weitzel, P
Tisdale, J
Wolff, EE
AF Vahidi, N.
Park, S.
Weitzel, P.
Tisdale, J.
Wolff, E. E.
TI CHARACTERIZATION OF THE PUTATIVE OVARIAN STEM CELL MARKER DDX4 BY MASS
SPECTROMETRY AND FUSION PROTEIN ANALYSIS OF C-TERMINUS EXPRESSION.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Vahidi, N.; Park, S.; Wolff, E. E.] NICHD, NIH, Bethesda, MD USA.
[Weitzel, P.; Tisdale, J.] NHLBI, NIH, Bethesda, MD 20892 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-306
BP E104
EP E104
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200307
ER
PT J
AU Zarek, SM
Schisterman, EF
Mitchell, EM
Lynch, A
Faraggi, D
Mumford, SL
AF Zarek, S. M.
Schisterman, E. F.
Mitchell, E. M.
Lynch, A.
Faraggi, D.
Mumford, S. L.
TI IS ANTI-MULLERIAN HORMONE (AMH) ASSOCIATED WITH PRETERM BIRTH? RESULTS
FROM THE EFFECTS OF ASPIRIN ON GESTATION AND REPRODUCTION (EAGER) TRIAL.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Zarek, S. M.; Schisterman, E. F.; Mitchell, E. M.; Mumford, S. L.] NIH, Rockville, MD USA.
[Lynch, A.] Univ Colorado, Aurora, CO USA.
[Faraggi, D.] Univ Haifa, IL-31999 Haifa, Israel.
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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-395
BP E269
EP E269
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201151
ER
PT J
AU Zarek, SM
Schisterman, EF
Mitchell, EM
Silver, RM
Segars, JH
Mumford, SL
AF Zarek, S. M.
Schisterman, E. F.
Mitchell, E. M.
Silver, R. M.
Segars, J. H.
Mumford, S. L.
TI ASSOCIATION OF ANTI-MULLERIAN HORMONE (AMH) AND PREGNANCY LOSS.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Zarek, S. M.; Schisterman, E. F.; Mitchell, E. M.; Segars, J. H.; Mumford, S. L.] NIH, Bethesda, MD 20892 USA.
[Silver, R. M.] Univ Utah, Salt Lake City, UT 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-398
BP E270
EP E270
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201154
ER
PT J
AU Zarek, SM
Mumford, SL
Segars, JH
Armstrong, AY
AF Zarek, S. M.
Mumford, S. L.
Segars, J. H.
Armstrong, A. Y.
TI COST EFFECTIVE ANALYSIS COMPARING A FREEZE-ALL PROTOCOL TO FRESH
BLASTOCYST EMBRYO TRANSFER IN NORMAL RESPONDERS
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Zarek, S. M.; Segars, J. H.; Armstrong, A. Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Mumford, S. L.] NICHD, Div Intramural Populat Hlth Res, Rockville, 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-306
BP E241
EP E241
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201062
ER
PT J
AU Zarek, SM
Brezina, PR
Mumford, SL
Plowden, TC
Coddington, CC
Segars, JH
AF Zarek, S. M.
Brezina, P. R.
Mumford, S. L.
Plowden, T. C.
Coddington, C. C.
Segars, J. H.
TI TRAINING OF REPRODUCTIVE ENDOCRINOLOGYAND INFERTILITY FELLOWS FOR EMBRYO
TRANSFER DID NOT RESULT IN A DECREMENT IN PREGNANCY.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Zarek, S. M.; Mumford, S. L.; Plowden, T. C.; Segars, J. H.] NIH, Bethesda, MD 20892 USA.
[Brezina, P. R.] Fertil Associates Memphis, Memphis, TN USA.
[Coddington, C. C.] Mayo Clin, Rochester, MN 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 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA P-273
BP E230
EP E230
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500201029
ER
PT J
AU Zarek, SM
Mitchell, EM
DeCherney, AH
Richter, KS
Devine, K
Browne, PE
O'Brien, JE
AF Zarek, S. M.
Mitchell, E. M.
DeCherney, A. H.
Richter, K. S.
Devine, K.
Browne, P. E.
O'Brien, J. E.
TI THE EFFECT OF DONOR OOCYTE RECIPIENT OBESITY ON LIVE BIRTH: AN ANALYSIS
OF 3,922 SHARED DONOR OOCYTE ASSISTED REPRODUCTIVE TECHNOLOGY (ART)
CYCLES.
SO FERTILITY AND STERILITY
LA English
DT Meeting Abstract
CT 70th Annual Meeting of the American-Society-for-Reproductive-Medicine
CY OCT 18-22, 2014
CL Honolulu, HI
SP Amer Soc Reprod Med
C1 [Zarek, S. M.; Mitchell, E. M.; DeCherney, A. H.; Devine, K.] NIH, Bethesda, MD 20892 USA.
[Richter, K. S.; Browne, P. E.; O'Brien, J. E.] Shady Grove Fertil, Rockville, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2014
VL 102
IS 3
SU S
MA O-8
BP E4
EP E4
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AQ0VG
UT WOS:000342500200009
ER
PT J
AU Yu, WS
McIntosh, C
Lister, R
Zhu, I
Han, YX
Ren, JK
Landsman, D
Lee, E
Briones, V
Terashima, M
Leighty, R
Ecker, JR
Muegge, K
AF Yu, Weishi
McIntosh, Carl
Lister, Ryan
Zhu, Iris
Han, Yixing
Ren, Jianke
Landsman, David
Lee, Eunice
Briones, Victorino
Terashima, Minoru
Leighty, Robert
Ecker, Joseph R.
Muegge, Kathrin
TI Genome-wide DNA methylation patterns in LSH mutant reveals de-repression
of repeat elements and redundant epigenetic silencing pathways
SO GENOME RESEARCH
LA English
DT Article
ID EMBRYONIC STEM-CELLS; NUCLEAR LAMINA INTERACTIONS; CYTOSINE METHYLATION;
FAMILY-MEMBER; SNF2 FAMILY; DIFFERENTIATION; CHROMATIN; GENE;
HYPOMETHYLATION; ARABIDOPSIS
AB Cytosine methylation is critical in mammalian development and plays a role in diverse biologic processes such as genomic imprinting, X chromosome inactivation, and silencing of repeat elements. Several factors regulate DNA methylation in early embryogenesis, but their precise role in the establishment of DNA methylation at a given site remains unclear. We have generated a comprehensive methylation map in fibroblasts derived from the murine DNA methylation mutant Hells(-/-) (helicase, lymphoid specific, also known as LSH). It has been previously shown that HELLS can influence de novo methylation of retroviral sequences and endogenous genes. Here, we describe that HELLS controls cytosine methylation in a nuclear compartment that is in part defined by lamin B1 attachment regions. Despite widespread loss of cytosine methylation at regulatory sequences, including promoter regions of protein-coding genes and noncoding RNA genes, overall relative transcript abundance levels in the absence of HELLS are similar to those in wild-type cells. A subset of promoter regions shows increases of the histone modification H3K27me3, suggesting redundancy of epigenetic silencing mechanisms. Furthermore, HELLS modulates CG methylation at all classes of repeat elements and is critical for repression of a subset of repeat elements. Overall, we provide a detailed analysis of gene expression changes in relation to DNA methylation alterations, which contributes to our understanding of the biological role of cytosine methylation.
C1 [Yu, Weishi; Han, Yixing; Ren, Jianke; Lee, Eunice; Briones, Victorino; Terashima, Minoru; Muegge, Kathrin] NCI, Ctr Canc Res, Mouse Canc Genet Program, Frederick, MD 21702 USA.
[McIntosh, Carl] NCI, Frederick Natl Lab Canc Res, BCGC, Frederick, MD 21702 USA.
[Lister, Ryan; Ecker, Joseph R.] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA.
[Lister, Ryan; Ecker, Joseph R.] Salk Inst Biol Studies, Genome Anal Lab, La Jolla, CA 92037 USA.
[Zhu, Iris; Landsman, David] NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
[Leighty, Robert] NCI, Frederick Natl Lab Canc Res, Data Management Serv Inc, Frederick, MD 21702 USA.
[Muegge, Kathrin] Leidos Biomed Res Inc, Basic Sci Program, Frederick Natl Lab, Frederick, MD 21702 USA.
RP Muegge, K (reprint author), NCI, Ctr Canc Res, Mouse Canc Genet Program, Frederick, MD 21702 USA.
EM Kathrin.Muegge@nih.gov
RI Lister, Ryan/B-5168-2012; Ecker, Joseph/B-9144-2008;
OI Lister, Ryan/0000-0001-6637-7239; Ecker, Joseph/0000-0001-5799-5895;
Landsman, David/0000-0002-9819-6675
FU National Cancer Institute, National Institutes of Health
[HHSN26120080001E]; Intramural Research Program of the NIH; National
Cancer Institute; Center for Cancer Research; National Library of
Medicine, NIH
FX We thank Lino Tessarolo and Michael Bustin for helpful suggestions on
the manuscript. We thank Karen Saylor for excellent animal technical
assistance. We thank Matthew Fivash and Xiangtao Liu for help on the use
of the R program, Jyoti Shetty, Yongmei Zhao, and Bao Tran from the NCI
Sequencing Facility, FNLCR, and the NIH Fellows Editorial Board for
suggestions on the manuscript. This project has been funded in whole or
in part with federal funds from the National Cancer Institute, National
Institutes of Health, under contract HHSN26120080001E. The content of
this publication does not necessarily reflect the views or policies of
the Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the US
Government. This research was supported by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research, and the National Library of Medicine, NIH. Frederick National
Laboratory for Cancer Research is accredited by AAALAC International and
follows the Public Health Service Policy for the Care and Use of
Laboratory Animals. Animal care was provided in accordance with the
procedures outlined in the "Guide for Care and Use of Laboratory
Animals" (National Research Council, 1996, National Academy Press,
Washington, DC).
NR 59
TC 16
Z9 17
U1 0
U2 8
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD OCT
PY 2014
VL 24
IS 10
BP 1613
EP 1623
DI 10.1101/gr.172015.114
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA AQ1LL
UT WOS:000342542800006
PM 25170028
ER
PT J
AU Ganguli, D
Chereji, RV
Iben, JR
Cole, HA
Clark, DJ
AF Ganguli, Dwaipayan
Chereji, Razvan V.
Iben, James R.
Cole, Hope A.
Clark, David J.
TI RSC-dependent constructive and destructive interference between opposing
arrays of phased nucleosomes in yeast
SO GENOME RESEARCH
LA English
DT Article
ID CHROMATIN-REMODELING COMPLEX; GENOME-WIDE; SACCHAROMYCES-CEREVISIAE;
EUKARYOTIC GENOME; ACTIVATION; ORGANIZATION; RESOLUTION; LOCATION;
REVEALS; REGIONS
AB RSC and SWI/SNF are related ATP-dependent chromatin remodeling machines that move nucleosomes, regulating access to DNA. We addressed their roles in nucleosome phasing relative to transcription start sites in yeast. SWI / SNF has no effect on phasing at the global level. In contrast, RSC depletion results in global nucleosome repositioning: Both upstream and downstream nucleosomal arrays shift toward the nucleosome-depleted region (NDR), with no change in spacing, resulting in a narrower and partly filled NDR. The global picture of RSC-depleted chromatin represents the average of a range of chromatin structures, with most genes showing a shift of the +1 or the -1 nucleosome into the NDR. Using RSC ChIP data reported by others, we show that RSC occupancy is highest on the coding regions of heavily transcribed genes, though not at their NDRs. We propose that RSC has a role in restoring chromatin structure after transcription. Analysis of gene pairs in different orientations demonstrates that phasing patterns reflect competition between phasing signals emanating from neighboring NDRs. These signals may be in phase, resulting in constructive interference and a regular array, or out of phase, resulting in destructive interference and fuzzy positioning. We propose a modified barrier model, in which a stable complex located at the NDR acts as a bidirectional phasing barrier. In RSC-depleted cells, this barrier has a smaller footprint, resulting in narrower NDRs. Thus, RSC plays a critical role in organizing yeast chromatin.
C1 [Ganguli, Dwaipayan; Chereji, Razvan V.; Iben, James R.; Cole, Hope A.; Clark, David J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Clark, DJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
EM clarkda@mail.nih.gov
OI Chereji, Razvan/0000-0002-0572-6412
FU Intramural Research Program of the NIH (NICHD)
FX This research was supported by the Intramural Research Program of the
NIH (NICHD). We thank Gary Felsenfeld, Tara Burke, Peter Eriksson, and
Josefina Ocampo for helpful comments on the manuscript. We thank the
Tufts University Core Facility for paired-end sequencing of the snf2
Delta strain and the NHLBI Core Facility (Yoshi Wakabayashi, Yan Luo,
Ting Ni, and Jun Zhu) for paired-end sequencing of the RSC strains. We
thank Marian Carlson for strains MCY3860 and MCY3647.
NR 60
TC 18
Z9 18
U1 0
U2 4
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD OCT
PY 2014
VL 24
IS 10
BP 1637
EP 1649
DI 10.1101/gr.177014.114
PG 13
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA AQ1LL
UT WOS:000342542800008
PM 25015381
ER
PT J
AU Khawaja, O
Maziarz, M
Biggs, ML
Longstreth, WT
Ix, JH
Kizer, JR
Zieman, S
Tracy, RP
Mozaffarian, D
Mukamal, KJ
Siscovick, DS
Djousse, L
AF Khawaja, Owais
Maziarz, Marlena
Biggs, Mary L.
Longstreth, William T., Jr.
Ix, Joachim H.
Kizer, Jorge R.
Zieman, Susan
Tracy, Russell P.
Mozaffarian, Dariush
Mukamal, Kenneth J.
Siscovick, David S.
Djousse, Luc
TI Plasma free fatty acids and risk of stroke in the Cardiovascular Health
Study
SO INTERNATIONAL JOURNAL OF STROKE
LA English
DT Article
DE epidemiology; free fatty acids; risk factors; stroke
ID INCIDENT STROKE; CYSTATIN-C; ASSOCIATION; DISEASE
AB Background Although free fatty acids have been positively associated with risk factors for stroke, the role of plasma free fatty acids in the development of stroke has not been elucidated in older adults.
Aims We sought to examine the association between plasma free fatty acids and incident stroke.
Methods Prospective cohort of 4369 men and women 65 years of age in the Cardiovascular Health Study. Plasma levels of free fatty acids were measured at the 1992-1993 examination and stroke events were adjudicated by a committee of experts including neurologists and neuroradiologists. Cox regression was used to estimate the relative risk of stroke associated with free fatty acids concentrations.
Results The average age among participants was 7552 years. During a median follow-up of 114 years, 732 incident strokes occurred. The crude incidence rates of stroke were 145, 149, and 176 per 1000 person-years across increasing tertiles of plasma free fatty acids. The adjusted hazard ratio (95% confidence interval) for incident stroke was 105 (097-114) per standard deviation increase in plasma free fatty acids. Restriction to ischemic stroke did not alter the results [hazard ratio (95% confidence interval): 104 (096-114) per standard deviation higher free fatty acids], and there was no effect modification by adiposity (P interaction=018) or by diabetes (P interaction=015).
Conclusion Our data did not show an association of plasma free fatty acids with incident stroke among community dwelling older adults.
C1 [Khawaja, Owais] Dartmouth Hitchcock Med Ctr, Sect Pulm & Crit Care Med, Lebanon, NH 03766 USA.
[Maziarz, Marlena; Biggs, Mary L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Longstreth, William T., Jr.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
[Ix, Joachim H.] Univ Calif San Diego, Nephrol Sect, Vet Affairs San Diego Healthcare Syst, San Diego, CA 92103 USA.
[Kizer, Jorge R.] Montefiore Med Ctr, Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY USA.
[Zieman, Susan] NIA, Bethesda, MD 20892 USA.
[Tracy, Russell P.] Univ Vermont, Coll Med, Dept Pathol, Colchester, VT USA.
[Mozaffarian, Dariush] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Mozaffarian, Dariush] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Mozaffarian, Dariush] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Dept Gen Med & Primary Care, Boston, MA 02215 USA.
[Mukamal, Kenneth J.; Djousse, Luc] Harvard Univ, Sch 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, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Djousse, Luc] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
[Djousse, Luc] Boston Vet Affairs Healthcare Syst, Boston, MA USA.
RP Khawaja, O (reprint author), Dartmouth Hitchcock Med Ctr, Sect Pulm & Crit Care Med, 1 Med Ctr Dr, Lebanon, NH 03766 USA.
EM oajaz@yahoo.com
RI Djousse, Luc/F-5033-2017
OI Djousse, Luc/0000-0002-9902-3047
FU NHLBI NIH HHS [R01 HL094555, HHSN268200800007C, HHSN268201200036C, N01
HC55222, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082,
N01HC85083, N01HC85086, R01 HL080295, R01HL094555, U01 HL080295]; NIA
NIH HHS [AG023629, R01 AG023629, R56 AG023629]; PHS HHS
[HHSN268200800007C, HHSN268201200036C]
NR 21
TC 2
Z9 2
U1 2
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1747-4930
EI 1747-4949
J9 INT J STROKE
JI Int. J. Stroke
PD OCT
PY 2014
VL 9
IS 7
BP 917
EP 920
DI 10.1111/ijs.12216
PG 4
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AQ1YT
UT WOS:000342581900022
PM 24447493
ER
PT J
AU Zhu, QY
Yamakuchi, M
Ture, S
Garcia-Hernandez, MD
Ko, KA
Modjeski, KL
LoMonaco, MB
Johnson, AB
O'Donnell, CJ
Takai, Y
Morrell, CN
Lowenstein, CJ
AF Zhu, Qiuyu
Yamakuchi, Munekazu
Ture, Sara
Garcia-Hernandez, Maria de la Luz
Ko, Kyung Ae
Modjeski, Kristina L.
LoMonaco, Michael B.
Johnson, Andrew B.
O'Donnell, Christopher J.
Takai, Yoshimi
Morrell, Craig N.
Lowenstein, Charles J.
TI Syntaxin-binding protein STXBP5 inhibits endothelial exocytosis and
promotes platelet secretion
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID VON-WILLEBRAND-FACTOR; WEIBEL-PALADE BODY;
ETHYLMALEIMIDE-SENSITIVE-FACTOR; SYNAPTIC VESICLE CYCLE; THROMBUS
FORMATION; NEUROTRANSMITTER RELEASE; MEMBRANE-FUSION; VENOUS
THROMBOEMBOLISM; CARDIOVASCULAR-DISEASE; REGULATES EXOCYTOSIS
AB In humans, vWF levels predict the risk of myocardial infarction and thrombosis; however, the factors that influence vWF levels are not completely understood. Recent genome-wide association studies (GWAS) have identified syntaxin-binding protein 5 (STXBP5) as a candidate gene linked to changes in vWF plasma levels, though the functional relationship between STXBPS and vWF is unknown. We hypothesized that STXBP5 inhibits endothelial cell exocytosis. We found that STXBP5 is expressed in human endothelial cells and colocalizes with and interacts with syntaxin 4. In human endothelial cells reduction of STXBP5 increased exocytosis of vWF and P-selectin. Mice lacking Stxbp5 had higher levels of vWF in the plasma, increased P-selectin translocation, and more platelet-endothelial interactions, which suggests that STXBP5 inhibits endothelial exocytosis. However, Stxbp5 KO mice also displayed hemostasis defects, including prolonged tail bleeding times and impaired mesenteric arteriole and carotid artery thrombosis. Furthermore, platelets from Stxbp5 KO mice had defects in platelet secretion and activation; thus, STXBP5 inhibits endothelial exocytosis but promotes platelet secretion. Our study reveals a vascular function for STXBP5, validates the functional relevance of a candidate gene identified by GWAS, and suggests that variation within STXBPS is a genetic risk for venous thromboembolic disease.
C1 [Zhu, Qiuyu; Yamakuchi, Munekazu; Ture, Sara; Garcia-Hernandez, Maria de la Luz; Ko, Kyung Ae; Modjeski, Kristina L.; LoMonaco, Michael B.; Morrell, Craig N.; Lowenstein, Charles J.] Univ Rochester, Med Ctr, Dept Med, Aab Cardiovasc Res Inst, Rochester, NY 14642 USA.
[Zhu, Qiuyu; Modjeski, Kristina L.] Univ Rochester, Sch Med & Dent, Dept Physiol & Pharmacol, Rochester, NY USA.
[Yamakuchi, Munekazu] Kagoshima Univ, Grad Sch Med & Dent, Dept Lab & Vasc Med, Kagoshima 890, Japan.
[Johnson, Andrew B.; O'Donnell, Christopher J.] NHLBI, Div Intramural Res, NIH, Framingham, MA USA.
[Johnson, Andrew B.; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[O'Donnell, Christopher J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiovasc, Boston, MA USA.
[Takai, Yoshimi] Kobe Univ, Grad Sch Med, Dept Biochem & Mol Biol, Kobe, Hyogo 657, Japan.
RP Lowenstein, CJ (reprint author), Box CVRI,601 Elmwood Ave, Rochester, NY 14642 USA.
EM charles_lowenstein@urmc.rochester.edu
RI Johnson, Andrew/G-6520-2013
FU NIH/NHLBI [R21 HL108372]; HHMI "Med-into-Grad" Fellowship in
Cardiovascular Sciences at the Aab Cardiovascular Research Institute,
University of Rochester; American Heart Association [14GRNT19020033,
0835446N, 13PRE17050105]
FX We thank Jun Miyoshi for Stxbp5 KO mice, Sriram Neelamegham for XS-vWF
protein, and David James for pMEX neo-3xFLAG-tomosyn (8)-ATG expression
plasmid. This work was supported by NIH/NHLBI grant R21 HL108372 (to
C.J. Lowenstein); by the HHMI "Med-into-Grad" Fellowship in
Cardiovascular Sciences at the Aab Cardiovascular Research Institute,
University of Rochester (to C.J. Lowenstein and Q Zhu); and by American
Heart Association grants 14GRNT19020033 (to C.J. Lowenstein), 0835446N
(to M. Yamakuchi), and 13PRE17050105 (to Q. Zhu).
NR 87
TC 17
Z9 17
U1 2
U2 4
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 OCT
PY 2014
VL 124
IS 10
BP 4503
EP 4516
DI 10.1172/JCI71245
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AQ2WG
UT WOS:000342649900042
PM 25244095
ER
PT J
AU Taylor, DH
Danis, M
Zafar, SY
Howie, LJ
Samsa, GP
Wolf, SP
Abernethy, AP
AF Taylor, Donald H., Jr.
Danis, Marion
Zafar, S. Yousuf
Howie, Lynn J.
Samsa, Gregory P.
Wolf, Steven P.
Abernethy, Amy P.
TI There Is a Mismatch Between the Medicare Benefit Package and the
Preferences of Patients With Cancer and Their Caregivers
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID CARE; EXPERIENCE
AB Purpose
To identify insured services that are most important to Medicare beneficiaries with cancer and their family caregivers when coverage is limited.
Methods
A total of 440 participants (patients, n = 246; caregivers, n = 194) were enrolled onto the CHAT (Choosing Health Plans All Together) study from August 2010 to March 2013. The exercise elicited preferences about what benefits Medicare should cover for patients with cancer in their last 6 months of life. Facilitated sessions lasted 2.5 hours, included 8 to 10 participants, and focused on choices about Medicare health benefits within the context of a resource-constrained environment.
Results
Six of 15 benefit categories were selected by > 80% of participants: cancer care, prescription drugs, primary care, home care, palliative care, and nursing home coverage. Only 12% of participants chose the maximum level of cancer benefits, a level of care commonly financed in the Medicare program. Between 40% and 50% of participants chose benefits not currently covered by Medicare: unrestricted cash, concurrent palliative care, and home-based long-term care. Nearly one in five participants picked some level of each of these three benefit categories and allocated on average 30% of their resources toward them.
Conclusion
The mismatch between covered benefits and participant preferences shows that addressing quality of life and the financial burden of care is a priority for a substantial subset of patients with cancer in the Medicare program. Patient and caregiver preferences can be elicited, and the choices they express could suggest potential for Medicare benefit package reform and flexibility. (C) 2014 by American Society of Clinical Oncology
C1 [Taylor, Donald H., Jr.] Duke Univ, Sanford Sch Publ Policy, Durham, NC 27708 USA.
[Zafar, S. Yousuf; Howie, Lynn J.; Abernethy, Amy P.] Duke Univ, Duke Clin Res Inst, Durham, NC 27708 USA.
[Samsa, Gregory P.; Wolf, Steven P.] Duke Univ, Med Ctr, Durham, NC 27708 USA.
[Danis, Marion] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Taylor, DH (reprint author), Duke Univ, Box 90253, Durham, NC 27708 USA.
EM don.taylor@duke.edu
FU Agency for Health Care Research and Quality [RO1 HS018360]; National
Institute of Nursing Research [1UC4NR012584]; Department of Bioethics,
an intramural program at the National Institutes of Health
FX Supported in part by Grants No. RO1 HS018360 from the Agency for Health
Care Research and Quality and No. 1UC4NR012584 from the National
Institute of Nursing Research and by the Department of Bioethics, an
intramural program at the National Institutes of Health.
NR 18
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT 1
PY 2014
VL 32
IS 28
BP 3163
EP +
DI 10.1200/JCO.2013.54.2605
PG 9
WC Oncology
SC Oncology
GA AQ3EB
UT WOS:000342671000012
PM 25154830
ER
PT J
AU Joffe, S
Miller, FG
AF Joffe, Steven
Miller, Franklin G.
TI Ethics of Cancer Clinical Trials in Low-Resource Settings
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; METASTATIC BREAST-CANCER;
DEVELOPING-COUNTRIES; PLACEBO; TRANSMISSION; PACLITAXEL; LAPATINIB
C1 [Joffe, Steven] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Miller, Franklin G.] NIH, Bethesda, MD 20892 USA.
RP Joffe, S (reprint author), Univ Penn, Perelman Sch Med, Dept Med Eth & Hlth Policy, 3401 Market St,Suite 320, Philadelphia, PA 19104 USA.
EM joffes@upenn.edu
NR 25
TC 5
Z9 5
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT 1
PY 2014
VL 32
IS 28
BP 3192
EP +
DI 10.1200/JCO.2014.56.9780
PG 6
WC Oncology
SC Oncology
GA AQ3EB
UT WOS:000342671000017
PM 25185082
ER
PT J
AU Hyman, DM
Eaton, AA
Gounder, MM
Ivy, SP
Iasonos, A
Spriggs, DR
AF Hyman, David M.
Eaton, Anne A.
Gounder, Mrinal M.
Ivy, S. Percy
Iasonos, Alexia
Spriggs, David R.
TI Improving Patient Selection for Phase I Oncology Trials Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID DESIGN
C1 [Hyman, David M.; Eaton, Anne A.; Gounder, Mrinal M.; Iasonos, Alexia; Spriggs, David R.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Hyman, David M.; Gounder, Mrinal M.] Weill Cornell Med Coll, New York, NY USA.
[Ivy, S. Percy] NCI, Bethesda, MD 20892 USA.
RP Hyman, DM (reprint author), Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
FU NCI NIH HHS [P30 CA008748]
NR 5
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT 1
PY 2014
VL 32
IS 28
BP 3199
EP U288
DI 10.1200/JCO.2014.56.5762
PG 2
WC Oncology
SC Oncology
GA AQ3EB
UT WOS:000342671000021
PM 25071117
ER
PT J
AU Gornick, MC
Ryan, KA
Kim, SYH
AF Gornick, Michele C.
Ryan, Kerry A.
Kim, Scott Y. H.
TI Impact of Non-Welfare Interests on Willingness to Donate to Biobanks: An
Experimental Survey
SO JOURNAL OF EMPIRICAL RESEARCH ON HUMAN RESEARCH ETHICS
LA English
DT Article
DE informed consent; non-welfare interests; blanket consent; public
attitudes; biobank donation
ID TIME GENERAL CONSENT; BIOLOGICAL SAMPLES; SURROGATE CONSENT; DEMENTIA
RESEARCH; ATTITUDES; SCIENCE; DEBATE; ETHICS; CANCER
AB The ethical debate surrounding biobanks has focused on protecting donors' welfare and privacy. However, little attention has been given to the ethical significance of donor interests that go beyond privacy and welfare (non-welfare interests [NWIs]), such as their concerns about the moral or religious implications of researchers using their donated samples. Using an experimental survey design with 1,276 participants recruited via Amazon Mechanical Turk (MTurk), we studied the potential impact of eight NWI scenarios on people's attitudes toward research studies being performed on samples donated to biobanks by assessing willingness to donate, attitudes toward disclosure of NWIs, impact of timing and format of disclosure (number of NWIs disclosed on a page), and participant factors associated with willingness to donate. Baseline willingness to donate to biobanks prior to any mention of NWIs was comparable with previous studies, at 85% to 89%. Most participants wanted NWI disclosures prior to donation to biobanks, but far fewer favored specific consent. Overall pattern of responses showed that as participants receive more information about NWIs, willingness to donate decreases in a scenario dependent manner. Specifically, NWI concerns about profit seeking research and insurance risk assessment had the strongest impact, even greater than controversial issues such as reproductive research, regardless of political, religious, and most other characteristics of respondents. Based on the results, a schema of NWI types is proposed that could be used for further research and policy discussions.
C1 [Gornick, Michele C.] VA Ann Arbor Ctr Clin Management Res, Ann Arbor, MI USA.
[Gornick, Michele C.] Univ Michigan, Dept Vet Affairs Hlth Serv Res & Dev, Ann Arbor, MI 48109 USA.
[Gornick, Michele C.; Ryan, Kerry A.] Univ Michigan, CBSSM, Ann Arbor, MI 48109 USA.
[Kim, Scott Y. H.] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
RP Kim, SYH (reprint author), NIH, Dept Bioeth, 10 Ctr Dr,1C118, Bethesda, MD 20892 USA.
EM Scott.kim@nih.gov
OI Ryan, Kerry/0000-0002-0582-3693
FU University of Michigan; Department of Veterans Affairs Advanced
Fellowship in Health Services Research Development
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This work
was supported by internal center research funds of the University of
Michigan. Michele C. Gornick is also supported by the Department of
Veterans Affairs Advanced Fellowship in Health Services Research &
Development.
NR 34
TC 5
Z9 5
U1 0
U2 10
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1556-2646
EI 1556-2654
J9 J EMPIR RES HUM RES
JI J. Empir. Res. Hum. Res. Ethics
PD OCT
PY 2014
VL 9
IS 4
BP 22
EP 33
DI 10.1177/1556264614544277
PG 12
WC Ethics; Medical Ethics
SC Social Sciences - Other Topics; Medical Ethics
GA AQ2SA
UT WOS:000342637300003
PM 25747294
ER
PT J
AU Cadman, ME
Murphy, JH
Brintnall-Karabelas, J
Squires, C
Whorton, K
Pao, M
AF Cadman, Mary Ellen
Murphy, Jean H.
Brintnall-Karabelas, Julie
Squires, Carol
Whorton, Katherine
Pao, Maryland
TI A Training Program for Improving the Informed Consent Discussion Between
Clinical Researchers and Their Subjects
SO JOURNAL OF EMPIRICAL RESEARCH ON HUMAN RESEARCH ETHICS
LA English
DT Article
DE informed consent training; communication skills; clinical research;
video
ID QUALITY
AB Although there are many training programs on informed consent, they seldom model the contextual factors that support the vital elements of communication, including presentation style, body language, providing a comfortable environment, utilizing clear language, and establishing overall rapport with the subject. A team of clinicians at the National Institute of Mental Health (NIMH) created a pilot program that consists of a video (http://www.youtube.com/watch?v=l26hdCD9g2I) and didactic presentation to train investigators to conduct informed consent discussions. Thirty-four physicians and eighty nurses were tested on the training content including these contextual factors. Both groups showed an increase in content knowledge after the training. An informed consent training program such as this is feasible and may improve both the knowledge and communication skills necessary for this important process.
C1 [Cadman, Mary Ellen; Murphy, Jean H.; Brintnall-Karabelas, Julie; Squires, Carol; Whorton, Katherine; Pao, Maryland] NIH, Bethesda, MD 20892 USA.
RP Cadman, ME (reprint author), NIMH, Human Subjects Protect Unit, Off Clin Director, 9000 Rockville Pike,Bldg 10,Room 3 N218, Bethesda, MD 20892 USA.
EM marycadman@mail.nih.gov
FU Office of the Clinical Director, National Institute of Mental Health
(NIMH)
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This study
was conducted with the support of the Office of the Clinical Director,
National Institute of Mental Health (NIMH).
NR 9
TC 0
Z9 0
U1 0
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1556-2646
EI 1556-2654
J9 J EMPIR RES HUM RES
JI J. Empir. Res. Hum. Res. Ethics
PD OCT
PY 2014
VL 9
IS 4
BP 71
EP 75
DI 10.1177/1556264614546096
PG 5
WC Ethics; Medical Ethics
SC Social Sciences - Other Topics; Medical Ethics
GA AQ2SA
UT WOS:000342637300008
ER
PT J
AU de Serres, F
Blanco, I
AF Serres, F. de
Blanco, I.
TI Role of alpha-1 antitrypsin in human health and disease
SO JOURNAL OF INTERNAL MEDICINE
LA English
DT Review
DE AAT deficiency; alpha-1 antitrypsin; hereditary disorder; therapy
ID PI-ASTERISK-S; ALPHA(1)-ANTITRYPSIN AUGMENTATION THERAPY; OBSTRUCTIVE
PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; ALPHA1-ANTITRYPSIN DEFICIENCY;
ANTITRYPSIN DEFICIENCY; REPLACEMENT THERAPY; LIVER-DISEASE;
LUNG-FUNCTION; ALPHA-1-PROTEINASE INHIBITOR
AB Alpha-1 antitrypsin (AAT) deficiency is an under-recognized hereditary disorder associated with the premature onset of chronic obstructive pulmonary disease, liver cirrhosis in children and adults, and less frequently, relapsing panniculitis, systemic vasculitis and other inflammatory, autoimmune and neoplastic diseases. Severe AAT deficiency mainly affects Caucasian individuals and has its highest prevalence (1:2000-1:5000 individuals) in Northern, Western and Central Europe. In the USA and Canada, the prevalence is 1: 5000-10000. Prevalence is five times lower in Latin American countries and is rare or nonexistent in African and Asian individuals. The key to successful diagnosis is by measuring serum AAT, followed by the determination of the phenotype or genotype if low concentrations are found. Case detection allows implementation of genetic counselling and, in selected cases, the application of augmentation therapy. Over the past decade, it has been demonstrated that AAT is a broad-spectrum anti-inflammatory, immunomodulatory, anti-infective and tissue-repair molecule. These new capacities are promoting an increasing number of clinical studies, new pharmacological formulations, new patent applications and the search for alternative sources of AAT (including transgenic and recombinant AAT) to meet the expected demand for treating a large number of diseases, inside and outside the context of AAT deficiency.
C1 [Serres, F. de] NIEHS, Natl Toxicol Program, Ctr Evaluat Risks Human Reprod, Res Triangle Pk, NC 27709 USA.
[Blanco, I.] Lung Fdn Breathe, Spanish Soc Pneumol SEPAR, Board Directors Alpha Antitrypsin Deficiency Span, Barcelona, Spain.
RP de Serres, F (reprint author), 632 Rock Creek Rd, Chapel Hill, NC 27514 USA.
EM deserres@bellsouth.net; ignablanco@yahoo.com
NR 143
TC 14
Z9 17
U1 2
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0954-6820
EI 1365-2796
J9 J INTERN MED
JI J. Intern. Med.
PD OCT
PY 2014
VL 276
IS 4
BP 311
EP 335
DI 10.1111/joim.12239
PG 25
WC Medicine, General & Internal
SC General & Internal Medicine
GA AQ3VT
UT WOS:000342722300001
PM 24661570
ER
PT J
AU Abbenhardt, C
McTiernan, A
Alfano, CM
Wener, MH
Campbell, KL
Duggan, C
Foster-Schubert, KE
Kong, A
Toriola, AT
Potter, JD
Mason, C
Xiao, L
Blackburn, GL
Bain, C
Ulrich, CM
AF Abbenhardt, C.
McTiernan, A.
Alfano, C. M.
Wener, M. H.
Campbell, K. L.
Duggan, C.
Foster-Schubert, K. E.
Kong, A.
Toriola, A. T.
Potter, J. D.
Mason, C.
Xiao, L.
Blackburn, G. L.
Bain, C.
Ulrich, C. M.
TI Effects of individual and combined dietary weight loss and exercise
interventions in postmenopausal women on adiponectin and leptin levels
(vol 274, pg 163, 2013)
SO JOURNAL OF INTERNAL MEDICINE
LA English
DT Correction
C1 [Abbenhardt, C.] Natl Ctr Tumor Dis, Heidelberg, Germany.
German Canc Res Ctr, Heidelberg, Germany.
Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
NCI, NIH, Bethesda, MD 20892 USA.
Univ Washington, Seattle, WA 98195 USA.
Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
Washington Univ, Sch Med, St Louis, MO USA.
Massey Univ, Wellington, New Zealand.
Harvard Univ, Sch Med, Boston, MA USA.
Univ Illinois, Chicago, IL USA.
RP Abbenhardt, C (reprint author), Natl Ctr Tumor Dis, Heidelberg, Germany.
NR 2
TC 0
Z9 0
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0954-6820
EI 1365-2796
J9 J INTERN MED
JI J. Intern. Med.
PD OCT
PY 2014
VL 276
IS 4
BP 418
EP 418
DI 10.1111/joim.12305
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA AQ3VT
UT WOS:000342722300011
ER
PT J
AU Wendler, D
Miller, F
AF Wendler, David
Miller, Franklin
TI The ethics of peer review in bioethics
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY; MANUSCRIPTS; IMPROVE; AUTHOR;
BLIND
AB A good deal has been written on the ethics of peer review, especially in the scientific and medical literatures. In contrast, we are unaware of any articles on the ethics of peer review in bioethics. Recognising this gap, we evaluate the extant proposals regarding ethical standards for peer review in general and consider how they apply to bioethics. We argue that scholars have an obligation to perform peer review based on the extent to which they personally benefit from the peer review process. We also argue, contrary to existing proposals and guidelines, that it can be appropriate for peer reviewers to benefit in their own scholarship from the manuscripts they review. With respect to bioethics in particular, we endorse double-blind review and suggest several ways in which the peer review process might be improved.
C1 [Wendler, David; Miller, Franklin] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Wendler, D (reprint author), NIH, Dept Bioeth, Ctr Clin, 10-1C118, Bethesda, MD 20892 USA.
EM dwendler@nih.gov
FU NIH intramural funds
FX Supported by NIH intramural funds.
NR 39
TC 1
Z9 1
U1 2
U2 12
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0306-6800
EI 1473-4257
J9 J MED ETHICS
JI J. Med. Ethics
PD OCT
PY 2014
VL 40
IS 10
BP 697
EP 701
DI 10.1136/medethics-2013-101364
PG 5
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA AQ1VH
UT WOS:000342570900015
PM 24131903
ER
PT J
AU Kulkarni, V
Rosati, M
Jalah, R
Ganneru, B
Alicea, C
Yu, L
Guan, YJ
LaBranche, C
Montefiori, DC
King, AD
Valentin, A
Pavlakis, GN
Felber, BK
AF Kulkarni, Viraj
Rosati, Margherita
Jalah, Rashmi
Ganneru, Brunda
Alicea, Candido
Yu, Lei
Guan, Yongjun
LaBranche, Celia
Montefiori, David C.
King, Alan D.
Valentin, Antonio
Pavlakis, George N.
Felber, Barbara K.
TI DNA vaccination by intradermal electroporation induces long-lasting
immune responses in rhesus macaques
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Article
DE avidity; binding antibody; cellular responses; DNA vaccine; durability
of responses; HIV; neutralizing antibody; SIV
ID GENOME; ALIGNMENT; RNA; SEQUENCES; MODEL; TOOL
AB Background A desirable HIV vaccine should induce protective long-lasting humoral and cellular immune responses. Methods Macaques were immunized by env DNA, selected from a panel of recently transmitted SIVmac251 Env using intradermal electroporation as vaccine delivery method and magnitude, breadth and longevity of humoral and cellular immune responses. Results The macaques developed high, long-lasting humoral immune responses with neutralizing capacity against homologous and heterologous Env. The avidity of the antibody responses was also preserved over 1-year follow-up. Analysis of cellular immune responses demonstrated induction of Env-specific memory T cells harboring granzyme B, albeit their overall levels were low. Similar to the humoral responses, the cellular immunity was persistent over the similar to 1-year follow-up. Conclusion These data show that vaccination by this intradermal DNA delivery regimen is able to induce potent and durable immune responses in macaques.
C1 [Kulkarni, Viraj; Jalah, Rashmi; Alicea, Candido; Felber, Barbara K.] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21702 USA.
[Rosati, Margherita; Ganneru, Brunda; Valentin, Antonio; Pavlakis, George N.] NCI, Human Retrovirus Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21702 USA.
[Yu, Lei; Guan, Yongjun] Univ Maryland, Sch Med, Dept Microbiol & Immunol, Inst Human Virol, Baltimore, MD 21201 USA.
[LaBranche, Celia; Montefiori, David C.] Duke Human Vaccine Inst, Durham, NC USA.
[King, Alan D.] Cyto Pulse Sci Inc, Glen Burnie, MD USA.
RP Felber, BK (reprint author), NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, POB B,Bldg 535,Room 209, Frederick, MD 21702 USA.
EM barbara.felber@nih.gov
FU Intramural NIH HHS [ZIA BC010350-14]; NIAID NIH HHS [R01AI087181, R01
AI087181]; PHS HHS [HHSN27201100016C]
NR 17
TC 2
Z9 2
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
BP 329
EP 340
DI 10.1111/jmp.12123
PG 12
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700006
PM 24810337
ER
PT J
AU Micci, L
Iriele, R
Alvarez, X
Ortiz, A
Midkiff, C
McGary, C
Davenport, M
Estes, J
Lackner, A
Silvestri, G
Paiardini, M
AF Micci, Luca
Iriele, Robin
Alvarez, Xavier
Ortiz, Alex
Midkiff, Cecily
McGary, Colleen
Davenport, Miles
Estes, Jacob
Lackner, Andrew
Silvestri, Guido
Paiardini, Mirko
TI EXPERIMENTAL CD4 DEPLETION PRIOR TO SIV INFECTION IN MACAQUES RESULTS IN
ENCEPHALITIS, MASSIVE MACROPHAGES AND MICROGLIA INFECTION, AND RAPID
TURNOVER OF INFECTED CELLS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Micci, Luca; Iriele, Robin; McGary, Colleen; Silvestri, Guido; Paiardini, Mirko] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Alvarez, Xavier; Midkiff, Cecily; Lackner, Andrew] Tulane Univ, Hlth Sci Ctr, Tulane Natl Primate Res Ctr, Covington, LA USA.
[Ortiz, Alex] NIAID, NIH, Bethesda, MD 20892 USA.
[Davenport, Miles] Univ New S Wales, Sydney, NSW, Australia.
[Estes, Jacob] NCI Frederick, AIDs Canc Virus Program, Frederick, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 4
BP 380
EP 380
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700017
ER
PT J
AU Ayala, V
Trivett, M
Keele, B
Barsov, E
Coren, L
Jain, S
Piatak, M
Estes, J
Gorelick, R
Chertova, E
Smedley, J
Lifson, J
Ott, D
Ohlen, C
AF Ayala, Victor
Trivett, Matthew
Keele, Brandon
Barsov, Eugene
Coren, Lori
Jain, Sumiti
Piatak, Michael
Estes, Jake
Gorelick, Robert
Chertova, Elena
Smedley, Jeremy
Lifson, Jeffrey
Ott, David
Ohlen, Claes
TI ADOPTIVE TRANSFER OF GENETICALLY ENGINEERED SIV-SPECIFIC T CELLS LIMITS
THE NUMBER OF SIV FOUNDER VIRUSES IN RHESUS MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Ayala, Victor; Trivett, Matthew; Keele, Brandon; Barsov, Eugene; Coren, Lori; Jain, Sumiti; Piatak, Michael; Estes, Jake; Gorelick, Robert; Chertova, Elena; Lifson, Jeffrey; Ott, David; Ohlen, Claes] SAIC Frederick Inc, AIDs & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Smedley, Jeremy] SAIC Frederick Inc, Lab Anim Sci Program, Frederick Natl Lab Canc Res, Frederick, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 10
BP 382
EP 383
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700023
ER
PT J
AU Haigwood, NL
Jaworski, JP
Kobie, J
Sutton, WF
Lewis, A
Axthelm, MK
Mascola, J
Graham, B
Hessell, AJ
AF Haigwood, Nancy L.
Jaworski, J. Pablo
Kobie, James
Sutton, William F.
Lewis, Anne
Axthelm, Michael K.
Mascola, John
Graham, Barney
Hessell, Ann J.
TI REDUCING VIRAL RESERVOIRS IN A NONHUMAN PRIMATE MODEL FOR
MOTHER-TO-CHILD-TRANSMISSION USING NEUTRALIZING ANTIBODIES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Haigwood, Nancy L.; Jaworski, J. Pablo; Sutton, William F.; Lewis, Anne; Axthelm, Michael K.; Hessell, Ann J.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Beaverton, OR USA.
[Haigwood, Nancy L.; Axthelm, Michael K.; Hessell, Ann J.] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Beaverton, OR USA.
[Haigwood, Nancy L.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Kobie, James] Univ Rochester, New York, NY USA.
[Mascola, John; Graham, Barney] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 8
BP 382
EP 382
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700021
ER
PT J
AU Hatziioannou, T
Bitzegeio, J
Raymond, A
Rodriguez, A
McNatt, M
Keele, B
Del Prete, G
Estes, J
Mac Trubey, C
Smedley, J
Piatak, M
Ramani, VNK
Lifson, JD
Bieniasz, PD
AF Hatziioannou, Theodora
Bitzegeio, Julia
Raymond, Alice
Rodriguez, Anthony
McNatt, Matthew
Keele, Brandon
Del Prete, Gregory
Estes, Jacob
Mac Trubey, C.
Smedley, Jeremy
Piatak, Michael, Jr.
Ramani, Vineet N. Kewal
Lifson, Jeffrey D.
Bieniasz, Paul D.
TI HIV-1 INDUCED AIDS IN MONKEYS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Hatziioannou, Theodora; Bitzegeio, Julia; Raymond, Alice; Rodriguez, Anthony; McNatt, Matthew; Bieniasz, Paul D.] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10021 USA.
[McNatt, Matthew; Bieniasz, Paul D.] Rockefeller Univ, Lab Retrovirol, New York, NY 10021 USA.
[Keele, Brandon; Del Prete, Gregory; Estes, Jacob; Mac Trubey, C.; Piatak, Michael, Jr.; Lifson, Jeffrey D.] SAIC Frederick Inc, AIDs & Canc Virus Program, Frederick Natl Lab, Frederick, MD USA.
[Smedley, Jeremy] SAIC Frederick Inc, Lab Anim Sci Program, Frederick Natl Lab, Frederick, MD USA.
[Ramani, Vineet N. Kewal] NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA.
[Bieniasz, Paul D.] Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 11
BP 383
EP 383
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700024
ER
PT J
AU Hao, XP
Morcock, D
Johnston, L
Smedley, J
Brenchley, JM
Lifson, J
Estes, JD
AF Hao, Xing Pei
Morcock, David
Johnston, Leslie
Smedley, Jeremy
Brenchley, Jason M.
Lifson, Jeffrey
Estes, Jacob D.
TI ESTABLISHMENT OF AN EXPERIMENTAL MODEL OF ACUTE COLITIS IN SIV-NEGATIVE
RHESUS MACAQUES: IMPACT OF GI EPITHELIAL DAMAGE ON SYSTEMIC IMMUNE
ACTIVATION IN THE ABSENCE OF LENTIVIRAL INFECTION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Hao, Xing Pei] SAIC Frederick Inc, Pathol & Histotechnol Lab, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Morcock, David; Johnston, Leslie; Lifson, Jeffrey; Estes, Jacob D.] SAIC Frederick Inc, AIDs & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Smedley, Jeremy] SAIC Frederick Inc, Lab Anim Sci Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Brenchley, Jason M.] NIID, Mol Microbiol Lab, NIH, Bethesda, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 17
BP 385
EP 386
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700030
ER
PT J
AU Bosinger, S
Ortiz, A
Folkner, K
Patel, N
Cervasi, B
Gill, K
Johnson, Z
Silvestri, G
AF Bosinger, Steve
Ortiz, Alexandra
Folkner, Kathryn
Patel, Nirav
Cervasi, Barbara
Gill, Kiran
Johnson, Zach
Silvestri, Guido
TI COMPREHENSIVE TRANSCRIPTOME ANALYSIS OF THE T CELL COMPARTMENT IN
PRIMATE HOSTS OF HIV AND SIV
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Bosinger, Steve; Folkner, Kathryn; Cervasi, Barbara; Gill, Kiran; Silvestri, Guido] Yerkes Natl Primate Res Ctr, Div Microbiol & Immunol, Atlanta, GA USA.
[Bosinger, Steve; Patel, Nirav; Johnson, Zach] Yerkes Natl Primate Res Ctr, Yerkes NonHuman Primate Genom Core, Atlanta, GA USA.
[Ortiz, Alexandra] NIAID, Mol Microbiol Lab, Viral Pathogenesis & Vaccine Sect, NIH, Atlanta, GA 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 19
BP 386
EP 386
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700032
ER
PT J
AU McGinnis, K
Nguyen, R
Song, KM
Roederer, M
Bolton, DL
AF McGinnis, Katie
Nguyen, Richard
Song, Kaimei
Roederer, Mario
Bolton, Diane L.
TI GENE EXPRESSION AND PHENOTYPIC ANALYSIS OF SIV PRODUCTIVELY INFECTED
CD4+T-CELLS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [McGinnis, Katie; Nguyen, Richard; Song, Kaimei; Roederer, Mario] NIAID, Immunotechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Bolton, Diane L.] Reed Army Inst Res, Us Mil HIV Res Program, Silver Spring, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 28
BP 390
EP 390
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700041
ER
PT J
AU Smedley, J
Turkbey, IB
Bernardo, ML
Del Prete, GQ
Estes, JD
Choyke, PL
Lifson, JD
Keele, BF
AF Smedley, Jeremy
Turkbey, I. Baris
Bernardo, Marcelino L.
Del Prete, Gregory Q.
Estes, Jacob D.
Choyke, Peter L.
Lifson, Jeffrey D.
Keele, Brandon F.
TI TRACKING THE LUMINAL EXPOSURE AND LYMPHATIC DRAINAGE OF INTRAVAGINAL AND
INTRARECTAL INOCULA
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Smedley, Jeremy] NCI, Lab Anim Sci Program, Bethesda, MD 20892 USA.
[Turkbey, I. Baris; Bernardo, Marcelino L.; Choyke, Peter L.] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
[Del Prete, Gregory Q.; Estes, Jacob D.; Lifson, Jeffrey D.; Keele, Brandon F.] SAIC Frederick Inc, AIDs & Canc Virus Program, Frederick Natl Lab, Frederick, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 29
BP 390
EP 390
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700042
ER
PT J
AU Shingai, M
Nishimura, Y
Klein, F
Mouquet, H
Donau, OK
Plishka, R
Buckler-White, A
Piatak, M
Lifson, JD
Nussenzweig, MC
Martin, MA
AF Shingai, Masashi
Nishimura, Yoshiaki
Klein, Florian
Mouquet, Hugo
Donau, Olivia K.
Plishka, Ronald
Buckler-White, Alicia
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Nussenzweig, Michel C.
Martin, Malcolm A.
TI ANTIBODY MEDIATED IMMUNOTHERAPY OF MACAQUES CHRONICALLY INFECTED WITH
SHIV SUPPRESSES VIREMIA
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Shingai, Masashi; Nishimura, Yoshiaki; Donau, Olivia K.; Plishka, Ronald; Buckler-White, Alicia; Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Klein, Florian; Nussenzweig, Michel C.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA.
[Mouquet, Hugo] Inst Pasteur, Dept Immunol, Lab Humoral Response Pathogens, Paris, France.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, AIDs & Canc Virus Program, Frederick, MD USA.
[Nussenzweig, Michel C.] Howard Hughes Med Inst, Chevy Chase, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 36
BP 393
EP 394
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700049
ER
PT J
AU Chowdhury, A
Estrada, PMD
Reuter, M
Hayes, T
Bosinger, SE
Paiardini, M
Estes, JD
Betts, M
Silvestri, G
AF Chowdhury, Ankita
Estrada, Perla M. del Rio
Reuter, Morgan
Hayes, Timothy
Bosinger, Steven E.
Paiardini, Mirko
Estes, Jacob D.
Betts, Michael
Silvestri, Guido
TI TROGOCYTOSIS BETWEEN TFH AND GERMINAL CENTER B CELLS DURING PRIMARY
IMMUNE RESPONSE IN PRIMATES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Chowdhury, Ankita; Estrada, Perla M. del Rio; Hayes, Timothy; Bosinger, Steven E.; Paiardini, Mirko; Silvestri, Guido] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Reuter, Morgan; Betts, Michael] Univ Penn, Perelman Sch Med, Dept Microbiol, Philadelphia, PA 19104 USA.
[Estes, Jacob D.] NCI, AIDs & Canc Virus Program, sAIC Frederick Inc, Frederick, MD 21701 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 39
BP 395
EP 395
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700052
ER
PT J
AU Foulds, KE
Keele, BF
Mason, RD
Welles, HC
Schmidt, SD
Mascola, JR
Roederer, M
AF Foulds, Kathryn E.
Keele, Brandon F.
Mason, Rosemarie D.
Welles, Hugh C.
Schmidt, Stephen D.
Mascola, John R.
Roederer, Mario
TI DIFFERENTIAL VACCINE EFFICACY BY VIRAL SPECIES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Foulds, Kathryn E.; Mason, Rosemarie D.; Welles, Hugh C.; Schmidt, Stephen D.; Mascola, John R.; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Keele, Brandon F.] Frederick Natl Lab, AIDs & Canc Virus Program, sAIC Frederick Inc, Frederick, MD USA.
OI Welles, Hugh/0000-0002-3336-1203
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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 44
BP 397
EP 397
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700057
ER
PT J
AU Sui, YJ
Hogg, A
Wang, YC
Frey, B
Yu, HF
Xia, Z
Venzon, D
Smedley, J
Gathuka, M
Klinman, D
Keele, BF
Langermann, S
Liu, LD
Franchini, G
Berzofsky, JA
AF Sui, Yong Jun
Hogg, Alison
Wang, Yichuan
Frey, Blake
Yu, Huifeng
Xia, Zheng
Venzon, David
Smedley, Jeremy
Gathuka, Mercy
Klinman, Dennis
Keele, Brandon F.
Langermann, Sol
Liu, Linda
Franchini, Genoveffa
Berzofsky, Jay A.
TI MUCOSAL ADJUVANTS AND MYELOID CELLS MODULATE VIRAL LOAD REDUCTION IN
SIVMAC251-INFECTION OF MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Sui, Yong Jun; Hogg, Alison; Wang, Yichuan; Frey, Blake; Yu, Huifeng; Xia, Zheng; Franchini, Genoveffa; Berzofsky, Jay A.] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Smedley, Jeremy; Gathuka, Mercy] NCI, Lab Anim Sci Program, NIH, Bethesda, MD 20892 USA.
[Klinman, Dennis] NCI, Expt Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Keele, Brandon F.] NCI, AIDs & Canc Virus Program, sAIC Frederick, NIH, Bethesda, MD 20892 USA.
[Langermann, Sol; Liu, Linda] Amplimmune Inc, Gaithersburg, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 45
BP 397
EP 397
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700058
ER
PT J
AU Nishimura, Y
Shingai, M
Donau, OK
Plishka, RJ
Buckler-White, A
Mascola, JR
Nabel, GJ
Nason, MC
Montefiori, D
Moldt, B
Poignard, P
Diskin, R
Bjorkman, PJ
Klein, F
Mouquet, H
Burton, DR
Nussenzweig, MC
Martin, MA
AF Nishimura, Yoshiaki
Shingai, Masashi
Donau, Olivia K.
Plishka, Ronald J.
Buckler-White, Alicia
Mascola, John R.
Nabel, Gary J.
Nason, Martha C.
Montefiori, David
Moldt, Brian
Poignard, Pascal
Diskin, Ron
Bjorkman, Pamela J.
Klein, Florian
Mouquet, Hugo
Burton, Dennis R.
Nussenzweig, Michel C.
Martin, Malcolm A.
TI PREEXPOSURE PASSIVE TRANSFER PREDICTS PLASMA ANTIBODY LEVELS TO PREVENT
HIV-1 AQUISITION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Nishimura, Yoshiaki; Shingai, Masashi; Donau, Olivia K.; Plishka, Ronald J.; Buckler-White, Alicia; Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Mascola, John R.; Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Nason, Martha C.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Montefiori, David] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
[Moldt, Brian; Poignard, Pascal; Burton, Dennis R.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Moldt, Brian; Poignard, Pascal; Burton, Dennis R.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
[Moldt, Brian; Poignard, Pascal; Burton, Dennis R.] Scripps Res Inst, Ctr HIV AIDs Vaccine Immunol & Immunogen Discover, La Jolla, CA 92037 USA.
[Diskin, Ron; Bjorkman, Pamela J.] CALTECH, Div Biol, Pasadena, CA 91125 USA.
[Bjorkman, Pamela J.; Nussenzweig, Michel C.] Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10021 USA.
[Klein, Florian; Mouquet, Hugo; Nussenzweig, Michel C.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA.
[Burton, Dennis R.] Ragon Inst Massachusetts Gen Hosp Massachusetts I, Boston, MA USA.
RI poignard, pascal/N-6678-2013
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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 47
BP 398
EP 398
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700060
ER
PT J
AU Byrareddy, SN
Dunbar, P
Little, D
Zhao, CX
Yang, GX
Sidell, N
Pierzchalski, K
Kane, MA
Arthos, J
Cicala, C
Mayne, A
Soares, MA
Villinger, F
Ansari, AA
AF Byrareddy, Siddappa N.
Dunbar, Paul
Little, Dawn
Zhao, Chunxia
Yang, Gui X.
Sidell, Neil
Pierzchalski, Keely
Kane, Maureen A.
Arthos, Jim
Cicala, Claudia
Mayne, Ann
Soares, Marcelo A.
Villinger, Francois
Ansari, Aftab A.
TI SPECIES-SPECIFIC DIFFERENCES IN THE REGULATION OF ALPHA4 BETA7 (alpha 4
beta 7) EXPRESSION IN VARIOUS NON HUMAN PRIMATES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Byrareddy, Siddappa N.; Dunbar, Paul; Little, Dawn; Mayne, Ann; Villinger, Francois; Ansari, Aftab A.] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
[Zhao, Chunxia; Villinger, Francois] Yerkes Natl Primate Ctr, Atlanta, GA USA.
[Yang, Gui X.; Sidell, Neil] Emory Univ, Sch Med, Dept Gynecol & Obstet, Atlanta, GA USA.
[Pierzchalski, Keely; Kane, Maureen A.] Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, Baltimore, MD 21201 USA.
[Arthos, Jim; Cicala, Claudia] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Soares, Marcelo A.] Univ Fed Rio de Janeiro, Lab Human Virol, BR-21941 Rio De Janeiro, Brazil.
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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 62
BP 404
EP 404
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700075
ER
PT J
AU Hayes, T
Bosinger, S
Chowdhury, A
Lawson, B
Cervasi, B
Gill, K
Paiardini, M
Estes, J
Silvestri, G
AF Hayes, Timothy
Bosinger, Steven
Chowdhury, Ankita
Lawson, Benton
Cervasi, Barbara
Gill, Kiran
Paiardini, Mirko
Estes, Jacob
Silvestri, Guido
TI MECHANISMS OF SIV SUPPRESSION BY CD8+LYMPHOCYTES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Hayes, Timothy; Bosinger, Steven; Chowdhury, Ankita; Lawson, Benton; Cervasi, Barbara; Gill, Kiran; Paiardini, Mirko; Silvestri, Guido] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Estes, Jacob] Frederick Natl Lab Canc Res, AIDs & Canc Virus Program, Frederick, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 61
BP 404
EP 404
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700074
ER
PT J
AU Adnan, S
Colantonio, AD
Yu, Y
Gillis, J
Wong, FE
Becker, EA
Piatak, M
Lifson, JD
O'Connor, SL
Johnson, RP
AF Adnan, Sama
Colantonio, Arnaud D.
Yu, Yi
Gillis, Jackie
Wong, Fay E.
Becker, Ericka A.
Piatak, Michael, Jr.
Lifson, Jeffrey D.
O'Connor, Shelby L.
Johnson, R. Paul
TI ESCAPE IN SIVDNEF REFOCUSES THE CD8 T CELL RESPONSE ON MORE CONSERVED
EPITOPES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Adnan, Sama; Colantonio, Arnaud D.; Yu, Yi; Gillis, Jackie; Wong, Fay E.; Johnson, R. Paul] Harvard Univ, Sch Med, New England Primate Res Ctr, Div Immunol, Southborough, MA 01772 USA.
[Becker, Ericka A.; O'Connor, Shelby L.] Univ Wisconsin, Wisconsin Natl Primate Res Ctr, Madison, WI USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] NCI, AIDs & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21701 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 71
BP 408
EP 408
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700084
ER
PT J
AU Felber, BK
Kulkarni, V
Valentin, A
Hu, XT
Rosati, M
Alicea, C
Sardesai, NY
Le Gall, S
Mothe, B
Brander, C
Rolland, M
Mullins, JI
Pavlakis, GN
AF Felber, Barbara K.
Kulkarni, Viraj
Valentin, Antonio
Hu, Xintao
Rosati, Margherita
Alicea, Candido
Sardesai, Niranjan Y.
Le Gall, Sylvie
Mothe, Beatriz
Brander, Christian
Rolland, Morgane
Mullins, James I.
Pavlakis, George N.
TI ALTERED IMMUNODOMINANCE HIERARCHY AND INCREASED T-CELL BREADTH UPON
HIV-1 CONSERVED ELEMENT DNA VACCINATION IN MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Felber, Barbara K.; Kulkarni, Viraj; Hu, Xintao; Alicea, Candido] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21701 USA.
[Valentin, Antonio; Rosati, Margherita; Pavlakis, George N.] NCI, Human Retrovirus Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21701 USA.
[Sardesai, Niranjan Y.] Inovio Pharmaceut Inc, Blue Bell, PA USA.
[Le Gall, Sylvie] MIT & Harvard, Ragon Inst MGH, Boston, MA USA.
[Mothe, Beatriz; Brander, Christian] Autonomous Univ Barcelona, IrsiCaixa AIDs Res Inst HIVACAT, Barcelona, Spain.
[Brander, Christian] ICREA, Barcelona, Spain.
[Rolland, Morgane; Mullins, James I.] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Mullins, James I.] Univ Washington, Seattle, WA 98195 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 75
BP 410
EP 410
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700088
ER
PT J
AU Pavlakis, GN
Jalah, R
Li, JY
Valentin, A
Rosati, M
Patel, V
Kulkarni, V
Alicea, C
Kelly, RB
Guan, YJ
Lifson, JD
Hirsch, VM
Venzon, D
Broderick, KE
Sardesai, NY
Fouts, TR
Pinter, A
Labranche, C
Montefiori, DC
Shen, S
Tomaras, GD
Felber, BK
AF Pavlakis, George N.
Jalah, Rashmi
Li, Jinyao
Valentin, Antonio
Rosati, Margherita
Patel, Vainav
Kulkarni, Viraj
Alicea, Candido
Kelly, Rachel Beach
Guan, Yong Jun
Lifson, Jeffrey D.
Hirsch, Vanessa M.
Venzon, David
Broderick, Kate E.
Sardesai, Niranjan Y.
Fouts, Timothy R.
Pinter, Abraham
Labranche, Celia
Montefiori, David C.
Shen, Shaunna
Tomaras, Georgia D.
Felber, Barbara K.
TI OPTIMIZATION OF SYSTEMIC AND MUCOSAL IMMUNE RESPONSES TO SIV AND HIV-1
ANTIGENS USING DIFFERENT PROTOCOLS OF DNA AND PROTEIN IMMUNIZATION IN
MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Pavlakis, George N.; Li, Jinyao; Valentin, Antonio; Rosati, Margherita; Patel, Vainav; Kelly, Rachel Beach] NCI, Human Retrovirus Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21701 USA.
[Jalah, Rashmi; Kulkarni, Viraj; Alicea, Candido; Kelly, Rachel Beach; Felber, Barbara K.] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21701 USA.
[Guan, Yong Jun] Inst Human Virol, Baltimore, MD USA.
[Lifson, Jeffrey D.] NCI, AIDs & Canc Virus Program, SAIC Frederick, Frederick, MD 21701 USA.
[Hirsch, Vanessa M.] NIAID, Viral Pathogenesis & Vaccine Sect, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Broderick, Kate E.; Sardesai, Niranjan Y.] Inovio Pharmaceut Inc, Blue Bell, PA USA.
[Fouts, Timothy R.] Univ Med & Dent New Jersey, Publ Hlth Res Inst, Newark, NJ 07103 USA.
[Pinter, Abraham] Profectus Biosci Inc, Baltimore, MD USA.
[Labranche, Celia; Montefiori, David C.; Shen, Shaunna; Tomaras, Georgia D.] Duke Univ, Med Ctr, Dept Surg, Lab AIDs Vaccine Res & Dev, Durham, NC 27710 USA.
RI Tomaras, Georgia/J-5041-2016; bebarta, vikhyat/K-3476-2015
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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 76
BP 410
EP 410
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700089
ER
PT J
AU Goode, D
Truong, R
Guerra-Perez, N
Arthos, J
Piatak, M
Lifson, JD
Blanchard, J
Gettie, A
Robbiani, M
Martinelli, E
AF Goode, Diana
Truong, Rosaline
Guerra-Perez, Natalia
Arthos, James
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Blanchard, James
Gettie, Agegnehu
Robbiani, Melissa
Martinelli, Elena
TI THE FREQUENCY OF alpha(4)beta(7)HIGH CD4+T CELLS IN BLOOD CORRELATES
WITH SIV INFECTION IN-VIVO RECTALLY AND EX-VIVO
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Goode, Diana; Truong, Rosaline; Guerra-Perez, Natalia; Robbiani, Melissa; Martinelli, Elena] Populat Council, Ctr Biomed Res, New York, NY 10021 USA.
[Arthos, James] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] NCI, AIDs & Canc Virus Program, SAIC Frederick, Frederick, MD 21701 USA.
[Blanchard, James] Tulane Natl Primate Res Ctr, Covington, LA USA.
[Gettie, Agegnehu] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10021 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 95
BP 418
EP 418
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700108
ER
PT J
AU Shen, XY
Williams, W
Yates, N
Francica, J
Reimann, K
Montefiori, D
McElrath, J
Seder, R
Tomaras, G
AF Shen, Xiaoying
Williams, William
Yates, Nicole
Francica, Joe
Reimann, Keith
Montefiori, David
McElrath, Julie
Seder, Robert
Tomaras, Georgia
TI HIV ENV-SPECIFIC IGG3 RESPONSES ARE DIFFERENTIALLY ELICITED IN NONHUMAN
PRIMATE BY ENV VACCINES WITH DIFFERENT ADJUVANTS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Shen, Xiaoying; Williams, William; Yates, Nicole; Tomaras, Georgia] Duke Univ, Duke Human Vaccine Inst, Durham, NC USA.
[Francica, Joe; Seder, Robert] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Reimann, Keith] Univ Massachusetts Med Sch, Worcester, MA USA.
[Montefiori, David] Duke Univ, Dept Surg, Durham, NC USA.
[McElrath, Julie] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 104
BP 421
EP 421
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700117
ER
PT J
AU Munson, P
Bratt, D
Agricola, B
Koday, M
Treants, M
Fuller, J
Kulkarni, V
Felber, BK
Pavlakis, GN
Liu, Y
Mullins, JI
Fuller, D
AF Munson, Paul
Bratt, Deborah
Agricola, Brian
Koday, Mike
Treants, Merika
Fuller, Jim
Kulkarni, Viraj
Felber, Barbara K.
Pavlakis, George N.
Liu, Yi
Mullins, James I.
Fuller, Deborah
TI THERAPEUTIC CONSERVED ELEMENTS (CE) DNA VACCINE INDUCES STRONG T-CELL
RESPONSES AGAINST HIGHLY CONSERVED VIRAL SEQUENCES IN THE SETTING OF
PRE-EXISTING IMMUNODOMINANT RESPONSES INDUCED BY CHRONIC VIRAL INFECTION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Munson, Paul; Treants, Merika; Fuller, Jim; Liu, Yi; Mullins, James I.; Fuller, Deborah] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Munson, Paul; Bratt, Deborah; Agricola, Brian; Koday, Mike; Treants, Merika; Fuller, Deborah] Univ Washington Natl Primate Res Ctr, Seattle, WA USA.
[Kulkarni, Viraj; Felber, Barbara K.] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21701 USA.
[Pavlakis, George N.] NCI, Human Retrovirus Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21701 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 110
BP 423
EP 424
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700123
ER
PT J
AU Richert-Spuhler, LE
Koday, M
Brenchley, JM
Estes, JD
Keele, BF
Klatt, NR
AF Richert-Spuhler, Laura E.
Koday, Michael
Brenchley, Jason M.
Estes, Jacob D.
Keele, Brandon F.
Klatt, Nichole R.
TI RAPID LOSS OF IL-17 AND IL-22 PRODUCING CD4+T CELLS AFTER SIV INFECTION
OF RHESUS MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Richert-Spuhler, Laura E.; Koday, Michael; Klatt, Nichole R.] Univ Washington, Dept Pharmaceut, Washington Natl Primate Res Ctr, Seattle, WA 98195 USA.
[Brenchley, Jason M.; Estes, Jacob D.] Natl Inst Infect Dis, Mol Microbiol Lab, NIH, Bethesda, MD USA.
[Keele, Brandon F.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, AIDs & Canc Virus Program, Frederick, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 109
BP 423
EP 423
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700122
ER
PT J
AU Jain, S
Barsov, E
Ayala, V
Trivett, M
Coren, L
Ohlen, C
Ott, D
AF Jain, Sumiti
Barsov, Eugene
Ayala, Victor
Trivett, Matthew
Coren, Lori
Ohlen, Claes
Ott, David
TI VIRUS-SPECIFIC CD4+T CELLS EXPRESSING CROSS-SPECIES TRIM 5-ALPHA GENES
RESTRICT SIV INFECTION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Jain, Sumiti; Barsov, Eugene; Ayala, Victor; Trivett, Matthew; Coren, Lori; Ohlen, Claes; Ott, David] SAIC Frederick Inc, AIDs & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 127
BP 430
EP 430
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700140
ER
PT J
AU Matsuda, K
Wu, F
Goeken, R
Riddick, N
Ourmanov, I
Plishka, R
Buckler-White, A
Hirsch, V
AF Matsuda, Kenta
Wu, Fan
Goeken, Robert
Riddick, Nadeene
Ourmanov, Ilnour
Plishka, Ronald
Buckler-White, Alicia
Hirsch, Vanessa
TI MUTATIONS AT CYTOPLASMIC TAIL OF GP41 ENHANCE REPLICATION OF SIVSME543-3
IN MACROPHAGES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Matsuda, Kenta; Wu, Fan; Goeken, Robert; Riddick, Nadeene; Ourmanov, Ilnour; Plishka, Ronald; Buckler-White, Alicia; Hirsch, Vanessa] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 126
BP 430
EP 430
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700139
ER
PT J
AU Riddick, NE
Goeken, RM
Whitted, S
Hirsch, VM
AF Riddick, Nadeene E.
Goeken, Robert M.
Whitted, Sonya
Hirsch, Vanessa M.
TI EXAMINATION OF CCR5 DEPENDENCE BY SIV DERIVED FROM NATURAL AND
NON-NATURAL HOSTS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Riddick, Nadeene E.; Goeken, Robert M.; Whitted, Sonya; Hirsch, Vanessa M.] NIAID, Mol Med Lab, NIH, Bethesda, MD 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 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2014
VL 43
IS 5
MA 128
BP 430
EP 430
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA AQ3EZ
UT WOS:000342673700141
ER
PT J
CA Nat Genetics
TI Genetic Risk Factors for Parkinson Disease
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Editorial Material
C1 [Nat Genetics] NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT
PY 2014
VL 55
IS 10
BP 21N
EP 22N
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AQ3SA
UT WOS:000342712600007
ER
PT J
AU Dwyer, JT
Saldanha, LG
Bailen, RA
Bailey, RL
Costello, RB
Betz, JM
Chang, FF
Goshorn, J
Andrews, KW
Pehrsson, PR
Milner, JA
Burt, VL
Gahche, JJ
Hardy, CJ
Emenaker, NJ
AF Dwyer, Johanna T.
Saldanha, Leila G.
Bailen, Richard A.
Bailey, Regan L.
Costello, Rebecca B.
Betz, Joseph M.
Chang, Florence F.
Goshorn, Jeanne
Andrews, Karen W.
Pehrsson, Pamela R.
Milner, John A.
Burt, Vicki L.
Gahche, Jaime J.
Hardy, Constance J.
Emenaker, Nancy J.
TI A Free New Dietary Supplement Label Database for Registered Dietitian
Nutritionists
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Editorial Material
ID UNITED-STATES; NATIONAL-HEALTH; AMERICA-NHANES; US ADULTS; ADOLESCENTS;
MINERALS; CHILDREN; FOOD; EAT
C1 [Dwyer, Johanna T.; Saldanha, Leila G.; Bailen, Richard A.; Bailey, Regan L.; Costello, Rebecca B.; Betz, Joseph M.] NIH, Dietary Supplement Analyt Methods & Reference Mat, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Chang, Florence F.; Goshorn, Jeanne] NIH, Biomed Informat Serv Branch, Specialized Informat Serv Div, Natl Lib Med, Bethesda, MD USA.
[Andrews, Karen W.; Pehrsson, Pamela R.; Milner, John A.] ARS, US Dept Agr Human, Nutr Res Ctr, Beltsville, MD USA.
[Burt, Vicki L.; Gahche, Jaime J.] Natl Ctr Hlth Stat, Hyattsville, MD 20782 USA.
[Hardy, Constance J.] US FDA, Ctr Food Sci & Nutr, College Pk, MD USA.
[Emenaker, Nancy J.] NCI, Canc Prevent Div, Nutr Sci Grp, Bethesda, MD USA.
RP Dwyer, JT (reprint author), NIH, Dietary Supplement Analyt Methods & Reference Mat, Off Dietary Supplements, Bldg 10, Bethesda, MD 20892 USA.
OI Dwyer, Johanna/0000-0002-0783-1769
FU Intramural CDC HHS [CC999999]
NR 21
TC 1
Z9 1
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
EI 2212-2680
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD OCT
PY 2014
VL 114
IS 10
BP 1512
EP +
DI 10.1016/j.jand.2014.04.015
PG 4
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AQ2JD
UT WOS:000342610700002
PM 24928780
ER
PT J
AU Eckhardt, CL
Lutz, T
Karanja, N
Jobe, JB
Maupome, G
Ritenbaugh, C
AF Eckhardt, Cara L.
Lutz, Tam
Karanja, Njeri
Jobe, Jared B.
Maupome, Gerardo
Ritenbaugh, Cheryl
TI Knowledge, Attitudes, and Beliefs that Can Influence Infant Feeding
Practices in American Indian Mothers
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Article
DE American Indian/Alaska Native; Breastfeeding; Infant feeding; Solid
foods; Knowledge, attitudes, and beliefs
ID OF-THE-LITERATURE; OBESITY PREVENTION; ALASKA NATIVES; BREAST; CHILDREN;
WEIGHT; ASSOCIATION; BEHAVIORS; COMMUNITY; TODDLERS
AB The promotion of healthy infant feeding is increasingly recognized as an important obesity-prevention strategy. This is relevant for American Indian populations that exhibit high levels of obesity and low compliance with infant feeding guidelines. The literature examining the knowledge, attitudes, and beliefs surrounding infant feeding within the American Indian population is sparse and focuses primarily on breastfeeding, with limited information on the introduction of solid foods and related practices that can be important in an obesity-prevention context. This research presents descriptive findings from a baseline knowledge, attitudes, and beliefs questionnaire on infant feeding and related behaviors administered to mothers (n=438) from five Northwest American Indian tribes that participated in the Prevention of Toddler Overweight and Teeth Health Study (PTOTS). Enrollment occurred during pregnancy or up to 6 months postpartum. The knowledge, attitudes, and beliefs questionnaire focused on themes of breastfeeding/formula feeding and introducing solid foods, with supplemental questions on physical activity. Knowledge questions were multiple choice or true/false. Attitudes and beliefs were assessed on Likert scales. Descriptive statistics included frequencies and percents and means and standard deviations. Most women knew basic breastfeeding recommendations and facts, but fewer recognized the broader health benefits of breastfeeding (eg, reducing diabetes risk) or knew when to introduce solid foods. Women believed breastfeeding to be healthy and perceived their social networks to agree. Attitudes and beliefs about formula feeding and social support were more ambivalent. This Work suggests opportunities to increase the perceived value of breastfeeding to include broader health benefits, increase knowledge about solid foods, and strengthen social support.
C1 [Eckhardt, Cara L.] Portland State Univ, Sch Community Hlth, Portland, OR 97201 USA.
[Lutz, Tam] Northwest Portland Area Indian Hlth Board, Portland, OR USA.
[Karanja, Njeri] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
[Jobe, Jared B.] NHLBI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Maupome, Gerardo] Indiana Univ, Sch Dent, Indianapolis, IN 46204 USA.
[Ritenbaugh, Cheryl] Univ Arizona, Dept Family & Community Med, Tucson, AZ USA.
RP Eckhardt, CL (reprint author), Portland State Univ, Sch Community Hlth, 506 SW Mill St,Suite 450, Portland, OR 97201 USA.
EM c.eckhardt@pdx.edu
OI Maupome, Gerardo/0000-0002-3590-0864
FU National Institutes of Health, through the National Heart, Lung, and
Blood Institute [U01 HL081624]
FX Funding and support for this project came from the National Institutes
of Health grant "Primordial Prevention of Overweight in Al Children"
(U01 HL081624), through the National Heart, Lung, and Blood Institute.
NR 30
TC 1
Z9 1
U1 3
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
EI 2212-2680
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD OCT
PY 2014
VL 114
IS 10
BP 1587
EP 1593
DI 10.1016/j.jand.2014.04.021
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AQ2JD
UT WOS:000342610700011
PM 24951434
ER
PT J
AU Gao, F
Kasprzak, WK
Szarko, C
Shapiro, BA
Simon, AE
AF Gao, Feng
Kasprzak, Wojciech K.
Szarko, Christine
Shapiro, Bruce A.
Simon, Anne E.
TI The 3 ' Untranslated Region of Pea Enation Mosaic Virus Contains Two
T-Shaped, Ribosome-Binding, Cap-Independent Translation Enhancers
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TURNIP CRINKLE VIRUS; MINUS-STRAND SYNTHESIS; RNA-RNA INTERACTION;
VIRAL-RNA; MESSENGER-RNA; PLANT-VIRUS; INITIATION; PROTEIN; REPLICATION;
TOMBUSVIRIDAE
AB Many plant viruses without 5' caps or 3' poly(A) tails contain 3' proximal, cap-independent translation enhancers (3'CITEs) that bind to ribosomal subunits or translation factors thought to assist in ribosome recruitment. Most 3'CITEs participate in a long-distance kissing-loop interaction with a 5' proximal hairpin to deliver ribosomal subunits to the 5' end for translation initiation. Pea enation mosaic virus (PEMV) contains two adjacent 3'CITEs in the center of its 703-nucleotide 3' untranslated region (3'UTR), the ribosome-binding, kissing-loop T-shaped structure (kl-TSS) and eukaryotic translation initiation factor 4E-binding Panicum mosaic virus-like translation enhance (PTE). We now report that PEMV contains a third, independent 3'CITE located near the 3' terminus. This 3'CITE is composed of three hairpins and two pseudoknots, similar to the TSS 3'CITE of the carmovirus Turnip crinkle virus (TCV). As with the TCV TSS, the PEMV 3'TSS is predicted to fold into a T-shaped structure that binds to 80S ribosomes and 60S ribosomal subunits. A small hairpin (kl-H) upstream of the 3'TSS contains an apical loop capable of forming a kissing-loop interaction with a 5' proximal hairpin and is critical for the accumulation of full-length PEMV in protoplasts. Although the kl-H and 3'TSS are dispensable for the translation of a reporter construct containing the complete PEMV 3'UTR in vitro, deleting the normally required kl-TSS and PTE 3'CITEs and placing the kl-H and 3'TSS proximal to the reporter termination codon restores translation to near wild-type levels. This suggests that PEMV requires three 3'CITEs for proper translation and that additional translation enhancers may have been missed if reporter constructs were used in 3'CITE identification.
IMPORTANCE
The rapid life cycle of viruses requires efficient translation of viral-encoded proteins. Many plant RNA viruses contain 3' cap-independent translation enhancers (3'CITEs) to effectively compete with ongoing host translation. Since only single 3'CITEs have been identified for the vast majority of individual viruses, it is widely accepted that this is sufficient for a virus's translational needs. Pea enation mosaic virus possesses a ribosome-binding 3'CITE that can connect to the 5' end through an RNA-RNA interaction and an adjacent eukaryotic translation initiation factor 4E-binding 3'CITE. We report the identification of a third 3'CITE that binds weakly to ribosomes and requires an upstream hairpin to form a bridge between the 3' and 5' ends. Although both ribosome-binding 3'CITEs are critical for virus accumulation in vivo, only the CITE closest to the termination codon of a reporter open reading frame is active, suggesting that artificial constructs used for 3'CITE identification may underestimate the number of CITEs that participate in translation.
C1 [Gao, Feng; Szarko, Christine; Simon, Anne E.] Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
[Kasprzak, Wojciech K.] Leidos Biomedical Res Inc, Frederick Natl Lab Canc Res, Basic Sci Program, Frederick, MD USA.
[Shapiro, Bruce A.] Natl Canc Inst, Basic Res Lab, Frederick, MD USA.
RP Simon, AE (reprint author), Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
EM shapirbr@mail.nih.gov; simona@umd.edu
RI Gao, Feng/K-4403-2015
FU NSF [MCB 1157906]; Frederick National Laboratory for Cancer Research,
National Institutes of Health [HHSN 261200800001E]; National Institutes
of Health, Center for Cancer Research
FX This study was supported by the NSF (MCB 1157906) to A. E. S. This
publication has been funded in part with federal funds from the
Frederick National Laboratory for Cancer Research, National Institutes
of Health, under contract HHSN 261200800001E to W. K. K. This research
was supported in part by the Intramural Research Program of the National
Institutes of Health, Center for Cancer Research, to B.A.S.
NR 63
TC 7
Z9 7
U1 3
U2 17
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 20
BP 11696
EP 11712
DI 10.1128/JVI.01433-14
PG 17
WC Virology
SC Virology
GA AQ3JH
UT WOS:000342688000007
PM 25100834
ER
PT J
AU Dowd, KA
Mukherjee, S
Kuhn, RJ
Pierson, TC
AF Dowd, Kimberly A.
Mukherjee, Swati
Kuhn, Richard J.
Pierson, Theodore C.
TI Combined Effects of the Structural Heterogeneity and Dynamics of
Flaviviruses on Antibody Recognition
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID WEST-NILE-VIRUS; DENGUE VIRUS; ENVELOPE PROTEIN; MEDIATED
NEUTRALIZATION; MONOCLONAL-ANTIBODIES; FUSION-LOOP; INFECTION;
TEMPERATURE; MATURATION; PRM
AB Flaviviruses are thought to sample an ensemble of structures at equilibrium. One consequence of a structurally dynamic virion is the observed time-dependent increases in neutralization sensitivity that can occur after prolonged incubation with antibody. Differences in how virus strains "breathe" may affect epitope exposure and contribute to the underlying mechanisms of strain-dependent neutralization sensitivity. Beyond the contribution of structural dynamics, flaviviruses exist as a structurally heterogeneous population due to an inefficient virion maturation process. Here, we investigate the interplay between virion maturation and structural dynamics that contributes to antibody-mediated neutralization. Using West Nile (WNV) and dengue (DENV) viruses produced under conditions that modify the extent of virion maturation, we investigated time-dependent changes in neutralization sensitivity associated with structural dynamics. Our results identify distinct patterns of neutralization against viruses that vary markedly with respect to the extent of virion maturation. Reducing the efficiency of virion maturation resulted in greater time-dependent changes in neutralization potency and a marked reduction in the stability of the particle at 37 degrees C compared to more mature virus. The fact that the neutralization sensitivity of WNV and DENV did not increase after prolonged incubation in the absence of antibody, regardless of virion maturation, suggests that the dynamic processes that govern epitope accessibility on infectious viruses are reversible. Against the backdrop of heterogeneous flavivirus structures, differences in the pathways by which viruses "breathe" represent an additional layer of complexity in understanding maturation state-dependent patterns of antibody recognition.
IMPORTANCE
Flaviviruses exist as a group of related structures at equilibrium that arise from the dynamic motion of E proteins that comprise the antigenic surface of the mature virion. This process has been characterized for numerous viruses and is referred to as viral "breathing." Additionally, flaviviruses are structurally heterogeneous due to an inefficient maturation process responsible for cleaving prM on the virion surface. Both of these mechanisms vary the exposure of antigenic sites available for antibody binding and impact the ability of antibodies to neutralize infection. We demonstrate that virions with inefficient prM cleavage "breathe" differently than their more mature counterparts, resulting in distinct patterns of neutralization sensitivity. Additionally, the maturation state was found to impact virus stability in solution. Our findings provide insight into the complex flavivirus structures that contribute to infection with the potential to impact antibody recognition.
C1 [Dowd, Kimberly A.; Mukherjee, Swati; Pierson, Theodore C.] NIAID, Viral Dis Lab, Viral Pathogenesis Sect, NIH, Bethesda, MD 20892 USA.
[Kuhn, Richard J.] Purdue Univ, Dept Biol Sci, Indiana, PA USA.
RP Pierson, TC (reprint author), NIAID, Viral Dis Lab, Viral Pathogenesis Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM piersontc@mail.nih.gov
FU National Institute of Allergy and Infectious Diseases
FX This work was funded by the Intramural Research Program of the National
Institute of Allergy and Infectious Diseases.
NR 56
TC 20
Z9 20
U1 0
U2 9
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 20
BP 11726
EP 11737
DI 10.1128/JVI.01140-14
PG 12
WC Virology
SC Virology
GA AQ3JH
UT WOS:000342688000009
PM 25078693
ER
PT J
AU Wolf, AI
Strauman, MC
Mozdzanowska, K
Whittle, JRR
Williams, KL
Sharpe, AH
Weiser, JN
Caton, AJ
Hensley, SE
Erikson, J
AF Wolf, Amaya I.
Strauman, Maura C.
Mozdzanowska, Krystyna
Whittle, James R. R.
Williams, Katie L.
Sharpe, Arlene H.
Weiser, Jeffrey N.
Caton, Andrew J.
Hensley, Scott E.
Erikson, Jan
TI Coinfection with Streptococcus pneumoniae Modulates the B Cell Response
to Influenza Virus
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID T-CELLS; ANTIBODY-RESPONSES; IMMUNE-RESPONSE; DENDRITIC CELLS; MOUSE
MODEL; MEMORY B; ALVEOLAR MACROPHAGES; PLASMA-CELL; A VIRUS; INFECTION
AB Pathogen-specific antibodies (Abs) protect against respiratory infection with influenza A virus (IAV) and Streptococcus pneumoniae and are the basis of effective vaccines. Sequential or overlapping coinfections with both pathogens are common, yet the impact of coinfection on the generation and maintenance of Ab responses is largely unknown. We report here that the B cell response to IAV is altered in mice coinfected with IAV and S. pneumoniae and that this response differs, depending on the order of pathogen exposure. In mice exposed to S. pneumoniae prior to IAV, the initial virus-specific germinal center (GC) B cell response is significantly enhanced in the lung-draining mediastinal lymph node and spleen, and there is an increase in CD4(+) T follicular helper (TFH) cell numbers. In contrast, secondary S. pneumoniae infection exaggerates early antiviral antibody-secreting cell formation, and at later times, levels of GCs, TFH cells, and antiviral serum IgG are elevated. Mice exposed to S. pneumoniae prior to IAV do not maintain the initially robust GC response in secondary lymphoid organs and exhibit reduced antiviral serum IgG with diminished virus neutralization activity a month after infection. Our data suggest that the history of pathogen exposures can critically affect the generation of protective antiviral Abs and may partially explain the differential susceptibility to and disease outcomes from IAV infection in humans.
IMPORTANCE
Respiratory tract coinfections, specifically those involving influenza A viruses and Streptococcus pneumoniae, remain a top global health burden. We sought to determine how S. pneumoniae coinfection modulates the B cell immune response to influenza virus since antibodies are key mediators of protection.
C1 [Wolf, Amaya I.; Strauman, Maura C.; Mozdzanowska, Krystyna; Williams, Katie L.; Caton, Andrew J.; Hensley, Scott E.; Erikson, Jan] Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
[Whittle, James R. R.] NIH, Vaccine Res Ctr, Bethesda, MD USA.
[Sharpe, Arlene H.] Harvard Univ, Sch Med, Dept Microbiol & Immunol, Boston, MA USA.
[Weiser, Jeffrey N.] Univ Penn, Dept Microbiol & Pediat, Philadelphia, PA 19104 USA.
RP Erikson, J (reprint author), Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA.
EM jan@wistar.org
OI Weiser, Jeffrey/0000-0001-7168-8090
FU Wistar Cancer Center [P30 CA10815]; NIH [U19AI083022, AI038446,
K22AI091651, T32CA09171]
FX This work was supported by The Wistar Cancer Center Core grant P30
CA10815 and NIH grants U19AI083022 to J.E. and A.J.C., AI038446 to J.
N.W., K22AI091651 to S.E.H., and T32CA09171 to A.I.W. and M.C.S.
NR 71
TC 6
Z9 7
U1 1
U2 15
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 20
BP 11995
EP 12005
DI 10.1128/JVI.01833-14
PG 11
WC Virology
SC Virology
GA AQ3JH
UT WOS:000342688000033
PM 25100838
ER
PT J
AU Vacchio, MS
Wang, L
Bouladoux, N
Carpenter, AC
Xiong, Y
Wohlfert, E
Song, KD
Belkaid, Y
Love, PE
Bosselut, R
AF Vacchio, Melanie S.
Wang, Lie
Bouladoux, Nicolas
Carpenter, Andrea C.
Xiong, Yumei
Wohlfert, Elizabeth
Song, Ki-Duk
Belkaid, Yasmine
Love, Paul E.
Bosselut, Remy
TI A ThPOK-LRF transcriptional node maintains the integrity and effector
potential of post-thymic CD4(+) T cells
SO NATURE IMMUNOLOGY
LA English
DT Article
ID ZINC-FINGER PROTEIN; CD4-CD8 LINEAGE DIFFERENTIATION; HELPER TYPE-1
CELLS; EXPRESSION; REPRESSION; COMMITMENT; THYMOCYTES; LIGAND; RUNX3;
GENE
AB The transcription factor ThPOK promotes CD4(+) T cell differentiation in the thymus. Here, using a mouse strain that allows post-thymic gene deletion, we show that ThPOK maintains CD4(+) T lineage integrity and couples effector differentiation to environmental cues after antigenic stimulation. ThPOK preserved the integrity and amplitude of effector responses and was required for proper differentiation of types 1 and 2 helper T cells in vivo by restraining the expression and function of Runx3, a nuclear factor crucial for cytotoxic T cell differentiation. The transcription factor LRF acts redundantly with ThPOK to prevent the transdifferentiation of mature CD4(+) T cells into CD8(+) T cells. As such, the ThPOK-LRF transcriptional module was essential for CD4(+) T cell integrity and responses.
C1 [Vacchio, Melanie S.; Wang, Lie; Carpenter, Andrea C.; Xiong, Yumei; Wohlfert, Elizabeth; Bosselut, Remy] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Bouladoux, Nicolas; Wohlfert, Elizabeth; Belkaid, Yasmine] NIAID, Mucosal Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Song, Ki-Duk; Love, Paul E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular & Dev Biol, Program Genom Differentiat, NIH, Bethesda, MD USA.
[Wohlfert, Elizabeth] SUNY Buffalo, Sch Med & Biomed Sci, Dept Microbiol & Immunol, Buffalo, NY 14260 USA.
[Song, Ki-Duk] Seoul Natl Univ, Ctr Agr Biomat, Seoul, South Korea.
RP Bosselut, R (reprint author), NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM remy@helix.nih.gov
FU US National Institutes of Health Intramural Research Programs of the
National Cancer Institute, Center for Cancer Research; National
Institute of Allergy and Infectious Diseases; Eunice Kennedy Shriver
National Institute of Child Health and Human Development
FX We thank T. Ciucci for experimental assistance and discussions; T.-A.
Lewis for animal care and genotyping; M. McGinty and Q. Xiao for
technical assistance; X. Wu for microarray analyses; D. Littman, P.P.
Pandolfi and S. Reiner for mice; M. Grigg for the T. gondii strain; J.
Grainger, T. Hand and S. Spencer for discussions; and J. Ashwell and J.
Brenchley for reading the manuscript. Supported by the US National
Institutes of Health Intramural Research Programs of the National Cancer
Institute, Center for Cancer Research, the National Institute of Allergy
and Infectious Diseases and the Eunice Kennedy Shriver National
Institute of Child Health and Human Development.
NR 56
TC 15
Z9 15
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
EI 1529-2916
J9 NAT IMMUNOL
JI Nat. Immunol.
PD OCT
PY 2014
VL 15
IS 10
BP 947
EP U192
DI 10.1038/ni.2960
PG 11
WC Immunology
SC Immunology
GA AQ1TR
UT WOS:000342564800010
PM 25129370
ER
PT J
AU Tropea, MM
Harper, BJA
Graninger, GM
Phillips, TM
Ferreyra, G
Mostowski, HS
Danner, RL
Suffredini, AF
Solomon, MA
AF Tropea, Margaret M.
Harper, Bonnie J. A.
Graninger, Grace M.
Phillips, Terry M.
Ferreyra, Gabriela
Mostowski, Howard S.
Danner, Robert L.
Suffredini, Anthony F.
Solomon, Michael A.
TI Isolation of a circulating CD45(-), CD34(dim) cell population and
validation of their endothelial phenotype
SO THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE Vascular cell markers; gene expression; flow cytometry; viability;
circulating endothelial cells
ID PERIPHERAL-BLOOD; PROGENITOR CELLS; MONOCLONAL-ANTIBODY; FLOW-CYTOMETRY;
APOPTOSIS; CANCER; CD146; ENUMERATION; BIOMARKERS; DAMAGE
AB Accurately detecting circulating endothelial cells (CECs) is important since their enumeration has been proposed as a biomarker to measure injury to the vascular endothelium. However, there is no single methodology for determining CECs in blood, making comparison across studies difficult. Many methods for detecting CECs rely on characteristic cell surface markers and cell viability indicators, but lack secondary validation. Here, a CEC population in healthy adult human subjects was identified by flow cytometry as CD45(-), CD34(dim) that is comparable to a previously described CD45-, CD31(bright) population. In addition, nuclear staining with 7-aminoactinomycin D (7-AAD) was employed as a standard technique to exclude dead cells. Unexpectedly, the CD45-, CD34(dim), 7-MD- CECs lacked surface detectable CD146, a commonly used marker of CECs. Furthermore, light microscopy revealed this cell population to be composed primarily of large cells without a clearly defined nucleus. Nevertheless, immunostains still demonstrated the presence of the lectin Ulex europaeus and von Willebrand factor. Ultramicro analytical immunochemistry assays for the endothelial cell proteins CD31, CD34, CD62E, CD105, CD141, CD144 and vWF indicated these cells possess an endothelial phenotype. However, only a small amount of RNA, which was mostly degraded, could be isolated from these cells. Thus the majority of CECs in healthy individuals as defined by CD45-, CD34(dim), and 7-AAD(-) have shed their CD146 surface marker and are senescent cells without an identifiable nucleus and lacking RNA of sufficient quantity and quality for transcriptomal analysis. This study highlights the importance of secondary validation of CEC identification.
C1 [Tropea, Margaret M.; Harper, Bonnie J. A.; Graninger, Grace M.; Ferreyra, Gabriela; Danner, Robert L.; Suffredini, Anthony F.; Solomon, Michael A.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Phillips, Terry M.] Natl Inst Biomed Imaging & Bioengn, Ultramicro Analyt Immunochem Unit, NIH, Bethesda, MD USA.
[Solomon, Michael A.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Mostowski, Howard S.] US FDA, Div Cell & Gene Therapy, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
RP Solomon, MA (reprint author), NIH, Dept Crit Care Med, Ctr Clin, Bldg 10,Room 2C145, Bethesda, MD 20892 USA.
EM msolomon@cc.nih.gov
FU Critical Care Medicine Department, Clinical Center Intramural
Research-Program
FX This work was funded by Critical Care Medicine Department, Clinical
Center Intramural Research-Program.
NR 43
TC 2
Z9 2
U1 0
U2 1
PU SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN
PI STUTTGART
PA HOLDERLINSTRASSE 3, D-70174 STUTTGART, GERMANY
SN 0340-6245
J9 THROMB HAEMOSTASIS
JI Thromb. Haemost.
PD OCT
PY 2014
VL 112
IS 4
BP 770
EP 780
DI 10.1160/TH14-01-0043
PG 11
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA AQ2YE
UT WOS:000342655100017
PM 25057108
ER
PT J
AU Edelman, EJ
Gordon, KS
Hogben, M
Crystal, S
Bryant, K
Justice, AC
Fiellin, DA
AF Edelman, E. J.
Gordon, K. S.
Hogben, M.
Crystal, S.
Bryant, K.
Justice, A. C.
Fiellin, D. A.
CA VACS Project Team
TI Sexual Partner Notification of HIV Infection Among a National United
States-Based Sample of HIV-Infected Men
SO AIDS AND BEHAVIOR
LA English
DT Article
DE HIV; Sexual partners; Sexually transmitted diseases/prevention and
control; Disease notification
ID REFERRAL SERVICES; HEALTH; EXPERIENCES; ATTITUDES; STD
AB Limited data exist on whether sexual partner notification practices among HIV-infected men, particularly those who have sex with men (MSM), vary by HIV viral load. We examined factors associated with complete (all partners) versus incomplete partner notification in 760 HIV-infected individuals across the United States, 49 % of whom were MSM. Thirty-four percent reported incomplete partner notification. Incomplete partner notification was more likely among black men, MSM, and those reporting casual partners and non-condom use. Partner notification practices did not vary by HIV viral load except among those with casual partners in whom a detectable viral load was associated with incomplete partner notification. Increased sexual partner notification among HIV-infected men, especially MSM, is needed.
C1 [Edelman, E. J.; Justice, A. C.; Fiellin, D. A.] Yale Univ, Yale Sch Med, New Haven, CT 06520 USA.
[Edelman, E. J.; Justice, A. C.; Fiellin, D. A.] Yale Univ, Ctr Interdisciplinary Res AIDS, New Haven, CT 06520 USA.
[Gordon, K. S.; Justice, A. C.] VA Connecticut Healthcare Syst, West Haven, CT USA.
[Hogben, M.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Crystal, S.] Rutgers State Univ, New Brunswick, NJ 08903 USA.
[Bryant, K.] NIAAA, Bethesda, MD USA.
RP Edelman, EJ (reprint author), Yale Univ, Yale Sch Med, POB 208025, New Haven, CT 06520 USA.
EM ejennifer.edelman@yale.edu
OI Fiellin, David/0000-0002-4006-010X
FU NIAAA NIH HHS [U01 AA013566, U01 AA020790, U10 AA013566, U10-AA13566,
U24 AA020794]; NIDA NIH HHS [K12 DA033312, K12DA033312-01A1]
NR 20
TC 4
Z9 4
U1 1
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1090-7165
EI 1573-3254
J9 AIDS BEHAV
JI AIDS Behav.
PD OCT
PY 2014
VL 18
IS 10
BP 1898
EP 1903
DI 10.1007/s10461-014-0799-7
PG 6
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA AP9UF
UT WOS:000342425000006
PM 24858394
ER
PT J
AU Tanofsky-Kraff, M
Shomaker, LB
Wilfley, DE
Young, JF
Sbrocco, T
Stephens, M
Ranzenhofer, LM
Elliott, C
Brady, S
Radin, RM
Vannucci, A
Bryant, EJ
Osborn, R
Berger, SS
Olsen, C
Kozlosky, M
Reynolds, JC
Yanovski, JA
AF Tanofsky-Kraff, Marian
Shomaker, Lauren B.
Wilfley, Denise E.
Young, Jami F.
Sbrocco, Tracy
Stephens, Mark
Ranzenhofer, Lisa M.
Elliott, Camden
Brady, Sheila
Radin, Rachel M.
Vannucci, Anna
Bryant, Edny J.
Osborn, Robyn
Berger, Sarah S.
Olsen, Cara
Kozlosky, Merel
Reynolds, James C.
Yanovski, Jack A.
TI Targeted prevention of excess weight gain and eating disorders in
high-risk adolescent girls: a randomized controlled trial
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID GROUP INTERPERSONAL PSYCHOTHERAPY; COGNITIVE-BEHAVIORAL THERAPY; ADULT
OBESITY; PSYCHOLOGICAL TREATMENTS; CHILDHOOD OVERWEIGHT; SHARED RISK;
DEPRESSION; CHILDREN; EFFICACY; MAINTENANCE
AB Background: The high prevalence and incidence of obesity and eating disorders in US adolescent girls are serious health problems. Because of the shared risk factors for obesity and eating disorders, a targeted prevention of both conditions is a priority.
Objective: We determined whether an adapted interpersonal psychotherapy prevention program is more efficacious for reducing excess weight gain and worsening disordered eating than health education in adolescent girls at high risk of obesity and eating disorders.
Design: A parallel-group, randomized controlled trial was conducted between September 2008 and January 2013 in a university-based laboratory and a federal research hospital. The study included 113 adolescent (12-17-y-old) girls deemed at high risk of adult obesity and eating disorders because of a body mass index (BMI) between the 75th and 97th percentiles and reports of episodes of a loss of control over their eating. Girls were randomly assigned to participate in an adapted interpersonal psychotherapy or a health-education group program for 12 weekly 90-mM group sessions. Follow-up assessments occurred immediately after group programs and at 6 and 12 mo.
Results: Participation in both conditions was associated with decreases in expected BMI gain, age-adjusted BMI metrics, the percentage of fat by using dual-energy X-ray absorptiometry, symptoms of depression and anxiety, and the frequency of loss-of-control eating over 12 mo of follow-up (Ps < 0.001) with no group difference. In follow-up analyses, interpersonal psychotherapy was more efficacious than health education at reducing objective binge eating at the 12-mo follow-up (P < 0.05).
Conclusions: The intervention with adolescent girls with loss-of-control eating is associated with lower age-adjusted BMI and percentage of adiposity as well as improved mood symptoms over 1 y. Interpersonal psychotherapy further reduced objective binge eating. Additional research is needed to elucidate the mechanisms by which physical and psychological improvements were observed. This trial was registered at clinicaltrials.gov as NCT00680979.
C1 [Tanofsky-Kraff, Marian; Shomaker, Lauren B.; Sbrocco, Tracy; Stephens, Mark; Ranzenhofer, Lisa M.; Elliott, Camden; Radin, Rachel M.; Vannucci, Anna; Bryant, Edny J.; Osborn, Robyn; Berger, Sarah S.; Olsen, Cara] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Kozlosky, Merel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hatfield Clin Res Ctr, Dept Nutr, NIH, Bethesda, MD USA.
[Reynolds, James C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hatfield Clin Res Ctr, Dept Nucl Med, NIH, Bethesda, MD USA.
[Tanofsky-Kraff, Marian; Shomaker, Lauren B.; Ranzenhofer, Lisa M.; Elliott, Camden; Brady, Sheila; Radin, Rachel M.; Vannucci, Anna; Berger, Sarah S.; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Obes, NIH, Bethesda, MD USA.
[Wilfley, Denise E.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
[Young, Jami F.] Rutgers State Univ, Piscataway Township, NJ USA.
RP Tanofsky-Kraff, M (reprint author), Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM marian.tanofsky-kraff@usuhs.edu
RI Stephens, Mark/A-2679-2015
FU National Institute of Diabetes and Digestive and Kidney Diseases
[1R01DK080906]; Uniformed Services University of the Health Sciences
[R072IC]; Eunice Kennedy Shriver National Institute of Child Health and
Human Development Intramural Research Program [ZIA-HO-00641]; National
Institute of Mental Health [1K24 MH070446]
FX Supported by the National Institute of Diabetes and Digestive and Kidney
Diseases (1R01DK080906; to MT-K), the Uniformed Services University of
the Health Sciences (grant R072IC; to MT-K), the Eunice Kennedy Shriver
National Institute of Child Health and Human Development Intramural
Research Program (ZIA-HO-00641; to JAY), and the National Institute of
Mental Health (1K24 MH070446; to DEW).
NR 49
TC 18
Z9 18
U1 7
U2 26
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 OCT
PY 2014
VL 100
IS 4
BP 1010
EP 1018
DI 10.3945/ajcn.114.092536
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AP7OT
UT WOS:000342267300005
PM 25240070
ER
PT J
AU Mills, JL
Fan, RZ
Brody, LC
Liu, AY
Ueland, PM
Wang, YF
Kirke, PN
Shane, B
Molloy, AM
AF Mills, James L.
Fan, Ruzong
Brody, Lawrence C.
Liu, Aiyi
Ueland, Per M.
Wang, Yifan
Kirke, Peadar N.
Shane, Barry
Molloy, Anne M.
TI Maternal choline concentrations during pregnancy and choline-related
genetic variants as risk factors for neural tube defects
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID PHOSPHATIDYLETHANOLAMINE N-METHYLTRANSFERASE; MASS-SPECTROMETRY;
FOLIC-ACID; PLASMA; FOLATE; HOMOCYSTEINE; POLYMORPHISM; POPULATION;
METABOLISM; BETAINE
AB Background: Low maternal choline intake and blood concentration may be risk factors for having a child with a neural tube defect (NTD); however, the data are inconsistent. This is an important question to resolve because choline, if taken periconceptionally, might add to the protective effect currently being achieved by folic acid.
Objective: We examined the relation between NTDs, choline status, and genetic polymorphisms reported to influence de novo choline synthesis to investigate claims that taking choline periconceptionafly could reduce NTD rates.
Design: Two study groups of pregnant women were investigated: women who had a current NTD-affected pregnancy (AP; n = 71) and unaffected controls (n = 214) and women who had an NTD in another pregnancy but not in the current pregnancy [nonaffected pregnancy (NAP); n = 98] and unaffected controls (n = 386). Blood samples to measure betaine and total choline concentrations and single nucleotide polymorphisms related to choline metabolism were collected at their first prenatal visit.
Results: Mean (+/- SD) plasma total choline concentrations in the AP (2.8 +/- 1.0 mmol/L) and control (2.9 +/- 0.9 mmol/L) groups did not differ significantly. Betaine concentrations were not significantly different between the 2 groups. Total choline and betaine in the NAP group did not differ from controls. Cases were significantly more likely to have the G allele of phosphatidylethanolamine-N-methyltransferase (PEMT; V175M, +5465 G>A) rs7946 (P = 0.02).
Conclusions: Our results indicate that maternal betaine and choline concentrations are not strongly associated with NTD risk. The association between PEMT rs7946 and NTDs requires confirmation. The addition of choline to folic acid supplements may not further reduce NTD risk.
C1 [Mills, James L.; Fan, Ruzong; Liu, Aiyi; Wang, Yifan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20892 USA.
[Brody, Lawrence C.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
[Ueland, Per M.] Univ Bergen, Dept Clin Sci, Bergen, Norway.
[Ueland, Per M.] Haukeland Hosp, Lab Clin Biochem, N-5021 Bergen, Norway.
[Kirke, Peadar N.] Hlth Res Board, Dublin, Ireland.
[Shane, Barry] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Molloy, Anne M.] Univ Dublin Trinity Coll, Sch Med, Dept Clin Med, Dublin 2, Ireland.
RP Mills, JL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, 6100 Bldg,7B03, Bethesda, MD 20892 USA.
EM jamesmills@nih.gov
RI Ueland, Per/C-7340-2013;
OI Molloy, Anne/0000-0002-1688-9049; Liu, Aiyi/0000-0002-6618-5082
FU Intramural Research Program, Eunice Kennedy Shriver National Institute
of Child Health and Human Development [N01HD33348]; Intramural Research
Program, National Human Genome Research Institute; Health Research
Board, Dublin, Ireland
FX Supported by the Intramural Research Program, Eunice Kennedy Shriver
National Institute of Child Health and Human Development (contract
N01HD33348), the Intramural Research Program, National Human Genome
Research Institute, and the Health Research Board, Dublin, Ireland.
NR 23
TC 3
Z9 3
U1 1
U2 16
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 OCT
PY 2014
VL 100
IS 4
BP 1069
EP 1074
DI 10.3945/ajcn.113.079319
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AP7OT
UT WOS:000342267300012
PM 25240073
ER
PT J
AU Salinas, CF
Irvine, AD
Itin, PH
Di Giovanna, JJ
Schneider, H
Clarke, AJ
McGovern, LS
Fete, M
AF Salinas, Carlos F.
Irvine, Alan D.
Itin, Peter H.
Di Giovanna, John J.
Schneider, Holm
Clarke, Angus J.
McGovern, Laura Sternesky
Fete, Mary
TI Second International Conference on a Classification of Ectodermal
Dysplasias: Development of a Multiaxis Model
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE ectodermal dysplasias; ectodermal dysplasias classification;
classification; multiaxial model; bioinformatics
ID MORPHOLOGY STANDARD TERMINOLOGY; ELEMENTS; REGION
AB Ectodermal dysplasias (EDs) comprise a large clinically and etiologically heterogeneous group of genetic disorders characterized by abnormalities in tissues derived from the embryonic ectoderm. Controversy exists over which syndromes should be classified as EDs and which should be excluded from the classification. The challenge will be to balance comprehensiveness within the classification with usability and accessibility so that the benefits truly serve the needs of researchers, health-care providers, and ultimately the individuals and families directly affected by EDs. The overarching goal of the Second International Conference was to develop a consensus on EDs classifications, with the ultimate goal of creating a system that integrates clinical and molecular knowledge, using an interactive Internet-based database that clinicians, researchers, and laymen can use. The Conference, brought together a group of experts from around the world, including a diverse health-care providers, researchers, patient advocate representatives, and administrators. The Conference was modeled after the 2008 conference, with plenary sessions, scientific updates, and small group discussions. Based on the present clinical knowledge, new molecular advances and both coupled with new bioinformatics developments, the participants agree to develop a multiaxis system approach for the classification of EDs. The multiaxis approach will include a clinical/phenotype axis, a gene-based axis, and a functional/pathways axis. The significance of the conference outcomes includes, a new classification approach that will foster a better understanding of EDs, open new fields of research and develop a nosologic approach that may have broad implications for classifying other hereditary conditions. (C) 2014 Wiley Periodicals, Inc.
C1 [Salinas, Carlos F.] Med Univ S Carolina, Coll Dent Med, Div Craniofacial Genet, Charleston, SC 29425 USA.
[Irvine, Alan D.] Our Ladys Childrens Hosp Crumlin, Natl Childrens Res Ctr & Paediat Dermatol, Dublin, Ireland.
[Itin, Peter H.] Univ Basel Hosp, Dept Dermatol, CH-4031 Basel, Switzerland.
[Di Giovanna, John J.] NCI, DNA Repair Sect, Dermatol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Schneider, Holm] Univ Erlangen Nuernberg, Childrens Hosp, Erlangen, Germany.
[Clarke, Angus J.] Cardiff Univ, Sch Med, Inst Med Genet, Dept Med Genet Haematol & Pathol, Cardiff CF10 3AX, S Glam, Wales.
[McGovern, Laura Sternesky] Altarum Inst, Washington, DC USA.
[Fete, Mary] Natl Fdn Ectodermal Dysplasias, Fairview Hts, IL USA.
RP Salinas, CF (reprint author), Med Univ S Carolina, 173 Ashley Ave,BSB 128,MSC 507, Charleston, SC 29425 USA.
EM salinasc@musc.edu
OI Irvine, Alan/0000-0002-9048-2044
FU National Foundation for Ectodermal Dysplasias (NFED); National Institute
of Dental and Craniofacial Research [1R13DEO23034-01]
FX Grant sponsor: National Foundation for Ectodermal Dysplasias (NFED);
Grant sponsor: National Institute of Dental and Craniofacial Research;
Grant number: 1R13DEO23034-01.
NR 23
TC 2
Z9 2
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2014
VL 164
IS 10
BP 2482
EP 2489
DI 10.1002/ajmg.a.36507
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA AP7TM
UT WOS:000342279600012
PM 24700551
ER
PT J
AU Butali, A
Mossey, P
Adeyemo, W
Eshete, M
Gaines, L
Braimah, R
Aregbesola, B
Rigdon, J
Emeka, C
Olutayo, J
Ogunlewe, O
Ladeinde, A
Abate, F
Hailu, T
Mohammed, I
Gravem, P
Deribew, M
Gesses, M
Adeyemo, A
Marazita, M
Murray, J
AF Butali, Azeez
Mossey, Peter
Adeyemo, Wasiu
Eshete, Mekonen
Gaines, Lauren
Braimah, Ramat
Aregbesola, Babatunde
Rigdon, Jennifer
Emeka, Christian
Olutayo, James
Ogunlewe, Olugbenga
Ladeinde, Akinola
Abate, Fikre
Hailu, Taye
Mohammed, Ibrahim
Gravem, Paul
Deribew, Milliard
Gesses, Mulualem
Adeyemo, Adebowale
Marazita, Mary
Murray, Jeffrey
TI Rare Functional Variants in Genome-Wide Association Identified Candidate
Genes for Nonsyndromic Clefts in the African Population
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE Africa; GWAS; rare variants
ID SUSCEPTIBILITY LOCUS; PALATE; LIP; RISK; LIP/PALATE; MUTATIONS;
IMPLICATE; SIGNALS; IMPACT; 10Q25
AB Nonsyndromic clefts of the lip and palate (NSCLP) are complex genetic traits. Together, they are classified as one of the most common birth defects with a prevalence of 1/700 live births. Genome-wide association studies (GWAS) for nonsyndromic cleft lip with or without cleft palate (NSCL[P]) revealed significant association for common single nucleotide polymorphisms near genes involved in craniofacial development i.e., MAFB, PAX7, VAX1, ARHGAP29 (ABCA4 locus), and IRF6. Sequencing of protein coding regions of the NSCL(P) GWAS candidate genes or adjacent genes suggest a role for rare functional variants. Replication studies in the African population did not observe any significant association with the GWAS candidate genes. On the other hand, the role of rare functional variants in GWAS candidate genes has not been evaluated in the African population. We obtained saliva samples from case triads in Nigeria and Ethiopia for Sanger sequencing of the GWAS candidate genes (MAFB, PAX7, VAX1, ARHGAP29, and IRF6) in order to identify rare functional variants. A total of 220 African samples (140 Nigerians and 80 Ethiopians) were sequenced and we found the following new rare variants-p. His165Asn in the MAFB gene, p.Asp428Asn in the PAX7, a splice-site variant that creates a new donor splice-site in PAX7. We also found three previously reported missense variants p. Gly466Ser in PAX7; p.Leu913Ser and Arg955His in ARHGAP29. No de novo mutations were found. Future genome-wide association and sequencing studies should be conducted using samples from Africa in order to identify new molecular genetic factors that contribute to the etiology of NSCLP. (C) 2014 Wiley Periodicals, Inc.
C1 [Butali, Azeez] Univ Iowa, Coll Dent, Dept Oral Pathol Radiol & Med, Iowa City, IA 52241 USA.
[Mossey, Peter] Univ Dundee, Dundee DD1 4HN, Scotland.
[Adeyemo, Wasiu; Emeka, Christian; Olutayo, James; Ogunlewe, Olugbenga; Ladeinde, Akinola] Univ Lagos, Lagos, Nigeria.
[Eshete, Mekonen; Abate, Fikre; Hailu, Taye; Mohammed, Ibrahim; Gravem, Paul; Deribew, Milliard; Gesses, Mulualem] Univ Addis Ababa, Addis Ababa, Ethiopia.
[Gaines, Lauren; Rigdon, Jennifer; Murray, Jeffrey] Univ Iowa, Dept Pediat, Iowa City, IA 52241 USA.
[Braimah, Ramat; Aregbesola, Babatunde] Obafemi Awolowo Univ, Ife, Nigeria.
[Adeyemo, Adebowale] NIH, Bethesda, MD 20892 USA.
[Marazita, Mary] Univ Pittsburgh, Pittsburgh, PA USA.
RP Butali, A (reprint author), Univ Iowa, Coll Dent, Dept Oral Pathol Radiol & Med, Iowa City, IA 52241 USA.
EM Azeez-butali@uiowa.edu
OI Mossey, Peter/0000-0002-9914-6901; Adeyemo,
Adebowale/0000-0002-3105-3231
FU NIDCR [K99/R00 DE022378, DE-08559, R37, DE-016148]
FX Grant sponsor: NIDCR K99/R00 DE022378; Grant number: DE-08559; Grant
sponsor: NIDCR R37; Grant number: DE-016148.
NR 25
TC 6
Z9 6
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2014
VL 164
IS 10
BP 2567
EP 2571
DI 10.1002/ajmg.a.36691
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA AP7TM
UT WOS:000342279600024
PM 25081408
ER
PT J
AU Heselmeyer-Haddad, KM
Garcia, LYB
Bradley, A
Hernandez, L
Hu, Y
Habermann, JK
Dumke, C
Thorns, C
Perner, S
Pestova, E
Burke, C
Chowdhury, SA
Schwartz, R
Schaffer, AA
Paris, PL
Ried, T
AF Heselmeyer-Haddad, Kerstin M.
Garcia, Lissa Y. Berroa
Bradley, Amanda
Hernandez, Leanora
Hu, Yue
Habermann, Jens K.
Dumke, Christoph
Thorns, Christoph
Perner, Sven
Pestova, Ekaterina
Burke, Catherine
Chowdhury, Salim A.
Schwartz, Russell
Schaeffer, Alejandro A.
Paris, Pamela L.
Ried, Thomas
TI Single-Cell Genetic Analysis Reveals Insights into Clonal Development of
Prostate Cancers and Indicates Loss of PTEN as a Marker of Poor
Prognosis
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID IN-SITU HYBRIDIZATION; GROWTH-FACTOR; C-MYC; TRANSCRIPTION ACTIVATION;
RADICAL PROSTATECTOMY; FUSION TRANSCRIPTS; COPY NUMBER; ERG;
PROGRESSION; EXPRESSION
AB Gauging the risk of developing progressive disease is a major challenge in prostate cancer patient management. We used genetic markers to understand genomic alteration dynamics during disease progression. By using a novel, advanced, multicolor fluorescence in situ hybridization approach, we enumerated copy numbers of six genes previously identified by array comparative genomic hybridization to be involved in aggressive prostate cancer [TBL1XR1, CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent radical prostatectomy cases. An ERG break-apart probe to detect TMPRSS2-ERG fusions was included. Subsequent hybridization of probe panels and cell relocation resulted in signal counts for all probes in each individual cell analyzed. Differences in the degree of chromosomal and genomic instability (ie, tumor heterogeneity) or the percentage of cells with TMPRSS2-ERG fusion between samples with or without progression were not observed. Tumors from patients that progressed had more chromosomal gains and losses, and towed a higher degree of selection for a predominant clonal pattern. PTEN loss was the most frequent aberration in progressers (57%), followed by TBL1XR1 gain (29%). MYC gain was observed in one progresser-which was the only lesion with an ERG gain, but no TMPRS52-ERG fusion. According to our results a probe set consisting of PTEN, MYC, and TBL1XR1 would detect progressers, with 86%, sensitivity specificity. This will be evaluated further in Larger studies.
C1 [Heselmeyer-Haddad, Kerstin M.; Garcia, Lissa Y. Berroa; Bradley, Amanda; Hernandez, Leanora; Hu, Yue; Ried, Thomas] NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Schaeffer, Alejandro A.] NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Habermann, Jens K.; Dumke, Christoph] Univ Lubeck, Sect Translat Surg Oncol & Biobanking, Dept Surg, Lubeck, Germany.
[Thorns, Christoph] Univ Lubeck, Inst Pathol, Lubeck, Germany.
[Thorns, Christoph] Campus Univ Lubeck, Univ Med Ctr Schleswig Holstein, Lubeck, Germany.
[Perner, Sven] Univ Hosp Bonn, Inst Pathol, Dept Prostate Canc Res, Bonn, Germany.
[Pestova, Ekaterina] Abbott Mol, Des Plaines, IL USA.
[Burke, Catherine; Paris, Pamela L.] Univ Calif San Francisco, Dept Urol, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Chowdhury, Salim A.] Carnegie Mellon Univ, Joint Carnegie Mellon Univ Pittsburgh, PhD Program Computat Biol, Pittsburgh, PA 15213 USA.
[Chowdhury, Salim A.] Carnegie Mellon Univ, Lane Ctr Computat Biol, Pittsburgh, PA 15213 USA.
[Schwartz, Russell] Carnegie Mellon Univ, Dept Biol Sci, Pittsburgh, PA 15213 USA.
RP Heselmeyer-Haddad, KM (reprint author), NCI, Genet Branch, Ctr Canc Res, NIH, 50 South Dr,Bldg 50,Room 1408, Bethesda, MD 20892 USA.
EM heselmek@mail.nih.gov
RI Habermann, Jens/E-2968-2010; Schwartz, Russell/A-1998-2016;
OI Schwartz, Russell/0000-0002-4970-2252; Pestova,
Katerina/0000-0001-8200-2621
FU Intramural Research Program of the NIH; National Cancer Institue; US
National Library of Medicine; NIH [CA140214, AI0763318, CA115484]
FX Supported in part by the Intramural Research Program of the NIH,
National Cancer Institue, US National Library of Medicine, and NIH R01
Awards CA140214, AI0763318, and CA115484.
NR 70
TC 10
Z9 11
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD OCT
PY 2014
VL 184
IS 10
BP 2671
EP 2686
DI 10.1016/j.ajpath.2014.06.030
PG 16
WC Pathology
SC Pathology
GA AP7SK
UT WOS:000342276800009
PM 25131421
ER
PT J
AU Stratman, AN
Mikelis, CM
Pezoa, SA
Pham, VN
Castranova, D
Davis, AE
Kilts, TM
Davis, GE
Gutkind, JS
Pan, WJ
Weinstein, BM
AF Stratman, Amber N.
Mikelis, Constantinos M.
Pezoa, Sofia A.
Pham, Van N.
Castranova, Daniel
Davis, Andrew E.
Kilts, Tina M.
Davis, George E.
Gutkind, J. Silvio
Pan Weijun
Weinstein, Brant M.
TI Anti-angiogenic effects of VEGF stimulation on endothelium deficient in
phosphoinositide recycling
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [Stratman, Amber N.; Mikelis, Constantinos M.; Pezoa, Sofia A.; Pham, Van N.; Castranova, Daniel; Davis, Andrew E.; Kilts, Tina M.; Gutkind, J. Silvio; Weinstein, Brant M.] NIH, Bethesda, MD 20892 USA.
[Davis, George E.] Univ Missouri, Columbia, MO USA.
[Pan Weijun] Chinese Acad Sci, Shanghai, Peoples R China.
[Pan Weijun] Shanghai Jiao Tong Univ, Sch Med, Shanghai 200030, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA G04
BP 947
EP 947
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100048
ER
PT J
AU Xie, ZH
Sek, A
Terai, K
Dudek, A
Druey, KM
AF Xie Zhihui (Sherry)
Sek, Albert
Terai, Koaru
Dudek, Arkadiusz
Druey, Kirk M.
TI Endothelium expression of ETA, a possible role of endothelin receptor A
in SCLS pathogenesis
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [Xie Zhihui (Sherry); Sek, Albert; Druey, Kirk M.] NIH, Bethesda, MD 20892 USA.
[Terai, Koaru; Dudek, Arkadiusz] Univ Minnesota, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA 024
BP 953
EP 953
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100068
ER
PT J
AU Shepherd, BT
James, J
Mukouyama, YS
AF Shepherd, Brian T.
James, Jennifer
Mukouyama, Yoh-suke
TI TGF beta signaling positively regulates lymphatic endothelial cell
sprouting in vitro
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [Shepherd, Brian T.; James, Jennifer; Mukouyama, Yoh-suke] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA 033
BP 954
EP 954
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100073
ER
PT J
AU Jin, XT
Freeman, S
Anzinger, J
Xu, Q
Fessler, M
Addadi, L
Kruth, HS
AF Jin Xueting
Freeman, Sebastian
Anzinger, Joshua
Xu Qing
Fessler, Michael
Addadi, Lia
Kruth, Howard S.
TI Extracellular unesterified cholesterol-rich microdomains generated by
macrophages and their function in reverse cholesterol transport
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [Jin Xueting; Freeman, Sebastian; Anzinger, Joshua; Xu Qing; Kruth, Howard S.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Fessler, Michael] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
[Addadi, Lia] Weizmann Inst Technol, Rehovot, Israel.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA 080
BP 965
EP 965
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100108
ER
PT J
AU James, JM
Shepherd, BT
Mukouyama, YS
AF James, Jennifer M.
Shepherd, Brian T.
Mukouyama, Yoh-suke
TI TGF beta signaling is required for lymphatic network development in
mouse skin
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [James, Jennifer M.; Shepherd, Brian T.; Mukouyama, Yoh-suke] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA 116
BP 973
EP 973
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100132
ER
PT J
AU Li, WL
Sajja, A
Mukouyama, YS
AF Li Wenling
Sajja, Aparna
Mukouyama, Yoh-suke
TI How does hypoxia influence nerve-controlled arterial branching
morphogenesis?
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [Li Wenling; Sajja, Aparna; Mukouyama, Yoh-suke] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA 117
BP 973
EP 973
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100133
ER
PT J
AU Yu, JA
Castranova, D
Pham, V
Weinstein, BM
AF Yu, Jianxin Alex
Castranova, Daniel
Pham Van
Weinstein, Brant M.
TI Single cell analysis of endothelial morphogenesis in vivo
SO ANGIOGENESIS
LA English
DT Meeting Abstract
C1 [Yu, Jianxin Alex; Castranova, Daniel; Pham Van; Weinstein, Brant M.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
EI 1573-7209
J9 ANGIOGENESIS
JI Angiogenesis
PD OCT
PY 2014
VL 17
IS 4
MA 118
BP 973
EP 973
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP9VE
UT WOS:000342428100134
ER
PT J
AU Glasheen, C
Hedden, SL
Forman-Hoffman, VL
Colpe, LJ
AF Glasheen, Cristie
Hedden, Sarra L.
Forman-Hoffman, Valerie L.
Colpe, Lisa J.
TI Cigarette smoking behaviors among adults with serious mental illness in
a nationally representative sample
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Smoking; Tobacco use disorder; Mental health; Mental disorders; Mentally
ill persons
ID NICOTINE DEPENDENCE
AB Purpose: This study updates nationally representative information on cigarette smoking behaviors among adults with mental illness, particularly serious mental illness (SMI), to serve as a new benchmark for smoking cessation initiatives.
Methods: Data are from the 2008-2012 National Surveys on Drug Use and Health. Prevalence estimates for past month daily smoking, heavy smoking, mean cigarettes consumed per day, nicotine dependence, past month quit ratio, and proportion of cigarettes consumed are presented by mental illness status.
Results: Adults with SMI were more likely than adults with any mental illness (AMI) but not SMI and adults without mental illness to engage in smoking behaviors. Adults with AMI but not SMI were more likely to engage in all smoking behaviors compared with adults without mental illness. The past month quit ratio was significantly lower among adults with SMI and among adults with AMI but not SMI than among adults without mental illness. Adults with SMI comprised 6.9% of past month smokers but consumed 8.7% of all cigarettes.
Conclusions: Adults with mental illness engage in more smoking behaviors and are less likely to quit than adults without mental illness. In this high-risk population, continued efforts to promote smoking cessation are needed. Published by Elsevier Inc.
C1 [Glasheen, Cristie; Forman-Hoffman, Valerie L.] RTI Int, Behav Hlth Epidemiol Program, Res Triangle Pk, NC USA.
[Hedden, Sarra L.] Ctr Behav Hlth Stat & Qual, Subst Abuse & Mental Hlth Serv Adm, Rockville, MD USA.
[Colpe, Lisa J.] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
RP Colpe, LJ (reprint author), NIMH, Div Serv & Intervent Res, 6001 Execut Blvd, Bethesda, MD 20892 USA.
EM lcolpe@mail.nih.gov
OI Glasheen, Cristie/0000-0003-4419-9659
FU Substance Abuse and Mental Health Services Administration (SAMHSA);
Center for Behavioral Health Statistics and Quality (CBHSQ); SAMHSA
[284-2010-0003C, 0212800.002]; National Institute of Mental Health
(NIMH)
FX The authors would like to thank Joseph Gfroerer for his review of the
report and Christine Davies and Julia Gable for their assistance with
the analyses. The National Survey on Drug Use and Health (NSDUH) is
funded by the Substance Abuse and Mental Health Services Administration
(SAMHSA), Center for Behavioral Health Statistics and Quality (CBHSQ).
This study was funded and approved under SAMHSA Contract No.
284-2010-0003C, Project No. 0212800.002, which was supported by funding
from the National Institute of Mental Health (NIMH). The views expressed
in this manuscript do not necessarily represent the views of the
National Institutes of Health or the Federal Government.
NR 18
TC 10
Z9 10
U1 1
U2 5
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 OCT
PY 2014
VL 24
IS 10
BP 776
EP 780
DI 10.1016/j.annepidem.2014.07.009
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AP8KY
UT WOS:000342329100011
PM 25169683
ER
PT J
AU Dai, DD
Huang, Q
Nussinov, R
Ma, BY
AF Dai, Dandan
Huang, Qiang
Nussinov, Ruth
Ma, Buyong
TI Promiscuous and specific recognition among ephrins and Eph receptors
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Article
DE Eph receptor tyrosine kinase; Conformational selection; Induced fit;
Protein-protein interaction; Energy landscape; Conformational dynamics
ID CONFORMATIONAL SELECTION; SUBSTRATE RECOGNITION; PROTEIN DYNAMICS; AXON
GUIDANCE; INDUCED FIT; BINDING; CELL; CANCER; NMR; MOLECULES
AB Eph-ephrin interactions control the signal transduction between cells and play an important role in carcinogenesis and other diseases. The interactions between Eph receptors and ephrins of the same subclass are promiscuous; there are cross-interactions between some subclasses, but not all. To understand how Eph-ephrin interactions can be both promiscuous and specific, we investigated sixteen energy landscapes of four Eph receptors (A2, A4, 132, and B4) interacting with four ephrin ligands (A1, A2, A5, and B2). We generated conformational ensembles and recognition energy landscapes starting from separated Eph and ephrin molecules and proceeding up to the formation of Eph-ephrin complexes. Analysis of the Eph-ephrin recognition trajectories and the co-evolution entropy of 400 ligand binding domains of Eph receptor and 241 ephrin ligands identified conserved residues during the recognition process. Our study correctly predicted the promiscuity and specificity of the interactions and provided insights into their recognition. The dynamic conformational changes during Eph-ephrin recognition can be described by progressive conformational selection and population shift events, with two dynamic salt bridges between EphB4 and ephrin-B2 contributing to the specific recognition. EphA3 cancer-related mutations lowered the binding energies. The specificity is not only controlled by the final stage of the interaction across the protein-protein interface, but also has large contributions from binding kinetics with the help of dynamic intermediates along the pathway from the separated Eph and ephrin to the Eph-ephrin complex. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Dai, Dandan; Huang, Qiang] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
[Nussinov, Ruth; Ma, Buyong] NCI, Basic Sci Program, Leidos Biomed Res Inc, Canc & Inflammat Program, 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 Huang, Q (reprint author), Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
EM huangqiang@fudan.edu.cn; mabuyong@mail.nih.gov
RI Ma, Buyong/F-9491-2011
OI Ma, Buyong/0000-0002-7383-719X
FU Federal funds from the National Cancer Institute, National Institutes of
Health [HHSN261200800001E]; Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research; Hi-tech Research
and Development Program of China [2008AA02Z311]; Shanghai Natural
Science Foundation [13ZR1402400]; Shanghai Leading Academic Discipline
Project [B111]
FX The authors are funded in whole or in part with Federal funds from the
National Cancer Institute, National Institutes of Health, under contract
number HHSN261200800001E. This research was supported (in part) by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research. Q. Huang was supported in part by the grants
from the Hi-tech Research and Development Program of China (No.
2008AA02Z311), the Shanghai Natural Science Foundation (No.
13ZR1402400), and the Shanghai Leading Academic Discipline Project
(B111).
NR 77
TC 5
Z9 5
U1 9
U2 22
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-9639
EI 0006-3002
J9 BBA-PROTEINS PROTEOM
JI BBA-Proteins Proteomics
PD OCT
PY 2014
VL 1844
IS 10
BP 1729
EP 1740
DI 10.1016/j.bbapap.2014.07.002
PG 12
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA AP7SF
UT WOS:000342276300001
PM 25017878
ER
PT J
AU Orban, T
Beam, CA
Xu, P
Moore, K
Jiang, Q
Deng, J
Muller, S
Gottlieb, P
Spain, L
Peakman, M
AF Orban, Tihamer
Beam, Craig A.
Xu, Ping
Moore, Keith
Jiang, Qi
Deng, Jun
Muller, Sarah
Gottlieb, Peter
Spain, Lisa
Peakman, Mark
CA Type 1 Diabet TrialNet Abatacept S
TI Reduction in CD4 Central Memory T-Cell Subset in Costimulation Modulator
Abatacept-Treated Patients With Recent-Onset Type 1 Diabetes Is
Associated With Slower C-Peptide Decline
SO DIABETES
LA English
DT Article
ID DOUBLE-BLIND; THERAPY; MELLITUS; TRIAL
AB We previously reported that continuous 24-month costimulation blockade by abatacept significantly slows the decline of beta-cell function after diagnosis of type 1 diabetes. In a mechanistic extension of that study, we evaluated peripheral blood immune cell subsets (CD4, CD8-naive, memory and activated subsets, myeloid and plasmacytoid dendritic cells, monocytes, B lymphocytes, CD4(+)CD25(high) regulatory T cells, and invariant NK T cells) by flow cytometry at baseline and 3, 6, 12, 24, and 30 months after treatment initiation to discover biomarkers of therapeutic effect. Using multivariable analysis and lagging of longitudinally measured variables, we made the novel observation in the placebo group that an increase in central memory (CM) CD4 T cells (CD4(+)CD45R0(+)CD62L(+)) during a preceding visit was significantly associated with C-peptide decline at the subsequent visit. These changes were significantly affected by abatacept treatment, which drove the peripheral contraction of CM CD4 T cells and the expansion of naive (CD45R0(-)CD62L(+)) CD4 T cells in association with a significantly slower rate of C-peptide decline. The findings show that the quantification of CM CD4 T cells can provide a surrogate immune marker for C-peptide decline after the diagnosis of type 1 diabetes and that costimulation blockade may exert its beneficial therapeutic effect via modulation of this subset.
C1 [Orban, Tihamer] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Beam, Craig A.; Xu, Ping; Muller, Sarah] Univ S Florida, Dept Pediat, Div Informat & Biostat, Tampa, FL 33620 USA.
[Moore, Keith; Jiang, Qi; Deng, Jun] David H Murdock Res Inst, Kannapolis, NC USA.
[Gottlieb, Peter] Univ Colorado, Barbara Davis Ctr Childhood Diabet, Aurora, CO USA.
[Spain, Lisa] Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA.
[Peakman, Mark] Kings Coll London, Sch Med, Peter Gorer Dept Immunobiol, London WC2R 2LS, England.
RP Orban, T (reprint author), Joslin Diabet Ctr, Boston, MA 02215 USA.
EM tihamer.orban@gmail.com
RI Krammel, Vera/N-4826-2014
OI Krammel, Vera/0000-0002-8273-8396
FU Type 1 Diabetes Trial Net Study Group; National Institutes of Health
through National Institute of Diabetes and Digestive and Kidney
Diseases; National Institute of Allergy and Infectious Diseases; The
Eunice Kennedy Shriver National Institute of Child Health and Human
Development [U01-DK-061010, U01-DK-061016, U01-DK-061034, U01-DK-061036,
U01-DK-061040, U01-DK-061041, U01-DK-061042, U01-DK-061055,
U01-DK-061058, U01-DK-084565, U01-DK-085453, U01-DK-085461,
U01-DK-085463, U01-DK-085466, U01-DK-085499, U01-DK-085505,
U01-DK-085509, HHSN267200800019C]; National Center for Research
Resources [UL1-RR-024131, UL1-RR-024139, UL1-RR-024153, UL1-RR-024975,
UL1-RR-024982, UL1-RR-025744, UL1-RR-025761, UL1-RR-025780,
UL1-RR-029890, UL1-RR-031986]; General Clinical Research Center Award
[M01-RR-00400]; Juvenile Diabetes Research Foundation International;
American Diabetes Association
FX The sponsor of the trial was the Type 1 Diabetes Trial Net Study Group.
The Type 1 Diabetes Trial Net Study Group is a clinical trials network
funded by the National Institutes of Health through the National
Institute of Diabetes and Digestive and Kidney Diseases, the National
Institute of Allergy and Infectious Diseases, and The Eunice Kennedy
Shriver National Institute of Child Health and Human Development through
cooperative agreements U01-DK-061010, U01-DK-061016, U01-DK-061034,
U01-DK-061036, U01-DK-061040, U01-DK-061041, U01-DK-061042,
U01-DK-061055, U01-DK-061058, U01-DK-084565, U01-DK-085453,
U01-DK-085461, U01-DK-085463, U01-DK-085466, U01-DK-085499,
U01-DK-085505, and U01-DK-085509 and contract HHSN267200800019C; the
National Center for Research Resources through Clinical Translational
Science Awards UL1-RR-024131, UL1-RR-024139, UL1-RR-024153,
UL1-RR-024975, UL1-RR-024982, UL1-RR-025744, UL1-RR-025761,
UL1-RR-025780, UL1-RR-029890, and UL1-RR-031986 and General Clinical
Research Center Award M01-RR-00400; the Juvenile Diabetes Research
Foundation International; and the American Diabetes Association.
NR 20
TC 13
Z9 13
U1 0
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
EI 1939-327X
J9 DIABETES
JI Diabetes
PD OCT
PY 2014
VL 63
IS 10
BP 3449
EP 3457
DI 10.2337/db14-0047
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AQ1FM
UT WOS:000342527300031
PM 24834977
ER
PT J
AU Horner-Johnson, W
Dobbertin, K
Lee, JC
Andresen, EM
AF Horner-Johnson, Willi
Dobbertin, Konrad
Lee, Jae Chul
Andresen, Elena M.
TI Rural disparities in receipt of colorectal cancer screening among adults
ages 50-64 with disabilities
SO DISABILITY AND HEALTH JOURNAL
LA English
DT Article
DE People with disabilities; Cancer screening; Rural population; Health
care disparities; Population surveillance
ID CONFRONT SUBSTANTIAL BARRIERS; EXPENDITURE PANEL SURVEY; FECAL
OCCULT-BLOOD; HEALTH-CARE; UNITED-STATES; MORTALITY; RISK; METAANALYSIS;
SERVICES; COLONOSCOPY
AB Background: Colorectal cancer is the third leading cause of cancer deaths in the United States. Early detection can reduce mortality; however, only 59% of U.S. adults age 50 and over meet recommended colorectal cancer screening guidelines. Studies in the general population have observed that rural residents are less likely to have received colorectal cancer screening than residents of urban areas.
Objective: To determine whether urban/rural disparities in colorectal cancer screening exist among people with disabilities, similar to the disparities found in the general population.
Methods: We analyzed Medical Expenditure Panel Survey annual data files from 2002 to 2008. We conducted logistic regression analyses to examine the relationship between urban/rural residence and ever having received screening for colorectal cancer (via colonoscopy, sigmoidoscopy, or fecal occult blood test).
Results: Among U.S. adults ages 50-64 with disabilities, those living in rural areas were significantly less likely to have ever received any type of screening for colorectal cancer. The urban/rural difference was statistically significant regardless of whether or not we controlled for demographic, socioeconomic, health, and health care access variables.
Conclusions: Disparity in screening for colorectal cancer places rural residents with disabilities at greater risk for late stage diagnosis and mortality relative to people with disabilities in urban areas. Thus, there is a need for strategies to improve screening among people with disabilities in rural areas. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Horner-Johnson, Willi; Dobbertin, Konrad; Andresen, Elena M.] Oregon Hlth & Sci Univ, Inst Dev & Disabil, Portland, OR 97239 USA.
[Lee, Jae Chul] Univ Delaware, Ctr Disabil Studies, Coll Educ & Human Dev, Newark, DE 19716 USA.
[Lee, Jae Chul] NIH, Dept Rehabil Med, Clin Res Ctr, Bethesda, MD USA.
RP Horner-Johnson, W (reprint author), Oregon Hlth & Sci Univ, Inst Dev & Disabil, 707 SW Gaines St, Portland, OR 97239 USA.
EM hornerjo@ohsu.edu
OI Horner-Johnson, Willi/0000-0003-3568-1400
FU Administration on Intellectual and Developmental Disabilities
[90DD0684]; National Center on Birth Defects and Developmental
Disabilities, Centers for Disease Control and Prevention [U59DD00942];
National Institute on Disability and Rehabilitation Research, U.S.
Department of Education [H133A080031]; Institute on Development &
Disability at Oregon Health & Science University
FX This work was supported in part by grant #90DD0684 from the
Administration on Intellectual and Developmental Disabilities;
cooperative agreement #U59DD00942 from the National Center on Birth
Defects and Developmental Disabilities, Centers for Disease Control and
Prevention; grant #H133A080031 from the National Institute on Disability
and Rehabilitation Research, U.S. Department of Education; and by the
Institute on Development & Disability at Oregon Health & Science
University.
NR 54
TC 5
Z9 5
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-6574
EI 1876-7583
J9 DISABIL HEALTH J
JI Disabil. Health J.
PD OCT
PY 2014
VL 7
IS 4
BP 394
EP 401
DI 10.1016/j.dhjo.2014.06.001
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health; Rehabilitation
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Rehabilitation
GA AP8LW
UT WOS:000342331500005
PM 25065974
ER
PT J
AU Hammond, GRV
Balla, T
AF Hammond, Gerald R. V.
Balla, Tamas
TI A tail of new lipids
SO EMBO JOURNAL
LA English
DT Editorial Material
AB The inositol lipids play many essential roles in eukaryotic physiology, although the action has usually focused on the special properties of their headgroup. Now, a study by Clark et al (2014) refocuses attention on the hydrophobic lipid tails, showing that these too exhibit unique biochemical properties-and are also likely to play a fundamental role in the biology of the lipid.
C1 [Hammond, Gerald R. V.; Balla, Tamas] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Signal Transduct, NIH, Bethesda, MD 20892 USA.
RP Hammond, GRV (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Signal Transduct, NIH, Bethesda, MD 20892 USA.
EM ballat@mail.nih.gov
RI Hammond, Gerald/A-5759-2016;
OI Hammond, Gerald/0000-0002-6660-3272; Balla, Tamas/0000-0002-9077-3335
NR 7
TC 0
Z9 0
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0261-4189
EI 1460-2075
J9 EMBO J
JI Embo J.
PD OCT 1
PY 2014
VL 33
IS 19
BP 2140
EP 2141
DI 10.15252/embj.201489773
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AQ0WL
UT WOS:000342503300003
PM 25180229
ER
PT J
AU Taieb, D
Kaliski, A
Boedeker, CC
Martucci, V
Fojo, T
Adler, JR
Pacak, K
AF Taieb, David
Kaliski, Alexandre
Boedeker, Carsten C.
Martucci, Victoria
Fojo, Tito
Adler, John R., Jr.
Pacak, Karel
TI Current Approaches and Recent Developments in the Management of Head and
Neck Paragangliomas
SO ENDOCRINE REVIEWS
LA English
DT Review
ID GLOMUS-JUGULARE TUMORS; QUALITY-OF-LIFE; POSITRON-EMISSION-TOMOGRAPHY;
CAROTID-BODY PARAGANGLIOMAS; MITOCHONDRIAL COMPLEX II; GAMMA-KNIFE
RADIOSURGERY; SDHB GENE-MUTATIONS; RADIATION-THERAPY; MALIGNANT
PHEOCHROMOCYTOMA; SUCCINATE-DEHYDROGENASE
AB Head and neck paragangliomas (HNPGLs) are rare neuroendocrine tumors belonging to the family of pheochromocytoma/paraganglioma neoplasms. Despite advances in understanding the pathogenesis of these tumors, the growth potential and clinical outcome of individual cases remains largely unpredictable. Over several decades, surgical resection has long been the treatment of choice for HNPGLs. However, increasing experience in various forms of radiosurgery has been reported to result in curative-like outcomes, even for tumors localized in the most inaccessible anatomical areas. The emergence of such new therapies challenges the traditional paradigm for the management of HNPGLs. This review will assist and guide physicians who encounter patients with such tumors, either from a diagnostic or therapeutic standpoint. This review will also particularly emphasize current and emerging knowledge in genetics, imaging, and therapeutic options as well as the health-related quality of life for patients with HNPGLs.
C1 [Taieb, David] Aix Marseille Univ, CERIMED, La Timone Univ Hosp, Dept Nucl Med, F-13385 Marseille, France.
[Kaliski, Alexandre] Besancon Univ Hosp, Dept Radiat Oncol, F-25030 Besancon, France.
[Boedeker, Carsten C.] HELIOS Hanseklinikum Stralsund, Dept Otorhinolaryngol Head & Neck Surg, D-18435 Stralsund, Germany.
[Boedeker, Carsten C.] Univ Hosp, Dept Otorhinolaryngol Head & Neck Surg, Freiburg, Germany.
[Martucci, Victoria; Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, Bethesda, MD 20892 USA.
[Fojo, Tito] NIH, Med Oncol Branch, Bethesda, MD 20892 USA.
[Adler, John R., Jr.] Stanford Univ, Stanford Hosp & Clin, Dept Neurosurg, Stanford, CA 94305 USA.
RP Taieb, D (reprint author), Aix Marseille Univ, CERIMED, La Timone Univ Hosp, Dept Nucl Med, 264 Rue St Pierre, F-13385 Marseille, France.
EM david.taieb@ap-hm.fr; karel@mail.nih.gov
FU Intramural Research Program of the Eucine Kennedy Shriver National
Institute of Child Health and Development; National Institute of
Neurological Disorders and Stroke at the National Intitutes of Health
FX This research was supported by the Intramural Research Program of the
Eucine Kennedy Shriver National Institute of Child Health and
Development and the National Institute of Neurological Disorders and
Stroke at the National Intitutes of Health.
NR 183
TC 20
Z9 20
U1 2
U2 9
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD OCT
PY 2014
VL 35
IS 5
BP 795
EP 819
DI 10.1210/er.2014-1026
PG 25
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AP8RJ
UT WOS:000342346200004
PM 25033281
ER
PT J
AU Deyo, RA
Dworkin, SF
Amtmann, D
Andersson, G
Borenstein, D
Carragee, E
Carrino, J
Chou, R
Cook, K
DeLitto, A
Goertz, C
Khalsa, P
Loeser, J
Mackey, S
Panagis, J
Rainville, J
Tosteson, T
Turk, D
Von Korff, M
Weiner, DK
AF Deyo, Richard A.
Dworkin, Samuel F.
Amtmann, Dagmar
Andersson, Gunnar
Borenstein, David
Carragee, Eugene
Carrino, John
Chou, Roger
Cook, Karon
DeLitto, Anthony
Goertz, Christine
Khalsa, Partap
Loeser, John
Mackey, Sean
Panagis, James
Rainville, James
Tosteson, Tor
Turk, Dennis
Von Korff, Michael
Weiner, Debra K.
TI Focus article: report of the NIH task force on research standards for
chronic low back pain
SO EUROPEAN SPINE JOURNAL
LA English
DT Article
DE Low back pain; Chronic low back pain; Research standards; Minimum
dataset; NIH Task Force
ID CLINICAL-PRACTICE GUIDELINE; DEFINING CHRONIC PAIN; INFORMATION-SYSTEM
PROMIS; FUNCTION ITEM BANK; QUALITY-OF-LIFE; PRIMARY-CARE; PROGNOSTIC
APPROACH; SCREENING TOOL; START BACK; OUTCOME MEASURES
AB Despite rapidly increasing intervention, functional disability due to chronic low back pain (cLBP) has increased in recent decades. We often cannot identify mechanisms to explain the major negative impact cLBP has on patients' lives. Such cLBP is often termed non-specific and may be due to multiple biologic and behavioral etiologies. Researchers use varied inclusion criteria, definitions, baseline assessments, and outcome measures, which impede comparisons and consensus. Therefore, NIH Pain Consortium charged a Research Task Force (RTF) to draft standards for research on cLBP. The resulting multidisciplinary panel recommended using 2 questions to define cLBP; classifying cLBP by its impact (defined by pain intensity, pain interference, and physical function); use of a minimum dataset to describe research participants (drawing heavily on the PROMIS methodology); reporting "responder analyses" in addition to mean outcome scores; and suggestions for future research and dissemination. The Pain Consortium has approved the recommendations, which investigators should incorporate into NIH grant proposals. The RTF believes that these recommendations will advance the field, help to resolve controversies, and facilitate future research addressing the genomic, neurologic, and other mechanistic substrates of chronic low back pain. We expect that the RTF recommendations will become a dynamic document and undergo continual improvement.
A task force was convened by the NIH Pain Consortium with the goal of developing research standards for chronic low back pain. The results included recommendations for definitions, a minimum dataset, reporting outcomes, and future research. Greater consistency in reporting should facilitate comparisons among studies and the development of phenotypes.
C1 [Deyo, Richard A.; Chou, Roger] Oregon Hlth & Sci Univ, Portland, OR 97239 USA.
[Dworkin, Samuel F.; Amtmann, Dagmar; Loeser, John; Turk, Dennis] Univ Washington, Seattle, WA 98195 USA.
[Andersson, Gunnar] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Borenstein, David] George Washington Univ, Washington, DC USA.
[Carragee, Eugene; Mackey, Sean] Stanford Univ, Stanford, CA 94305 USA.
[Carrino, John] Johns Hopkins Univ, Baltimore, MD USA.
[Cook, Karon] Northwestern Univ, Evanston, IL USA.
[DeLitto, Anthony; Weiner, Debra K.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[DeLitto, Anthony; Weiner, Debra K.] Univ Pittsburgh, Pittsburgh, PA USA.
[Goertz, Christine] Palmer Coll Chiropract, Davenport, IA USA.
[Khalsa, Partap] Natl Ctr Complementary & Alternat Med, Bethesda, MD USA.
[Panagis, James] NIAMSD, Bethesda, MD 20892 USA.
[Rainville, James] New England Baptist Hosp, Roxbury Crossing, MA USA.
[Tosteson, Tor] Dartmouth Coll, Hanover, NH USA.
[Von Korff, Michael] Grp Hlth Res Inst, Seattle, WA USA.
RP Deyo, RA (reprint author), Oregon Hlth & Sci Univ, 3181 SW Sam Jackson Pk Rd,Mail Code FM, Portland, OR 97239 USA.
EM deyor@ohsu.edu
FU National Center for Complementary and Alternative Medicine; National
Institute for Arthritis, Musculoskeletal, and Skin Diseases
FX This study was supported by the National Center for Complementary and
Alternative Medicine and the National Institute for Arthritis,
Musculoskeletal, and Skin Diseases.
NR 123
TC 13
Z9 13
U1 8
U2 20
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0940-6719
EI 1432-0932
J9 EUR SPINE J
JI Eur. Spine J.
PD OCT
PY 2014
VL 23
IS 10
BP 2028
EP 2045
DI 10.1007/s00586-014-3540-3
PG 18
WC Clinical Neurology; Orthopedics
SC Neurosciences & Neurology; Orthopedics
GA AQ0EI
UT WOS:000342455200002
PM 25212440
ER
PT J
AU Bartness, TJ
Liu, Y
Shrestha, YB
Ryu, V
AF Bartness, Timothy J.
Liu, Yang
Shrestha, Yogendra B.
Ryu, Vitaly
TI Neural innervation of white adipose tissue and the control of lipolysis
SO FRONTIERS IN NEUROENDOCRINOLOGY
LA English
DT Review
DE Pseudorabies virus; Herpes simplex virus-1; Siberian hamsters; Rats;
Mice; Humans; Denervation; Norepinephrine turnover; Insulin; Leptin
ID SYMPATHETIC-NERVOUS-SYSTEM; HORMONE-SENSITIVE LIPASE;
HEART-RATE-VARIABILITY; ATRIAL-NATRIURETIC-PEPTIDE;
BETA-ADRENERGIC-RECEPTORS; SHORT-DAY RESPONSES; FAT-CELL LIPOLYSIS;
CENTRAL SENSORY CIRCUITS; VAGAL AFFERENT-FIBERS; GENE-RELATED PEPTIDE
AB White adipose tissue (WAT) is innervated by the sympathetic nervous system (SNS) and its activation is necessary for lipolysis. WAT parasympathetic innervation is not supported. Fully-executed SNS-norepinephrine (NE)-mediated WAT lipolysis is dependent on beta-adrenoceptor stimulation ultimately hinging on hormone sensitive lipase and perilipin A phosphorylation. WAT sympathetic drive is appropriately measured electrophysiologically and neurochemically (NE turnover) in non-human animals and this drive is fat pad-specific preventing generalizations among WAT depots and non-WAT organs. Leptin-triggered SNS-mediated lipolysis is weakly supported, whereas insulin or adenosine inhibition of SNS/NE-mediated lipolysis is strongly supported. In addition to lipolysis control, increases or decreases in WAT SNS drive/NE inhibit and stimulate white adipocyte proliferation, respectively. WAT sensory nerves are of spinal-origin and sensitive to local leptin and increases in sympathetic drive, the latter implicating lipolysis. Transsynaptic viral tract tracers revealed WAT central sympathetic and sensory circuits including SNS-sensory feedback loops that may control lipolysis. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Bartness, Timothy J.; Liu, Yang; Ryu, Vitaly] Georgia State Univ, Dept Biol, Ctr Obes Reversal, Atlanta, GA 30302 USA.
[Bartness, Timothy J.; Liu, Yang; Ryu, Vitaly] Georgia State Univ, Ctr Behav Neurosci, Atlanta, GA 30302 USA.
[Liu, Yang; Shrestha, Yogendra B.; Ryu, Vitaly] NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Bartness, TJ (reprint author), Georgia State Univ, Dept Biol, 24 Peachtree Ctr Ave NE, Atlanta, GA 30302 USA.
EM bartness@gsu.edu
FU National Institutes of Health Research Grant [R37 DK 35254]
FX This research was supported, in part, by National Institutes of Health
Research Grant R37 DK 35254 to TJB.
NR 322
TC 33
Z9 33
U1 3
U2 26
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-3022
EI 1095-6808
J9 FRONT NEUROENDOCRIN
JI Front. Neuroendocrinol.
PD OCT
PY 2014
VL 35
IS 4
BP 473
EP 493
DI 10.1016/j.yfrne.2014.04.001
PG 21
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA AQ1GB
UT WOS:000342528800006
PM 24736043
ER
PT J
AU Liu, SH
Sun, XH
Wang, ML
Hou, YY
Zhan, Y
Jiang, YH
Liu, ZJ
Cao, XW
Chen, PF
Liu, Z
Chen, X
Tao, Y
Xu, C
Mao, J
Cheng, CY
Li, CF
Hu, YM
Wang, LS
Chin, YE
Shi, YF
Siebenlist, U
Zhang, XR
AF Liu, Sanhong
Sun, Xiaohua
Wang, Mingliang
Hou, Yingyong
Zhan, Yu
Jiang, Yuhang
Liu, Zhanjie
Cao, Xinwei
Chen, Pengfei
Liu, Zhi
Chen, Xi
Tao, Yu
Xu, Chen
Mao, Jie
Cheng, Chunyan
Li, Cuifeng
Hu, Yiming
Wang, Lunshan
Chin, Y. Eugene
Shi, Yufang
Siebenlist, Ulrich
Zhang, Xiaoren
TI A microRNA 221-and 222-Mediated Feedback Loop Maintains Constitutive
Activation of NF kappa B and STAT3 in Colorectal Cancer Cells
SO GASTROENTEROLOGY
LA English
DT Article
DE microRNA 221; microRNA 222; Colon Cancer; Carcinogenesis
ID COLITIS-ASSOCIATED CANCER; COLON-CANCER; IKK-ALPHA; INFLAMMATION;
EXPRESSION; PATHWAY; TUMORIGENESIS; TRANSLATION; PROGRESSION;
DIFFERENTIATION
AB BACKGROUND & AIMS: Constitutive activation of the transcription factors nuclear factor kappa B (NF-kappa B) and STAT3 is involved in the development and progression of human colorectal cancer (CRC). Little is known about how these factors become activated in cancer cells. We investigated whether microRNA miR-221 and miR-222 regulate NF-kappa B and signal transducer and activator of transcription 3 (STAT3) activation in human CRC cell lines. METHODS: CRC cell lines (HCT116 and RKO) were transfected with miR-221 or miR-222 mimics or inhibitors. The activity levels of NF-kappa B and STAT3 were measured in dual luciferase reporter assays. We used immunoblot and real-time polymerase chain reaction analyses to measure protein and messenger RNA (mRNA) levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. Mice were given injections of azoxymethane, followed by dextran sodium sulfate, along with control lentivirus or those expressing mRNAs that bind miR-221 and miR-222 (miR-221/miR-222 sponge). The levels of miR-221 and miR-222 as well as RelA, STAT3, and PDLIM2 mRNAs were measured in 57 paired CRC and adjacent nontumor tissues from patients. RESULTS: In CRC cell lines, mimics of miR-221 and miR-222 activated NF-kappa B and STAT3, further increasing expression of miR-221 and miR-222. miR-221 and miR-222 bound directly to the coding region of RelA mRNA, increasing its stability. miR-221 and miR-222 also reduced the ubiquitination and degradation of the RelA and STAT3 proteins by binding to the 3' untranslated region of PDLIM2 mRNA (PDLIM2 is a nuclear ubiquitin E3 ligase for RelA and STAT3). Incubation of CRC cells with miR-221 and miR-222 inhibitors reduced their proliferation and colony formation compared with control cells. In mice with colitis, injection of lentiviruses expressing miR-221/miR-222 sponges led to formation of fewer tumors than injection of control lentiviruses. Human CRC tissues had higher levels of miR-221 and miR-222 than nontumor colon tissues; increases correlated with increased levels of RelA and STAT3 mRNAs. Levels of PDLIM2 mRNA were lower in CRC than nontumor tissues. CONCLUSIONS: In human CRC cells, miR-221 and miR-222 act in a positive feedback loop to increase expression levels of RelA and STAT3. Antagonism of miR-221 and miR-222 reduces growth of colon tumors in mice with colitis.
C1 [Liu, Sanhong; Sun, Xiaohua; Zhan, Yu; Jiang, Yuhang; Liu, Zhanjie; Cao, Xinwei; Chen, Pengfei; Liu, Zhi; Chen, Xi; Tao, Yu; Mao, Jie; Cheng, Chunyan; Li, Cuifeng; Hu, Yiming; Wang, Lunshan; Chin, Y. Eugene; Shi, Yufang; Zhang, Xiaoren] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai 200031, Peoples R China.
[Liu, Sanhong; Sun, Xiaohua; Zhan, Yu; Jiang, Yuhang; Liu, Zhanjie; Cao, Xinwei; Chen, Pengfei; Liu, Zhi; Chen, Xi; Tao, Yu; Mao, Jie; Cheng, Chunyan; Li, Cuifeng; Hu, Yiming; Wang, Lunshan; Chin, Y. Eugene; Shi, Yufang; Zhang, Xiaoren] Shanghai Jiao Tong Univ, Sch Med, Shanghai 200031, Peoples R China.
[Wang, Mingliang] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, Shanghai 200031, Peoples R China.
[Hou, Yingyong; Xu, Chen] Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200433, Peoples R China.
[Siebenlist, Ulrich] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Zhang, XR (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai 200031, Peoples R China.
EM xrzhang@sibs.ac.cn
FU National Basic Research Program [2014CB541904, 2011CB946102,
2014CB943600]; National Natural Science Foundation of China [31370881,
90919017, 30972695]; Knowledge Innovation Project of Chinese Academy of
Sciences [KSCX1-YW-22]
FX Supported by grants from the National Basic Research Program
(2014CB541904, 2011CB946102, 2014CB943600), the National Natural Science
Foundation of China (31370881, 90919017 and 30972695), and the Knowledge
Innovation Project of Chinese Academy of Sciences (KSCX1-YW-22).
NR 38
TC 29
Z9 32
U1 5
U2 21
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2014
VL 147
IS 4
BP 847
EP U231
DI 10.1053/j.gastro.2014.06.006
PG 24
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ0SO
UT WOS:000342493200028
PM 24931456
ER
PT J
AU Yi, CJ
Yang, E
Lai, SH
Gai, N
Liu, C
Liu, ST
Zimmerman, SL
Lima, JAC
Bluemke, DA
AF Yi, Colin J.
Yang, Eunice
Lai, Shenghan
Gai, Neville
Liu, Chia
Liu, Songtao
Zimmerman, Stefan L.
Lima, Joao A. C.
Bluemke, David A.
TI Progression of diffuse myocardial fibrosis assessed by cardiac magnetic
resonance T-1 mapping
SO INTERNATIONAL JOURNAL OF CARDIOVASCULAR IMAGING
LA English
DT Article
DE Cardiac magnetic resonance imaging; Diffuse myocardial fibrosis; Late
gadolinium enhancement; T-1 mapping; Non-ischemic and ischemic
cardiomyopathy
ID LOOK-LOCKER; HYPERTROPHIC CARDIOMYOPATHY; DILATED CARDIOMYOPATHY;
HYPERTENSIVE PATIENTS; GD-DTPA; INFARCTION; ASSOCIATION; DYSFUNCTION;
RECOVERY; ENHANCEMENT
AB To evaluate long-term changes in diffuse myocardial fibrosis using cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) and T-1 mapping. Patients with chronic stable cardiomyopathy and stable clinical status (n = 52) underwent repeat CMR at a 6 month or greater follow up interval and had LGE and left ventricular (LV) T-1 mapping CMR. Diffuse myocardial fibrosis (excluding areas of focal myocardial scar) was assessed by post gadolinium myocardial T-1 times. Mean baseline age of 52 patients (66 % male) was 35 +/- A 19 years with a mean interval between CMR examinations of 2.0 +/- A 0.8 years. CMR parameters, including LV mass and ejection fraction, showed no change at follow-up CMR (p > 0.05). LVT1 times (excluding focal scar) decreased over the study interval (from 468 +/- A 106 to 434 +/- A 82 ms, p = 0.049). 38 Patients had no visual LGE-, while 14 were LGE+. For LGE- patients, greater change in LV mass and end systolic volume index were associated with change in T-1 time (beta = -2.03 ms/g/m(2), p = 0.035 and beta = 2.1 ms/mL/m(2), p = 0.029, respectively). For LGE+ patients, scar size was stable between CMR1 and CMR2 (10.7 +/- A 13.8 and 11.5 +/- A 13.9 g, respectively, p = 0.32). These results suggest that diffuse myocardial fibrosis, as assessed by T-1 mapping, progresses over time in patients with chronic stable cardiomyopathy.
C1 [Yi, Colin J.; Yang, Eunice; Gai, Neville; Liu, Chia; Liu, Songtao; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Yang, Eunice; Lai, Shenghan; Zimmerman, Stefan L.; Lima, Joao A. C.; Bluemke, David A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Bluemke, DA (reprint author), NIH, 10 Ctr Dr,Rm 10-1C355, Bethesda, MD 20892 USA.
EM dbluemke@jhmi.edu
FU Intramural NIH HHS [ZIA CL090019-04, ZIA EB000072-04]
NR 35
TC 2
Z9 4
U1 0
U2 11
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1569-5794
EI 1573-0743
J9 INT J CARDIOVAS IMAG
JI Int. J. Cardiovasc. Imaging
PD OCT
PY 2014
VL 30
IS 7
BP 1339
EP 1346
DI 10.1007/s10554-014-0459-z
PG 8
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA AQ0DS
UT WOS:000342453600018
PM 24903343
ER
PT J
AU Spreafico, A
Chi, KN
Sridhar, SS
Smith, DC
Carducci, MA
Kavsak, P
Wong, TS
Wang, LS
Ivy, SP
Mukherjee, SD
Kollmannsberger, CK
Sukhai, MA
Takebe, N
Kamel-Reid, S
Siu, LL
Hotte, SJ
AF Spreafico, Anna
Chi, Kim N.
Sridhar, Srikala S.
Smith, David C.
Carducci, Michael A.
Kavsak, Peter
Wong, Tracy S.
Wang, Lisa
Ivy, S. Percy
Mukherjee, Som Dave
Kollmannsberger, Christian K.
Sukhai, Mahadeo A.
Takebe, Naoko
Kamel-Reid, Suzanne
Siu, Lillian L.
Hotte, Sebastien J.
TI A randomized phase II study of cediranib alone versus cediranib in
combination with dasatinib in docetaxel resistant, castration resistant
prostate cancer patients
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Cediranib; Dasatinib; Castration resistant prostate cancer; Quality of
life; Bone turnover marker
ID ADVANCED SOLID TUMORS; MITOXANTRONE PLUS PREDNISONE; TYROSINE KINASE
INHIBITOR; POTENT ANTITUMOR-ACTIVITY; GROWTH-FACTOR RECEPTOR-2; CHRONIC
MYELOID-LEUKEMIA; QUALITY-OF-LIFE; DOUBLE-BLIND; OPEN-LABEL; ENDOTHELIAL
PERMEABILITY
AB Background Activation of the vascular endothelial growth factor receptor (VEGFR) and the oncogenic Src pathway has been implicated in the development of castration-resistant prostate cancer (CRPC) in preclinical models. Cediranib and dasatinib are multi-kinase inhibitors targeting VEGFR and Src respectively. Phase II studies of cediranib and dasatinib in CRPC have shown single agent activity. Methods Docetaxel-pretreated CRPC patients were randomized to arm A: cediranib alone (20 mg/day) versus arm B: cediranib (20 mg/day) plus dasatinib (100 mg/day) given orally on 4-week cycles. Primary endpoint was 12-week progression-free survival (PFS) as per the Prostate Cancer Clinical Trials Working Group (PCWG2). Patient reported outcomes were evaluated using Functional Assessment of Cancer Therapy-Prostate (FACT-P) and Present Pain Intensity (PPI) scales. Correlative studies of bone turnover markers (BTM), including bone alkaline phosphate (BAP) and serum beta-C telopeptide (B-CTx) were serially assayed. Results A total of 22 patients, 11 per arm, were enrolled. Baseline demographics were similar in both arms. Median number of cycles =4 in arm A (range 1-12) and 2 in arm B (range 1-9). Twelve-week PFS was 73 % in arm A versus 18 % in arm B (p = 0.03). Median PFS in months (arm A versus B) was: 5.2 versus 2.6 (95 % CI: 1.9-6.5 versus 1.4-not reached). Most common grade 3 toxicities were hypertension, anemia and thrombocytopenia in arm A and hypertension, diarrhea and fatigue in arm B. One treatment-related death (retroperitoneal hemorrhage) was seen in arm A. FACT-P and PPI scores did not significantly change in either arm. No correlation between BTM and PFS was seen in either arm. Conclusions Although limited by small numbers, this randomized study showed that the combination of VEGFR and Src targeted therapy did not result in improved efficacy and may be associated with a worse outcome than VEGFR targeted therapy alone in patients with CRPC. ClinicalTrials.gov number: NCT01260688.
C1 [Spreafico, Anna; Sridhar, Srikala S.; Wong, Tracy S.; Wang, Lisa; Sukhai, Mahadeo A.; Kamel-Reid, Suzanne; Siu, Lillian L.] Princess Margaret Canc Ctr, Toronto, ON, Canada.
[Chi, Kim N.; Kollmannsberger, Christian K.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Smith, David C.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Carducci, Michael A.] Johns Hopkins Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Kavsak, Peter; Mukherjee, Som Dave; Hotte, Sebastien J.] Juravinski Canc Ctr, Hamilton, ON, Canada.
[Ivy, S. Percy] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Takebe, Naoko] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
RP Hotte, SJ (reprint author), Juravinski Canc Ctr, 699 Concession St, Hamilton, ON, Canada.
EM sebastien.hotte@jcc.hhsc.ca
FU US National Cancer Institute [PJC-002/CTEP 8476, U01-CA132123]
FX This study (PJC-002/CTEP 8476), supported by the US National Cancer
Institute, is led by the Princess Margaret Hospital Phase I Consortium
(U01-CA132123), with participation from the University of Chicago Phase
II Consortium (N01-CM-2011-00071) and the Johns Hopkins Kimmel Cancer
Center Phase I Consortium (U01-CA70095).
NR 83
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U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD OCT
PY 2014
VL 32
IS 5
BP 1005
EP 1016
DI 10.1007/s10637-014-0106-5
PG 12
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA AP9PK
UT WOS:000342411500022
PM 24788563
ER
PT J
AU Sugui, JA
Peterson, SW
Figat, A
Hansen, B
Samson, RA
Mellado, E
Cuenca-Estrella, M
Kwon-Chung, KJ
AF Sugui, Janyce A.
Peterson, Stephen W.
Figat, Abigail
Hansen, Bryan
Samson, Robert A.
Mellado, Emilia
Cuenca-Estrella, Manuel
Kwon-Chung, Kyung J.
TI Genetic Relatedness versus Biological Compatibility between Aspergillus
fumigatus and Related Species
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID SECTION FUMIGATI; SP NOV.; GALLERIA-MELLONELLA; LENTULUS; VIRIDINUTANS;
RECOGNITION; DIVERSITY; VIRULENCE; COMPLEX; SUSCEPTIBILITY
AB Aspergillus section Fumigati contains 12 clinically relevant species. Among these Aspergillus species, A. fumigatus is the most frequent agent of invasive aspergillosis, followed by A. lentulus and A. viridinutans. Genealogical concordance and mating experiments were performed to examine the relationship between phylogenetic distance and mating success in these three heterothallic species. Analyses of 19 isolates from section Fumigati revealed the presence of three previously unrecognized species within the broadly circumscribed species A. viridinutans. A single mating type was found in the new species Aspergillus pseudofelis and Aspergillus pseudoviridinutans, but in Aspergillus parafelis, both mating types were present. Reciprocal interspecific pairings of all species in the study showed that the only successful crosses occurred with the MAT1-2 isolates of both A. parafelis and A. pseudofelis. The MAT1-2 isolate of A. parafelis was fertile when paired with the MAT1-1 isolates of A. fumigatus, A. viridinutans, A. felis, A. pseudoviridinutans, and A. wyomingensis but was not fertile with the MAT1-1 isolate of A. lentulus. The MAT1-2 isolates of A. pseudofelis were fertile when paired with the MAT1-1 isolate of A. felis but not with any of the other species. The general infertility in the interspecies crossings suggests that genetically unrelated species are also biologically incompatible, with the MAT1-2 isolates of A. parafelis and A. pseudofelis being the exception. Our findings underscore the importance of genealogical concordance analysis for species circumscription, as well as for accurate species identification, since misidentification of morphologically similar pathogens with differences in innate drug resistance may be of grave consequences for disease management.
C1 [Sugui, Janyce A.; Figat, Abigail; Kwon-Chung, Kyung J.] NIAID, Mol Microbiol Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Peterson, Stephen W.] USDA, Natl Ctr Agr Utilizat Res, Peoria, IL USA.
[Hansen, Bryan] NIAID, Electron Microscopy Unit, Res Technol Branch, Rocky Mt Labs,NIH, Hamilton, MT USA.
[Samson, Robert A.] CBS KNAW Fungal Biodivers Ctr, Dept Appl & Ind Mycol, Utrecht, Netherlands.
[Mellado, Emilia; Cuenca-Estrella, Manuel] Inst Salud Carlos III, Ctr Nacl Microbiol, Madrid, Spain.
RP Kwon-Chung, KJ (reprint author), NIAID, Mol Microbiol Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jkchung@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This work was supported by the Intramural program of the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health.
NR 52
TC 9
Z9 9
U1 4
U2 17
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0095-1137
EI 1098-660X
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD OCT
PY 2014
VL 52
IS 10
BP 3707
EP 3721
DI 10.1128/JCM.01704-14
PG 15
WC Microbiology
SC Microbiology
GA AP9AX
UT WOS:000342371700026
PM 25100816
ER
PT J
AU Jena, AB
DePasse, JW
Prasad, V
AF Jena, Anupam B.
DePasse, Jacqueline W.
Prasad, Vinay
TI The Declining Demand for Hospital Care as a Rationale for Duty Hour
Reform
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
ID INTERNS; TIME
AB The regulation of duty hours of physicians in training remains among the most hotly debated subjects in medical education. Although recent duty hour reforms have been chiefly motivated by concerns about resident well-being and medical errors attributable to resident fatigue, the debate surrounding duty hour reform has infrequently involved discussion of one of the most important secular changes in hospital care that has affected nearly all developed countries over the last 3 decades: the declining demand for hospital care. For example, in 1980, we show that resident physicians in US teaching hospitals provided, on average, 1,302 inpatient days of care per resident physician compared to 593 inpatient days in 2011, a decline of 54 %. This decline in the demand for hospital care by residents provides an under-recognized economic rationale for reducing residency duty hours, a rationale based solely on supply and demand considerations. Work hour reductions and growing requirements for outpatient training can be seen as an appropriate response to the shrinking demand for hospital care across the health-care sector.
C1 [Jena, Anupam B.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Jena, Anupam B.] NBER, Cambridge, MA 02138 USA.
[Jena, Anupam B.; DePasse, Jacqueline W.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Jena, Anupam B.; DePasse, Jacqueline W.; Prasad, Vinay] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Jena, AB (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM jena@hcp.med.harvard.edu
OI Prasad, Vinay/0000-0002-6110-8221
FU NIH HHS [DP5 OD017897, 1DP5OD017897-01]
NR 9
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD OCT
PY 2014
VL 29
IS 10
BP 1400
EP 1403
DI 10.1007/s11606-014-2901-2
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA AQ0DV
UT WOS:000342453900021
PM 24866469
ER
PT J
AU Bishop, SL
Farmer, C
Thurm, A
AF Bishop, S. L.
Farmer, C.
Thurm, A.
TI EARLY MOTOR MILESTONE MARKERS OF DEVELOPMENTAL TRAJECTORIES: AGE OF
WALKING IN AUTISM SPECTRUM DISORDERS (ASD) VS. NON-ASD
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Meeting Abstract
DE gross motor milestones; walking; intellectual disability; autism
spectrum disorder; developmental disability
C1 [Bishop, S. L.] Weill Cornell Med Coll, White Plains, NY USA.
[Farmer, C.; Thurm, A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0964-2633
EI 1365-2788
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD OCT
PY 2014
VL 58
IS 10
BP 883
EP 883
PG 1
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
Neurology; Psychiatry; Rehabilitation
GA AP5YA
UT WOS:000342153400003
ER
PT J
AU Raznahan, A
Lee, NR
Greenstein, D
Wallace, GL
Blumenthal, J
Clasen, L
Giedd, JN
AF Raznahan, A.
Lee, N. R.
Greenstein, D.
Wallace, G. L.
Blumenthal, J.
Clasen, L.
Giedd, J. N.
TI NEUROANATOMICALLY PHENOTYPING SEX CHROMOSOME ANEUPLOIDIES AS MODELS OF
GENETIC RISK FOR AUTISTIC BEHAVIORS
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Meeting Abstract
DE Aneuploidy; Cortical Thickness; Surface Area; Pseudoautosomal
C1 [Raznahan, A.; Lee, N. R.; Greenstein, D.; Blumenthal, J.; Clasen, L.; Giedd, J. N.] NIMH, Sect Brain Imaging, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Wallace, G. L.] George Washington Univ, Dept Speech & Hearing Sci, Washington, DC 20052 USA.
RI Giedd, Jay/J-9644-2015; Lee, Nancy/M-7492-2016
OI Giedd, Jay/0000-0003-2002-8978; Lee, Nancy/0000-0002-6663-0713
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 0964-2633
EI 1365-2788
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD OCT
PY 2014
VL 58
IS 10
BP 887
EP 887
PG 1
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
Neurology; Psychiatry; Rehabilitation
GA AP5YA
UT WOS:000342153400018
ER
PT J
AU Neelavalli, J
Mody, S
Yeo, L
Jella, PK
Korzeniewski, SJ
Saleem, S
Katkuri, Y
Bahado-Singh, RO
Hassan, SS
Haacke, EM
Romero, R
Thomason, ME
AF Neelavalli, Jaladhar
Mody, Swati
Yeo, Lami
Jella, Pavan Kumar
Korzeniewski, Steven J.
Saleem, Sheena
Katkuri, Yashwanth
Bahado-Singh, Ray O.
Hassan, Sonia S.
Haacke, E. Mark
Romero, Roberto
Thomason, Moriah E.
TI MR Venography of the Fetal Brain Using Susceptibility Weighted Imaging
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE fetal imaging; pregnancy; cerebral; gradient echo; phase; veins
ID DIFFUSE AXONAL INJURY; OXYGEN-SATURATION; ISCHEMIC-STROKE;
CEREBRAL-PALSY; 3 TESLA; CONTRAST; CHILDREN; PHASE; MICROBLEEDS; LESIONS
AB Purpose: To evaluate the feasibility of performing fetal brain magnetic resonance venography using susceptibility weighted imaging (SWI).
Materials and Methods: After obtaining informed consent, pregnant women in the second and third trimester were imaged using a modified SWI sequence. Fetal SWI acquisition was repeated when fetal or maternal motion was encountered. The median and maximum number of times an SWI sequence was repeated was four and six respectively. All SWI image data were systematically evaluated by a pediatric neuroradiologist for image quality using an ordinal scoring scheme: 1. diagnostic; 2. diagnostic with artifacts; and 3. nondiagnostic. The best score in an individual fetus was used for further statistical analysis. Visibility of venous vasculature was also scored using a dichotomous variable. A subset of SWI data was re-evaluated by the first and independently by a second pediatric neuroradiologist. Kappa coefficients were computed to assess intra-rater and inter-rater reliability.
Results: SWI image data from a total of 22 fetuses were analyzed. Median gestational age and interquartile range of the fetuses imaged were 32 (29.9-34.9) weeks. In 68.2% of the cases (n = 15), there was no artifact; 22.7% (n = 5) had minor artifacts and 9.1% (n = 2) of the data was of nondiagnostic quality. Cerebral venous vasculature was visible in 86.4% (n = 19) of the cases. Substantial agreement (Kappa = 0.73; 95% confidence interval 0.44-1.00)) was observed for intra-rater reliability and moderate agreement (Kappa = 0.48; 95% confidence interval 0.19-0.77) was observed for inter-rater reliability.
Conclusion: It is feasible to perform fetal brain venography in humans using SWI.
C1 [Neelavalli, Jaladhar; Jella, Pavan Kumar; Katkuri, Yashwanth; Haacke, E. Mark] Wayne State Univ, Dept Radiol, Detroit, MI USA.
[Mody, Swati; Saleem, Sheena] Childrens Hosp Michigan, Dept Pediat Imaging, Detroit, MI 48201 USA.
[Yeo, Lami; Korzeniewski, Steven J.; Bahado-Singh, Ray O.; Hassan, Sonia S.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Yeo, Lami; Korzeniewski, Steven J.; Hassan, Sonia S.; Romero, Roberto; Thomason, Moriah E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Bethesda, MD USA.
[Yeo, Lami; Korzeniewski, Steven J.; Hassan, Sonia S.; Romero, Roberto; Thomason, Moriah E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NIH, Detroit, MI USA.
[Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Thomason, Moriah E.] Wayne State Univ, Dept Pediat, Merrill Palmer Skillman Inst Child & Family Dev, Detroit, MI 48202 USA.
RP Neelavalli, J (reprint author), Univ Hlth Ctr, 4201 St Antoine,5E-12, Detroit, MI 48201 USA.
EM jaladhar@wayne.edu
OI Saleem, Sheena/0000-0002-6772-4981
FU NHLBI [1R42HL112580-01A1]; Perinatal Research Initiative of the Wayne
State University School of Medicine, Detroit, Michigan
FX Contract grant sponsor: NHLBI; Contract grant number: 1R42HL112580-01A1;
Contract grant sponsor: Perinatal Research Initiative of the Wayne State
University School of Medicine, Detroit, Michigan.
NR 49
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U1 3
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-1807
EI 1522-2586
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD OCT
PY 2014
VL 40
IS 4
BP 949
EP 957
DI 10.1002/jmri.24476
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AP8QA
UT WOS:000342342500024
PM 24989457
ER
PT J
AU Kim, JS
Oh, YS
Lee, KS
Song, IU
Park, IS
Yang, DW
Koo, JS
Goldstein, DS
AF Kim, Joong-Seok
Oh, Yoon-Sang
Lee, Kwang-Soo
Song, In-Uk
Park, In-Seok
Yang, Dong-Won
Koo, Ja-Seong
Goldstein, David S.
TI Carotid artery thickening and neurocirculatory abnormalities in de novo
Parkinson disease
SO JOURNAL OF NEURAL TRANSMISSION
LA English
DT Article
DE Parkinson disease; Carotid; Intima-media thickness; Orthostatic
hypotension; Supine hypertension; Nocturnal blood pressure; Non-dipping;
Baroreflex
ID NOCTURNAL BLOOD-PRESSURE; ORTHOSTATIC HYPOTENSION; HYPERTENSION;
PATHOGENESIS; PREVALENCE; THICKNESS; ADULTS
AB Cognitive dysfunction constitutes a major non-motor manifestation of Parkinson disease (PD), but the mechanisms remain incompletely understood. Neurocirculatory abnormalities such as supine hypertension (SH) and orthostatic hypotension (OH), white matter hyperintensities upon magnetic resonance imaging, and dementia are inter-related in PD, even in patients with early, levodopa-untreated disease. These abnormalities might in turn be associated with carotid atherosclerosis which, by a variety of interacting means could contribute to repeated episodes of cerebral hypo- and hyper-perfusion. We investigated inter-correlations among neurocirculatory and carotid sonographic measurements [intimal-medial thickness (IMT) and wall:lumen ratios (WLR)] in 65 patients with levodopa-untreated, de novo PD who underwent tilt table testing and 24-h ambulatory blood pressure monitoring. Increased mean IMT and WLR were associated with OH and supine and overnight blood pressures. Across individuals the orthostatic fall in systolic pressure was correlated with both IMT and WLR. Since arteriosclerosis would be expected to splint carotid sinus baroreceptors, complex positive interactions among carotid wall thickening, SH, and OH may result in myriad episodes of cerebral hypo- and hyper-perfusion, contributing to microvascular injury and consequently to the cognitive dysfunction attending PD.
C1 [Kim, Joong-Seok; Oh, Yoon-Sang; Lee, Kwang-Soo; Song, In-Uk; Park, In-Seok; Yang, Dong-Won; Koo, Ja-Seong] Catholic Univ Korea, Dept Neurol, Coll Med, Seoul St Marys Hosp, Seoul 137701, South Korea.
[Goldstein, David S.] NINDS, Clin Neurocardiol Sect, Clin Neurosci Program, Div Intramural Res,NIH, Bethesda, MD 20892 USA.
RP Kim, JS (reprint author), Catholic Univ Korea, Dept Neurol, Coll Med, Seoul St Marys Hosp, 505 Banpo Dong, Seoul 137701, South Korea.
EM neuronet@catholic.ac.kr; goldsteind@ninds.nih.gov
FU Division of Intramural Research of the NINDS; Seoul St. Mary's Hospital
Clinical Medicine Research Program through Catholic University of Korea
FX Dr. Goldstein is supported by the Division of Intramural Research of the
NINDS.; This research was supported by Seoul St. Mary's Hospital
Clinical Medicine Research Program years of 2013 through the Catholic
University of Korea.
NR 37
TC 4
Z9 4
U1 0
U2 7
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0300-9564
EI 1435-1463
J9 J NEURAL TRANSM
JI J. Neural Transm.
PD OCT
PY 2014
VL 121
IS 10
BP 1259
EP 1268
DI 10.1007/s00702-014-1203-5
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ0DR
UT WOS:000342453500005
PM 24692006
ER
PT J
AU Yakel, JL
AF Yakel, Jerrel L.
TI Nicotinic ACh receptors in the hippocampal circuit; functional
expression and role in synaptic plasticity
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Review
ID STRATUM-ORIENS INTERNEURONS; CENTRAL CHOLINERGIC SYSTEM; LONG-TERM
POTENTIATION; CENTRAL-NERVOUS-SYSTEM; BETA-AMYLOID PEPTIDE;
ACETYLCHOLINE-RECEPTORS; RAT HIPPOCAMPAL; ALZHEIMERS-DISEASE;
BETA-AMYLOID(1-42) PEPTIDE; CALCIUM PERMEABILITY
AB Acetylcholine (ACh) can regulate neuronal excitability in the hippocampus, an important area in the brain for learning and memory, by acting on both nicotinic (nAChRs) and muscarinic ACh receptors. The primary cholinergic input to the hippocampus arises from the medial septum and diagonal band of Broca (MS-DBB), and we investigated how their activation regulated hippocampal synaptic plasticity. We found that activation of these endogenous cholinergic inputs can directly induce different forms of hippocampal synaptic plasticity with a timing precision in themillisecond range. Furthermore, we observed a prolonged enhancement of excitability both pre- and postsynaptically. Lastly we found that the presence of the alpha 7 nAChR subtype to both pre- and postsynaptic sites appeared to be required to induce this plasticity. We propose that alpha 7 nAChRs coordinate pre- and postsynaptic activities to induce glutamatergic synaptic plasticity, and thus provide a novel mechanism underlying physiological neuronal communication that could lead to timing-dependent synaptic plasticity in the hippocampus.
C1 [Yakel, Jerrel L.] NIEHS, Neurobiol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Yakel, JL (reprint author), NIEHS, F2-08,POB 12233,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM yakel@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences
FX This work was supported by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences.
NR 92
TC 10
Z9 11
U1 1
U2 23
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3751
EI 1469-7793
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD OCT 1
PY 2014
VL 592
IS 19
BP 4147
EP 4153
DI 10.1113/jphysiol.2014.273896
PG 7
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA AQ0ZE
UT WOS:000342510400007
PM 24860170
ER
PT J
AU Johnston, A
McBain, CJ
Fisahn, A
AF Johnston, April
McBain, Chris J.
Fisahn, Andre
TI 5-Hydroxytryptamine(1A) receptor-activation hyperpolarizes pyramidal
cells and suppresses hippocampal gamma oscillations via Kir3 channel
activation
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID IN-VITRO; SEROTONIN RECEPTOR; 5-HT1A RECEPTORS; K+ CHANNELS; G-PROTEINS;
NEURONS; RAT; MODULATION; EXPRESSION; FREQUENCY
AB Rhythmic cortical neuronal oscillations in the gamma frequency band (30-80 Hz, gamma oscillations) have been associated with cognitive processes such as sensory perception and integration, attention, learning, and memory. Gamma oscillations are disrupted in disorders for which cognitive deficits are hallmark symptoms such as schizophrenia and Alzheimer's disease. In vitro, various neurotransmitters have been found to modulate gamma oscillations. Serotonin (5-HT) has long been known to be important for both behavioural and cognitive functions such as learning and memory. Multiple 5-HT receptor subtypes are expressed in the CA3 region of the hippocampus and high doses of 5-HT reduce the power of induced gamma oscillations. Hypothesizing that 5-HT may have cell-and receptor subtype-specific modulatory effects, we investigated the receptor subtypes, cell types and cellular mechanisms engaged by 5-HT in the modulation of gamma oscillations in mice and rats. We found that 5-HT decreases the power of kainate-induced hippocampal gamma oscillations in both species via the 5-HT1A receptor subtype. Whole-cell patch clamp recordings demonstrated that this decrease was caused by a hyperpolarization of CA3 pyramidal cells and a reduction of their firing frequency, but not by alteration of inhibitory neurotransmission. Finally, our results show that the effect on pyramidal cells is mediated via the G protein-coupled receptor inwardly rectifying potassium channel Kir3. Our findings suggest this novel cellular mechanism as a potential target for therapies that are aimed at alleviating cognitive decline by helping the brain to maintain or re-establish normal gamma oscillation levels in neuropsychiatric and neurodegenerative disorders.
C1 [Johnston, April; Fisahn, Andre] Karolinska Inst, Ctr Alzheimer Res, Dept NVS, Div Neurogeriatr,Neuronal Oscillat Lab, S-14186 Stockholm, Sweden.
[Johnston, April; McBain, Chris J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Fisahn, A (reprint author), Karolinska Inst, Ctr Alzheimer Res, Dept Neurobiol Care Sci & Soc, Div Neurogeriatr,Neuronal Oscillat Lab, Retzius Vag 8, S-17177 Stockholm, Sweden.
EM andre.fisahn@ki.se
FU Karolinska Institute-NIH; National Institutes of Health; Swedish
Research Council; Swedish Medical Association; Swedish Brain Foundation;
Strategic Program in Neurosciences at the Karolinska Institute
FX This work was supported by a Karolinska Institute-NIH PhD studentship
(A.J.), the National Institutes of Health (C.J.M) and the Swedish
Research Council, the Swedish Medical Association, the Swedish Brain
Foundation and the Strategic Program in Neurosciences at the Karolinska
Institute (A.F.).
NR 36
TC 10
Z9 11
U1 2
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3751
EI 1469-7793
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD OCT 1
PY 2014
VL 592
IS 19
BP 4187
EP 4199
DI 10.1113/jphysiol.2014.279083
PG 13
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA AQ0ZE
UT WOS:000342510400011
PM 25107925
ER
PT J
AU Raznahan, A
AF Raznahan, Armin
TI Sizing Up the Search for Autism Spectrum Disorder (ASD) Risk Markers
During Prenatal and Early Postnatal Life
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID BRAIN OVERGROWTH
C1 [Raznahan, Armin] NIMH, Bethesda, MD 20892 USA.
[Raznahan, Armin] NIH, Intramural Res Program, Bethesda, MD 20892 USA.
RP Raznahan, A (reprint author), NIMH, NIH, Child Psychiat Branch, Room 4C108,Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM raznahana@mail.nih.gov
FU Intramural NIH HHS [Z99 MH999999]
NR 10
TC 0
Z9 0
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
EI 1527-5418
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2014
VL 53
IS 10
BP 1045
EP 1047
DI 10.1016/j.jaac.2014.07.010
PG 3
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA AP9MO
UT WOS:000342404100003
PM 25245346
ER
PT J
AU Kaffenberger, BH
Zuo, RC
Gru, A
Plotner, AN
Sweeney, SA
Devine, SM
Hymes, SR
Cowen, EW
AF Kaffenberger, Benjamin H.
Zuo, Rena C.
Gru, Alejandro
Plotner, Alisha N.
Sweeney, Sarah A.
Devine, Steven M.
Hymes, Sharon R.
Cowen, Edward W.
TI Graft-versus-host disease-associated angiomatosis: A
clinicopathologically distinct entity
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Article
DE angioendotheliomatosis; angiomatosis; eruptive angiomas;
graft-versus-host disease; sclerosis; sclerotic; vascular tumors
ID VASCULAR PROLIFERATIONS; ERUPTIVE ANGIOMAS; SKIN; RADIOTHERAPY; TUMORS;
ANGIOENDOTHELIOMATOSIS; TRANSPLANTATION; CYCLOSPORINE; ENDOTHELIUM;
MANAGEMENT
AB Background: Chronic graft-versus-host disease (GVHD) may present with various cutaneous manifestations. Isolated case reports describe eruptive angiomas in this setting.
Objective: We sought to provide a clinical and pathologic description of vascular proliferations in patients with GVHD.
Methods: Cases of documented GVHD associated with vascular proliferations were collected from the National Institutes of Health, Ohio State University, and MD Anderson Cancer Center.
Results: Eleven patients with a diagnosis of GVHD who developed vascular proliferations were identified. All patients manifested sclerotic type chronic GVHD of the skin. Vascular lesions were first documented a median of 44 months after transplantation and occurred primarily on the lower extremities or trunk. Histopathology revealed anastomosing networks of thin-walled vascular proliferations in a vague lobular growth pattern, with overlying epidermal acanthosis, peripheral collarette, ulceration, and disorganized fibroblast-rich and fibrotic stroma. Improvement was noted in 1 patient treated with propranolol and sirolimus and 1 patient with electrocautery.
Limitations: Given the retrospective nature of the study, the overall incidence of vascular lesions in patients with GVHD is unknown. Histopathology was present for review on only 3 of 11 patients.
Conclusion: The phenomenon of vascular lesions appears to be relatively specific for sclerotic type chronic GVHD when compared with other fibrosing diseases. We propose the term "graft-versus-host disease-associated angiomatosis'' to describe this entity.
C1 [Kaffenberger, Benjamin H.; Gru, Alejandro; Plotner, Alisha N.] Ohio State Univ, Div Dermatol, Wexner Med Ctr, Columbus, OH 43221 USA.
[Gru, Alejandro] Ohio State Univ, Div Dermatopathol, Wexner Med Ctr, Columbus, OH 43221 USA.
[Zuo, Rena C.; Cowen, Edward W.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Sweeney, Sarah A.; Hymes, Sharon R.] Univ Texas MD Anderson Canc Ctr, Dept Dermatol, Houston, TX USA.
[Devine, Steven M.] Ohio State Univ, James Canc Hosp, Div Blood & Marrow Transplantat, Columbus, OH 43221 USA.
RP Kaffenberger, BH (reprint author), Ohio State Univ, Div Dermatol, 2012 Kenny Rd,2nd Floor, Columbus, OH 43221 USA.
EM Benjamin.Kaffenberger@osumc.edu
RI Kaffenberger, Benjamin/N-2732-2014
OI Kaffenberger, Benjamin/0000-0001-8079-0011
FU National Institutes of Health (NIH), National Cancer Institute; NIH
Medical Research Scholars Program; NIH; Pfizer Inc; Doris Duke
Charitable Foundation; Alexandria Real Estate Equities Inc; Howard
Hughes Medical Institute
FX Supported in part by the Intramural Research Program of the National
Institutes of Health (NIH), National Cancer Institute and the NIH
Medical Research Scholars Program, a public-private partnership
supported jointly by the NIH and generous contributions to the
Foundation for the NIH from Pfizer Inc, the Doris Duke Charitable
Foundation, the Alexandria Real Estate Equities Inc and Mr and Mrs Joel
S. Marcus, and the Howard Hughes Medical Institute, as well as other
private donors.
NR 29
TC 3
Z9 3
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD OCT
PY 2014
VL 71
IS 4
BP 745
EP 753
DI 10.1016/j.jaad.2014.05.034
PG 9
WC Dermatology
SC Dermatology
GA AP6FJ
UT WOS:000342172700052
PM 24993601
ER
PT J
AU Hofmann, JN
Purdue, MP
AF Hofmann, Jonathan N.
Purdue, Mark P.
TI CKD and Risk of Renal Cell Carcinoma: A Causal Association?
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Editorial Material
ID KIDNEY-TRANSPLANTATION; CANCER-RISK; DISEASE; DIALYSIS
C1 [Hofmann, Jonathan N.; Purdue, Mark P.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Hofmann, JN (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E132,MSC 9771, Bethesda, MD 20892 USA.
EM hofmannjn@mail.nih.gov
RI Purdue, Mark/C-9228-2016
OI Purdue, Mark/0000-0003-1177-3108
FU Intramural NIH HHS
NR 15
TC 3
Z9 3
U1 0
U2 6
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD OCT
PY 2014
VL 25
IS 10
BP 2147
EP 2148
DI 10.1681/ASN.2014040376
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA AP9ML
UT WOS:000342403800003
PM 24876123
ER
PT J
AU Wetmore, JB
Calvet, JP
Yu, ASL
Lynch, CF
Wang, CJ
Kasiske, BL
Engels, EA
AF Wetmore, James B.
Calvet, James P.
Yu, Alan S. L.
Lynch, Charles F.
Wang, Connie J.
Kasiske, Bertram L.
Engels, Eric A.
TI Polycystic Kidney Disease and Cancer after Renal Transplantation
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID C-MYC; PROTOONCOGENE EXPRESSION; CYSTIC-DISEASE; GENETICS
AB Autosomal dominant polycystic kidney disease (ADPKD), the most common form of polycystic kidney disease (PKD), is a disorder with characteristics of neoplasia. However, it is not known whether renal transplant recipients with PKD have an increased risk of cancer. Data from the Scientific Registry of Transplant Recipients, which contains information on all solid organ transplant recipients in the United States, were linked to 15 population-based cancer registries in the United States. For PKD recipients, we compared overall cancer risk with that in the general population. We also compared cancer incidence in PKD versus non-PKD renal transplant recipients using Poisson regression, and we determined incidence rate ratios (IRRs) adjusted for age, sex, race/ethnicity, dialysis duration, and time since transplantation. The study included 10,166 kidney recipients with PKD and 107,339 without PKD. Cancer incidence in PKD recipients was 1233.6 per 100,000 person-years, 48% higher than expected in the general population (standardized incidence ratio, 1.48; 95% confidence interval [95% CI], 1.37 to 1.60), whereas cancer incidence in non-PKD recipients was 1119.1 per 100,000 person-years. The unadjusted incidence was higher in PKD than in non-PKD recipients (IRR, 1.10; 95% CI, 1.01 to 1.20). However, PKD recipients were older (median age at transplantation, 51 years versus 45 years for non-PKD recipients), and after multivariable adjustment, cancer incidence was lower in PKD recipients than in others (IRR, 0.84; 95% CI, 0.77 to 0.91). The reason for the lower cancer risk in PKD recipients is not known but may relate to biologic characteristics of ADPKD or to cancer risk behaviors associated with ADPKD.
C1 [Wetmore, James B.; Yu, Alan S. L.; Wang, Connie J.] Univ Kansas, Sch Med, Dept Med, Div Nephrol, Kansas City, KS USA.
[Wetmore, James B.; Calvet, James P.; Yu, Alan S. L.; Wang, Connie J.] Univ Kansas, Sch Med, Kidney Inst, Kansas City, KS USA.
[Calvet, James P.] Univ Kansas, Sch Med, Dept Biochem & Mol Biol, Kansas City, KS USA.
[Calvet, James P.] Univ Kansas, Sch Med, Dept Canc Biol, Kansas City, KS USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Kasiske, Bertram L.] Hennepin Cty Med Ctr, Div Nephrol, Dept Med, Minneapolis, MN 55415 USA.
[Engels, Eric A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Wetmore, JB (reprint author), Hennepin Cty Med Ctr, Div Nephrol, 701 Pk Ave, Minneapolis, MN 55415 USA.
EM james.wetmore@hcmed.org
FU National Cancer Institute; Arbor Research Collaborative for Health in
Ann Arbor, Michigan [HHSH234200537009C]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: California
[1U58 DP000807-01]; National Program of Cancer Registries of the Centers
for Disease Control and Prevention: Colorado [U58 DP000848-04]; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: Georgia [5U58DP003875-01]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: Illinois
[5658DP000805-04]; National Program of Cancer Registries of the Centers
for Disease Control and Prevention: Michigan [5U58DP000812-03]; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: New Jersey [1US58/DP0039311-01]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: New York
[U58DP003879]; National Program of Cancer Registries of the Centers for
Disease Control and Prevention: North Carolina [U58DP000832]; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: Texas [5U58DP000824-04]; National Cancer Institute:
California [HHSN261201000036C, HHSN261201000035C, HHSN261201000034C];
National Cancer Institute: Connecticut [HHSN261201000024C]; National
Cancer Institute: Hawaii [HHSN261201000037C, N01-PC-35137,
N01-PC-35139]; National Cancer Institute: Iowa [HSN261201000032C,
N01-PC-35143]; National Cancer Institute: New Jersey [HHSN261201000027C,
N01-PC-2010-0027]; National Cancer Institute: Seattle-Puget Sound
[N01-PC-35142]; National Cancer Institute: Utah [HHSN261201000026C];
state of California (Cancer Surveillance Improvement Initiative), Texas
[14-2491]; state of Colorado (Cancer Surveillance Improvement
Initiative), Texas [14-2491]; state of Connecticut (Cancer Surveillance
Improvement Initiative), Texas [14-2491]; state of Illinois (Cancer
Surveillance Improvement Initiative), Texas [14-2491]; state of Iowa
(Cancer Surveillance Improvement Initiative), Texas [14-2491]; state of
New Jersey (Cancer Surveillance Improvement Initiative), Texas
[14-2491]; state of New York (Cancer Surveillance Improvement
Initiative), Texas [14-2491]; Washington; Fred Hutchinson Cancer
Research Center in Seattle, Washington
FX The views expressed in this paper are those of the authors and should
not be interpreted to reflect the views or policies of the National
Cancer Institute, Health Resources and Services Administration, SRTR,
cancer registries, or their contractors. This research was supported in
part by the Intramural Research Program of the National Cancer
Institute.; During the initial period when registry linkages were
performed, the SRTR was managed by Arbor Research Collaborative for
Health in Ann Arbor, Michigan (contract HHSH234200537009C). Beginning in
September 2010, the SRTR was managed by Minneapolis Medical Research
Foundation in Minneapolis, Minnesota (HHSH250201000018C). The following
cancer registries were supported by the National Program of Cancer
Registries of the Centers for Disease Control and Prevention: California
(agreement 1U58 DP000807-01), Colorado (U58 DP000848-04), Georgia
(5U58DP003875-01), Illinois (5658DP000805-04), Michigan
(5U58DP000812-03), New Jersey (1US58/DP0039311-01), New York
(U58DP003879), North Carolina (U58DP000832), and Texas
(5U58DP000824-04). The following cancer registries were supported by the
Surveillance, Epidemiology, and End Result Program of the National
Cancer Institute: California (contracts HHSN261201000036C,
HHSN261201000035C, and HHSN261201000034C), Connecticut
(HHSN261201000024C), Hawaii (HHSN261201000037C, N01-PC-35137, and
N01-PC-35139), Iowa (HSN261201000032C and N01-PC-35143), New Jersey
(HHSN261201000027C, N01-PC-2010-0027), Seattle-Puget Sound
(N01-PC-35142), and Utah (HHSN261201000026C). Additional support was
provided by the states of California, Colorado, Connecticut, Illinois,
Iowa, New Jersey, New York (Cancer Surveillance Improvement Initiative
14-2491), Texas, and Washington, as well as the Fred Hutchinson Cancer
Research Center in Seattle, Washington.
NR 26
TC 15
Z9 15
U1 0
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD OCT
PY 2014
VL 25
IS 10
BP 2335
EP 2341
DI 10.1681/ASN.2013101122
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AP9ML
UT WOS:000342403800022
PM 24854270
ER
PT J
AU Shaikh, QN
Memon, AA
Kamal, AK
AF Shaikh, Quratulain Nauman
Memon, Adeel Ali
Kamal, Ayeesha Kamran
TI Early magnetic resonance imaging in transient ischaemic attack and minor
stroke
SO JOURNAL OF THE PAKISTAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
C1 [Shaikh, Quratulain Nauman; Memon, Adeel Ali; Kamal, Ayeesha Kamran] Aga Khan Univ, Stroke Res Team, Clin Res Training Program, Fogarty Int Ctr, Karachi, Pakistan.
RP Kamal, AK (reprint author), Aga Khan Univ, Stroke Res Team, Clin Res Training Program, Fogarty Int Ctr, Karachi, Pakistan.
EM ayeesha.kamal@aku.edu
FU FIC NIH HHS [D43TW008660]
NR 4
TC 0
Z9 0
U1 0
U2 0
PU PAKISTAN MEDICAL ASSOC
PI KARACHI
PA PMA HOUSE, AGA KHAN III RD, KARACHI, 00000, PAKISTAN
SN 0030-9982
J9 J PAK MED ASSOC
JI J. Pak. Med. Assoc.
PD OCT
PY 2014
VL 64
IS 10
BP 1207
EP 1207
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA AP8MN
UT WOS:000342333200026
PM 25823169
ER
PT J
AU Reddy, U
Abuhamad, A
Levine, D
Saade, G
AF Reddy, Uma
Abuhamad, Alfred
Levine, Deborah
Saade, George
TI Fetal Imaging: Executive Summary of a Joint Eunice Kennedy Shriver
National Institute of Child Health and Human Development, Society for
Maternal-Fetal Medicine, American Institute of Ultrasound in Medicine,
American College of Obstetricians and Gynecologists, American College of
Radiology, Society for Pediatric Radiology, and Society of Radiologists
in Ultrasound Fetal Imaging Workshop Reply
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Letter
C1 [Reddy, Uma] NICHHD, Bethesda, MD 20892 USA.
[Abuhamad, Alfred] Eastern Virginia Med Sch, Med Grp, Norfolk, VA 23501 USA.
[Levine, Deborah] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Saade, George] Univ Texas Med Branch, Galveston, TX 77555 USA.
RP Reddy, U (reprint author), NICHHD, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
EI 1550-9613
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD OCT
PY 2014
VL 33
IS 10
BP 1877
EP 1877
DI 10.7863/ultra.33.10.1877
PG 1
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA AQ0MP
UT WOS:000342477700024
PM 25253840
ER
PT J
AU An, L
Li, SZ
Wood, ET
Reich, DS
Shen, J
AF An, Li
Li, Shizhe
Wood, Emily T.
Reich, Daniel S.
Shen, Jun
TI N-Acetyl-Aspartyl-Glutamate Detection in the Human Brain at 7 Tesla by
Echo Time Optimization and Improved Wiener Filtering
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE NAAG; GAMMA simulation; Wiener filter; TE optimization
ID IN-VIVO; MAGNETIC-RESONANCE; NAAG; SPECTROSCOPY; METABOLITES;
RESOLUTION; MRS; ACETYLASPARTYLGLUTAMATE; QUANTIFICATION; SCHIZOPHRENIA
AB PurposeTo report enhanced signal detection for measuring N-acetyl-aspartyl-glutamate (NAAG) in the human brain at 7 Tesla by echo time (TE) -optimized point-resolved spectroscopy (PRESS) and improved Wiener filtering.
MethodsUsing a highly efficient in-house developed numerical simulation program, a PRESS sequence with (TE1, TE2)=(26, 72) ms was found to maximize the NAAG signals relative to the overlapping Glu signals. A new Wiener filtering water reference deconvolution method was developed to reduce broadening and distortions of metabolite peaks caused by B-0 inhomogeneity and eddy currents.
ResultsMonte Carlo simulation results demonstrated that the new Wiener filtering method offered higher spectral resolution, reduced spectral artifacts, and higher accuracy in NAAG quantification compared with the original Wiener filtering method. In vivo spectra and point spread functions of signal distortion confirmed that the new Wiener filtering method lead to improved spectral resolution and reduced spectral artifacts.
ConclusionTE-optimized PRESS in combination with a new Wiener filtering method made it possible to fully use both the NAAG singlet signal at 2.05 ppm and the NAAG multiplet signal at 2.18 ppm in the quantification of NAAG. A more accurate characterization of lineshape distortion for Wiener filtering needs B-0 field maps and segmented anatomical images to exclude contribution from cerebral spinal fluid. Magn Reson Med 72:903-912, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [An, Li; Li, Shizhe; Shen, Jun] NIMH, NIH, Bethesda, MD 20892 USA.
[Wood, Emily T.; Reich, Daniel S.] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Wood, Emily T.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
RP An, L (reprint author), Bldg 10,Room 3D46,10 Ctr Dr,MSC 1216, Bethesda, MD 20892 USA.
EM li.an@nih.gov
RI Reich, Daniel/E-5701-2010;
OI Reich, Daniel/0000-0002-2628-4334; Wood, Emily/0000-0003-0395-4849
FU NIH, NIMH; NINDS
FX We thank Mr. Christopher Johnson and Mrs. Maria Ferraris Araneta for
recruiting and caring for the healthy volunteers. This work was
supported by the intramural programs of the NIH, NIMH, and NINDS.
NR 26
TC 4
Z9 4
U1 0
U2 29
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0740-3194
EI 1522-2594
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD OCT
PY 2014
VL 72
IS 4
BP 903
EP 912
DI 10.1002/mrm.25007
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AP8PZ
UT WOS:000342342300002
PM 24243344
ER
PT J
AU Zhang, Y
Shen, J
AF Zhang, Yan
Shen, Jun
TI Smoothness of In Vivo Spectral Baseline Determined by Mean-Square Error
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE baseline; smoothness; spectral fitting; root-mean-square error;
Cramer-Rao lower bound; Fisher matrix; bias
ID MAGNETIC-RESONANCE-SPECTROSCOPY; REGULARIZED LINESHAPE DECONVOLUTION;
PROTON MR SPECTROSCOPY; TE-AVERAGED PRESS; HUMAN BRAIN; AUTOMATED
QUANTITATION; H-1-NMR SPECTRA; PRIOR KNOWLEDGE; DOMAIN METHODS;
NMR-SPECTRA
AB PurposeA nonparametric smooth line is usually added to the spectral model to account for background signals in vivo magnetic resonance spectroscopy (MRS). The assumed smoothness of the baseline significantly influences quantitative spectral fitting. In this paper, a method is proposed to minimize baseline influences on the estimated spectral parameters.
MethodsThe nonparametric baseline function with a given smoothness was treated as a function of spectral parameters. Its uncertainty was measured by root-mean-square error (RMSE). The proposed method was demonstrated with a simulated spectrum and in vivo spectra of both short echo time and averaged echo times. The estimated in vivo baselines were compared with the metabolite-nulled spectra and the LCModel-estimated baselines. The accuracies of estimated baseline and metabolite concentrations were further verified via cross-validation.
ResultsAn optimal smoothness condition was found that led to the minimal baseline RMSE. In this condition, the best fit was balanced against minimal baseline influences on metabolite concentration estimates.
ConclusionBaseline RMSE can be used to indicate estimated baseline uncertainties and serve as the criterion for determining the baseline smoothness of in vivo MRS. Magn Reson Med 72:913-922, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Zhang, Yan; Shen, Jun] NIMH, MR Spect Core Facil, NIH, Rockville, MD 20892 USA.
[Shen, Jun] NIMH, Mol Imaging Branch, NIH, Rockville, MD 20892 USA.
RP Zhang, Y (reprint author), NIMH, MR Spect Core Facil, Bldg 10,Room 2D50,9000 Rockville Pike, Rockville, MD 20892 USA.
EM zhangya@mail.nih.gov
FU National Institute of Mental Health, National Institutes of Health
FX Grant sponsor: Intramural Research Program of the National Institute of
Mental Health, National Institutes of Health.
NR 33
TC 3
Z9 3
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0740-3194
EI 1522-2594
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD OCT
PY 2014
VL 72
IS 4
BP 913
EP 922
DI 10.1002/mrm.25013
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AP8PZ
UT WOS:000342342300003
PM 24259436
ER
PT J
AU Hassett, MJ
Ritzwoller, DP
Taback, N
Carroll, N
Cronin, AM
Ting, GV
Schrag, D
Warren, JL
Hornbrook, MC
Weeks, JC
AF Hassett, Michael J.
Ritzwoller, Debra P.
Taback, Nathan
Carroll, Nikki
Cronin, Angel M.
Ting, Gladys V.
Schrag, Deb
Warren, Joan L.
Hornbrook, Mark C.
Weeks, Jane C.
TI Validating Billing/Encounter Codes as Indicators of Lung, Colorectal,
Breast, and Prostate Cancer Recurrence Using 2 Large Contemporary
Cohorts
SO MEDICAL CARE
LA English
DT Article
DE cancer; recurrence; administrative data; applied methods
ID SEER-MEDICARE DATA; RACIAL-DIFFERENCES; FREE SURVIVAL; OLDER WOMEN;
STAGE; COMORBIDITY; POPULATION; OUTCOMES; SURGERY; THERAPY
AB Background: A substantial proportion of cancer-related mortality is attributable to recurrent, not de novo metastatic disease, yet we know relatively little about these patients. To fill this gap, investigators often use administrative codes for secondary malignant neoplasm or chemotherapy to identify recurrent cases in population-based datasets. However, these algorithms have not been validated in large, contemporary, routine care cohorts.
Objective: To evaluate the validity of secondary malignant neoplasm and chemotherapy codes as indicators of recurrence after definitive local therapy for stage I-III lung, colorectal, breast, and prostate cancer.
Research Design, Subjects, and Measures: We assessed the sensitivity, specificity, and positive predictive value (PPV) of these codes 14 and 60 months after diagnosis using 2 administrative datasets linked with gold-standard recurrence status information: CanCORS/Medicare (diagnoses 2003-2005) and HMO/Cancer Research Network (diagnoses 2000-2005).
Results: We identified 929 CanCORS/Medicare patients and 5298 HMO/CRN patients. Sensitivity, specificity, and PPV ranged widely depending on which codes were included and the type of cancer. For patients with lung, colorectal, and breast cancer, the combination of secondary malignant neoplasm and chemotherapy codes was the most sensitive (75%-85%); no code-set was highly sensitive and highly specific. For prostate cancer, no code-set offered even moderate sensitivity (<= 19%).
Conclusions: Secondary malignant neoplasm and chemotherapy codes could not identify recurrent cancer without some risk of misclassification. Findings based on existing algorithms should be interpreted with caution. More work is needed to develop a valid algorithm that can be used to characterize outcomes and define patient cohorts for comparative effectiveness research studies.
C1 [Hassett, Michael J.; Schrag, Deb; Weeks, Jane C.] Dana Farber Canc Inst, Dept Med Oncol, Ctr Outcomes & Policy Res, Boston, MA 02215 USA.
[Hassett, Michael J.; Schrag, Deb; Weeks, Jane C.] Harvard Univ, Sch Med, Boston, MA USA.
[Ritzwoller, Debra P.; Carroll, Nikki] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO USA.
[Taback, Nathan] Univ Toronto, Div Biostat, Toronto, ON, Canada.
[Cronin, Angel M.; Ting, Gladys V.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Warren, Joan L.] NCI, Bethesda, MD 20892 USA.
[Hornbrook, Mark C.] Kaiser Permanente Northwest, Ctr Hlth Res, Portland, OR USA.
RP Hassett, MJ (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Ctr Outcomes & Policy Res, 450 Brookline Ave, Boston, MA 02215 USA.
EM michael_hassett@dfci.harvard.edu
FU National Cancer Institute [RC2 CA148185-01]; NCI (Cancer Research
Network) [U19 CA79689]; American Society of Clinical Oncology; Susan G.
Komen for the Cure; National Cancer Institute (NCI) [U01 CA093344];
Dana-Farber Cancer Institute/Cancer Research Network [U01 CA093332];
Harvard Medical School/Northern California Cancer Center [U01 CA093324];
University of Iowa [U01 CA01013]; University of North Carolina [U01
CA093326]; Department of Veterans Affairs [VA HSRD CRS 02 164]
FX Supported by a grant from the National Cancer Institute (RC2 CA148185-01
to J.C.W. and D. P. R.) and an NCI cooperative agreement (U19 CA79689,
Cancer Research Network). The American Society of Clinical Oncology
(Career Development Award) and Susan G. Komen for the Cure (Career
Catalyst Award) provided salary support to M.J.H. The work of the
CanCORS consortium was supported by grants from the National Cancer
Institute (NCI) to the Statistical Coordinating Center (U01 CA093344)
and to the Primary Data Collection and Research Centers (Dana-Farber
Cancer Institute/Cancer Research Network U01 CA093332; Harvard Medical
School/Northern California Cancer Center U01 CA093324; University of
Iowa U01 CA01013; University of North Carolina U01 CA093326); and by a
Department of Veterans Affairs grant to the Durham VA Medical Center VA
HSRD CRS 02 164.
NR 23
TC 14
Z9 14
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD OCT
PY 2014
VL 52
IS 10
BP E65
EP E73
PG 9
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA AP9CK
UT WOS:000342375800001
PM 23222531
ER
PT J
AU Rus, H
Tegla, CA
Nguyen, V
Cudrici, CD
Badea, TC
Rus, V
AF Rus, Horea
Tegla, Cosmin A.
Vingh Nguyen
Cudrici, Cornelia D.
Badea, Tudor C.
Rus, Violeta
TI Response gene to complement-32 is essential for TGF-beta mediated Th17
differentiation
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 25th International Complement Workshop
CY SEP 14-18, 2014
CL Rio de Janeiro, BRAZIL
C1 [Rus, Horea; Tegla, Cosmin A.; Vingh Nguyen; Cudrici, Cornelia D.; Rus, Violeta] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Badea, Tudor C.] NEI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 2014
VL 61
IS 2
SI SI
MA 071
BP 241
EP 242
PG 2
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA AP7NZ
UT WOS:000342265300090
ER
PT J
AU Sae-Ueng, U
Li, D
Zuo, XB
Huffman, JB
Homa, FL
Rau, D
Evilevitch, A
AF Sae-Ueng, Udom
Li, Dong
Zuo, Xiaobing
Huffman, Jamie B.
Homa, Fred L.
Rau, Donald
Evilevitch, Alex
TI Solid-to-fluid DNA transition inside HSV-1 capsid close to the
temperature of infection
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID HERPES-SIMPLEX-VIRUS; IN-VITRO; EJECTION; PHAGE; BACTERIOPHAGE;
PRESSURE; FORCES; DYNAMICS; VIRIONS; GENOME
AB DNA in the human Herpes simplex virus type 1 (HSV-1) capsid is packaged to a tight density. This leads to tens of atmospheres of internal pressure responsible for the delivery of the herpes genome into the cell nucleus. In this study we show that, despite its liquid crystalline state inside the capsid, the DNA is fluid-like, which facilitates its ejection into the cell nucleus during infection. We found that the sliding friction between closely packaged DNA strands, caused by interstrand repulsive interactions, is reduced by the ionic environment of epithelial cells and neurons susceptible to herpes infection. However, variations in the ionic conditions corresponding to neuronal activity can restrict DNA mobility in the capsid, making it more solid-like. This can inhibit intranuclear DNA release and interfere with viral replication. In addition, the temperature of the human host (37 degrees C) induces a disordering transition of the encapsidated herpes genome, which reduces interstrand interactions and provides genome mobility required for infection.
C1 [Sae-Ueng, Udom; Li, Dong; Evilevitch, Alex] Carnegie Mellon Univ, Dept Phys, Pittsburgh, PA 15213 USA.
[Zuo, Xiaobing] Argonne Natl Lab, Adv Photon Source, Xray Sci Div, Argonne, IL 60439 USA.
[Huffman, Jamie B.; Homa, Fred L.] Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA USA.
[Rau, Donald] NIH, Lab Phys & Struct Biol, Program Phys Biol, Bethesda, MD USA.
[Evilevitch, Alex] Lund Univ, Dept Biochem & Struct Biol, Lund, Sweden.
RP Evilevitch, A (reprint author), Carnegie Mellon Univ, Dept Phys, Pittsburgh, PA 15213 USA.
EM alexe@cmu.edu
RI Evilevitch, Alex/P-3103-2014; Li, Dong/D-9221-2015
OI Evilevitch, Alex/0000-0002-0245-9574; Li, Dong/0000-0002-5282-6918
FU Swedish Research Council, VR grant [622-2008-726]; US National Science
Foundation grant [CHE-1152770]; Public Health Service Grant from the US
National Institutes of Health (NIH) [AI060836]; McWilliams Fellowship in
the Mellon College of Science; Intramural Research Program of the
National Institutes of Child Health and Human Development-NIH; US
Department of Energy [DE-AC02-06CH11357]
FX We acknowledge T. Liu and I. Shefer for their substantial help with the
manuscript preparation. We also thank B. Jonsson for discussions that
have been inspiring for this work. We are grateful to G. Berry, M.
Widom, P. LeDuc, M. Deserno and L. Walker for providing critically
important feedback on data analysis. We acknowledge J. Shaw, B.
Pittenger and M. Thompson from Bruker Nano Surfaces Division for
outstanding support with AFM measurements. We thank A. Templeton for
help with proofreading. The SAXS experiments were performed at beamline
12ID-B of the Advanced Photon Source at Argonne National Laboratory. We
acknowledge the Advanced Photon Source, which is an Office of Science
User Facility operated by Argonne National Laboratory for the US
Department of Energy under contract no. DE-AC02-06CH11357. This work was
supported by the Swedish Research Council, VR grant 622-2008-726 (A.E.)
and US National Science Foundation grant CHE-1152770 (A.E.). Support was
also provided by the Public Health Service Grant AI060836 from the US
National Institutes of Health (NIH) (F.L.H.) and by the McWilliams
Fellowship in the Mellon College of Science (to U.S.). This work was
partially supported by the Intramural Research Program of the National
Institutes of Child Health and Human Development-NIH (to D.R.).
NR 54
TC 6
Z9 6
U1 3
U2 21
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
EI 1552-4469
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD OCT
PY 2014
VL 10
IS 10
BP 861
EP +
DI 10.1038/NCHEMBIO.1628
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AQ0GV
UT WOS:000342462100013
PM 25195012
ER
PT J
AU Al Olama, AA
Kote-Jarai, Z
Berndt, SI
Conti, DV
Schumacher, F
Han, Y
Benlloch, S
Hazelett, DJ
Wang, ZM
Saunders, E
Leongamornlert, D
Lindstrom, S
Jugurnauth-Little, S
Dadaev, T
Tymrakiewicz, M
Stram, DO
Rand, K
Wan, P
Stram, A
Sheng, X
Pooler, LC
Park, K
Xia, L
Tyrer, J
Kolonel, LN
Le Marchand, L
Hoover, RN
Machiela, MJ
Yeager, M
Burdette, L
Chung, CC
Hutchinson, A
Yu, K
Goh, C
Ahmed, M
Govindasami, K
Guy, M
Tammela, TLJ
Auvinen, A
Wahlfors, T
Schleutker, J
Visakorpi, T
Leinonen, KA
Xu, JF
Aly, M
Donovan, J
Travis, RC
Key, TJ
Siddiq, A
Canzian, F
Khaw, KT
Takahashi, A
Kubo, M
Pharoah, P
Pashayan, N
Weischer, M
Nordestgaard, BG
Nielsen, SF
Klarskov, P
Roder, MA
Iversen, P
Thibodeau, SN
McDonnell, SK
Schaid, DJ
Stanford, JL
Kolb, S
Holt, S
Knudsen, B
Coll, AH
Gapstur, SM
Diver, WR
Stevens, VL
Maier, C
Luedeke, M
Herkommer, K
Rinckleb, AE
Strom, SS
Pettaway, C
Yeboah, ED
Tettey, Y
Biritwum, RB
Adjei, AA
Tay, E
Truelove, A
Niwa, S
Choklcalingam, AP
Cannon-Albright, L
Cybulski, C
Wokolorczyk, D
Kluzniak, W
Park, J
Sellers, T
Lin, HY
Isaacs, WB
Partin, AW
Brenner, H
Dieffenbach, AK
Stegmaier, C
Chen, C
Giovannucci, EL
Ma, J
Stampfer, M
Penney, KL
Mucci, L
John, EM
Ingles, SA
Kittles, RA
Murphy, AB
Pandha, H
Michael, A
Kierzek, AM
Blot, W
Signorello, LB
Zheng, W
Albanes, D
Virtamo, J
Weinstein, S
Nemesure, B
Carpten, J
Leske, C
Wu, SY
Hennis, A
Kibel, AS
Rybicki, BA
Neslund-Dudas, C
Hsing, AW
Chu, L
Goodman, PJ
Klein, EA
Zheng, SL
Batra, J
Clements, J
Spurdle, A
Teixeira, MR
Paulo, P
Maia, S
Slavov, C
Kaneva, R
Mitev, V
Witte, JS
Casey, G
Gillanders, EM
Seminara, D
Riboli, E
Hamdy, FC
Coetzee, GA
Li, QY
Freedman, ML
Hunter, DJ
Muir, K
Gronberg, H
Nea, DE
Southey, M
Giles, GG
Severi, G
Cook, MB
Nakagawa, H
Wiklund, F
Kraft, P
Chanock, SJ
Henderson, BE
Easton, DF
Eeles, RA
Haiman, CA
AF Al Olama, Ali Amin
Kote-Jarai, Zsofia
Berndt, Sonja I.
Conti, David V.
Schumacher, Fredrick
Han, Ying
Benlloch, Sara
Hazelett, Dennis J.
Wang, Zhaoming
Saunders, Ed
Leongamornlert, Daniel
Lindstrom, Sara
Jugurnauth-Little, Sara
Dadaev, Tokhir
Tymrakiewicz, Malgorzata
Stram, Daniel O.
Rand, Kristin
Wan, Peggy
Stram, Alex
Sheng, Xin
Pooler, Loreall C.
Park, Karen
Xia, Lucy
Tyrer, Jonathan
Kolonel, Laurence N.
Le Marchand, Loic
Hoover, Robert N.
Machiela, Mitchell J.
Yeager, Merideth
Burdette, Laurie
Chung, Charles C.
Hutchinson, Amy
Yu, Kai
Goh, Chee
Ahmed, Mahbubl
Govindasami, Koveela
Guy, Michelle
Tammela, Teuvo L. J.
Auvinen, Anssi
Wahlfors, Tlina
Schleutker, Johanna
Visakorpi, Tapio
Leinonen, Katri A.
Xu, Jianfeng
Aly, Markus
Donovan, Jenny
Travis, Ruth C.
Key, Tim J.
Siddiq, Afshan
Canzian, Federico
Khaw, Kay-Tee
Takahashi, Atsushi
Kubo, Michiaki
Pharoah, Paul
Pashayan, Nora
Weischer, Maren
Nordestgaard, Borge G.
Nielsen, Sune F.
Klarskov, Peter
Roder, Martin Andreas
Iversen, Peter
Thibodeau, Stephen N.
McDonnell, Shannon K.
Schaid, Daniel J.
Stanford, Janet L.
Kolb, Suzanne
Holt, Sarah
Knudsen, Beatrice
Coll, Antonio Hurtado
Gapstur, Susan M.
Diver, W. Ryan
Stevens, Victoria L.
Maier, Christiane
Luedeke, Manuel
Herkommer, Kathleen
Rinckleb, Antje E.
Strom, Sara S.
Pettaway, Curtis
Yeboah, Edward D.
Tettey, Yao
Biritwum, Richard B.
Adjei, Andrew A.
Tay, Evelyn
Truelove, Ann
Niwa, Shelley
Choklcalingam, Anand P.
Cannon-Albright, Lisa
Cybulski, Cezary
Wokolorczyk, Dominika
Kluzniak, Wojciech
Park, Jong
Sellers, Thomas
Lin, Hui-Yi
Isaacs, William B.
Partin, Alan W.
Brenner, Hermann
Dieffenbach, Aida Karina
Stegmaier, Christa
Chen, Constance
Giovannucci, Edward L.
Ma, Jing
Stampfer, Meir
Penney, Kathryn L.
Mucci, Lorelei
John, Esther M.
Ingles, Sue A.
Kittles, Rick A.
Murphy, Adam B.
Pandha, Hardev
Michael, Agnieszka
Kierzek, Andrzej M.
Blot, William
Signorello, Lisa B.
Zheng, Wei
Albanes, Demetrius
Virtamo, Jarmo
Weinstein, Stephanie
Nemesure, Barbara
Carpten, John
Leske, Cristina
Wu, Suh-Yuh
Hennis, Anselm
Kibel, Adam S.
Rybicki, Benjamin A.
Neslund-Dudas, Christine
Hsing, Ann W.
Chu, Lisa
Goodman, Phyllis J.
Klein, Eric A.
Zheng, S. Lilly
Batra, Jyotsna
Clements, Judith
Spurdle, Amanda
Teixeira, Manuel R.
Paulo, Paula
Maia, Sofia
Slavov, Chavdar
Kaneva, Radka
Mitev, Vanio
Witte, John S.
Casey, Graham
Gillanders, Elizabeth M.
Seminara, Daniella
Riboli, Elio
Hamdy, Freddie C.
Coetzee, Gerhard A.
Li, Qiyuan
Freedman, Matthew L.
Hunter, David J.
Muir, Kenneth
Gronberg, Henrik
Nea, David E.
Southey, Melissa
Giles, Graham G.
Severi, Gianluca
Cook, Michael B.
Nakagawa, Hidewaki
Wiklund, Fredrik
Kraft, Peter
Chanock, Stephen J.
Henderson, Brian E.
Easton, Douglas F.
Eeles, Rosalind A.
Haiman, Christopher A.
CA Breast Prostate Canc Cohort Consor
Practical Prostate Canc Associatio
COGS Consortium
GAME-ON ELLIPSE Consortium
TI A meta-analysis of 87,040 individuals identifies 23 new susceptibility
loci for prostate cancer
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COMMON VARIANTS; MYOSIN VI; RISK; JAPANESE;
GLIOMA; 22Q13; MEN
AB Genome-wide association studies (GWAS) have identified 76 variants associated with prostate cancer risk predominantly in populations of European ancestry. To identify additional susceptibility loci for this common cancer, we conducted a meta-analysis of >10 million SNPs in 43,303 prostate cancer cases and 43,737 controls from studies in populations of European, African, Japanese and Latino ancestry. Twenty-three new susceptibility loci were identified at association P < 5 x 10(-8); 15 variants were identified among men of European ancestry, 7 were identified in multi-ancestry analyses and 1 was associated with early-onset prostate cancer. These 23 variants, in combination with known prostate cancer risk variants, explain 33% of the familial risk for this disease in European-ancestry populations. These findings provide new regions for investigation into the pathogenesis of prostate cancer and demonstrate the usefulness of combining ancestrally diverse populations to discover risk loci for disease.
C1 [Al Olama, Ali Amin; Benlloch, Sara; Tyrer, Jonathan; Easton, Douglas F.] Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
[Kote-Jarai, Zsofia; Saunders, Ed; Leongamornlert, Daniel; Jugurnauth-Little, Sara; Dadaev, Tokhir; Tymrakiewicz, Malgorzata; Goh, Chee; Ahmed, Mahbubl; Govindasami, Koveela; Guy, Michelle; Eeles, Rosalind A.] Inst Canc Res, London SW3 6JB, England.
[Berndt, Sonja I.; Wang, Zhaoming; Hoover, Robert N.; Machiela, Mitchell J.; Yeager, Merideth; Burdette, Laurie; Chung, Charles C.; Hutchinson, Amy; Yu, Kai; Cook, Michael B.; Chanock, Stephen J.] Natl Canc Inst, US NIH, Div Canc Epidemiol & Genet, Bethesda, MD USA.
[Conti, David V.; Schumacher, Fredrick; Han, Ying; Hazelett, Dennis J.; Stram, Daniel O.; Rand, Kristin; Wan, Peggy; Stram, Alex; Sheng, Xin; Pooler, Loreall C.; Park, Karen; Xia, Lucy; Ingles, Sue A.; Casey, Graham; Coetzee, Gerhard A.; Henderson, Brian E.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Conti, David V.; Schumacher, Fredrick; Hazelett, Dennis J.; Stram, Daniel O.; Ingles, Sue A.; Casey, Graham; Coetzee, Gerhard A.; Henderson, Brian E.; Haiman, Christopher A.] Univ So Calif, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Wang, Zhaoming] SAIC Frederick Inc, Natl Canc Inst, Div Canc Epidemiol & Genet, Canc Genom Res Lab, Frederick, MD USA.
[Lindstrom, Sara; Chen, Constance; Hunter, David J.; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Genet Epidemiol & Stat Genet, Boston, MA 02115 USA.
[Kolonel, Laurence N.; Le Marchand, Loic] Univ Hawaii, Ctr Canc, Program Epidemiol, Honolulu, HI 96822 USA.
[Tammela, Teuvo L. J.] Univ Tampere, Tampere Univ Hosp, Dept Urol, FIN-33101 Tampere, Finland.
[Tammela, Teuvo L. J.] Univ Tampere, Sch Med, FIN-33101 Tampere, Finland.
[Auvinen, Anssi] Univ Tampere, Sch Hlth Sci, Dept Epidemiol, FIN-33101 Tampere, Finland.
[Wahlfors, Tlina; Schleutker, Johanna] Univ Tampere, BioMediTech, Tampere, Finland.
[Wahlfors, Tlina; Schleutker, Johanna] Univ Tampere, FimLab Labs, Tampere, Finland.
[Schleutker, Johanna] Univ Turku, Inst Biomed, Dept Biochem Med, Turku, Finland.
[Visakorpi, Tapio; Leinonen, Katri A.] Univ Tampere, BioMediTech, Inst Biomed Technol, Tampere, Finland.
[Visakorpi, Tapio; Leinonen, Katri A.] Tampere Univ Hosp, Tampere, Finland.
[Xu, Jianfeng; Zheng, S. Lilly] Wake Forest Sch Med, Ctr Canc Genom, Winston Salem, NC USA.
[Aly, Markus; Gronberg, Henrik; Wiklund, Fredrik] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Aly, Markus] Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden.
[Donovan, Jenny] Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
[Travis, Ruth C.; Key, Tim J.] Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England.
[Siddiq, Afshan] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Genom Common Dis, London, England.
[Canzian, Federico] German Canc Res Ctr, Genom Epidemiol Grp, Heidelberg, Germany.
[Khaw, Kay-Tee] Univ Cambridge, Clin Gerontol Unit, Cambridge, England.
[Takahashi, Atsushi] RIKEN, Ctr Integrat Med Sci, Lab Stat Anal, Yokohama, Kanagawa, Japan.
[Kubo, Michiaki] RIKEN, Ctr Integrat Med Sci, Lab Genotyping Dev, Yokohama, Kanagawa, Japan.
[Pharoah, Paul; Pashayan, Nora] Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Oncol, Cambridge, England.
[Weischer, Maren; Nordestgaard, Borge G.; Nielsen, Sune F.] Copenhagen Univ Hosp, Herlev Hosp, Dept Clin Biochem, Herlev, Denmark.
[Nordestgaard, Borge G.; Nielsen, Sune F.] Univ Copenhagen, Fac Hlth & Med Sci, Herlev, Denmark.
[Klarskov, Peter] Copenhagen Univ Hosp, Herlev Hosp, Dept Urol, Herlev, Denmark.
[Roder, Martin Andreas; Iversen, Peter] Copenhagen Univ Hosp, Rigshosp, Copenhagen Prostate Canc Ctr, Dept Urol, Copenhagen, Denmark.
[Thibodeau, Stephen N.; McDonnell, Shannon K.; Schaid, Daniel J.] Mayo Clin, Rochester, MN USA.
[Stanford, Janet L.; Kolb, Suzanne] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Stanford, Janet L.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Holt, Sarah] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Knudsen, Beatrice] Cedars Sinai, Translat Pathol, Los Angeles, CA USA.
[Coll, Antonio Hurtado] Prostate Ctr, Vancouver, BC, Canada.
[Gapstur, Susan M.; Diver, W. Ryan] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Maier, Christiane; Luedeke, Manuel] Univ Hosp Ulm, Dept Urol, Ulm, Germany.
[Herkommer, Kathleen] Tech Univ Munich, Klinikum Rechts Isar, Dept Urol, D-80290 Munich, Germany.
[Rinckleb, Antje E.; Strom, Sara S.] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Pettaway, Curtis] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA.
[Yeboah, Edward D.; Tettey, Yao; Biritwum, Richard B.; Adjei, Andrew A.; Tay, Evelyn] Univ Ghana, Sch Med, Accra, Ghana.
[Yeboah, Edward D.; Tettey, Yao; Biritwum, Richard B.; Adjei, Andrew A.; Tay, Evelyn] Korle Bu Teaching Hosp, Accra, Ghana.
[Truelove, Ann; Niwa, Shelley] Westat Corp, Rockville, MD USA.
[Choklcalingam, Anand P.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Cannon-Albright, Lisa] Univ Utah, Sch Med, Dept Med, Div Genet Epidemiol, Salt Lake City, UT USA.
[Cannon-Albright, Lisa] Vet Affairs Med Ctr, George E Wahlen Dept, Salt Lake City, UT 84148 USA.
[Cybulski, Cezary; Wokolorczyk, Dominika; Kluzniak, Wojciech] Pomeranian Med Univ, Int Hereditary Canc Ctr, Dept Genet & Pathol, Szczecin, Poland.
[Park, Jong; Sellers, Thomas] H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
[Lin, Hui-Yi] H Lee Moffitt Canc Ctr & Res Inst, Dept Biostat & Bioinformat, Tampa, FL USA.
[Isaacs, William B.; Partin, Alan W.] Johns Hopkins Hosp & Med Inst, James Buchanan Brady Urol Inst, Baltimore, MD USA.
[Brenner, Hermann; Dieffenbach, Aida Karina] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
[Brenner, Hermann; Dieffenbach, Aida Karina] German Canc Consortium, Heidelberg, Germany.
[Stegmaier, Christa] Saarland Canc Registry, Saarbrucken, Germany.
[Giovannucci, Edward L.; Stampfer, Meir; Penney, Kathryn L.; Mucci, Lorelei; Signorello, Lisa B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Ma, Jing; Stampfer, Meir; Penney, Kathryn L.; Mucci, Lorelei; Signorello, Lisa B.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Div Network Med, Boston, MA 02115 USA.
[John, Esther M.; Hsing, Ann W.; Chu, Lisa] Cancer Prevent Inst Calif, Fremont, CA USA.
[John, Esther M.; Hsing, Ann W.; Chu, Lisa] Stanford Univ, Sch Med, Stanford Canc Inst, Stanford, CA 94305 USA.
[Kittles, Rick A.] Univ Illinois, Dept Med, Chicago, IL USA.
[Murphy, Adam B.] Northwestern Univ, Dept Urol, Chicago, IL 60611 USA.
[Pandha, Hardev; Michael, Agnieszka; Kierzek, Andrzej M.] Univ Surrey, Fac Hlth & Med Sci, Guildford, Surrey, England.
[Blot, William] Int Epidemiol Inst, Rockville, MD USA.
[Blot, William; Zheng, Wei] Vanderbilt Univ, Sch Med, Vanderbilt Epidemiol Ctr, Dept Med,Div Epidemiol, Nashville, TN 37235 USA.
[Albanes, Demetrius; Weinstein, Stephanie] US Natl Inst Hlth, Natl Canc Inst, Div Canc Epidemiol & Genet, Nutr Epidemiol Branch, Bethesda, MD USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Nemesure, Barbara; Leske, Cristina; Wu, Suh-Yuh; Hennis, Anselm] SUNY Stony Brook, Dept Prevent Med, Stony Brook, NY 11794 USA.
[Hennis, Anselm] Translat Genom Res Inst, Phoenix, AZ USA.
[Kibel, Adam S.] Univ W Indies, Chron Dis Res Ctr, Bridgetown, Barbados.
[Rybicki, Benjamin A.; Neslund-Dudas, Christine] Brigham & Womens Hosp, Dana Farber Canc Inst, Div Urol Surg, Boston, MA 02115 USA.
[Goodman, Phyllis J.] Henry Ford Hosp, Dept Publ Hlth Sci, Detroit, MI 48202 USA.
[Klein, Eric A.] Fred Hutchinson Canc Res Ctr, Ctr Stat, Southwest Oncol Grp, Seattle, WA 98104 USA.
[Batra, Jyotsna; Clements, Judith] Cleveland Clin, Glickman Urol & Kidney Inst, Dept Urol, Cleveland, OH 44106 USA.
[Spurdle, Amanda] Queensland Univ Technol, Inst Hlth & Biomed Innovat, Australian Prostate Canc Res Ctr Queensland, Brisbane, Qld 4001, Australia.
[Teixeira, Manuel R.; Paulo, Paula; Maia, Sofia] Queensland Univ Technol, Sch Biomed Sci, Translat Res Inst, Brisbane, Qld 4001, Australia.
[Teixeira, Manuel R.] QIMR Berghofer Med Res Inst, Mol Canc Epidemiol Lab, Brisbane, Qld, Australia.
[Slavov, Chavdar] Portuguese Oncol Inst, Dept Genet, Oporto, Portugal.
[Kaneva, Radka; Mitev, Vanio] Univ Porto, Biomed Sci Inst, Oporto, Portugal.
[Witte, John S.] Med Univ Sofia, Dept Urol, Sofia, Bulgaria.
[Witte, John S.] Med Univ Sofia, Mol Med Ctr, Dept Med Chem & Biochem, Sofia, Bulgaria.
[Witte, John S.] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
[Witte, John S.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Gillanders, Elizabeth M.; Seminara, Daniella] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Riboli, Elio] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
[Hamdy, Freddie C.] Univ Oxford, Nuffield Dept Surg Sci, Oxford, England.
[Li, Qiyuan; Freedman, Matthew L.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Muir, Kenneth] Univ Manchester, Inst Populat Hlth, Manchester, Lancs, England.
[Muir, Kenneth] Univ Warwick, Warwick Med Sch, Coventry CV4 7AL, W Midlands, England.
[Nea, David E.] Canc Res UK, Li Ka Shing Ctr, Cambridge Res Inst, Cambridge, England.
[Nea, David E.] Univ Cambridge, Addenbrookes Hosp, Dept Oncol, Cambridge CB2 2QQ, England.
[Southey, Melissa] Univ Melbourne, Dept Pathol, Genet Epidemiol Lab, Parkville, Vic 3052, Australia.
[Giles, Graham G.; Severi, Gianluca] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[Giles, Graham G.] Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Biostat & Epidemiol, Melbourne, Vic, Australia.
[Severi, Gianluca] Human Genet Fdn, Turin, Italy.
[Nakagawa, Hidewaki] RIKEN, Ctr Integrat Med Sci, Lab Genome Sequencing Anal, Tokyo, Japan.
[Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Eeles, Rosalind A.] Royal Marsden Natl Hlth Serv NHS Fdn Trust, London, England.
[Eeles, Rosalind A.] Royal Marsden Natl Hlth Serv NHS Fdn Trust, Sutton, Surrey, England.
RP Haiman, CA (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
EM rosalind.eeles@icr.ac.uk; haiman@usc.edu
RI Albanes, Demetrius/B-9749-2015; Spurdle, Amanda/A-4978-2011; Cook,
Michael/A-5641-2009; Paulo, Paula/F-1441-2016; Teixeira,
Manuel/E-4885-2011; Kubo, Michiaki/N-7947-2015; Batra,
Jyotsna/B-4130-2011; Brenner, Hermann/B-4627-2017;
OI albright, lisa/0000-0003-2602-3668; Machiela,
Mitchell/0000-0001-6538-9705; Giles, Graham/0000-0003-4946-9099;
Clements, Judith/0000-0001-6026-1964; Spurdle,
Amanda/0000-0003-1337-7897; Cook, Michael/0000-0002-0533-7302; Paulo,
Paula/0000-0001-8387-2127; Teixeira, Manuel/0000-0002-4896-5982;
Brenner, Hermann/0000-0002-6129-1572; Roder, Martin
Andreas/0000-0002-0019-5333; Kierzek, Andrzej/0000-0002-2605-9057;
Eeles, Rosalind/0000-0002-3698-6241; Hazelett,
Dennis/0000-0003-0749-9935; Leongamornlert, Daniel/0000-0002-3486-3168
FU Cancer Research UK [10118, 10124, 13065, 14136]; Medical Research
Council [G0401527, G0900871, G1000143]; NCI NIH HHS [U01 CA098216, P30
CA042014, P30 CA068485, P30 CA076292, P50 CA140388, R01 CA056678, R01
CA068578, R01 CA072818, R01 CA082664, R01 CA084979, R01 CA088164, R01
CA092447, R01 CA092579, R01 CA128813, R01 CA128978, R01 CA136924, R37
CA054281, RC2 CA148085, U01 CA063464, U01 CA089600, U01 CA098233, U01
CA098710, U01 CA098758, U01 CA127298, U01 CA136792, U10 CA037429, U19
CA148065, U19 CA148112, U19 CA148537, UG1 CA189974, UM1 CA182883]; NHGRI
NIH HHS [U01 HG004446, U01 HG004726]; NIEHS NIH HHS [P30 ES007784, R01
ES011126]; NIGMS NIH HHS [S06 GM008016]; Prostate Cancer UK [G2011/36,
G2012/48]
NR 29
TC 103
Z9 103
U1 3
U2 31
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2014
VL 46
IS 10
BP 1103
EP 1109
DI 10.1038/ng.3094
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA AQ1PU
UT WOS:000342554100013
PM 25217961
ER
PT J
AU Hysi, PG
Cheng, CY
Springelkamp, H
Macgregor, S
Bailey, JNC
Wojciechowski, R
Vitart, V
Nag, A
Hewitt, AW
Hohn, R
Venturini, C
Mirshahi, A
Ramdas, WD
Thorleifsson, G
Vithana, E
Khor, CC
Stefansson, AB
Liao, JM
Haines, JL
Amin, N
Wang, YX
Wild, PS
Ozel, AB
Li, JZ
Fleck, BW
Zeller, T
Staffieri, SE
Teo, YY
Cuellar-Partida, G
Luo, XY
Allingham, RR
Richards, JE
Senft, A
Karssen, LC
Zheng, YF
Bellenguez, C
Xu, L
Iglesias, AI
Wilson, JF
Kang, JH
van Leeuwen, EM
Jonsson, V
Thorsteinsdottir, U
Despriet, DDG
Ennis, S
Moroi, SE
Martin, NG
Jansonius, NM
Yazar, S
Tai, ES
Amouyel, P
Kirwan, J
van Koolwijk, LME
Hauser, MA
Jonasson, F
Leo, P
Loomis, SJ
Fogarty, R
Rivadeneira, F
Kearns, L
Lackner, KJ
de Jong, PTVM
Simpson, CL
Pennell, CE
Oostra, BA
Uitterlinden, AG
Saw, SM
Lotery, AJ
Bailey-Wilson, JE
Hofman, A
Vingerling, JR
Maubaret, C
Pfeiffer, N
Wolfs, RCW
Lemij, HG
Young, TL
Pasquale, LR
Delcourt, C
Spector, TD
Klaver, CCW
Small, KS
Burdon, KP
Stefansson, K
Wong, TY
Viswanathan, A
Mackey, DA
Craig, JE
Wiggs, JL
van Duijn, CM
Hammond, CJ
Aung, T
AF Hysi, Pirro G.
Cheng, Ching-Yu
Springelkamp, Henriet
Macgregor, Stuart
Bailey, Jessica N. Cooke
Wojciechowski, Robert
Vitart, Veronique
Nag, Abhishek
Hewitt, Alex W.
Hohn, Rene
Venturini, Cristina
Mirshahi, Alireza
Ramdas, Wishal D.
Thorleifsson, Gudmar
Vithana, Eranga
Khor, Chiea-Chuen
Stefansson, Arni B.
Liao, Jiemin
Haines, Jonathan L.
Amin, Najaf
Wang, Ya Xing
Wild, Philipp S.
Ozel, Ayse B.
Li, Jun Z.
Fleck, Brian W.
Zeller, Tanja
Staffieri, Sandra E.
Teo, Yik-Ying
Cuellar-Partida, Gabriel
Luo, Xiaoyan
Allingham, R. Rand
Richards, Julia E.
Senft, Andrea
Karssen, Lennart C.
Zheng, Yingfeng
Bellenguez, Celine
Xu, Liang
Iglesias, Adriana I.
Wilson, James F.
Kang, Jae H.
van Leeuwen, Elisabeth M.
Jonsson, Vesteinn
Thorsteinsdottir, Unnur
Despriet, Dominiek D. G.
Ennis, Sarah
Moroi, Sayoko E.
Martin, Nicholas G.
Jansonius, Nomdo M.
Yazar, Seyhan
Tai, E-Shyong
Amouyel, Philippe
Kirwan, James
van Koolwijk, Leonieke M. E.
Hauser, Michael A.
Jonasson, Fridbert
Leo, Paul
Loomis, Stephanie J.
Fogarty, Rhys
Rivadeneira, Fernando
Kearns, Lisa
Lackner, Karl J.
de Jong, Paulus T. V. M.
Simpson, Claire L.
Pennell, Craig E.
Oostra, Ben A.
Uitterlinden, Andre G.
Saw, Seang-Mei
Lotery, Andrew J.
Bailey-Wilson, Joan E.
Hofman, Albert
Vingerling, Johannes R.
Maubaret, Cecilia
Pfeiffer, Norbert
Wolfs, Roger C. W.
Lemij, Hans G.
Young, Terri L.
Pasquale, Louis R.
Delcourt, Cecile
Spector, Timothy D.
Klaver, Caroline C. W.
Small, Kerrin S.
Burdon, Kathryn P.
Stefansson, Kari
Wong, Tien-Yin
Viswanathan, Ananth
Mackey, David A.
Craig, Jamie E.
Wiggs, Janey L.
van Duijn, Cornelia M.
Hammond, Christopher J.
Aung, Tin
CA BMES GWAS Grp
NEIGHBORHOOD Consortium
Wellcome Trust Case Control Conso
TI Genome-wide analysis of multi-ancestry cohorts identifies new loci
influencing intraocular pressure and susceptibility to glaucoma
SO NATURE GENETICS
LA English
DT Article
ID OPEN-ANGLE GLAUCOMA; CENTRAL CORNEAL THICKNESS; COMMON VARIANTS;
ASSOCIATION; METAANALYSIS; POPULATION; EXPRESSION; REDUCTION; TRIAL;
RISK
AB Elevated intraocular pressure (IOP) is an important risk factor in developing glaucoma, and variability in IOP might herald glaucomatous development or progression. We report the results of a genome-wide association study meta-analysis of 18 population cohorts from the International Glaucoma Genetics Consortium (IGGC), comprising 35,296 multi-ancestry participants for IOP. We confirm genetic association of known loci for IOP and primary open-angle glaucoma (POAG) and identify four new IOP-associated loci located on chromosome 3q25.31 within the FNDC3B gene (P = 4.19 x 10(-8) for rs6445055), two on chromosome 9 (P = 2.80 x 10(-11) for rs2472493 near ABCA1 and P = 6.39 x 10(-11) for rs8176693 within ABO) and one on chromosome 11p11.2 (best P = 1.04 x 10(-11) for rs747782). Separate meta-analyses of 4 independent POAG cohorts, totaling 4,284 cases and 95,560 controls, showed that 3 of these loci for IOP were also associated with POAG.
C1 [Hysi, Pirro G.; Small, Kerrin S.] Kings Coll London, Dept Twin Res & Genet Epidemiol, London, England.
[Cheng, Ching-Yu; Nag, Abhishek; Vithana, Eranga; Liao, Jiemin; Zheng, Yingfeng; Saw, Seang-Mei; Wong, Tien-Yin; Aung, Tin] Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore.
[Cheng, Ching-Yu; Vithana, Eranga; Khor, Chiea-Chuen; Liao, Jiemin; Wong, Tien-Yin; Aung, Tin] Natl Univ Singapore, Dept Ophthalmol, Singapore 117548, Singapore.
[Cheng, Ching-Yu; Vithana, Eranga; Khor, Chiea-Chuen; Liao, Jiemin; Teo, Yik-Ying; Zheng, Yingfeng; Tai, E-Shyong; Saw, Seang-Mei; Wong, Tien-Yin; Aung, Tin] Natl Univ Hlth Syst, Singapore, Singapore.
[Cheng, Ching-Yu; Teo, Yik-Ying; Zheng, Yingfeng; Tai, E-Shyong; Saw, Seang-Mei; Wong, Tien-Yin] Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore.
[Cheng, Ching-Yu; Vithana, Eranga; Tai, E-Shyong; Saw, Seang-Mei] Duke Natl Univ Singapore, Grad Sch Med, Singapore, Singapore.
[Springelkamp, Henriet; Ramdas, Wishal D.; Richards, Julia E.; Despriet, Dominiek D. G.; Vingerling, Johannes R.; Wolfs, Roger C. W.; Klaver, Caroline C. W.] Erasmus MC, Dept Ophthalmol, Rotterdam, Netherlands.
[Springelkamp, Henriet; Ramdas, Wishal D.; Amin, Najaf; Karssen, Lennart C.; Iglesias, Adriana I.; van Leeuwen, Elisabeth M.; van Koolwijk, Leonieke M. E.; Rivadeneira, Fernando; Uitterlinden, Andre G.; Hofman, Albert; Vingerling, Johannes R.; Klaver, Caroline C. W.; van Duijn, Cornelia M.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Macgregor, Stuart; Cuellar-Partida, Gabriel; Martin, Nicholas G.] Royal Brisbane Hosp, QIMR Berghofer Med Res Inst, Brisbane, Qld 4029, Australia.
[Bailey, Jessica N. Cooke; Haines, Jonathan L.] Case Western Reserve Univ, Dept Epidemiol & Biostat, Cleveland, OH 44106 USA.
[Wojciechowski, Robert] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Wojciechowski, Robert; Simpson, Claire L.; Bailey-Wilson, Joan E.] Natl Human Genome Res Inst, US Natl Inst Hlth, Baltimore, MD USA.
[Vitart, Veronique] Univ Edinburgh, Inst Genet & Mol Med, MRC, Human Genet Unit, Edinburgh, Midlothian, Scotland.
[Hewitt, Alex W.; Staffieri, Sandra E.; Kearns, Lisa; Mackey, David A.] Univ Melbourne, Royal Victorian Eye & Ear Hosp, Ctr Eye Res Australia, Melbourne, Vic, Australia.
[Hohn, Rene; Mirshahi, Alireza; Pfeiffer, Norbert] Univ Med Ctr Mainz, Dept Ophthalmol, Mainz, Germany.
[Venturini, Cristina] UCL, Inst Ophthalmol, London, England.
[Thorleifsson, Gudmar; Thorsteinsdottir, Unnur; Stefansson, Kari] deCODE Amgen, Reykjavik, Iceland.
[Khor, Chiea-Chuen] Genome Inst Singapore, Div Human Genet, Singapore, Singapore.
[Stefansson, Arni B.] Eye Clin, Reykjavik, Iceland.
[Wang, Ya Xing; Xu, Liang] Capital Univ Med Sci, Beijing Tongren Hosp, Beijing Inst Ophthalmol, Beijing, Peoples R China.
[Wild, Philipp S.] Univ Med Ctr Mainz, Dept Internal Med 2, Mainz, Germany.
[Ozel, Ayse B.; Li, Jun Z.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Fleck, Brian W.] Natl Hlth Serv NHS Princess Alexandra Eye Pavil, Edinburgh, Midlothian, Scotland.
[Zeller, Tanja] Univ Heart Ctr Hamburg, Clin Gen & Intervent Cardiol, Hamburg, Germany.
[Teo, Yik-Ying] Natl Univ Singapore, Dept Stat & Appl Probabil, Singapore 117548, Singapore.
[Luo, Xiaoyan; Young, Terri L.] Duke Univ, Duke Eye Ctr, Durham, NC USA.
[Allingham, R. Rand; Hauser, Michael A.] Duke Univ, Med Ctr, Dept Ophthalmol, Durham, NC 27710 USA.
[Senft, Andrea] Univ Hosp Schleswig Holstein, Inst Med Biometry & Stat, Lubeck, Germany.
[Bellenguez, Celine; Amouyel, Philippe] INSERM, UMR 774, F-59045 Lille, France.
[Bellenguez, Celine; Amouyel, Philippe] Univ Lille 2, Lille, France.
[Bellenguez, Celine; Amouyel, Philippe] Inst Pasteur, F-59019 Lille, France.
[Wilson, James F.] Univ Edinburgh, Sch Med, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
[Kang, Jae H.; Pasquale, Louis R.] Harvard Univ, Sch Med, Channing Div Network Med, Boston, MA USA.
[Jonsson, Vesteinn] Landspitali Natl Univ Hosp, Dept Ophthalmol, Reykjavik, Iceland.
[Ennis, Sarah] Univ Southampton, Fac Med, Human Genet & Genom Med, Southampton SO9 5NH, Hants, England.
[Moroi, Sayoko E.] Univ Michigan, Dept Ophthalmol & Visual Sci, Ann Arbor, MI 48109 USA.
[Jansonius, Nomdo M.] Univ Groningen, Univ Med Ctr Groningen, Dept Ophthalmol, Groningen, Netherlands.
[Yazar, Seyhan; Mackey, David A.] Univ Western Australia, Lions Eye Inst, Ctr Ophthalmol & Visual Sci, Perth, WA 6009, Australia.
[Tai, E-Shyong] Natl Univ Singapore, Dept Med, Singapore 117548, Singapore.
[Amouyel, Philippe] Univ Lille, Ctr Hosp Reg, Lille, France.
[Kirwan, James] Portsmouth Hosp NHS Trust, Dept Ophthalmol, Portsmouth, Hants, England.
[Hauser, Michael A.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Jonasson, Fridbert] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Leo, Paul] Univ Queensland, Diamantina Inst, Woollongabba, Qld, Australia.
[Loomis, Stephanie J.; Pasquale, Louis R.; Wiggs, Janey L.] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Loomis, Stephanie J.; Pasquale, Louis R.; Wiggs, Janey L.] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Fogarty, Rhys; Burdon, Kathryn P.; Craig, Jamie E.] Flinders Univ S Australia, Dept Ophthalmol, Adelaide, SA 5001, Australia.
[Rivadeneira, Fernando; Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Rivadeneira, Fernando; Uitterlinden, Andre G.; Hofman, Albert] Netherlands Consortium Healthy Ageing, Netherlands Genom Initiat, The Hague, Netherlands.
[Lackner, Karl J.] Inst Clin Chem, Mainz, Germany.
[Lackner, Karl J.] Lab Med, Mainz, Germany.
[de Jong, Paulus T. V. M.] Netherlands Inst Neurosci, Amsterdam, Netherlands.
[de Jong, Paulus T. V. M.] Leiden Univ, Med Ctr, Dept Ophthalmol, Leiden, Netherlands.
[de Jong, Paulus T. V. M.] Acad Med Ctr, Dept Ophthalmol, Amsterdam, Netherlands.
[Pennell, Craig E.] Univ Western Australia, Sch Womens & Infants Hlth, Perth, WA 6009, Australia.
[Oostra, Ben A.] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Lotery, Andrew J.] Univ Southampton, Fac Med, Southampton SO9 5NH, Hants, England.
[Maubaret, Cecilia; Delcourt, Cecile] Univ Bordeaux, ISPED, Bordeaux, France.
[Maubaret, Cecilia; Delcourt, Cecile] INSERM, Ctr INSERM Epidemiol Biostat Bordeaux U897, Bordeaux, France.
[Lemij, Hans G.] Rotterdam Eye Hosp, Glaucoma Serv, Rotterdam, Netherlands.
[Viswanathan, Ananth] Moorfields Eye Hosp NHS Fdn Trust, Biomed Res Ctr, NIHR, London, England.
RP Aung, T (reprint author), Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore.
EM chris.hammond@kcl.ac.uk; aung_tin@yahoo.co.uk
RI Delcourt, Cecile/I-2627-2013; Macgregor, Stuart/C-6442-2009; Cuellar
Partida, Gabriel/P-3701-2014; Wilson, James F/A-5704-2009; Rivadeneira,
Fernando/O-5385-2015; Hewitt, Alex/D-1936-2013; wang, YA
XING/K-9671-2016; Mackey, David/H-5340-2014; Cuellar Partida,
Gabriel/C-6686-2017;
OI Delcourt, Cecile/0000-0002-2099-0481; Macgregor,
Stuart/0000-0001-6731-8142; Wilson, James F/0000-0001-5751-9178;
Rivadeneira, Fernando/0000-0001-9435-9441; Hewitt,
Alex/0000-0002-5123-5999; Wojciechowski, Robert/0000-0002-9593-4652;
wang, YA XING/0000-0003-2749-7793; Mackey, David/0000-0001-7914-4709;
Cuellar Partida, Gabriel/0000-0001-7648-4097; Yazar,
Seyhan/0000-0003-0994-6196; Bailey-Wilson, Joan/0000-0002-9153-2920;
Hohn, Rene /0000-0003-2870-1469; Small, Kerrin/0000-0003-4566-0005;
Khor, Chiea Chuen/0000-0002-1128-4729; Hammond,
Christopher/0000-0002-3227-2620; Tai, E Shyong/0000-0003-2929-8966;
Karssen, Lennart C./0000-0002-1959-342X; Martin,
Nicholas/0000-0003-4069-8020
FU Chief Scientist Office [CZB/4/438, CZB/4/710]; Department of Health
[SRF/01/010]; Medical Research Council [MC_PC_U127561128]; NEI NIH HHS
[K08 EY022943, P30 EY014104, R01 EY015473, R01 EY022124, R01 EY022305,
R01 EY023512]; NHGRI NIH HHS [U01 HG004728]
NR 28
TC 46
Z9 47
U1 2
U2 22
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2014
VL 46
IS 10
BP 1126
EP 1130
DI 10.1038/ng.3087
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA AQ1PU
UT WOS:000342554100017
PM 25173106
ER
PT J
AU Canna, SW
de Jesus, AA
Gounil, S
Brooks, SR
Marrero, B
Liu, Y
DiMattia, MA
Zaal, KJM
Sanchez, GAM
Kim, H
Chapelle, D
Plass, N
Huang, Y
Villarinol, AV
Biancotto, A
Fleisher, TA
Duncan, JA
O'Shea, JJ
Benseler, S
Grom, A
Deng, ZM
Laxer, RM
Goldbach-Mansky, R
AF Canna, Scott W.
de Jesus, Adriana A.
Gounil, Sushanth
Brooks, Stephen R.
Marrero, Bernadette
Liu, Yin
DiMattia, Michael A.
Zaal, Kristien J. M.
Sanchez, Gina A. Montealegre
Kim, Hanna
Chapelle, Dawn
Plass, Nicole
Huang, Yan
Villarinol, Alejandro V.
Biancotto, Angelique
Fleisher, Thomas A.
Duncan, Joseph A.
O'Shea, John J.
Benseler, Susanne
Grom, Alexei
Deng, Zuoming
Laxer, Ronald M.
Goldbach-Mansky, Raphaela
TI An activating NLRC4 inflammasome mutation causes autoinflammation with
recurrent macrophage activation syndrome
SO NATURE GENETICS
LA English
DT Article
ID JUVENILE IDIOPATHIC ARTHRITIS; CYTOKINE PROFILES; BLAU-SYNDROME;
DISEASE; INTERLEUKIN-18; MECHANISM; REVEALS; HETEROGENEITY;
PATHOGENESIS; DEFICIENCY
AB Inflammasomes are innate immune sensors that respond to pathogen- and damage-associated signals with caspase-1 activation, interleukin (11)-1 beta and IL-18 secretion, and macrophage pyroptosis. The discovery that dominant gain-of-function mutations in NLRP3 cause the cryopyrin-associated periodic syndromes (CAPS) and trigger spontaneous inflammasome activation and IL-1 beta oversecretion led to successful treatment with IL-1-blocking agents(1). Herein we report a de novo missense mutation (c.1009A>T, encoding p.Thr337Ser) affecting the nucleotide-binding domain of the inflammasome component NLRC4 that causes early-onset recurrent fever flares and macrophage activation syndrome (MAS). Functional analyses demonstrated spontaneous inflammasome formation and production of the inflammasome-dependent cytokines IL-1 beta and IL-18, with the latter exceeding the levels seen in CAPS. The NLRC4 mutation caused constitutive caspase-1 cleavage in cells transduced with mutant NLRC4 and increased production of IL-18 in both patient-derived and mutant NLRC4 transduced macrophages. Thus, we describe a new monoallelic inflammasome defect that expands the monogenic autoinflammatory disease spectrum to include MAS and suggests new targets for therapy.
C1 [Canna, Scott W.; Gounil, Sushanth; Villarinol, Alejandro V.; O'Shea, John J.] Natl Inst Arthrit & Musculoskeletal & Skin Dis NI, Mol Immunol & Inflammat Branch, US Natl Inst Hlth NIH, Bethesda, MD USA.
[de Jesus, Adriana A.; Marrero, Bernadette; Liu, Yin; Kim, Hanna; Chapelle, Dawn; Plass, Nicole; Huang, Yan; Goldbach-Mansky, Raphaela] NIAMS, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD 20892 USA.
[Brooks, Stephen R.; Deng, Zuoming] NIAMS, Biodata Min & Discovery Sect, Off Sci & Technol, NIH, Bethesda, MD USA.
[DiMattia, Michael A.] NIAMS, Lab Struct Biol, NIH, Bethesda, MD USA.
[Zaal, Kristien J. M.] NIAMS, Light Imaging Sect, Off Sci & Technol, NIH, Bethesda, MD USA.
[Sanchez, Gina A. Montealegre; Chapelle, Dawn; Plass, Nicole] NIAMS, Office Clin Director, NIH, Bethesda, MD USA.
[Biancotto, Angelique] NHLBI, Ctr Human Immunol, NIH, Bethesda, MD USA.
[Fleisher, Thomas A.] NIH, Dept Lab, Ctr Clin, Bethesda, MD 20892 USA.
[Duncan, Joseph A.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
[Benseler, Susanne] Alberta Childrens Prov Gen Hosp, Calgary, AB, Canada.
[Benseler, Susanne] Univ Calgary, Calgary, AB, Canada.
[Grom, Alexei] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Grom, Alexei] Univ Cincinnati, Cincinnati, OH USA.
[Laxer, Ronald M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
RP Canna, SW (reprint author), NIAMS, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD 20892 USA.
EM scott.canna@nih.gov; goldbacr@mail.nih.gov
OI Kim, Hanna/0000-0002-0595-6533; Villarino, Alejandro/0000-0001-8068-2176
FU Intramural Research Program of the National Institute of Arthritis and
Musculoskeletal and Skin Diseases of the US National Institutes of
Health; Arthritis National Research Foundation
FX The authors are grateful to O. Navarro and G. Somers for assistance with
data acquisition and to H. Convery and the patient and her family for
assistance with research coordination. This research was supported by
the Intramural Research Program of the National Institute of Arthritis
and Musculoskeletal and Skin Diseases of the US National Institutes of
Health. S.W.C. was also supported by the Arthritis National Research
Foundation.
NR 38
TC 103
Z9 107
U1 4
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2014
VL 46
IS 10
BP 1140
EP 1146
DI 10.1038/ng.3089
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA AQ1PU
UT WOS:000342554100020
PM 25217959
ER
PT J
AU Ramasamy, A
Trabzuni, D
Guelfi, S
Varghese, V
Smith, C
Walker, R
De, T
Coin, L
de Silva, R
Cookson, MR
Singleton, AB
Hardy, J
Ryten, M
Weale, ME
AF Ramasamy, Adaikalavan
Trabzuni, Daniah
Guelfi, Sebastian
Varghese, Vibin
Smith, Colin
Walker, Robert
De, Tisham
Coin, Lachlan
de Silva, Rohan
Cookson, Mark R.
Singleton, Andrew B.
Hardy, John
Ryten, Mina
Weale, Michael E.
CA UK Brain Expression Consortium
North Amer Brain Expression Consor
TI Genetic variability in the regulation of gene expression in ten regions
of the human brain
SO NATURE NEUROSCIENCE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; HUMAN PREFRONTAL CORTEX; ALZHEIMERS-DISEASE;
SMOKING-BEHAVIOR; COMMON VARIANTS; LUNG-CANCER; SUSCEPTIBILITY;
METAANALYSIS; LOCUS; CD2AP
AB Germ-line genetic control of gene expression occurs via expression quantitative trait loci (eQTLs). We present a large, exon-specific eQTL data set covering ten human brain regions. We found that cis-eQTL signals (within 1 Mb of their target gene) were numerous, and many acted heterogeneously among regions and exons. Co-regulation analysis of shared eQTL signals produced well-defined modules of region-specific co-regulated genes, in contrast to standard coexpression analysis of the same samples. We report cis-eQTL signals for 23.1% of catalogued genome-wide association study hits for adult-onset neurological disorders. The data set is publicly available via public data repositories and via http://www.braineac.org/. Our study increases our understanding of the regulation of gene expression in the human brain and will be of value to others pursuing functional follow-up of disease-associated variants.
C1 [Ramasamy, Adaikalavan; Varghese, Vibin; Ryten, Mina; Weale, Michael E.] Guys Hosp, Kings Coll London, Dept Med & Mol Genet, London SE1 9RT, England.
[Ramasamy, Adaikalavan; Trabzuni, Daniah; Guelfi, Sebastian; de Silva, Rohan; Hardy, John; Ryten, Mina] UCL, Inst Neurol, Dept Mol Neurosci, Reta Lila Weston Res Labs, London, England.
[Trabzuni, Daniah] King Faisal Specialist Hosp & Res Ctr, Dept Genet, Riyadh 11211, Saudi Arabia.
[Smith, Colin; Walker, Robert] Univ Edinburgh, Dept Neuropathol, MRC Sudden Death Brain Bank Project, Edinburgh, Midlothian, Scotland.
[De, Tisham] Univ London Imperial Coll Sci Technol & Med, Fac Med, Sch Publ Hlth, London, England.
[Coin, Lachlan] Univ Queensland, Inst Mol Biosci, St Lucia, Qld, Australia.
[Cookson, Mark R.; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Ryten, M (reprint author), Guys Hosp, Kings Coll London, Dept Med & Mol Genet, London SE1 9RT, England.
EM mina.ryten@ucl.ac.uk; michael.weale@kcl.ac.uk
RI Hardy, John/C-2451-2009; Singleton, Andrew/C-3010-2009; de Silva,
Rohan/C-1734-2008; Ramasamy, Adaikalavan/G-2632-2010; Weale,
Michael/F-2587-2010; Coin, Lachlan/A-9001-2014
OI de Silva, Rohan/0000-0002-5052-5775; Ramasamy,
Adaikalavan/0000-0002-7598-2892; Weale, Michael/0000-0003-4593-1186;
Coin, Lachlan/0000-0002-4300-455X
FU US National Institute of Neurological Disorders and Stroke [U24
NS072026]; National Institute on Aging [P30 AG19610]; Arizona Department
of Health Services [211002]; Arizona Biomedical Research Commission
[4001, 0011, 05-901, 1001]; Michael J. Fox Foundation for Parkinson's
Research; UK Medical Research Council (MRC) through the MRC Sudden Death
Brain Bank [G0901254, G0802462]; King Faisal Specialist Hospital and
Research Centre, Saudi Arabia; Intramural Research Program of the US
National Institute on Aging, National Institutes of Health, Department
of Health and Human Services [ZO1 AG000947]; National Institute for
Health Research (NIHR) Biomedical Research Centre based at Guy's and St
Thomas' National Health Service (NHS) Foundation Trust; King's College
London
FX We are grateful to the Banner Sun Health Research Institute Brain and
Body Donation Program of Sun City, Arizona for the provision of human
biospecimens. The Brain and Body Donation Program is supported by the US
National Institute of Neurological Disorders and Stroke (U24 NS072026
National Brain and Tissue Resource for Parkinson's Disease and Related
Disorders), the National Institute on Aging (P30 AG19610 Arizona
Alzheimer's Disease Core Center), the Arizona Department of Health
Services (contract 211002, Arizona Alzheimer's Research Center), the
Arizona Biomedical Research Commission (contracts 4001, 0011, 05-901 and
1001 to the Arizona Parkinson's Disease Consortium) and the Michael J.
Fox Foundation for Parkinson's Research. We would like to thank AROS
Applied Biotechnology AS company laboratories and Affymetrix for their
input. H. Jonvik, L. Stanyer, J. Toombs and M. Gaskin provided
invaluable assistance in helping with Our computer infrastructure and in
sample handling and databasing. We thank A. Pittman for discussions.
This work was supported by the UK Medical Research Council (MRC) through
the MRC Sudden Death Brain Bank (C.S.), a Project Grant (G0901254 to
J.H. and M.E.W) and Training Fellowship (G0802462 to M.R.). D.T. was
supported by the King Faisal Specialist Hospital and Research Centre,
Saudi Arabia. This work was also supported in part by the Intramural
Research Program of the US National Institute on Aging, National
Institutes of Health, Department of Health and Human Services; project
ZO1 AG000947. We acknowledge support from the National Institute for
Health Research (NIHR) Biomedical Research Centre based at Guy's and St
Thomas' National Health Service (NHS) Foundation Trust and King's
College London. The views expressed are those of the authors and not
necessarily those of the NHS, the NIHR or the Department of Health.
NR 46
TC 107
Z9 107
U1 1
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
EI 1546-1726
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD OCT
PY 2014
VL 17
IS 10
BP 1418
EP 1428
DI 10.1038/nn.3801
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA AP8KD
UT WOS:000342327000023
PM 25174004
ER
PT J
AU Fields, RD
Araque, A
Johansen-Berg, H
Lim, SS
Lynch, G
Nave, KA
Nedergaard, M
Perez, R
Sejnowski, T
Wake, H
AF Fields, R. Douglas
Araque, Alfonso
Johansen-Berg, Heidi
Lim, Soo-Siang
Lynch, Gary
Nave, Klaus-Armin
Nedergaard, Maiken
Perez, Ray
Sejnowski, Terrence
Wake, Hiroaki
TI Glial Biology in Learning and Cognition
SO NEUROSCIENTIST
LA English
DT Article
DE memory; astrocyte; microglia; oligodendrocyte; myelin; synaptic
plasticity; neuron-glia interactions
ID EMERGING ROLES; ASTROCYTES; MEMORY; NEUROGENESIS; MYELINATION;
POTENTIALS; MODULATION; PLASTICITY; DYNAMICS; BRAIN
AB Neurons are exquisitely specialized for rapid electrical transmission of signals, but some properties of glial cells, which do not communicate with electrical impulses, are well suited for participating in complex cognitive functions requiring broad spatial integration and long-term temporal regulation. Astrocytes, microglia, and oligodendrocytes all have biological properties that could influence learning and cognition. Myelination by oligodendrocytes increases conduction velocity, affecting spike timing and oscillations in neuronal activity. Astrocytes can modulate synaptic transmission and may couple multiple neurons and synapses into functional assemblies. Microglia can remove synapses in an activity-dependent manner altering neural networks. Incorporating glia into a bicellular mechanism of nervous system function may help answer long-standing questions concerning the cellular mechanisms of learning and cognition.
C1 [Fields, R. Douglas] NICHD, NIH, Bethesda, MD 20904 USA.
[Araque, Alfonso] CSIC, Inst Cajal, E-28002 Madrid, Spain.
[Johansen-Berg, Heidi] John Radcliffe Hosp, Oxford OX3 9DU, England.
[Lim, Soo-Siang] Natl Sci Fdn, Arlington, VA 22230 USA.
[Lynch, Gary] Univ Calif Irvine, Irvine, CA USA.
[Nave, Klaus-Armin] Max Planck Inst Expt Med, D-37075 Gottingen, Germany.
[Nedergaard, Maiken] Univ Rochester, Rochester, NY USA.
[Perez, Ray] Off Naval Res, Arlington, VA 22217 USA.
[Sejnowski, Terrence] Salk Inst Biol Studies, La Jolla, CA USA.
[Wake, Hiroaki] Natl Inst Basic Biol, Okazaki, Aichi 444, Japan.
RP Fields, RD (reprint author), NICHD, NIH, Bldg 35,Room 2A211,MSC 3713, Bethesda, MD 20904 USA.
EM fieldsd@mail.nih.gov
OI Araque, Alfonso/0000-0003-3840-1144
FU NICHD; NSF [SMA-1330402, SMA-1258562]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This study
was supported by funds for intramural research, NICHD and NSF grants
SMA-1330402 and SMA-1258562 to R. Douglas Fields and Beth Stevens,
Harvard University.
NR 33
TC 25
Z9 27
U1 6
U2 34
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-8584
EI 1089-4098
J9 NEUROSCIENTIST
JI Neuroscientist
PD OCT
PY 2014
VL 20
IS 5
BP 426
EP 431
DI 10.1177/1073858413504465
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AQ2TB
UT WOS:000342640800005
PM 24122821
ER
PT J
AU Sun, DQ
Zhou, X
Lin, FR
Francis, HW
Carey, JP
Chien, WW
AF Sun, Daniel Q.
Zhou, Xin
Lin, Frank R.
Francis, Howard W.
Carey, John P.
Chien, Wade W.
TI Racial Difference in Cochlear Pigmentation Is Associated With Hearing
Loss Risk
SO OTOLOGY & NEUROTOLOGY
LA English
DT Article
DE Cochlea; Hearing loss; Melanin; Race; Temporal bone
ID STRIA VASCULARIS; INTERMEDIATE CELLS; INNER-EAR; MELANIN; NOISE;
MELANOCYTES; RACE/ETHNICITY; PREVALENCE; DEAFNESS; ADULTS
AB Objectives: The goals of this study are to characterize the distribution of melanin pigmentation in the human cochlea and to investigate differences in pigment content between races.
Methods: Human temporal bone specimens from the Johns Hopkins Temporal Bone Collection were examined. Demographic, clinical, and audiometric data were analyzed. Melanin pigmentation in the cochlea was quantified in each specimen.
Results: Nineteen African-American (AA) and 27 Caucasian specimens were selected for the study. The mean ages were 64 and 70 years for AA and Caucasian specimens, respectively (p = 0.21). At all cochlear turns, AA specimens contained significantly more pigmentation in the stria vascularis (p = 0.0003) and Rosenthal's canal (p < 0.0001) compared with Caucasian specimens. Strial melanin content increased significantly with age. Cochlear pigmentation content was not associated with sex or hearing thresholds.
Conclusion: Melanin pigmentation is significantly more abundant in AA cochleae than in Caucasian cochleae. This study provides a detailed description of pigmentation in the cochlea and may help to explain the observed racial differences in hearing thresholds.
C1 [Sun, Daniel Q.; Lin, Frank R.; Francis, Howard W.; Carey, John P.; Chien, Wade W.] Dept Otolaryngol Head & Neck Surg, Baltimore, MD USA.
[Zhou, Xin] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Chien, Wade W.] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA.
RP Sun, DQ (reprint author), Johns Hopkins Outpatient Ctr, Dept Otolaryngol Head & Neck Surg, 6th Floor,601 N Caroline St, Baltimore, MD 21287 USA.
EM danthesun@hotmail.com
NR 27
TC 5
Z9 5
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1531-7129
EI 1537-4505
J9 OTOL NEUROTOL
JI Otol. Neurotol.
PD OCT
PY 2014
VL 35
IS 9
BP 1509
EP 1514
PG 6
WC Clinical Neurology; Otorhinolaryngology
SC Neurosciences & Neurology; Otorhinolaryngology
GA AQ0JG
UT WOS:000342468700008
PM 25166018
ER
PT J
AU Laiyemo, AO
Adebogun, AO
Doubeni, CA
Ricks-Santi, L
McDonald-Pinkett, S
Young, PE
Cash, BD
Klabunde, CN
AF Laiyemo, Adeyinka O.
Adebogun, Akeem O.
Doubeni, Chyke A.
Ricks-Santi, Luisel
McDonald-Pinkett, Shelly
Young, Patrick E.
Cash, Brooks D.
Klabunde, Carrie N.
TI Influence of provider discussion and specific recommendation on
colorectal cancer screening uptake among U.S. adults
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Colon cancer; Screening; Colonoscopy; Stool blood test; Sigmoidoscopy;
HINTS
ID HEALTH INTERVIEW SURVEY; ADHERENCE; PATTERNS
AB Objectives. It is unclear if provider recommendations regarding colorectal cancer (CRC) screening modalities affect patient compliance. We evaluated provider-patient communications about CRC screening with and without a specific screening modality recommendation on patient compliance with screening guidelines.
Methods. We used the 2007 Health Information National Trends Survey (HINTS) and identified 4283 respondents who were at least 50 years of age and answered questions about their communication with their care providers and CRC screening uptake. We defined being compliant with CRC screening as the use of fecal occult blood testing (FOBT) within 1 year, sigmoidoscopy within 5 years, or colonoscopy within 10 years. We used survey weights in all analyses.
Results. CRC screening discussions occurred with 3320 (76.2%) respondents. Approximately 95% of these discussions were with physicians. Overall, 2793 (62.6%) respondents were current with CRC screening regardless of the screening modality. Discussion about screening (odds ratio (OR) = 8.83; 95% confidence interval (CI): 720-10.84) and providers making a specific recommendation about screening modality rather than leaving it to the patient to decide (OR = 2.04; 95% Cl: 1.54-2.68) were associated with patient compliance with CRC screening guidelines.
Conclusion. Compliance with CRC screening guidelines is improved when providers discuss options and make specific screening test recommendations. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Laiyemo, Adeyinka O.; Adebogun, Akeem O.; McDonald-Pinkett, Shelly] Howard Univ, Coll Med, Dept Med, Washington, DC 20060 USA.
[Laiyemo, Adeyinka O.] NCI, Biometry Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Doubeni, Chyke A.] Perelman Sch Med, Dept Family Med & Community Hlth, Philadelphia, PA USA.
[Doubeni, Chyke A.] Univ Penn, Leonard Davis Inst Hlth Econ, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Doubeni, Chyke A.] Univ Penn, Perelman Sch Med, Ctr Publ Hlth Initiat, Philadelphia, PA 19104 USA.
[McDonald-Pinkett, Shelly] Hampton Univ, Dept Biol Sci, Canc Res Ctr, Hampton, VA 23668 USA.
[Young, Patrick E.; Cash, Brooks D.] Walter Reed Natl Mil Med Ctr, Dept Med, Bethesda, MD USA.
[Klabunde, Carrie N.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
RP Laiyemo, AO (reprint author), Howard Univ, Coll Med, Dept Med, Div Gastroenterol, 2041 Georgia Ave NW, Washington, DC 20060 USA.
EM adeyinka.laiyemo@howard.edu
OI Doubeni, Chyke/0000-0001-7495-0285
FU National Center for Advancing Translational Sciences [KL2TR000102-04,
UL1RT000101]; National Cancer Institute of the National Institutes of
Health [5K01CA127118, U01CA151736]
FX Grant support: Dr Laiyemo is supported by a grant award from the
National Center for Advancing Translational Sciences (KL2TR000102-04 and
UL1RT000101). The content is solely the responsibility of the authors
and does not necessarily represent the official views of the National
Center for Advancing Translational Sciences and the National Institutes
of Health.; Dr. Doubeni is supported by grant numbers 5K01CA127118 and
U01CA151736 from the National Cancer Institute of the National
Institutes of Health.
NR 17
TC 11
Z9 11
U1 1
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
EI 1096-0260
J9 PREV MED
JI Prev. Med.
PD OCT
PY 2014
VL 67
BP 1
EP 5
DI 10.1016/j.ypmed.2014.06.022
PG 5
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA AP7KD
UT WOS:000342255300001
PM 24967957
ER
PT J
AU Marcus, PM
Ogden, SL
Gren, LH
Childs, JC
Pretzel, SM
Lamerato, LE
Walsh, K
Rozjabek, HM
Mabie, J
Thomas, B
Riley, T
AF Marcus, Pamela M.
Ogden, Sheryl L.
Gren, Lisa H.
Childs, Jeffery C.
Pretzel, Shannon M.
Lamerato, Lois E.
Walsh, Kayo
Rozjabek, Heather M.
Mabie, Jerome
Thomas, Brett
Riley, Tom
TI Non-compliance with the initial screening exam visit in the Prostate,
Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Mass screening; Adherence; Compliance; Cancer; Randomized controlled
trial as subject
ID ADHERENCE; MORTALITY; PARTICIPATION; PREDICTORS
AB Objective. Identify predictors of non-compliance with first round screening exams in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
Method. The PLCO was conducted from 1993 to 2011 at 10 US institutions. A total of 154,897 healthy men and women ages 55-74 years were randomized. Intervention arm participants were invited to receive gender-appropriate screening exams for prostate, lung, colorectal and ovarian cancer. Using intervention-arm data (73,036 participants), non-compliance percentages for 13 covariates were calculated, as were unadjusted and adjusted odds ratios (ORs), and 95% confidence intervals. Covariates included demographic factors as well as factors specific to PLCO (e.g., method of consent, distance from screening center).
Results. The rate of non-compliance was 11% overall but varied by screening center. Significant associations were observed for most covariates but indicated modest increases or decreases in odds. An exception was the use of a two-step consent process (consented intervention arm participants for exams after randomization) relative to a one-step process (consented all participants prior to randomization) (OR: 2.2, 95% CI: 2.0-2.5). Non-compliance percentages increased with further distance from screening centers, but ORs were not significantly different from 1.
Conclusions. Many factors modestly influenced compliance. Consent process was the strongest predictor of compliance. Published by Elsevier Inc.
C1 [Marcus, Pamela M.; Rozjabek, Heather M.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Ogden, Sheryl L.] Univ Colorado, Ctr Canc, Colorado Colorectal Screening Program, Aurora, CO 80045 USA.
[Gren, Lisa H.] Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT 84108 USA.
[Childs, Jeffery C.] Univ Utah, Div Oncol, Salt Lake City, UT 84112 USA.
[Pretzel, Shannon M.] Univ Colorado, Aurora, CO 80045 USA.
[Lamerato, Lois E.] Henry Ford Hlth Syst, Dept Publ Hlth Sci, Detroit, MI 48202 USA.
[Walsh, Kayo] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Rozjabek, Heather M.] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19102 USA.
[Mabie, Jerome; Thomas, Brett; Riley, Tom] Informat Management Syst, Rockville, MD 20852 USA.
RP Marcus, PM (reprint author), NCI, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Room 4E-608, Bethesda, MD 20892 USA.
EM marcusp@mail.nih.gov; Sheryl.ogden@ucdenver.edu; Lisa.gren@hsc.utah.edu;
jeff.childs@hsc.utah.edu; Shannon.pretzel@ucdenver.edu;
llamera1@hfhs.org; walsh@hcp.med.harvard.edu;
heather.rozjabek@gmail.com; mabiej@imsweb.com; thomasb@imsweb.com;
rileyt@imsweb.com
FU Division of Cancer Prevention, National Cancer Institute [N01-CN-25476,
N01-CN-25514, N01-CN-25522, N01-CN-25515, N01-CN-25512, N01-CN-25513,
N01-CN-25516, N01-CN-25511, N01-CN-25524, N01-CN-25518, N01-CN-75022,
N02-CN-55203-76, N02-CN-35001-45]
FX Supported by contracts from the Division of Cancer Prevention, National
Cancer Institute, to the coordinating center (N01-CN-25476 to Westat,
Inc.), the ten screening centers (N01-CN-25514 to the University of
Colorado Anschutz Medical Campus (Denver Metro area); N01-CN-25522 to
Georgetown University Medical Center (Washington, DC metro area);
N01-CN-25515 to the Pacific Health Research and Education Institute
(Honolulu, HI); N01-CN-25512 to the Henry Ford Health System (Detroit,
MI); N01-CN-25513 to the University of Minnesota School of Public Health
(Minneapolis/St Paul, MN); N01-CN-25516 to Washington University School
of Medicine (St. Louis, MO); N01-CN-25511 to the University of Pittsburg
Medical Center (Pittsburgh, PA); N01-CN-25524 to the University of Utah
Health Sciences Center (Salt Lake City, UT); N01-CN-25518 to the
Marshfield Clinic Research Foundation (Marshfield, WI); N01-CN-75022 to
the University of Alabama at Birmingham (Birmingham, AL); and
N02-CN-55203-76 and N02-CN-35001-45 to Information Management Services,
Inc. (Rockville, MD)).
NR 12
TC 1
Z9 1
U1 0
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
EI 1096-0260
J9 PREV MED
JI Prev. Med.
PD OCT
PY 2014
VL 67
BP 82
EP 88
DI 10.1016/j.ypmed.2014.07.013
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA AP7KD
UT WOS:000342255300013
PM 25038532
ER
PT J
AU Jayanthi, S
Koppolu, BP
Smith, SG
Jalah, R
Bear, J
Rosati, M
Pavlakis, GN
Felber, BK
Zaharoff, DA
Kumar, TKS
AF Jayanthi, Srinivas
Koppolu, Bhanu Prasanth
Smith, Sean G.
Jalah, Rashmi
Bear, Jenifer
Rosati, Margherita
Pavlakis, George N.
Felber, Barbara K.
Zaharoff, David A.
Kumar, Thallapuranam Krishnaswamy Suresh
TI Efficient production and purification of recombinant human
interleukin-12 (IL-12) overexpressed in mammalian cells without affinity
tag
SO PROTEIN EXPRESSION AND PURIFICATION
LA English
DT Article
DE Interleukin-12; Heparin Sepharose; HEK293; Cytokine; Purification;
Bioactivity
ID GROWTH-FACTOR RECEPTOR; HEPARIN-BINDING; IN-VIVO; CHICKEN
INTERLEUKIN-12; ADAPTIVE IMMUNITY; ESCHERICHIA-COLI; PROTEIN; CYTOKINE;
CHROMATOGRAPHY; ANTITUMOR
AB Interleukin-12 is a heterodimeric, pro-inflammatory cytokine that is a key driver of cell-mediated immunity. Clinical interest in IL-12 is significant due to its potent anti-tumor activity and efficacy in controlling certain infectious diseases such as Leishmaniasis and Listeria infection. For clinical applications, the ease of production and purification of IL-12 and the associated cost continues to be a consideration. In this context, we report a simple and effective heparin-affinity based purification of recombinant human IL-12 (hIL-12) from the serum-free supernatants of stable IL-12-transduced HEK293 cells. Fractionation of culture supernatants on heparin Sepharose columns revealed that hIL-12 elutes as a single peak in 500 mM NaCl. Coomassie staining and Western blot analysis showed that hIL-12 eluted in 500 mM NaCl is homogeneous. Purity of hIL-12 was ascertained by RP-HPLC and ESI-MS analysis, and found to be similar to 98%. Western blot analysis, using monoclonal antibodies, demonstrated that the crucial inter-subunit disulfide bond linking the p35 and p40 subunits is intact in the purified hIL-12. Results of far UV circular dichroism, steady-state tryptophan fluorescence, and differential scanning calorimetry experiments suggest that purified hIL-12 is in its stable native conformation. Enzyme linked immunosorbent assays (ELISAs) and bioactivity studies demonstrate that hIL-12 is obtained in high yields (0.31 +/- 0.05 mg/mL of the culture medium) and is also fully bioactive. Isothermal titration calorimetry data show that IL-12 exhibits a moderate binding affinity (K-d(app) = 69 +/- 1 mu M) to heparin. The purification method described in this study is expected to provide greater impetus for research on the role of heparin in the regulation of the function of IL-12. In addition, the results of this study provide an avenue to obtain high amounts of IL-12 required for structural studies which are aimed at the development of novel IL-12-based therapeutics. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Jayanthi, Srinivas; Kumar, Thallapuranam Krishnaswamy Suresh] Univ Arkansas, Dept Chem & Biochem, Fayetteville, AR 72701 USA.
[Koppolu, Bhanu Prasanth; Smith, Sean G.; Zaharoff, David A.] Univ Arkansas, Dept Biomed Engn, Fayetteville, AR 72701 USA.
[Jalah, Rashmi; Bear, Jenifer; Felber, Barbara K.] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Frederick, MD 21702 USA.
[Rosati, Margherita; Pavlakis, George N.] NCI, Human Retrovirus Sect, Vaccine Branch, Frederick, MD 21702 USA.
RP Zaharoff, DA (reprint author), Univ Arkansas, Dept Biomed Engn, Fayetteville, AR 72701 USA.
EM zaharoff@uark.edu; sthalla@uark.edu
RI Koppolu, Bhanu prasanth/H-1313-2016; Kumar, Suresh
Thallapuranam/R-5606-2016;
OI Koppolu, Bhanu prasanth/0000-0001-9570-3902; Kumar, Suresh
Thallapuranam/0000-0001-7262-1373; Zaharoff, David/0000-0001-6885-6727;
Jayanthi, Srinivas/0000-0001-7357-760X
FU National Institutes of Health (USA) [NCRR COBRE Grant] [1 P20 RR15569,
P30 GM103450, K22 CA131567, R01 CA172631, R15 CA176648]; Department of
Energy [DE-FG02-01ER15161]; National Science Foundation (USA); Arkansas
Biosciences Institute (USA); Intramural Research Program of the National
Cancer Institute, National Institutes of Health (NCI/NIH)
FX This work was supported in part by grants from the National Institutes
of Health (USA) [NCRR COBRE Grant 1 P20 RR15569 (T.K.S.K.), P30 GM103450
(T.K.S.K.), K22 CA131567 (D.A.Z.), R01 CA172631 (D.A.Z. and T.K.S.K),
R15 CA176648, the Department of Energy (Grant DE-FG02-01ER15161
(T.K.S.K.), National Science Foundation (USA) and the Arkansas
Biosciences Institute (USA) (T.K.S.K. and D.A.Z.), by the Intramural
Research Program of the National Cancer Institute, National Institutes
of Health (NCI/NIH) (G.N.P. and B.K.F.). We thank C. Bergamaschi and
J.J.S. Cadwell for discussions, and B. Chowdhury for technical
assistance.
NR 62
TC 1
Z9 2
U1 6
U2 27
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-5928
EI 1096-0279
J9 PROTEIN EXPRES PURIF
JI Protein Expr. Purif.
PD OCT
PY 2014
VL 102
BP 76
EP 84
DI 10.1016/j.pep.2014.07.002
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AQ0OC
UT WOS:000342481600011
PM 25123642
ER
PT J
AU Wainer, IW
AF Wainer, Irving W.
TI Are basal D-serine plasma levels a predictive biomarker for the rapid
antidepressant effects of ketamineand ketamine metabolites?
SO PSYCHOPHARMACOLOGY
LA English
DT Letter
ID MAMMALIAN TARGET; RAPAMYCIN
C1 [Wainer, Irving W.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Wainer, Irving W.] Mitchell Woods Pharmaceut, Shelton, CT 06484 USA.
RP Wainer, IW (reprint author), Mitchell Woods Pharmaceut, 4 Corp Dr,Suite 287, Shelton, CT 06484 USA.
EM Wainerir@grc.nia.nih.gov
NR 7
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2014
VL 231
IS 20
BP 4083
EP 4084
DI 10.1007/s00213-014-3736-6
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AQ0EE
UT WOS:000342454800015
PM 25209678
ER
PT J
AU Yoon, JH
Abdelmohsen, K
Gorospe, M
AF Yoon, Je-Hyun
Abdelmohsen, Kotb
Gorospe, Myriam
TI Functional interactions among microRNAs and long noncoding RNAs
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Post-transcriptional gene regulation; Ribonucleoprotein complex;
RNA-binding protein; mRNA stability; Translation
ID EMBRYONIC STEM-CELLS; REPRESSIVE COMPLEX 2; TUMOR-SUPPRESSOR;
MESSENGER-RNAS; CIRCULAR RNAS; HUMAN GENOME; MUSCLE DIFFERENTIATION;
ANTISENSE RNA; GENE; TRANSLATION
AB In mammals, the vast majority of transcripts expressed are noncoding RNAs, ranging from short RNAs (including microRNAs) to long RNAs spanning up to hundreds of kb. While the actions of microRNAs as destabilizers and repressors of the translation of protein-coding transcripts (mRNAs) have been studied in detail, the influence of microRNAs on long noncoding RNA (lncRNA) function is only now coming into view. Conversely, the influence of lncRNAs upon microRNA function is also rapidly emerging. In some cases, lncRNA stability is reduced through the interaction of specific miRNAs. In other cases, lncRNAs can act as microRNA decoys, with the sequestration of microRNAs favoring expression of repressed target mRNAs. Other lncRNAs derepress gene expression by competing with miRNAs for interaction with shared target mRNAs. Finally, some lncRNAs can produce miRNAs, leading to repression of target mRNAs. These microRNA-lncRNA regulatory paradigms modulate gene expression patterns that drive major cellular processes (such as cell differentiation, proliferation, and cell death) which are central to mammalian physiologic and pathologic processes. We review and summarize the types of microRNA-lncRNA crosstalk identified to-date and discuss their influence on gene expression programs. Published by Elsevier Ltd.
C1 [Yoon, Je-Hyun; Abdelmohsen, Kotb; Gorospe, Myriam] NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Yoon, JH (reprint author), NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM yoonjehyun@gmail.com; myriamgorospe@nih.gov
FU National Institute on Aging Intramural Research Program, National
Institutes of Health
FX JHY, KA, and MG were supported by the National Institute on Aging
Intramural Research Program, National Institutes of Health.
NR 72
TC 48
Z9 53
U1 6
U2 53
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 OCT
PY 2014
VL 34
BP 9
EP 14
DI 10.1016/j.semcdb.2014.05.015
PG 6
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA AP4YN
UT WOS:000342086700003
PM 24965208
ER
PT J
AU Bonnemaison, M
Back, N
Lin, YM
Bonifacino, JS
Mains, R
Eipper, B
AF Bonnemaison, Mathilde
Back, Nils
Lin, Yimo
Bonifacino, Juan S.
Mains, Richard
Eipper, Betty
TI AP-1A Controls Secretory Granule Biogenesis and Trafficking of Membrane
Secretory Granule Proteins
SO TRAFFIC
LA English
DT Article
DE carboxypeptidase D; PAM; peptide hormone; regulated secretion; TGN
ID ALPHA-AMIDATING MONOOXYGENASE; TRANS-GOLGI NETWORK; MANNOSE 6-PHOSPHATE
RECEPTORS; ATT-20 CELLS; NEUROENDOCRINE CELLS; SORTING SIGNALS;
METALLOCARBOXYPEPTIDASE D; CYTOPLASMIC DOMAIN; COATED VESICLES; PAM
EXPRESSION
AB The adaptor protein 1A complex (AP-1A) transports cargo between the trans-Golgi network (TGN) and endosomes. In professional secretory cells, AP-1A also retrieves material from immature secretory granules (SGs). The role of AP-1A in SG biogenesis was explored using AtT-20 corticotrope tumor cells expressing reduced levels of the AP-1A 1A subunit. A twofold reduction in 1A resulted in a decrease in TGN cisternae and immature SGs and the appearance of regulated secretory pathway components in non-condensing SGs. Although basal secretion of endogenous SG proteins was unaffected, secretagogue-stimulated release was halved. The reduced 1A levels interfered with the normal trafficking of carboxypeptidase D (CPD) and peptidylglycine -amidating monooxygenase-1 (PAM-1), integral membrane enzymes that enter immature SGs. The non-condensing SGs contained POMC products and PAM-1, but not CPD. Based on metabolic labeling and secretion experiments, the cleavage of newly synthesized PAM-1 into PHM was unaltered, but PHM basal secretion was increased in sh-1A PAM-1 cells. Despite lacking a canonical AP-1A binding motif, yeast two-hybrid studies demonstrated an interaction between the PAM-1 cytosolic domain and AP-1A. Coimmunoprecipitation experiments with PAM-1 mutants revealed an influence of the luminal domains of PAM-1 on this interaction. Thus, AP-1A is crucial for normal SG biogenesis, function and composition.
C1 [Bonnemaison, Mathilde; Eipper, Betty] Univ Connecticut, Ctr Hlth, Dept Mol Biol & Biophys, Farmington, CT 06030 USA.
[Back, Nils] Univ Helsinki, Inst Biomed Anat, FIN-00014 Helsinki, Finland.
[Lin, Yimo; Bonifacino, Juan S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
[Mains, Richard; Eipper, Betty] Univ Connecticut, Ctr Hlth, Dept Neurosci, Farmington, CT 06030 USA.
RP Eipper, B (reprint author), Univ Connecticut, Ctr Hlth, Dept Mol Biol & Biophys, Farmington, CT 06030 USA.
EM eipper@uchc.edu
OI Back, Nils/0000-0001-9992-3726; Bonifacino, Juan S./0000-0002-5673-6370
FU National Institutes of Health [DK32949]; Scoville Endowment; Janice and
Rodney Reynolds Endowment; Liv och Halsa Foundation; Magnus Ehrnrooth
Foundation; Perklen Foundation; Intramural Program of NICHD, NIH
FX We thank Darlene D'Amato and Yanping Wang for their constant technical
support. We thank Dr. Kurutihalli Vishwanatha and Megan Miller for their
helpful comments on the manuscript. We thank Dr. Lloyd Fricker for his
generous gift of carboxypeptidase D antibodies and Dr. Ann Cowan for
guidance with our fluorescence imaging experiments. We thank the
Electron Microscopy Unit of the Institute of Biotechnology, University
of Helsinki for providing laboratory facilities. This work was supported
by the National Institutes of Health (DK32949), Scoville Endowment,
Janice and Rodney Reynolds Endowment, Liv och Halsa Foundation, the
Magnus Ehrnrooth Foundation, the Perklen Foundation and the Intramural
Program of NICHD, NIH. The authors declare they have no conflicts of
interest.
NR 92
TC 11
Z9 11
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-9219
EI 1600-0854
J9 TRAFFIC
JI Traffic
PD OCT
PY 2014
VL 15
IS 10
BP 1099
EP 1121
DI 10.1111/tra.12194
PG 23
WC Cell Biology
SC Cell Biology
GA AP8SJ
UT WOS:000342348900005
PM 25040637
ER
PT J
AU Hofer, CB
Harris, DR
de Oliveira, RH
de Abreu, TF
Kakehasi, F
Pilotto, JH
Ruz, NP
Krauss, MR
Hazra, R
AF Hofer, Cristina B.
Harris, D. Robert
de Oliveira, Ricardo Hugo
de Abreu, Thalita F.
Kakehasi, Fabiana
Pilotto, Jose Henrique
Ruz, Noris Pavia
Krauss, Margot R.
Hazra, Rohan
TI Short Communication: Kidney Dysfunction Among HIV-Infected Children in
Latin America and the Caribbean
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ANTIRETROVIRAL THERAPY; PROTEINURIA;
ADOLESCENTS; INFANTS; COHORT
AB Renal toxicity is a concern in HIV-infected children receiving antiretrovirals. However, the prevalence [1.7%; 95% confidence interval (CI): 1.0-2.6%] and incidence of kidney dysfunction (0.17 cases/100 person-years; 95% CI: 0.04-0.30) were rare in this multicenter cohort study of 1,032 perinatally HIV-infected Latin American and Caribbean children followed from 2002 to 2011.
C1 [Hofer, Cristina B.] Univ Fed Rio de Janeiro, Dept Prevent Med, Rio De Janeiro, Brazil.
[Harris, D. Robert; Krauss, Margot R.] Westat Corp, Rockville, MD USA.
[de Oliveira, Ricardo Hugo; de Abreu, Thalita F.] Univ Fed Rio de Janeiro, Inst Puericultura & Pediat Martagao Gesteira, Rio De Janeiro, Brazil.
[Kakehasi, Fabiana] Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil.
[Pilotto, Jose Henrique] Hosp Geral Nova Iguacu, Inst Oswaldo Cruz, Nova Iguacu, Brazil.
[Ruz, Noris Pavia] Hosp Infantil Mexico Dr Federico Gomez, Mexico City, DF, Mexico.
[Hazra, Rohan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, NIH, Bethesda, MD USA.
RP Hofer, CB (reprint author), Ilha Fundao, R Bruno Lobo 50, BR-22460010 Rio De Janeiro, Brazil.
EM cbhofer@hucff.ufrj.br
FU NICHD [N01-HD-3-3345, HHSN267200800001C, N01-HD-8-0001]
FX Supported by NICHD Contract N01-HD-3-3345 (2002-2007) and by NICHD
Contract HHSN267200800001C (NICHD Control: N01-HD-8-0001) (2007-2012).
NR 10
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT 1
PY 2014
VL 30
IS 10
BP 966
EP 969
DI 10.1089/aid.2013.0276
PG 4
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA AP8TR
UT WOS:000342352500007
PM 24866283
ER
PT J
AU Swerdlow, SH
Jaffe, ES
Brousset, P
Chan, JKC
de Leval, L
Gaulard, P
Harris, NL
Pileri, S
Weiss, LM
AF Swerdlow, Steven H.
Jaffe, Elaine S.
Brousset, Pierre
Chan, John K. C.
de Leval, Laurence
Gaulard, Philippe
Harris, Nancy Lee
Pileri, Stefano
Weiss, Lawrence M.
CA Int Lymphoma Study Grp
TI Cytotoxic T-cell and NK-cell Lymphomas Current Questions and
Controversies
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE cytotoxic T-cell lymphoma; gamma delta T cells; natural killer cells;
enteropathy-associated T-cell lymphoma
ID EPSTEIN-BARR-VIRUS; NATURAL-KILLER-CELL; NON-HODGKINS-LYMPHOMA; DISTINCT
CLINICOPATHOLOGICAL ENTITY; GAMMA-DELTA; NASAL-TYPE; ALPHA-BETA;
CELIAC-DISEASE; LYMPHOPROLIFERATIVE DISORDER; GASTROINTESTINAL-TRACT
AB The cytotoxic T-cell and natural killer (NK)-cell lymphomas and related disorders are important but relatively rare lymphoid neoplasms that frequently are a challenge for practicing pathologists. This selective review, based on a meeting of the International Lymphoma Study Group, briefly reviews T-cell and NK-cell development and addresses questions related to the importance of precise cell lineage (alpha beta-type T cell, gamma delta T cell, or NK cell), the implications of Epstein-Barr virus infection, the significance of anatomic location including nodal disease, and the question of further categorization of enteropathy-associated T-cell lymphomas. Finally, developments subsequent to the 2008 World Health Organization Classification, including the recognition of indolent NK-cell and T-cell disorders of the gastrointestinal tract are presented.
C1 [Swerdlow, Steven H.] Univ Pittsburgh, Sch Med, Dept Pathol, Div Hematopathol, Pittsburgh, PA USA.
[Jaffe, Elaine S.] NCI, Bethesda, MD 20892 USA.
[Harris, Nancy Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Weiss, Lawrence M.] Clarient Diagnost Serv Inc, Aliso Viejo, CA USA.
[Brousset, Pierre] IUC T Oncopole, Toulouse, France.
[Gaulard, Philippe] Univ Paris Est, Hop Henri Mondor, Dept Pathol, Inserm,U955, Creteil, France.
[Chan, John K. C.] Queen Elizabeth Hosp, Hong Kong, Hong Kong, Peoples R China.
[de Leval, Laurence] Univ Hosp Lausanne CHUV, Inst Pathol, Lausanne, Switzerland.
[Pileri, Stefano] Univ Bologna, Sch Med, St Orsola Policlin, Bologna, Italy.
RP Swerdlow, SH (reprint author), UPMC Hlth Syst UPMC Presbyterian, Div Hematopathol, Dept Pathol, 200 Lothrop St Room G-335, Pittsburgh, PA 15213 USA.
EM swerdlowsh@upmc.edu
NR 100
TC 18
Z9 18
U1 3
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD OCT
PY 2014
VL 38
IS 10
BP E60
EP E71
PG 12
WC Pathology; Surgery
SC Pathology; Surgery
GA AP3TY
UT WOS:000342001800001
PM 25025449
ER
PT J
AU Ellefsen, KN
Concheiro, M
Beck, O
Gorelick, DA
Pirard, S
Huestis, MA
AF Ellefsen, Kayla N.
Concheiro, Marta
Beck, Olof
Gorelick, David A.
Pirard, Sandrine
Huestis, Marilyn A.
TI Quantification of cocaine and metabolites in exhaled breath by liquid
chromatography-high-resolution mass spectrometry following controlled
administration of intravenous cocaine
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Cocaine; Exhaled breath; LC-HRMS; Metabolites; SensAbues
ID ORAL FLUID; METHADONE; DRUGS; ABUSE; PHARMACOKINETICS; DISPOSITION;
PARTICLES; CANNABIS; USERS
AB Breath has been investigated as an alternative matrix for detecting recent cocaine intake; however, there are no controlled cocaine administration studies that investigated the drug's disposition into breath. Breath was collected from 10 healthy adult cocaine users by asking them to breathe into a SensAbues device for 3 min before and up to 22 h following 25 mg intravenous (IV) cocaine dosing on days 1, 5, and 10, and assayed with a validated liquid chromatography-high-resolution mass spectrometry (LC-HRMS) method to quantify breath cocaine, benzoylecgonine (BE), ecgonine methyl ester (EME), and norcocaine. The assay was linear from 25 to 1,000 pg/filter, extraction efficiencies were 83.6-126 %, intra- and inter-assay imprecision was < 10.6 %, and bias was between -8.5 and 16.8 %. No endogenous or exogenous interferences were observed for more than 75 tested. Analytes were generally stable under short-term storage conditions. Ion suppression was less than 46 %. Of breath specimens collected after controlled cocaine administration, 2.6 % were positive for cocaine (26.1-66 pg/filter, 1-9.5 h), 0.72 % BE (83.3-151 pg/filter, 6.5-12.5 h), and 0.72 % EME (50-69.1 pg/filter, 6.5-12.5 h); norcocaine was not detected. Methanolic extraction of the devices themselves, after filters were removed, yielded 19.2 % positive cocaine tests (25.2-36.4 pg/device, 10 min-22 h) and 4.3 % positive BE tests (26.4-93.7 pg/device, 10 min-22 h), explaining differences between the two extraction techniques. These results suggest that the device reflects the drug in oral fluid as well as lung microparticles, while the filter reflects only drug-laden microparticles. A sensitive and specific method for cocaine, BE, EME, and norcocaine quantification in breath was developed and validated. Cocaine in breath identifies recent cocaine ingestion, but its absence does not preclude recent use.
C1 [Ellefsen, Kayla N.; Concheiro, Marta; Pirard, Sandrine; Huestis, Marilyn A.] NIDA, NIH, Baltimore, MD 21224 USA.
[Ellefsen, Kayla N.] Univ Maryland, Toxicol Program, Baltimore, MD 21201 USA.
[Beck, Olof] Karolinska Inst, S-17177 Stockholm, Sweden.
[Gorelick, David A.] Univ Maryland, Sch Med, Dept Psychiat, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), NIDA, NIH, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
OI Beck, Olof/0000-0002-3546-8872
FU Intramural Research Program (IRP), National Institute on Drug Abuse
(NIDA), National Institutes of Health (NIH)
FX This work was supported by the Intramural Research Program (IRP),
National Institute on Drug Abuse (NIDA), National Institutes of Health
(NIH). The authors acknowledge the contributions of the clinical staff
of the NIDA-IRP and the Clinical Research Unit, Johns Hopkins Bayview
Medical Center, as well as the University of Maryland, Baltimore, a
member of the Graduate Partnership Program, NIH.
NR 28
TC 9
Z9 9
U1 5
U2 25
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
EI 1618-2650
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD OCT
PY 2014
VL 406
IS 25
BP 6213
EP 6223
DI 10.1007/s00216-014-8051-x
PG 11
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA AP6YK
UT WOS:000342224300013
PM 25129634
ER
PT J
AU Patel, D
Ellis, R
Howard, B
Boufraqech, M
Gara, SK
Zhang, LS
Quezado, MM
Nilubol, N
Kebebew, E
AF Patel, Dhaval
Ellis, Ryan
Howard, Brandi
Boufraqech, Myriem
Gara, Sudheer Kumar
Zhang, Lisa
Quezado, Martha M.
Nilubol, Naris
Kebebew, Electron
TI Analysis of IGF and IGFBP as Prognostic Serum Biomarkers for
Adrenocortical Carcinoma
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; FACTOR-II; BINDING PROTEIN-2; FACTOR SYSTEM;
INSULIN; TUMORS; EXPRESSION; PROGRESSION; CANCER; TUMORIGENESIS
AB Adrenocortical carcinoma (ACC) lacks diagnostic and prognostic biomarkers to guide treatment. A consistently dysregulated pathway in ACC is the IGF signaling pathway, specifically overexpression of IGF2, IGF-I-receptor, and IGFBP2. The objective of this study was to perform a comprehensive analysis of serum IGF and IGFBP levels and to determine their utility as diagnostic and prognostic biomarkers in ACC.
Preoperative serum samples from 53 patients who underwent surgery for adrenocortical adenomas, 3 patients who underwent initial surgery for ACC, 16 patients who underwent reoperative surgery for ACC, and 5 healthy volunteer controls were analyzed. The serum concentration of IGF1, IGF2, IGFBP1, IGFBP2, and IGFBP3 was determined by enzyme-linked immunosorbent assay.
No difference in the levels of IGF2 (p = .231) and IGFBP2 (p = .511) was observed between patients with ACC, benign adrenocortical tumors, and healthy volunteers. IGF1, IGFBP1, and IGFBP3 levels were not detected. High IGFBP2 levels were associated with better overall survival (OS) (p = .001) and showed a trend toward better abdominal progression-free (APFS) survival (p = .070) in patients with ACC. A subanalysis of patients undergoing reoperation for recurrent ACC showed better OS with high levels of IGFBP2 (p = .003) and a trend toward better APFS (p = .107). There was no significant difference in IGF2 and IGFBP2 levels by extent of disease.
IGF2 and IGFBP2 are not elevated in the serum of patients with ACC compared with patients with benign neoplasms and healthy volunteers. Elevated serum IGFBP2 is associated with better survival in patients with ACC and those undergoing reoperative surgery for recurrent ACC.
C1 [Patel, Dhaval; Howard, Brandi; Boufraqech, Myriem; Gara, Sudheer Kumar; Zhang, Lisa; Nilubol, Naris; Kebebew, Electron] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Ellis, Ryan] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Quezado, Martha M.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Patel, D (reprint author), NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
EM divot999@gmail.com
RI Gara, Sudheer Kumar/E-8084-2016; Boufraqech, Myriem/E-4823-2016;
OI Patel, Dhaval/0000-0002-5744-568X
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX We thank the staff and patients at the NIH for providing the serum
samples used in these studies. We are also very thankful to Tito Fojo,
MD, at the NIH, for referring his patients to the Endocrine Oncology
Branch for surgery. This research was supported by the intramural
research program of the Center for Cancer Research, National Cancer
Institute, National Institutes of Health.
NR 35
TC 3
Z9 4
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD OCT
PY 2014
VL 21
IS 11
BP 3541
EP 3547
DI 10.1245/s10434-014-3768-5
PG 7
WC Oncology; Surgery
SC Oncology; Surgery
GA AP5UT
UT WOS:000342144900031
PM 24833102
ER
PT J
AU Hughes, RC
AF Hughes, Robert C.
TI JUSTIFYING COMMUNITY BENEFIT REQUIREMENTS IN INTERNATIONAL RESEARCH
SO BIOETHICS
LA English
DT Article
DE community; fair benefits; reasonable availability; exploitation;
international research
ID RISKS
AB It is widely agreed that foreign sponsors of research in low- and middle-income countries (LMICs) are morally required to ensure that their research benefits the broader host community. There is no agreement, however, about how much benefit or what type of benefit research sponsors must provide, nor is there agreement about what group of people is entitled to benefit. To settle these questions, it is necessary to examine why research sponsors have an obligation to benefit the broader host community, not only their subjects. Justifying this claim is not straightforward. There are three justifications for an obligation to benefit host communities that each apply to some research, but not to all. Each requires a different amount of benefit, and each requires benefit to be directed toward a different group. If research involves significant net risk to LMIC subjects, research must provide adequate benefit to people in LMICs to avoid an unjustified appeal to subjects' altruism. If research places significant burdens on public resources, research must provide fair compensation to the community whose public resources are burdened. If research is for profit, research sponsors must contribute adequately to the upkeep of public goods from which they benefit in order to avoid the wrong of free-riding, even if their use of these public goods is not burdensome.
C1 [Hughes, Robert C.] Univ Calif Los Angeles, Los Angeles, CA 90095 USA.
[Hughes, Robert C.] NIH, Bioeth Dept, Bethesda, MD USA.
RP Hughes, RC (reprint author), Univ Calif Los Angeles, Sch Law, 385 Charles E Young Dr East,Room 3468, Los Angeles, CA 90095 USA.
EM hughes@law.ucla.edu
FU Intramural Research Program of the NIH, Clinical Center
FX I am grateful to Joseph Millum, Seema Shah, David Wendler, and Alan
Wertheimer for helpful comments on previous drafts of this article. This
work was completed as part of the author's duties as a fellow of the US
National Institutes of Health and was supported by the Intramural
Research Program of the NIH, Clinical Center. The views expressed here
are the author's and do not reflect the policies and positions of the
NIH, the US Public Health Service, or the US Department of Health and
Human Services.
NR 24
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-9702
EI 1467-8519
J9 BIOETHICS
JI Bioethics
PD OCT
PY 2014
VL 28
IS 8
BP 397
EP 404
DI 10.1111/bioe.12002
PG 8
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA AP6RW
UT WOS:000342206300003
PM 23025255
ER
PT J
AU Tannenbaum, J
AF Tannenbaum, Julie
TI THE PROMISE AND PERIL OF THE PHARMACOLOGICAL ENHANCER MODAFINIL
SO BIOETHICS
LA English
DT Article
DE Modafinil; enhancement; quality of life; conditional goods
ID COGNITIVE PERFORMANCE; WAKEFULNESS; DRUGS
AB The neuro-enhancement Modafinil promises to dramatically increase users' waking hours without much sacrifice to clarity of thought and without serious side effects (inducing addiction). For Modafinil to be advantageous, its usage must enable access to goods that themselves improve the quality of one's life. I draw attention to a variety of conditions that must be met for an experience, activity or object to improve the quality of one's life, such as positional, relational, and saturation conditions, as well as it's being good for its own sake. I discuss and describe the contexts in which widespread usage (legal or not) of Modafinil would undermine these conditions being met, and thus users would fail to significantly improve the quality of their lives and would in fact potentially make both themselves and nonusers worse off in important respects thus far overlooked by critics. In the right contexts, where free time is protected and prolonged, Modafinil does have a variety of potential benefits including, most interestingly, a distinctive form of agency possible only in free time. The potential disadvantages and advantages highlighted in this article are relevant not only to public institutions deciding whether to legalize Modafinil's use as an enhancement but also to individuals deciding whether to use it illegally, as well as to the questions of how and whether to alter key features of one's context (e.g. regulating work hours or extending social services) rather than, or in addition, to regulating the use of enhancement drugs such as Modafinil.
C1 [Tannenbaum, Julie] Pomona Coll, Claremont, CA 91711 USA.
[Tannenbaum, Julie] NIH, Dept Bioeth, Bethesda, MD USA.
RP Tannenbaum, J (reprint author), Pomona Coll, 551 N Coll Ave, Claremont, CA 91711 USA.
EM julie.tannenbaum@pomona.edu
FU California State University; Northridge's Faculty Fellowship; Brocher
Foundation
FX Work on this article was made possible by a grant from California State
University, Northridge's Faculty Fellowship and Grant Program and the
Brocher Foundation. I also want to thank Stavroula Glezakos, Michael
Green, Agnieszka Jaworska, Govind Persad, Seema Shah, Yannig Luthra and
audience members at American Society for Bioethics and Humanities and
California State University, Long Beach for helpful feedback on earlier
versions.
NR 35
TC 1
Z9 1
U1 3
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-9702
EI 1467-8519
J9 BIOETHICS
JI Bioethics
PD OCT
PY 2014
VL 28
IS 8
BP 436
EP 445
DI 10.1111/bioe.12008
PG 10
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA AP6RW
UT WOS:000342206300008
PM 23278474
ER
PT J
AU Jacobsen, PB
Le-Rademacher, J
Jim, H
Syrjala, K
Wingard, JR
Logan, B
Wu, J
Majhail, NS
Wood, W
Rizzo, JD
Geller, NL
Kitko, C
Faber, E
Abidi, MH
Slater, S
Horowitz, MM
Lee, SJ
AF Jacobsen, Paul B.
Le-Rademacher, Jennifer
Jim, Heather
Syrjala, Karen
Wingard, John R.
Logan, Brent
Wu, Juan
Majhail, Navneet S.
Wood, William
Rizzo, J. Douglas
Geller, Nancy L.
Kitko, Carrie
Faber, Edward
Abidi, Muneer H.
Slater, Susan
Horowitz, Mary M.
Lee, Stephanie J.
TI Exercise and Stress Management Training Prior to Hematopoietic Cell
Transplantation: Blood and Marrow Transplant Clinical Trials Network
(BMT CTN) 0902
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Autologous hematopoietic cell transplantation; Allogeneic hematopoietic
cell transplantation; Exercise; Stress management; Quality of life
ID QUALITY-OF-LIFE; HEMATOLOGICAL MALIGNANCIES; CANCER SURVIVORS; AEROBIC
EXERCISE; BREAST-CANCER; PHYSICAL PERFORMANCE; RANDOMIZED-TRIAL; ADULT
PATIENTS; PROGRAM; CHEMOTHERAPY
AB Studies show that engaging patients in exercise and/or stress management techniques during hematopoietic cell transplantation (HCT) improves quality of life. The Blood and Marrow Transplant Clinical Trials Network tested the efficacy of training patients to engage in self-directed exercise and stress management during HCT. The study randomized 711 patients at 21 centers to receive 1 of 4 training interventions before HCT: a self-directed exercise program, a self-administered stress management program, both, or neither. Participants completed self-reported assessments at enrollment and up to 180 days after HCT. Randomization was stratified by center and transplant type. There were no differences in the primary endpoints of the Physical Component Summary and Mental Component Summary scales of the Medical Outcomes Study Short Form 36 at day +100 among the groups, based on an intention-to-treat analysis. There also were no differences in overall survival, days of hospitalization through day +100 post-HCT, or in other patient-reported outcomes, including treatment-related distress, sleep quality, pain, and nausea. Patients randomized to training in stress management reported more use of those techniques, but patients randomized to training in exercise did not report more physical activity. Although other studies have reported efficacy of more intensive interventions, brief training in an easy-to-disseminate format for either self-directed exercise or stress management was not effective in our trial. (C) 2014 American Society for Blood and Marrow Transplantation.
C1 [Jacobsen, Paul B.; Jim, Heather] H Lee Moffitt Canc Ctr & Res Inst, Dept Hlth Outcomes & Behav, Tampa, FL USA.
[Le-Rademacher, Jennifer; Logan, Brent] Med Coll Wisconsin, Div Biostat, Milwaukee, WI 53226 USA.
[Syrjala, Karen; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Wingard, John R.] Univ Florida, Coll Med, Dept Med, Div Hematol Oncol, Gainesville, FL USA.
[Wu, Juan] EMMES Corp, Washington, DC USA.
[Majhail, Navneet S.] Cleveland Clin, Blood & Marrow Transplant Program, Cleveland, OH 44106 USA.
[Wood, William] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Rizzo, J. Douglas; Horowitz, Mary M.] Med Coll Wisconsin, Dept Med, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Geller, Nancy L.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Kitko, Carrie] Univ Michigan, Pediat Blood & Marrow Transplant Program, Ann Arbor, MI 48109 USA.
[Faber, Edward] Univ Nebraska Med Ctr, Div Hematol Oncol, Omaha, NE USA.
[Abidi, Muneer H.] Wayne State Univ, Dept Med Oncol, Karmanos Canc Inst, Detroit, MI USA.
[Slater, Susan] Oregon Hlth & Sci Univ, Knight Canc Inst, Ctr Hematol Malignancies, Portland, OR 97201 USA.
RP Lee, SJ (reprint author), Fred Hutchinson Canc Res Ctr, D5-290,POB 19024, Seattle, WA 98109 USA.
EM sjlee@fhcrc.org
OI Abidi, Muneer/0000-0002-9936-6031; Wood, William/0000-0001-7439-2543
FU National Heart, Lung, and Blood Institute; National Cancer Institute
[U10HL069294]
FX This work was supported by the National Heart, Lung, and Blood Institute
and the National Cancer Institute (Grant U10HL069294).
NR 56
TC 12
Z9 12
U1 4
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2014
VL 20
IS 10
BP 1530
EP 1536
DI 10.1016/j.bbmt.2014.05.027
PG 7
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA AP5KC
UT WOS:000342117100010
PM 24910380
ER
PT J
AU Saber, W
Le Rademacher, J
Sekeres, M
Logan, B
Lewis, M
Mendizabal, A
Leifer, E
Appelbaum, FR
Horowitz, MM
Nakamura, R
Cutler, CS
AF Saber, Wael
Le Rademacher, Jennifer
Sekeres, Mikkael
Logan, Brent
Lewis, Moira
Mendizabal, Adam
Leifer, Eric
Appelbaum, Frederick R.
Horowitz, Mary M.
Nakamura, Ryotaro
Cutler, Corey S.
TI Multicenter Biologic Assignment Trial Comparing Reduced-Intensity
Allogeneic Hematopoietic Cell Transplant to Hypomethylating Therapy or
Best Supportive Care in Patients Aged 50 to 75 with Intermediate-2 and
High-Risk Myelodysplastic Syndrome: Blood and Marrow Transplant Clinical
Trials Network #1102 Study Rationale, Design, and Methods
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Biologic assignment; MDS; Transplantation
ID ACUTE MYELOID-LEUKEMIA; PROGNOSTIC SCORING SYSTEM; ACUTE MYELOGENOUS
LEUKEMIA; PHASE-III; MYELOPROLIFERATIVE DISORDERS; DECISION-ANALYSIS;
OLDER PATIENTS; UNITED-STATES; 1ST REMISSION; AZACITIDINE
AB The introduction of reduced-intensity conditioning (RIC) regimens made it possible to offer allogeneic hematopoietic cell transplantation (alloHCT) to older patients with myelodysplastic syndromes (MDS). However, the relative risks and benefits of alloHCT compared with novel nontransplant therapies continue to be the source of considerable uncertainty. We will perform a prospective biologic assignment trial to compare RIC alloHCT with nontransplant therapies based on donor availability. Primary outcome is 3-year overall survival. Secondary outcomes include leukemia-free survival, quality of life, and cost-effectiveness. Four hundred patients will be enrolled over roughly 3 years. Planned subgroup analyses will evaluate key biologic questions, such as the impact of age and response to hypomethylating agents on treatment effects. Findings from this study potentially may set a new standard of care for older MDS patients who are considered candidates for alloHCT. (C) 2014 American Society for Blood and Marrow Transplantation.
C1 [Saber, Wael; Le Rademacher, Jennifer; Logan, Brent; Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Sekeres, Mikkael] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
[Lewis, Moira; Mendizabal, Adam] EMMES Corp, Rockville, MD USA.
[Leifer, Eric] NHLBI, Bethesda, MD 20892 USA.
[Appelbaum, Frederick R.] Univ Washington, Fred Hutchinson Canc Res Ctr, Sch Med, Seattle, WA 98195 USA.
[Nakamura, Ryotaro] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Cutler, Corey S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Saber, W (reprint author), Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, 9200 W Wisconsin Ave,Suite C5500, Milwaukee, WI 53226 USA.
EM wsaber@mcw.edu
FU National Heart, Lung, and Blood Institute [U10 HL069294]; National
Cancer Institute (NCI) of the National Institutes of Health; NCI [U24
CA076518]; NHLBI; National Institute of Allergy and Infectious Diseases;
Health Resources and Services Administration of the US Department of
Health and Human Services [HHSH250201200016 C]; Office of Naval Research
[N00014-12-1-0142, N00014-13-1-0039]; Allos Therapeutics, Inc.; Amgen,
Inc.; Ariad Pharmaceuticals; Be The Match Foundation; Blue Cross and
Blue Shield Association; Celgene; Fresenius-Biotech North America, Inc.;
Gamida Cell Teva Joint Venture Ltd.; Genentech, Inc.; Gentium SpA;
Genzyme Corporation; GlaxoSmithKline; HistoGenetics, Inc.; Kiadis
Pharma; The Leukemia & Lymphoma Society; The Medical College of
Wisconsin; Merck Co., Inc.; Millennium: The Takeda Oncology Co.;
Milliman USA, Inc.; Miltenyi Biotec, Inc.; National Marrow Donor
Program; Onyx Pharmaceuticals; Optum Healthcare Solutions, Inc.; Osiris
Therapeutics, Inc.; Otsuka America Pharmaceutical, Inc.; Remedy
Informatics; Sanofi US; Seattle Genetics; Sigma-Tau Pharmaceuticals;
Soligenix, Inc.; StemCyte, A Global Cord Blood Therapeutics Co.;
Stemsoft Software, Inc.; Swedish Orphan Biovitrum; Tarix
Pharmaceuticals; Terumo BCT; Teva Neuroscience, Inc.; Texas Instruments
Inc.; Well Point, Inc.
FX Financial disclosure: The design and conduct of the BMT CTN 1102 is
supported by Grant/Cooperative Agreement U10 HL069294 from the National
Heart, Lung, and Blood Institute and the National Cancer Institute (NCI)
of the National Institutes of Health. Data collection on alloHCT
recipients will be through the CIBMTR, which is supported by Public
Health Service Grant/Cooperative Agreement U24 CA076518 from the NCI,
the NHLBI, and the National Institute of Allergy and Infectious
Diseases; contract HHSH250201200016 C with the Health Resources and
Services Administration of the US Department of Health and Human
Services; grants N00014-12-1-0142 and N00014-13-1-0039 from the Office
of Naval Research; and grants from Allos Therapeutics, Inc.; Amgen,
Inc.; Anonymous donation to the Medical College of Wisconsin; Ariad
Pharmaceuticals; Be The Match Foundation; Blue Cross and Blue Shield
Association; Celgene;Fresenius-Biotech North America, Inc.; Gamida Cell
Teva Joint Venture Ltd.; Genentech, Inc.; Gentium SpA; Genzyme
Corporation; GlaxoSmithKline; HistoGenetics, Inc.; Kiadis Pharma; The
Leukemia & Lymphoma Society; The Medical College of Wisconsin; Merck &
Co., Inc.; Millennium: The Takeda Oncology Co.; Milliman USA, Inc.;
Miltenyi Biotec, Inc.; National Marrow Donor Program; Onyx
Pharmaceuticals; Optum Healthcare Solutions, Inc.; Osiris Therapeutics,
Inc.; Otsuka America Pharmaceutical, Inc.; Remedy Informatics; Sanofi
US; Seattle Genetics; Sigma-Tau Pharmaceuticals; Soligenix, Inc.;
StemCyte, A Global Cord Blood Therapeutics Co.; Stemsoft Software, Inc.;
Swedish Orphan Biovitrum; Tarix Pharmaceuticals; Terumo BCT; Teva
Neuroscience, Inc.; Texas Instruments Inc.; and Well Point, Inc.. The
views expressed in this article do not reflect the official policy or
position of the National Institutes of Health, the Department of the
Navy, the Department of Defense, or any other agency of the US
Government.
NR 49
TC 6
Z9 6
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2014
VL 20
IS 10
BP 1566
EP 1572
DI 10.1016/j.bbmt.2014.06.010
PG 7
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA AP5KC
UT WOS:000342117100015
PM 24972249
ER
PT J
AU Auer, H
Mobley, JA
Ayers, LW
Bowen, J
Chuaqui, RF
Johnson, LA
Livolsi, VA
Lubensky, IA
McGarvey, D
Monovich, LC
Moskaluk, CA
Rumpel, CA
Sexton, KC
Washington, MK
Wiles, KR
Grizzle, WE
Ramirez, NC
AF Auer, H.
Mobley, J. A.
Ayers, L. W.
Bowen, J.
Chuaqui, R. F.
Johnson, L. A.
Livolsi, V. A.
Lubensky, I. A.
McGarvey, D.
Monovich, L. C.
Moskaluk, C. A.
Rumpel, C. A.
Sexton, K. C.
Washington, M. K.
Wiles, K. R.
Grizzle, W. E.
Ramirez, N. C.
TI The effects of frozen tissue storage conditions on the integrity of RNA
and protein
SO BIOTECHNIC & HISTOCHEMISTRY
LA English
DT Article
DE assays; human tissues; proteomics; RNA; storage; temperatures
ID PROSTATE-CANCER; MASS-SPECTROMETRY; STATISTICAL-MODEL; DATABASE SEARCH;
IDENTIFICATIONS; ADENOCARCINOMA; EXPRESSION; DIAGNOSIS; HEDGEHOG;
SURFACE
AB Unfixed tissue specimens most frequently are stored for long term research uses at either -80 degrees C or in vapor phase liquid nitrogen (VPLN). There is little information concerning the effects such long term storage on tissue RNA or protein available for extraction. Aliquots of 49 specimens were stored for 5-12 years at -80 degrees C or in VPLN. Twelve additional paired specimens were stored for 1 year under identical conditions. RNA was isolated from all tissues and assessed for RNA yield, total RNA integrity and mRNA integrity. Protein stability was analyzed by surface-enhanced or matrix-assisted laser desorption ionization time of flight mass spectrometry (SELDI-TOF-MS, MALDI-TOF-MS) and nano-liquid chromatography electrospray ionization tandem mass spectrometry (nLC-ESI-MS/MS). RNA yield and total RNA integrity showed significantly better results for -80 degrees C storage compared to VPLN storage; the transcripts that were preferentially degraded during VPLN storage were these involved in antigen presentation and processing. No consistent differences were found in the SELDI-TOF-MS, MALDI-TOF-MS or nLC-ESI-MS/MS analyses of specimens stored for more than 8 years at -80 degrees C compared to those stored in VPLN. Long term storage of human research tissues at -80 degrees C provides at least the same quality of RNA and protein as storage in VPLN.
C1 [Auer, H.] Inst Res Biomed, Funct Genom Core, Barcelona, Spain.
[Mobley, J. A.] Univ Alabama Birmingham, Dept Surg, Birmingham, AL 35294 USA.
[Ayers, L. W.; Johnson, L. A.] Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA.
[Bowen, J.; Monovich, L. C.; Ramirez, N. C.] Nationwide Childrens Hosp, Dept Pathol & Lab Med, Columbus, OH USA.
[Chuaqui, R. F.; Lubensky, I. A.] NCI, Canc Diag Program, PIRB, Rockville, MD USA.
[Livolsi, V. A.; McGarvey, D.] Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Moskaluk, C. A.; Rumpel, C. A.] Univ Virginia, Dept Pathol, Charlottesville, VA 22903 USA.
[Sexton, K. C.; Grizzle, W. E.] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA.
[Washington, M. K.; Wiles, K. R.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
RP Grizzle, WE (reprint author), Univ Alabama Birmingham, Dept Pathol, Div Anat Pathol, ZRB 408,1720 Second Ave South, Birmingham, AL 35294 USA.
EM wgrizzle@uab.edu
FU Cooperative Human Tissue Network (CHTN); University of Alabama at
Birmingham Mass Spectrometry/Proteomics (MSP); Tissue Procurement Shared
Facilities of the University of Alabama at Birmingham Comprehensive
Cancer Center
FX Drs. Ramirez and Grizzle are co-senior authors on this manuscript.
Supported by all the individual grants of the Cooperative Human Tissue
Network (CHTN) and the University of Alabama at Birmingham Mass
Spectrometry/Proteomics (MSP) and Tissue Procurement Shared Facilities
of the University of Alabama at Birmingham Comprehensive Cancer Center.
NR 17
TC 3
Z9 4
U1 0
U2 3
PU INFORMA HEALTHCARE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 1052-0295
EI 1473-7760
J9 BIOTECH HISTOCHEM
JI Biotech. Histochem.
PD OCT
PY 2014
VL 89
IS 7
BP 518
EP 528
DI 10.3109/10520295.2014.904927
PG 11
WC Biotechnology & Applied Microbiology; Cell Biology
SC Biotechnology & Applied Microbiology; Cell Biology
GA AP6BL
UT WOS:000342162400006
PM 24799092
ER
PT J
AU Fagundes, CP
Jaremka, LM
Glaser, R
Alfano, CM
Povoski, SP
Lipari, AM
Agnese, DM
Yee, LD
Carson, WE
Farrar, WB
Malarkey, WB
Chen, M
Kiecolt-Glaser, JK
AF Fagundes, Christopher P.
Jaremka, Lisa M.
Glaser, Ronald
Alfano, Catherine M.
Povoski, Stephen P.
Lipari, Adele M.
Agnese, Doreen M.
Yee, Lisa D.
Carson, William E., III
Farrar, William B.
Malarkey, William B.
Chen, Mm
Kiecolt-Glaser, Janice K.
TI Attachment anxiety is related to Epstein-Barr virus latency
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE Psychoneuroimmunology; Close relationships; Attachment theory;
Attachment anxiety; Stress; Herpesvirus; Immune system
ID STEADY-STATE EXPRESSION; SOCIAL SUPPORT; HERPESVIRUS LATENCY; ADULT
ATTACHMENT; FOLLOW-UP; CYTOMEGALOVIRUS-INFECTION;
CARDIOVASCULAR-DISEASE; PHYSICAL HEALTH; GENE-EXPRESSION; IMMUNE-SYSTEM
AB Attachment theory provides a framework for understanding individual differences in chronic interpersonal stress. Attachment anxiety, a type of relationship insecurity characterized by worry about rejection and abandonment, is a chronic interpersonal stressor. Stress impacts cellular immunity, including herpesvirus reactivation. We investigated whether attachment anxiety was related to the expression of a latent herpesvirus, Epstein-Barr virus (EBV), when individuals were being tested for breast or colon cancer and approximately 1 year later. Participants (N = 183) completed a standard attachment questionnaire and provided blood to assess EBV viral capsid antigen (VCA) IgG antibody titers. Individuals with more attachment anxiety had higher EBV VCA IgG antibody titers than those with less attachment anxiety. The strength of the association between attachment anxiety and antibody titers was the same at both assessments. This study is the first to show an association between latent herpesvirus reactivation and attachment anxiety. Because elevated herpesvirus antibody titers reflect poorer cellular immune system control over the latent virus, these data suggest that high attachment anxiety is associated with cellular immune dysregulation. (C) 2014 Published by Elsevier Inc.
C1 [Fagundes, Christopher P.] Univ Texas MD Anderson Canc Ctr, Dept Hlth Dispar, Houston, TX 77030 USA.
[Jaremka, Lisa M.; Glaser, Ronald; Chen, Mm; Kiecolt-Glaser, Janice K.] Ohio State Univ, Coll Med, Inst Behav Med Res, Columbus, OH 43210 USA.
[Alfano, Catherine M.] NCI, Off Canc Survivorship, NIH, Bethesda, MD 20892 USA.
[Povoski, Stephen P.; Agnese, Doreen M.; Yee, Lisa D.; Carson, William E., III; Farrar, William B.] Ohio State Univ, Coll Med, Dept Surg, Columbus, OH 43210 USA.
[Lipari, Adele M.] Ohio State Univ, Coll Med, Dept Radiol, Columbus, OH 43210 USA.
[Carson, William E., III] Ohio State Univ, Coll Med, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Malarkey, William B.] Ohio State Univ, Coll Med, Inst Behav Med Res, Dept Internal Med, Columbus, OH 43210 USA.
[Malarkey, William B.] Ohio State Univ, Coll Med, Inst Behav Med Res, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Malarkey, William B.; Kiecolt-Glaser, Janice K.] Ohio State Univ, Coll Med, Ctr Comprehens Canc, Inst Behav Med Res, Columbus, OH 43210 USA.
[Malarkey, William B.; Kiecolt-Glaser, Janice K.] Ohio State Univ, Coll Med, Dept Psychiat, Columbus, OH 43210 USA.
RP Fagundes, CP (reprint author), UT MD Anderson Canc Ctr, Dept Hlth Dispar Res, Unit 1440,Rm FCT 9-5016,POB 301402, Houston, TX 77230 USA.
EM CPFagundes@mdanderson.org
RI Kiecolt-Glaser, Janice/A-3236-2009; Carson, William/E-2846-2011;
Povoski, Stephen/E-3887-2011; Agnese, Doreen/I-1351-2012
OI Kiecolt-Glaser, Janice/0000-0003-4900-9578;
FU American Cancer Society [PF-11-007-01-CPPB, PF-12-040-01-CPPB]; NIH
[CA131029, CA126857, CA16058]; National Center for Advancing
Translational Sciences [UL1TR000090]
FX Work on this project was supported in part by American Cancer Society
Postdoctoral Fellowship Grants PF-11-007-01-CPPB and PF-12-040-01-CPPB
and NIH grants CA131029, CA126857, and CA16058. Finally, the project was
also supported by Award Number UL1TR000090 from the National Center for
Advancing Translational Sciences. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Center for Advancing Translational
Sciences or the National Institutes of Health.
NR 74
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Z9 6
U1 1
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
EI 1090-2139
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD OCT
PY 2014
VL 41
BP 232
EP 238
DI 10.1016/j.bbi.2014.04.002
PG 7
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA AP2MD
UT WOS:000341905400026
PM 24945717
ER
PT J
AU Mena, E
Lindenberg, ML
Turkbey, BI
Shih, J
Logan, J
Adler, S
Wong, K
Wilson, W
Choyke, PL
Kurdziel, KA
AF Mena, Esther
Lindenberg, Maria Liza
Turkbey, Baris I.
Shih, Joanna
Logan, Jean
Adler, Stephen
Wong, Karen
Wilson, Wyndham
Choyke, Peter L.
Kurdziel, Karen A.
TI A Pilot Study of the Value of F-18-Fluoro-Deoxy-Thymidine PET/CT in
Predicting Viable Lymphoma in Residual F-18-FDG Avid Masses After
Completion of Therapy
SO CLINICAL NUCLEAR MEDICINE
LA English
DT Article
DE PET imaging; F-18-FLT; F-18-FDG; lymphoma; residual mass; PET/CT
ID POSITRON-EMISSION-TOMOGRAPHY; B-CELL LYMPHOMA; THE-ART THERAPEUTICS;
HODGKINS-LYMPHOMA; IMAGING PROLIFERATION; RESPONSE ASSESSMENT;
MALIGNANT-LYMPHOMA; THYMIDINE ANALOGS; LUNG-TUMORS; CANCER
AB Background: Despite its success in diagnosing and staging lymphoma, F-18-FDG PET/CT can be falsely positive in areas of posttreatment inflammation. 3'-F-18-fluoro-3'-deoxy-l-thymidine (F-18-FLT) is a structural analog of the DNA constituent thymidine; its uptake correlates with cellular proliferation. This pilot study evaluates the ability of F-18-FLT PET/CT to distinguish viable lymphoma from posttreatment inflammatory changes in F-18-FDG avid residual masses.
Methods: Twenty-one patients with lymphoma with at least 1 F-18-FDG avid residual mass after therapy underwent F-18-FLT PET/CT imaging. F-18-FDG and F-18-FLT uptake values were compared, including quantitative pharmacokinetic parameters extracted from the F-18-FLT time activity curves generated from dynamic data using graphical and nonlinear compartmental modeling.
Results: The true nature of the residual mass was confirmed by biopsy in 12 patients (8 positive and 4 negative for viable lymphoma and by follow-up CT and/or repeat F-18-FDG PET/CT imaging over 1 year); among the remaining 9 patients, 7 lesions resolved or decreased and 2 showed growth indicative of lymphoma. F-18-FLT PET SUVest.max was significantly higher in tumors than in benign lesions (5.5 [2.2] vs 1.7 [0.6]; P < 0.0001), whereas the difference in F-18-FDG SUVs was not significant (malignant, 7.8 [3.8] vs benign, 5.4 [2.4]; P = 0.11). All of the benign lesions had an F-18-FLT SUVest.max of less than 3.0.
Conclusions: F-18-FLT shows improved specificity over F-18-FDG in distinguishing residual lymphoma from posttreatment inflammation and may be useful in the evaluation of patients with residual F-18-FDG-positive masses after completing therapy.
C1 [Mena, Esther; Lindenberg, Maria Liza; Turkbey, Baris I.; Wong, Karen; Choyke, Peter L.; Kurdziel, Karen A.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Shih, Joanna] NCI, Biometr Res Branch, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
[Logan, Jean] Brookhaven Natl Labs, Upton, NY USA.
[Adler, Stephen] SAIC Contractor NCI, Ft Detrick Frederick, MD USA.
[Wilson, Wyndham] NCI, Lymphoma Therapeut Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Kurdziel, KA (reprint author), NCI, Mol Imaging Program, Bldg 10,Room B3B69F, Bethesda, MD 20892 USA.
EM kurdziek@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 34
TC 4
Z9 5
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0363-9762
EI 1536-0229
J9 CLIN NUCL MED
JI Clin. Nucl. Med.
PD OCT
PY 2014
VL 39
IS 10
BP 874
EP 881
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AP5AK
UT WOS:000342091900013
PM 25144214
ER
PT J
AU Ambrosius, WT
Sink, KM
Foy, CG
Berlowitz, DR
Cheung, AK
Cushman, WC
Fine, LJ
Goff, DC
Johnson, KC
Killeen, AA
Lewis, CE
Oparil, S
Reboussin, DM
Rocco, MV
Snyder, JK
Williamson, JD
Wright, JT
Whelton, PK
AF Ambrosius, Walter T.
Sink, Kaycee M.
Foy, Capri G.
Berlowitz, Dan R.
Cheung, Alfred K.
Cushman, William C.
Fine, Lawrence J.
Goff, David C., Jr.
Johnson, Karen C.
Killeen, Anthony A.
Lewis, Cora E.
Oparil, Suzanne
Reboussin, David M.
Rocco, Michael V.
Snyder, Joni K.
Williamson, Jeff D.
Wright, Jackson T., Jr.
Whelton, Paul K.
CA SPRINT Study Res Grp
TI The design and rationale of a multicenter clinical trial comparing two
strategies for control of systolic blood pressure: The Systolic Blood
Pressure Intervention Trial (SPRINT)
SO CLINICAL TRIALS
LA English
DT Article
DE Randomized clinical trial; major adverse cardiovascular outcomes; blood
pressure targets; hypertension; stroke; cardiovascular; kidney;
cognition; brain structure and function; geriatrics
ID CORONARY-HEART-DISEASE; MILD COGNITIVE IMPAIRMENT; FEMALE SEXUAL
FUNCTION; STROKE RISK-FACTORS; DOUBLE-BLIND; ALZHEIMERS-DISEASE;
ISCHEMIC-STROKE; KIDNEY-DISEASE; GLOBAL BURDEN; RENAL-DISEASE
AB Background: High blood pressure is an important public health concern because it is highly prevalent and a risk factor for adverse health outcomes, including coronary heart disease, stroke, decompensated heart failure, chronic kidney disease, and decline in cognitive function. Observational studies show a progressive increase in risk associated with blood pressure above 115/75 mm Hg. Prior research has shown that reducing elevated systolic blood pressure lowers the risk of subsequent clinical complications from cardiovascular disease. However, the optimal systolic blood pressure to reduce blood pressure-related adverse outcomes is unclear, and the benefit of treating to a level of systolic blood pressure well below 140 mm Hg has not been proven in a large, definitive clinical trial.
Purpose: To describe the design considerations of the Systolic Blood Pressure Intervention Trial (SPRINT) and the baseline characteristics of trial participants.
Methods: The Systolic Blood Pressure Intervention Trial is a multicenter, randomized, controlled trial that compares two strategies for treating systolic blood pressure: one targets the standard target of <140 mm Hg, and the other targets a more intensive target of <120 mm Hg. Enrollment focused on volunteers of age >= 50 years (no upper limit) with an average baseline systolic blood pressure >= 130 mm Hg and evidence of cardiovascular disease, chronic kidney disease, 10-year Framingham cardiovascular disease risk score >= 15%, or age >= 75 years. The Systolic Blood Pressure Intervention Trial recruitment also targeted three pre-specified subgroups: participants with chronic kidney disease (estimated glomerular filtration rate <60 mL/min/1.73 m(2)), participants with a history of cardiovascular disease, and participants 75 years of age or older. The primary outcome is first the occurrence of a myocardial infarction (MI), acute coronary syndrome, stroke, heart failure, or cardiovascular disease death. Secondary outcomes include all-cause mortality, decline in kidney function or development of end-stage renal disease, incident dementia, decline in cognitive function, and small-vessel cerebral ischemic disease.
Results: Between 8 November 2010 and 15 March 2013, Systolic Blood Pressure Intervention Trial recruited and randomized 9361 people at 102 clinics, including 3331 women, 2648 with chronic kidney disease, 1877 with a history of cardiovascular disease, 3962 minorities, and 2636 >= 75 years of age.
Limitations: Although the overall recruitment target was met, the numbers recruited in the high-risk subgroups were lower than planned.
Conclusions: The Systolic Blood Pressure Intervention Trial will provide important information on the risks and benefits of intensive blood pressure treatment targets in a diverse sample of high-risk participants, including those with prior cardiovascular disease, chronic kidney disease, and those aged >= 75 years.
C1 [Ambrosius, Walter T.; Reboussin, David M.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC 27157 USA.
[Sink, Kaycee M.; Williamson, Jeff D.] Wake Forest Sch Med, Dept Internal Med, Sect Gerontol & Geriatr Med, Winston Salem, NC 27157 USA.
[Foy, Capri G.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Social Sci & Hlth Policy, Winston Salem, NC 27157 USA.
[Berlowitz, Dan R.] Bedford Vet Affairs Hosp, Ctr Healthcare Org & Implementat Res, Bedford, MA USA.
[Cheung, Alfred K.] Univ Utah, Dept Internal Med, Salt Lake City, UT 84112 USA.
[Cheung, Alfred K.] Vet Affairs Salt Lake City Healthcare Syst, Salt Lake City, UT USA.
[Cushman, William C.] Vet Affairs Med Ctr, Prevent Med Sect, Memphis, TN USA.
[Fine, Lawrence J.; Snyder, Joni K.] NHLBI, Clin Applicat & Prevent Branch, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Goff, David C., Jr.] Colorado Sch Publ Hlth, Dept Epidemiol, Aurora, CO USA.
[Johnson, Karen C.] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Memphis, TN USA.
[Killeen, Anthony A.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Lewis, Cora E.] Univ Alabama Birmingham, Dept Med, Div Prevent Med, Birmingham, AL 35294 USA.
[Oparil, Suzanne] Univ Alabama Birmingham, Dept Med, Div Cardiovasc Dis, Birmingham, AL 35294 USA.
[Rocco, Michael V.] Wake Forest Sch Med, Dept Internal Med, Nephrol Sect, Winston Salem, NC 27157 USA.
[Wright, Jackson T., Jr.] Case Western Reserve Univ, Dept Med, Div Nephrol & Hypertens, Cleveland, OH 44106 USA.
[Whelton, Paul K.] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA 70118 USA.
RP Ambrosius, WT (reprint author), Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC 27157 USA.
EM wambrosi@wakehealth.edu
RI Bhatt, Udayan/E-2754-2011
FU National Heart, Lung, and Blood Institute, the National Institute of
Diabetes and Digestive and Kidney Diseases, the National Institute on
Aging and the National Institute of Neurological Disorders and Stroke
[HHSN268200900040C]; Wake Forest University Claude D. Pepper Older
Americans Independence Center [P30-AG21332]; NCATS, CWRU [UL1TR000439];
NCRR, OSU [UL1RR025755]; NCRR, U Penn [UL1RR024134]; NCATS
[UL1TR000003]; CTSA, Boston [UL1 RR025771]; CTSA, Stanford [UL1
TR000093]; NCATS, Stanford [UL1 TR000093]; NCRR, Tufts [UL1RR025752];
NCATS, Tufts [UL1 TR000073, UL1 TR001064]; University of Illinois
[UL1TR000050]; UT Southwestern [9U54TR000017-06]; University of Utah
[UL1TR000105-05]; Vanderbilt University [UL1 TR000445]; University of
CA, Davis [UL1 TR000002]; University of Florida [UL1 TR000064];
University of Michigan [UL1TR000433]; NHLBI [Y1-HV-0514-01]; NIDDK
[Y1-HV-0514-01]; NIA [Y1-HV-0514-01]; NINDS [Y1-HV-0514-01]
FX The Systolic Blood Pressure Intervention Trial is funded in whole or in
part with Federal funds from the National Heart, Lung, and Blood
Institute, the National Institute of Diabetes and Digestive and Kidney
Diseases, the National Institute on Aging and the National Institute of
Neurological Disorders and Stroke, under Contract Number:
HHSN268200900040C. In addition, the trial is/was supported by the
following awards: WFU Coordinating Center Publication Acknowledgement:
Wake Forest University Claude D. Pepper Older Americans Independence
Center (P30-AG21332); CWRU Clinical Center Network Publication
Acknowledgements: CWRU: UL1TR000439 (NCATS); OSU: UL1RR025755 (NCRR);
and U Penn: UL1RR024134 (NCRR) and UL1TR000003 (NCATS); Utah Clinical
Center Network Publication Acknowledgments: Boston: UL1 RR025771 (CTSA);
Stanford: UL1 TR000093 (CTSA) and UL1 TR000093 (NCATS); Tufts:
UL1RR025752 (NCRR), UL1 TR000073 and UL1 TR001064 (NCATS); University of
Illinois: UL1TR000050 (CIC); UT Southwestern: 9U54TR000017-06 (CTSA);
University of Utah: UL1TR000105-05 (CTSA); Vanderbilt University: UL1
TR000445 (NCATS); University of CA, Davis: UL1 TR000002 (CTSA);
University of Florida: UL1 TR000064 (NCATS); University of Michigan:
UL1TR000433 (MICHR); VA Clinical Center Network Publication
Acknowledgments: Y1-HV-0514-01 (NHLBI, NIDDK, NIA, and NINDS).
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PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2014
VL 11
IS 5
BP 532
EP 546
DI 10.1177/1740774514537404
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AP1GJ
UT WOS:000341815600004
PM 24902920
ER
PT J
AU Rosas, SR
Schouten, JT
Dixon, D
Varghese, S
Cope, MT
Marci, J
Kagan, JM
AF Rosas, Scott R.
Schouten, Jeffrey T.
Dixon, Dennis
Varghese, Suresh
Cope, Marie T.
Marci, Joe
Kagan, Jonathan M.
TI Evaluating protocol lifecycle time intervals in HIV/AIDS clinical trials
SO CLINICAL TRIALS
LA English
DT Article
DE Survival analysis; HIV/AIDS Clinical Trials; protocol development;
protocol implementation; time-based analyses
ID THERAPY EVALUATION PROGRAM; CANCER; IMPACT; PERFORMANCE
AB Background: Identifying efficacious interventions for the prevention and treatment of human diseases depends on the efficient development and implementation of controlled clinical trials. Essential to reducing the time and burden of completing the clinical trial lifecycle is determining which aspects take the longest, delay other stages, and may lead to better resource utilization without diminishing scientific quality, safety, or the protection of human subjects.
Purpose: In this study, we modeled time-to-event data to explore relationships between clinical trial protocol development and implementation times, as well as to identify potential correlates of prolonged development and implementation.
Methods: We obtained time interval and participant accrual data from 111 interventional clinical trials initiated between 2006 and 2011 by National Institutes of Health's HIV/AIDS Clinical Trials Networks. We determined the time (in days) required to complete defined phases of clinical trial protocol development and implementation. Kaplan-Meier estimates were used to assess the rates at which protocols reached specified terminal events, stratified by study purpose (therapeutic, prevention) and phase group (pilot/phase I, phase II, and phase III/IV). We also examined several potential correlates to prolonged development and implementation intervals.
Results: Even though phase grouping did not determine development or implementation times of either therapeutic or prevention studies, overall we observed wide variation in protocol development times. Moreover, we detected a trend toward phase III/IV therapeutic protocols exhibiting longer developmental (median 2 1/2 years) and implementation times (. 3 years). We also found that protocols exceeding the median number of days for completing the development interval had significantly longer implementation.
Limitations: The use of a relatively small set of protocols may have limited our ability to detect differences across phase groupings. Some timing effects present for a specific study phase may have been masked by combining protocols into phase groupings. Presence of informative censoring, such as withdrawal of some protocols from development if they began showing signs of lost interest among investigators, complicates interpretation of Kaplan-Meier estimates. Because this study constitutes a retrospective examination over an extended period of time, it does not allow for the precise identification of relative factors impacting timing.
Conclusion: Delays not only increase the time and cost to complete clinical trials but they also diminish their usefulness by failing to answer research questions in time. We believe that research analyzing the time spent traversing defined intervals across the clinical trial protocol development and implementation continuum can stimulate business process analyses and re-engineering efforts that could lead to reductions in the time from clinical trial concept to results, thereby accelerating progress in clinical research.
C1 [Rosas, Scott R.; Cope, Marie T.] Concept Syst Inc, Ithaca, NY 14850 USA.
[Schouten, Jeffrey T.] Fred Hutchinson Canc Res Ctr, Off HIV AIDS Network Coordinat, Seattle, WA 98104 USA.
[Varghese, Suresh] Digital Infuz Inc, Gaithersburg, MD USA.
[Marci, Joe] US Govt, Div Acquired Immunodeficiency Syndrome, Natl Inst Allergy & Infect Dis, NIH,Dept Hlth & Human Serv, Bethesda, MD USA.
[Kagan, Jonathan M.] US Govt, Div Clin Res, Natl Inst Allergy & Infect Dis, NIH,Dept Hlth & Human Serv, Bethesda, MD USA.
RP Rosas, SR (reprint author), Concept Syst Inc, Ithaca, NY 14850 USA.
EM srosas@conceptsystems.com
OI Rosas, Scott/0000-0001-5212-1478
FU United States Government Department of Health and Human Services,
National Institutes of Health (NIH), National Institute of Allergy and
Infectious Diseases (NIAID) under "Leadership Group for [U01AI068614,
N01AI-50022]
FX This project has been funded in whole or in part with funds from the
United States Government Department of Health and Human Services,
National Institutes of Health (NIH), National Institute of Allergy and
Infectious Diseases (NIAID), under (a) Grant U01AI068614, "Leadership
Group for a Global HIV Vaccine Clinical Trials Network" (Office of
HIV/AIDS Network Coordination) to the Fred Hutchinson Cancer Research
Center, and (b) a subcontract to Concept Systems, Inc., under Contract
N01AI-50022, "HIV Clinical Research Support Services."
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PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2014
VL 11
IS 5
BP 553
EP 559
DI 10.1177/1740774514540814
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AP1GJ
UT WOS:000341815600006
PM 24980279
ER
PT J
AU Jacobs, SR
Weiner, BJ
Reeve, BB
Weinberger, M
Minasian, LM
Good, MJ
AF Jacobs, Sara R.
Weiner, Bryan J.
Reeve, Bryce B.
Weinberger, Morris
Minasian, Lori M.
Good, Marjorie J.
TI Organizational and physician factors associated with patient enrollment
in cancer clinical trials
SO CLINICAL TRIALS
LA English
DT Article
DE Cancer; clinical trial enrollment; Community Clinical Oncology Program;
National Cancer Institute Oncology Research Program; organizational
design features; Structural Equation Modeling
ID ONCOLOGY PROGRAM; FRAMEWORK; BARRIERS
AB Background: Our purpose was to identify physicians' individual characteristics, attitudes, and organizational contextual factors associated with higher enrollment of patients in cancer clinical trials among physician participants in the National Cancer Institute's Community Clinical Oncology Program (CCOP). We hypothesized that physicians' individual characteristics, such as age, medical specialty, tenure, CCOP organizational factors (i.e. policies and procedures to encourage enrollment), and attitudes toward participating in CCOP would directly determine enrollment. We also hypothesized that physicians' characteristics and CCOP organizational factors would influence physicians' attitudes toward participating in CCOP, which in turn would predict enrollment.
Methods: We evaluated enrollment in National Cancer Institute-sponsored cancer clinical trials in 2011 among 481 physician participants using Structural Equation Modeling. The data sources include CCOP Annual Progress Reports, two surveys of CCOP administrators and physician participants, and the American Medical Association Masterfile.
Results: Physicians with more positive attitudes toward participating in CCOP enrolled more patients than physicians with less positive attitudes. In addition, physicians who practiced in CCOPs that had more supportive policies and practices in place to encourage enrollment (i.e. offered trainings, provided support to screen and enroll patients, gave incentives to enroll patients, instituted minimum accrual expectations) also significantly enrolled more patients. Physician status as CCOP Principal Investigator had a positive direct effect on enrollment, while physician age and non-oncology medical specialty had negative direct effects on enrollment. Neither physicians' characteristics nor CCOP organizational factors indirectly influenced enrollment through an effect on physician attitudes.
Conclusion: We examined whether individual physicians' characteristics and attitudes, as well as CCOP organizational factors, influenced patient enrollment in cancer clinical trials among CCOP physicians. Physician attitudes and CCOP organizational factors had positive direct effects, but not indirect effects, on physician enrollment of patients. Our results could be used to develop physician-directed strategies aimed at increasing involvement in clinical research. For example, administrators may want to ensure physicians have access to support staff to help screen and enroll patients or institute minimum accrual expectations. Our results also highlight the importance of recruiting physicians for volunteer clinical research programs whose attitudes and values align with programmatic goals. Given that physician involvement is a key determinant of patient enrollment in clinical trials, these interventions could expand the overall number of patients involved in cancer research. These strategies will be increasingly important as the CCOP network continues to evolve.
C1 [Jacobs, Sara R.; Weiner, Bryan J.; Reeve, Bryce B.; Weinberger, Morris] Univ N Carolina, Dept Hlth Policy & Management, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Jacobs, Sara R.] RTI Int, Publ Hlth Res Div, Durham, NC 27709 USA.
[Weiner, Bryan J.] Univ N Carolina, Cecil G Sheps Ctr Hlth Serv Res, Chapel Hill, NC USA.
[Reeve, Bryce B.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Weinberger, Morris] Durham Ctr Hlth Serv Res Primary Care, Dept Vet Affairs, Durham, NC USA.
[Minasian, Lori M.; Good, Marjorie J.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Jacobs, SR (reprint author), RTI Int, Publ Hlth Res Div, 3040 E Cornwallis Rd, Durham, NC 27709 USA.
EM sjacobs@rti.org
FU National Cancer Institute at the National Institutes of Health
[R25CA116339, R01CA 124402]; VA HSR&D Senior Research Career Scientist
Award [RCS 91-408]
FX This work was supported by the National Cancer Institute at the National
Institutes of Health (R25CA116339 and R01CA 124402). In addition, Dr
Weinberger was funded by a VA HSR&D Senior Research Career Scientist
Award (RCS 91-408).
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PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2014
VL 11
IS 5
BP 565
EP 575
DI 10.1177/1740774514536000
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AP1GJ
UT WOS:000341815600008
PM 24902923
ER
PT J
AU Crow, SJ
Swanson, SA
le Grange, D
Feig, EH
Merikangas, KR
AF Crow, Scott J.
Swanson, Sonja A.
le Grange, Daniel
Feig, Emily H.
Merikangas, Kathleen R.
TI Suicidal behavior in adolescents and adults with bulimia nervosa
SO COMPREHENSIVE PSYCHIATRY
LA English
DT Article
ID COMORBIDITY-SURVEY-REPLICATION; WEIGHT CONTROL BEHAVIORS; MULTIPLE
PURGING METHODS; EATING-DISORDERS; ANOREXIA-NERVOSA; BIPOLAR DISORDER;
PREVALENCE; SUPPLEMENT; INPATIENTS; SUBTYPES
AB Background: Recent evidence suggests increased risk for mortality in bulimia nervosa (BN). However, little is yet known about suicidal behavior in BN.
Aims: To examine frequency and correlates of suicidal ideation and attempts in adolescents and adults with BN in two population-based samples.
Method: A total of 10,123 adolescents and 2980 adults in two nationally representative surveys of mental disorder were queried regarding eating disorder symptoms and suicidal ideation and attempts.
Results: Less than 1 percent (0.9%) of adolescents and 1.0% of adults met the criteria for BN. Suicidal ideation was more common among adolescents with BN (53.0%) compared with those with binge eating disorder (BED) (34.4%), other psychopathology (21.3%) or no psychopathology (3.8%). Similar trends emerged for the association between BN and self-reported suicidal plans or attempts. Among adults, suicidality was more common in BN than in the no psychopathology group, but not significantly different from the anorexia nervosa (AN), BED, or other psychopathology subgroups.
Conclusion: There is a high risk of suicidal ideation and behavior among those with BN. These results underscore the importance of addressing suicide risk in adolescents and adults with eating disorder symptoms. (C) 2014 Published by Elsevier Inc.
C1 [Crow, Scott J.] Dept Psychiat, Minneapolis, MN USA.
[Swanson, Sonja A.; Feig, Emily H.; Merikangas, Kathleen R.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
[Swanson, Sonja A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[le Grange, Daniel] Univ Chicago, Dept Psychiat & Behav Neurosci, Chicago, IL 60637 USA.
RP Merikangas, KR (reprint author), NIMH, Genet Epidemiol Res Branch, Bethesda, MD 20892 USA.
EM Merikank@mail.nih.gov
NR 29
TC 10
Z9 10
U1 1
U2 21
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0010-440X
EI 1532-8384
J9 COMPR PSYCHIAT
JI Compr. Psychiat.
PD OCT
PY 2014
VL 55
IS 7
BP 1534
EP 1539
DI 10.1016/j.comppsych.2014.05.021
PG 6
WC Psychiatry
SC Psychiatry
GA AP5LX
UT WOS:000342121800009
PM 25070478
ER
PT J
AU Roth, MY
Shih, G
Ilani, N
Wang, C
Page, ST
Bremner, WJ
Swerdloff, RS
Sitruk-Ware, R
Blithe, DL
Amory, JK
AF Roth, Mara Y.
Shih, Grace
Ilani, Niloufar
Wang, Christina
Page, Stephanie T.
Bremner, William J.
Swerdloff, Ronald S.
Sitruk-Ware, Regine
Blithe, Diana L.
Amory, John K.
TI Acceptability of a transdermal gel-based male hormonal contraceptive in
a randomized controlled trail
SO CONTRACEPTION
LA English
DT Article
DE Contraception; Acceptability; Testosterone; Nestorone; Spermatogenesis
ID TESTOSTERONE-INDUCED AZOOSPERMIA; MALE-FERTILITY CONTROL; MULTINATIONAL
SURVEY; NORMAL MEN; EFFICACY; NESTORONE(R); COMBINATION; SUPPRESSION;
PROGESTIN; SPERMATOGENESIS
AB Objective: Fifty percent of pregnancies in the United States are unintended despite numerous contraceptive methods available to women. The only male contraceptive methods, vasectomy and condoms, are used by 10% and 16% of couples, respectively. Prior studies have shown efficacy of male hormonal contraceptives in development, but few have evaluated patient acceptability and potential use if commercially available. The objective of this study is to determine if a transdermal gel-based male hormonal contraceptive regimen, containing testosterone and Nestorone (R) gels, would be acceptable to study participants as a primary contraceptive method.
Study Design: As part of a three-arm, 6-month, double-blind, randomized controlled trial of testosterone and nestorone gels at two academic medical centers, subjects completed a questionnaire to assess the acceptability of the regimen. Of the 99 men randomized, 79 provided data for analysis.
Results: Overall, 56% (44/79) of men were satisfied or extremely satisfied with this gel-based method of contraception, and 51% (40/79) reported that they would recommend this method to others. One third of subjects (26/79) reported that they would use this as their primary method of contraception if it were commercially available today. However, men with concerns about sexually transmitted disease were significantly less satisfied than men without such concerns (p=0.03).
Conclusions: A majority of the men who volunteered to participate in this trial of an experimental male hormonal contraceptive were satisfied with this transdermal male hormonal contraceptive. If commercially available, a combination of topical nesterone and testosterone gels could provide a reversible, effective method of contraception that is appealing to men. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Roth, Mara Y.; Page, Stephanie T.; Bremner, William J.; Amory, John K.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Shih, Grace] Univ Washington, Dept Family Med, Seattle, WA 98195 USA.
[Ilani, Niloufar; Wang, Christina; Swerdloff, Ronald S.] Harbor UCLA, Med Ctr, Torrance, CA USA.
[Ilani, Niloufar; Wang, Christina; Swerdloff, Ronald S.] Los Angeles Biomed Res Inst, Dept Med, Torrance, CA USA.
[Sitruk-Ware, Regine] Populat Council, Ctr Biomed Res, New York, NY 10021 USA.
[Blithe, Diana L.] NICHD, Contracept Discovery & Dev Branch, Bethesda, MD USA.
RP Roth, MY (reprint author), Univ Washington, 1959 NE Pacific St,Box 357138, Seattle, WA 98195 USA.
EM mylang@u.washington.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HHSN 2752004033691, HHSN 2751008060044U]; Population
Council; Eunice Kennedy Skiver National Institute of Child Health and
Human Development [U54 HD-42454]; Cooperative Contraceptive Research
Centers Program [K12 HD053984, K23 HD073164-02]; Endocrinology,
Metabolism and Nutrition training Grant [T32 DK007571]; UCLA Clinical
and Translational Science Institute at Harbor-UCLA Medical Center
[UL1TR000124]; Los Angeles Biomedical Research Institute
FX The study was supported by the Eunice Kennedy Shriver National Institute
of Child Health and Human Development contracts HHSN 2752004033691 and
HHSN 2751008060044U and the Population Council. The University of
Washington site was supported by the Eunice Kennedy Skiver National
Institute of Child Health and Human Development through cooperative
agreement U54 HD-42454 as part of the Cooperative Contraceptive Research
Centers Program and through K12 HD053984 and K23 HD073164-02. The Los
Angeles Center was supported by the Endocrinology, Metabolism and
Nutrition training Grant (T32 DK007571) and the UCLA Clinical and
Translational Science Institute (UL1TR000124) at Harbor-UCLA Medical
Center and Los Angeles Biomedical Research Institute.
NR 27
TC 11
Z9 12
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0010-7824
EI 1879-0518
J9 CONTRACEPTION
JI Contraception
PD OCT
PY 2014
VL 90
IS 4
BP 407
EP 412
DI 10.1016/j.contraception.2014.05.013
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AP5KL
UT WOS:000342118000007
PM 24981149
ER
PT J
AU Kalil, AC
Sun, JF
AF Kalil, Andre C.
Sun, Junfeng
TI Bayesian Methodology for the Design and Interpretation of Clinical
Trials in Critical Care Medicine: A Primer for Clinicians
SO CRITICAL CARE MEDICINE
LA English
DT Review
DE Bayes; clinical trial; critical care
ID SURVIVING SEPSIS CAMPAIGN; RISK SURGICAL-PATIENTS; CONTINUAL
REASSESSMENT METHOD; RANDOMIZED CONTROLLED-TRIALS; MAXIMIZING OXYGEN
DELIVERY; CORONARY-ARTERY-DISEASE; GOAL-DIRECTED THERAPY; SEPTIC SHOCK;
NETWORK METAANALYSIS; PROSPECTIVE COHORT
AB Objectives: To review Bayesian methodology and its utility to clinical decision making and research in the critical care field.
Data Source and Study Selection: Clinical, epidemiological, and biostatistical studies on Bayesian methods in PubMed and Embase from their inception to December 2013.
Data Synthesis: Bayesian methods have been extensively used by a wide range of scientific fields, including astronomy, engineering, chemistry, genetics, physics, geology, paleontology, climatology, cryptography, linguistics, ecology, and computational sciences. The application of medical knowledge in clinical research is analogous to the application of medical knowledge in clinical practice. Bedside physicians have to make most diagnostic and treatment decisions on critically ill patients every day without clear-cut evidence-based medicine (more subjective than objective evidence). Similarly, clinical researchers have to make most decisions about trial design with limited available data. Bayesian methodology allows both subjective and objective aspects of knowledge to be formally measured and transparently incorporated into the design, execution, and interpretation of clinical trials. In addition, various degrees of knowledge and several hypotheses can be tested at the same time in a single clinical trial without the risk of multiplicity. Notably, the Bayesian technology is naturally suited for the interpretation of clinical trial findings for the individualized care of critically ill patients and for the optimization of public health policies.
Conclusions: We propose that the application of the versatile Bayesian methodology in conjunction with the conventional statistical methods is not only ripe for actual use in critical care clinical research but it is also a necessary step to maximize the performance of clinical trials and its translation to the practice of critical care medicine.
C1 [Kalil, Andre C.] Univ Nebraska Med Ctr, Dept Internal Med, Div Infect Dis, Omaha, NE 68198 USA.
[Sun, Junfeng] NIH, Dept Crit Care, Bethesda, MD 20892 USA.
RP Kalil, AC (reprint author), Univ Nebraska Med Ctr, Dept Internal Med, Div Infect Dis, Omaha, NE 68198 USA.
EM akalil@unmc.edu
NR 108
TC 6
Z9 6
U1 0
U2 27
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD OCT
PY 2014
VL 42
IS 10
BP 2267
EP 2277
DI 10.1097/CCM.0000000000000576
PG 11
WC Critical Care Medicine
SC General & Internal Medicine
GA AP7BC
UT WOS:000342231500015
PM 25226118
ER
PT J
AU Jaswal, DS
Leung, JM
Sun, JF
Cui, XZ
Li, Y
Kern, S
Welsh, J
Natanson, C
Eichacker, PQ
AF Jaswal, Dharmvir S.
Leung, Janice M.
Sun, Junfeng
Cui, Xizhong
Li, Yan
Kern, Steven
Welsh, Judith
Natanson, Charles
Eichacker, Peter Q.
TI Tidal Volume and Plateau Pressure Use for Acute Lung Injury From 2000 to
Present: A Systematic Literature Review
SO CRITICAL CARE MEDICINE
LA English
DT Review
DE acute lung injury; acute respiratory distress syndrome; mechanical
ventilation; tidal volume
ID RESPIRATORY-DISTRESS-SYNDROME; RANDOMIZED CONTROLLED-TRIAL;
END-EXPIRATORY PRESSURE; INTENSIVE-CARE-UNIT; FREQUENCY OSCILLATORY
VENTILATION; PROTECTIVE MECHANICAL VENTILATION; ADAPTIVE SUPPORT
VENTILATION; CONTROLLED CLINICAL-TRIAL; CRITICALLY-ILL PATIENTS;
PREDICTED BODY-WEIGHT
AB Objective: Since publication of the Respiratory Management of Acute Lung Injury and Acute Respiratory Distress Syndrome (ARMA) trial in 2000, use of tidal volume (V-T) less than or equal to 6 mL/ kg predicted body weight with corresponding plateau airway pressures (P-Plat) less than or equal to 30 cm H2O has been advocated for acute lung injury. However, compliance with these recommendations is unknown. We therefore investigated V-T (mL/ kg predicted body weight) and P-Plat (cm H2O) practices reported in studies of acute lung injury since ARMA using a systematic literature review (i.e., not a meta-analysis).
Data Sources: PubMed, Scopus, and EMBASE.
Study Selection: Randomized controlled trials and nonrandomized studies enrolling patients with acute lung injury from May 2000 to June 2013 and reporting V-T.
Data Extraction: Whether the study was a randomized controlled trial or a nonrandomized study and performed or not at an Acute Respiratory Distress Syndrome Network center; in randomized controlled trials, the pre- and postrandomization V-T (mL/kg predicted body weight) and P-Plat (cm H2O) and whether a V-T protocol was used postrandomization; in nonrandomized studies, baseline V-T and P-Plat.
Data Synthesis: Twenty-two randomized controlled trials and 71 nonrandomized studies were included. Since 2000 at acute respiratory distress syndrome Network centers , routine V-T was similar comparing randomized controlled trials and nonrandomized studies (p = 0.25) and unchanged over time (p = 0.75) with a mean value of 6.81 (95% CI, 6.45, 7.18). At non-acute respiratory distress syndrome Network centers, routine V-T was also similar when comparing randomized controlled trials and nonrandomized studies (p = 0.71), but decreased (p = 0.001); the most recent estimate for it was 6.77 (6.22, 7.32). All V-T estimates were significantly greater than 6 (p <= 0.02). In randomized controlled trials employing V-T protocols, routine V-T was reduced in both acute respiratory distress syndrome Network (n = 4) and non-acute respiratory distress syndrome Network (n = 11) trials (p <= 0.01 for both), but even postrandomization was greater than 6 (6.47 [6.29, 6.65] and 6.80 [6.42, 7.17], respectively; p <= 0.0001 for both). In 59 studies providing data, routine P-Plat, averaged across acute respiratory distress syndrome Network or non-acute respiratory distress syndrome Network centers, was significantly less than 30 (p <= 0.02).
Conclusions: For clinicians treating acute lung injury since 2000, achieving V-T less than or equal to 6 mL/kg predicted body weight may not have been as attainable or important as P-Plat less than or equal to 30 cm H2O. If so, there may be equipoise to test if V-T less than or equal to 6 mL/kg predicted body weight are necessary to improve acute lung injury outcome.
C1 [Jaswal, Dharmvir S.; Leung, Janice M.; Sun, Junfeng; Cui, Xizhong; Li, Yan; Kern, Steven; Natanson, Charles; Eichacker, Peter Q.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Welsh, Judith] Natl Inst Hlth Lib, NIH, Bethesda, MD USA.
RP Eichacker, PQ (reprint author), NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
EM peichacker@mail.cc.nih.gov
FU Division of Intramural Research of the Clinical Center at the National
Institutes of Health; National Institutes of Health (NIH)
FX Supported, in part, by the Division of Intramural Research of the
Clinical Center at the National Institutes of Health.; Drs. Jaswal, Li,
Natanson, and Eichacker received support for article research from the
National Institutes of Health (NIH) and disclosed government work. Dr.
Leung lectured for Astra-Zeneca (Speaking Honoraria). Dr. Sun disclosed
government work. Dr. Cui received support for article research from the
NIH. Dr. Kern received support for article research from the NIH. Dr.
Welsh has disclosed that she does not have any potential conflicts of
interest.
NR 129
TC 10
Z9 12
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD OCT
PY 2014
VL 42
IS 10
BP 2278
EP 2289
DI 10.1097/CCM.0000000000000504
PG 12
WC Critical Care Medicine
SC General & Internal Medicine
GA AP7BC
UT WOS:000342231500016
PM 25098333
ER
PT J
AU Estrada, A
Ramnitz, MS
Gafni, RI
AF Estrada, Andrea
Ramnitz, Mary Scott
Gafni, Rachel I.
TI Bone densitometry in children and adolescents
SO CURRENT OPINION IN OBSTETRICS & GYNECOLOGY
LA English
DT Review
DE bone density; dual-energy X-ray absorptiometry; fractures; juvenile
osteoporosis; quantitative computed tomography
ID X-RAY ABSORPTIOMETRY; PEDIATRIC OFFICIAL POSITIONS; QUANTITATIVE
COMPUTED-TOMOGRAPHY; VERTEBRAL FRACTURE ASSESSMENT; MONITORING
TIME-INTERVAL; GE LUNAR PRODIGY; MINERAL DENSITY; DISTAL RADIUS;
ANOREXIA-NERVOSA; BODY-COMPOSITION
AB Purpose of review
Abnormalities in bone health are increasingly recognized in the pediatric population. Although the methodologies for assessing bone mineral density were originally developed for adults, great strides have been made in recent years, improving their applicability to children. Understanding these technologies, their interpretation, utility, and limitations is critical when assessing a child or adolescent with a suspected abnormality in bone mineral density.
Recent findings
Improved normative databases that address some of the confounding variables in the growing and maturing child have solidified dual-energy X-ray absorptiometry as the preferred method for the assessment of bone mineral density in children. Consensus statements by expert panels now provide specific guidance to clinicians seeking to evaluate children with fractures or at risk for fractures. Although still primarily a research tool, continued development of quantitative computed tomography applications in pediatrics suggests there may be a complementary role for clinical use in the future.
Summary
In the child or adolescent with a significant fracture history or a potential for fractures because of an underlying cause, clinicians now have guidelines and normative data to better focus their evaluation. Likewise, researchers can use this information to improve clinical trial design and interpretation of results.
C1 [Estrada, Andrea; Ramnitz, Mary Scott] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Estrada, Andrea; Ramnitz, Mary Scott; Gafni, Rachel I.] NIDCR, NIH, Bethesda, MD 20892 USA.
RP Gafni, RI (reprint author), NIDCR, NIH, Bldg 30,Room 228,30 Convent Dr MSC 4320, Bethesda, MD 20892 USA.
EM gafnir@mail.nih.gov
FU NIH/NIDCR/NICHD
FX Research in the authors' laboratory is supported by the Intramural
Research Program of NIH/NIDCR/NICHD. This manuscript reflects the
opinions of the authors and not those of the National Institutes of
Health or the United States Federal Government.
NR 47
TC 1
Z9 2
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-872X
EI 1473-656X
J9 CURR OPIN OBSTET GYN
JI Curr. Opin. Obstet. Gynecol.
PD OCT
PY 2014
VL 26
IS 5
BP 339
EP 346
DI 10.1097/GCO.0000000000000100
PG 8
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AP1NB
UT WOS:000341836200003
PM 25144595
ER
PT J
AU Mena, E
Owenius, R
Turkbey, B
Sherry, R
Bratslavsky, G
Macholl, S
Miller, M
Somer, EJ
Lindenberg, L
Adler, S
Shih, J
Choyke, P
Kurdziel, K
AF Mena, Esther
Owenius, Rikard
Turkbey, Baris
Sherry, Richard
Bratslavsky, Gennady
Macholl, Sven
Miller, Matthew P.
Somer, Ed J.
Lindenberg, Liza
Adler, Stephen
Shih, Joanna
Choyke, Peter
Kurdziel, Karen
TI [F-18]Fluciclatide in the in vivo evaluation of human melanoma and renal
tumors expressing alpha(v)beta(3) and alpha(v)beta(5) integrins
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Alpha(v)beta(3) integrins; Alpha(v)beta(5) integrins;
[F-18]Fluciclatide; PET; Angiogenesis; Melanoma; Renal cell carcinoma
ID POSITRON-EMISSION-TOMOGRAPHY; ANTI-ANGIOGENIC THERAPIES; BREAST-CANCER
PATIENTS; CELL CARCINOMA; RGD PEPTIDES; PHASE-II; F-18-AH111585; PET;
BIODISTRIBUTION; ALPHA-V-BETA-3
AB Purpose [F-18]Fluciclatide is an integrin-targeted PET radiopharmaceutical. alpha(v)beta(3) and alpha(v)beta(5) are upregulated in tumor angiogenesis as well as on some tumor cell surfaces. Our aim was to use [F-18]fluciclatide (formerly known as [F-18]AH111585) for PET imaging of angiogenesis in melanoma and renal tumors and compare with tumor integrin expression.
Methods Eighteen evaluable patients with solid tumors >= 2.0 cm underwent [F-18]fluciclatide PET/CT. All patients underwent surgery and tumor tissue samples were obtained. Immunohistochemical (IHC) staining with mouse monoclonal antibodies and diaminobenzidine (DAB) was applied to snap-frozen tumor specimens, and additional IHC was done on formalin-fixed paraffin-embedded samples. DAB optical density (OD) data from digitized whole-tissue sections were compared with PET SUV80% max, and Patlak influx rate constant (K (i)) data, tumor by tumor.
Results Tumors from all 18 patients demonstrated measurable [F-18]fluciclatide uptake. At the final dynamic time-point (55 min after injection), renal malignancies (in 11 patients) demonstrated an average SUV80% max of 6.4 +/- 2.0 (range 3.8 - 10.0), while the average SUV80% max for metastatic melanoma lesions (in 6 patients) was 3.0 +/- 2.0 (range 0.7 - 6.5). There was a statistically significant difference in [F-18]fluciclatide uptake between chromophobe and nonchromophobe renal cell carcinoma (RCCs, with SUV80% max of 8.2 +/- 1.8 and 5.4 +/- 1.4 (P = 0.020) and tumor-to-normal kidney (T/N) ratios of 1.5 +/- 0.4 and 0.9 +/- 0.2, respectively (P = 0.029). The highest Pearson's correlation coefficients were obtained when comparing Patlak K-i and alpha(v)beta(5) OD when segregating the patient population between melanoma and RCC (r = 0.83 for K-i vs. melanoma and r = 0.91 for K-i vs. RCC). SUV80% max showed a moderate correlation with alpha(v)beta(5) and alpha(v)beta(3) OD.
Conclusion [F-18]Fluciclatide PET imaging was well tolerated and demonstrated favorable characteristics for imaging alpha(v)beta(3) and alpha(v)beta(5) expression in melanoma and RCC. Higher uptake was observed in chromophobe than in nonchromophobe RCC. [F-18]Fluciclatide may be a useful radiotracer to improve knowledge of integrin expression.
C1 [Mena, Esther; Turkbey, Baris; Lindenberg, Liza; Choyke, Peter; Kurdziel, Karen] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Owenius, Rikard] GE Healthcare Life Sci, Uppsala, Sweden.
[Sherry, Richard] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Bratslavsky, Gennady] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Macholl, Sven; Miller, Matthew P.; Somer, Ed J.] GE Healthcare Life Sci, Amersham, England.
[Adler, Stephen] NCI Frederick, CMRP SAIC Frederick Inc, Clin Res Directorate, Frederick, MD 21702 USA.
[Shih, Joanna] NCI, Biometr Res Branch, DCTD, NIH, Rockville, MD USA.
[Lindenberg, Liza] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
RP Lindenberg, L (reprint author), NCI, Mol Imaging Program, 10 Ctr Dr,MSC 1182,Bldg 10,Room B3B69, Bethesda, MD 20892 USA.
EM liza.lindenberg@nih.gov
FU GE Healthcare
FX We thank Adrian Smith, Derek Grant, Brian Higley and Ian Wilson from GE
Healthcare, and Tanya Ledezma and Karen Yamamoto for support. We also
thank Earl Henry for consultancy with the statistical analyses. This
trial was sponsored by GE Healthcare.
NR 36
TC 15
Z9 15
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
EI 1619-7089
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD OCT
PY 2014
VL 41
IS 10
BP 1879
EP 1888
DI 10.1007/s00259-014-2791-x
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AP2PF
UT WOS:000341914900007
PM 24973039
ER
PT J
AU Rondonotti, E
Koulaouzidis, A
Karargyris, A
Giannakou, A
Fini, L
Soncini, M
Pennazio, M
Douglas, S
Shams, A
Lachlan, N
Zahid, A
Mandelli, G
Girelli, C
AF Rondonotti, Emanuele
Koulaouzidis, Anastasios
Karargyris, Alexandros
Giannakou, Andry
Fini, Lucia
Soncini, Marco
Pennazio, Marco
Douglas, Sarah
Shams, Aman
Lachlan, Neil
Zahid, Ali
Mandelli, Giovanna
Girelli, Carlo
TI Utility of 3-dimensional image reconstruction in the diagnosis of
small-bowel masses in capsule endoscopy (with video)
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID OPERATING CHARACTERISTIC CURVES; DOUBLE-BALLOON ENTEROSCOPY;
COST-EFFECTIVENESS; COLOR ENHANCEMENT; LESIONS; SYSTEM; CHROMOENDOSCOPY;
AGREEMENT; SOFTWARE; TUMORS
AB Background: In small-bowel capsule endoscopy (SBCE), differentiating masses (ie, lesions of higher probability for neoplasia) requiring more aggressive intervention from bulges (essentially, false-positive findings) is a challenging task; recently, software that enables 3-dimensional (3D) reconstruction has become available.
Objective: To evaluate whether "coupling" 3D reconstructed video clips with the standard 2-dimensional (s2D) counterparts helps in distinguishing masses from bulges.
Design: Three expert and 3 novice SBCE readers, blind to others and in a random order, reviewed the s2D video clips and subsequently the s2D clips coupled with their 3D reconstruction (2D+3D).
Setting: Multicenter study in 3 community hospitals in Italy and a university hospital in Scotland.
Patients: Thirty-two deidentified 5-minute video clips, containing mucosal bulging (19) or masses (13).
Intervention: 3D reconstruction of s2D SBCE video clips.
Main Outcome Measure: Differentiation of masses from bulges with s2D and 2D+3D video clips, estimated by the area under the receiver operating characteristic curve (AUC); interobserver agreement.
Results: AUC for experts and novices for s2D video clips was .74 and .5, respectively (P = .0053). AUC for experts and novices with 2D+3D was .70 (compared with s2D: P = .245) and .57 (compared s2D: P = .049), respectively. AUC for experts and novices with 2D+3D was similar (P = .1846). The interobserver agreement was good for both experts and novices with the s2D (k = .71 and .54, respectively) and the 2D+3D video clips (k = .58 in both groups).
Limitations: Few, short video clips; fixed angle of 3D reconstruction.
Conclusions: The adjunction of a 3D reconstruction to the s2D video reading platform does not improve the performance of expert SBCE readers, although it significantly increases the performance of novices in distinguishing masses from bulging.
C1 [Rondonotti, Emanuele; Mandelli, Giovanna] Osped Valduce, Gastroenterol Unit, Como, Italy.
[Koulaouzidis, Anastasios; Douglas, Sarah; Shams, Aman; Lachlan, Neil; Zahid, Ali] Royal Infirm Edinburgh NHS Trust, Endoscopy Unit, Ctr Liver & Digest Disorders, Edinburgh, Midlothian, Scotland.
[Karargyris, Alexandros] NIH, Natl Lib Med, Bethesda, MD 20892 USA.
[Giannakou, Andry] Open Univ Cyprus, Fac Econ & Management, Nicosia, Cyprus.
[Fini, Lucia] Busto Arsizio Hosp, Gastroenterol & Digest Endoscopy Unit, Dept Internal Med, Busto Arsizio, Italy.
[Soncini, Marco] San Carlo Borromeo Hosp, Gastroenterol Unit, Dept Internal Med, Milan, Italy.
[Pennazio, Marco] San Giovanni Battista Univ, Teaching Hosp, Dept Med, Div Gastroenterol, Turin, Italy.
RP Rondonotti, E (reprint author), Osped Valduce, Gastroenterol Unit, Como, Italy.
NR 39
TC 11
Z9 11
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
EI 1097-6779
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD OCT
PY 2014
VL 80
IS 4
BP 642
EP 651
DI 10.1016/j.gie.2014.04.057
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AP6CZ
UT WOS:000342166400012
PM 24998466
ER
PT J
AU Drozdovitch, V
Brill, AB
Mettler, FA
Beckner, WM
Goldsmith, SJ
Gross, MD
Hays, MT
Kirchner, PT
Langan, JK
Reba, RC
Smith, GT
Bouville, A
Linet, MS
Melo, DR
Lee, C
Simon, SL
AF Drozdovitch, Vladimir
Brill, Aaron B.
Mettler, Fred A., Jr.
Beckner, William M.
Goldsmith, Stanley J.
Gross, Milton D.
Hays, Marguerite T.
Kirchner, Peter T.
Langan, James K.
Reba, Richard C.
Smith, Gary T.
Bouville, Andre
Linet, Martha S.
Melo, Dunstana R.
Lee, Choonsik
Simon, Steven L.
TI NUCLEAR MEDICINE PRACTICES IN THE 1950s THROUGH THE MID-1970s AND
OCCUPATIONAL RADIATION DOSES TO TECHNOLOGISTS FROM DIAGNOSTIC
RADIOISOTOPE PROCEDURES
SO HEALTH PHYSICS
LA English
DT Article
DE dose assessment; historical profiles; nuclear medicine; radiation;
medical
ID US RADIOLOGIC TECHNOLOGISTS; FOCUS GROUP INTERVIEWS; DOSIMETRY;
PHANTOMS; HEALTH
AB Data on occupational radiation exposure from nuclear medicine procedures for the time period of the 1950s through the 1970s is important for retrospective health risk studies of medical personnel who conducted those activities. However, limited information is available on occupational exposure received by physicians and technologists who performed nuclear medicine procedures during those years. To better understand and characterize historical radiation exposures to technologists, the authors collected information on nuclear medicine practices in the 1950s, 1960s, and 1970s. To collect historical data needed to reconstruct doses to technologists, a focus group interview was held with experts who began using radioisotopes in medicine in the 1950s and the 1960s. Typical protocols and descriptions of clinical practices of diagnostic radioisotope procedures were defined by the focus group and were used to estimate occupational doses received by personnel, per nuclear medicine procedure, conducted in the 1950s to 1960s using radiopharmaceuticals available at that time. The radionuclide activities in the organs of the reference patient were calculated using the biokinetic models described in ICRP Publication 53. Air kerma rates as a function of distance from a reference patient were calculated by Monte Carlo radiation transport calculations using a hybrid computational phantom. Estimates of occupational doses to nuclear medicine technologists per procedure were found to vary from less than 0.01 mu Sv (thyroid scan with 1.85 MBq of administered I-131-iodide) to 0.4 mu Sv (brain scan with 26 MBq of Hg-203-chlormerodin). Occupational doses for the same diagnostic procedures starting in the mid-1960s but using Tc-99m were also estimated. The doses estimated in this study show that the introduction of Tc-99m resulted in an increase in occupational doses per procedure.
C1 [Drozdovitch, Vladimir; Bouville, Andre; Linet, Martha S.; Lee, Choonsik; Simon, Steven L.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Brill, Aaron B.] Vanderbilt Univ, Nashville, TN 37232 USA.
[Mettler, Fred A., Jr.] New Mexico VA Hlth Care Syst, Radiol & Nucl Med Serv, Albuquerque, NM 87108 USA.
[Beckner, William M.] Natl Council Radiat Protect & Measurements, Bethesda, MD USA.
[Goldsmith, Stanley J.] New York Presbyterian Hosp, Weill Cornell Med Ctr, Dept Nucl Med, New York, NY 10065 USA.
[Gross, Milton D.] Dept Vet Affairs Hlth Syst, Nucl Med Serv, Ann Arbor, MI 48105 USA.
[Gross, Milton D.] Dept Vet Affairs Hlth Syst, Radiat Serv, Ann Arbor, MI 48105 USA.
[Hays, Marguerite T.] Dept Vet Affairs Hlth Syst, Palo Alto, CA USA.
[Kirchner, Peter T.] Natl Inst Biomed Imaging & Biomed Engn, NIH, DHHS, Bethesda, MD 20892 USA.
[Langan, James K.] Johns Hopkins Univ, Med Ctr, Baltimore, MD 21287 USA.
[Reba, Richard C.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Smith, Gary T.] Tennessee Valley Healthcare Syst, Dept Nucl Med, Dept Vet Affairs, Nashville, TN 37212 USA.
[Melo, Dunstana R.] Inst Radioprotecao & Dosimetria, BR-22780160 Rio De Janeiro, RJ, Brazil.
RP Drozdovitch, V (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 9609 Med Ctr Dr,Room 7E548,MSC 9778, Bethesda, MD 20892 USA.
EM drozdovv@mail.nih.gov
RI Lee, Choonsik/C-9023-2015
OI Lee, Choonsik/0000-0003-4289-9870
FU Division of Cancer Epidemiology and Genetics, NCI, NIH
FX This study was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, NCI, NIH. The authors are
grateful to Abigail Ukwuani, Kathleen Stine, Jenna Nober, and Denise
Duong (NCI), who aided in the organizing and conducting of the focus
group meeting, and Sara Schonfeld and Rebecca Imran (NCI) for valuable
assistance during the focus group meeting. Special thanks to Michael
Schwerin for valuable help in preparation of the focus group discussion.
NR 37
TC 2
Z9 2
U1 2
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0017-9078
EI 1538-5159
J9 HEALTH PHYS
JI Health Phys.
PD OCT
PY 2014
VL 107
IS 4
BP 300
EP 310
DI 10.1097/HP.0000000000000107
PG 11
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA AP2EC
UT WOS:000341884300003
PM 25162420
ER
PT J
AU Torjesen, AA
Sigurdsson, S
Westenberg, JJM
Gotal, JD
Bell, V
Aspelund, T
Launer, LJ
de Roos, A
Gudnason, V
Harris, TB
Mitchell, GF
AF Torjesen, Alyssa A.
Sigurdsson, Sigurdur
Westenberg, Jos J. M.
Gotal, John D.
Bell, Vanessa
Aspelund, Thor
Launer, Lenore J.
de Roos, Albert
Gudnason, Vilmundur
Harris, Tamara B.
Mitchell, Gary F.
TI Pulse Pressure Relation to Aortic and Left Ventricular Structure in the
Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study
SO HYPERTENSION
LA English
DT Article
DE blood pressure; hypertension; magnetic resonance imaging; pulse wave
analysis; vascular stiffness
ID ISOLATED SYSTOLIC HYPERTENSION; WAVE REFLECTION; INPUT IMPEDANCE;
HEART-FAILURE; NORMAL LIMITS; DIMENSIONS; STIFFNESS; DIAMETER; VELOCITY;
SIZE
AB High pulse pressure, a major cardiovascular risk factor, has been attributed to medial elastic fiber degeneration and aortic dilation, which transfers hemodynamic load to stiffer collagen. However, recent studies suggest higher pulse pressure is instead associated with smaller aortic diameter. Thus, we sought to elucidate relations of pulse pressure with aortic stiffness and aortic and cardiac dimensions. We used magnetic resonance imaging to examine relationships of pulse pressure with lumen area and wall stiffness and thickness in the thoracic aorta and left ventricular structure in 526 participants (72-94 years of age, 295 women) in the community-based Age, Gene/Environment Susceptibility-Reykjavik Study. In a multivariable model that adjusted for age, sex, height, weight, and standard vascular risk factors, central pulse pressure had a negative relationship with aortic lumen area (all effects expressed as mm Hg/SD; B=-8.1 +/- 1.2; P<0.001) and positive relationships with left ventricular end-diastolic volume (B=3.8 +/- 1.0; P<0.001), carotid-femoral pulse wave velocity (B=3.6 +/- 1.0; P<0.001), and aortic wall area (B=3.0 +/- 1.2; P=0.015). Higher pulse pressure in older people is associated with smaller aortic lumen area and greater aortic wall stiffness and thickness and left ventricular volume. Relationships of larger ventricular volume and smaller aortic lumen with higher pulse pressure suggest mismatch in hemodynamic load accommodation by the heart and aorta in older people.
C1 [Torjesen, Alyssa A.; Gotal, John D.; Bell, Vanessa] Cardiovasc Engn Inc, Norwood, MA 02062 USA.
[Sigurdsson, Sigurdur; Aspelund, Thor; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Westenberg, Jos J. M.; de Roos, Albert] Leiden Univ, Med Ctr, Leiden, Netherlands.
[Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
[Launer, Lenore J.; Harris, Tamara B.] NIA, NIH, Bethesda, MD 20892 USA.
RP Mitchell, GF (reprint author), Cardiovasc Engn Inc, 1 Edgewater Dr,Suite 201A, Norwood, MA 02062 USA.
EM GaryFMitchell@mindspring.com
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
FU National Institutes of Health [N01-AG-12100]; National Institute on
Aging Intramural Research Program; Hjartavernd (the Icelandic Heart
Association); Althingi (the Icelandic Parliament); National Institutes
of Health, National Heart, Lung, and Blood Institute [HL094898]
FX This work was supported by National Institutes of Health (contract
N01-AG-12100); the National Institute on Aging Intramural Research
Program; Hjartavernd (the Icelandic Heart Association); the Althingi
(the Icelandic Parliament); and a grant from the National Institutes of
Health, National Heart, Lung, and Blood Institute (grant no. HL094898).
NR 32
TC 13
Z9 13
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
EI 1524-4563
J9 HYPERTENSION
JI Hypertension
PD OCT
PY 2014
VL 64
IS 4
BP 756
EP +
DI 10.1161/HYPERTENSIONAHA.114.03870
PG 17
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP3PB
UT WOS:000341988000013
PM 25024287
ER
PT J
AU Wuthrick, EJ
Curran, WJ
Camphausen, K
Lin, A
Glass, J
Evans, J
Andrews, DW
Axelrod, R
Shi, WY
Werner-Wasik, M
Haacke, EM
Hillman, GG
Dicker, AP
AF Wuthrick, Evan J.
Curran, Walter J., Jr.
Camphausen, Kevin
Lin, Alexander
Glass, Jon
Evans, James
Andrews, David W.
Axelrod, Rita
Shi, Wenyin
Werner-Wasik, Maria
Haacke, E. Mark
Hillman, Gilda G.
Dicker, Adam P.
TI A Pilot Study of Hypofractionated Stereotactic Radiation Therapy and
Sunitinib in Previously Irradiated Patients With Recurrent High-Grade
Glioma
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; IONIZING-RADIATION; TUMOR VASCULATURE;
PROGENITOR CELLS; TYROSINE KINASE; PHASE-II; RADIOTHERAPY; RECRUITMENT;
CANCER; ANGIOGENESIS
AB Purpose/Objective(s): Angiogenic blockade with irradiation may enhance the therapeutic ratio of radiation therapy (RT) through vascular normalization. We sought to determine the safety and toxicity profile of continuous daily-dosed sunitinib when combined with hypofractionated stereotactic RT (fSRT) for recurrent high-grade gliomas (rHGG).
Methods and Materials: Eligible patients had malignant high-grade glioma that recurred or progressed after primary surgery and RT. All patients received a minimum of a 10-day course of fSRT, had World Health Organization performance status of 0 to 1, and a life expectancy of >3 months. During fSRT, sunitinib was administered at 37.5 mg daily. The primary endpoint was acute toxicity, and response was assessed via serial magnetic resonance imaging.
Results: Eleven patients with rHGG were enrolled. The fSRT doses delivered ranged from 30 to 42 Gy in 2.5- to 3.75-Gy fractions. The median follow-up time was 40 months. Common acute toxicities included hematologic disorders, fatigue, hypertension, and elevated liver transaminases. Sunitinib and fSRT were well tolerated. One grade 4 mucositis toxicity occurred, and no grade 4 or 5 hypertensive events or intracerebral hemorrhages occurred. One patient had a nearly complete response, and 4 patients had stable disease for >9 months. Two patients (18%) remain alive and progression-free >3 years from enrollment. The 6-month progression-free survival was 45%.
Conclusions: Sunitinib at a daily dose of 37.5 mg given concurrently with hypofractionated stereotactic reirradiation for rHGG yields acceptable toxicities and an encouraging 6-month progression-free survival. (C) 2014 Elsevier Inc.
C1 [Wuthrick, Evan J.; Curran, Walter J., Jr.; Lin, Alexander; Shi, Wenyin; Werner-Wasik, Maria; Dicker, Adam P.] Thomas Jefferson Univ, Sidney Kimmel Med Coll, Dept Radiat Oncol, Philadelphia, PA 19107 USA.
[Axelrod, Rita] Thomas Jefferson Univ, Sidney Kimmel Med Coll, Dept Med Oncol, Philadelphia, PA 19107 USA.
[Glass, Jon; Evans, James; Andrews, David W.] Thomas Jefferson Univ, Sidney Kimmel Med Coll, Dept Neurol Surg, Philadelphia, PA 19107 USA.
[Camphausen, Kevin] NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA.
[Hillman, Gilda G.] Wayne State Univ, Sch Med, Dept Radiat Oncol, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
[Haacke, E. Mark] Wayne State Univ, Sch Med, Dept Radiol, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
[Haacke, E. Mark] Wayne State Univ, Sch Med, Dept Biomed Engn, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
RP Wuthrick, EJ (reprint author), James Canc Hosp, Dept Radiat Med, 300 West 10th Ave, Columbus, OH 43210 USA.
EM evan.wuthrick@osumc.edu
OI Dicker, Adam/0000-0003-0733-3337; Shi, Wenyin/0000-0002-6336-3912
FU Pfizer Incorporated; Pfizer grant IIR [GA61818Z9]
FX Supported by an unrestricted grant from Pfizer Incorporated to A. P. D.
and Pfizer grant IIR No. GA61818Z9 to G. H.
NR 33
TC 6
Z9 6
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2014
VL 90
IS 2
BP 369
EP 375
DI 10.1016/j.ijrobp.2014.05.034
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA AP3RI
UT WOS:000341994400020
PM 25104067
ER
PT J
AU McEvoy, JW
Nasir, K
DeFilippis, AP
Lima, JAC
Bluemke, DA
Hundley, WG
Barr, RG
Budoff, MJ
Szklo, M
Navas-Acien, A
Polak, JF
Blumenthal, RS
Post, WS
Blaha, MJ
AF McEvoy, J. W.
Nasir, K.
DeFilippis, A. P.
Lima, J. A. C.
Bluemke, D. A.
Hundley, W. G.
Barr, R. G.
Budoff, M. J.
Szklo, M.
Navas-Acien, A.
Polak, J. F.
Blumenthal, R. S.
Post, W. S.
Blaha, M. J.
TI The Relationship of Cigarette Smoking with Inflammation and Subclinical
Vascular Disease: The Multi-Ethnic Study of Atherosclerosis
SO IRISH JOURNAL OF MEDICAL SCIENCE
LA English
DT Meeting Abstract
C1 [McEvoy, J. W.; Nasir, K.; DeFilippis, A. P.; Blumenthal, R. S.; Blaha, M. J.] Johns Hopkins Univ, Ciccarone Ctr Prevent Heart Dis, Baltimore, MD USA.
[Nasir, K.] Baptist Hlth South Florida, Ctr Wellness & Prevent, Miami Beach, FL USA.
[DeFilippis, A. P.] Univ Louisville, Rudd Heart & Lung Ctr, Div Cardiol, Louisville, KY 40292 USA.
[Lima, J. A. C.; Blumenthal, R. S.] Johns Hopkins Univ, Div Cardiol, Baltimore, MD USA.
[Bluemke, D. A.] NIH, Bethesda, MD 20892 USA.
[Hundley, W. G.] Wake Forest Univ Hlth Ctr, Winston Salem, NC USA.
[Barr, R. G.] Columbia Univ Med Ctr, Div Gen Med, Div Pulm Allergy & Crit Care, Dept Med, New York, NY USA.
[Barr, R. G.] Columbia Univ Med Ctr, Dept Epidemiol, New York, NY USA.
[Budoff, M. J.] Univ Calif Los Angeles, Harbor UCLA, Los Angeles Biomed Res Inst, Los Angeles, CA USA.
[Szklo, M.; Navas-Acien, A.; Post, W. S.; Blaha, M. J.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Polak, J. F.] Tufts Univ Sch Med, Tufts Med Ctr, Dept Radiol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0021-1265
EI 1863-4362
J9 IRISH J MED SCI
JI Irish J. Med. Sci.
PD OCT
PY 2014
VL 183
SU 8
MA 52
BP S421
EP S421
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA AP4VQ
UT WOS:000342077600053
ER
PT J
AU Loth, AK
Drabick, DAG
Leibenluft, E
Hulvershorn, LA
AF Loth, Annemarie K.
Drabick, Deborah A. G.
Leibenluft, Ellen
Hulvershorn, Leslie A.
TI Do Childhood Externalizing Disorders Predict Adult Depression? A
Meta-Analysis
SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY
LA English
DT Article
DE Depression; Externalizing disorders; Conduct; Meta-analysis; Childhood
predictors
ID LIFE-COURSE-PERSISTENT; 14-YEAR FOLLOW-UP; DEVELOPMENTAL PSYCHOPATHOLOGY
PERSPECTIVE; OPPOSITIONAL DEFIANT DISORDER; LIMITED ANTISOCIAL PATHWAYS;
EARLY ADOLESCENT BOYS; CONDUCT DISORDER; PSYCHIATRIC-DISORDERS; ANXIETY
DISORDERS; MAJOR DEPRESSION
AB Childhood externalizing disorders have been linked to adult affective disorders, although some studies fail to substantiate this finding. Multiple longitudinal cohort studies identifying childhood psychopathology and their association with adult psychiatric illness have been published. To examine the association between childhood externalizing symptoms or disorders and the development of adult depression across cohorts, a meta-analysis was performed. Potential studies were identified using a PubMed search through November 2013. All published, prospective, longitudinal, community-sampled cohort studies of children (a parts per thousand currency sign 13 years) with externalizing symptoms or disorders (aggression, conduct problems, oppositional defiant disorder, conduct disorder), reassessed in adulthood (a parts per thousand yen 18 years) for depressive disorders (major depressive disorder, depressive disorder NOS, or dysthymic disorder) were included. A random effects model was used to summarize the pooled effect sizes. Ancillary analyses considered covariates that could account for variance among studies. Ten studies representing eight cohorts of children initially assessed at age 13 or younger (N = 17,712) were included in the meta-analysis. Childhood externalizing behavior was associated with adult depressive disorders (OR = 1.52, 95 % confidence interval = 1.27-1.80, p < 0.0001). Utilizing Orwin's Fail-safe N approach, 263 studies with a mean odds ratio of 1.0 would have to be added to the analysis before the cumulative effect would become trivial. Externalizing psychopathology in childhood is associated with the development of unipolar depressive disorders in adulthood.
C1 [Loth, Annemarie K.; Hulvershorn, Leslie A.] Indiana Univ Sch Med, Riley Hosp Children, Dept Psychiat, Indianapolis, IN 46202 USA.
[Drabick, Deborah A. G.] Temple Univ, Dept Psychol, Philadelphia, PA 19122 USA.
[Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, NIH,US Dept HHS, Bethesda, MD 20892 USA.
RP Hulvershorn, LA (reprint author), Indiana Univ Sch Med, Riley Hosp Children, Dept Psychiat, 705 Riley Hosp Dr,Room 4300, Indianapolis, IN 46202 USA.
EM lhulvers@iupui.edu
FU Intramural NIH HHS; NIDA NIH HHS [K12 DA000357]; NIMH NIH HHS
[K01MH0737, K01 MH073717]
NR 48
TC 6
Z9 6
U1 4
U2 24
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0091-0627
EI 1573-2835
J9 J ABNORM CHILD PSYCH
JI J. Abnorm. Child Psychol.
PD OCT
PY 2014
VL 42
IS 7
BP 1103
EP 1113
DI 10.1007/s10802-014-9867-8
PG 11
WC Psychology, Clinical; Psychology, Developmental
SC Psychology
GA AP6GY
UT WOS:000342176800004
PM 24652486
ER
PT J
AU Loth, AK
Drabick, DAG
Leibenluft, E
Hulvershorn, LA
AF Loth, Annemarie K.
Drabick, Deborah A. G.
Leibenluft, Ellen
Hulvershorn, Leslie A.
TI Do Childhood Externalizing Disorders Predict Adult Depression? A
Meta-Analysis (vol 42, pg 1103, 2014)
SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY
LA English
DT Correction
C1 [Loth, Annemarie K.; Hulvershorn, Leslie A.] Indiana Univ Sch Med, Riley Hosp Children, Dept Psychiat, Indianapolis, IN 46202 USA.
[Drabick, Deborah A. G.] Temple Univ, Dept Psychol, Philadelphia, PA 19122 USA.
[Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, NIH,US Dept HHS, Bethesda, MD 20892 USA.
RP Hulvershorn, LA (reprint author), Indiana Univ Sch Med, Riley Hosp Children, Dept Psychiat, 705 Riley Hosp Dr,Room 4300, Indianapolis, IN 46202 USA.
EM lhulvers@iupui.edu
NR 1
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0091-0627
EI 1573-2835
J9 J ABNORM CHILD PSYCH
JI J. Abnorm. Child Psychol.
PD OCT
PY 2014
VL 42
IS 7
BP 1115
EP 1116
DI 10.1007/s10802-014-9876-7
PG 2
WC Psychology, Clinical; Psychology, Developmental
SC Psychology
GA AP6GY
UT WOS:000342176800005
ER
PT J
AU Terracciano, A
Scuteri, A
Strait, J
Sutin, AR
Meirelles, O
Marongiu, M
Orru, M
Pilia, MG
Ferrucci, L
Cucca, F
Schlessinger, D
Lakatta, E
AF Terracciano, Antonio
Scuteri, Angelo
Strait, James
Sutin, Angelina R.
Meirelles, Osorio
Marongiu, Michele
Orru, Marco
Pilia, Maria Grazia
Ferrucci, Luigi
Cucca, Francesco
Schlessinger, David
Lakatta, Edward
TI Are personality traits associated with white-coat and masked
hypertension?
SO JOURNAL OF HYPERTENSION
LA English
DT Article
DE ambulatory blood pressure; antagonism; antihypertensive medications;
anxiety; conscientiousness; masked hypertension; monitoring;
personality; white-coat hypertension
ID AMBULATORY BLOOD-PRESSURE; PSYCHOLOGICAL DISTRESS; 5-FACTOR MODEL;
ANXIETY; RISK; POPULATION; HOME; PREDICTORS; DEPRESSION; LONGEVITY
AB Objectives: Anxiety and other psychological dispositions are thought to be associated with blood pressure. This study tests whether personality traits have long-term associations with masked and white-coat effects.
Methods: A community-based sample of 2838 adults from Sardinia (Italy) completed the Revised NEO Personality Inventory, and 7 years later, blood pressure was assessed in the clinic and with ambulatory monitoring. Logistic regressions were used to test whether anxiety, neuroticism, extraversion, openness, agreeableness, and conscientiousness predicted the white-coat and masked hypertension phenomena. Age, sex, and antihypertensive medication use were tested as moderators.
Results: Significant interactions were found between personality traits and antihypertensive medications in predicting masked and white-coat effects. Only among those taking antihypertensive medication, higher anxiety was associated with a higher risk of pseudo-resistant hypertension due to white-coat effect (odds ratio 1.39, 95% confidence interval 1.01-1.91) and higher conscientiousness was associated with a lower risk of masked uncontrolled hypertension (odds ratio 0.70, 95% confidence interval 0.49-0.99). There were no significant interactions with age or sex.
Conclusions: Among those on antihypertensive medications, anxious individuals were more likely to have pseudo-resistant hypertension due to white-coat effect and less conscientious individuals were at increased risk of masked uncontrolled hypertension. Particularly among anxious and less conscientious individuals, ambulatory monitoring may improve the tailoring of pharmacological treatments.
C1 [Terracciano, Antonio; Sutin, Angelina R.] Florida State Univ, Coll Med, Tallahassee, FL 32306 USA.
[Terracciano, Antonio; Strait, James; Sutin, Angelina R.; Meirelles, Osorio; Ferrucci, Luigi; Schlessinger, David; Lakatta, Edward] NIA, NIH, Baltimore, MD 21224 USA.
[Scuteri, Angelo] Hosp San Raffaele Pisana IRCCS, Rome, Italy.
[Marongiu, Michele; Pilia, Maria Grazia; Cucca, Francesco] CNR, Ist Neurogenet & Neurofarmacol, Cagliari, Italy.
[Orru, Marco] Presidio Osped A Businco, Unita Operat Complessa Cardiol, Cagliari, Italy.
RP Terracciano, A (reprint author), Florida State Univ, Dept Geriatr, Coll Med, 1115 West Call St, Tallahassee, FL 32306 USA.
EM antonio.terracciano@med.fsu.edu
OI Marongiu, Michele/0000-0002-7289-9815
FU Intramural Research Program of the NIH, National Institute on Aging;
NIA-NIH [NO1-AG-1-2109]
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute on Aging. Funding was also provided
through contract NO1-AG-1-2109 from the NIA-NIH.
NR 45
TC 9
Z9 9
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0263-6352
EI 1473-5598
J9 J HYPERTENS
JI J. Hypertens.
PD OCT
PY 2014
VL 32
IS 10
BP 1987
EP 1992
DI 10.1097/HJH.0000000000000289
PG 6
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP1NW
UT WOS:000341838500012
PM 25186529
ER
PT J
AU Shimbo, D
Wang, L
Lamonte, MJ
Allison, M
Wellenius, GA
Bavry, AA
Martin, LW
Aragaki, A
Newman, JD
Swica, Y
Rossouw, JE
Manson, JE
Wassertheil-Smoller, S
AF Shimbo, Daichi
Wang, Lu
Lamonte, Michael J.
Allison, Matthew
Wellenius, Gregory A.
Bavry, Anthony A.
Martin, Lisa W.
Aragaki, Aaron
Newman, Jonathan D.
Swica, Yael
Rossouw, Jacques E.
Manson, JoAnn E.
Wassertheil-Smoller, Sylvia
TI The effect of hormone therapy on mean blood pressure and visit-to-visit
blood pressure variability in postmenopausal women: results from the
Women's Health Initiative randomized controlled trials
SO JOURNAL OF HYPERTENSION
LA English
DT Article
DE blood pressure; hormone therapy; hypertension; postmenopause; women
ID REPLACEMENT THERAPY; AORTIC STIFFNESS; HYPERTENSION; ESTROGEN; DESIGN;
ATHEROSCLEROSIS; STROKE; RISK; DISTENSIBILITY; METAANALYSIS
AB Objectives: Mean and visit-to-visit variability (VVV) of blood pressure (BP) are associated with an increased cardiovascular disease risk. We examined the effect of hormone therapy on mean and VVV of BP in postmenopausal women from the Women's Health Initiative (WHI) randomized controlled trials.
Methods: BP was measured at baseline and annually in the two WHI hormone therapy trials, in which 10 739 and 16 608 postmenopausal women were randomized to conjugated equine estrogens (CEEs, 0.625 mg/day) or placebo, and CEEs and medroxyprogesterone acetate (MPA, 2.5 mg/day) or placebo, respectively.
Results: At the first annual visit (year 1), mean SBP was 1.04 mmHg [95% confidence interval (CI) 0.58, 1.50] and 1.35 mmHg (95% CI 0.99, 1.72) higher in the CEEs and CEEs and MPA arms, respectively, compared with the corresponding placebos. These effects remained stable after year 1. CEEs also increased the VVV of SBP (ratio of VVV in CEEs vs. placebo, 1.03; P < 0.001), whereas CEEs and MPA did not (ratio of VVV in CEEs and MPA vs. placebo, 1.01; P = 0.20). After accounting for study drug adherence, the effects of CEEs and CEEs and MPA on mean SBP increased at year 1, and the differences in the CEEs and CEEs and MPA arms vs. placebos also continued to increase after year 1. Further, both CEEs and CEEs and MPA significantly increased the VVV of SBP (ratio of VVV in CEEs vs. placebo, 1.04; P < 0.001; ratio of VVV in CEEs and MPA vs. placebo, 1.05; P < 0.001).
Conclusion: Among postmenopausal women, CEEs and CEEs and MPA at conventional doses increased mean and VVV of SBP.
C1 [Shimbo, Daichi; Newman, Jonathan D.] Columbia Univ, Med Ctr, Dept Med, New York, NY 10032 USA.
[Wang, Lu; Manson, JoAnn E.] Harvard Univ, Brigham & Womens Hosp, Div Prevent Med, Sch Med, Boston, MA 02115 USA.
[Lamonte, Michael J.] SUNY Buffalo, Dept Social & Prevent Med, Sch Publ Hlth & Hlth Profess, Buffalo, NY 14260 USA.
[Allison, Matthew] Univ Calif San Diego, Dept Family & Prevent Med, San Diego, CA 92103 USA.
[Wellenius, Gregory A.] Brown Univ, Dept Epidemiol, Providence, RI 02912 USA.
[Bavry, Anthony A.] Univ Florida, Dept Med, North Florida South Georgia Vet Hlth Syst, Gainesville, FL USA.
[Martin, Lisa W.] George Washington Univ, Div Cardiol, Washington, DC USA.
[Aragaki, Aaron] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Swica, Yael] Columbia Univ, Med Ctr, Ctr Family & Community Med, New York, NY 10032 USA.
[Rossouw, Jacques E.] NHLBI, Bethesda, MD 20892 USA.
[Wassertheil-Smoller, Sylvia] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
RP Shimbo, D (reprint author), Columbia Univ, Med Ctr, 622 West 168th St,PH 9-310, New York, NY 10032 USA.
EM ds2231@columbia.edu
RI Wellenius, Gregory/A-7105-2012;
OI Wellenius, Gregory/0000-0003-0427-7376; Allison,
Matthew/0000-0003-0777-8272
FU National Heart, Lung, and Blood Institute, National Institutes of
Health, U.S. Department of Health and Human Services [N01WH22110, 24152,
32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122,
42107-26, 42129-32, 44221]
FX The WHI program is funded by the National Heart, Lung, and Blood
Institute, National Institutes of Health, U.S. Department of Health and
Human Services through contracts N01WH22110, 24152, 32100-2, 32105-6,
32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, and
44221. The Supplemental Digital Content http://links.lww.com/HJH/A370
contains additional WHI administrative information.
NR 37
TC 5
Z9 5
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0263-6352
EI 1473-5598
J9 J HYPERTENS
JI J. Hypertens.
PD OCT
PY 2014
VL 32
IS 10
BP 2071
EP 2081
DI 10.1097/HJH.0000000000000287
PG 11
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AP1NW
UT WOS:000341838500023
PM 24991872
ER
PT J
AU Shen, JY
Hilgenbrink, AR
Xia, W
Feng, Y
Dimitrov, DS
Lockwood, MB
Amato, RJ
Low, PS
AF Shen, Jiayin
Hilgenbrink, Andrew R.
Xia, Wei
Feng, Yang
Dimitrov, Dimiter S.
Lockwood, Michael B.
Amato, Robert J.
Low, Philip S.
TI Folate receptor-beta constitutes a marker for human proinflammatory
monocytes
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE inflammatory subset; folate targeting; immunotherapy; inflammation
ID RHEUMATOID-ARTHRITIS; FUNCTIONAL-CHARACTERIZATION; ALTERNATIVE
ACTIVATION; POSITIVE MACROPHAGES; EXPRESSION; CELLS; CCR2;
IMMUNOTHERAPY; HETEROGENEITY; MIGRATION
AB Activated macrophages are commonly involved in the pathogenesis of inflammatory and autoimmune diseases and have been frequently reported to overexpress FR-. Although FR-targeted therapies aimed at eliminating activated macrophages have shown promise for treating inflammatory diseases, little work has been performed to evaluate whether other hematopoietic cells might also express FR-. Analysis of peripheral blood cells with a mAb to human FR- reveals that only monocytes express FR-. Molecular characterization of these circulating monocytes further demonstrates that solely the classic/proinflammatory subset (CD14(high)CD16(-)) expresses the FR and that only CD14(high)CD16(-) FR-(+) monocytes also display the ability to bind folate-linked molecules. Confirmation that this subset of monocytes indeed constitutes the proinflammatory subpopulation was obtained by demonstrating coexpression of FR- with other proinflammatory markers, including CCR2 and HLA-DR. Synovial monocytes from the joints of patients with RA were also shown to express FR-. As inhibition of the chemotaxis of proinflammatory monocytes into sites of inflammation has been explored frequently as a means of controlling autoimmune diseases, demonstration that FR- is uniquely expressed on this proinflammatory subpopulation offers a new strategy to suppress migration of inflammatory monocytes into sites of inflammation.
C1 [Shen, Jiayin; Hilgenbrink, Andrew R.; Xia, Wei; Low, Philip S.] Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.
[Feng, Yang; Dimitrov, Dimiter S.] NCI, Prot Interact Grp, Ctr Canc & Inflammat Program, NIH, Frederick, MD 21701 USA.
[Lockwood, Michael B.] Clarian Arnett Hlth, Dept Rheumatol, Lafayette, IN USA.
[Amato, Robert J.] Univ Texas Hlth Sci Ctr Houston, Sch Med, Dept Internal Med, Mem Hermann Canc Ctr,Div Oncol, Houston, TX 77030 USA.
RP Low, PS (reprint author), Purdue Univ, Dept Chem, 560 Oval Dr, W Lafayette, IN 47907 USA.
EM plow@purdue.edu
FU Endocyte (West Lafayette, IN, USA)
FX This work was supported by a grant from Endocyte (West Lafayette, IN,
USA). We thank Jill Hutchcroft (Cell Separation Facility of Bindley
Bioscience) for her assistance in cell sorting.
NR 40
TC 10
Z9 10
U1 1
U2 13
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
EI 1938-3673
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT
PY 2014
VL 96
IS 4
BP 563
EP 570
DI 10.1189/jlb.2AB0713-372R
PG 8
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA AP6YD
UT WOS:000342223600007
PM 25015955
ER
PT J
AU Wang, M
You, Q
Lor, K
Chen, FF
Gao, B
Ju, C
AF Wang, Meng
You, Qiang
Lor, Kenton
Chen, Fangfang
Gao, Bin
Ju, Cynthia
TI Chronic alcohol ingestion modulates hepatic macrophage populations and
functions in mice
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE M1 macrophages; M2 macrophages; Kupffer cells
ID MYELOID SUPPRESSOR-CELLS; LIVER-INJURY; KUPFFER CELLS; INFILTRATING
MACROPHAGES; MONOCYTES; INFLAMMATION; DISEASE; ACTIVATION;
DIFFERENTIATION; PATHWAY
AB Hepatic Macs, consisting of resident KCs and infiltrating monocytes/IMs, are thought to play an important role in the pathogenesis of ALD. Previous work has focused on KCs or studied hepatic Macs as one cell population. The aim of the current study is to distinguish IMs from KCs and to compare their phenotypes and functions. We show here that a 4-week ethanol feeding of C57BL/6J mice causes recruitment of IMs into the liver. KCs and IMs can be distinguished based on their differential expression of F4/80 and CD11b. IMs can be divided further into two subsets based on their differential expression of Ly6C. KCs and two subsets of IMs were separately purified by FACS. The phagocytosis abilities and the expression profiles of genes related to various functions were compared among different populations of hepatic Macs. Ly6C(low) IMs exhibit an anti-inflammatory and tissue-protective phenotype; in contrast, Ly6C(hi) IMs exhibit a proinflammatory, tissue-damaging phenotype. The ratio of Ly6C(hi)/Ly6C(low) increases when mice chronically fed ethanol were binged, which significantly enhanced liver injury. Moreover, upon phagocytosis of apoptotic hepatocytes, Ly6C(hi) IMs switch to Ly6C(low) IMs. Taken together, chronic ethanol feeding induces the recruitment of two subsets of hepatic IMs, which play different or even opposite roles in regulating liver inflammation and repair. These findings may not only increase our understanding of the complex functions of Macs in the pathogenesis of ALD but also help us to identify novel therapeutic targets for the treatment of this disease.
C1 [Wang, Meng; Lor, Kenton; Ju, Cynthia] Univ Colorado, Skaggs Sch Pharm & Pharmaceut Sci, Aurora, CO 80045 USA.
[Ju, Cynthia] Univ Colorado, Aurora, CO 80045 USA.
[You, Qiang] Nanjing Med Univ, Dept Biotherapy, Affiliated Hosp 2, Nanjing, Jiangsu, Peoples R China.
[Chen, Fangfang] Jilin Univ, Dept Gastrointestinal Surg, China Japan Union Hosp, Changchun, Peoples R China.
[Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD USA.
RP Ju, C (reprint author), Univ Colorado, Skaggs Sch Pharm, Anschutz Med Campus,C238,12850 East Montview Blvd, Aurora, CO 80045 USA.
EM cynthia.ju@ucdenver.edu
FU [U01AA021723]
FX This work was supported by U01AA021723 (to C.J. and B. G.). We thank Dr.
Karen Helm for assistance with FACSort.
NR 47
TC 18
Z9 19
U1 0
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
EI 1938-3673
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT
PY 2014
VL 96
IS 4
BP 657
EP 665
DI 10.1189/jlb.6A0114-004RR
PG 9
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA AP6YD
UT WOS:000342223600016
PM 25030420
ER
PT J
AU Ward, R
Zucca, FA
Duyn, JH
Crichton, RR
Zecca, L
AF Ward, Roberta
Zucca, Fabio A.
Duyn, Jeff H.
Crichton, Robert R.
Zecca, Luigi
TI The role of iron in brain ageing and neurodegenerative disorders
SO LANCET NEUROLOGY
LA English
DT Review
ID RESTLESS LEGS SYNDROME; AMYLOID-PRECURSOR-PROTEIN; HEME OXYGENASE-1
EXPRESSION; MILD COGNITIVE IMPAIRMENT; CENTRAL-NERVOUS-SYSTEM; OXIDATIVE
DNA-DAMAGE; X-RAY-MICROANALYSIS; PARKINSONS-DISEASE; SUBSTANTIA-NIGRA;
ALZHEIMERS-DISEASE
AB In the CNS, iron in several proteins is involved in many important processes such as oxygen transportation, oxidative phosphorylation, myelin production, and the synthesis and metabolism of neurotransmitters. Abnormal iron homoeostasis can induce cellular damage through hydroxyl radical production, which can cause the oxidation and modification of lipids, proteins, carbohydrates, and DNA. During ageing, different iron complexes accumulate in brain regions associated with motor and cognitive impairment. In various neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, changes in iron homoeostasis result in altered cellular iron distribution and accumulation. MRI can often identify these changes, thus providing a potential diagnostic biomarker of neurodegenerative diseases. An important avenue to reduce iron accumulation is the use of iron chelators that are able to cross the blood-brain bather, penetrate cells, and reduce excessive iron accumulation, thereby affording neuroprotection.
C1 [Ward, Roberta] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Ctr Neuroinflammat & Neurodegenerat, Dept Med, London, England.
[Ward, Roberta; Crichton, Robert R.] Catholic Univ Louvain, Fac Sci, Louvain La Neuve, Belgium.
[Zucca, Fabio A.; Zecca, Luigi] Natl Res Council Italy, Inst Biomed Technol, Milan, Italy.
[Duyn, Jeff H.] NINDS, Adv MRI Sect, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
RP Zecca, L (reprint author), Natl Res Council Italy, Inst Biomed Technol, I-20090 Segrate, MI, Italy.
EM luigi.zecca@itb.cnr.it
RI Zucca, Fabio/O-4368-2015
OI Zucca, Fabio/0000-0003-1230-1129
FU Italian Ministry of Education, University; Research-National Research
Programme (PNR)-CNR Flagship "InterOmics" Project [PB . P05]; PNR-CNR
Ageing program; MIUR-Medical Research in Italy Project [RBNE08ZZN7]
FX FAZ and LZ were supported by Italian Ministry of Education, University,
and Research-National Research Programme (PNR)-CNR Flagship "InterOmics"
Project (PB . P05), by PNR-CNR Ageing program 2012-14, and by
MIUR-Medical Research in Italy Project (RBNE08ZZN7). We thank Francesca
A Cupaioli for her assistance in bibliographic research.
NR 223
TC 98
Z9 104
U1 15
U2 92
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1474-4422
EI 1474-4465
J9 LANCET NEUROL
JI Lancet Neurol.
PD OCT
PY 2014
VL 13
IS 10
BP 1045
EP 1060
PG 16
WC Clinical Neurology
SC Neurosciences & Neurology
GA AP3EZ
UT WOS:000341959700019
PM 25231526
ER
PT J
AU Hughey, CC
Wasserman, DH
Lee-Young, RS
Lantier, L
AF Hughey, Curtis C.
Wasserman, David H.
Lee-Young, Robert S.
Lantier, Louise
TI Approach to assessing determinants of glucose homeostasis in the
conscious mouse
SO MAMMALIAN GENOME
LA English
DT Article
ID HIGH-FAT DIET; MUSCLE INSULIN-RESISTANCE; MELANOCORTIN-4 RECEPTOR GENE;
DOSE-RESPONSE CURVES; OB-OB MICE; METABOLIC SYNDROME; IN-VIVO; KNOCKOUT
MICE; C57BL/6J MICE; FRAMESHIFT MUTATION
AB Obesity and type 2 diabetes lessen the quality of life of those afflicted and place considerable burden on the healthcare system. Furthermore, the detrimental impact of these pathologies is expected to persist or even worsen. Diabetes is characterized by impaired insulin action and glucose homeostasis. This has led to a rapid increase in the number of mouse models of metabolic disease being used in the basic sciences to assist in facilitating a greater understanding of the metabolic dysregulation associated with obesity and diabetes, the identification of therapeutic targets, and the discovery of effective treatments. This review briefly describes the most frequently utilized models of metabolic disease. A presentation of standard methods and technologies on the horizon for assessing metabolic phenotypes in mice, with particular emphasis on glucose handling and energy balance, is provided. The article also addresses issues related to study design, selection and execution of metabolic tests of glucose metabolism, the presentation of data, and interpretation of results.
C1 [Hughey, Curtis C.; Wasserman, David H.; Lantier, Louise] Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
[Wasserman, David H.; Lantier, Louise] Vanderbilt Univ, Sch Med, Mouse Metab Phenotyping Ctr, Nashville, TN 37232 USA.
[Lee-Young, Robert S.] Baker IDI Heart & Diabet Inst, Div Metab & Obes, Cellular & Mol Metab Lab, Melbourne, Vic 3004, Australia.
RP Hughey, CC (reprint author), Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, 823 Light Hall,2215 Garland Ave, Nashville, TN 37232 USA.
EM curtis.hughey.1@vanderbilt.edu
FU Canadian Diabetes Association; National Institutes of Health [DK059637,
DK050277, DK054902]
FX This work was supported by the Canadian Diabetes Association (CCH), and
National Institutes of Health Grants DK059637 (Mouse Metabolic
Phenotyping Center; DHW), DK050277 (DHW), and DK054902 (DHW).
NR 140
TC 3
Z9 4
U1 3
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-8990
EI 1432-1777
J9 MAMM GENOME
JI Mamm. Genome
PD OCT
PY 2014
VL 25
IS 9-10
SI SI
BP 522
EP 538
DI 10.1007/s00335-014-9533-z
PG 17
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA AP6FT
UT WOS:000342173700015
PM 25074441
ER
PT J
AU Liu, CH
Sastre, A
Conroy, R
Seto, B
Pettigrew, RI
AF Liu, Christina H.
Sastre, Antonio
Conroy, Richard
Seto, Belinda
Pettigrew, Roderic I.
TI NIH Workshop on Clinical Translation of Molecular Imaging Probes and
Technology-Meeting Report
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Article
DE Molecular Imaging probes; Human translation; Disease targets; Regulatory
science
ID POSITRON-EMISSION-TOMOGRAPHY; MRI CONTRAST AGENT; MAGNETIC-RESONANCE
ANGIOGRAPHY; RESEARCH-AND-DEVELOPMENT; KINASE GENE-EXPRESSION;
COMPUTED-TOMOGRAPHY; PROSTATE-CANCER; MYOCARDIAL-INFARCTION;
ALZHEIMERS-DISEASE; ATHEROSCLEROTIC PLAQUES
AB A workshop on "Clinical Translation of Molecular Imaging Probes and Technology" was held August 2, 2013 in Bethesda, Maryland, organized and supported by the National Institute of Biomedical Imaging and Bioengineering (NIBIB). This workshop brought together researchers, clinicians, representatives from pharmaceutical companies, molecular probe developers, and regulatory science experts. Attendees met to talk over current challenges in the discovery, validation, and translation of molecular imaging (MI) probes for key clinical applications. Participants also discussed potential strategies to address these challenges. The workshop consisted of 4 sessions, with 14 presentations and 2 panel discussions. Topics of discussion included (1) challenges and opportunities for clinical research and patient care, (2) advances in molecular probe design, (3) current approaches used by industry and pharmaceutical companies, and (4) clinical translation of MI probes. In the presentations and discussions, there were general agreement that while the barriers for validation and translation of MI probes remain high, there are pressing clinical needs and development opportunities for targets in cardiovascular, cancer, endocrine, neurological, and inflammatory diseases. The strengths of different imaging modalities, and the synergy of multimodality imaging, were highlighted. Participants also underscored the continuing need for close interactions and collaborations between academic and industrial partners, and federal agencies in the imaging probe development process.
C1 [Liu, Christina H.; Sastre, Antonio; Conroy, Richard; Seto, Belinda; Pettigrew, Roderic I.] Natl Inst Biomed Imaging & Bioengn, Bethesda, MD 20892 USA.
RP Liu, CH (reprint author), Natl Inst Biomed Imaging & Bioengn, 6707 Democracy Blvd,Suite 200, Bethesda, MD 20892 USA.
EM Christina.liu@nih.gov
RI Conroy, Richard/D-1979-2009;
OI Conroy, Richard/0000-0002-8896-6090; Liu, Christina/0000-0002-5723-177X
NR 95
TC 1
Z9 1
U1 0
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1536-1632
EI 1860-2002
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD OCT
PY 2014
VL 16
IS 5
BP 595
EP 604
DI 10.1007/s11307-014-0746-z
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AP5RG
UT WOS:000342135800001
PM 24833042
ER
PT J
AU Guitart, X
Navarro, G
Moreno, E
Yano, H
Cai, NS
Sanchez-Soto, M
Kumar-Barodia, S
Naidu, YT
Mallol, J
Cortes, A
Lluis, C
Canela, EI
Casado, V
McCormick, PJ
Ferre, S
AF Guitart, Xavier
Navarro, Gemma
Moreno, Estefania
Yano, Hideaki
Cai, Ning-Sheng
Sanchez-Soto, Marta
Kumar-Barodia, Sandeep
Naidu, Yamini T.
Mallol, Josefa
Cortes, Antoni
Lluis, Carme
Canela, Enric I.
Casado, Vicent
McCormick, Peter J.
Ferre, Sergi
TI Functional Selectivity of Allosteric Interactions within G
Protein-Coupled Receptor Oligomers: The Dopamine D-1-D-3 Receptor
Heterotetramer
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID ADENYLYL-CYCLASE; HETEROMERIZATION; INTERFACE; RELEVANCE; TARGETS;
BRAIN; FORMS; D-1
AB The dopamine D-1 receptor-D-3 receptor (D1R-D3R) heteromer is being considered as a potential therapeutic target for neuropsychiatric disorders. Previous studies suggested that this heteromer could be involved in the ability of D3R agonists to potentiate locomotor activation induced by D1R agonists. It has also been postulated that its overexpression plays a role in L-dopa-induced dyskinesia and in drug addiction. However, little is known about its biochemical properties. By combining bioluminescence resonance energy transfer, bimolecular complementation techniques, and cell-signaling experiments in transfected cells, evidence was obtained for a tetrameric stoichiometry of the D1R-D3R heteromer, constituted by two interacting D1R and D3R homodimers coupled to G(s) and G(i) proteins, respectively. Coactivation of both receptors led to the canonical negative interaction at the level of adenylyl cyclase signaling, to a strong recruitment of beta-arrestin-1, and to a positive cross talk of D1R and D3R agonists at the level of mitogen-activated protein kinase (MAPK) signaling. Furthermore, D1R or D3R antagonists counteracted beta-arrestin-1 recruitment and MAPK activation induced by D3R and D1R agonists, respectively (cross-antagonism). Positive cross talk and cross-antagonism at the MAPK level were counteracted by specific synthetic peptides with amino acid sequences corresponding to D1R transmembrane (TM) domains TM5 and TM6, which also selectively modified the quaternary structure of the D1R-D3R heteromer, as demonstrated by complementation of hemiproteins of yellow fluorescence protein fused to D1R and D3R. These results demonstrate functional selectivity of allosteric modulations within the D1R-D3R heteromer, which can be involved with the reported behavioral synergism of D1R and D3R agonists.
C1 [Guitart, Xavier; Yano, Hideaki; Cai, Ning-Sheng; Sanchez-Soto, Marta; Kumar-Barodia, Sandeep; Naidu, Yamini T.; Ferre, Sergi] NIDA, Intramural Res Program, NIH, Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
[Navarro, Gemma; Moreno, Estefania; Mallol, Josefa; Cortes, Antoni; Lluis, Carme; Canela, Enric I.; Casado, Vicent; McCormick, Peter J.] Univ Barcelona, Fac Biol, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Barcelona, Spain.
[Navarro, Gemma; Moreno, Estefania; Mallol, Josefa; Cortes, Antoni; Lluis, Carme; Canela, Enric I.; Casado, Vicent; McCormick, Peter J.] Univ Barcelona, Fac Biol, Dept Biochem & Mol Biol, Barcelona, Spain.
[McCormick, Peter J.] Univ E Anglia, Sch Pharm, Norwich NR4 7TJ, Norfolk, England.
RP Ferre, S (reprint author), NIDA, Integrat Neurobiol Sect, Intramural Res Program, NIH,Dept Hlth & Human Serv, Triad Technol Bldg,333 Cassell Dr, Baltimore, MD 21224 USA.
EM sferre@intra.nida.nih.gov
RI Casado, Vicent/K-1660-2014; Canela, Enric I./M-8726-2013; McCormick,
Peter/E-7387-2012
OI Canela, Enric I./0000-0003-4992-7440; McCormick,
Peter/0000-0002-2225-5181
FU National Institutes of Health National Institute on Drug Addiction;
Michael J. Fox Foundation for Parkinson's Research [RRIA]; Spanish
Ministerio de Ciencia y Tecnologia [SAF2011-23813, SAF2009-07276];
Government of Catalonia [2009-SGR-12]; Centro de Investigacion Biom
medica en Red Sobre Enfermedades Neurodegenerativas [CB06/05/0064];
Ramon y Cajal fellowship
FX This work was supported by intramural funds of the National Institutes
of Health National Institute on Drug Addiction; grants from Michael J.
Fox Foundation for Parkinson's Research [RRIA 2010], Spanish Ministerio
de Ciencia y Tecnologia [SAF2011-23813 and SAF2009-07276], and
Government of Catalonia [2009-SGR-12]; and a grant [CB06/05/0064] from
Centro de Investigacion Biom medica en Red Sobre Enfermedades
Neurodegenerativas. P.J.M. was supported through a Ramon y Cajal
fellowship.
NR 30
TC 27
Z9 27
U1 0
U2 9
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
EI 1521-0111
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD OCT
PY 2014
VL 86
IS 4
BP 417
EP 429
DI 10.1124/mol.114.093096
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AP4QN
UT WOS:000342063100007
PM 25097189
ER
PT J
AU Aguayo, LG
Castro, P
Mariqueo, T
Munoz, B
Xiong, W
Zhang, L
Lovinger, DM
Homanics, GE
AF Aguayo, Luis G.
Castro, Patricio
Mariqueo, Trinidad
Munoz, Braulio
Xiong, Wei
Zhang, Li
Lovinger, David M.
Homanics, Gregg E.
TI Altered Sedative Effects of Ethanol in Mice with alpha 1 Glycine
Receptor Subunits that are Insensitive to G beta gamma Modulation
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
ID ACTIVATED CL-CURRENT; ION-CHANNEL; NEURONS; MUTATIONS; CELLS;
POTENTIATION; INHIBITION; KNOCKOUT; GABA(A); ALCOHOL
AB Alcohol abuse and alcoholism are major health problems and one of the leading preventable causes of death. Before achieving better treatments for alcoholism, it is necessary to understand the critical actions of alcohol on membrane proteins that regulate fundamental functions in the central nervous system. After generating a genetically modified knock-in (KI) mouse having a glycine receptor (GlyR) with phenotypical silent mutations at KK385/386AA, we studied its cellular and in vivo ethanol sensitivity. Analyses with western blotting and immunocytochemistry indicated that the expression of alpha 1 GlyRs in nervous tissues and spinal cord neurons (SCNs) were similar between WT and KI mice. The analysis of synaptic currents recorded from KI mice showed that the glycinergic synaptic transmission had normal properties, but the sensitivity to ethanol was significantly reduced. Furthermore, the glycine-evoked current in SCNs from KI was resistant to ethanol and G-protein activation by GTP-gamma-S. In behavioral studies, KI mice did not display the foot-clasping behavior upon lifting by the tail and lacked an enhanced startle reflex response that are characteristic of other glycine KI mouse lines with markedly impaired glycine receptor function. The most notable characteristic of the KI mice was their significant lower sensitivity to ethanol (similar to 40%), expressed by shorter times in loss of righting reflex (LORR) in response to a sedative dose of ethanol (3.5 g/Kg). These data provide the first evidence to link a molecular site in the GlyR with the sedative effects produced by intoxicating doses of ethanol.
C1 [Aguayo, Luis G.; Castro, Patricio; Mariqueo, Trinidad; Munoz, Braulio] Univ Concepcion, Dept Physiol, Neurophysiol Lab, Concepcion 4030001, Chile.
[Xiong, Wei; Zhang, Li; Lovinger, David M.] NIAAA, Lab Integrat Neurosci, NIH, Bethesda, MD USA.
[Homanics, Gregg E.] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA USA.
[Homanics, Gregg E.] Univ Pittsburgh, Dept Pharmacol, Pittsburgh, PA 15261 USA.
[Homanics, Gregg E.] Univ Pittsburgh, Dept Biol Chem, Pittsburgh, PA USA.
RP Aguayo, LG (reprint author), Univ Concepcion, Dept Physiol, POB 160C, Concepcion 4030001, Chile.
EM laguayo@udec.cl; HomanicsGE@anes.upmc.edu
FU NIH [AA17875]; Division of Intramural Clinical and Biological Research
of NIAAA
FX We thank Carolyn Ferguson and Lauren J Aguayo for expert technical
assistance. This work was supported by an NIH grant AA17875 awarded to
LGA and GEH. The work of WX, LZ and DML was supported by the Division of
Intramural Clinical and Biological Research of NIAAA. All reagents and
materials used for this work are commercially available.
NR 42
TC 10
Z9 11
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD OCT
PY 2014
VL 39
IS 11
BP 2538
EP 2548
DI 10.1038/npp.2014.100
PG 11
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AP6PZ
UT WOS:000342201000005
PM 24801766
ER
PT J
AU Ciccocioppo, R
Stopponi, S
Economidou, D
Kuriyama, M
Kinoshita, H
Heilig, M
Roberto, M
Weiss, F
Teshima, K
AF Ciccocioppo, Roberto
Stopponi, Serena
Economidou, Daina
Kuriyama, Makoto
Kinoshita, Hiroshi
Heilig, Markus
Roberto, Marisa
Weiss, Friedbert
Teshima, Koji
TI Chronic Treatment with Novel Brain-Penetrating Selective NOP Receptor
Agonist MT-7716 Reduces Alcohol Drinking and Seeking in the Rat
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
ID CORTICOTROPIN-RELEASING-FACTOR; DRUG-ASSOCIATED STIMULI; ORPHANIN-FQ
NOCICEPTIN; PLACE PREFERENCE; INDUCED REINSTATEMENT; NUCLEUS-ACCUMBENS;
OPIOID RECEPTORS; BED NUCLEUS; STRESS; BEHAVIOR
AB Since its discovery, the nociceptin/orphanin FQ (N/OFQ)-NOP receptor system has been extensively investigated as a promising target to treat alcoholism. Encouraging results obtained with the endogenous ligand N/OFQ stimulated research towards the development of novel brain-penetrating NOP receptor agonists with a pharmacological and toxicological profile compatible with clinical development. Here we describe the biochemical and alcohol-related behavioral effects of the novel NOP receptor agonist MT-7716. MT-7716 has high affinity for human NOP receptors expressed in HEK293 cells with a Ki value of 0.21 nM. MT-7716 concentration-dependently stimulated GTP gamma S-35 binding with an EC50 value of 0.30 nM and its efficacy was similar to N/OFQ, suggesting that MT7716 is a full agonist at NOP receptors. In the two bottle choice test MT-7716 (0, 0.3, 1, and 3 mg/kg, bid) given orally for 14 days dose-dependently decreased voluntary alcohol intake in Marchigian Sardinian rats. The effect became gradually stronger following repeated administration, and was still significant 1 week after discontinuation of the drug. Oral naltrexone (30 mg/kg, bid) for 14 days also reduced ethanol intake; however, the effect decreased over the treatment period and rapidly disappeared when drug treatment was discontinued. MT-7716 is also effective for preventing reinstatement caused by both ethanol-associated environmental stimuli and stress. Finally, to investigate the effect of MT-7716 on alcohol withdrawal symptoms, Wistar rats were withdrawn from a 7-day alcohol liquid diet. MT-7716 significantly attenuated somatic alcohol withdrawal symptoms. Together these findings indicate that MT-7716 is a promising candidate for alcoholism treatment remaining effective with chronic administration.
C1 [Ciccocioppo, Roberto; Stopponi, Serena; Economidou, Daina] Univ Camerino, Sch Pharm, Pharmacol Unit, I-62032 Camerino, Italy.
[Kuriyama, Makoto; Kinoshita, Hiroshi; Teshima, Koji] Mitsubishi Tanabe Pharma Corp, Dept CNS 2, Div Res, Pharmacol Res Labs 1, Yokohama, Kanagawa, Japan.
[Heilig, Markus] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Roberto, Marisa] Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA.
[Weiss, Friedbert] Scripps Res Inst, Dept Mol & Cellular Neurosci, La Jolla, CA 92037 USA.
RP Ciccocioppo, R (reprint author), Univ Camerino, Sch Pharm, Pharmacol Unit, Via Madonna Carceri, I-62032 Camerino, Italy.
EM roberto.ciccocioppo@unicam.it
OI Heilig, Markus/0000-0003-2706-2482
FU NIH [AA014351, AA017447]; Mitsubishi Tanabe Pharma Corporation
FX This study was supported by NIH AA014351 (FW) and AA017447 (MR). Support
was also provided by the Mitsubishi Tanabe Pharma Corporation (grant to
RC).
NR 65
TC 13
Z9 13
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD OCT
PY 2014
VL 39
IS 11
BP 2601
EP 2610
DI 10.1038/npp.2014.113
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AP6PZ
UT WOS:000342201000011
PM 24863033
ER
PT J
AU Park, TS
Abate-Daga, D
Zhang, L
Zheng, ZL
Morgan, RA
AF Park, Tristen S.
Abate-Daga, Daniel
Zhang, Ling
Zheng, Zhili
Morgan, Richard A.
TI Gamma-Retroviral Vector Design for the Co-Expression of Artificial
microRNAs and Therapeutic Proteins
SO NUCLEIC ACID THERAPEUTICS
LA English
DT Article
ID ENGINEERED T-CELLS; CHIMERIC ANTIGEN RECEPTOR; CANCER-IMMUNOTHERAPY;
SHRNA LIBRARIES; GENE-THERAPY; IN-VIVO; EXPRESSION; RNA; LYMPHOCYTES;
MIRNAS
AB To generate gamma-retroviral vectors for stable conjoint expression of artificial microRNAs (amiR) and therapeutic genes in primary human lymphocytes, and to identify the design parameters that are key for successful vector generation. Gamma-retroviral vectors were designed to co-express both amiRs and a linked reporter gene, truncated CD34 (tCD34). Artificial miRs based on microRNAs miR-16, miR-142, miR-146b, miR-150, miR155, and miR-223 were inserted into sites within the intron of the vector and tested for tCD34 expression by flow cytometry (FACS). Different constructs were assembled with amiRs targeted to knockdown expression of suppressor of cytokine signaling 1 (SOCS1) or programmed cell death 1 (PDCD1, PD-1). Three of the six amiRs maintained tCD34 expression. Expansion of primary human T cells transduced with these amiR vectors, as well as transgene expression, were equivalent to control engineered T cells over a 40-day period. Knockdown of SOCS1 RNA and PD-1 expression by FACS was shown to vary between constructs, dependent on either the specific short interfering RNA sequence used in the amiR, or the microRNA backbone and location in the vector intron. Gamma-retroviral vectors that both efficiently knockdown endogenous gene expression and maintain linked transgene production can be produced, but empirical vector evaluations were best suited for optimal construct analysis.
C1 [Park, Tristen S.; Abate-Daga, Daniel; Zhang, Ling; Zheng, Zhili; Morgan, Richard A.] NCI, Surg Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Abate-Daga, D (reprint author), NCI, Surg Branch, CRC, Bldg 10,Room 3W-3864,10 Ctr Dr, Bethesda, MD 20892 USA.
EM daniel.abate-daga@nih.gov
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health, Bethesda Maryland
FX The authors would like to thank Arnold Mixon and Shawn Farid for
technical support with FACS analysis. This work was supported by the
intramural program of the Center for Cancer Research, National Cancer
Institute, National Institutes of Health, Bethesda Maryland.
NR 43
TC 1
Z9 1
U1 0
U2 7
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 2159-3337
EI 2159-3345
J9 NUCLEIC ACID THER
JI Nucl. Acid Ther.
PD OCT
PY 2014
VL 24
IS 5
BP 356
EP 363
DI 10.1089/nat.2014.0486
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Medicine,
Research & Experimental
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Research &
Experimental Medicine
GA AP5HA
UT WOS:000342109100005
PM 25019196
ER
PT J
AU Burotto, M
Szabo, E
AF Burotto, Mauricio
Szabo, Eva
TI PPAR gamma in head and neck cancer prevention
SO ORAL ONCOLOGY
LA English
DT Article
DE Head and neck cancer; Oral carcinoma; PPAR gamma (peroxisome
proliferator-activated receptor gamma); Pioglitazone
ID ACTIVATED RECEPTOR-GAMMA; CELL LUNG-CANCER; ORAL PREMALIGNANT LESIONS;
2ND PRIMARY TUMORS; HUMAN-PAPILLOMAVIRUS; RANDOMIZED-TRIAL;
MALIGNANT-TRANSFORMATION; INSULIN SENSITIVITY; DIABETIC-PATIENTS;
BETA-CAROTENE
AB Head and neck cancer is a major source of morbidity and mortality worldwide. Intervention during the early phases of carcinogenesis represents a promising new strategy for curbing the devastating effects of this disease and its primary treatment modalities, surgery and radiation with or without concomitant chemotherapy. This review focuses on the peroxisome proliferator-activated receptor gamma (PPAR gamma) as a target for chemoprevention of oral cancer. Accumulating data suggest that ligands of PPAR gamma, which include the thiazolidinedione class of agents approved for the treatment of diabetes, inhibit cancer cell growth in vitro and in animal carcinogenesis models, providing the rationale for testing this approach in populations at risk for head and neck cancer. Published by Elsevier Ltd.
C1 [Burotto, Mauricio] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Szabo, Eva] NCI, Lung & Upper Aerodigest Canc Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
RP Szabo, E (reprint author), NCI, LUACRG, DCP, NIH, 9609 Med Ctr Dr,Room 5E-102, Bethesda, MD 20892 USA.
EM szaboe@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 71
TC 3
Z9 3
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD OCT
PY 2014
VL 50
IS 10
BP 924
EP 929
DI 10.1016/j.oraloncology.2013.12.020
PG 6
WC Oncology; Dentistry, Oral Surgery & Medicine
SC Oncology; Dentistry, Oral Surgery & Medicine
GA AP6AS
UT WOS:000342160500010
PM 24434068
ER
PT J
AU Vander Broek, R
Snow, GE
Chen, Z
Van Waes, C
AF Vander Broek, Robert
Snow, Grace E.
Chen, Zhong
Van Waes, Carter
TI Chemoprevention of head and neck squamous cell carcinoma through
inhibition of NF-kappa B signaling
SO ORAL ONCOLOGY
LA English
DT Article
DE Nuclear factor-kappa B (NF-kappa B); Head and neck cancer;
Chemoprevention; Epidermal growth factor receptor (EGFR);
Phosphatidylinositol 3-kinase (PI3K); Retinoids; Mammalian target of
rapamycin (mTOR); Curcumin; Cyclooxygenase (COX) inhibitors; Green tea
extract (GTE)
ID GROWTH-FACTOR-RECEPTOR; ORAL PREMALIGNANT LESIONS; SELECTIVE
CYCLOOXYGENASE-2 INHIBITOR; LYOPHILIZED BLACK-RASPBERRIES; CURCUMIN
SUPPRESSES GROWTH; INDUCED MAMMALIAN TARGET; NECROSIS-FACTOR-ALPHA;
13-CIS RETINOIC ACID; EPSTEIN-BARR-VIRUS; BREAST-CANCER CELL
AB Nuclear factor-kappa B (NF-kappa B) transcription factors regulate cellular processes such as inflammation and cell survival. The NF-kappa B pathway is often activated with development and progression of head and neck squamous cell carcinoma (HNSCC). As such, NF-kappa B represents an attractive target for chemoprevention. HNSCC involves progression of lesions from premalignant to malignant, providing a window of opportunity for intervention with chemopreventive agents. Appropriate chemopreventive agents should be inexpensive, nontoxic, and target important pathways involved in the development of HNSCC. Several such agents that inhibit the NF-kappa B pathway have been investigated in HNSCC. Retinoids have been studied most extensively but have shown limited potential in human trials. Epidermal growth factor receptor inhibitors and PI3K-mTOR inhibitors may benefit a subset of patients. Other agents such as green tea extract and curcumin are appealing because they are generally regarded as safe. In contrast, there is evidence that Vitamin E supplementation may actually increase mortality of cancer patients. Repurposed drugs such as cyclooxygenase (COX) inhibitors and antidiabetic drugs are an emerging area of interest. Future research to develop agents with lower toxicity and higher specificity for the NF-kappa B pathway, and to target these therapies to individual patient genetic signatures should help to increase the utility of chemoprevention in HSNCC. Published by Elsevier Ltd.
C1 [Vander Broek, Robert; Snow, Grace E.; Chen, Zhong; Van Waes, Carter] NIDCD, Tumor Biol Sect, Head & Neck Surg Branch, NIH, Bethesda, MD 20892 USA.
[Vander Broek, Robert; Snow, Grace E.] NIH, Med Res Scholars Program, Bethesda, MD 20892 USA.
RP Van Waes, C (reprint author), NIDCD, NIH, Bldg 10-CRC,4-2732,10 Ctr Dr, Bethesda, MD 20892 USA.
EM vanwaesc@nidcd.nih.gov
FU NIH Medical Research; NIH; Pfizer Inc; [ZIA-DC-000016]
FX RVB and GES are supported through the NIH Medical Research Scholars
Program, a public-private partnership supported jointly by the NIH and
generous contributions to the Foundation for the NIH from Pfizer Inc,
The Leona M. and Harry B. Helmsley Charitable Trust, and the Howard
Hughes Medical Institute, as well as other private donors. For a
complete list, please visit
http://www.fnih.org/work/programs-development/medical-research-scholarsp
rogram. ZC and CVW are supported by intramural project ZIA-DC-000016.
NR 208
TC 3
Z9 3
U1 1
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD OCT
PY 2014
VL 50
IS 10
BP 930
EP 941
DI 10.1016/j.oraloncology.2013.10.005
PG 12
WC Oncology; Dentistry, Oral Surgery & Medicine
SC Oncology; Dentistry, Oral Surgery & Medicine
GA AP6AS
UT WOS:000342160500011
PM 24177052
ER
PT J
AU Fan, JH
Wang, JB
Qu, CX
Zhang, YQ
Taylor, PR
Abnet, CC
Dawsey, SM
Qiao, YL
AF Fan, J. -H.
Wang, J. -B.
Qu, C. -X.
Zhang, Y. -Q.
Taylor, P. R.
Abnet, C. C.
Dawsey, S. M.
Qiao, Y. -L.
TI Association between oral leukoplakia and upper gastrointestinal cancers:
A 28-year follow-up study in the Linxian General Population Trial
SO ORAL ONCOLOGY
LA English
DT Article
DE Oral leukoplakia; Esophageal squamous cell carcinoma; Gastric cardia
carcinoma; Gastric non-cardia carcinoma; Linxian General Population
Trial
ID SQUAMOUS-CELL CARCINOMA; EPIDERMAL-GROWTH-FACTOR; GASTRIC CANCERS;
ESOPHAGEAL CANCER; INCIDENT ESOPHAGEAL; INCREASED RISK; BETA-CAROTENE;
TOOTH LOSS; CHINA; POLYMORPHISMS
AB Background: Oral leukoplakia is a precancerous disorder that is common among residents in Linxian. However, the associations between oral leukoplakia and upper gastrointestinal cancers have not been reported. We investigated the relationships between oral leukoplakia and upper gastrointestinal cancers in the Linxian General Population Trial cohort.
Methods: The Linxian General Population Trial cohort, with 29,584 healthy adults enrolled in 1985 and followed through the end of 2012. With collected baseline data, hazard ratios (HR) and 95% confidence intervals (95% CI) for developing upper gastrointestinal cancers were estimated using Cox proportional hazard models.
Results: During 28 years of follow-up, we confirmed a total of 2924 incident esophageal squamous cell carcinoma (ESCC) cases, 1644 gastric cardia cancers and 590 gastric non-cardia cancers. Overall, participants with oral leukoplakia had significantly higher risk of developing ESCC (HR = 1.18, 95% CI: 1.08, 1.29). Among individuals <= 52 years old at baseline, oral leukoplakia was associated with elevated risk of ESCC (HR = 1.31, 95% CI: 1.15, 1.49). No significant associations were observed for gastric cardia or non-cardia cancers in either all subjects or subgroups.
Conclusions: Oral leukoplakia was associated with increased risk of ESCC, particularly in younger population. Future studies are needed to confirm these findings. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Fan, J. -H.; Wang, J. -B.; Qu, C. -X.; Zhang, Y. -Q.; Qiao, Y. -L.] Chinese Acad Med Sci, Canc Inst Hosp, Dept Canc Epidemiol, Beijing 100021, Peoples R China.
[Fan, J. -H.; Wang, J. -B.; Qu, C. -X.; Zhang, Y. -Q.; Qiao, Y. -L.] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Wang, J. -B.] Zhejiang Univ, Sch Publ Hlth, Dept Epidemiol & Hlth Stat, Hangzhou 310003, Zhejiang, Peoples R China.
[Taylor, P. R.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Abnet, C. C.; Dawsey, S. M.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Qiao, YL (reprint author), Chinese Acad Med Sci, Canc Inst Hosp, Dept Canc Epidemiol, 17 South Pan Jia Yuan Lane, Beijing 100021, Peoples R China.
EM qiaoy@cicams.ac.cn
RI Abnet, Christian/C-4111-2015; Qiao, You-Lin/B-4139-2012
OI Abnet, Christian/0000-0002-3008-7843; Qiao, You-Lin/0000-0001-6380-0871
FU CCR NIH HHS [N01RC47701]; Intramural NIH HHS; NCI NIH HHS [N01-SC-91030]
NR 31
TC 0
Z9 0
U1 2
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD OCT
PY 2014
VL 50
IS 10
BP 971
EP 975
DI 10.1016/j.oraloncology.2014.07.009
PG 5
WC Oncology; Dentistry, Oral Surgery & Medicine
SC Oncology; Dentistry, Oral Surgery & Medicine
GA AP6AS
UT WOS:000342160500016
PM 25132090
ER
PT J
AU Smith, JP
Cooper, TK
McGovern, CO
Gilius, EL
Zhong, Q
Liao, JG
Molinolo, AA
Gutkind, JS
Matters, GL
AF Smith, Jill P.
Cooper, Timothy K.
McGovern, Christopher O.
Gilius, Evan L.
Zhong, Qing
Liao, Jiangang
Molinolo, Alfredo A.
Gutkind, J. Silvio
Matters, Gail L.
TI Cholecystokinin Receptor Antagonist Halts Progression of Pancreatic
Cancer Precursor Lesions and Fibrosis in Mice
SO PANCREAS
LA English
DT Article
DE transgenic; proglumide; Kras; PanIN lesions; fibrosis
ID GASTRIN GENE-EXPRESSION; STELLATE CELLS; EXOCRINE SECRETION; STIMULATES
GROWTH; DOWN-REGULATION; MOUSE MODELS; ADENOCARCINOMA; IDENTIFICATION;
PEPTIDE; MICROENVIRONMENT
AB Objectives: Exogenous administration of cholecystokinin (CCK) induces hypertrophy and hyperplasia of the pancreas with an increase in DNA content. We hypothesized that endogenous CCK is involved in the malignant progression of pancreatic intraepithelial neoplasia (PanIN) lesions and the fibrosis associated with pancreatic cancer.
Methods: The presence of CCK receptors in early PanIN lesions was examined by immunohistochemistry in mouse and human pancreas. Pdx1-Cre/LSL-Kras(G12D) transgenic mice were randomized to receive either untreated drinking water or water supplemented with a CCK receptor antagonist (proglumide, 0.1 mg/mL). Pancreas from the mice were removed and examined histologically for number and grade of PanINs after 1, 2, or 4 months of antagonist therapy.
Results: Both CCK-A and CCK-B receptors were identified in early stage PanINs from mouse and human pancreas. The grade of PanIN lesions was reversed, and progression to advanced lesions arrested in mice treated with proglumide compared with the controls (P = 0.004). Furthermore, pancreatic fibrosis was significantly reduced in antagonist-treated animals compared with vehicle (P < 0.001).
Conclusions: These findings demonstrate that endogenous CCK is in part responsible for the development and progression of pancreatic cancer. The use of CCK receptor antagonists may have a role in cancer prophylaxis in high-risk subjects and may reduce fibrosis in the microenvironment.
C1 [Smith, Jill P.] NIDDKD, NIH, Bethesda, MD USA.
[Smith, Jill P.; McGovern, Christopher O.; Gilius, Evan L.; Matters, Gail L.] Penn State Univ, Coll Med, Dept Med, Hershey, PA USA.
[Cooper, Timothy K.; Zhong, Qing] Penn State Univ, Coll Med, Dept Comparat Med & Pathol, Hershey, PA USA.
[Liao, Jiangang] Penn State Univ, Coll Med, Dept Publ Hlth Sci, Hershey, PA USA.
[Molinolo, Alfredo A.; Gutkind, J. Silvio] Penn State Univ, Coll Med, Dept Biochem & Mol Biol, Hershey, PA USA.
[Matters, Gail L.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
RP Smith, JP (reprint author), Georgetown Univ, 3800 Reservoir Rd,NW,2 Main, Washington, DC 20007 USA.
EM jps261@georgetown.edu
FU NIH [R01 CA117926]; Robert Sullivan Foundation; V-Foundation for Cancer
Research
FX This work was funded by the NIH R01 CA117926 grant and Robert Sullivan
Foundation award to J.P.S. We recognize additional support from The
V-Foundation for Cancer Research.
NR 62
TC 4
Z9 4
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD OCT
PY 2014
VL 43
IS 7
BP 1050
EP 1059
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AP4US
UT WOS:000342074900011
PM 25058882
ER
PT J
AU Baumann, MH
AF Baumann, Michael H.
TI Awash in a sea of 'bath salts': implications for biomedical research and
public health
SO ADDICTION
LA English
DT Editorial Material
DE Bath salts; cathinone; dopamine; mephedrone; methylone; MDPV;
transporter
ID SYNTHETIC CATHINONES; LIQUID-CHROMATOGRAPHY; DESIGNER CATHINONES;
MASS-SPECTROMETRY; LEGAL HIGHS; PHARMACOLOGY; MEPHEDRONE;
METHYLENEDIOXYPYROVALERONE; STIMULANTS; ANALOGS
C1 NIDA, DDRU, IRP, Baltimore, MD 21224 USA.
RP Baumann, MH (reprint author), NIDA, DDRU, IRP, 333 Cassell Dr,Suite 4400, Baltimore, MD 21224 USA.
EM mbaumann@mail.nih.gov
FU Intramural NIH HHS [Z99 DA999999]
NR 18
TC 10
Z9 10
U1 1
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0965-2140
EI 1360-0443
J9 ADDICTION
JI Addiction
PD OCT
PY 2014
VL 109
IS 10
BP 1577
EP 1579
DI 10.1111/add.12601
PG 3
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA AO9AO
UT WOS:000341648000001
PM 24984975
ER
PT J
AU Suls, J
AF Suls, Jerry
TI An Informative Failure to Replicate-the Type D is Distressed: a Comment
on Meyer et al.
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Editorial Material
ID D PERSONALITY; MORTALITY; RISK
C1 NCI, Behav Res Program, Bethesda, MD 20892 USA.
RP Suls, J (reprint author), NCI, Behav Res Program, 9609 Med Ctr Dr MSC 9761, Bethesda, MD 20892 USA.
EM jerry.suls@nih.gov
NR 8
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
EI 1532-4796
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD OCT
PY 2014
VL 48
IS 2
BP 140
EP 141
DI 10.1007/s12160-014-9628-5
PG 2
WC Psychology, Multidisciplinary
SC Psychology
GA AP1EF
UT WOS:000341808600002
PM 24817016
ER
PT J
AU Lv, QW
Chen, T
Zhang, W
Shi, Q
Zheng, WJ
Lipsky, PE
Zhang, X
AF Lv, Qian-wen
Chen, Tao
Zhang, Wen
Shi, Qun
Zheng, Wen-jie
Lipsky, Peter E.
Zhang, Xuan
TI TwHF versus methotrexate in the treatment of rheumatoid arthritis:
response to Landewe's comment on the TRIFRA study
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Letter
ID WILFORDII HOOK-F
C1 [Lv, Qian-wen; Zhang, Wen; Shi, Qun; Zheng, Wen-jie; Zhang, Xuan] Chinese Acad Med Sci, Dept Rheumatol & Clin Immunol, Peking Union Med Coll Hosp, Beijing 100730, Peoples R China.
[Lv, Qian-wen; Zhang, Wen; Shi, Qun; Zheng, Wen-jie; Zhang, Xuan] Peking Union Med Coll, Beijing 100730, Peoples R China.
[Chen, Tao] Nanjing Med Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Nanjing, Jiangsu, Peoples R China.
[Zhang, Xuan] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Zhang, X (reprint author), Chinese Acad Med Sci, Dept Rheumatol & Clin Immunol, Peking Union Med Coll Hosp, Beijing 100730, Peoples R China.
EM peterlipsky@comcast.net; zxpumch2003@sina.com
OI zhang, xuan/0000-0001-8775-1699
NR 4
TC 0
Z9 0
U1 0
U2 1
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD OCT
PY 2014
VL 73
IS 10
BP E63
EP U26
DI 10.1136/annrheumdis-2014-206156
PG 2
WC Rheumatology
SC Rheumatology
GA AP0XK
UT WOS:000341789500004
PM 25063826
ER
PT J
AU Blasio, A
Rice, KC
Sabino, V
Cottone, P
AF Blasio, Angelo
Rice, Kenner C.
Sabino, Valentina
Cottone, Pietro
TI Characterization of a shortened model of diet alternation in female
rats: effects of the CB1 receptor antagonist rimonabant on food intake
and anxiety-like behavior
SO BEHAVIOURAL PHARMACOLOGY
LA English
DT Article
DE diet cycling; eating disorders; female; palatable food; rat; rimonabant;
withdrawal
ID ELEVATED PLUS-MAZE; BASE-LINE ANXIETY; PALATABLE FOOD; PREFERRED FOOD;
CANNABINOID RECEPTOR; INTERMITTENT ACCESS; EATING-DISORDERS; LIMITED
ACCESS; DARK SIDE; AMYGDALA
AB The prevalence of eating disorders and obesity in western societies is epidemic and increasing in severity. Preclinical research has focused on the development of animal models that can mimic the maladaptive patterns of food intake observed in certain forms of eating disorders and obesity. This study was aimed at characterizing a recently established model of palatable diet alternation in female rats. For this purpose, females rats were fed either continuously with a regular chow diet (Chow/Chow) or intermittently with a regular chow diet for 2 days and a palatable, high-sucrose diet for 1 day (Chow/Palatable). Following diet cycling, rats were administered rimonabant (0, 0.3, 1, 3 mg/kg intraperitoneally) during access to either palatable diet or chow diet and were assessed for food intake and body weight. Finally, rats were pretreated with rimonabant (0, 3 mg/kg, intraperitoneally) and tested in the elevated plus maze during withdrawal from the palatable diet. Female rats with alternating access to palatable food cycled their intake, overeating during access to the palatable diet and undereating upon returning to the regular chow diet. Rimonabant treatment resulted in increased chow hypophagia and anxiety-like behavior in Chow/Palatable rats. No effect of drug treatment was observed on the compulsive eating of palatable food in the diet-cycled rats. The results of this study suggest that withdrawal from alternating access to the palatable diet makes individuals vulnerable to the anxiogenic effects of rimonabant and provides etiological factors potentially responsible for the emergence of severe psychiatric side-effects following rimonabant treatment in obese patients. (C) 2014 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Blasio, Angelo; Sabino, Valentina; Cottone, Pietro] Boston Univ, Sch Med, Dept Pharmacol, Lab Addict Disorders, Boston, MA 02118 USA.
[Blasio, Angelo; Sabino, Valentina; Cottone, Pietro] Boston Univ, Sch Med, Dept Psychiat, Lab Addict Disorders, Boston, MA 02118 USA.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, Rockville, MD USA.
[Rice, Kenner C.] NIAAA, Rockville, MD 20852 USA.
RP Cottone, P (reprint author), Boston Univ, Sch Med, Dept Pharmacol, Lab Addict Disorders, 72 E Concord St,R-618, Boston, MA 02118 USA.
EM cottone@bu.edu
RI Sabino, Valentina/F-5290-2012; Cottone, Pietro/F-5291-2012
OI Sabino, Valentina/0000-0002-6680-1279; Cottone,
Pietro/0000-0003-1320-1672
FU National Institute of Mental Health (NIMH), the National Institute on
Drug Abuse (NIDA) [MH091945, MH093650, DA030425]; Peter Paul Career
Development Professorship; Boston University's Undergraduate Research
Opportunities Program (UROP); NIH Intramural Research Program of the
National Institute on Drug Abuse (NIDA); NIH Intramural Research Program
of National Institute of Alcohol Abuse and Alcoholism (NIAAA)
FX The authors thank Anika Begum and Alyssa C. DiLeo for their technical
assistance. This publication was made possible by grant numbers
MH091945, MH093650, and DA030425 from the National Institute of Mental
Health (NIMH), the National Institute on Drug Abuse (NIDA), by the Peter
Paul Career Development Professorship (P. C.), and by Boston
University's Undergraduate Research Opportunities Program (UROP). A
portion of this work was supported by the NIH Intramural Research
Programs of the National Institute on Drug Abuse (NIDA) and the National
Institute of Alcohol Abuse and Alcoholism (NIAAA).
NR 50
TC 2
Z9 2
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0955-8810
EI 1473-5849
J9 BEHAV PHARMACOL
JI Behav. Pharmacol.
PD OCT
PY 2014
VL 25
IS 7
BP 609
EP 617
DI 10.1097/FBP.0000000000000059
PG 9
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA AP0PE
UT WOS:000341763500001
PM 25011007
ER
PT J
AU Shultz, JM
Garfin, DR
Espinel, Z
Araya, R
Oquendo, MA
Wainberg, ML
Chaskel, R
Gaviria, SL
Ordonez, AE
Espinola, M
Wilson, FE
Garcia, NM
Ceballos, AMG
Garcia-Barcena, Y
Verdeli, H
Neria, Y
AF Shultz, James M.
Garfin, Dana Rose
Espinel, Zelde
Araya, Ricardo
Oquendo, Maria A.
Wainberg, Milton L.
Chaskel, Roberto
Gaviria, Silvia L.
Ordonez, Anna E.
Espinola, Maria
Wilson, Fiona E.
Munoz Garcia, Natalia
Gomez Ceballos, Angela Milena
Garcia-Barcena, Yanira
Verdeli, Helen
Neria, Yuval
TI Internally Displaced "Victims of Armed Conflict" in Colombia: The
Trajectory and Trauma Signature of Forced Migration
SO CURRENT PSYCHIATRY REPORTS
LA English
DT Article
DE Internal displacement; Internally displaced persons; Victims of armed
conflict; Humanitarian crisis; Complex emergency; Forced displacement;
Forced migration; Trauma signature analysis; TSIG
ID POSTTRAUMATIC-STRESS-DISORDER; QUALITY-OF-LIFE; MENTAL-HEALTH; NORTHERN
UGANDA; PSYCHOLOGICAL DISTRESS; INCOME COUNTRIES; WAR; ASSOCIATION;
POPULATIONS; DEPRESSION
AB While conflict-induced forced migration is a global phenomenon, the situation in Colombia, South America, is distinctive. Colombia has ranked either first or second in the number of internally displaced persons for 10 years, a consequence of decades of armed conflict compounded by high prevalence of drug trafficking. The displacement trajectory for displaced persons in Colombia proceeds through a sequence of stages: (1) pre-expulsion threats and vulnerability, (2) expulsion, (3) migration, (4) initial adaptation to relocation, (5) protracted resettlement (the end point for most forced migrants), and, rarely, (6) return to the community of origin. Trauma signature analysis, an evidence-based method that elucidates the physical and psychological consequences associated with exposures to harm and loss during disasters and complex emergencies, was used to identify the psychological risk factors and potentially traumatic events experienced by conflict-displaced persons in Colombia, stratified across the phases of displacement. Trauma and loss are experienced differentially throughout the pathway of displacement.
C1 [Shultz, James M.] Univ Miami, Miller Sch Med, DEEP Ctr, Miami, FL 33136 USA.
[Garfin, Dana Rose] Univ Calif Irvine, Dept Psychol & Social Behav, Irvine, CA USA.
[Espinel, Zelde] Univ Miami, Miller Sch Med, Dept Psychiat & Behav Hlth, Miami, FL 33136 USA.
[Espinel, Zelde] Jackson Mem Hosp, Miami, FL 33136 USA.
[Araya, Ricardo] London Sch Hyg & Trop Med, Ctr Global Mental Hlth, London WC1, England.
[Oquendo, Maria A.; Wainberg, Milton L.; Verdeli, Helen; Neria, Yuval] Columbia Univ, Dept Psychiat, New York, NY USA.
[Oquendo, Maria A.; Wainberg, Milton L.; Verdeli, Helen; Neria, Yuval] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Chaskel, Roberto] Univ Los Andes, Univ Bosque, Hosp Mil Cent, Fdn Santa Fe Bogota, Bogota, Colombia.
[Gaviria, Silvia L.] Univ CES, Dept Psychiat, Medellin, Colombia.
[Ordonez, Anna E.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Espinola, Maria] Harvard Univ, Sch Med, Dept Psychiat, McLean Hosp, Boston, MA 02115 USA.
[Wilson, Fiona E.] Univ Edinburgh, Dept Clin & Hlth Psychol, Edinburgh, Midlothian, Scotland.
[Munoz Garcia, Natalia] Univ Los Andes, Sch Social Sci, Program Clin & Hlth Psychol, Bogota, Colombia.
[Gomez Ceballos, Angela Milena] Univ Los Andes, Program Publ Hlth, Sch Med, Bogota, Colombia.
[Gomez Ceballos, Angela Milena] Univ Los Andes, Program Publ Hlth, Sch Govt, Bogota, Colombia.
[Garcia-Barcena, Yanira] Louis Calder Mem Lib, Leonard M Miller Sch Med, Dept Hlth Informat, Miami, FL USA.
[Verdeli, Helen] Columbia Univ, Teachers Coll, New York, NY 10027 USA.
[Neria, Yuval] Columbia Univ, Dept Epidemiol, New York, NY USA.
RP Shultz, JM (reprint author), 251 174 St 2319, Sunny Isles Beach, FL USA.
EM jamesmichaelshultz@gmail.com; dgarfin@uci.edu; z.espinel@med.miami.edu;
riaraya.psych@gmail.com; mao4@columbia.edu; mlw35@columbia.edu;
rchaskel@gmail.com; sgaviria1@une.net.co; anna.ordonez@nih.gov;
mfe@bu.edu; fiona.e.wilson@nhslothian.scot.nhs.uk;
n.munoz12@uniandes.edu.co; am.gomez14@unandes.edu.co;
jennygarcia@miami.edu; verdeli@tc.edu; ny126@columbia.edu
FU NIMH NIH HHS [R25 MH060482, T32 MH096724]
NR 103
TC 2
Z9 2
U1 4
U2 38
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3812
EI 1535-1645
J9 CURR PSYCHIAT REP
JI Curr. Psychiatry Rep.
PD OCT
PY 2014
VL 16
IS 10
AR 475
DI 10.1007/s11920-014-0475-7
PG 16
WC Psychiatry
SC Psychiatry
GA AP1KG
UT WOS:000341827500003
PM 25135775
ER
PT J
AU Punthakee, Z
Miller, M
Simmons, D
Riddle, M
Ismail-Beigi, F
Brillon, D
Bergenstal, R
Savage, P
Hramiak, I
Largay, J
Sood, A
Gerstein, H
AF Punthakee, Zubin
Miller, Michael E.
Simmons, Debra L.
Riddle, Matthew C.
Ismail-Beigi, Faramarz
Brillon, David J.
Bergenstal, Richard M.
Savage, Peter J.
Hramiak, Irene
Largay, Joseph F.
Sood, Ajay
Gerstein, Hertzel C.
CA ACCORD Grp Investigators
TI Durable change in glycaemic control following intensive management of
type 2 diabetes in the ACCORD clinical trial
SO DIABETOLOGIA
LA English
DT Article
DE Intensive glucose lowering; Long-term glycaemic control;
Post-intervention follow-up; Type 2 diabetes
ID IMPAIRED GLUCOSE-TOLERANCE; LIFE-STYLE INTERVENTION; BETA-CELL FUNCTION;
BARIATRIC SURGERY; GASTRIC BYPASS; THERAPY; INSULIN; PRESERVATION;
PREVENTION; OUTCOMES
AB Aims/hypothesis We aimed to determine the persistence of glycaemic control 1 year after a limited period of intensive glycaemic management of type 2 diabetes.
Methods 4119 ACCORD Trial participants randomised to target HbA(1c) <6.0% (42 mmol/mol) for 4.0 +/- 1.2 years were systematically transitioned to target HbA(1c) 7.0-7.9% (53-63 mmol/mol) and followed for an additional 1.1 +/- 0.2 years. Characteristics of participants with HbA(1c) <6.5% (48 mmol/mol) or >= 6.5% at transition were compared. Changes in BMI and glucose-lowering medications were compared between those ending with HbA(1c) <6.5% vs >= 6.5%. Poisson models were used to assess the independent effect of attaining HbA(1c) <6.5% before transition on ending with HbA(1c) <6.5%.
Results Participants with pre-transition HbA(1c) <6.5% were older with shorter duration diabetes and took less insulin but more non-insulin glucose-lowering agents than those with higher HbA(1c). A total of 823 participants achieved a final HbA(1c) <6.5%, and had greater post-transition reductions in BMI, insulin dose and secretagogue and acarbose use than those with higher HbA(1c) (p<0.0001). HbA(1c) <6.5% at transition predicted final HbA(1c) <6.5% (crude RR 4.9 [95% CI 4.0, 5.9]; RR 3.9 [95% CI 3.2, 4.8] adjusted for demographics, co-interventions, pre-intervention HbA(1c), BMI and glucose-lowering medication, and post-transition change in both BMI and glucose-lowering medication). Progressively lower pre-transition HbA(1c) levels were associated with a greater likelihood of maintaining a final HbA(1c) of <6.5%. Follow-up duration was not associated with post-transition rise in HbA(1c).
Conclusions/interpretation Time-limited intensive glycaemic management using a combination of agents that achieves HbA(1c) levels below 6.5% in established diabetes is associated with glycaemic control more than 1 year after therapy is relaxed.
C1 [Punthakee, Zubin; Gerstein, Hertzel C.] McMaster Univ, Dept Med, Hamilton, ON L8S 4K1, Canada.
[Miller, Michael E.] Wake Forest Univ, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Simmons, Debra L.] Univ Utah, Sch Med, Dept Internal Med, Div Endocrinol, Salt Lake City, UT USA.
[Simmons, Debra L.] VA Salt Lake City Hlth Care Syst, Salt Lake City, UT USA.
[Riddle, Matthew C.] Oregon Hlth & Sci Univ, Div Endocrinol Diabet & Clin Nutr, Portland, OR 97201 USA.
[Ismail-Beigi, Faramarz; Sood, Ajay] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
[Ismail-Beigi, Faramarz] Cleveland VA Med Ctr, Cleveland, OH USA.
[Brillon, David J.] Cornell Univ, Weill Cornell Med Coll, Div Endocrinol, New York, NY 10021 USA.
[Bergenstal, Richard M.] Int Diabet Ctr Pk Nicollet, Minneapolis, MN USA.
[Savage, Peter J.] NIDDK, NIH, Bethesda, MD USA.
[Hramiak, Irene] Western Univ, Dept Med, London, ON, Canada.
[Largay, Joseph F.] Univ N Carolina, Dept Med, Div Endocrinol, Chapel Hill, NC USA.
[Sood, Ajay] Louis Stokes VA Med Ctr, Cleveland, OH USA.
RP Punthakee, Z (reprint author), McMaster Univ, Dept Med, 1280 Main St W, Hamilton, ON L8S 4K1, Canada.
EM zubin.punthakee@mcmaster.ca
FU National Heart, Lung, and Blood Institute [N01-HC-95178, N01-HC-95179,
N01-HC-95180, N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184,
IAA-Y1-HC-9035, IAA-Y1- HC-1010]; National Institutes of Health,
National Institute of Diabetes and Digestive and Kidney Diseases;
National Institute on Aging; National Eye Institute; Centers for Disease
Control and Prevention; General Clinical Research Centers
FX The ACCORD Trial was supported by grants (N01-HC-95178, N01-HC-95179,
N01-HC-95180, N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184,
IAA-Y1-HC-9035 and IAA-Y1- HC-1010) from the National Heart, Lung, and
Blood Institute, by other components of the National Institutes of
Health, including the National Institute of Diabetes and Digestive and
Kidney Diseases, the National Institute on Aging, and the National Eye
Institute, by the Centers for Disease Control and Prevention, and by
General Clinical Research Centers. The following companies provided
study medications, equipment, or supplies: Abbott Laboratories, Amylin
Pharmaceutical, AstraZeneca, Bayer HealthCare, Closer Healthcare,
GlaxoSmithKline, King Pharmaceuticals, Merck, Novartis, Novo Nordisk,
Omron Healthcare, Sanofi-Aventis and Schering-Plough.
NR 24
TC 2
Z9 2
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
EI 1432-0428
J9 DIABETOLOGIA
JI Diabetologia
PD OCT
PY 2014
VL 57
IS 10
BP 2030
EP 2037
DI 10.1007/s00125-014-3318-5
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AO9VZ
UT WOS:000341708900004
PM 24985147
ER
PT J
AU Kim, KS
Egan, JM
Jang, HJ
AF Kim, Ki-Suk
Egan, Josephine M.
Jang, Hyeung-Jin
TI Denatonium induces secretion of glucagon-like peptide-1 through
activation of bitter taste receptor pathways
SO DIABETOLOGIA
LA English
DT Article
DE Bitter taste receptor; GLP-1; Incretin; PYY; Type 2 diabetesmellitus;
alpha-gustducin
ID SWEET TASTE; FOOD-INTAKE; PANCREATIC-POLYPEPTIDE; DIABETES-MELLITUS;
STC-1 CELLS; GUT HORMONE; GUSTDUCIN; FAMILY; EXPRESSION; TYPE-2
AB Aims/hypothesis This study was designed to ascertain whether human enteroendocrine cells express bitter taste receptors, and whether activation of these receptors with bitter-tasting ligands induces secretion of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY).
Methods We used human enteroendocrine NCI-H716 cells, isolated duodenal segments from mice, and whole mice as our experimental systems for investigating stimuli and mechanisms underlying GLP-1- and PYY-stimulated release. We measured hormone levels by ELISA and determined bitter taste receptor expression by real-time quantitative PCR. We adopted a pharmacological approach using inhibitors and enhancers of downstream signalling pathways known to be involved in bitter taste transduction in taste bud cells to investigate these pathways in NCI-H716 cells.
Results Using a pharmacological approach, we identified signalling pathways triggered by the denatonium benzoate (DB)-activated bitter receptors. This involved activation of alpha-gustducin (G alpha gust)-the specific G-protein subunit that is also present in taste bud cells-reduction of intracellular cAMP levels and enhancement of phospholipase C (PLC) activity, which ultimately led to increased intracellular calcium concentrations and hormone release. Gavage of DB, followed by gavage of glucose, to db/db mice stimulated GLP-1 and subsequent insulin secretion, leading to lower blood glucose levels.
Conclusions/interpretation Our study demonstrates that activation of gut-expressed bitter taste receptors stimulates GLP-1 secretion in a PLC-dependent manner. In diabetic mice, DB (a ligand of bitter taste receptor cells), when given via gavage, lowers blood glucose levels in diabetic mice after oral glucose administration, through increased secretion of GLP-1.
C1 [Kim, Ki-Suk; Jang, Hyeung-Jin] Kyung Hee Univ, Coll Korean Med, Dept Biochem, Seoul 130701, South Korea.
[Egan, Josephine M.] NIA, NIH, Baltimore, MD 21224 USA.
RP Jang, HJ (reprint author), Kyung Hee Univ, Coll Korean Med, Dept Biochem, Seoul 130701, South Korea.
EM hjjang@khu.ac.kr
FU Intramural Research Program of the National Institute on Aging/National
Institutes of Health; National Institute on Deafness and Other
Communication Disorders/National Institutes of Health [DC003055]
FX This work was supported by the Intramural Research Program of the
National Institute on Aging/National Institutes of Health and by
National Institute on Deafness and Other Communication
Disorders/National Institutes of Health (grants DC003055).
NR 41
TC 21
Z9 21
U1 2
U2 27
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
EI 1432-0428
J9 DIABETOLOGIA
JI Diabetologia
PD OCT
PY 2014
VL 57
IS 10
BP 2117
EP 2125
DI 10.1007/s00125-014-3326-5
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AO9VZ
UT WOS:000341708900014
PM 25016595
ER
PT J
AU Wallen, GR
Brooks, AT
Whiting, B
Clark, R
Krumlauf, MC
Yang, L
Schwandt, ML
George, DT
Ramchandani, VA
AF Wallen, Gwenyth R.
Brooks, Alyssa T.
Whiting, Barbara
Clark, Rosa
Krumlauf, Michael C.
Yang, Li
Schwandt, Melanie L.
George, David T.
Ramchandani, Vijay A.
TI The Prevalence of Sleep Disturbance in Alcoholics Admitted for Treatment
A Target for Chronic Disease Management
SO FAMILY & COMMUNITY HEALTH
LA English
DT Article
DE actigraphy; addiction; alcohol; insomnia; sleep disturbances
ID RECOVERING ALCOHOLICS; PSYCHIATRIC-DISORDERS; DAYTIME SLEEPINESS;
SUBSTANCE-ABUSE; INSOMNIA; RELAPSE; SCALE; ADOLESCENTS; WITHDRAWAL;
DEPENDENCE
AB Prolonged and heavy use of alcohol is associated with persistent sleep disturbances. Objective and subjective measures of sleep quantity and quality were collected on 164 individuals undergoing detoxification. A high prevalence of sleep disturbance was found in this sample. Sleep quality improved by week 4 but continued to be altered, signaling a target area for recovery management. This study supports the high prevalence of sleep disturbance in individuals undergoing alcohol treatment. Health promotion strategies in an addiction recovery model should address quality-of-life enhancements for individuals and their families including optimizing sleep quality and duration through sustained recovery.
C1 [Wallen, Gwenyth R.; Brooks, Alyssa T.; Krumlauf, Michael C.; Yang, Li] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Whiting, Barbara; Clark, Rosa; Schwandt, Melanie L.; George, David T.; Ramchandani, Vijay A.] NIAAA, NIH, Bethesda, MD USA.
RP Wallen, GR (reprint author), NIH, Ctr Clin, Bldg 10,Room 2B09, Bethesda, MD 20892 USA.
EM gwallen@cc.nih.gov
RI Schwandt, Melanie/L-9866-2016
FU Intramural NIH HHS [Z99 CL999999]
NR 32
TC 3
Z9 3
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0160-6379
EI 1550-5057
J9 FAM COMMUNITY HEALTH
JI Fam. Community Health
PD OCT-DEC
PY 2014
VL 37
IS 4
BP 288
EP 297
DI 10.1097/FCH.0000000000000040
PG 10
WC Family Studies; Public, Environmental & Occupational Health
SC Family Studies; Public, Environmental & Occupational Health
GA AO8TB
UT WOS:000341626400006
PM 25167069
ER
PT J
AU de Maturana, EL
Ibanez-Escriche, N
Gonzalez-Recio, O
Marenne, G
Mehrban, H
Chanock, SJ
Goddard, ME
Malats, N
AF Lopez de Maturana, Evangelina
Ibanez-Escriche, Noelia
Gonzalez-Recio, Oscar
Marenne, Gaelle
Mehrban, Hossein
Chanock, Stephen J.
Goddard, Michael E.
Malats, Nuria
TI Next generation modeling in GWAS: comparing different genetic
architectures
SO HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; URINARY-BLADDER CANCER; BAYESIAN LASSO; ADULT
HEIGHT; MISSING HERITABILITY; RISK; LOCI; PREDICTION; SUSCEPTIBILITY;
REGRESSION
AB The continuous advancement in genotyping technology has not been accompanied by the application of innovative statistical methods, such as multi-marker methods (MMM), to unravel genetic associations with complex traits. Although the performance of MMM has been widely explored in a prediction context, little is known on their behavior in the quantitative trait loci (QTL) detection under complex genetic architectures. We shed light on this still open question by applying Bayes A (BA) and Bayesian LASSO (BL) to simulated and real data. Both methods were compared to the single marker regression (SMR). Simulated data were generated in the context of six scenarios differing on effect size, minor allele frequency (MAF) and linkage disequilibrium (LD) between QTLs. These were based on real SNP genotypes in chromosome 21 from the Spanish Bladder Cancer Study. We show how the genetic architecture dramatically affects the behavior of the methods in terms of power, type I error and accuracy of estimates. Markers with high MAF are easier to detect by all methods, especially if they have a large effect on the phenotypic trait. A high LD between QTLs with either large or small effects differently affects the power of the methods: it impairs QTL detection with BA, irrespectively of the effect size, although boosts that of small effects with BL and SMR. We demonstrate the convenience of applying MMM rather than SMR because of their larger power and smaller type I error. Results from real data when applying MMM suggest novel associations not detected by SMR.
C1 [Lopez de Maturana, Evangelina; Marenne, Gaelle; Malats, Nuria] Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid 28029, Spain.
[Ibanez-Escriche, Noelia; Mehrban, Hossein] Res Inst & Agr Technol IRTA, Lleida 25198, Spain.
[Gonzalez-Recio, Oscar; Goddard, Michael E.] Agribio, Dept Environm & Primary Ind, Biosci Res Div, Bundoora, Vic 3083, Australia.
[Gonzalez-Recio, Oscar] Dairy Futures Cooperat Res Ctr, Bundoora, Vic 3083, Australia.
[Mehrban, Hossein] Univ Shahrekord, Dept Anim Sci, Shahrekord 8818634141, Iran.
[Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, US Dept HHS, Bethesda, MD 20892 USA.
[Goddard, Michael E.] Univ Melbourne, Dept Food & Agr Syst, Melbourne, Vic, Australia.
RP de Maturana, EL (reprint author), Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, C MelchorFernandezAlmagro 3, Madrid 28029, Spain.
EM melopezdm@cnio.es
RI Ibanez, Noelia/H-2988-2014; Malats, Nuria/H-7041-2015; Gonzalez-Recio,
Oscar/C-8553-2016;
OI Ibanez, Noelia/0000-0002-6221-3576; Malats, Nuria/0000-0003-2538-3784;
Gonzalez-Recio, Oscar/0000-0002-9106-4063; Lopez de Maturana,
Evangelina/0000-0001-9425-3911; Goddard, Michael/0000-0001-9917-7946
NR 44
TC 5
Z9 5
U1 3
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
EI 1432-1203
J9 HUM GENET
JI Hum. Genet.
PD OCT
PY 2014
VL 133
IS 10
BP 1235
EP 1253
DI 10.1007/s00439-014-1461-1
PG 19
WC Genetics & Heredity
SC Genetics & Heredity
GA AP1KP
UT WOS:000341828900003
ER
PT J
AU Kelley, MJ
Shi, JX
Ballew, B
Hyland, PL
Li, WQ
Rotunno, M
Alcorta, DA
Liebsch, NJ
Mitchell, J
Bass, S
Roberson, D
Boland, J
Cullen, M
He, J
Burdette, L
Yeager, M
Chanock, SJ
Parry, DM
Goldstein, AM
Yang, XHR
AF Kelley, Michael J.
Shi, Jianxin
Ballew, Bari
Hyland, Paula L.
Li, Wen-Qing
Rotunno, Melissa
Alcorta, David A.
Liebsch, Norbert J.
Mitchell, Jason
Bass, Sara
Roberson, David
Boland, Joseph
Cullen, Michael
He, Ji
Burdette, Laurie
Yeager, Meredith
Chanock, Stephen J.
Parry, Dilys M.
Goldstein, Alisa M.
Yang, Xiaohong R.
TI Characterization of T gene sequence variants and germline duplications
in familial and sporadic chordoma
SO HUMAN GENETICS
LA English
DT Article
ID TRANSCRIPTION FACTOR; BRACHYURY; PROTEIN; POPULATION; SURVIVAL; COMPLEX
AB Chordoma is a rare bone cancer that is believed to originate from notochordal remnants. We previously identified germline T duplication as a major susceptibility mechanism in several chordoma families. Recently, a common genetic variant in T (rs2305089) was significantly associated with the risk of sporadic chordoma. We sequenced all T exons in 24 familial cases and 54 unaffected family members from eight chordoma families (three with T duplications), 103 sporadic cases, and 160 unrelated controls. We also measured T copy number variation in all sporadic cases. We confirmed the association between the previously reported variant rs2305089 and risk of familial [odds ratio (OR) = 2.6, 95 % confidence interval (CI) = 0.93, 7.25, P = 0.067] and sporadic chordoma (OR = 2.85, 95 % CI = 1.89, 4.29, P < 0.0001). We also identified a second common variant, rs1056048, that was strongly associated with chordoma in families (OR = 4.14, 95 % CI = 1.43, 11.92, P = 0.0086). Among sporadic cases, another common variant (rs3816300) was significantly associated with risk when jointly analyzed with rs2305089. The association with rs3816300 was significantly stronger in cases with early age onset. In addition, we identified three rare variants that were only observed among sporadic chordoma cases, all of which have potential functional relevance based on in silico predictions. Finally, we did not observe T duplication in any sporadic chordoma case. Our findings further highlight the importance of the T gene in the pathogenesis of both familial and sporadic chordoma and suggest a complex susceptibility related to T.
C1 [Kelley, Michael J.; Alcorta, David A.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27705 USA.
[Kelley, Michael J.] Durham Vet Affairs Med Ctr, Durham, NC 27705 USA.
[Shi, Jianxin; Ballew, Bari; Hyland, Paula L.; Li, Wen-Qing; Rotunno, Melissa; Mitchell, Jason; Bass, Sara; Roberson, David; Boland, Joseph; Cullen, Michael; He, Ji; Burdette, Laurie; Yeager, Meredith; Chanock, Stephen J.; Parry, Dilys M.; Goldstein, Alisa M.; Yang, Xiaohong R.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Liebsch, Norbert J.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Mitchell, Jason; Bass, Sara; Roberson, David; Boland, Joseph; Cullen, Michael; He, Ji; Burdette, Laurie; Yeager, Meredith] SAIC Frederick Inc, Canc Genom Res Lab, Bethesda, MD 20892 USA.
RP Yang, XHR (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
EM royang@mail.nih.gov
RI Li, Wenqing/N-2293-2014
OI Li, Wenqing/0000-0002-1283-4091
FU National Cancer Institute, Division of Cancer Epidemiology and Genetics,
National Institutes of Health; Department of Veterans Affairs, Veterans
Health Administration, Office of Research and Development, Biomedical
Laboratory Research and Development program; Chordoma Foundation
FX We thank Deborah Zametkin for her outstanding skills as a research
nurse; Drs. Gladys M. Glenn and Mary L. McMaster for their careful
clinical evaluations of patients and family members; Dr. Nicholas J.
Patronas for reviewing the MR images; Cancer Genomics Research
Laboratory for sequencing and bioinformatic analyses; and, especially,
the patients and their families for their participation. This work was
supported by the Intramural Research Program of the National Cancer
Institute, Division of Cancer Epidemiology and Genetics, National
Institutes of Health, and by the Department of Veterans Affairs,
Veterans Health Administration, Office of Research and Development,
Biomedical Laboratory Research and Development program, and a grant from
the Chordoma Foundation (M.J.K.).
NR 21
TC 10
Z9 10
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
EI 1432-1203
J9 HUM GENET
JI Hum. Genet.
PD OCT
PY 2014
VL 133
IS 10
BP 1289
EP 1297
DI 10.1007/s00439-014-1463-z
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA AP1KP
UT WOS:000341828900006
PM 24990759
ER
PT J
AU Rada, B
Park, JJ
Sil, P
Geiszt, M
Leto, TL
AF Rada, Balazs
Park, Jonathan J.
Sil, Payel
Geiszt, Miklos
Leto, Thomas L.
TI NLRP3 inflammasome activation and interleukin-1 beta release in
macrophages require calcium but are independent of calcium-activated
NADPH oxidases
SO INFLAMMATION RESEARCH
LA English
DT Article
DE Calcium; Duox; Macrophage; Inflammasome; NADPH oxidase
ID CHRONIC GRANULOMATOUS-DISEASE; NALP3 INFLAMMASOME; HYDROGEN-PEROXIDE;
OXIDATIVE STRESS; MOLECULAR-MECHANISMS; MYELOID CELLS; HOST-DEFENSE;
IL-1-BETA; SECRETION; DUOX1
AB We studied the involvement of calcium and calcium-activated NADPH oxidases in NLRP3 inflammasome activation and IL-1 beta release to better understand inflammasome signaling in macrophages.
Human volunteer blood donors were recruited to isolate monocytes to differentiate them into macrophages. Wild-type or DUOX1-deficient C57/B6 mice were used to prepare bone marrow-derived macrophages.
Murine or human macrophages were treated in vitro with NLRP3 inflammasome agonists (ATP, silica crystals) or calcium agonists (thapsigargin, ionomycin) in calcium-containing or calcium-free medium.
Intracellular calcium changes were followed by measuring FURA2-based fluorescence. Gene expression changes were measured by quantitative real-time PCR. Protein expression was assessed by western blotting. Enzymatic activity was measured by fluorescence caspase-1 activity assay. IL-1 beta release was determined by ELISA. ELISA data were analyzed by ANOVA and Tukey's post hoc test.
Our data show that calcium is essential for IL-1 beta release in human macrophages. Increases in cytosolic calcium alone lead to IL-1 beta secretion. Calcium removal blocks caspase-1 activation. Human macrophages express Duox1, a calcium-regulated NADPH oxidase that produces reactive oxygen species. However, Duox1-deficient murine macrophages show normal IL-1 beta release.
Human macrophage inflammasome activation and IL-1 beta secretion requires calcium but does not involve NADPH oxidases.
C1 [Rada, Balazs; Park, Jonathan J.; Leto, Thomas L.] NIAID, Lab Host Def, NIH, Rockville, MD 20852 USA.
[Rada, Balazs; Sil, Payel] Univ Georgia, Dept Infect Dis, Coll Vet Med, Athens, GA 30602 USA.
[Geiszt, Miklos] Semmelweis Univ, Fac Med, Dept Physiol, H-1085 Budapest, Hungary.
[Geiszt, Miklos] Semmelweis Univ, Lendulet Peroxidase Enzyme Res Grp, H-1085 Budapest, Hungary.
[Geiszt, Miklos] Hungarian Acad Sci, Budapest, Hungary.
RP Leto, TL (reprint author), NIAID, Lab Host Def, NIH, 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM radab@uga.edu; jon.j.park@gmail.com; payel@uga.edu;
geiszt.miklos@med.semmelweis-univ.hu; tleto@nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute of Allergy and Infectious Diseases
FX This study was supported by funds from the Intramural Research Program
of the National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 54
TC 9
Z9 9
U1 0
U2 12
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1023-3830
EI 1420-908X
J9 INFLAMM RES
JI Inflamm. Res.
PD OCT
PY 2014
VL 63
IS 10
BP 821
EP 830
DI 10.1007/s00011-014-0756-y
PG 10
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA AP2PO
UT WOS:000341916000003
PM 25048991
ER
PT J
AU Persoskie, A
Ferrer, RA
Klein, WMP
AF Persoskie, Alexander
Ferrer, Rebecca A.
Klein, William M. P.
TI Association of cancer worry and perceived risk with doctor avoidance: an
analysis of information avoidance in a nationally representative US
sample
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Information avoidance; Doctor avoidance; Risk perception; Worry; Cancer
ID FORCE RECOMMENDATION STATEMENT; BREAST-CANCER; HEALTH INFORMATION;
PERCEPTIONS; CARE; METAANALYSIS; BEHAVIORS; SERVICES; IMPACT;
VACCINATION
AB Fear of receiving bad news about one's health can lead people to avoid seeking out health information that, ironically, may be crucial for health maintenance. Using a nationally representative US sample, the present study examined whether perceived likelihood of developing cancer and worry about cancer were associated with reports of avoiding visits to one's doctor, in respondents under and over age 50. Cancer worry, but not perceived risk of cancer, predicted doctor avoidance in respondents aged 50 and older, whereas the opposite pattern held for respondents under age 50. Moreover, in respondents aged 50 and older, cancer worry and perceived cancer risk interacted such that cancer worry was linked to doctor avoidance only when respondents also perceived a high likelihood of cancer. The latter result is consistent with the notion that worry may motivate information seeking when people expect information to dispel worry and information avoidance when the information is seen as highly likely to confirm one's fears. Findings suggest a need for communication strategies that can influence worry and perceived risk differentially. Research should also assess the effectiveness of other behavioral strategies (e.g., automatic scheduling of appointments) as a means for reducing doctor avoidance.
C1 [Persoskie, Alexander; Ferrer, Rebecca A.; Klein, William M. P.] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Persoskie, A (reprint author), NCI, Behav Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Floor 3 East Tower, Bethesda, MD 20892 USA.
EM persoskieai@mail.nih.gov
NR 64
TC 11
Z9 11
U1 3
U2 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
EI 1573-3521
J9 J BEHAV MED
JI J. Behav. Med.
PD OCT
PY 2014
VL 37
IS 5
BP 977
EP 987
DI 10.1007/s10865-013-9537-2
PG 11
WC Psychology, Clinical
SC Psychology
GA AP1LB
UT WOS:000341830300015
PM 24072430
ER
PT J
AU Singh, NS
Habicht, KL
Dossou, KSS
Shimmo, R
Wainer, IW
Moaddel, R
AF Singh, N. S.
Habicht, K-L.
Dossou, K. S. S.
Shimmo, R.
Wainer, I. W.
Moaddel, R.
TI Multiple protein stationary phases: A review
SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL
AND LIFE SCIENCES
LA English
DT Review
DE Bioaffinity chromatography; G-protein coupled receptors; Ligand-gated
ion channels; ATP-binding cassette transporters
ID HUMAN SERUM-ALBUMIN; AFFINITY-CHROMATOGRAPHY COLUMN; IMMOBILIZED
P-GLYCOPROTEIN; OPEN-TUBULAR COLUMN; BENZODIAZEPINE BINDING;
STEREOCHEMICAL ASPECTS; COUPLED RECEPTORS; IDENTIFICATION; TECHNOLOGIES;
THYROXINE
AB Cellular membrane affinity chromatography stationary phases have been extensively used to characterize immobilized proteins and provide a direct measurement of multiple binding sites, including orthosteric and allosteric sites. This review will address the utilization of immobilized cellular and tissue fragments to characterize multiple transmembrane proteins co-immobilized onto a stationary phase. This approach will be illustrated by demonstrating that multiple transmembrane proteins were immobilized from cell lines and tissue fragments. In addition, the immobilization of individual compartments/organelles within a cell will be discussed and the changes in the proteins binding/kinetics based on their location. Published by Elsevier B.V.
C1 [Singh, N. S.; Dossou, K. S. S.; Wainer, I. W.; Moaddel, R.] NIA, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
[Habicht, K-L.; Shimmo, R.] Tallinn Univ, Dept Nat Sci, Inst Math & Nat Sci, EE-10120 Tallinn, Estonia.
RP Moaddel, R (reprint author), NIA, Bioanalyt & Drug Discovery Unit, Lab Clin Invest, NIH, Suite 100,8B131 Biomed Res Ctr,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM moaddelru@grc.nia.nih.gov
RI Singh, Nagendra/K-8966-2015
FU Intramural Research Program of the National Institute on Aging, NIH;
European Union through the European Regional Development Fund [TK114];
Estonian Ministry of Education and Research [SF0130010s12]; European
Social Fund's Doctoral Studies and Internationalisation Programme DoRa
FX This work was supported in part by the Intramural Research Program of
the National Institute on Aging, NIH. K-L.H. and R.S. were supported by
the European Union through the European Regional Development Fund
(Center of Excellence "Mesosystems: Theory and Applications", TK114) and
by the Estonian Ministry of Education and Research under targeted
financing No. SF0130010s12. K-L.H. was also supported by European Social
Fund's Doctoral Studies and Internationalisation Programme DoRa, which
is carried out by Foundation Archimedes.
NR 35
TC 5
Z9 5
U1 0
U2 36
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-0232
EI 1873-376X
J9 J CHROMATOGR B
JI J. Chromatogr. B
PD OCT 1
PY 2014
VL 968
SI SI
BP 64
EP 68
DI 10.1016/j.jchromb.2014.04.005
PG 5
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA AO7UX
UT WOS:000341559200009
PM 24780640
ER
PT J
AU Singh, N
Ravichandran, S
Spelman, K
Fugmann, SD
Moaddel, R
AF Singh, N.
Ravichandran, S.
Spelman, K.
Fugmann, S. D.
Moaddel, R.
TI The identification of a novel SIRT6 modulator from Trigonella
foenum-graecum using ligand fishing with protein coated magnetic beads
SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL
AND LIFE SCIENCES
LA English
DT Article
DE SIRT6; Fenugreek seed extract; Orientin; Ligand fishing; Magnetic beads
ID EXTRACTS; SEEDS; ACID; DEACETYLASE; DISEASE; GLUCOSE; RATS
AB SIRT6 is a histone deacetylase that has been proposed as a potential therapeutic target for metabolic disorders and the prevention of age-associated diseases. Thus the identification of compounds that modulate SIRT6 activity could be of great therapeutic importance. We have previously developed an H3K9 deacetylation guided assay with SIRT6 coated magnetic beads (SIRT6-MB). With the developed assay, we identified quercetin, naringenin and vitexin as SIRT6 inhibitors from T. foenum-graecum seed extract using a candidate approach. Currently, the predominant method for the identification of active compounds from a plant extract is carried out through a dereplication process. A novel targeted approach for the direct identification of active compounds from a complex matrix could save time and resources. Herein, we report the application of the SIRT6-MB for 'fishing' experiments utilizing T. foenum-graecum seed extract. In which orientin, and seventeen other compounds were identified as SIRT6 binders. This is the first use of this method for 'fishing' out active ligands from a botanical matrix, and sets the basis for the identification of active compounds from a complex matrix. Published by Elsevier B.V.
C1 [Singh, N.; Moaddel, R.] NIA, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
[Ravichandran, S.] Frederick Natl Lab Canc Res, Adv Biomed Comp Ctr, Informat Syst Program, Frederick, MD 21702 USA.
[Spelman, K.] Hlth Educ & Res Bot Med, Ashland, OR 97520 USA.
[Fugmann, S. D.] Chang Gung Univ, Dept Biomed Sci, Kwei Shan, Taiwan.
RP Moaddel, R (reprint author), NIA, Bioanalyt & Drug Discovery Unit, Lab Clin Investigat, NIH,Biomed Res Ctr, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM moaddelru@grc.nia.nih.gov
RI Singh, Nagendra/K-8966-2015
FU NIA Intramural Research Program; National Cancer Institute/National
Institutes of Health [HHSN261200800001E]
FX This work was supported in part by funds from the NIA Intramural
Research Program (RM), and from the National Cancer Institute/National
Institutes of Health contract no. HHSN261200800001E (SR). 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. There are no financial conflicts.
NR 28
TC 11
Z9 12
U1 2
U2 23
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-0232
EI 1873-376X
J9 J CHROMATOGR B
JI J. Chromatogr. B
PD OCT 1
PY 2014
VL 968
SI SI
BP 105
EP 111
DI 10.1016/j.jchromb.2014.03.016
PG 7
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA AO7UX
UT WOS:000341559200015
PM 24704183
ER
PT J
AU Martin, S
Wolters, PL
Baldwin, A
Roderick, MC
Toledo-Tamula, MA
Gillespie, A
Widemann, B
AF Martin, Staci
Wolters, Pamela L.
Baldwin, Andrea
Roderick, Marie Claire
Toledo-Tamula, Mary Anne
Gillespie, Andrea
Widemann, Brigitte
TI Attitudes About Internet Support Groups Among Adolescents and Young
Adults with Neurofibromatosis Type 1 and their Parents
SO JOURNAL OF GENETIC COUNSELING
LA English
DT Article
DE Neurofibromatosis Type 1; internet support groups; survey; social
support; youth; parents
ID SOCIAL SUPPORT; PLEXIFORM NEUROFIBROMAS; CHILDREN; DISEASE; HEALTH;
INDIVIDUALS; DEPRESSION; EPILEPSY; CANCER; LIFE
AB Youth with neurofibromatosis type 1 (NF1) have multiple, complex symptoms associated with physical, social-emotional, and cognitive difficulties. In addition, caring for a child with NF1 can be extremely challenging for parents. Since research with other chronic illness populations suggests that social support, including internet support groups (ISGs), can be beneficial, this survey study aimed to determine the attitudes and preferences of adolescents and young adults with NF1 and parents of a child with NF1 regarding ISGs. Thirty patients and 30 caregivers completed a 24-item survey about ISGs. Many patients and parents are not aware of any ISGs for NF1, but are interested in using one in the future for a variety of reasons, including to get answers to their questions about NF1, to find out about research studies, and to discuss problems and concerns about NF1. Specific concerns of interest include physical, social-emotional, and cognitive aspects of NF1. ISGs have potential as a social support intervention within the NF1 community. ISGs for the NF1 population should include patients with NF1 (or parents of children with NF1) as well as a health professional, and both chat rooms and discussion boards likely would be well-received.
C1 [Martin, Staci; Wolters, Pamela L.; Baldwin, Andrea; Roderick, Marie Claire; Gillespie, Andrea; Widemann, Brigitte] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Roderick, Marie Claire] Inst Psychol Sci, Arlington, VA USA.
[Toledo-Tamula, Mary Anne] SAIC Frederick Inc, Clin Res Directorate CMRP, Frederick Natl Lab Canc Res, Frederick, MD USA.
RP Martin, S (reprint author), NCI, Pediat Oncol Branch, Bldg 82,Room 107 9030 Old Georgetown Rd, Bethesda, MD 20892 USA.
EM martins@mail.nih.gov
FU National Institutes of Health, National Cancer Institute; National
Cancer Institute, National Institutes of Health [HHSN261200800001E]
FX The authors wish to extend their appreciation to the individuals who
participated in this survey study. This research was supported by the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute. In addition, 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.
NR 30
TC 0
Z9 0
U1 1
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1059-7700
EI 1573-3599
J9 J GENET COUNS
JI J. Genet. Couns.
PD OCT
PY 2014
VL 23
IS 5
BP 796
EP 804
DI 10.1007/s10897-014-9688-5
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA AP1OO
UT WOS:000341840500012
PM 24469442
ER
PT J
AU Schulden, JD
Painter, TM
Song, BW
Valverde, E
Borman, MA
Monroe-Spencer, K
Bautista, G
Saleheen, H
Voetsch, AC
Heffelfinger, JD
AF Schulden, Jeffrey D.
Painter, Thomas M.
Song, Binwei
Valverde, Eduardo
Borman, Mary Ann
Monroe-Spencer, Kyle
Bautista, Greg
Saleheen, Hassan
Voetsch, Andrew C.
Heffelfinger, James D.
TI HIV Testing Histories and Risk Factors Among Migrants and Recent
Immigrants Who Received Rapid HIV Testing from Three Community-Based
Organizations
SO JOURNAL OF IMMIGRANT AND MINORITY HEALTH
LA English
DT Article
DE HIV; STD; Migrants; Immigrants; Rapid HIV testing; HIV prevention
ID SEXUALLY-TRANSMITTED-DISEASES; INJECTION-DRUG USERS; MEXICAN MIGRANTS;
UNITED-STATES; DAY LABORERS; NORTH-CAROLINA; FOREIGN-BORN; SEX WORKERS;
CONDOM USE; INFECTION
AB Migrants and recent immigrants in the US constitute a large population that is vulnerable to HIV. From March 2005 to February 2007, three community-based organizations conducted rapid HIV testing among migrants in five states. Participants were asked to complete a survey on sociodemographics, HIV-risk behaviors, and HIV-testing histories with the aim of understanding factors associated with HIV testing. Among 5,247 persons tested, 6 (0.1 %) were HIV-positive. Among 3,135 persons who completed surveys, more than half had never been tested for HIV previously (59 %). Participants reported high levels of HIV-risk behaviors in the past year, including 2 or more sex partners (45 %), sex while high/drunk (30 %), and transactional sex (29 %). Multivariate analysis identified several factors independently associated with decreased likelihood of prior HIV testing, including poor spoken English. Continued efforts are needed to ensure that migrant populations have improved access to HIV testing and prevention services. Understanding factors associated with migrants' lack of previous HIV testing may help focus these efforts.
C1 [Schulden, Jeffrey D.] NIDA, NIH, Bethesda, MD 20892 USA.
[Painter, Thomas M.; Song, Binwei; Valverde, Eduardo; Voetsch, Andrew C.; Heffelfinger, James D.] Ctr Dis Control & Prevent CDC, Natl Ctr HIV AIDS Viral Hepatitis STD & TB Preven, Atlanta, GA USA.
[Borman, Mary Ann] United Migrant Opportun Serv, Milwaukee, WI USA.
[Monroe-Spencer, Kyle; Bautista, Greg] AIDGwinnett, Lawrenceville, GA USA.
[Saleheen, Hassan] Connecticut Childrens Med Ctr, Hartford, CT USA.
RP Schulden, JD (reprint author), NIDA, NIH, 6001 Execut Blvd,MSC 9589, Bethesda, MD 20892 USA.
EM schuldenj@nida.nih.gov
NR 71
TC 5
Z9 5
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1912
EI 1557-1920
J9 J IMMIGR MINOR HEALT
JI J. Immigr. Minor. Health
PD OCT
PY 2014
VL 16
IS 5
BP 798
EP 810
DI 10.1007/s10903-013-9811-y
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AO9PJ
UT WOS:000341687400004
PM 23512324
ER
PT J
AU Chung, HY
Gu, MG
Buehler, E
MacDonald, MR
Rice, CM
AF Chung, Hyo-Young
Gu, Meigang
Buehler, Eugen
MacDonald, Margaret R.
Rice, Charles M.
TI Seed Sequence-Matched Controls Reveal Limitations of Small Interfering
RNA Knockdown in Functional and Structural Studies of Hepatitis C Virus
NS5A-MOBKL1B Interaction
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ORGAN SIZE CONTROL; HIPPO PATHWAY; NS5A PROTEIN; CELL-CULTURE;
NONSTRUCTURAL PROTEIN; CRYSTAL-STRUCTURE; DEPENDENT MANNER; DOMAIN-II;
REPLICATION; GROWTH
AB Hepatitis C virus (HCV) is a widespread human pathogen causing liver cirrhosis and cancer. Similar to the case for other viruses, HCV depends on host and viral factors to complete its life cycle. We used proteomic and yeast two-hybrid approaches to elucidate host factors involved in HCV nonstructural protein NS5A function and found that MOBKL1B interacts with NS5A. Initial experiments with small interfering RNA (siRNA) knockdown suggesting a role in HCV replication led us to examine the interaction using biochemical and structural approaches. As revealed by a cocrystal structure of a core MOBKL1B-NS5A peptide complex at 1.95 angstrom, NS5A binds to a hydrophobic patch on the MOBKL1B surface. Biosensor binding assays identified a highly conserved, 18-amino-acid binding site in domain II of NS5A, which encompasses residues implicated in cyclophilin A (CypA)dependent HCV RNA replication. However, a CypA-independent HCV variant had reduced replication in MOBKL1B knockdown cells, even though its NS5A does not interact with MOBKL1B. These discordant results prompted more extensive studies of MOBKL1B gene knockdowns, which included additional siRNAs and specifically matched seed sequence siRNA controls. We found that reduced virus replication after treating cells with MOBKL1B siRNA was actually due to off-target inhibition, which indicated that the initial finding of virus replication dependence on the MOBKL1B-NS5A interaction was incorrect. Ultimately, using several approaches, we found no relationship of the MOBKL1B-NS5A interaction to virus replication. These findings collectively serve as a reminder to investigators and scientific reviewers of the pervasive impact of siRNA off-target effects on interpretation of biological data.
IMPORTANCE
Our study illustrates an underappreciated shortcoming of siRNA gene knockdown technology. We initially identified a cellular protein, MOBKL1B, as a binding partner with the NS5A protein of hepatitis C virus (HCV). MOBKL1B siRNA, but not irrelevant RNA, treatment was associated with both reduced virus replication and the absence of MOBKL1B. Believing that HCV replication depended on the MOBKL1B-NS5A interaction, we carried out structural and biochemical analyses. Unexpectedly, an HCV variant lacking the MOBKL1B-NS5A interaction could not replicate after cells were treated with MOBKL1B siRNA. By repeating the MOBKL1B siRNA knockdowns and including seed sequence-matched siRNA instead of irrelevant siRNA as a control, we found that the MOBKL1B siRNAs utilized had off-target inhibitory effects on virus replication. Collectively, our results suggest that stricter controls must be utilized in all RNA interference (RNAi)-mediated gene knockdown experiments to ensure sound conclusions and a reliable scientific knowledge database.
C1 [Chung, Hyo-Young; Gu, Meigang; MacDonald, Margaret R.; Rice, Charles M.] Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, New York, NY 10021 USA.
[Buehler, Eugen] Natl Ctr Adv Translat Sci, Div Preclin Innovat, NIH, Bethesda, MD USA.
RP Rice, CM (reprint author), Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, 1230 York Ave, New York, NY 10021 USA.
EM ricec@mail.rockefeller.edu
FU National Cancer Institute of the National Institutes of Health
[R01CA057973]; Greenberg Medical Research Institute; Starr Foundation;
Merck postdoctoral fellowship at the Rockefeller University
FX The research reported in this publication was supported by the National
Cancer Institute of the National Institutes of Health under award number
R01CA057973 (C.M.R.). Additional financial support was provided by the
Greenberg Medical Research Institute and the Starr Foundation (to
C.M.R). H.C. was supported in part by a Merck postdoctoral fellowship at
the Rockefeller University.
NR 48
TC 11
Z9 11
U1 0
U2 9
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 19
BP 11022
EP 11033
DI 10.1128/JVI.01582-14
PG 12
WC Virology
SC Virology
GA AP1ZX
UT WOS:000341872700003
PM 25031347
ER
PT J
AU Taylor, KG
Woods, TA
Winkler, CW
Carmody, AB
Peterson, KE
AF Taylor, Katherine G.
Woods, Tyson A.
Winkler, Clayton W.
Carmody, Aaron B.
Peterson, Karin E.
TI Age-Dependent Myeloid Dendritic Cell Responses Mediate Resistance to La
Crosse Virus-Induced Neurological Disease
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TOLL-LIKE RECEPTOR-3; ALPHAVIRUS REPLICATION; INNATE IMMUNITY;
INFECTIONS; SYSTEM; ENCEPHALITIS; ATTENUATION; MOLECULE; CHILDREN; MOUSE
AB La Crosse virus (LACV) is the major cause of pediatric viral encephalitis in the United States; however, the mechanisms responsible for age-related susceptibility in the pediatric population are not well understood. Our current studies in a mouse model of LACV infection indicated that differences in myeloid dendritic cell (mDC) responses between weanling and adult mice accounted for susceptibility to LACV-induced neurological disease. We found that type I interferon (IFN) responses were significantly stronger in adult than in weanling mice. Production of these IFNs required both endosomal Toll-like receptors (TLRs) and cytoplasmic RIG-I-like receptors (RLRs). Surprisingly, IFN expression was not dependent on plasmacytoid DCs (pDCs) but rather was dependent on mDCs, which were found in greater number and induced stronger IFN responses in adults than in weanlings. Inhibition of these IFN responses in adults resulted in susceptibility to LACV-induced neurological disease, whereas postinfection treatment with type I IFN provided protection in young mice. These studies provide a definitive mechanism for age-related susceptibility to LACV encephalitis, where mDCs in young mice are insufficiently activated to control peripheral virus replication, thereby allowing virus to persist and eventually cause central nervous system (CNS) disease.
IMPORTANCE
La Crosse virus (LACV) is the primary cause of pediatric viral encephalitis in the United States. Although the virus infects both adults and children, over 80% of the reported neurological disease cases are in children. To understand why LACV causes neurological disease primarily in young animals, we used a mouse model where weanling mice, but not adult mice, develop neurological disease following virus infection. We found that an early immune response cell type, myeloid dendritic cells, was critical for protection in adult animals and that these cells were reduced in young animals. Activation of these cells during virus infection or after treatment with type I interferon in young animals provided protection from LACV. Thus, this study demonstrates a reason for susceptibility to LACV infection in young animals and shows that early therapeutic treatment in young animals can prevent neurological disease.
C1 [Taylor, Katherine G.; Woods, Tyson A.; Winkler, Clayton W.; Carmody, Aaron B.; Peterson, Karin E.] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Peterson, KE (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
EM petersonka@niaid.nih.gov
RI Peterson, Karin/D-1492-2016
OI Peterson, Karin/0000-0003-4177-7249
FU Division of Intramural Research, National Institutes of Health, National
Institute of Allergy and Infectious Diseases
FX This work was supported by the Division of Intramural Research, National
Institutes of Health, National Institute of Allergy and Infectious
Diseases.
NR 38
TC 7
Z9 7
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 19
BP 11070
EP 11079
DI 10.1128/JVI.01866-14
PG 10
WC Virology
SC Virology
GA AP1ZX
UT WOS:000341872700007
PM 25008929
ER
PT J
AU Bhardwaj, N
Maldarelli, F
Mellors, J
Coffin, JM
AF Bhardwaj, Neeru
Maldarelli, Frank
Mellors, John
Coffin, John M.
TI HIV-1 Infection Leads to Increased Transcription of Human Endogenous
Retrovirus HERV-K (HML-2) Proviruses In Vivo but Not to Increased Virion
Production
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN BREAST-CANCER; SUPPRESSIVE ANTIRETROVIRAL THERAPY; T-CELL
RESPONSES; RHEUMATOID-ARTHRITIS; HIV-1-INFECTED INDIVIDUALS; INSERTIONAL
POLYMORPHISMS; IMMUNE ACTIVATION; RNA TITERS; EXPRESSION; IDENTIFICATION
AB Recent studies suggest that human endogenous retrovirus group K (HERV-K) provirus expression plays a role in the pathogenesis of HIV-1 infection. In particular, RNA from the HML-2 subgroup of HERV-K proviruses has been reported to be highly expressed at the cellular level and detectable in the plasma of HIV-1-infected patients, suggestive of virion production and, perhaps, replication. In this study, we developed an HML-2-specific quantitative-PCR assay that detects 51 of the 89 known HML-2 proviruses in the human genome. Plasma and peripheral blood mononuclear cells (PBMCs) from HIV-negative controls and HIV-1-infected patients were collected for analysis of HML-2 RNA expression. Contrary to previous reports, we did not detect high levels of HML-2 RNA in the plasma of HIV-1-infected patients, but we did observe a significant increase of HML-2 RNA in total PBMCs compared to HIV-negative controls. The level of HML-2 expression in PBMCs does not appear to be related to patient use of antiretrovirals or to HIV-1 plasma RNA, cellular RNA, or cellular DNA levels. To investigate the source of HML-2 RNA expression, patient PBMCs were sorted into CD3(+) CD4(+), CD3(+) CD8(+), CD3(+) CD14(+), and CD3(+) CD20(+) cell subsets and then analyzed for HML-2 RNA levels. No single cell subset was enriched for HML-2 RNA expression in HIV-1-infected patients, but there appears to be substantial variability in the level of HML-2 expression depending on the cell type.
IMPORTANCE
Here, we report that human endogenous retrovirus group K (HERV-K) (HML-2) proviruses are expressed at significantly higher levels in peripheral blood mononuclear cells (PBMCs) from patients with HIV-1 infection than in those from uninfected individuals. However, contrary to previous reports, this expression did not lead to detectable virions in the plasma of these patients. In addition, we found that HML-2 proviruses were expressed in multiple blood cell types from HIV-1-infected individuals, and the magnitude of HML-2 expression was not related to HIV-1 disease markers in this patient cohort. These findings may have implications for HML-2-based therapies targeting HIV-1 infection.
C1 [Bhardwaj, Neeru; Coffin, John M.] Tufts Univ, Sackler Sch Grad Biomed Sci, Grad Program Mol Microbiol, Boston, MA 02111 USA.
[Maldarelli, Frank] NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21701 USA.
[Mellors, John] Univ Pittsburgh, Div Infect Dis, Pittsburgh, PA USA.
RP Coffin, JM (reprint author), Tufts Univ, Sackler Sch Grad Biomed Sci, Grad Program Mol Microbiol, Boston, MA 02111 USA.
EM john.coffin@tufts.edu
FU National Cancer Institute [R37 CA 089441]; Leidos through the National
Cancer Institute [25XS119]; Howard Hughes Medical Institute (HHMI) Med
into Grad Scholar; HHMI through the Med into Grad Initiative; F. M.
Kirby Foundation
FX This work was supported by research grant R37 CA 089441 from the
National Cancer Institute and by Leidos contract 25XS119 to J.M. through
the National Cancer Institute. N.B. was a Howard Hughes Medical
Institute (HHMI) Med into Grad Scholar supported in part by a grant to
Tufts University from HHMI through the Med into Grad Initiative and the
recipient of a travel award from the Tufts/Brown/Life Span Center for
AIDS Research. J.M.C. was a Research Professor of the American Cancer
Society with support from the F. M. Kirby Foundation.
NR 70
TC 16
Z9 17
U1 0
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 19
BP 11108
EP 11120
DI 10.1128/JVI.01623-14
PG 13
WC Virology
SC Virology
GA AP1ZX
UT WOS:000341872700010
PM 25056891
ER
PT J
AU Erlandson, KJ
Cotter, CA
Charity, JC
Martens, C
Fischer, ER
Ricklefs, SM
Porcella, SF
Moss, B
AF Erlandson, Karl J.
Cotter, Catherine A.
Charity, James C.
Martens, Craig
Fischer, Elizabeth R.
Ricklefs, Stacy M.
Porcella, Stephen F.
Moss, Bernard
TI Duplication of the A17L Locus of Vaccinia Virus Provides an Alternate
Route to Rifampin Resistance
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MEMBRANE TOPOLOGY; EXTERNAL SCAFFOLD; ENVELOPE PROTEIN; GENE-PRODUCT;
DNA HELICASE; A19 PROTEIN; MORPHOGENESIS; PHOSPHORYLATION; BIOGENESIS;
PARTICLES
AB Specific gene duplications can enable double-stranded DNA viruses to adapt rapidly to environmental pressures despite the low mutation rate of their high-fidelity DNA polymerases. We report on the rapid positive selection of a novel vaccinia virus genomic duplication mutant in the presence of the assembly inhibitor rifampin. Until now, all known rifampin-resistant vaccinia virus isolates have contained missense mutations in the D13L gene, which encodes a capsid-like scaffold protein required for stabilizing membrane curvature during the early stage of virion assembly. Here we describe a second pathway to rifampin resistance involving A17, a membrane protein that binds and anchors D13 to the immature virion. After one round of selection, a rifampin-resistant virus that contained a genomic duplication in the A17L-A21L region was recovered. The mutant had both C-terminally truncated and full-length A17L open reading frames. Expression of the truncated A17 protein was retained when the virus was passaged in the presence of rifampin but was lost in the absence of the drug, suggesting that the duplication decreased general fitness. Both forms of A17 were bound to the virion membrane and associated with D13. Moreover, insertion of an additional truncated or inducible full-length A17L open reading frame into the genome of the wild-type virus was sufficient to confer rifampin resistance. In summary, this report contains the first evidence of an alternate mechanism for resistance of poxviruses to rifampin, indicates a direct relationship between A17 levels and the resistance phenotype, and provides further evidence of the ability of double-stranded DNA viruses to acquire drug resistance through gene duplication.
IMPORTANCE
The present study provides the first evidence of a new mechanism of resistance of a poxvirus to the antiviral drug rifampin. In addition, it affirms the importance of the interaction between the D13 scaffold protein and the A17 membrane protein for assembly of virus particles. Resistance to rifampin was linked to a partial duplication of the gene encoding the A17 protein, similar to the resistance to hydroxyurea enabled by duplication of the gene encoding the small subunit of ribonucleotide reductase and of the K3L gene to allow adaptation to the antiviral action of protein kinase R. Gene duplication may provide a way for poxviruses and other DNA viruses with high-fidelity DNA polymerases to adjust rapidly to changes in the environment.
C1 [Erlandson, Karl J.; Cotter, Catherine A.; Charity, James C.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Martens, Craig; Fischer, Elizabeth R.; Ricklefs, Stacy M.; Porcella, Stephen F.] NIAID, Res Technol Sect, Rocky Mt Labs, NIH, Hamilton, MT USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases; National Institute of General Medical Sciences
FX This research was supported by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases. K.J.E. received
support from a PRAT fellowship provided by the National Institute of
General Medical Sciences.
NR 40
TC 4
Z9 4
U1 0
U2 23
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2014
VL 88
IS 19
BP 11576
EP 11585
DI 10.1128/JVI.00618-14
PG 10
WC Virology
SC Virology
GA AP1ZX
UT WOS:000341872700048
PM 25078687
ER
PT J
AU Pergoli, L
Favero, C
Pfeiffer, RM
Tarantini, L
Calista, D
Cavalleri, T
Angelici, L
Consonni, D
Bertazzi, PA
Pesatori, AC
Landi, MT
Bollati, V
AF Pergoli, Laura
Favero, Chiara
Pfeiffer, Ruth M.
Tarantini, Letizia
Calista, Donato
Cavalleri, Tommaso
Angelici, Laura
Consonni, Dario
Bertazzi, Pier A.
Pesatori, Angela C.
Landi, Maria T.
Bollati, Valentina
TI Blood DNA methylation, nevi number, and the risk of melanoma
SO MELANOMA RESEARCH
LA English
DT Article
DE cutaneous malignant melanoma; methylation; nevi; pyrosequencing
ID CUTANEOUS MALIGNANT-MELANOMA; GENOME-WIDE ASSOCIATION; TERT PROMOTER
MUTATIONS; POPULATION-BASED SAMPLE; GERMLINE EPIMUTATION; FAMILIAL
MELANOMA; SPORADIC MELANOMA; PERIPHERAL-BLOOD; DYSPLASTIC NEVI; PRONE
FAMILIES
AB Germline mutations determining increased cutaneous malignant melanoma (CMM) risk have been identified in familial and sporadic CMM cases, but they account only for a small proportion of CMM cases. Recent evidence suggests that germline epimutations (e.g. DNA methylation alterations), which can be inherited similarly to genomic mutations and can be detected in normal body cells (including blood), might increase susceptibility to cancer. The aim of the study was to identify germline epimutations of genes that were found to be mutated in familial CMM (p16(INK4a), p14(ARF), CDK4, MC1R, hTERT), immune and inflammatory genes (ICAM-1, TNF alpha), DNA mismatch repair gene (MLH1), and repetitive elements (ALU, LINE-1, HERV-w). We measured DNA methylation using bisulfite pyrosequencing in peripheral blood mononuclear cells from 167 CMM cases and 164 sex-matched and age-matched controls. We used multivariable logistic regression models to evaluate the association between methylation levels and CMM status or presence of dysplastic nevi. We found an association between the risk of CMM and peripheral blood mononuclear cell methylation levels of TNF alpha [odds ratio (OR) = 1.11, 95% confidence interval (CI) = 1.03-1.18], CDK4 (OR = 0.76, 95% CI = 0.64-0.91), and MLH1 (OR = 1.12, 95% CI = 1.02-1.22). In control participants, the risk of developing dysplastic nevi was associated with methylation levels of TNF alpha (OR = 0.81, 95% CI = 0.69-0.95), hTERT (OR = 0.90, 95% CI = 0.82-0.99), and ALU (OR = 1.56, 95% CI = 1.02-2.39). Epimutations in CMM susceptibility genes and in genes involved in response to oxidative damage are associated with the risk of developing CMM or dysplastic nevi. Further studies measuring methylation levels of these genes in prospectively collected samples are warranted to further elucidate their role in the development and progression of CMM. (C) 2014 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Pergoli, Laura; Favero, Chiara; Tarantini, Letizia; Cavalleri, Tommaso; Angelici, Laura; Bertazzi, Pier A.; Pesatori, Angela C.; Bollati, Valentina] Univ Milan, Dept Clin Sci & Community Hlth, Ctr Mol & Genet Epidemiol, I-20122 Milan, Italy.
[Consonni, Dario; Bertazzi, Pier A.; Pesatori, Angela C.; Bollati, Valentina] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Epidemiol Unit, Milan, Italy.
[Calista, Donato] Bufalini Hosp, Dermatol Unit, Cesena, Italy.
[Pfeiffer, Ruth M.; Landi, Maria T.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Bollati, V (reprint author), Univ Milan, Dept Clin Sci & Community Hlth, Ctr Mol & Genet Epidemiol, Via San Barnaba 8, I-20122 Milan, Italy.
EM valentina.bollati@unimi.it
RI Consonni, Dario/K-7943-2016; bertazzi, pietro alberto/D-5039-2017;
OI Consonni, Dario/0000-0002-8935-3843; bertazzi, pietro
alberto/0000-0003-3475-2449; pesatori, angela/0000-0002-0261-3252;
Bollati, Valentina/0000-0002-0370-9598
FU Associazione Italiana Ricerca sul Cancro (AIRC) [MFAG 10361]
FX This work was supported by Associazione Italiana Ricerca sul Cancro
(AIRC) (MFAG 10361) to Valentina Bollati.
NR 48
TC 6
Z9 6
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0960-8931
EI 1473-5636
J9 MELANOMA RES
JI Melanoma Res.
PD OCT
PY 2014
VL 24
IS 5
BP 480
EP 487
DI 10.1097/CMR.0000000000000112
PG 8
WC Oncology; Dermatology; Medicine, Research & Experimental
SC Oncology; Dermatology; Research & Experimental Medicine
GA AP3MG
UT WOS:000341979500010
PM 25026000
ER
PT J
AU Yuan, S
Tang, H
Xing, JY
Fan, XQ
Cai, XY
Li, Q
Han, P
Luo, YH
Zhang, ZJ
Jiang, B
Dou, YL
Gorospe, M
Wang, WG
AF Yuan, Shuai
Tang, Hao
Xing, Junyue
Fan, Xiuqin
Cai, Xiaoyu
Li, Qiu
Han, Pei
Luo, Yuhong
Zhang, Zhuojun
Jiang, Bin
Dou, Yali
Gorospe, Myriam
Wang, Wengong
TI Methylation by NSun2 Represses the Levels and Function of MicroRNA 125b
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID METHYLTRANSFERASE MISU NSUN2; RIBOSOMAL-RNA METHYLATIONS;
PIWI-INTERACTING RNAS; MESSENGER-RNA; ESCHERICHIA-COLI; NONCODING RNA;
EXPRESSION; STABILITY; BIOGENESIS; INITIATION
AB Methylation is a prevalent posttranscriptional modification of RNAs. However, whether mammalian microRNAs are methylated is unknown. Here, we show that the tRNA methyltransferase NSun2 methylates primary (pri-miR-125b), precursor (pre-miR-125b), and mature microRNA 125b (miR-125b) in vitro and in vivo. Methylation by NSun2 inhibits the processing of pri-miR-125b2 into pre-miR-125b2, decreases the cleavage of pre-miR-125b2 into miR-125, and attenuates the recruitment of RISC by miR-125, thereby repressing the function of miR-125b in silencing gene expression. Our results highlight the impact of miR-125b function via methylation by NSun2.
C1 [Yuan, Shuai; Tang, Hao; Xing, Junyue; Fan, Xiuqin; Cai, Xiaoyu; Li, Qiu; Han, Pei; Zhang, Zhuojun; Jiang, Bin; Wang, Wengong] Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Beijing 100871, Peoples R China.
[Luo, Yuhong] Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China.
[Dou, Yali] Univ Michigan, Dept Pathol & Biol Chem, Ann Arbor, MI 48109 USA.
[Gorospe, Myriam] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
RP Wang, WG (reprint author), Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Beijing 100871, Peoples R China.
EM wwg@bjmu.edu.cn
FU National Science Foundation of China [81230008, 91339114]; Ministry of
Education of People's Republic of China (111 project) [B07001]; National
Institute on Aging-IRP, National Institutes of Health
FX This work was supported by grants 81230008 and 91339114 from the
National Science Foundation of China and grant B07001 (111 project) from
the Ministry of Education of People's Republic of China. M.G. was
supported by the National Institute on Aging-IRP, National Institutes of
Health.
NR 36
TC 18
Z9 20
U1 0
U2 11
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD OCT
PY 2014
VL 34
IS 19
BP 3630
EP 3641
DI 10.1128/MCB.00243
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AP1UM
UT WOS:000341857100007
PM 25047833
ER
PT J
AU Jin, QH
Wang, CC
Kuang, XH
Feng, XS
Sartorelli, V
Ying, H
Ge, K
Dent, SYR
AF Jin, Qihuang
Wang, Chaochen
Kuang, Xianghong
Feng, Xuesong
Sartorelli, Vittorio
Ying, Hao
Ge, Kai
Dent, Sharon Y. R.
TI Gcn5 and PCAF Regulate PPAR gamma and Prdm16 Expression To Facilitate
Brown Adipogenesis
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID ADIPOCYTE DIFFERENTIATION; TRANSCRIPTIONAL CONTROL; BINDING PROTEIN;
CODING REGIONS; IN-VIVO; FAT; ACETYLATION; SWITCH; ACETYLTRANSFERASES;
RECRUITMENT
AB The acetyltransferase Gcn5 is critical for embryogenesis and shows partial functional redundancy with its homolog PCAF. However, the tissue-and cell lineage-specific functions of Gcn5 and PCAF are still not well defined. Here we probe the functions of Gcn5 and PCAF in adipogenesis. We found that the double knockout (DKO) of Gcn5/PCAF inhibits expression of the master adipogenic transcription factor gene PPAR gamma, thereby preventing adipocyte differentiation. The adipogenesis defects in Gcn5/PCAF DKO cells are rescued by ectopic expression of peroxisome proliferator-activated receptor gamma (PPAR gamma), suggesting Gcn5/PCAF act upstream of PPAR gamma to facilitate adipogenesis. The requirement of Gcn5/PCAF for PPAR gamma expression was unexpectedly bypassed by prolonged treatment with an adipogenic inducer, 3-isobutyl-1-methylxanthine (IBMX). However, neither PPAR gamma ectopic expression nor prolonged IBMX treatment rescued defects in Prdm16 expression in DKO cells, indicating that Gcn5/PCAF are essential for normal Prdm16 expression. Gcn5/PCAF regulate PPAR gamma and Prdm16 expression at different steps in the transcription process, facilitating RNA polymerase II recruitment to Prdm16 and elongation of PPAR gamma transcripts. Overall, our study reveals that Gcn5/PCAF facilitate adipogenesis through regulation of PPAR gamma expression and regulate brown adipogenesis by influencing Prdm16 expression.
C1 [Jin, Qihuang; Kuang, Xianghong; Dent, Sharon Y. R.] Univ Texas MD Anderson Canc Ctr, Ctr Canc Epigenet, Dept Mol Carcinogenesis, Smithville, TX USA.
[Jin, Qihuang; Wang, Chaochen; Ge, Kai] NIDDK, Lab Endocrinol & Receptor Biol, NIH, Bethesda, MD 20892 USA.
[Feng, Xuesong; Sartorelli, Vittorio] NIAMSD, Lab Muscle Stem Cells & Gene Regulat, NIH, Bethesda, MD 20892 USA.
[Ying, Hao] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Shanghai, Peoples R China.
RP Ge, K (reprint author), NIDDK, Lab Endocrinol & Receptor Biol, NIH, Bethesda, MD 20892 USA.
EM kaig@niddk.nih.gov; sroth@mdanderson.org
FU National Cancer Institute [5 P30 CA16672-32]; NIGMS/NIH [R01 067718];
Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases, National Institutes of Health; CAS/SAFEA
International Partnership Program for Creative Research Teams
FX Mouse experiments were facilitated by the Science Park Research Animal
facility, which is partly supported by a Cancer Center Support (CORE)
grant (5 P30 CA16672-32, DePinho as the principal investigator) from the
National Cancer Institute. This study was supported by NIGMS/NIH R01
067718 to S.Y.R.D.; by the Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health, to K.G.; and by CAS/SAFEA International
Partnership Program for Creative Research Teams to H.Y.
NR 39
TC 10
Z9 11
U1 1
U2 14
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD OCT
PY 2014
VL 34
IS 19
BP 3746
EP 3753
DI 10.1128/MCB.00622-14
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AP1UM
UT WOS:000341857100015
PM 25071153
ER
PT J
AU Colt, JS
Friesen, MC
Stewart, PA
Donguk, P
Johnson, A
Schwenn, M
Karagas, MR
Armenti, K
Waddell, R
Verrill, C
Ward, MH
Freeman, LEB
Moore, LE
Koutros, S
Baris, D
Silverman, DT
AF Colt, Joanne S.
Friesen, Melissa C.
Stewart, Patricia A.
Donguk, Park
Johnson, Alison
Schwenn, Molly
Karagas, Margaret R.
Armenti, Karla
Waddell, Richard
Verrill, Castine
Ward, Mary H.
Freeman, Laura E. Beane
Moore, Lee E.
Koutros, Stella
Baris, Dalsu
Silverman, Debra T.
TI A case-control study of occupational exposure to metalworking fluids and
bladder cancer risk among men
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID POLYCYCLIC AROMATIC-HYDROCARBONS; LOWER URINARY-TRACT; MORTALITY;
WORKERS; TOBACCO; SMOKING; COHORT; STATES; OILS
AB Objectives Metalworking has been associated with an excess risk of bladder cancer in over 20 studies. Metalworking fluids (MWFs) are suspected as the responsible exposure, but epidemiological data are limited. We investigated this association among men in the New England Bladder Cancer Study using state-of-the-art, quantitative exposure assessment methods.
Methods Cases (n=895) and population controls (n=1031) provided occupational histories during personal interviews. For selected jobs, exposure-oriented modules were administered to collect information on use of three MWF types: (1) straight (mineral oil, additives), (2) soluble (mineral oil, water, additives) and (3) synthetic (water, organics, additives) or semisynthetic (hybrid of soluble and synthetic). We computed ORs and 95% CIs relating bladder cancer risk to a variety of exposure metrics, adjusting for smoking and other factors. Non-metalworkers who had held jobs with possible exposure to mineral oil were analysed separately.
Results Bladder cancer risk was elevated among men who reported using straight MWFs (OR=1.7, 95% CI 1.1 to 2.8); risk increased monotonically with increasing cumulative exposure (p=0.041). Use of soluble MWFs was associated with a 50% increased risk (95% CI 0.96 to 2.5). ORs were non-significantly elevated for synthetic/semisynthetic MWFs based on a small number of exposed men. Non-metalworkers holding jobs with possible exposure to mineral oil had a 40% increased risk (95% CI 1.1 to 1.8).
Conclusions Exposure to straight MWFs was associated with a significantly increased bladder cancer risk, as was employment in non-metalworking jobs with possible exposure to mineral oil. These findings strengthen prior evidence for mineral oil as a bladder carcinogen.
C1 [Colt, Joanne S.; Friesen, Melissa C.; Stewart, Patricia A.; Ward, Mary H.; Freeman, Laura E. Beane; Moore, Lee E.; Koutros, Stella; Baris, Dalsu; Silverman, Debra T.] NCI, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Stewart, Patricia A.] Stewart Exposure Assessments LLC, Arlington, VA USA.
[Donguk, Park] Korea Natl Open Univ, Seoul, South Korea.
[Johnson, Alison] Vermont Canc Registry, Burlington, VT USA.
[Schwenn, Molly; Verrill, Castine] Maine Canc Registry, Augusta, ME USA.
[Karagas, Margaret R.; Waddell, Richard] Geisel Sch Med Dartmouth, Hanover, NH USA.
[Armenti, Karla] New Hampshire Dept Hlth & Human Serv, Concord, NH 03301 USA.
RP Colt, JS (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E140, Bethesda, MD 20892 USA.
EM coltj@mail.nih.gov
RI Friesen, Melissa/A-5362-2009
FU National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics [N02-CP-01037]
FX This study was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics (contract number N02-CP-01037).
NR 47
TC 9
Z9 11
U1 4
U2 10
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1351-0711
EI 1470-7926
J9 OCCUP ENVIRON MED
JI Occup. Environ. Med.
PD OCT
PY 2014
VL 71
IS 10
BP 667
EP 674
DI 10.1136/oemed-2013-102056
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AP1SC
UT WOS:000341850500003
PM 25201311
ER
PT J
AU Fargo, KN
Aisen, P
Albert, M
Au, R
Corrada, MM
DeKosky, S
Drachman, D
Fillit, H
Gitlin, L
Haas, M
Herrup, K
Kawas, C
Khachaturian, AS
Khachaturian, ZS
Klunk, W
Knopman, D
Kukull, WA
Lamb, B
Logsdon, RG
Maruff, P
Mesulam, M
Mobley, W
Mohs, R
Morgan, D
Nixon, RA
Paul, S
Petersen, R
Plassman, B
Potter, W
Reiman, E
Reisberg, B
Sano, M
Schindler, R
Schneider, LS
Snyder, PJ
Sperling, RA
Yaffe, K
Bain, LJ
Thies, WH
Carrillo, MC
AF Fargo, Keith N.
Aisen, Paul
Albert, Marilyn
Au, Rhoda
Corrada, Maria M.
DeKosky, Steven
Drachman, David
Fillit, Howard
Gitlin, Laura
Haas, Magali
Herrup, Karl
Kawas, Claudia
Khachaturian, Ara S.
Khachaturian, Zaven S.
Klunk, William
Knopman, David
Kukull, Walter A.
Lamb, Bruce
Logsdon, Rebecca G.
Maruff, Paul
Mesulam, Marsel
Mobley, William
Mohs, Richard
Morgan, David
Nixon, Ralph A.
Paul, Steven
Petersen, Ronald
Plassman, Brenda
Potter, William
Reiman, Eric
Reisberg, Barry
Sano, Mary
Schindler, Rachel
Schneider, Lon S.
Snyder, Peter J.
Sperling, Reisa A.
Yaffe, Kristine
Bain, Lisa J.
Thies, William H.
Carrillo, Maria C.
CA Alzheimer's Assoc Natl Plan
TI 2014 Report on the Milestones for the US National Plan to Address
Alzheimer's Disease
SO ALZHEIMERS & DEMENTIA
LA English
DT Editorial Material
DE Policy; National Plan to Address Alzheimer's Disease; Milestones
ID AFRICAN-AMERICANS; HYPOTHETICAL MODEL; DYNAMIC BIOMARKERS;
DRUG-DEVELOPMENT; CLINICAL-TRIALS; DEMENTIA; RECRUITMENT; PREVALENCE;
CHALLENGES; DIAGNOSIS
AB With increasing numbers of people with Alzheimer's and other dementias across the globe, many countries have developed national plans to deal with the resulting challenges. In the United States, the National Alzheimer's Project Act, signed into law in 2011, required the creation of such a plan with annual updates thereafter. Pursuant to this, the US Department of Health and Human Services (HHS) released the National Plan to Address Alzheimer's Disease in 2012, including an ambitious research goal of preventing and effectively treating Alzheimer's disease by 2025. To guide investments, activities, and the measurement of progress toward achieving this 2025 goal, in its first annual plan update (2013) HHS also incorporated into the plan a set of short, medium and long-term milestones. HHS further committed to updating these milestones on an ongoing basis to account for progress and setbacks, and emerging opportunities and obstacles. To assist HHS as it updates these milestones, the Alzheimer's Association convened a National Plan Milestone Workgroup consisting of scientific experts representing all areas of Alzheimer's and dementia research. The workgroup evaluated each milestone and made recommendations to ensure that they collectively constitute an adequate work plan for reaching the goal of preventing and effectively treating Alzheimer's by 2025. This report presents these Workgroup recommendations. (C) 2014 The Alzheimer's Association.
C1 [Fargo, Keith N.; Thies, William H.; Carrillo, Maria C.] Alzheimers Assoc, Div Med & Sci Relat, Chicago, IL 60631 USA.
[Aisen, Paul; Mobley, William] Univ Calif San Diego, Sch Med, Dept Neurosci, San Diego, CA 92103 USA.
[Albert, Marilyn] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
[Au, Rhoda] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Au, Rhoda] Boston Univ, Sch Med, Framingham Heart Study, Boston, MA 02118 USA.
[Corrada, Maria M.] Univ Calif Irvine, Dept Neurol, Irvine, CA 92717 USA.
[Corrada, Maria M.] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
[DeKosky, Steven] Univ Virginia, Dept Neurol, Charlottesville, VA USA.
[DeKosky, Steven] Univ Pittsburgh, Dept Radiol, Pittsburgh, PA 15260 USA.
[DeKosky, Steven] Univ Pittsburgh, Dept Neurol, Pittsburgh, PA 15260 USA.
[Drachman, David] Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA USA.
[Fillit, Howard] Icahn Sch Med Mt Sinai, Dept Geriatr & Palliat Med, Alzheimers Drug Discovery Fdn, New York, NY 10029 USA.
[Fillit, Howard] Icahn Sch Med Mt Sinai, Dept Neurosci, New York, NY 10029 USA.
Johns Hopkins Univ, Dept Community Publ Hlth, Baltimore, MD USA.
[Gitlin, Laura] Johns Hopkins Univ, Dept Psychiat, Baltimore, MD USA.
[Haas, Magali] Orion Bionetworks, Cambridge, MA USA.
[Herrup, Karl] Hong Kong Univ Sci & Technol, Div Life Sci, Kowloon, Hong Kong, Peoples R China.
[Herrup, Karl] Hong Kong Univ Sci & Technol, State Key Lab Mol Neurosci, Kowloon, Hong Kong, Peoples R China.
[Kawas, Claudia] Univ Calif Irvine, Dept Neurobiol & Behav, Dept Neurol, Irvine, CA USA.
[Kawas, Claudia] Univ Calif Irvine, Inst Memory Impairments & Neurol Disorders, Irvine, CA USA.
[Khachaturian, Ara S.] Natl Biomed Res Eth Council, Rockville, MD USA.
[Khachaturian, Zaven S.] PAD2020, Rockville, MD USA.
[Klunk, William] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Knopman, David; Petersen, Ronald] Mayo Clin, Coll Med, Alzheimers Dis Res Ctr, Dept Neurol, Rochester, MN USA.
[Kukull, Walter A.] Univ Washington, NACC, Seattle, WA 98195 USA.
[Kukull, Walter A.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Lamb, Bruce] Cleveland Clin, Lerner Res Inst, Dept Neurosci, Cleveland, OH 44106 USA.
[Logsdon, Rebecca G.] Univ Washington, Dept Psychosocial & Community Hlth, Seattle, WA 98195 USA.
[Maruff, Paul] Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Melbourne, Vic, Australia.
[Maruff, Paul] CogState Ltd, Melbourne, Vic, Australia.
[Mesulam, Marsel] Northwestern Univ, Feinberg Sch Med, Dept Neurol, Chicago, IL 60611 USA.
[Mesulam, Marsel] Northwestern Univ, Feinberg Sch Med, Alzheimers Dis Ctr, Chicago, IL 60611 USA.
[Mohs, Richard] Eli Lilly & Co, Neurosci Early Clin Dev, Indianapolis, IN 46285 USA.
[Morgan, David] Univ S Florida, Byrd Alzheimers Inst, Tampa, FL USA.
[Nixon, Ralph A.] NYU, Dept Psychiat, Langone Med Ctr, New York, NY 10016 USA.
[Nixon, Ralph A.] NYU, Dept Cell Biol, Langone Med Ctr, New York, NY 10016 USA.
[Nixon, Ralph A.] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA.
[Paul, Steven] Fdn Natl Inst Hlth, Bethesda, MD USA.
[Plassman, Brenda] Duke Univ, Dept Psychiat & Behav Sci, Durham, NC USA.
[Potter, William] Fdn Natl Inst Hlth, Neuroscience Steering Comm Biomarkers Consortium, Phoenix, AZ USA.
[Reiman, Eric] Univ Arizona, Coll Med, Banner Alzheimers Inst, Phoenix, AZ USA.
[Reiman, Eric] Univ Arizona, Coll Med, Dept Psychiat, Phoenix, AZ USA.
[Reisberg, Barry] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Reisberg, Barry] NYU, Sch Med, Alzheimers Dis Res Ctr, New York, NY USA.
[Schindler, Rachel] Pfizer Inc, New York, NY USA.
[Schneider, Lon S.] Univ So Calif, Dept Psychiat & Behav Sci, Los Angeles, CA USA.
[Schneider, Lon S.] Univ So Calif, Keck Sch Med, Dept Neurol, Los Angeles, CA 90033 USA.
[Schneider, Lon S.] Univ So Calif, Leonard Davis Sch Gerontol, Los Angeles, CA USA.
[Snyder, Peter J.] Brown Univ, Alpert Med Sch, Dept Neurol, Providence, RI 02912 USA.
[Snyder, Peter J.] Rhode Isl Hosp, Dept Neurol, Providence, RI USA.
[Sperling, Reisa A.] Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Sperling, Reisa A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Yaffe, Kristine] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Carrillo, MC (reprint author), Alzheimers Assoc, Div Med & Sci Relat, Chicago, IL 60631 USA.
EM mcarrillo@alz.org
OI Reisberg, Barry/0000-0002-9104-7423; Kukull, Walter/0000-0001-8761-9014;
corrada, maria/0000-0002-8168-8593; Maruff, Paul/0000-0002-6947-9537
NR 48
TC 14
Z9 14
U1 4
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1552-5260
EI 1552-5279
J9 ALZHEIMERS DEMENT
JI Alzheimers. Dement.
PD OCT
PY 2014
VL 10
IS 5
SU 1
BP S430
EP S452
DI 10.1016/j.jalz.2014.08.103
PG 23
WC Clinical Neurology
SC Neurosciences & Neurology
GA CZ0WW
UT WOS:000366828100023
ER
PT J
AU Lahiri, DK
Maloney, B
Long, JM
Greig, NH
AF Lahiri, Debomoy K.
Maloney, Bryan
Long, Justin M.
Greig, Nigel H.
TI Lessons from a BACE1 inhibitor trial: Off-site but not off base
SO ALZHEIMERS & DEMENTIA
LA English
DT Article
DE Aging; Animal model; Brain disorder; CNS; Dementia; Demyelination; Drug
trial; Liver damage; Human studies; Melatonin; Neuronal death;
Sialylation; Secretase; Side effects; ROS
ID INDUCED LIVER-INJURY; AMYLOID PRECURSOR PROTEIN; ALZHEIMERS
BETA-SECRETASE; LEARN MODEL; IN-VIVO; DISEASE; GENE; CLEAVAGE; MICE;
MECHANISMS
AB Alzheimer's disease (AD) is characterized by formation of neuritic plaque primarily composed of a small filamentous protein called amyloid-beta peptide (A beta). The rate-limiting step in the production of Ab is the processing of A beta precursor protein (APP) by beta-site APP-cleaving enzyme (BACE1). Hence, BACE1 activity plausibly plays a rate-limiting role in the generation of potentially toxic Ab within brain and the development of AD, thereby making it an interesting drug target. A phase II trial of the promising LY2886721 inhibitor of BACE1 was suspended in June 2013 by Eli Lilly and Co., due to possible liver toxicity. This outcome was apparently a surprise to the study's team, particularly since BACE1 knockout mice and mice treated with the drug did not show such liver toxicity. Lilly proposed that the problem was not due to LY2886721 anti-BACE1 activity. We offer an alternative hypothesis, whereby anti-BACE1 activity may induce apparent hepatotoxicity through inhibiting BACE1's processing of beta-galactoside alpha-2,6-sialyltransferase I (STGal6 I). In knockout mice, paralogues, such as BACE2 or cathepsin D, could partially compensate. Furthermore, the short duration of animal studies and short lifespan of study animals could mask effects that would require several decades to accumulate in humans. Inhibition of hepatic BACE1 activity in middle-aged humans would produce effects not detectable in mice. We present a testable model to explain the off-target effects of LY2886721 and highlight more broadly that so-called off-target drug effects might actually represent off-site effects that are not necessarily off-target. Consideration of this concept in forthcoming drug design, screening, and testing programs may prevent such failures in the future. (C) 2014 The Alzheimer's Association. All rights reserved.
C1 [Lahiri, Debomoy K.; Maloney, Bryan; Long, Justin M.] Indiana Univ Sch Med, Inst Psychiat Res, Dept Psychiat, Mol Neurogenet Lab, Indianapolis, IN 46202 USA.
[Lahiri, Debomoy K.] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Greig, Nigel H.] NIA, Lab Translat Gerontol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Lahiri, DK (reprint author), Indiana Univ Sch Med, Inst Psychiat Res, Dept Psychiat, Mol Neurogenet Lab, Indianapolis, IN 46202 USA.
EM dlahiri@iupui.edu
RI Maloney, Bryan/C-4924-2011
OI Maloney, Bryan/0000-0003-2364-9649
FU Alzheimer's Association (Zenith Award and IIRG); National Institutes of
Health [AG18379, AG18884, AG042804]; Intramural Research Program of the
National Institute on Aging, NIH
FX The authors appreciate grant support from the Alzheimer's Association
(Zenith Award and IIRG) and from the National Institutes of Health
(Grants AG18379, and AG042804) to D.K.L. N.H.G. is supported by the
Intramural Research Program of the National Institute on Aging, NIH.
NR 61
TC 16
Z9 16
U1 3
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1552-5260
EI 1552-5279
J9 ALZHEIMERS DEMENT
JI Alzheimers. Dement.
PD OCT
PY 2014
VL 10
IS 5
SU 1
BP S411
EP S419
DI 10.1016/j.jalz.2013.11.004
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA CZ0WW
UT WOS:000366828100020
PM 24530026
ER
PT J
AU Chisari, C
Fanciullacci, C
Lamola, G
Rossi, B
Cohen, LG
AF Chisari, C.
Fanciullacci, C.
Lamola, G.
Rossi, B.
Cohen, L. G.
TI NIBS-driven brain plasticity
SO ARCHIVES ITALIENNES DE BIOLOGIE
LA English
DT Article
DE Plasticity; Non-invasive brain stimulation (NIBS); Neuromodulation;
Transcranial magnetic stimulation (TMS); Transcranial direct current
stimulation (tDCS)
ID TRANSCRANIAL MAGNETIC STIMULATION; HUMAN MOTOR CORTEX;
THETA-BURST-STIMULATION; PAIRED ASSOCIATIVE STIMULATION; RANDOM NOISE
STIMULATION; ACUTE ISCHEMIC-STROKE; CORTICAL STIMULATION; SYNAPTIC
PLASTICITY; SKILL ACQUISITION; FUNCTION RECOVERY
AB Through plasticity the brain is able to change its function and to rearrange following injury or environmental changes. In recent years, it was shown that non-invasive brain stimulation (NIBS) techniques, especially transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) can contribute to understand how these plastic changes occur. Additionally, the literature suggests that TMS and tDCS may be used as interventional strategies to improve neurorehabilitation efforts and arguably recovery of motor function after brain lesions. This review focuses on the use of NIBS in experimental protocols for evaluation and modulation of brain plasticity, the factors contributing to the inter-individual variability of response, proposed mechanisms and difficulties in translating findings from small proof of principle studies through the pipeline to clinical practice.
C1 [Chisari, C.; Fanciullacci, C.; Lamola, G.; Rossi, B.] Univ Hosp Pisa, Unit Neurorehabil, I-56124 Pisa, Italy.
[Cohen, L. G.] Natl Inst Neurol Disorders & Stroke, Human Cort Physiol & Neurorehabil Sect, NIH, Bethesda, MD USA.
RP Chisari, C (reprint author), Univ Hosp Pisa, Unit Neurorehabil, Via Paradisa 2, I-56124 Pisa, Italy.
EM c.chisari@ao-pisa.toscana.it
OI Lamola, Giuseppe/0000-0003-3949-9788
NR 92
TC 5
Z9 5
U1 0
U2 2
PU PISA UNIV PRESS
PI PISA
PA LUNGARNO A PACINOTTI 43, 56100 PISA, ITALY
SN 0003-9829
J9 ARCH ITAL BIOL
JI Arch. Ital. Biol.
PD OCT-DEC
PY 2014
VL 152
IS 4
SI SI
BP 247
EP 258
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA DB3UV
UT WOS:000368439000005
PM 25987184
ER
PT J
AU Clark, PJ
Ghasem, PR
Mika, A
Daya, HE
Herrera, JJ
Greenwood, BN
Fleshner, M
AF Clark, Peter J.
Ghasem, Parsa R.
Mika, Agnieszka
Daya, Heidi E.
Herrera, Jonathan J.
Greenwood, Benjamin N.
Fleshner, Monika
TI Wheel running alters patterns of uncontrollable stress-induced cfos mRNA
expression in rat dorsal striatum direct and indirect pathways: A
possible role for plasticity in adenosine receptors
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Exercise; Striatum; Adenosine; Dopamine; Stress; Running
ID ANTAGONIST MSX-3 REVERSES; COCAINE-SEEKING BEHAVIOR; BRAIN-BARRIER
TRANSPORT; DOPAMINE D-1 RECEPTORS; NUCLEUS-ACCUMBENS CORE; NF-KAPPA-B;
A(2A) RECEPTORS; A(1) RECEPTORS; BASAL GANGLIA; PC12 CELLS
AB Emerging evidence indicates that adenosine is a major regulator of striatum activity, in part, through the antagonistic modulation of dopaminergic function. Exercise can influence adenosine and dopamine activity, which may subsequently promote plasticity in striatum adenosine and dopamine systems. Such changes could alter activity of medium spiny neurons and impact striatum function. The purpose of this study was twofold. The first was to characterize the effect of long-term wheel running on adenosine 1 (A(1)R), adenosine 2A (A(2A)R), dopamine 1 (D1R), and dopamine 2 (D2R) receptor mRNA expression in adult rat dorsal and ventral striatum structures using in situ hybridization. The second was to determine if changes to adenosine and dopamine receptor mRNA from running are associated with altered cfos mRNA induction in dynorphin- (direct pathway) and enkephalin- (indirect pathway) expressing neurons of the dorsal striatum following stress exposure. We report that chronic running, as well as acute uncontrollable stress, reduced A(1)R and A(2A)R mRNA levels in the dorsal and ventral striatum. Running also modestly elevated D2R mRNA levels in striatum regions. Finally, stress-induced cfos was potentiated in dynorphin and attenuated in enkephalin expressing neurons of running rats. These data suggest striatum adenosine and dopamine systems are targets for neuroplasticity from exercise, which may contribute to changes in direct and indirect pathway activity. These findings may have implications for striatum mediated motor and cognitive processes, as well as exercise facilitated stress-resistance. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Clark, Peter J.; Ghasem, Parsa R.; Mika, Agnieszka; Daya, Heidi E.; Herrera, Jonathan J.; Greenwood, Benjamin N.; Fleshner, Monika] Univ Colorado, Boulder, CO 80309 USA.
[Daya, Heidi E.] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA.
RP Clark, PJ (reprint author), NIA, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM peter.clark@nih.gov
OI DAY, HEIDI/0000-0002-5683-3496
FU National Institutes of Mental Health [068283]
FX Special thanks to University of Colorado Boulder Animal Care facility.
This work was supported by National Institutes of Mental Health Grant
068283.
NR 132
TC 3
Z9 3
U1 1
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD OCT 1
PY 2014
VL 272
BP 252
EP 263
DI 10.1016/j.bbr.2014.07.006
PG 12
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA AO6NQ
UT WOS:000341469200030
PM 25017571
ER
PT J
AU Zingone, A
Wang, WX
Corrigan-Cummins, M
Wu, SP
Plyler, R
Korde, N
Kwok, M
Manasanch, EE
Tageja, N
Bhutani, M
Mulquin, M
Zuchlinski, D
Yancey, MA
Roschewski, M
Zhang, Y
Roccaro, AM
Ghobrial, IM
Calvo, KR
Landgren, O
AF Zingone, Adriana
Wang, Weixin
Corrigan-Cummins, Meghan
Wu, S. Peter
Plyler, Ryan
Korde, Neha
Kwok, Mary
Manasanch, Elisabet E.
Tageja, Nishant
Bhutani, Manisha
Mulquin, Marcia
Zuchlinski, Diamond
Yancey, Mary Ann
Roschewski, Mark
Zhang, Yong
Roccaro, Aldo M.
Ghobrial, Irene M.
Calvo, Katherine R.
Landgren, Ola
TI Altered cytokine and chemokine profiles in multiple myeloma and its
precursor disease
SO CYTOKINE
LA English
DT Article
DE Multiple myeloma; Chemokines; CXCL8
ID UNDETERMINED SIGNIFICANCE; MONOCLONAL GAMMOPATHY; PROGRESSION; CELLS;
TRANSACTIVATION; MIGRATION; RECEPTOR; CANCER; RISK
AB Currently, no reliable biomarkers are available to predict transformation from smoldering myeloma (SMM) to multiple myeloma (MM). Using an ultrasensitive enzyme-linked immunosorbent assay (ELISA) we assessed the levels of a broad range of cytokines and chemokines in the peripheral blood (PB) and bone marrow (BM) supernatant collected from 14 SMM and 38 MM patients and compared to healthy donors. We found significantly increased levels of key cytokines, in particular CXCL8 (IL-8), associated with progressive disease state (controls -> SMM -> MM). Cytokine profiles were found similar in PB and BM. Five of fourteen SMM patients (36%) progressed to MM.
Our findings, although based on a limited number of patients, suggest that serum-based cytokines may have a future role as biomarkers for disease progression and could potentially be assessed as novel targets for treatment. Published by Elsevier Ltd.
C1 [Zingone, Adriana; Wu, S. Peter; Korde, Neha; Kwok, Mary; Manasanch, Elisabet E.; Tageja, Nishant; Bhutani, Manisha; Mulquin, Marcia; Zuchlinski, Diamond; Yancey, Mary Ann; Roschewski, Mark; Landgren, Ola] NCI, Lymphoid Malignancies Branch, NIH, Bethesda, MD 20892 USA.
[Wang, Weixin; Corrigan-Cummins, Meghan; Plyler, Ryan; Calvo, Katherine R.] NIH, Hematol Serv, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Zhang, Yong; Roccaro, Aldo M.; Ghobrial, Irene M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Landgren, Ola] Mem Sloan Kettering Canc Ctr, Myeloma Serv, New York, NY 10065 USA.
RP Landgren, O (reprint author), Mem Sloan Kettering Canc Ctr, Myeloma Serv, 1275 York Ave, New York, NY 10065 USA.
EM landgrec@mskcc.org
OI Roccaro, Aldo/0000-0002-1872-5128
FU Intramural NIH HHS [Z99 CA999999]
NR 15
TC 3
Z9 3
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2014
VL 69
IS 2
BP 294
EP 297
DI 10.1016/j.cyto.2014.05.017
PG 4
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA AO6RB
UT WOS:000341478100019
PM 25043675
ER
PT J
AU Coulon, A
Ferguson, ML
de Turris, V
Palangat, M
Chow, CC
Larson, DR
AF Coulon, Antoine
Ferguson, Matthew L.
de Turris, Valeria
Palangat, Murali
Chow, Carson C.
Larson, Daniel R.
TI Kinetic competition during the transcription cycle results in stochastic
RNA processing
SO ELIFE
LA English
DT Article
ID PRE-MESSENGER-RNA; REAL-TIME; GENE-EXPRESSION; IN-VIVO; CORRELATION
SPECTROSCOPY; SPLICING KINETICS; GLOBAL ANALYSIS; LIVING CELLS; REVEALS;
DYNAMICS
AB Synthesis of mRNA in eukaryotes involves the coordinated action of many enzymatic processes, including initiation, elongation, splicing and cleavage. Kinetic competition between these processes has been proposed to determine RNA fate, yet such coupling has never been observed in vivo on single transcripts. Here, we use dual-color single-molecule RNA imaging in living human cells to construct a complete kinetic profile of transcription and splicing of the beta-globin gene. We find that kinetic competition results in multiple competing pathways for pre-mRNA splicing. Splicing of the terminal intron occurs stochastically both before and after transcript release, indicating there is not a strict quality control checkpoint. The majority of pre-mRNAs are spliced after release, while diffusing away from the site of transcription. A single missense point mutation (S34F) in the essential splicing factor U2AF1 which occurs in human cancers perturbs this kinetic balance and defers splicing to occur entirely post-release.
C1 [Coulon, Antoine; Chow, Carson C.] NIDDK, NIH, Bethesda, MD USA.
[Ferguson, Matthew L.; Palangat, Murali; Larson, Daniel R.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[de Turris, Valeria] Ist Italiano Tecnol, Ctr Life Nanosci IIT Sapienza, Rome, Italy.
RP Larson, DR (reprint author), 41 Lib Dr, Bethesda, MD 20892 USA.
EM dan.larson@nih.gov
RI Larson, Daniel/B-9829-2008; Coulon, Antoine/A-9006-2012; Ferguson,
Matthew/C-4140-2014;
OI Larson, Daniel/0000-0001-9253-3055; Ferguson,
Matthew/0000-0003-0760-757X; de Turris, Valeria/0000-0003-0872-185X
NR 61
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PU ELIFE SCIENCES PUBLICATIONS LTD
PI CAMBRIDGE
PA SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND
SN 2050-084X
J9 ELIFE
JI eLife
PD OCT 1
PY 2014
VL 3
AR e03939
DI 10.7554/eLife.03939
PG 60
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AR2JI
UT WOS:000343409900004
ER
PT J
AU Ju, YS
Futreal, CA
Gerstung, M
Martincorena, I
Nik-Zainal, S
Ramakrishna, M
Davies, HR
Papaemmanuil, E
Gundem, G
Shlien, A
Bolli, N
Behjati, S
Tarpey, PS
Nangalia, J
Massie, CE
Butler, AP
Teague, JW
Vassiliou, GS
Green, AR
Du, MQ
Unnikrishnan, A
Pimanda, JE
Teh, BT
Munshi, N
Greaves, M
Vyas, P
El-Naggar, AK
Santarius, T
Collins, VP
Grundy, R
Taylor, JA
Hayes, DN
Malkin, D
Foster, CS
Warren, AY
Whitaker, HC
Brewer, D
Eeles, R
Cooper, C
Neal, D
Visakorpi, T
Isaacs, WB
Bova, GS
Flanagan, AM
Futreal, PA
Lynch, AG
Chinnery, PF
McDermott, U
Stratton, MR
Campbell, PJ
AF Ju, Young Seok
Alexandrov, Ludmil B.
Gerstung, Moritz
Martincorena, Inigo
Nik-Zainal, Serena
Ramakrishna, Manasa
Davies, Helen R.
Papaemmanuil, Elli
Gundem, Gunes
Shlien, Adam
Bolli, Niccolo
Behjati, Sam
Tarpey, Patrick S.
Nangalia, Jyoti
Massie, Charles E.
Butler, Adam P.
Teague, Jon W.
Vassiliou, George S.
Green, Anthony R.
Du, Ming-Qing
Unnikrishnan, Ashwin
Pimanda, John E.
Teh, Bin Tean
Munshi, Nikhil
Greaves, Mel
Vyas, Paresh
El-Naggar, Adel K.
Santarius, Tom
Collins, V. Peter
Grundy, Richard
Taylor, Jack A.
Hayes, D. Neil
Malkin, David
Foster, Christopher S.
Warren, Anne Y.
Whitaker, Hayley C.
Brewer, Daniel
Eeles, Rosalind
Cooper, Colin
Neal, David
Visakorpi, Tapio
Isaacs, William B.
Bova, G. Steven
Flanagan, Adrienne M.
Futreal, P. Andrew
Lynch, Andy G.
Chinnery, Patrick F.
McDermott, Ultan
Stratton, Michael R.
Campbell, Peter J.
CA ICGC Breast Canc Grp
ICGC Chronic Myeloid Disorders Grp
ICGC Prostate Canc Grp
TI Origins and functional consequences of somatic mitochondrial DNA
mutations in human cancer
SO ELIFE
LA English
DT Article
ID 21 BREAST CANCERS; POPULATION-GENETICS; POLYMERASE-GAMMA;
LAGGING-STRAND; HUMAN-DISEASE; STEM-CELLS; GENOME; HETEROPLASMY;
REPLICATION; EVOLUTION
AB Recent sequencing studies have extensively explored the somatic alterations present in the nuclear genomes of cancers. Although mitochondria control energy metabolism and apoptosis, the origins and impact of cancer-associated mutations in mitochondrial DNA (mtDNA) are unclear. Here, we analysed somatic alterations in mtDNA from 1,675 tumors across 31 histologies. We identified 1,907 somatic substitutions, which exhibited dramatic replicative strand bias, predominantly C>T and A>G on the mitochondrial heavy strand. This strand-asymmetric signature differs from those found in nuclear cancer genomes but matches the inferred germline process shaping primate mtDNA sequence content. Numbers of mtDNA mutations showed considerable heterogeneity across tumor types. Missense mutations were selectively neutral and often gradually drifted towards homoplasmy over time. In contrast, mutations resulting in protein truncation undergo negative selection and were almost exclusively heteroplasmic. Our findings indicate that the endogenous mutational mechanism has far greater impact than any other external mutagens in mitochondria, and is fundamentally linked to mtDNA replication.
C1 [Ju, Young Seok; Alexandrov, Ludmil B.; Gerstung, Moritz; Martincorena, Inigo; Nik-Zainal, Serena; Ramakrishna, Manasa; Davies, Helen R.; Papaemmanuil, Elli; Gundem, Gunes; Shlien, Adam; Bolli, Niccolo; Behjati, Sam; Tarpey, Patrick S.; Nangalia, Jyoti; Massie, Charles E.; Butler, Adam P.; Teague, Jon W.; Vassiliou, George S.; Futreal, P. Andrew; Stratton, Michael R.; ICGC Breast Canc Grp; ICGC Chronic Myeloid Disorders Grp] Wellcome Trust Sanger Inst, Canc Genome Project, Hinxton CB10 1SA, England.
[Nangalia, Jyoti; Massie, Charles E.; Vassiliou, George S.; Green, Anthony R.; Du, Ming-Qing; Santarius, Tom; Collins, V. Peter; Warren, Anne Y.; McDermott, Ultan; Campbell, Peter J.] Cambridge Univ Hosp NHS Trust, Cambridge, England.
[Nangalia, Jyoti; Massie, Charles E.; Vassiliou, George S.; Green, Anthony R.; Campbell, Peter J.] Univ Cambridge, Dept Hematol, Cambridge, England.
[Unnikrishnan, Ashwin; Pimanda, John E.] Univ New S Wales, Lowy Canc Res Ctr, Sydney, NSW, Australia.
[Teh, Bin Tean] Natl Canc Ctr, Lab Canc Epigenome, Singapore, Singapore.
[Teh, Bin Tean] Duke Nus Grad Med Sch, Singapore, Singapore.
[Munshi, Nikhil] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Greaves, Mel; Brewer, Daniel; Eeles, Rosalind; Cooper, Colin] Inst Canc Res, Sutton, Surrey, England.
[Vyas, Paresh] Univ Oxford, Weatherall Inst Mol Med, Oxford, England.
[El-Naggar, Adel K.; Futreal, P. Andrew] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Grundy, Richard] Univ Nottingham, Childrens Brain Tumor Res Ctr, Nottingham NG7 2RD, England.
[Taylor, Jack A.] NIH, Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
[Hayes, D. Neil] Univ N Carolina, Chapel Hill, NC 27515 USA.
[Malkin, David] Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Whitaker, Hayley C.; Neal, David; ICGC Prostate Canc Grp] Univ Cambridge, Canc Res UK Cambridge Inst, Cambridge, England.
[Foster, Christopher S.] Univ Liverpool, London, England.
[Foster, Christopher S.] HCA Pathol Labs, London, England.
[Brewer, Daniel; Cooper, Colin] Univ E Anglia, Norwich NR4 7TJ, Norfolk, England.
[Visakorpi, Tapio; Bova, G. Steven] Univ Tampere, Inst Biomed Technol, FIN-33101 Tampere, Finland.
[Visakorpi, Tapio; Bova, G. Steven] Univ Tampere, BioMediTech, FIN-33101 Tampere, Finland.
[Isaacs, William B.] Johns Hopkins Univ, Baltimore, MD USA.
[Flanagan, Adrienne M.] Royal Natl Orthopaed Hosp, Stanmore, Middx, England.
[Flanagan, Adrienne M.] UCL, UCL Canc Inst, London, England.
[Chinnery, Patrick F.] Univ Newcastle, Inst Med Genet, Wellcome Ctr Mitochondrial Res, Newcastle Upon Tyne, Tyne & Wear, England.
RP Campbell, PJ (reprint author), Wellcome Trust Sanger Inst, Canc Genome Project, Hinxton CB10 1SA, England.
EM pc8@sanger.ac.uk
RI Ju, Young Seok/E-1324-2012; Bolli, Niccolo/D-4057-2011;
OI taylor, jack/0000-0001-5303-6398; Ju, Young Seok/0000-0002-5514-4189;
Bolli, Niccolo/0000-0002-1018-5139; Ehinger, Anna/0000-0001-9225-7396;
Gerstung, Moritz/0000-0001-6709-963X; Eeles,
Rosalind/0000-0002-3698-6241; Vassiliou, George/0000-0003-4337-8022;
Vyas, Paresh/0000-0003-3931-0914; McDermott, Ultan/0000-0001-9032-4700;
Martin, Sancha/0000-0001-6213-5259; Unnikrishnan,
Ashwin/0000-0001-5168-8755; Massie, Charlie/0000-0003-2314-4843
FU Wellcome Trust; British Lung Foundation; Health Innovation Challenge
Fund; Kay Kendall Leukaemia Fund; Chordoma Foundation; Adenoid Cystic
Carcinoma Research Foundation; EMBO long-term fellowship [ALTF
1203-2012, ALTF 1287-2012]; National Institute for Health Research
(NIHR) UCLH Biomedical Research Centre; Leukaemia Lymphoma Research;
Cancer Research UK; Leukemia Lymphoma Society; European Union (BASIS);
National Cancer Research Prostate Cancer: Mechanisms of Progression and
Treatment (PROMPT) collaborative [G0500966/75466]; Intramural Research
Program of the NIH, National Institute of Environmental Health Sciences
FX Data used in this manuscript are described in the supplementary
materials (Supplementary file 1). We thank Thomas Bleazard at Faculty of
Medical and Human Sciences, University of Manchester for discussion and
assistance with manuscript preparation. We would like to thank The
Cancer Genome Atlas (TCGA) Project Team and their specimen donors for
providing sequencing data. This work was supported by the Wellcome
Trust, the British Lung Foundation, the Health Innovation Challenge
Fund, the Kay Kendall Leukaemia Fund, the Chordoma Foundation and the
Adenoid Cystic Carcinoma Research Foundation. Y.S.J and I.M. are
supported by EMBO long-term fellowship (ALTF 1203-2012 and ALTF
1287-2012, respectively). P.J.C. is a Wellcome Trust Senior Clinical
Fellow. Support was provided to A.M.F. by the National Institute for
Health Research (NIHR) UCLH Biomedical Research Centre. A.R.G. receives
support from Leukaemia Lymphoma Research, Cancer Research UK and the
Leukemia Lymphoma Society. Samples from Addenbrooke's Hospital were
collected with support from the NIHR Cambridge Biomedical Resource
Centre. The ICGC Breast Cancer Consortium was supported by a grant from
the European Union (BASIS) and the Wellcome Trust. The ICGC Prostate
Cancer Consortium was funded by Cancer Research UK. We would also like
to acknowledge the support of the National Cancer Research Prostate
Cancer: Mechanisms of Progression and Treatment (PROMPT) collaborative
(grant code G0500966/75466) which has funded tissue and urine
collections in Cambridge. This research was supported in part by the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences (J.A.T.). We obtained informed consent and
consent to publish from participants enrolled.
NR 59
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PI CAMBRIDGE
PA SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND
SN 2050-084X
J9 ELIFE
JI eLife
PD OCT 1
PY 2014
VL 3
AR e02935
DI 10.7554/eLife.02935
PG 53
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AR2JI
UT WOS:000343409900003
ER
PT J
AU Jurek, B
Slattery, DA
Liu, Y
Aguilera, G
Van den Burg, EH
Neumann, ID
AF Jurek, B.
Slattery, D. A.
Liu, Y.
Aguilera, G.
Van den Burg, E. H.
Neumann, I. D.
TI Oxytocin controls the CRF gene via CRTC3: implications for
stress-related disorders
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 27th Congress of the European-College-of-Neuropsychopharmacology (ECNP)
CY OCT 18-21, 2014
CL Berlin, GERMANY
SP European Coll Neuropsychopharmacol
C1 [Jurek, B.; Slattery, D. A.; Van den Burg, E. H.; Neumann, I. D.] Univ Regensburg, Dept Neurobiol & Anim Physiol, D-93053 Regensburg, Germany.
[Liu, Y.; Aguilera, G.] NICHHD, Sect Endocrine Physiol, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 1
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD OCT
PY 2014
VL 24
SU 2
MA P.4.a.008
BP S580
EP S581
PG 2
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CT5LM
UT WOS:000362851800063
ER
PT J
AU Pfarr, S
Meinhardt, MW
Klee, ML
Schonig, K
Vengeliene, V
Hope, BT
Bartsch, D
Spanagel, R
Sommer, WH
AF Pfarr, S.
Meinhardt, M. W.
Klee, M. L.
Schoenig, K.
Vengeliene, V.
Hope, B. T.
Bartsch, D.
Spanagel, R.
Sommer, W. H.
TI Losing control: excessive alcohol seeking after selective inactivation
of cue-responsive neurons in the infralimbic cortex
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 27th Congress of the European-College-of-Neuropsychopharmacology (ECNP)
CY OCT 18-21, 2014
CL Berlin, GERMANY
SP European Coll Neuropsychopharmacol
C1 [Pfarr, S.; Meinhardt, M. W.; Klee, M. L.; Vengeliene, V.; Spanagel, R.; Sommer, W. H.] Cent Inst Mental Hlth, Psychopharmacol, Mannheim, Germany.
[Schoenig, K.; Bartsch, D.] Cent Inst Mental Hlth, Mol Biol, Mannheim, Germany.
[Hope, B. T.] IRP NIDA NIH, Behav Neurosci Branch, Baltimore, MD USA.
NR 3
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PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD OCT
PY 2014
VL 24
SU 2
MA P.6.a.016
BP S662
EP S662
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CT5LM
UT WOS:000362851800198
ER
PT J
AU Potter, WZ
AF Potter, W. Z.
TI Making better early go/no-go decisions in drug development progress in
the NIMH FAST-FAIL programme
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 27th ECNP Congress
CY OCT 18-21, 2014
CL Berlin, GERMANY
SP ECNP
C1 [Potter, W. Z.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD OCT
PY 2014
VL 24
SU 2
MA E.05.02
BP S150
EP S150
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CO7FF
UT WOS:000359324300109
ER
PT J
AU Vitiello, B
AF Vitiello, B.
TI Should we expect smaller effect sizes in paediatric clinical trials?
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 27th ECNP Congress
CY OCT 18-21, 2014
CL Berlin, GERMANY
SP ECNP
C1 [Vitiello, B.] NIMH, DSIR, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
EI 1873-7862
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD OCT
PY 2014
VL 24
SU 2
MA S.17.03
BP S133
EP S133
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CO7FF
UT WOS:000359324300064
ER
PT J
AU Felker, GM
Ahmad, T
Anstrom, KJ
Adams, KF
Cooper, LS
Ezekowitz, JA
Fiuzat, M
Houston-Miller, N
Januzzi, JL
Leifer, ES
Mark, DB
Desvigne-Nickens, P
Paynter, G
Pina, IL
Whellan, DJ
O'Connor, CM
AF Felker, G. Michael
Ahmad, Tariq
Anstrom, Kevin J.
Adams, Kirkwood F.
Cooper, Lawton S.
Ezekowitz, Justin A.
Fiuzat, Mona
Houston-Miller, Nancy
Januzzi, James L.
Leifer, Eric S.
Mark, Daniel B.
Desvigne-Nickens, Patrice
Paynter, Gayle
Pina, Ileana L.
Whellan, David J.
O'Connor, Christopher M.
TI Rationale and Design of the GUIDE-IT Study Guiding Evidence Based
Therapy Using Biomarker Intensified Treatment in Heart Failure
SO JACC-HEART FAILURE
LA English
DT Article
DE biomarkers; clinical trial; heart failure
ID BRAIN-NATRIURETIC PEPTIDE; RANDOMIZED CLINICAL-TRIALS; VAL-HEFT;
SYSTOLIC DYSFUNCTION; DISEASE MANAGEMENT; PRIMARY-CARE; IMPROVE HF; BNP;
CARDIOLOGY; MORTALITY
AB OBJECTIVES The GUIDE-IT (Guiding Evidence Based Therapy Using Biomarker Intensified Treatment in Heart Failure) study is designed to determine the safety, efficacy, and cost-effectiveness of a strategy of adjusting therapy with the goal of achieving and maintaining a target N-terminal pro-B-type natriuretic peptide (NT-proBNP) level of < 1,000 pg/ml compared with usual care in high-risk patients with systolic heart failure (HF).
BACKGROUND Elevations in natriuretic peptide (NP) levels provide key prognostic information in patients with HF. Therapies proven to improve outcomes in patients with HF are generally associated with decreasing levels of NPs, and observational data show that decreases in NP levels over time are associated with favorable outcomes. Results from smaller prospective, randomized studies of this strategy thus far have been mixed, and current guidelines do not recommend serial measurement of NP levels to guide therapy in patients with HF.
METHODS GUIDE-IT is a prospective, randomized, controlled, unblinded, multicenter clinical trial designed to randomize approximately 1,100 high-risk subjects with systolic HF (left ventricular ejection fraction <= 40%) to either usual care (optimized guideline-recommended therapy) or a strategy of adjusting therapy with the goal of achieving and maintaining a target NT-proBNP level of < 1,000 pg/ml. Patients in either arm of the study are followed up at regular intervals and after treatment adjustments for a minimum of 12 months. The primary endpoint of the study is time to cardiovascular death or first hospitalization for HF. Secondary endpoints include time to cardiovascular death and all-cause mortality, cumulative mortality, health-related quality of life, resource use, cost-effectiveness, and safety.
CONCLUSIONS The GUIDE-IT study is designed to definitively assess the effects of an NP-guided strategy in high-risk patients with systolic HF on clinically relevant endpoints of mortality, hospitalization, quality of life, and medical resource use. (C) 2014 by the American College of Cardiology Foundation.
C1 [Felker, G. Michael; Ahmad, Tariq; Fiuzat, Mona; Mark, Daniel B.; O'Connor, Christopher M.] Duke Univ, Med Ctr, Div Cardiol, Durham, NC 27710 USA.
[Felker, G. Michael; Ahmad, Tariq; Anstrom, Kevin J.; Fiuzat, Mona; Mark, Daniel B.; Paynter, Gayle; O'Connor, Christopher M.] Duke Univ, Med Ctr, Div Cardiol, Duke Clin Res Inst, Durham, NC 27710 USA.
[Adams, Kirkwood F.] Univ N Carolina, Div Cardiol, Chapel Hill, NC USA.
[Cooper, Lawton S.; Leifer, Eric S.; Desvigne-Nickens, Patrice] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Ezekowitz, Justin A.] Univ Alberta, Div Cardiol, Edmonton, AB T6G 2M7, Canada.
[Houston-Miller, Nancy] Stanford Univ, Div Cardiol, Palo Alto, CA 94304 USA.
[Januzzi, James L.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Pina, Ileana L.] Montefiore Einstein Med Ctr, Div Cardiol, Bronx, NY USA.
[Whellan, David J.] Thomas Jefferson Univ, Div Cardiol, Philadelphia, PA 19107 USA.
RP Felker, GM (reprint author), Duke Clin Res Inst, DUMC Box 3850, Durham, NC 27710 USA.
EM michael.felker@duke.edu
OI Mark, Daniel/0000-0001-6340-8087
FU National Heart Lung and Blood Institute [1R01HL105448-01A1,
1R01HL105451-01A1, 1R01HL105457-01A1]; Roche Diagnostics; BG Medicine;
Critical Diagnostics; Daland Fellowship; National Institutes of Health;
Alere Inc.; Siemens; Singulex; Thermo Fisher Scientific; Sphingotec;
Amgen; Zensun; AstraZeneca; Gilead; Eli Lilly; Bristol-Myers Squibb; AGA
Medical
FX The GUIDE-IT study is funded by grants 1R01HL105448-01A1,
1R01HL105451-01A1, and 1R01HL105457-01A1 from the National Heart Lung
and Blood Institute. Substudies for echocardiography as well as the
GUIDE-IT biobank were funded by a grant from Roche Diagnostics. Dr.
Felker has received research funding from Roche Diagnostics, BG
Medicine, and Critical Diagnostics and has served as a consultant for
Roche Diagnostics, Singulex, and HDL. Dr. Ahmad has received support
from the Daland Fellowship in Clinical Investigation. Dr. Anstrom has
served as a consultant for Abbott Vascular, AstraZeneca, Bristol-Myers
Squibb, Gilead, Pfizer Inc., GlaxoSmithKline, Promedior, and Ikria; has
served a member of data and safety monitoring boards for the National
Institutes of Health, University of North Carolina, University of Miami,
Forest Laboratories, Pfizer Inc., GlaxoSmithKline, and Vertex
Pharmaceuticals; and is part owner of Biscardia, Inc. Dr. Adams has
received research funding from Roche Diagnostics and Critical
Diagnostics and has served as a consultant for Roche Diagnostics. Dr.
Ezekowitz has received research funding from the National Institutes of
Health and Alere Inc. Dr. Fiuzat has served as a consultant for Roche
Diagnostics and has received research funding from Roche Diagnostics, BG
Medicine, and Critical Diagnostics. Dr. Januzzi has served as a
consultant for Critical Diagnostics and Novartis and has received
research funding from Critical Diagnostics, Roche Diagnostics, Siemens,
Singulex, Thermo Fisher Scientific, Sphingotec, Amgen, and Zensun. Dr.
Mark has received grant funding from AstraZeneca, Gilead, Eli Lilly,
Bristol-Myers Squibb, and AGA Medical; and has served as a consultant
for Janssen, Medtronic, and Somahlution. Dr. O'Connor has served as a
consultant for Roche Diagnostics and has received research funding from
Roche Diagnostics, BG Medicine, and Critical Diagnostics. All other
authors have reported that they have no relationships relevant to the
contents of this paper to disclose. John R. Teerlink, MD, served as
Guest Editor for this paper.
NR 44
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PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2213-1779
EI 2213-1787
J9 JACC-HEART FAIL
JI JACC-Heart Fail.
PD OCT
PY 2014
VL 2
IS 5
BP 457
EP 465
DI 10.1016/j.jchf.2014.05.007
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA CX4DK
UT WOS:000365648500006
PM 25194287
ER
PT J
AU Ahmad, T
Fiuzat, M
Pencina, MJ
Geller, NL
Zannad, F
Cleland, JGF
Snider, JV
Blankenberg, S
Adams, KF
Redberg, RF
Kim, JB
Mascette, A
Mentz, RJ
O'Connor, CM
Felker, GM
Januzzi, JL
AF Ahmad, Tariq
Fiuzat, Mona
Pencina, Michael J.
Geller, Nancy L.
Zannad, Faiez
Cleland, John G. F.
Snider, James V.
Blankenberg, Stephan
Adams, Kirkwood F.
Redberg, Rita F.
Kim, Jae B.
Mascette, Alice
Mentz, Robert J.
O'Connor, Christopher M.
Felker, G. Michael
Januzzi, James L.
TI Charting a Roadmap for Heart Failure Biomarker Studies
SO JACC-HEART FAILURE
LA English
DT Article
DE biomarkers; heart failure; studies
ID NATRIURETIC-PEPTIDE-MEASUREMENTS; BNP MEASUREMENTS USEFUL;
DIAGNOSTIC-ACCURACY; PREDICTION MODELS; RANDOMIZED-TRIAL; RISK
PREDICTION; THERAPY; RECLASSIFICATION; ROSUVASTATIN; MANAGEMENT
AB Heart failure is a syndrome with a pathophysiological basis that can be traced to dysfunction in several interconnected molecular pathways. Identification of biomarkers of heart failure that allow measurement of the disease on a molecular level has resulted in enthusiasm for their use in prognostication and selection of appropriate therapies. However, despite considerable amounts of information available on numerous biomarkers, inconsistent research methodologies and lack of clinical correlations have made bench-to-bedside translations rare and left the literature with countless publications of varied quality. There is a need for a systematic and collaborative approach aimed at definitively studying the clinical benefits of novel biomarkers. In this review, on the basis of input from academia, industry, and governmental agencies, we propose a systematized approach based on adherence to specific quality measures for studies looking to augment current prediction model or use biomarkers to tailor therapeutics. We suggest that study quality, rather than results, should determine publication and propose a system for grading biomarker studies. We outline the need for collaboration between clinical investigators and statisticians to introduce more advanced statistical methodologies into the field of biomarkers that would allow for data from a large number of variables to be distilled into clinically actionable information. Lastly, we propose the creation of a heart failure biomarker consortium that would allow for a comprehensive list of biomarkers to be concomitantly analyzed in a pooled sample of randomized clinical trials and hypotheses to be generated for testing in biomarker-guided trials. Such a consortium could collaborate in sharing samples to identify biomarkers, undertake meta-analyses on completed trials, and spearhead clinical trials to test the clinical utility of new biomarkers. (C) 2014 by the American College of Cardiology Foundation.
C1 [Ahmad, Tariq; Fiuzat, Mona; Pencina, Michael J.; Mentz, Robert J.; O'Connor, Christopher M.; Felker, G. Michael; Januzzi, James L.] Duke Univ, Med Ctr, Div Cardiol, Durham, NC 27710 USA.
[Ahmad, Tariq; Fiuzat, Mona; O'Connor, Christopher M.; Felker, G. Michael] Duke Clin Res Inst, Durham, NC USA.
[Geller, Nancy L.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Zannad, Faiez; Mascette, Alice] Nancy Univ, Nancy, France.
[Cleland, John G. F.] Univ Hull, Kingston Upon Hull, Yorks, England.
[Snider, James V.] Crit Diagnost, San Diego, CA USA.
[Blankenberg, Stephan] Johannes Gutenberg Univ Mainz, D-55122 Mainz, Germany.
[Adams, Kirkwood F.] Univ N Carolina, Div Cardiol, Chapel Hill, NC USA.
[Redberg, Rita F.] UCSF, Div Cardiol, San Francisco, CA USA.
[Kim, Jae B.] Amgen Inc, Thousand Oaks, CA USA.
[Mascette, Alice] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Januzzi, James L.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Januzzi, JL (reprint author), Massachusetts Gen Hosp, Div Cardiol, 32 Fruit St,Yawkey 5984, Boston, MA 02114 USA.
EM jjanuzzi@partners.org
OI Cleland, John/0000-0002-1471-7016
FU BG Medicine; Critical Diagnostics; Roche Diagnostics; Thermo Fisher;
Singulex; Siemens AG
FX Drs. Fiuzat and O'Connor have received research funding from BG
Medicine, Critical Diagnostics, and Roche Diagnostics. Dr. Pencina
served as a data safety and monitoring board member for DC Devices and
the Cardiovascular Clinical Science Foundation; and served as a
consultant for BioVentrix. Dr. Zannad has received research funding from
BG Medicine and Roche Diagnostics; and served as a consultant for BG
Medicine. Dr. Cleland has received research funding from Roche
Diagnostics. Dr. Snider is an employee of Critical Diagnostics. Dr. Kim
is an employee of Amgen. Dr. Mentz has received honoraria from
Bristol-Myers Squibb and Novartis. Dr. Felker has received research
funding from BG Medicine, Critical Diagnostics, and Roche Diagnostics;
and has served as a consultant for BG Medicine and Roche Diagnostics.
Dr. Januzzi has served as an advisor or consultant for Critical
Diagnostics; and has received research funding from Critical
Diagnostics, Roche Diagnostics, BG Medicine, Thermo Fisher, Singulex,
and Siemens AG. All other authors have reported that they have no
relationships relevant to the contents of this paper to disclose. John
R. Teerlink, MD, served as Guest Editor for this article.
NR 50
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U1 3
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PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2213-1779
EI 2213-1787
J9 JACC-HEART FAIL
JI JACC-Heart Fail.
PD OCT
PY 2014
VL 2
IS 5
BP 477
EP 488
DI 10.1016/j.jchf.2014.02.005
PG 12
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA CX4DK
UT WOS:000365648500009
PM 24929535
ER
PT J
AU Pendergast, LL
Scharf, RJ
Rasmussen, ZA
Seidman, JC
Schaefer, BA
Svensen, E
Tofail, F
Koshy, B
Kosek, M
Rasheed, MA
Roshan, R
Maphula, A
Shrestha, R
Murray-Kolb, LE
AF Pendergast, Laura L.
Scharf, Rebecca J.
Rasmussen, Zeba A.
Seidman, Jessica C.
Schaefer, Barbara A.
Svensen, Erling
Tofail, Fahmida
Koshy, Beena
Kosek, Margaret
Rasheed, Muneera A.
Roshan, Reeba
Maphula, Angelina
Shrestha, Rita
Murray-Kolb, Laura E.
CA MAL-ED Network Investigators
TI Postpartum depressive symptoms across time and place: Structural
invariance of the Self-Reporting Questionnaire among women from the
international, multi-site MAL-ED study
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE Postpartum depression; Self-Reporting Questionnaire; Validity; Low-and
middle-income countries; MAL-ED
ID MATERNAL DEPRESSION; POSTNATAL-DEPRESSION; LANGUAGE-DEVELOPMENT; INFANT
DEVELOPMENT; FUTURE-DIRECTIONS; CHILD-DEVELOPMENT; PRIMARY-CARE;
MOTHERS; VALIDATION; DISORDER
AB Background: The Self-Reporting Questionnaire (SRQ) is a screening instrument that has been shown to be an effective measure of depression in postpartum women and is widely used in developing nations.
Methods: The SRQ was administered to 2028 mothers from eight nations at two time points: one and six months postpartum. All data were obtained from the Interactions of Malnutrition and Enteric Infections: Consequences for Child Health and Development (MAL-ED) study. The sample included women from MAL-ED sites in Bangladesh, Brazil, India, Nepal, Pakistan, Peru, South Africa, and Tanzania. This study examined three aspects of validity of SRQ scores including (a) structural validity, (b) cross-cultural invariance, and (c) invariance over time.
Results: A 16-item, one-factor structure with items reflecting somatic symptoms removed was deemed to be superior to the original structure in this postpartum population. Although differential item functioning (DIF) across sites was evident the one-factor model was a good fit to the data from seven sites, and the structure was invariant across the one- and six-month time points.
Limitations: Findings are based on data from self-report scales. No information about the clinical status of the participants was available.
Conclusions: Overall, findings support the validity of a modified model of the SRQ among postpartum women. Somatic symptoms (e.g., headaches, not sleeping well) may not reflect internalizing problems in a postpartum population. Implications for researchers and practitioners are discussed. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Pendergast, Laura L.] Temple Univ, Sch Psychol Program, Philadelphia, PA 19122 USA.
[Scharf, Rebecca J.] Univ Virginia, Charlottesville, VA 22903 USA.
[Rasmussen, Zeba A.; Seidman, Jessica C.] Fogarty Int Ctr, Washington, DC USA.
[Schaefer, Barbara A.; Murray-Kolb, Laura E.] Penn State Univ, University Pk, PA 16802 USA.
[Svensen, Erling] Univ Bergen, N-5020 Bergen, Norway.
[Svensen, Erling] Haydom Lutheran Hosp, Moshi, Tanzania.
[Tofail, Fahmida] Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh.
[Koshy, Beena; Roshan, Reeba] Christian Med Coll & Hosp, Vellore, Tamil Nadu, India.
[Kosek, Margaret] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21218 USA.
[Rasheed, Muneera A.] Aga Khan Univ, Karachi, Pakistan.
[Maphula, Angelina] Univ Venda, Thohoyandou, South Africa.
[Shrestha, Rita] Tribuhvan Univ, Inst Med, Kathmandu, Nepal.
RP Pendergast, LL (reprint author), Temple Univ, Sch Psychol Program, Ritter Annex 265,1301 Cecil B Moore Ave, Philadelphia, PA 19122 USA.
EM Laura.Pendergast@temple.edu
RI Strand, Tor/D-9836-2016;
OI Strand, Tor/0000-0002-4038-151X; Mohan, Venkata
Raghava/0000-0001-5787-7223; Kang, Gagandeep/0000-0002-3656-564X
FU Bill and Melinda Gates Foundation
FX The donor for this study - the Bill and Melinda Gates Foundation through
an award to the Foundation for the National Institutes of Health - had
no role in the design, analysis or writing of this report.
NR 63
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U1 4
U2 17
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
EI 1573-2517
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD OCT 1
PY 2014
VL 167
BP 178
EP 186
DI 10.1016/j.jad.2014.05.039
PG 9
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA AO4UA
UT WOS:000341335700028
PM 24981251
ER
PT J
AU Shivva, V
Cox, P
Clarke, K
Veech, RL
Tucker, IG
Duffull, SB
AF Shivva, Vittal
Cox, Pete
Clarke, Kieran
Veech, Richard L.
Tucker, Ian G.
Duffull, Stephen B.
TI A Population Pharmacokinetic Model for D-beta-Hydroxybutyrate Following
Administration of Ketone Monoester
SO JOURNAL OF PHARMACOKINETICS AND PHARMACODYNAMICS
LA English
DT Meeting Abstract
C1 [Shivva, Vittal; Tucker, Ian G.; Duffull, Stephen B.] Univ Otago, Sch Pharm, Dunedin, New Zealand.
[Cox, Pete; Clarke, Kieran] Univ Oxford, Dept Physiol Anat & Genet, Oxford, England.
[Veech, Richard L.] NIAAA, Lab Metab Control, NIH, Rockville, MD 20852 USA.
NR 2
TC 0
Z9 0
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 OCT
PY 2014
VL 41
SU 1
MA M-007
BP S9
EP S10
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA V45QB
UT WOS:000209830000009
ER
PT J
AU Redd, AD
Tobian, AAR
AF Redd, Andrew D.
Tobian, Aaron A. R.
TI The death of HIV long-term non-progression?
SO LANCET HIV
LA English
DT Editorial Material
ID NONPROGRESSORS; INFECTION
C1 [Redd, Andrew D.] NIAID, Immunoregulat Lab, Div Intramural Res, NIH, Baltimore, MD USA.
[Redd, Andrew D.; Tobian, Aaron A. R.] Johns Hopkins Univ, Dept Med, Baltimore, MD 21287 USA.
[Tobian, Aaron A. R.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21287 USA.
RP Tobian, AAR (reprint author), Johns Hopkins Univ, Dept Med, Baltimore, MD 21287 USA.
EM atobian1@jhmi.edu
NR 10
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2352-3018
J9 LANCET HIV
JI Lancet HIV
PD OCT
PY 2014
VL 1
IS 1
BP E8
EP E9
DI 10.1016/S2352-3018(14)70019-0
PG 2
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CU8JC
UT WOS:000363787300005
PM 26423818
ER
PT J
AU Gulley, SP
Rasch, EK
Chan, L
AF Gulley, Stephen P.
Rasch, Elizabeth K.
Chan, Leighton
TI Difference, Disparity, and Disability A Comparison of Health, Insurance
Coverage, and Health Service Use on the Basis of Race/Ethnicity Among US
Adults With Disabilities, 2006-2008
SO MEDICAL CARE
LA English
DT Article
DE United States; disabled persons; health care disparities; population
groups; health services accessibility
AB Background: In the United States, research on health disparities has begun to include people with disabilities as a minority population. However, there is a gap in our knowledge of whether, and to what extent, racial and ethnic disparities may affect the health or health care access of people with disabilities.
Objectives: We examined potential disparities in overall health, insurance coverage status, and health service use between non-Hispanic whites, non-Hispanic blacks, and Hispanics, among a nationally representative US sample of adults with and without disabilities (N = 63,257), using both bivariate and multivariate methods. We tested 2 definitions of disparity.
Results: Under the more conservative definition, we confirmed the presence of both racial and ethnic disparities in overall health, total annual health care visits, and the percentage reporting no doctor visit during the year among people with less severe disabilities; Hispanics also evidenced a disparity in rates uninsured relative to non-Hispanic whites in this group. Racial/ethnic disparities were less common among persons with more severe disabilities that affected activities of daily living or instrumental activities.
Conclusions: We conclude that the reduction of disparities between the populations of people with and without disabilities will require specific attention to racial and ethnic disparities in health, insurance coverage, and service use.
C1 [Gulley, Stephen P.] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA USA.
[Gulley, Stephen P.; Rasch, Elizabeth K.; Chan, Leighton] NIH, Dept Rehabil Med, Clin Res Ctr, 6100 Execut Blvd,Suite 3C01,MSC 7515, Bethesda, MD 20892 USA.
RP Gulley, SP (reprint author), NIH, Dept Rehabil Med, Mark O Hatfield Clin Res Ctr, 6100 Execut Blvd,Suite 3C01,MSC 7515, Bethesda, MD 20892 USA.
EM gulley@brandeis.edu
FU National Institutes of Health
FX Supported by the National Institutes of Health intramural research
program.
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U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD OCT
PY 2014
VL 52
IS 10
SU 3
BP S9
EP S16
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA V45TK
UT WOS:000209838700003
PM 25222647
ER
PT J
AU Mondul, AM
Moore, SC
Weinstein, SJ
Mannisto, S
Sampson, JN
Albanes, D
AF Mondul, Alison M.
Moore, Steven C.
Weinstein, Stephanie J.
Mannisto, Satu
Sampson, Joshua N.
Albanes, Demetrius
TI 1-Stearoylglycerol is associated with risk of prostate cancer: results
from a serum metabolomic profiling analysis
SO METABOLOMICS
LA English
DT Article
DE Metabolomics; Prostatic neoplasms; Prospective study; Nested
case-control study; Early detection; Biomarker
ID SYSTEMS
AB Although prostate cancer is the most commonly diagnosed cancer among men in developed populations, recent recommendations against routine prostate-specific antigen screening have cast doubt on its utility for early detection. We compared the metabolomic profiles of prospectively collected fasting serum from 74 prostate cancer cases and 74 controls selected from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of male smokers. Circulating 1-stearoylglycerol (1-SG, or 1-monostearin) was statistically significantly inversely associated with risk of prostate cancer after Bonferroni correction for multiple comparisons (i.e., 420 identified metabolites) (OR 0.34, 95 % CI 0.20-0.58, p 6.3 x 10(-5)). The magnitude of this association did not differ by disease aggressiveness and was observed for cases diagnosed up to 23 years after blood collection. Similar but somewhat weaker prostate cancer risk signals were also evident for glycerol and alpha-ketoglutarate. In this population, men with higher serum 1-SG were less likely to develop prostate cancer, supporting a role for dysregulation of lipid metabolism in this malignancy. Additional studies are needed to retest the association and to examine 1-SG for its potential as a prostate cancer early detection marker.
C1 [Mondul, Alison M.; Moore, Steven C.; Weinstein, Stephanie J.; Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Mannisto, Satu] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Sampson, Joshua N.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Mondul, AM (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 9609 Med Ctr Dr,6E328, Bethesda, MD 20892 USA.
EM mondulam@mail.nih.gov; daa@nih.gov
RI Albanes, Demetrius/B-9749-2015; Moore, Steven/D-8760-2016
OI Moore, Steven/0000-0002-8169-1661
FU National Cancer Institute at the National Institutes of Health (U.S.
Public Health Service); U.S. Public Health Service [N01-CN-45165,
N01-RC-45035, N01-RC-37004, HHSN261201000006C, HHSN261200800001E]
FX This work was supported by the Intramural Research Program of the
National Cancer Institute at the National Institutes of Health (U.S.
Public Health Service), and U.S. Public Health Service contracts
N01-CN-45165, N01-RC-45035, N01-RC-37004, HHSN261201000006C,
HHSN261200800001E.
NR 16
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U1 1
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1573-3882
EI 1573-3890
J9 METABOLOMICS
JI Metabolomics
PD OCT
PY 2014
VL 10
IS 5
BP 1036
EP 1041
DI 10.1007/s11306-014-0643-0
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AO5YH
UT WOS:000341422600023
PM 25254003
ER
PT J
AU Zhou, QF
Lam, KH
Zheng, HR
Qiu, WB
Shung, KK
AF Zhou, Qifa
Lam, Kwok Ho
Zheng, Hairong
Qiu, Weibao
Shung, K. Kirk
TI Piezoelectric single crystal ultrasonic transducers for biomedical
applications
SO PROGRESS IN MATERIALS SCIENCE
LA English
DT Review
DE Ultrasonic transducer; Single crystal; Biomedical applications
ID MEDICAL IMAGING APPLICATIONS; LITHIUM-NIOBATE CRYSTALS; 1-3 COMPOSITE
TRANSDUCER; HIGH-FREQUENCY; PASSIVE MATERIALS; DIELECTRIC-PROPERTIES;
PHASE-BOUNDARY; MHZ ULTRASOUND; IN-VIVO; GROWTH
AB Piezoelectric single crystals, which have excellent piezoelectric properties, have extensively been employed for various sensors and actuators applications. In this paper, the state-of-art in piezoelectric single crystals for ultrasonic transducer applications is reviewed. Firstly, the basic principles and design considerations of piezoelectric ultrasonic transducers will be addressed. Then, the popular piezoelectric single crystals used for ultrasonic transducer applications, including LiNbO3 (LN), PMN-PT and PIN-PMN-PT, will be introduced. After describing the preparation and performance of the single crystals, the recent development of both the single-element and array transducers fabricated using the single crystals will be presented. Finally, various biomedical applications including eye imaging, intravascular imaging, blood flow measurement, photoacoustic imaging and microbeam applications of the single crystal transducers will be discussed. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Zhou, Qifa; Shung, K. Kirk] Univ So Calif, NIH, Resource Ctr Med Ultrason Transducer Technol, Dept Biomed Engn, Los Angeles, CA 90089 USA.
[Lam, Kwok Ho] Hong Kong Polytech Univ, Dept Elect Engn, Hunghom, Hong Kong, Peoples R China.
[Zheng, Hairong; Qiu, Weibao] Chinese Acad Sci, Shenzhen Inst Adv Technol, Paul C Lauterbur Res Ctr Biomed Imaging, Shenzhen 518055, Peoples R China.
RP Zhou, QF (reprint author), Univ So Calif, NIH, Resource Ctr Med Ultrason Transducer Technol, Dept Biomed Engn, Los Angeles, CA 90089 USA.
EM qifazhou@usc.edu; hr.zheng@siat.ac.cn
RI Lam, K.H./B-7765-2014
OI Lam, K.H./0000-0003-1456-9049
FU National Institute of Health(NIH) [P41-EB02182, R01CA157277-01,
R01EB010090]; National Science Foundation of China (NSFC) [11325420,
61302038]; Hong Kong Polytechnic University [1-ZVCG]
FX This work has been supported by National Institute of Health(NIH) Grants
Nos. P41-EB02182, R01CA157277-01 and R01EB010090. This work has also
been partially supported by National Science Foundation of China (NSFC
Grant Nos. 11325420 and 61302038). This work was also supported by The
Hong Kong Polytechnic University strategic plan (No. 1-ZVCG).
NR 108
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Z9 27
U1 18
U2 135
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0079-6425
J9 PROG MATER SCI
JI Prog. Mater. Sci.
PD OCT
PY 2014
VL 66
BP 87
EP 111
DI 10.1016/j.pmatsci.2014.06.001
PG 25
WC Materials Science, Multidisciplinary
SC Materials Science
GA AO6OU
UT WOS:000341472200002
PM 25386032
ER
PT J
AU Davies, B
Hatton, E
Hussin, J
Altemose, N
Pratto, F
Moralli, D
Gupta, A
Biggs, D
Brick, K
Green, C
Camerini-Otero, D
Myers, S
Donnelly, P
AF Davies, Benjamin
Hatton, Edouard
Hussin, Julie
Altemose, Nicolas
Pratto, Florencia
Moralli, Daniela
Gupta, Anjali
Biggs, Daniel
Brick, Kevin
Green, Catherine
Camerini-Otero, Daniel
Myers, Simon
Donnelly, Peter
TI Reprogramming meiotic recombination in the mouse
SO TRANSGENIC RESEARCH
LA English
DT Meeting Abstract
C1 [Davies, Benjamin; Hatton, Edouard; Hussin, Julie; Altemose, Nicolas; Moralli, Daniela; Gupta, Anjali; Biggs, Daniel; Green, Catherine; Myers, Simon; Donnelly, Peter] Wellcome Trust Ctr Human Genet, Oxford, England.
[Pratto, Florencia; Brick, Kevin; Camerini-Otero, Daniel] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-8819
EI 1573-9368
J9 TRANSGENIC RES
JI Transgenic Res.
PD OCT
PY 2014
VL 23
IS 5
MA 65
BP 854
EP 854
PG 1
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AO6BY
UT WOS:000341434600077
ER
PT J
AU Romeo, C
Myers, P
Goulding, E
Martin, NP
AF Romeo, Charles
Myers, Page
Goulding, Eugenia
Martin, Negin P.
TI En masse lentiviral gene delivery to mouse single-cell embryos via laser
perforation of the zona pellucida
SO TRANSGENIC RESEARCH
LA English
DT Meeting Abstract
C1 [Romeo, Charles; Martin, Negin P.] NIEHS, NIH, DHHS, Lab Neurobiol, Bethesda, MD USA.
[Myers, Page] NIEHS, NIH, DHHS, Vet Med Branch, Bethesda, MD USA.
[Goulding, Eugenia] NIEHS, NIH, DHHS, Lab Reprod & Dev Toxicol, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-8819
EI 1573-9368
J9 TRANSGENIC RES
JI Transgenic Res.
PD OCT
PY 2014
VL 23
IS 5
MA 73
BP 857
EP 857
PG 1
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AO6BY
UT WOS:000341434600085
ER
PT J
AU Richie, C
Baweke, L
Slaughter, D
Vasudevan, K
Harvey, B
Pickel, J
AF Richie, Christopher
Baweke, Lenegereshe
Slaughter, David
Vasudevan, Kuzhalini
Harvey, Brandon
Pickel, Jim
TI Producing multiple-component transgene systems in rats
SO TRANSGENIC RESEARCH
LA English
DT Meeting Abstract
C1 [Richie, Christopher; Harvey, Brandon] NIDA, NIH, Baltimore, MD USA.
[Baweke, Lenegereshe; Slaughter, David; Vasudevan, Kuzhalini; Pickel, Jim] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-8819
EI 1573-9368
J9 TRANSGENIC RES
JI Transgenic Res.
PD OCT
PY 2014
VL 23
IS 5
MA 89
BP 863
EP 864
PG 2
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AO6BY
UT WOS:000341434600101
ER
PT J
AU Zhou, Y
Baweke, L
Dallstream, A
Vasudevan, K
Paulson, M
Feng, GP
Pickel, J
AF Zhou, Yang
Baweke, Lenegereshe
Dallstream, Alice
Vasudevan, Kuzhalini
Paulson, Madeline
Feng, Guoping
Pickel, Jim
TI CRISPR/Cas9 nuclease-mediated targeting in marmosets, rats and mice
SO TRANSGENIC RESEARCH
LA English
DT Meeting Abstract
C1 [Zhou, Yang; Feng, Guoping] McGovern Inst, Boston, MA USA.
[Baweke, Lenegereshe; Dallstream, Alice; Vasudevan, Kuzhalini; Paulson, Madeline; Pickel, Jim] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-8819
EI 1573-9368
J9 TRANSGENIC RES
JI Transgenic Res.
PD OCT
PY 2014
VL 23
IS 5
MA 140
BP 882
EP 883
PG 2
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AO6BY
UT WOS:000341434600152
ER
PT J
AU Liu, CY
Xie, W
Gui, CY
Du, YB
AF Liu, Chengyu
Xie, Wen
Gui, Changyun
Du, Yubin
TI Characterization of a novel dwarf and obese mouse line generated by the
gene trapping method
SO TRANSGENIC RESEARCH
LA English
DT Meeting Abstract
C1 [Liu, Chengyu; Xie, Wen; Gui, Changyun; Du, Yubin] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-8819
EI 1573-9368
J9 TRANSGENIC RES
JI Transgenic Res.
PD OCT
PY 2014
VL 23
IS 5
MA 189
BP 902
EP 902
PG 1
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AO6BY
UT WOS:000341434600201
ER
PT J
AU Choi, H
Kim, MG
Cummins, TM
Hwang, JY
Shung, KK
AF Choi, Hojong
Kim, Min Gon
Cummins, Thomas M.
Hwang, Jae Youn
Shung, K. Kirk
TI Power MOSFET-Diode-Based Limiter for High-Frequency Ultrasound Systems
SO ULTRASONIC IMAGING
LA English
DT Article
DE limiter; transducer; ultrasound system; MOSFET; pulser
AB The purpose of the limiter circuits used in the ultrasound imaging systems is to pass low-voltage echo signals generated by ultrasonic transducers while preventing high-voltage short pulses transmitted by pulsers from damaging front-end circuits. Resistor-diode-based limiters (a 50 Omega resistor with a single cross-coupled diode pair) have been widely used in pulse-echo measurement and imaging system applications due to their low cost and simple architecture. However, resistor-diode-based limiters may not be suited for high-frequency ultrasound transducer applications since they produce large signal conduction losses at higher frequencies. Therefore, we propose a new limiter architecture utilizing power MOSFETs, which we call a power MOSFET-diode-based limiter. The performance of a power MOSFET-diode-based limiter was evaluated with respect to insertion loss (IL), total harmonic distortion (THD), and response time (RT). We compared these results with those of three other conventional limiter designs and showed that the power MOSFET-diode-based limiter offers the lowest IL (-1.33 dB) and fastest RT (0.10 mu s) with the lowest suppressed output voltage (3.47 Vp-p) among all the limiters at 70 MHz. A pulse-echo test was performed to determine how the new limiter affected the sensitivity and bandwidth of the transducer. We found that the sensitivity and bandwidth of the transducer were 130% and 129% greater, respectively, when combined with the new power MOSFET-diode-based limiter versus the resistor-diode-based limiter. Therefore, these results demonstrate that the power MOSFET-diode-based limiter is capable of producing lower signal attenuation than the three conventional limiter designs at higher frequency operation.
C1 [Choi, Hojong; Kim, Min Gon; Cummins, Thomas M.; Shung, K. Kirk] Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
[Choi, Hojong; Kim, Min Gon; Cummins, Thomas M.; Shung, K. Kirk] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
[Hwang, Jae Youn] Daegu Gyeongbuk Inst Sci & Technol, Dept Informat & Commun Engn, Taegu, South Korea.
RP Choi, H (reprint author), Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
EM hojongch@usc.edu
FU National Institute of Health [P41-EB02182]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This
project was supported by National Institute of Health Grant P41-EB02182.
NR 15
TC 3
Z9 3
U1 1
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0161-7346
EI 1096-0910
J9 ULTRASONIC IMAGING
JI Ultrason. Imaging
PD OCT
PY 2014
VL 36
IS 4
BP 317
EP 330
DI 10.1177/0161734614524180
PG 14
WC Acoustics; Engineering, Biomedical; Radiology, Nuclear Medicine &
Medical Imaging
SC Acoustics; Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA AO7AE
UT WOS:000341503400005
PM 24626565
ER
PT J
AU Dutagaci, B
Becker-Baldus, J
Faraldo-Gomez, JD
Glaubitz, C
AF Dutagaci, Bercem
Becker-Baldus, Johanna
Faraldo-Gomez, Jose D.
Glaubitz, Clemens
TI Ceramide-lipid interactions studied by MD simulations and solid-state
NMR
SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES
LA English
DT Article
DE Ceramide; DMPC; MAS NMR; MD simulation; Lipid raft
ID X-RAY-SCATTERING; N-ACYL CHAIN; PHOSPHATIDYLCHOLINE BILAYERS;
PHOSPHOLIPID MEMBRANE; SIMPLE SPHINGOLIPIDS; DOMAINS; SPECTROSCOPY;
RAFTS; SPHINGOMYELIN; LIPOSOMES
AB Ceramides play a key modulatory role in many cellular processes, which results from their effect on the structure and dynamics of biological membranes. In this study, we investigate the influence of C16-ceramide (C16) on the biophysical properties of DMPC lipid bilayers using solid-state NMR and atomistic molecular dynamics (MD) simulations. MD simulations and NMR measurements were carried out for a pure DMPC bilayer and for a 20% DMPC-C16 mixture. Calculated key structural properties, namely area per lipid, chain order parameters, and mass density profiles, indicate that C16 has an ordering effect on the DMPC bilayer. Furthermore, the simulations predict that specific hydrogen-bonds form between DMPC and C16 molecules. Multi-nuclear solid-state NMR was used to verify these theoretical predictions. Chain order parameters extracted from C-13-H-1 dipole couplings were measured for both lipid and ceramide and follow the trend suggested by the MD simulations. Furthermore, H-1-MAS NMR experiments showed a direct contact between ceramide and lipids. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Dutagaci, Bercem; Becker-Baldus, Johanna; Glaubitz, Clemens] Goethe Univ Frankfurt, Inst Biophys Chem, D-60438 Frankfurt, Germany.
[Faraldo-Gomez, Jose D.] NHLBI, Theoret Mol Biophys Sect, NIH, Bethesda, MD 20892 USA.
RP Glaubitz, C (reprint author), Goethe Univ Frankfurt, Inst Biophys Chem, Max von Laue Str 9, D-60438 Frankfurt, Germany.
EM glaubitz@em.uni-frankfurt.de
RI Faraldo-Gomez, Jose/H-7127-2016; Fachbereich14, Dekanat/C-8553-2015;
OI Glaubitz, Clemens/0000-0002-3554-6586
FU Center for Biomolecular Magnetic Resonance (BMRZ); Lipid Signaling
Forschungszentrum Frankfurt (Liff); Intramural Research Program of the
NIH, NHLBI
FX This work was funded by the Center for Biomolecular Magnetic Resonance
(BMRZ), and the Lipid Signaling Forschungszentrum Frankfurt (Liff) and
was supported in part (JDF-G) by the Intramural Research Program of the
NIH, NHLBI.
NR 49
TC 4
Z9 4
U1 1
U2 34
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0005-2736
EI 0006-3002
J9 BBA-BIOMEMBRANES
JI Biochim. Biophys. Acta-Biomembr.
PD OCT
PY 2014
VL 1838
IS 10
BP 2511
EP 2519
DI 10.1016/j.bbamem.2014.05.024
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA AO0CB
UT WOS:000340975600018
PM 24882733
ER
PT J
AU Bai, Y
Lathia, JD
Zhang, PS
Flavahan, W
Rich, JN
Mattson, MP
AF Bai, Yun
Lathia, Justin D.
Zhang, Peisu
Flavahan, William
Rich, Jeremy N.
Mattson, Mark P.
TI Molecular Targeting of TRF2 Suppresses the Growth and Tumorigenesis of
Glioblastoma Stem Cells
SO GLIA
LA English
DT Article
DE cancer stem cells; glioblastoma; telomeres; transcriptional repression
ID ADHESION MOLECULE; GENE-EXPRESSION; ADJUVANT TEMOZOLOMIDE; GLIOMA-CELLS;
HUMAN BRAIN; REST; CANCER; TUMOR; P53; DNA
AB Glioblastoma is the most prevalent primary brain tumor and is essentially universally fatal within 2 years of diagnosis. Glioblastomas contain cellular hierarchies with self-renewing glioblastoma stem cells (GSCs) that are often resistant to chemotherapy and radiation therapy. GSCs express high amounts of repressor element 1 silencing transcription factor (REST), which may contribute to their resistance to standard therapies. Telomere repeat-binding factor 2 (TRF2) stablizes telomeres and REST to maintain self-renewal of neural stem cells and tumor cells. Here we show viral vector-mediated delivery of shRNAs targeting TRF2 mRNA depletes TRF2 and REST from GSCs isolated from patient specimens. As a result, GSC proliferation is reduced and the level of proteins normally expressed by postmitotic neurons (L1CAM and beta 3-tubulin) is increased, suggesting that loss of TRF2 engages a cell differentiation program in the GSCs. Depletion of TRF2 also sensitizes GSCs to temozolomide, a DNA-alkylating agent currently used to treat glioblastoma. Targeting TRF2 significantly increased the survival of mice bearing GSC xenografts. These findings reveal a role for TRF2 in the maintenance of REST-associated proliferation and chemotherapy resistance of GSCs, suggesting that TRF2 is a potential therapeutic target for glioblastoma.
C1 [Bai, Yun] Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Cell Biol, Beijing 100191, Peoples R China.
[Bai, Yun; Zhang, Peisu; Mattson, Mark P.] Natl Inst Aging Intramural Res Program, Neurosci Lab, Baltimore, MD USA.
[Lathia, Justin D.; Flavahan, William] Cleveland Clin Fdn, Lerner Res Inst, Dept Cellular & Mol Med, Cleveland, OH 44195 USA.
[Rich, Jeremy N.] Cleveland Clin Fdn, Lerner Res Inst, Dept Stem Cell Biol & Regenerat Med, Cleveland, OH 44195 USA.
RP Mattson, MP (reprint author), Natl Inst Aging Intramural Res Program, Lab Neurosci, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mark.mattson@nih.gov
FU National Natural Sciences Foundation of China [81272432, 31070948];
Intramural Research Program of the National Institute on Aging (NIH)
FX Grant sponsor: National Natural Sciences Foundation of China; Grant
numbers: 81272432; 31070948; Grant sponsor: Intramural Research Program
of the National Institute on Aging (NIH).
NR 67
TC 4
Z9 6
U1 0
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-1491
EI 1098-1136
J9 GLIA
JI Glia
PD OCT
PY 2014
VL 62
IS 10
BP 1687
EP 1698
DI 10.1002/glia.22708
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA AN8IA
UT WOS:000340846600009
PM 24909307
ER
PT J
AU Wells, EA
Donovan, DM
Daley, DC
Doyle, SR
Brigham, G
Garrett, SB
Ingalsbe, MH
Hatch-Maillette, MA
Perl, HI
Walker, R
AF Wells, Elizabeth A.
Donovan, Dennis M.
Daley, Dennis C.
Doyle, Suzanne R.
Brigham, Greg
Garrett, Sharon B.
Ingalsbe, Michelle H.
Hatch-Maillette, Mary A.
Perl, Harold I.
Walker, Robrina
TI Is level of exposure to a 12-step facilitation therapy associated with
treatment outcome?
SO JOURNAL OF SUBSTANCE ABUSE TREATMENT
LA English
DT Article
DE 12-Step; 12-Step facilitation; Treatment exposure; Intensive referral;
Cocaine; Methamphetamine
ID ALCOHOLICS-ANONYMOUS PARTICIPATION; COLLABORATIVE-COCAINE-TREATMENT;
COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CLINICAL-TRIAL; SELF-HELP
GROUPS; SUBSTANCE USE; OUTPATIENT TREATMENT; NATIONAL-INSTITUTE; RELAPSE
PREVENTION; DEPENDENT PATIENTS
AB This study examined whether level of exposure to Stimulant Abuser Groups to Engage in 12-Step (STAGE-12), a 12-Step facilitative therapy, is related to treatment outcome. Data were from a large National Drug Abuse Treatment Clinical Trials Network (CTN) study comparing STAGE-12 combined with treatment-as-usual (TAU) to TAU alone. These analyses include only those randomized to STAGE-12 (n = 234). Assessments occurred at baseline and 30, 60, 90, and 180 days following randomization. High-exposure patients (n = 158; attended at least 2 of 3 individual, and 3 of 5 group, sessions), compared to those with less exposure (n = 76), demonstrated: (1) higher odds of self-reported abstinence from, and lower rates of, stimulant and non-stimulant drug use; (2) lower probabilities of stimulant-positive urines; (3) more days of attending and lower odds of not attending 12-Step meetings; (4) greater likelihood of reporting no drug problems; (5) more days of duties at meetings; and (6) more types of 12-Step activities. Many of these differences declined over time, but several were still significant by the last follow-up. Treatment and research implications are discussed. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Wells, Elizabeth A.] Univ Washington, Sch Social Work, Seattle, WA 98105 USA.
[Wells, Elizabeth A.; Donovan, Dennis M.; Doyle, Suzanne R.; Garrett, Sharon B.; Ingalsbe, Michelle H.; Hatch-Maillette, Mary A.] Univ Washington, Inst Alcohol & Drug Abuse, Seattle, WA 98105 USA.
[Donovan, Dennis M.] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98105 USA.
[Daley, Dennis C.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA.
[Daley, Dennis C.] Western Psychiat Inst & Clin, Pittsburgh, PA USA.
[Brigham, Greg] Maryhaven Inc, Columbus, OH USA.
[Perl, Harold I.] NIDA, Bethesda, MD 20892 USA.
[Walker, Robrina] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
RP Wells, EA (reprint author), Univ Washington, Sch Social Work, 4101 15th Ave NE, Seattle, WA 98105 USA.
EM bwells@uw.edu
OI Brigham, Gregory/0000-0003-1150-4493
FU NIDA NIH HHS [U10 DA013714, U10 DA013727, U10 DA013732, U10 DA020024,
U10DA13714, U10DA13727, U10DA13732, U10DA20024, U10DA13045, U10
DA013036, U10 DA013045, U10 DA013720, U10 DA020036, U10DA13036,
U10DA13720, U10DA20036, UG1 DA020024]
NR 51
TC 2
Z9 2
U1 5
U2 25
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0740-5472
J9 J SUBST ABUSE TREAT
JI J. Subst. Abus. Treat.
PD OCT
PY 2014
VL 47
IS 4
BP 265
EP 274
DI 10.1016/j.jsat.2014.06.003
PG 10
WC Psychology, Clinical; Substance Abuse
SC Psychology; Substance Abuse
GA AO0GB
UT WOS:000340986000004
PM 25064421
ER
PT J
AU Grunseich, C
Zukosky, K
Kats, IR
Ghosh, L
Harmison, GG
Bott, LC
Rinaldi, C
Chen, KL
Chen, GB
Boehm, M
Fischbeck, KH
AF Grunseich, Christopher
Zukosky, Kristen
Kats, Ilona R.
Ghosh, Laboni
Harmison, George G.
Bott, Laura C.
Rinaldi, Carlo
Chen, Ke-lian
Chen, Guibin
Boehm, Manfred
Fischbeck, Kenneth H.
TI Stem cell-derived motor neurons from spinal and bulbar muscular atrophy
patients
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE Spinal and bulbar muscular atrophy; Induced pluripotent stem cells;
Motor neuron disease; Androgen receptor
ID ANDROGEN RECEPTOR-GENE; MOUSE MODEL; HDAC6; AGGREGATION; ACETYLATION;
DEACETYLASE; EXPRESSION; GENERATION; MUTATIONS; DISEASE
AB Spinal and bulbar muscular atrophy (SBMA, Kennedy's disease) is a motor neuron disease caused by polyglutamine repeat expansion in the androgen receptor. Although degeneration occurs in the spinal cord and muscle, the exact mechanism is not clear. Induced pluripotent stem cells from spinal and bulbar muscular atrophy patients provide a useful model for understanding the disease mechanism and designing effective therapy. Stem cells were generated from six patients and compared to control lines from three healthy individuals. Motor neurons from four patients were differentiated from stem cells and characterized to understand disease-relevant phenotypes. Stem cells created from patient fibroblasts express less androgen receptor than control cells, but show androgen-dependent stabilization and nuclear translocation. The expanded repeat in several stem cell clones was unstable, with either expansion or contraction. Patient stem cell clones produced a similar number of motor neurons compared to controls, with or without androgen treatment. The stem cell-derived motor neurons had immunoreactivity for HB9, Isl1, ChAT, and SMI-32, and those with the largest repeat expansions were found to have increased acetylated a-tubulin and reduced HDAC6. Reduced HDAC6 was also found in motor neuron cultures from two other patients with shorter repeats. Evaluation of stably transfected mouse cells and SBMA spinal cord showed similar changes in acetylated a-tubulin and HDAC6. Perinuclear lysosomal enrichment, an HDAC6 dependent process, was disrupted in motor neurons from two patients with the longest repeats. SBMA stem cells present new insights into the disease, and the observations of reduced androgen receptor levels, repeat instability, and reduced HDAC6 provide avenues for further investigation of the disease mechanism and development of effective therapy. Published by Elsevier Inc.
C1 [Grunseich, Christopher; Zukosky, Kristen; Kats, Ilona R.; Ghosh, Laboni; Harmison, George G.; Bott, Laura C.; Rinaldi, Carlo; Chen, Ke-lian; Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Bott, Laura C.] Karolinska Inst, Dept Cell & Mol Biol, S-17177 Solna, Sweden.
[Chen, Guibin; Boehm, Manfred] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Grunseich, C (reprint author), NINDS, Neurogenet Branch, NIH, 2A-1000 Bldg 35,35 Convent Dr, Bethesda, MD 20892 USA.
EM christopher.grunseich@nih.gov; kristen.perkins@nih.gov;
Ilona.kats@nih.gov; labonighosh@gmail.com; george.harmison@nih.gov;
laura.bott@nih.gov; carlo.rinaldi@nih.gov; chenk@ninds.nih.gov;
guibin.chen@nih.gov; manfred.boehm@nih.gov; kf@ninds.nih.gov
FU National Center for Regenerative Medicine; National Institute of
Neurological Disorders and Stroke; NIH
FX This work was supported by intramural funding from the National Center
for Regenerative Medicine and the National Institute of Neurological
Disorders and Stroke, NIH.
NR 33
TC 20
Z9 20
U1 1
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD OCT
PY 2014
VL 70
BP 12
EP 20
DI 10.1016/j.nbd.2014.05.038
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA AN6FW
UT WOS:000340691400002
PM 24925468
ER
PT J
AU Masneuf, S
Lowery-Gionta, E
Colacicco, G
Pleil, KE
Li, C
Crowley, N
Flynn, S
Holmes, A
Kash, T
AF Masneuf, Sophie
Lowery-Gionta, Emily
Colacicco, Giovanni
Pleil, Kristen E.
Li, Chia
Crowley, Nicole
Flynn, Shaun
Holmes, Andrew
Kash, Thomas
TI Glutamatergic mechanisms associated with stress-induced amygdala
excitability and anxiety-related behavior
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Stress; Basolateral amygdala; GluN1; GluK1; Glutamate; C57BL/6J
ID MEDIATED FEAR EXTINCTION; GAMMA-AMINOBUTYRIC-ACID; BASOLATERAL AMYGDALA;
STRIA TERMINALIS; MOUSE STRAINS; BED NUCLEUS; MICE; FACILITATION;
RELEASE; NEURONS
AB The neural factors underlying individual differences in susceptibility to chronic stress remain poorly understood. Preclinical studies demonstrate that mouse strains vary greatly in anxiety-related responses to chronic stress in a manner paralleled by differential stress-induced changes in glutamatergic signaling in the basolateral amygdala (BLA). Previous work has also shown that alterations in the amygdala gene expression of the GluN1 NMDA and the GluK1 kainate receptors are associated with stress-induced alterations in anxiety-like behavior in the C57BL/6J mouse strain. Using in vivo behavioral pharmacological and ex vivo physiological approaches, the aim of the current study was to further elucidate changes in glutamate neurotransmission in the BLA caused by stress and to test the functional roles of GluN1 and GluK1 in mediating stress-related changes in behavior. Results showed that stress-induced alterations in anxiety-like behavior (light/dark exploration test) were absent following bilateral infusion of the GluK1 agonist ATPA into the BLA. Intra-BLA infusion of the competitive NMDA antagonist AP5 produced a generalized behavioral disinhibition/locomotor hyperactivity, irrespective of stress. Slice electrophysiological recordings showed that ATPA augmented BLA GABAergic neurotransmission and that stress increased the amplitude of network-dependent spontaneous excitatory postsynaptic currents and amplitude of GABAergic miniature inhibitory postsynaptic currents in BLA. These findings could indicate stress-induced BLA glutamatergic neuronal network hyperexcitability and a compensatory increase in GABAergic neurotransmission, suggesting that GluK1 agonism augmented GABAergic inhibition to prevent behavioral sequelae of stress. Current data could have implications for developing novel therapeutic approaches, including GluK1 agonists, for stress-related anxiety disorders. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Masneuf, Sophie; Colacicco, Giovanni; Flynn, Shaun; Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, NIH, Bethesda, MD USA.
[Lowery-Gionta, Emily; Pleil, Kristen E.; Li, Chia; Crowley, Nicole; Kash, Thomas] Univ N Carolina, Sch Med, Dept Pharmacol, Lab Mol Neurophysiol,Bowles Ctr Alcohol Studies, Chapel Hill, NC 27515 USA.
RP Kash, T (reprint author), Univ N Carolina, Sch Med, Dept Pharmacol, Lab Mol Neurophysiol,Bowles Ctr Alcohol Studies, Chapel Hill, NC 27515 USA.
EM thomas_kash@med.unc.edu
FU U.S. Department of Defense Award [W81XWH-10-1-0999]; National Institute
on Alcohol Abuse and Alcoholism intramural research program; Bowles
Center for Alcohol Studies
FX We are grateful to Olena Bukalo for critical comments. Research
supported by the U.S. Department of Defense Award W81XWH-10-1-0999 to
TLK and AH (administered by The Henry M. Jackson Foundation for the
Advancement of Military Medicine Inc.), the National Institute on
Alcohol Abuse and Alcoholism intramural research program (AH) and the
Bowles Center for Alcohol Studies (TLK).
NR 45
TC 8
Z9 9
U1 0
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
EI 1873-7064
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD OCT
PY 2014
VL 85
BP 190
EP 197
DI 10.1016/j.neuropharm.2014.04.015
PG 8
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA AN8KR
UT WOS:000340853600021
PM 24796255
ER
PT J
AU Christopoulos, A
Changeux, JP
Catterall, WA
Fabbro, D
Burris, TP
Cidlowski, JA
Olsen, RW
Peters, JA
Neubig, RR
Pin, JP
Sexton, PM
Kenakin, TP
Ehlert, FJ
Spedding, M
Langmead, CJ
AF Christopoulos, Arthur
Changeux, Jean-Pierre
Catterall, William A.
Fabbro, Doriano
Burris, Thomas P.
Cidlowski, John A.
Olsen, Richard W.
Peters, John A.
Neubig, Richard R.
Pin, Jean-Philippe
Sexton, Patrick M.
Kenakin, Terry P.
Ehlert, Frederick J.
Spedding, Michael
Langmead, Christopher J.
TI International Union of Basic and Clinical Pharmacology. XC. Multisite
Pharmacology: Recommendations for the Nomenclature of Receptor
Allosterism and Allosteric Ligands
SO PHARMACOLOGICAL REVIEWS
LA English
DT Review
ID PROTEIN-COUPLED RECEPTORS; GATED ION CHANNELS; NICOTINIC
ACETYLCHOLINE-RECEPTORS; THYROID-HORMONE RECEPTOR; GATING MODIFIER
TOXINS; NEURONAL CALCIUM-CHANNEL; AMINO-ACID SUBSTITUTIONS; MULTIPLE
BINDING-SITES; GROWTH-FACTOR RECEPTOR; NUCLEAR-RECEPTOR
AB Allosteric interactions play vital roles in metabolic processes and signal transduction and, more recently, have become the focus of numerous pharmacological studies because of the potential for discovering more target-selective chemical probes and therapeutic agents. In addition to classic early studies on enzymes, there are now examples of small molecule allosteric modulators for all superfamilies of receptors encoded by the genome, including ligand-and voltage-gated ion channels, G protein-coupled receptors, nuclear hormone receptors, and receptor tyrosine kinases. As a consequence, a vast array of pharmacologic behaviors has been ascribed to allosteric ligands that can vary in a target-, ligand-, and cell-/tissue-dependent manner. The current article presents an overview of allostery as applied to receptor families and approaches for detecting and validating allosteric interactions and gives recommendations for the nomenclature of allosteric ligands and their properties.
C1 [Christopoulos, Arthur; Sexton, Patrick M.; Langmead, Christopher J.] Monash Univ, Monash Inst Pharmaceut Sci, Parkville, Vic 3052, Australia.
[Christopoulos, Arthur; Sexton, Patrick M.; Langmead, Christopher J.] Monash Univ, Monash Inst Pharmaceut Sci, Dept Pharmacol, Parkville, Vic 3052, Australia.
[Changeux, Jean-Pierre] Inst Pasteur, Coll France, Paris, France.
[Changeux, Jean-Pierre] Inst Pasteur, CNRS URA 2182, Paris, France.
[Catterall, William A.] Univ Washington, Sch Med, Dept Pharmacol, Seattle, WA USA.
[Fabbro, Doriano] PIQUR Therapeut AG, Basel, Switzerland.
[Burris, Thomas P.] St Louis Univ, Sch Med, Dept Pharmacol & Physiol Sci, St Louis, LA 63103 USA.
[Cidlowski, John A.] Natl Inst Environm Hlth Sci, Mol Endocrinol Grp, Signal Transduct Lab, Res Triangle Pk, NC USA.
Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA USA.
[Pin, Jean-Philippe] Univ Dundee, Sch Med, Div Neurosci, Dundee DD1 4HN, Scotland.
[Neubig, Richard R.] Michigan State Univ, Dept Pharmacol & Toxicol, E Lansing, MI 48824 USA.
[Pin, Jean-Philippe] CNRS, Inst Genom Fonct, Montpellier, France.
[Kenakin, Terry P.] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC USA.
[Ehlert, Frederick J.] Univ Calif Irvine, Dept Pharmacol, Irvine, CA 92717 USA.
[Spedding, Michael] Res Solut SARL, Paris, France.
RP Christopoulos, A (reprint author), Monash Univ, Monash Inst Pharmaceut Sci, 399 Royal Parade, Parkville, Vic 3052, Australia.
EM arthur.christopoulos@monash.edu
RI Burris, Thomas/B-3886-2016; Sexton, Patrick/B-1319-2008;
OI Burris, Thomas/0000-0003-2922-4449; Sexton, Patrick/0000-0001-8902-2473;
Spedding, Michael/0000-0002-1248-8221; Christopoulos,
Arthur/0000-0003-4442-3294
NR 302
TC 51
Z9 51
U1 3
U2 36
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0031-6997
EI 1521-0081
J9 PHARMACOL REV
JI Pharmacol. Rev.
PD OCT
PY 2014
VL 66
IS 4
BP 918
EP 947
DI 10.1124/pr.114.008862
PG 30
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AN8YQ
UT WOS:000340892400001
PM 25026896
ER
PT J
AU Stroud, LR
Papandonatos, GD
Rodriguez, D
McCallum, M
Salisbury, AL
Phipps, MG
Lester, B
Huestis, MA
Niaura, R
Padbury, JF
Marsit, CJ
AF Stroud, Laura R.
Papandonatos, George D.
Rodriguez, Daniel
McCallum, Meaghan
Salisbury, Amy L.
Phipps, Maureen G.
Lester, Barry
Huestis, Marilyn A.
Niaura, Raymond
Padbury, James F.
Marsit, Carmen J.
TI Maternal smoking during pregnancy and infant stress response: Test of a
prenatal programming hypothesis
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE Smoking; Tobacco; Pregnancy; Infant; Cortisol; Stress; Epigenetic;
Programming; Placenta; NR3C1
ID NICOTINE IN-UTERO; GLUCOCORTICOID-RECEPTOR; NEWBORN NEUROBEHAVIOR;
TOBACCO EXPOSURE; DNA METHYLATION; NEUROENDOCRINE RESPONSE;
BRAIN-DEVELOPMENT; BIRTH-WEIGHT; CORD BLOOD; CORTISOL
AB Background: Maternal smoking during pregnancy (MSDP) is associated with early and long-term neurobehavioral deficits; however mechanisms remain unknown. We tested the hypothesis that MSDP programs the hypothalamic pituitary adrenocortical (HPA) axis of the offspring leading to adverse outcomes. In an intensive, prospective study, we investigated associations between MSDP and infant cortisol stress response and explored whether alterations in cortisol response were mediated by epigenetic modulation of the placental glucocorticoid receptor gene (NR3C1).
Methods: Participants were 100 healthy mother-infant pairs (53% MSDP-exposed; 42% female) from a low income, racially/ethnically diverse sample (55% minorities). MSDP was assessed by timeline followback interview verified by saliva and meconium cotinine. Infant cortisol responses to a neurobehavioral exam were assessed seven times over the first postnatal month. Methylation of placental NR3C1 promoter exon 1F was assessed using bisulfite pyrosequencing in a subsample (n = 45).
Results: MSDP-exposed infants showed significantly and persistently attenuated basal and reactive cortisol levels over the first postnatal month vs. unexposed infants. Exploratory analyses revealed that MSDP was associated with altered methylation of the placental NR3C1 promoter; degree of methylation of the placental NR3C1 was associated with infant basal and reactive cortisol over the first postnatal month and mediated effects of MSDP on infant basal cortisol.
Conclusions: Results provide initial support for our hypothesis that MSDP programs offspring HPA (dys)regulation. Epigenetic regulation of placental GR may serve as a novel underlying mechanism. Results may have implications for delineating pathways to adverse outcomes from MSDP. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Stroud, Laura R.; Salisbury, Amy L.; Lester, Barry] Brown Univ, Warren Alpert Med Sch, Dept Psychiat & Human Behav, Providence, RI 02906 USA.
[Stroud, Laura R.] Miriam Hosp, Ctr Behav & Prevent Med, Providence, RI 02906 USA.
[Papandonatos, George D.] Brown Univ, Sch Publ Hlth, Dept Biostat, Providence, RI 02903 USA.
[Rodriguez, Daniel] La Salle Univ, Sch Nursing & Hlth Sci, Dept Publ Hlth & Nutr, Philadelphia, PA 19141 USA.
[McCallum, Meaghan] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA.
[Salisbury, Amy L.; Lester, Barry; Padbury, James F.] Brown Univ, Warren Alpert Med Sch, Dept Pediat, Providence, RI 02906 USA.
[Salisbury, Amy L.; Phipps, Maureen G.; Lester, Barry; Padbury, James F.] Women & Infants Hosp Rhode Isl, Providence, RI 02905 USA.
[Phipps, Maureen G.] Brown Univ, Warren Alpert Med Sch, Dept Obstet & Gynecol, Providence, RI 02905 USA.
[Huestis, Marilyn A.] NIDA, Intramural Res Branch, NIH, Baltimore, MD 21224 USA.
[Niaura, Raymond] Amer Legacy Fdn, Schroeder Inst Tobacco Res & Policy Studies, Washington, DC 20036 USA.
[Marsit, Carmen J.] Dartmouth Coll, Dept Pharmacol & Toxicol, Hanover, NH 03755 USA.
RP Stroud, LR (reprint author), Brown Univ, Ctr Behav & Prevent Med, Dept Psychiat & Human Behav, Miriam Hosp, 164 Summit Ave, Providence, RI 02906 USA.
EM Laura_Stroud@brown.edu
OI Marsit, Carmen/0000-0003-4566-150X; Papandonatos,
George/0000-0001-6770-932X
FU National Institutes of Health [R01 DA019558, R01 DA031188]; Flight
Attendant Medical Research Institute Clinical Innovator Award
FX Preparation of this manuscript was supported by the National Institutes
of Health (R01 DA019558 and R01 DA031188 to L.R.S.) and the Flight
Attendant Medical Research Institute Clinical Innovator Award to L.R.S.
The funding agencies had no further role in study design; in the
collection, analysis and interpretation of data; in the writing of the
report; and in the decision to submit the paper for publication.
NR 61
TC 19
Z9 19
U1 0
U2 13
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 OCT
PY 2014
VL 48
BP 29
EP 40
DI 10.1016/j.psyneuen.2014.05.017
PG 12
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA AN8JR
UT WOS:000340851000004
PM 24999830
ER
PT J
AU Luger, TM
Suls, J
Vander Weg, MW
AF Luger, Tana M.
Suls, Jerry
Vander Weg, Mark W.
TI How robust is the association between smoking and depression in adults?
A meta-analysis using linear mixed-effects models
SO ADDICTIVE BEHAVIORS
LA English
DT Review
DE Smoking; Depression; Meta-analysis; Measurement
ID CORONARY-HEART-DISEASE; CIGARETTE-SMOKING; MAJOR DEPRESSION; TOBACCO
SMOKING; MENTAL-HEALTH; RISK-FACTORS; PSYCHIATRIC-DISORDERS;
UNIVERSITY-STUDENTS; CHINESE-AMERICANS; SOCIAL SUPPORT
AB Introduction: Our objective was to use meta-analytic techniques to assess the strength of the overall relationship and role of potential moderators in the association between smoking and depression in adults.
Methods: Two popular health and social science databases (PubMed and PsycINFO) were systematically searched to identify studies which examined the association between adult smoking behavior and major depressive disorder (MDD) or depressive symptoms. A total of 85 relevant studies were selected for inclusion. Studies were analyzed using a linear mixed effects modeling package ("Ime4" for R) and the Comprehensive Meta-Analysis program version 2.
Results: Multiple nested linear mixed-effects models were compared. The best fitting models were those that included only random study effects and smoking status. In cross-sectional studies, current smokers were more likely to be depressed than never smokers (OR = 1.50, CI = 1.39-1.60), and current smokers were more likely to be depressed than former smokers (OR = 1.76, CI = 1.48-2.09). The few available prospective studies, that used the requisite statistical adjustments, also showed smokers at baseline had greater odds of incident depression at follow-up than never smokers (OR = 1.62, CI = 1.10-2.40).
Conclusions: In cross-sectional studies, smoking was associated with a nearly two-fold increased risk of depression relative to both never smokers and former smokers. In the smaller set of prospective studies, the odds of subsequent depression were also higher for current than never smokers. Attesting to its robustness, the relationship between smoking and depression was exhibited across several moderators. Findings could help health care providers to more effectively anticipate co-occurring health issues of their patients. Several methodological recommendations for future research are offered. Published by Elsevier Ltd.
C1 [Luger, Tana M.] Ctr Healthcare Org & Implementat Res, Bedford, MA 02117 USA.
[Suls, Jerry] NCI, Behav Res Program, Bethesda, MD 20892 USA.
[Vander Weg, Mark W.] Univ Iowa, Dept Psychol, Iowa City, IA 52242 USA.
[Vander Weg, Mark W.] Comprehens Access & Delivery Res & Evaluat Ctr, Iowa City, IA 52246 USA.
[Vander Weg, Mark W.] Univ Iowa, Dept Internal Med, Carver Coll Med, Iowa City, IA 52242 USA.
RP Luger, TM (reprint author), 200 Springs Rd,Bldg 70 152, Bedford, MA 02117 USA.
EM Tana.Luger2@va.gov; jerry.suls@nih.gov; mark-vanderweg@uiowa.edu
NR 111
TC 25
Z9 25
U1 5
U2 32
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4603
EI 1873-6327
J9 ADDICT BEHAV
JI Addict. Behav.
PD OCT
PY 2014
VL 39
IS 10
BP 1418
EP 1429
DI 10.1016/j.addbeh.2014.05.011
PG 12
WC Psychology, Clinical; Substance Abuse
SC Psychology; Substance Abuse
GA AN1BY
UT WOS:000340318900009
PM 24935795
ER
PT J
AU Dalsgaard, TK
Triquigneaux, M
Deterding, L
Summers, FA
Mortensen, G
Mason, RP
AF Dalsgaard, Trine K.
Triquigneaux, Mathilde
Deterding, Leesa
Summers, Fiona A.
Mortensen, Grith
Mason, Ronald P.
TI Oxidation of alpha-lactalbumin after a lactoperoxidase-catalysed
reaction: An oxidomics approach applying immuno-spin trapping and mass
spectrometry
SO INTERNATIONAL DAIRY JOURNAL
LA English
DT Article; Proceedings Paper
CT 8th NIZO Dairy Conference
CY SEP 11-13, 2013
CL Papendal, NETHERLANDS
ID PROTEIN RADICAL FORMATION; MILK-PROTEINS; ANTIOXIDANT ACTIVITY;
CROSS-LINKING; IMMUNOCHEMICAL DETECTION; HYDROGEN-PEROXIDE; LIPID
OXIDATION; WHEY; PHOTOOXIDATION; IDENTIFICATION
AB Free radicals were characterised by mass spectrometry (MS) and immuno-spin trapping on alpha-lactalbumin (alpha-lac) after a lactoperoxidase (LPO)-catalysed reaction. Although spin traps have historically been used for electron spin resonance (ESR) studies, here free radicals were detected by immuno-spin trapping using the spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO), Western blotting, and MS; the latter yields information about the location of radical formation in the protein structure. Radical formation was highly specific towards Tyr residues; DMPO-trapped radicals were detected at Tyr18 and Tyr50, and the results also indicated a radical on Tyr36. These three oxidation sites on alpha-lac are all exposed on the surface of the protein, indicating that accessibility for LPO or DMPO was important. Applying immunospin trapping in combination with MS is a good approach to understand how different oxidation mechanisms affect the generation of radicals on proteins, and this oxidomics approach has future potential in food science. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Dalsgaard, Trine K.] Aarhus Univ, Fac Sci & Technol, Dept Food Sci, DK-8830 Tjele, Denmark.
[Triquigneaux, Mathilde; Summers, Fiona A.; Mason, Ronald P.] NIH, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
[Deterding, Leesa] NIEHS, Lab Struct Biol, NIH, Res Triangle Pk, NC 27709 USA.
[Mortensen, Grith] Arla Foods, Strateg Innovat Ctr, DK-8220 Brabrand, Denmark.
RP Dalsgaard, TK (reprint author), Aarhus Univ, Fac Sci & Technol, Dept Food Sci, POB 50, DK-8830 Tjele, Denmark.
EM trine.dalsgaard@agrsci.dk
FU Danish Agency of Science, Technology and Innovation; Protein as
Antioxidants - Effect of Protein Structure
FX This study was supported by a postdoctoral grant, Protein as
Antioxidants - Effect of Protein Structure, awarded by The Danish Agency
of Science, Technology and Innovation.
NR 31
TC 0
Z9 0
U1 2
U2 27
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0958-6946
EI 1879-0143
J9 INT DAIRY J
JI Int. Dairy J.
PD OCT
PY 2014
VL 38
IS 2
SI SI
BP 154
EP 159
DI 10.1016/j.idairyj.2013.11.005
PG 6
WC Food Science & Technology
SC Food Science & Technology
GA AN1GZ
UT WOS:000340332000011
ER
PT J
AU Yang, Y
Wu, QJ
Xie, L
Chow, WH
Rothman, N
Li, HL
Gao, YT
Zheng, W
Shu, XO
Xiang, YB
AF Yang, Yang
Wu, Qi-Jun
Xie, Li
Chow, Wong-Ho
Rothman, Nat
Li, Hong-Lan
Gao, Yu-Tang
Zheng, Wei
Shu, Xiao-Ou
Xiang, Yong-Bing
TI Prospective cohort studies of association between family history of
liver cancer and risk of liver cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE family history of liver cancer; liver cancer; cohort studies;
meta-analysis
ID HEPATITIS-B-VIRUS; HEPATOCELLULAR-CARCINOMA RISK; PANCREATIC-CANCER;
CIGARETTE-SMOKING; UNITED-STATES; SUSCEPTIBILITY LOCUS; HAIMEN-CITY;
CARRIERS; POLYMORPHISM; EPIDEMIOLOGY
AB Uncertainty remains on the relationship between a family history of liver cancer and liver cancer risk in prospective cohort studies in a general population. Thus, we examined this association in 133,014 participants in the Shanghai Women's and Men's Health Studies. Family history of liver cancer was categorized through dichotomous and proportional score approaches. Hazard ratios (HRs) and 95% confidence intervals (CIs) were derived using the Cox proportional hazards models with adjustment for potential confounders. A meta-analysis of observational studies through December 2013 on liver cancer risk in relation to family history of liver cancer was also performed. Study-specific risk estimates were combined using fixed or random effects models depending on whether significant heterogeneity was detected. For the Shanghai Women's and Men's Health Studies, 299 liver cancer cases were identified during follow-up through 2010. Family history of liver cancer was associated with liver cancer risk using both binary indicator (HR=2.60, 95% CI: 1.77-3.80) and proportional score (high-risk vs. minimal-risk category: HR=3.03, 95% CI: 1.73-5.31), with increasing HRs for increasing score categories. The meta-analysis also showed an increased risk for those with a family history of liver cancer (relative risk=2.55, 95% CI: 2.05-3.16). Family history of liver cancer was related to increased risk of liver cancer in Chinese population. This risk is particularly high for those with an affected mother. The "dose-response" of risk with an increasing family history score of liver cancer might further facilitate future cancer prevention programs on identifying individuals with the highest potential liver cancer risk.
C1 [Yang, Yang; Wu, Qi-Jun; Xie, Li; Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Shanghai Canc Inst,State Key Lab Oncogene & Relat, Shanghai 200032, Peoples R China.
[Yang, Yang; Wu, Qi-Jun; Xie, Li; Li, Hong-Lan; Gao, Yu-Tang; Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Epidemiol,Shanghai Canc Inst, Shanghai 200032, Peoples R China.
[Chow, Wong-Ho] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Div Canc Prevent & Populat Sci, Houston, TX 77030 USA.
[Rothman, Nat] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Zheng, Wei; Shu, Xiao-Ou] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Div Epidemiol,Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
RP Xiang, YB (reprint author), Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Shanghai Canc Inst, 25,Lane 2200,Xie Tu Rd, Shanghai 200032, Peoples R China.
EM ybxiang@shsci.org
FU State Key Project Specialized for Infectious Diseases of China
[2008ZX10002-015, 2012ZX10002008-002]; United States National Institutes
of Health [R37 CA070867, R01 CA82729]
FX Grant sponsor: State Key Project Specialized for Infectious Diseases of
China; Grant numbers: 2008ZX10002-015, 2012ZX10002008-002; Grant
sponsor: United States National Institutes of Health; Grant numbers: R37
CA070867, R01 CA82729
NR 61
TC 6
Z9 7
U1 0
U2 29
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2014
VL 135
IS 7
BP 1605
EP 1614
DI 10.1002/ijc.28792
PG 10
WC Oncology
SC Oncology
GA AN3XA
UT WOS:000340520800013
PM 24535817
ER
PT J
AU Freedman, DM
Wu, JC
Daugherty, SE
Kuncl, RW
Enewold, LR
Pfeiffer, RM
AF Freedman, D. Michal
Wu, Jincao
Daugherty, Sarah E.
Kuncl, Ralph W.
Enewold, Lindsey R.
Pfeiffer, Ruth M.
TI The risk of amyotrophic lateral sclerosis after cancer in US elderly
adults: A population-based prospective study
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE cancer; amyotrophic lateral sclerosis; Medicare; SEER Program
ID MOTOR-NEURON DISEASE; PARKINSONS-DISEASE; UNITED-STATES; MEDICARE DATA;
ASSOCIATION; MORTALITY
AB Although epidemiologic studies have examined the risk of amyotrophic lateral sclerosis (ALS) in relation to cancer, none have been large population-based studies using incident ALS and adjusting for medical surveillance. Addressing those limitations, all first primary cancer cases from the Surveillance, Epidemiology and End Results (SEER) Program (1992-2005), linked to Medicare claims data were used. Cases were followed from cancer diagnosis until the earliest date of ALS diagnosis, a break in Medicare claims data, death, age 85 or December 31, 2005. A comparison group from a 5% random Medicare sample in the SEER areas who were cancer-free and censored as above, or until a cancer diagnosis were selected. ALS outcomes were derived from medical claims. The proportional hazards models to estimate ALS hazard ratios (HRs), using age as the time scale, adjusting for sex, race and physician visits, and stratifying the baseline hazard on birth year and SEER registry were used. A total of 303 ALS cases were ascertained in cancer patients (2,154,062 person-years) compared with 246 ALS cases (2,467,634 person-years) in the reference population. There was no overall relationship between cancer and ALS (HR = 0.99; 95% CI = 0.81-1.22), nor by gender or race. Except for an elevated ALS risk in the first year after a leukemia diagnosis, the relationship between site-specific cancers and ALS was null after correcting for multiple comparisons. Having a cancer diagnosis was not associated with an overall risk of incident ALS. The short-term ALS risk after leukemia may reflect screening or reporting errors.
C1 [Freedman, D. Michal; Wu, Jincao; Daugherty, Sarah E.; Pfeiffer, Ruth M.] NCI, US Dept HHS, NIH, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
[Kuncl, Ralph W.] Univ Redlands, Dept Biol, Redlands, CA 92373 USA.
[Enewold, Lindsey R.] NCI, US Dept HHS, NIH, Div Canc Control & Populat Sci, Rockville, MD USA.
RP Freedman, DM (reprint author), NCI, US Dept HHS, NIH, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM freedmam@mail.nih.gov
FU National Institutes of Health, National Cancer Institute; U.S. Public
Health Service
FX Grant sponsors: Intramural Research Program of the National Institutes
of Health, National Cancer Institute and the U.S. Public Health Service
NR 20
TC 9
Z9 9
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2014
VL 135
IS 7
BP 1745
EP 1750
DI 10.1002/ijc.28795
PG 6
WC Oncology
SC Oncology
GA AN3XA
UT WOS:000340520800028
PM 24550098
ER
PT J
AU Di Biagio, A
Rusconi, S
Marzocchetti, A
Signori, A
Schiavetti, I
Bruzzone, B
Monno, L
Punzi, G
Colao, MG
Penco, G
Zazzi, M
De Luca, A
AF Di Biagio, Antonio
Rusconi, Stefano
Marzocchetti, Angela
Signori, Alessio
Schiavetti, Irene
Bruzzone, Bianca
Monno, Laura
Punzi, Grazia
Colao, Maria Grazia
Penco, Giovanni
Zazzi, Maurizio
De Luca, Andrea
CA ARCA Collaborative Grp
TI The Role of Baseline HIV-1 RNA, Drug Resistance, and Regimen Type as
Determinants of Response to First-Line Antiretroviral Therapy
SO JOURNAL OF MEDICAL VIROLOGY
LA English
DT Article
DE HIV-1 RNA; CD4; drug resistance; drug regimen; wGSS; N(n)RTI backbone
ID HIV-1-INFECTED PATIENTS; COLLABORATIVE ANALYSIS; INFECTED ADULTS; VIRAL
LOAD; CELL COUNTS; EFAVIRENZ; INDIVIDUALS; PROGRESSION; INITIATION;
PROGNOSIS
AB The factors influencing virological response to first-line combined antiretroviral therapy (cART) in an Italian cohort of HIV-1-infected patients were examined. Eligible patients were those enrolled in a national prospective observational cohort (Antiretroviral Resistance Cohort Analysis), starting first-line cART between 2001 and 2011 and who had at least one follow-up of HIV-1 RNA. The primary endpoint was virological success, defined as the first viral load <50 copies/ml. Time to events were analyzed by Kaplan-Meier analysis and Cox proportional hazard model. One thousand three hundred five patients met the study inclusion criteria. In a multivariable model adjusting for transmission mode, presence of transmitted drug resistance, baseline CD4(+) cell count, viral subtype, and type of NRTI backbone employed, independent predictors of virological success were higher baseline viral load (>= 500,000 vs. <100,000 HR 0.52; P < 0.001), a weighted genotypic susceptibility score (wGSS) < 3 (HR 0.58; P = 0.003), male sex (HR 0.76 P = 0.001), and type of initial third drug employed (integrase inhibitor vs. boosted protease inhibitors HR 3.23; P < 0.001). In the subset with HIV-1 RNA >100,000 copies/ml, virologic success was only associated with the use of integrase inhibitors in the first cART regimen. Independent predictors of immunological success were baseline CD4(+) cell count and wGSS <3. High baseline HIV-1 RNA, predicted activity of the first-line regimen based on genotypic resistance testing, gender, and use of new agents were found to predict time to achieve virological success. The type of initial nucleoside analog backbone was not found to predict virological response. (C) 2014 Wiley Periodicals, Inc.
C1 [Di Biagio, Antonio] Natl Canc Inst, IRCCS San Martino IST, Clin Infect Dis, Genoa, Italy.
[Rusconi, Stefano] Univ Milan, Clin Infect Dis, DIBIC Luigi Sacco, I-20157 Milan, Italy.
[Marzocchetti, Angela; De Luca, Andrea] Univ Cattolica Sacro Cuore, Inst Clin Infect Dis, I-00168 Rome, Italy.
[Signori, Alessio; Schiavetti, Irene] Univ Genoa, Dept Hlth Sci, Biostat Unit, Genoa, Italy.
[Bruzzone, Bianca] Natl Canc Inst, Hyg Unit, IRCCS San Martino IST, Genoa, Italy.
[Monno, Laura; Punzi, Grazia] Univ Bari, Clin Infect Dis, Bari, Italy.
[Colao, Maria Grazia] AOU Careggi, Inst Virol, Florence, Italy.
[Penco, Giovanni] EO Galliera, Dept Infect Dis, Genoa, Italy.
[Zazzi, Maurizio] Univ Siena, Dept Med Biotechnol, I-53100 Siena, Italy.
[De Luca, Andrea] Univ Hosp Siena, Univ Div Infect Dis, Siena, Italy.
RP Rusconi, S (reprint author), Univ Milan, Clin Infect Dis, DIBIC Luigi Sacco, Via GB Grassi 74, I-20157 Milan, Italy.
EM stefano.rusconi@unimi.it
RI De Luca, Andrea/G-8810-2011;
OI Zazzi, Maurizio/0000-0002-0344-6281; MONNO, Laura/0000-0002-2713-4258;
Signori, Alessio/0000-0001-6289-9144; Di Biagio,
Antonio/0000-0003-1436-5089
FU Abbott; Bristol-Myers Squibb; Gilead; Janssen-Cilag; Merck Sharp Dohme;
Roche; ViiV; Pfizer; ViiV Healthcare; Abbott Molecular; Siemens
Diagnostics; Teva Pharmaceuticals
FX ADB did not receive any financial support for his contribution to this
study, but he has received prior research funding and/or consultancy
honoraria from Abbott, Bristol-Myers Squibb, Gilead, Janssen-Cilag,
Merck Sharp & Dohme, Roche, and ViiV. SR has received research funding
from Pfizer and have been involved in advisory boards or educational
courses supported by the following companies: Abbott, Boehringer
Ingelheim, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, now ViiV
Healthcare, Merck Sharp & Dohme and Janssen-Cilag. BB has received
consultancy honoraria from Abbott, Bristol-Myers Squibb, Gilead,
Janssen-Cilag, Merck Sharp & Dohme and ViiV. MZ has received research
funding from ViiV Healthcare and Abbott Molecular, has been member of
the speakers bureau of Janssen-Cilag and Merck Sharp & Dohme, and has
been member of advisory boards for Merck Sharp & Dohme and Abbott
Molecular. ADL has received research funding from ViiV Healthcare, is
member of the speakers bureau of Gilead, has been member of advisory
boards for Gilead, Janssen-Cilag, Siemens Diagnostics, ViiV Healthcare,
and Teva Pharmaceuticals, and has received consultancy honoraria from
Gilead and Janssen-Cilag.
NR 27
TC 5
Z9 5
U1 0
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0146-6615
EI 1096-9071
J9 J MED VIROL
JI J. Med. Virol.
PD OCT
PY 2014
VL 86
IS 10
BP 1648
EP 1655
DI 10.1002/jmv.24017
PG 8
WC Virology
SC Virology
GA AN4EN
UT WOS:000340540500002
PM 25042976
ER
PT J
AU Kolb, EA
Gorlick, R
Billups, CA
Hawthorne, T
Kurmasheva, RT
Houghton, PJ
Smith, MA
AF Kolb, E. Anders
Gorlick, Richard
Billups, Catherine A.
Hawthorne, Thomas
Kurmasheva, Raushan T.
Houghton, Peter J.
Smith, Malcolm A.
TI Initial Testing (Stage 1) of Glembatumumab Vedotin (CDX-011) by the
Pediatric Preclinical Testing Program
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE antibody-drug conjugate; developmental therapeutics; osteosarcoma;
preclinical testing
ID ANTIBODY-DRUG CONJUGATE; HIGH-DOSE METHOTREXATE; ADJUVANT CHEMOTHERAPY;
THERAPEUTIC TARGET; BREAST-CANCER; DC-HIL; OSTEOSARCOMA; MELANOMA;
GPNMB; GLYCOPROTEIN
AB Background. Glembatumumab vedotin is an antibody-auristatin conjugate that targets cells expressing the transmembrane glycoprotein NMB (GPNMB, also known as osteoactivin). It has entered clinical evaluation for adult cancers that express GPNMB, including melanoma and breast cancer. Procedures. Glembatumumab vedotin was administered intravenously at a dose of 2.5 mg/kg using a weekly x 3 schedule, and its antitumor activity was evaluated against selected Pediatric Preclinical Testing Program (PPTP) solid tumor xenografts using standard PPTP response metrics. Results. Among PPTP xenografts, GPNMB was primarily expressed on the osteosarcoma xenografts, all of which expressed GPNMB at the RNA level, although at varying levels. Protein expression assessed by immunohistochemistry (IHC) showed variation across the osteosarcoma xenografts with one model showing no tumor cell expression. Glembatumumab vedotin induced statistically significant differences (P < 0.05) in event-free survival (EFS) distribution compared to control in each of the six osteosarcoma models studied. Three of six osteosarcoma xenografts demonstrated a maintained complete response (MCR). Two other xenografts showed progressive disease with growth delay, while the final xenograft showed progressive disease with no growth delay. Two of the osteosarcoma xenografts with MCRs showed the highest GPNMB expression at the RNA level. Conversely, the xenograft with the lowest GPNMB mRNA expression had the poorest response to glembatumumab vedotin. Two rhabdomyosarcoma xenografts that did not express GPNMB showed limited responses to glembatumumab vedotin. Conclusions. Glembatumumab vedotin yielded high-level activity against three of six osteosarcoma xenografts, with evidence for response being related to GPNMB expression levels. (C) 2014 Wiley Periodicals, Inc.
C1 [Kolb, E. Anders] Alfred I DuPont Hosp Children, Wilmington, DE 19803 USA.
[Gorlick, Richard] Childrens Hosp Montefiore, Bronx, NY USA.
[Billups, Catherine A.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Hawthorne, Thomas] Celldex Therapeut, Needham, MA USA.
[Kurmasheva, Raushan T.; Houghton, Peter J.] Nationwide Childrens Hosp, Columbus, OH USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Kolb, EA (reprint author), Alfred I DuPont Hosp Children, Dept Oncol, 1600 Rockland Rd, Wilmington, DE 19803 USA.
EM eakolb@nemours.org
FU National Cancer Institute [NO1-CM-42216, CA21765, CA108786]
FX Grant sponsor: National Cancer Institute; Grant numbers: NO1-CM-42216;
CA21765; CA108786
NR 29
TC 8
Z9 9
U1 0
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD OCT
PY 2014
VL 61
IS 10
BP 1816
EP 1821
DI 10.1002/pbc.25099
PG 6
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA AN4ET
UT WOS:000340541100020
PM 24912408
ER
PT J
AU Garg, NK
Dwivedi, P
Jain, A
Tyagi, S
Sahu, T
Tyagi, RK
AF Garg, Neeraj K.
Dwivedi, Priya
Jain, Ashay
Tyagi, Shikha
Sahu, Tejram
Tyagi, Rajeev K.
TI Development of novel carrier(s) mediated tuberculosis vaccine: More than
a tour de force
SO EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Review
DE Tuberculosis; Liposomes; Microparticle; Nanoparticles; Mucosal vaccine;
PLGA
ID T-CELL RESPONSE; ENHANCED PROTECTIVE EFFICACY;
MYCOBACTERIUM-TUBERCULOSIS; DNA VACCINE; IMMUNE-RESPONSE; DENDRITIC
CELLS; CALMETTE-GUERIN; IN-VIVO; ALVEOLAR MACROPHAGES; SUBUNIT
VACCINATION
AB Despite worldwide availability of the vaccines against most of the infectious diseases, BCG and various programs such as Directly Observed Treatment Short course (DOTS) to prevent tuberculosis still remains one of the most deadly forms of the disease affecting millions of people globally. The evolution of multi drug resistant strains (MDR) has increased the complexity further. Although currently available marketed BCG vaccine has shown sufficient protection against childhood tuberculosis, it has failed to prevent the most common form of disease i.e., pulmonary tuberculosis in adults. However, various vaccine candidates have already entered phase I clinical trials and have shown promising outcomes. The most prominent amongst them is the heterologous prime-boost approach, which shows a great promise towards designing and development of a new efficacious tuberculosis vaccine. It has also been shown that the use of various viral and non-viral vectors as carriers for the potential vaccine candidates will further boost their effect on subsequent immunization. In this review, we briefly summarize the potential of a few novel nano-carriers for developing effective vaccination strategies against tuberculosis. Published by Elsevier B.V.
C1 [Garg, Neeraj K.; Jain, Ashay] Panjab Univ, UGC Ctr Adv Studies, Univ Inst Pharmaceut Sci, Drug Delivery Res Grp, Chandigarh 160014, India.
[Garg, Neeraj K.; Jain, Ashay] Dr Hari Singh Gour Vishwavidyalaya, Dept Pharmaceut Sci, Sagar 470003, MP, India.
[Dwivedi, Priya] TRS Coll, Dept Biotechnol, Rewa 486001, MP, India.
[Tyagi, Shikha] UP Tech Univ, IMS Engn Coll, Dept Biotechnol, Lucknow, Uttar Pradesh, India.
[Sahu, Tejram] NIAID, NIH, Rockville, MD USA.
[Tyagi, Rajeev K.] Georgia Regents Univ, Coll Dent Med, Dept Periodont, Augusta, GA USA.
RP Garg, NK (reprint author), Panjab Univ, UGC Ctr Adv Studies, Univ Inst Pharmaceut Sci, Drug Delivery Res Grp, Chandigarh 160014, India.
EM neerajombiotech@gmail.com; rtyagi@gru.edu
OI Sahu, Tejram/0000-0002-0912-7660
FU Council of Scientific and Industrial Research-Human Resource Development
Group (CSIR-HRDG), Department of Biotechnology (DBT), New Delhi, India
FX The research work is supported by various grants from Council of
Scientific and Industrial Research-Human Resource Development Group
(CSIR-HRDG), Department of Biotechnology (DBT), New Delhi, India. The
authors have no other relevant affiliations or financial involvement
with any other organization or entity with a financial interest in or
financial conflict with the subject matter or material discussed in the
manuscript apart from those disclosed. No writing assistance was taken
in this manuscript.
NR 111
TC 0
Z9 1
U1 2
U2 51
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0928-0987
EI 1879-0720
J9 EUR J PHARM SCI
JI Eur. J. Pharm. Sci.
PD OCT 1
PY 2014
VL 62
BP 227
EP 242
DI 10.1016/j.ejps.2014.05.028
PG 16
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AN0VG
UT WOS:000340301500027
PM 24909731
ER
PT J
AU Pletnikova, O
Sloane, KL
Renton, AE
Traynor, BJ
Crain, BJ
Reid, T
Zu, T
Ranum, LPW
Troncoso, JC
Rabins, PV
Onyike, CU
AF Pletnikova, Olga
Sloane, Kelly L.
Renton, Alan E.
Traynor, Bryan J.
Crain, Barbara J.
Reid, Tammy
Zu, Tao
Ranum, Laura P. W.
Troncoso, Juan C.
Rabins, Peter V.
Onyike, Chiadi U.
TI Hippocampal sclerosis dementia with the C9ORF72 hexanucleotide repeat
expansion
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE C9ORF72 hexanucleotide repeat expansion; Hippocampal sclerosis;
Dementia; Frontotemporal dementia
ID AMYOTROPHIC-LATERAL-SCLEROSIS; FRONTOTEMPORAL LOBAR DEGENERATION;
ALZHEIMERS-DISEASE; GGGGCC REPEAT; RISK-FACTOR; TRANSLATION; ALS;
NEURODEGENERATION; MUTATIONS; C9FTD/ALS
AB Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are the main syndromes of the chromosome 9 ORF72 (C9ORF72) hexanucleotide repeat expansion, but studies have shown a substantial phenotypic diversity that includes psychiatric presentations. This study describes hippocampal sclerosis dementia (HSD) in carriers of the C9ORF72 mutation. We compared clinical and neuropathological features of HSD in carriers and noncarriers autopsied at Johns Hopkins. Carriers presented with amnesia, agitation, dissocial behavior, and impaired self-care, whereas noncarriers showed little agitation. The groups were not dissimilar in cognitive or motor dysfunction. Neuropathological examination of carriers showed cerebellar neuronal inclusions positive for ubiquitin, p62, and ubiquilin-2, and negative for TAR DNA-binding protein 43. Noncarriers did not have cerebellar inclusions. C9ORF72 repeat-associated non-ATG translation was confirmed by immunohistochemistry. These observations broaden the C9ORF72 phenotype and place HSD in the FTD spectrum. The amnesic phenotype of HSD, which is consistent with the focal hippocampal atrophy, should be included in clinical categorizations of FTD. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Pletnikova, Olga; Crain, Barbara J.; Troncoso, Juan C.] Johns Hopkins Univ, Dept Pathol, Div Neuropathol, Baltimore, MD USA.
[Sloane, Kelly L.; Rabins, Peter V.; Onyike, Chiadi U.] Johns Hopkins Univ Hosp, Dept Psychiat & Behav Sci, Div Geriatr Psychiat & Neuropsychiatry, Baltimore, MD 21287 USA.
[Renton, Alan E.; Traynor, Bryan J.] NIH, NIA, Neurogenet Lab, Neuromuscular Dis Res Unit, Bethesda, MD USA.
[Traynor, Bryan J.] Johns Hopkins Univ, Brain Sci Inst, Baltimore, MD USA.
[Reid, Tammy; Zu, Tao; Ranum, Laura P. W.] Univ Florida, Coll Med, Ctr NeuroGenet, Dept Mol Genet & Microbiol, Gainesville, FL USA.
[Reid, Tammy; Zu, Tao; Ranum, Laura P. W.] Univ Florida, Coll Med, Genet Inst, Dept Neurol, Gainesville, FL USA.
[Troncoso, Juan C.] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
RP Onyike, CU (reprint author), Johns Hopkins Univ Hosp, Dept Psychiat & Behav Sci, Div Geriatr Psychiat & Neuropsychiatry, 600 N Wolfe St,Meyer 279, Baltimore, MD 21287 USA.
EM conyike1@johnshopkins.edu
FU Intramural Research Program of the National Institutes of Health,
National Institute on Aging [Z01-AG000949-02]; Johns Hopkins Alzheimer's
Disease Research Center (National Institutes on Aging) [P50AG05146];
Samuel I. Newhouse Foundation; Robert Hall family; Richman Family
professorship; Jane Tanger Black Fund for Young-Onset Dementia Research;
W.F. Keck Foundation; ALS Association; Target ALS
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Aging
(Z01-AG000949-02); the Johns Hopkins Alzheimer's Disease Research Center
(National Institutes on Aging grant P50AG05146); the Samuel I. Newhouse
Foundation; the Robert Hall family; the Richman Family professorship;
the Jane Tanger Black Fund for Young-Onset Dementia Research; the W.F.
Keck Foundation; the ALS Association; and Target ALS.
NR 42
TC 2
Z9 2
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2014
VL 35
IS 10
AR 2419e.17
DI 10.1016/j.neurobiolaging.2014.04.009
PG 5
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AM3EK
UT WOS:000339735100028
PM 24819148
ER
PT J
AU Sassi, C
Guerreiro, R
Gibbs, R
Ding, JH
Lupton, MK
Troakes, C
Lunnon, K
Al-Sarraj, S
Brown, KS
Medway, C
Lord, J
Turton, J
Mann, D
Snowden, J
Neary, D
Harris, J
Bras, J
Morgan, K
Powell, JF
Singleton, A
Hardy, J
AF Sassi, Celeste
Guerreiro, Rita
Gibbs, Raphael
Ding, Jinhui
Lupton, Michelle K.
Troakes, Claire
Lunnon, Katie
Al-Sarraj, Safa
Brown, Kristelle S.
Medway, Chirstopher
Lord, Jenny
Turton, James
Mann, David
Snowden, Julie
Neary, David
Harris, Jeniffer
Bras, Jose
Morgan, Kevin
Powell, John F.
Singleton, Andrew
Hardy, John
CA ARUK Consortium
TI Exome sequencing identifies 2 novel presenilin 1 mutations (p.L166V and
p.S230R) in British early-onset Alzheimer's disease
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Early-onset Alzheimer's disease; APP; PSEN1; PSEN2; British cohort
ID PRECURSOR PROTEIN GENE; APP; GENERATION
AB Early-onset Alzheimer's disease (EOAD) represents 1%-2% of the Alzheimer's disease (AD) cases, and it is generally characterized by a positive family history and a rapidly progressive symptomatology. Rare coding and fully penetrant variants in amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) are the only causative mutations reported for autosomal dominant AD. Thus, in this study we used exome sequencing data to rapidly screen rare coding variability in APP, PSEN1, and PSEN2, in a British cohort composed of 47 unrelated EOAD cases and 179 elderly controls, neuropathologically proven. We report 2 novel and likely pathogenic variants in PSEN1 (p.L166V and p.S230R). A comprehensive catalog of rare pathogenic variants in the AD Mendelian genes is pivotal for a premortem diagnosis of autosomal dominant EOAD and for the differential diagnosis with other early onset dementias such as frontotemporal dementia (FTD) and Creutzfeldt-Jakob disease (CJD). (C) 2014 The Authors. Published by Elsevier Inc. All rights reserved(.)
C1 [Sassi, Celeste; Guerreiro, Rita; Gibbs, Raphael; Bras, Jose; Hardy, John] UCL, Inst Neurol, London, England.
[Sassi, Celeste; Guerreiro, Rita; Gibbs, Raphael; Ding, Jinhui; Singleton, Andrew] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Lupton, Michelle K.; Troakes, Claire; Lunnon, Katie; Al-Sarraj, Safa; Powell, John F.] Kings Coll London, Inst Psychiat, London, England.
[Brown, Kristelle S.; Medway, Chirstopher; Lord, Jenny; Turton, James; Morgan, Kevin] Univ Nottingham, Queens Med Ctr, Inst Genet, Sch Mol Med Sci, Nottingham NG7 2RD, England.
[Mann, David] Univ Manchester, Inst Brain Behav & Mental Hlth, Manchester, Lancs, England.
[Snowden, Julie; Neary, David; Harris, Jeniffer] Greater Manchester Neurosci Ctr, Cerebral Funct Unit, Manchester, Lancs, England.
RP Sassi, C (reprint author), NIH, Neurogenet Lab, 35 Convent Dr, Bethesda, MD 20892 USA.
EM celeste.sassi.10@ucl.ac.uk
RI Pickering-Brown, Stuart/D-4008-2009; Troakes, Claire/K-4346-2015;
Lunnon, Katie/C-4638-2012; Guerreiro, Rita/A-1327-2011; Hardy,
John/C-2451-2009; Singleton, Andrew/C-3010-2009; Bras, Jose/A-1428-2011;
Powell, John/G-4412-2011
OI Pickering-Brown, Stuart/0000-0003-1561-6054; Lunnon,
Katie/0000-0001-7570-6065; Bras, Jose/0000-0001-8186-0333; Snowden,
Julie/0000-0002-3976-4310; Powell, John/0000-0001-6124-439X
FU Alzheimer's Research UK; Medical Research Council; Wellcome Trust;
Wellcome Trust/MRC Joint Call in Neurodegeneration Award [WT089698];
National Institute for Health Research Biomedical Research Unit in
Dementia at University College London Hospitals, University College
London; National Institutes of Health Research; Wellcome Trust Medical
Research Council; Fondation pour la Recherche sur Alzheimer; Big
Lottery; Intramural Research Program of the National Institute on Aging,
National Institutes of Health (Department of Health and Human Services)
[ZO1 AG000950-10]; Intramural Research Program of the National Institute
of Neurological Disease and Stroke, National Institutes of Health
(Department of Health and Human Services) [ZO1 AG000950-10]; ARUK; ABBUK
Ltd; [P50 AG016574]; [U01 AG006786]; [R01 AG18023]
FX This study was supported by the Alzheimer's Research UK, the Medical
Research Council, the Wellcome Trust, the Wellcome Trust/MRC Joint Call
in Neurodegeneration Award (WT089698) to the UK Parkinson's Disease
Consortium (whose members are from the University College London
Institute of Neurology, the University of Sheffield, and the MRC Protein
Phosphorylation Unit at the University of Dundee), grants (P50 AG016574,
U01 AG006786, and R01 AG18023), the National Institute for Health
Research Biomedical Research Unit in Dementia at University College
London Hospitals, University College London; the National Institutes of
Health Research, the Wellcome Trust Medical Research Council, an
anonymous charitable foundation, the Fondation pour la Recherche sur
Alzheimer, the Big Lottery (to Dr Morgan); a fellowship from Alzheimer's
Research UK (to Dr Guerreiro); and the Intramural Research Programs of
the National Institute on Aging and the National Institute of
Neurological Disease and Stroke, National Institutes of Health
(Department of Health and Human Services Project number, ZO1
AG000950-10). The MRC London Neurodegenerative Diseases Brain Bank and
the Manchester Brain Bank from Brains for Dementia Research are jointly
funded from ARUK and AS via ABBUK Ltd.
NR 16
TC 2
Z9 3
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2014
VL 35
IS 10
AR 2422.e13
DI 10.1016/j.neurobiolaging.2014.04.026
PG 4
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AM3EK
UT WOS:000339735100036
PM 24880964
ER
PT J
AU Van Doormaal, PTC
Ticozzi, N
Gellera, C
Ratti, A
Taroni, F
Chio, A
Calvo, A
Mora, G
Restagno, G
Traynor, BJ
Birve, A
Lemmens, R
Van Es, MA
Saris, CGJ
Blauw, HM
Van Vught, PWJ
Groen, EJN
Corrado, L
Mazzini, L
Del Bo, R
Corti, S
Waibel, S
Meyer, T
Ludolph, AC
Goris, A
Van Damme, P
Robberecht, W
Shatunov, A
Fogh, I
Andersen, PM
D'Alfonso, S
Hardiman, O
Cronin, S
Rujescu, D
Al-Chalabi, A
Landers, JE
Silani, V
Van den Berg, LH
Veldink, JH
AF Van Doormaal, Perry T. C.
Ticozzi, Nicola
Gellera, Cinzia
Ratti, Antonia
Taroni, Franco
Chio, Adriano
Calvo, Andrea
Mora, Gabriele
Restagno, Gabriella
Traynor, Bryan J.
Birve, Anna
Lemmens, Robin
Van Es, Michael A.
Saris, Christiaan G. J.
Blauw, Hylke M.
Van Vught, Paul W. J.
Groen, Ewout J. N.
Corrado, Lucia
Mazzini, Letizia
Del Bo, Roberto
Corti, Stefania
Waibel, Stefan
Meyer, Thomas
Ludolph, Albert C.
Goris, An
Van Damme, Philip
Robberecht, Wim
Shatunov, Aleksey
Fogh, Isabella
Andersen, Peter M.
D'Alfonso, Sandra
Hardiman, Orla
Cronin, Simon
Rujescu, Dan
Al-Chalabi, Ammar
Landers, John E.
Silani, Vincenzo
Van den Berg, Leonard H.
Veldink, Jan H.
TI Analysis of the KIFAP3 gene in amyotrophic lateral sclerosis: a
multicenter survival study
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Amyotrophic lateral sclerosis; Kinesin-associated protein 3 gene;
KIFAP3; Genome-wide association study
AB Sporadic amyotrophic lateral sclerosis is a multifactorial disease of environmental and genetic origin. In a previous large multicenter genome wide study, common genetic variation in the Kinesin-Associated Protein 3 (KIFAP3) gene (rs1541160) was reported to have a significant effect on survival in amyotrophic lateral sclerosis patients. However, this could not be replicated in 3 smaller independent cohorts. We conducted a large multicenter multivariate survival analysis (n = 2362) on the effect of genetic variation in rs1541160. The previously reported beneficial genotype did not show a significant improvement in survival in this patient group. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Van Doormaal, Perry T. C.; Van Es, Michael A.; Saris, Christiaan G. J.; Blauw, Hylke M.; Van Vught, Paul W. J.; Groen, Ewout J. N.; Van den Berg, Leonard H.; Veldink, Jan H.] Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Dept Neurol, Utrecht, Netherlands.
[Ticozzi, Nicola; Ratti, Antonia; Silani, Vincenzo] IRCCS, Ist Auxologico Italiano, Neurol Unit, Neurosci Lab, Milan, Italy.
[Ticozzi, Nicola; Ratti, Antonia; Del Bo, Roberto; Corti, Stefania; Silani, Vincenzo] Univ Studi Milano, Dino Ferrari Ctr, Dept Pathophysiol & Transplantat, Milan, Italy.
[Gellera, Cinzia; Taroni, Franco] IRCCS, Carlo Besta Neurol Inst, Neurodegenerat & Metab Dis, Genet Unit, Milan, Italy.
[Chio, Adriano; Calvo, Andrea] Univ Turin, Dept Neurol Sci, Turin, Italy.
[Mora, Gabriele] IRCCS, ALS Ctr, Salvatore Maugeri Fdn, Milan, Italy.
[Restagno, Gabriella] Citta Salute Scienza Hosp, Genet Mol Lab, Turin, Italy.
[Traynor, Bryan J.] Natl Inst Aging, Neurogenet Lab, Neuromuscular Dis Res Grp, Bethesda, MD USA.
[Birve, Anna; Andersen, Peter M.] Umea Univ, Inst Pharmacol & Clin Neurosci, Umea, Sweden.
[Lemmens, Robin; Goris, An; Van Damme, Philip; Robberecht, Wim] Univ Leuven, LIND, Leuven, Belgium.
[Lemmens, Robin; Van Damme, Philip; Robberecht, Wim] Flanders Inst Biotechnol VIB, Vesalius Res Ctr Ctr VRC, Leuven, Belgium.
[Lemmens, Robin; Van Damme, Philip; Robberecht, Wim] Univ Leuven, Univ Hosp Leuven, Dept Clin & Expt Neurol, Leuven, Belgium.
[Corrado, Lucia; D'Alfonso, Sandra] Univ Piemonte Orientale, IRCAD, Dept Hlth Sci, Novara, Italy.
[Mazzini, Letizia] Avogadro Univ & Maggiore Carita Hosp, Dept Neurol, Novara, Italy.
[Del Bo, Roberto; Corti, Stefania] IRCCS, Fdn Ca Granda Osped Maggiore Policlin, Neurol Unit, Milan, Italy.
[Waibel, Stefan; Ludolph, Albert C.] Univ Ulm, Dept Neurol, D-89069 Ulm, Germany.
[Meyer, Thomas] Humboldt Univ, Charite Univ Hosp, Dept Neurol, Berlin, Germany.
[Goris, An] Katholieke Univ Leuven, Sect Expt Neurol, Lab Neuroimmunol, Leuven, Belgium.
[Shatunov, Aleksey; Fogh, Isabella; Al-Chalabi, Ammar] Kings Coll London, Inst Psychiat, Dept Clin Neurosci, London, England.
[Hardiman, Orla] Trinity Coll Dublin, Inst Neurosci, Dublin, Ireland.
[Hardiman, Orla; Cronin, Simon] Beaumont Hosp, Dept Neurol, Dublin, Ireland.
[Cronin, Simon] Royal Coll Surgeons Ireland, Dept Clin Neurol Sci, Dublin, Ireland.
[Rujescu, Dan] Univ Halle, Dept Psychiat, Halle, Germany.
[Landers, John E.] Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA USA.
RP Veldink, JH (reprint author), Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Dept Neurol, Utrecht, Netherlands.
EM j.h.veldink@umcutrecht.nl
RI GELLERA, CINZIA/J-7887-2016; Van Damme, Philip/A-6464-2009; D'Alfonso,
Sandra/K-7295-2014; Goris, An/F-2943-2010; Calvo, Andrea/K-4141-2016;
Corti, Stefania/K-6034-2016; Ticozzi, Nicola/K-8094-2016; Groen,
Ewout/L-5081-2016;
OI Silani, Vincenzo/0000-0002-7698-3854; GELLERA,
CINZIA/0000-0002-3582-665X; Hardiman, Orla/0000-0003-2610-1291; Van
Damme, Philip/0000-0001-6384-0611; D'Alfonso,
Sandra/0000-0002-3983-9925; Goris, An/0000-0002-1276-6682; Calvo,
Andrea/0000-0002-5122-7243; Corti, Stefania/0000-0001-5425-969X;
Ticozzi, Nicola/0000-0001-5963-7426; Groen, Ewout/0000-0002-2330-9444;
Chio, Adriano/0000-0001-9579-5341
FU Medical Research Council [G0600974]; NINDS NIH HHS [R01 NS065847]
NR 0
TC 1
Z9 1
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2014
VL 35
IS 10
AR 2420.e13
DI 10.1016/j.neurobiolaging.2014.04.014
PG 2
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AM3EK
UT WOS:000339735100031
PM 24838185
ER
PT J
AU Yotter, RA
Doshi, J
Clark, V
Sojkova, J
Zhou, Y
Wong, DF
Ferrucci, L
Resnick, SM
Davatzikos, C
AF Yotter, Rachel A.
Doshi, Jimit
Clark, Vanessa
Sojkova, Jitka
Zhou, Yun
Wong, Dean F.
Ferrucci, Luigi
Resnick, Susan M.
Davatzikos, Christos
TI Memory decline shows stronger associations with estimated spatial
patterns of amyloid deposition progression than total amyloid burden
(vol 34, pg 2835, 2013)
SO NEUROBIOLOGY OF AGING
LA English
DT Correction
C1 [Yotter, Rachel A.; Doshi, Jimit; Clark, Vanessa; Davatzikos, Christos] Univ Penn, Dept Radiol, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.
[Sojkova, Jitka; Resnick, Susan M.] NIA, Lab Behav Neurosci, Baltimore, MD 21224 USA.
[Sojkova, Jitka; Zhou, Yun; Wong, Dean F.] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
RP Yotter, RA (reprint author), Univ Penn, Dept Radiol, Ctr Biomed Image Comp & Analyt, Philadelphia, PA 19104 USA.
EM rachel.yotter@uphs.upenn.edu
NR 1
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 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2014
VL 35
IS 10
AR e25
DI 10.1016/j.neurobiolaging.2014.04.005
PG 1
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AM3EK
UT WOS:000339735100003
ER
PT J
AU Bolandzadeh, N
Liu-Ambrose, T
Aizenstein, H
Harris, T
Launer, L
Yaffe, K
Kritchevsky, SB
Newman, A
Rosano, C
AF Bolandzadeh, Niousha
Liu-Ambrose, Teresa
Aizenstein, Howard
Harris, Tamara
Launer, Lenore
Yaffe, Kristine
Kritchevsky, Stephen B.
Newman, Anne
Rosano, Caterina
TI Pathways linking regional hyperintensities in the brain and slower gait
SO NEUROIMAGE
LA English
DT Article
DE White matter hyperintensities; Mobility; Cognitive function; Executive
function; Gait speed; Mediation
ID WHITE-MATTER LESIONS; RANDOMIZED CONTROLLED-TRIAL; MILD COGNITIVE
IMPAIRMENT; FUNCTIONING OLDER-ADULTS; VASCULAR RISK-FACTORS;
ABNORMALITIES; POPULATION; DECLINE; PEOPLE; SPEED
AB Importance: Cerebral white matter hyperintensities (WMHs) are involved in the evolution of impaired mobility and executive functions. Executive functions and mobility are also associated. Thus WMHs may impair mobility directly, by disrupting mobility-related circuits, or indirectly, by disrupting circuits responsible for executive functions. Understanding the mechanisms underlying impaired mobility in late life will increase our capacity to develop effective interventions.
Objective: To identify regional WMHs most related to slower gait and to examine whether these regional WMHs directly impact mobility, or indirectly by executive functions.
Design: Cross-sectional study. Twenty-one WMH variables (i.e., total WMH volume and WMHs in 20 tracts), gait speed, global cognition (Modified Mini-Mental State Examination; 3MS), and executive functions and processing speed (Digit-Symbol Substitution Test; DSST) were assessed. An L1-L2 regularized regression (i.e., Elastic Net model) identified the WMH variables most related to slower gait Multivariable linear regression models quantified the association between these WMH variables and gait speed. Formal tests of mediation were also conducted.
Setting: Community-based sample.
Participants: Two hundred fifty-three adults (mean age: 83 years, 58% women, 41% black).
Main Outcome Measure: Gait speed.
Results: In older adults with an average gait speed of 0.91 m/sec, total WMH volume, WMHs located in the right anterior thalamic radiation (ATRR) and frontal corpus callosum (CCF) were most associated with slower gait. There was a >10% slower gait for each standard deviation of WMH in CCF, ATRR or total brain (standardized beta in m/sec [p value]: -0.11 [p = 0.046], -0.15 [p = 0.007] and -0.14 [p = 0.010], respectively). These associations were substantially and significantly attenuated after adjustment for DSST. This effect was stronger for WMH in CCF than for ATRR or total WMH (standardized beta in m/sec [p value]: -0.07 [p = 0.190], -0.12 [p = 0.024] and -0.10 [p = 0.049], respectively). Adjustment for 3MS did not change these associations. The mediation analyses also found that DSST significantly mediated the associations between WMHs and gait speed. Our models were adjusted for age, sex, BMI, quadriceps strength, years of education, standing height, and prevalent hypertension.
Conclusion: The impact, direct or indirect, of WMHs on gait speed depended on their location and was mediated by executive function. Thus, multi-faceted interventions targeting executive control functions as well as motor functions, such as balance and strength training, are candidates to the maintenance of mobility across the lifespan. (C) 2014 Elsevier Inc All rights reserved.
C1 [Bolandzadeh, Niousha; Liu-Ambrose, Teresa] Univ British Columbia, Fac Med, Dept Phys Therapy, Aging Mobil & Cognit Neurosci Lab, Vancouver, BC V5Z 1M9, Canada.
[Bolandzadeh, Niousha; Liu-Ambrose, Teresa] Univ British Columbia, Brain Res Ctr, Vancouver, BC V5Z 1M9, Canada.
[Bolandzadeh, Niousha] Univ British Columbia, Fac Med, Dept Med, Expt Med Grad Program, Vancouver, BC V5Z 1M9, Canada.
[Aizenstein, Howard] Univ Pittsburgh, Fac Med, Geriatr Psychiat Neuroimaging Lab, Pittsburgh, PA USA.
[Harris, Tamara; Launer, Lenore] Natl Inst Aging, Lab Epidemiol & Populat Sci, Bethesda, MD USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Kritchevsky, Stephen B.] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Newman, Anne; Rosano, Caterina] Univ Pittsburgh, Ctr Aging & Populat Hlth, Sch Publ Hlth, Pittsburgh, PA 15222 USA.
RP Rosano, C (reprint author), Univ Pittsburgh, Ctr Aging & Populat Hlth, Sch Publ Hlth, Pittsburgh, PA 15222 USA.
EM RosanoC@edc.pitt.edu
RI Newman, Anne B./C-6408-2013;
OI Newman, Anne B./0000-0002-0106-1150; Rosano,
Caterina/0000-0002-0909-1506; Rosano, Caterina/0000-0002-4271-6010
FU National Institute on Aging (NIA) [N01-AG-6-2101, N01-AG-6-2013,
N01-AG-6-2106]; NIA [R01-AG028050]; NINR [R01-NR012459, K23 AG28966, R01
AG029232, R01 AG037451, P30 AG024827]; Intramural Research Program of
the National Institute of Health (NIH) NIA; Heart and Stroke Foundation
of Canada
FX This research was supported by National Institute on Aging (NIA) grant
contracts N01-AG-6-2101, N01-AG-6-2013, N01-AG-6-2106, NIA grant
R01-AG028050, and NINR grant R01-NR012459, and K23 AG28966, R01
AG029232, R01 AG037451, and P30 AG024827. This research was also
supported in part by the Intramural Research Program of the National
Institute of Health (NIH) NIA. N.B. was supported by Heart and Stroke
Foundation of Canada for her PhD studies. T.L.A. is a Canada Research
Chair in Physical Activity, Mobility and Cognitive Neuroscience. C.R.
had full access to all of the data in study and responsibility for the
integrity of the data and the accuracy of the data analysis.
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PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD OCT 1
PY 2014
VL 99
BP 7
EP 13
DI 10.1016/j.neuroimage.2014.05.017
PG 7
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AM4XR
UT WOS:000339860000002
PM 24841418
ER
PT J
AU Debas, K
Carrier, J
Barakat, M
Marrelec, G
Bellec, P
Tahar, AH
Karni, A
Ungerleider, LG
Benali, H
Doyon, J
AF Debas, Karen
Carrier, Julie
Barakat, Marc
Marrelec, Guillaume
Bellec, Pierre
Tahar, Abdallah Hadj
Karni, Avi
Ungerleider, Leslie G.
Benali, Habib
Doyon, Julien
TI Off-line consolidation of motor sequence learning results in greater
integration within a cortico-striatal functional network
SO NEUROIMAGE
LA English
DT Article
DE Functional connectivity; Consolidation; Sleep; Motor learning; fMRI;
Networks
ID EXPERIENCE-DEPENDENT CHANGES; INDEPENDENT COMPONENT ANALYSIS;
EYE-MOVEMENT SLEEP; RESTING-STATE; BASAL GANGLIA; BRAIN; MEMORY; SKILL;
FMRI; CONNECTIVITY
AB The consolidation of motor sequence learning is known to depend on sleep. Work in our laboratory and others have shown that the striatum is associated with this off-line consolidation process. In this study, we aimed to quantify the sleep-dependent dynamic changes occurring at the network level using a measure of functional integration. We directly compared changes in connectivity before and after sleep or the simple passage of daytime. As predicted, the results revealed greater integration within the cortico-striatal network after sleep, but not an equivalent daytime period. Importantly, a similar pattern of results was also observed using a data-driven approach; the increase in integration being specific to a cortico-striatal network, but not to other known functional networks. These findings reveal, for the first time, a new signature of motor sequence consolidation: a greater between-regions interaction within the cortico-striatal system. (C) 2014 Elsevier Inc All rights reserved.
C1 [Debas, Karen; Carrier, Julie; Barakat, Marc; Marrelec, Guillaume; Bellec, Pierre; Tahar, Abdallah Hadj; Doyon, Julien] Univ Montreal, Inst Geriatr, Ctr Rech, Funct Neuroimaging Unit, Quebec City, PQ, Canada.
[Carrier, Julie] Hop Sacre Coeur Montreal, Ctr Etud Sommeil & Rythmes Biol, Quebec City, PQ, Canada.
[Debas, Karen; Carrier, Julie; Barakat, Marc; Doyon, Julien] Univ Montreal, Dept Psychol, Quebec City, PQ, Canada.
[Marrelec, Guillaume; Benali, Habib; Doyon, Julien] Univ Paris 06, Ctr Hosp Univ Pitie Salpetriere, INSERM, Unite Mixte Rech S 678, Paris, France.
[Karni, Avi] Univ Haifa, Brain Behav Ctr, Lab Funct Brain Imaging & Learning Res, IL-31999 Haifa, Israel.
[Ungerleider, Leslie G.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Doyon, J (reprint author), Funct Neuroimaging Unit, 4565 Queen Mary St,Room M-7836, Montreal, PQ H3W 1W5, Canada.
EM julien.doyon@umontreal.ca
OI Bellec, Pierre/0000-0002-9111-0699
FU Canadian Institutes of Health Research [86463]; Fonds de recherche du
Quebec sante [20882]
FX Support for this research was provided by a Canadian Institutes of
Health Research (86463) grant to JD, JC, AHT, AK, HB and LGU, and by a
fellowship from the Fonds de recherche du Quebec sante to KD (folder
number # 20882). The authors are grateful to Vo An Nguyen, Estelle
Breton and Laurence Girouard for their help in data acquisition.
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U2 25
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD OCT 1
PY 2014
VL 99
BP 50
EP 58
DI 10.1016/j.neuroimage.2014.05.022
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AM4XR
UT WOS:000339860000006
PM 24844748
ER
PT J
AU Yang, Z
Huang, ZR
Gonzalez-Castillo, J
Dai, R
Northoff, G
Bandettini, P
AF Yang, Zhi
Huang, Zirui
Gonzalez-Castillo, Javier
Dai, Rui
Northoff, Georg
Bandettini, Peter
TI Using fMRI to decode true thoughts independent of intention to conceal
SO NEUROIMAGE
LA English
DT Article
DE Dorsolateral prefrontal cortex; fMRI; Multivariate pattern analysis;
Searchlight; Deception
ID FUNCTIONAL MAGNETIC-RESONANCE; DORSOLATERAL PREFRONTAL CORTEX;
PERCEPTUAL DECISION-MAKING; VOXEL PATTERN-ANALYSIS; HUMAN BRAIN;
DECEPTION EVIDENCE; MEMORY; FACES; MRI; ACTIVATION
AB Multi-variate pattern analysis (MVPA) applied to BOLD-fMRI has proven successful at decoding complicated fMRI signal patterns associated with a variety of cognitive processes. One cognitive process, not yet investigated, is the mental representation of "Yes/No" thoughts that precede the actual overt response to a binary "Yes/No" question. In this study, we focus on examining: (1) whether spatial patterns of the hemodynamic response carry sufficient information to allow reliable decoding of "Yes/No" thoughts; and (2) whether decoding of "Yes/No" thoughts is independent of the intention to respond honestly or dishonestly. To achieve this goal, we conducted two separate experiments. Experiment 1, collected on a 3T scanner, examined the whole brain to identify regions that carry sufficient information to permit significantly above-chance prediction of "Yes/No" thoughts at the group level. In Experiment 2, collected on a 7T scanner, we focused on the regions identified in Experiment 1 to examine the capability of achieving high decoding accuracy at the single subject level. A set of regions - namely right superior temporal gyrus, left supra-marginal gyrus, and left middle frontal gyrus - exhibited high decoding power. Decoding accuracy for these regions increased with trial averaging. When 18 trials were averaged, the median accuracies were 82.5%, 77.5%, and 79.5%, respectively. When trials were separated according to deceptive intentions (set via experimental cues), and classifiers were trained on honest trials, but tested on trials where subjects were asked to deceive, the median accuracies of these regions still reached 66%, 75%, and 78.5%. These results provide evidence that concealed "Yes/No" thoughts are encoded in the BOLD signal, retaining some level of independence from the subject's intentions to answer honestly or dishonestly. These findings also suggest the theoretical possibility for more efficient brain-computer interfaces where subjects only need to think their answers to communicate. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Yang, Zhi; Huang, Zirui] Chinese Acad Sci Lincui Rd, Inst Psychol, Key Lab Behav Sci, Beijing 100101, Peoples R China.
[Yang, Zhi; Gonzalez-Castillo, Javier; Bandettini, Peter] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD USA.
[Huang, Zirui; Northoff, Georg] Univ Ottawa, Mind Brain Imaging & Neuroeth Res Unit, Ottawa, ON K1Z 7K4, Canada.
[Huang, Zirui; Dai, Rui; Northoff, Georg] Hangzhou Normal Univ, Ctr Cognit & Brain Disorders, Hangzhou 310015, Zhejiang, Peoples R China.
[Dai, Rui] S China Normal Univ, Inst Life Sci, Guangzhou 510631, Guangdong, Peoples R China.
RP Yang, Z (reprint author), Chinese Acad Sci Lincui Rd, Inst Psychol, Key Lab Behav Sci, 16 Lincui Rd, Beijing 100101, Peoples R China.
EM yangz@psych.ac.cn
OI Yang, Zhi/0000-0002-2222-2312; Gonzalez-Castillo,
Javier/0000-0002-6520-5125
FU National Science Foundation of China (NSFC) [81270023]; Foundation of
Beijing Key Laboratory of Mental Disorders [2014JSJB03]; NIMH
FX The authors would like to thank Drs. Xuchu Weng, Gang Chen, John X.
Zhang, Yi Jiang, Wen Zhou, Xi-Nian Zuo, Sundeep Teki, Chaogan Yan, and
Ms. Laura Buchanan for their help in improving the manuscript We thank
Ms. Lijuan Cheng for helps in collecting the data in Experiment 1. This
work was supported by the National Science Foundation of China (NSFC,
No. 81270023 to ZY), the Foundation of Beijing Key Laboratory of Mental
Disorders (2014JSJB03 to ZY), and the NIMH Intramural research program
(ZY, JGC, and PAB).
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PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD OCT 1
PY 2014
VL 99
BP 80
EP 92
DI 10.1016/j.neuroimage.2014.05.034
PG 13
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AM4XR
UT WOS:000339860000009
PM 24844742
ER
PT J
AU Chen, G
Adleman, NE
Saad, ZS
Leibenluft, E
Cox, RW
AF Chen, Gang
Adleman, Nancy E.
Saad, Ziad S.
Leibenluft, Ellen
Cox, Robert W.
TI Applications of multivariate modeling to neuroimaging group analysis: A
comprehensive alternative to univariate general linear model
SO NEUROIMAGE
LA English
DT Article
ID REPEATED-MEASURES DESIGNS; FMRI
AB All neuroimaging packages can handle group analysis with t-tests or general linear modeling (GLM). However, they are quite hamstrung when there are multiple within-subject factors or when quantitative covariates are involved in the presence of a within-subject factor. In addition, sphericity is typically assumed for the variance-co-variance structure when there are more than two levels in a within-subject factor. To overcome such limitations in the traditional AN(C)OVA and GLM, we adopt a multivariate modeling (MVM) approach to analyzing neuroimaging data at the group level with the following advantages: a) there is no limit on the number of factors as long as sample sizes are deemed appropriate; b) quantitative covariates can be analyzed together with within-subject factors; c) when a within-subject factor is involved, three testing methodologies are provided: traditional univariate testing (UVT) with sphericity assumption (UVT-UC) and with correction when the assumption is violated (UVT-SC), and within-subject multivariate testing (MVT-WS); d) to correct for sphericity violation at the voxel level, we propose a hybrid testing (FIT) approach that achieves equal or higher power via combining traditional sphericity correction methods (Greenhouse-Geisser and Huynh-Feldt) with MVT-WS.
To validate the MVM methodology, we performed simulations to assess the controllability for false positives and power achievement. A real FMRI dataset was analyzed to demonstrate the capability of the MVM approach. The methodology has been implemented into an open source program 3dMVM in AFNI, and all the statistical tests can be performed through symbolic coding with variable names instead of the tedious process of dummy coding. Our data indicates that the severity of sphericity violation varies substantially across brain regions. The differences among various modeling methodologies were addressed through direct comparisons between the MVM approach and some of the GLM implementations in the field, and the following two issues were raised: a) the improper formulation of test statistics in some univariate GLM implementations when a within-subject factor is involved in a data structure with two or more factors, and b) the unjustified presumption of uniform sphericity violation and the practice of estimating the variance-covariance structure through pooling across brain regions. Published by Elsevier Inc.
C1 [Chen, Gang; Saad, Ziad S.; Cox, Robert W.] NIMH, Sci & Stat Comp Core, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Adleman, Nancy E.] Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA.
[Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, NIH,Dept Hlth & Human Serv, Bethesda, MD USA.
RP Chen, G (reprint author), NIMH, Sci & Stat Comp Core, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM gangchen@mail.nih.gov
OI Chen, Gang/0000-0002-2960-089X
FU NIMH Intramural Research Program of the NIH/HHS, USA; NINDS Intramural
Research Program of the NIH/HHS, USA
FX Our work benefited significantly from the statistical computational
language and environment R, its many packages, and the support of the R
community. All the plots were created in R using the base graphics
library. Special thanks are due to Henrik Singmann for his assistance in
the technical details of the R package afex. We would also like to thank
Donald McLaren for his help in running SPM and the GLM Flex package. The
research and writing of the paper were supported by the NIMH and NINDS
Intramural Research Programs of the NIH/HHS, USA.
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U2 12
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD OCT 1
PY 2014
VL 99
BP 571
EP 588
DI 10.1016/j.neuroimage.2014.06.027
PG 18
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AM4XR
UT WOS:000339860000055
PM 24954281
ER
PT J
AU Ardeshirpour, Y
Hassan, M
Zielinski, R
Horton, JA
Capala, J
Gandjbakhche, AH
Chernomordik, V
AF Ardeshirpour, Yasaman
Hassan, Moinuddin
Zielinski, Rafal
Horton, Jason A.
Capala, Jacek
Gandjbakhche, Amir H.
Chernomordik, Victor
TI In Vivo Assessment of HER2 Receptor Density in HER2-positive Tumors by
Near-infrared Imaging, Using Repeated Injections of the Fluorescent
Probe
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Article
DE Fluorescence imaging; Near-infrared optical imaging; Targeted
fluorescent probe; Affibody; Cancer treatment; Cancer diagnostics; Human
epidermal growth factor receptor
ID BREAST-CANCER; EXPRESSION; QUANTIFICATION; THERAPY; PET
AB HER2 overexpression and amplification of the HER2/neu gene have been found in approximately 25% of invasive breast carcinomas. They are associated with a poor prognosis and resistance to therapy in breast cancer patients. Up to now, clinical evaluation of human epidermal growth factor receptor 2 (HER2) expression is based on ex vivo methods (immuno histochemistry (I H C) or fluorescence in situ hybridization (FISH) staining of biopsied tissue). Our goal is to realize "image and treat" paradigm using targeted fluorescent probes to evaluate expression levels of cell biomarkers responsible for cancer progression and to monitor the efficacy of corresponding monoclonal antibody treatments. We used fluorescent Affibody-based probes for in vivo analysis of HER2 receptors using near-infrared optical imaging that do not interfere with binding of the therapeutic agents to these receptors. We have analyzed two types of breast carcinoma xenografts with significant differences in HER2 expression (3+ and 2+ according to classification) in the mouse model. Using our kinetic model to analyze the temporal variations of the fluorescence intensity in the tumor area after two subsequent injections allowed us to assess quantitatively the difference in HER2 expression levels for two tumor types (BT-474 and MD-MBA-361). This result was substantiated by ELISA ex vivo assays of HER2 expression in the same tumors.
C1 [Ardeshirpour, Yasaman; Hassan, Moinuddin; Gandjbakhche, Amir H.; Chernomordik, Victor] NICHHD, NIH, Bethesda, MD 20892 USA.
[Hassan, Moinuddin; Horton, Jason A.] US FDA, Div Phys, Off Sci & Engn Labs, CDRH, Silver Spring, MD 20993 USA.
[Zielinski, Rafal; Capala, Jacek] NCI, NIH, Bethesda, MD 20892 USA.
[Zielinski, Rafal] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Gandjbakhche, AH (reprint author), NICHHD, NIH, Bldg 9,9 Mem Dr, Bethesda, MD 20892 USA.
EM gandjbaa@mail.nih.gov
FU Intramural Research Program of National Cancer Institute, NIH;
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, NIH
FX This research is supported by the Intramural Research Program of
National Cancer Institute, NIH, and Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, NIH.
NR 19
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U1 0
U2 33
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1533-0346
EI 1533-0338
J9 TECHNOL CANCER RES T
JI Technol. Cancer Res. Treat.
PD OCT
PY 2014
VL 13
IS 5
BP 427
EP 434
DI 10.7785/tcrt.2013.600265
PG 8
WC Oncology
SC Oncology
GA AL0IB
UT WOS:000338809500007
PM 24000992
ER
PT J
AU Dey, B
Lagenaur, LA
Lusso, P
AF Dey, Barna
Lagenaur, Laurel A.
Lusso, Paolo
TI Protein-Based HIV-1 Microbicides
SO CURRENT HIV RESEARCH
LA English
DT Article
DE Antiviral; entry inhibitor; HIV; live vector; Lactobacillus;
microbicide; mucosal transmission; prevention; protein
ID HUMAN-IMMUNODEFICIENCY-VIRUS; GP120 ENVELOPE GLYCOPROTEIN; HUMAN
MONOCLONAL-ANTIBODIES; PROXIMAL EXTERNAL REGION; VAGINAL SHIV CHALLENGE;
BROADLY NEUTRALIZING ANTIBODIES; LACTOBACILLUS-REUTERI RC-14; HUMAN
CERVICAL TISSUE; CD4 BINDING-SITE; CYANOVIRIN-N
AB Although the development of a protective vaccine remains the most effective strategy for the global control of HIV/AIDS, another practical form of medical intervention would be a microbicide capable of preventing HIV-1 transmission at the mucosal level. A broad spectrum of antiviral molecules have demonstrated in vitro efficacy in proof-of-principle studies, and a selected few have already been tested in pre-clinical and clinical microbicide trials. Nevertheless, major hurdles remain to be overcome and there is still much uncertainty about the choice of inhibitors, formulations and administration vehicles for obtaining a safe and effective microbicide.
A special category of HIV-1 microbicides are those based on proteins or peptides that interfere with the earliest steps in the viral infectious cycle. Besides a high degree of target specificity and a limited, if any, systemic absorption, protein-based microbicides offer the unique advantage of being suitable to in vivo expression by engineered bacteria or viral vectors, which might ensure prolonged protection without the need for planned, intercourse-coordinated application. In this respect, vaginal or rectal microbiota such as Lactobacillus spp. represent ideal expression systems as they would not only produce the inhibitor of choice at the mucosal surface, but also easily blend within the resident microflora and offer additional valuable homeostatic effects.
C1 [Dey, Barna] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Lusso, Paolo] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Lagenaur, Laurel A.] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Lagenaur, Laurel A.] Osel Inc, Mountain View, CA 94043 USA.
RP Dey, B (reprint author), NIAID, Viral Dis Lab, NIH, Bldg 33,Rm 1E19A,33 North Dr,MSC 3210, Bethesda, MD 20892 USA.
EM bdey@mail.nih.gov
FU NIAID, NIH
FX This work was supported by the Intramural Research Program of the NIAID,
NIH.
NR 233
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U2 81
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1570-162X
EI 1873-4251
J9 CURR HIV RES
JI Curr. HIV Res.
PD OCT
PY 2014
VL 11
IS 7
SI SI
BP 576
EP 594
PG 19
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA AD0XS
UT WOS:000332958300010
ER
PT J
AU Blumenthal, GM
Gills, JJ
Ballas, MS
Bernstein, WB
Komiya, T
Dechowdhury, R
Morrow, B
Root, H
Chun, G
Helsabeck, C
Steinberg, SM
LoPiccolo, J
Kawabata, S
Gardner, ER
Figg, WD
Dennis, PA
AF Blumenthal, Gideon M.
Gills, Joell J.
Ballas, Marc S.
Bernstein, Wendy B.
Komiya, Takefumi
Dechowdhury, Roopa
Morrow, Betsy
Root, Hyejeong
Chun, Guinevere
Helsabeck, Cynthia
Steinberg, Seth M.
LoPiccolo, Jaclyn
Kawabata, Shigeru
Gardner, Erin R.
Figg, William D.
Dennis, Phillip A.
TI A phase I trial of the HIV protease inhibitor nelfinavir in adults with
solid tumors
SO ONCOTARGET
LA English
DT Article
DE Nelfinavir; phase I clinical trial; AKT; endoplasmic reticulum stress;
neuroendocrine
ID CELL LUNG-CANCER; PANCREATIC NEUROENDOCRINE TUMORS; MULTIPLE-MYELOMA
CELLS; VITRO; VIVO; CHEMORADIATION; PATHWAY
AB Nelfinavir is an HIV protease inhibitor being repurposed as an anti-cancer agent in preclinical models and in small oncology trials, yet the MTD of nelfinavir has not been determined. Therefore, we conducted a Phase Ia study to establish the maximum tolerated dose (MTD) and dose limiting toxicities (DLT) of nelfinavir in subjects with advanced solid tumors. Adults with refractory cancers were given oral nelfinavir twice daily with pharmacokinetic and pharmacodynamic analyses. Twenty-eight subjects were enrolled. Nelfinavir was generally well tolerated. Common adverse events included diarrhea, anemia, and lymphopenia, which were mostly mild. The DLT was rapid-onset neutropenia that was reversible. The MTD was established at 3125 mg twice daily. In an expansion cohort at the MTD, one of 11 (9%) evaluable subjects had a confirmed partial response. This, plus two minor responses, occurred in subjects with neuroendocrine tumors of the midgut or pancreatic origin. Thirty-six percent of subjects had stable disease for more than 6 months. In peripheral blood mononuclear cells, Nelfinavir inhibited AKT and induced markers of ER stress. In summary, nelfinavir is well tolerated in cancer patients at doses 2.5 times the FDA-approved dose for HIV management and showed preliminary activity in tumors of neuroendocrine origin.
C1 [Blumenthal, Gideon M.; Ballas, Marc S.; Bernstein, Wendy B.; Komiya, Takefumi; Dechowdhury, Roopa; Morrow, Betsy; Root, Hyejeong; Chun, Guinevere; Helsabeck, Cynthia; LoPiccolo, Jaclyn; Gardner, Erin R.; Figg, William D.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Gills, Joell J.; Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
[Kawabata, Shigeru; Dennis, Phillip A.] Johns Hopkins Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
RP Dennis, PA (reprint author), Johns Hopkins Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
EM pdennis@jhmi.edu
RI Figg Sr, William/M-2411-2016
FU intramural program of the National Cancer Institute at the National
Institutes of Health
FX This work was supported by the intramural program of the National Cancer
Institute at the National Institutes of Health.
NR 35
TC 11
Z9 11
U1 1
U2 2
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 30
PY 2014
VL 5
IS 18
BP 8161
EP 8172
PG 12
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA AZ1YI
UT WOS:000348030900016
PM 25327558
ER
PT J
AU Kim, EM
Park, JK
Hwang, SG
Kim, WJ
Liu, ZG
Kang, SW
Um, HD
AF Kim, Eun Mi
Park, Jong Kuk
Hwang, Sang-Gu
Kim, Wun-Jae
Liu, Zheng-Gang
Kang, Sang Won
Um, Hong-Duck
TI Nuclear and cytoplasmic p53 suppress cell invasion by inhibiting
respiratory Complex-I activity via Bcl-2 family proteins
SO ONCOTARGET
LA English
DT Article
DE p53; Bcl-2 family proteins; respiratory complex-I; cell invasion
ID WILD-TYPE P53; MATRIX METALLOPROTEINASE-2; GAMMA-IRRADIATION; TUMOR
PROGRESSION; BREAST-CANCER; CARCINOMA; APOPTOSIS; OVEREXPRESSION;
MITOCHONDRIA; BINDING
AB Although the p53 tumor suppressor/transcription factor often accumulates in the cytoplasm of healthy cells, limited information is available on the cytoplasmic function of p53. Here, we show that cytoplasmic p53 suppresses cell invasion by reducing mitochondrial reactive oxygen species (ROS) levels. Analysis revealed that this function is mediated by Bcl-2 family proteins: Cytoplasmic p53 binds Bcl-w, liberating Bax, which then binds ND5, a subunit of respiratory complex-I, thereby suppressing complex-I activity and thus ROS production. The G13289A mutation of ND5, identified in cancer patients, prevents Bax/ND5 interactions and promotes ROS production and cell invasion. We also showed that Bcl-X-L and Bak can substitute for Bcl-w and Bax, respectively, regulating complex-I activity and supporting the cytoplasmic function of p53; nuclear p53 also suppresses complex-I activity by inducing Bax expression. Studies in animal models support the notion that p53 and Bcl-2 family proteins exhibit these functions in vivo. This study demonstrates a link between p53 and Bcl-2 proteins as regulators of ROS production and cellular invasiveness, and reveals complex-I, especially ND5, as their functional target.
C1 [Kim, Eun Mi; Park, Jong Kuk; Hwang, Sang-Gu; Um, Hong-Duck] Korea Inst Radiol & Med Sci, Div Radiat Canc Biol, Seoul, South Korea.
[Kim, Eun Mi; Kang, Sang Won] Ewha Womans Univ Seoul, Div Life & Pharmaceut Sci, Seoul, South Korea.
[Kim, Wun-Jae] Chungbuk Natl Univ, Coll Med, Dept Urol, Cheongju, South Korea.
[Liu, Zheng-Gang] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Um, HD (reprint author), Korea Inst Radiol & Med Sci, Div Radiat Canc Biol, Seoul, South Korea.
EM hdum@kcch.re.kr
FU National Research Foundation of Korea (NRF) grant - Korean government
(MSIP) [2012M2A2A7010459, 2012R1A2A2A01045978, 2008-0062611]
FX This work was supported by the National Research Foundation of Korea
(NRF) grant funded by the Korean government (MSIP) (2012M2A2A7010459,
2012R1A2A2A01045978, 2008-0062611).
NR 44
TC 9
Z9 9
U1 0
U2 2
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 30
PY 2014
VL 5
IS 18
BP 8452
EP 8465
PG 14
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA AZ1YI
UT WOS:000348030900038
PM 25115399
ER
PT J
AU Dobbin, ZC
Katre, AA
Steg, AD
Erickson, BK
Shah, MM
Alvarez, RD
Conner, MG
Schneider, D
Chen, DQ
Landen, CN
AF Dobbin, Zachary C.
Katre, Ashwini A.
Steg, Adam D.
Erickson, Britt K.
Shah, Monjri M.
Alvarez, Ronald D.
Conner, Michael G.
Schneider, David
Chen, Dongquan
Landen, Charles N.
TI Using heterogeneity of the patient-derived xenograft model to identify
the chemoresistant population in ovarian cancer
SO ONCOTARGET
LA English
DT Article
DE Ovarian Cancer; Patient-derived xenograft; cancer stem cells;
chemoresistance; animal models of cancer
ID HUMAN TUMOR XENOGRAFTS; STEM-CELLS; ALDEHYDE DEHYDROGENASE; IN-VITRO;
EXPRESSION; GENE; THERAPY; CD133; TRANSPLANTATION; ADENOCARCINOMA
AB A cornerstone of preclinical cancer research has been the use of clonal cell lines. However, this resource has underperformed in its ability to effectively identify novel therapeutics and evaluate the heterogeneity in a patient's tumor. The patient-derived xenograft (PDX) model retains the heterogeneity of patient tumors, allowing a means to not only examine efficacy of a therapy, but also basic tenets of cancer biology in response to treatment. Herein we describe the development and characterization of an ovarian-PDX model in order to study the development of chemoresistance. We demonstrate that PDX tumors are not simply composed of tumor-initiating cells, but recapitulate the original tumor's heterogeneity, oncogene expression profiles, and clinical response to chemotherapy. Combined carboplatin/paclitaxel treatment of PDX tumors enriches the cancer stem cell populations, but persistent tumors are not entirely composed of these populations. RNA-Seq analysis of six pair of treated PDX tumors compared to untreated tumors demonstrates a consistently contrasting genetic profile after therapy, suggesting similar, but few, pathways are mediating chemoresistance. Pathways and genes identified by this methodology represent novel approaches to targeting the chemoresistant population in ovarian cancer
C1 [Dobbin, Zachary C.; Katre, Ashwini A.; Steg, Adam D.; Erickson, Britt K.; Shah, Monjri M.; Alvarez, Ronald D.] Univ Alabama Birmingham, Dept Obstet & Gynecol, Div Gynecol Oncol, Birmingham, AL USA.
[Dobbin, Zachary C.] Univ Alabama Birmingham, NIH Med Scientist Training Program, Birmingham, AL USA.
[Conner, Michael G.] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL USA.
[Schneider, David] Univ Alabama Birmingham, Dept Biochem & Mol Genet, Birmingham, AL USA.
[Chen, Dongquan] Univ Alabama Birmingham, Dept Med, Div Preventat Med, Birmingham, AL USA.
[Landen, Charles N.] Univ Virginia, Div Gynecol Oncol, Dept Obstet & Gynecol, Charlottesville, VA 22904 USA.
RP Landen, CN (reprint author), Univ Virginia, Div Gynecol Oncol, Dept Obstet & Gynecol, Charlottesville, VA 22904 USA.
EM clanden@virginia.edu
FU UAB Medical Scientist Training Program [NIGMS T32GM008361]; Norma
Livingston Ovarian Cancer Foundation; University of Alabama at
Birmingham Center for Clinical and Translational Science [5UL1RR025777];
Department of Defense Ovarian Cancer Research Academy [OC093443]
FX Funding support provided in part by UAB Medical Scientist Training
Program (NIGMS T32GM008361) to ZCD; and by the Norma Livingston Ovarian
Cancer Foundation, the University of Alabama at Birmingham Center for
Clinical and Translational Science (5UL1RR025777), and the Department of
Defense Ovarian Cancer Research Academy (OC093443) to CNL.
NR 47
TC 21
Z9 21
U1 0
U2 5
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 30
PY 2014
VL 5
IS 18
BP 8750
EP 8764
PG 15
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA AZ1YI
UT WOS:000348030900061
PM 25209969
ER
PT J
AU Scher, AI
Ross, GW
Sigurdsson, S
Garcia, M
Gudmundsson, LS
Sveinbojrnsdottir, S
Wagner, AK
Gudnason, V
Launer, LJ
AF Scher, Ann I.
Ross, G. Webster
Sigurdsson, Sigurdur
Garcia, Melissa
Gudmundsson, Larus S.
Sveinboejrnsdottir, Sigurlaug
Wagner, Amy K.
Gudnason, Vilmundur
Launer, Lenore J.
TI Midlife migraine and late-life parkinsonism AGES-Reykjavik Study
SO NEUROLOGY
LA English
DT Article
ID RESTLESS LEGS SYNDROME; TRAUMATIC BRAIN-INJURY; CHRONIC DAILY HEADACHE;
MOVEMENT-DISORDERS; DISEASE; IRON; METAANALYSIS; DOPAMINE; RISK;
DYSFUNCTION
AB Objective: In the present study, we tested the hypothesis that having migraine in middle age is related to late-life parkinsonism and a related disorder, restless legs syndrome (RLS), also known as Willis-Ekbom disease (WED).
Methods: The AGES-Reykjavik cohort (born 1907-1935) has been followed since 1967. Headaches were classified based on symptoms assessed in middle age. From 2002 to 2006, 5,764 participants were reexamined to assess symptoms of parkinsonism, diagnosis of Parkinson disease (PD), family history of PD, and RLS/WED.
Results: Subjects with midlife migraine, particularly migraine with aura (MA), were in later life more likely than others to report parkinsonian symptoms (odds ratio [OR] MA = 3.6 [95% CI 2.7-4.8]) and diagnosed PD (ORMA = 2.5 [95% CI 1.2-5.2]). Women with MA were more likely than others to have a parent (ORMA = 2.26 [95% CI 1.3-4.0]) or sibling (ORMA = 1.78 [95% CI 1.1-2.9]) with PD. Late-life RLS/WED was increased for headache generally. Associations were independent of cardiovascular disease and MRI-evident presumed ischemic lesions.
Conclusions: These findings suggest there may be a common vulnerability to, or consequences of, migraine and multiple indicators of parkinsonism. Additional genetic and longitudinal observational studies are needed to identify candidate pathways that may account for the comorbid constellation of symptoms.
C1 [Scher, Ann I.] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD 20814 USA.
[Scher, Ann I.; Garcia, Melissa; Launer, Lenore J.] NIA, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
[Ross, G. Webster] Vet Affairs Pacific Islands Hlth Care Syst, Honolulu, HI USA.
[Ross, G. Webster] Pacific Hlth Res & Educ Inst, Honolulu, HI USA.
[Sigurdsson, Sigurdur; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Gudmundsson, Larus S.] Univ Iceland, Sch Hlth Sci, Reykjavik, Iceland.
[Gudnason, Vilmundur] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Sveinboejrnsdottir, Sigurlaug] Broomfield Hosp, Dept Neurol, Chelmsford, Essex, England.
[Wagner, Amy K.] Univ Pittsburgh, Dept Phys Med & Rehabil, Pittsburgh, PA 15260 USA.
RP Scher, AI (reprint author), Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD 20814 USA.
EM ascher@usuhs.mil
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
FU NIH [N01-AG-12100]; National Institute on Aging Intramural Program,
Hjartavernd (the Icelandic Heart Association); Althingi (the Icelandic
Parliament)
FX The AGES-Reykjavik Study was supported by NIH N01-AG-12100, the National
Institute on Aging Intramural Program, Hjartavernd (the Icelandic Heart
Association), and the Althingi (the Icelandic Parliament). The views
expressed in this work are those of the authors and do not necessarily
reflect the official policy or position of the Department of Defense or
the US Government.
NR 40
TC 4
Z9 4
U1 0
U2 8
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 SEP 30
PY 2014
VL 83
IS 14
BP 1246
EP 1252
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA AT3UN
UT WOS:000344860700010
PM 25230997
ER
PT J
AU Katagiri, S
Akahori, M
Sergeev, Y
Yoshitake, K
Ikeo, K
Furuno, M
Hayashi, T
Kondo, M
Ueno, S
Tsunoda, K
Shinoda, K
Kuniyoshi, K
Tsurusaki, Y
Matsumoto, N
Tsuneoka, H
Iwata, T
AF Katagiri, Satoshi
Akahori, Masakazu
Sergeev, Yuri
Yoshitake, Kazutoshi
Ikeo, Kazuho
Furuno, Masaaki
Hayashi, Takaaki
Kondo, Mineo
Ueno, Shinji
Tsunoda, Kazushige
Shinoda, Kei
Kuniyoshi, Kazuki
Tsurusaki, Yohinori
Matsumoto, Naomichi
Tsuneoka, Hiroshi
Iwata, Takeshi
TI Whole Exome Analysis Identifies Frequent CNGA1 Mutations in Japanese
Population with Autosomal Recessive Retinitis Pigmentosa
SO PLOS ONE
LA English
DT Article
ID CGMP-GATED CHANNEL; RHODOPSIN GENE; MISSENSE MUTATION; ARRESTIN GENE;
ALPHA-SUBUNIT; HEARING-LOSS; EYS GENE; ORTHOLOG; DYSTROPHIES; FAMILY
AB Objective: The purpose of this study was to investigate frequent disease-causing gene mutations in autosomal recessive retinitis pigmentosa (arRP) in the Japanese population.
Methods: In total, 99 Japanese patients with non-syndromic and unrelated arRP or sporadic RP (spRP) were recruited in this study and ophthalmic examinations were conducted for the diagnosis of RP. Among these patients, whole exome sequencing analysis of 30 RP patients and direct sequencing screening of all CNGA1 exons of the other 69 RP patients were performed.
Results: Whole exome sequencing of 30 arRP/spRP patients identified disease-causing gene mutations of CNGA1 (four patients), EYS (three patients) and SAG (one patient) in eight patients and potential disease-causing gene variants of USH2A (two patients), EYS (one patient), TULP1 (one patient) and C2orf71 (one patient) in five patients. Screening of an additional 69 arRP/spRP patients for the CNGA1 gene mutation revealed one patient with a homozygous mutation.
Conclusions: This is the first identification of CNGA1 mutations in arRP Japanese patients. The frequency of CNGA1 gene mutation was 5.1% (5/99 patients). CNGA1 mutations are one of the most frequent arRP-causing mutations in Japanese patients.
C1 [Katagiri, Satoshi; Akahori, Masakazu; Iwata, Takeshi] Natl Hosp Org, Tokyo Med Ctr, Natl Inst Sensory Organs, Div Mol & Cellular Biol, Tokyo, Japan.
[Katagiri, Satoshi; Hayashi, Takaaki; Tsuneoka, Hiroshi] Jikei Univ, Sch Med, Dept Ophthalmol, Tokyo, Japan.
[Sergeev, Yuri] NEI, NIH, Bethesda, MD 20892 USA.
[Yoshitake, Kazutoshi; Ikeo, Kazuho] Natl Inst Genet, Lab DNA Data Anal, Shizuoka, Japan.
[Furuno, Masaaki] RIKEN, Ctr Life Sci Technol, Div Genom Technol, Life Sci Accelerator Technol Grp, Yokohama, Kanagawa, Japan.
[Kondo, Mineo] Mie Univ, Grad Sch Med, Dept Ophthalmol, Tsu, Mie 514, Japan.
[Ueno, Shinji] Nagoya Univ, Grad Sch Med, Dept Ophthalmol, Nagoya, Aichi 4648601, Japan.
[Tsunoda, Kazushige] Natl Inst Sensory Organs, Lab Visual Physiol, Tokyo, Japan.
[Shinoda, Kei] Teikyo Univ, Sch Med, Dept Ophthalmol, Tokyo 173, Japan.
[Kuniyoshi, Kazuki] Kinki Univ, Fac Med, Dept Ophthalmol, Osaka, Japan.
[Tsurusaki, Yohinori; Matsumoto, Naomichi] Yokohama City Univ, Dept Human Genet, Yokohama, Kanagawa 232, Japan.
RP Iwata, T (reprint author), Natl Hosp Org, Tokyo Med Ctr, Natl Inst Sensory Organs, Div Mol & Cellular Biol, Tokyo, Japan.
EM iwatatakeshi@kankakuki.go.jp
RI Ueno, Shinji/M-5063-2014;
OI Katagiri, Satoshi/0000-0001-7787-8194
FU Ministry of Health, Labor, and Welfare of Japan [13803661]; Ministry of
Education, Culture, Sports, Science, and Technology of Japan [25462744,
25462738]; Vehicle Racing Commemorative Foundation; RIKEN Omics Science
Center MEXT
FX This study was supported by the grants to T.I. from the Ministry of
Health, Labor, and Welfare of Japan (13803661); to M.A. and T.H. from
the Ministry of Education, Culture, Sports, Science, and Technology of
Japan (Grant-in-Aid for Scientific Research C, 25462744 and 25462738);
to T.H. from the Vehicle Racing Commemorative Foundation; and to M.F.
from the Research Grant for RIKEN Omics Science Center MEXT. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 35
TC 12
Z9 13
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 30
PY 2014
VL 9
IS 9
AR e108721
DI 10.1371/journal.pone.0108721
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AR6CW
UT WOS:000343671700148
PM 25268133
ER
PT J
AU Van Rie, A
Clouse, K
Hanrahan, C
Selibas, K
Sanne, I
Williams, S
Kim, P
Bassett, J
AF Van Rie, Annelies
Clouse, Kate
Hanrahan, Colleen
Selibas, Katerina
Sanne, Ian
Williams, Sharon
Kim, Peter
Bassett, Jean
TI High Uptake of Systematic HIV Counseling and Testing and TB Symptom
Screening at a Primary Care Clinic in South Africa
SO PLOS ONE
LA English
DT Article
ID ANTIRETROVIRAL THERAPY; TUBERCULOSIS-CONTROL; PREVALENCE; FACILITIES;
DIAGNOSIS; COMMUNITY
AB Background: Timely diagnosis and treatment of tuberculosis (TB) and HIV is important to reduce morbidity and mortality, and break the cycle of ongoing transmission.
Methods: We performed an implementation research study to develop a model for systematic TB symptom screening and HIV counseling and testing (HCT) for all adult clients at a primary care clinic and prospectively evaluate the 6-month coverage and yield, and 18-month sustainability at a primary care clinic in Johannesburg, South Africa.
Results: During the first 6 months, 26,515 visits occurred among 12,078 adults. The proportion of adults aware of their HIV status was 43.7% at the start of the first visit, increased to 84.6% at the end of the first visit, and to 90% at end of any visit during the first 6 months. During these 6 months, 1042 clients were newly diagnosed with HIV. HIV prevalence was 22.9% among those newly tested, and 58.9% among all adult clinic clients. High coverage of systematic HCT was sustained across all 18 months. Coverage of systematic HIV-stratified TB symptom screening during first 6-months was also high (89.6%) but only 35.0% of those symptomatic were screened by sputum. During these 6-months, 90 clients had a positive Xpert MTB/RIF assay, corresponding to a TB prevalence of 0.4% among all 23,534 clients TB symptom-screened and 2.8% among the 3,284 clients with a positive TB symptom screen. The initial high coverage of TB symptom screening was not sustained, with coverage of TB symptom screening dropping after the first six months to 70% and assessment by sputum dropping to 15%.
Conclusion: Routine, systematic HCT and HIV-stratified TB symptom screening is feasible at primary care level. Systematic HCT doubled the proportion of clients with known HIV status. While HCT was sustainable, coverage of systematic TB screening dropped significantly after the first 6 months of implementation.
C1 [Van Rie, Annelies; Clouse, Kate; Hanrahan, Colleen] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Selibas, Katerina; Sanne, Ian] Univ Witwatersrand, Clin HIV Res Unit, Johannesburg, South Africa.
[Williams, Sharon; Kim, Peter] NIAID, NIH, Bethesda, MD 20892 USA.
[Bassett, Jean] Witkoppen Hlth & Welf Ctr, Johannesburg, South Africa.
RP Van Rie, A (reprint author), Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
EM Vanrie@email.unc.edu
RI Van Rie, Annelies/C-2082-2017;
OI Van Rie, Annelies/0000-0001-7666-3263; Clouse, Kate/0000-0002-0190-7398
FU PEPFAR; National Institutes of Health [UM1 AI069463]; United States
Agency for International Development [674-A-00-08-00007,
674-A-12-00020]; Welfare Center [674-A-12-00033]
FX This work was supported by PEPFAR and the National Institutes of Health
grant UM1 AI069463, and by the United States Agency for International
Development grants to Right to Care: 674-A-00-08-00007 and
674-A-12-00020, and to Witkoppen Health and Welfare Center:
674-A-12-00033. The funders had no role in data collection, analysis, or
decision to publish.
NR 23
TC 3
Z9 3
U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 30
PY 2014
VL 9
IS 9
AR e105428
DI 10.1371/journal.pone.0105428
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AR6CW
UT WOS:000343671700005
PM 25268851
ER
PT J
AU Yong, KJ
Milenic, DE
Baidoo, KE
Brechbiel, MW
AF Yong, Kwon Joong
Milenic, Diane E.
Baidoo, Kwamena E.
Brechbiel, Martin W.
TI Impact of alpha-Targeted Radiation Therapy on Gene Expression in a
Pre-Clinical Model for Disseminated Peritoneal Disease when Combined
with Paclitaxel
SO PLOS ONE
LA English
DT Article
ID CELL-CYCLE ARREST; SPINDLE CHECKPOINT; CANCER; RADIOIMMUNOTHERAPY;
APOPTOSIS; REPAIR; BRCA1; POTENTIATION; MICROTUBULE; MECHANISMS
AB To better understand the molecular basis of the enhanced cell killing effected by the combined modality of paclitaxel and Pb-212-trastuzumab (Pac/Pb-212-trastuzumab), gene expression in LS-174T i.p. xenografts was investigated 24 h after treatment. Employing a real time quantitative PCR array (qRT-PCR array), 84 DNA damage response genes were quantified. Differentially expressed genes following therapy with Pac/Pb-212-trastuzumab included those involved in apoptosis (BRCA1, CIDEA, GADD45 alpha, GADD45 gamma, GML, IP6K3, PCBP4, PPP1R15A, RAD21, and p73), cell cycle (BRCA1, CHK1, CHK2, GADD45 alpha, GML, GTSE1, NBN, PCBP4, PPP1R15A, RAD9A, and SESN1), and damaged DNA repair (ATRX, BTG2, EXO1, FEN1, IGHMBP2, OGG1, MSH2, MUTYH, NBN, PRKDC, RAD21, and p73). This report demonstrates that the increased stressful growth arrest conditions induced by the Pac/Pb-212-trastuzumab treatment suppresses cell proliferation through the regulation of genes which are involved in apoptosis and damaged DNA repair including single and double strand DNA breaks. Furthermore, the study demonstrates that Pb-212-trastuzumab potentiation of cell killing efficacy results from the perturbation of genes related to the mitotic spindle checkpoint and BASC (BRCA1-associated genome surveillance complex), suggesting cross-talk between DNA damage repair and the spindle damage response.
C1 [Yong, Kwon Joong; Milenic, Diane E.; Baidoo, Kwamena E.; Brechbiel, Martin W.] NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Brechbiel, MW (reprint author), NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
EM martinwb@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research; AREVA Med LLC
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research, and AREVA Med LLC. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 44
TC 1
Z9 1
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 30
PY 2014
VL 9
IS 9
AR e108511
DI 10.1371/journal.pone.0108511
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AR6CW
UT WOS:000343671700103
PM 25268703
ER
PT J
AU McCrindle, BW
Li, JS
Manlhiot, C
Tweddell, JS
Giglia, TM
Massicotte, MP
Monagle, P
Krishnamurthy, R
Mahaffey, KW
Michelson, AD
Verdun, N
Almond, CS
Newburger, JW
Brandao, LR
Esmon, CT
Manco-Johnson, MJ
Ichord, R
Ortel, TL
Chan, AK
Portman, R
Rose, M
Strony, J
Kaltman, JR
AF McCrindle, Brian W.
Li, Jennifer S.
Manlhiot, Cedric
Tweddell, James S.
Giglia, Therese M.
Massicotte, M. Patricia
Monagle, Paul
Krishnamurthy, Rajesh
Mahaffey, Kenneth W.
Michelson, Alan D.
Verdun, Nicole
Almond, Christopher S.
Newburger, Jane W.
Brandao, Leonardo R.
Esmon, Charles T.
Manco-Johnson, Marilyn J.
Ichord, Rebecca
Ortel, Thomas L.
Chan, Anthony K.
Portman, Ron
Rose, Martin
Strony, John
Kaltman, Jonathan R.
TI Challenges and Priorities for Research A Report From the National Heart,
Lung, and Blood Institute (NHLBI)/National Institutes of Health (NIH)
Working Group on Thrombosis in Pediatric Cardiology and Congenital Heart
Disease
SO CIRCULATION
LA English
DT Article
DE antithrombotic agents; cardiology; pediatrics; thrombosis
ID MAGNETIC-RESONANCE ANGIOGRAPHY; CARDIOPULMONARY BYPASS; CLINICAL-TRIALS;
KAWASAKI-DISEASE; PRIMARY THROMBOPROPHYLAXIS; DEVELOPMENTAL HEMOSTASIS;
VENOUS THROMBOEMBOLISM; CARDIOVASCULAR-DISEASE; CIRCULATORY SUPPORT;
ORAL ANTICOAGULANTS
C1 [McCrindle, Brian W.; Manlhiot, Cedric; Brandao, Leonardo R.] Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Li, Jennifer S.; Ortel, Thomas L.] Duke Univ, Med Ctr, Durham, NC USA.
[Tweddell, James S.] Med Coll Wisconsin, Childrens Hosp Wisconsin, Milwaukee, WI 53226 USA.
[Giglia, Therese M.; Ichord, Rebecca] Univ Penn, Childrens Hosp Philadelphia, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Massicotte, M. Patricia] Univ Alberta, Stollery Childrens Hosp, Edmonton, AB, Canada.
[Monagle, Paul] Univ Melbourne, Royal Childrens Hosp, Murdoch Childrens Res Inst, Melbourne, Vic, Australia.
[Krishnamurthy, Rajesh] Texas Childrens Hosp, Baylor Coll Med, Houston, TX 77030 USA.
[Mahaffey, Kenneth W.] Stanford Univ, Dept Med, Sch Med, Stanford, CA 94305 USA.
[Michelson, Alan D.; Almond, Christopher S.; Newburger, Jane W.] Harvard Univ, Sch Med, Boston Childrens Hosp, Boston, MA USA.
[Verdun, Nicole] George Washington Univ, Childrens Natl Med Ctr, Washington, DC USA.
[Esmon, Charles T.] Oklahoma Med Res Fdn, Coagulat Biol Lab, Oklahoma City, OK 73104 USA.
[Manco-Johnson, Marilyn J.] Univ Colorado, Childrens Hosp Colorado, Aurora, CO USA.
[Chan, Anthony K.] McMaster Univ, McMaster Childrens Hosp, Hamilton, ON, Canada.
[Portman, Ron] Bristol Myers Squibb Co, Princeton, NJ USA.
[Rose, Martin] US FDA, Div Cardiovasc & Renal Protocol, Silver Spring, MD USA.
[Strony, John] Merck, Whitehouse Stn, NJ USA.
[Kaltman, Jonathan R.] NHLBI, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
RP McCrindle, BW (reprint author), Univ Toronto, Labatt Family Heart Ctr, Dept Pediat, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM brian.mccrindle@sickkids.ca
FU NIH/NHLBI, Bethesda MD
FX Funding for the Working Group meeting was provided by the NIH/NHLBI,
Bethesda MD.
NR 75
TC 11
Z9 11
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD SEP 30
PY 2014
VL 130
IS 14
BP 1192
EP 1203
DI 10.1161/CIRCULATIONAHA.113.008428
PG 12
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AQ8CA
UT WOS:000343048800012
PM 25266860
ER
PT J
AU Zhang, CL
Tobias, DK
Chavarro, JE
Bao, W
Wang, D
Ley, SH
Hu, FB
AF Zhang, Cuilin
Tobias, Deirdre K.
Chavarro, Jorge E.
Bao, Wei
Wang, Dong
Ley, Sylvia H.
Hu, Frank B.
TI Adherence to healthy lifestyle and risk of gestational diabetes
mellitus: prospective cohort study
SO BMJ-BRITISH MEDICAL JOURNAL
LA English
DT Article
ID PHYSICAL-ACTIVITY; PREGNANT-WOMEN; INCREASING PREVALENCE; SEDENTARY
BEHAVIORS; CHRONIC DISEASE; DIETARY; QUESTIONNAIRE; OBESITY;
HYPERGLYCEMIA; WEIGHT
AB Objective To quantify the association between a combination of healthy lifestyle factors before pregnancy (healthy body weight, healthy diet, regular exercise, and not smoking) and the risk of gestational diabetes.
Design Prospective cohort study.
Setting Nurses' Health Study II, United States.
Participants 20 136 singleton live births in 14 437 women without chronic disease.
Main outcome measure Self reported incident gestational diabetes diagnosed by a physician, validated by medical records in a previous study.
Results Incident first time gestational diabetes was reported in 823 pregnancies. Each lifestyle factor measured was independently and significantly associated with risk of gestational diabetes. The combination of three low risk factors (non-smoker, >= 150 minutes a week of moderate to vigorous physical activity, and healthy eating (top two fifths of Alternate Healthy Eating Index-2010 adherence score)) was associated with a 41% lower risk of gestational diabetes compared with all other pregnancies (relative risk 0.59, 95% confidence interval 0.48 to 0.71). Addition of body mass index (BMI) <25 before pregnancy (giving a combination of four low risk factors) was associated with a 52% lower risk of gestational diabetes compared with all other pregnancies (relative risk 0.48, 0.38 to 0.61). Compared with pregnancies in women who did not meet any of the low risk lifestyle factors, those meeting all four criteria had an 83% lower risk of gestational diabetes (relative risk 0.17, 0.12 to 0.25). The population attributable risk percentage of the four risk factors in combination (smoking, inactivity, overweight, and poor diet) was 47.5% (95% confidence interval 35.6% to 56.6%). A similar population attributable risk percentage (49.2%) was observed when the distributions of the four low risk factors from the US National Health and Nutrition Examination Survey (2007-10) data were applied to the calculation.
Conclusions Adherence to a low risk lifestyle before pregnancy is associated with a low risk of gestational diabetes and could be an effective strategy for the prevention of gestational diabetes.
C1 [Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20852 USA.
[Tobias, Deirdre K.; Chavarro, Jorge E.; Wang, Dong; Ley, Sylvia H.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Tobias, Deirdre K.; Chavarro, Jorge E.; Wang, Dong; Ley, Sylvia H.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Chavarro, Jorge E.; Hu, Frank B.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.
[Chavarro, Jorge E.; Hu, Frank B.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Zhang, CL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20852 USA.
EM zhangcu@mail.nih.gov
OI Bao, Wei/0000-0002-7301-5786
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health [HHSN275201000020C]; National
Institutes of Health [DK58845, CA50385, P30 DK46200, UM1 CA176726];
American Diabetes Association [7-12-MN-34]
FX This study was supported by the intramural research program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health (contract No
HHSN275201000020C). The Nurses' Health Study II was funded by research
grants DK58845, CA50385, P30 DK46200, and UM1 CA176726 from the National
Institutes of Health and by an American Diabetes Association Award
7-12-MN-34.
NR 38
TC 19
Z9 20
U1 2
U2 35
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1756-1833
J9 BMJ-BRIT MED J
JI BMJ-British Medical Journal
PD SEP 30
PY 2014
VL 349
AR g5450
DI 10.1136/bmj.g5450
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA AQ3CA
UT WOS:000342665100001
PM 25269649
ER
PT J
AU Daye, PM
Optican, LM
AF Daye, Pierre M.
Optican, Lance M.
TI Saccade detection using a particle filter
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE Catch-up saccade; Smooth pursuit; Eye drift; Microsaccades; Bayesian
estimator
ID COMPLEX 2-DIMENSIONAL TRAJECTORIES; HEAD-UNRESTRAINED CONDITIONS;
PREDICTIVE SMOOTH-PURSUIT; CATCH-UP SACCADES; EYE-MOVEMENTS; NEURAL
INTEGRATOR; SLOW SACCADES; TARGET MOTION; TRACKING; MONKEY
AB Background: When healthy subjects track a moving target, "catch-up" saccades are triggered to compensate for the non-perfect tracking gain. The evaluation of the pursuit and/or saccade kinematics requires that saccade and pursuit components be separated from the eye movement trace. A similar situation occurs when analyzes eye movements of patients that could contain eye drifts between saccades. This task is especially difficult, because the range of saccadic amplitudes goes from microsaccades (less than 1 degrees) to large exploratory saccades (40 degrees).
New method: In this paper we proposed a new algorithm to detect saccades based on a particle filter. The new method suppresses the baseline velocity component linked to smooth pursuit (or to eye drifts) and thus permits a constant threshold during a trial despite the smooth pursuit behavior. It also accounts for a wide range of saccade amplitudes.
Results: The new method is validated with five different paradigms, microsaccades, microsaccades plus saccades with drift, linear target motion, non-linear target motion and free viewing. The sensitivity of the method to signal noise is analyzed.
Comparison with existing methods: Traditional saccade detection algorithms using a velocity (or acceleration or jerk) threshold can be inadequate because of the baseline velocity component linked to the smooth pursuit (especially if the target motion is non-linear, i.e. not constant velocity) or to eye drifts between saccades.
Conclusions: The new method detects saccades in challenging situations involving eye movements between saccades (smooth pursuit and/or eye drifts) and unfiltered recordings. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Daye, Pierre M.] Univ Paris 06, INSERM UMRS 975, CNRS 7225, ICM, F-75013 Paris, France.
[Daye, Pierre M.; Optican, Lance M.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP Daye, PM (reprint author), Univ Paris 06, INSERM UMRS 975, CNRS 7225, ICM, F-75013 Paris, France.
EM pierre.daye@gmail.com
OI Daye, Pierre/0000-0002-0586-396X
NR 33
TC 5
Z9 5
U1 3
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
EI 1872-678X
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD SEP 30
PY 2014
VL 235
BP 157
EP 168
DI 10.1016/j.jneumeth.2014.06.020
PG 12
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AP7PO
UT WOS:000342269400018
PM 25043508
ER
PT J
AU Ma, XR
Xu, LY
Gavrilova, O
Mueller, E
AF Ma, Xinran
Xu, Lingyan
Gavrilova, Oksana
Mueller, Elisabetta
TI Role of forkhead box protein A3 in age-associated metabolic decline
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE obesity; diabetes
ID BROWN ADIPOSE-TISSUE; NUCLEAR FACTOR 3-GAMMA; INSULIN-RESISTANCE;
ADIPOCYTE DIFFERENTIATION; GLUCOSE-HOMEOSTASIS; ENERGY-EXPENDITURE;
TRANSCRIPTION; MICE; FAT; PGC-1-ALPHA
AB Aging is associated with increased adiposity and diminished thermogenesis, but the critical transcription factors influencing these metabolic changes late in life are poorly understood. We recently demonstrated that the winged helix factor forkhead box protein A3 (Foxa3) regulates the expansion of visceral adipose tissue in high-fat diet regimens; however, whether Foxa3 also contributes to the increase in adiposity and the decrease in brown fat activity observed during the normal aging process is currently unknown. Here we report that during aging, levels of Foxa3 are significantly and selectively up-regulated in brown and inguinal white fat depots, and that midage Foxa3-null mice have increased white fat browning and thermogenic capacity, decreased adipose tissue expansion, improved insulin sensitivity, and increased longevity. Foxa3 gain-of-function and loss-of-function studies in inguinal adipose depots demonstrated a cell-autonomous function for Foxa3 in white fat tissue browning. Furthermore, our analysis revealed that the mechanisms of Foxa3 modulation of brown fat gene programs involve the suppression of peroxisome proliferator activated receptor gamma coactivtor 1 alpha (PGC1 alpha) levels through interference with cAMP responsive element binding protein 1-mediated transcriptional regulation of the PGC1 alpha promoter. Overall, our data demonstrate a role for Foxa3 in energy expenditure and in age-associated metabolic disorders.
C1 [Ma, Xinran; Xu, Lingyan; Mueller, Elisabetta] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
[Gavrilova, Oksana] NIDDK, Mouse Metab Core, NIH, Bethesda, MD 20892 USA.
RP Mueller, E (reprint author), NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
EM elisabettam@niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX We thank Pasha Sarraf for discussions and comments on the manuscript;
Tatyana Chanturiya and Ruifeng Tan for technical assistance; Klaus
Kaestner for the gift of the Foxa3-null mice; and Jeffrey Kopp, Hidefumi
Wakashin, and Shashi Shivrastav for sharing the Seahorse Instrument.
This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health.
NR 41
TC 8
Z9 8
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD SEP 30
PY 2014
VL 111
IS 39
BP 14289
EP 14294
DI 10.1073/pnas.1407640111
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AP8SW
UT WOS:000342350200064
PM 25225406
ER
PT J
AU Iwashita, M
AF Iwashita, Motoko
TI Phasic activation of ventral tegmental neurons increases response and
pattern similarity in prefrontal cortex neurons
SO ELIFE
LA English
DT Article
ID NIGRAL DOPAMINE NEURONS; IN-VIVO; FIRING PATTERN; MODULATION; SELECTION;
RELEASE; RAT
AB Dopamine is critical for higher neural processes and modifying activity of the prefrontal cortex (PFC). However, dopamine contribution to the modification of neural representation is largely unknown. Using in vivo two-photon population Ca2+ imaging in awake mice, I investigated how neural representation of visual input to PFC neurons is regulated by dopamine. Phasic stimulation of dopaminergic neurons in the ventral tegmental area (VTA) evoked prolonged Ca2+ transients, lasting similar to 30 seconds in layer 2/3 neurons of PFC, which are regulated by dopamine D1 receptor-dependent pathway. Furthermore, only a conditioning protocol with visual sensory input applied 0.5 second before the VTA dopaminergic input could evoke enhanced Ca2+ transients and increased pattern similarity (or establish a neural representation) of PFC neurons to the same sensory input. By increasing both the level of neuronal response and pattern similarity, dopaminergic input may establish robust and reliable cortical representation.
C1 NIMH, US Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Iwashita, M (reprint author), NIMH, US Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 30
TC 0
Z9 1
U1 2
U2 2
PU ELIFE SCIENCES PUBLICATIONS LTD
PI CAMBRIDGE
PA SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND
SN 2050-084X
J9 ELIFE
JI eLife
PD SEP 30
PY 2014
VL 3
AR e02726
DI 10.7554/eLife.02726
PG 29
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AR2IZ
UT WOS:000343408800006
ER
PT J
AU Jacobs, JH
Viboud, C
Tchetgen, ET
Schwartz, J
Steiner, C
Simonsen, L
Lipsitch, M
AF Jacobs, Jessica Hartman
Viboud, Cecile
Tchetgen, Eric Tchetgen
Schwartz, Joel
Steiner, Claudia
Simonsen, Lone
Lipsitch, Marc
TI The Association of Meningococcal Disease with Influenza in the United
States, 1989-2009
SO PLOS ONE
LA English
DT Article
ID RESPIRATORY SYNCYTIAL VIRUS; A VIRUS; NEISSERIA-MENINGITIDIS; EPIDEMIC
INFLUENZA; INFECTIONS; ENGLAND; MODELS; WALES; BOOTSTRAP; SCHOOL
AB Importance and Objective: Prior influenza infection is a risk factor for invasive meningococcal disease. Quantifying the fraction of meningococcal disease attributable to influenza could improve understanding of viral-bacterial interaction and indicate additional health benefits to influenza immunization.
Design, Setting and Participants: A time series analysis of the association of influenza and meningococcal disease using hospitalizations in 9 states from 1989-2009 included in the State Inpatient Databases from the Agency for Healthcare Research and Quality and the proportion of positive influenza tests by subtype reported to the Centers for Disease Control. The model accounts for the autocorrelation of meningococcal disease and influenza between weeks, temporal trends, co-circulating respiratory syncytial virus, and seasonality. The influenza-subtype-attributable fraction was estimated using the model coefficients. We analyzed the synchrony of seasonal peaks in hospitalizations for influenza, respiratory syncytial virus, and meningococcal disease.
Results and Conclusions: In 19 of 20 seasons, influenza peaked <= 2 weeks before meningococcal disease, and peaks were highly correlated in time (rho = 0.95; P<.001). H3N2 and H1N1 peaks were highly synchronized with meningococcal disease while pandemic H1N1, B, and respiratory syncytial virus were not. Over 20 years, 12.8% (95% CI, 9.1-15.0) of meningococcal disease can be attributable to influenza in the preceding weeks with H3N2 accounting for 5.2% (95% CI, 3.0-6.5), H1N1 4.3% (95% CI, 2.6-5.6), B 3.0% (95% CI, 0.8-4.9) and pH1N1 0.2% (95% CI, 0-0.4). During the height of influenza season, weekly attributable fractions reach 59%. While vaccination against meningococcal disease is the most important prevention strategy, influenza vaccination could provide further protection, particularly in young children where the meningococcal disease vaccine is not recommended or protective against the most common serogroup.
C1 [Jacobs, Jessica Hartman; Tchetgen, Eric Tchetgen; Schwartz, Joel; Lipsitch, Marc] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Ctr Communicable Dis Dynam, Boston, MA 02115 USA.
[Viboud, Cecile; Simonsen, Lone] NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Tchetgen, Eric Tchetgen] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Schwartz, Joel] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Steiner, Claudia] Agcy Healthcare Res & Qual, Ctr Delivery Org & Markets, Rockville, MD USA.
[Simonsen, Lone] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Global Hlth, Washington, DC USA.
[Lipsitch, Marc] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Lipsitch, M (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Ctr Communicable Dis Dynam, Boston, MA 02115 USA.
EM mlipsitc@hsph.harvard.edu
OI Simonsen, Lone/0000-0003-1535-8526
FU National Institute Of General Medical Sciences [U54GM088558]
FX The project described was supported by the National Institute Of General
Medical Sciences [Award Number U54GM088558]. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institute Of General Medical Sciences,
the National Institutes of Health, or the Agency for Healthcare Research
and Quality. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 46
TC 4
Z9 4
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 29
PY 2014
VL 9
IS 9
AR e107486
DI 10.1371/journal.pone.0107486
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AU6XR
UT WOS:000345745400023
PM 25265409
ER
PT J
AU Sarwar, UN
Novik, L
Enama, ME
Plummer, SA
Koup, RA
Nason, MC
Bailer, RT
McDermott, AB
Roederer, M
Mascola, JR
Ledgerwood, JE
Graham, BS
AF Sarwar, Uzma N.
Novik, Laura
Enama, Mary E.
Plummer, Sarah A.
Koup, Richard A.
Nason, Martha C.
Bailer, Robert T.
McDermott, Adrian B.
Roederer, Mario
Mascola, John R.
Ledgerwood, Julie E.
Graham, Barney S.
CA VRC 015 Study Team
TI Homologous Boosting with Adenoviral Serotype 5 HIV Vaccine (rAd5) Vector
Can Boost Antibody Responses despite Preexisting Vector-Specific
Immunity in a Randomized Phase I Clinical Trial
SO PLOS ONE
LA English
DT Article
ID T-CELL RESPONSES; DNA VACCINE; HEALTHY-ADULTS; NEUTRALIZING ANTIBODY;
IMMUNOGENICITY EVALUATION; CANDIDATE VACCINE; MALARIA VACCINE; NEEDLE;
SAFETY; INJECTION
AB Background: Needle-free delivery improves the immunogenicity of DNA vaccines but is also associated with more local reactogenicity. Here we report the first comparison of Biojector and needle administration of a candidate rAd5 HIV vaccine.
Methods: Thirty-one adults, 18-55 years, 20 naive and 11 prior rAd5 vaccine recipients were randomized to receive single rAd5 vaccine via needle or Biojector IM injection at 10(10) PU in a Phase I open label clinical trial. Solicited reactogenicity was collected for 5 days; clinical safety and immunogenicity follow-up was continued for 24 weeks.
Results: Overall, injections by either method were well tolerated. There were no serious adverse events. Frequency of any local reactogenicity was 16/16 (100%) for Biojector compared to 11/15 (73%) for needle injections. There was no difference in HIV Env-specific antibody response between Biojector and needle delivery. Env-specific antibody responses were more than 10-fold higher in subjects receiving a booster dose of rAd5 vaccine than after a single dose delivered by either method regardless of interval between prime and boost.
Conclusions: Biojector delivery did not improve antibody responses to the rAd5 vaccine compared to needle administration. Homologous boosting with rAd5 gene-based vectors can boost insert-specific antibody responses despite pre-existing vector-specific immunity.
C1 [Sarwar, Uzma N.; Novik, Laura; Enama, Mary E.; Plummer, Sarah A.; Koup, Richard A.; Bailer, Robert T.; McDermott, Adrian B.; Roederer, Mario; Mascola, John R.; Ledgerwood, Julie E.; Graham, Barney S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Nason, Martha C.] NIAID, Biostat Res Branch, Div Clin Res, NIH, Bethesda, MD 20892 USA.
RP Graham, BS (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM bgraham@mail.nih.gov
OI Richie, Thomas/0000-0002-2946-5456
FU U.S. Government
FX This study was supported by U.S. Government funding for the intramural
research conducted by the National Institute of Allergy and Infectious
Diseases. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 35
TC 5
Z9 5
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 29
PY 2014
VL 9
IS 9
AR e106240
DI 10.1371/journal.pone.0106240
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AU6XR
UT WOS:000345745400008
PM 25264782
ER
PT J
AU Shigehiro, T
Kasai, T
Murakami, M
Sekhar, SC
Tominaga, Y
Okada, M
Kudoh, T
Mizutani, A
Murakami, H
Salomon, DS
Mikuni, K
Mandai, T
Hamada, H
Seno, M
AF Shigehiro, Tsukasa
Kasai, Tomonari
Murakami, Masaharu
Sekhar, Sreeja C.
Tominaga, Yuki
Okada, Masashi
Kudoh, Takayuki
Mizutani, Akifumi
Murakami, Hiroshi
Salomon, David S.
Mikuni, Katsuhiko
Mandai, Tadakatsu
Hamada, Hiroki
Seno, Masaharu
TI Efficient Drug Delivery of Paclitaxel Glycoside: A Novel Solubility
Gradient Encapsulation into Liposomes Coupled with Immunoliposomes
Preparation
SO PLOS ONE
LA English
DT Article
ID BREAST-CANCER CELLS; ANTI-HER2 IMMUNOLIPOSOMES; FORMULATIONS;
NANOPARTICLES; EFFICACY; TAXOIDS; TUMORS; EGFR
AB Although the encapsulation of paclitaxel into liposomes has been extensively studied, its significant hydrophobic and uncharged character has generated substantial difficulties concerning its efficient encapsulation into the inner water core of liposomes. We found that a more hydrophilic paclitaxel molecule, 7-glucosyloxyacetylpaclitaxel, retained tubulin polymerization stabilization activity. The hydrophilic nature of 7-glucosyloxyacetylpaclitaxel allowed its efficient encapsulation into the inner water core of liposomes, which was successfully accomplished using a remote loading method with a solubility gradient between 40% ethylene glycol and Cremophor EL/ethanol in PBS. Trastuzumab was then conjugated onto the surface of liposomes as immunoliposomes to selectively target human epidermal growth factor receptor-2 (HER2)-overexpressing cancer cells. In vitro cytotoxicity assays revealed that the immunoliposomes enhanced the toxicity of 7-glucosyloxyacetylpaclitaxel in HER2-overexpressing cancer cells and showed more rapid suppression of cell growth. The immunoliposomes strongly inhibited the tumor growth of HT-29 cells xenografted in nude mice. Notably, mice survived when treated with the immunoliposomes formulation, even when administered at a lethal dose of 7glucosyloxyacetylpaclitaxel in vivo. This data successfully demonstrates immunoliposomes as a promising candidate for the efficient delivery of paclitaxel glycoside.
C1 [Shigehiro, Tsukasa; Kasai, Tomonari; Murakami, Masaharu; Sekhar, Sreeja C.; Tominaga, Yuki; Okada, Masashi; Kudoh, Takayuki; Mizutani, Akifumi; Murakami, Hiroshi; Seno, Masaharu] Okayama Univ, Grad Sch Nat Sci & Technol, Dept Biotechnol, Okayama 7008530, Japan.
[Salomon, David S.] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Mikuni, Katsuhiko] Ensuiko Sugar Refining Co Ltd, Tokyo, Japan.
[Mandai, Tadakatsu] Kurashiki Univ Sci & Arts, Fac Life Sci, Kurashiki, Okayama, Japan.
[Hamada, Hiroki] Okayama Univ Sci, Fac Sci, Okayama, Japan.
RP Hamada, H (reprint author), Okayama Univ Sci, Fac Sci, Okayama, Japan.
EM hamada@dls.ous.ac.jp; mseno@okayama-u.ac.jp
RI SENO, Masaharu /B-2092-2011; hamada, hiroki/A-4276-2009
OI SENO, Masaharu /0000-0001-8547-6259;
FU Ministry of Education, Culture, Sports, Science and Technology of Japan
[23650598, 25242045, 26640079, 24510151, 24501315]; Japan Society for
the Promotion of Science; Ensuiko Sugar Refining Co., Ltd. (Tokyo,
Japan)
FX This study was partly supported by Grant-in-Aid for Challenging
Exploratory Research No. 23650598 (MS), 25242045 (MS), and 26640079
(MS); Grant-in-Aid for Scientific Research (C) Nos. 24510151 (T. Kasai)
and 24501315 (AM) from the Ministry of Education, Culture, Sports,
Science and Technology of Japan (http://www.mext.go.jp); and from the
Japan Society for the Promotion of Science (http://www.jsps.go.jp). This
research was funded by a commercial company, Ensuiko Sugar Refining Co.,
Ltd. (Tokyo, Japan). Ensuiko Sugar Refining Co., Ltd. had a role in the
study design. The other funders had no role in study design. All funders
had no role in data collection and analysis, decision to publish, or
preparation of the manuscript in this study.
NR 33
TC 5
Z9 5
U1 2
U2 16
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 SEP 29
PY 2014
VL 9
IS 9
AR e107976
DI 10.1371/journal.pone.0107976
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AU6XR
UT WOS:000345745400036
PM 25264848
ER
PT J
AU Pilkington, GR
Purzycka, KJ
Bear, J
Le Grice, SFJ
Felber, BK
AF Pilkington, Guy R.
Purzycka, Katarzyna J.
Bear, Jenifer
Le Grice, Stuart F. J.
Felber, Barbara K.
TI Gammaretrovirus mRNA expression is mediated by a novel, bipartite
post-transcriptional regulatory element
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; MURINE LEUKEMIA-VIRUS; UNSPLICED VIRAL
TRANSCRIPTS; SIMIAN RETROVIRUS TYPE-1; REV RESPONSE ELEMENT; LONG
TERMINAL REPEAT; MAMMARY-TUMOR VIRUS; ROUS-SARCOMA-VIRUS; HTLV-I REX;
NUCLEAR EXPORT
AB Post-transcriptional regulatory mechanisms of several complex and simple retroviruses and retroelements have been elucidated, with the exception of the gammaretrovirus family. We found that, similar to the other retroviruses, gag gene expression of MuLV and XMRV depends on post-transcriptional regulation mediated via an RNA sequence overlapping the pro-pol open reading frame, termed the Post-Transcriptional Element (PTE). PTE function can be replaced by heterologous RNA export elements, e.g. CTE of simian type D retroviruses. Alternatively, Gag particle production is achieved using an RNA/codon optimized gag gene. PTE function is transferable and can replace HIV Rev-RRE-regulated expression of HIV gag. Analysis of PTE by SHAPE revealed a highly structured RNA comprising seven stem-loop structures, with the 5' and 3' stem-loops forming an essential bipartite signal. MuLV and XMRV PTE share 98% identity and have highly similar RNA structures, with changes mostly located to single-stranded regions. PTE identification strongly suggests that all retroviruses and retroelements share common strategies of post-transcriptional gene regulation to produce Gag. Expression depends on complex RNA structures embedded within retroviral mRNA, in coding regions or the 3' untranslated region. These specific structures serve as recognition signals for either cellular or viral proteins.
C1 [Pilkington, Guy R.; Bear, Jenifer; Felber, Barbara K.] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21702 USA.
[Purzycka, Katarzyna J.; Le Grice, Stuart F. J.] NCI, RT Biochem Sect, Drug Resistance Program, Frederick, MD 21702 USA.
[Purzycka, Katarzyna J.] Polish Acad Sci, Inst Bioorgan Chem, PL-61704 Poznan, Poland.
RP Felber, BK (reprint author), NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21702 USA.
EM legrices@mail.nih.gov; Barbara.felber@nih.gov
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health (NCI/NIH); HOMING [PLUS/2012-6/12]; Intramural
Research Program NIH/NCI
FX Intramural Research Program of the National Cancer Institute, National
Institutes of Health (NCI/NIH) [to S.F.J.L., B.K.F.].; HOMING
[PLUS/2012-6/12 to K.J.P.]. Funding for open access charge: Intramural
Research Program NIH/NCI.
NR 73
TC 4
Z9 4
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP 29
PY 2014
VL 42
IS 17
BP 11092
EP 11106
DI 10.1093/nar/gku798
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AU7JG
UT WOS:000345776200024
PM 25190459
ER
PT J
AU Czerwinska, J
Poznanski, J
Debski, J
Bukowy, Z
Bohr, VA
Tudek, B
Speina, E
AF Czerwinska, Jolanta
Poznanski, Jaroslaw
Debski, Janusz
Bukowy, Zuzanna
Bohr, Vilhelm A.
Tudek, Barbara
Speina, Elzbieta
TI Catalytic activities of Werner protein are affected by adduction with
4-hydroxy-2-nonenal
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID BASE EXCISION-REPAIR; JAPANESE POPULATION; LIPID-PEROXIDATION; RECQ
HELICASES; WRN GENE; MYOCARDIAL-INFARCTION; NUCLEAR-LOCALIZATION;
POLYMORPHIC VARIANT; ALZHEIMERS-DISEASE; OXIDATIVE STRESS
AB 4-Hydroxy-2-nonenal (HNE) is a reactive alpha,beta-unsaturated aldehyde generated during oxidative stress and subsequent peroxidation of polyunsaturated fatty acids. Here, Werner protein (WRN) was identified as a novel target for modification by HNE. Werner syndrome arises through mutations in the WRN gene that encodes the RecQ DNA helicase which is critical for maintaining genomic stability. This hereditary disease is associated with chromosomal instability, premature aging and cancer predisposition. WRN appears to participate in the cellular response to oxidative stress and cells devoid of WRN display elevated levels of oxidative DNA damage. We demonstrated that helicase/ATPase and exonuclease activities of HNE-modified WRN protein were inhibited both in vitro and in immunocomplexes purified from the cell extracts. Sites of HNE adduction in human WRN were identified at Lys577, Cys727, His1290, Cys1367, Lys1371 and Lys1389. We applied in silico modeling of the helicase and RQC domains of WRN protein with HNE adducted to Lys577 and Cys727 and provided a potential mechanism of the observed deregulation of the protein catalytic activities. In light of the obtained results, we postulate that HNE adduction to WRN is a post-translational modification, which may affect WRN conformational stability and function, contributing to features and diseases associated with premature senescence.
C1 [Czerwinska, Jolanta; Poznanski, Jaroslaw; Debski, Janusz; Bukowy, Zuzanna; Tudek, Barbara; Speina, Elzbieta] Polish Acad Sci, Inst Biochem & Biophys, PL-02106 Warsaw, Poland.
[Bohr, Vilhelm A.] NIA, NIH, Baltimore, MD 21224 USA.
[Tudek, Barbara] Univ Warsaw, Inst Genet & Biotechnol, PL-02106 Warsaw, Poland.
RP Speina, E (reprint author), Polish Acad Sci, Inst Biochem & Biophys, Pawinskiego 5a, PL-02106 Warsaw, Poland.
EM elasp@ibb.waw.pl
RI Poznanski, Jarek/F-7705-2014; Debski, Janusz/D-8138-2015; Debski,
Janusz/I-4721-2015
OI Poznanski, Jarek/0000-0003-2684-1775; Debski,
Janusz/0000-0002-0171-7797; Debski, Janusz/0000-0002-8898-7692
FU National Science Center [UMO-2012/05/B/NZ5/01392]; Intramural Research
Program of the National Institutes of Health, USA
FX National Science Center [UMO-2012/05/B/NZ5/01392]. Intramural Research
Program of the National Institutes of Health, USA. Funding for open
access charge: National Science Center [UMO-2012/05/B/NZ5/01392].
NR 68
TC 1
Z9 1
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP 29
PY 2014
VL 42
IS 17
BP 11119
EP 11135
DI 10.1093/nar/gku783
PG 17
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AU7JG
UT WOS:000345776200026
PM 25170083
ER
PT J
AU Adhikari, D
Diril, MK
Busayavalasa, K
Risal, S
Nakagawa, S
Lindkvist, R
Shen, Y
Coppola, V
Tessarollo, L
Kudo, NR
Kaldis, P
Liu, K
AF Adhikari, Deepak
Diril, M. Kasim
Busayavalasa, Kiran
Risal, Sanjiv
Nakagawa, Shoma
Lindkvist, Rebecca
Shen, Yan
Coppola, Vincenzo
Tessarollo, Lino
Kudo, Nobuaki R.
Kaldis, Philipp
Liu, Kui
TI Mastl is required for timely activation of APC/C in meiosis I and Cdk1
reactivation in meiosis II
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID PROTEIN PHOSPHATASE 2A; CELL-CYCLE REGULATION; XENOPUS EGG EXTRACTS;
GREATWALL KINASE; MEIOTIC MATURATION; MOUSE OOCYTES; MITOTIC
PROGRESSION; MITOSIS; PHOSPHORYLATION; CHECKPOINT
AB In mitosis, the Greatwall kinase (called microtubule-associated serine/threonine kinase like [Mastl] in mammals) is essential for prometaphase entry or progression by suppressing protein phosphatase 2A (PP2A) activity. PP2A suppression in turn leads to high levels of Cdk1 substrate phosphorylation. We have used a mouse model with an oocyte-specific deletion of Mastl to show that Mastl-null oocytes resume meiosis I and reach metaphase I normally but that the onset and completion of anaphase I are delayed. Moreover, after the completion of meiosis I, Mastl-null oocytes failed to enter meiosis II (MII) because they reassembled a nuclear structure containing decondensed chromatin. Our results show that Mastl is required for the timely activation of anaphase-promoting complex/cyclosome to allow meiosis I exit and for the rapid rise of Cdk1 activity that is needed for the entry into MII in mouse oocytes.
C1 [Adhikari, Deepak; Busayavalasa, Kiran; Risal, Sanjiv; Lindkvist, Rebecca; Shen, Yan; Liu, Kui] Univ Gothenburg, Dept Chem & Mol Biol, S-40530 Gothenburg, Sweden.
[Diril, M. Kasim; Kaldis, Philipp] ASTAR, Inst Mol & Cell Biol, Singapore 138673, Singapore.
[Nakagawa, Shoma; Kudo, Nobuaki R.] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Inst Reprod & Dev Biol, Dept Surg & Canc, London W12 0NN, England.
[Coppola, Vincenzo; Tessarollo, Lino] NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA.
[Kaldis, Philipp] Natl Univ Singapore, Dept Biochem, Singapore 117599, Singapore.
RP Kaldis, P (reprint author), ASTAR, Inst Mol & Cell Biol, Singapore 138673, Singapore.
EM kaldis@imcb.a-star.edu.sg; kui.liu@gu.se
RI ASTAR, IMCB/E-2320-2012;
OI Kudo, Nobuaki/0000-0001-8134-1242; Kaldis, Philipp/0000-0002-7247-7591
FU Jane and Dan Olssons Foundation; LUA/ALF-medel Vastra Gotalandsregionen,
AFA Insurance; Swedish Research Council; Swedish Cancer Foundation;
Biomedical Research Council of A*STAR, Singapore; Medical Research
Council; Genesis Research Trust
FX This study was supported by grants (to K. Liu) from the Jane and Dan
Olssons Foundation, the LUA/ALF-medel Vastra Gotalandsregionen, AFA
Insurance, the Swedish Research Council, and the Swedish Cancer
Foundation; by funding (to P. Kaldis) from the Biomedical Research
Council of A*STAR, Singapore; and by funding (to N.R. Kudo) from the
Medical Research Council and the Genesis Research Trust.
NR 57
TC 11
Z9 11
U1 0
U2 13
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD SEP 29
PY 2014
VL 206
IS 7
BP 843
EP 853
DI 10.1083/jcb.201406033
PG 11
WC Cell Biology
SC Cell Biology
GA AQ1KE
UT WOS:000342539500006
PM 25246615
ER
PT J
AU Kong, D
Farmer, V
Shukla, A
James, J
Gruskin, R
Kiriyama, S
Loncarek, J
AF Kong, Dong
Farmer, Veronica
Shukla, Anil
James, Jana
Gruskin, Richard
Kiriyama, Shigeo
Loncarek, Jadranka
TI Centriole maturation requires regulated Plk1 activity during two
consecutive cell cycles
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID CENTROSOME DUPLICATION CYCLE; PROTEIN; MOTHER; CEP152; PROCENTRIOLE;
CILIOGENESIS; CENTROBIN; INTERACTS; SCAFFOLD; DOCKING
AB Newly formed centrioles in cycling cells undergo a maturation process that is almost two cell cycles long before they become competent to function as microtubule-organizing centers and basal bodies. As a result, each cell contains three generations of centrioles, only one of which is able to form cilia. It is not known how this long and complex process is regulated. We show that controlled Plk1 activity is required for gradual biochemical and structural maturation of the centrioles and timely appendage assembly. Inhibition of Plk1 impeded accumulation of appendage proteins and appendage formation. Unscheduled Plk1 activity, either in cycling or interphase-arrested cells, accelerated centriole maturation and appendage and cilia formation on the nascent centrioles, erasing the age difference between centrioles in one cell. These findings provide a new understanding of how the centriole cycle is regulated and how proper cilia and centrosome numbers are maintained in the cells.
C1 [Kong, Dong; Farmer, Veronica; Shukla, Anil; James, Jana; Gruskin, Richard; Kiriyama, Shigeo; Loncarek, Jadranka] NCI, Lab Prot Dynam & Signaling, Ctr Canc Res Frederick, NIH, Frederick, MD 21702 USA.
RP Loncarek, J (reprint author), NCI, Lab Prot Dynam & Signaling, Ctr Canc Res Frederick, NIH, Frederick, MD 21702 USA.
EM jadranka.loncarek@nih.gov
RI Kong, Dong/O-4465-2016;
OI Kong, Dong/0000-0002-7144-3808; Shukla, Anil/0000-0001-7797-7299
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute, Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health; National Cancer Institute, Center for
Cancer Research.
NR 32
TC 14
Z9 15
U1 1
U2 10
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD SEP 29
PY 2014
VL 206
IS 7
BP 855
EP 865
DI 10.1083/jcb.201407087
PG 11
WC Cell Biology
SC Cell Biology
GA AQ1KE
UT WOS:000342539500007
PM 25246616
ER
PT J
AU Horiuchi, A
Tanaka, N
AF Horiuchi, Akira
Tanaka, Naoki
TI Improving quality measures in colonoscopy and its therapeutic
intervention
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Colonoscopy; Polypectomy; Hemostasis; Endoscopic decompression;
Colorectal polyp; Colonic diverticular bleeding; Colorectal obstruction;
Gastrointestinal endoscopy
ID SMALL COLORECTAL POLYPS; TRANSANAL DRAINAGE TUBE; COLD SNARE
POLYPECTOMY; HOT BIOPSY FORCEPS; ADENOMA DETECTION; SCREENING
COLONOSCOPY; CONVENTIONAL POLYPECTOMY; WITHDRAWAL TIMES; DETECTION
RATES; CANCER
AB Colonoscopy with polypectomy has been shown to reduce the risk of colon cancer. The critical element in the quality of colonoscopy in terms of polyp detection and removal continues to be the performance of the endoscopist, independent of patient-related factors. Improved results in terms of polyp detection and complete removal have implications regarding the development of screening and surveillance intervals and the reduction of interval cancers after negative colonoscopy. Advances in colonoscopy techniques such as high-definition colonoscopy, hood-assisted colonoscopy and dye-based chromoendoscopy have improved the detection of small and flat-type colorectal polyps. Virtual chromoendoscopy has not proven to improve polyp detection but may be useful to predict polyp pathology. The majority of polyps can be removed endoscopically. Available polypectomy techniques include cold forceps polypectomy, cold snare polypectomy, conventional polypectomy, endoscopic mucosal resection and endoscopic submucosal dissection. The preferred choice depends on the polyp size and characteristics. Other useful techniques include colonoscopic hemostasis for acute colonic diverticular bleeding, endoscopic decompression using colonoscopic stenting, and transanal tube placement for colorectal obstruction. Here we review the current knowledge concerning the improvement of quality measures in colonoscopy and colonoscopy-related therapeutic interventions. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
C1 [Horiuchi, Akira] Showa Inan Gen Hosp, Ctr Digest Dis, Komagane 3994117, Japan.
[Tanaka, Naoki] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
RP Horiuchi, A (reprint author), Showa Inan Gen Hosp, Ctr Digest Dis, 3230 Akaho, Komagane 3994117, Japan.
EM horiuchi.akira@sihp.jp
NR 56
TC 3
Z9 3
U1 0
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 28
PY 2014
VL 20
IS 36
BP 13027
EP 13034
DI 10.3748/wjg.v20.i36.13027
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AR9GK
UT WOS:000343880900024
PM 25278696
ER
PT J
AU Beydoun, MA
Nalls, MA
Canas, JA
Evans, MK
Zonderman, AB
AF Beydoun, May A.
Nalls, Michael A.
Canas, J. Atilio
Evans, Michele K.
Zonderman, Alan B.
TI Gene polymorphisms and gene scores linked to low serum carotenoid status
and their associations with metabolic disturbance and depressive
symptoms in African-American adults
SO BRITISH JOURNAL OF NUTRITION
LA English
DT Article
DE Gene polymorphisms; Gene risk scores; Carotenoids; Metabolic
disturbance; Depressive symptoms
ID DENSITY-LIPOPROTEIN CHOLESTEROL; NUTRITION EXAMINATION SURVEY; 3RD
NATIONAL-HEALTH; SINGLE NUCLEOTIDE POLYMORPHISMS; MULTILOCUS GENOTYPE
DATA; DIABETES-MELLITUS; APO-B-516C/T POLYMORPHISM; US ADULTS;
ANTIOXIDANT CONCENTRATIONS; CARDIOVASCULAR-DISEASE
AB Gene polymorphisms provide a means to obtain unconfounded associations between carotenoids and various health outcomes. In the present study, we tested whether gene polymorphisms and gene scores linked to low serum carotenoid status are related to metabolic disturbance and depressive symptoms in African-American adults residing in Baltimore city, MD, using cross-sectional data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study (age range 30-64 years, n 873-994). We examined twenty-four SNP of various gene loci that were previously shown to be associated with low serum carotenoid status (SNPlcar). Gene risk scores were created: five low specific-carotenoid risk scores (LSCRS: alpha-carotene, beta-carotene, lutein+zeaxanthin, beta-cryptoxanthin and lycopene) and one low total-carotenoid risk score (LTCRS: total carotenoids). SNPlcar, LSCRS and LTCRS were entered as predictors for a number of health outcomes. These included obesity, National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome and its components, elevated homeostatic model assessment of insulin resistance, C-reactive protein, hyperuricaemia and elevated depressive symptoms (EDS, Center for Epidemiologic Studies-Depression score >= 16). Among the key findings, SNPlcar were not associated with the main outcomes after correction for multiple testing. However, an inverse association was found between the LTCRS and HDL-cholesterol (HDL-C) dyslipidaemia. Specifically, the alpha-carotene and beta-cryptoxanthin LSCRS were associated with a lower odds of HDL-C dyslipidaemia. However, the beta-cryptoxanthin LSCRS was linked to a higher odds of EDS, with a linear dose-response relationship. In summary, gene risk scores linked to low serum carotenoids had mixed effects on HDL-C dyslipidaemia and EDS. Further studies using larger African-American population samples are needed.
C1 [Beydoun, May A.; Evans, Michele K.; Zonderman, Alan B.] NIA, Lab Epidemiol & Populat Sci, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
[Nalls, Michael A.] NIA, Neurogenet Lab, NIH, Baltimore, MD 21224 USA.
[Canas, J. Atilio] Nemours Childrens Clin, Jacksonville, FL USA.
RP Beydoun, MA (reprint author), NIA, Lab Epidemiol & Populat Sci, NIH, Biomed Res Ctr, IRP 251,Bayview Blvd,Suite 100,Room 04B118, Baltimore, MD 21224 USA.
EM baydounm@mail.nih.gov
OI Zonderman, Alan B/0000-0002-6523-4778
FU Intramural Research Program of the NIH, National Institute on Aging
FX The present study was fully supported by the Intramural Research Program
of the NIH, National Institute on Aging.
NR 70
TC 2
Z9 2
U1 0
U2 7
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 0007-1145
EI 1475-2662
J9 BRIT J NUTR
JI Br. J. Nutr.
PD SEP 28
PY 2014
VL 112
IS 6
BP 992
EP 1003
DI 10.1017/S0007114514001706
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AP3JD
UT WOS:000341970800016
PM 25201307
ER
PT J
AU Baker, SG
Schuit, E
Steyerberg, EW
Pencina, MJ
Vickers, A
Moons, KGM
Mol, BJ
Lindeman, KS
AF Baker, Stuart G.
Schuit, Ewoud
Steyerberg, Ewout W.
Pencina, Michael J.
Vickers, Andew
Moons, Karel G. M.
Mol, Ben W. J.
Lindeman, Karen S.
TI How to interpret a small increase in AUC with an additional risk
prediction marker: decision analysis comes through
SO STATISTICS IN MEDICINE
LA English
DT Article
DE AUC; cesarean section; decision curves; receiver operating
characteristic curves; relative utility curves
ID RELATIVE UTILITY CURVES; DIAGNOSTIC-TESTS; MODELS; RECLASSIFICATION;
PERFORMANCE; IMPROVEMENT; SURVIVAL; TIME
AB An important question in the evaluation of an additional risk prediction marker is how to interpret a small increase in the area under the receiver operating characteristic curve (AUC). Many researchers believe that a change in AUC is a poor metric because it increases only slightly with the addition of a marker with a large odds ratio. Because it is not possible on purely statistical grounds to choose between the odds ratio and AUC, we invoke decision analysis, which incorporates costs and benefits. For example, a timely estimate of the risk of later non-elective operative delivery can help a woman in labor decide if she wants an early elective cesarean section to avoid greater complications from possible later non-elective operative delivery. A basic risk prediction model for later non-elective operative delivery involves only antepartum markers. Because adding intrapartum markers to this risk prediction model increases AUC by 0.02, we questioned whether this small improvement is worthwhile. A key decision-analytic quantity is the risk threshold, here the risk of later non-elective operative delivery at which a patient would be indifferent between an early elective cesarean section and usual care. For a range of risk thresholds, we found that an increase in the net benefit of risk prediction requires collecting intrapartum marker data on 68 to 124 women for every correct prediction of later non-elective operative delivery. Because data collection is non-invasive, this test tradeoff of 68 to 124 is clinically acceptable, indicating the value of adding intrapartum markers to the risk prediction model. Copyright (C) 2014 John Wiley & Sons, Ltd.
C1 [Baker, Stuart G.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Schuit, Ewoud; Moons, Karel G. M.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
[Schuit, Ewoud] Univ Amsterdam, Acad Med Ctr, Dept Obstet & Gynecol, NL-1105 AZ Amsterdam, Netherlands.
[Steyerberg, Ewout W.] Erasmus MC, Dept Publ Hlth, Rotterdam, Netherlands.
[Pencina, Michael J.] Duke Univ, Dept Biostat, Durham, NC 27706 USA.
[Vickers, Andew] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Mol, Ben W. J.] Univ Adelaide, Sch Pediat & Reprod Hlth, Robinson Inst, Adelaide, SA, Australia.
[Lindeman, Karen S.] Johns Hopkins UniversityBaltimore, Dept Anesthesiol CCM, Baltimore, MD USA.
RP Baker, SG (reprint author), NCI, Biometry Res Branch, Canc Prevent Div, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
OI Vickers, Andrew/0000-0003-1525-6503
FU Intramural NIH HHS [Z99 CA999999]; NCI NIH HHS [P30 CA008748]
NR 31
TC 9
Z9 9
U1 2
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD SEP 28
PY 2014
VL 33
IS 22
BP 3946
EP 3959
DI 10.1002/sim.6195
PG 14
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA AP1JH
UT WOS:000341824600013
PM 24825728
ER
PT J
AU Haflidadottir, S
Jonasson, JG
Norland, H
Einarsdottir, SO
Kleiner, DE
Lund, SH
Bjornsson, ES
AF Haflidadottir, Svanhildur
Jonasson, Jon G.
Norland, Helga
Einarsdottir, Sylvia O.
Kleiner, David E.
Lund, Sigrun H.
Bjornsson, Einar S.
TI Long term follow-up and liver-related death rate in patients with
non-alcoholic and alcoholic related fatty liver disease
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE NAFLD; AFLD; Fibrosis; Prognosis; Mortality
ID MORTALITY; CIRRHOSIS; RISK; PROGNOSIS; STEATOHEPATITIS; EPIDEMIOLOGY;
PREVALENCE; STEATOSIS; OUTCOMES; COHORT
AB Background: Few studies have compared the prognosis and liver-related mortality in patients with NAFLD (nonalcoholic fatty liver disease) and AFLD (alcoholic fatty liver disease). We aimed to investigate the etiology and liver-related mortality of patients with liver biopsy verified fatty liver disease in a population based setting.
Methods: In this retrospective study, all patients who underwent a liver biopsy 1984-2009 at the National University Hospital of Iceland were identified through a computerized pathological database with the code for fatty liver. Only patients with NAFLD and AFLD were included and medical records reviewed. The patients were linked to the Hospital Discharge Register, the Causes of Death Registry and Centre for Addiction Medicine.
Results: A total of 151 had NAFLD and 94 AFLD with median survival of 24 years and 20 years, respectively (p = NS). A total of 10/151 (7%) patients developed cirrhosis in the NAFLD group and 19/94 (20%) in AFLD group (p = 0.03). The most common cause of death in the NAFLD group was cardiovascular disease (48%). Liver disease was the most common cause of death in the AFLD group (36%), whereas liver-related death occurred in 7% of the NAFLD group. The mean liver-related death rate among the general population during the study period was 0.1% of all deaths. There was a significantly worse survival for patients in the AFLD group compared to the NAFLD group after adjusting for gender, calendar year of diagnosis and age at diagnosis (HR 2.16, p = 0.009). The survival for patients with moderate to severe fibrosis was significantly worse than for patients with mild fibrosis after adjusting for gender, calendar year of diagnosis and age at diagnosis (HR 2.09, p = 0.01).
Conclusions: Patients with fatty liver disease showed a markedly higher risk of developing liver-related death compared to the general population. The AFLD group had higher liver-related mortality and had a worse survival than the NAFLD group. Patients with more severe fibrosis at baseline showed a worse survival than patients with none or mild fibrosis at baseline.
C1 [Haflidadottir, Svanhildur; Bjornsson, Einar S.] Natl Univ Hosp Iceland, Sect Gastroenterol & Hepatol, Dept Internal Med, IS-101 Reykjavik, Iceland.
[Jonasson, Jon G.; Einarsdottir, Sylvia O.] Natl Univ Hosp Reykjavik, Dept Pathol, Reykjavik, Iceland.
[Jonasson, Jon G.; Norland, Helga; Lund, Sigrun H.; Bjornsson, Einar S.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Lund, Sigrun H.] Univ Iceland, Ctr Publ Hlth, Reykjavik, Iceland.
RP Bjornsson, ES (reprint author), Natl Univ Hosp Iceland, Sect Gastroenterol & Hepatol, Dept Internal Med, Hringbraut 11D, IS-101 Reykjavik, Iceland.
EM einarsb@landspitali.is
RI Lund, Sigrun Helga/K-9144-2015
OI Lund, Sigrun Helga/0000-0002-3806-2296
FU NIH, National Cancer Institute; University Hospital of Iceland Research
Fund
FX Funding Acknowledgement: This research was supported in part by the
Intramural Research Program of the NIH, National Cancer Institute. Study
was also supported by the University Hospital of Iceland Research Fund.
NR 27
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Z9 13
U1 5
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD SEP 27
PY 2014
VL 14
AR 166
DI 10.1186/1471-230X-14-166
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AQ3MQ
UT WOS:000342698500001
PM 25260964
ER
PT J
AU Kim, JY
Hwang, JY
Lee, DY
Song, EH
Park, KJ
Kim, GH
Jeong, EA
Lee, YJ
Go, MJ
Kim, DJ
Lee, SS
Kim, BJ
Song, J
Roh, GS
Gao, B
Kim, WH
AF Kim, Ji Yeon
Hwang, Joo-Yeon
Lee, Dae Yeon
Song, Eun Hyun
Park, Keon Jae
Kim, Gyu Hee
Jeong, Eun Ae
Lee, Yoo Jeong
Go, Min Jin
Kim, Dae Jin
Lee, Seong Su
Kim, Bong-Jo
Song, Jihyun
Roh, Gu Seob
Gao, Bin
Kim, Won-Ho
TI Chronic Ethanol Consumption Inhibits Glucokinase Transcriptional
Activity by Atf3 and Triggers Metabolic Syndrome in Vivo
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NF-KAPPA-B; PANCREATIC BETA-CELLS; ALCOHOL-CONSUMPTION;
INSULIN-RESISTANCE; GENE-EXPRESSION; LIVER-DISEASE; FACTOR PDX-1; FATTY
LIVER; GLUCOSE; ACTIVATION
AB Chronic ethanol consumption induces pancreatic beta-cell dysfunction through glucokinase (Gck) nitration and down-regulation, leading to impaired glucose tolerance and insulin resistance, but the underlying mechanism remains largely unknown. Here, we demonstrate that Gck gene expression and promoter activity in pancreatic beta-cells were suppressed by chronic ethanol exposure in vivo and in vitro, whereas expression of activating transcription factor 3 (Atf3) and its binding to the putative Atf/Creb site (from -287 to -158 bp) on the Gck promoter were up-regulated. Furthermore, in vitro ethanol-induced Atf3 inhibited the positive effect of Pdx-1 on Gck transcriptional regulation, enhanced recruitment of Hdac1/2 and histone H3 deacetylation, and subsequently augmented the interaction of Hdac1/Pdx-1 on the Gck promoter, which were diminished by Atf3 siRNA. In vivo Atf3-silencing reversed ethanol-mediated Gck down-regulation and beta-cell dysfunction, followed by the amelioration of impaired glucose tolerance and insulin resistance. Together, we identified that ethanol-induced Atf3 fosters beta-cell dysfunction via Gck down-regulation and that its loss ameliorates metabolic syndrome and could be a potential therapeutic target in treating type 2 diabetes. The Atf3 gene is associated with the induction of type 2 diabetes and alcohol consumption-induced metabolic impairment and thus may be the major negative regulator for glucose homeostasis.
C1 [Kim, Ji Yeon; Lee, Dae Yeon; Song, Eun Hyun; Park, Keon Jae; Kim, Gyu Hee; Jeong, Eun Ae; Lee, Yoo Jeong; Song, Jihyun; Kim, Won-Ho] Natl Inst Hlth, Ctr Biomed Sci, Div Metab Dis, Cheongwon Gun 363951, Chungbuk, South Korea.
[Hwang, Joo-Yeon; Go, Min Jin; Kim, Bong-Jo] Natl Inst Hlth, Div Struct & Funct Genom, Ctr Genom Sci, Cheongwon Gun 363951, Chungbuk, South Korea.
[Kim, Dae Jin] Catholic Univ, Coll Med, Dept Psychiat, Puchon 420743, South Korea.
[Lee, Seong Su] Catholic Univ, Coll Med, Dept Endocrinol, Puchon 420743, South Korea.
[Roh, Gu Seob] Gyeongsang Natl Univ, Inst Hlth Sci, Dept Anat & Neurobiol, Jinju 660751, Gyeongnam, South Korea.
[Lee, Dae Yeon] Korea Univ, Dept Biotechnol, Coll Life Sci & Biotechnol, Seoul 136701, South Korea.
[Park, Keon Jae] Chungbuk Natl Univ, Div Cardiol, Dept Internal Med, Sch Med, Cheongju 361763, South Korea.
[Gao, Bin] NIAAA, Lab Liver Dis, Bethesda, MD 20892 USA.
RP Kim, WH (reprint author), Natl Inst Hlth, Ctr Biomed Sci, Div Metab Dis, 187 Osong Saengmyeong2 Ro, Cheongwon Gun 363951, Chungbuk, South Korea.
EM jhkwh@nih.go.kr
OI song, jihyun/0000-0003-0420-2374
FU Korean National Institutes of Health [4845-302-210-13]
FX This work was authored, in whole or in part, by National Institutes of
Health staff. This work was supported by Research Grant 4845-302-210-13
from the Korean National Institutes of Health.
NR 39
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U1 0
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 26
PY 2014
VL 289
IS 39
BP 27065
EP 27079
DI 10.1074/jbc.M114.585653
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AQ5MS
UT WOS:000342853900034
PM 25074928
ER
PT J
AU Barnable, P
Calenda, G
Ouattara, L
Gettie, A
Blanchard, J
Jean-Pierre, N
Kizima, L
Rodriguez, A
Abraham, C
Menon, R
Seidor, S
Cooney, ML
Roberts, KD
Sperling, R
Piatak, M
Lifson, JD
Fernandez-Romero, JA
Zydowsky, TM
Robbiani, M
Teleshova, N
AF Barnable, Patrick
Calenda, Giulia
Ouattara, Louise
Gettie, Agegnehu
Blanchard, James
Jean-Pierre, Ninochka
Kizima, Larisa
Rodriguez, Aixa
Abraham, Ciby
Menon, Radhika
Seidor, Samantha
Cooney, Michael L.
Roberts, Kevin D.
Sperling, Rhoda
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Fernandez-Romero, Jose A.
Zydowsky, Thomas M.
Robbiani, Melissa
Teleshova, Natalia
TI A MIV-150/Zinc Acetate Gel Inhibits SHIV-RT Infection in Macaque Vaginal
Explants
SO PLOS ONE
LA English
DT Article
ID ALTERED IMMUNE FUNCTION; ZINC; MICROBICIDE; TRANSMISSION; RESISTANCE;
EFFICACY; TYPE-1; SEMEN; LOAD
AB To extend our observations that single or repeated application of a gel containing the NNRTI MIV-150 (M) and zinc acetate dihydrate (ZA) in carrageenan (CG) (MZC) inhibits vaginal transmission of simian/human immunodeficiency virus (SHIV)-RT in macaques, we evaluated safety and anti-SHIV-RT activity of MZC and related gel formulations ex vivo in macaque mucosal explants. In addition, safety was further evaluated in human ectocervical explants. The gels did not induce mucosal toxicity. A single ex vivo exposure to diluted MZC (1:30, 1:100) and MC (1:30, the only dilution tested), but not to ZC gel, up to 4 days prior to viral challenge, significantly inhibited SHIV-RT infection in macaque vaginal mucosa. MZC's activity was not affected by seminal plasma. The antiviral activity of unformulated MIV-150 was not enhanced in the presence of ZA, suggesting that the antiviral activity of MZC was mediated predominantly by MIV-150. In vivo administration of MZC and CG significantly inhibited ex vivo SHIV-RT infection (51-62% inhibition relative to baselines) of vaginal (but not cervical) mucosa collected 24 h post last gel exposure, indicating barrier effect of CG. Although the inhibitory effect of MZC (65-74%) did not significantly differ from CG (32-45%), it was within the range of protection (similar to 75%) against vaginal SHIV-RT challenge 24 h after gel dosing. Overall, the data suggest that evaluation of candidate microbicides in macaque explants can inform macaque efficacy and clinical studies design. The data support advancing MZC gel for clinical evaluation.
C1 [Barnable, Patrick; Calenda, Giulia; Ouattara, Louise; Jean-Pierre, Ninochka; Kizima, Larisa; Rodriguez, Aixa; Abraham, Ciby; Menon, Radhika; Seidor, Samantha; Cooney, Michael L.; Roberts, Kevin D.; Fernandez-Romero, Jose A.; Zydowsky, Thomas M.; Robbiani, Melissa; Teleshova, Natalia] Populat Council, New York, NY 10021 USA.
[Gettie, Agegnehu] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10021 USA.
[Blanchard, James] Tulane Univ, Tulane Natl Primate Res Ctr, Covington, LA USA.
[Sperling, Rhoda] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] Frederick Natl Lab Canc Res, SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick, MD USA.
RP Teleshova, N (reprint author), Populat Council, 1230 York Ave, New York, NY 10021 USA.
EM nteleshova@popcouncil.org
FU United States Agency for International Development (USAID)
[GPO-A-00-04-00019-00]; Swedish Ministry of Foreign Affairs (SMFA);
Primate Center base grant [P51 OD011104-51]; National Cancer Institute,
National Institutes of Health (NIH) [HHSN261200800001E]
FX This work was supported by the United States Agency for International
Development (USAID) Cooperative Agreement GPO-A-00-04-00019-00, by the
Swedish Ministry of Foreign Affairs (SMFA) and Primate Center base grant
P51 OD011104-51. This research is made possible by the generous support
of the American people through the USAID and supported in part with
federal funds from the National Cancer Institute, National Institutes of
Health (NIH), under contract HHSN261200800001E (J.D.L.). The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 29
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U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 26
PY 2014
VL 9
IS 9
AR e108109
DI 10.1371/journal.pone.0108109
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AQ3IP
UT WOS:000342685600047
PM 25259616
ER
PT J
AU Hoenen, T
Feldmann, H
AF Hoenen, Thomas
Feldmann, Heinz
TI Ebolavirus in West Africa, and the use of experimental therapies or
vaccines
SO BMC BIOLOGY
LA English
DT Article
ID NONHUMAN-PRIMATES; HEMORRHAGIC-FEVER; VIRUS; MANAGEMENT; OUTBREAK;
INFECTIONS; DISEASE
AB Response to the current ebolavirus outbreak based on traditional control measures has so far been insufficient to prevent the virus from spreading rapidly. This has led to urgent discussions on the use of experimental therapies and vaccines untested in humans and existing in limited quantities, raising political, strategic, technical and ethical questions.
C1 [Hoenen, Thomas; Feldmann, Heinz] NIAID, Virol Lab, Div Intramural Res, NIH, Hamilton, MT 59840 USA.
RP Feldmann, H (reprint author), NIAID, Virol Lab, Div Intramural Res, NIH, 903 S 4th St, Hamilton, MT 59840 USA.
EM feldmannh@niaid.nih.gov
OI Hoenen, Thomas/0000-0002-5829-6305
FU NIH, NIAID
FX The authors thank Allison Groseth for critical reading of the
manuscript. This work was supported by the Intramural Research Program
of the NIH, NIAID.
NR 20
TC 9
Z9 10
U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1741-7007
J9 BMC BIOL
JI BMC Biol.
PD SEP 26
PY 2014
VL 12
AR 80
DI 10.1186/s12915-014-0080-6
PG 6
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AP9BF
UT WOS:000342372500001
PM 25286348
ER
PT J
AU Kuehn, HS
Ouyang, WM
Lo, B
Deenick, EK
Niemela, JE
Avery, DT
Schickel, JN
Tran, DQ
Stoddard, J
Zhang, Y
Frucht, DM
Dumitriu, B
Scheinberg, P
Folio, LR
Frein, CA
Price, S
Koh, C
Heller, T
Seroogy, CM
Huttenlocher, A
Rao, VK
Su, HC
Kleiner, D
Notarangelo, LD
Rampertaap, Y
Olivier, KN
McElwee, J
Hughes, J
Pittaluga, S
Oliveira, JB
Meffre, E
Fleisher, TA
Holland, SM
Lenardo, MJ
Tangye, SG
Uzel, G
AF Kuehn, Hye Sun
Ouyang, Weiming
Lo, Bernice
Deenick, Elissa K.
Niemela, Julie E.
Avery, Danielle T.
Schickel, Jean-Nicolas
Tran, Dat Q.
Stoddard, Jennifer
Zhang, Yu
Frucht, David M.
Dumitriu, Bogdan
Scheinberg, Phillip
Folio, Les R.
Frein, Cathleen A.
Price, Susan
Koh, Christopher
Heller, Theo
Seroogy, Christine M.
Huttenlocher, Anna
Rao, V. Koneti
Su, Helen C.
Kleiner, David
Notarangelo, Luigi D.
Rampertaap, Yajesh
Olivier, Kenneth N.
McElwee, Joshua
Hughes, Jason
Pittaluga, Stefania
Oliveira, Joao B.
Meffre, Eric
Fleisher, Thomas A.
Holland, Steven M.
Lenardo, Michael J.
Tangye, Stuart G.
Uzel, Gulbu
TI Immune dysregulation in human subjects with heterozygous germline
mutations in CTLA4
SO SCIENCE
LA English
DT Article
ID REGULATORY T-CELLS; COMMON VARIABLE IMMUNODEFICIENCY; B-CELLS;
METASTATIC MELANOMA; AUTOIMMUNE-DISEASE; TOLERANCE; LYMPHOPROLIFERATION;
ACCUMULATION; ACTIVATION; MECHANISMS
AB Cytotoxic T lymphocyte antigen-4 (CTLA-4) is an inhibitory receptor found on immune cells. The consequences of mutations in CTLA4 in humans are unknown. We identified germline heterozygous mutations in CTLA4 in subjects with severe immune dysregulation from four unrelated families. Whereas Ctla4 heterozygous mice have no obvious phenotype, human CTLA4 haploinsufficiency caused dysregulation of FoxP3(+) regulatory T (T-reg) cells, hyperactivation of effector T cells, and lymphocytic infiltration of target organs. Patients also exhibited progressive loss of circulating B cells, associated with an increase of predominantly autoreactive CD21(lo) B cells and accumulation of B cells in nonlymphoid organs. Inherited human CTLA4 haploinsufficiency demonstrates a critical quantitative role for CTLA-4 in governing T and B lymphocyte homeostasis.
C1 [Kuehn, Hye Sun; Niemela, Julie E.; Stoddard, Jennifer; Fleisher, Thomas A.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Ouyang, Weiming; Frucht, David M.] US FDA, Lab Cell Biol, Div Monoclonal Antibodies, Off Biotechnol Prod,Ctr Drug Evaluat & Res, Bethesda, MD 20892 USA.
[Lo, Bernice; Price, Susan; Rao, V. Koneti; Lenardo, Michael J.] NIAID, Mol Dev Immune Syst Sect, Immunol Lab, Bethesda, MD 20892 USA.
[Lo, Bernice; Zhang, Yu; Price, Susan; Rao, V. Koneti; Su, Helen C.; Holland, Steven M.; Lenardo, Michael J.] NIAID, Clin Genom Program, Bethesda, MD 20892 USA.
[Deenick, Elissa K.; Avery, Danielle T.; Tangye, Stuart G.] Garvan Inst Med Res, Immunol & Immunodeficiency Grp, Div Immunol, Sydney, NSW 2010, Australia.
[Deenick, Elissa K.; Tangye, Stuart G.] Univ New S Wales, Fac Med, St Vincents Clin Sch, Sydney, NSW 2010, Australia.
[Schickel, Jean-Nicolas; Meffre, Eric] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06511 USA.
[Tran, Dat Q.] Univ Texas Med Sch, Dept Pediat, Houston, TX 77030 USA.
[Zhang, Yu; Su, Helen C.] NIAID, Immunol Dis Unit, Lab Host Defenses, Bethesda, MD 20892 USA.
[Dumitriu, Bogdan; Scheinberg, Phillip] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
[Folio, Les R.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Frein, Cathleen A.] Frederick Natl Lab Canc Res, Clin Res Directorate, Clin Monitoring Res Program, Leidos Biomed Res Inc, Frederick, MD 21702 USA.
[Koh, Christopher; Heller, Theo] NIDDK, Liver Dis Branch, Bethesda, MD 20892 USA.
[Seroogy, Christine M.; Huttenlocher, Anna] Univ Wisconsin, Dept Pediat, Madison, WI 53706 USA.
[Huttenlocher, Anna] Univ Wisconsin, Dept Med Microbiol & Immunol, Madison, WI 53706 USA.
[Kleiner, David; Pittaluga, Stefania] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Notarangelo, Luigi D.] Harvard Univ, Sch Med, Childrens Hosp, Div Immunol, Boston, MA 02117 USA.
[Notarangelo, Luigi D.] Harvard Univ, Sch Med, Childrens Hosp, Manton Ctr Orphan Dis Res, Boston, MA USA.
[Rampertaap, Yajesh; Olivier, Kenneth N.; Holland, Steven M.; Uzel, Gulbu] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[McElwee, Joshua; Hughes, Jason] Merck & Co Inc, Merck Res Labs, Boston, MA 02130 USA.
[Oliveira, Joao B.] Inst Med Integral Prof Fernando Figueira IMIP, BR-50070 Recife, PE, Brazil.
RP Fleisher, TA (reprint author), NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
EM tfleishe@cc.nih.gov; lenardo@nih.gov; guzel@niaid.nih.gov
RI Su, Helen/H-9541-2015; Notarangelo, Luigi/F-9718-2016;
OI Su, Helen/0000-0002-5582-9110; Notarangelo, Luigi/0000-0002-8335-0262;
Oliveira, Joao/0000-0001-9388-8173; Niemela, Julie/0000-0003-4197-3792;
Lo, Bernice/0000-0002-1087-6845; Deenick, Elissa/0000-0002-9271-0004
FU Intramural Research Program, NIH Clinical Center; Division of Intramural
Research, National Institute of Allergy and Infectious Diseases;
National Cancer Institute [HHSN261200800001E]; National Institute of
Allergy and Infectious Diseases [5R01HL113304-01, AI071087, AI095848,
AI061093]; National Health and Medical Research Council of Australia;
Cancer Council NSW
FX We thank the referring physicians, as well as the patients and families.
The data are tabulated in the main paper and in the supplementary
materials. Supported by the Intramural Research Program, NIH Clinical
Center (H. S. K., T. A. F., J.S., J.E.N., L. R. F.); the Division of
Intramural Research, National Institute of Allergy and Infectious
Diseases (B. L., Y.Z., V. K. R., H. C. S., Y.R., K.N.O., S.Pr., S. M.
H., M.J.L., G. U.); the National Cancer Institute under contract
HHSN261200800001E (C. A. F.); National Institute of Allergy and
Infectious Diseases grant 5R01HL113304-01 (D. Q. T.); the National
Health and Medical Research Council of Australia (E. K. D., S. G. T.);
Cancer Council NSW (S. G. T.); and National Institute of Allergy and
Infectious Diseases grants AI071087, AI095848, and AI061093 (E. M.). The
content of this publication does not necessarily reflect the views or
policies of the U.S. Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government. The sequencing data are deposited in
dbGaP under accession no. phs000797.v1.p1.
NR 28
TC 124
Z9 126
U1 6
U2 27
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD SEP 26
PY 2014
VL 345
IS 6204
BP 1623
EP 1627
DI 10.1126/science.1255904
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AP6CG
UT WOS:000342164500049
PM 25213377
ER
PT J
AU Hsu, CW
Zhao, JH
Huang, RL
Hsieh, JH
Hamm, J
Chang, XQ
Houck, K
Xia, MH
AF Hsu, Chia-Wen
Zhao, Jinghua
Huang, Ruili
Hsieh, Jui-Hua
Hamm, Jon
Chang, Xiaoqing
Houck, Keith
Xia, Menghang
TI Quantitative High-Throughput Profiling of Environmental Chemicals and
Drugs that Modulate Farnesoid X Receptor
SO SCIENTIFIC REPORTS
LA English
DT Article
ID BILE-ACID-BINDING; NUCLEAR RECEPTOR; BETA-TUBULIN; NATURAL-PRODUCT;
CANCER CELLS; FXR; ANTAGONIST; LIGAND; IDENTIFICATION; EXPRESSION
AB The farnesoid X receptor (FXR) regulates the homeostasis of bile acids, lipids, and glucose. Because endogenous chemicals bind and activate FXR, it is important to examine which xenobiotic compounds would disrupt normal receptor function. We used a cell-based human FXR beta-lactamase (Bla) reporter gene assay to profile the Tox21 10K compound collection of environmental chemicals and drugs. Structure-activity relationships of FXR-active compounds revealed by this screening were then compared against the androgen receptor, estrogen receptor alpha, peroxisome proliferator-activated receptors delta and gamma, and the vitamin D receptor. We identified several FXR-active structural classes including anthracyclines, benzimidazoles, dihydropyridines, pyrethroids, retinoic acids, and vinca alkaloids. Microtubule inhibitors potently decreased FXR reporter gene activity. Pyrethroids specifically antagonized FXR transactivation. Anthracyclines affected reporter activity in all tested assays, suggesting non-specific activity. These results provide important information to prioritize chemicals for further investigation, and suggest possible modes of action of compounds in FXR signaling.
C1 [Hsu, Chia-Wen; Zhao, Jinghua; Huang, Ruili; Xia, Menghang] NIH, Natl Ctr Advancing Translat Sci, Bethesda, MD 20892 USA.
[Hsieh, Jui-Hua] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
[Hamm, Jon; Chang, Xiaoqing] Integrated Lab Syst Inc, Morrisville, NC USA.
[Houck, Keith] US EPA, Res Triangle Pk, NC 27711 USA.
RP Xia, MH (reprint author), NIH, Natl Ctr Advancing Translat Sci, Bldg 10, Bethesda, MD 20892 USA.
EM mxia@mail.nih.gov
FU U.S. Environmental Protection Agency [Y3-HG-7026-03]; National
Toxicology Program [Y2-ES-7020-01]
FX This work was supported by the U.S. Environmental Protection Agency
(Interagency agreement #Y3-HG-7026-03) and the National Toxicology
Program (Interagency agreement #Y2-ES-7020-01). We thank Misha Itkin,
Danielle VanLeer, Paul Shinn for compound management, Tongan Zhao for
informatics support, and Sam Michael for technical support of the
screening process. We also thank Dave Allen, Kevin Crofton, Raymond
Tice, and Stephen Ferguson for reviewing the manuscript. The views
expressed in this paper are those of the authors and do not necessarily
reflect the statements, opinions, views, conclusions, or policies of the
National Institute of Environmental Health Sciences (NIEHS), the U.S.
Environmental Protection Agency, the National Center for Advancing
Translational Sciences (NCATS), National Institutes of Health (NIH), or
the United States government.
NR 77
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U1 4
U2 19
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD SEP 26
PY 2014
VL 4
AR 6437
DI 10.1038/srep06437
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AP8WY
UT WOS:000342361300001
PM 25257666
ER
PT J
AU Tovo-Rodrigues, L
Roux, A
Hutz, MH
Rohde, LA
Woods, AS
AF Tovo-Rodrigues, L.
Roux, A.
Hutz, M. H.
Rohde, L. A.
Woods, A. S.
TI FUNCTIONAL CHARACTERIZATION OF G-PROTEIN-COUPLED RECEPTORS: A
BIOINFORMATICS APPROACH
SO NEUROSCIENCE
LA English
DT Article
DE GPCR; disordered proteins; pest motifs; noncovalent interactions; linear
motifs
ID ADENOSINE A(2A) RECEPTORS; RESONANCE ENERGY-TRANSFER; CANNABINOID CB1
RECEPTOR; DOPAMINE D2 RECEPTORS; ASSISTED-LASER-DESORPTION/IONIZATION;
SYNAPTIC VESICLE EXOCYTOSIS; DELTA-OPIOID RECEPTORS; HIGHER-ORDER
OLIGOMERS; SRC-FAMILY KINASES; RAT STRIATUM
AB Complex molecular and cellular mechanisms regulate G protein-coupled receptors (GPCRs). It is suggested that proteins intrinsically disordered regions (IDRs) are to play a role in GPCR's intra and extracellular regions plasticity, due to their potential for post-translational modification and interaction with other proteins. These regions are defined as lacking a stable three-dimensional (3D) structure. They are rich in hydrophilic and charged, amino acids and are capable to assume different conformations which allow them to interact with multiple partners. In this study we analyzed 75 GPCR involved in synaptic transmission using computational tools for sequence-based prediction of IDRs within a protein. We also evaluated putative ligand-binding motifs using receptor sequences. The disorder analysis indicated that neurotransmitter GPCRs have a significant amount of disorder in their N-terminus, third intracellular loop (3IL) and C-terminus. About 31%, 39% and 53% of human GPCR involved in synaptic transmission are disordered in these regions. Thirty-three percent of receptors show at least one predicted PEST motif, this being statistically greater than the estimate for the rest of human GPCRs. About 90% of the receptors had at least one putative site for dimerization in their 3IL or C-terminus. ELM instances sampled in these domains were 14-3-3, SH3, SH2 and PDZ motifs. In conclusion, the increased flexibility observed in GPCRs, added to the enrichment of linear motifs, PEST and heteromerization sites, maybe critical for the nervous system's functional plasticity. Published by Elsevier Ltd. on behalf of IBRO.
C1 [Tovo-Rodrigues, L.; Hutz, M. H.] Univ Fed Rio Grande do Sul, Dept Genet, Porto Alegre, RS, Brazil.
[Tovo-Rodrigues, L.; Roux, A.; Woods, A. S.] NIDA, Struct Biol Unit, Integrat Neurosci Branch, IRP,NIH, Baltimore, MD 21224 USA.
[Rohde, L. A.] Univ Fed Rio Grande do Sul, Child & Adolescent Psychiat Div, Dept Psychiat, Porto Alegre, RS, Brazil.
RP Woods, AS (reprint author), NIDA, IRP, NIH, Johns Hopkins Sch Med, 333 Cassell Dr,Room 1120, Baltimore, MD 21224 USA.
EM awoods@mail.nih.gov
RI Rohde, Luis Augusto/A-6426-2008;
OI Rohde, Luis Augusto/0000-0002-4552-4188; Hutz, Mara/0000-0002-9146-1229
FU Conselho Nacional de Desenvolvimento Cientifico e Tecnologico, CNPq,
(Brazilian National Science Foundation); Intramural Research Program of
the National Institute on Drug Abuse, NIH
FX The authors thank the Conselho Nacional de Desenvolvimento Cientifico e
Tecnologico, CNPq, (Brazilian National Science Foundation), for partial
financial support through the "Ciencia sem Fronteiras" program. This
research was supported by the Intramural Research Program of the
National Institute on Drug Abuse, NIH.
NR 209
TC 7
Z9 7
U1 2
U2 24
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
EI 1873-7544
J9 NEUROSCIENCE
JI Neuroscience
PD SEP 26
PY 2014
VL 277
BP 764
EP 779
DI 10.1016/j.neuroscience.2014.06.049
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA AO6VA
UT WOS:000341488700067
PM 24997265
ER
PT J
AU Cohen, JE
Lee, PR
Fields, RD
AF Cohen, Jonathan E.
Lee, Philip R.
Fields, R. Douglas
TI Systematic identification of 3 '-UTR regulatory elements in
activity-dependent mRNA stability in hippocampal neurons
SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE 3 '-UTR; activity-dependent plasticity; miRNA; mRNA stability
ID LARGE GENE LISTS; LOCAL TRANSLATION; MICROARRAY DATA; EXPRESSION;
TRANSCRIPTION; TRANSPORT; MICRORNAS; SYNAPSE; SPECIFICITY; MECHANISMS
AB Ongoing neuronal activity during development and plasticity acts to refine synaptic connections and contributes to the induction of plasticity and ultimately long-term memory storage. Activity-dependent, post-transcriptional control of mRNAs occurs through transport to axonal and dendritic compartments, local translation and mRNA stability. We have identified a mechanism that contributes to activity-dependent regulation of mRNA stability during synaptic plasticity in rat hippocampal neurons. In this study, we demonstrate rapid, post-transcriptional control over process-enriched mRNAs by neuronal activity. Systematic analysis of the 3'-UTRs of destabilized transcripts, identifies enrichment in sequence motifs corresponding to microRNA (miRNA)-binding sites. The miRNAs that were identified, miR-326-3p/miR-330-5p, miR-485-5p, miR-666-3p and miR-761 are predicted to regulate networks of genes important in plasticity and development. We find that these miRNAs are developmentally regulated in the hippocampus, many increasing by postnatal day 14. We further find that miR-485-5p controls NGF-induced neurite outgrowth in PC12 cells, tau expression and axonal development in hippocampal neurons. miRNAs can function at the synapse to rapidly control and affect short- and long-term changes at the synapse. These processes likely occur during refinement of synaptic connections and contribute to the induction of plasticity and learning and memory.
C1 [Cohen, Jonathan E.; Lee, Philip R.; Fields, R. Douglas] Eunice Kennedy Shriver Natl Inst Child & Human De, Sect Nervous Syst Dev & Plast, NIH, Bethesda, MD 20892 USA.
RP Fields, RD (reprint author), Eunice Kennedy Shriver Natl Inst Child & Human De, Sect Nervous Syst Dev & Plast, NIH, Bldg 35,Room 2A211, Bethesda, MD 20892 USA.
EM fieldsd@mail.nih.gov
RI Moyal, Elizabeth/A-9802-2015
OI Moyal, Elizabeth/0000-0002-6593-9276
FU intramural research programme at National Institutes of Health, National
Institute of Child Health and Human Development
FX This work was supported by the intramural research programme at National
Institutes of Health, National Institute of Child Health and Human
Development.
NR 55
TC 3
Z9 3
U1 1
U2 11
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8436
EI 1471-2970
J9 PHILOS T R SOC B
JI Philos. Trans. R. Soc. B-Biol. Sci.
PD SEP 26
PY 2014
VL 369
IS 1652
AR 20130509
DI 10.1098/rstb.2013.0509
PG 12
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA AO1LS
UT WOS:000341074200006
ER
PT J
AU Biswas, S
Choudhary, P
Elias, SC
Miura, K
Milne, KH
de Cassan, SC
Collins, KA
Halstead, FD
Bliss, CM
Ewer, KJ
Osier, FH
Hodgson, SH
Duncan, CJA
O'Hara, GA
Long, CA
Hill, AVS
Draper, SJ
AF Biswas, Sumi
Choudhary, Prateek
Elias, Sean C.
Miura, Kazutoyo
Milne, Kathryn H.
de Cassan, Simone C.
Collins, Katharine A.
Halstead, Fenella D.
Bliss, Carly M.
Ewer, Katie J.
Osier, Faith H.
Hodgson, Susanne H.
Duncan, Christopher J. A.
O'Hara, Geraldine A.
Long, Carole A.
Hill, Adrian V. S.
Draper, Simon J.
TI Assessment of Humoral Immune Responses to Blood-Stage Malaria Antigens
following ChAd63-MVA Immunization, Controlled Human Malaria Infection
and Natural Exposure
SO PLOS ONE
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; APICAL MEMBRANE ANTIGEN-1; MEROZOITE
SURFACE PROTEIN-1; SUBUNIT VACCINE IMMUNOGENICITY; IN-VITRO GROWTH;
IMMUNOGLOBULIN-G; RECOMBINANT ADENOVIRUS; ANTIBODY-RESPONSES; VECTORED
VACCINES; ADJUVANT VACCINES
AB The development of protective vaccines against many difficult infectious pathogens will necessitate the induction of effective antibody responses. Here we assess humoral immune responses against two antigens from the blood-stage merozoite of the Plasmodium falciparum human malaria parasite - MSP1 and AMA1. These antigens were delivered to healthy malaria-naive adult volunteers in Phase Ia clinical trials using recombinant replication-deficient viral vectors - ChAd63 to prime the immune response and MVA to boost. In subsequent Phase IIa clinical trials, immunized volunteers underwent controlled human malaria infection (CHMI) with P. falciparum to assess vaccine efficacy, whereby all but one volunteer developed low-density blood-stage parasitemia. Here we assess serum antibody responses against both the MSP1 and AMA1 antigens following i) ChAd63-MVA immunization, ii) immunization and CHMI, and iii) primary malaria exposure in the context of CHMI in unimmunized control volunteers. Responses were also assessed in a cohort of naturally-immune Kenyan adults to provide comparison with those induced by a lifetime of natural malaria exposure. Serum antibody responses against MSP1 and AMA1 were characterized in terms of i) total IgG responses before and after CHMI, ii) responses to allelic variants of MSP1 and AMA1, iii) functional growth inhibitory activity (GIA), iv) IgG avidity, and v) isotype responses (IgG1-4, IgA and IgM). These data provide the first in-depth assessment of the quality of adenovirus-MVA vaccine-induced antibody responses in humans, along with assessment of how these responses are modulated by subsequent low-density parasite exposure. Notable differences were observed in qualitative aspects of the human antibody responses against these malaria antigens depending on the means of their induction and/or exposure of the host to the malaria parasite. Given the continued clinical development of viral vectored vaccines for malaria and a range of other diseases targets, these data should help to guide further immuno-monitoring studies of vaccine-induced human antibody responses.
C1 [Biswas, Sumi; Choudhary, Prateek; Elias, Sean C.; Milne, Kathryn H.; de Cassan, Simone C.; Collins, Katharine A.; Halstead, Fenella D.; Bliss, Carly M.; Ewer, Katie J.; Hodgson, Susanne H.; Hill, Adrian V. S.; Draper, Simon J.] Univ Oxford, Jenner Inst, Oxford, England.
[Miura, Kazutoyo; Long, Carole A.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Osier, Faith H.] KEMRI Ctr Geog Med Res, Kilifi, Kenya.
[Hodgson, Susanne H.; Duncan, Christopher J. A.; O'Hara, Geraldine A.] Univ Oxford, Churchill Hosp, Jenner Inst, Ctr Clin Vaccinol & Trop Med, Oxford, England.
RP Biswas, S (reprint author), Univ Oxford, Jenner Inst, Oxford, England.
EM sumi.biswas@ndm.ox.ac.uk
RI Draper, Simon/F-1758-2011; Ewer, Katie/B-4328-2011;
OI Draper, Simon/0000-0002-9415-1357; Ewer, Katie/0000-0001-9827-9836;
Osier, Faith/0000-0001-7133-5375; Collins, Katharine/0000-0002-7080-2215
FU UK Medical Research Council (MRC) [G0700735]; EMVDA (European Malaria
Vaccine Development Association); European Commission
[LSHP-CT-2007-037506]; UK National Institute of Health Research through
the Oxford Biomedical Research Centre [084113/Z/07/Z]; EVIMalaR -
European Community [242095]; PATH Malaria Vaccine Initiative; Intramural
Program of the National Institutes of Health, National Institute of
Allergy and Infectious Diseases; Wellcome Trust Research Training
Fellowship [097940/Z/11/Z]
FX This work was supported by the UK Medical Research Council (MRC;
http://www.mrc.ac.uk) [grant number G0700735]; the EMVDA (European
Malaria Vaccine Development Association; http://www.emvda.org), a
European Commission FP6-funded consortium [LSHP-CT-2007-037506]; the UK
National Institute of Health Research through the Oxford Biomedical
Research Centre (http://[084113/Z/07/Z]; and by EVIMalaR
(http://www.evimalar.org) funded by the European Community's Seventh
Framework Programme (FP7/2007-2013) [Grant agreement No. 242095]. The
GIA work was supported by the PATH Malaria Vaccine Initiative
(http://www.malariavaccine.org) and the Intramural Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases (http://www.niaid.nih.gov). SHH holds a Wellcome
Trust Research Training Fellowship (097940/Z/11/Z). AVSH and SJD are
Jenner Investigators (http://www.jenner.ac.uk). SB is a NDM Leadership
Fellow (http://www.ndm.ox.ac.uk) and Junior Research Fellow of St
Catherine's College, Oxford University (http://www.stcatz.ox.ac.uk). SJD
is a UK MRC Career Development Fellow [G1000527] and Lister Institute
Research Prize Fellow (http://www.lister-institute.org.uk). The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 83
TC 23
Z9 24
U1 1
U2 4
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 SEP 25
PY 2014
VL 9
IS 9
AR e107903
DI 10.1371/journal.pone.0107903
PG 17
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AT3UZ
UT WOS:000344862300041
PM 25254500
ER
PT J
AU Boyd, A
Ribeiro, JMC
Nutman, TB
AF Boyd, Alexis
Ribeiro, Jose M. C.
Nutman, Thomas B.
TI Human CD117 (cKit)+ Innate Lymphoid Cells Have a Discrete
Transcriptional Profile at Homeostasis and Are Expanded during Filarial
Infection
SO PLOS ONE
LA English
DT Article
ID DENDRITIC CELLS; TYPE-2 IMMUNITY; EXPRESSION; GROWTH; T(H)2; INHIBITION;
CARCINOMA; RESPONSES; PARASITES; EPS8
AB Since innate lymphoid cells (ILCs) have been found to play a role in the immune response to helminth parasites in rodents, we sought to determine their role in human helminth infection. By developing multicolor flow cytometry-based methods to identify and enumerate circulating ILCs and their subsets, we were able to identify a subset of cKit+ ILCs defined as Lineage (Lin)-/CD45+/cKit+/CD127+ that were significantly expanded in the filarial-infected individuals (p = 0.0473) as were those cKit+ ILCs that produced IL-13. Additionally, the frequency of these cKit+ ILCs correlated with the frequency of IL-17 producing CD4+ T cells (Th17 cells; p = 0.025). To investigate the function of cKit+ ILCs, sorted, highly purified human ILCs were subjected to transcriptional profiling by RNAseq and compared to appropriate control cells. These cKit+ ILCs expressed TLRs, a broad range of cytokines/cytokine receptors and MHC Class II molecules suggesting that these ILCs sense pathogens independent of other cell types. Functional analysis revealed expanded cKit+ ILC-specific transcription and ILC-specific microRNA precursors.
C1 [Boyd, Alexis; Nutman, Thomas B.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Ribeiro, Jose M. C.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD USA.
RP Nutman, TB (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM tnutman@niaid.nih.gov
OI Ribeiro, Jose/0000-0002-9107-0818
FU Division of Intramural Research, NIAID, NIH
FX This study was funded entirely 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 29
TC 11
Z9 11
U1 0
U2 3
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 SEP 25
PY 2014
VL 9
IS 9
AR e108649
DI 10.1371/journal.pone.0108649
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AT3UZ
UT WOS:000344862300101
PM 25255226
ER
PT J
AU Takakusagi, Y
Matsumoto, S
Saito, K
Matsuo, M
Kishimoto, S
Wojtkowiak, JW
DeGraff, W
Kesarwala, AH
Choudhuri, R
Devasahayam, N
Subramanian, S
Munasinghe, JP
Gillies, RJ
Mitchell, JB
Hart, CP
Krishna, MC
AF Takakusagi, Yoichi
Matsumoto, Shingo
Saito, Keita
Matsuo, Masayuki
Kishimoto, Shun
Wojtkowiak, Jonathan W.
DeGraff, William
Kesarwala, Aparna H.
Choudhuri, Rajani
Devasahayam, Nallathamby
Subramanian, Sankaran
Munasinghe, Jeeva P.
Gillies, Robert J.
Mitchell, James B.
Hart, Charles P.
Krishna, Murali C.
TI Pyruvate Induces Transient Tumor Hypoxia by Enhancing Mitochondrial
Oxygen Consumption and Potentiates the Anti-Tumor Effect of a
Hypoxia-Activated Prodrug TH-302
SO PLOS ONE
LA English
DT Article
ID HYPERBARIC-OXYGEN; CYCLING HYPOXIA; CANCER-THERAPY; MICE;
MICROVASCULATURE; PHARMACOKINETICS; FLUCTUATIONS; MISONIDAZOLE;
IRRADIATION; CARCINOMA
AB Background: TH-302 is a hypoxia-activated prodrug (HAP) of bromo isophosphoramide mustard that is selectively activated within hypoxic regions in solid tumors. Our recent study showed that intravenously administered bolus pyruvate can transiently induce hypoxia in tumors. We investigated the mechanism underlying the induction of transient hypoxia and the combination use of pyruvate to potentiate the anti-tumor effect of TH-302.
Methodology/Results: The hypoxia-dependent cytotoxicity of TH-302 was evaluated by a viability assay in murine SCCVII and human HT29 cells. Modulation in cellular oxygen consumption and in vivo tumor oxygenation by the pyruvate treatment was monitored by extracellular flux analysis and electron paramagnetic resonance (EPR) oxygen imaging, respectively. The enhancement of the anti-tumor effect of TH-302 by pyruvate treatment was evaluated by monitoring the growth suppression of the tumor xenografts inoculated subcutaneously in mice. TH-302 preferentially inhibited the growth of both SCCVII and HT29 cells under hypoxic conditions (0.1% O-2), with minimal effect under aerobic conditions (21% O-2). Basal oxygen consumption rates increased after the pyruvate treatment in SCCVII cells in a concentration-dependent manner, suggesting that pyruvate enhances the mitochondrial respiration to consume excess cellular oxygen. In vivo EPR oxygen imaging showed that the intravenous administration of pyruvate globally induced the transient hypoxia 30 min after the injection in SCCVII and HT29 tumors at the size of 500-1500 mm(3). Pretreatment of SCCVII tumor bearing mice with pyruvate 30 min prior to TH-302 administration, initiated with small tumors (similar to 550 mm(3)), significantly delayed tumor growth.
Conclusions/Significance: Our in vitro and in vivo studies showed that pyruvate induces transient hypoxia by enhancing mitochondrial oxygen consumption in tumor cells. TH-302 therapy can be potentiated by pyruvate pretreatment if started at the appropriate tumor size and oxygen concentration.
C1 [Takakusagi, Yoichi; Matsumoto, Shingo; Saito, Keita; Matsuo, Masayuki; Kishimoto, Shun; DeGraff, William; Choudhuri, Rajani; Devasahayam, Nallathamby; Subramanian, Sankaran; Mitchell, James B.; Krishna, Murali C.] NCI, Radiat Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Wojtkowiak, Jonathan W.; Gillies, Robert J.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Kesarwala, Aparna H.] NCI, Radiat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Munasinghe, Jeeva P.] NINDS, Bethesda, MD 20892 USA.
[Hart, Charles P.] Threshold Pharmaceut, San Francisco, CA USA.
RP Krishna, MC (reprint author), NCI, Radiat Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
EM murali@helix.nih.gov
OI Gillies, Robert/0000-0002-8888-7747; Hart, Charles/0000-0003-4440-726X
FU Intramural Research Program, Center for Cancer Research, National Cancer
Institute, National Institutes of Health (NIH)
FX This research was supported by the Intramural Research Program, Center
for Cancer Research, National Cancer Institute, National Institutes of
Health (NIH). The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 35
TC 5
Z9 6
U1 1
U2 15
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 SEP 25
PY 2014
VL 9
IS 9
AR e107995
DI 10.1371/journal.pone.0107995
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AT3UZ
UT WOS:000344862300050
PM 25254649
ER
PT J
AU Sun, XP
Wheeler, CT
Yolitz, J
Laslo, M
Alberico, T
Sun, YN
Song, QS
Zou, SG
AF Sun, Xiaoping
Wheeler, Charles T.
Yolitz, Jason
Laslo, Mara
Alberico, Thomas
Sun, Yaning
Song, Qisheng
Zou, Sige
TI A Mitochondrial ATP Synthase Subunit Interacts with TOR Signaling to
Modulate Protein Homeostasis and Lifespan in Drosophila
SO CELL REPORTS
LA English
DT Article
ID DIETARY-RESTRICTION; CALORIC RESTRICTION; OXIDATIVE STRESS;
RHESUS-MONKEYS; RNAI SCREEN; FRUIT-FLY; MELANOGASTER; LONGEVITY;
MACRONUTRIENTS; EXTENSION
AB Diet composition is a critical determinant of lifespan, and nutrient imbalance is detrimental to health. However, how nutrients interact with genetic factors to modulate lifespan remains elusive. We investigated how diet composition influences mitochondrial ATP synthase subunit d (ATPsyn-d) in modulating lifespan in Drosophila. ATPsyn-d knockdown extended lifespan in females fed low carbohydrate-to-protein (C:P) diets but not the high C: P ratio diet. This extension was associated with increased resistance to oxidative stress; transcriptional changes in metabolism, proteostasis, and immune genes; reduced protein damage and aggregation, and reduced phosphorylation of S6K and ERK in TOR and mitogenactivated protein kinase (MAPK) signaling, respectively. ATPsyn-d knockdown did not extend lifespan in females with reduced TOR signaling induced genetically by Tsc2 overexpression or pharmacologically by rapamycin. Our data reveal a link among diet, mitochondria, and MAPK and TOR signaling in aging and stresses the importance of considering genetic background and diet composition in implementing interventions for promoting healthy aging.
C1 [Sun, Xiaoping; Wheeler, Charles T.; Yolitz, Jason; Laslo, Mara; Alberico, Thomas; Sun, Yaning; Zou, Sige] NIA, Translat Gerontol Branch, Baltimore, MD 21224 USA.
[Song, Qisheng] Univ Missouri, Div Plant Sci, Columbia, MO 65211 USA.
RP Zou, SG (reprint author), NIA, Translat Gerontol Branch, Baltimore, MD 21224 USA.
EM zous@mail.nih.gov
FU Intramural Research Program of the NIA, NIH [AG000365-09]
FX We thank E. Spangler for critical reading of the manuscript; J. Tower,
V. Monnier, D. Pan, and T. P. Neufeld for reagents; and Bloomington and
Vienna stock centers for fly stocks. This study was supported by the
Intramural Research Program of the NIA, NIH, to S.Z. (grant number
AG000365-09).
NR 41
TC 10
Z9 10
U1 0
U2 23
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 SEP 25
PY 2014
VL 8
IS 6
BP 1781
EP 1792
DI 10.1016/j.celrep.2014.08.022
PG 12
WC Cell Biology
SC Cell Biology
GA AR9BZ
UT WOS:000343867400019
PM 25220459
ER
PT J
AU McDevitt, RA
Tiran-Cappello, A
Shen, H
Balderas, I
Britt, JP
Marino, RAM
Chung, SL
Richie, CT
Harvey, BK
Bonci, A
AF McDevitt, Ross A.
Tiran-Cappello, Alix
Shen, Hui
Balderas, Israela
Britt, Jonathan P.
Marino, Rosa A. M.
Chung, Stephanie L.
Richie, Christopher T.
Harvey, Brandon K.
Bonci, Antonello
TI Serotonergic versus Nonserotonergic Dorsal Raphe Projection Neurons:
Differential Participation in Reward Circuitry
SO CELL REPORTS
LA English
DT Article
ID VENTRAL TEGMENTAL AREA; INTRACRANIAL SELF-STIMULATION;
PARA-CHLOROPHENYLALANINE; AFFERENT-PROJECTIONS; DOPAMINERGIC-NEURONS;
GABAERGIC NEURONS; NUCLEUS-ACCUMBENS; GRAY-MATTER; IN-VITRO; RAT
AB The dorsal raphe nucleus (DRN) contains the largest group of serotonin-producing neurons in the brain and projects to regions controlling reward. Although pharmacological studies suggest that serotonin inhibits reward seeking, electrical stimulation of the DRN strongly reinforces instrumental behavior. Here, we provide a targeted assessment of the behavioral, anatomical, and electrophysiological contributions of serotonergic and nonserotonergic DRN neurons to reward processes. To explore DRN heterogeneity, we used a simultaneous two-vector knockout/optogenetic stimulation strategy, as well as cre-induced and cre-silenced vectors in several cre-expressing transgenic mouse lines. We found that the DRN is capable of reinforcing behavior primarily via nonserotonergic neurons, for which the main projection target is the ventral tegmental area (VTA). Furthermore, these nonserotonergic projections provide glutamatergic excitation of VTA dopamine neurons and account for a large majority of the DRN-VTA pathway. These findings help to resolve apparent discrepancies between the roles of serotonin versus the DRN in behavioral reinforcement.
C1 [McDevitt, Ross A.; Tiran-Cappello, Alix; Shen, Hui; Balderas, Israela; Britt, Jonathan P.; Marino, Rosa A. M.; Chung, Stephanie L.; Richie, Christopher T.; Harvey, Brandon K.; Bonci, Antonello] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Tiran-Cappello, Alix] Ecole Normale Super Lyon, Dept Biol, F-69007 Lyon, France.
[Balderas, Israela] Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City 04510, DF, Mexico.
[Bonci, Antonello] Univ Calif San Francisco, Ernest Gallo Clin & Res Ctr, Emeryville, CA 94608 USA.
[Bonci, Antonello] Johns Hopkins Univ, Sch Med, Solomon H Snyder Neurosci Inst, Baltimore, MD 21205 USA.
RP Bonci, A (reprint author), NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM antonello.bonci@nih.gov
RI Britt, Jonathan/D-8877-2011
OI Britt, Jonathan/0000-0003-3044-9565
FU Intramural Research Program of the National Institute on Drug Abuse
FX This research was supported by the Intramural Research Program of the
National Institute on Drug Abuse. We are grateful to Dr. Karl Deisseroth
for providing cre-ON ChR2 plasmid DNA; Dr. Zheng-Xiong Xi for assistance
with mouse self-administration; Dr. Francois Vautier and Joni McKenzie
for assistance with transgenic mouse colonies; Zachary Fusfeld,
Christina Hatch, India J. Kawata, and Martha Zemen for assistance with
surgery and behavioral testing; Doug Howard and Lowella Fortuno for
assistance with cre-OFF vector preparation; and the NIDA Optogenetic and
Transgenic Technology Core for production of other vectors.
NR 54
TC 40
Z9 42
U1 1
U2 9
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 SEP 25
PY 2014
VL 8
IS 6
BP 1857
EP 1869
DI 10.1016/j.celrep.2014.08.037
PG 13
WC Cell Biology
SC Cell Biology
GA AR9BZ
UT WOS:000343867400025
PM 25242321
ER
PT J
AU Rhee, DY
Cho, DY
Zhai, B
Slattery, M
Ma, LJ
Mintseris, J
Wong, CY
White, KP
Celniker, SE
Przytycka, TM
Gygi, SP
Obar, RA
Artavanis-Tsakonas, S
AF Rhee, David Y.
Cho, Dong-Yeon
Zhai, Bo
Slattery, Matthew
Ma, Lijia
Mintseris, Julian
Wong, Christina Y.
White, Kevin P.
Celniker, Susan E.
Przytycka, Teresa M.
Gygi, Steven P.
Obar, Robert A.
Artavanis-Tsakonas, Spyros
TI Transcription Factor Networks in Drosophila melanogaster
SO CELL REPORTS
LA English
DT Article
ID DNA-BINDING SPECIFICITY; PROTEIN-INTERACTION MAP; EMBRYONIC STEM-CELLS;
REGULATORY NETWORKS; FUNCTIONAL MODULES; GENETIC CIRCUITRY;
MASS-SPECTROMETRY; GAGA FACTOR; NOTCH; EXPRESSION
AB Specific cellular fates and functions depend on differential gene expression, which occurs primarily at the transcriptional level and is controlled by complex regulatory networks of transcription factors (TFs). TFs act through combinatorial interactions with other TFs, cofactors, and chromatin-remodeling proteins. Here, we define protein-protein interactions using a coaffinity purification/mass spectrometry method and study 459 Drosophila melanogaster transcription-related factors, representing approximately half of the established catalog of TFs. We probe this network in vivo, demonstrating functional interactions for many interacting proteins, and test the predictive value of our data set. Building on these analyses, we combine regulatory network inference models with physical interactions to define an integrated network that connects combinatorial TF protein interactions to the transcriptional regulatory network of the cell. We use this integrated network as a tool to connect the functional network of genetic modifiers related to mastermind, a transcriptional cofactor of the Notch pathway.
C1 [Rhee, David Y.; Zhai, Bo; Mintseris, Julian; Wong, Christina Y.; Gygi, Steven P.; Obar, Robert A.; Artavanis-Tsakonas, Spyros] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Cho, Dong-Yeon; Przytycka, Teresa M.] Natl Lib Med, Computat Biol Branch, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
[Slattery, Matthew; Ma, Lijia; White, Kevin P.] Univ Chicago, Inst Genom & Syst Biol, Chicago, IL 60637 USA.
[Celniker, Susan E.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Berkeley Drosophila Genome Project, Berkeley, CA 94720 USA.
[Artavanis-Tsakonas, Spyros] Biogen Idec Inc, Cambridge, MA 02142 USA.
RP Artavanis-Tsakonas, S (reprint author), Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
EM sartavanis@cb.med.harvard.edu
FU NIH [5RO1HG003616]; NHGRI [P41HG3487]; Intramural Research Program of
the National Library of Medicine, NIH
FX We thank Mark Kankel, Mat Sowa, Jean-Francois Rual, and members of
S.A.-T.'s lab for helpful discussions and comments. This work was
supported by a grant from the NIH (5RO1HG003616) to S.A.-T. Generation
of the clone set was supported by a grant from the NHGRI (P41HG3487) to
S.E.C. D.-Y.C. and T.M.P. were supported by the Intramural Research
Program of the National Library of Medicine, NIH.
NR 76
TC 15
Z9 15
U1 0
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 SEP 25
PY 2014
VL 8
IS 6
BP 2031
EP 2043
DI 10.1016/j.celrep.2014.08.038
PG 13
WC Cell Biology
SC Cell Biology
GA AR9BZ
UT WOS:000343867400038
PM 25242320
ER
PT J
AU Sherman, MH
Yu, RT
Engle, DD
Ding, N
Atkins, AR
Tiriac, H
Collisson, EA
Connor, F
Van Dyke, T
Kozlov, S
Martin, P
Tseng, TW
Dawson, DW
Donahue, TR
Masamune, A
Shimosegawa, T
Apte, MV
Wilson, JS
Ng, B
Lau, SL
Gunton, JE
Wahl, GM
Hunter, T
Drebin, JA
O'Dwyer, PJ
Liddle, C
Tuveson, DA
Downes, M
Evans, RM
AF Sherman, Mara H.
Yu, Ruth T.
Engle, Dannielle D.
Ding, Ning
Atkins, Annette R.
Tiriac, Herve
Collisson, Eric A.
Connor, Frances
Van Dyke, Terry
Kozlov, Serguei
Martin, Philip
Tseng, Tiffany W.
Dawson, David W.
Donahue, Timothy R.
Masamune, Atsushi
Shimosegawa, Tooru
Apte, Minoti V.
Wilson, Jeremy S.
Ng, Beverly
Lau, Sue Lynn
Gunton, Jenny E.
Wahl, Geoffrey M.
Hunter, Tony
Drebin, Jeffrey A.
O'Dwyer, Peter J.
Liddle, Christopher
Tuveson, David A.
Downes, Michael
Evans, Ronald M.
TI Vitamin D Receptor-Mediated Stromal Reprogramming Suppresses
Pancreatitis and Enhances Pancreatic Cancer Therapy
SO CELL
LA English
DT Article
ID DUCTAL ADENOCARCINOMA; STELLATE CELLS; MOUSE MODEL; TUMOR-STROMA; MICE
LACKING; IN-VIVO; PROGRESSION; GROWTH; FIBROBLASTS; GEMCITABINE
AB The poor clinical outcome in pancreatic ductal adenocarcinoma (PDA) is attributed to intrinsic chemoresistance and a growth-permissive tumor micro-environment. Conversion of quiescent to activated pancreatic stellate cells (PSCs) drives the severe stromal reaction that characterizes PDA. Here, we reveal that the vitamin D receptor (VDR) is expressed in stroma from human pancreatic tumors and that treatment with the VDR ligand calcipotriol markedly reduced markers of inflammation and fibrosis in pancreatitis and human tumor stroma. We show that VDR acts as a master transcriptional regulator of PSCs to reprise the quiescent state, resulting in induced stromal remodeling, increased intratumoral gemcitabine, reduced tumor volume, and a 57% increase in survival compared to chemotherapy alone. This work describes a molecular strategy through which transcriptional reprogramming of tumor stroma enables chemotherapeutic response and suggests vitamin D priming as an adjunct in PDA therapy.
C1 [Sherman, Mara H.; Yu, Ruth T.; Ding, Ning; Atkins, Annette R.; Tseng, Tiffany W.; Wahl, Geoffrey M.; Downes, Michael; Evans, Ronald M.] Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA.
[Engle, Dannielle D.; Tiriac, Herve; Tuveson, David A.] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
[Collisson, Eric A.] Univ Calif San Francisco, Dept Med Hematol & Oncol, San Francisco, CA 94143 USA.
[Connor, Frances] Canc Res UK Cambridge Res Inst, Li Ka Shing Ctr, Cambridge CB2 0RE, England.
[Van Dyke, Terry] NCI, Ctr Adv Preclin Res, Frederick, MD 21702 USA.
[Kozlov, Serguei; Martin, Philip] Leidos Biomed Inc, Frederick Natl Lab Canc Res, Ctr Adv Preclin Res, Frederick, MD 21702 USA.
[Dawson, David W.; Donahue, Timothy R.] Univ Calif Los Angeles, David Geffen Sch Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[Masamune, Atsushi; Shimosegawa, Tooru] Tohoku Univ, Grad Sch Med, Div Gastroenterol, Sendai, Miyagi 9808574, Japan.
[Apte, Minoti V.; Wilson, Jeremy S.] Univ New S Wales, South Western Sydney Clin Sch, Fac Med, Pancreat Res Grp, Sydney, NSW 2052, Australia.
[Ng, Beverly; Lau, Sue Lynn; Gunton, Jenny E.] Garvan Inst Med Res, Diabet & Transcript Factors Grp, Sydney, NSW 2010, Australia.
[Ng, Beverly; Gunton, Jenny E.] Univ New S Wales, St Vincents Clin Sch, Sydney, NSW 2052, Australia.
[Lau, Sue Lynn; Gunton, Jenny E.] Univ Sydney, Fac Med, Sydney, NSW 2052, Australia.
[Lau, Sue Lynn; Gunton, Jenny E.] Westmead Hosp, Dept Endocrinol & Diabet, Sydney, NSW 2145, Australia.
[Hunter, Tony] Salk Inst Biol Studies, Mol & Cell Biol Lab, La Jolla, CA 92037 USA.
[Drebin, Jeffrey A.] Hosp Univ Penn, Dept Surg, Philadelphia, PA 19104 USA.
[O'Dwyer, Peter J.] Hosp Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Liddle, Christopher] Westmead Millennium Inst, Storr Liver Unit, Westmead, NSW 2145, Australia.
[Liddle, Christopher] Univ Sydney, Westmead Hosp, Westmead, NSW 2145, Australia.
[Evans, Ronald M.] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA.
RP Downes, M (reprint author), Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA.
EM downes@salk.edu; evans@salk.edu
RI Wilson, Jeremy/I-4586-2013;
OI Wilson, Jeremy/0000-0003-2355-8632; Apte, Minoti/0000-0003-0194-8939
FU Ruth L. Kirchstein National Research Service [T32-CA009370]; NIH
[HL105278, DK0577978, DK090962, CA014195, ES010337]; Helmsley Charitable
Trust; Samuel Waxman Cancer Research Foundation; Stand Up to Cancer
Dream Team Translational Cancer Research Grant; Program of the
Entertainment Industry Foundation [SU2C-AACR-DT0509]; National Health
and Medical Research Council of Australia [512354, 632886, 1043199];
Cancer Council of NSW; Japan Society for the Promotion of Science
[23591008]; Lustgarten Foundation
FX We thank E. Ong and C. Brondos for administrative support; M. Baran, T.
Guerin, J. Schlomer, J. Kalen, L. Riffel, P. Mackin, S. Kaufman, J.
Alvarez, and H. Juguilon for technical assistance; and D. von Hoff and
T. Bapiro for discussion. We thank T. Guerin and J. Schlomer for
efficacy studies done at the Center for Advanced Preclinical Research
(CAPR), the Center for Cancer Research, the National Cancer Institute.
M.H.S. was supported by a Ruth L. Kirchstein National Research Service
Award (T32-CA009370). This work was funded by grants from the NIH
(HL105278, DK0577978, DK090962, CA014195, and ES010337), the Helmsley
Charitable Trust, and the Samuel Waxman Cancer Research Foundation.
R.M.E. and M.D. are supported in part by a Stand Up to Cancer Dream Team
Translational Cancer Research Grant, a Program of the Entertainment
Industry Foundation (SU2C-AACR-DT0509). C.L. and M.D. are funded by
grants from the National Health and Medical Research Council of
Australia Project Grants 512354, 632886 and 1043199. M.A. and J.W. are
funded by grants from the Cancer Council of NSW. A.M. is supported by
Grant-in-Aid from Japan Society for the Promotion of Science (23591008).
R.M.E. is an investigator of the Howard Hughes Medical Institute and
March of Dimes Chair in Molecular and Developmental Biology at the Salk
Institute and supported by a grant from The Lustgarten Foundation.
NR 62
TC 133
Z9 135
U1 12
U2 80
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD SEP 25
PY 2014
VL 159
IS 1
BP 80
EP 93
DI 10.1016/j.cell.2014.08.007
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AQ8QQ
UT WOS:000343095000011
PM 25259922
ER
PT J
AU Cioffi, CL
Dobri, N
Freeman, EE
Conlon, MP
Chen, P
Stafford, DG
Schwarz, DMC
Golden, KC
Zhu, L
Kitchen, DB
Barnes, KD
Racz, B
Qin, Q
Michelotti, E
Cywin, CL
Martin, WH
Pearson, PG
Johnson, G
Petrukhin, K
AF Cioffi, Christopher L.
Dobri, Nicoleta
Freeman, Emily E.
Conlon, Michael P.
Chen, Ping
Stafford, Douglas G.
Schwarz, Daniel M. C.
Golden, Kathy C.
Zhu, Lei
Kitchen, Douglas B.
Barnes, Keith D.
Racz, Boglarka
Qin, Qiong
Michelotti, Enrique
Cywin, Charles L.
Martin, William H.
Pearson, Paul G.
Johnson, Graham
Petrukhin, Konstantin
TI Design, Synthesis, and Evaluation of Nonretinoid Retinol Binding Protein
4 Antagonists for the Potential Treatment of Atrophic Age-Related
Macular Degeneration and Stargardt Disease
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID PIGMENT EPITHELIAL-CELLS; VITAMIN-A METABOLISM; FUNDUS AUTOFLUORESCENCE;
GEOGRAPHIC ATROPHY; LIPOFUSCIN ACCUMULATION; 3-DIMENSIONAL STRUCTURE;
INSULIN-RESISTANCE; MOUSE MODEL; IN-VIVO; A2E
AB Accumulation of lipofuscin in the retina is associated with pathogenesis of atrophic age-related macular degeneration and Stargardt disease. Lipofuscin bisretinoids (exemplified by N-retinylidene-N-retinylethanolamine) seem to mediate lipofuscin toxicity. Synthesis of lipofuscin bisretinoids depends on the influx of retinol from serum to the retina. Compounds antagonizing the retinol-dependent interaction of retinol-binding protein 4 (RBP4) with transthyretin in the serum would reduce serum RBP4 and retinol and inhibit bisretinoid formation. We recently showed that A1120 (3), a potent carboxylic acid based RBP4 antagonist, can significantly reduce lipofuscin bisretinoid formation in the retinas of Abca4(-/-). mice. As part of the NIH Blueprint Neurotherapeutics Network project we undertook the in vitro exploration to identify novel conformationally flexible and constrained RBP4 antagonists with improved potency and metabolic stability. We also demonstrate that upon acute and chronic dosing in rats, 43, a potent cyclopentyl fused pyrrolidine antagonist, reduced circulating plasma RBP4 protein levels by approximately 60%.
C1 [Cioffi, Christopher L.; Freeman, Emily E.; Conlon, Michael P.; Chen, Ping; Stafford, Douglas G.; Schwarz, Daniel M. C.; Golden, Kathy C.; Zhu, Lei; Kitchen, Douglas B.; Barnes, Keith D.] Albany Mol Res Inc, Dept Med Chem, Rensselaer, NY 12144 USA.
[Dobri, Nicoleta; Racz, Boglarka; Qin, Qiong; Petrukhin, Konstantin] Columbia Univ, Med Ctr, Dept Ophthalmol, New York, NY 10032 USA.
[Johnson, Graham] NuPharmAdvise LLC, Sanbornton, NH 03269 USA.
[Pearson, Paul G.] Pearson Pharma Partners, Westlake Village, CA 91361 USA.
[Martin, William H.] WHM Consulting LLC, Lyme, CT 06371 USA.
[Michelotti, Enrique] NIMH, NIH, Bethesda, MD 20892 USA.
[Cywin, Charles L.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Cioffi, CL (reprint author), Albany Mol Res Inc, Dept Med Chem, East Campus,C Wing, Rensselaer, NY 12144 USA.
EM christopher.cioffi@amriglobal.com; kep4@cumc.columbia.edu
OI Kitchen, Douglas/0000-0001-8988-759X
FU NIH [U01 NS074476, P30 EY019007]; Research To Prevent Blindness (New
York, NY); National Institute of Neurological Disorders and Stroke,
Neurosciences Blueprint Program, National Institutes of Health,
Department of Health and Human Services [HHSN271201100013C]
FX This study was supported by NIH Grants U01 NS074476 (to K.P.) and P30
EY019007 (Core Support for Vision Research) and unrestricted funds from
Research To Prevent Blindness (New York, NY) to the Department of
Ophthalmology, Columbia University, NY. The authors thank The Burch
Family Foundation, the Mary Jaharis-John Catsimatidis Scholarship Fund,
the Kaplen Foundation, and the Eye Surgery Fund for gifts supporting
this study. This project has also been funded in whole or in part with
federal funds from the National Institute of Neurological Disorders and
Stroke, Neurosciences Blueprint Program, National Institutes of Health,
Department of Health and Human Services, under Contract No.
HHSN271201100013C.
NR 66
TC 6
Z9 7
U1 1
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD SEP 25
PY 2014
VL 57
IS 18
BP 7731
EP 7757
DI 10.1021/jm5010013
PG 27
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA AP9JN
UT WOS:000342396200019
PM 25210858
ER
PT J
AU Schiering, C
Krausgruber, T
Chomka, A
Frohlich, A
Adelmann, K
Wohlfert, EA
Pott, J
Griseri, T
Bollrath, J
Hegazy, AN
Harrison, OJ
Owens, BMJ
Lohning, M
Belkaid, Y
Fallon, PG
Powrie, F
AF Schiering, Chris
Krausgruber, Thomas
Chomka, Agnieszka
Froehlich, Anja
Adelmann, Krista
Wohlfert, Elizabeth A.
Pott, Johanna
Griseri, Thibault
Bollrath, Julia
Hegazy, Ahmed N.
Harrison, Oliver J.
Owens, Benjamin M. J.
Loehning, Max
Belkaid, Yasmine
Fallon, Padraic G.
Powrie, Fiona
TI The alarmin IL-33 promotes regulatory T-cell function in the intestine
SO NATURE
LA English
DT Article
ID AMELIORATES EXPERIMENTAL COLITIS; INFLAMMATORY-BOWEL-DISEASE;
TRANSCRIPTION FACTOR FOXP3; ULCERATIVE-COLITIS; DEPENDENT COLITIS;
SOLUBLE ST2; CYTOKINE; MICE; RESPONSES; COMPLEX
AB FOXP3+ regulatory T cells (T-reg cells) are abundant in the intestine, where they prevent dysregulated inflammatory responses to self and environmental stimuli. It is now appreciated that T-reg cells acquire tissue-specific adaptations that facilitate their survival and function(1); however, key host factors controlling theT(reg) response in the intestine are poorly understood. The interleukin (IL)-1 family member IL-33 is constitutively expressed in epithelial cells at barrier sites(2), where it functions as an endogenous danger signal, or alarmin, in response to tissue damage(3). Recent studies in humans have described high levels of IL-33 in inflamed lesions of inflammatory bowel disease patients(4-7), suggesting a role for this cytokine in disease pathogenesis. In the intestine, both protective and pathological roles for IL-33 have been described in murine models of acute colitis(8-11), but its contribution to chronic inflammation remains ill defined. Here we show in mice that the IL-33 receptor ST2 is preferentially expressed on colonic T-reg cells, where it promotes T-reg function and adaptation to the inflammatory environment. IL-33 signalling in T cells stimulates T-reg responses in several ways. First, it enhances transforming growth factor (TGF)-beta 1-mediated differentiation of T-reg cells and, second, it provides a necessary signal for T-reg-cell accumulation and maintenance in inflamed tissues. Strikingly, IL-23, a key pro-inflammatory cytokine in the pathogenesis of inflammatory bowel disease, restrained T-reg responses through inhibition of IL-33 responsiveness. These results demonstrate a hitherto unrecognized link between an endogenous mediator of tissue damage and a major anti-inflammatory pathway, and suggest that the balance between IL-33 and IL-23 may be a key controller of intestinal immune responses.
C1 [Schiering, Chris; Krausgruber, Thomas; Chomka, Agnieszka; Adelmann, Krista; Griseri, Thibault; Bollrath, Julia; Hegazy, Ahmed N.; Owens, Benjamin M. J.; Powrie, Fiona] Univ Oxford, John Radcliffe Hosp, Translat Gastroenterol Unit, Nuffield Dept Clin Med,Expt Med Div, Oxford OX3 9DU, England.
[Froehlich, Anja; Loehning, Max] Charite, Dept Rheumatol & Clin Immunol, D-10117 Berlin, Germany.
[Froehlich, Anja; Loehning, Max] German Rheumatism Res Ctr DRFZ, D-10117 Berlin, Germany.
[Wohlfert, Elizabeth A.; Belkaid, Yasmine] NIAID, Program Barrier Immun & Repair, Mucosal Immunol Sect, Lab Parasit Dis,NIH, Bethesda, MD 20892 USA.
[Pott, Johanna; Harrison, Oliver J.] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
[Fallon, Padraic G.] Univ Dublin Trinity Coll, Trinity Biomed Sci Inst, Dublin 2, Ireland.
RP Powrie, F (reprint author), Univ Oxford, John Radcliffe Hosp, Translat Gastroenterol Unit, Nuffield Dept Clin Med,Expt Med Div, Oxford OX3 9DU, England.
EM fiona.powrie@path.ox.ac.uk
OI Krausgruber, Thomas/0000-0002-1374-0329; Fallon,
Padraic/0000-0002-8401-7293; Stockenhuber, Krista/0000-0003-3608-064X;
Schiering, Chris/0000-0001-7902-6024
FU Wellcome Trust; Fondation Louis Jeantet; European Molecular Biology
Organization long-term fellowship [ALTF 116-2012]; Science Foundation
Ireland; Volkswagen Foundation (Lichtenberg Program); BMBF
(e:Bio/T-Sys); Oxford-UCB Pharma Postdoctoral Fellowship
FX C. S., K. A., A. C., O.J.H. and F. P. are supported by the Wellcome
Trust. F. P. is also supported by the Fondation Louis Jeantet. A.N.H. is
supported by a European Molecular Biology Organization long-term
fellowship (ALTF 116-2012). P. G. F. is supported by Science Foundation
Ireland. M. L. and A. F. are supported by the Volkswagen Foundation
(Lichtenberg Program) and BMBF (e:Bio/T-Sys). B.M.J.O. is supported by
an Oxford-UCB Pharma Postdoctoral Fellowship. We thank all members of
the Oxford Translational Gastroenterology Unit for assistance and
support. We are grateful to H. Ferry and K. Alford for essential flow
cytometry support and the staff of the University of Oxford for animal
care. We are also grateful to D. Baban for conducting microarray
hybridizations.
NR 36
TC 155
Z9 157
U1 9
U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD SEP 25
PY 2014
VL 513
IS 7519
BP 564
EP +
DI 10.1038/nature13577
PG 17
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AP4VB
UT WOS:000342075800044
PM 25043027
ER
PT J
AU Al-Herz, W
Bousfiha, A
Casanova, JL
Chatila, T
Conley, ME
Cunningham-Rundlee, C
Etzioni, A
Franco, JL
Gaspar, HB
Holland, SM
Klein, C
Nonoyama, S
Ochs, HD
Oksenhendler, E
Picard, C
Puck, JM
Sullivan, K
Tang, MLK
AF Al-Herz, Waleed
Bousfiha, Aziz
Casanova, Jean-Laurent
Chatila, Talal
Conley, Mary Ellen
Cunningham-Rundlee, Charlotte
Etzioni, Amos
Franco, Jose Luis
Gaspar, H. Bobby
Holland, Steven M.
Klein, Christoph
Nonoyama, Shigeaki
Ochs, Hans D.
Oksenhendler, Erik
Picard, Capucine
Puck, Jennifer M.
Sullivan, Kate
Tang, Mimi L. K.
TI Primary immunodeficency diseases: an update on the classification from
the International Union of Immunological Societies Expert Committee for
Primary Immunodeficiency (vol 5, 162,2014)
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Correction
DE immunodeficiency; classification; gene defects; genotype; IUIS
C1 [Al-Herz, Waleed] Kuwait Univ, Dept Pediat, Kuwait, Kuwait.
[Al-Herz, Waleed] Al Sabah Hosp, Dept Pediat, Allergy & Clin Immunol Unit, Kuwait, Kuwait.
[Bousfiha, Aziz] King Hassan II Univ, Ibn Rochd Med Sch, Casablanca Childrens Hosp, Clin Immunol Unit, Casablanca, Morocco.
[Casanova, Jean-Laurent; Conley, Mary Ellen] Rockefeller Univ, Rockefeller Branch, St Giles Lab Human Genet Infect Dis, New York, NY USA.
[Casanova, Jean-Laurent; Picard, Capucine] Univ Paris 05, Necker Med Sch, Imagine Inst, INSERM,Necker Branch,Lab Human Genet Infect Dis,U, Paris, France.
[Chatila, Talal] Childrens Hosp Boston, Div Immunol, Boston, MA USA.
[Cunningham-Rundlee, Charlotte] Mt Sinai Sch Med, Dept Med & Pediat, New York, NY USA.
[Franco, Jose Luis] Technion Israel Inst Technol, Meyer Childrens Hosp, Haifa, Israel.
[Franco, Jose Luis] Univ Antioquia, Grp Primary Immunodeficiencies, Medellin, Colombia.
[Gaspar, H. Bobby] UCL Inst Child Hlth, London, England.
[Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Klein, Christoph] Univ Munich, Dr Von Hauner Childrens Hosp, Munich, Germany.
[Nonoyama, Shigeaki] Natl Def Med Coll, Dept Pediat, Saitama, Japan.
[Ochs, Hans D.] Univ Washington, Seattle Childrens Res Inst, Dept Pediat, Seattle, WA 98195 USA.
[Oksenhendler, Erik] Hop St Louis, AP HP, Dept Clin Immunol, Paris, France.
[Oksenhendler, Erik] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
[Picard, Capucine] Hop Necker Enfants Malad, AP HP, CEDI, Paris, France.
[Puck, Jennifer M.] Univ Calif San Francisco, Benioff Childrens Hosp, Dept Pediat, San Francisco, CA 94143 USA.
[Sullivan, Kate] Childrens Hosp Philadelphia, Dept Pediat, Div Allergy Immunol, Philadelphia, PA 19104 USA.
[Tang, Mimi L. K.] Murdoch Childrens Res Inst, Melbourne, Vic, Australia.
[Tang, Mimi L. K.] Univ Melbourne, Dept Paediat, Melbourne, Vic, Australia.
[Tang, Mimi L. K.] Royal Childrens Hosp, Dept Allergy & Immunol, Melbourne, Vic, Australia.
RP Gaspar, HB (reprint author), UCL Inst Child Hlth, London, England.
EM h.gaspar@ucl.ac.uk
NR 1
TC 1
Z9 2
U1 0
U2 4
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 24
PY 2014
VL 5
AR 460
DI 10.3389/fimmu.2014.00460
PG 6
WC Immunology
SC Immunology
GA CI0TE
UT WOS:000354450100001
ER
PT J
AU Konishi, Y
Yang, LB
He, P
Lindholm, K
Lu, B
Li, R
Shen, Y
AF Konishi, Yoshihiro
Yang, Li-Bang
He, Ping
Lindholm, Kristina
Lu, Bai
Li, Rena
Shen, Yong
TI Deficiency of GDNF Receptor GFR alpha 1 in Alzheimer's Neurons Results
in Neuronal Death
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE neurodegeneration; neuron
ID HUMAN CEREBRAL-CORTEX; NEUROTROPHIC FACTOR; IN-VITRO; NEURODEGENERATIVE
DISORDERS; AMYLOID HYPOTHESIS; PARKINSONS-DISEASE; NEURITE OUTGROWTH;
FAMILY; BRAIN; GENERATION
AB We have recently developed aged cortical neuron cultures from autopsied human brains with Alzheimer's disease (AD). During the culturing process, we found that glutamatergic cortical neurons from the AD brain lacked a response to glial cell line-derived neurotrophic factor (GDNF), including no axonal regrowth, and were starting to undergo apoptosis. Here we showed that, in cortical neurons from age- and gender-matched cognitively normal control (NC) subjects (NC neurons), GDNF enhanced the expression of GDNF family receptor subtype alpha 1 (GFR alpha 1), but not the other three subtypes (GFR alpha 2, GFR alpha 3, and GFR alpha 4), whereas GDNF failed to induce GFR alpha 1 expression in cortical neurons from the AD brain (AD neurons). The exogenous introduction of GFR alpha 1, but not of its binding partner alpha 1-neural cell adhesion molecule, or RET into AD neurons restored the effect of GDNF on neuronal survival. Moreover, between NC and AD neurons, the AMPA receptor blocker CNQX and the NMDA receptor blocker AP-5 had opposite effects on the GFR alpha 1 expression induced by GDNF. In NC neurons, the presence of glutamate receptors was necessary for GDNF-linked GFR alpha 1 expression, while in AD neurons the absence of glutamate receptors was required for GFR alpha 1 expression by GDNF stimulation. These results suggest that, in AD neurons, specific impairments of GFR alpha 1, which may be linked to glutamatergic neurotransmission, shed light on developing potential therapeutic strategies for AD by upregulation of GFR alpha 1 expression.
C1 [Konishi, Yoshihiro; Yang, Li-Bang; He, Ping; Lindholm, Kristina; Shen, Yong] Roskamp Inst, Haldeman Lab Mol & Cellular Neurobiol, Sarasota, FL 34243 USA.
[Li, Rena] Roskamp Inst, Ctr Hormone Adv Sci & Educ, Sarasota, FL 34243 USA.
[Lu, Bai] NICHD, Sect Synapt Dev, NIH, Bethesda, MD 20892 USA.
[Konishi, Yoshihiro] Natl Tottori Med Ctr, Dept Clin Res, Tottori 6890203, Japan.
[Li, Rena] Beijing Inst Brain Disorders, Beijing 100069, Peoples R China.
[Shen, Yong] Roskamp Inst, Ctr Adv Therapeut Strategies Brain Disorders, Sarasota, FL 34243 USA.
[Shen, Yong] Univ Florida, Coll Med, Dept Neurol, Gainesville, FL 32610 USA.
[Shen, Yong] Univ Sci & Technol, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
[Shen, Yong] Univ Sci & Technol, Med Res Ctr, Hefei 230027, Anhui, Peoples R China.
RP Shen, Y (reprint author), Roskamp Inst, 2040 Whitfield Ave, Sarasota, FL 34243 USA.
EM rli@rfdn.org; yshen@rfdn.org
FU National Institutes of Health [RO1AG025888, RO1032441, RO1025888S];
Arizona Biomedical Research Commission [ABRC002]; Alzheimer's
Association [IIRG-07-59510, IIRG-09-61521, NIRG-08-91471]; American
Health Assistance Foundation [G2006-118]; Research Resource Network
(RRN) of the National organization in Japan
FX This work was supported by National Institutes of Health Grants
RO1AG025888, RO1032441, and RO1025888S; by Arizona Biomedical Research
Commission ABRC002; by the Alzheimer's Association Zenith Award II
Initiated Research Grants IIRG-07-59510 and IIRG-09-61521 and New
Investigator Research Grant NIRG-08-91471; by American Health Assistance
Foundation Grant G2006-118; and a grant from the Research Resource
Network (RRN) of the National organization in Japan.
NR 47
TC 12
Z9 13
U1 2
U2 9
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 SEP 24
PY 2014
VL 34
IS 39
BP 13127
EP 13138
DI 10.1523/JNEUROSCI.2582-13.2014
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA AQ9CR
UT WOS:000343140000017
PM 25253858
ER
PT J
AU Xiao, Q
Liao, LD
Matthews, CE
Chow, WH
Davis, F
Schwartz, K
Purdue, M
Hofmann, JN
Colt, J
AF Xiao, Qian
Liao, Linda
Matthews, Charles E.
Chow, Wong-Ho
Davis, Faith
Schwartz, Kendra
Purdue, Mark
Hofmann, Jonathan N.
Colt, Joanne
TI Physical activity and renal cell carcinoma among black and white
Americans: a case-control study
SO BMC CANCER
LA English
DT Article
DE Renal cell carcinoma; Physical activities; Racial differences;
Case-control study
ID BODY-MASS INDEX; RISK-FACTORS; KIDNEY CANCER; REPRODUCTIVE FACTORS;
AFRICAN-AMERICANS; UNITED-STATES; OBESITY; WEIGHT; COHORT; HYPERTENSION
AB Background: Renal cell carcinoma (RCC) has a higher incidence in blacks than in whites. Physical activity may influence the risk of renal cell cancer, but the evidence is inconsistent. No previous study has investigated this relationship in the black population.
Methods: We examined the association between self-reported physical activity at different ages and risk of RCC in a population based case-control study of 1217 cases (361 black, 856 white) and 1235 controls (523 black, 712 white) frequency-matched on age, race, and gender. Multivariate-adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated using unconditional logistic regression.
Results: Among whites, increased risks of RCC were observed among participants reporting low levels of transportation-related activity in their 20's (OR (<1 hr/wk vs > 7 hr/wk) (95% CI): 1.42 (1.10, 1.83)) and leisure time activity in their 50's (OR (<1 hr/wk vs > 7 hr/wk) (95% CI): 1.49 (1.00, 2.20)). We found no association between physical activity and RCC risk among blacks.
Conclusion: Our results suggest that physical activity may be inversely associated with RCC risk in whites, but there was no evidence of such an association in blacks. As this is the first study evaluating the effect of physical activity on RCC risk among blacks, further investigations are needed to clarify the relationship in this population.
C1 [Xiao, Qian; Liao, Linda; Matthews, Charles E.; Purdue, Mark; Hofmann, Jonathan N.; Colt, Joanne] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Chow, Wong-Ho] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Davis, Faith] Univ Alberta, Sch Publ Hlth, Edmonton, AB T6G 2M7, Canada.
[Schwartz, Kendra] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Schwartz, Kendra] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Detroit, MI USA.
RP Xiao, Q (reprint author), NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
EM qian.xiao@nih.gov
RI matthews, Charles/E-8073-2015;
OI matthews, Charles/0000-0001-8037-3103; Liao, Linda/0000-0002-1923-5294
FU National Institutes of Health; National Cancer Institute [N02-CP-10128,
N02-CP-11004, N02-CP-11161]
FX Supported by the Intramural Research Program of the National Institutes
of Health and the National Cancer Institute with contracts N02-CP-10128
(Westat, Inc.), N02-CP-11004 (Wayne State University), and N02-CP-11161
(University of Illinois at Chicago).
NR 30
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD SEP 24
PY 2014
VL 14
AR 707
DI 10.1186/1471-2407-14-707
PG 7
WC Oncology
SC Oncology
GA AQ0IM
UT WOS:000342466600001
PM 25253394
ER
EF