FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Kucharski, AJ
Mills, HL
Donnelly, CA
Riley, S
AF Kucharski, Adam J.
Mills, Harriet L.
Donnelly, Christl A.
Riley, Steven
TI Transmission Potential of Influenza A(H7N9) Virus, China, 2013-2014
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID LIVE-POULTRY MARKETS; INFECTION
AB To determine transmission potential of influenza A(H7N9) virus, we used symptom onset data to compare 2 waves of infection in China during 2013-2014. We found evidence of increased transmission potential in the second wave and showed that live bird market closure was significantly less effective in Guangdong than in other regions.
C1 [Kucharski, Adam J.] Univ London London Sch Hyg & Trop Med, London WC1E 7HT, England.
[Kucharski, Adam J.] NIH, Bethesda, MD 20892 USA.
[Kucharski, Adam J.; Mills, Harriet L.; Donnelly, Christl A.; Riley, Steven] Univ London Imperial Coll Sci Technol & Med, London, England.
RP Kucharski, AJ (reprint author), Univ London London Sch Hyg & Trop Med, Dept Infect Dis Epidemiol, Keppel St, London WC1E 7HT, England.
EM adam.kucharski@lshtm.ac.uk
OI Donnelly, Christl/0000-0002-0195-2463
FU Wellcome Trust [093488/Z/10/Z]; Medical Research Council (United
Kingdom) [MR/J008761/1, MR/K021524/1]; National Institute for General
Medical Sciences (United States) [MIDAS U01 GM110721-01]; European Union
Seventh Framework Programme [278433-PREDEMICS]; Fogarty International
Center (United States) [R01 TW008246-01]; Research and Policy for
Infectious Disease Dynamics program from Fogarty International Center
with the Science and Technology Directorate, Department of Homeland
Security.
FX This work was funded by the Wellcome Trust (project grant
093488/Z/10/Z); the Medical Research Council (United Kingdom, project
grant MR/J008761/1; Fellowship MR/K021524/1); National Institute for
General Medical Sciences (United States, MIDAS U01 GM110721-01); the
European Union Seventh Framework Programme (FP7/2007-2013) under grant
agreement no. 278433-PREDEMICS; the Fogarty International Center (United
States, R01 TW008246-01); and the Research and Policy for Infectious
Disease Dynamics program also from Fogarty International Center with the
Science and Technology Directorate, Department of Homeland Security.
NR 14
TC 7
Z9 8
U1 0
U2 8
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD MAY
PY 2015
VL 21
IS 5
BP 852
EP 855
DI 10.3201/eid2105.141137
PG 4
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CG9BW
UT WOS:000353610400016
PM 25897624
ER
PT J
AU Prescott, J
Bushmaker, T
Fischer, R
Miazgowicz, K
Judson, S
Munster, VJ
AF Prescott, Joseph
Bushmaker, Trenton
Fischer, Robert
Miazgowicz, Kerri
Judson, Seth
Munster, Vincent J.
TI Postmortem Stability of Ebola Virus
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID HEMORRHAGIC-FEVER; CONGO; TRANSMISSION; RISK
AB The ongoing Ebola virus outbreak in West Africa has highlighted questions regarding stability of the virus and detection of RNA from corpses. We used Ebola virus infected macaques to model humans who died of Ebola virus disease. Viable virus was isolated <= 7 days posteuthanasia; viral RNA was detectable for 10 weeks.
C1 [Prescott, Joseph; Bushmaker, Trenton; Fischer, Robert; Miazgowicz, Kerri; Judson, Seth; Munster, Vincent J.] NIH, Hamilton, MT USA.
RP Munster, VJ (reprint author), NIAID, Rocky Mt Labs, 903 S 4th St, Hamilton, MT 59840 USA.
EM munstervj@niaid.nih.gov
OI Fischer, Robert/0000-0002-1816-472X; Munster,
Vincent/0000-0002-2288-3196
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This study was supported by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 12
TC 21
Z9 21
U1 1
U2 19
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD MAY
PY 2015
VL 21
IS 5
BP 856
EP 859
DI 10.3201/eid2105.150041
PG 4
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CG9BW
UT WOS:000353610400017
PM 25897646
ER
PT J
AU Bae, WK
Kang, K
Yu, JH
Yoo, KH
Factor, VM
Kaji, K
Matter, M
Thorgeirsson, S
Hennighausen, L
AF Bae, Woo Kyun
Kang, Keunsoo
Yu, Ji Hoon
Yoo, Kyung Hyun
Factor, Valentina M.
Kaji, Kosuke
Matter, Matthias
Thorgeirsson, Snorri
Hennighausen, Lothar
TI The methyltransferases enhancer of zeste homolog (EZH) 1 and EZH2
control hepatocyte homeostasis and regeneration
SO FASEB JOURNAL
LA English
DT Article
DE H3-K27 trimethylation; liver regeneration; fibrosis
ID STEM-CELLS; GROUP PROTEINS; POLYCOMB; COMPLEX; CANCER; LIVER;
PROLIFERATION; METHYLATION; MEMORY; BMI-1
AB To investigate the role of enhancer of zeste homolog (EZH) 1 and EZH2 in liver homeostasis, mice were generated that carried Ezh1(-/-) and EZH2(fl/fl) alleles and an Alb-Cre transgene. Only the combined loss of EZH1 and EZH2 in mouse hepatocytes caused a depletion of global trimethylation on Lys 27 of histone H3 (H3K27me3) marks and the specific loss of over similar to 1900 genes at 3 mo of age. Ezh1(-/-),Ezh2(fl/fl)Alb-Cre mice exhibited progressive liver abnormalities manifested by the development of regenerative nodules and concomitant periportal fibrosis, inflammatory infiltration, and activation of A6-positive hepatic progenitor cells at 8 mo of age. In response to chronic treatment with carbon tetrachloride, all experimental mice, but none of the controls (n = 27 each), showed increased hepatic degeneration associated with liver dysfunction and reduced ability to proliferate. After two-thirds partial hepatectomy, mutant mice (n = 5) displayed increased liver injury and a blunted regenerative response. Genome-wide analyses at 3 mo of age identified 51 genes that had lost H3K27me3 marks, and their expression was significantly increased. These genes were involved in regulation of cell survival, fibrosis, and proliferation. H3K27me3 levels and liver physiology were unaffected in mice lacking either EZH1 globally or EZH2 specifically in hepatocytes. This work demonstrates a critical redundancy of EZH1 and EZH2 in maintaining hepatic homeostasis and regeneration.
C1 [Bae, Woo Kyun; Kang, Keunsoo; Yu, Ji Hoon; Yoo, Kyung Hyun; Hennighausen, Lothar] NIDDK, Lab Genet & Physiol, Bethesda, MD 20892 USA.
[Factor, Valentina M.; Kaji, Kosuke; Matter, Matthias; Thorgeirsson, Snorri] NCI, Ctr Canc Res, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Bae, Woo Kyun] Chonnam Natl Univ, Sch Med, Dept Internal Med, Kwangju, South Korea.
[Kang, Keunsoo] Dankook Univ, Dept Microbiol, Cheonan, South Korea.
[Yu, Ji Hoon] Daegu Gyeongbuk Med Innovat Fdn, New Drug Dev Ctr, Taegu, South Korea.
RP Bae, WK (reprint author), NIDDK, Lab Genet & Physiol, NIH, 8 Ctr Dri,Room 101, Bethesda, MD 20892 USA.
EM drwookyun@chonnam.ac.kr; lotharh@mail.nih.gov
FU NIH NIDDK
FX The authors thank Harold Smith [U.S. National Institutes of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases'
(NIDDK) genomics core] for conducting next-generation sequencing.
Alexander Tarakhovsky (Rockefeller University, New York, NY, USA)
provided Ezh2 floxed mice. Ezh1 mutant mice were generated at the
Research Institute of Molecular Pathology (Vienna, Austria) by Donal
O'Carroll (laboratory of Thomas Jenuwein) with the help of Maria Sibilia
(Laboratory of Erwin Wagner). The research was supported by the
Intramural Research Program of the NIH NIDDK. The authors declare no
conflicts of interest.
NR 28
TC 5
Z9 5
U1 1
U2 6
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD MAY
PY 2015
VL 29
IS 5
BP 1653
EP 1662
DI 10.1096/fj.14-261537
PG 10
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA CH5ZJ
UT WOS:000354114600005
PM 25477280
ER
PT J
AU Schenkel, LC
Singh, RK
Michel, V
Zeisel, SH
da Costa, KA
Johnson, AR
Mudd, HS
Bakovic, M
AF Schenkel, Laila C.
Singh, Ratnesh K.
Michel, Vera
Zeisel, Steven H.
da Costa, Kerry-Ann
Johnson, Amy R.
Mudd, Harvey S.
Bakovic, Marica
TI Mechanism of choline deficiency and membrane alteration in postural
orthostatic tachycardia syndrome primary skin fibroblasts
SO FASEB JOURNAL
LA English
DT Article
DE choline transport; CTL1/SLC44A1; mitochondria; phospholipids
ID TRANSPORTER-LIKE PROTEIN-1; RAT-LIVER MITOCHONDRIA; ONE-CARBON
METABOLITES; MASS-SPECTROMETRY; S-ADENOSYLMETHIONINE;
PHOSPHATIDYLETHANOLAMINE; CELLS; NUTRIENT; WOMEN; PHOSPHATIDYLCHOLINE
AB Fibroblasts from a patient with postural orthostatic tachycardia syndrome (POTS), who presented with low plasma choline and betaine, were studied to determine the metabolic characteristics of the choline deficiency. Choline is required for the synthesis of the phospholipid phosphatidylcholine (PC) and for betaine, an important osmoregulator. Here, choline transport, lipid homeostasis, and mitochondria function were analyzed in skin fibroblasts from POTS and compared with control cells. The choline transporter-like protein 1/solute carrier 44A1 (CTL1/SLC44A1) and mRNA expression were 2-3 times lower in POTS fibroblasts, and choline uptake was reduced 60% (P < 0.05). Disturbances of membrane homeostasis were observed by reduced ratios between PC:phosphatidylethanolamine and sphingomyelin:cholesterol, as well as by modified phospholipid fatty acid composition. Choline deficiency also impaired mitochondria function, which was observed by a reduction in oxygen consumption, mitochondrial potential, and glycolytic activity. When POTS cells were treated with choline, transporter was up-regulated, and uptake of choline increased, offering an option for patient treatment. The characteristics of the POTS fibroblasts described here represent a first model of choline and CTL1/SLC44A1 deficiency, in which choline transport, membrane homeostasis, and mitochondrial function are impaired.Schenkel, L. C., Singh, R. K., Michel, V., Zeisel, S. H., da Costa, K.-A., Johnson, A. R., Mudd, H. S., Bakovic, M. Mechanism of choline deficiency and membrane alteration in postural orthostatic tachycardia syndrome primary skin fibroblasts.
C1 [Schenkel, Laila C.; Singh, Ratnesh K.; Michel, Vera; Bakovic, Marica] Univ Guelph, Dept Human Hlth & Nutr Sci, Guelph, ON N1G 2W1, Canada.
[Zeisel, Steven H.] Univ N Carolina, Inst Nutr Res, Kannapolis, NC USA.
[Zeisel, Steven H.; Johnson, Amy R.] Univ N Carolina, Dept Nutr, Chapel Hill, NC USA.
[da Costa, Kerry-Ann] Toxicol Serv Inc, Chapel Hill, NC USA.
[Mudd, Harvey S.] NIMH, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Bakovic, M (reprint author), Univ Guelph, Dept Human Hlth & Nutr Sci, Anim Sci & Nutr Bldg,Room 346,50 Stone Rd East, Guelph, ON N1G 2W1, Canada.
EM mbakovic@uoguelph.ca
OI Schenkel, Laila Cigana/0000-0003-4939-6790
FU National Sciences and Engineering Research Council of Canada; Ontario
Ministry of Agriculture, Food and Rural Affairs
FX All the authors wish to acknowledge Dr. Harvey S. Mudd (1927-2014) who
assembled this team of scientists to examine the metabolic disorder
presented in this paper in order to understand it and give the patient
possible treatment options. Dr. Mudd was a thoughtful and generous
collaborator, and this paper brings to fruition his tireless efforts,
although he did not live to see its completion. The authors acknowledge
the support of Michael Leadley and the Analytical Facility for Bioactive
Molecules, Sick Kids Centre, Toronto, in assisting with the lipidomics
analysis. This study was supported by operating grants from the National
Sciences and Engineering Research Council of Canada and the Ontario
Ministry of Agriculture, Food and Rural Affairs (to M.B.).
NR 43
TC 1
Z9 1
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD MAY
PY 2015
VL 29
IS 5
BP 1663
EP 1675
DI 10.1096/fj.14-258566
PG 13
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA CH5ZJ
UT WOS:000354114600006
PM 25466896
ER
PT J
AU Deplanche, M
El-Aouar, RA
Alekseeva, L
Ladier, E
Jardin, J
Henry, G
Azevedo, V
Miyoshi, A
Beraud, L
Laurent, F
Lina, G
Vandenesch, F
Steghens, JP
Le Loir, Y
Otto, M
Gotz, F
Berkova, N
AF Deplanche, Martine
El-Aouar Filho, Rachid Aref
Alekseeva, Ludmila
Ladier, Emilie
Jardin, Julien
Henry, Gwenaele
Azevedo, Vasco
Miyoshi, Anderson
Beraud, Laetitia
Laurent, Frederic
Lina, Gerard
Vandenesch, Francois
Steghens, Jean-Paul
Le Loir, Yves
Otto, Michael
Goetz, Friedrich
Berkova, Nadia
TI Phenol-soluble modulin alpha induces G2/M phase transition delay in
eukaryotic HeLa cells
SO FASEB JOURNAL
LA English
DT Article
DE Staphylococcus aureus; cell cycle alteration; defensins; toxin; innate
immune response
ID BETA-DEFENSIN 2; STAPHYLOCOCCUS-AUREUS; EPITHELIAL-CELLS; INFECTION;
CYCLE; EXPRESSION; PROTEINS; INHIBIT; SKIN
AB Staphylococcus aureus is a gram-positive bacterium responsible for a wide range of infections. Host cell cycle alteration is a sophisticated mechanism used by pathogens to hijack the defense functions of host cells. We previously demonstrated that S. aureus MW2 (USA400) bacteria induced a G2/M phase transition delay in HeLa cells. We demonstrate here that this activity is triggered by culture supernatant compounds. Using size exclusion chromatography of the MW2 supernatant, followed by mass spectroscopy analysis of corresponding peaks, we identified phenol-soluble modulin (PSM) peptides as the likely candidates for this effect. Indeed, synthetic PSM1 and PSM3 caused a G2/M phase transition delay. The implication of PSM in cell cycle alteration was confirmed by comparison of S. aureus Los Angeles County clone (LAC) wild-type with the isogenic mutant LACpsm, which lacks the psm operon encoding PSM1-4. PSM-induced G2/M transition delay correlated with a decrease in the defensin genes expression suggesting a diminution of antibacterial functions of epithelial cells. By testing the supernatant of S. aureus human clinical isolates, we found that the degree of G2/M phase transition delay correlated with PSM1 production. We show that PSMs secreted by S. aureus alter the host cell cycle, revealing a newly identified mechanism for fostering an infection.
C1 [Deplanche, Martine; El-Aouar Filho, Rachid Aref; Alekseeva, Ludmila; Ladier, Emilie; Jardin, Julien; Henry, Gwenaele; Le Loir, Yves; Berkova, Nadia] INRA, STLO, UMR1253, Agrocampus Ouest, 65 Rue St Brieuc, F-35042 Rennes, France.
[Deplanche, Martine; El-Aouar Filho, Rachid Aref; Alekseeva, Ludmila; Ladier, Emilie; Jardin, Julien; Henry, Gwenaele; Le Loir, Yves; Berkova, Nadia] Agrocampus Ouest, UMR1253, STLO, Rennes, France.
[El-Aouar Filho, Rachid Aref; Azevedo, Vasco; Miyoshi, Anderson] Univ Fed Minas Gerais, Inst Ciencias Biol, Belo Horizonte, MG, Brazil.
[Alekseeva, Ludmila] Shemyakin Ovchinnikov Inst Bioorgan Chem, Moscow, Russia.
[Beraud, Laetitia; Laurent, Frederic; Lina, Gerard; Vandenesch, Francois] Univ Lyon 1, CNRS, INSERM U111, Ctr Int Rech Infectiol,Unite Mixtes Rech5308, F-69365 Lyon, France.
[Laurent, Frederic; Lina, Gerard; Vandenesch, Francois; Steghens, Jean-Paul] Hosp Civil Lyon, Lyon, France.
[Otto, Michael] NIH, Lab Human Bacterial Pathogenesis, Bethesda, MD 20892 USA.
[Goetz, Friedrich] Univ Tubingen, Microbial Genet, Tubingen, Germany.
RP Berkova, N (reprint author), INRA, STLO, UMR1253, Agrocampus Ouest, 65 Rue St Brieuc, F-35042 Rennes, France.
EM nadia.berkova@rennes.inra.fr
RI JARDIN, Julien/A-3241-2012; vasco, azevedo/F-4315-2011; Vandenesch,
Francois/C-7209-2014
OI JARDIN, Julien/0000-0003-0520-9391; vasco, azevedo/0000-0002-4775-2280;
Vandenesch, Francois/0000-0001-9412-7106
FU French National Institute for Agricultural Research (INRA) [P10552];
U.S. National Institutes of Health, National Institute of Allergy and
Infectious Diseases' Intramural Research Program; German Research
Foundation [SFB766]; Coordenacao de Aperfeicoamento de Pessoal de Nivel
Superior (CAPES; Brazil); France-Russia Bilateral Collaboration
FX The authors thank Gail Wagman and Mary Bret for revising the English.
This work was supported by French National Institute for Agricultural
Research (INRA), Ruminflame P10552 (to N.B., M.D., J.J., G.H., and
Y.L.L.), the U.S. National Institutes of Health, National Institute of
Allergy and Infectious Diseases' Intramural Research Program (to M.O.),
and the German Research Foundation, SFB766 (to F.G.). R.A.E.-A.F. is a
recipient of a Ph.D. fellowship from Coordenacao de Aperfeicoamento de
Pessoal de Nivel Superior (CAPES; Brazil), and L.A. is a recipient of a
postdoctoral fellowship (France-Russia Bilateral Collaboration). The
authors declare no conflicts of interest.
NR 34
TC 6
Z9 6
U1 2
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD MAY
PY 2015
VL 29
IS 5
BP 1950
EP 1959
DI 10.1096/fj.14-260513
PG 10
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA CH5ZJ
UT WOS:000354114600029
PM 25648996
ER
PT J
AU Eisenberg, ML
Chen, Z
Ye, AJ
Louis, GMB
AF Eisenberg, Michael L.
Chen, Zhen
Ye, Aijun
Louis, Germaine M. Buck
TI Relationship between physical occupational exposures and health on semen
quality: data from the Longitudinal Investigation of Fertility and the
Environment (LIFE) Study
SO FERTILITY AND STERILITY
LA English
DT Article
DE Male infertility; oligospermia; workplace; comorbidity; health
ID MALE-INFERTILITY; REPRODUCTIVE HORMONES; LIPID CONCENTRATIONS;
DIABETES-MELLITUS; COUPLE FECUNDITY; UNITED-STATES; MEN; PREVALENCE;
COHORT; MORTALITY
AB Objective: To study the relationship among occupation, health, and semen quality in a cohort of men attempting to conceive.
Design: Observational prospective cohort.
Setting: Not applicable.
Patient(s): A total of 501 couples discontinuing contraception were followed for 1 year while trying to conceive; 473 men (94%) provided one semen sample, and 80% provided a second sample.
Intervention(s): None.
Main Outcome Measure(s): Semen data obtained through at-home semen collection with next-day analysis/quantification.
Result(s): In all, complete data were available for 456 men, with a mean age of 31.8 years. Work-related heavy exertion was consistently associated with lower semen concentration and total sperm count. Thirteen percent of men who reported heavy exertion displayed oligospermia, compared with 6% who did not report workplace exertion. Shift work, night work, vibration, noise, heat, and prolonged sitting were not associated with semen quality. Men with high blood pressure had significantly lower strict morphology scores compared with normotensive men (17% vs. 21%). In contrast, hyperlipidemia, diabetes, and composite of total comorbidities were not associated with semen quality. The number of medications a man was taking as a proxy of health status was associated with semen quality. There was a negative association between number of medications and sperm count.
Conclusion(s): A negative relationship among occupational exertion, hypertension, and the number of medications with semen quality was identified. As these are potentially modifiable factors, further research should determine whether treatment or cessation may improve male fecundity. (C) 2015 by American Society for Reproductive Medicine.
C1 [Eisenberg, Michael L.] Stanford Univ, Dept Urol, Stanford, CA 94305 USA.
[Eisenberg, Michael L.] Stanford Univ, Dept Obstet & Gynecol, Stanford, CA 94305 USA.
[Chen, Zhen; Louis, Germaine M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Rockville, MD USA.
[Ye, Aijun] Glotec, Rockville, MD USA.
RP Eisenberg, ML (reprint author), Stanford Univ, Sch Med, Dept Urol, 300 Pasteur Dr, Stanford, CA 94305 USA.
EM eisenberg@stanford.edu
OI Eisenberg, Michael/0000-0001-5482-0141; Buck Louis,
Germaine/0000-0002-1774-4490
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [N01-HD-3-3355, N01-HD-3-3356, N01-HD-3-3358]
FX Intramural research of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development (contract nos. N01-HD-3-3355,
N01-HD-3-3356, and N01-HD-3-3358).
NR 37
TC 8
Z9 9
U1 2
U2 9
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 MAY
PY 2015
VL 103
IS 5
BP 1271
EP 1277
DI 10.1016/j.fertnstert.2015.02.010
PG 7
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA CH2GM
UT WOS:000353843700031
PM 25765658
ER
PT J
AU Rigler, SL
Kay, DM
Sicko, RJ
Fan, RZ
Liu, AY
Caggana, M
Browne, ML
Druschel, CM
Romitti, PA
Brody, LC
Mills, JL
AF Rigler, Shannon L.
Kay, Denise M.
Sicko, Robert J.
Fan, Ruzong
Liu, Aiyi
Caggana, Michele
Browne, Marilyn L.
Druschel, Charlotte M.
Romitti, Paul A.
Brody, Lawrence C.
Mills, James L.
TI Novel copy-number variants in a population-based investigation of
classic heterotaxy
SO GENETICS IN MEDICINE
LA English
DT Article
DE BMP2 gene; congenital heart disease; copy-number variant; heterotaxy;
MNDA gene
ID CONGENITAL HEART-DISEASE; LEFT-RIGHT ASYMMETRY; ATRIOVENTRICULAR
SEPTAL-DEFECTS; CARDIOVASCULAR MALFORMATIONS; MISSENSE MUTATIONS; HUMAN
GENOME; GENE; ZEBRAFISH; MOUSE; IDENTIFICATION
AB Purpose: Heterotaxy is a clinically and genetically heterogeneous disorder. We investigated whether screening cases restricted to a classic phenotype would result in the discovery of novel, potentially causal copy-number variants.
Methods: We identified 77 cases of classic heterotaxy from all live births in New York State during 1998-2005. DNA extracted from each infant's newborn dried blood spot was genotyped with a microarray containing 2.5 million single-nucleotide polymorphisms. Copy-number variants were identified with PennCNV and cnvPartition software. Candidates were selected for follow-up if they were absent in unaffected controls, contained 10 or more consecutive probes, and had minimal overlap with variants published in the Database of Genomic Variants.
Results: We identified 20 rare copy-number variants including a deletion of BMP2, which has been linked to laterality disorders in mice but not previously reported in humans. We also identified a large, terminal deletion of 10q and a microdeletion at 1q23.1 involving the MNDA gene; both are rare variants suspected to be associated with heterotaxy.
Conclusion: Our findings implicate rare copy-number variants in classic heterotaxy and highlight several candidate gene regions for further investigation. We also demonstrate the efficacy of copy-number variant genotyping in blood spots using microarrays.
C1 [Rigler, Shannon L.; Fan, Ruzong; Liu, Aiyi; Mills, James L.] Eunice Kennedy Shriver Natl Inst Hlth & Human Dev, Div Intramural Populat Hlth Res, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Rigler, Shannon L.] Walter Reed Natl Mil Med Ctr, Dept Neonatol, Bethesda, MD USA.
[Kay, Denise M.; Sicko, Robert J.; Caggana, Michele] New York State Dept Hlth, Div Genet, Wadsworth Ctr, Albany, NY USA.
[Browne, Marilyn L.; Druschel, Charlotte M.] New York State Dept Hlth, Congenital Malformat Registry, Albany, NY USA.
[Browne, Marilyn L.; Druschel, Charlotte M.] SUNY Albany, Sch Publ Hlth, Dept Epidemiol & Biostat, Rensselaer, NY USA.
[Romitti, Paul A.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Brody, Lawrence C.] NHGRI, Genome Technol Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Rigler, SL (reprint author), Eunice Kennedy Shriver Natl Inst Hlth & Human Dev, Div Intramural Populat Hlth Res, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM shannon.rigler@med.navy.mil
OI Liu, Aiyi/0000-0002-6618-5082
FU National Institutes of Health, Eunice Kennedy Shriver National Institute
of Child Health and Human Development [HHSN275201100001I, HHSN27500005];
National Institutes of Health, Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD) [N01-DK-73431]; National
Human Genome Research Institute; Wellcome Trust
FX This work was funded by the Intramural Research Program of the National
Institutes of Health, Eunice Kennedy Shriver National Institute of Child
Health and Human Development (contracts HHSN275201100001I and
HHSN27500005; NICHD contract N01-DK-73431) and the National Human Genome
Research Institute. Funding for the DECIPHER project was provided by the
Wellcome Trust. We thank Michael Tsai and Natalie Weir at the Minnesota
Core Laboratories and the staff at the Biomedical Genomics Center
Facility at the University of Minnesota for microarray genotyping; Emily
C. McGrath, Adam C. Gearhart, April J. Atkins, Deborah K. West, and Zoe
Edmunds at the Wadsworth Center, New York State Department of Health,
for Sanger sequencing and laboratory and technical assistance; Sandra D.
Richardson at the Congenital Malformations Registry, New York State
Department of Health, for data management; Matthew Shudt and Zhen Zhang
at the Wadsworth Center Applied Genomic Technologies Core for
next-generation sequencing; and Nathan Pankratz, University of
Minnesota, and Karl G. Hill, Social Development Research Group,
University of Washington, for generously sharing population B-allele
frequency and GC content files for PennCNV software. This study makes
use of data generated by the DECIPHER Consortium. A full list of centers
that contributed to the generation of the data is available from
http://decipher.sanger.ac.uk and via email from decipher@sanger.ac.uk.
Those who carried out the original analysis and collection of the data
bear no responsibility for the further analysis or interpretation. Some
data used for comparison in this article were obtained from the
International Standards for Cytogenomic Arrays Consortium database
(http://www.iscaconsortium.org), which generates this information using
the National Center for Biotechnology Information's database of genomic
structural variation (dbVar, http://www.ncbi.nlm.nih.gov/dbvar/), study
nstd37. Samples and associated phenotype data were provided by
International Standards for Cytogenomic Arrays Consortium member
laboratories.
NR 39
TC 6
Z9 6
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD MAY
PY 2015
VL 17
IS 5
BP 348
EP 357
DI 10.1038/gim.2014.112
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA CH5SZ
UT WOS:000354096900004
PM 25232849
ER
PT J
AU Lawrence, MG
Uzel, G
AF Lawrence, Monica G.
Uzel, Gulbu
TI 6-Year-Old Boy with Recurrent Sinopulmonary Infections and
Lymphadenopathy
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE
LA English
DT Editorial Material
DE Hyper-IgM syndrome; Nodular lymphoid hyperplasia; Epstein-Barr virus
(EBV); Cytomegalovirus (CMV); Activated p110 delta
ID MUTATIONS; DEFICIENCY; IMMUNODEFICIENCY; PI3K; GENE
C1 [Lawrence, Monica G.] Univ Virginia, Dept Med, Div Allergy Asthma & Immunol, Charlottesville, VA USA.
[Uzel, Gulbu] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
RP Uzel, G (reprint author), NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
EM guzel@niaid.nih.gov
FU Intramural NIH HHS
NR 11
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2213-2198
EI 2213-2201
J9 J ALLER CL IMM-PRACT
JI J. Allergy Clin. Immunol.-Pract.
PD MAY-JUN
PY 2015
VL 3
IS 3
BP 461
EP +
DI 10.1016/j.jaip.2014.10.017
PG 4
WC Allergy; Immunology
SC Allergy; Immunology
GA CH7JS
UT WOS:000354212900031
PM 25956317
ER
PT J
AU Tykvart, J
Barinka, C
Svoboda, M
Navratil, V
Soucek, R
Hubalek, M
Hradilek, M
Sacha, P
Lubkowski, J
Konvalinka, J
AF Tykvart, Jan
Barinka, Cyril
Svoboda, Michal
Navratil, Vaclav
Soucek, Radko
Hubalek, Martin
Hradilek, Martin
Sacha, Pavel
Lubkowski, Jacek
Konvalinka, Jan
TI Structural and Biochemical Characterization of a Novel Aminopeptidase
from Human Intestine
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID GLUTAMATE-CARBOXYPEPTIDASE-II; REACTION-MECHANISM; EXPRESSION;
PEPTIDASE; CRYSTALLOGRAPHY; INHIBITION; PROTEINS; ENZYME; RAT
AB N-acetylated alpha-linked acidic dipeptidase-like protein (NAALADase L), encoded by the NAALADL1 gene, is a close homolog of glutamate carboxypeptidase II, a metallopeptidase that has been intensively studied as a target for imaging and therapy of solid malignancies and neuropathologies. However, neither the physiological functions nor structural features of NAALADase L are known at present. Here, we report a thorough characterization of the protein product of the human NAALADL1 gene, including heterologous overexpression and purification, structural and biochemical characterization, and analysis of its expression profile. By solving the NAALADase L x-ray structure, we provide the first experimental evidence that it is a zinc-dependent metallopeptidase with a catalytic mechanism similar to that of glutamate carboxypeptidase II yet distinct substrate specificity. Aproteome-based assay revealed that the NAALADL1 gene product possesses previously unrecognized aminopeptidase activity but no carboxy-or endopeptidase activity. These findings were corroborated by site-directed mutagenesis and identification of bestatin as a potent inhibitor of the enzyme. Analysis of NAALADL1 gene expression at both the mRNA and protein levels revealed the small intestine as the major site of protein expression and points toward extensive alternative splicing of the NAALADL1 gene transcript. Taken together, our data imply that the NAALADL1 gene product's primary physiological function is associated with the final stages of protein/peptide digestion and absorption in the human digestive system. Based on these results, we suggest a new name for this enzyme: human ileal aminopeptidase (HILAP).
C1 [Tykvart, Jan; Svoboda, Michal; Navratil, Vaclav; Soucek, Radko; Hubalek, Martin; Hradilek, Martin; Sacha, Pavel; Konvalinka, Jan] Acad Sci Czech Republic, Inst Organ Chem & Biochem, Gilead Sci & IOCB Res Ctr, CR-16610 Prague 6, Czech Republic.
[Tykvart, Jan; Navratil, Vaclav; Sacha, Pavel; Konvalinka, Jan] Charles Univ Prague, Fac Nat Sci, Dept Biochem, Prague 2, Czech Republic.
[Svoboda, Michal] Charles Univ Prague, Fac Nat Sci, Dept Phys & Macromol Chem, Prague 2, Czech Republic.
[Barinka, Cyril] Acad Sci Czech Republic, Inst Biotechnol, Prague 4, Czech Republic.
[Lubkowski, Jacek] NCI, Ctr Canc Res, Macromol Crystallog Lab, NIH, Frederick, MD 21702 USA.
RP Konvalinka, J (reprint author), Acad Sci Czech Republic, Inst Organ Chem & Biochem, Vvi, Flemingovo 2, Prague 16610 6, Czech Republic.
EM jan.konvalinka@uochb.cas.cz
RI Barinka, Cyril/G-9803-2014; Hubalek, Martin/H-1400-2014; Tykvart,
Jan/G-6770-2014; Sacha, Pavel/G-9729-2014;
OI Tykvart, Jan/0000-0002-6938-1513; Sacha, Pavel/0000-0001-6198-9826;
Konvalinka, Jan/0000-0003-0695-9266
FU Grant Agency of the Czech Republic [P304-12-0847]; InterBioMed Project
from Ministry of Education of the Czech Republic [LO 1302]; National
Institutes of Health, NCI, Center for Cancer Research, Intramural
Research Program; European Regional Development Fund
[CZ.1.05/1.1.00/02.0109]; United States Department of Energy
[W-31-109-Eng38]; EMBO [1978, 249220]
FX This work was supported by Grant Agency of the Czech Republic (Grant
P304-12-0847) and InterBioMed Project LO 1302 from the Ministry of
Education of the Czech Republic. This work was also supported in part by
the National Institutes of Health, NCI, Center for Cancer Research,
Intramural Research Program (to J. L.) and also in part by project
"BIOCEV" (CZ.1.05/1.1.00/02.0109) from the European Regional Development
Fund (to C. B.). The use of the Advanced Photon Source was supported by
United States Department of Energy Contract W-31-109-Eng38.; Supported
by EMBO Installation Grant 1978 and Installation Research Grant Project
249220.
NR 31
TC 2
Z9 2
U1 2
U2 17
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 MAY 1
PY 2015
VL 290
IS 18
BP 11321
EP 11336
DI 10.1074/jbc.M114.628149
PG 16
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CH0OA
UT WOS:000353719400010
PM 25752612
ER
PT J
AU Wang, SM
Yin, LY
Zhang, Y
Fan, JH
Chang, IJ
Dawsey, SM
Taylor, PR
Abnet, CC
Qiao, YL
AF Wang, Shao-Ming
Yin, Liang-Yu
Zhang, Yu
Fan, Jin-Hu
Chang, Irene J.
Dawsey, Sanford M.
Taylor, Philip R.
Abnet, Christian C.
Qiao, You-Lin
TI Multivitamin and mineral supplementation is associated with the
reduction of fracture risk and hospitalization rate in Chinese adult
males: a randomized controlled study
SO JOURNAL OF BONE AND MINERAL METABOLISM
LA English
DT Article
DE Multivitamin supplementation; Fracture risk; Hospitalization rate;
Nutritional intervention trial
ID VITAMIN-D SUPPLEMENTATION; OSTEOPOROSIS-RELATED FRACTURES;
HIP-FRACTURES; GASTRIC CANCERS; ELDERLY-WOMEN; WORLDWIDE PREVALENCE;
POSTMENOPAUSAL WOMEN; CONTROLLED-TRIAL; ESOPHAGEAL; CALCIUM
AB Controversy exists in the literature regarding the efficacy of bone health-related nutrients, especially calcium and vitamin D, in preventing fractures. The aim of our present study was to determine the effect of multivitamin and mineral supplementation on fracture incidence among 3,318 participants from a nutritional intervention trial in Linxian, China. A total of 1,461 men and 1,857 women were enrolled and randomized to daily supplementation with 26 vitamins and minerals tablet or placebo pills for 6 years, followed by a 16-year post-interventional follow-up. The dates, sites, and causes of the fractures were collected retrospectively via a standardized questionnaire. Cox proportional hazard model was used to estimate hazard ratios and 95 % confidence intervals of fracture incidence in the intervention versus the placebo group. A total of 221 fractures (57 in men and 164 in women) occurred during the entire study period of 21 years and 9 months. In men, the supplement reduced the risk of fracture by 63 % during the trial period, and this protective effect was sustained and statistically significant when analysis included both the trial period and 5- or 10-year post-intervention follow-up (years 0-11, P = 0.04; years 0-16, P = 0.02, respectively). The protection against fracture was not apparent > 10 years after cessation of the intervention. In women, no significant effect of supplementation on fracture incidence was seen in any of the study periods. These results demonstrate that a 6-year multivitamin and mineral intervention was associated with significant reduction of fracture risk and fracture-related hospitalization in men, but not in women.
C1 [Wang, Shao-Ming; Yin, Liang-Yu; Zhang, Yu; Fan, Jin-Hu; Qiao, You-Lin] Chinese Acad Med Sci, Canc Inst Hosp, Dept Epidemiol, Beijing 100021, Peoples R China.
[Chang, Irene J.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Dawsey, Sanford M.; Taylor, Philip R.; Abnet, Christian C.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Abnet, Christian C.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Qiao, YL (reprint author), Chinese Acad Med Sci, Canc Inst Hosp, Dept Epidemiol, 17 South Panjiayuan Lane, Beijing 100021, Peoples R China.
EM abnetc@mail.nih.gov; 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 NIH [NHHSN261200477001C]; Cancer Institute of the Chinese Academy of
Medical Sciences; Chinese Academy of Medical Sciences; Intramural
Research Program of the US National Cancer Institute, NIH
FX Shao-Ming Wang was involved in the writing and revising of the
manuscript and part of the data analysis, Liang-Yu Yin was involved in
the writing and revising of the manuscript, Zhang Yu was involved in the
study design, data collection, data analysis and writing of the
manuscript, and Jin-Hu Fan was involved in the study design, data
collection and data analysis. Irene J. Chang was involved in revising
the draft. Sanford M. Dawsey and Philip R. Taylor participated in the
study design, data-analysis and revision of the manuscript, and
Christian C. Abnet and You-Lin Qiao supervised the entire study as the
principle investigators. All the authors contributed to the data
interpretation and manuscript revisions and approved the final version
of the manuscript. This study was supported in part by NIH contracts
NHHSN261200477001C with the Cancer Institute of the Chinese Academy of
Medical Sciences; by additional funds from the Chinese Academy of
Medical Sciences; and by funds from the Intramural Research Program of
the US National Cancer Institute, NIH.
NR 49
TC 0
Z9 0
U1 1
U2 9
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 0914-8779
EI 1435-5604
J9 J BONE MINER METAB
JI J. Bone Miner. Metab.
PD MAY
PY 2015
VL 33
IS 3
BP 294
EP 302
DI 10.1007/s00774-014-0589-3
PG 9
WC Endocrinology & Metabolism; Medicine, Research & Experimental
SC Endocrinology & Metabolism; Research & Experimental Medicine
GA CH8OH
UT WOS:000354295200007
PM 24849736
ER
PT J
AU Mehta, GU
Montgomery, BK
Raghavan, P
Sharma, S
Nieman, LK
Patronas, N
Oldfield, EH
Chittiboina, P
AF Mehta, Gautam U.
Montgomery, Blake K.
Raghavan, Pooja
Sharma, Susmeeta
Nieman, Lynnette K.
Patronas, Nicholas
Oldfield, Edward H.
Chittiboina, Prashant
TI Different imaging characteristics of concurrent pituitary adenomas in a
patient with Cushing's disease
SO JOURNAL OF CLINICAL NEUROSCIENCE
LA English
DT Article
DE Cushing's disease; Delayed MRI; Fluid attenuated inversion recovery
imaging; Pituitary adenoma; Transsphenoidal surgery
ID SERIES; BRAIN; GLAND
AB We report a patient with Cushing's disease (CD) and two pituitary adenomas that demonstrated different imaging characteristics and therefore suggest an alternative imaging strategy for these patients. A 42-year-old woman presented with signs and symptoms of CD. Biochemical evaluation confirmed hypercortisolemia and suggested CD. On pituitary MRI with spoiled gradient recalled acquisition in the steady-state and T1-weighted spin echo protocols, a 5 mm hypoenhancing region typical for a pituitary adenoma was identified on the left. However, after surgical resection the patient remained hypercortisolemic and pathology revealed a non-functional adenoma. At early repeat surgical exploration a 10 mm adenoma was found in the right side of the gland. Postoperatively the patient became hypocortisolemic and pathology demonstrated an adrenocorticotropic hormone (ACTH)-staining adenoma. On review of the initial MRI this tumor corresponded to a region of contrast retention best visualized on delayed fluid attenuated inversion recovery (FLAIR) imaging. While the incidentaloma in this case demonstrated classical imaging characteristics of a pituitary adenoma the larger ACTH-secreting tumor was best appreciated by contrast retention. This suggests a role for delayed postcontrast FLAIR imaging in the preoperative evaluation of CD. ACTH-secreting tumors causing CD cause significant morbidity. Due to their small size, a pituitary adenoma is frequently not identified on imaging despite endocrinologic testing suggesting CD. Regardless of improvements in MRI, many tumors are only identified at surgical exploration. Published by Elsevier Ltd.
C1 [Mehta, Gautam U.; Montgomery, Blake K.; Oldfield, Edward H.; Chittiboina, Prashant] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20814 USA.
[Raghavan, Pooja; Sharma, Susmeeta; Nieman, Lynnette K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Reprod Endocrinol, NIH, Bethesda, MD USA.
[Patronas, Nicholas] NIH, Diagnost Radiol, Walter Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Oldfield, Edward H.] Univ Virginia, Hlth Sci Ctr, Dept Neurosurg, Charlottesville, VA 22908 USA.
RP Chittiboina, P (reprint author), NINDS, Surg Neurol Branch, NIH, Room 3D20,10 Ctr Dr, Bethesda, MD 20814 USA.
EM prashant.chittiboina@nih.gov
OI Mehta, Gautam/0000-0002-8009-6430
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke at the National Institutes of Health (NIH); NIH
Medical Research Scholars Program - NIH
FX This research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke at the National
Institutes of Health (NIH) and 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 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 14
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0967-5868
EI 1532-2653
J9 J CLIN NEUROSCI
JI J. Clin. Neurosci.
PD MAY
PY 2015
VL 22
IS 5
BP 891
EP 894
DI 10.1016/j.jocn.2015.01.001
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CH3KL
UT WOS:000353929500021
PM 25827866
ER
PT J
AU Kubagawa, H
Carroll, MC
Jacob, CO
Lang, KS
Lee, KH
Mak, T
McAndrews, M
Morse, HC
Nolan, GP
Ohno, H
Richter, GH
Seal, R
Wang, JY
Wiestner, A
Coligan, JE
AF Kubagawa, Hiromi
Carroll, Michael C.
Jacob, Chaim O.
Lang, Karl S.
Lee, Kyeong-Hee
Mak, Tak
McAndrews, Monica
Morse, Herbert C., III
Nolan, Garry P.
Ohno, Hiroshi
Richter, Guenther H.
Seal, Ruth
Wang, Ji-Yang
Wiestner, Adrian
Coligan, John E.
TI Nomenclature of Toso, Fas Apoptosis Inhibitory Molecule 3, and IgM FcR
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MU-R; IMMUNE-RESPONSES; T-CELLS; DENDRITIC CELLS; B-CELLS; RECEPTOR;
ACTIVATION; BINDING; DEATH; GRANULOCYTES
AB Hiromi Kubagawa and John E. Coligan coordinated an online meeting to define an appropriate nomenclature for the cell surface glycoprotein presently designated by different names: Toso, Fas apoptosis inhibitory molecule 3 (FAIM3), and IgM FcR (Fc mu R). FAIM3 and Faim3 are the currently approved symbols for the human and mouse genes, respectively, in the National Center for Biotechnology Information, Ensembl, and other databases. However, recent functional results reported by several groups of investigators strongly support a recommendation for renaming FAIM3/Faim3 as FCMR/Fcmr, a name better reflecting its physiological function as the FcR for IgM. Participants included 12 investigators involved in studying Toso/FAIM3(Faim3)/F mu R, representatives from the Human Genome Nomenclature Committee (Ruth Seal) and the Mouse Genome Nomenclature Committee (Monica McAndrews), and an observer from the IgM research field (Michael Carroll). In this article, we provide a brief background of the key research on the Toso/FAIM3(Faim3)/Fc mu R proteins, focusing on the ligand specificity and functional activity, followed by a brief summary of discussion about adopting a single name for this molecule and its gene and a resulting recommendation for genome nomenclature committees.
C1 [Kubagawa, Hiromi] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA.
[Carroll, Michael C.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Jacob, Chaim O.] Univ So Calif, Sch Med, Dept Med, Los Angeles, CA 90033 USA.
[Lang, Karl S.] Univ Duisburg Essen, Inst Immunol, D-45147 Essen, Germany.
[Lee, Kyeong-Hee] Hannover Med Sch, Inst Clin Chem, D-30625 Hannover, Germany.
[Mak, Tak] Univ Hlth Network, Princess Margaret Canc Ctr, Campbell Family Inst Breast Canc Res, Toronto, ON M5T 2M9, Canada.
[McAndrews, Monica] Jackson Lab, Mouse Genome Informat, Bar Harbor, ME 04609 USA.
[Morse, Herbert C., III; Coligan, John E.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Nolan, Garry P.] Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA.
[Ohno, Hiroshi] RIKEN, Ctr Integrat Med Sci, Lab Intestinal Ecosyst, Yokohama, Kanagawa 2300045, Japan.
[Richter, Guenther H.] Tech Univ Munich, Klinikum Rechts Isar, Kinderklin, D-81664 Munich, Germany.
[Seal, Ruth] European Bioinformat Inst, Human Genome Org Gene Nomenclature Comm, Hinxton CB10 1SD, Cambs, England.
[Wang, Ji-Yang] Fudan Univ, Sch Basic Med Sci, Dept Immunol, Shanghai 200032, Peoples R China.
[Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Kubagawa, H (reprint author), Deutsch Rheuma Forschungszentrum Berlin, Charitepl, D-10117 Berlin, Germany.
EM hiromi.kubagawa@drfz.de; JCOLIGAN@niaid.nih.gov
RI Ohno, Hiroshi/L-7899-2014; Lang, Karl/R-2505-2016;
OI Ohno, Hiroshi/0000-0001-8776-9661; Seal, Ruth/0000-0002-7545-6817
FU National Institutes of Health/National Institute of Allergy and
Infectious Diseases [R21AI094625]; National Human Genome Research
Institute [U41HG003345]; Wellcome Trust [099129/Z/12/Z]
FX This work was supported in part by National Institutes of
Health/National Institute of Allergy and Infectious Diseases Grant
R21AI094625 (to H.K.), the National Institutes of Health/National
Institute of Allergy and Infectious Diseases Intramural Research
Programs (to H.C.M. and J.E.C.), and National Human Genome Research
Institute Grant U41HG003345 and Wellcome Trust Grant 099129/Z/12/Z (to
R.S.).
NR 24
TC 1
Z9 1
U1 2
U2 6
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4055
EP 4057
DI 10.4049/jimmunol.1500222
PG 3
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400001
PM 25888699
ER
PT J
AU Wang, J
Shirota, Y
Bayik, D
Shirota, H
Tross, D
Gulley, JL
Wood, LV
Berzofsky, JA
Klinman, DM
AF Wang, Jing
Shirota, Yuko
Bayik, Defne
Shirota, Hidekazu
Tross, Debra
Gulley, James L.
Wood, Lauren V.
Berzofsky, Jay A.
Klinman, Dennis M.
TI Effect of TLR Agonists on the Differentiation and Function of Human
Monocytic Myeloid-Derived Suppressor Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TUMOR-ASSOCIATED MACROPHAGES; CARCINOMA PATIENTS; IMMUNE-RESPONSE;
T-CELLS; IMMUNOSUPPRESSIVE ACTIVITY; ANTITUMOR IMMUNITY; INNATE
IMMUNITY; CANCER-PATIENTS; IN-VIVO; ACTIVATION
AB Tumors persist by occupying immunosuppressive microenvironments that inhibit the activity of tumoricidal T and NK cells. Monocytic myeloid-derived suppressor cells (mMDSC) are an important component of this immunosuppressive milieu. We find that the suppressive activity of mMDSC isolated from cancer patients can be reversed by treatment with TLR7/8 agonists, which induce human mMDSC to differentiate into tumoricidal M1-like macrophages. In contrast, agonists targeting TLR1/2 cause mMDSC to mature into immunosuppressive M2-like macrophages. These two populations of macrophage are phenotypically and functionally discrete and differ in gene expression profile. The ability of TLR7/8 agonists to reverse mMDSC-mediated immune suppression suggests that they might be useful adjuncts for tumor immunotherapy.
C1 [Wang, Jing; Shirota, Yuko; Bayik, Defne; Shirota, Hidekazu; Tross, Debra; Klinman, Dennis M.] NCI, Canc & Inflammat Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Gulley, James L.] NCI, Genitourinary Malignancies Branch, Bethesda, MD 20892 USA.
[Wood, Lauren V.; Berzofsky, Jay A.] NCI, Vaccine Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Klinman, DM (reprint author), Frederick Natl Lab Canc Res, Bldg 567,Room 205, Frederick, MD 21702 USA.
EM klinmand@mail.nih.gov
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
FU Intramural NIH HHS [Z01 BC010852-01]
NR 56
TC 5
Z9 5
U1 1
U2 9
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4215
EP 4221
DI 10.4049/jimmunol.1402004
PG 7
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400020
PM 25825448
ER
PT J
AU Ding, XL
Yan, YP
Li, X
Li, K
Ciric, B
Yang, JX
Zhang, Y
Wu, S
Xu, H
Chen, WJ
Lovett-Racke, AE
Zhang, GX
Rostami, A
AF Ding, Xiaoli
Yan, Yaping
Li, Xing
Li, Ke
Ciric, Bogoljub
Yang, Jingxian
Zhang, Yuan
Wu, Shuai
Xu, Hui
Chen, Wanjun
Lovett-Racke, Amy E.
Zhang, Guang-Xian
Rostami, Abdolmohamad
TI Silencing IFN-gamma Binding/Signaling in Astrocytes versus Microglia
Leads to Opposite Effects on Central Nervous System Autoimmunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID T-CELL RESPONSES; INTERFERON-GAMMA; MULTIPLE-SCLEROSIS;
ENCEPHALOMYELITIS; ACTIVATION; EAE; EXPRESSION; MICE; PATHOGENESIS;
INDUCTION
AB IFN-gamma, the hallmark cytokine of Th1 cells, plays an important role in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Thus far, the role of IFN-gamma in EAE has been largely studied through its effects on immune cells, whereas much less is known about its effects on CNS cells, especially in vivo. In this study, we dissected the in vivo effects and mechanisms of IFN-gamma binding/signaling in astrocytes and microglia, and found that IFN-gamma signaling in these cell types has opposite effects in EAE pathogenesis. Silencing IFN-gamma binding/signaling in astrocytes alleviated EAE, whereas in microglia, and likely in some infiltrating macrophages, it increased disease severity. Silencing IFN-gamma signaling in astrocytes resulted in diminished expression of chemokines and fewer inflammatory cells infiltrating into the CNS, whereas blocking IFN-gamma binding/signaling in microglia, probably infiltrating macrophages as well, increased disease severity through augmented activation and proliferation of microglia. Further, blocking IFN-gamma binding/signaling in astrocytes alleviated both Th1- and Th17-mediated adoptive EAE, indicating an important role for IFN-gamma signaling in astrocytes in autoimmune CNS inflammation. Thus, our study defines novel mechanisms of action of IFN-gamma in EAE pathogenesis, and also highlights an opportunity for development of multiple sclerosis therapies directed at CNS cells.
C1 [Ding, Xiaoli; Yan, Yaping; Li, Xing; Li, Ke; Ciric, Bogoljub; Yang, Jingxian; Zhang, Yuan; Wu, Shuai; Xu, Hui; Zhang, Guang-Xian; Rostami, Abdolmohamad] Thomas Jefferson Univ, Dept Neurol, Philadelphia, PA 19107 USA.
[Ding, Xiaoli; Yan, Yaping] Shaanxi Normal Univ, Coll Life Sci, Natl Engn Lab Resource Dev Endangered Crude Drugs, Key Lab Minist Educ Med Resources & Nat Pharmaceu, Xian 710062, Peoples R China.
[Yang, Jingxian] Liaoning Univ Tradit Chinese Med, Dept Pharmacol, Dalian 110847, Peoples R China.
[Chen, Wanjun] Natl Inst Dent & Craniofacial Res, Mucosal Immunol Sect, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA.
[Lovett-Racke, Amy E.] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
RP Rostami, A (reprint author), Thomas Jefferson Univ, Dept Neurol, 900 Walnut St,JHN 300, Philadelphia, PA 19107 USA.
EM Guang-Xian.Zhang@jefferson.edu; a.m.rostami@jefferson.edu
RI Lovett-Racke, Amy/E-3545-2011
FU National Multiple Sclerosis Society; National Institutes of Health;
Groff Foundation; Chinese National Natural Science Foundation
[81100888]; Fundamental Research Funds for the Central Universities of
China [GK261001027]
FX This work was supported by the National Multiple Sclerosis Society, the
National Institutes of Health, the Groff Foundation, the Chinese
National Natural Science Foundation (Grant 81100888 to X.D. and Y.Y.)
and the Fundamental Research Funds for the Central Universities of China
(Grant GK261001027 to X.D. and Y.Y.).
NR 52
TC 10
Z9 10
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4251
EP 4264
DI 10.4049/jimmunol.1303321
PG 14
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400024
PM 25795755
ER
PT J
AU Metidji, A
Rieder, SA
Glass, DD
Cremer, I
Punkosdy, GA
Shevach, EM
AF Metidji, Amina
Rieder, Sadiye Amcaoglu
Glass, Deborah Dacek
Cremer, Isabelle
Punkosdy, George A.
Shevach, Ethan M.
TI IFN-alpha/beta Receptor Signaling Promotes Regulatory T Cell Development
and Function under Stress Conditions
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID PERSISTENT LCMV INFECTION; I INTERFERONS; CLONAL EXPANSION; MEMORY
FORMATION; CUTTING EDGE; ACTIVATION; EXPRESSION; DISTINCT; STIMULATION;
EFFECTOR
AB Type I IFNs are a family of cytokines with antiviral and immunomodulatory properties. Although the antiviral effects of IFNs are well characterized, their immunomodulatory properties are less clear. To specifically address the effects of type I IFNs on T regulatory cells (Tregs), we studied mixed bone marrow chimeras between wild-type and IFN-alpha/beta receptor (IFNAR) knockout (KO) mice, and heterozygous female mice expressing a Treg-specific deletion of the IFNAR. In these two models, IFNAR signaling promotes the development of the Treg lineage in the thymus and their survival in the periphery. IFNAR KO Tregs had a higher expression of the proapoptotic gene Bim and higher frequency of active caspase-positive cells. IFNAR KO Tregs from chimeric mice displayed a more naive phenotype, accompanied by lower levels of CD25 and phosphorylated STAT5. Therefore, in Tregs, IFNAR signaling may directly or indirectly affect phosphorylation of STAT5. In mixed chimeras with Scurfy fetal liver, Tregs derived from IFNAR KO bone marrow were unable to control T effector cell activation and tissue inflammation. Under stress conditions or in a competitive environment, IFNAR signaling may be required to maintain Treg homeostasis and function.
C1 [Metidji, Amina; Rieder, Sadiye Amcaoglu; Glass, Deborah Dacek; Punkosdy, George A.; Shevach, Ethan M.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Metidji, Amina; Cremer, Isabelle] Univ Paris 06, F-75005 Paris, France.
[Cremer, Isabelle] INSERM, Ctr Rech Cordeliers, F-75006 Paris, France.
[Cremer, Isabelle] Univ Paris 05, F-75006 Paris, France.
RP Shevach, EM (reprint author), NIAID, Immunol Lab, NIH, Bldg 10,Room 11N315,10 Ctr Dr,MSC 1892, Bethesda, MD 20892 USA.
EM eshevach@niaid.nih.gov
FU Intramural Program of the National Institute of Allergy and Infectious
Diseases
FX This work was supported by the Intramural Program of the National
Institute of Allergy and Infectious Diseases.
NR 48
TC 9
Z9 10
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4265
EP 4276
DI 10.4049/jimmunol.1500036
PG 12
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400025
PM 25795758
ER
PT J
AU Ainsua-Enrich, E
Serrano-Candelas, E
Alvarez-Errico, D
Picado, C
Sayos, J
Rivera, J
Martin, M
AF Ainsua-Enrich, Erola
Serrano-Candelas, Eva
Alvarez-Errico, Damiana
Picado, Cesar
Sayos, Joan
Rivera, Juan
Martin, Margarita
TI The Adaptor 3BP2 Is Required for KIT Receptor Expression and Human Mast
Cell Survival
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID FC-EPSILON-RI; TRANSCRIPTION FACTOR GATA-3; C-KIT; PROTEIN 3BP2; ANTIGEN
RECEPTOR; TYROSINE KINASE; GENE-EXPRESSION; T-CELLS; M-CSF; ACTIVATION
AB SH3-binding protein 2 (3BP2) is a cytoplasmic adaptor protein that acts as a positive regulator in mast cell Fc epsilon RI-dependent signaling. The KIT receptor whose ligand is the stem cell factor is necessary for mast cell development, proliferation, and survival as well as for optimal IgE-dependent signal. Activating mutations in KIT have been associated with several diseases including mastocytosis. In the present work, we found that 3BP2 silencing impairs KIT signaling pathways, thus affecting phosphoinositide 3-kinase and MAPK pathways in human mast cells (huMCs) from HMC-1, LAD2 (huMC lines), and CD34(+)-derived mast cells. Unexpectedly, silencing of 3BP2 reduces KIT expression in normal huMCs as well as in HMC-1 cells where KIT is mutated, thus increasing cellular apoptosis and caspase-3/7 activity. 3BP2 silencing reduces KIT transcription expression levels. Interestingly, 3BP2 silencing decreased microphthalmia-associated transcription factor (MITF) expression, a transcription factor involved in KIT expression. Reconstitution of 3BP2 in knockdown cells leads to reversal of KIT expression as well as survival phenotype. Accordingly MITF reconstitution enhances KIT expression levels in 3BP2-silenced cells. Moreover, downregulation of KIT expression by miRNA-221 overexpression or the proteasome inhibitor bortezomib also reduced 3BP2 and MITF expression. Furthermore, KIT tyrosine activity inhibition reduced 3BP2 and MITF expression, demonstrating again a tight and reciprocal relationship between these molecules. Taken together, our results show that 3BP2 regulates huMC survival and participates in KIT-mediated signal transduction by directly controlling KIT receptor expression, suggesting its potential as a therapeutic target in mast cell-mediated inflammatory diseases and deregulated KIT disorders.
C1 [Ainsua-Enrich, Erola; Serrano-Candelas, Eva; Alvarez-Errico, Damiana; Martin, Margarita] Univ Barcelona, Fac Med, Biochem Unit, E-08036 Barcelona, Spain.
[Ainsua-Enrich, Erola; Serrano-Candelas, Eva; Alvarez-Errico, Damiana; Picado, Cesar; Martin, Margarita] Inst Invest Biomed August Pi & Sunyer, Lab Immunoallergia Resp Clin & Expt, Barcelona 08036, Spain.
[Picado, Cesar] Inst Hlth Carlos III, Networking Res Ctr Resp Dis, Madrid 28029, Spain.
[Sayos, Joan] Autonomous Univ Barcelona, Mol Biol & Biochem Res Ctr Nanomed, Immunobiol Grp, E-08035 Barcelona, Spain.
[Sayos, Joan] Inst Hlth Carlos III, Networking Res Ctr Bioengn Biomat & Nanomed, Madrid 28029, Spain.
[Rivera, Juan] NIAMSD, Mol Immunol Sect, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
RP Martin, M (reprint author), Univ Barcelona, Fac Med, Biochem Unit, Carrer Casanova 143, E-08036 Barcelona, Spain.
EM martin_andorra@ub.edu
RI Sayos, Joan/B-6119-2009; Serrano Candelas, Eva/I-1892-2015;
OI Sayos, Joan/0000-0002-4664-3461; Serrano Candelas,
Eva/0000-0002-8929-5364; Martin, Margarita/0000-0002-9245-4899
FU Fondo de Investigaciones Sanitarias, Ministerio de Economia y
Competitividad (Spain) [PI1200332]; Miguel Servet contract from the
Fondo de Investigaciones Sanitarias, Instituto de Salud Carlos III
[CP06/00058]; Intramural Research Program within the National Institute
of Arthritis and Musculoskeletal and Skin Diseases of the National
Institutes of Health
FX This work was supported by Grant PI1200332 from the Fondo de
Investigaciones Sanitarias, Ministerio de Economia y Competitividad
(Spain). J.S. is supported by a Miguel Servet contract from the Fondo de
Investigaciones Sanitarias, Instituto de Salud Carlos III (CP06/00058).
Work done in J.R.'s laboratory is supported by the Intramural Research
Program within the National Institute of Arthritis and Musculoskeletal
and Skin Diseases of the National Institutes of Health.
NR 59
TC 1
Z9 1
U1 1
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4309
EP 4318
DI 10.4049/jimmunol.1402887
PG 10
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400029
PM 25810396
ER
PT J
AU Singh, SP
Zhang, HH
Tsang, H
Gardina, PJ
Myers, TG
Nagarajan, V
Lee, CH
Farber, JM
AF Singh, Satya P.
Zhang, Hongwei H.
Tsang, Hsinyi
Gardina, Paul J.
Myers, Timothy G.
Nagarajan, Vijayaraj
Lee, Chang Hoon
Farber, Joshua M.
TI PLZF Regulates CCR6 and Is Critical for the Acquisition and Maintenance
of the Th17 Phenotype in Human Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID ROR-GAMMA-T; ACUTE PROMYELOCYTIC LEUKEMIA; GENOME-WIDE ASSOCIATION;
RHEUMATOID-ARTHRITIS; TRANSCRIPTIONAL REPRESSION; INTERLEUKIN 22;
RECEPTOR CCR6; T-H-17 CELLS; RISK LOCI; DIFFERENTIATION
AB Th17 cells, which express the chemokine receptor CCR6, are implicated in many immune-mediated disorders, such as psoriasis and multiple sclerosis. We found that expression levels of CCR6 on human effector/memory CD4(+) T cells reflect a continuum of Th17 differentiation. By evaluating the transcriptome in cells with increasing CCR6, we detected progressive upregulation of ZBTB16, which encodes the broad complex, tramtrack, bric-a-brac-zinc finger transcription factor promyelocytic leukemia zinc finger protein (PLZF). Using chromatin immunoprecipitation for modified histones, p300, and PLZF, we identified enhancer-like sites at -9/-10 and -13/-14 kb from the upstream transcription start site of CCR6 that bind PLZF in CCR6(+) cells. For Th cells from adult blood, both in the CCR6(+) memory population and in naive cells activated ex vivo, knockdown of ZBTB16 downregulated CCR6 and other Th17-associated genes. ZBTB16 and RORC (which encodes the "master regulator" RORgt) cross-regulate each other, and PLZF binds at the RORC promoter in CCR6(+) cells. In naive Th cells from cord blood, ZBTB16 expression was confined to CD161(+) cells, which are Th17 cell precursors. ZBTB16 was not expressed in mouse Th17 cells, and Th17 cells could be made from luxoid mice, which harbor an inactivating mutation in Zbtb16. These studies demonstrate a role for PLZF as an activator of transcription important both for Th17 differentiation and the maintenance of the Th17 phenotype in human cells, expand the role of PLZF as a critical regulator in the human adaptive immune system, and identify a novel, essential element in a regulatory network that is of significant therapeutic interest.
C1 [Singh, Satya P.; Zhang, Hongwei H.; Tsang, Hsinyi; Lee, Chang Hoon; Farber, Joshua M.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Gardina, Paul J.; Myers, Timothy G.] NIAID, Technol Branch, NIH, Bethesda, MD 20892 USA.
[Nagarajan, Vijayaraj] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
RP Farber, JM (reprint author), NIAID, Lab Mol Immunol, NIH, Bldg 10,Room 11N-111,10 Ctr Dr,MSC 1886, Bethesda, MD 20892 USA.
EM jfarber@niaid.nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 66
TC 5
Z9 5
U1 1
U2 6
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4350
EP 4361
DI 10.4049/jimmunol.1401093
PG 12
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400033
PM 25833398
ER
PT J
AU Enqvist, M
Ask, EH
Forslund, E
Carlsten, M
Abrahamsen, G
Beziat, V
Andersson, S
Schaffer, M
Spurkland, A
Bryceson, Y
Onfelt, B
Malmberg, KJ
AF Enqvist, Monika
Ask, Eivind Heggernes
Forslund, Elin
Carlsten, Mattias
Abrahamsen, Greger
Beziat, Vivien
Andersson, Sandra A
Schaffer, Marie
Spurkland, Anne
Bryceson, Yenan
Onfelt, Bjorn
Malmberg, Karl-Johan
TI Coordinated Expression of DNAM-1 and LFA-1 in Educated NK Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID NATURAL-KILLER-CELLS; MHC CLASS-I; LIPID RAFT RECRUITMENT; INHIBITORY
RECEPTORS; CYTOMEGALOVIRUS-INFECTION; ADHESION MOLECULE; FLOW-CYTOMETRY;
TARGET-CELLS; SELF-MHC; T-CELL
AB The functional capacity of NK cells is dynamically tuned by integrated signals from inhibitory and activating cell surface receptors in a process termed NK cell education. However, the understanding of the cellular and molecular mechanisms behind this functional tuning is limited. In this study, we show that the expression of the adhesion molecule and activation receptor DNAX accessory molecule 1 (DNAM-1) correlates with the quantity and quality of the inhibitory input by HLA class I-specific killer cell Ig-like receptors and CD94/NKG2A as well as with the magnitude of functional responses. Upon target cell recognition, the conformational state of LFA-1 changed in educated NK cells, associated with rapid colocalization of both active LFA-1 and DNAM-1 at the immune synapse. Thus, the coordinated expression of LFA-1 and DNAM-1 is a central component of NK cell education and provides a potential mechanism for controlling cytotoxicity by functionally mature NK cells.
C1 [Enqvist, Monika; Carlsten, Mattias; Beziat, Vivien; Andersson, Sandra A; Schaffer, Marie; Bryceson, Yenan; Malmberg, Karl-Johan] Karolinska Inst, Ctr Infect Med, Dept Med, S-14186 Stockholm, Sweden.
[Ask, Eivind Heggernes; Malmberg, Karl-Johan] Univ Oslo, Inst Clin Med, KG Jebsen Ctr Canc Immunotherapy, N-0316 Oslo, Norway.
[Ask, Eivind Heggernes; Malmberg, Karl-Johan] Oslo Univ Hosp, Inst Canc Res, Dept Canc Immunol, N-0310 Oslo, Norway.
[Forslund, Elin; Onfelt, Bjorn] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, S-17177 Stockholm, Sweden.
[Carlsten, Mattias] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Abrahamsen, Greger; Spurkland, Anne] Univ Oslo, Inst Basic Med Sci, N-0317 Oslo, Norway.
[Onfelt, Bjorn] Royal Inst Technol, Dept Appl Phys, Sci Life Lab, S-10691 Stockholm, Sweden.
RP Malmberg, KJ (reprint author), Karolinska Inst, Ctr Infect Med, F59, S-14186 Stockholm, Sweden.
EM kalle.malmberg@ki.se
RI Beziat, Vivien/G-2971-2011;
OI Beziat, Vivien/0000-0002-4020-824X; Malmberg,
Karl-Johan/0000-0002-8718-9373; Spurkland, Anne/0000-0003-4421-0766;
Bryceson, Yenan/0000-0002-7783-9934; Carlsten,
Mattias/0000-0001-9815-0012
FU Swedish Research Council; Swedish Children's Cancer Society; Swedish
Cancer Society; Karolinska Institutet; Wenner-Gren Foundation; Anders
Jahres Foundation; Norwegian Cancer Society; Norwegian Research Council;
South-Eastern Norway Regional Health Authority; European Research
Council; K.G. Jebsen Center for Cancer Immunotherapy
FX This work was supported by grants from the Swedish Research Council, the
Swedish Children's Cancer Society, the Swedish Cancer Society, the
Karolinska Institutet, the Wenner-Gren Foundation, the Anders Jahres
Foundation, the Norwegian Cancer Society, the Norwegian Research
Council, the South-Eastern Norway Regional Health Authority, the
European Research Council, and the K.G. Jebsen Center for Cancer
Immunotherapy.
NR 50
TC 15
Z9 15
U1 4
U2 13
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
IS 9
BP 4518
EP 4527
DI 10.4049/jimmunol.1401972
PG 10
WC Immunology
SC Immunology
GA CH0QN
UT WOS:000353727400050
PM 25825444
ER
PT J
AU Zhang, YH
Wahl, LM
AF Zhang, Yahong
Wahl, Larry M.
TI Cytokine-induced monocyte MMP-1 is negatively regulated by GSK-3 through
a p38 MAPK-mediated decrease in ERK1/2 MAPK activation
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE signal transduction; inflammation; connective tissue
ID GLYCOGEN-SYNTHASE KINASE-3; MATRIX-METALLOPROTEINASE EXPRESSION;
MACROPHAGE COLLAGENASE PRODUCTION; BETA-CATENIN; CANCER-CELLS;
DIFFERENTIAL REGULATION; SIGNALING PATHWAY; XENOPUS EMBRYOS; INHIBITION;
RECEPTOR
AB Elucidation of the signal transduction events leading to the production of MMPs by monocytes/macrophages may provide insights into the mechanisms involved in the destruction of connective tissue associated with chronic inflammatory lesions. Here, we show that GSK-3 is a negative regulator of cytokine-induced MMP-1 production by monocytes. Inhibition of monocyte GSK-3 pharmacologically with SB216763 or GSK-3 beta siRNA caused a significant enhancement of MMP-1 by TNF-alpha- and GM-CSF-activated monocytes, indicating that induction of MMP-1 by TNF-alpha and GM-CSF involved phosphorylation/inactivation of GSK-3. TNF-alpha- and GM-CSF-induced phosphorylation of GSK-3 and subsequent MMP-1 production was blocked with the PKC inhibitor Go6976 but not by the AKT1/2 inhibitor AKT VIII, showing that cytokine phosphorylation of GSK-3 occurs primarily through a PKC pathway. Inhibition of GSK-3 resulted in decreased phosphorylation of p38 MAPK with a corresponding increase in phosphorylation of ERK1/2 MAPK. Enhanced MMP-1 production by treatment with SB216763 was a result of increased ERK1/2 activation, as demonstrated by inhibition of MMP-1 by PD98059, a specific ERK1/2 inhibitor. Conversely, the p38 MAPK inhibitor SB203580 enhanced cytokine activation of ERK1/2 and the production of MMP-1 similar to that of SB216763. These findings demonstrate that the degree of cytokine-mediated phosphorylation/inhibition of GSK-3 determines the level of MMP-1 production through amechanism involving decreased activation of p38 MAPK, a negative regulator of ERK1/2 required for cytokine-induced production of MMP-1 by monocytes.
C1 [Zhang, Yahong; Wahl, Larry M.] NIDCR, NIH, Bethesda, MD 20892 USA.
RP Wahl, LM (reprint author), NIDCR, NIH, 30 Convent Dr,Bldg 30,Room 109, Bethesda, MD 20892 USA.
EM lwahl@mail.nih.gov
FU National Institute of Dental and Craniofacial Research U.S. National
Institutes of Health
FX This study was supported by intramural funds of the National Institute
of Dental and Craniofacial Research U.S. National Institutes of Health.
NR 49
TC 1
Z9 1
U1 0
U2 3
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 MAY
PY 2015
VL 97
IS 5
BP 921
EP 927
DI 10.1189/jlb.3A0413-235R
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA CH3BK
UT WOS:000353900500010
PM 25714802
ER
PT J
AU Zheng, B
Bernier, M
Zhang, XH
Suzuki, T
Nie, CQ
Li, YH
Zhang, Y
Song, LL
Shi, HJ
Liu, Y
Zheng, CY
Wen, JK
AF Zheng, Bin
Bernier, Michel
Zhang, Xin-hua
Suzuki, Toru
Nie, Chan-quan
Li, Yong Hui
Zhang, Yong
Song, Li-li
Shi, Hui-jing
Liu, Yan
Zheng, Cui-ying
Wen, Jin-kun
TI miR-200c-SUMOylated KLF4 feedback loop acts as a switch in
transcriptional programs that control VSMC proliferation
SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
LA English
DT Letter
DE miR-200c; Ubc9; SUMOylation; KLF4; VSMC; Proliferation
ID SMOOTH-MUSCLE-CELLS; MEDIATES NUCLEAR-LOCALIZATION; GENE-EXPRESSION;
DOWN-REGULATION; CANCER-CELLS; PROMOTER ACTIVITY; IN-VIVO; SUMOYLATION;
GROWTH; ALPHA
AB The regulation of vascular smooth muscle cell (VSMC) proliferation is an important issue because it has major implications for the prevention of pathological vascular conditions. Using microRNA array screen, we found the expression levels of 200 unique miRNAs in hyperplasic tissues. Among them, miR-200c expression substantially was down-regulated. The objective of this work was to assess the function of miR-200c and SUMOylated Kruppel-like transcription factor 4 (KLF4) in the regulation of VSMC proliferation in both cultured cells and animal models of balloon injury. Under basal conditions, we found that miR-200c inhibited the expression of KLF4 and the SUMO-conjugating enzyme Ubc9. Upon PDGF-BB treatment, Ubc9 interacted with and promoted the SUMOylation of KLF4, which allowed the recruitment of transcriptional corepressors (e.g., nuclear receptor corepressor (NCoR) and HDAC2) to the miR-200c promoter. The reduction in miR-200c levels led to increased target gene expression (e.g., Ubc9 and KLF4), which further repressed miR-200c levels and accelerated VSMC proliferation. These results demonstrate that induction of a miR-200c-SUMOylated KLF4 feedback loop is a significant aspect of the PDGF-BB proliferative response in VSMCs and that targeting Ubc9 represents a novel approach for the prevention of restenosis. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Zheng, Bin; Zhang, Xin-hua; Nie, Chan-quan; Li, Yong Hui; Song, Li-li; Shi, Hui-jing; Liu, Yan; Zheng, Cui-ying; Wen, Jin-kun] Hebei Med Univ, Dept Biochem & Mol Biol, Shijiazhuang 050017, Peoples R China.
[Bernier, Michel] NIA, Lab Clin Invest, NIH, Baltimore, MD 21224 USA.
[Suzuki, Toru] Univ Tokyo, Dept Cardiovasc Med, Tokyo, Japan.
[Zhang, Yong] Hebei Med Univ, Dept Urinary Surg, Hosp 2, Shijiazhuang 050000, Peoples R China.
RP Zheng, B (reprint author), Hebei Med Univ, Dept Biochem & Mol Biol, 361 Zhongshan East Rd, Shijiazhuang 050017, Peoples R China.
EM doublezb@sina.com; wjk@hebmu.edu.cn
FU Intramural NIH HHS
NR 45
TC 8
Z9 8
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2828
EI 1095-8584
J9 J MOL CELL CARDIOL
JI J. Mol. Cell. Cardiol.
PD MAY
PY 2015
VL 82
BP 201
EP 212
DI 10.1016/j.yjmcc.2015.03.011
PG 12
WC Cardiac & Cardiovascular Systems; Cell Biology
SC Cardiovascular System & Cardiology; Cell Biology
GA CH6KO
UT WOS:000354145700023
PM 25791170
ER
PT J
AU Sun, N
Finkel, T
AF Sun, Nuo
Finkel, Toren
TI Cardiac mitochondria: A surprise about size
SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
LA English
DT Editorial Material
ID ENDOPLASMIC-RETICULUM; HEART-FAILURE; CELL-DEATH; FUSION; DYNAMICS;
FISSION; OPA1; FRAGMENTATION; DYSFUNCTION; MORPHOLOGY
C1 [Sun, Nuo; Finkel, Toren] NHLBI, Ctr Mol Med, Bethesda, MD 20892 USA.
RP Finkel, T (reprint author), NIH, Bldg 10-CRC 5-3330,10 Ctr Dr, Bethesda, MD 20892 USA.
EM finkelt@nih.gov
FU Intramural NIH HHS
NR 27
TC 1
Z9 1
U1 1
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2828
EI 1095-8584
J9 J MOL CELL CARDIOL
JI J. Mol. Cell. Cardiol.
PD MAY
PY 2015
VL 82
BP 213
EP 215
DI 10.1016/j.yjmcc.2015.01.009
PG 3
WC Cardiac & Cardiovascular Systems; Cell Biology
SC Cardiovascular System & Cardiology; Cell Biology
GA CH6KO
UT WOS:000354145700024
PM 25626176
ER
PT J
AU Lyoo, CH
Ikawa, M
Liow, JS
Zoghbi, SS
Morse, CL
Pike, VW
Fujita, M
Innis, RB
Kreisl, WC
AF Lyoo, Chul Hyoung
Ikawa, Masamichi
Liow, Jeih-San
Zoghbi, Sami S.
Morse, Cheryl L.
Pike, Victor W.
Fujita, Masahiro
Innis, Robert B.
Kreisl, William Charles
TI Cerebellum Can Serve As a Pseudo-Reference Region in Alzheimer Disease
to Detect Neuroinflammation Measured with PET Radioligand Binding to
Translocator Protein
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE Alzheimer disease; neuroinflammation; C-11-PBR28; positron emission
tomography; ratio method
ID PERIPHERAL BENZODIAZEPINE-RECEPTOR; MILD COGNITIVE IMPAIRMENT;
POSITRON-EMISSION-TOMOGRAPHY; IN-VIVO; ASSOCIATION WORKGROUPS;
DIAGNOSTIC GUIDELINES; NATIONAL INSTITUTE; BRAIN; TSPO; POLYMORPHISM
AB Alzheimer disease (AD) is associated with an increase in the brain of the 18-kDa translocator protein (TSPO), which is overexpressed in activated microglia and reactive astrocytes. Measuring the density of TSPO with PET typically requires absolute quantitation with arterial blood sampling, because a reference region devoid of TSPO does not exist in the brain. We sought to determine whether a simple ratio method could substitute for absolute quantitation of binding with C-11-PBR28, a second-generation radioligand for TSPO. Methods: C-11-PBR28 PET imaging was performed in 21 healthy controls, 11 individuals with mild cognitive impairment, and 25 AD patients. Group differences in C-11-PBR28 binding were compared using 2 methods. The first was the gold standard method of calculating total distribution volume (VT), using the 2-tissue-compartment model with the arterial input function, corrected for plasma-free fraction of radiotracer (fP). The second method used a ratio of brain uptake in target regions to that in cerebellum-that is, standardized uptake value ratio (SUVR). Results: Using absolute quantitation, we confirmed that TSPO binding (VT/fP) was greater in AD patients than in healthy controls in expected temporoparietal regions and was not significantly different among the 3 groups in the cerebellum. When the cerebellum was used as a pseudo-reference region, the SUVR method detected greater binding in AD patients than controls in the same regions as absolute quantification and in 1 additional region, suggesting SUVR may have greater sensitivity. Coefficients of variation of SUVR measurements were about two-thirds lower than those of absolute quantification, and the resulting statistical significance was much higher for SUVR when comparing AD and healthy controls (e.g., P < 0.0005 for SUVR vs. P = 0.023 for V-T/fP in combined middle and inferior temporal cortex). Conclusion: To measure TSPO density in AD patients and control subjects, a simple ratio method SUVR can substitute for, and may even be more sensitive than, absolute quantitation. The SUVR method is expected to improve subject tolerability by allowing shorter scanning time and not requiring arterial catheterization. In addition, this ratio method allows smaller sample sizes for comparable statistical significance because of the relatively low variability of the ratio values.
C1 [Lyoo, Chul Hyoung] Yonsei Univ, Coll Med, Gangnam Severance Hosp, Dept Nephrol, Seoul 120749, South Korea.
[Lyoo, Chul Hyoung; Ikawa, Masamichi; Liow, Jeih-San; Zoghbi, Sami S.; Morse, Cheryl L.; Pike, Victor W.; Fujita, Masahiro; Innis, Robert B.; Kreisl, William Charles] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Kreisl, William Charles] Columbia Univ, Med Ctr, Taub Inst Res Alzheimers Dis & Aging Brain, New York, NY USA.
RP Kreisl, WC (reprint author), Taub Inst, Dept Neurol, 622 W 168th St,PH 19th Floor, New York, NY 10032 USA.
EM kreislw@mail.nih.gov
FU Intramural Research Program of the National Institute of Mental Health,
National Institutes of Health (IRP-NIMH-NIH); American Academy of
Neurology Foundation [NCT00613119, 08-M-0066]
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This project was funded in part by the Intramural Research
Program of the National Institute of Mental Health, National Institutes
of Health (IRP-NIMH-NIH), and a fellowship award from the American
Academy of Neurology Foundation, under clinicaltrials.gov identifier
NCT00613119 (protocol # 08-M-0066). No other potential conflict of
interest relevant to this article was reported.
NR 25
TC 23
Z9 23
U1 0
U2 5
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY 1
PY 2015
VL 56
IS 5
BP 701
EP 706
DI 10.2967/jnumed.114.146027
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CH2CB
UT WOS:000353831000015
PM 25766898
ER
PT J
AU Grady, PA
Rosenbaum, LM
AF Grady, Patricia A.
Rosenbaum, Louise M.
TI The Science of Caregiver Health
SO JOURNAL OF NURSING SCHOLARSHIP
LA English
DT Editorial Material
ID INTERVENTIONS; METAANALYSIS
C1 [Grady, Patricia A.; Rosenbaum, Louise M.] NINR, NIH, Bethesda, MD 20892 USA.
RP Grady, PA (reprint author), NINR, NIH, Bethesda, MD 20892 USA.
EM rosenbauml@mail.nih.gov
FU Intramural NIH HHS [Z99 NR999999]
NR 6
TC 2
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6546
EI 1547-5069
J9 J NURS SCHOLARSHIP
JI J. Nurs. Scholarsh.
PD MAY
PY 2015
VL 47
IS 3
BP 197
EP 199
DI 10.1111/jnu.12137
PG 3
WC Nursing
SC Nursing
GA CH4ER
UT WOS:000353986300002
PM 25809219
ER
PT J
AU Jenkins, J
Calzone, KA
Caskey, S
Culp, S
Weiner, M
Badzek, L
AF Jenkins, Jean
Calzone, Kathleen A.
Caskey, Sarah
Culp, Stacey
Weiner, Marsha
Badzek, Laurie
TI Methods of Genomic Competency Integration in Practice
SO JOURNAL OF NURSING SCHOLARSHIP
LA English
DT Article
DE Champions; competency; education; genomics; nursing
ID NURSING PRACTICE
AB PurposeGenomics is increasingly relevant to health care, necessitating support for nurses to incorporate genomic competencies into practice. The primary aim of this project was to develop, implement, and evaluate a year-long genomic education intervention that trained, supported, and supervised institutional administrator and educator champion dyads to increase nursing capacity to integrate genomics through assessments of program satisfaction and institutional achieved outcomes.
DesignLongitudinal study of 23 Magnet Recognition Program (R) Hospitals (21 intervention, 2 controls) participating in a 1-year new competency integration effort aimed at increasing genomic nursing competency and overcoming barriers to genomics integration in practice.
MethodsChampion dyads underwent genomic training consisting of one in-person kick-off training meeting followed by monthly education webinars. Champion dyads designed institution-specific action plans detailing objectives, methods or strategies used to engage and educate nursing staff, timeline for implementation, and outcomes achieved. Action plans focused on a minimum of seven genomic priority areas: champion dyad personal development; practice assessment; policy content assessment; staff knowledge needs assessment; staff development; plans for integration; and anticipated obstacles and challenges. Action plans were updated quarterly, outlining progress made as well as inclusion of new methods or strategies. Progress was validated through virtual site visits with the champion dyads and chief nursing officers. Descriptive data were collected on all strategies or methods utilized, and timeline for achievement. Descriptive data were analyzed using content analysis.
FindingsThe complexity of the competency content and the uniqueness of social systems and infrastructure resulted in a significant variation of champion dyad interventions.
ConclusionsNursing champions can facilitate change in genomic nursing capacity through varied strategies but require substantial training in order to design and implement interventions.
Clinical RelevanceGenomics is critical to the practice of all nurses. There is a great opportunity and interest to address genomic knowledge deficits in the practicing nurse workforce as a strategy to improve patient outcomes. Exemplars of champion dyad interventions designed to increase nursing capacity focus on improving education, policy, and healthcare services.
C1 [Jenkins, Jean] NHGRI, Genom Healthcare Branch, Div Policy Commun & Educ, NIH, Bethesda, MD 20892 USA.
[Calzone, Kathleen A.] NCI, Res, NIH, Ctr Canc Res,Genet Branch, Bethesda, MD 20892 USA.
[Caskey, Sarah; Culp, Stacey; Badzek, Laurie] W Virginia Univ, Sch Nursing, Morgantown, WV 26506 USA.
[Weiner, Marsha] Keiser Univ, Sarasota, FL USA.
RP Jenkins, J (reprint author), NHGRI, Genom Healthcare Branch, Div Policy Commun & Educ, NIH, Bldg 31 Rm 4B09, Bethesda, MD 20892 USA.
EM jean.jenkins@nih.gov
FU National Council of State Boards of Nursing; West Virginia University;
Intramural Research Program of the National Institutes of Health,
National Cancer Institute; National Human Genome Research Institute,
Division of Policy, Communications, and Education
FX This research was funded through a grant from the National Council of
State Boards of Nursing, and supported by West Virginia University and
the Intramural Research Program of the National Institutes of Health,
National Cancer Institute, and National Human Genome Research Institute,
Division of Policy, Communications, and Education.
NR 15
TC 3
Z9 3
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6546
EI 1547-5069
J9 J NURS SCHOLARSHIP
JI J. Nurs. Scholarsh.
PD MAY
PY 2015
VL 47
IS 3
BP 200
EP 210
DI 10.1111/jnu.12131
PG 11
WC Nursing
SC Nursing
GA CH4ER
UT WOS:000353986300003
PM 25808828
ER
PT J
AU Kirrane, EF
Bowman, C
Davis, JA
Hoppin, JA
Blair, A
Chen, HL
Patel, MM
Sandler, DP
Tanner, CM
Vinikoor-Imler, L
Ward, MH
Luben, TJ
Kamel, F
AF Kirrane, Ellen F.
Bowman, Christal
Davis, J. Allen
Hoppin, Jane A.
Blair, Aaron
Chen, Honglei
Patel, Molini M.
Sandler, Dale P.
Tanner, Caroline M.
Vinikoor-Imler, Lisa
Ward, Mary H.
Luben, Thomas J.
Kamel, Freya
TI Associations of Ozone and PM2.5 Concentrations With Parkinson's Disease
Among Participants in the Agricultural Health Study
SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID FINE PARTICULATE MATTER; LONG-TERM EXPOSURE; AIR-POLLUTION; COGNITIVE
FUNCTION; CARDIOVASCULAR MORTALITY; OXIDATIVE STRESS; OLDER-ADULTS; US
ADULTS; BRAIN; COHORT
AB Objective: This study describes associations of ozone and fine particulate matter with Parkinson's disease observed among farmers in North Carolina and Iowa. Methods: We used logistic regression to determine the associations of these pollutants with self-reported, doctor-diagnosed Parkinson's disease. Daily predicted pollutant concentrations were used to derive surrogates of long-term exposure and link them to study participants' geocoded addresses. Results: We observed positive associations of Parkinson's disease with ozone (odds ratio = 1.39; 95% CI: 0.98 to 1.98) and fine particulate matter (odds ratio = 1.34; 95% CI: 0.93 to 1.93) in North Carolina but not in Iowa. Conclusions: The plausibility of an effect of ambient concentrations of these pollutants on Parkinson's disease risk is supported by experimental data demonstrating damage to dopaminergic neurons at relevant concentrations. Additional studies are needed to address uncertainties related to confounding and to examine temporal aspects of the associations we observed.
C1 [Kirrane, Ellen F.; Bowman, Christal; Davis, J. Allen; Patel, Molini M.; Vinikoor-Imler, Lisa; Luben, Thomas J.] US EPA, Natl Ctr Environm Assessment, Off Res & Dev, Res Triangle Pk, NC 27709 USA.
[Hoppin, Jane A.; Chen, Honglei; Sandler, Dale P.; Kamel, Freya] NIEHS, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Blair, Aaron; Ward, Mary H.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Rockville, MD USA.
[Tanner, Caroline M.] San Francisco VA Med Ctr, Parkinsons Dis Res Educ & Clin Ctr, San Francisco, CA USA.
[Tanner, Caroline M.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
RP Kirrane, EF (reprint author), US EPA, Natl Ctr Environm Assessment, Off Res & Dev, 109 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM kirrane.ellen@epa.gov
OI Kamel, Freya/0000-0001-5052-6615; Sandler, Dale/0000-0002-6776-0018;
Chen, Honglei/0000-0003-3446-7779
FU intramural research program of the National Institutes of Health;
National Institute of Environmental Health Sciences [Z01-ES049030];
National Cancer Institute [Z01-CP010119]
FX This work was supported in part by the intramural research program of
the National Institutes of Health, the National Institute of
Environmental Health Sciences (Z01-ES049030), and National Cancer
Institute (Z01-CP010119). Data were obtained from Agricultural Health
Study data release versions P1REL0906.00 (for phase 1), P2REL0907.00
(phase 2), and P3RREL0901 (phase 3). The views expressed in this article
are those of the authors and do not necessarily represent the views or
policies of the US Environmental Protection Agency. Dr Caroline Tanner
has served as a consultant to Pfizer Pharmaceuticals, a manufacturer of
treatments for Parkinson's disease. No other potential conflicts of
interest were declared.
NR 46
TC 5
Z9 5
U1 3
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1076-2752
EI 1536-5948
J9 J OCCUP ENVIRON MED
JI J. Occup. Environ. Med.
PD MAY
PY 2015
VL 57
IS 5
BP 509
EP 517
DI 10.1097/JOM.0000000000000451
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CH7NY
UT WOS:000354225000006
PM 25951420
ER
PT J
AU Bunt, CW
Burke, HB
Towbin, AJ
Hoang, A
Stephens, MB
Fontelo, P
Liu, F
Gimbel, RW
AF Bunt, Christopher W.
Burke, Harry B.
Towbin, Alexander J.
Hoang, Albert
Stephens, Mark B.
Fontelo, Paul
Liu, Fang
Gimbel, Ronald W.
TI Point-of-Care Estimated Radiation Exposure and Imaging Guidelines Can
Reduce Pediatric Radiation Burden
SO JOURNAL OF THE AMERICAN BOARD OF FAMILY MEDICINE
LA English
DT Article
DE Clinical Decision Support Systems; Decision Making; Evidence-Based
Medicine; Radiation; Radiology
ID CT
AB Introduction: The steady increase in the use of computed tomography (CT) has particular concerns for children. Family physicians must often select pediatric imaging without any decision support. We hypothesized that point-of-care decision support would lead to the selection of imaging that lowered radiation exposure and improved guideline congruence.
Methods: Our double-blind, randomized simulation included family physicians in the Military Health System. Participants initially reviewed a pediatric hematuria scenario and selected imaging without decision support. Participants were subsequently randomized to either receive imaging-appropriateness guidelines and then estimated radiation exposure information or receive estimated radiation information then guidelines; imaging selections were required after each step. The primary outcome was the selected imaging modality with point-of-care decision support.
Results: The first arm increased CT ordering after viewing the guidelines (P = .008) but then decreased it after reviewing radiation exposure information (P = .007). In the second arm radiation information decreased CT and plain film use (P = not significant), with a subsequent increase in ultrasound and CT after the guideline presentation (P = .05).
Conclusions: Decision support during a simulated pediatric scenario helped family physicians select imaging that lowered radiation exposure and was aligned with current guidelines, especially when presented with radiation information after guideline review. This information could help inform electronic medical record design.
C1 [Bunt, Christopher W.; Stephens, Mark B.] Uniformed Serv Univ Hlth Sci, Dept Family Med, Bethesda, MD 20814 USA.
[Burke, Harry B.; Hoang, Albert] Uniformed Serv Univ Hlth Sci, Dept Med, Bethesda, MD 20814 USA.
[Towbin, Alexander J.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat Radiol, Cincinnati, OH 45229 USA.
[Fontelo, Paul; Liu, Fang] Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD USA.
[Gimbel, Ronald W.] Clemson Univ, Dept Publ Hlth Sci, Clemson, SC USA.
RP Bunt, CW (reprint author), Uniformed Serv Univ Hlth Sci, Dept Family Med, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM christopher.bunt@usuhs.edu
OI Bunt, Christopher/0000-0002-5130-6902; Towbin,
Alexander/0000-0003-1729-5071
FU Uniformed Services University [R02930.4]; US Department of Defense
Patient Safety Program
FX Intramural funding was provided by the Uniformed Services University
(grant no. R02930.4) and the US Department of Defense Patient Safety
Program.
NR 11
TC 1
Z9 1
U1 0
U2 1
PU AMER BOARD FAMILY MEDICINE
PI LEXINGTON
PA 2228 YOUNG DR, LEXINGTON, KY 40505 USA
SN 1557-2625
EI 1558-7118
J9 J AM BOARD FAM MED
JI J. Am. Board Fam. Med.
PD MAY-JUN
PY 2015
VL 28
IS 3
BP 343
EP 350
DI 10.3122/jabfm.2015.03.140251
PG 8
WC Primary Health Care; Medicine, General & Internal
SC General & Internal Medicine
GA CH8HR
UT WOS:000354277700009
PM 25957367
ER
PT J
AU Recuenco, MC
Ohmori, T
Tanigawa, S
Taguchi, A
Fujimura, S
Conti, MA
Wei, QZ
Kiyonari, H
Abe, T
Adelstein, RS
Nishinakamura, R
AF Recuenco, Mariam C.
Ohmori, Tomoko
Tanigawa, Shunsuke
Taguchi, Atsuhiro
Fujimura, Sayoko
Conti, Mary Anne
Wei, Qize
Kiyonari, Hiroshi
Abe, Takaya
Adelstein, Robert S.
Nishinakamura, Ryuichi
TI Nonmuscle Myosin II Regulates the Morphogenesis of Metanephric
Mesenchyme-Derived Immature Nephrons
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID KIDNEY DEVELOPMENT; AFRICAN-AMERICANS; HEAVY-CHAIN; MURINE HOMOLOG;
RENAL-DISEASE; MYH9; GENE; CELLS; PROLIFERATION; EXPRESSION
AB The kidney develops from reciprocal interactions between the metanephric mesenchyme and ureteric bud. The mesenchyme transforms into epithelia and forms complicated nephron structures, whereas the ureteric bud extends its pre-existing epithelial ducts. Although the roles are well established for extracellular stimuli, such as Wnt and Notch, it is unclear how the intracellular cytoskeleton regulates these morphogenetic processes. Myh9 and Myh10 encode nonmuscle myosin II heavy chains, and Myh9 mutations in humans are implicated in congenital kidney diseases and focal segmental glomerulosclerosis in adults. Here, we analyzed the roles of Myh9 and Myh10 in the developing kidney. Ureteric bud-specific depletion of Myh9 resulted in no apparent phenotypes, whereas mesenchyme-specific Myh9 deletion caused proximal tubule dilations and renal failure. Mesenchyme-specific Myh9/Myh10 mutant mice died shortly after birth and showed a severe defect in nephron formation. The nascent mutant nephrons failed to form a continuous lumen, which likely resulted from impaired apical constriction of the elongating tubules. In addition, nephron progenitors lacking Myh9/Myh10 or the possible interactor Kif26b were less condensed at midgestation and reduced at birth. Taken together, nonmuscle myosin II regulates the morphogenesis of immature nephrons derived from the metanephric mesenchyme and the maintenance of nephron progenitors. Our data also suggest that Myh9 deletion in mice results in failure to maintain renal tubules but not in glomerulosclerosis.
C1 [Recuenco, Mariam C.; Ohmori, Tomoko; Tanigawa, Shunsuke; Taguchi, Atsuhiro; Nishinakamura, Ryuichi] Kumamoto Univ, Dept Kidney Dev, Kumamoto 8600811, Japan.
[Fujimura, Sayoko] Kumamoto Univ, Inst Mol Embryol & Genet, Liaison Lab Res Promot Ctr, Kumamoto 8600811, Japan.
[Conti, Mary Anne; Wei, Qize; Adelstein, Robert S.] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
[Kiyonari, Hiroshi; Abe, Takaya] RIKEN Ctr Dev Biol, Lab Anim Resources & Genet Engn, Kobe, Hyogo, Japan.
RP Nishinakamura, R (reprint author), Kumamoto Univ, Inst Mol Embryol & Genet, Dept Kidney Dev, 2-2-1 Honjo, Kumamoto 8600811, Japan.
EM ryuichi@kumamoto-u.ac.jp
RI Kiyonari, Hiroshi/N-7936-2015;
OI Taguchi, Atsuhiro/0000-0003-1741-2987; Adelstein,
Robert/0000-0002-8683-2144
FU KAKENHI from the Ministry of Education, Culture, Sports, Science and
Technology, Japan [24112518, 24790851]
FX This study was supported by KAKENHI Grants 24112518 and 24790851 from
the Ministry of Education, Culture, Sports, Science and Technology,
Japan.
NR 33
TC 3
Z9 3
U1 0
U2 2
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 MAY
PY 2015
VL 26
IS 5
BP 1081
EP 1091
DI 10.1681/ASN.2014030281
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA CH2PX
UT WOS:000353868200012
PM 25168025
ER
PT J
AU Woodard, T
Sigurdsson, S
Gotal, JD
Torjesen, AA
Inker, LA
Aspelund, T
Eiriksdottir, G
Gudnason, V
Harris, TB
Launer, LJ
Levey, AS
Mitchell, GF
AF Woodard, Todd
Sigurdsson, Sigurdur
Gotal, John D.
Torjesen, Alyssa A.
Inker, Lesley A.
Aspelund, Thor
Eiriksdottir, Gudny
Gudnason, Vilmundur
Harris, Tamara B.
Launer, Lenore J.
Levey, Andrew S.
Mitchell, Gary F.
TI Mediation Analysis of Aortic Stiffness and Renal Microvascular Function
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; PULSE-WAVE VELOCITY; GLOMERULAR-FILTRATION-RATE;
ARTERIAL STIFFNESS; GENE/ENVIRONMENT SUSCEPTIBILITY; MORTALITY;
PULSATILITY; REYKJAVIK; PRESSURE; SURVIVAL
AB Aortic stiffening, assessed by carotid-femoral pulse wave velocity, is associated with CKD. Transmission of excessive flow pulsatility into the low-impedance renal microvasculature may mediate this association. However, direct analyses of macrovascular-microvascular relations in the kidney are limited. Using arterial tonometry, iohexol clearance, and magnetic resonance imaging, we related arterial stiffness, GFR, urinary albumin excretion, and potential mediators, including renal artery pulsatility index, renal vascular resistance, and arterial volume in the cortex, in 367 older adults (ages 72-92 years) participating in the Age, Gene/Environment Susceptibility-Reykjavik Study. In a model adjusted for age, sex, heart rate, and body size, aortic stiffness was related to GFR (Slope of regression B=-2.28 +/- 0.85 ml/min per SD, P=0.008) but not urine albumin (P=0.09). After accounting for pulsatility index, the relation between aortic stiffness and GFR was no longer significant (P=0.10). Mediation analysis showed that 34% of the relation between aortic stiffness and GFR was mediated by pulsatility index (95% confidence interval of indirect effect, -1.35 to -0.29). An additional 20% or 36% of the relation was mediated by lower arterial volume in the cortex or higher renal vascular resistance, respectively, when offered as mediators downstream from higher pulsatility index (95% confidence interval of indirect effect including arterial volume in the cortex, -2.22 to -0.40; 95% confidence interval of indirect effect including renal vascular resistance, -2.51 to -0.76). These analyses provide the first evidence that aortic stiffness may contribute to lower GFR by transferring excessive flow pulsatility into the susceptible renal microvasculature, leading to dynamic constriction or vessel loss.
C1 [Woodard, Todd; Gotal, John D.; Torjesen, Alyssa A.; Mitchell, Gary F.] Cardiovasc Engn Inc, Norwood, MA 02062 USA.
[Sigurdsson, Sigurdur; Aspelund, Thor; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Inker, Lesley A.; Levey, Andrew S.] Tufts Med Ctr, Dept Med, William B Schwartz Div Nephrol, Boston, MA USA.
[Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Harris, Tamara B.; Launer, Lenore J.] 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; Aspelund, Thor/C-5983-2008
OI Gudnason, Vilmundur/0000-0001-5696-0084; Aspelund,
Thor/0000-0002-7998-5433
FU National Institutes of Health [N01-AG-12100]; National Institute on
Aging Intramural Research Program; Althingi (the Icelandic Parliament);
National Institutes of Health National Heart, Lung and Blood Institute
[HL094898]; National Institutes of Health National Institute of Diabetes
and Digestive and Kidney Diseases [DK082447]; Hjartavernd (the Icelandic
Heart Association)
FX This work was supported by National Institutes of Health Grant
N01-AG-12100, the National Institute on Aging Intramural Research
Program, Hjartavernd (the Icelandic Heart Association), the Althingi
(the Icelandic Parliament), National Institutes of Health National
Heart, Lung and Blood Institute Grant HL094898, and National Institutes
of Health National Institute of Diabetes and Digestive and Kidney
Diseases Grant DK082447.
NR 29
TC 16
Z9 17
U1 0
U2 2
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 MAY
PY 2015
VL 26
IS 5
BP 1181
EP 1187
DI 10.1681/ASN.2014050450
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA CH2PX
UT WOS:000353868200021
PM 25294231
ER
PT J
AU Badirou, I
Pan, J
Souquere, S
Legrand, C
Pierron, G
Wang, A
Eckly, A
Roy, A
Gachet, C
Vainchenker, W
Chang, Y
Leon, C
AF Badirou, I.
Pan, J.
Souquere, S.
Legrand, C.
Pierron, G.
Wang, A.
Eckly, A.
Roy, A.
Gachet, C.
Vainchenker, W.
Chang, Y.
Leon, C.
TI Distinct localizations and roles of non-muscle myosin II during
proplatelet formation and platelet release
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE megakaryocyte; Non-muscle myosin type IIA; Non-muscle myosin type IIB;
platelet; stem cell
ID RESTRICTED MYH9 INACTIVATION; CONTRACTILE RING; ISOFORM; MICE;
POLYPLOIDIZATION; INHIBITION; EXPRESSION; DEFECTS; RUNX1; TAIL
AB BackgroundAt the end of maturation, megakaryocytes (MKs) form long cytoplasmic extensions called proplatelets (PPT). Enormous changes in cytoskeletal structures cause PPT to extend further, to re-localize organelles such as mitochondria and to fragment, leading to platelet release. Two non-muscle myosin IIs (NMIIs) are expressed in MKs; however, only NMII-A (MYH9), but not NMII-B (MYH10), is expressed in mature MKs and is implicated in PPT formation.
ObjectivesTo provide invivo evidence on the specific role of NMII-A and IIB in MK PPT formation.
MethodsWe studied two transgenic mouse models in which non-muscle myosin heavy chain (NMHC) II-A was genetically replaced either by II-B or by a chimeric NMHCII that combined the head domain of II-A with the rod and tail domains of II-B.
Results and ConclusionsThis work demonstrates that the kinetic properties of NM-IIA, depending on the N-terminal domain, render NMII-A the better NMII candidate to control PPT formation. Furthermore, the carboxyl-terminal domain determines myosin II localization in the constriction region of PPT and is responsible for the specific role of NMII in platelet release.
C1 [Badirou, I.; Pan, J.; Legrand, C.; Eckly, A.; Roy, A.; Gachet, C.; Vainchenker, W.; Chang, Y.; Leon, C.] INSERM, Villejuif, France.
[Badirou, I.; Pan, J.; Souquere, S.; Legrand, C.; Pierron, G.; Roy, A.; Vainchenker, W.; Chang, Y.] Univ Paris Sud, F-94275 Le Kremlin Bicetre, France.
[Badirou, I.; Pan, J.; Souquere, S.; Legrand, C.; Pierron, G.; Roy, A.; Vainchenker, W.; Chang, Y.] Inst Gustave Roussy, Villejuif, France.
[Souquere, S.; Pierron, G.] CNRS, Villejuif, France.
[Wang, A.] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
[Eckly, A.; Gachet, C.; Leon, C.] Etab Francais Sang Alsace, Strasbourg, France.
[Eckly, A.; Gachet, C.; Leon, C.] Univ Strasbourg, Fac Med, Strasbourg, France.
[Eckly, A.; Gachet, C.; Leon, C.] Federat Med Translat, Strasbourg, France.
RP Chang, Y (reprint author), INSERM, U1009, Villejuif, France.
EM yunhua.chang-marchand@inserm.fr
RI leon, catherine/G-6473-2015; Gachet, Christian/H-9156-2016
OI leon, catherine/0000-0002-8597-9929;
FU INSERM; Agence Nationale de la Recherche (ANR Jeune chercheur); la Ligue
Nationale Contre le Cancer; ANR; China Scholarship Council; la Societe
Francaise d'Hematologie; la Fondation de la Recherche Medicale (FRM)
FX This work was supported by INSERM, by the Agence Nationale de la
Recherche (ANR Jeune chercheur) (Y. Chang), and by grants from la Ligue
Nationale Contre le Cancer (Equipe labellisee 2012). I. Badirou was
supported by the ANR, and J. Pan by the China Scholarship Council and la
Societe Francaise d'Hematologie. A. Roy is supported by a grant from la
Fondation de la Recherche Medicale (FRM). We thank L. Lodier, J. Weber
and P. Laeuffer for their technical help.
NR 19
TC 1
Z9 2
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
EI 1538-7836
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD MAY
PY 2015
VL 13
IS 5
BP 851
EP 859
DI 10.1111/jth.12887
PG 9
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CH8AU
UT WOS:000354259000021
PM 25736522
ER
PT J
AU Dimichele, DM
Lacroix-Desmazes, S
Peyvandi, F
Srivastava, A
Rosendaal, FR
AF Dimichele, D. M.
Lacroix-Desmazes, S.
Peyvandi, F.
Srivastava, A.
Rosendaal, F. R.
CA Subcomm Factor VIII Factor IX Rare
TI Design of clinical trials for new products in hemophilia: communication
from the SSC of the ISTH
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
ID FACTOR-VIII PRODUCTS; INHIBITOR DEVELOPMENT; EUROPEAN GUIDELINES;
EVOLUTION; CHILDREN
C1 [Dimichele, D. M.] NHLBI, Div Blood Dis & Resources, NIH, Bethesda, MD 20892 USA.
[Lacroix-Desmazes, S.] Univ Paris 05, Univ Paris 06, Ctr Rech Cordeliers, INSERM,UMR S 1138, Paris, France.
[Peyvandi, F.] Univ Milan, Angelo Bianchi Bonomi Hemophilia & Thrombosis Ctr, Fdn IRCCS Ca Granda Osped Maggiore Policlin, Fdn Luigi Villa, Milan, Italy.
[Peyvandi, F.] Univ Milan, Dept Pathophysiol & Transplantat, Milan, Italy.
[Srivastava, A.] Christian Med Coll & Hosp, Dept Hematol, Vellore, Tamil Nadu, India.
[Rosendaal, F. R.] Leiden Univ, Dept Clin Epidemiol, Med Ctr, Leiden, Netherlands.
[Rosendaal, F. R.] Leiden Univ, Dept Thrombosis & Haemostasis, Med Ctr, Leiden, Netherlands.
RP Dimichele, DM (reprint author), NHLBI, Div Blood Dis & Resources, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM donna.dimichele@nih.gov
OI Peyvandi, Flora/0000-0001-7423-9864
FU Novo Nordisk; Biotest; Kedrion Biopharma; CSL Behring; LFB; Grifols;
Bayer; Baxter; Biokit; Alnylam; Octapharma
FX F. Peyvandi reports grants and personal fees from Novo Nordisk, Biotest,
and Kedrion Biopharma and personal fees from CSL Behring, LFB, Grifols,
Bayer, Baxter, Biokit, Alnylam and Octapharma outside the submitted
work. All other authors state that they have no conflict of interest.
NR 14
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
EI 1538-7836
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD MAY
PY 2015
VL 13
IS 5
BP 876
EP 879
DI 10.1111/jth.12882
PG 4
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CH8AU
UT WOS:000354259000024
PM 25728341
ER
PT J
AU Kusek, JW
AF Kusek, John W.
TI Is it time to tip your glass to prevent CKD?
SO KIDNEY INTERNATIONAL
LA English
DT Editorial Material
ID CHRONIC KIDNEY-DISEASE; ALCOHOL-CONSUMPTION; FUNCTION DECLINE;
FOLLOW-UP; RISK; POPULATION; MEN
AB Chronic kidney disease (CKD) is a major global medical and public health challenge. On the basis primarily of a modest number of prospective epidemiological studies, it appears that alcohol consumption reduces the risk of CKD in the general population. Our understanding of the potential benefits of alcohol consumption with regard to CKD is likely to evolve in the future and will be informed primarily by observational epidemiological studies.
C1 NIDDK, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
RP Kusek, JW (reprint author), NIDDK, Div Kidney Urol & Hematol Dis, NIH, Room 617,6707 Democracy Blvd,Two Democracy Plaza, Bethesda, MD 20892 USA.
EM kusekj@extra.niddk.nih.gov
FU Intramural NIH HHS [Z99 DK999999]
NR 9
TC 0
Z9 0
U1 1
U2 2
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 MAY
PY 2015
VL 87
IS 5
BP 877
EP 879
DI 10.1038/ki.2015.54
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA CH5HS
UT WOS:000354066900003
PM 25951066
ER
PT J
AU Gorski, M
Tin, A
Garnaas, M
McMahon, GM
Chu, AY
Tayo, BO
Pattaro, C
Teumer, A
Chasman, DI
Chalmers, J
Hamet, P
Tremblay, J
Woodward, M
Aspelund, T
Eiriksdottir, G
Gudnason, V
Harris, TB
Launer, LJ
Smith, AV
Mitchell, BD
O'Connell, JR
Shuldiner, AR
Coresh, J
Li, M
Freudenberger, P
Hofer, E
Schmidt, H
Schmidt, R
Holliday, EG
Mitchell, P
Wang, JJ
de Boer, IH
Li, G
Siscovick, DS
Kutalik, Z
Corre, T
Vollenweider, P
Waeber, G
Gupta, J
Kanetsky, PA
Hwang, SJ
Olden, M
Yang, Q
de Andrade, M
Atkinson, EJ
Kardia, SLR
Turner, ST
Stafford, JM
Ding, JZ
Liu, YM
Barlassina, C
Cusi, D
Salvi, E
Staessen, JA
Ridker, PM
Grallert, H
Meisinger, C
Muller-Nurasyid, M
Kramer, BK
Kramer, H
Rosas, SE
Nolte, IM
Penninx, BW
Snieder, H
Del Greco, MF
Franke, A
Nothlings, U
Lieb, W
Bakker, SJL
Gansevoort, RT
van der Harst, P
Dehghan, A
Franco, OH
Hofman, A
Rivadeneira, F
Sedaghat, S
Uitterlinden, AG
Coassin, S
Haun, M
Kollerits, B
Kronenberg, F
Paulweber, B
Aumann, N
Endlich, K
Pietzner, M
Volker, U
Rettig, R
Chouraki, V
Helmer, C
Lambert, JC
Metzger, M
Stengel, B
Lehtimaki, T
Lyytikainen, LP
Raitakari, O
Johnson, A
Parsa, A
Bochud, M
Heid, IM
Goessling, W
Kottgen, A
Kao, WHL
Fox, CS
Boger, CA
AF Gorski, Mathias
Tin, Adrienne
Garnaas, Maija
McMahon, Gearoid M.
Chu, Audrey Y.
Tayo, Bamidele O.
Pattaro, Cristian
Teumer, Alexander
Chasman, Daniel I.
Chalmers, John
Hamet, Pavel
Tremblay, Johanne
Woodward, Marc
Aspelund, Thor
Eiriksdottir, Gudny
Gudnason, Vilmundur
Harris, Tamara B.
Launer, Lenore J.
Smith, Albert V.
Mitchell, Braxton D.
O'Connell, Jeffrey R.
Shuldiner, Alan R.
Coresh, Josef
Li, Man
Freudenberger, Paul
Hofer, Edith
Schmidt, Helena
Schmidt, Reinhold
Holliday, Elizabeth G.
Mitchell, Paul
Wang, Jie Jin
de Boer, Ian H.
Li, Guo
Siscovick, David S.
Kutalik, Zoltan
Corre, Tanguy
Vollenweider, Peter
Waeber, Gerard
Gupta, Jayanta
Kanetsky, Peter A.
Hwang, Shih-Jen
Olden, Matthias
Yang, Qiong
de Andrade, Mariza
Atkinson, Elizabeth J.
Kardia, Sharon L. R.
Turner, Stephen T.
Stafford, Jeanette M.
Ding, Jingzhong
Liu, Yongmei
Barlassina, Cristina
Cusi, Daniele
Salvi, Erika
Staessen, Jan A.
Ridker, Paul M.
Grallert, Harald
Meisinger, Christa
Mueller-Nurasyid, Martina
Kraemer, Bernhard K.
Kramer, Holly
Rosas, Sylvia E.
Nolte, Ilja M.
Penninx, Brenda W.
Snieder, Harold
Del Greco, M. Fabiola
Franke, Andre
Noethlings, Ute
Lieb, Wolfgang
Bakker, Stephan J. L.
Gansevoort, Ron T.
van der Harst, Pim
Dehghan, Abbas
Franco, Oscar H.
Hofman, Albert
Rivadeneira, Fernando
Sedaghat, Sanaz
Uitterlinden, Andre G.
Coassin, Stefan
Haun, Margot
Kollerits, Barbara
Kronenberg, Florian
Paulweber, Bernhard
Aumann, Nicole
Endlich, Karlhans
Pietzner, Mike
Voelker, Uwe
Rettig, Rainer
Chouraki, Vincent
Helmer, Catherine
Lambert, Jean-Charles
Metzger, Marie
Stengel, Benedicte
Lehtimaki, Terho
Lyytikainen, Leo-Pekka
Raitakari, Olli
Johnson, Andrew
Parsa, Afshin
Bochud, Murielle
Heid, Iris M.
Goessling, Wolfram
Kottgen, Anna
Kao, W. H. Linda
Fox, Caroline S.
Boeger, Carsten A.
TI Genome-wide association study of kidney function decline in individuals
of European descent
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE chronic kidney disease; genome-wide association study; kidney function
decline; kidney development; population genetics; single nucleotide
polymorphism; zebrafish
ID GLOMERULAR-FILTRATION-RATE; STAGE RENAL-DISEASE; SYNDROME TYPE 1D;
HYPERTENSIVE NEPHROSCLEROSIS; DIABETIC-NEPHROPATHY; DEAFNESS DFNB12;
MORTALITY RISK; MOUSE MODEL; GENE; PROGRESSION
AB Genome-wide association studies (GWASs) have identified multiple loci associated with cross-sectional eGFR, but a systematic genetic analysis of kidney function decline over time is missing. Here we conducted a GWAS meta-analysis among 63,558 participants of European descent, initially from 16 cohorts with serial kidney function measurements within the CKDGen Consortium, followed by independent replication among additional participants from 13 cohorts. In stage 1 GWAS meta-analysis, single-nucleotide polymorphisms (SNPs) at MEOX2, GALNT11, IL1RAP, NPPA, HPCAL1, and CDH23 showed the strongest associations for at least one trait, in addition to the known UMOD locus, which showed genome-wide significance with an annual change in eGFR. In stage 2 meta-analysis, the significant association at UMOD was replicated. Associations at GALNT11 with Rapid Decline (annual eGFR decline of 3 ml/min per 1.73m(2) or more), and CDH23 with eGFR change among those with CKD showed significant suggestive evidence of replication. Combined stage 1 and 2 meta-analyses showed significance for UMOD, GALNT11, and CDH23. Morpholino knockdowns of galnt11 and cdh23 in zebrafish embryos each had signs of severe edema 72 h after gentamicin treatment compared with controls, but no gross morphological renal abnormalities before gentamicin administration. Thus, our results suggest a role in the deterioration of kidney function for the loci GALNT11 and CDH23, and show that the UMOD locus is significantly associated with kidney function decline.
C1 [Gorski, Mathias; Olden, Matthias; Heid, Iris M.] Univ Regensburg, Inst Epidemiol & Prevent Med, Dept Genet Epidemiol, D-93053 Regensburg, Germany.
[Gorski, Mathias; Boeger, Carsten A.] Univ Hosp Regensburg, Dept Nephrol, D-93042 Regensburg, Germany.
[Tin, Adrienne; Coresh, Josef; Li, Man; Kottgen, Anna; Kao, W. H. Linda] Johns Hopkins Univ, Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Garnaas, Maija] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Genet,Dept Med, Boston, MA 02115 USA.
[McMahon, Gearoid M.] Brigham & Womens Hosp, Div Nephrol, Boston, MA 02115 USA.
[McMahon, Gearoid M.] Harvard Univ, Sch Med, Boston, MA USA.
[McMahon, Gearoid M.; Hwang, Shih-Jen; Olden, Matthias; Yang, Qiong; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Chu, Audrey Y.; Chasman, Daniel I.; Ridker, Paul M.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Tayo, Bamidele O.; Kramer, Holly] Loyola Univ Chicago, Loyola Med Ctr, Dept Publ Hlth Serv, Maywood, IL USA.
[Pattaro, Cristian; Del Greco, M. Fabiola] Univ Lubeck, European Acad Bozen Bolzano EURAC, Ctr Biomed, Bolzano, Italy.
[Teumer, Alexander; Voelker, Uwe] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Genom, Dept Funct Genom, Greifswald, Germany.
[Chalmers, John; Woodward, Marc] Univ Sydney, George Inst Global Hlth, Sydney, NSW 2006, Australia.
[Hamet, Pavel] Univ Montreal, Ctr Hosp, Ctr Rech, Montreal, PQ, Canada.
[Tremblay, Johanne] CHUM Res Center, Montreal, PQ, Canada.
[Aspelund, Thor; Eiriksdottir, Gudny; Gudnason, Vilmundur; Smith, Albert V.] Icelandic Heart Assoc, Res Inst, Kopavogur, Iceland.
[Aspelund, Thor; Gudnason, Vilmundur; Smith, Albert V.] Univ Iceland, Reykjavik, Iceland.
[Harris, Tamara B.; Launer, Lenore J.] NIA, Intramural Res Program, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Mitchell, Braxton D.; O'Connell, Jeffrey R.; Shuldiner, Alan R.; Parsa, Afshin] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[Mitchell, Braxton D.; O'Connell, Jeffrey R.; Shuldiner, Alan R.; Parsa, Afshin] Univ Maryland, Sch Med, Program Personalized & Genom Med, Baltimore, MD 21201 USA.
[Mitchell, Braxton D.; Shuldiner, Alan R.] Univ Maryland, Sch Med, Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21201 USA.
[Coresh, Josef; Kao, W. H. Linda] Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Freudenberger, Paul; Schmidt, Helena] Med Univ Graz, Inst Mol Biol & Biochem, Graz, Austria.
[Hofer, Edith] Med Univ Graz, Inst Med Informat Stat & Documentat, Dept Neurol, Graz, Austria.
[Schmidt, Reinhold] Med Univ Graz, Dept Neurol, Graz, Austria.
[Holliday, Elizabeth G.] Univ Newcastle, CReDITSS, HMRI, Ctr Clin Epidemiol & Biostat, Callaghan, NSW 2308, Australia.
[Mitchell, Paul; Wang, Jie Jin] Univ Sydney, Westmead Hosp, Westmead Millennium Inst, Ctr Vis Res, Sydney, NSW 2006, Australia.
[de Boer, Ian H.] Univ Washington, Seattle, WA 98195 USA.
[Li, Guo; Siscovick, David S.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Siscovick, David S.] New York Acad Med, New York, NY USA.
[Kutalik, Zoltan; Corre, Tanguy] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
[Kutalik, Zoltan] Swiss Inst Bioinformat, Dept Med Genet, Lausanne, Switzerland.
[Vollenweider, Peter; Waeber, Gerard] Univ Lausanne Hosp, Dept Internal Med, Lausanne, Switzerland.
[Gupta, Jayanta; Kanetsky, Peter A.] Univ Penn, Perelman Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Yang, Qiong] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[de Andrade, Mariza; Atkinson, Elizabeth J.; Turner, Stephen T.] Mayo Clin, Rochester, MN USA.
[Kardia, Sharon L. R.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Stafford, Jeanette M.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Ding, Jingzhong] Wake Forest Sch Med, Dept Internal Med, Winston Salem, NC USA.
[Liu, Yongmei] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Epidemiol & Prevent, Winston Salem, NC USA.
[Barlassina, Cristina; Cusi, Daniele; Salvi, Erika] Univ Milan, Dept Hlth Sci, Milan, Italy.
[Cusi, Daniele] San Paolo Hosp, Div Nephrol, Milan, Italy.
[Staessen, Jan A.] Maastricht Univ, Dept Epidemiol, NL-6200 MD Maastricht, Netherlands.
[Staessen, Jan A.] Univ Leuven, Dept Cardiovasc Sci, Div Hypertens & Cardiovasc Rehabil, Studies Coordinating Ctr, Leuven, Belgium.
[Grallert, Harald; Meisinger, Christa] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, Neuherberg, Germany.
[Grallert, Harald] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Res Unit Mol Epidemiol, Neuherberg, Germany.
[Grallert, Harald] German Ctr Diabet Res, Neuherberg, Germany.
[Mueller-Nurasyid, Martina] DZHK German Ctr Cardiovasc Res, Partner Site Munich Heart Alliance, Munich, Germany.
[Mueller-Nurasyid, Martina; Heid, Iris M.] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Genet Epidemiol, Neuherberg, Germany.
[Mueller-Nurasyid, Martina] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Mueller-Nurasyid, Martina] Univ Munich, Univ Hosp Grosshadern, Dept Med 1, Munich, Germany.
[Kraemer, Bernhard K.] Heidelberg Univ, Univ Med Ctr Mannheim, Dept Med 5, Mannheim, Germany.
[Rosas, Sylvia E.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Rosas, Sylvia E.] Harvard Univ, Sch Med, Beth Israel Med Ctr, Boston, MA USA.
[Nolte, Ilja M.; Snieder, Harold] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
[Nolte, Ilja M.; Snieder, Harold] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol FA40, Unit Genet Epidemiol & Bioinformat, NL-9713 AV Groningen, Netherlands.
[Penninx, Brenda W.] Vrije Univ Amsterdam, Med Ctr, EMGO Inst, Dept Psychiat, Amsterdam, Netherlands.
[Penninx, Brenda W.] NESDA, EMGO Inst Vumc, Amsterdam, Netherlands.
[Franke, Andre] Inst Clin Mol Biol, Kiel, Germany.
[Noethlings, Ute] Univ Hosp Schleswig Holstein, Popgen Biobank, Kiel, Germany.
[Noethlings, Ute] Univ Kiel, Inst Expt Med, Epidemiol Sect, Kiel, Germany.
[Lieb, Wolfgang] Univ Kiel, Inst Epidemiol, Kiel, Germany.
[Lieb, Wolfgang] Univ Kiel, Biobank Popgen, Kiel, Germany.
[Bakker, Stephan J. L.; Gansevoort, Ron T.] Univ Groningen, Univ Med Ctr Groningen, Dept Nephrol, Groningen, Netherlands.
[van der Harst, Pim] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, Groningen, Netherlands.
[Dehghan, Abbas; Hofman, Albert; Rivadeneira, Fernando; Sedaghat, Sanaz; Uitterlinden, Andre G.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Coassin, Stefan; Haun, Margot; Kollerits, Barbara; Kronenberg, Florian] Med Univ Innsbruck, Div Genet Epidemiol, A-6020 Innsbruck, Austria.
[Paulweber, Bernhard] Paracelsus Private Med Univ Salzburg, Dept Internal Med 1, Salzburg, Austria.
[Aumann, Nicole] Univ Med Greifswald, Inst Community Med, Dept SHIP KEF, Greifswald, Germany.
[Endlich, Karlhans] Univ Med Greifswald, Inst Anat & Cell Biol, Greifswald, Germany.
[Pietzner, Mike] Univ Med Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
[Rettig, Rainer] Ernst Moritz Arndt Univ Greifswald, Inst Physiol, Greifswald, Germany.
[Chouraki, Vincent] Univ Lille Nord France, Inst Pasteur Lille, INSERM, U744,CHR&U Lille,Serv Epidemiol Reg,CHRU, Lille, France.
[Helmer, Catherine] Univ Bordeaux 2, ISPED, INSERM, U897, F-33076 Bordeaux, France.
[Lambert, Jean-Charles] Univ Lille Nord France, Inst Pasteur Lille, INSERM, U744, Lille, France.
[Stengel, Benedicte] Univ Paris 11, INSERM, U1018, CESP Team 10, Villejuif, France.
[Lehtimaki, Terho; Lyytikainen, Leo-Pekka] Fimlab Labs, Dept Clin Chem, Tampere, Finland.
[Raitakari, Olli] Turku Univ Hosp, Dept Clin Physiol, FIN-20520 Turku, Finland.
[Raitakari, Olli] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Johnson, Andrew] NHLBI, Cardiovasc Epidemiol & Human Genom Branch, Framingham Heart Study, Framingham, MA USA.
[Bochud, Murielle] Univ Lausanne Hosp, Inst Social & Prevent Med IUMSP, Epalinges, Switzerland.
[Goessling, Wolfram] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Genet, Boston, MA 02115 USA.
[Goessling, Wolfram] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Gastroenterol, Boston, MA 02115 USA.
[Goessling, Wolfram] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Goessling, Wolfram] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Goessling, Wolfram] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Kottgen, Anna] Freiburg Univ Clin, Div Renal, Freiburg, Germany.
[Fox, Caroline S.] Brigham & Womens Hosp, Dept Endocrinol, Boston, MA 02115 USA.
RP Boger, CA (reprint author), Univ Hosp Regensburg, Dept Nephrol, Franz Josef Strauss Allee 11, D-93042 Regensburg, Germany.
EM carsten.boeger@klinik.uni-regensburg.de
RI Lyytikainen, Leo-Pekka/C-8544-2016; Stengel, Benedicte/G-5730-2015;
Cossette, Suzanne/I-8008-2016; Lambert, jean-charles/A-9553-2014; Smith,
Albert/K-5150-2015; Bochud, Murielle/A-3981-2010; Johnson,
Andrew/G-6520-2013; Franke, Andre/B-2151-2010; Lieb,
Wolfgang/C-1990-2012; Rivadeneira, Fernando/O-5385-2015; lambert,
jean-charles/F-8787-2013; Kronenberg, Florian/B-1736-2008; Colaus,
PsyColaus/K-6607-2013; Grallert, Harald/B-3424-2013; HELMER,
Catherine/I-6581-2015; Bakker, Stephan/J-4023-2015; Staessen,
Jan/A-1065-2011; Gudnason, Vilmundur/K-6885-2015; Aspelund,
Thor/C-5983-2008; Woodward, Mark/D-8492-2015; Wang, Jie Jin/P-1499-2014;
Mitchell, Paul/P-1498-2014
OI Goessling, Wolfram/0000-0001-9972-1569; Meisinger,
Christa/0000-0002-9026-6544; Salvi, Erika/0000-0002-2724-2291; Mitchell,
Braxton/0000-0003-4920-4744; Dehghan, Abbas/0000-0001-6403-016X;
Lyytikainen, Leo-Pekka/0000-0002-7200-5455; Lambert,
jean-charles/0000-0003-0829-7817; Smith, Albert/0000-0003-1942-5845;
Bochud, Murielle/0000-0002-5727-0218; Franke, Andre/0000-0003-1530-5811;
McMahon, Gearoid/0000-0002-7723-2198; Rivadeneira,
Fernando/0000-0001-9435-9441; Kronenberg, Florian/0000-0003-2229-1120;
HELMER, Catherine/0000-0002-5169-7421; Bakker,
Stephan/0000-0003-3356-6791; Staessen, Jan/0000-0002-3026-1637;
Gudnason, Vilmundur/0000-0001-5696-0084; Aspelund,
Thor/0000-0002-7998-5433; Wang, Jie Jin/0000-0001-9491-4898;
FU NIH [N01-AG-1-2100, R01 AG18728, R01 HL088119, U01 GM074518-04, U01
HL072515-06, U01 HL084756, K12RR023250, NIH P30 DK072488]; NIA
Intramural Research Program, Hjartavernd (the Icelandic Heart
Association); Althingi (the Icelandic Parliament); University of
Maryland General Clinical Research Center [M01 RR 16500]; Baltimore
Veterans Administration Medical Center Geriatrics Research and Education
Clinical Center; National Heart, Lung, and Blood Institute
[HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
HHSN268201100011C, HHSN268201100012C, R01HL087641, R01HL59367,
R01HL086694]; National Human Genome Research Institute [U01HG004402];
National Institutes of Health [HHSN268200625226C]; component of the
National Institutes of Health and NIH Roadmap for Medical Research
[UL1RR025005]; (Emmy Noether Programme) of the German Research
Foundation [KO3598/2- 1]; Austrian Science Fond (FWF) [P20545-P05,
P20545-P05 and P13180]
FX AGES: This study has been funded by NIH contract N01-AG-1-2100, the NIA
Intramural Research Program, Hjartavernd (the Icelandic Heart
Association), and the Althingi (the Icelandic Parliament). The study is
approved by the Icelandic National Bioethics Committee, VSN: 00-063. We
are indebted to the participants for their willingness to participate in
the study.; AMISH: The Amish studies are supported by grants and
contracts from the NIH including R01 AG18728 (Amish Longevity Study),
R01 HL088119 (Amish Calcification Study), U01 GM074518-04 (PAPI Study),
U01 HL072515-06 (HAPI Study), U01 HL084756 and NIH K12RR023250
(University of Maryland MCRDP), NIH P30 DK072488 (Clinical Nutrition
Research Unit), the University of Maryland General Clinical Research
Center, grant M01 RR 16500, and the Baltimore Veterans Administration
Medical Center Geriatrics Research and Education Clinical Center. We
thank our Amish research volunteers for their long-standing partnership
in research, and the research staff at the Amish Research Clinic for
their hard work and dedication.; The Atherosclerosis Risk in Communities
Study is carried out as a collaborative study supported by National
Heart, Lung, and Blood Institute contracts (HHSN268201100005C,
HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and
HHSN268201100012C), R01HL087641, R01HL59367, and R01HL086694; National
Human Genome Research Institute contract U01HG004402; and National
Institutes of Health contract HHSN268200625226C. We thank the staff and
participants of the ARIC study for their important contributions.
Infrastructure was partly supported by Grant Number UL1RR025005, a
component of the National Institutes of Health and NIH Roadmap for
Medical Research. AK was supported by the grant KO3598/2- 1 (Emmy
Noether Programme) of the German Research Foundation.; ASPS: The
research reported in this article was funded by the Austrian Science
Fond (FWF) grant number P20545-P05 and P13180. The Medical University of
Graz supports the databank of the ASPS. The authors thank the staff and
the participants of the ASPS for their valuable contributions. We thank
Birgit Reinhart for her long-term administrative commitment and Ing
Johann Semmler for the technical assistance at creating the DNA bank.
NR 53
TC 15
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U1 2
U2 16
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 MAY
PY 2015
VL 87
IS 5
BP 1017
EP 1029
DI 10.1038/ki.2014.361
PG 13
WC Urology & Nephrology
SC Urology & Nephrology
GA CH5HS
UT WOS:000354066900019
PM 25493955
ER
PT J
AU Roschewski, M
Dunleavy, K
Pittaluga, S
Moorhead, M
Pepin, F
Kong, K
Shovlin, M
Jaffe, ES
Staudt, LM
Lai, C
Steinberg, SM
Chen, CC
Zheng, JB
Willis, TD
Faham, M
Wilson, WH
AF Roschewski, Mark
Dunleavy, Kieron
Pittaluga, Stefania
Moorhead, Martin
Pepin, Francois
Kong, Katherine
Shovlin, Margaret
Jaffe, Elaine S.
Staudt, Louis M.
Lai, Catherine
Steinberg, Seth M.
Chen, Clara C.
Zheng, Jianbiao
Willis, Thomas D.
Faham, Malek
Wilson, Wyndham H.
TI Circulating tumour DNA and CT monitoring in patients with untreated
diffuse large B-cell lymphoma: a correlative biomarker study
SO LANCET ONCOLOGY
LA English
DT Article
ID DOSE-ADJUSTED EPOCH; FDG-PET; RITUXIMAB; TOMOGRAPHY; THERAPY; INTERIM;
TRANSPLANTATION; CLASSIFICATION; CHEMOTHERAPY; LEUKEMIA
AB Background Diff use large-B-cell lymphoma is curable, but when treatment fails, outcome is poor. Although imaging can help to identify patients at risk of treatment failure, they are often imprecise, and radiation exposure is a potential health risk. We aimed to assess whether circulating tumour DNA encoding the clonal immunoglobulin gene sequence could be detected in the serum of patients with diffuse large-B-cell lymphoma and used to predict clinical disease recurrence after frontline treatment.
Methods We used next-generation DNA sequencing to retrospectively analyse cell-free circulating tumour DNA in patients assigned to one of three treatment protocols between May 8, 1993, and June 6, 2013. Eligible patients had diffuse large-B-cell lymphoma, no evidence of indolent lymphoma, and were previously untreated. We obtained serial serum samples and concurrent CT scans at specified times during most treatment cycles and up to 5 years of follow-up. VDJ gene segments of the rearranged immunoglobulin receptor genes were amplified and sequenced from pretreatment specimens and serum circulating tumour DNA encoding the VDJ rearrangements was quantitated.
Findings Tumour clonotypes were identified in pretreatment specimens from 126 patients who were followed up for a median of 11 years (IQR 6.8-14.2). Interim monitoring of circulating tumour DNA at the end of two treatment cycles in 108 patients showed a 5-year time to progression of 41.7% (95% CI 22.2-60.1) in patients with detectable circulating tumour DNA and 80.2% (69.6-87.3) in those without detectable circulating tumour DNA (p<0.0001). Detectable interim circulating tumour DNA had a positive predictive value of 62.5% (95% CI 40.6-81.2) and a negative predictive value of 79.8% (69.6-87.8). Surveillance monitoring of circulating tumour DNA was done in 107 patients who achieved complete remission. A Cox proportional hazards model showed that the hazard ratio for clinical disease progression was 228 (95% CI 51-1022) for patients who developed detectable circulating tumour DNA during surveillance compared with patients with undetectable circulating tumour DNA (p<0.0001). Surveillance circulating tumour DNA had a positive predictive value of 88.2% (95% CI 63.6-98.5) and a negative predictive value of 97.8% (92.2-99.7) and identified risk of recurrence at a median of 3.5 months (range 0-200) before evidence of clinical disease.
Interpretation Surveillance circulating tumour DNA identifies patients at risk of recurrence before clinical evidence of disease in most patients and results in a reduced disease burden at relapse. Interim circulating tumour DNA is a promising biomarker to identify patients at high risk of treatment failure.
C1 [Roschewski, Mark; Dunleavy, Kieron; Shovlin, Margaret; Staudt, Louis M.; Lai, Catherine; Wilson, Wyndham H.] NCI, Lymphoid Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Off Clin Director, Ctr Canc Res, Bethesda, MD 20892 USA.
[Moorhead, Martin; Pepin, Francois; Kong, Katherine; Zheng, Jianbiao; Willis, Thomas D.; Faham, Malek] Adapt Biotechnol, San Francisco, CA USA.
[Chen, Clara C.] NIH, Div Nucl Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Wilson, WH (reprint author), NCI, Lymphoma Therapeut Sect, Lymphoid Malignancies Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM wilsonw@mail.nih.gov
FU National Cancer Institute; Adaptive Biotechnologies
FX This study was funded by the National Cancer Institute and Adaptive
Biotechnologies.
NR 30
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U1 4
U2 20
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 MAY
PY 2015
VL 16
IS 5
BP 541
EP 549
DI 10.1016/S1470-2045(15)70106-3
PG 9
WC Oncology
SC Oncology
GA CH3DW
UT WOS:000353908200048
PM 25842160
ER
PT J
AU Lowy, DR
Herrero, R
Hildesheim, A
AF Lowy, Douglas R.
Herrero, Rolando
Hildesheim, Allan
CA IARC NCI Workshop Primary Endpoin
TI Primary endpoints for future prophylactic human papillomavirus vaccine
trials: towards infection and immunobridging
SO LANCET ONCOLOGY
LA English
DT Article
ID INTRAEPITHELIAL NEOPLASIA; CERVICAL-CANCER; AS04-ADJUVANTED VACCINE; HPV
INFECTION; ANTIBODY-RESPONSES; PARTICLE VACCINE; 2-DOSE SCHEDULE;
DOUBLE-BLIND; GRADE 3; WOMEN
AB Although available human papillomavirus (HPV) vaccines have high efficacy against incident infection and disease caused by HPV types that they specifically target, new vaccine trials continue to be needed. The goals of these trials could include change of vaccine dose or route of administration (or both), development of second-generation vaccines, and the regional manufacture of biosimilar vaccines. We summarise present thinking about primary endpoints for HPV vaccine trials as developed at an experts workshop convened by the International Agency for Research on Cancer and the US National Cancer Institute in September, 2013. Efficacy trials that have led to licensure for cervical cancer prevention have used the disease endpoint of cervical intraepithelial neoplasia grade 2 or worse (CIN2+). However, on the basis of experience from the trials and present knowledge of HPV infection, future efficacy trials for new vaccines can be safely streamlined by the use of persistent HPV infection, which occurs more frequently than CIN2+, and can be more reproducibly measured as a primary endpoint. Immunobridging trials can be sufficient to ascertain immunological non-inferiority for licensure for alternate dosing schedules, bridging to age 26 years or younger, and biosimilar vaccines, with post-licensure surveillance confirming effectiveness. These recommendations are intended to help stimulate continued vaccine development while ensuring appropriate assessment of safety and efficacy.
C1 [Lowy, Douglas R.] NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
[Herrero, Rolando] Int Agcy Res Canc, Prevent & Implementat Grp, Sect Early Detect & Prevent, F-69372 Lyon, France.
[Hildesheim, Allan] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Lowy, DR (reprint author), NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
EM lowyd@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU Intramural Research Program, National Cancer Institute, National
Institutes of Health
FX This Series paper was borne out of the International Agency for Research
on Cancer and the US National Cancer Institute workshop on Primary
Endpoints for Prophylactic HPV Vaccine Trials. We thank Gary Clifford,
Linda Eckert, Aimee Kreimer, Suzanne Kruger-Kjaer, Lauri Markowitz,
Pieter Neels, Martyn Plummer, Jeff Roberts, Rengaswamy Sankaranarayanan,
Mahboobeh Safaeian, Vivien Davis Tsu, Elizabeth R Unger, Salvatore
Vaccarella, Sholom Wacholder, and Christopher Wild. DRL and AH are
employed by the National Cancer Institute, National Institutes of
Health. This Series paper is supported in part by the Intramural
Research Program, National Cancer Institute, National Institutes of
Health.
NR 44
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U1 2
U2 9
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 MAY
PY 2015
VL 16
IS 5
BP E226
EP E233
PG 8
WC Oncology
SC Oncology
GA CH3DW
UT WOS:000353908200024
PM 25943067
ER
PT J
AU Schiller, JT
Muller, M
AF Schiller, John T.
Mueller, Martin
TI Next generation prophylactic human papillomavirus vaccines
SO LANCET ONCOLOGY
LA English
DT Article
ID VIRUS-LIKE PARTICLES; INTRAEPITHELIAL NEOPLASIA; VACCINATION PROGRAM;
IMMUNE-RESPONSES; QUADRIVALENT VACCINE; CERVICAL-CANCER; HPV VACCINES;
YOUNG-WOMEN; L1; IMMUNOGENICITY
AB The two licensed bivalent and quadrivalent human papillomavirus (HPV) L1 (the major papillomavirus virion protein) virus-like particle (VLP) vaccines are regarded as safe, effective, and well established prophylactic vaccines. However, they have some inherent limitations, including a fairly high production and delivery cost, virus-type restricted protection, and no reported therapeutic activity, which might be addressed with the development of alternative dosing schedules and vaccine products. A change from a three-dose to a two-dose protocol for the licensed HPV vaccines, especially in younger adolescents (aged 9-13 years), is underway in several countries and is likely to become the future norm. Preliminary evidence suggests that recipients of HPV vaccines might derive prophylactic benefits from one dose of the bivalent vaccine. Substantial interest exists in both the academic and industrial sectors in the development of second-generation L1 VLP vaccines in terms of cost reduction-eg, by production in Escherichia coli or alternative types of yeast. However, Merck's nonavalent vaccine, produced via the Saccharomyces cerevisiae production system that is also used for their quadrivalent vaccine, is the first second-generation HPV VLP vaccine to be available on the market. By contrast, other pharmaceutical companies are developing microbial vectors that deliver L1 genes. These two approaches would add an HPV component to existing live attenuated vaccines for measles and typhoid fever. Prophylactic vaccines that are based on induction of broadly cross-neutralising antibodies to L2, the minor HPV capsid protein, are also being developed both as simple monomeric fusion proteins and as virus-like display vaccines. The strong interest in developing the next generation of vaccines, particularly by manufacturers in middle-to-high income countries, increases the likelihood that vaccine production will become decentralised with the hope that effective HPV vaccines will be made increasingly available in low-resource settings where they are most needed.
C1 [Schiller, John T.] NCI, NIH, Bethesda, MD 20892 USA.
[Mueller, Martin] Deutsch Krebsforschungszentrum, Heidelberg, Germany.
RP Schiller, JT (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM schillej@mail.nih.gov
FU Merck
FX JTS in an inventor on US Government-owned patents related to
papillomavirus virus-like particle vaccines licensed to Merck and
GlaxoSmithKline (GSK), and patents related to papillomavirus L2 vaccines
licensed to Sanofi Pasteur and GSK. MM is an inventor and in receipt of
royalties of patents related to virus-like particle vaccines owned by
Loyola University Chicago (Chicago, USA) and licensed to GSK. MM is an
inventor of Trx-L2 vaccines and received personal fees from Merck for
analyses of clinical trial sera.
NR 72
TC 12
Z9 15
U1 4
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD MAY
PY 2015
VL 16
IS 5
BP E217
EP E225
PG 9
WC Oncology
SC Oncology
GA CH3DW
UT WOS:000353908200023
PM 25943066
ER
PT J
AU Rao, M
AF Rao, Mahendra
TI National Institutes of Health: A Catalyst in Advancing Regenerative
Medicine Science Into Practice
SO MAYO CLINIC PROCEEDINGS
LA English
DT Article
ID PERSONALIZED GENOMIC MEDICINE; PLURIPOTENT STEM-CELLS; THERAPY
AB The stem cell domain of the regenerative medicine field has seen fundamental changes initiated by seminal discoveries in cell biology, genetic engineering, and whole genome sequencing. Many of these discoveries were funded in part by the National Institutes of Health (NIH), and the NIH remains a leader in supporting research in the United States. However, as the field has developed, the NIH has responded proactively to identify roadblocks and to develop solutions that will accelerate translation of basic discoveries to the clinical setting. These activities range from organizing specialized workshops and coordinating activities among international organizations and the different arms of the government to funding small-scale industry. In addition, the NIH has been a key driver in providing needed infrastructure in areas in which the private sector has been unable to, or does not believe it can, invest. These activities of the NIH are as important as its traditional funding role, and I believe they have contributed to the innovation and rapid pace of discovery in this field. (C) 2015 Mayo Foundation for Medical Education and Research
C1 [Rao, Mahendra] NIH, Ctr Regenerat Med, Bethesda, MD 20892 USA.
RP Rao, M (reprint author), New York Stem Cell Fdn, 1995 Broadway,Ste 600, New York, NY 10023 USA.
EM mrao@qthera.com
NR 29
TC 1
Z9 1
U1 2
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-6196
EI 1942-5546
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD MAY
PY 2015
VL 90
IS 5
BP 672
EP 679
DI 10.1016/j.mayocp.2013.05.038
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA CH2TG
UT WOS:000353876900017
PM 25939939
ER
PT J
AU Cornelis, MC
Byrne, EM
Esko, T
Nalls, MA
Ganna, A
Paynter, N
Monda, KL
Amin, N
Fischer, K
Renstrom, F
Ngwa, JS
Huikari, V
Cavadino, A
Nolte, IM
Teumer, A
Yu, K
Marques-Vidal, P
Rawal, R
Manichaikul, A
Wojczynski, MK
Vink, JM
Zhao, JH
Burlutsky, G
Lahti, J
Mikkila, V
Lemaitre, RN
Eriksson, J
Musani, SK
Tanaka, T
Geller, F
Luan, J
Hui, J
Magi, R
Dimitriou, M
Garcia, ME
Ho, WK
Wright, MJ
Rose, LM
Magnusson, PKE
Pedersen, NL
Couper, D
Oostra, BA
Hofman, A
Ikram, MA
Tiemeier, HW
Uitterlinden, AG
van Rooij, FJA
Barroso, I
Johansson, I
Xue, L
Kaakinen, M
Milani, L
Power, C
Snieder, H
Stolk, RP
Baumeister, SE
Biffar, R
Gu, F
Bastardot, F
Kutalik, Z
Jacobs, DR
Forouhi, NG
Mihailov, E
Lind, L
Lindgren, C
Michaelsson, K
Morris, A
Jensen, M
Khaw, KT
Luben, RN
Wang, JJ
Mannisto, S
Perala, MM
Kahonen, M
Lehtimaki, T
Viikari, J
Mozaffarian, D
Mukamal, K
Psaty, BM
Doring, A
Heath, AC
Montgomery, GW
Dahmen, N
Carithers, T
Tucker, KL
Ferrucci, L
Boyd, HA
Melbye, M
Treur, JL
Mellstrom, D
Hottenga, JJ
Prokopenko, I
Tonjes, A
Deloukas, P
Kanoni, S
Lorentzon, M
Houston, DK
Liu, Y
Danesh, J
Rasheed, A
Mason, MA
Zonderman, AB
Franke, L
Kristal, BS
Karjalainen, J
Reed, DR
Westra, HJ
Evans, MK
Saleheen, D
Harris, TB
Dedoussis, G
Curhan, G
Stumvoll, M
Beilby, J
Pasquale, LR
Feenstra, B
Bandinelli, S
Ordovas, JM
Chan, AT
Peters, U
Ohlsson, C
Gieger, C
Martin, NG
Waldenberger, M
Siscovick, DS
Raitakari, O
Eriksson, JG
Mitchell, P
Hunter, DJ
Kraft, P
Rimm, EB
Boomsma, DI
Borecki, IB
Loos, RJF
Wareham, NJ
Vollenweider, P
Caporaso, N
Grabe, HJ
Neuhouser, ML
Wolffenbuttel, BHR
Hu, FB
Hypponen, E
Jarvelin, MR
Cupples, LA
Franks, PW
Ridker, PM
van Duijn, CM
Heiss, G
Metspalu, A
North, KE
Ingelsson, E
Nettleton, JA
van Dam, RM
Chasman, DI
AF Cornelis, M. C.
Byrne, E. M.
Esko, T.
Nalls, M. A.
Ganna, A.
Paynter, N.
Monda, K. L.
Amin, N.
Fischer, K.
Renstrom, F.
Ngwa, J. S.
Huikari, V.
Cavadino, A.
Nolte, I. M.
Teumer, A.
Yu, K.
Marques-Vidal, P.
Rawal, R.
Manichaikul, A.
Wojczynski, M. K.
Vink, J. M.
Zhao, J. H.
Burlutsky, G.
Lahti, J.
Mikkila, V.
Lemaitre, R. N.
Eriksson, J.
Musani, S. K.
Tanaka, T.
Geller, F.
Luan, J.
Hui, J.
Maegi, R.
Dimitriou, M.
Garcia, M. E.
Ho, W-K
Wright, M. J.
Rose, L. M.
Magnusson, P. K. E.
Pedersen, N. L.
Couper, D.
Oostra, B. A.
Hofman, A.
Ikram, M. A.
Tiemeier, H. W.
Uitterlinden, A. G.
van Rooij, F. J. A.
Barroso, I.
Johansson, I.
Xue, L.
Kaakinen, M.
Milani, L.
Power, C.
Snieder, H.
Stolk, R. P.
Baumeister, S. E.
Biffar, R.
Gu, F.
Bastardot, F.
Kutalik, Z.
Jacobs, D. R., Jr.
Forouhi, N. G.
Mihailov, E.
Lind, L.
Lindgren, C.
Michaelsson, K.
Morris, A.
Jensen, M.
Khaw, K-T
Luben, R. N.
Wang, J. J.
Mannisto, S.
Perala, M-M
Kahonen, M.
Lehtimaki, T.
Viikari, J.
Mozaffarian, D.
Mukamal, K.
Psaty, B. M.
Doering, A.
Heath, A. C.
Montgomery, G. W.
Dahmen, N.
Carithers, T.
Tucker, K. L.
Ferrucci, L.
Boyd, H. A.
Melbye, M.
Treur, J. L.
Mellstrom, D.
Hottenga, J. J.
Prokopenko, I.
Toenjes, A.
Deloukas, P.
Kanoni, S.
Lorentzon, M.
Houston, D. K.
Liu, Y.
Danesh, J.
Rasheed, A.
Mason, M. A.
Zonderman, A. B.
Franke, L.
Kristal, B. S.
Karjalainen, J.
Reed, D. R.
Westra, H-J
Evans, M. K.
Saleheen, D.
Harris, T. B.
Dedoussis, G.
Curhan, G.
Stumvoll, M.
Beilby, J.
Pasquale, L. R.
Feenstra, B.
Bandinelli, S.
Ordovas, J. M.
Chan, A. T.
Peters, U.
Ohlsson, C.
Gieger, C.
Martin, N. G.
Waldenberger, M.
Siscovick, D. S.
Raitakari, O.
Eriksson, J. G.
Mitchell, P.
Hunter, D. J.
Kraft, P.
Rimm, E. B.
Boomsma, D. I.
Borecki, I. B.
Loos, R. J. F.
Wareham, N. J.
Vollenweider, P.
Caporaso, N.
Grabe, H. J.
Neuhouser, M. L.
Wolffenbuttel, B. H. R.
Hu, F. B.
Hyppoenen, E.
Jarvelin, M-R
Cupples, L. A.
Franks, P. W.
Ridker, P. M.
van Duijn, C. M.
Heiss, G.
Metspalu, A.
North, K. E.
Ingelsson, E.
Nettleton, J. A.
van Dam, R. M.
Chasman, D. I.
CA Coffee & Caffeine Genetics Consort
Int Parkinson's Dis Genomics Conso
North Amer Brain Expression Consor
UK Brain Expression Consortium
TI Genome-wide meta-analysis identifies six novel loci associated with
habitual coffee consumption
SO MOLECULAR PSYCHIATRY
LA English
DT Article
ID CAFFEINE; PROTEIN; VARIANTS; RECEPTOR; BRAIN; GLUCOKINASE; INVOLVEMENT;
BINDING; BDNF
AB Coffee, a major dietary source of caffeine, is among the most widely consumed beverages in the world and has received considerable attention regarding health risks and benefits. We conducted a genome-wide (GW) meta-analysis of predominately regular-type coffee consumption (cups per day) among up to 91 462 coffee consumers of European ancestry with top single-nucleotide polymorphisms (SNPs) followed-up in similar to 30 062 and 7964 coffee consumers of European and African-American ancestry, respectively. Studies from both stages were combined in a trans-ethnic meta-analysis. Confirmed loci were examined for putative functional and biological relevance. Eight loci, including six novel loci, met GW significance (log(10)Bayes factor (BF) > 5.64) with per-allele effect sizes of 0.03-0.14 cups per day. Six are located in or near genes potentially involved in pharmacokinetics (ABCG2, AHR, POR and CYP1A2) and pharmacodynamics (BDNF and SLC6A4) of caffeine. Two map to GCKR and MLXIPL genes related to metabolic traits but lacking known roles in coffee consumption. Enhancer and promoter histone marks populate the regions of many confirmed loci and several potential regulatory SNPs are highly correlated with the lead SNP of each. SNP alleles near GCKR, MLXIPL, BDNF and CYP1A2 that were associated with higher coffee consumption have previously been associated with smoking initiation, higher adiposity and fasting insulin and glucose but lower blood pressure and favorable lipid, inflammatory and liver enzyme profiles (P < 5x10(-8)). Our genetic findings among European and African-American adults reinforce the role of caffeine in mediating habitual coffee consumption and may point to molecular mechanisms underlying inter-individual variability in pharmacological and health effects of coffee.
C1 [Cornelis, M. C.; Mozaffarian, D.; Curhan, G.; Pasquale, L. R.; Chan, A. T.; Hunter, D. J.; Rimm, E. B.; Hu, F. B.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02215 USA.
[Cornelis, M. C.; Jensen, M.; Mozaffarian, D.; Rimm, E. B.; Hu, F. B.; Franks, P. W.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02215 USA.
[Byrne, E. M.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4072, Australia.
[Esko, T.; Fischer, K.; Maegi, R.; Milani, L.; Mihailov, E.; Metspalu, A.] Univ Tartu, Estonian Genome Ctr, EE-50090 Tartu, Estonia.
[Esko, T.] Childrens Hosp Boston, Div Endocrinol, Boston, MA USA.
[Esko, T.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02215 USA.
[Esko, T.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Nalls, M. A.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Ganna, A.; Magnusson, P. K. E.; Pedersen, N. L.] Karolinska Inst, Dept Med Epidemiol & Biostat, Karolinska, Sweden.
[Paynter, N.; Rose, L. M.; Ridker, P. M.; Chasman, D. I.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02215 USA.
[Monda, K. L.; Heiss, G.; North, K. E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Amin, N.; Hofman, A.; Ikram, M. A.; Tiemeier, H. W.; Uitterlinden, A. G.; van Rooij, F. J. A.; van Duijn, C. M.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Renstrom, F.; Franks, P. W.] Lund Univ, Dept Clin Sci, Malmo, Sweden.
[Ngwa, J. S.; Xue, L.; Cupples, L. A.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Huikari, V.; Kaakinen, M.; Jarvelin, M-R] Univ Oulu, Inst Hlth Sci, Oulu, Finland.
[Cavadino, A.; Power, C.; Hyppoenen, E.] UCL, Inst Child Hlth, Ctr Paediat Epidemiol & Biostat, Ctr Epidemiol Child Hlth,MRC, London, England.
[Nolte, I. M.; Snieder, H.; Stolk, R. P.] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
[Teumer, A.] Univ Med Greifswald, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[Yu, K.; Gu, F.; Caporaso, N.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Marques-Vidal, P.] Univ Lausanne Hosp, Inst Social & Prevent Med, Lausanne, Switzerland.
[Rawal, R.; Gieger, C.] Helmholtz Zentrum Munchen, Inst Genet Epidemiol, Munich, Germany.
[Manichaikul, A.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Wojczynski, M. K.; Borecki, I. B.] Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
[Vink, J. M.; Treur, J. L.; Hottenga, J. J.; Boomsma, D. I.] Vrije Univ Amsterdam, Dept Biol Psychol Netherlands Twin Register, Amsterdam, Netherlands.
[Zhao, J. H.; Luan, J.; Forouhi, N. G.; Loos, R. J. F.; Wareham, N. J.] Univ Cambridge, Epidemiol Unit, MRC, Cambridge, England.
[Burlutsky, G.; Wang, J. J.; Mitchell, P.] Univ Sydney, Dept Ophthalmol, Ctr Vis Res, Sydney, NSW 2006, Australia.
[Burlutsky, G.; Wang, J. J.; Mitchell, P.] Univ Sydney, Westmead Millennium Inst, Sydney, NSW 2006, Australia.
[Lahti, J.] Univ Helsinki, Inst Behav Sci, Helsinki, Finland.
[Lahti, J.; Eriksson, J. G.] Folkhalsan Res Ctr, Helsinki, Finland.
[Mikkila, V.] Univ Helsinki, Dept Food & Environm Sci, Helsinki, Finland.
[Mikkila, V.; Raitakari, O.] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Mikkila, V.; Raitakari, O.] Turku Univ Hosp, FIN-20520 Turku, Finland.
[Lemaitre, R. N.; Psaty, B. M.; Siscovick, D. S.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Eriksson, J.; Mellstrom, D.; Lorentzon, M.; Ohlsson, C.] Univ Gothenburg, Sahlgrenska Acad, Inst Med, Ctr Bone & Arthrit Res, Gothenburg, Sweden.
[Musani, S. K.] Univ Mississippi, Med Ctr, Jackson, MI USA.
[Tanaka, T.; Ferrucci, L.] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
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[Hui, J.; Beilby, J.] Busselton Populat Med Res Fdn Inc, Busselton, WA, Australia.
[Hui, J.; Beilby, J.] PathWest Lab Med, Nedlands, WA, Australia.
[Hui, J.; Beilby, J.] Univ Western Australia, Sch Pathol & Lab Med, Nedlands, WA 6009, Australia.
[Hui, J.] Univ Western Australia, Sch Populat Hlth, Nedlands, WA 6009, Australia.
[Dimitriou, M.; Dedoussis, G.] Harokopio Univ, Athens, Greece.
[Garcia, M. E.; Harris, T. B.] NIA, Lab Epidemiol & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Ho, W-K; Khaw, K-T; Luben, R. N.; Danesh, J.; Saleheen, D.] Univ Cambridge, Inst Publ Hlth, Dept Publ Hlth & Primary Care, Cambridge, England.
[Wright, M. J.; Montgomery, G. W.; Martin, N. G.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
[Couper, D.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Oostra, B. A.] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Ikram, M. A.] Erasmus MC, Dept Radiol, Rotterdam, Netherlands.
[Ikram, M. A.] Erasmus MC, Dept Neurol, Rotterdam, Netherlands.
[Tiemeier, H. W.] Erasmus MC, Dept Psychiat, Rotterdam, Netherlands.
[Uitterlinden, A. G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Barroso, I.; Deloukas, P.] Wellcome Trust Sanger Inst, Cambridge, England.
[Barroso, I.] Univ Cambridge, Metab Res Labs, Cambridge, England.
[Barroso, I.] NIHR Cambridge Biomed Res Ctr, Cambridge, England.
[Johansson, I.] Umea Univ, Dept Odontol, Umea, Sweden.
[Kaakinen, M.; Jarvelin, M-R] Univ Oulu, Bioctr Oulu, Oulu, Finland.
[Kaakinen, M.; Jarvelin, M-R] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Biostat, MRC Hlth Protect Agcy HPE, Ctr Environm & Hlth,Sch Publ Hlth, London SW7 2AZ, England.
[Baumeister, S. E.] Univ Med Greifswald, Inst Community Med, Greifswald, Germany.
[Biffar, R.] Univ Med Greifswald, Ctr Oral Hlth, Dept Prosthodont Gerodontol & Biomat, Greifswald, Germany.
[Bastardot, F.; Vollenweider, P.] CHU Vaudois, Dept Internal Med, Lausanne, Switzerland.
[Bastardot, F.; Stumvoll, M.] Univ Lausanne, Lausanne, Switzerland.
[Kutalik, Z.] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
[Kutalik, Z.] CHU Vaudois, Inst Social & Prevent Med IUMSP, CH-1011 Lausanne, Switzerland.
[Kutalik, Z.] Swiss Inst Bioinformat, Lausanne, Switzerland.
[Jacobs, D. R., Jr.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Lind, L.; Ingelsson, E.] Uppsala Univ, Dept Med Sci, Mol Epidemiol & Sci Life Lab, Uppsala, Sweden.
[Lindgren, C.; Morris, A.; Prokopenko, I.; Ingelsson, E.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Michaelsson, K.] Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
[Mannisto, S.; Perala, M-M] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Kahonen, M.] Tampere Univ Hosp, Dept Clin Physiol, Tampere, Finland.
[Kahonen, M.; Lehtimaki, T.] Univ Tampere, Sch Med, FIN-33101 Tampere, Finland.
[Lehtimaki, T.] Univ Tampere, Fimlab Labs, Dept Clin Chem, FIN-33101 Tampere, Finland.
[Viikari, J.] Univ Turku, Dept Med, Turku, Finland.
[Viikari, J.] Turku Univ Hosp, FIN-20520 Turku, Finland.
[Mozaffarian, D.; Rimm, E. B.; Hu, F. B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Mozaffarian, D.] Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
[Mukamal, K.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Psaty, B. M.; Siscovick, D. S.] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Psaty, B. M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Psaty, B. M.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Doering, A.] Helmholtz Zentrum Munchen, Inst Epidemiol, Munich, Germany.
[Heath, A. C.] Washington Univ, Dept Psychiat, St Louis, MO USA.
[Dahmen, N.] Johannes Gutenberg Univ Mainz, Dept Psychiat, Mainz, Germany.
[Carithers, T.] Univ Mississippi, Sch Appl Sci, Oxford, MS USA.
[Tucker, K. L.] Univ MA Lowell, Clin Lab & Nutr Sci, Lowell, MA USA.
[Prokopenko, I.] Univ London Imperial Coll Sci Technol & Med, Dept Genom Common Dis, London, England.
[Toenjes, A.; Stumvoll, M.] Univ Leipzig, Dept Med, D-04109 Leipzig, Germany.
[Toenjes, A.; Stumvoll, M.] Univ Leipzig, IFB Adipos Dis, D-04109 Leipzig, Germany.
[Deloukas, P.; Kanoni, S.] Queen Mary Univ London, William Harvey Res Inst, Barts & London Sch Med & Dent, London, England.
[Deloukas, P.] King Abdulaziz Univ, Jeddah 21413, Saudi Arabia.
[Houston, D. K.] Wake Forest Sch Med, Winston Salem, NC USA.
[Houston, D. K.; Liu, Y.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Rasheed, A.; Saleheen, D.] Ctr Noncommunicable Dis, Karachi, Pakistan.
[Mason, M. A.; Evans, M. K.] NIA, Hlth Dispar Res Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
[Zonderman, A. B.] NIA, Lab Personal & Cognit, NIH, Baltimore, MD 21224 USA.
[Franke, L.; Karjalainen, J.; Westra, H-J] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
[Kristal, B. S.] Brigham & Womens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Kristal, B. S.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Reed, D. R.] Monell Chem Senses Ctr, Philadelphia, PA 19104 USA.
[Pasquale, L. R.] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Bandinelli, S.] Azienda Sanitaria Firenze, Geriatr Unit, Florence, Italy.
[Ordovas, J. M.] Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[Chan, A. T.] MA Gen Hosp, Div Gastroenterol, Boston, MA USA.
[Peters, U.; Neuhouser, M. L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Waldenberger, M.] Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, Munich, Germany.
[Raitakari, O.] Turku Univ Hosp, Dept Clin Physiol & Nucl Med, FIN-20520 Turku, Finland.
[Eriksson, J. G.] Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland.
[Eriksson, J. G.] Univ Helsinki, Cent Hosp, Unit Gen Practice, Helsinki, Finland.
[Hunter, D. J.; Kraft, P.] Harvard Univ, Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA 02115 USA.
[Loos, R. J. F.] Icahn Sch Med Mt Sinai, Genet Obes & Related Metab Traits Program, New York, NY 10029 USA.
[Loos, R. J. F.] Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.
[Grabe, H. J.] Univ Med Greifswald, HELIOS Hosp Stralsund, Dept Psychiat & Psychotherapy, Greifswald, Germany.
[Wolffenbuttel, B. H. R.] Univ Groningen, Dept Endocrinol, Univ Med Ctr Groningen, Groningen, Netherlands.
[Hyppoenen, E.] Univ S Australia, Sch Populat Hlth, Adelaide, SA 5001, Australia.
[Hyppoenen, E.] South Australian Hlth & Med Res Inst, Adelaide, SA, Australia.
[Jarvelin, M-R] Natl Inst Hlth & Welf, Dept Children & Young People & Families, Oulu, Finland.
[Jarvelin, M-R] Oulu Univ Hosp, Unit Primary Care, Oulu, Finland.
[Cupples, L. A.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Franks, P. W.] Umea Univ, Med Sect, Dept Publ Hlth & Clin Med, Umea, Sweden.
[van Duijn, C. M.] Netherlands Consortium Hlth Ageing, Leiden, Netherlands.
[van Duijn, C. M.] Natl Genom Initiat, Leiden, Netherlands.
[Nettleton, J. A.] Univ Texas Hlth Sci Ctr Houston, Div Epidemiol Human Genet & Environm Sci, Houston, TX 77030 USA.
[van Dam, R. M.] Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore.
[van Dam, R. M.] Natl Univ Singapore, Dept Med, Yong Loo Lin Sch Med, Singapore 117548, Singapore.
[van Dam, R. M.] Natl Univ Hlth Syst, Singapore, Singapore.
RP Cornelis, MC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 401 Pk Dr, Boston, MA 02215 USA.
EM mcorneli@hsph.harvard.edu; dchasman@research.bwh.harvard.edu
RI Colaus, PsyColaus/K-6607-2013; Waldenberger, Melanie/B-5355-2014;
Prokopenko, Inga/H-3241-2014; Wright, Margaret/A-4560-2016; Hypponen,
Elina/B-2596-2014; Deloukas, Panos/B-2922-2013; Franke,
Lude/P-7036-2016; Karjalainen, Juha/P-8624-2016; Magnusson,
Patrik/C-4458-2017;
OI Eriksson, Johan/0000-0002-2516-2060; Zonderman, Alan
B/0000-0002-6523-4778; corvol, jean-christophe/0000-0001-7325-0199;
Lahti, Jari/0000-0002-4310-5297; Ganna, Andrea/0000-0002-8147-240X;
Tiemeier, Henning/0000-0002-4395-1397; Plagnol,
Vincent/0000-0002-5597-9215; Ikram, Mohammad Arfan/0000-0003-0372-8585;
Esko, Tonu/0000-0003-1982-6569; Gieger, Christian/0000-0001-6986-9554;
van Dam, Rob/0000-0002-7354-8734; Mannisto, Satu/0000-0002-8668-3046;
Mellstrom, Dan/0000-0003-2761-3723; Luben, Robert/0000-0002-5088-6343;
Wolffenbuttel, Bruce H.R./0000-0001-9262-6921; Forouhi,
Nita/0000-0002-5041-248X; Jarvelin, Marjo-Riitta/0000-0002-2149-0630;
Waldenberger, Melanie/0000-0003-0583-5093; Prokopenko,
Inga/0000-0003-1624-7457; Wright, Margaret/0000-0001-7133-4970;
Hypponen, Elina/0000-0003-3670-9399; Deloukas,
Panos/0000-0001-9251-070X; Franke, Lude/0000-0002-5159-8802; Kaakinen,
Marika/0000-0002-9228-0462; HO, WEANG KEE/0000-0002-8269-7344; Magi,
Reedik/0000-0002-2964-6011
NR 43
TC 19
Z9 20
U1 5
U2 46
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD MAY
PY 2015
VL 20
IS 5
BP 647
EP 656
DI 10.1038/mp.2014.107
PG 10
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA CH0JS
UT WOS:000353706400016
ER
PT J
AU Corrigan-Curay, J
O'Reilly, M
Kohn, DB
Cannon, PM
Bao, G
Bushman, FD
Carroll, D
Cathomen, T
Joung, JK
Roth, D
Sadelain, M
Scharenberg, AM
von Kalle, C
Zhang, F
Jambou, R
Rosenthal, E
Hassani, M
Singh, A
Porteus, MH
AF Corrigan-Curay, Jacqueline
O'Reilly, Marina
Kohn, Donald B.
Cannon, Paula M.
Bao, Gang
Bushman, Frederic D.
Carroll, Dana
Cathomen, Toni
Joung, J. Keith
Roth, David
Sadelain, Michel
Scharenberg, Andrew M.
von Kalle, Christof
Zhang, Feng
Jambou, Robert
Rosenthal, Eugene
Hassani, Morad
Singh, Aparna
Porteus, Matthew H.
TI Genome Editing Technologies: Defining a Path to Clinic
SO MOLECULAR THERAPY
LA English
DT News Item
ID ZINC-FINGER NUCLEASES; ACUTE LYMPHOBLASTIC-LEUKEMIA; RAG-MEDIATED
RECOMBINATION; MAMMALIAN-CELLS; GENE-THERAPY; IN-VITRO; T-CELLS; DNA;
SPECIFICITY; CHALLENGES
C1 [Corrigan-Curay, Jacqueline; O'Reilly, Marina; Jambou, Robert; Rosenthal, Eugene; Hassani, Morad; Singh, Aparna] NIH, Bethesda, MD 20892 USA.
[Kohn, Donald B.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Cannon, Paula M.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Bao, Gang] Georgia Inst Technol, Atlanta, GA 30332 USA.
[Bushman, Frederic D.; Roth, David] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Carroll, Dana] Univ Utah, Sch Med, Salt Lake City, UT USA.
[Cathomen, Toni] Univ Med Ctr, Freiberg, Germany.
[Joung, J. Keith] Massachusetts Gen Hosp, Charlestown, MA USA.
[Joung, J. Keith] Harvard Univ, Sch Med, Boston, MA USA.
[Sadelain, Michel] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Scharenberg, Andrew M.] Seattle Childrens Res Inst, Seattle, WA USA.
[Scharenberg, Andrew M.] Univ Washington, Sch Med, Seattle, WA USA.
[von Kalle, Christof] Natl Ctr Tumor Dis, Heidelberg, Germany.
[von Kalle, Christof] German Canc Res Ctr, Heidelberg, Germany.
[Zhang, Feng] MIT, Cambridge, MA 02139 USA.
[Zhang, Feng] Harvard Univ, Cambridge, MA 02138 USA.
[Porteus, Matthew H.] Stanford Univ, Stanford, CA 94305 USA.
RP Corrigan-Curay, J (reprint author), NIH, Off Sci Policy, 6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM corrigaja@nhlbi.nih.gov
OI Cathomen, Toni/0000-0002-7757-4630
NR 43
TC 25
Z9 25
U1 2
U2 14
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
EI 1525-0024
J9 MOL THER
JI Mol. Ther.
PD MAY
PY 2015
VL 23
IS 5
BP 796
EP 806
DI 10.1038/mt.2015.54
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA CH3LW
UT WOS:000353933200002
PM 25943494
ER
PT J
AU Gowdy, KM
Madenspacher, JH
Azzam, KM
Gabor, KA
Janardhan, KS
Aloor, JJ
Fessler, MB
AF Gowdy, K. M.
Madenspacher, J. H.
Azzam, K. M.
Gabor, K. A.
Janardhan, K. S.
Aloor, J. J.
Fessler, M. B.
TI Key role for scavenger receptor B-I in the integrative physiology of
host defense during bacterial pneumonia
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID COMMUNITY-ACQUIRED PNEUMONIA; HIGH-DENSITY-LIPOPROTEIN; VITAMIN-E;
SR-BI; ALVEOLAR EPITHELIUM; ENDOTHELIAL-CELLS; ESCHERICHIA-COLI; HDL
RECEPTOR; LUNG INJURY; INFECTION
AB Scavenger receptor B-I (SR-BI) is a multirecognition receptor that regulates cholesterol trafficking and cardiovascular inflammation. Although it is expressed by neutrophils (PMNs) and lung-resident cells, no role for SR-BI has been defined in pulmonary immunity. Herein, we report that, compared with SR-BI+/+ counterparts, SR-BI-/- mice suffer markedly increased mortality during bacterial pneumonia associated with higher bacterial burden in the lung and blood, deficient induction of the stress glucocorticoid corticosterone, higher serum cytokines, and increased organ injury. SR-BI-/- mice had significantly increased PMN recruitment and cytokine production in the infected airspace. This was associated with defective hematopoietic cell-dependent clearance of lipopolysaccharide from the airspace and increased cytokine production by SR-BI-/- macrophages. Corticosterone replacement normalized alveolar neutrophilia but not alveolar cytokines, bacterial burden, or mortality, suggesting that adrenal insufficiency derepresses PMN trafficking to the SR-BI-/- airway in a cytokine-independent manner. Despite enhanced alveolar neutrophilia, SR-BI-/- mice displayed impaired phagocytic killing. Bone marrow chimeras revealed this defect to be independent of the dyslipidemia and adrenal insufficiency of SR-BI-/- mice. During infection, SR-BI-/- PMNs displayed deficient oxidant production and CD11b externalization, and increased surface L-selectin, suggesting defective activation. Taken together, SR-BI coordinates several steps in the integrated neutrophilic host defense response to pneumonia.
C1 [Gowdy, K. M.; Madenspacher, J. H.; Azzam, K. M.; Gabor, K. A.; Aloor, J. J.; Fessler, M. B.] NIEHS, Div Intramural Res, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
[Janardhan, K. S.] NIEHS, Cellular & Mol Pathol Branch, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
[Janardhan, K. S.] NIH, Integrated Lab Syst Inc, Res Triangle Pk, NC USA.
RP Gowdy, KM (reprint author), NIEHS, Div Intramural Res, Lab Resp Biol, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM kymberly.gowdy@nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01 ES102005]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences (Z01 ES102005). We thank Drs Donald Cook and Seddon
Thomas for manuscript review and Ralph Wilson, Debra King, Ligon Perrow,
Maria Sifre, Carl Bortner, and CJ Tucker for their technical assistance.
NR 49
TC 2
Z9 2
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
EI 1935-3456
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD MAY
PY 2015
VL 8
IS 3
BP 559
EP 571
DI 10.1038/mi.2014.88
PG 13
WC Immunology
SC Immunology
GA CH5OR
UT WOS:000354085700011
PM 25336169
ER
PT J
AU Schindler, C
Chen, Y
Pu, J
Guo, XL
Bonifacino, JS
AF Schindler, Christina
Chen, Yu
Pu, Jing
Guo, Xiaoli
Bonifacino, Juan S.
TI EARP is a multisubunit tethering complex involved in endocytic recycling
SO NATURE CELL BIOLOGY
LA English
DT Article
ID TRANS-GOLGI NETWORK; SYNTAXIN 6; RETROGRADE TRANSPORT; STRUCTURE
PREDICTION; HIPPOCAMPAL-NEURONS; GLUCOSE-TRANSPORT; 3T3-L1 ADIPOCYTES;
STRUCTURAL BASIS; SNARE COMPLEXES; CELL-MIGRATION
AB Recycling of endocytic receptors to the cell surface involves passage through a series of membrane-bound compartments by mechanisms that are poorly understood. In particular, it is unknown if endocytic recycling requires the function of multisubunit tethering complexes, as is the case for other intracellular trafficking pathways. Herein we describe a tethering complex named endosome-associated recycling protein (EARP) that is structurally related to the previously described Golgi-associated retrograde protein (GARP) complex. The two complexes share the Ang2, Vps52 and Vps53 subunits, but EARP contains an uncharacterized protein, syndetin, in place of the Vps54 subunit of GARP. This change determines differential localization of EARP to recycling endosomes and GARP to the Golgi complex. EARP interacts with the target SNARE syntaxin 6 and various cognate SNAREs. Depletion of syndetin or syntaxin 6 delays recycling of internalized transferrin to the cell surface. These findings implicate EARP in canonical membrane-fusion events in the process of endocytic recycling.
C1 [Schindler, Christina; Chen, Yu; Pu, Jing; Guo, Xiaoli; Bonifacino, Juan S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
RP Bonifacino, JS (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
EM bonifacinoj@helix.nih.gov
OI Bonifacino, Juan S./0000-0002-5673-6370
FU Intramural Program of NICHD, NIH [ZIA HD001607]
FX We thank X. Zhu and N. Tsal for technical assistance, J. Presley for
discussions and R. Mattera and D. Gershlick for critical review of the
manuscript. This work is funded by the Intramural Program of NICHD, NIH
(ZIA HD001607).
NR 63
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
EI 1476-4679
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD MAY
PY 2015
VL 17
IS 5
BP 639
EP U229
DI 10.1038/ncb3129
PG 22
WC Cell Biology
SC Cell Biology
GA CH1HG
UT WOS:000353771500012
PM 25799061
ER
PT J
AU Kang, XL
Lu, ZG
Cui, CH
Deng, M
Fan, YQ
Dong, BJ
Han, X
Xie, FC
Tyner, JW
Coligan, JE
Collins, RH
Xiao, XS
You, MJ
Zhang, CC
AF Kang, Xunlei
Lu, Zhigang
Cui, Changhao
Deng, Mi
Fan, Yuqi
Dong, Baijun
Han, Xin
Xie, Fuchun
Tyner, Jeffrey W.
Coligan, John E.
Collins, Robert H.
Xiao, Xiangshu
You, M. James
Zhang, Cheng Cheng
TI The ITIM-containing receptor LAIR1 is essential for acute myeloid
leukaemia development
SO NATURE CELL BIOLOGY
LA English
DT Article
ID HEMATOPOIETIC STEM-CELLS; IG-LIKE RECEPTOR-1; TYROSINE-PHOSPHATASE
SHP-1; PROTEIN-KINASE-I; VIVO; BINDING; TRANSPLANTATION; IDENTIFICATION;
MALIGNANCIES; RENEWAL
AB Conventional strategies are not particularly successful in the treatment of leukaemia, and identification of signalling pathways crucial to the activity of leukaemia stem cells will provide targets for the development of new therapies. Here we report that certain receptors containing the immunoreceptor tyrosine-based inhibition motif (ITIM) are crucial for the development of acute myeloid leukaemia (AML). Inhibition of expression of the ITIM-containing receptor LAIR1 does not affect normal haematopoiesis but abolishes leukaemia development. LAIR1 induces activation of SHP-1, which acts as a phosphatase-independent signalling adaptor to recruit CAMK1 for activation of downstream CREB in AML cells. The LAIR1-SHP-1-CAMK1-CREB pathway sustains the survival and self-renewal of AML stem cells. Intervention in the signalling initiated by ITIM-containing receptors such as LAIR1 may result in successful treatment of AML.
C1 [Kang, Xunlei; Lu, Zhigang; Cui, Changhao; Deng, Mi; Fan, Yuqi; Zhang, Cheng Cheng] Univ Texas SW Med Ctr Dallas, Dept Physiol, Dallas, TX 75390 USA.
[Kang, Xunlei; Lu, Zhigang; Cui, Changhao; Deng, Mi; Fan, Yuqi; Zhang, Cheng Cheng] Univ Texas SW Med Ctr Dallas, Dept Dev Biol, Dallas, TX 75390 USA.
[Dong, Baijun; You, M. James] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Div Pathol & Lab Med, Houston, TX 77030 USA.
[Han, Xin] Univ Texas MD Anderson Canc Ctr, Dept Lab Med, Div Pathol & Lab Med, Houston, TX 77030 USA.
[Xie, Fuchun; Xiao, Xiangshu] Oregon Hlth & Sci Univ, Knight Canc Inst, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Tyner, Jeffrey W.] Oregon Hlth & Sci Univ, Knight Canc Inst, Cell & Dev Biol, Portland, OR 97239 USA.
[Coligan, John E.] NIAID, Receptor Cell Biol Sect, NIH, Rockville, MD 20852 USA.
[Collins, Robert H.] Univ Texas SW Med Ctr Dallas, Internal Med, Dallas, TX 75390 USA.
[You, M. James] Univ Texas Grad Sch Biomed Sci Houston, Houston, TX 77030 USA.
[Cui, Changhao] Dalian Univ Technol, Sch Life Sci & Med, Panjin 124221, Liaoning, Peoples R China.
RP Zhang, CC (reprint author), Univ Texas SW Med Ctr Dallas, Dept Physiol, Dallas, TX 75390 USA.
EM Alec.Zhang@UTSouthwestern.edu
FU NIH [1R01CA172268]; Leukemia & Lymphoma Society [1024-14, TRP-6024-14,
CPRIT RP140402]; March of Dimes Foundation [1-FY14-201]; Robert A. Welch
Foundation [I-1834]; When Everyone Survives Foundation; V Foundation for
Cancer Research; William Lawrence and Blanche Hughes Fund; National
Cancer Institute [4 R00CA151457-03]; Leukemia Lymphoma Society; Susan G.
Komen Foundation [RO1GM087305]; National Institute Allergy and
Infectious Diseases; NIH/NCI [R01 CA164346]; Ladies Leukemia Leaque,
Developmental Research Awards in Leukemia [SPORE CA100632]; Center for
Inflammation and Cancer; IRG; Center for Genetics and Genomics; Sister
Institution Network fund; Physician Scientist Award of the Univmsity of
Texas MD Anderson Care Center
FX We would lie to thank II. Saya from Keio University School of Medicine
for the pMX-IG N-Myc vector. We appreciate the support of staff of the
tissue bank at the Department of Hematopathology, the University of
Texas MD Anderson Cancer Center. Support to C.C.Z. was from NIH grant
1R01CA172268, Leukemia & Lymphoma Society Awards 1024-14 and
TRP-6024-14, CPRIT RP140402, March of Dimes Foundation grant 1-FY14-201,
Robert A. Welch Foundation grant I-1834, and When Everyone Survives
Foundation. J.W.T. is supported by grants from the V Foundation for
Cancer Research, the William Lawrence and Blanche Hughes Fund, and the
National Cancer Institute (4 R00CA151457-03), and the Leukemia Lymphoma
Society. X.X. is supported by Susan G. Komen Foundation and RO1GM087305.
J.W.C. is supported by the intramural program of the National Institute
Allergy and Infectious Diseases. M.J.Y. is supported in part by NIH/NCI
R01 CA164346, Ladies Leukemia Leaque, Developmental Research Awards in
Leukemia SPORE CA100632, and Center for Inflammation and Cancer, IRG,
Center for Genetics and Genomics, Sister Institution Network fund and
Physician Scientist Award of the Univmsity of Texas MD Anderson Care
Center.
NR 57
TC 14
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U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
EI 1476-4679
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD MAY
PY 2015
VL 17
IS 5
BP 665
EP U286
DI 10.1038/nch3158
PG 28
WC Cell Biology
SC Cell Biology
GA CH1HG
UT WOS:000353771500014
PM 25915125
ER
PT J
AU Kroeze, WK
Sassano, MF
Huang, XP
Lansu, K
McCorvy, JD
Giguere, PM
Sciaky, N
Roth, BL
AF Kroeze, Wesley K.
Sassano, Maria F.
Huang, Xi-Ping
Lansu, Katherine
McCorvy, John D.
Giguere, Patrick M.
Sciaky, Noah
Roth, Bryan L.
TI PRESTO-Tango as an open-source resource for interrogation of the
druggable human GPCRome
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; BETA-ARRESTIN BINDING; OPIOID RECEPTOR;
SCREENING ASSAY; ACTIVATION; CELLS; SUBTYPES; IDENTIFICATION;
DOPAMINE-D-2; PHARMACOLOGY
AB G protein-coupled receptors (GPCRs) are essential mediators of cellular signaling and are important targets of drug action. Of the approximately 350 nonolfactory human GPCRs, more than 100 are still considered to be 'orphans' because their endogenous ligands remain unknown. Here, we describe a unique open-source resource that allows interrogation of the druggable human GPCRome via a G protein-independent beta-arrestin-recruitment assay. We validate this unique platform at more than 120 nonorphan human GPCR targets, demonstrate its utility for discovering new ligands for orphan human GPCRs and describe a method (parallel receptorome expression and screening via transcriptional output, with transcriptional activation following arrestin translocation (PRESTO-Tango)) for the simultaneous and parallel interrogation of the entire human nonolfactory GPCRome.
C1 [Kroeze, Wesley K.; Sassano, Maria F.; Huang, Xi-Ping; Lansu, Katherine; McCorvy, John D.; Giguere, Patrick M.; Sciaky, Noah; Roth, Bryan L.] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Kroeze, Wesley K.; Sassano, Maria F.; Huang, Xi-Ping; Roth, Bryan L.] Univ N Carolina, NIMH, Psychoact Drug Screening Program, Chapel Hill, NC USA.
[Roth, Bryan L.] Univ N Carolina, Program Neurosci, Chapel Hill, NC USA.
[Roth, Bryan L.] Univ N Carolina, Div Chem Biol & Med Chem, Chapel Hill, NC USA.
RP Roth, BL (reprint author), Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA.
EM bryan_roth@med.unc.edu
RI Roth, Bryan/F-3928-2010
FU US National Institutes of Health [R01DA27170, UO1MH104974]; US National
Institute of Mental Health Psychoactive Drug Screening Program; Michael
Hooker Distinguished Professorship; University of North Carolina
Department of Pharmacology Training Program [NIH 5-T32-GM007040]
FX This work was supported by US National Institutes of Health grant
R01DA27170 (B.L.R., M.F.S. and W.K.K.) and UO1MH104974 (B.L.R., W.K.K.,
M.F.S. and K.L.), the US National Institute of Mental Health
Psychoactive Drug Screening Program (B.L.R., M.F.S., W.K.K. and X.-P.H.)
and the Michael Hooker Distinguished Professorship (B.L.R.). K.L. was
supported by the University of North Carolina Department of Pharmacology
Training Program (NIH 5-T32-GM007040). The authors thank R. Stevens and
S. Katrich for allowing us to use and modify their GPCRome tree (Fig. 6)
from ref. 49. We thank R. Axel (Columbia University) for providing HTLA
cells.
NR 50
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U1 0
U2 5
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 MAY
PY 2015
VL 22
IS 5
BP 362
EP U28
DI 10.1038/nsmb.3014
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA CH5SD
UT WOS:000354094700008
PM 25895059
ER
PT J
AU Gonzalez, I
Munita, R
Agirre, E
Dittmer, TA
Gysling, K
Misteli, T
Luco, RF
AF Gonzalez, Inma
Munita, Roberto
Agirre, Eneritz
Dittmer, Travis A.
Gysling, Katia
Misteli, Tom
Luco, Reini F.
TI A lncRNA regulates alternative splicing via establishment of a
splicing-specific chromatin signature
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID LONG NONCODING RNA; HISTONE H3; TRIMETHYLATION; TRANSCRIPTION;
EXPRESSION; COMPLEXES
AB Alternative pre-mRNA splicing is a highly cell type-specific process essential to generating protein diversity. However, the mechanisms responsible for the establishment and maintenance of heritable cell-specific alternative-splicing programs are poorly understood. Recent observations point to a role of histone modifications in the regulation of alternative splicing. Here we report a new mechanism of chromatin-mediated splicing control involving a long noncoding RNA (lncRNA). We have identified an evolutionarily conserved nuclear antisense lncRNA, generated from within the human FGFR2 locus, that promotes epithelial-specific alternative splicing of FGFR2. The lncRNA acts through recruitment of Polycomb-group proteins and the histone demethylase KDM2a to create a chromatin environment that impairs binding of a repressive chromatin-splicing adaptor complex important for mesenchymal-specific splicing. Our results uncover a new function for lncRNAs in the establishment and maintenance of cell-specific alternative splicing via modulation of chromatin signatures.
C1 [Gonzalez, Inma; Agirre, Eneritz; Luco, Reini F.] CNRS, Inst Human Genet, ATIP AVENIR Team, UPR 1142, Montpellier, France.
[Munita, Roberto; Gysling, Katia] Pontificia Univ Catolica Chile, Fac Biol Sci, Santiago, Chile.
[Dittmer, Travis A.; Misteli, Tom] NCI, NIH, Bethesda, MD 20892 USA.
RP Luco, RF (reprint author), CNRS, Inst Human Genet, ATIP AVENIR Team, UPR 1142, Montpellier, France.
EM mistelit@mail.nih.gov; reini.luco@igh.cnrs.fr
FU Intramural Research Program of the US National Institutes of Health,
National Cancer Institute, Center for Cancer Research; French Fondation
de la Recherche Medical starting grant [AJE201132]; Fondation ARC pour
la Recherche sur le Cancer under the program ATIP-AVENIR; European
EpiGeneSys network of excellence; Chilean Millennium Science Initiative
grant [P10/063-F]
FX We thank V.J. Bardwell (University of Minnesota), R. Carstens
(University of Pennsylvania), C.S. Duckett (University of Michigan), M.
Garcia-Blanco (Duke University), K. Helin (Biotech Research and
Innovation Centre, University of Copenhagen), H. Kimura (Osaka
University), H. Koseki (RIKEN Center for Integrative Medical Sciences),
R. Klose (Oxford University), D. Reinberg (New York University School of
Medicine), K. Tominaga (Jichi Medical School) and D. Haber
(Massachusetts General Hospital) for reagents; A. Farcas (R. Klose
laboratory) for developing the anti-KDM2b antibody; S. Martinez (R.F.L.
laboratory) for establishing the epithelial-to-mesenchymal-transition
system; and P. Scaffidi, N. Rascovan, K. Meaburn and R. Klose for
discussions and critical reading of the manuscript. This work was
supported by the Intramural Research Program of the US National
Institutes of Health, National Cancer Institute, Center for Cancer
Research (T.M., R.F.L. and T.A.D.), the French Fondation de la Recherche
Medical starting grant AJE201132 (R.F.L., I.G. and E.A.), the Fondation
ARC pour la Recherche sur le Cancer under the program ATIP-AVENIR
(I.G.), the European EpiGeneSys network of excellence (E.A.) and the
Chilean Millennium Science Initiative grant P10/063-F (R.M. and K.G.).
NR 34
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U1 5
U2 25
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 MAY
PY 2015
VL 22
IS 5
BP 370
EP U111
DI 10.1038/nsmb.3005
PG 10
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA CH5SD
UT WOS:000354094700009
PM 25849144
ER
PT J
AU Basselin, M
Ramadan, E
Chen, M
Rapoport, SI
AF Basselin, Mireille
Ramadan, Epolia
Chen, Mei
Rapoport, Stanley I.
TI Anti-Inflammatory Effects of Chronic Aspirin on Brain Arachidonic Acid
Metabolites (Retraction of vol 36, pg 139, 2011)
SO NEUROCHEMICAL RESEARCH
LA English
DT Correction
C1 [Basselin, Mireille; Ramadan, Epolia; Chen, Mei; Rapoport, Stanley I.] NIA, NIH, Brain Physiol & Metab Sect, Bethesda, MD 20892 USA.
RP Ramadan, E (reprint author), NIA, NIH, Brain Physiol & Metab Sect, Bldg 9,Room 1S126,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ramadanir@mail.nih.gov
NR 1
TC 0
Z9 0
U1 2
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-3190
EI 1573-6903
J9 NEUROCHEM RES
JI Neurochem. Res.
PD MAY
PY 2015
VL 40
IS 5
BP 1094
EP 1094
DI 10.1007/s11064-015-1583-4
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CH5SH
UT WOS:000354095100023
ER
PT J
AU Zhu, J
Qu, YQ
Ma, T
Li, R
Du, YZ
Huang, SH
Shung, KK
Zhou, QF
Chen, ZP
AF Zhu, Jiang
Qu, Yueqiao
Ma, Teng
Li, Rui
Du, Yongzhao
Huang, Shenghai
Shung, K. Kirk
Zhou, Qifa
Chen, Zhongping
TI Imaging and characterizing shear wave and shear modulus under orthogonal
acoustic radiation force excitation using OCT Doppler variance method
SO OPTICS LETTERS
LA English
DT Article
ID OPTICAL COHERENCE TOMOGRAPHY; IN-VIVO; ELASTOGRAPHY; TISSUE; ULTRASOUND;
STRAIN
AB We report on a novel acoustic radiation force orthogonal excitation optical coherence elastography (ARFOE-OCE) technique for imaging shear wave and quantifying shear modulus under orthogonal acoustic radiation force (ARF) excitation using the optical coherence tomography (OCT) Doppler variance method. The ARF perpendicular to the OCT beam is produced by a remote ultrasonic transducer. A shear wave induced by ARF excitation propagates parallel to the OCT beam. The OCT Doppler variance method, which is sensitive to the transverse vibration, is used to measure the ARF-induced vibration. For analysis of the shear modulus, the Doppler variance method is utilized to visualize shear wave propagation instead of Doppler OCT method, and the propagation velocity of the shear wave is measured at different depths of one location with the M scan. In order to quantify shear modulus beyond the OCT imaging depth, we move ARF to a deeper layer at a known step and measure the time delay of the shear wave propagating to the same OCT imaging depth. We also quantitatively map the shear modulus of a cross-section in a tissue-equivalent phantom after employing the B scan. (C) 2015 Optical Society of America
C1 [Zhu, Jiang; Qu, Yueqiao; Li, Rui; Du, Yongzhao; Huang, Shenghai; Chen, Zhongping] Univ Calif Irvine, Beckman Laser Inst, Irvine, CA 92612 USA.
[Qu, Yueqiao; Chen, Zhongping] Univ Calif Irvine, Dept Biomed Engn, Irvine, CA 92697 USA.
[Ma, Teng; Shung, K. Kirk; Zhou, Qifa] Univ So Calif, Ultrason Transducer Resource Ctr, Dept Biomed Engn, NIH, Los Angeles, CA 90089 USA.
RP Chen, ZP (reprint author), Univ Calif Irvine, Beckman Laser Inst, 1002 Hlth Sci Rd East, Irvine, CA 92612 USA.
EM z2chen@uci.edu
RI Zhu, Jiang/O-4869-2016
OI Zhu, Jiang/0000-0002-2601-4967
FU National Institutes of Health [R01EB-10090, R01HL-125084, R01HL-105215,
R01EY-021529, P41-EB002182, P41-EB015890]
FX This work was supported by the National Institutes of Health under
grants R01EB-10090, R01HL-125084, R01HL-105215, R01EY-021529,
P41-EB002182, P41-EB015890. Dr. Zhongping Chen has a financial interest
in OCT Medical Inc, which, however, did not support this work.
NR 20
TC 5
Z9 6
U1 0
U2 9
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 0146-9592
EI 1539-4794
J9 OPT LETT
JI Opt. Lett.
PD MAY 1
PY 2015
VL 40
IS 9
BP 2099
EP 2102
DI 10.1364/OL.40.002099
PG 4
WC Optics
SC Optics
GA CH3IQ
UT WOS:000353924600056
PM 25927794
ER
PT J
AU Wang, EA
McGinms, KA
Goulet, J
Bryant, K
Gibert, C
Leaf, DA
Mattocks, K
Fiellin, LE
Vogenthaler, N
Justice, AC
Fiellin, DA
AF Wang, Emily A.
McGinms, Kathleen A.
Goulet, Joseph
Bryant, Kendall
Gibert, Cynthia
Leaf, David A.
Mattocks, Kristin
Fiellin, Lynn E.
Vogenthaler, Nicholas
Justice, Amy C.
Fiellin, David A.
CA Vet Aging Cohort Study Project Tea
TI Food Insecurity and Health: Data from the Veterans Aging Cohort Study
SO PUBLIC HEALTH REPORTS
LA English
DT Article
ID HIV-INFECTED INDIVIDUALS; MENTAL-HEALTH; HOUSING INSTABILITY; WELFARE
RECIPIENTS; INSUFFICIENCY; CARE; MORTALITY; ADULTS; CHILDREN; DISEASE
AB Objective. Food insecurity may be a modifiable and independent risk factor for worse control of medical conditions, but it has not been explored among veterans. We determined the prevalence of, and factors independently associated with, food insecurity among veterans in the Veterans Aging Cohort Study (VACS).
Methods. Using data from VACS from 2002-2008, we determined the prevalence of food insecurity among veterans who have accessed health care in the Veterans Health Administration (VA) as defined by "concern about having enough food for you or your family in the past month." We used multivariable logistic regression to determine factors independently associated with food insecurity and tests of trend to measure the association between food insecurity and control of hypertension, diabetes, HIV, and depression.
Results. Of the 6,709 veterans enrolled in VACS, 1,624 (24%) reported being food insecure. Food insecurity was independently associated with being African American, earning <$25,000/year, recent homelessness, marijuana use, and depression. Being food insecure was also associated with worse control of hypertension, diabetes, HIV and depression (p<0.001).
Conclusion. Food insecurity is prevalent and associated with worse control of medical conditions among veterans who have accessed care in the VA.
C1 [Wang, Emily A.; Goulet, Joseph; Fiellin, Lynn E.; Justice, Amy C.; Fiellin, David A.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[McGinms, Kathleen A.; Goulet, Joseph; Justice, Amy C.] VA Connecticut Healthcare Syst, West Haven, CT USA.
[Bryant, Kendall] NIAAA, NIH, Rockville, MD 20852 USA.
[Gibert, Cynthia] VA Med Ctr, Washington, DC USA.
[Gibert, Cynthia] George Washington Univ, Med Ctr, Washington, DC 20037 USA.
[Leaf, David A.] Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
[Mattocks, Kristin] VA Cent Western Massachusetts, Northampton, MA USA.
[Mattocks, Kristin] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Vogenthaler, Nicholas] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA.
[Justice, Amy C.; Fiellin, David A.] Yale Univ, Sch Publ Hlth, Ctr Interdisciplinary Res AIDS, New Haven, CT 06510 USA.
RP Wang, EA (reprint author), Yale Univ, Sch Med, Gen Internal Med, Harkness Hall Bldg A,367 Cedar St,Ste 410A, New Haven, CT 06510 USA.
EM emily.wang@yale.edu
OI Fiellin, David/0000-0002-4006-010X; Goulet, Joseph/0000-0002-0842-804X
FU National Institute on Alcohol Abuse and Alcoholism [U01-AA-13566,
U10-AA-13566]; National Institute on Aging (NIA) [K23-AG00826]; Robert
Wood Johnson Generalist Faculty Scholar Award; NIA, National Institute
of Mental Health; Veterans Health Administration Health Services
Research & Development Research Enhancement Award Program (REAP) PRIME
Project [REA-08-266]; National Heart, Lung, and Blood Institute
[K23-HL103720]; Yale Clinical Center of Investigation's Clinical &
Translations Science Awards Grant [UL1 RR024139]
FX The sponsor had no role in the design and conduct of the study;
collection, management, analysis, and interpretation of the data; and
preparation, review, or approval of the manuscript. The Veterans Aging
Cohort Study (VACS) is funded by the National Institute on Alcohol Abuse
and Alcoholism (#U01-AA-13566 and #U10-AA-13566); the National Institute
on Aging (NIA) (#K23-AG00826); and the Robert Wood Johnson Generalist
Faculty Scholar Award, an interagency agreement among the NIA, National
Institute of Mental Health, and Veterans Health Administration Health
Services Research & Development Research Enhancement Award Program
(REAP) PRIME Project (#REA-08-266). Emily Wang receives salary support
from a career development award from the National Heart, Lung, and Blood
Institute (#K23-HL103720) and the Yale Clinical Center of
Investigation's Clinical & Translations Science Awards Grant (#UL1
RR024139). The Institutional Review Boards at the Veterans Health
Administrations in Atlanta, Georgia; Baltimore, Maryland; Bronx, New
York; Manhattan/Brooklyn, New York; Houston, Texas; Los Angeles,
California; Pittsburgh, Pennsylvania; and Washington, D.C., approved the
study, and all participants provided written informed consent prior to
enrollment.
NR 33
TC 7
Z9 7
U1 3
U2 11
PU ASSOC SCHOOLS PUBLIC HEALTH
PI WASHINGTON
PA 1900 M ST NW, STE 710, WASHINGTON, DC 20036 USA
SN 0033-3549
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD MAY-JUN
PY 2015
VL 130
IS 3
BP 261
EP 268
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CH5JJ
UT WOS:000354071600013
PM 25931630
ER
PT J
AU Bataller, R
Gao, B
AF Bataller, Ramon
Gao, Bin
TI Liver Fibrosis in Alcoholic Liver Disease
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE alcoholic hepatitis; hepatic stellate cells; steatohepatitis; animal
models
ID INDUCED HEPATIC-FIBROSIS; HEPATOCELLULAR-CARCINOMA; NONALCOHOLIC
STEATOHEPATITIS; GENETIC POLYMORPHISMS; STELLATE CELLS; UNITED-STATES;
RISK-FACTORS; CIRRHOSIS; INJURY; METAANALYSIS
AB Excessive alcohol consumption causes a wide spectrum of liver disease, ranging from simple steatosis to severe forms of liver injury such as steatohepatitis, liver fibrosis, cirrhosis, and liver cancer. Moreover, alcohol consumption also accelerates liver fibrosis in patients with other types of liver diseases such as viral hepatitis and nonalcoholic fatty liver disease. Virtually all clinical complications of alcoholic liver disease occur in patients with established fibrosis and cirrhosis, thus making fibrosis a key parameter for treatment and prognosis of patients. Here, the authors review diagnosis, management, and antifibrotic therapy of alcoholic liver fibrosis. They discuss both the unique features of alcoholic liver fibrosis and the similarities to liver fibrosis from other etiologies, and review molecular pathogenesis and animal models. Finally, future directions for basic and clinical research on alcoholic liver fibrosis are proposed.
C1 [Bataller, Ramon] Univ N Carolina, Dept Med, Div Gastroenterol & Hepatol, Chapel Hill, NC 27599 USA.
[Gao, Bin] NIAAA, Lab Liver Dis, Natl Inst Hlth, Bethesda, MD USA.
RP Bataller, R (reprint author), Univ N Carolina, Dept Med, Div Gastroenterol & Hepatol, Chapel Hill, NC 27599 USA.
EM ramon_bataller@med.unc.edu
NR 102
TC 16
Z9 16
U1 3
U2 17
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
EI 1098-8971
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD MAY
PY 2015
VL 35
IS 2
BP 146
EP 156
DI 10.1055/s-0035-1550054
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CH9PM
UT WOS:000354368100006
PM 25974900
ER
PT J
AU Liu, WL
Zhang, K
Locatis, C
Ackerman, M
AF Liu, Wei-Li
Zhang, Kai
Locatis, Craig
Ackerman, Michael
TI Cloud and Traditional Videoconferencing Technology for Telemedicine and
Distance Learning
SO TELEMEDICINE AND E-HEALTH
LA English
DT Article
DE telecommunications; distance learning; cloud computing; technology;
telemedicine
AB Introduction: Cloud-based videoconferencing versus traditional systems are described for possible use in telemedicine and distance learning. Materials and Methods: Differences between traditional and cloud-based videoconferencing systems are examined, and the methods for identifying and testing systems are explained. Findings are presented characterizing the cloud conferencing genre and its attributes versus traditional H.323 conferencing. Results: Because the technology is rapidly evolving and needs to be evaluated in reference to local needs, it is strongly recommended that this or other reviews not be considered substitutes for personal hands-on experience. Conclusions: This review identifies key attributes of the technology that can be used to appraise the relevance of cloud conferencing technology and to determine whether migration from traditional technology to a cloud environment is warranted. An evaluation template is provided for assessing systems appropriateness.
C1 [Liu, Wei-Li; Zhang, Kai; Locatis, Craig; Ackerman, Michael] Natl Lib Med, Off High Performance Comp & Commun, Bethesda, MD 20894 USA.
RP Liu, WL (reprint author), Natl Lib Med, Off High Performance Comp & Commun, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM wliu@mail.nih.gov
FU National Institutes of Health/National Library of Medicine intramural
research program
FX This review was supported by the National Institutes of Health/National
Library of Medicine intramural research program. The authors acknowledge
the contributions of Willis Nguyen, a student intern who helped install
and test the programs.
NR 9
TC 1
Z9 1
U1 1
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1530-5627
EI 1556-3669
J9 TELEMED E-HEALTH
JI Telemed. e-Health
PD MAY 1
PY 2015
VL 21
IS 5
BP 422
EP 426
DI 10.1089/tmj.2014.0121
PG 5
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA CH5UA
UT WOS:000354099600011
PM 25785761
ER
PT J
AU Zeng, PB
Ma, LL
Gao, Z
Wang, JX
Liu, J
Huang, XW
Yang, QZ
Cao, R
Wen, XQ
Zhu, LL
Ma, HL
Yang, ZD
Lee, TH
Brambilla, D
Yuan, M
Glynn, S
Ness, P
Kleinman, S
Busch, M
Shan, H
AF Zeng, Peibin
Ma, Lili
Gao, Zhan
Wang, Jingxing
Liu, Jing
Huang, Xianwei
Yang, Qizhi
Cao, Ruan
Wen, Xiuqiong
Zhu, Lili
Ma, Hongli
Yang, Zhendong
Lee, Tzong-Hae
Brambilla, Donald
Yuan, Michelle
Glynn, Simone
Ness, Paul
Kleinman, Steve
Busch, Michael
Shan, Hua
CA Int Component NHLBI Recipient
TI A study of seroprevalence and rates of asymptomatic viremia of severe
fever with thrombocytopenia syndrome virus among Chinese blood donors
SO TRANSFUSION
LA English
DT Article
ID SHANDONG PROVINCE; INFECTION; BUNYAVIRUS; ASSAY; TRANSMISSION;
ANTIBODIES; CONTACT
AB BackgroundSevere fever with thrombocytopenia syndrome virus (SFTSV), an emerging tick-borne pathogen that can cause fatal severe fever with thrombocytopenia syndrome, was first identified in China in 2009. Limited evidence suggests that SFTSV can be transmitted between humans via blood contact, raising concerns over transfusion safety. A study of donor samples from three Chinese blood centers was conducted to investigate the seroprevalence and rate of SFTSV viremia among Chinese blood donors.
Study Design and MethodsFrom April 16 to October 31, 2012, a total of 17,208 plasma samples were collected from donors at Xinyang (located in an SFTSV-endemic area), Mianyang, and Luoyang Blood Centers. Assessment of anti-SFTSV total antibody was performed on all samples using enzyme-linked immunosorbent assay. Repeat-reactive samples were tested for SFTSV RNA using reverse transcription (RT)-real-time polymerase chain reaction (PCR) assay with Taqman probes. In addition, 9960 of the Xinyang samples were tested in pools of 4 by the same PCR method and each of the samples in a reactive pool was tested individually.
ResultsDonor seroreactivity rates were as follows: Xinyang, 0.54% (80/14,752); Mianyang, 0.27% (3/1130); and Luoyang, 0.28% (3/1326). All seroreactive samples were negative on RT-PCR single-sample testing. Two RT-PCR-reactive donor samples were identified, both with estimated viral loadof less than20plaque-forming units/mL. The RNA prevalence rate for SFTSV among donors in Xinyang was 0.02%.
ConclusionThis was the first multiregion study of SFTSV sero- and viral prevalence among Chinese blood donors. Viral prevalence was low and no seroreactive sample was viremic, suggesting a limited impact of SFTSV on blood safety in China.
C1 [Zeng, Peibin; Ma, Lili; Gao, Zhan; Wang, Jingxing] Chinese Acad Med Sci, Inst Blood Transfus, Chengdu 610052, Sichuan, Peoples R China.
[Liu, Jing; Ness, Paul; Shan, Hua] Johns Hopkins Univ Hosp, Dept Transfus Med, Baltimore, MD 21287 USA.
[Huang, Xianwei; Yang, Qizhi] Xinyang Blood Ctr, Xinyang, Peoples R China.
[Cao, Ruan; Wen, Xiuqiong] Mianyang Blood Ctr, Mianyang, Peoples R China.
[Zhu, Lili; Ma, Hongli] Luoyang Blood Ctr, Luoyang, Peoples R China.
[Yang, Zhendong; Busch, Michael] Xinyang 154 Mil Hosp, Xinyang, Peoples R China.
[Lee, Tzong-Hae] Blood Syst Res Inst, San Francisco, CA USA.
[Brambilla, Donald; Yuan, Michelle] RTI Int, Rockville, MD USA.
[Glynn, Simone] NHLBI, Bethesda, MD 20892 USA.
[Kleinman, Steve] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
RP Zeng, PB (reprint author), Chinese Acad Med Sci, Inst Blood Transfus, Chengdu 610052, Sichuan, Peoples R China.
EM zengpeibin@live.cn
FU NHLBI Recipient Epidemiology and Donor Evaluation Study-III [X101222002]
FX This work was supported by the NHLBI Recipient Epidemiology and Donor
Evaluation Study-III (X101222002).
NR 24
TC 3
Z9 3
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0041-1132
EI 1537-2995
J9 TRANSFUSION
JI Transfusion
PD MAY
PY 2015
VL 55
IS 5
BP 965
EP 971
DI 10.1111/trf.12953
PG 7
WC Hematology
SC Hematology
GA CH8JB
UT WOS:000354281500009
PM 25496479
ER
PT J
AU Custer, B
Kessler, D
Vahidnia, F
Leparc, G
Krysztof, DE
Shaz, B
Kamel, H
Glynn, S
Dodd, RY
Stramer, SL
AF Custer, Brian
Kessler, Debra
Vahidnia, Farnaz
Leparc, German
Krysztof, David E.
Shaz, Beth
Kamel, Hany
Glynn, Simone
Dodd, Roger Y.
Stramer, Susan L.
CA NHLBI Retrovirus Epidemiology
TI Risk factors for retrovirus and hepatitis virus infections in accepted
blood donors
SO TRANSFUSION
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; B-VIRUS; UNITED-STATES; RESIDUAL RISK;
BEHAVIORAL-CHARACTERISTICS; NATIONAL-HEALTH; PREVALENCE; EPIDEMIOLOGY;
DONATION; EXPERIENCE
AB BackgroundRisk factor surveillance among infected blood donors provides information on the effectiveness of eligibility assessment and is critical for reducing risk of transfusion-transmitted infection.
Study Design and MethodsAmerican Red Cross, Blood Systems, Inc., New York Blood Center, and OneBlood participated in a case-control study from 2010 to 2013. Donors with serologic and nucleic acid testing (NAT) or NAT-only confirmed human immunodeficiency virus (HIV), hepatitisB virus (HBV), hepatitisC virus (HCV), or serology-confirmed human T-lymphotropic virus (HTLV) infections (cases) and donors with false-positive results (controls) were interviewed for putative behavioral and demographic risks. Frequencies and adjusted odds ratios (AORs) from multivariable logistic regression analyses for each exposure in cases compared to controls are reported.
ResultsIn the study, 196 HIV, 292 HBV, 316 HCV, and 198 HTLV cases, and 1587 controls were interviewed. For HIV, sex with an HIV+ person (AOR, 132; 95% confidence interval [CI], 27-650) and male-male sex (AOR, 62; 95% CI, 27-140) were primary risk factors. For HBV, first-time donor status (AOR, 16; 95% CI, 10-27), sex with an injection drug user (IDU; AOR, 11; 95% CI, 5-28), and black race (AOR, 11; 95% CI, 6-19) were primary. For HCV, IDU (AOR, 42; 95% CI, 13-136), first time (AOR, 18; 95% CI, 10-30), and a family member with hepatitis (AOR, 15; 95% CI, 6-40) were primary. For HTLV, sex with an IDU (AOR, 22; 95% CI, 10-48), 55 years old or more (AOR, 21; 95% CI, 8-52], and first time (AOR, 15; 95% CI, 9-24) were primary.
ConclusionsDespite education efforts and risk screening, individuals with deferrable risks still donate; they may fail to understand or ignore or do not believe they have risk. Recipients have potential transfusion-transmitted infection risk because of nondisclosure by donors.
C1 [Custer, Brian; Vahidnia, Farnaz] Blood Syst Res Inst, San Francisco, CA 94118 USA.
[Custer, Brian] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
[Kessler, Debra; Shaz, Beth] New York Blood Ctr, New York, NY 10021 USA.
[Leparc, German] OneBlood, Tampa, FL USA.
[Krysztof, David E.; Stramer, Susan L.] Amer Red Cross, Sci Support Off, Gaithersburg, MD USA.
[Kamel, Hany] Blood Syst Inc, Scottsdale, AZ USA.
[Glynn, Simone] NHLBI, NIH, Rockville, MD USA.
[Dodd, Roger Y.] Amer Red Cross, Holland Lab, Rockville, MD USA.
RP Custer, B (reprint author), Blood Syst Res Inst, 270 Masonic Ave, San Francisco, CA 94118 USA.
EM bcuster@bloodsystems.org
OI Vahidnia, Farnaz/0000-0003-1130-4643
FU Retrovirus Epidemiology Donor Study-II (REDS-II) - National Heart, Lung
and Blood Institute, National Institutes of Health [HHSN26820041717]
FX This study was funded by research contract HHSN26820041717 from the
Retrovirus Epidemiology Donor Study-II (REDS-II) sponsored by the
National Heart, Lung and Blood Institute, National Institutes of Health.
NR 37
TC 13
Z9 13
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0041-1132
EI 1537-2995
J9 TRANSFUSION
JI Transfusion
PD MAY
PY 2015
VL 55
IS 5
BP 1098
EP 1107
DI 10.1111/trf.12951
PG 10
WC Hematology
SC Hematology
GA CH8JB
UT WOS:000354281500027
PM 25470984
ER
PT J
AU Hall, EC
Engels, EA
Pfeiffer, RM
Segev, DL
AF Hall, Erin C.
Engels, Eric A.
Pfeiffer, Ruth M.
Segev, Dorry L.
TI Association of Antibody Induction Immunosuppression With Cancer After
Kidney Transplantation
SO TRANSPLANTATION
LA English
DT Article
ID POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDER; NON-HODGKIN-LYMPHOMA;
UNITED-STATES; RENAL-TRANSPLANTATION; DEPLETIONAL INDUCTION;
RISK-FACTORS; RECIPIENTS; EPIDEMIOLOGY; ALEMTUZUMAB; SEROSTATUS
AB Background. Induction immunosuppression is a main stay of rejection prevention after transplantation. Studies have suggested a connection between antibody induction agents and cancer development, potentially limiting important immunosuppression protocols. Methods. We used a linkage of U.S. transplantation data and cancer registries to explore the relationship between induction and cancer after transplantation. A total of 111,857 kidney recipients (1987-2009) in the Transplant Cancer Match Study, which links the Scientific Registry for Transplant Recipients and U.S. Cancer Registries, were included. Poisson regression models were used to estimate adjusted incidence rate ratios (aIRR) of non-Hodgkin lymphoma (NHL) and other cancers with increased incidence after transplantation (lung, colorectal, kidney, and thyroid cancers, plus melanoma). Results. Two thousand seven hundred sixty-three cancers of interest were identified. Muromonab-CD3 was associated with increased NHL (aIRR, 1.37; 95% CI, 1.06-1.76). Alemtuzumab was associated with increased NHL (aIRR, 1.79; 95% CI, 1.02-3.14), colorectal cancer (aIRR, 2.46; 95% CI, 1.03-5.91), and thyroid cancer (aIRR, 3.37; 95% CI, 1.55-7.33). Polyclonal induction was associated with increased melanoma (aIRR, 1.50; 95% CI, 1.06-2.14). Conclusion. Our findings highlight the relative safety with regard to cancer risk of themost common induction therapies, the need for surveillance of patients treated with alemtuzumab, and the possible role for increased melanoma screening for those patients treated with polyclonal anti-T-cell induction.
C1 [Hall, Erin C.; Segev, Dorry L.] Johns Hopkins Sch Med, Dept Surg, Baltimore, MD USA.
[Hall, Erin C.; Engels, Eric A.; Pfeiffer, Ruth M.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Segev, Dorry L.] Johns Hopkins Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
RP Segev, DL (reprint author), Johns Hopkins Med Inst, Transplant Surg, 720 Rutland Ave,Ross 771B, Baltimore, MD 21205 USA.
EM dorry@jhmi.edu
FU National Cancer Institute; National Institute of Health; Sanofi
Pharmaceuticals; Arbor Research Collaborative for Health in Ann Arbor,
MI [HHSH234200537009C]; National Program of Cancer Registries ofthe
Centers for Disease Control and Prevention: California [1U58
DP000807-01]; National Program of Cancer Registries ofthe Centers for
Disease Control and Prevention: Colorado [U58 DP000848-04]; National
Program of Cancer Registries ofthe Centers for Disease Control and
Prevention: Georgia [5U58DP000817-05]; National Program of Cancer
Registries ofthe Centers for Disease Control and Prevention: Illinois
[5658DP000805-04]; National Program of Cancer Registries ofthe Centers
for Disease Control and Prevention: Michigan [5U58DP000812-03]; National
Program of Cancer Registries ofthe Centers for Disease Control and
Prevention: New Jersey [5U58/DP000808-05]; National Program of Cancer
Registries ofthe Centers for Disease Control and Prevention: New York
[150351]; National Program of Cancer Registries ofthe Centers for
Disease Control and Prevention: North Carolina [U58DP000832]; National
Program of Cancer Registries ofthe 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 [N01-PC-35143]; National
Cancer Institute: New Jersey [HHSN261201000027C N01-PC-54405]; National
Cancer Institute: Seattle-Puget Sound [N01-PC-35142]; National Cancer
Institute: Utah [HHSN261201000026C]; state of California; state of
Colorado; state of Connecticut; state of Illinois; state of Iowa; state
of New Jersey; state of New York (Cancer Surveillance Improvement
Initiative) [14-2491]; state of Texas; state of Washington; Fred
Hutchinson Cancer Research Center in Seattle, WA
FX E.A.E. and R.M.P. were supported by Intramural Research Program
(National Cancer Institute). E.C.H. was supported by a National
Institute of Health training grant. D.L.S. was supported by Sanofi
Pharmaceuticals (Investigator-Initiated Grant).; During the initial
period when registry linkages were performed, the SRTR was managed by
Arbor Research Collaborative for Health in Ann Arbor, MI (contract
HHSH234200537009C); beginning in September 2010, the SRTR was managed by
Minneapolis Medical Research Foundation in Minneapolis, MN
(HHSH250201000018C). The following cancer registries were supported by
the National Program of Cancer Registries ofthe Centers for Disease
Control and Prevention: California (agreement 1U58 DP000807-01),
Colorado (U58 DP000848-04), Georgia (5U58DP000817-05), Illinois
(5658DP000805-04), Michigan (5U58DP000812-03), New Jersey
(5U58/DP000808-05), New York (150351), North Carolina (U58DP000832), and
Texas (5U58DP000824-04). The following cancer registries were supported
by the SEER Program of the National Cancer Institute: California
(contracts HHSN261201000036C, HHSN261201000035C, and HHSN261201000034C),
Connecticut (HHSN261201000024C), Hawaii (HHSN261201000037C,
N01-PC-35137, and N01-PC-35139), Iowa (N01-PC-35143), New Jersey
(HHSN261201000027C N01-PC-54405), Seattle-Puget Sound (N01-PC-35142),
and Utah (HHSN261201000026C). Additional support was provided by the
states of California, Colorado, Connecticut, Illinois, Iowa, New Jersey,
New York (Cancer Surveillance Improvement Initiative 14-2491), Texas,
and Washington, as well as the Fred Hutchinson Cancer Research Center in
Seattle, WA.
NR 28
TC 9
Z9 11
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD MAY
PY 2015
VL 99
IS 5
BP 1051
EP 1057
DI 10.1097/TP.0000000000000449
PG 7
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA CH3WW
UT WOS:000353962700032
PM 25340595
ER
PT J
AU Sanchez-Martin, D
Sorensen, MD
Lykkemark, S
Sanz, L
Kristensen, P
Ruoslahti, E
Alvarez-Vallina, L
AF Sanchez-Martin, David
Sorensen, Morten Draeby
Lykkemark, Simon
Sanz, Laura
Kristensen, Peter
Ruoslahti, Erkki
Alvarez-Vallina, Luis
TI Selection strategies for anticancer antibody discovery: searching off
the beaten path
SO TRENDS IN BIOTECHNOLOGY
LA English
DT Review
DE therapeutic antibodies; tumor-associated antigens; phage display;
advanced phage selections
ID PHAGE DISPLAY LIBRARY; SINGLE-CHAIN FV; LASER CAPTURE MICRODISSECTION;
CELL-SURFACE ANTIGENS; IN-VIVO SELECTION; CANCER CELLS; TUMOR-ANTIGENS;
COLORECTAL-CANCER; PERIPHERAL-BLOOD; HETEROGENEOUS POPULATION
AB Antibody-based drugs represent one of the most successful and promising therapeutic approaches in oncology. Large combinatorial phage antibody libraries are available for the identification of therapeutic antibodies and various technologies exist for their further conversion into multivalent and multispecific formats optimized for the desired pharmacokinetics and the pathological context. However, there is no technology for antigen profiling of intact tumors to identify tumor markers targetable with antibodies. Such constraints have led to a relative paucity of tumor-associated antigens for antibody targeting in oncology. Here we review novel approaches aimed at the identification of antibody-targetable, accessible antigens in intact tumors. We hope that such advanced selection approaches will be useful in the development of next-generation antibody therapies for cancer.
C1 [Sanchez-Martin, David] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Sorensen, Morten Draeby] Spanish Natl Canc Res Ctr CNIO, Madrid 28029, Spain.
[Sorensen, Morten Draeby] Aarhus Univ, Dept Mol Biol & Genet, DK-8000 Aarhus C, Denmark.
[Lykkemark, Simon] Aarhus Univ, Dept Clin Med, DK-8000 Aarhus C, Denmark.
[Lykkemark, Simon] Aarhus Univ, Sinodanish Ctr, DK-8000 Aarhus C, Denmark.
[Sanz, Laura; Alvarez-Vallina, Luis] Hosp Univ Puerta Hierro, Mol Immunol Unit, Madrid 28222, Majadahonda, Spain.
[Kristensen, Peter; Alvarez-Vallina, Luis] Aarhus Univ, Dept Engn, DK-8000 Aarhus C, Denmark.
[Ruoslahti, Erkki] Sanford Burnham Med Res Inst, Ctr Canc, La Jolla, CA 92037 USA.
[Ruoslahti, Erkki] Univ Calif Santa Barbara, Ctr Nanomed, Santa Barbara, CA 93106 USA.
[Alvarez-Vallina, Luis] Univ Calif Santa Barbara, Dept Cell Mol & Dev Biol, Santa Barbara, CA 93106 USA.
RP Alvarez-Vallina, L (reprint author), Hosp Univ Puerta Hierro, Mol Immunol Unit, Madrid 28222, Majadahonda, Spain.
EM lav@eng.au.dk
RI Sanz, Laura/F-8542-2010; Sanchez-Martin, David/C-9927-2013;
OI Sanz, Laura/0000-0002-3119-3218; Sanchez-Martin,
David/0000-0002-2712-4762; Kristensen, Peter/0000-0001-7205-6853;
Lykkemark, Simon/0000-0001-8920-6926
FU Ministerio de Economia y Competitividad [BIO2011-22738]; Novo Nordisk
Foundation [11019]; National Cancer Institute; Fondo de Investigacion
Snitaria/Instituto de Salud Carlos III [PI13/00090]; Comunidad de Madrid
[S2010/BMD-2312]; Danish Cancer Society; Lundbeck Foundation
[R126-2012-12143]; Danish Council for Independent Research - Technology
and Production Sciences [09-065063, 0602-02377B]; Danish Cancer Society
[R40-A2115]
FX L.A-V. was supported by grants from the Ministerio de Economia y
Competitividad (BIO2011-22738) and the Novo Nordisk Foundation (11019).
E.R. was supported by grants from the National Cancer Institute. L.S.
was supported by grants from the Fondo de Investigacion
Snitaria/Instituto de Salud Carlos III (PI13/00090) and the Comunidad de
Madrid (S2010/BMD-2312). M.D.S. was supported by a grant from the Danish
Cancer Society. P.K. was supported by grants from the Lundbeck
Foundation (R126-2012-12143), the Danish Council for Independent
Research - Technology and Production Sciences (09-065063 and
0602-02377B), and the Danish Cancer Society (R40-A2115).
NR 90
TC 5
Z9 5
U1 2
U2 15
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0167-7799
J9 TRENDS BIOTECHNOL
JI Trends Biotechnol.
PD MAY
PY 2015
VL 33
IS 5
BP 292
EP 301
DI 10.1016/j.tibtech.2015.02.008
PG 10
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA CH6PG
UT WOS:000354157900007
PM 25819764
ER
PT J
AU Lee, PC
Rietsch, A
AF Lee, Pei-Chung
Rietsch, Arne
TI Fueling type III secretion
SO TRENDS IN MICROBIOLOGY
LA English
DT Review
DE T3SS; needle complex; flagellum; proton motive force; ATPase
ID PROTON MOTIVE FORCE; YERSINIA-ENTEROCOLITICA; FLAGELLAR FILAMENTS;
EXPORT APPARATUS; PROTEIN EXPORT; ANGSTROM RESOLUTION; ESCHERICHIA-COLI;
FLII ATPASE; SYSTEM; TRANSLOCATION
AB Type Ill secretion systems (T3SSs) are complex nanomachines that export proteins from the bacterial cytoplasm across the cell envelope in a single step. They are at the core of the machinery used to assemble the bacterial flagellum, and the needle complex many Gram-negative pathogens use to inject effector proteins into host cells and cause disease. Several models have been put forward to explain how this export is energized, and the mechanism has been the subject of considerable debate. Here we present an overview of these models and discuss their relative merits. Recent evidence suggests that the proton motive force (pmf) is the primary energy source for type Ill secretion, although contribution from refolding of secreted proteins has not been ruled out. The mechanism by which the pmf is converted to protein export remains enigmatic.
C1 [Lee, Pei-Chung] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
[Rietsch, Arne] Case Western Reserve Univ, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA.
RP Rietsch, A (reprint author), Case Western Reserve Univ, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA.
EM arne.rietsch@case.edu
OI Rietsch, Arne/0000-0002-1556-7064
FU NIAID NIH HHS [R21 AI107131]
NR 40
TC 9
Z9 9
U1 0
U2 14
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0966-842X
EI 1878-4380
J9 TRENDS MICROBIOL
JI Trends Microbiol.
PD MAY
PY 2015
VL 23
IS 5
BP 296
EP 300
DI 10.1016/j.tim.2015.01.012
PG 5
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA CH6MS
UT WOS:000354151300009
PM 25701111
ER
PT J
AU Spagnolo, PA
Colloca, L
Heilig, M
AF Spagnolo, Primavera A.
Colloca, Luana
Heilig, Markus
TI The Role of Expectation in the Therapeutic Outcomes of Alcohol and Drug
Addiction Treatments
SO ALCOHOL AND ALCOHOLISM
LA English
DT Article
ID SUBSTANCE-ABUSE TREATMENT; PLACEBO; REWARD; ATTITUDES; ADOPTION
AB Throughout history, patient-physician relationships have been acknowledged as an important component of the therapeutic effects of any pharmacological treatment. Here, we discuss the role of physicians' expectations in influencing the therapeutic outcomes of alcohol and drug addiction pharmacological treatments. As largely demonstrated, such expectations and attitudes may contribute to produce placebo and nocebo effects that in turn affect the course of the disease and the response to the therapy. This article is aimed at discussing the current insights into expectations, placebo and nocebo mechanisms and their impact on the therapeutic outcomes of alcohol and drug addiction treatments; with the goal of informing physicians and other health care providers about the potentially widespread implications for clinical practice and for a successful treatment regimen.
C1 [Spagnolo, Primavera A.; Heilig, Markus] NIAAA, Lab Clin & Translat Studies, Bethesda, MD 20892 USA.
[Colloca, Luana] Univ Maryland, Sch Nursing, Pain & Translat Symptom Sci, Baltimore, MD 21201 USA.
[Colloca, Luana] Univ Maryland, UM Ctr Adv Chron Pain Res, Baltimore, MD 21201 USA.
[Colloca, Luana] Univ Maryland, Dept Anesthesiol, Sch Med, Baltimore, MD 21201 USA.
RP Spagnolo, PA (reprint author), NIAAA, Lab Clin & Translat Studies, NIH, Clin Res Ctr, Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM vera.spagnolo@nih.gov
NR 27
TC 0
Z9 0
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0735-0414
EI 1464-3502
J9 ALCOHOL ALCOHOLISM
JI Alcohol Alcohol.
PD MAY-JUN
PY 2015
VL 50
IS 3
BP 282
EP 285
DI 10.1093/alcalc/agv015
PG 4
WC Substance Abuse
SC Substance Abuse
GA CH2AY
UT WOS:000353827100004
PM 25761920
ER
PT J
AU Emadi, A
Faramand, R
Carter-Cooper, B
Tolu, S
Ford, LA
Lapidus, RG
Wetzler, M
Wang, ES
Etemadi, A
Griffiths, EA
AF Emadi, Ashkan
Faramand, Rawan
Carter-Cooper, Brandon
Tolu, Seda
Ford, Laurie A.
Lapidus, Rena G.
Wetzler, Meir
Wang, Eunice S.
Etemadi, Arash
Griffiths, Elizabeth A.
TI Presence of isocitrate dehydrogenase mutations may predict clinical
response to hypomethylating agents in patients with acute myeloid
leukemia
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID MYELODYSPLASTIC SYNDROMES; IDH2 MUTATIONS; OLDER PATIENTS; INTENSIVE
CHEMOTHERAPY; DECITABINE; AML; DIFFERENTIATION; THERAPY; ADULTS;
AZACITIDINE
AB Mutations in IDH1 and IDH2 occur in 15-20% of AML cases, resulting in the production of 2-hydroxyglutarate, which promotes aberrant hypermethylation of DNA in leukemic cells. Although these mutations have been shown to have prognostic implications for patients with AML, optimal treatment strategies have yet to be defined. We retrospectively identified forty-two patients with AML treated with DNA methyltransferase inhibitors (DNMTIs) decitabine (n=36) or azacitidine (n=6) and performed analysis of stored samples for the presence of IDH1 and IDH2 mutations. Of the forty-two samples analyzed, seven (16.7%) had IDH mutations. Thirteen patients (31%) achieved remission [(complete remission (CR)/complete remission with incomplete count recovery (CRi)/partial response (PR)] after treatment with a DNMTI, five of seven (71.4%) with IDH mutations and eight of thirty-five (22.9%) without IDH mutations (P=0.01). When adjusted for age at diagnosis, sex, bone marrow blast percentage and cytogenetic, the odds of achieving response after administration of a DNMTI among patients with an IDH mutation was 14.2 when compared to patients without an IDH mutation (95%CI: 1.3-150.4). IDH1 and IDH2 mutations may predict a favorable response to DNMTI in patients with AML. Am. J. Hematol. 90:E77-E79, 2015. (c) 2015 Wiley Periodicals, Inc.
C1 [Emadi, Ashkan; Faramand, Rawan; Carter-Cooper, Brandon; Tolu, Seda; Lapidus, Rena G.] Univ Maryland, Sch Med, Dept Internal Med, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Ford, Laurie A.; Wetzler, Meir; Wang, Eunice S.; Griffiths, Elizabeth A.] SUNY Buffalo, Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14260 USA.
[Etemadi, Arash] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Emadi, A (reprint author), Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Leukemia & Hematol Malignancies,Med, 22 South Greene St,Room N9E24, Baltimore, MD 21201 USA.
EM aemadi@umm.eduand; elizabeth.griffiths@roswellpark.org
RI Etemadi, Arash/C-1386-2016
OI Etemadi, Arash/0000-0002-3458-1072
FU National Cancer Institute [CA 16056]; Emadi Research Foundation Account
at University of Maryland Greenebaum Cancer Center (UMGCC); Leonard S.
LuVullo Endowment for Leukemia Research; Nancy C. Cully Endowment for
Leukemia Research; Babcock Family Endowment; Heidi Leukemia Research
Fund, Buffalo, NY; Roswell Park Alliance Foundation; Louis M. Sklarow
Memorial Fund
FX Contract grant sponsor: National Cancer Institute Grant; Contract grant
number: CA 16056.; Contract grant sponsors: Emadi Research Foundation
Account at University of Maryland Greenebaum Cancer Center (UMGCC).;
Contract grant sponsor: the Leonard S. LuVullo Endowment for Leukemia
Research.; Contract grant sponsor: the Nancy C. Cully Endowment for
Leukemia Research.; Contract grant sponsor: the Babcock Family
Endowment.; Contract grant sponsor: the Heidi Leukemia Research Fund,
Buffalo, NY.; Contract grant sponsor: Roswell Park Alliance Foundation;
the Louis M. Sklarow Memorial Fund.
NR 27
TC 17
Z9 19
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD MAY
PY 2015
VL 90
IS 5
BP E77
EP E79
DI 10.1002/ajh.23965
PG 3
WC Hematology
SC Hematology
GA CG6FS
UT WOS:000353393300001
PM 25651001
ER
PT J
AU Jennings, BL
Moore, JA
Pingili, AK
Estes, AM
Fang, XR
Kanu, A
Gonzalez, FJ
Malik, KU
AF Jennings, Brett L.
Moore, Joseph A.
Pingili, Ajeeth K.
Estes, Anne M.
Fang, Xiao R.
Kanu, Alie
Gonzalez, Frank J.
Malik, Kafait U.
TI Disruption of the cytochrome P-450 1B1 gene exacerbates renal
dysfunction and damage associated with angiotensin II-induced
hypertension in female mice
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE angiotensin II; cytochrome P-450 1B1-deficient female mice; kidney
dysfunction; increased oxidative stress; reduced antioxidant activity
ID BLOOD-PRESSURE REGULATION; MESSENGER-RNA EXPRESSION; NITRIC-OXIDE
SYNTHASE; SMOOTH-MUSCLE-CELLS; SEX-DIFFERENCES; SUPEROXIDE-PRODUCTION;
OXIDATIVE STRESS; MESANGIAL CELLS; PULMONARY-HYPERTENSION;
COLLAGEN-SYNTHESIS
AB Recently, we demonstrated in female mice that protection against ANG II-induced hypertension and associated cardiovascular changes depend on cytochrome P-450 (CYP) 1B1. The present study was conducted to determine if Cyp1b1 gene disruption ameliorates renal dysfunction and organ damage associated with ANG II-induced hypertension in female mice. ANG II (700 ng.kg(-1).min(-1)) infused by miniosmotic pumps for 2 wk in female Cyp1b1(+/+) mice did not alter water consumption, urine output, Na+ excretion, osmolality, or protein excretion. However, in Cyp1b1(-/-) mice, ANG II infusion significantly increased (P < 0.05) water intake (5.50 +/- 0.42 ml/24 h with vehicle vs. 8.80 +/- 0.60 ml/24 h with ANG II), urine output (1.44 +/- 0.37 ml/24 h with vehicle vs. 4.30 +/- 0.37 ml/24 h with ANG II), and urinary Na+ excretion (0.031 +/- 0.016 mmol/24 h with vehicle vs. 0.099 +/- 0.010 mmol/24 h with ANG II), decreased osmolality (2,630 +/- 79 mosM/kg with vehicle vs. 1,280 +/- 205 mosM/kg with ANG II), and caused proteinuria (2.60 +/- 0.30 mg/24 h with vehicle vs. 6.96 +/- 0.55 mg/24 h with ANG II). Infusion of ANG II caused renal fibrosis, as indicated by an accumulation of renal interstitial alpha-smooth muscle actin, collagen, and transforming growth factor-beta in Cyp1b1(-/-) but not Cyp1b1(+/+) mice. ANG II also increased renal production of ROS and urinary excretion of thiobarburic acid-reactive substances and reduced the activity of antioxidants and urinary excretion of nitrite/nitrate and the 17 beta-estradiol metabolite 2-methoxyestradiol in Cyp1b1(-/-) but not Cyp1b1(+/+) mice. These data suggest that Cyp1b1 plays a critical role in female mice in protecting against renal dysfunction and end-organ damage associated with ANG II-induced hypertension, in preventing oxidative stress, and in increasing activity of antioxidant systems, most likely via generation of 2-methoxyestradiol from 17 beta-estradiol.
C1 [Jennings, Brett L.; Moore, Joseph A.; Pingili, Ajeeth K.; Estes, Anne M.; Fang, Xiao R.; Malik, Kafait U.] Univ Tennessee, Dept Pharmacol, Coll Med, Hlth Sci Ctr, Memphis, TN 38163 USA.
[Kanu, Alie] Univ Tennessee, Dept Physiol, Coll Med, Hlth Sci Ctr, Memphis, TN 38163 USA.
[Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
RP Malik, KU (reprint author), Univ Tennessee, Dept Pharmacol, Coll Med, Hlth Sci Ctr, 874 Union Ave, Memphis, TN 38163 USA.
EM kmalik@uthsc.edu
FU National Heart, Lung, and Blood Institute Grants [R01-HL-19134-38-39,
K01-HL-96410-04]; American Society of Pharmacology and Experimental
Therapeutics
FX This work was supported by National Heart, Lung, and Blood Institute
Grants R01-HL-19134-38-39 (to K. U. Malik) and K01-HL-96410-04 (to A.
Kanu). J. A. Moore was supported by a summer student fellowship from the
American Society of Pharmacology and Experimental Therapeutics.
NR 65
TC 2
Z9 2
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
EI 1522-1466
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD MAY 1
PY 2015
VL 308
IS 9
BP F981
EP F992
DI 10.1152/ajprenal.00597.2014
PG 12
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA CH3VD
UT WOS:000353957700004
PM 25694484
ER
PT J
AU Davis, AS
Taubenberger, JK
Bray, M
AF Davis, A. Sally
Taubenberger, Jeffery K.
Bray, Mike
TI The use of nonhuman primates in research on seasonal, pandemic and avian
influenza, 1893-2014
SO ANTIVIRAL RESEARCH
LA English
DT Review
DE Influenza A virus; Nonhuman primate; Experimental infection;
Coinfection; Pneumonia; Pathogenesis
ID A H5N1 VIRUS; EXPERIMENTAL RESPIRATORY-INFECTIONS; DEPENDENT CELLULAR
CYTOTOXICITY; POLYRIBOCYTIDYLIC ACID COMPLEX; MACAQUES
MACACA-FASCICULARIS; GORILLA-GORILLA-GORILLA; SQUIRREL-MONKEYS;
CYNOMOLGUS-MACAQUES; H1N1 INFLUENZA; RHESUS-MONKEYS
AB Attempts to reproduce the features of human influenza in laboratory animals date from the early 1890s, when Richard Pfeiffer inoculated apes with bacteria recovered from influenza patients and produced a mild respiratory illness. Numerous studies employing nonhuman primates (NHPs) were performed during the 1918 pandemic and the following decade. Most used bacterial preparations to infect animals, but some sought a filterable agent for the disease. Since the viral etiology of influenza was established in the early 1930s, studies in NHPs have been supplemented by a much larger number of experiments in mice, ferrets and human volunteers. However, the emergence of a novel swine-origin H1N1 influenza virus in 1976 and the highly pathogenic H5N1 avian influenza virus in 1997 stimulated an increase in NHP research, because these agents are difficult to study in naturally infected patients and cannot be administered to human volunteers. In this paper, we review the published literature on the use of NHPs in influenza research from 1893 through the end of 2014. The first section summarizes observational studies of naturally occurring influenza-like syndromes in wild and captive primates, including serologic investigations. The second provides a chronological account of experimental infections of NHPs, beginning with Pfeiffer's study and covering all published research on seasonal and pandemic influenza viruses, including vaccine and antiviral drug testing. The third section reviews experimental infections of NHPs with avian influenza viruses that have caused disease in humans since 1997. The paper concludes with suggestions for further studies to more clearly define and optimize the role of NHPs as experimental animals for influenza research. Published by Elsevier B.V.
C1 [Davis, A. Sally; Taubenberger, Jeffery K.] NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Davis, A. Sally] Kansas State Univ, Coll Vet Med, Dept Diagnost Med & Pathobiol, Manhattan, KS 66506 USA.
[Bray, Mike] NIAID, Div Clin Res, NIH, Bethesda, MD 20892 USA.
RP Taubenberger, JK (reprint author), NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, 33 North Dr,Room 3E19A-2 MSC 3203, Bethesda, MD 20892 USA.
EM taubenbergerj@niaid.nih.gov
OI Davis, Anne/0000-0001-5711-3936
FU Intramural Research Program of NIAID
FX This work was supported by the Intramural Research Program of NIAID.
NR 249
TC 8
Z9 8
U1 2
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
EI 1872-9096
J9 ANTIVIR RES
JI Antiviral Res.
PD MAY
PY 2015
VL 117
BP 75
EP 98
DI 10.1016/j.antiviral.2015.02.011
PG 24
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA CH0TH
UT WOS:000353734800010
PM 25746173
ER
PT J
AU Imrich, R
Alevizos, I
Bebris, L
Goldstein, DS
Holmes, CS
Illei, GG
Nikolov, NP
AF Imrich, Richard
Alevizos, Ilias
Bebris, Lolita
Goldstein, David S.
Holmes, Courtney S.
Illei, Gabor G.
Nikolov, Nikolay P.
TI Predominant Glandular Cholinergic Dysautonomia in Patients With Primary
Sjogren's Syndrome
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID DOUBLE-BLIND; FAILURE; NEUROPATHY; SYMPTOMS; DISEASE; TRIAL
AB Objective. The autonomic nervous system (ANS) modulates exocrine gland function. Available data show poor correlation between the degree of function and destruction of the exocrine glands in primary Sjogren's syndrome (SS), suggesting that other mechanisms, such as autonomic dysfunction, may be important in these patients. The aim of this study was to perform a comprehensive analysis of sympathoneural and sympathetic cholinergic function in well-characterized patients with primary SS.
Methods. Twenty-one patients with primary SS (mean +/- SEM age 44.2 +/- 2.8 years) and 13 healthy control subjects (mean +/- SEM age 50.8 +/- 1.9 years) were assessed during orthostasis and intravenous injection of edrophonium (10 mg). The postganglionic sympathetic cholinergic system was evaluated by assessing sweat production by means of the Quantitative Sudomotor Axon Reflex Test (QSART). Tests of gastric emptying were used to assess the gastrointestinal ANS in primary SS patients.
Results. The velocity index and the acceleration index were significantly higher (P < 0.05) in patients with primary SS as compared to controls, both before and during the orthostatic and edrophonium tests. Findings of other hemodynamic and neurochemical parameters did not differ between primary SS patients and controls during the orthostasis and edrophonium test; however, the edrophonium-induced saliva increment was lower in primary SS patients (P = 0.002). Abnormally low sweat production was found in 4 primary SS patients but in none of the controls, as determined by the QSART. Gastric emptying was delayed in 53% of primary SS patients.
Conclusion. We observed subtle differences in several ANS domains, including the gastrointestinal and sympathocholinergic systems, suggesting the presence of a complex ANS dysfunction in primary SS. The impact was greatest on the exocrine glands, with subtle differences in the cardiac parasympathetic function that were independent of glandular inflammation and atrophy, suggesting an alternative mechanism of disease pathogenesis in primary SS.
C1 [Imrich, Richard] Slovak Acad Sci, Inst Expt Endocrinol, Bratislava 83101, Slovakia.
[Alevizos, Ilias; Bebris, Lolita; Illei, Gabor G.; Nikolov, Nikolay P.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
[Goldstein, David S.; Holmes, Courtney S.] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA.
RP Imrich, R (reprint author), Slovak Acad Sci, Inst Expt Endocrinol, Ctr Mol Med, Vlarska 3-7, Bratislava 83101, Slovakia.
EM richard.imrich@savba.sk
FU Intramural Research Program of the National Institute of Dental and
Craniofacial Research; National Institute of Neurological Disorders and
Stroke, NIH
FX Supported by the Intramural Research Program of the National Institute
of Dental and Craniofacial Research and the National Institute of
Neurological Disorders and Stroke, NIH.
NR 28
TC 1
Z9 1
U1 0
U2 4
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 MAY
PY 2015
VL 67
IS 5
BP 1345
EP 1352
DI 10.1002/art.39044
PG 8
WC Rheumatology
SC Rheumatology
GA CH1IV
UT WOS:000353775900025
PM 25622919
ER
PT J
AU Paczesny, S
Hakim, FT
Pidala, J
Cooke, KR
Lathrop, J
Griffith, LM
Hansen, J
Jagasia, M
Miklos, D
Pavletic, S
Parkman, R
Russek-Cohen, E
Flowers, MED
Lee, S
Martin, P
Vogelsang, G
Walton, M
Schultz, KR
AF Paczesny, Sophie
Hakim, Frances T.
Pidala, Joseph
Cooke, Kenneth R.
Lathrop, Julia
Griffith, Linda M.
Hansen, John
Jagasia, Madan
Miklos, David
Pavletic, Steven
Parkman, Robertson
Russek-Cohen, Estelle
Flowers, Mary E. D.
Lee, Stephanie
Martin, Paul
Vogelsang, Georgia
Walton, Marc
Schultz, Kirk R.
TI National Institutes of Health Consensus Development Project on Criteria
for Clinical Trials in Chronic Graft-versus-Host Disease: III. The 2014
Biomarker Working Group Report
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Chronic graft-versus-host disease; Biomarkers; National Institutes of
Health; Consensus
ID STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION; REGULATORY
T-CELLS; PARAFFIN-EMBEDDED TISSUE; CHILDRENS ONCOLOGY GROUP; SERUM
CYTOKINE LEVELS; PREDICT CHRONIC GVHD; PERIPHERAL-BLOOD; GENE
POLYMORPHISMS; INCIDENTAL FINDINGS
AB Biology-based markers to confirm or aid in the diagnosis or prognosis of chronic graft-versus-host disease (GVHD) after allogeneic hematopoietic cell transplantation or monitor its progression are critically needed to facilitate evaluation of new therapies. Biomarkers have been defined as any characteristic that is objectively measured and evaluated as an indicator of a normal biological or pathogenic process, or of a pharmacologic response to a therapeutic intervention. Applications of biomarkers in chronic GVHD clinical trials or patient management include the following: (1) diagnosis and assessment of chronic GVHD disease activity, including distinguishing irreversible damage from continued disease activity; (2) prognostic risk to develop chronic GVHD; and (3) prediction of response to therapy. Sample collection for chronic GVHD biomarkers studies should be well documented following established quality control guidelines for sample acquisition, processing, preservation, and testing, at,intervals that are both calendar and event driven. The consistent therapeutic treatment of subjects and standardized documentation needed to support biomarker studies are most likely to be provided in prospective clinical trials. To date, no chronic GVHD biomarkers have been qualified for use in clinical applications. Since our previous chronic GVHD Biomarkers Working Group report in 2005, an increasing number of chronic GVHD candidate biomarkers are available for further investigation. This paper provides a 4-part framework for biomarker investigations: identification, verification, qualification, and application with terminology based on Food and Drug Administration and European Medicines Agency guidelines. (C) 2015 American Society for Blood and Marrow Transplantation.
C1 [Paczesny, Sophie] Indiana Univ Med, Dept Pediat & Immunol, Indianapolis, IN USA.
[Hakim, Frances T.; Pavletic, Steven] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Pidala, Joseph] H Lee Moffitt Canc Ctr & Res Inst, Blood & Marrow Transplantat, Tampa, FL USA.
[Cooke, Kenneth R.; Vogelsang, Georgia] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Dept Oncol, Baltimore, MD USA.
[Lathrop, Julia] Ctr Devices & Radiol Hlth Food & Drug Adm, Off Vitro Diagnost & Radiol Hlth, Silver Spring, MD USA.
[Griffith, Linda M.] NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
[Hansen, John; Flowers, Mary E. D.; Lee, Stephanie; Martin, Paul] Univ Washington, Sch Med, Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98195 USA.
[Hansen, John; Flowers, Mary E. D.; Lee, Stephanie; Martin, Paul] Univ Washington, Sch Med, Div Med Oncol, Seattle, WA 98195 USA.
[Jagasia, Madan] Vanderbilt Univ, Med Ctr, Dept Med, Div Hematol Oncol, Nashville, TN USA.
[Miklos, David] Stanford Univ, Stanford Bone Marrow Transplant Cellular Therapy, Stanford, CA 94305 USA.
[Parkman, Robertson] Univ So Calif, Childrens Hosp Los Angeles, Dept Pediat, Los Angeles, CA USA.
[Russek-Cohen, Estelle] Ctr Biol Food & Drug Adm, Div Biostat, Silver Spring, MD USA.
[Walton, Marc] Ctr Drug Evaluat & Res Food & Drug Adm, Off Translat Sci, Silver Spring, MD USA.
[Schultz, Kirk R.] BC Childrens Hosp, Michael Cuccione Childhood Canc Res Program, Vancouver, BC, Canada.
[Schultz, Kirk R.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
RP Paczesny, S (reprint author), 1044 W Walnut St,Room R4-425, Indianapolis, IN 46202 USA.
EM sophpacz@iu.edu
FU National Institutes of Health's (NIH's) National Cancer Institute,
Center for Cancer Research, Intramural Research Program and Division of
Cancer Treatment and Diagnosis, Cancer Therapy Evaluation Program;
Office of Rare Disease Research, National Center for Advancing
Translational Sciences; Division of Allergy, Immunology and
Transplantation, National Institute of Allergy and Infectious Diseases;
National Heart, Lung, and Blood Institute, Division of Blood Diseases
and Resources; Office of Rare Diseases Research/National Center for
Advancing Translational Sciences and National Cancer Institute
FX This project Was supported by the National Institutes of Health's
(NIH's) National Cancer Institute, Center for Cancer Research,
Intramural Research Program and Division of Cancer Treatment and
Diagnosis, Cancer Therapy Evaluation Program; Office of Rare Disease
Research, National Center for Advancing Translational Sciences; Division
of Allergy, Immunology and Transplantation, National Institute of
Allergy and Infectious Diseases; National Heart, Lung, and Blood
Institute, Division of Blood Diseases and Resources. The authors
acknowledge the following individuals and organizations that, by their
participation, made this project possible: American Society for Blood
and Marrow Transplantation, Center for International Bone and Marrow
Transplant Research, US Chronic GVHD Consortium (supported by Office of
Rare Diseases Research/National Center for Advancing Translational
Sciences and National Cancer Institute), German-Austrian-Swiss chronic
GVHD Consortium, National Marrow Donor Program, the Health Resources and
Services Administration, Division of Transplantation, US Department of
Human Health and Services, Canadian Blood and Marrow Transplant Group,
European Group for Blood and Marrow Transplantation, Pediatric Blood and
Marrow Transplant Consortium, and the representatives of the Brazilian
Chronic GVHD consortium (Drs. Maria Claudia Moreira, Marcia de Matos
Silva and Vaneuza Funke) and Deutsche Jose Carreras Leukamie-Stiftung.
The authors thank Dr. Joseph Antin (Dana Farber Cancer Center, Boston,
MA), Dr. Hildegard Greinix (Medical University of Vienna, Vienna,
Austria), and Dr. Gerard Socie (University Paris VII & AP-HP, Hospital
Saint Louis, Paris, France) for their critical review of the manuscript.
The organizers are in debt to patients and patient and research advocacy
groups, who made this process much more meaningful by their engagement.
Acknowledgement goes to the Meredith Cowden GVHD foundation for
facilitating the initial planning meeting in Cleveland in November of
2013 in conjunction with the National GVHD Symposium. The project group
also recognizes the contributions of numerous colleagues in the field of
blood and marrow transplantation in the United States and
internationally, medical specialists and consultants, the pharmaceutical
industry, and the NIH and US Food and Drug Administration professional
staff for their intellectual input, dedication, and enthusiasm on the
road to completion of these documents. For their expert contributions to
this 2014 NIH Biomarkers Consensus Working Group document, special
acknowledgements to Ms. Licia Masuch, Ms. Kristie Bradley, and Ms. Linda
Henson for assistance in the manuscript preparation. The opinions
expressed are those of the authors and do not represent the position of
the National Cancer Institute; the National Heart, Lung and Blood
Institute; the National Institute of Allergy and Infectious Diseases;
the National Institutes of Health; the Food and Drug Administration; or
the United States government.
NR 97
TC 15
Z9 15
U1 0
U2 3
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 MAY
PY 2015
VL 21
IS 5
BP 780
EP 792
DI 10.1016/j.bbna.2015.01.003
PG 13
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA CH2LM
UT WOS:000353856700002
PM 25644957
ER
PT J
AU Chokshi, P
Anandi, P
Jain, N
Dunavin, N
Le, RQ
Ito, S
Barrett, J
Battiwalla, M
AF Chokshi, Puja
Anandi, Prathima
Jain, Natasha
Dunavin, Neil
Le, Robert Q.
Ito, Sawa
Barrett, John
Battiwalla, Minoo
TI Minor ABO Incompatibility Does Not Impact Nonrelapse Mortality in T
Cell-Depleted Human Leukocyte Antigen-Matched Sibling Transplantation
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Letter
ID BONE-MARROW-TRANSPLANTATION; TISSUE DISTRIBUTION
C1 [Chokshi, Puja; Anandi, Prathima; Jain, Natasha; Dunavin, Neil; Le, Robert Q.; Ito, Sawa; Barrett, John; Battiwalla, Minoo] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Battiwalla, M (reprint author), NHLBI, Hematol Branch, NIH, 10-CRC,Rm 3-5330,10 Ctr Dr, Bethesda, MD 20892 USA.
EM minoo.battiwalla@nih.gov
NR 7
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD MAY
PY 2015
VL 21
IS 5
BP 954
EP 955
DI 10.1016/j.bbmt.2015.02.020
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA CH2LM
UT WOS:000353856700023
PM 25711513
ER
PT J
AU Wang, QS
Qian, L
Chen, SH
Chu, CH
Wilson, B
Oyarzabal, E
Ali, S
Robinson, B
Rao, D
Hong, JS
AF Wang, Qingshan
Qian, Li
Chen, Shih-Heng
Chu, Chun-Hsien
Wilson, Belinda
Oyarzabal, Esteban
Ali, Syed
Robinson, Bonnie
Rao, Deepa
Hong, Jau-Shyong
TI Post-treatment with an ultra-low dose of NADPH oxidase inhibitor
diphenyleneiodonium attenuates disease progression in multiple
Parkinson's disease models
SO BRAIN
LA English
DT Article
DE Parkinson's disease; microglia; NADPH oxidase; neuroinflammation;
superoxide
ID DOPAMINERGIC NEURODEGENERATION; MPTP MODEL; CHRONIC NEUROINFLAMMATION;
MICROGLIAL ACTIVATION; REACTIVE MICROGLIOSIS; OXIDATIVE STRESS;
ALPHA-SYNUCLEIN; ANIMAL-MODEL; NOX ENZYMES; NEUROPROTECTION
AB Nicotinamide adenine dinucleotide phosphate oxidase, a key superoxide-producing enzyme, plays a critical role in microglia-mediated chronic neuroinflammation and subsequent progressive dopaminergic neurodegeneration in Parkinson's disease. Although nicotinamide adenine dinucleotide phosphate oxidase-targeting anti-inflammatory therapy for Parkinson's disease has been proposed, its application in translational research remains limited. The aim of this study was to obtain preclinical evidence supporting this therapeutic strategy by testing the efficacy of an ultra-low dose of the nicotinamide adenine dinucleotide phosphate oxidase inhibitor diphenyleneiodonium in both endotoxin (lipopolysaccharide)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice using post-treatment regimens. Our data revealed that post-treatment with diphenyleneiodonium significantly attenuated progressive dopaminergic degeneration and improved rotarod activity. Remarkably, post-treatment with diphenyleneiodonium 10 months after lipopolysaccharide injection when mice had 30% loss of nigral dopaminergic neurons, showed high efficacy in protecting the remaining neuronal population and restoring motor function. Diphenyleneiodonium-elicited neuroprotection was associated with the inhibition of microglial activation, a reduction in the expression of proinflammatory factors and an attenuation of alpha-synuclein aggregation. A pathophysiological evaluation of diphenyleneiodonium-treated mice, including assessment of body weight, organs health, and neuronal counts, revealed no overt signs of toxicity. In summary, infusion of ultra-low dose diphenyleneiodonium potently reduced microglia-mediated chronic neuroinflammation by selectively inhibiting nicotinamide adenine dinucleotide phosphate oxidase and halted the progression of neurodegeneration in mouse models of Parkinson's disease. The robust neuroprotective effects and lack of apparent toxic side effects suggest that diphenyleneiodonium at ultra-low dose may be a promising candidate for future clinical trials in Parkinson's disease patients.
C1 [Wang, Qingshan; Qian, Li; Chen, Shih-Heng; Chu, Chun-Hsien; Wilson, Belinda; Oyarzabal, Esteban; Hong, Jau-Shyong] NIEHS, Neuropharmacol Sect, Neurobiol Lab, Res Triangle Pk, NC 27709 USA.
[Ali, Syed; Robinson, Bonnie] US FDA, Neurochem Lab, Div Neurotoxicol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
[Rao, Deepa] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Wang, QS (reprint author), NIEHS, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM wangq4@niehs.nih.gov; hong3@niehs.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences
NR 49
TC 5
Z9 6
U1 0
U2 13
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
EI 1460-2156
J9 BRAIN
JI Brain
PD MAY 1
PY 2015
VL 138
BP 1247
EP 1262
DI 10.1093/brain/awv034
PN 5
PG 16
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CH2DB
UT WOS:000353834100022
PM 25716193
ER
PT J
AU Maity, TK
Venugopalan, A
Linnoila, I
Cultraro, CM
Giannakou, A
Nemati, R
Zhang, X
Webster, JD
Ritt, D
Ghosal, S
Hoschuetzky, H
Simpson, RM
Biswas, R
Politi, K
Morrison, DK
Varmus, HE
Guha, U
AF Maity, Tapan K.
Venugopalan, Abhilash
Linnoila, Ilona
Cultraro, Constance M.
Giannakou, Andreas
Nemati, Roxanne
Zhang, Xu
Webster, Joshua D.
Ritt, Daniel
Ghosal, Sarani
Hoschuetzky, Heinz
Simpson, R. Mark
Biswas, Romi
Politi, Katerina
Morrison, Deborah K.
Varmus, Harold E.
Guha, Udayan
TI Loss of MIG6 Accelerates Initiation and Progression of Mutant Epidermal
Growth Factor Receptor-Driven Lung Adenocarcinoma
SO CANCER DISCOVERY
LA English
DT Article
ID KINASE DOMAIN; EGF RECEPTOR; ACQUIRED-RESISTANCE; DOWN-REGULATION;
GENE-MUTATIONS; MESENCHYMAL TRANSITION; ACTIVATING MUTATIONS;
NEVER-SMOKERS; CANCER; GEFITINIB
AB Somatic mutations in the EGFR kinase domain drive lung adenocarcinoma. We have previously identified MIG6, an inhibitor of ERBB signaling and a potential tumor suppressor, as a target for phosphorylation by mutant EGFRs. Here, we demonstrate that MIG6 is a tumor suppressor for the initiation and progression of mutant EGFR-driven lung adenocarcinoma in mouse models. Mutant EGFR-induced lung tumor formation was accelerated in Mig6-deficient mice, even with Mig6 haploinsufficiency. We demonstrate that constitutive phosphorylation of MIG6 at Y394/Y395 in EGFR-mutant human lung adenocarcinoma cell lines is associated with an increased interaction of MIG6 with mutant EGFR, which may stabilize EGFR protein. MIG6 also fails to promote mutant EGFR degradation. We propose a model whereby increased tyrosine phosphorylation of MIG6 decreases its capacity to inhibit mutant EGFR. Nonetheless, the residual inhibition is sufficient for MIG6 to delay mutant EGFR-driven tumor initiation and progression in mouse models.
SIGNIFICANCE: This study demonstrates that MIG6 is a potent tumor suppressor for mutant EGFR-driven lung tumor initiation and progression in mice and provides a possible mechanism by which mutant EGFR can partially circumvent this tumor suppressor in human lung adenocarcinoma. (C) 2015 AACR.
C1 [Maity, Tapan K.; Venugopalan, Abhilash; Cultraro, Constance M.; Nemati, Roxanne; Zhang, Xu; Ghosal, Sarani; Biswas, Romi; Guha, Udayan] NCI, Thorac & Gastrointestinal Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Linnoila, Ilona] NCI, Cell & Canc Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Giannakou, Andreas; Politi, Katerina; Varmus, Harold E.; Guha, Udayan] Mem Sloan Kettering Canc Ctr, Canc Biol & Genet Program, New York, NY 10021 USA.
[Webster, Joshua D.; Simpson, R. Mark] NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Ritt, Daniel; Morrison, Deborah K.] NCI, Lab Cell & Dev Signaling, Frederick, MD 21701 USA.
[Hoschuetzky, Heinz] NanoTools, Teningen, Germany.
RP Guha, U (reprint author), NCI, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM udayan.guha@nih.gov
FU National Cancer Institute Center for Cancer Research (NCI-CCR)
Intramural Research Program [ZIA BC 011259]; K99 Career Transition Award
[K99CA140792]; [PO1 CA129243]
FX This work was supported by the National Cancer Institute Center for
Cancer Research (NCI-CCR) Intramural Research Program ZIA BC 011259 (to
U. Guha), a K99 Career Transition Award (K99CA140792; to U. Guha), and
PO1 CA129243 (to H.E. Varmus).
NR 60
TC 7
Z9 7
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD MAY
PY 2015
VL 5
IS 5
BP 534
EP 549
DI 10.1158/2159-8290.CD-14-0750
PG 16
WC Oncology
SC Oncology
GA CH0HI
UT WOS:000353700000025
PM 25735773
ER
PT J
AU Wibom, C
Spath, F
Dahlin, AM
Langseth, H
Hovig, E
Rajaraman, P
Johannesen, TB
Andersson, U
Melin, B
AF Wibom, Carl
Spath, Florentin
Dahlin, Anna M.
langseth, HilDe
Hovig, Eivind
Rajaraman, Preetha
Johannesen, Tom Borge
Andersson, Ulrika
Melin, Beatrice
TI Investigation of Established Genetic Risk Variants for Glioma in
Prediagnostic Samples from a Population-Based Nested Case-Control Study
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; NERVOUS-SYSTEM TUMORS; JANUS-SERUM-BANK;
TELOMERE LENGTH; CAPILLARY-ELECTROPHORESIS; CANCER SUSCEPTIBILITY;
1ST-DEGREE RELATIVES; IONIZING-RADIATION; BRAIN; GLIOBLASTOMA
AB Background: Although glioma etiology is poorly understood in general, growing evidence indicates a genetic component. Four large genome-wide association studies (GWAS) have linked common genetic variants with an increased glioma risk. However, to date, these studies are based largely on a case-control design, where cases have been recruited at the time of or after diagnosis. They may therefore suffer from a degree of survival bias, introduced when rapidly fatal cases are not included.
Methods: To confirm glioma risk variants in a prospective setting, we have analyzed 11 previously identified risk variants in a set of prediagnostic serum samples with 598 cases and 595 matched controls. Serum samples were acquired from The Janus Serum Bank, a Norwegian population-based biobank reserved for cancer research.
Results: We confirmed the association with glioma risk for variants within five genomic regions: 8q24.21 (CCDC26), 9p21.3 (CDKN2B-AS1), 11q23.3 (PHLDB1), 17p13.1 (TP53), and 20q13.33 (RTEL1). However, previously identified risk variants within the 7p11.2 (EGFR) region were not confirmed by this study.
Conclusions: Our results indicate that the risk variants that were confirmed by this study are truly associated with glioma risk and may, consequently, affect gliomagenesis. Though the lack of positive confirmation of EGFR risk variants may be attributable to relatively limited statistical power, it nevertheless raises the question whether they truly are risk variants or markers for glioma prognosis.
Impact: Our findings indicate the need for further studies to clarify the role of glioma risk loci with respect to prolonged survival versus etiology. (C) 2015 AACR.
C1 [Wibom, Carl; Spath, Florentin; Dahlin, Anna M.; Andersson, Ulrika; Melin, Beatrice] Umea Univ, Dept Radiat Sci, Oncol, S-90187 Umea, Sweden.
[Wibom, Carl; Dahlin, Anna M.] Umea Univ, Computat Life Sci Cluster CLiC, S-90187 Umea, Sweden.
[langseth, HilDe] Canc Registry Norway, Inst Populat Based Canc Res, Dept Res, Oslo, Norway.
[Hovig, Eivind] Norwegian Radium Hosp, Inst Canc Res, Dept Tumor Biol, Oslo, Norway.
[Hovig, Eivind] Univ Oslo, Dept Informat, N-0316 Oslo, Norway.
[Rajaraman, Preetha] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Johannesen, Tom Borge] Canc Registry Norway, Inst Populat Based Canc Res, Oslo, Norway.
RP Wibom, C (reprint author), Umea Univ, Computat Life Sci Cluster CLiC, KBC Bldg,4th Floor, S-90187 Umea, Sweden.
EM carl.wibom@onkologi.umu.se
RI Hovig, Eivind/H-2474-2011
OI Hovig, Eivind/0000-0002-9103-1077
FU Acta Oncologica foundation through the Royal Swedish Academy of Science;
Swedish Research Council; Swedish Cancer Foundation; Northern Sweden
Cancer Foundation; Umea University Young investigator reward; Umea
Hospital Cutting Edge Grant
FX B. Melin was supported by grants from Acta Oncologica foundation through
the Royal Swedish Academy of Science (salary), The Swedish Research
Council, Swedish Cancer Foundation, Northern Sweden Cancer Foundation,
Umea University Young investigator reward, and Umea Hospital Cutting
Edge Grant.
NR 32
TC 3
Z9 3
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2015
VL 24
IS 5
BP 810
EP 816
DI 10.1158/1055-9965.EPI-14-1106
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CH0IK
UT WOS:000353702800006
PM 25713050
ER
PT J
AU Kuhs, KAL
Hildesheim, A
Trabert, B
Kemp, TJ
Purdue, MP
Wentzensen, N
Katki, HA
Pinto, LA
Loftfield, E
Safaeian, M
Chaturvedi, AK
Shiels, MS
AF Kuhs, Krystle A. Lang
Hildesheim, Allan
Trabert, Britton
Kemp, Troy J.
Purdue, Mark P.
Wentzensen, Nicolas
Katki, Hormuzd A.
Pinto, Ligia A.
Loftfield, Erikka
Safaeian, Mahboobeh
Chaturvedi, Anil K.
Shiels, Meredith S.
TI Association between Regular Aspirin Use and Circulating Markers of
Inflammation: A Study within the Prostate, Lung, Colorectal, and Ovarian
Cancer Screening Trial
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID NON-HODGKIN-LYMPHOMA; C-REACTIVE PROTEIN; LOW-DOSE ASPIRIN; TUMOR
ANGIOGENESIS; RANDOMIZED-TRIALS; SERUM-LEVELS; RISK; CYTOKINES;
CLOPIDOGREL; METASTASIS
AB Background: Regular aspirin use may decrease cancer risk by reducing chronic inflammation. However, associations between aspirin use and circulating markers of inflammation have not been well studied.
Methods: Serum levels of 78 inflammatory markers were measured in 1,819 55-to 74-year-old men and women in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Data were combined from three completed case-control studies and reweighted to the PLCO screening arm. Self-reported aspirin and ibuprofen use (number of tablets taken per day/week/month) over the previous 12 months was collected at baseline. Associations between (i) nonregular (< 4 tablets/month), (ii) low (1-4 tablets/week), (iii) moderate (1 tablet/day), or (iv) high (2+tablets/day) regular aspirin or ibuprofen use and marker levels were assessed with weighted logistic regression.
Results: Aspirin use was nominally associated with (P-trend across categories <= 0.05) decreased levels of chemokine C-C motif ligand 15 [CCL15; OR, 0.5; 95% confidence intervals (CI), 0.3-0.8; moderate versus nonregular use]; soluble vascular endothelial growth factor receptor 2 (sVEGFR2; OR, 0.7; 95% CI, 0.4-1.0); soluble tumor necrosis factor receptor 1 (sTNFR1; OR, 0.6; 95% CI, 0.4-0.9) and increased levels of CCL13 (OR, 1.3; 95% CI, 0.8-2.1); CCL17 (OR, 1.1; 95% CI, 0.7-1.9) and interleukin 4 (IL4; OR, 1.6; 95% CI, 0.9-2.8). Trends were not statistically significant following correction for multiple comparisons. Likewise, no statistically significant associations were observed between ibuprofen use and marker levels.
Conclusions: No significant associations were observed between regular aspirin use and the inflammatory markers assessed.
Impact: Additional studies are needed to better understand the relationship between aspirin use, chronic inflammation, and cancer risk. (C) 2015 AACR.
C1 [Kuhs, Krystle A. Lang; Hildesheim, Allan; Trabert, Britton; Purdue, Mark P.; Wentzensen, Nicolas; Katki, Hormuzd A.; Loftfield, Erikka; Safaeian, Mahboobeh; Chaturvedi, Anil K.; Shiels, Meredith S.] NCI, NIH, Bethesda, MD 20892 USA.
[Kemp, Troy J.; Pinto, Ligia A.] Leidos Biomed Res Inc, HPV Immunol Lab, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Purdue, Mark P.] Ontario Inst Canc Res, Toronto, ON, Canada.
RP Kuhs, KAL (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6-E210, Bethesda, MD 20892 USA.
EM Krystle.Kuhs@nih.gov
RI Hildesheim, Allan/B-9760-2015; Purdue, Mark/C-9228-2016; Trabert,
Britton/F-8051-2015; Chaturvedi, Anil/J-2024-2015
OI Hildesheim, Allan/0000-0003-0257-2363; Purdue, Mark/0000-0003-1177-3108;
Chaturvedi, Anil/0000-0003-2696-8899
FU Intramural Research Program of the National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Cancer Institute (all authors received).
NR 40
TC 2
Z9 3
U1 1
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2015
VL 24
IS 5
BP 825
EP 832
DI 10.1158/1055-9965.EPI-14-1363
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CH0IK
UT WOS:000353702800008
PM 25713025
ER
PT J
AU Ochs-Balcom, HM
Phillips, LS
Nichols, HB
Martinez, E
Thompson, B
Ojeifo, J
Rebbeck, TR
AF Ochs-Balcom, Heather M.
Phillips, Lynette S.
Nichols, Hazel B.
Martinez, Elena
Thompson, Beti
Ojeifo, John
Rebbeck, Timothy R.
TI Building a Funded Research Program in Cancer Health Disparities:
Considerations for Young Investigators
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Editorial Material
AB A workshop entitled "Building a funded research program in cancer health disparities" was held at the 38th Annual American Society of Preventive Oncology (ASPO) Meeting. Organized by the Junior Members Interest Group, the session addressed topics relevant to career development for cancer disparities investigators. Such considerations include the development of research programs on a backdrop of existing multi- and transdisciplinary teams, recognizing opportunities for advancing their research, given the growth of consortia-related research, and development of effective community-based partnerships. Key strategies for developing a sustainable career in cancer health disparities in the current environment include the need to effectively engage with communities, appreciate the value of team science and develop cross-discipline collaborations, and navigate the use and utility of consortia for disparities research. Academic considerations related to earning tenure and promotion that may be faced by the junior investigator in cancer health disparities were also discussed. This report may serve to both educate and provide lessons for early-stage investigators who wish to tackle complex scientific questions while developing their careers in cancer health disparities. (C) 2015 AACR.
C1 [Ochs-Balcom, Heather M.] SUNY Buffalo, Sch Publ Hlth & Hlth Profess, Dept Epidemiol & Environm Hlth, Buffalo, NY 14214 USA.
[Phillips, Lynette S.] Kent State Univ, Coll Publ Hlth, Kent, OH 44242 USA.
[Nichols, Hazel B.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
[Martinez, Elena] Univ Calif San Diego, Family & Prevent Med, La Jolla, CA 92093 USA.
[Thompson, Beti] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Thompson, Beti] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
[Ojeifo, John] Ctr Reduce Canc Hlth Dispar, Divers Training Branch, NIH, Bethesda, MD USA.
[Rebbeck, Timothy R.] Univ Penn, Perelman Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Rebbeck, Timothy R.] Univ Penn, Perelman Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RP Ochs-Balcom, HM (reprint author), SUNY Buffalo, 270 Farber Hall, Buffalo, NY 14214 USA.
EM hmochs2@buffalo.edu
FU NIH/NCI [K07CA136969]; Susan G. Komen for the Cure [KG090937]
FX The authors thank the members of the ASPO Junior Members Interest Group,
especially Drs. Marlyn Allicock, Tomi Akinyemiju, Adana Llanos, and
Kathryn Roysewho helped organize the session, as well as Heidi Sahel for
session logistics. Dr. Ochs-Balcom received grant support from the
NIH/NCI (K07CA136969) and Susan G. Komen for the Cure (KG090937).
NR 5
TC 1
Z9 1
U1 2
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD MAY
PY 2015
VL 24
IS 5
BP 882
EP 885
DI 10.1158/1055-9965.EPI-15-0136
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA CH0IK
UT WOS:000353702800018
PM 25934837
ER
PT J
AU Medina-Echeverz, J
Ma, C
Duffy, AG
Eggert, T
Hawk, N
Kleiner, DE
Korangy, F
Greten, TF
AF Medina-Echeverz, Jose
Ma, Chi
Duffy, Austin G.
Eggert, Tobias
Hawk, Nga
Kleiner, David E.
Korangy, Firouzeh
Greten, Tim F.
TI Systemic Agonistic Anti-CD40 Treatment of Tumor-Bearing Mice Modulates
Hepatic Myeloid-Suppressive Cells and Causes Immune-Mediated Liver
Damage
SO CANCER IMMUNOLOGY RESEARCH
LA English
DT Article
ID MONOCLONAL-ANTIBODY THERAPY; A-INDUCED HEPATITIS;
HEPATOCELLULAR-CARCINOMA; ANTITUMOR VACCINE; REACTIVE OXYGEN; MURINE
MODELS; CD40 ANTIBODY; CANCER; IMMUNOTHERAPY; MICROENVIRONMENT
AB Immune-stimulatory mAbs are currently being evaluated as antitumor agents. Although overall toxicity from these agents appears to be moderate, liver toxicities have been reported and are not completely understood. We studied the effect of systemic CD40 antibody treatment on myeloid cells in the spleen and liver. Naive and tumor-bearing mice were treated systemically with agonistic anti-CD40 antibody. Immune cell subsets in the liver and spleen, serum transaminases, and liver histologies were analyzed after antibody administration. Nox2(-/-), Cd40(-/-), and bone marrow chimeric mice were used to study the mechanism by which agonistic anti-CD40 mediates its effects in vivo. Suppressor function of murine and human tumor-induced myeloid-derived suppressor cells (MDSC) was studied upon CD40 ligation. Agonistic CD40 antibody caused liver damage within 24 hours after injection in two unrelated tumor models and mice strains. Using bone marrow chimeras, we demonstrate that CD40 antibody-induced hepatitis in tumor-bearing mice was dependent on the presence of CD40-expressing hematopoietic cells. Agonistic CD40 ligation-dependent liver damage was induced by the generation of reactive oxygen species. Furthermore, agonistic CD40 antibody resulted in increased CD80-positive and CD40-positive liver CD11b(+)Gr-1(+) immature myeloid cells. CD40 ligation on tumor-induced murine and human CD14(+)HLA-DRlow peripheral blood mononuclear cells from patients with cancer reduced their immune suppressor function. Collectively, agonistic CD40 antibody treatment activated tumor-induced myeloid cells, caused myeloid-dependent hepatotoxicity, and ameliorated the suppressor function of murine and human MDSC. Collectively, our data suggest that CD40 may mature immunosuppressive myeloid cells and thereby cause liver damage in mice with an accumulation of tumor-induced hepatic MDSC. (c) 2015 AACR.
C1 [Medina-Echeverz, Jose; Ma, Chi; Duffy, Austin G.; Eggert, Tobias; Korangy, Firouzeh; Greten, Tim F.] NCI, Gastrointestinal Malignancy Sect, Thorac & Gastrointestinal Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Hawk, Nga] NIH, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Greten, TF (reprint author), NCI, NIH, 10 Ctr Dr,Bldg 10,Room 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM tim.greten@nih.gov
FU Intramural Research Program of the NCI, NIH
FX This work was supported by the Intramural Research Program of the NCI,
NIH.
NR 51
TC 5
Z9 5
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2326-6066
EI 2326-6074
J9 CANCER IMMUNOL RES
JI Cancer Immunol. Res.
PD MAY
PY 2015
VL 3
IS 5
BP 557
EP 566
DI 10.1158/2326-6066.CIR-14-0182
PG 10
WC Oncology; Immunology
SC Oncology; Immunology
GA CH0HX
UT WOS:000353701500016
PM 25637366
ER
PT J
AU Greene, MH
Mai, PL
AF Greene, Mark H.
Mai, Phuong L.
TI The Fallopian Tube: From Back Stage to Center Stage
SO CANCER PREVENTION RESEARCH
LA English
DT Editorial Material
ID REDUCING SALPINGO-OOPHORECTOMY; GYNECOLOGIC-ONCOLOGY-GROUP;
OVARIAN-CANCER; INTRAEPITHELIAL CARCINOMA; MUTATION CARRIERS; BRCA2
MUTATION; RISK; WOMEN; FAMILIES; FIMBRIA
AB The recognition that a significant fraction of what historically has been classified as ovarian cancer is, in fact, a malignancy that arises in the fallopian tube mucosa comprises a paradigm shift in our understanding of these neoplasms. New etiologic and management opportunities have been created by this insight, both for women at increased genetic risk of ovarian cancer by virtue of being BRCA1/2 mutation carriers and, perhaps, for women in the general population as well. Cancer (C) 2015 AACR.
C1 [Greene, Mark H.; Mai, Phuong L.] NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, Rockville, MD 20850 USA.
RP Greene, MH (reprint author), NCI, Clin Genet Branch, NIH, 9609 Med Ctr Dr,Room 6E-454, Rockville, MD 20850 USA.
EM greenem@mail.nih.gov
FU Intramural NIH HHS [ZIA CP010144-15]
NR 24
TC 1
Z9 1
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD MAY
PY 2015
VL 8
IS 5
BP 339
EP 341
DI 10.1158/1940-6207.CAPR-15-0072
PG 3
WC Oncology
SC Oncology
GA CH0IY
UT WOS:000353704300001
PM 25802341
ER
PT J
AU St Croix, B
AF St Croix, Brad
TI CD146: the unveiling of a pro-angiogenic netrin receptor
SO CELL RESEARCH
LA English
DT Editorial Material
AB Netrin-1, a classic neuronal guidance cue, can promote angiogenesis under certain developmental and pathological conditions, but key receptors on vascular endothelium have remained elusive. A recent study published in Cell Research by Tu et al. reveals that CD146, an endothelial receptor of the immunoglobulin superfamily, binds netrin-1 with high affinity and may play an important role in regulating angiogenesis.
C1 NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA.
RP St Croix, B (reprint author), NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA.
EM stcroix@ncifcrf.gov
NR 12
TC 1
Z9 1
U1 0
U2 5
PU INST BIOCHEMISTRY & CELL BIOLOGY
PI SHANGHAI
PA SIBS, CAS, 319 YUEYANG ROAD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1001-0602
EI 1748-7838
J9 CELL RES
JI Cell Res.
PD MAY
PY 2015
VL 25
IS 5
BP 533
EP 534
DI 10.1038/cr.2015.42
PG 2
WC Cell Biology
SC Cell Biology
GA CH3GP
UT WOS:000353917500003
PM 25849249
ER
PT J
AU Boyiadzis, M
Arora, M
Klein, JP
Hassebroek, A
Hemmer, M
Urbano-Ispizua, A
Antin, JH
Bolwell, BJ
Cahn, JYY
Cairo, MS
Cutler, CS
Flowers, ME
Gale, RP
Herzig, R
Isola, LM
Jacobsohn, DA
Jagasia, MH
Klumpp, TR
Lee, SJ
Petersdorf, EW
Santarone, S
Spellman, SR
Schouten, HC
Verdonck, LF
Wingard, JR
Weisdorf, DJ
Horowitz, MM
Pavletic, SZ
AF Boyiadzis, Michael
Arora, Mukta
Klein, John P.
Hassebroek, Anna
Hemmer, Michael
Urbano-Ispizua, Alvaro
Antin, Joseph H.
Bolwell, Brian J.
Cahn, Jean-Yves Y.
Cairo, Mitchell S.
Cutler, Corey S.
Flowers, Mary E.
Gale, Robert P.
Herzig, Roger
Isola, Luis M.
Jacobsohn, David A.
Jagasia, Madan H.
Klumpp, Thomas R.
Lee, Stephanie J.
Petersdorf, Effie W.
Santarone, Stella
Spellman, Stephen R.
Schouten, Harry C.
Verdonck, Leo F.
Wingard, John R.
Weisdorf, Daniel J.
Horowitz, Mary M.
Pavletic, Steven Z.
TI Impact of Chronic Graft-versus-Host Disease on Late Relapse and Survival
on 7,489 Patients after Myeloablative Allogeneic Hematopoietic Cell
Transplantation for Leukemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; UNRELATED DONOR TRANSPLANTATION;
HLA-IDENTICAL SIBLINGS; LEUKOCYTE INFUSIONS; MYELOID-LEUKEMIA; EUROPEAN
GROUP; MORTALITY; BLOOD
AB Purpose: Malignancy relapse remains a major obstacle for successful allogeneic hematopoietic cell transplantation (HCT). Chronic graft-versus-host disease (cGVHD) is associated with fewer relapses. However, when studying effects of cGVHD on relapse, it is difficult to separate from acute GVHD effects as most cases of cGVHD occur within the first year after transplant at the time when acute GVHD is still active.
Experimental Design: This study based on CIBMTR registry data investigated cGVHD and its association with the incidence of late relapse and survival in 7,489 patients with acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), and myelodysplastic syndromes (MDS), who were leukemia free at 12 months after myeloablative allogeneic HCT.
Results: Forty-seven percent of the study population was diagnosed with cGVHD at 12 months after transplant. The protective effect of cGVHD on late relapse was present only in patients with CML [RR, 0.47; 95% confidence interval (CI), 0.37-0.59; P < 0.0001). cGVHD was significantly associated with higher risk of treatment-related mortality (TRM; RR, 2.43; 95% CI, 2.09-2.82; P < 0.0001) and inferior overall survival (RR, 1.56; 95% CI, 1.41-1.73; P < 0.0001) for all diseases. In patients with CML, all organ sites and presentation types of cGVHD were equally associated with lower risk of late relapse.
Conclusions: These results indicate that clinically relevant antileukemia effects of cGVHD on late relapses are present only in CML but not in AML, ALL, or MDS. Chronic GVHD in patients who are 1-year survivors after myeloablative allogeneic HCT is primarily associated with higher TRM and inferior survival. (C) 2014 AACR.
C1 [Boyiadzis, Michael] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15232 USA.
[Arora, Mukta; Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
[Klein, John P.; Hemmer, Michael; Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Hassebroek, Anna; Spellman, Stephen R.] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
[Urbano-Ispizua, Alvaro] Hosp Clinic, Inst Hematol & Oncol, Boston, MA USA.
[Antin, Joseph H.; Cutler, Corey S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bolwell, Brian J.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Cahn, Jean-Yves Y.] CHU Grenoble, Hop Michallon, F-38043 Grenoble, France.
[Cairo, Mitchell S.] New York Med Coll, Valhalla, NY 10595 USA.
[Flowers, Mary E.; Lee, Stephanie J.; Petersdorf, Effie W.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Gale, Robert P.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Herzig, Roger] Univ Louisville, Hosp James Brown Canc Ctr, Louisville, KY 40292 USA.
[Isola, Luis M.] Mt Sinai Med Ctr, Miami, FL USA.
[Jacobsohn, David A.] Childrens Hosp, Natl Med Ctr, Washington, DC 20010 USA.
[Jagasia, Madan H.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Klumpp, Thomas R.] Temple Bone Marrow Transplant Program, Philadelphia, PA USA.
[Santarone, Stella] Osped Civile BMT Ctr, Pescara, Italy.
[Schouten, Harry C.] Acad Ziekenhuis Maastricht, Maastricht, Netherlands.
[Verdonck, Leo F.] Isala Clin, Zwolle, Netherlands.
[Wingard, John R.] Shands HealthCare, Gainesville, FL USA.
[Wingard, John R.] Univ Florida, Gainesville, FL USA.
[Pavletic, Steven Z.] NCI, Bethesda, MD 20892 USA.
RP Boyiadzis, M (reprint author), Univ Pittsburgh, Inst Canc, UPMC Canc Pavil,5150 Ctr Ave,Suite 564, Pittsburgh, PA 15232 USA.
EM boyiadzism@upmc.edu
FU National Cancer Institute (NCI) [U24-CA76518]; National Heart, Lung, and
Blood Institute (NHLBI); National Institute of Allergy and Infectious
Diseases (NIAID); NHLBI [5U01HL069294]; Health Resources and Services
Administration (HRSA/DHHS) [HHSH234200637015C]; Office of Naval Research
[N00014-06-1-0704, N00014-08-1-0058]; Allos, Inc.; Amgen, Inc.;
Angioblast; Be the Match Foundation; Blue Cross and Blue Shield
Association; Buchanan Family Foundation; CaridianBCT; Celgene
Corporation; CellGenix, GmbH; Children's Leukemia Research Association;
Fresenius Biotech North America, Inc.; Gamida Cell Teva Joint Venture
Ltd.; Genentech, Inc.; Genzyme Corporation; GlaxoSmithKline;
HistoGenetics, Inc.; Kiadis Pharma; Leukemia & Lymphoma Society; Medical
College of Wisconsin; Merck Co, Inc.; Millennium: The Takeda Oncology
Co.; Milliman USA, Inc.; Miltenyi Biotec, Inc.; National Marrow Donor
Program; Optum Healthcare Solutions, Inc.; Osiris Therapeutics, Inc.;
Otsuka America Pharmaceutical, Inc.; RemedyMD; Sanofi; Seattle Genetics;
Sigma-Tau Pharmaceuticals; Soligenix, Inc.; StemCyte, A Global Cord
Blood Therapeutics Co.; Stemsoft Software, Inc.; Swedish Orphan
Biovitrum; Tarix Pharmaceuticals; Teva Neuroscience, Inc.; THERAKOS,
Inc.; Wellpoint, Inc.
FX The CIBMTR is supported by Public Health Service grant/cooperative
agreement U24-CA76518 from the National Cancer Institute (NCI), the
National Heart, Lung, and Blood Institute (NHLBI) and the National
Institute of Allergy and Infectious Diseases (NIAID); a
grant/cooperative agreement 5U01HL069294 from NHLBI and NCI; a contract
HHSH234200637015C with Health Resources and Services Administration
(HRSA/DHHS); two grants N00014-06-1-0704 and N00014-08-1-0058 from the
Office of Naval Research; and grants from Allos, Inc.; Amgen, Inc.;
Angioblast; Anonymous donation to the Medical College of Wisconsin;
Ariad; Be the Match Foundation; Blue Cross and Blue Shield Association;
Buchanan Family Foundation; CaridianBCT; Celgene Corporation; CellGenix,
GmbH; Children's Leukemia Research Association; Fresenius Biotech North
America, Inc.; Gamida Cell Teva Joint Venture Ltd.; Genentech, Inc.;
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; Optum Healthcare Solutions, Inc.; Osiris Therapeutics, Inc.;
Otsuka America Pharmaceutical, Inc.; RemedyMD; Sanofi; Seattle Genetics;
Sigma-Tau Pharmaceuticals; Soligenix, Inc.; StemCyte, A Global Cord
Blood Therapeutics Co.; Stemsoft Software, Inc.; Swedish Orphan
Biovitrum; Tarix Pharmaceuticals; Teva Neuroscience, Inc.; THERAKOS,
Inc.; and Wellpoint, Inc.
NR 22
TC 15
Z9 15
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD MAY 1
PY 2015
VL 21
IS 9
BP 2020
EP 2028
DI 10.1158/1078-0432.CCR-14-0586
PG 9
WC Oncology
SC Oncology
GA CH0KK
UT WOS:000353708200009
PM 25348512
ER
PT J
AU Jain, S
Jirau-Serrano, X
Zullo, KM
Scotto, L
Palermo, CF
Sastra, SA
Olive, KP
Cremers, S
Thomas, T
Wei, Y
Zhang, Y
Bhagat, G
Amengual, JE
Deng, CC
Karan, C
Realubit, R
Bates, SE
O'Connor, OA
AF Jain, Salvia
Jirau-Serrano, Xavier
Zullo, Kelly M.
Scotto, Luigi
Palermo, Carmine F.
Sastra, Stephen A.
Olive, Kenneth P.
Cremers, Serge
Thomas, Tiffany
Wei, Ying
Zhang, Yuan
Bhagat, Govind
Amengual, Jennifer E.
Deng, Changchun
Karan, Charles
Realubit, Ronald
Bates, Susan E.
O'Connor, Owen A.
TI Preclinical Pharmacologic Evaluation of Pralatrexate and Romidepsin
Confirms Potent Synergy of the Combination in a Murine Model of Human
T-cell Lymphoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PROTEASOME INHIBITOR BORTEZOMIB; SEZARY-SYNDROME; MOUSE MODEL; IN-VITRO;
MICE; GROWTH; METHOTREXATE; SUPERIOR; TUMORS
AB Purpose: T-cell lymphomas (TCL) are aggressive diseases, which carry a poor prognosis. The emergence of new drugs for TCL has created a need to survey these agents in a rapid and reproducible fashion, to prioritize combinations which should be prioritized for clinical study. Mouse models of TCL that can be used for screening novel agents and their combinations are lacking. Developments in noninvasive imaging modalities, such as surface bioluminescence (SBL) and three-dimensional ultrasound (3D-US), are challenging conventional approaches in xenograft modeling relying on caliper measurements. The recent approval of pralatrexate and romidepsin creates an obvious combination that could produce meaningful activity in TCL, which is yet to be studied in combination.
Experimental Design: High-throughput screening and multi-modality imaging approach of SBL and 3D-US in a xenograft NOG mouse model of TCL were used to explore the in vitro and in vivo activity of pralatrexate and romidepsin in combination. Corresponding mass spectrometry-based pharmacokinetic and immunohistochemistry-based pharmacodynamic analyses of xenograft tumors were performed to better understand a mechanistic basis for the drug: drug interaction.
Results: In vitro, pralatrexate and romidepsin exhibited concentration-dependent synergism in combination against a panel of TCL cell lines. In aNOG murine model of TCL, the combination of pralatrexate and romidepsin exhibited enhanced efficacy compared with either drug alone across a spectrum of tumors using complementary imaging modalities, such as SBL and 3D-US.
Conclusions: Collectively, these data strongly suggest that the combination of pralatrexate and romidepsin merits clinical study in patients with TCLs. (C) 2015 AACR.
C1 [Jain, Salvia] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Jirau-Serrano, Xavier; Zullo, Kelly M.; Scotto, Luigi; Amengual, Jennifer E.; Deng, Changchun; O'Connor, Owen A.] Columbia Univ, Med Ctr, Ctr Lymphoid Malignancies, New York, NY 10019 USA.
[Jirau-Serrano, Xavier; Zullo, Kelly M.; Scotto, Luigi; Sastra, Stephen A.; Olive, Kenneth P.; Amengual, Jennifer E.; Deng, Changchun; O'Connor, Owen A.] Columbia Univ, Med Ctr, Herbert Irving Comprehens Canc Ctr, New York, NY 10019 USA.
[Palermo, Carmine F.; Sastra, Stephen A.; Olive, Kenneth P.; Cremers, Serge; Thomas, Tiffany; Bhagat, Govind] Columbia Univ, Med Ctr, Dept Pathol & Cell Biol, New York, NY 10019 USA.
[Palermo, Carmine F.; Sastra, Stephen A.; Olive, Kenneth P.; Cremers, Serge] Irving Inst Clin & Translat Res, New York, NY USA.
[Palermo, Carmine F.; Sastra, Stephen A.; Olive, Kenneth P.; Cremers, Serge; Amengual, Jennifer E.; Deng, Changchun; O'Connor, Owen A.] Columbia Univ, Med Ctr, Dept Med, New York, NY 10019 USA.
[Wei, Ying; Zhang, Yuan] Columbia Univ, Med Ctr, Dept Biostat, New York, NY 10019 USA.
[Karan, Charles; Realubit, Ronald] Columbia Univ, Med Ctr, Dept Syst Biol, High Throughput Screening Facil, New York, NY 10019 USA.
[Bates, Susan E.] NCI, Dev Therapeut Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP O'Connor, OA (reprint author), Columbia Univ, Med Ctr, 51 West 51st St, New York, NY 10019 USA.
EM oo2130@columbia.edu
OI Bhagat, Govind/0000-0001-6250-048X
FU Columbia University Lymphoma Research Fund; [S 10 RR025482-01AS10]
FX The authors thank the Columbia University Lymphoma Research Fund for
support. Imaging studies were performed in collaboration with the Small
Animal Imaging Shared Resource within the Herbert Irving Comprehensive
Cancer Center (NCI 3 P30 CA13696). The Vexo 2100 ultrasound was
purchased from a Small Instrumentation Grant (S 10 RR025482-01AS10).
NR 29
TC 6
Z9 6
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD MAY 1
PY 2015
VL 21
IS 9
BP 2096
EP 2106
DI 10.1158/1078-0432.CCR-14-2249
PG 11
WC Oncology
SC Oncology
GA CH0KK
UT WOS:000353708200017
PM 25677697
ER
PT J
AU Weykamp, C
John, G
Gillery, P
English, E
Ji, LN
Lenters-Westra, E
Little, RR
Roglic, G
Sacks, DB
Takei, I
AF Weykamp, Cas
John, Garry
Gillery, Philippe
English, Emma
Ji, Linong
Lenters-Westra, Erna
Little, Randie R.
Roglic, Gojka
Sacks, David B.
Takei, Izumi
CA IFCC Task Force Implementation HbA
TI Investigation of 2 Models to Set and Evaluate Quality Targets for Hb
A(1c): Biological Variation and Sigma-Metrics
SO CLINICAL CHEMISTRY
LA English
DT Article
ID ANALYTICAL BIAS; IMPRECISION; HBA(1C); NUMBER; LIMITS; GOALS
AB BACKGROUND: A major objective of the IFCC Task Force on Implementation of HbA(1c) Standardization is to develop a model to define quality targets for glycated hemoglobin (Hb A(1c)).
METHODS: Two generic models, biological variation and sigma-metrics, are investigated. We selected variables in the models for Hb A(1c) and used data of external quality assurance/proficiency testing programs to evaluate the suitability of the models to set and evaluate quality targets within and between laboratories.
RESULTS: In the biological variation model, 48% of individual laboratories and none of the 26 instrument groups met the minimum performance criterion. In the sigma-metrics model, with a total allowable error (TAE) set at 5 mmol/mol (0.46% NGSP), 77% of the individual laboratories and 12 of 26 instrument groups met the 2 sigma criterion.
CONCLUSIONS: The biological variation and sigma-metrics models were demonstrated to be suitable for setting and evaluating quality targets within and between laboratories. The sigma-metrics model is more flexible, as both the TAE and the risk of failure can be adjusted to the situation for example, requirements related to diagnosis/monitoring or international authorities. With the aim of reaching (inter)national consensus on advice regarding quality targets for Hb A,5, the Task Force suggests the sigma-metrics model as the model of choice, with default values of 5 mmol/mol (0.46%) for TAE and risk levels of 2 sigma and 4 sigma for routine laboratories and laboratories performing clinical trials, respectively. These goals should serve as a starting point for discussion with international stakeholders in the field of diabetes. (C) 2015 American Association for Clinical Chemistry
C1 [Weykamp, Cas] Locat Queen Beatrix Hosp, Dept Clin Chem, Winterswijk, Netherlands.
[Weykamp, Cas] Locat Queen Beatrix Hosp, European Reference Lab, Winterswijk, Netherlands.
[John, Garry] Norfolk & Norwich Univ Hosp, Norwich, Norfolk, England.
[Gillery, Philippe] Univ Hosp Reims, Lab Pediat Biol & Res, Reims, France.
[English, Emma] Univ Nottingham, Royal Derby Hosp, Sch Med, Derby, England.
[Ji, Linong] Peking Univ, Peoples Hosp, Beijing 100871, Peoples R China.
[Lenters-Westra, Erna] Isala Clin, Dept Clin Chem, Zwolle, Netherlands.
[Lenters-Westra, Erna] European Reference Lab, Location Isala, Zwolle, Netherlands.
[Little, Randie R.] Univ Missouri, Sch Med, Dept Pathol, Columbia, MO 65212 USA.
[Little, Randie R.] Univ Missouri, Sch Med, Dept Child Hlth, Columbia, MO 65212 USA.
[Roglic, Gojka] WHO, Dept Management Noncommunicable Dis, CH-1211 Geneva, Switzerland.
[Sacks, David B.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
[Takei, Izumi] Ichikawa Gen Hosp, Diabet & Endocrine Dept, Ichikawa, Japan.
RP Weykamp, C (reprint author), Queen Beatrix Hosp, Dept Clin Chem, Beatrixpk 1, NL-7101 BN Winterswijk, Netherlands.
EM c.w.weykamp@skbwinterswijk.nl
FU Intramural Research Program of the NIH
FX D.B. Sacks, Intramural Research Program of the NIH.
NR 19
TC 16
Z9 16
U1 0
U2 1
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
EI 1530-8561
J9 CLIN CHEM
JI Clin. Chem.
PD MAY
PY 2015
VL 61
IS 5
BP 752
EP 759
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA CH2GR
UT WOS:000353844200015
PM 25737535
ER
PT J
AU Rogers, T
Lederman, RJ
AF Rogers, Toby
Lederman, Robert J.
TI Interventional CMR: Clinical Applications and Future Directions
SO CURRENT CARDIOLOGY REPORTS
LA English
DT Article
DE Interventional cardiovascularMRI; Structural heart disease; MRI
catheterization; Cardiac electrophysiology; Electrophysiology mapping
and ablation.; Cardiovascular catheterization; Real-time MRI
ID CONGENITAL HEART-DISEASE; REAL-TIME MRI; CARDIOVASCULAR
MAGNETIC-RESONANCE; RADIOFREQUENCY ABLATION LESIONS; PULMONARY
VASCULAR-RESISTANCE; ARTERY STENT PLACEMENT; CARDIAC-CATHETERIZATION;
ANIMAL-MODEL; SWINE MODEL; IN-VIVO
AB Interventional cardiovascular magnetic resonance (iCMR) promises to enable radiation-free catheterization procedures and to enhance contemporary image guidance for structural heart and electrophysiological interventions. However, clinical translation of exciting pre-clinical interventions has been limited by availability of devices that are safe to use in the magnetic resonance (MR) environment. We discuss challenges and solutions for clinical translation, including MR-conditional and MR-safe device design, and how to configure an interventional suite. We review the recent advances that have already enabled diagnostic MR right heart catheterization and simple electrophysiologic ablation to be performed in humans and explore future clinical applications.
C1 [Rogers, Toby; Lederman, Robert J.] NHLBI, Cardiovasc & Pulm Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
RP Lederman, RJ (reprint author), NHLBI, Cardiovasc & Pulm Branch, Div Intramural Res, NIH, Bldg 10,Room 2c713, Bethesda, MD 20892 USA.
EM lederman@nih.gov
OI lederman, robert/0000-0003-1202-6673; Rogers, Toby/0000-0002-6043-3137
FU Division of Intramural Research, National Heart Lung and Blood
Institute, National Institutes of Health [Z01-HL005062]
FX This work was supported by the Division of Intramural Research, National
Heart Lung and Blood Institute, National Institutes of Health
(Z01-HL005062).
NR 84
TC 3
Z9 3
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3782
EI 1534-3170
J9 CURR CARDIOL REP
JI Curr. Cardiol. Rep.
PD MAY
PY 2015
VL 17
IS 5
AR 31
DI 10.1007/s11886-015-0580-1
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA CG2XE
UT WOS:000353138200001
PM 25894793
ER
PT J
AU Garriock, RJ
Chalamalasetty, RB
Kennedy, MW
Canizales, LC
Lewandoski, M
Yamaguchi, TP
AF Garriock, Robert J.
Chalamalasetty, Ravindra B.
Kennedy, Mark W.
Canizales, Lauren C.
Lewandoski, Mark
Yamaguchi, Terry P.
TI Lineage tracing of neuromesodermal progenitors reveals novel
Wnt-dependent roles in trunk progenitor cell maintenance and
differentiation
SO DEVELOPMENT
LA English
DT Article
DE Neural progenitor; Neuromesodermal progenitor; Wnt signaling; Brachyury;
Paraxial mesoderm; Sox2
ID BETA-CATENIN GENE; AXIAL STEM-CELLS; PRIMITIVE STREAK; MOUSE EMBRYO;
WNT/BETA-CATENIN; MESODERMAL TISSUES; AVIAN GASTRULATION; TAIL BUD;
FATE; MICE
AB In the development of the vertebrate body plan, Wnt3a is thought to promote the formation of paraxial mesodermal progenitors (PMPs) of the trunk region while suppressing neural specification. Recent lineage-tracing experiments have demonstrated that these trunk neural progenitors and PMPs derive from a common multipotent progenitor called the neuromesodermal progenitor (NMP). NMPs are known to reside in the anterior primitive streak (PS) region; however, the extent to which NMPs populate the PS and contribute to the vertebrate body plan, and the precise role that Wnt3a plays in regulating NMP self-renewal and differentiation are unclear. To address this, we used cell-specific markers (Sox2 and T) and tamoxifen-induced Cre recombinase-based lineage tracing to locate putative NMPs in vivo. We provide functional evidence for NMP location primarily in the epithelial PS, and to a lesser degree in the ingressed PS. Lineage-tracing studies in Wnt3a/beta-catenin signaling pathway mutants provide genetic evidence that trunk progenitors normally fated to enter the mesodermal germ layer can be redirected towards the neural lineage. These data, combined with previous PS lineage-tracing studies, support a model that epithelial anterior PS cells are Sox2(+)T(+) multipotent NMPs and form the bulk of neural progenitors and PMPs of the posterior trunk region. Finally, we find that Wnt3a/beta-catenin signaling directs trunk progenitors towards PMP fates; however, our data also suggest that Wnt3a positively supports a progenitor state for both mesodermal and neural progenitors.
C1 [Garriock, Robert J.; Chalamalasetty, Ravindra B.; Kennedy, Mark W.; Canizales, Lauren C.; Lewandoski, Mark; Yamaguchi, Terry P.] NCI Frederick, Ctr Canc Res, Canc & Dev Biol Lab, Cell Signaling Vertebrate Dev Sect,NIH, Frederick, MD 21702 USA.
RP Yamaguchi, TP (reprint author), NCI Frederick, Ctr Canc Res, Canc & Dev Biol Lab, Cell Signaling Vertebrate Dev Sect,NIH, Frederick, MD 21702 USA.
EM yamagute@mail.nih.gov
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. Deposited in PMC for release after 12 months.
NR 46
TC 15
Z9 16
U1 1
U2 6
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
EI 1477-9129
J9 DEVELOPMENT
JI Development
PD MAY 1
PY 2015
VL 142
IS 9
BP 1628
EP 1638
DI 10.1242/dev.111922
PG 11
WC Developmental Biology
SC Developmental Biology
GA CG8UY
UT WOS:000353591300008
PM 25922526
ER
PT J
AU Anderson, AL
Li, SH
Markova, D
Holmes, TH
Chiang, N
Kahn, R
Campbell, J
Dickerson, DL
Galloway, GP
Haning, W
Roache, JD
Stock, C
Elkashef, AM
AF Anderson, Ann L.
Li, Shou-Hua
Markova, Denka
Holmes, Tyson H.
Chiang, Nora
Kahn, Roberta
Campbell, Jan
Dickerson, Daniel L.
Galloway, Gantt P.
Haning, William
Roache, John D.
Stock, Christopher
Elkashef, Ahmed M.
TI Bupropion for the treatment of methamphetamine dependence in non-daily
users: A randomized, double-blind, placebo-controlled trial
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE Bupropion; Methamphetamine; Substance-related disorders; Drug therapy;
Medication adherence; Patient acuity
ID ABUSE; INTERVIEW
AB Aim: Bupropion was tested for efficacy to achieve methamphetamine (MA) abstinence in dependent, non-daily users.
Methods: A randomized, double-blind, placebo-controlled trial, with 12-week treatment and 4-week follow-up, was conducted with 204 treatment-seeking participants having MA dependence per DSM-IV, who used MA on a less-than-daily basis. 104 were randomized to matched placebo and 100 to bupropion, sustained-release 150 mg, twice daily. Participants were seen three times weekly to obtain urine for MA and bupropion assays, study assessments, and thrice weekly, 90-min, group psychotherapy. There was no biomarker for placebo adherence. The primary outcome was achievement of abstinence throughout the last two weeks of treatment; 'success' requiring at least two urine samples during each of Weeks 11 and 12, and all samples MA-negative (<300 ng/mL).
Results: Bupropion and placebo groups did not differ significantly in the percentage achieving abstinence for the last 2 weeks of treatment (chi-square, p = 0.32). Subgroup analysis of participants with lower baseline MA use (<= 18 of last 30 days before consent) also revealed no difference in success between groups (p = 0.73). Medication adherence per protocol (detectable bupropion, >5 ng/mL, in >= 50% of urine samples from Study Weeks 1-10 and >= 66% of urine samples from Weeks 11 to 12) was achieved by 47% of participants taking bupropion.
Conclusions: These data indicate that bupropion did not increase abstinence in dependent participants who were using MA less-than-daily. Medication non-adherence was a limitation in this trial. Psychosocial therapy remains the mainstay of treatment for MA dependence. Further research on subgroups who may respond to bupropion may be warranted. Published by Elsevier Ireland Ltd.
C1 [Anderson, Ann L.; Li, Shou-Hua; Chiang, Nora; Kahn, Roberta] NIDA, NIH, Div Pharmacotherapies & Med Consequences, Bethesda, MD 20892 USA.
[Markova, Denka] Medivation Inc, San Francisco, CA USA.
[Holmes, Tyson H.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford Ctr Sleep Sci & Med, Stanford, CA 94305 USA.
[Campbell, Jan] Univ Kansas, Kansas City, KS USA.
[Dickerson, Daniel L.] Univ Calif Los Angeles, Integrated Subst Abuse Programs, Los Angeles, CA USA.
[Galloway, Gantt P.] St Lukes Hosp, San Francisco, CA USA.
[Haning, William] Univ Hawaii, Honolulu, HI 96822 USA.
[Roache, John D.] UTX, Hlth Sci Ctr, San Antonio, TX USA.
[Stock, Christopher] VA Hlth Care Syst, Salt Lake City, UT USA.
[Elkashef, Ahmed M.] Natl Rehabil Ctr, Abu Dhabi, U Arab Emirates.
RP Anderson, AL (reprint author), NIDA, NIH, DPMCDA, 6001 Execut Blvd,Rm 4149, Bethesda, MD 20892 USA.
EM aa135m@nih.gov
FU Nat'l Institutes of Health - Nat'l Institute on Drug Abuse
[N01DA-05-8857]; NIDA through the Department of Veterans Affairs [1
Y01-DA-40032]
FX This study was funded by Nat'l Institutes of Health - Nat'l Institute on
Drug Abuse contract: N01DA-05-8857. NIDA had a major role in study
design, analysis and interpretation of the data, and writing and
submitting this manuscript for publication.; THH received partial salary
support from NIDA through the Department of Veterans Affairs Cooperative
Studies Program (Interagency Agreement) 1 Y01-DA-40032.
NR 19
TC 8
Z9 8
U1 2
U2 8
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
EI 1879-0046
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD MAY 1
PY 2015
VL 150
BP 170
EP 174
DI 10.1016/j.drugalcdep.2015.01.036
PG 5
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA CG8YF
UT WOS:000353600900023
PM 25818061
ER
PT J
AU He, S
Bergman, J
Zhang, YM
Weusten, B
Xue, LY
Qin, XM
Dou, LZ
Liu, Y
Fleischer, D
Lu, N
Dawsey, SM
Wang, GQ
AF He, Shun
Bergman, Jacques
Zhang, Yueming
Weusten, Bas
Xue, Liyan
Qin, Xiumin
Dou, Lizhou
Liu, Yong
Fleischer, David
Lu, Ning
Dawsey, Sanford M.
Wang, Gui-Qi
TI Endoscopic radiofrequency ablation for early esophageal squamous cell
neoplasia: report of safety and effectiveness from a large prospective
trial
SO ENDOSCOPY
LA English
DT Article
ID GRADE INTRAEPITHELIAL NEOPLASIA; SUBMUCOSAL DISSECTION; MUCOSAL
RESECTION; BARRETTS-ESOPHAGUS; CARCINOMA; CANCER; DYSPLASIA; OUTCOMES;
CHINA; LINXIAN
AB Background and study aims: Endoscopic radiofrequency ablation (RFA) is an established therapy for Barrett's esophagus. Preliminary reports, limited by low patient numbers, also suggest a possible role for RFA in early esophageal squamous cell neoplasia (ESCN). The aim of this study was to evaluate the safety and effectiveness of RFA for early ESCN (moderate/high grade intraepithelial neoplasia [MGIN/HGIN] and early flat-type esophageal squamous cell carcinoma [ESCC]).
Patients and methods: This prospective cohort study included patients with at least one flat (type 0-IIb) unstained lesion (USL) on Lugol's chromoendoscopy and a consensus diagnosis of MGIN, HGIN, or early ESCC. RFA was used at baseline to treat all USLs, and then biopsy (and focal RFA if USL persisted) was performed every 3 months until all biopsies were negative for MGIN, HGIN, and ESCC. The main outcome measurements were complete response at 3 and 12 months (absence of MGIN, HGIN, and ESCC), neoplastic progression, and adverse events.
Results: A total of 96 patients participated (MGIN 45, HGIN 42, early ESCC 9). At 3 and 12 months, 73% (70/96) and 84% (81/96), respectively, showed a complete response. Two patients (2 %) progressed (MGIN to HGIN; HGIN to T1m2 ESCC); both were treated endoscopically and achieved complete response. Stricture occurred in 20 patients (21 %), all after circumferential RFA. Lugol's + RFA 12J/cm(2) (single application, no cleaning) was the favored baseline circumferential RFA technique (82% 12-month complete response [14/17], 6% stricture [6/17]).
Conclusion: In patients with early ESCN, RFA was associated with a high complete response rate and an acceptable safety profile.
C1 [He, Shun; Zhang, Yueming; Qin, Xiumin; Dou, Lizhou; Liu, Yong; Wang, Gui-Qi] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Endoscopy, Beijing 100021, Peoples R China.
[He, Shun; Zhang, Yueming; Xue, Liyan; Qin, Xiumin; Dou, Lizhou; Liu, Yong; Lu, Ning; Wang, Gui-Qi] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Bergman, Jacques; Weusten, Bas] Univ Amsterdam, Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1105 AZ Amsterdam, Netherlands.
[Weusten, Bas] St Antonius Hosp, Dept Gastroenterol, Nieuwegein, Netherlands.
[Xue, Liyan; Lu, Ning] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Pathol, Beijing 100021, Peoples R China.
[Fleischer, David] Mayo Clin, Div Gastroenterol & Hepatol, Scottsdale, AZ USA.
[Dawsey, Sanford M.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Wang, GQ (reprint author), Chinese Acad Med Sci, Canc Inst & Hosp, Dept Endoscopy, 17 Panjiayuan, Beijing 100021, Peoples R China.
EM wangguiq@126.com
FU Covidien GI Solutions; Olympus Medical
FX Dr. Bergman has received medical supplies for study purposes and
unrestricted grant aid for training programs from Covidien GI Solutions
(formerly BARRX Medical). He has also received an unrestricted grant
from Olympus Medical. Dr. Wang has received medical supplies for study
purposes from Covidien GI Solutions (formerly BARRX Medical).
NR 39
TC 5
Z9 7
U1 1
U2 3
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0013-726X
EI 1438-8812
J9 ENDOSCOPY
JI Endoscopy
PD MAY
PY 2015
VL 47
IS 5
BP 398
EP 408
DI 10.1055/s-0034-1391285
PG 11
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA CG8MP
UT WOS:000353562400003
PM 25668428
ER
PT J
AU Kono, M
Proia, RL
AF Kono, Mari
Proia, Richard L.
TI Imaging S1P1 activation in vivo
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Review
DE Signaling; Sphingolipid; Sphingosine-1-phosphate; GPCR; Inflammation;
Homeostasis
ID PROTEIN-COUPLED RECEPTOR; PERSISTENT STAT3 ACTIVATION;
MULTIPLE-SCLEROSIS; ENDOTHELIAL-CELLS; VASCULAR MATURATION; FINGOLIMOD
FTY720; SPHINGOSINE-1-PHOSPHATE; EXPRESSION; MICE; INFLAMMATION
AB Sphingosine-1-phosphate receptor 1 (S1P1) is a G protein-coupled receptor that is activated by the sphingolipid ligand sphingosine-1-phosphate (S1P). S1P1 is widely expressed across tissues and, when activated, has broad functions in the immune, vascular and nervous systems. In several diseases in which inflammation plays a critical role, S1P1 activation has been found to be involved in pathogenesis. However, the details of S1P1 activation in vivo under different physiologic conditions are not well understood. Here we describe how a new in vivo methodology to identify S1P1 activation has helped increase understanding of the manner in which this signaling molecule functions both in homeostasis and during inflammation. Published by Elsevier Inc.
C1 [Kono, Mari; Proia, Richard L.] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Proia, RL (reprint author), NIDDK, Genet Dev & Dis Branch, Bldg 10,Room 9D-06,10 Ctr DR MSC 1821, Bethesda, MD 20892 USA.
EM richardp@intra.niddk.nih.gov
FU National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases
FX We thank Linda Raab for editing and helpful comments on the manuscript.
This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases.
NR 29
TC 0
Z9 0
U1 0
U2 5
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4827
EI 1090-2422
J9 EXP CELL RES
JI Exp. Cell Res.
PD MAY 1
PY 2015
VL 333
IS 2
BP 178
EP 182
DI 10.1016/j.yexcr.2014.11.023
PG 5
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA CG9UR
UT WOS:000353666100004
PM 25498971
ER
PT J
AU Liu, SX
Wang, Y
Worley, PF
Mattson, MP
Gaiano, N
AF Liu, Shuxi
Wang, Yue
Worley, Paul F.
Mattson, Mark P.
Gaiano, Nicholas
TI The Canonical Notch Pathway Effector RBP-J Regulates Neuronal Plasticity
and Expression of GABA Transporters in Hippocampal Networks
SO HIPPOCAMPUS
LA English
DT Article
DE RBP-J; canonical Notch signaling; GABA transporter; neuronal plasticity;
learning and memory
ID SYNAPTIC PLASTICITY; MOUSE-BRAIN; SIGNALING PATHWAY; GENE KNOCKOUT;
MEMORY; LOCALIZATION; RECOGNITION; CELLS; GAT-3
AB Activation of the Notch pathway in neurons is essential for learning and memory in various species from invertebrates to mammals. However, it remains unclear how Notch signaling regulates neuronal plasticity, and whether the transcriptional regulator and canonical pathway effector RBP-J plays a role. Here, we report that conditional disruption of RBP-J in the postnatal hippocampus leads to defects in long-term potentiation, long-term depression, and in learning and memory. Using gene expression profiling and chromatin immunoprecipitation, we identified two GABA transporters, GAT2 and BGT1, as putative Notch/RBP-J pathway targets, which may function downstream of RBP-J to limit the accumulation of GABA in the Schaffer collateral pathway. Our results reveal an essential role for canonical Notch/RBP-J signaling in hippocampal synaptic plasticity and suggest that role, at least in part, is mediated by the regulation of GABAergic signaling. (c) 2014 Wiley Periodicals, Inc.
C1 [Liu, Shuxi; Gaiano, Nicholas] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Neuroregenerat Program, Baltimore, MD USA.
[Liu, Shuxi; Worley, Paul F.; Gaiano, Nicholas] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Wang, Yue; Mattson, Mark P.] NIA, Neurosci Lab, NIH, Baltimore, MD 21224 USA.
[Worley, Paul F.; Mattson, Mark P.; Gaiano, Nicholas] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
[Gaiano, Nicholas] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
RP Liu, SX (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
EM shuxi.liu@nih.hhs.gov; Mark.mattson@nih.gov
FU Institute for Cell Engineering at Johns Hopkins University; Young
Investigator Award from the Brain and Behavior Research Foundation;
James S. McDonnell Foundation; National Institute of Mental Health;
Intramural Research Program of the National Institute on Aging, National
Institutes of Health
FX Grant sponsor: Institute for Cell Engineering at Johns Hopkins
University (N.G.), a Young Investigator Award from the Brain and
Behavior Research Foundation (N.G.), the James S. McDonnell Foundation
(N.G.), the National Institute of Mental Health (P.W.), and the
Intramural Research Program of the National Institute on Aging, National
Institutes of Health.
NR 30
TC 3
Z9 3
U1 1
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1050-9631
EI 1098-1063
J9 HIPPOCAMPUS
JI Hippocampus
PD MAY
PY 2015
VL 25
IS 5
BP 670
EP 678
DI 10.1002/hipo.22402
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA CH4BF
UT WOS:000353975200011
PM 25515406
ER
PT J
AU Liu, Q
Du, X
Hong, XF
Li, TM
Zheng, B
He, L
Wang, YN
Otto, M
Li, M
AF Liu, Qian
Du, Xin
Hong, Xufen
Li, Tianming
Zheng, Bing
He, Lei
Wang, Yanan
Otto, Michael
Li, Min
TI Targeting Surface Protein SasX by Active and Passive Vaccination To
Reduce Staphylococcus aureus Colonization and Infection
SO INFECTION AND IMMUNITY
LA English
DT Article
ID NASAL CARRIAGE; VIRULENCE DETERMINANT; DISEASE; EXPRESSION; VARIANT;
ALPHA
AB SasX is a recently described surface protein of Staphylococcus aureus that is linked to the epidemic success of hospital-associated methicillin-resistant clones, in particular in Asia. It enhances nasal colonization and virulence in skin and lung infection models. Here, we evaluated the potential of SasX as a vaccine component in passive and active immunization efforts using mouse infection models. We found that SasX induced a specific immune response predominantly based on IgG1 antibodies. Active immunization with recombinant SasX or passive immunization with rabbit polyclonal anti-SasX IgG significantly decreased the size of lesions caused by Staphylococcus aureus in a skin infection model. Furthermore, active immunization reduced acute lung injury in a lung infection model. Moreover, active or passive immunization significantly reduced Staphylococcus aureus colonization in a nasal colonization model. Finally, anti-SasX IgG enhanced the susceptibility of Staphylococcus aureus to killing by human neutrophils. We conclude that SasX is a potential target for therapeutics or vaccines designed to moderate colonization and infection by sasX-positive epidemic strains of Staphylococcus aureus.
C1 [Liu, Qian; Li, Tianming; Zheng, Bing; He, Lei; Wang, Yanan; Li, Min] Shanghai Jiao Tong Univ, Dept Lab Med, Renji Hosp, Sch Med, Shanghai 200030, Peoples R China.
[Du, Xin; Hong, Xufen] Fudan Univ, Dept Lab Med, Huashan Hosp, Shanghai Med Coll, Shanghai 200433, Peoples R China.
[Wang, Yanan] NIAID, Pathogen Mol Genet Sect, Lab Human Bacterial Pathogenesis, NIH, Bethesda, MD 20892 USA.
RP Otto, M (reprint author), NIAID, Pathogen Mol Genet Sect, Lab Human Bacterial Pathogenesis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM motto@niaid.nih.gov; ruth_limin@126.com
OI Otto, Michael/0000-0002-2222-4115
FU National Natural Science Foundation of China [81322025, 81171623,
81371875]; Shanghai Shuguang Talent Project [12SG03]; Shanghai Committee
of Science and Technology, China [14140901000]; Foundation for
Innovative Research Groups of the National Natural Science Foundation of
China [81421001]; Intramural Research Program of the National Institute
of Allergy and Infectious Diseases, National Institutes of Health
FX This study was supported by the National Natural Science Foundation of
China (grants 81322025, 81171623, and 81371875), Shanghai Shuguang
Talent Project (12SG03), the Shanghai Committee of Science and
Technology, China (14140901000), and the Foundation for Innovative
Research Groups of the National Natural Science Foundation of China
(grant no. 81421001) (to M.L.) and the Intramural Research Program of
the National Institute of Allergy and Infectious Diseases, the National
Institutes of Health (to M.O.).
NR 27
TC 3
Z9 4
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD MAY
PY 2015
VL 83
IS 5
BP 2168
EP 2174
DI 10.1128/IAI.02951-14
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CG0TJ
UT WOS:000352982600040
PM 25776748
ER
PT J
AU Winnenburg, R
Sorbello, A
Bodenreider, O
AF Winnenburg, Rainer
Sorbello, Alfred
Bodenreider, Olivier
TI Exploring adverse drug events at the class level
SO JOURNAL OF BIOMEDICAL SEMANTICS
LA English
DT Article
DE Adverse drug events; Drug classes; Anatomical Therapeutic Chemical (ATC)
drug classification system; Class effect; Heat maps; Pharmacovigilance
ID REPORTING SYSTEM
AB Background: While the association between a drug and an adverse event (ADE) is generally detected at the level of individual drugs, ADEs are often discussed at the class level, i.e., at the level of pharmacologic classes (e.g., in drug labels). We propose two approaches, one visual and one computational, to exploring the contribution of individual drugs to the class signal.
Methods: Having established a dataset of ADEs from MEDLINE, we aggregate drugs into ATC classes and ADEs into high-level MeSH terms. We compute statistical associations between drugs and ADEs at the drug level and at the class level. Finally, we visualize the signals at increasing levels of resolution using heat maps. We also automate the exploration of drug-ADE associations at the class level using clustering techniques.
Results: Using our visual approach, we were able to uncover known associations, e.g., between fluoroquinolones and tendon injuries, and between statins and rhabdomyolysis. Using our computational approach, we systematically analyzed 488 associations between a drug class and an ADE.
Conclusions: The findings gained from our exploratory techniques should be of interest to the curators of ADE repositories and drug safety professionals. Our approach can be applied to different drug-ADE datasets, using different drug classification systems and different signal detection algorithms.
C1 [Winnenburg, Rainer] Stanford Univ, Ctr Biomed Informat Res, Stanford, CA 94305 USA.
[Sorbello, Alfred] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Bodenreider, Olivier] Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, NIH, Bethesda, MD 20892 USA.
RP Bodenreider, O (reprint author), Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, NIH, Bethesda, MD 20892 USA.
EM obodenreider@mail.nih.gov
FU Intramural Research Program of the NIH, National Library of Medicine
(NLM); US Food and Drug Administration (FDA) through the Center for Drug
Evaluation and Research (CDER) Critical Path Program [XLM12011 001];
Office of Translational Sciences at CDER; U.S. Department of Energy;
National Library of Medicine
FX A preliminary version of this work was presented to the Vaccine and Drug
Ontology Studies (VDOS-2014) workshop. This work was supported by the
Intramural Research Program of the NIH, National Library of Medicine
(NLM). This work also received support from the US Food and Drug
Administration (FDA) through the Center for Drug Evaluation and Research
(CDER) Critical Path Program [interagency agreement with NLM (XLM12011
001)] and from the Office of Translational Sciences at CDER. While
conducting this research, RW was supported by an appointment to the NLM
Research Participation Program administered by the Oak Ridge Institute
for Science and Education through an interagency agreement between the
U.S. Department of Energy and the National Library of Medicine. The
authors want to thank Ana Szarfman, Rave Harpaz and Anna Ripple for
useful discussions.
NR 24
TC 2
Z9 2
U1 2
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2041-1480
J9 J BIOMED SEMANT
JI J. Biomed. Semant.
PD MAY 1
PY 2015
VL 6
AR 18
DI 10.1186/s13326-015-0017-1
PG 10
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA CH0BP
UT WOS:000353684200001
PM 25937884
ER
PT J
AU Dubey, JP
Sykes, JE
Shelton, GD
Sharp, N
Verma, SK
Calero-Bernal, R
Viviano, J
Sundar, N
Khan, A
Grigg, ME
AF Dubey, Jitender P.
Sykes, Jane E.
Shelton, G. Diane
Sharp, Nick
Verma, Shiv K.
Calero-Bernal, Rafael
Viviano, Jenifer
Sundar, Natarajan
Khan, Asis
Grigg, Michael E.
TI Sarcocystis caninum and Sarcocystis svanai n. spp. (Apicomplexa:
Sarcocystidae) Associated with Severe Myositis and Hepatitis in the
Domestic Dog (Canis familiaris)
SO JOURNAL OF EUKARYOTIC MICROBIOLOGY
LA English
DT Article
DE Canada; dog; USA
ID BEARS URSUS-MARITIMUS; MUSCULAR SARCOCYSTOSIS; NEURONA; ENCEPHALITIS;
INFECTION; SCHIZONTS; PARASITE
AB There are several reports of Sarcocystis sarcocysts in muscles of dogs, but these species have not been named. Additionally, there are two reports of Sarcocystis neurona in dogs. Here, we propose two new names, Sarcocystis caninum, and Sarcocystis svanai for sarcocysts associated with clinical muscular sarcocystosis in four domestic dogs (Canis familiaris), one each from Montana and Colorado in the USA, and two from British Columbia, Canada. Only the sarcocyst stage was identified. Most of the sarcocysts identified were S. caninum. Sarcocysts were studied using light microscopy, transmission electron microscopy (TEM), and polymerase chain reaction. Based on collective results two new species, S. caninum and S. svanai were designated. Sarcocystis caninum and S. svanai were structurally distinct. Sarcocystis caninum sarcocysts were up to 1.2mm long and up to 75m wide. By light microscopy, the sarcocyst wall was relatively thin and smooth. By TEM, the sarcocyst wall was type 9, 1-2m thick, and contained villar protrusions that lacked microtubules. Bradyzoites in sections were 7-9m long. Sarcocysts of S. svanai were few and were identified by TEM. Sarcocystis svanai sarcocysts were type 1, thin walled (<0.5m), and the wall lacked villar protrusions but had tiny blebs that did not invaginate. DNA was extracted either from infected frozen muscle biopsies or formalin-fixed paraffin-embedded sections. Dogs were either singly infected with S. caninum or multiply co-infected with S. caninum and S. svanai (the result of a mixed infection) based on multilocus DNA sequencing and morphology. BLASTn analysis established that the sarcocysts identified in these dogs were similar to, but not identical to Sarcocystis canis or Sarcocystis arctosi, parasites found to infect polar bears (Ursus maritimus) or brown bears (Ursus arctosi), respectively. However, the S. caninum sequence showed 100% identify over the 18S rRNA region sequenced to that of S. arctica, a parasite known to infect Arctic foxes (Vulpes lagopus).
C1 [Dubey, Jitender P.; Verma, Shiv K.; Calero-Bernal, Rafael] ARS, Anim Parasit Dis Lab, USDA, Beltsville Agr Res Ctr, Beltsville, MD 20705 USA.
[Sykes, Jane E.] Univ Calif Davis, Sch Vet Med, Dept Med & Epidemiol, Davis, CA 95616 USA.
[Shelton, G. Diane] Univ Calif San Diego, Dept Pathol, La Jolla, CA 92093 USA.
[Sharp, Nick] Canada West Vet Specialists, Vancouver, BC V6R 1E5, Canada.
[Viviano, Jenifer] US Army, Joint Pathol Ctr, Vet Pathol Serv, Silver Spring, MD 20910 USA.
[Sundar, Natarajan; Khan, Asis; Grigg, Michael E.] NIAID, Mol Parasitol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Dubey, JP (reprint author), BARC, Anim Parasit Dis Lab, USDA, Bldg 1001, Beltsville, MD 20705 USA.
EM jitender.dubey@ars.usda.gov
FU NIH; NIAID; Department of Employment and Innovation of the Regional
Government of Extremadura, Spain [PO12010]; European Social Fund
[PO12010]
FX The authors thank Dr. Eric Hoberg for his helpful suggestions concerning
taxonomy, and Mr. Efrain Perez, Joint Pathology Center, Veterinary
Services, U.S. Army, Silver Spring, Maryland for excellent technical
help with electron microscopy. This study was financially support in
part by the Intramural Research Program of the NIH and NIAID. M.E.G. is
a scholar of the Canadian Institute for Advanced Research Integrated
Microbial Biodiversity Program.; R. Calero-Bernal is a postdoctoral
fellow (ref. PO12010) funded by the Department of Employment and
Innovation of the Regional Government of Extremadura, Spain and the
European Social Fund.
NR 24
TC 2
Z9 2
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5234
EI 1550-7408
J9 J EUKARYOT MICROBIOL
JI J. Eukaryot. Microbiol.
PD MAY-JUN
PY 2015
VL 62
IS 3
BP 307
EP 317
DI 10.1111/jeu.12182
PG 11
WC Microbiology
SC Microbiology
GA CG8IQ
UT WOS:000353551300004
PM 25256157
ER
PT J
AU Gai, ND
Butman, JA
AF Gai, Neville D.
Butman, John A.
TI Reduced Scan Time Three-Dimensional FLAIR Using Modulated Inversion and
Repetition Time
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE 3D FLAIR; modulated repetition time; modulated inversion time; scan time
reduction; variable repetition time
ID REFOCUSING FLIP ANGLES; SEQUENCES; OPTIMIZATION; BRAIN; TESLA; T1
AB BackgroundThe purpose of this study is to design and evaluate a new reduced scan time three-dimensional (3D) FLuid Attenuated Inversion Recovery (FLAIR) sequence.
MethodsThe 3D FLAIR sequence was modified so that the repetition time was modulated in a predetermined smooth manner (3D mFLAIR). Inversion times were adjusted accordingly to maintain cerebrospinal fluid (CSF) suppression. Simulations were performed to determine SNR for gray matter (GM), white matter (WM), and CSF. Fourteen volunteers were imaged using the modified and product sequence. SNR measurements were performed in GM, WM, and CSF. Mean value and the 95% confidence interval ([CI]) were assessed. Scan time for the 3D FLAIR and 3D mFLAIR sequences was measured.
ResultsThere was no statistically significant difference in the SNR measured in GM (P value=0.5; mean SNR=42.8 [CI]: 38.2-45.5 versus 42.2 [CI]: 38.3-46.1 for 3D FLAIR and 3D mFLAIR, respectively) and WM (P value=0.25; mean SNR=32.1 [CI]: 30.3-33.8 versus 32.9 [CI]: 31.1-34.7). Scan time reduction greater than 30% was achieved for the given parameter set with the 3D mFLAIR sequence.
ConclusionScan time for 3D FLAIR can be effectively reduced by modulating repetition and inversion time in a predetermined manner while maintaining the SNR and CNR of a constant TR sequence. J. Magn. Reson. Imaging 2015;41:1440-1446. (c) 2014 Wiley Periodicals, Inc.
C1 [Gai, Neville D.; Butman, John A.] NIH, Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
RP Gai, ND (reprint author), NIH, Radiol & Imaging Sci RAD&IS, Ctr Clin, 9000 Rockville Pike,Bldg 10 Room 1C502, Bethesda, MD 20892 USA.
EM gaind@cc.nih.gov
RI Butman, John/J-2780-2013
OI Butman, John/0000-0002-1547-9195
FU Intramural Research Program of the NIH Clinical Center
FX This work was supported by the Intramural Research Program of the NIH
Clinical Center.
NR 12
TC 0
Z9 0
U1 0
U2 2
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 MAY
PY 2015
VL 41
IS 5
BP 1440
EP 1446
DI 10.1002/jmri.24679
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CG9ND
UT WOS:000353641600032
PM 24979311
ER
PT J
AU Gold, B
Cankovic, M
Furtado, LV
Meier, F
Gocke, CD
AF Gold, Bert
Cankovic, Milena
Furtado, Larissa V.
Meier, Frederick
Gocke, Christopher D.
TI Do Circulating Tumor Cells, Exosomes, and Circulating Tumor Nucleic
Acids Have Clinical Utility? A Report of the Association for Molecular
Pathology
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Article
ID LUNG-CANCER PATIENTS; METASTATIC BREAST-CANCER; K-RAS MUTATIONS;
RESISTANT PROSTATE-CANCER; PRIMARY COLORECTAL CANCERS; SERUM MICRORNA
EXPRESSION; PLASMA DNA; PERIPHERAL-BLOOD; PANCREATIC-CANCER;
MICROSATELLITE ALTERATIONS
AB Diagnosing and screening for tumors through noninvasive means represent an important paradigm shift in precision medicine. In contrast to tissue biopsy, detection of circulating tumor cells (CTCs) and circulating tumor nucleic acids provides a minimally invasive method for predictive and prognostic marker detection. This allows early and serial assessment of metastatic disease, including follow-up during remission, characterization of treatment effects, and clonal evolution. Isolation and characterization of CTCs and circulating tumor DNA (ctDNA) are likely to improve cancer diagnosis, treatment, and minimal residual disease monitoring. However, more trials are required to validate the clinical utility of precise molecular markers for a variety of tumor types. This review focuses on the clinical utility of CTCs and ctDNA testing in patients with solid tumors, including somatic and epigenetic alterations that can be detected. A comparison of methods used to isolate and detect CTCs and some of the intricacies of the characterization of the ctDNA are also provided.
C1 [Gold, Bert; Cankovic, Milena; Furtado, Larissa V.; Meier, Frederick; Gocke, Christopher D.] Circulating Tumor Cells Working Grp, Clin Practice Comm, Associat Mol Pathol, Bethesda, MD USA.
[Gold, Bert] NIH, Ctr Canc Res, Frederick, MD 21702 USA.
[Cankovic, Milena; Meier, Frederick] Henry Ford Hosp, Dept Pathol, Detroit, MI 48202 USA.
[Furtado, Larissa V.] Univ Chicago, Med Ctr, Dept Pathol, Chicago, IL 60637 USA.
[Gocke, Christopher D.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
RP Gold, B (reprint author), NIH, Ctr Canc Res, 1050 Boyles St, Frederick, MD 21702 USA.
EM bert.gold@nih.gov
FU Association for Molecular Pathology; Intramural Research Program of the
National Cancer Institute, NIH
FX Supported in part by the Association for Molecular Pathology and the
Intramural Research Program of the National Cancer Institute, NIH.
NR 221
TC 21
Z9 22
U1 4
U2 36
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD MAY
PY 2015
VL 17
IS 3
BP 209
EP 224
DI 10.1016/j.jmoldx.2015.02.001
PG 16
WC Pathology
SC Pathology
GA CH2GO
UT WOS:000353843900001
PM 25908243
ER
PT J
AU Janssen, I
Millo, C
Ling, A
Chen, C
Herscovitch, P
Pacak, K
AF Janssen, I.
Millo, C.
Ling, A.
Chen, C.
Herscovitch, P.
Pacak, K.
TI Comparison of Ga-68-DOTATATE PET/CT with other functional imaging
studies in head and neck paragangliomas: preliminary results
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Meeting Abstract
CT 3rd Theranostics World Congress on Gallium-68 and PRRT
CY MAR 12-14, 2015
CL Johns Hopkins Med Campus, Baltimore, MD
SP Soc Nucl Med & Mol Imaging, Johns Hopkins Univ
HO Johns Hopkins Med Campus
C1 [Janssen, I.; Millo, C.; Ling, A.; Chen, C.; Herscovitch, P.; Pacak, K.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD MAY 1
PY 2015
VL 56
SU 2
MA 34
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CH1XO
UT WOS:000353816700035
ER
PT J
AU Miljkovic, MD
Emuron, D
Rhodes, L
Abraham, J
Miller, K
AF Miljkovic, Milos D.
Emuron, Dennis
Rhodes, Lori
Abraham, Joseph
Miller, Kenneth
TI "Allow Natural Death" versus "Do Not Resuscitate": What Do Patients with
Advanced Cancer Choose?
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; LIFE; CARE; COMMUNICATION; VIDEO
AB Background: Many patients with advanced cancer at our hospital request full resuscitative efforts at the end of life. We assessed the knowledge and attitudes of these patients towards end-of-life (EOL) care, and their preferences about "Do Not Resuscitate" (DNR), "Allow Natural Death" (AND), and "full code" orders.
Methods: The first 100 consenting adult patients with advanced cancer were surveyed regarding their diagnosis, prognosis, and attitudes about critical care and resuscitation. They were then presented with hypothetical scenarios in which a decision on their code status had to be made if they had one year, six months, or one month left to live. Half were given a choice between being "full code" and "DNR," and half could choose between "full code" and "AND."
Results: All 93 of the participants who completed the survey were considered by their attending physician to have a terminal illness, but only 42% of these interviewees believed they were terminally ill. In addition, only 25% of participants thought that their primary oncologist knew their EOL wishes. Participants were equally likely to choose either of the "no code" options in all hypothetical scenarios (p>0.54), regardless of age, sex, race, type of cancer, education, or income level. A similar proportion of patients who had a living will chose "AND" and "DNR" orders instead of "full code" in all the scenarios (47%-74% and 63%-71%). In contrast, among patients who did not have a living will, 52% chose "DNR," while 19% opted for "AND."
Conclusions: We hypothesized that "AND" orders may be more acceptable to patients with advanced cancer, but there was no statistically significant difference in acceptability between "AND" and "DNR" orders.
C1 [Miljkovic, Milos D.] US Naval Hosp, NCI, Med Oncol Serv, Bethesda, MD 20814 USA.
[Emuron, Dennis] Sinai Hosp, Dept Internal Med, Baltimore, MD 21215 USA.
[Rhodes, Lori] Sinai Hosp, Alvin & Lois Lapidus Canc Inst, Baltimore, MD 21215 USA.
[Abraham, Joseph] Apex Epidemiol, Baltimore, MD USA.
[Miller, Kenneth] Sinai Hosp, Alvin & Lois Lapidus Canc Inst, Div Hematol Med Oncol, Baltimore, MD 21215 USA.
RP Miljkovic, MD (reprint author), US Naval Hosp, NCI, Med Oncol Serv, 10 Ctr Dr,Room 12N226, Bethesda, MD 20814 USA.
EM milos@miljko.org
RI Miljkovic, Milos/F-7685-2011
OI Miljkovic, Milos/0000-0001-5848-6320
NR 14
TC 3
Z9 3
U1 0
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
EI 1557-7740
J9 J PALLIAT MED
JI J. Palliat. Med.
PD MAY 1
PY 2015
VL 18
IS 5
BP 457
EP 460
DI 10.1089/jpm.2014.0369
PG 4
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA CH0LC
UT WOS:000353710300013
PM 25825919
ER
PT J
AU Lowitz, J
Keil, MF
AF Lowitz, Judith
Keil, Margaret F.
TI Cushing Syndrome: Establishing a Timely Diagnosis
SO JOURNAL OF PEDIATRIC NURSING-NURSING CARE OF CHILDREN & FAMILIES
LA English
DT Editorial Material
ID QUALITY-OF-LIFE; CHILDREN; ADOLESCENTS; CURE
C1 [Keil, Margaret F.] NIH, Ctr Clin, Dept Nursing, Bethesda, MD 20892 USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Endocrinol & Genet, NIH, Bethesda, MD USA.
RP Keil, MF (reprint author), NIH, Ctr Clin, Dept Nursing, Bethesda, MD 20892 USA.
EM keilm@mail.nih.gov
FU Intramural Research Program of National Institutes of Health, Eunice
Kennedy Shriver NICHD
FX This work was supported in part by the Intramural Research Program of
National Institutes of Health, Eunice Kennedy Shriver NICHD. We thank
Kathy Feigenbaum, Carol VanRyzin, and Dr. Barbara Jordan for their
review and comments.
NR 10
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 0882-5963
J9 J PEDIATR NURS
JI J. Pediatr. Nurs.
PD MAY-JUN
PY 2015
VL 30
IS 3
BP 528
EP 530
DI 10.1016/j.pedn.2015.02.006
PG 3
WC Nursing; Pediatrics
SC Nursing; Pediatrics
GA CH2BL
UT WOS:000353829000018
PM 25724858
ER
PT J
AU Davis, AS
Gantz, MG
Do, B
Shankaran, S
Hamrick, SEG
Kennedy, KA
Tyson, JE
Chalak, LF
Laptook, AR
Goldstein, RF
Hintz, SR
Das, A
Higgins, RD
Ball, MB
Hale, EC
Van Meurs, KP
AF Davis, A. S.
Gantz, M. G.
Do, B.
Shankaran, S.
Hamrick, S. E. G.
Kennedy, K. A.
Tyson, J. E.
Chalak, L. F.
Laptook, A. R.
Goldstein, R. F.
Hintz, S. R.
Das, A.
Higgins, R. D.
Ball, M. B.
Hale, E. C.
Van Meurs, K. P.
CA Eunice Kennedy Shriver Natl Inst C
Human Dev Neonatal Res Network
TI Serial aEEG recordings in a cohort of extremely preterm infants:
feasibility and safety
SO JOURNAL OF PERINATOLOGY
LA English
DT Article
ID AMPLITUDE-INTEGRATED ELECTROENCEPHALOGRAPHY; HYPOXIC-ISCHEMIC
ENCEPHALOPATHY; BACKGROUND PATTERNS; BRAIN-FUNCTION; 1ST WEEK; TERM;
PREDICTS; BIRTH; LIFE; HEMORRHAGE
AB OBJECTIVE: Amplitude-integrated electroencephalography (aEEG) monitoring is increasing in the neonatal population, but the safety and feasibility of performing aEEG in extremely preterm infants have not been systematically evaluated.
STUDY DESIGN: Inborn infants 230/7 to 286/7 weeks gestation or birth weight 401 to 1000 g were eligible. Serial, 6-h aEEG recordings were obtained from first week of life until 36 weeks postmenstrual age. Adverse events were documented, and surveys evaluated the impact of the aEEGs on routine care. Success of performing aEEGs according to protocol and aEEG quality were assessed.
RESULT: A total of 102 infants were enrolled, with 755 recordings performed. 83% of recordings were performed according to schedule, and 96% were without adverse event. Bedside nurses reported no interference with routine care for 89% of recordings. 92% of recordings had acceptable signal quality.
CONCLUSION: Serial aEEG monitoring is safe in preterm infants, with few adverse events and general acceptance by nursing staff.
C1 [Davis, A. S.; Hintz, S. R.; Ball, M. B.; Van Meurs, K. P.] Stanford Univ, Sch Med, Dept Pediat, Div Neonatal & Dev Med, Palo Alto, CA 94304 USA.
[Davis, A. S.; Hintz, S. R.; Ball, M. B.; Van Meurs, K. P.] Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA.
[Gantz, M. G.; Do, B.] RTI Int, Social Stat & Environm Sci Unit, Res Triangle Pk, NC USA.
[Shankaran, S.] Wayne State Univ, Sch Med, Dept Pediat, Detroit, MI 48201 USA.
[Hamrick, S. E. G.; Hale, E. C.] Emory Univ, Sch Med, Dept Pediat, Childrens Healthcare Atlanta, Atlanta, GA USA.
[Kennedy, K. A.; Tyson, J. E.] Univ Texas Houston, Med Sch Houston, Dept Pediat, Houston, TX USA.
[Chalak, L. F.] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
[Laptook, A. R.] Brown Univ, Women & Infants Hosp, Dept Pediat, Providence, RI 02908 USA.
[Goldstein, R. F.] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
[Das, A.] RTI Int, Social Stat & Environm Sci Unit, Rockville, MD USA.
[Higgins, R. D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Inst Hlth, Bethesda, MD USA.
RP Davis, AS (reprint author), Stanford Univ, Sch Med, Dept Pediat, Div Neonatal & Dev Med, 750 Welch Rd,Suite 315, Palo Alto, CA 94304 USA.
EM alexisdavismd@gmail.com
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Child Health and Human Development
FX We are indebted to our medical and nursing colleagues and to the infants
and their parents who agreed to take part in this study. A complete list
of investigators who participated in this study are listed in the
Appendix. The National Institutes of Health and the Eunice Kennedy
Shriver National Institute of Child Health and Human Development
provided grant support for this study.
NR 35
TC 0
Z9 0
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0743-8346
EI 1476-5543
J9 J PERINATOL
JI J. Perinatol.
PD MAY
PY 2015
VL 35
IS 5
BP 373
EP 378
DI 10.1038/jp.2014.217
PG 6
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA CG8NP
UT WOS:000353565200013
PM 25474559
ER
PT J
AU O'Connor, GM
Vivian, JP
Gostick, E
Pymm, P
Lafont, BAP
Price, DA
Rossjohn, J
Brooks, AG
McVicar, DW
AF O'Connor, Geraldine M.
Vivian, Julian P.
Gostick, Emma
Pymm, Phillip
Lafont, Bernard A. P.
Price, David A.
Rossjohn, Jamie
Brooks, Andrew G.
McVicar, Daniel W.
TI Peptide-Dependent Recognition of HLA-B*57:01 by KIR3DS1
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NATURAL-KILLER-CELL; IMMUNOGLOBULIN-LIKE RECEPTOR; HLA-B;
CRYSTAL-STRUCTURE; HIV-INFECTION; BW4 EPITOPE; NK CELLS; BINDING;
COMPLEX; KIR
AB Killer cell immunoglobulin-like receptors (KIRs) play an important role in the activation of natural killer (NK) cells, which in turn contribute to the effective immune control of many viral infections. In the context of HIV infection, the closely related KIR3DL1 and KIR3DS1 molecules, in particular, have been associated with disease outcome. Inhibitory signals via KIR3DL1 are disrupted by downregulation of HLA class I ligands on the infected cell surface and can also be impacted by changes in the presented peptide repertoire. In contrast, the activatory ligands for KIR3DS1 remain obscure. We used a structure-driven approach to define the characteristics of HLA class I-restricted peptides that interact with KIR3DL1 and KIR3DS1. In the case of HLAB*57:01, we used this knowledge to identify bona fide HIV-derived peptide epitopes with similar properties. Two such peptides facilitated productive interactions between HLA-B* 57:01 and KIR3DS1. These data reveal the presence of KIR3DS1 ligands within the HIV-specific peptide repertoire presented by a protective HLA class I allotype, thereby enhancing our mechanistic understanding of the processes that enable NK cells to impact disease outcome.
IMPORTANCE
Natural killer (NK) cells are implicated as determinants of immune control in many viral infections, but the precise molecular mechanisms that initiate and control these responses are unclear. The activating receptor KIR3DS1 in combination with HLA-Bw4 has been associated with better outcomes in HIV infection. However, evidence of a direct interaction between these molecules is lacking. In this study, we demonstrate that KIR3DS1 recognition of HLA-Bw4 is peptide dependent. We also identify HIV-derived peptide epitopes presented by the protective HLA-B*57:01 allotype that facilitate productive interactions with KIR3DS1. Collectively, these findings suggest a mechanism whereby changes in the peptide repertoire associated with viral infection provide a trigger for KIR3DS1 engagement and NK cell activation.
C1 [O'Connor, Geraldine M.; McVicar, Daniel W.] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Vivian, Julian P.; Pymm, Phillip; Rossjohn, Jamie] Monash Univ, Sch Biomed Sci, Dept Biochem & Mol Biol, Clayton, Vic, Australia.
[Vivian, Julian P.; Pymm, Phillip; Rossjohn, Jamie] Monash Univ, Australian Res Council Ctr Excellence Adv Mol Ima, Clayton, Vic, Australia.
[Gostick, Emma; Price, David A.; Rossjohn, Jamie] Cardiff Univ, Sch Med, Inst Infect & Immun, Cardiff CF10 3AX, S Glam, Wales.
[Lafont, Bernard A. P.] NIAID, Nonhuman Primate Immunogenet & Cellular Immunol U, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Price, David A.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Brooks, Andrew G.] Univ Melbourne, Dept Microbiol & Immunol, Parkville, Vic 3052, Australia.
RP McVicar, DW (reprint author), NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA.
EM mcvicard@mail.nih.gov
RI Price, David/C-7876-2013; McVicar, Daniel/G-1970-2015;
OI Price, David/0000-0001-9416-2737; Brooks, Andrew/0000-0002-4085-9683;
Rossjohn, Jamie/0000-0002-2020-7522
FU Intramural AIDS Targeted Antiviral Program of the National Institutes of
Health; National Health and Medical Research Council of Australia
(NHMRC); Association for International Cancer Research; Intramural
Research Program of the National Institutes of Health, National Cancer
Institute and National Institute of Allergy and Infectious Diseases
FX This work was supported by the Intramural AIDS Targeted Antiviral
Program of the National Institutes of Health, the National Health and
Medical Research Council of Australia (NHMRC), the Association for
International Cancer Research (J.R. and A.G.B.), and the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute and National Institute of Allergy and Infectious Diseases.
J.P.V. is an Australian Research Council DECRA Fellow, D.A.P. is a
Wellcome Trust Senior Investigator, and J.R. is an NHMRC Australia
Fellow.
NR 47
TC 18
Z9 18
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2015
VL 89
IS 10
BP 5213
EP 5221
DI 10.1128/JVI.03586-14
PG 9
WC Virology
SC Virology
GA CG5KB
UT WOS:000353329300004
PM 25740999
ER
PT J
AU Georgiev, IS
Joyce, MG
Yang, YP
Sastry, M
Zhang, BS
Baxa, U
Chen, RTE
Druz, A
Lees, CR
Narpala, S
Schon, A
Van Galen, J
Chuang, GY
Gorman, J
Harned, A
Pancera, M
Stewart-Jones, GBE
Cheng, C
Freire, E
McDermott, AB
Mascola, JR
Kwong, PD
AF Georgiev, Ivelin S.
Joyce, M. Gordon
Yang, Yongping
Sastry, Mallika
Zhang, Baoshan
Baxa, Ulrich
Chen, Rita E.
Druz, Aliaksandr
Lees, Christopher R.
Narpala, Sandeep
Schoen, Arne
Van Galen, Joseph
Chuang, Gwo-Yu
Gorman, Jason
Harned, Adam
Pancera, Marie
Stewart-Jones, Guillaume B. E.
Cheng, Cheng
Freire, Ernesto
McDermott, Adrian B.
Mascola, John R.
Kwong, Peter D.
TI Single-Chain Soluble BG505.SOSIP gp140 Trimers as Structural and
Antigenic Mimics of Mature Closed HIV-1 Env
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID BROADLY NEUTRALIZING ANTIBODIES; VIRUS ENVELOPE GLYCOPROTEIN; HUMAN
MONOCLONAL-ANTIBODIES; VACCINE DEVELOPMENT; CONFORMATIONAL-CHANGES;
GP41-GP120 INTERFACE; PRECURSOR CLEAVAGE; DEPENDENT EPITOPE;
RECEPTOR-BINDING; TYPE-1 ENVELOPE
AB Similar to other type I fusion machines, the HIV-1 envelope glycoprotein (Env) requires proteolytic activation; specifically, cleavage of a gp160 precursor into gp120 and gp41 subunits creates an N-terminal gp41 fusion peptide and permits folding from an immature uncleaved state to a mature closed state. While the atomic-level consequences of cleavage for HIV-1 Env are still being determined, the uncleaved state is antigenically distinct from the mature closed state, and cleavage has been reported to be essential for mimicry of the mature viral spike by soluble versions of Env. Here we report the redesign of a current state-of-the-art soluble Env mimic, BG505.SOSIP, to make it cleavage independent. Specifically, we replaced the furin cleavage site between gp120 and gp41 with Gly-Ser linkers of various lengths. The resultant linked gp120-gp41 constructs, termed single-chain gp140 (sc-gp140), exhibited different levels of structural and antigenic mimicry of the parent cleaved BG505.SOSIP. When constructs were subjected to negative selection to remove subspecies recognized by poorly neutralizing antibodies, trimers of high antigenic mimicry of BG505.SOSIP could be obtained; negative-stain electron microscopy indicated these to resemble the mature closed state. Higher proportions of BG505.SOSIP-trimer mimicry were observed in sc-gp140s with linkers of 6 or more residues, with a linker length of 15 residues exhibiting especially promising traits. Overall, flexible linkages between gp120 and gp41 in BG505.SOSIP can thus substitute for cleavage, and sc-gp140s that closely mimicked the vaccine-preferred mature closed state of Env could be obtained.
IMPORTANCE
The trimeric HIV-1 envelope glycoprotein (Env) is the sole target of virus-directed neutralizing antibody responses and a primary focus of vaccine design. Soluble mimics of Env have proven challenging to obtain and have been thought to require proteolytic cleavage into two-component subunits, gp120 and gp41, to achieve structural and antigenic mimicry of mature Env spikes on virions. Here we show that replacement of the cleavage site between gp120 and gp41 in a lead soluble gp140 construct, BG505.SOSIP, with flexible linkers can result in molecules that do not require cleavage to fold efficiently into the mature closed state. Our results provide insights into the impact of cleavage on HIV-1 Env folding. In some contexts such as genetic immunization, optimized cleavage-independent soluble gp140 constructs may have utility over the parental BG505.SOSIP, as they would not require furin cleavage to achieve mimicry of mature Env spikes on virions.
C1 [Georgiev, Ivelin S.; Joyce, M. Gordon; Yang, Yongping; Sastry, Mallika; Zhang, Baoshan; Chen, Rita E.; Druz, Aliaksandr; Lees, Christopher R.; Narpala, Sandeep; Van Galen, Joseph; Chuang, Gwo-Yu; Gorman, Jason; Pancera, Marie; Stewart-Jones, Guillaume B. E.; Cheng, Cheng; McDermott, Adrian B.; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Baxa, Ulrich; Harned, Adam] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Electron Microscopy Lab, Canc Res Technol Program, Frederick, MD USA.
[Schoen, Arne; Freire, Ernesto] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
RP Kwong, PD (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM pdkwong@nih.gov
FU Intramural Research Program of the Vaccine Research Center, National
Institute of Allergy and Infectious Diseases; Frederick National
Laboratory for Cancer Research, National Institutes of Health
[HHSN261200800001E]; National Institutes of Health [GM056550]; National
Science Foundation [MCB-1157506]
FX Support for this study was provided by the following: the Intramural
Research Program of the Vaccine Research Center, National Institute of
Allergy and Infectious Diseases; federal funds from the Frederick
National Laboratory for Cancer Research, National Institutes of Health,
under contract HHSN261200800001E; and grants from the National
Institutes of Health (GM056550 to E.F.) and from the National Science
Foundation (MCB-1157506 to E.F.).
NR 63
TC 24
Z9 25
U1 0
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 MAY
PY 2015
VL 89
IS 10
BP 5318
EP 5329
DI 10.1128/JVI.03451-14
PG 12
WC Virology
SC Virology
GA CG5KB
UT WOS:000353329300013
PM 25740988
ER
PT J
AU Pesne, V
Li, QS
Sodroski, C
Hsu, CS
Liang, TJ
AF Pesne, Veronique
Li, Qisheng
Sodroski, Catherine
Hsu, Ching-Sheng
Liang, T. Jake
TI Dynamic Interaction of Stress Granules, DDX3X, and IKK-alpha Mediates
Multiple Functions in Hepatitis C Virus Infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID BOX RNA HELICASE; CORE PROTEIN; DEPENDENT TRANSLATION; PROCESSING
BODIES; LIPID DROPLET; CELLULAR DDX3; REPLICATION; INNATE; GENOME; HCV
AB The ubiquitous ATP-dependent RNA helicase DDX3X is involved in many cellular functions, including innate immunity, and is a pivotal host factor for hepatitis C virus (HCV) infection. Recently, we showed that DDX3X specifically recognizes the HCV 3' untranslated region (UTR), leading to the activation of IKK-alpha and a cascade of lipogenic signaling to facilitate lipid droplet biogenesis and viral assembly (Q. Li, V. Pene, S. Krishnamurthy, H. Cha, and T. J. Liang, Nat Med 19:722-729, 2013, http://dx.doi.org/10.1038/nm.3190). The interaction of DDX3X with HCV core protein seems to be dispensable for its proviral role. In this study, through systematic imaging and biochemical and virologic approaches, we identified a dynamic association between DDX3X and various cellular compartments and viral elements mediating multiple functions of DDX3X in productive HCV infection. Upon HCV infection, the HCV 3' UTR interacts with DDX3X and IKK-alpha, which redistribute to speckle-like cytoplasmic structures shown to be stress granules (SGs). As viral proteins accumulate in infected cells, DDX3X granules together with SG-associated proteins redistribute and colocalize with HCV core protein around lipid droplets (LDs). IKK-alpha, however, does not relocate to the LD but translocates to the nucleus. In HCV-infected cells, various HCV nonstructural proteins also interact or colocalize with DDX3X in close proximity to SGs and LDs, consistent with the tight juxtaposition of the replication complex and the assembly site at the surface of LDs. Short interfering RNA (siRNA)-mediated silencing of DDX3X and multiple SG components markedly inhibits HCV infection. Our data suggest that DDX3X initiates a multifaceted cellular program involving dynamic associations with HCV RNA and proteins, IKK-alpha, SG, and LD surfaces for its crucial role in the HCV life cycle.
IMPORTANCE
DDX3X is a proviral host factor for HCV infection. Recently, we showed that DDX3X binds to the HCV 3' UTR, activating IKK-alpha and cellular lipogenesis to facilitate viral assembly (Q. Li et al., Nat Med 19:722-729, 2013, http://dx.doi.org/10.1038/nm.3190). Here, we report associations of DDX3X with various cellular compartments and viral elements that mediate its multiple functions in the HCV life cycle. Upon infection, the HCV 3' UTR redistributes DDX3X and IKK-alpha to speckle-like cytoplasmic structures shown to be SGs. Subsequently, interactions between DDX3X, SG, and HCV proteins facilitate the translocation of DDX3X-SG complexes to the LD surface. HCV nonstructural proteins are shown to colocalize with DDX3X in close proximity to SGs and LDs, consistent with the tight juxtaposition of the HCV replication complex and assembly site at the LD surface. Our data demonstrate that DDX3X initiates a multifaceted cellular program involving dynamic associations with HCV elements, IKK-alpha, SGs, and LDs for its critical role in HCV infection.
C1 [Pesne, Veronique; Li, Qisheng; Sodroski, Catherine; Hsu, Ching-Sheng; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Li, QS (reprint author), NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
EM liqisheng@niddk.nih.gov; jakel@bdg10.niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), U.S. National Institutes of Health (NIH)
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), U.S. National Institutes of Health (NIH).
NR 58
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2015
VL 89
IS 10
BP 5462
EP 5477
DI 10.1128/JVI.03197-14
PG 16
WC Virology
SC Virology
GA CG5KB
UT WOS:000353329300026
ER
PT J
AU Stenholm, S
Shardell, M
Bandinelli, S
Guralnik, JM
Ferrucci, L
AF Stenholm, Sari
Shardell, Michelle
Bandinelli, Stefania
Guralnik, Jack M.
Ferrucci, Luigi
TI Physiological Factors Contributing to Mobility Loss Over 9 Years of
Follow-Up-Results From the InCHIANTI Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Physical functioning; Mobility loss; Physiological markers; Muscle
strength; Central nervous system; Random survival forest
ID PHYSICAL PERFORMANCE BATTERY; LOWER-EXTREMITY FUNCTION; MAINTAINING
MOBILITY; RISK-FACTORS; FUNCTIONAL STATUS; OLDER-ADULTS; GAIT SPEED;
LATE-LIFE; DISABILITY; DECLINE
AB Background. Mobility is an essential aspect of everyday life and enables autonomy and participation. Although many risk factors for mobility loss have been previously described, their relative importance and independent contributions to the long-term risk of losing mobility have not been well defined.
Methods. This study is based on 1,013 men and women aged >= 65 years enrolled in 1998-2000 and followed for 9 years through 2007-2008 in the population-based InCHIANTI (Invecchiare in Chianti, aging in the Chianti area) study. We considered 44 different measures assessed at baseline to explore six subsystems: (i) central nervous system, (ii) peripheral nervous system, (iii) muscles, (iv) bone and joints, (v) energy production and delivery, and (vi) perceptual system. The outcome was incident mobility loss defined as self-report of inability to walk 400 m or climb and descend 10 steps without help from another person. Random survival forest analysis was used to rank the candidate predictors by their importance.
Results. The most important physiological markers predicting mobility loss that emerged from the random survival forest modeling were older age among women (81-95 vs 65-68 years, hazard ratio [HR] 9.60 [95% CI 3.35, 27.50]), weaker ankle dorsiflexion strength (lowest vs highest quintile, HR 5.25 [95% CI 2.35, 11.72]), low hip flexion range of motion (lowest vs highest quintile, HR 2.30 [95% CI 1.20, 4.41]), presence of primitive reflexes (yes vs no, HR 1.47 [95% CI 1.03, 2.09]), and tremor (yes vs no, HR 1.91 [95% CI 1.18, 3.07]).
Conclusion. Prevention of mobility loss with aging should focus on prevention and treatment of neuromuscular impairments.
C1 [Stenholm, Sari] Univ Turku, Dept Publ Hlth, FI-20014 Turku, Finland.
[Stenholm, Sari] Univ Tampere, Sch Hlth Sci, FIN-33101 Tampere, Finland.
[Shardell, Michelle; Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
[Guralnik, Jack M.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
RP Stenholm, S (reprint author), Univ Turku, Dept Publ Hlth, FI-20014 Turku, Finland.
EM sari.stenholm@utu.fi
FU Academy of Finland [264944, 273850]; National Institute on Aging,
National Institutes of Health, Baltimore, Maryland; Italian Ministry of
Health [ICS110.1/RF97.71]; U.S. National Institute on Aging [263 MD
9164, 263 MD 821336, N.1-AG-1-1, N.1-AG-1-2111, N01-AG-5-0002, 1 Z01
AG001050-01]
FX This work was supported by grants from the Academy of Finland (264944
and 273850) and in part by the Intramural research program of the
National Institute on Aging, National Institutes of Health, Baltimore,
Maryland. The InCHIANTI study baseline (1998-2000) was supported as a
"targeted project" (ICS110.1/RF97.71) by the Italian Ministry of Health
and in part by the U.S. National Institute on Aging (contracts: 263 MD
9164 and 263 MD 821336); the InCHIANTI Follow-up 1 (2001-2003) was
funded by the U.S. National Institute on Aging (contracts: N.1-AG-1-1
and N.1-AG-1-2111); the InCHIANTI Follow-up 2 study (2004-2006) was
financed by the U.S. National Institute on Aging (contract:
N01-AG-5-0002); and the InCHIANTI Follow-up 3 study (2007-2008) was
financed by the U.S. National Institute on Aging (contract: 1 Z01
AG001050-01). The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 22
TC 2
Z9 2
U1 4
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2015
VL 70
IS 5
BP 591
EP 597
DI 10.1093/gerona/glv004
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA CH3AX
UT WOS:000353899100006
PM 25748030
ER
PT J
AU Chen, DS
Betz, J
Yaffe, K
Ayonayon, HN
Kritchevsky, S
Martin, KR
Harris, TB
Purchase-Helzner, E
Satterfield, S
Xue, QL
Pratt, S
Simonsick, EM
Lin, FR
AF Chen, David S.
Betz, Joshua
Yaffe, Kristine
Ayonayon, Hilsa N.
Kritchevsky, Stephen
Martin, Kathryn R.
Harris, Tamara B.
Purchase-Helzner, Elizabeth
Satterfield, Suzanne
Xue, Qian-Li
Pratt, Sheila
Simonsick, Eleanor M.
Lin, Frank R.
CA Hlth ABC Study
TI Association of Hearing Impairment with Declines in Physical Functioning
and the Risk of Disability in Older Adults
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Physical function; Physical performance; Epidemiology
ID LOWER-EXTREMITY FUNCTION; GAIT SPEED DECLINE; PERFORMANCE BATTERY;
BODY-COMPOSITION; UNITED-STATES; SUBSEQUENT DISABILITY; VESTIBULAR
FUNCTION; PROGNOSTIC VALUE; HEALTH; SURVIVAL
AB Background: Identifying factors associated with functional declines in older adults is important given the aging of the population. We investigated if hearing impairment is independently associated with objectively measured declines in physical functioning in a community-based sample of older adults.
Methods: Prospective observational study of 2,190 individuals from the Health, Aging, and Body Composition study. Participants were followed annually for up to 11 visits. Hearing was measured with pure-tone audiometry. Physical functioning and gait speed were measured with the Short Physical Performance Battery (SPPB). Incident disability and requirement for nursing care were assessed semiannually through self-report.
Results: In a mixed-effects model, greater hearing impairment was associated with poorer physical functioning. At both Visit 1 and Visit 11, SPPB scores were lower in individuals with mild (10.14 [95% CI 10.04-10.25], p < .01; 7.35 [95% CI 7.12-7.58], p < .05) and moderate or greater hearing impairment (10.04 [95% CI 9.90-10.19], p < .01; 7.00 [95% CI 6.69-7.32], p < .01) than scores in normal hearing individuals (10.36 [95% CI 10.26-10.46]; 7.71 [95% CI 7.49-7.92]). We observed that women with moderate or greater hearing impairment had a 31% increased risk of incident disability (Hazard ratio [HR] = 1.31 [95% CI 1.08-1.60], p < .01) and a 31% increased risk of incident nursing care requirement (HR = 1.31 [95% CI 1.05-1.62], p = .02) compared to women with normal hearing.
Conclusions: Hearing impairment is independently associated with poorer objective physical functioning in older adults, and a 31% increased risk for incident disability and need for nursing care in women.
C1 [Chen, David S.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Chen, David S.; Betz, Joshua; Xue, Qian-Li; Lin, Frank R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
[Yaffe, Kristine; Ayonayon, Hilsa N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Kritchevsky, Stephen] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Martin, Kathryn R.; Harris, Tamara B.] NIA, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
[Martin, Kathryn R.; Harris, Tamara B.] NIA, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA.
[Martin, Kathryn R.] Univ Aberdeen, Sch Med & Dent, Epidemiol Grp, Aberdeen, Scotland.
[Purchase-Helzner, Elizabeth] Suny Downstate Med Ctr, Dept Epidemiol & Biostat, Brooklyn, NY 11203 USA.
[Satterfield, Suzanne] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[Xue, Qian-Li] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Pratt, Sheila] VA Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA USA.
[Pratt, Sheila] Univ Pittsburgh, Dept Commun Sci & Disorders, Pittsburgh, PA USA.
[Simonsick, Eleanor M.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
[Lin, Frank R.] Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21205 USA.
[Lin, Frank R.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
RP Lin, FR (reprint author), Johns Hopkins Ctr Aging & Hlth, 2024 Monument St,Suite 2-700, Baltimore, MD 21287 USA.
EM flin1@jhmi.edu
OI Betz, Joshua/0000-0003-4488-9799
FU NIH [K23DC011279]; Eleanor Schwartz Charitable Foundation; Triological
Society/American College of Surgeons; National Institute on Aging (NIA)
[N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106]; NIA [R01-AG028050]; NINR
[R01NR012459]; NIH, National Institute on Aging
FX This manuscript was supported in part by NIH K23DC011279, the Eleanor
Schwartz Charitable Foundation, and a Triological Society/American
College of Surgeons Clinician Scientist Award, as well as National
Institute on Aging (NIA) Contracts N01-AG-6-2101; N01-AG-6-2103;
N01-AG-6-2106; NIA grant R01-AG028050, NINR grant R01NR012459, and the
Intramural Research Program of the NIH, National Institute on Aging.
NR 44
TC 14
Z9 15
U1 4
U2 15
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD MAY
PY 2015
VL 70
IS 5
BP 654
EP 661
DI 10.1093/gerona/glu207
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA CH3AX
UT WOS:000353899100016
PM 25477427
ER
PT J
AU Brown, P
Gipson, C
AF Brown, Patricia
Gipson, Chester
TI A word from OLAW and USDA
SO LAB ANIMAL
LA English
DT Editorial Material
C1 [Brown, Patricia] HHS, NIH, OD, OER,OLAW, Washington, DC 20201 USA.
[Gipson, Chester] USDA, APHIS, AC, Washington, DC USA.
RP Brown, P (reprint author), HHS, NIH, OD, OER,OLAW, Washington, DC 20201 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
EI 1548-4475
J9 LAB ANIMAL
JI Lab Anim.
PD MAY
PY 2015
VL 44
IS 5
BP 168
EP 168
PG 1
WC Veterinary Sciences
SC Veterinary Sciences
GA CH2QK
UT WOS:000353869500015
PM 25897933
ER
PT J
AU Cameron, D
Higgins, DM
Stehning, C
Kouwenhoven, M
Bouhrara, M
Frenneaux, MP
Dawson, DK
Redpath, TW
AF Cameron, Donnie
Higgins, David M.
Stehning, Christian
Kouwenhoven, Marc
Bouhrara, Mustapha
Frenneaux, Michael P.
Dawson, Dana K.
Redpath, Thomas W.
TI Selection of magnetization catalyzation and readout methods for modified
Look-Locker inversion recovery: A T-1 mapping primer
SO MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE T-1 mapping; Tissue characterization; Steady-state free precession;
Transient signal oscillations
ID MOLLI; RESONANCE; HEART; EXPERIENCE; SEQUENCE; SSFP
AB Background: The purpose of this work was to evaluate different magnetization preparation and readout sequences for modified Look-Locker inversion recovery (MOLLI) toward improved T-1 mapping in the heart. Elements investigated include: catalyzation sequences to prepare the magnetization before readout, alternate k-space trajectories, a spoiled gradient recalled echo readout, and a 5b(3b)3b MOLLI sampling scheme ('b' denoting beats).
Methods: Conventional 3b(3b)3b(3b)5b MOLLI with a linear k-space trajectory was compared to four variants in simulations, in vitro and in vivo (at 3T). Variants were centric conventional MOLLI, centric-paired conventional MOLLI, linear 5b(3b)3b MOLLI and spoiled gradient recalled echo MOLLI. Each of these was applied with three magnetization catalyzation methods, and T-1 measurement accuracy and precision were evaluated in simulations via a Monte Carlo algorithm, in a set of calibrated phantoms, and in ten healthy volunteers. Contrast-to-noise, heart rate dependence and B-1 + dependence were also evaluated.
Results: A linear k-space trajectory was superior in vitro to centric and centric-paired trajectories. Of the catalyzation methods, preparation of transverse magnetization only using a linearly increasing flip angle catalyzation improved MOLLI T-1 measurement accuracy, precision, and map quality versus methods that include catalyzation of the longitudinal magnetization. The 5b(3b)3b MOLLI scheme offered comparable native T-1 measurement accuracy and precision to conventional MOLLI, despite its shortened acquisition.
Conclusions: MOLLI T-1 measurement accuracy, precision, and map quality depend on the method of catalyzation of magnetization prior to image acquisition, as well as on the readout method and MOLLI sampling scheme used. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Cameron, Donnie; Frenneaux, Michael P.; Dawson, Dana K.; Redpath, Thomas W.] Univ Aberdeen, Aberdeen, Scotland.
[Higgins, David M.] Philips Healthcare, Guildford, Surrey, England.
[Stehning, Christian] Philips Res, Hamburg, Germany.
[Kouwenhoven, Marc] Philips Healthcare, Best, Netherlands.
[Bouhrara, Mustapha] NIA, NIH, Baltimore, MD 21224 USA.
RP Cameron, D (reprint author), Harbor Hosp, NIA, 3001 Hanover St, Baltimore, MD 21225 USA.
EM d.cameron.09@aberdeen.ac.uk; david.higgins@philips.com;
christian.stehning@philips.com; marc.kouwenhoven@philips.com;
mustapha.bouhrara2@nih.gov; m.p.frenneaux@abdn.ac.uk;
dana.dawson@abdn.ac.uk; t.redpath@abdn.ac.uk
NR 30
TC 1
Z9 1
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0730-725X
EI 1873-5894
J9 MAGN RESON IMAGING
JI Magn. Reson. Imaging
PD MAY
PY 2015
VL 33
IS 4
BP 363
EP 373
DI 10.1016/j.mri.2015.02.004
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CG9VW
UT WOS:000353669200001
PM 25660643
ER
PT J
AU Ebong, IA
Watson, KE
Goff, DC
Bluemke, DA
Srikanthan, P
Horwich, T
Bertoni, AG
AF Ebong, Imo A.
Watson, Karol E.
Goff, David C., Jr.
Bluemke, David A.
Srikanthan, Preethi
Horwich, Tamara
Bertoni, Alain G.
TI Association of menopause age and N-terminal pro brain natriuretic
peptide: the Multi-Ethnic Study of Atherosclerosis
SO MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY
LA English
DT Article
DE Menopause; N-Terminal pro brain natriuretic peptide; Sex hormones
ID LEFT-VENTRICULAR HYPERTROPHY; INCIDENT HEART-FAILURE;
CARDIOVASCULAR-DISEASE; NATURAL MENOPAUSE; RISK-FACTORS;
MOLECULAR-MECHANISMS; POSTMENOPAUSAL WOMEN; METABOLIC SYNDROME;
DIABETES-MELLITUS; MORTALITY
AB Objective: Menopause age can affect the risk of developing cardiovascular disease (CVD). The purpose of this study was to investigate the associations of early menopause (menopause occurring before age 45 y) and menopause age with N-terminal pro brain natriuretic peptide (NT-proBNP), a potential risk marker of CVD and heart failure.
Methods: Our cross-sectional study included 2,275 postmenopausal women, aged 45 to 85 years and without clinical CVD (2000-2002), fromthe Multi-Ethnic Study ofAtherosclerosis. Participants were classified as having or not having early menopause. NT-proBNP was log-transformed. Multivariable linear regression was used for analysis.
Results: Five hundred sixty-one women had early menopause. The median (25th-75th percentiles) NT-proBNP value was 79.0 (41.1-151.6) pg/mL for all participants, 83.4 (41.4-164.9) pg/mL for women with early menopause, and 78.0 (40.8-148.3) pg/mL for women without early menopause. The mean (SD) age was 65 (10.1) and 65 (8.9) years for women with and without early menopause, respectively. No significant interactions between menopause age and ethnicity were observed. In multivariable analysis, early menopause was associated with a 10.7% increase in NT-proBNP levels, whereas each 1-year increase in menopause age was associated with a 0.7% decrease in NT-proBNP levels.
Conclusions: Early menopause is associated with greater NT-proBNP levels, whereas each 1-year increase in menopause age is associated with lower NT-proBNP levels, in postmenopausal women.
C1 [Ebong, Imo A.] Loma Linda Univ, Med Ctr, Inst Transplantat, Loma Linda, CA 92354 USA.
[Watson, Karol E.; Horwich, Tamara] Univ Calif Los Angeles, David Geffen Sch Med, Div Cardiol, Los Angeles, CA 90095 USA.
[Goff, David C., Jr.] Colorado Sch Publ Hlth, Aurora, CO USA.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Srikanthan, Preethi] Univ Calif Los Angeles, David Geffen Sch Med, Div Gen Internal Med & Hlth Serv Res, Los Angeles, CA 90095 USA.
[Bertoni, Alain G.] Wake Forest Univ, Bowman Gray Sch Med, Dept Med, Winston Salem, NC 27103 USA.
[Bertoni, Alain G.] Wake Forest Univ, Bowman Gray Sch Med, Dept Epidemiol, Winston Salem, NC USA.
RP Ebong, IA (reprint author), Loma Linda Univ, Med Ctr, Inst Transplantat, Suite 101,25865 Barton Rd, Loma Linda, CA 92354 USA.
EM momoebong4@gmail.com
OI Bluemke, David/0000-0002-8323-8086
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95160,
N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165,
N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169]
FX The Multi-Ethnic Study of Atherosclerosis was supported by contracts
N01-HC-95159 through N01-HC-95169 from the National Heart, Lung, and
Blood Institute.
NR 57
TC 1
Z9 1
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1072-3714
EI 1530-0374
J9 MENOPAUSE
JI Menopause-J. N. Am. Menopause Soc.
PD MAY
PY 2015
VL 22
IS 5
BP 527
EP 533
DI 10.1097/gme.0000000000000342
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CG9ZB
UT WOS:000353677500009
PM 25290536
ER
PT J
AU Lasota, J
Felisiak-Golabek, A
Aly, FZ
Wang, ZF
Thompson, LDR
Miettinen, M
AF Lasota, Jerzy
Felisiak-Golabek, Anna
Aly, F. Zahra
Wang, Zeng-Feng
Thompson, Lester D. R.
Miettinen, Markku
TI Nuclear expression and gain-of-function beta-catenin mutation in
glomangiopericytoma (sinonasal-type hemangiopericytoma): insight into
pathogenesis and a diagnostic marker
SO MODERN PATHOLOGY
LA English
DT Article
ID SOLITARY FIBROUS TUMORS; CYCLIN D1; DIFFERENTIAL-DIAGNOSIS; MYOID
DIFFERENTIATION; CARCINOMA-CELLS; GLOMUS TUMORS; ACTIVATION; CANCER;
GENE; IMMUNOHISTOCHEMISTRY
AB Glomangiopericytoma (sinonasal-type hemangiopericytoma) is a rare mesenchymal neoplasm with myoid phenotype (smooth muscle actin-positive), which distinguishes this tumor from soft tissue hemangiopericytoma/solitary fibrous tumor. Molecular genetic changes underlying the pathogenesis of glomangiopericytoma are not known. In this study, 13 well-characterized glomangiopericytomas were immunohistochemically evaluated for beta-catenin expression. All analyzed tumors showed strong expression and nuclear accumulation of beta-catenin. Following this observation, beta-catenin glycogen serine kinase-3 beta phosphorylation region, encoded by exon 3, was PCR amplified in all cases and evaluated for mutations using Sanger sequencing. Heterozygous mutations were identified in 12 of 13 tumors. All mutations consisted of single-nucleotide substitutions: three in codon 32 (c.94G4C (n = 2) and c.95A4T), four in codon 33 (two each c.98C4G and c.98C4T), two in codon 37 (c.109T4G), one in codon 41 (c.121A4G), and two in codon 45 (c.133T4C). At the protein level, these substitutions would lead to p.D32H, p.D32V, p.S33C, p.S33F, p.S37A, p.T41A, and p.S45L mutations, respectively. Previously, similar mutations have been reported in different types of cancers and shown to trigger activation of beta-catenin signaling. All analyzed glomangiopericytomas showed prominent nuclear expression of cyclin D1, as previously shown for tumors with nuclear expression of beta-catenin as a sign of oncogenic activation. These results demonstrate that mutational activation of b beta-catenin and associated cyclin D1 overexpression may be central events in the pathogenesis of glomangiopericytoma. In additon, nuclear accumulation of beta-catenin is a diagnostic marker for glomangiopericytoma.
C1 [Lasota, Jerzy; Felisiak-Golabek, Anna; Wang, Zeng-Feng; Miettinen, Markku] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Aly, F. Zahra] Univ Arizona, Dept Pathol, Tucson, AZ USA.
[Thompson, Lester D. R.] So Calif Permanente Med Grp, Dept Pathol, Woodland Hills, CA USA.
RP Lasota, J (reprint author), NCI, Pathol Lab, 9000 Rockville Pike,Bldg 10,Room B1B47, Bethesda, MD 20892 USA.
EM jerzy.lasota@nih.gov
RI Thompson, Lester/J-8404-2016
OI Thompson, Lester/0000-0003-3714-1432
NR 28
TC 8
Z9 9
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD MAY
PY 2015
VL 28
IS 5
BP 715
EP 720
DI 10.1038/modpathol.2014.161
PG 6
WC Pathology
SC Pathology
GA CH1IE
UT WOS:000353774200011
PM 25431235
ER
PT J
AU Stalnaker, TA
Cooch, NK
Schoenbaum, G
AF Stalnaker, Thomas A.
Cooch, Nisha K.
Schoenbaum, Geoffrey
TI What the orbitofrontal cortex does not do
SO NATURE NEUROSCIENCE
LA English
DT Review
ID VENTROMEDIAL PREFRONTAL CORTEX; DOPAMINE NEURONS ENCODE; FRONTAL-LOBE
DAMAGE; VENTRAL TEGMENTAL AREA; DECISION-MAKING; BASOLATERAL AMYGDALA;
REWARD VALUE; REINFORCER DEVALUATION; RHESUS-MONKEYS; ECONOMIC VALUE
AB The number of papers about the orbitofrontal cortex (OFC) has grown from 1 per month in 1987 to a current rate of over 50 per month. This publication stream has implicated the OFC in nearly every function known to cognitive neuroscience and in most neuropsychiatric diseases. However, new ideas about OFC function are typically based on limited data sets and often ignore or minimize competing ideas or contradictory findings. Yet true progress in our understanding of an area's function comes as much from invalidating existing ideas as proposing new ones. Here we consider the proposed roles for OFC, critically examining the level of support for these claims and highlighting the data that call them into question.
C1 [Stalnaker, Thomas A.; Cooch, Nisha K.; Schoenbaum, Geoffrey] US Natl Inst Hlth, Natl Inst Drug Abuse Intramural Res Program, Baltimore, MD 21224 USA.
RP Schoenbaum, G (reprint author), US Natl Inst Hlth, Natl Inst Drug Abuse Intramural Res Program, Baltimore, MD 21224 USA.
EM geoffrey.schoenbaum@nih.gov
OI Schoenbaum, Geoffrey/0000-0001-8180-0701
FU National Institute on Drug Abuse; National Institute of Mental Health;
National Institute on Aging; National Institute on Drug Abuse at the
Intramural Research Program
FX The authors would like to thank C. Padoa-Schioppa, J. Wallis and P.
Rudebeck for critical readings of earlier versions. This work was
supported by grants to G.S. from the National Institute on Drug Abuse,
the National Institute of Mental Health and the National Institute on
Aging while G.S. was employed at the University of Maryland, Baltimore,
and by funding from the National Institute on Drug Abuse at the
Intramural Research Program. The opinions expressed in this article are
the authors' own and do not reflect the view of the US National
Institutes of Health, the Department of Health and Human Services, or
the United States government.
NR 150
TC 55
Z9 57
U1 12
U2 57
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
EI 1546-1726
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD MAY
PY 2015
VL 18
IS 5
BP 620
EP 627
DI 10.1038/nn.3982
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA CG9LN
UT WOS:000353636900007
PM 25919962
ER
PT J
AU Wang, DV
Yau, HJ
Broker, CJ
Tsou, JH
Bonci, A
Ikemoto, S
AF Wang, Dong V.
Yau, Hau-Jie
Broker, Carl J.
Tsou, Jen-Hui
Bonci, Antonello
Ikemoto, Satoshi
TI Mesopontine median raphe regulates hippocampal ripple oscillation and
memory consolidation
SO NATURE NEUROSCIENCE
LA English
DT Article
ID URETHANE-ANESTHETIZED RAT; THETA-RHYTHM; PREFRONTAL CORTEX; SPATIAL
MEMORY; SEROTONERGIC CONTROL; NUCLEUS; NEURONS; BRAIN; DORSAL; SLEEP
AB Sharp wave-associated field oscillations (similar to 200 Hz) of the hippocampus, referred to as ripples, are believed to be important for consolidation of explicit memory. Little is known about how ripples are regulated by other brain regions. We found that the median raphe region (MnR) is important for regulating hippocampal ripple activity and memory consolidation. We performed in vivo simultaneous recording in the MnR and hippocampus of mice and found that, when a group of MnR neurons was active, ripples were absent. Consistently, optogenetic stimulation of MnR neurons suppressed ripple activity and inhibition of these neurons increased ripple activity. Notably, using a fear conditioning procedure, we found that photostimulation of MnR neurons interfered with memory consolidation. Our results demonstrate a critical role of the MnR in regulating ripples and memory consolidation.
C1 [Wang, Dong V.; Yau, Hau-Jie; Broker, Carl J.; Tsou, Jen-Hui; Bonci, Antonello; Ikemoto, Satoshi] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Ikemoto, S (reprint author), NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM satoshi.ikemoto@nih.gov
OI YAU, HAU-JIE/0000-0001-7454-7971; Ikemoto, Satoshi/0000-0002-0732-7386
FU Intramural Research Program of NIDA; Ministry of Science and Technology,
Taiwan [MOST 103-2911-I-038-501]
FX We thank the National Institute on Drug Abuse (NIDA) Optogenetics and
Transgenetic Technology Core for producing AAVs, E. Deneris (Case
Western Reserve University) for providing the ePet-Cre mouse line, R.
Cachope, J. Cheer, C. Mejias-Aponte, M. Moralas, A. Kesner, A. Ilango,
C. Yang, D. Nguyen and M. Vatsan for technical assistance, and S.-C.
Lin, Y. Shaham, G. Schoenbaum and A. Saul for reading and critical
discussions. This research was supported by the Intramural Research
Program of NIDA and the grant MOST 103-2911-I-038-501 from the Ministry
of Science and Technology, Taiwan.
NR 51
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U1 2
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
EI 1546-1726
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD MAY
PY 2015
VL 18
IS 5
BP 728
EP +
DI 10.1038/nn.3998
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA CG9LN
UT WOS:000353636900020
PM 25867120
ER
PT J
AU Wang, Z
Wang, F
Hida, N
Kiesewetter, DO
Tian, J
Niu, G
Chen, XY
AF Wang, Zhe
Wang, Fu
Hida, Naoki
Kiesewetter, Dale O.
Tian, Jie
Niu, Gang
Chen, Xiaoyuan
TI Design of a functional cyclic HSV1-TK reporter and its application to
PET imaging of apoptosis
SO NATURE PROTOCOLS
LA English
DT Article
ID SIMPLEX-VIRUS TYPE-1; POSITRON-EMISSION-TOMOGRAPHY; THYMIDINE KINASE;
CELL-DEATH; GENE-EXPRESSION; REAL-TIME; TRANSGENIC MICE; CANCER-CELLS;
ANNEXIN-V; IN-VITRO
AB Positron emission tomography (PET) is a sensitive and noninvasive imaging method that is widely used to explore molecular events in living subjects. PET can precisely and quantitatively evaluate cellular apoptosis, which has a crucial role in various physiological and pathological processes. In this protocol, we describe the design and use of an engineered cyclic herpes simplex virus 1-thymidine kinase (HSV1-TK) PET reporter whose kinase activity is specifically switched on by apoptosis. The expression of cyclic TK (cTK) in healthy cells leads to inactive product, whereas the activation of apoptosis through the caspase-3 pathway cleaves cTK, thus restoring its activity and enabling PET imaging. In addition to detailing the design and construction of the cTK plasmid in this protocol, we include assays for evaluating the function and specificity of the cTK reporter in apoptotic cells, such as assays for measuring the cell uptake of PET tracer in apoptotic cells, correlating doxorubicin (Dox)-induced cell apoptosis to cTK function recovery, and in vivo PET imaging of cancer cell apoptosis, and we also include corresponding data acquisition methods. The time to build the entire cTK reporter is similar to 2-3 weeks. The selection of a stable cancer cell line takes similar to 4-6 weeks. The time to implement assays regarding cTK function in apoptotic cells and the in vivo imaging varies depending on the experiment. The cyclization strategy described in this protocol can also be adapted to create other reporter systems for broad biomedical applications.
C1 [Wang, Zhe; Hida, Naoki; Kiesewetter, Dale O.; Niu, Gang; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
[Wang, Fu; Tian, Jie] Xidian Univ, Sch Life Sci & Technol, Xian, Peoples R China.
RP Chen, XY (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
EM gang.niu@nih.gov; shawn.chen@nih.gov
RI Song, Jiangdian/L-6992-2016; Tian, Jie/H-1190-2011;
OI Song, Jiangdian/0000-0002-3355-9930; Tian, Jie/0000-0003-0498-0432;
Wang, Fu/0000-0001-9222-0833
FU Center for Neuroscience and Regeneration Medicine Program at the Henry
M. Jackson Foundation; National Institute of Biomedical Imaging and
Bioengineering, US National Institutes of Health (NIH)
FX This work was supported, in part, by the Center for Neuroscience and
Regeneration Medicine Program at the Henry M. Jackson Foundation, and by
the Intramural Research Program of the National Institute of Biomedical
Imaging and Bioengineering, US National Institutes of Health (NIH). We
thank T. Ozawa (University of Tokyo) for providing us with the cDNAs of
DnaE and PEST.
NR 50
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U1 4
U2 21
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 MAY
PY 2015
VL 10
IS 5
BP 807
EP 821
DI 10.1038/nprot.2015.048
PG 15
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA CH1KJ
UT WOS:000353780000011
PM 25927390
ER
PT J
AU Mailankody, S
Korde, N
Lesokhin, AM
Lendvai, N
Hassoun, H
Stetler-Stevenson, M
Landgren, O
AF Mailankody, Sham
Korde, Neha
Lesokhin, Alexander M.
Lendvai, Nikoletta
Hassoun, Hani
Stetler-Stevenson, Maryalice
Landgren, Ola
TI Minimal residual disease in multiple myeloma: bringing the bench to the
bedside
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Review
ID STEM-CELL TRANSPLANTATION; MULTIPARAMETER FLOW-CYTOMETRY; COMPLETE
RESPONSE; PERIPHERAL-BLOOD; BONE-MARROW; CANCER; PCR; HETEROGENEITY;
DEXAMETHASONE; LENALIDOMIDE
AB Outcomes for patients with multiple myeloma (MM) have improved substantially in the past decade, with improvements in both progression-free survival and overall survival. Many patients are now achieving a complete response to treatment, and consequently highly sensitive assays are needed for detection of minimal residual disease (MRD) in patients with MM. Results of multicolour flow cytometry and deep-sequencing studies suggest that among patients achieving a complete response, MRD-negative status is associated with significant improvements in progression-free survival and overall survival. Despite the increasing need for MRD testing in patients with MM, considerable heterogeneity in techniques for MRD detection hinders the clinical interpretation of their results. The criteria used to define MRD, strengths and weaknesses of the major types of tests (flow cytometry versus molecular testing), and the optimal sample type (bone marrow aspirate versus peripheral blood) are all unresolved dilemmas in MRD testing. This Review presents an overview of the various techniques for MRD detection in patients with MM. In addition, this article discusses challenges and opportunities for the routine use of MRD testing, possible future directions for clinical trials and implications for drug approval processes.
C1 [Mailankody, Sham] NCI, Multiple Myeloma Sect, Lymphoid Malignancies Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice] NCI, Flow Cytometry Lab, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Korde, Neha; Lesokhin, Alexander M.; Lendvai, Nikoletta; Hassoun, Hani; 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
FU National Cancer Institute, Bethesda, MD, USA
FX S.M. and M.S.-S. gratefully acknowledge support from the Intramural
Research Program of the National Cancer Institute, Bethesda, MD, USA.
NR 43
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U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4774
EI 1759-4782
J9 NAT REV CLIN ONCOL
JI Nat. Rev. Clin. Oncol.
PD MAY
PY 2015
VL 12
IS 5
BP 286
EP U139
DI 10.1038/nrclinonc.2014.239
PG 10
WC Oncology
SC Oncology
GA CH1LP
UT WOS:000353783400007
PM 25622976
ER
PT J
AU Tsai, MS
Lee, ML
Chang, CY
Fan, HH
Yu, IS
Chen, YT
You, JY
Chen, CY
Chang, FC
Hsiao, JH
Khorkova, O
Liou, HH
Yanagawa, Y
Lee, LJ
Lin, SW
AF Tsai, Ming-Shian
Lee, Meng-Larn
Chang, Chun-Yun
Fan, Hsiang-Hsuan
Yu, I-Shing
Chen, You-Tzung
You, Jhih-Yi
Chen, Chun-Yu
Chang, Fang-Chia
Hsiao, Jane H.
Khorkova, Olga
Liou, Horng-Huei
Yanagawa, Yuchio
Lee, Li-Jen
Lin, Shu-Wha
TI Functional and structural deficits of the dentate gyrus network coincide
with emerging spontaneous seizures in an Scn1a mutant Dravet Syndrome
model during development
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE SCN1A; Dravet syndrome; Epilepsy; Mouse model
ID GABAERGIC SYNAPTIC-TRANSMISSION; HYPERTHERMIA-INDUCED SEIZURES;
EXPERIMENTAL FEBRILE SEIZURES; SEVERE MYOCLONIC EPILEPSY; MOUSE MODEL;
PYRAMIDAL NEURONS; RAT HIPPOCAMPUS; INHIBITORY INTERNEURONS;
ELECTRICAL-STIMULATION; CORTICAL INTERNEURONS
AB Dravet syndrome (DS) is characterized by severe infant-onset myoclonic epilepsy along with delayed psychomotor development and heightened premature mortality. A primary monogenic cause is mutation of the SCN1A gene, which encodes the voltage-gated sodium channel subunit Na(v)1:1. The nature and timing of changes caused by SCN1A mutation in the hippocampal dentate gyrus (DG) network, a core area for gating major excitatory input to hippocampus and a classic epileptogenic zone, are not well known. In particularly, it is still not clear whether the developmental deficit of this epileptogenic neural network temporally matches with the progress of seizure development. Here, we investigated the emerging functional and structural deficits of the DG network in a novel mouse model (scn1a(E1099X/+)) that mimics the genetic deficit of human DS. Scn1a(E1099X/+) (Het) mice, similarly to human DS patients, exhibited early spontaneous seizures and were more susceptible to hyperthermia-induced seizures starting at postnatal week (PW) 3, with seizures peaking at PW4. During the same period, the Het DG exhibited a greater reduction of Na(v)1.1-expressing GABAergic neurons compared to other hippocampal areas. Het DG GABAergic neurons showed altered action potential kinetics, reduced excitability, and generated fewer spontaneous inhibitory inputs into DG granule cells. The effect of reduced inhibitory input to DC granule cells was exacerbated by heightened spontaneous excitatory transmission and elevated excitatory release probability in these cells. In addition to electrophysiological deficit, we observed emerging morphological abnormalities of DG granule cells. Het granule cells exhibited progressively reduced dendritic arborization and excessive spines, which coincided with imbalanced network activity and the developmental onset of spontaneous seizures. Taken together, our results establish the existence of significant structural and functional developmental deficits of the DG network and the temporal correlation between emergence of these deficits and the onset of seizures in Net animals. Most importantly, our results uncover the developmental deficits of neural connectivity in Net mice. Such structural abnormalities likely further exacerbate network instability and compromise higher-order cognitive processing later in development, and thus highlight the multifaceted impacts of Scn1a deficiency on neural development. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Tsai, Ming-Shian; You, Jhih-Yi; Chen, Chun-Yu; Lin, Shu-Wha] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Dept Clin Lab Sci & Med Biotechnol, Taipei 100, Taiwan.
[Lee, Meng-Larn; Chang, Fang-Chia] Natl Taiwan Univ, Dept Vet Med, Taipei 100, Taiwan.
[Chang, Chun-Yun] NIDA, Intramural Res Program, Baltimore, MD 21224 USA.
[Fan, Hsiang-Hsuan; Chen, You-Tzung] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Grad Inst Med Genom & Prote, Taipei 100, Taiwan.
[Yu, I-Shing] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Lab Anim Ctr, Taipei 100, Taiwan.
[Hsiao, Jane H.; Khorkova, Olga] OPKO Hlth Inc, Miami, FL 33137 USA.
[Liou, Horng-Huei] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Dept Neurol, Taipei 100, Taiwan.
[Yanagawa, Yuchio] Gunma Univ, Grad Sch Med, Dept Genet & Behav Neurosci, Maebashi, Gumma 3718511, Japan.
[Yanagawa, Yuchio] JST, CREST, Maebashi, Gumma 3718511, Japan.
[Lee, Li-Jen] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Grad Inst Anat & Cell Biol, Taipei 100, Taiwan.
[Lee, Li-Jen] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Grad Inst Brain & Mind Sci, Taipei 100, Taiwan.
[Lin, Shu-Wha] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Coll Med, Dept Lab Med, Taipei 100, Taiwan.
[Lin, Shu-Wha] Natl Taiwan Univ, Ctr Genom Med, Taipei 100, Taiwan.
RP Lee, LJ (reprint author), Natl Taiwan Univ, Coll Med, Grad Inst Anat & Cell Biol, 1 Sect 1,Ren Ai Rd, Taipei 100, Taiwan.
EM ljlee@ntu.edu.tw; mtshuwha@ntu.edu.tw
OI LEE, LI-JEN/0000-0001-9108-3654; CHEN, YOU-TZUNG/0000-0001-6510-3420;
LIN, SHU-WHA/0000-0001-6748-5581
FU National Taiwan University [103R7152]; Ministry of Science and
Technology [MOST 103-2321-B-002-018]; Ministry of Health and Welfare in
Taiwan [MOHW103-TDU-PB-211-133008]; MEXT of Japan; Takeda Science
Foundation
FX Funding for this study was provided by National Taiwan University
(103R7152), the Ministry of Science and Technology (MOST
103-2321-B-002-018), and the Ministry of Health and Welfare in Taiwan
(MOHW103-TDU-PB-211-133008) for SW Lin, and the MEXT of Japan and Takeda
Science Foundation for Y Yanagawa.
NR 66
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U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD MAY
PY 2015
VL 77
BP 35
EP 48
DI 10.1016/j.nbd.2015.02.010
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA CG9CO
UT WOS:000353612200004
PM 25725421
ER
PT J
AU Messer, K
White, MM
Strong, DR
Wang, B
Shi, Y
Conway, KP
Pierce, JP
AF Messer, Karen
White, Martha M.
Strong, David R.
Wang, Baoguang
Shi, Yuyan
Conway, Kevin P.
Pierce, John P.
TI Trends in Use of Little Cigars or Cigarillos and Cigarettes among U.S.
Smokers, 2002-2011
SO NICOTINE & TOBACCO RESEARCH
LA English
DT Article
ID TOBACCO PRODUCTS; UNITED-STATES; ADOLESCENTS; PREVALENCE; CALIFORNIA;
PATTERNS; EXPLAINS; SMOKING
AB Objectives: Little cigars and cigarillos may resemble cigarettes, but may be less expensive and can be purchased singly and in flavored varieties. We used two major U.S. surveys to investigate use of cigarillos and cigarettes.
Methods: The 2010/2011 Tobacco Use Supplement to the Current Population Survey ascertained cigar use by brand and type (little cigars/cigarillos or large/regular). The annual National Survey on Drug Use and Health (NSDUH) assessed cigar use by brand, 2002-2011. We used the available data to classify cigars by type among males in the NSDUH.
Results: Estimated prevalence of little cigar use among male cigar smokers was similar using the two surveys. From 2002 to 2011, past-30-day cigarette smoking declined for all age groups and genders, but among young adult men (aged 18-25) little cigar smoking remained steady at nearly 9%. "Cigarette and/or cigar" smoking was 44% among young adult men in 2011, and was consistently 6 percentage points higher than cigarette-only smoking, from 2002 to 2011. Over 60% of male and 70% of female adolescent/young adult cigar smokers also smoked cigarettes in 2011. Most male adolescents preferred little cigars to traditional cigars. Among males, most lower income or less educated cigar smokers preferred little cigars, compared to only 16% of those with higher education.
Conclusions: These patterns indicate that little cigar/cigarillo use may promote initiation and maintenance of cigarette smoking, particularly among younger and less advantaged populations. Population-level data are urgently needed to better assess type of cigar smoked and reasons for use.
C1 [Messer, Karen; White, Martha M.; Strong, David R.; Shi, Yuyan; Pierce, John P.] Univ Calif San Diego, Canc Prevent & Control Div, Moores UCSD Canc Ctr, La Jolla, CA 92093 USA.
[Wang, Baoguang] US FDA, Ctr Tobacco Prod, Rockville, MD 20857 USA.
[Conway, Kevin P.] Natl Inst Drug Abuse, Div Epidemiol Serv & Prevent Res, Rockville, MD USA.
RP Messer, K (reprint author), Univ Calif San Diego, Div Biostat, Dept Family & Prevent Med, 3855 Hlth Sci Dr,0901, La Jolla, CA 92093 USA.
EM kmesser@ucsd.edu
OI Conway, Kevin/0000-0002-7638-339X
FU National Institute on Drug Abuse, National Institutes of Health; Food
and Drug Administration; Department of Health and Human Services
[HHSN271201100027C]; UC Tobacco-Related Disease Research Program
[21RT-0135, 21XT-0076]; National Cancer Institute [1R01CA172058-01]
FX This project has been funded in whole or in part with Federal funds from
the National Institute on Drug Abuse, National Institutes of Health, and
the Food and Drug Administration, Department of Health and Human
Services, under Contract No. HHSN271201100027C, UC Tobacco-Related
Disease Research Program grants 21RT-0135 and 21XT-0076, and National
Cancer Institute grant No. 1R01CA172058-01. The views and opinions
expressed in this presentation are those of the authors only and do not
necessarily represent the views, official policy or position of the U.S.
Department of Health and Human Services or any of its affiliated
institutions or agencies.
NR 26
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U1 3
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1462-2203
EI 1469-994X
J9 NICOTINE TOB RES
JI Nicotine Tob. Res.
PD MAY
PY 2015
VL 17
IS 5
BP 515
EP 523
DI 10.1093/ntr/ntu179
PG 9
WC Substance Abuse; Public, Environmental & Occupational Health
SC Substance Abuse; Public, Environmental & Occupational Health
GA CH3CL
UT WOS:000353904000003
PM 25239955
ER
PT J
AU Ekenga, CC
Parks, CG
Wilson, LE
Sandler, DP
AF Ekenga, Christine C.
Parks, Christine G.
Wilson, Lauren E.
Sandler, Dale P.
TI Leisure-time physical activity in relation to occupational physical
activity among women
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Physical activity; Workplace; Women
AB Objective. The objective of this study is to examine the association between occupational physical activity and leisure-time physical activity among US women in the Sister Study.
Methods. We conducted a cross-sectional study of 26,334 women who had been employed in their current job for at least 1 year at baseline (2004-2009). Occupational physical activity was self-reported and leisure-time physical activity was estimated in metabolic equivalent hours per week. Log multinomial regression was used to evaluate associations between occupational (sitting, standing, manually active) and leisure-time (insufficient, moderate, high) activity. Models were adjusted for age, race/ethnicity, education, income, geographic region, and body mass index.
Results. Only 54% of women met or exceeded minimum recommended levels of leisure-time physical activity (moderate 32% and high 22%). Women who reported sitting (prevalence ratio (PR) = 0.82, 95% confidence interval (CI): 0.74-0.92) or standing (PR = 0.84, 95% CI: 0.75-0.94) most of the time at work were less likely to meet the requirements for high leisure-time physical activity than manually active workers. Associations were strongest among women living in the Northeast and the South.
Conclusion. In this nationwide study, low occupational activity was associated with lower leisure-time physical activity. Women who are not active in the workplace may benefit from strategies to promote leisure-time physical activity. Published by Elsevier Inc.
C1 [Ekenga, Christine C.; Parks, Christine G.; Wilson, Lauren E.; Sandler, Dale P.] NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Ekenga, CC (reprint author), NIEHS, Epidemiol Branch, POB 12233,Mail Drop A3-05,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM christine.ekenga@nih.gov
OI Parks, Christine/0000-0002-5734-3456; Sandler, Dale/0000-0002-6776-0018;
Wilson, Lauren/0000-0002-5953-2293
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01ES044005]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences (Z01ES044005). The authors would like to thank Drs.
Katie O'Brien and Quaker Harmon for their helpful comments.
NR 11
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U1 1
U2 6
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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 MAY
PY 2015
VL 74
BP 93
EP 96
DI 10.1016/j.ypmed.2015.03.003
PG 4
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CH1AX
UT WOS:000353754600015
PM 25773471
ER
PT J
AU Djousse, L
Petrone, AB
Blackshear, C
Griswold, M
Harman, JL
Clark, CR
Talegawkar, S
Hickson, DA
Gaziano, JM
Dubbert, PM
Correa, A
Tucker, KL
Taylor, HA
AF Djousse, Luc
Petrone, Andrew B.
Blackshear, Chad
Griswold, Michael
Harman, Jane L.
Clark, Cheryl R.
Talegawkar, Sameera
Hickson, DeMarc A.
Gaziano, J. Michael
Dubbert, Patricia M.
Correa, Adolfo
Tucker, Katherine L.
Taylor, Herman A.
TI Prevalence and changes over time of ideal cardiovascular health metrics
among African-Americans: The Jackson Heart Study
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Epidemiology; Cardiovascular disease; Risk factors; Diet
ID ATHEROSCLEROSIS RISK; PHYSICAL-ACTIVITY; DISEASE INCIDENCE; US ADULTS;
ASSOCIATION; MORTALITY; COMMUNITIES; WOMEN; POPULATION; UPDATE
AB Objectives. The aim of this study is to assess the prevalence and changes over time of ideal Life's Simple Seven (LSS) in African-Americans.
Methods. Prospective cohort of 5301 African-Americans from the Jackson Heart Study OHS) from 2000 to 2013. Each of the LSS metrics was categorized as poor, intermediate, or ideal.
Results. Among men, the prevalence of having 0, 1, 2, 3, 4, 5, 6, and 7 ideal LSS was 3.3%, 23.0%, 33.5%, 24.7%, 11.6%, 3.6%, 0.3%, and 0%, respectively. Corresponding values for women were 1.7%, 26.3%, 33.1%, 22.8%, 11.9%, 3.7%, 0.6%, and 0%. Prevalence of ideal diet was 0.9%. The proportions of those meeting LSS ideal recommendations for cholesterol and fasting glucose declined from the first through third JHS visits across all age groups, whereas prevalence of ideal BMI declined only in participants <40 years at a given visit. Prevalence of ideal blood pressure did not change over time and being ideal on physical activity improved from the first [18.3% (95% CI: 17.3% to 19.3%)] to third visit [24.8% (95% CI: 23.3% to 26.3%)].
Conclusions. Our data show a low prevalence of ideal LSS (especially diet, physical activity, and obesity) in the JHS and a slight improvement in adherence to physical activity recommendations over time. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Djousse, Luc; Petrone, Andrew B.; Clark, Cheryl R.; Gaziano, J. Michael] Brigham & Womens Hosp, Boston, MA 02120 USA.
[Djousse, Luc; Gaziano, J. Michael] Boston VA Healthcare Syst, Boston, MA USA.
[Djousse, Luc; Clark, Cheryl R.; Gaziano, J. Michael] Harvard Univ, Sch Med, Boston, MA USA.
[Blackshear, Chad; Griswold, Michael; Hickson, DeMarc A.; Correa, Adolfo; Taylor, Herman A.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Harman, Jane L.] NHLBI, Bethesda, MD 20892 USA.
[Talegawkar, Sameera] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Dubbert, Patricia M.] South Cent VA MIRECC, Little Rock, AR USA.
[Dubbert, Patricia M.] Little Rock GRECC, Little Rock, AR USA.
[Tucker, Katherine L.] Univ Massachusetts Lowell, Lowell, MA USA.
[Taylor, Herman A.] Jackson State Univ, Jackson, MS USA.
[Taylor, Herman A.] Tougaloo Coll, Jackson, MS USA.
RP Djousse, L (reprint author), Brigham & Womens Hosp, Div Aging, 1620 Tremont St,3rd Floor, Boston, MA 02120 USA.
EM ldjousse@rics.bwh.harvard.edu
RI Djousse, Luc/F-5033-2017
OI Djousse, Luc/0000-0002-9902-3047
FU National Heart, Lung, and Blood Institute [HHSN268201300046C,
HHSN268201300047C, HHSN268201300048C, HHSN268201300049C,
HHSN268201300050C]; National Institute on Minority Health and Health
Disparities; National Health Institutes [R21 NR013231]; American
Diabetes Association [13BGIA17080036]
FX The Jackson Heart Study is supported by contracts HHSN268201300046C,
HHSN268201300047C, HHSN268201300048C, HHSN268201300049C, and
HHSN268201300050C from the National Heart, Lung, and Blood Institute and
the National Institute on Minority Health and Health Disparities. This
project was also supported by grant R21 NR013231 from the National
Health Institutes. Dr. Talegawkar was supported by grant 13BGIA17080036
from the American Diabetes Association.
NR 35
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U2 3
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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 MAY
PY 2015
VL 74
BP 111
EP 116
DI 10.1016/j.ypmed.2015.02.006
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CH1AX
UT WOS:000353754600018
PM 25712326
ER
PT J
AU Blanchard, HC
Taha, AY
Rapoport, SI
Yuan, ZX
AF Blanchard, Helene C.
Taha, Ameer Y.
Rapoport, Stanley I.
Yuan, Zhi-Xin
TI Low-dose aspirin (acetylsalicylate) prevents increases in brain PGE(2),
15-epi-lipoxin A4 and 8-isoprostane concentrations in 9 month-old HIV-1
transgenic rats, a model for HIV-1 associated neurocognitive disorders
SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
LA English
DT Review
DE HIV-1; PGE(2); 8-Isoprostane; Brain; Chronic aspirin; Rat
ID OXIDATIVE STRESS; INFECTED PATIENTS; ANTIRETROVIRAL THERAPY;
ALZHEIMERS-DISEASE; ANTI-INFLAMMATION; ASTROCYTOMA-CELLS; ACID;
CYCLOOXYGENASE-2; ACTIVATION; MARKERS
AB Background: Older human immunodeficiency virus (HIV)-1 transgenic rats are a model for HIV-1 associated neurocognitive disorders (HAND). They show behavioral changes, neuroinflammation, neuronal loss, and increased brain arachidonic acid (AA) enzymes. Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.
Hypothesis: Chronic low-dose ASA will downregulate brain AA metabolism in HIV-1 transgenic rats.
Methods: Nine month-old HIV-1 transgenic and wildtype rats were given 42 days of 10 mg/kg/day ASA or nothing in drinking water; eicosanoids were measured using ELISAs on microwaved brain extracts.
Results: Brain 15-epi-lipoxin A4 and 8-isoprostane concentrations were significantly higher in HIV-1 transgenic than wildtype rats; these differences were prevented by ASA. ASA reduced prostaglandin E-2 and leukotriene B-4 concentrations in HIV-1 Tg but not wildtype rats. Thromboxane B-2, 15-HETE, lipoxin A4 and resolvin D-1 concentrations were unaffected by genotype or treatment.
Conclusion: Chronic low-dose ASA reduces AA-metabolite markers of neuroinflammation and oxidative stress in a rat model for HAND. Published by Elsevier Ltd.
C1 [Blanchard, Helene C.; Taha, Ameer Y.; Rapoport, Stanley I.; Yuan, Zhi-Xin] NIA, Brain Physiol & Metab Sect, Neurosci Lab, NIH, Bethesda, MD 20892 USA.
RP Rapoport, SI (reprint author), NIA, Brain Physiol & Metab Sect, Neurosci Lab, NIH, Bldg 9,Room 1S128,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sir@mail.nih.gov
FU Intramural Research Program of the National Institute on Aging
FX The authors thank Lisa Chang and Mei Chen for skillful technical
assistance. The research was supported by the Intramural Research
Program of the National Institute on Aging. The authors declare no
conflict of interest.
NR 65
TC 5
Z9 6
U1 0
U2 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0952-3278
EI 1532-2823
J9 PROSTAG LEUKOTR ESS
JI Prostaglandins Leukot. Essent. Fatty Acids
PD MAY
PY 2015
VL 96
BP 25
EP 30
DI 10.1016/j.plefa.2015.01.002
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
GA CH0RV
UT WOS:000353731000004
PM 25638779
ER
PT J
AU Tandon, M
Gallo, A
Jang, S
Cotrim, A
Alevizos, I
AF Tandon, M.
Gallo, A.
Jang, S.
Cotrim, A.
Alevizos, I.
TI Metagenomic Analysis of Salivary Exosome Transcriptomes from Patients
with Primary Sjogren's Syndrome Using RNA-Seq
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Tandon, M.; Gallo, A.; Jang, S.; Cotrim, A.; Alevizos, I.] Natl Inst Dent & Craniofacial Res, Sjogrens Syndrome Clin, Mol Physiol & Therapeut Branch, 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 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S3.14
BP 351
EP 351
PG 1
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300049
ER
PT J
AU Teos, L
Zhang, J
Hak, J
Swaim, W
Ambrus, J
Grisius, M
Cotrim, A
Jang, S
Bebris, L
Illei, G
Yule, D
Ambudkar, I
Alevizos, I
AF Teos, L.
Zhang, J.
Hak, J.
Swaim, W.
Ambrus, J.
Grisius, M.
Cotrim, A.
Jang, S.
Bebris, L.
Illei, G.
Yule, D.
Ambudkar, I.
Alevizos, I.
TI IP3R Deficit in Acinar Cells Underlies Loss of Salivary Gland Fluid
Secretion in the Autoimmune Exocrinopathy, Sjogren's Syndrome
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Teos, L.; Grisius, M.; Cotrim, A.; Jang, S.; Bebris, L.; Illei, G.; Alevizos, I.] NIDCR, Sjogrens Syndrome & Salivary Gland Dysfunct Unit, MPTB, NIH, Bethesda, MD 20892 USA.
[Teos, L.; Swaim, W.; Ambudkar, I.] NIDCR, Secretory & Physiol Sect, MPTB, NIH, Bethesda, MD 20892 USA.
[Zhang, J.; Hak, J.; Yule, D.] Univ Rochester, Med Ctr, Sch Med & Dent, Rochester, NY 14642 USA.
[Ambrus, J.] SUNY Buffalo, Sch Med & Biomed Sci, Dept Med, Div Allergy Immunol & Rheumatol, Buffalo, NY 14203 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 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S4.11
BP 359
EP 360
PG 2
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300066
ER
PT J
AU Lai, Z
Yin, H
Cabrera-Perez, J
Glenton, P
Patel, A
Swaim, W
Zheng, C
Nguyen, CQ
Nyberg, F
Chiorini, JA
AF Lai, Z.
Yin, H.
Cabrera-Perez, J.
Glenton, P.
Patel, A.
Swaim, W.
Zheng, C.
Nguyen, C. Q.
Nyberg, F.
Chiorini, J. A.
TI Aquaporin Gene Therapy Corrects Exocrine Gland Dysfunction and
Inflammation in Mouse Model of Sjogren's Syndrome
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Lai, Z.; Yin, H.; Cabrera-Perez, J.; Patel, A.; Swaim, W.; Zheng, C.; Chiorini, J. A.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD USA.
[Lai, Z.; Nyberg, F.] Uppsala Univ, Div Biol Res Drug Dependence, Dept Pharmaceut Biosci, S-75124 Uppsala, Sweden.
[Glenton, P.; Nguyen, C. Q.] Univ Florida, Dept Pathol & Infect Dis, Gainesville, FL 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 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S12.6
BP 423
EP 423
PG 1
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300188
ER
PT J
AU Perez, P
Teos, L
Tandon, M
Kazmi, S
Gallo, A
Illei, G
Alevizos, I
AF Perez, P.
Teos, L.
Tandon, M.
Kazmi, S.
Gallo, A.
Illei, G.
Alevizos, I.
TI Downregulation of MicroRNA-183 in Sjogren's Syndrome Minor Salivary
Glands; Implications in the Control of ezrin Expression and Salivary
Gland Function
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Perez, P.; Teos, L.; Tandon, M.; Kazmi, S.; Gallo, A.; Illei, G.; Alevizos, I.] NIDCR, MPTB, 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 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S12.11
BP 426
EP 426
PG 1
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300193
ER
PT J
AU Weller, ML
Gardener, MR
Bogus, ZC
Smith, MA
Astorri, E
Michael, DG
Michael, DA
Zheng, C
Burbelo, PD
Lai, Z
Wilson, PA
Swaim, W
Handelman, B
Afione, SA
Bombardieri, M
Chiorini, JA
AF Weller, M. L.
Gardener, M. R.
Bogus, Z. C.
Smith, M. A.
Astorri, E.
Michael, D. G.
Michael, D. A.
Zheng, C.
Burbelo, P. D.
Lai, Z.
Wilson, P. A.
Swaim, W.
Handelman, B.
Afione, S. A.
Bombardieri, M.
Chiorini, J. A.
TI Hepatitis Delta Virus Detected in Salivary Glands of Sjogren's Syndrome
Patients and Induces a Sjogren's Syndrome Phenotype in vivo
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Weller, M. L.; Gardener, M. R.; Bogus, Z. C.; Smith, M. A.; Michael, D. G.; Zheng, C.; Lai, Z.; Swaim, W.; Handelman, B.; Afione, S. A.; Chiorini, J. A.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD USA.
[Astorri, E.; Bombardieri, M.] Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, Ctr Expt Med & Rheumatol, London, England.
[Burbelo, P. D.] Natl Inst Dent & Craniofacial Res, Dent Clin Res Core, NIH, Bethesda, MD USA.
[Wilson, P. A.] NIH, Natl Intramural Database, Div Enterprise & Custom Applicat, Ctr Informat Technol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S12.13
BP 427
EP 427
PG 1
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300195
ER
PT J
AU Faustman, DL
Alevizos, I
AF Faustman, D. L.
Alevizos, I.
TI Investigation of Repeat BCG Vaccinations in Autoimmunity: Rationale and
Phase I Trial in Sjogren's Syndrome
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Faustman, D. L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Immunobiol Lab, Boston, MA USA.
[Alevizos, I.] NIDCR, Sjogrens Syndrome Clin, NIH, Bethesda, 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 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S13.3
BP 428
EP 429
PG 2
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300198
ER
PT J
AU Jang, SI
Ong, HL
Alevizos, I
Ambudkar, IS
AF Jang, S-I
Ong, H-L
Alevizos, I.
Ambudkar, I. S.
TI Calcium-Calcineurin-NFAT Signaling Pathway Regulates AQP5 Expression in
Primary Salivary Gland Acinar Cells
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT 13th International Symposium on Sjogren's Syndrome
CY MAY 19-22, 2015
CL Bergen, NORWAY
C1 [Jang, S-I; Alevizos, I.] NIDCR, Sjogrens Syndrome & Salivary Gland Dysfunct Unit, MPTB, NIH, Bethesda, MD 20892 USA.
[Jang, S-I; Ong, H-L; Ambudkar, I. S.] NIDCR, Secretory & Physiol Sect, MPTB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-9475
EI 1365-3083
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD MAY
PY 2015
VL 81
IS 5
MA S13.8
BP 431
EP 431
PG 1
WC Immunology
SC Immunology
GA CG6HV
UT WOS:000353401300203
ER
PT J
AU Insel, TR
Cuthbert, BN
AF Insel, Thomas R.
Cuthbert, Bruce N.
TI Brain disorders? Precisely
SO SCIENCE
LA English
DT Editorial Material
ID RESEARCH DOMAIN CRITERIA; MENTAL-DISORDERS; MEDICINE; HEALTH
C1 [Insel, Thomas R.; Cuthbert, Bruce N.] NIMH, NIH, Bethesda, MD 20892 USA.
RP Insel, TR (reprint author), NIMH, NIH, Bethesda, MD 20892 USA.
EM tinsel@mail.nih.gov
NR 15
TC 55
Z9 56
U1 3
U2 26
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 MAY 1
PY 2015
VL 348
IS 6234
BP 499
EP 500
DI 10.1126/science.aab2358
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CH1JR
UT WOS:000353778100020
PM 25931539
ER
PT J
AU Palesch, YY
Yeatts, SD
Tomsick, TA
Foster, LD
Demchuk, AM
Khatri, P
Hill, MD
Jauch, EC
Jovin, TG
Yan, B
von Kummer, R
Molina, CA
Goyal, M
Schonewille, WJ
Mazighi, M
Engelter, ST
Anderson, C
Spilker, J
Carrozzella, J
Ryckborst, KJ
Janis, LS
Simpson, A
Simpson, KN
Broderick, JP
AF Palesch, Yuko Y.
Yeatts, Sharon D.
Tomsick, Thomas A.
Foster, Lydia D.
Demchuk, Andrew M.
Khatri, Pooja
Hill, Michael D.
Jauch, Edward C.
Jovin, Tudor G.
Yan, Bernard
von Kummer, Ruediger
Molina, Carlos A.
Goyal, Mayank
Schonewille, Wouter J.
Mazighi, Mikael
Engelter, Stefan T.
Anderson, Craig
Spilker, Judith
Carrozzella, Janice
Ryckborst, Karla J.
Janis, L. Scott
Simpson, Annie
Simpson, Kit N.
Broderick, Joseph P.
CA Interventional Management Stroke I
TI Twelve-Month Clinical and Quality-of-Life Outcomes in the Interventional
Management of Stroke III Trial
SO STROKE
LA English
DT Article
DE acute stroke; endovascular procedures; randomized trial; tPA
ID ACUTE ISCHEMIC-STROKE; ENDOVASCULAR THERAPY; RANDOMIZED-TRIAL; POOLED
ANALYSIS; TIME; EQ-5D; SCORE; RECANALIZATION; THROMBECTOMY; REPERFUSION
AB Background and Purpose-Randomized trials have indicated a benefit for endovascular therapy in appropriately selected stroke patients at 3 months, but data regarding outcomes at 12 months are currently lacking.
Methods-We compared functional and quality-of-life outcomes at 12 months overall and by stroke severity in stroke patients treated with intravenous tissue-type plasminogen activator followed by endovascular treatment as compared with intravenous tissue-type plasminogen activator alone in the Interventional Management of Stroke III Trial. The key outcome measures were a modified Rankin Scale score <= 2 (functional independence) and the Euro-QoL EQ-5D, a health-related quality-of-life measure.
Results-656 subjects with moderate-to-severe stroke (National Institutes of Health Stroke Scale >= 8) were enrolled at 58 centers in the United States (41 sites), Canada (7), Australia (4), and Europe (6). There was an interaction between treatment group and stroke severity in the repeated measures analysis of modified Rankin Scale <= 2 outcome (P=0.039). In the 204 participants with severe stroke (National Institutes of Health Stroke Scale >= 20), a greater proportion of the endovascular group had a modified Rankin Scale <= 2 (32.5%) at 12 months as compared with the intravenous tissue-type plasminogen activator group (18.6%, P=0.037); no difference was seen for the 452 participants with moderately severe strokes (55.6% versus 57.7%). In participants with severe stroke, the endovascular group had 35.2 (95% confidence interval: 2.1, 73.3) more quality-adjusted-days over 12 months as compared with intravenous tissue-type plasminogen activator alone.
Conclusions-Endovascular therapy improves functional outcome and health-related quality-of-life at 12 months after severe ischemic stroke.
C1 [Tomsick, Thomas A.; Khatri, Pooja; Spilker, Judith; Carrozzella, Janice; Broderick, Joseph P.] Univ Cincinnati, Dept Neurol, Inst Neurosci, Acad Hlth Ctr, Cincinnati, OH 45267 USA.
[Tomsick, Thomas A.; Khatri, Pooja; Spilker, Judith; Carrozzella, Janice; Broderick, Joseph P.] Univ Cincinnati, Dept Rehabil Med & Radiol, Inst Neurosci, Acad Hlth Ctr, Cincinnati, OH 45267 USA.
[Palesch, Yuko Y.; Yeatts, Sharon D.; Foster, Lydia D.; Simpson, Annie; Simpson, Kit N.] Med Univ S Carolina, Dept Publ Hlth Sci, Charleston, SC USA.
[Jauch, Edward C.] Med Univ S Carolina, Div Emergency Med, Charleston, SC USA.
[Demchuk, Andrew M.; Hill, Michael D.; Goyal, Mayank; Ryckborst, Karla J.] Univ Calgary, Dept Clin Neurosci, Seaman Family MR Res Ctr, Calgary Stroke Program,Hotchkiss Brain Inst, Calgary, AB, Canada.
[Demchuk, Andrew M.; Hill, Michael D.; Goyal, Mayank; Ryckborst, Karla J.] Univ Calgary, Dept Radiol, Seaman Family MR Res Ctr, Calgary Stroke Program,Hotchkiss Brain Inst, Calgary, AB, Canada.
[Jovin, Tudor G.] Univ Pittsburgh, Med Ctr, Stroke Inst, Pittsburgh, PA USA.
[Yan, Bernard] Univ Melbourne, Royal Melbourne Hosp, Melbourne Brain Ctr, Melbourne, Vic 3050, Australia.
[von Kummer, Ruediger] Dresden Univ, Stroke Ctr, Dept Neuroradiol, Univ Hosp, Dresden, Germany.
[Molina, Carlos A.] Hosp Univ Vall Hebron, Dept Neurol, Neurovasc Unit, Barcelona, Spain.
[Schonewille, Wouter J.] Univ Med Ctr Utrecht, Dept Neurol, Utrecht, Netherlands.
[Schonewille, Wouter J.] Rudolf Magnus Inst Neurosci, NL-3508 TA Utrecht, Netherlands.
[Schonewille, Wouter J.] St Antonius Hosp, Nieuwegein, Netherlands.
[Mazighi, Mikael] Lariboisiere Hosp, Dept Neurol, Paris, France.
[Mazighi, Mikael] Lariboisiere Hosp, Stroke Ctr, Paris, France.
[Engelter, Stefan T.] Univ Basel Hosp, Dept Neurol, CH-4031 Basel, Switzerland.
[Anderson, Craig] Univ Sydney, Royal Prince Alfred Hosp, George Inst Global Hlth, Sydney, NSW 2006, Australia.
[Janis, L. Scott] NINDS, NIH, Bethesda, MD 20892 USA.
RP Broderick, JP (reprint author), Univ Cincinnati, Dept Neurol, Inst Neurosci, 260 Stetson St,Suite 2300,POB 670525, Cincinnati, OH 45267 USA.
EM joseph.broderick@uc.edu
FU National Institute of Health/NINDS [U01NS052220, U01NS054630,
U01NS077304]
FX National Institute of Health/NINDS Grant Numbers: University of
Cincinnati U01NS052220 and Medical University of South Carolina
U01NS054630 and U01NS077304. Genentech Inc. supplied study drug used for
intra-arterial tPA in the Endovascular group. EKOS Corp., Concentric
Inc., Cordis Neurovascular, Inc. supplied study catheters during
Protocol Versions 1-3. In the United States, IMS III investigator
meeting support was provided in part by Genentech Inc, EKOS Corp., and
Concentric Inc. In Europe, IMS III investigator meeting support was
provided in part by Boehringer Ingelheim. Y.Y. Palesch, S.D. Yeatts,
L.D. Foster, A. Simpson, K.N. Simpson, J.P. Broderick were responsible
for the analyses used in this article. Y.Y. Palesch and J.P. Broderick
had full access to all of the data in the study and take responsibility
for the integrity of the data and the accuracy of the data analysis.
NR 33
TC 5
Z9 5
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD MAY
PY 2015
VL 46
IS 5
BP 1321
EP 1327
DI 10.1161/STROKEAHA.115.009180
PG 7
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA CG8LR
UT WOS:000353559800044
PM 25858239
ER
PT J
AU Abdul-Rahim, AH
Fulton, RL
Sucharew, H
Kleindorfer, D
Khatri, P
Broderick, JP
Lees, KR
AF Abdul-Rahim, A. H.
Fulton, R. L.
Sucharew, H.
Kleindorfer, D.
Khatri, P.
Broderick, J. P.
Lees, K. R.
CA VISTA Collaborators
TI National Institutes of Health Stroke Scale Item Profiles as Predictor of
Patient Outcome: External Validation on Independent Trial Data (vol 46,
pg 395, 2015)
SO STROKE
LA English
DT Correction
C1 [Abdul-Rahim, A. H.; Fulton, R. L.; Sucharew, H.; Kleindorfer, D.; Khatri, P.; Broderick, J. P.; Lees, K. R.] NIH, Bethesda, MD 20892 USA.
RP Abdul-Rahim, AH (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
RI Sucharew, Heidi/M-4338-2015
NR 1
TC 0
Z9 0
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD MAY
PY 2015
VL 46
IS 5
BP E128
EP E128
DI 10.1161/STR.0000000000000066
PG 1
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA CG8LR
UT WOS:000353559800014
ER
PT J
AU Degoma, EM
Salavati, A
Shinohara, RT
Saboury, B
Pollan, L
Schoen, M
Torigian, DA
Mohler, ER
Dunbar, RL
Litt, HI
Woo, J
Rader, DJ
Alavi, A
Mehta, NN
AF deGoma, Emil M.
Salavati, Ali
Shinohara, Russell T.
Saboury, Babak
Pollan, Laura
Schoen, Marisa
Torigian, Drew A.
Mohler, Emile R.
Dunbar, Richard L.
Litt, Harold I.
Woo, John
Rader, Daniel J.
Alavi, Abass
Mehta, Nehal N.
TI A Pilot Trial to Examine the Effect of High-Dose Niacin on Arterial Wall
Inflammation Using Fluorodeoxyglucose Positron Emission Tomography
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Atherosclerosis; positron emission tomography; fluorodeoxyglucose;
lipids; niacin
ID ACUTE CORONARY SYNDROME; LOW-DENSITY-LIPOPROTEIN; ATHEROSCLEROTIC PLAQUE
INFLAMMATION; TRANSIENT ISCHEMIC ATTACK; EXTENDED-RELEASE NIACIN;
NICOTINIC-ACID; STATIN THERAPY; FDG-PET/CT; SECONDARY PREVENTION;
RANDOMIZED-TRIALS
AB Rationale and Objectives: Although studies have reported direct inhibition of inflammatory pathways with niacin, the effect of niacin on arterial wall inflammation remains unknown. We examined the effect of niacin on arterial F-18-fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography (CT).
Materials and Methods: Nine statin-treated patients with coronary disease were randomized to niacin 6000 mg/day or placebo. FDG-PET/CT and lipids were assessed at-baseline and at 12 weeks. FOG was quantified in the aorta, right carotid artery, and left carotid artery as the target-to-background ratio (TBR) and target-to-background difference (TBD).
Results: Eight patients completed the study. No significant changes in FOG measured by aortic, left carotid, or right carotid TBR or TBD were seen in either group. Compared to baseline, niacin-treated subjects exhibited a significant 29% reduction in low-density lipoprotein cholesterol (LDL-C; 95% confidence interval [CI], -50% to 8%; P = .01) and a nonsignificant 29% reduction in LDL particle number (LDL-P; 95% CI, -58% to 0.2%; P = .07). A nonsignificant 11% increase in HDL-C (95% CI, -15% to 37%; P = .30) and 8% decrease in HDL-P (95% CI, -44% to 28%; P = .51) were observed with niacin treatment. In a pooled analysis, changes in LDL-P were positively correlated with FOG uptake in the aorta (TBR r = 0.66, P = .08; TBD r = 0.75, P = .03), left carotid (TBR r = 0.65, P = .08; TBD r = 0.74, P = .03), and right carotid (TBR r = 0.54, P = .17; TBD r = 0.61, P = .11).
Conclusions: In this pilot study, adding niacin to statin therapy did not affect arterial wall inflammation measured by FDG-PET/CT. However, an association between changes in arterial FOG uptake and LDL-P was observed. Larger studies are needed to definitively examine the effect of niacin on arterial wall inflammation.
C1 [deGoma, Emil M.; Mohler, Emile R.] Univ Penn, Div Cardiovasc Med, Perelman Ctr Adv Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Salavati, Ali; Saboury, Babak; Torigian, Drew A.; Alavi, Abass] Univ Penn, Div Nucl Med, Dept Radiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Shinohara, Russell T.; Dunbar, Richard L.] Univ Penn, Dept Biostat & Epidemiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Pollan, Laura; Schoen, Marisa; Rader, Daniel J.] Univ Penn, Div Translat Med & Human Genet, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Torigian, Drew A.; Litt, Harold I.; Woo, John] Univ Penn, Dept Radiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Mehta, Nehal N.] NHLBI, Sect Inflammat & Cardiometab Dis, Bethesda, MD USA.
RP Degoma, EM (reprint author), Univ Penn, Div Cardiovasc Med, Perelman Ctr Adv Med, Perelman Sch Med, 3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM deGoma@uphs.upenn.edu
FU Perelman School of Medicine at the University of Pennsylvania Schiffrin
Award; Division of Radiology Pilot Grant (PRODEV); Foundation of the
National Lipid Association; Division of Intramural Research grant
[HL-Z00000]; National Institute of Neurological Disorders and Stroke
[R01NS085211]
FX E.M.D. was supported by the Perelman School of Medicine at the
University of Pennsylvania Schiffrin Award, the Division of Radiology
Pilot Grant (PRODEV), and the Foundation of the National Lipid
Association. N.N.M. was supported by the Division of Intramural Research
grant HL-Z00000. R.T.S. was supported by R01NS085211 from the National
Institute of Neurological Disorders and Stroke.
NR 55
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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 1076-6332
EI 1878-4046
J9 ACAD RADIOL
JI Acad. Radiol.
PD MAY
PY 2015
VL 22
IS 5
BP 600
EP 609
DI 10.1016/j.acra.2014.12.015
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CG2AZ
UT WOS:000353078600008
PM 25708866
ER
PT J
AU Turkbey, B
Hoyt, RF
Agarwal, HK
Bernardo, M
Sankineni, S
Johnson, L
Grant, KB
Rais-Bahrami, S
Kobayashi, H
Wood, BJ
Pinto, PA
Griffiths, GL
Choyke, PL
AF Turkbey, Baris
Hoyt, Robert F., Jr.
Agarwal, Harsh K.
Bernardo, Marcelino
Sankineni, Sandeep
Johnson, Linda
Grant, Kinzya B.
Rais-Bahrami, Soroush
Kobayashi, Hisataka
Wood, Bradford J.
Pinto, Peter A.
Griffiths, Gary L.
Choyke, Peter L.
TI Magnetic Resonance Sentinel Lymph Node Imaging of the Prostate with
Gadofosveset Trisodium-Albumin: Preliminary Results in a Canine Model
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Gadofosveset trisodium; lymph node; MRI; human serum albumin
ID HUMAN SERUM-ALBUMIN; CANCER; DISSECTION; LYMPHOGRAPHY; METASTASES;
CARCINOMA; SIZE; 3T; CT
AB Rationale and Objectives: To determine if intraprostatic injection of gadofosveset trisodium mixed with human serum albumin (HSA) can identify sentinel lymph nodes (LNs) draining the prostate on magnetic resonance imaging (MRI) in a canine model.
Materials and Methods: Three male canines weighing between 25.7 and 41.3 kg were anesthetized, placed in a 3-T MRI, and a needle was placed transrectally into one side of the prostate using a commercially available intrarectal needle guide. Gadofosveset trisodium pre-mixed with 10% HSA was then administered at doses ranging from 0.1 to 2.5 mL. T1W MRI was performed immediately after injection, and two readers evaluated images for visualization of LNs draining the prostate.
Results: Intraprostatic injection of 0.2 mL gadofosveset trisodium premixed with HSA identified the draining periprostatic LNs in all cases. Delayed images demonstrated upper echelon nodes in the pelvis and the abdomen. Higher volume injections resulted in excessive periprostatic extravasation, whereas lower volume injections resulted in suboptimal visualization of LNs.
Conclusions: We demonstrate that gadofosveset trisodium (premixed with 10% HSA) injected intraprostatically at 0.2 mL visualized LNs draining the prostate. This approach can be readily adapted for clinical applications such as sentinel LN imaging in prostate cancer patients before surgery.
C1 [Turkbey, Baris; Agarwal, Harsh K.; Bernardo, Marcelino; Sankineni, Sandeep; Johnson, Linda; Grant, Kinzya B.; Kobayashi, Hisataka; Choyke, Peter L.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Hoyt, Robert F., Jr.] NHLBI, Lab Anim Med & Surg, NIH, Bethesda, MD 20892 USA.
[Hoyt, Robert F., Jr.] Leidos Biomed Res Inc, Lab Anim Sci Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Agarwal, Harsh K.] Philips Res North Amer, Briarcliff Manor, NY USA.
[Rais-Bahrami, Soroush; Pinto, Peter A.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Wood, Bradford J.; Pinto, Peter A.] NCI, Ctr Intervent Oncol, NIH, Bethesda, MD 20892 USA.
[Wood, Bradford J.; Pinto, Peter A.] NIH, Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Griffiths, Gary L.] Leidos Biomed Res Inc, Clin Res Directorate, Clin Monitoring Res Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
RP Turkbey, B (reprint author), NCI, Mol Imaging Program, NIH, 10 Ctr Dr,MSC 1182 Bldg 10,Room B3B85, Bethesda, MD 20892 USA.
EM turkbeyi@mail.nih.gov
OI Rais-Bahrami, Soroush/0000-0001-9466-9925
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract no. HHSN261200800001E. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 24
TC 6
Z9 6
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
EI 1878-4046
J9 ACAD RADIOL
JI Acad. Radiol.
PD MAY
PY 2015
VL 22
IS 5
BP 646
EP 652
DI 10.1016/j.acra.2014.12.021
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA CG2AZ
UT WOS:000353078600014
PM 25683498
ER
PT J
AU Adeyemi, EI
Giedd, JN
Lee, NR
AF Adeyemi, Elizabeth I.
Giedd, Jay N.
Lee, Nancy Raitano
TI A Case Study of Brain Morphometry in Triplets Discordant for Down
Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE down syndrome; trisomy 21; magnetic resonance imaging; cortical
thickness; cortical surface area
ID HIGH-RESOLUTION MRI; CHILDREN; GROWTH; CORTEX
AB Down syndrome, the most common genetic cause of intellectual disability, offers the opportunity to explore the associations between genetics and both neuroanatomic and neuropsychological phenotypes. This case report summarizes the findings of a neuroimaging and neuropsychology study of two adolescent females with Down syndrome and their same-sex discordant triplet siblings (one from each family; n=4). Using high-resolution magnetic resonance imaging and surface based morphometric approaches, we offer the first in vivo report of cortical surface area reductions and increases in the thickness of the cortical sheet in youth with Down syndrome relative to their typically developing same-sex triplet siblings. (c) 2015 Wiley Periodicals, Inc.
C1 [Adeyemi, Elizabeth I.; Giedd, Jay N.; Lee, Nancy Raitano] NIMH, Sect Brain Imaging, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Giedd, Jay N.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Lee, Nancy Raitano] Drexel Univ, Dept Psychol, Philadelphia, PA 19104 USA.
RP Adeyemi, EI (reprint author), NIMH, Child Psychiat Branch, NIH, 10 Ctr Dr,Bldg 10,Room 4C110,MSC 1367, Bethesda, MD 20892 USA.
EM eadeyemi1@gmail.com
RI Giedd, Jay/J-9644-2015; Lee, Nancy/M-7492-2016
OI Giedd, Jay/0000-0003-2002-8978; Lee, Nancy/0000-0002-6663-0713
FU National Institutes of Health, National Institute of Mental Health
[NCT00001246, 89-M-0006]
FX Grant sponsor: National Institutes of Health, National Institute of
Mental Health; Grant number: NCT00001246; Protocol ID 89-M-0006.
NR 20
TC 0
Z9 0
U1 1
U2 5
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 MAY
PY 2015
VL 167
IS 5
BP 1107
EP 1110
DI 10.1002/ajmg.a.36820
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA CG3HY
UT WOS:000353171900019
PM 25820455
ER
PT J
AU van Ravesteyn, NT
van Lier, L
Schechter, CB
Ekwueme, DU
Royalty, J
Miller, JW
Near, AM
Cronin, KA
Heijnsdijk, EAM
Mandelblatt, JS
de Koning, HJ
AF van Ravesteyn, Nicolien T.
van Lier, Lisanne
Schechter, Clyde B.
Ekwueme, Donatus U.
Royalty, Janet
Miller, Jacqueline W.
Near, Aimee M.
Cronin, Kathleen A.
Heijnsdijk, Eveline A. M.
Mandelblatt, Jeanne S.
de Koning, Harry J.
TI Transition From Film to Digital Mammography Impact for Breast Cancer
Screening Through the National Breast and Cervical Cancer Early
Detection Program
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID COST-EFFECTIVENESS; RANDOMIZED-TRIALS; UNITED-STATES; INSURANCE STATUS;
RACE; PERFORMANCE; BENEFITS; WOMEN; RATES; CONSEQUENCES
AB Introduction: The National Breast and Cervical Cancer Early Detection Program (NBCCEDP) provides mammograms and diagnostic services for low-income, uninsured women aged 40-64 years. Mammography facilities within the NBCCEDP gradually shifted from plain-film to digital mammography. The purpose of this study is to assess the impact of replacing film with digital mammography on health effects (deaths averted, life-years gained [LYG]); costs (for screening and diagnostics); and number of women reached.
Methods: NBCCEDP 2010 data and data representative of the program's target population were used in two established microsimulation models. Models simulated observed screening behavior including different screening intervals (annual, biennial, irregular) and starting ages (40, 50 years) for white, black, and Hispanic women. Model runs were performed in 2012.
Results: The models predicted 8.0-8.3 LYG per 1,000 film screens for black women, 5.9-7.5 for white women, and 4.0-4.5 for Hispanic women. For all race/ethnicity groups, digital mammography had more LYG than film mammography (2%-4%), but had higher costs (34%-35%). Assuming a fixed budget, 25%-26% fewer women could be served, resulting in 22%-24% fewer LYG if all mammograms were converted to digital. The loss in LYG could be reversed to an 8%-13% increase by only including biennial screening.
Conclusions: Digital could result in slightly more LYG than film mammography. However, with a fixed budget, fewer women may be served with fewer LYG. Changes in the program, such as only including biennial screening, will increase LYG/screen and could offset the potential decrease in LYG when shifting to digital mammography. (C) 2015 American Journal of Preventive Medicine. All rights reserved.
C1 [van Ravesteyn, Nicolien T.; van Lier, Lisanne; Heijnsdijk, Eveline A. M.; de Koning, Harry J.] Univ Med Ctr, Erasmus MC, Dept Publ Hlth, Rotterdam, Netherlands.
[van Lier, Lisanne] Vrije Univ Amsterdam, Dept Gen Practice & Elderly Care Med, Med Ctr, Amsterdam, Netherlands.
[Schechter, Clyde B.] Albert Einstein Coll Med, Dept Family & Social Med, Bronx, NY USA.
[Schechter, Clyde B.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY USA.
[Ekwueme, Donatus U.; Royalty, Janet; Miller, Jacqueline W.] CDC, Atlanta, GA 30333 USA.
[Near, Aimee M.; Mandelblatt, Jeanne S.] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC USA.
[Cronin, Kathleen A.] NCI, Stat Res & Applicat Branch, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
RP van Ravesteyn, NT (reprint author), Erasmus MC, Dept Publ Hlth, POB 2040, NL-3000 CA Rotterdam, Netherlands.
EM n.vanravesteyn@erasmusmc.nl
FU National Cancer Institute (NCI)-funded Breast Cancer Surveillance
Consortium [HHSN261201100031C]; Interagency Agreement from CDC to the
NCI [U01CA115337-10S1]; NCI [U01CA152958, U01CA088283, KO5CA96940];
Department of Defense [BC043120]
FX We thank the National Comprehensive Cancer Network investigators for use
of data on treatment dissemination. We thank the Breast Cancer
Surveillance Consortium (BCSC) investigators for the data they have
provided for this study. BCSC data collection was supported by the
National Cancer Institute (NCI)-funded Breast Cancer Surveillance
Consortium (Grant No. HHSN261201100031C). A list of the BCSC
investigators and procedures for requesting BCSC data for research
purposes are provided at: breastscreening.cancer.gov/. Drs. Mandelblatt
and de Koning contributed equally to this work as senior authors. This
study was supported by an Interagency Agreement from CDC to the NCI and
funded under Grant No. U01CA115337-10S1.; This study was also supported
in part by the NCI (Grant Nos. U01CA152958, U01CA088283; grant No.
KO5CA96940 [JM]) and the Department of Defense (Grant No. BC043120
[JM]). Model results are the sole responsibility of the authors. The
findings and conclusions in this report are those of the authors and do
not necessarily represent the official position of CDC.
NR 33
TC 0
Z9 0
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD MAY
PY 2015
VL 48
IS 5
BP 535
EP 542
DI 10.1016/j.amepre.2014.11.010
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA CG1XO
UT WOS:000353069300008
PM 25891052
ER
PT J
AU Chattopadhyay, PK
Roederer, M
AF Chattopadhyay, P. K.
Roederer, M.
TI A Mine Is a Terrible Thing to Waste: High Content, Single Cell
Technologies for Comprehensive Immune Analysis
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Review
ID HUMAN T-CELLS; POLYCHROMATIC FLOW-CYTOMETRY; MASS CYTOMETRY; PHENOTYPIC
ANALYSIS; GENE-EXPRESSION; RESPONSES; HETEROGENEITY; QUALITY; SUBSET;
VISUALIZATION
AB In recent years, an incredible variety of single cell technologies have become available to analyze immune responses. These technologies include polychromatic flow cytometry, mass cytometry, highly multiplexed single cell qPCR, RNA sequencing, microtools, and high-resolution imaging. In this article, we review these platforms, describing their power and limitations for comprehensive analysis of the immune system. We relate the properties of these technologies to the various cellular states relevant to an immune response, in order to address which technologies are most appropriate for which settings.
C1 [Chattopadhyay, P. K.; Roederer, M.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP Chattopadhyay, PK (reprint author), NIH, Vaccine Res Ctr, Bldg 10, Bethesda, MD 20892 USA.
OI Chattopadhyay, Pratip/0000-0002-5457-9666
NR 60
TC 6
Z9 6
U1 0
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
EI 1600-6143
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD MAY
PY 2015
VL 15
IS 5
BP 1155
EP 1161
DI 10.1111/ajt.13193
PG 7
WC Surgery; Transplantation
SC Surgery; Transplantation
GA CG5ML
UT WOS:000353335900008
PM 25708158
ER
PT J
AU Smith, MC
Crist, RM
Clogston, JD
McNeil, SE
AF Smith, Mackensie C.
Crist, Rachael M.
Clogston, Jeffrey D.
McNeil, Scott E.
TI Quantitative analysis of PEG-functionalized colloidal gold nanoparticles
using charged aerosol detection
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Polyethylene glycol (PEG); Surface characterization; Charged aerosol
detector; Gold nanoparticles; Stability; Displacement; Dissolution
ID POLYETHYLENE-GLYCOL; COLORIMETRIC ASSAY; CANCER-THERAPY; PARTICLE-SIZE;
SURFACE; QUANTIFICATION; PEGYLATION; PHARMACOKINETICS; PHARMACEUTICALS;
TRANSLATION
AB Surface characteristics of a nanoparticle, such as functionalization with polyethylene glycol (PEG), are critical to understand and achieve optimal biocompatibility. Routine physicochemical characterization such as UV-vis spectroscopy (for gold nanoparticles), dynamic light scattering, and zeta potential are commonly used to assess the presence of PEG. However, these techniques are merely qualitative and are not sensitive enough to distinguish differences in PEG quantity, density, or presentation. As an alternative, two methods are described here which allow for quantitative measurement of PEG on PEGylated gold nanoparticles. The first, a displacement method, utilizes dithiothreitol to displace PEG from the gold surface. The dithiothreitol-coated gold nanoparticles are separated from the mixture via centrifugation, and the excess dithiothreitol and dissociated PEG are separated through reversed-phase high-performance liquid chromatography (RP-HPLC). The second, a dissolution method, utilizes potassium cyanide to dissolve the gold nanoparticles and liberate PEG. Excess CN-, Au(CN)(2) (-), and free PEG are separated using RP-HPLC. In both techniques, the free PEG can be quantified against a standard curve using charged aerosol detection. The displacement and dissolution methods are validated here using 2-, 5-, 10-, and 20-kDa PEGylated 30-nm colloidal gold nanoparticles. Further value in these techniques is demonstrated not only by quantitating the total PEG fraction but also by being able to be adapted to quantitate the free unbound PEG and the bound PEG fractions. This is an important distinction, as differences in the bound and unbound PEG fractions can affect biocompatibility, which would not be detected in techniques that only quantitate the total PEG fraction.
C1 [Smith, Mackensie C.; Crist, Rachael M.; Clogston, Jeffrey D.; McNeil, Scott E.] Leidos Biomed Res Inc, Nanotechnol Characterizat Lab, Canc Res Technol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
RP Clogston, JD (reprint author), Leidos Biomed Res Inc, Nanotechnol Characterizat Lab, Canc Res Technol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
EM clogstonj@mail.nih.gov
RI Crist, Rachael/K-7603-2012; Nanotechnology Characterization Lab,
NCL/K-8454-2012
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX The authors are grateful to Sarah Anderson, Matthew Hansen, and Simona
Colantonio for TEM, ICP-MS, and MALDI-TOF MS analysis, respectively, and
Joseph Meyer for graphic illustrations. 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 US Government.
NR 48
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Z9 5
U1 5
U2 55
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 MAY
PY 2015
VL 407
IS 13
BP 3705
EP 3716
DI 10.1007/s00216-015-8589-2
PG 12
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA CG4CS
UT WOS:000353230400016
PM 25749798
ER
PT J
AU Kaplan, RM
Howard, VJ
Safford, MM
Howard, G
AF Kaplan, Robert M.
Howard, Virginia J.
Safford, Monika M.
Howard, George
TI Educational attainment and longevity: results from the REGARDS US
national cohort study of blacks and whites
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Educational attainment; Life expectancy; All-cause mortality;
Prospective cohort
ID HEALTHY LIFE EXPECTANCY; ADULT MORTALITY; UNITED-STATES; RISK-FACTORS;
AGE; COUNTRIES; INEQUALITIES; GRADIENT; GENDER; INCOME
AB Background: Educational attainment may be an important determinant of life expectancy. However, few studies have prospectively evaluated the relationship between educational attainment and life expectancy using adjustments for other social, behavioral, and biological factors.
Method: The data were from the REasons for Geographic and Racial Differences in Stroke study that enrolled 30,239 black and white adults (>= 45 years) between 2003 and 2007. Demographic and cardiovascular risk information was collected and participants were followed for health outcomes. Educational attainment was categorized as less than high school education, high school graduate, some college, or college graduate. Proportional hazards analysis was used to characterize survival by level of education.
Results: Educational attainment and follow-up data were available on 29,657(98%) of the participants. Over 6.3 years of follow-up, 3673 participants died. There was a monotonically increasing risk of death with lower levels of educational attainment. The same monotonic relationship held with adjustments for age, race, sex, cardiovascular risk factors, and health behaviors. The unadjusted hazard ratio for those without a high school education in comparison with college graduates was 2.89 (95% CI =2.64-3.18). Although adjustment for income, health behaviors, and cardiovascular risk factors attenuated the relationship, the same consistent pattern was observed after adjustment. The relationship between educational attainment and longevity was similar for black and white participants. The monotonic relationship between educational attainment and longevity was observed for all age groups, except for those aged 85 years or more.
Conclusions: Educational attainment is a significant predictor of longevity. Other factors including age, race, income, health behaviors, and cardiovascular risk factors only partially explain the relationship. Published by Elsevier Inc.
C1 [Kaplan, Robert M.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Howard, Virginia J.] Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL USA.
[Safford, Monika M.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
[Howard, George] Univ Alabama Birmingham, Dept Biostat, Birmingham, AL 35294 USA.
RP Kaplan, RM (reprint author), Agcy Healthcare Res & Qual, 540 Gaither Rd, Rockville, MD 20850 USA.
EM rmkaplan@ucla.edu
FU National Institute of Neurological Disorders and Stroke, National
Institutes of Health (NIH) [U01 NS041588]; American Reinvestment and
Recovery Act supplement; Department of Health and Human Services
FX This research was supported by a cooperative agreement U01 NS041588 from
the National Institute of Neurological Disorders and Stroke, National
Institutes of Health (NIH), Department of Health and Human Services, and
also an American Reinvestment and Recovery Act supplement. The content
is solely the responsibility of the authors and does not necessarily
represent the official views and positions of the National Institute of
Neurological Disorders and Stroke or the National Institutes of Health.
NR 25
TC 2
Z9 3
U1 3
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
EI 1873-2585
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD MAY
PY 2015
VL 25
IS 5
BP 323
EP 328
DI 10.1016/j.annepidem.2015.01.017
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CG5XI
UT WOS:000353368800003
PM 25791026
ER
PT J
AU Alonso, A
Huang, XM
Mosley, TH
Heiss, G
Chen, HL
AF Alonso, Alvaro
Huang, Xuemei
Mosley, Thomas H.
Heiss, Gerardo
Chen, Honglei
TI Heart Rate Variability and the Risk of Parkinson Disease: The
Atherosclerosis Risk in Communities Study
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID PATHOPHYSIOLOGY; DEGENERATION
AB ObjectiveAutonomic dysfunction frequently occurs in the context of Parkinson disease (PD) and may precede onset of motor symptoms. Limited data exist on the prospective association of heart rate variability (HRV), a marker of autonomic function, with PD risk.
MethodsWe included 12,162 participants of the Atherosclerosis Risk in Communities study, a community-based cohort, without a diagnosis of PD at baseline (1987-1989) and with available HRV data (mean age=54 years, 57% women). A 2-minute electrocardiogram was used to measure HRV. Incident PD was identified through 2008 from multiple sources, and adjudicated. Multivariable Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of PD by quartiles of HRV measurements.
ResultsDuring a mean follow-up of 18 years, we identified 78 incident PD cases. Lower values of the root mean square of successive differences in normal-to-normal R-R intervals (rMSSD) and standard deviation of normal-to-normal R-R intervals (SDNN), markers of parasympathetic activity and total variability, respectively, were associated with higher PD risk during follow-up. In multivariate models, the HR (95% CI) of PD in the bottom quartiles of rMSSD and SDNN compared to the top quartiles were 2.1 (1.0-4.3) and 2.9 (1.4-6.1), respectively. Other measures of cardiac autonomic function, including mean R-R interval and frequency-domain measurements, were not associated with PD risk.
InterpretationIn this prospective cohort, decreased HRV was associated with an increased risk of PD. Assessment of cardiac autonomic function may help identify individuals at risk for PD. Ann Neurol 2015;77:877-883
C1 [Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
[Huang, Xuemei] Penn State Milton S Hershey Med Ctr, Dept Neurol, Hershey, PA USA.
[Huang, Xuemei] Penn State Milton S Hershey Med Ctr, Dept Neurosurg, Hershey, PA USA.
[Huang, Xuemei] Penn State Milton S Hershey Med Ctr, Dept Pharmacol, Hershey, PA USA.
[Huang, Xuemei] Penn State Milton S Hershey Med Ctr, Dept Radiol, Hershey, PA USA.
[Huang, Xuemei] Penn State Milton S Hershey Med Ctr, Dept Kinesiol, Hershey, PA USA.
[Huang, Xuemei] Penn State Milton S Hershey Med Ctr, Hershey Brain Anal Res Lab Neurodegenerat Disorde, Hershey, PA USA.
[Mosley, Thomas H.] Univ Mississippi, Med Ctr, Div Geriatr Med, Jackson, MS 39216 USA.
[Heiss, Gerardo] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Chen, Honglei] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Alonso, A (reprint author), Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, 1300 S 2nd St,Suite 300, Minneapolis, MN 55454 USA.
EM alonso@umn.edu
RI Alonso, Alvaro/A-4917-2010;
OI Alonso, Alvaro/0000-0002-2225-8323; Chen, Honglei/0000-0003-3446-7779
FU NIH National Heart, Lung, and Blood Institute [HHSN268201100005C,
HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
HHSN268201100009C, HHSN268201100010C, HHSN268201100011C,
HHSN268201100012C]; NIH, the National Institute of Environmental Health
Sciences [Z01-ES101986]; NIH, National Institute of Neurological
Diseases and Stroke [NS060722, NS082151]; National Institute of
Environmental Health Sciences [ES019672]; National Institute of Aging
[AG21491]
FX The Atherosclerosis Risk in Communities study has been carried out as a
collaborative study supported by NIH National Heart, Lung, and Blood
Institute contracts (HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C). This study
was supported in part by the Intramural Program of the NIH, the National
Institute of Environmental Health Sciences (Z01-ES101986). X.H. is
currently supported by NIH, National Institute of Neurological Diseases
and Stroke (NS060722 and NS082151), and National Institute of
Environmental Health Sciences (ES019672), as well as a K23 award
(National Institute of Aging (AG21491)) at the conception of this work.
NR 22
TC 11
Z9 11
U1 0
U2 6
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 MAY
PY 2015
VL 77
IS 5
BP 877
EP 883
DI 10.1002/ana.24393
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CG4EF
UT WOS:000353235400015
PM 25707861
ER
PT J
AU Wang, T
Cunningham, A
Dokun, AO
Hazarika, S
Houston, K
Chen, L
Lye, RJ
Spolski, R
Leonard, WJ
Annex, BH
AF Wang, Tao
Cunningham, Alexis
Dokun, Ayotunde O.
Hazarika, Surovi
Houston, Kevin
Chen, Lingdan
Lye, R. John
Spolski, Rosanne
Leonard, Warren J.
Annex, Brian H.
TI Loss of Interleukin-21 Receptor Activation in Hypoxic Endothelial Cells
Impairs Perfusion Recovery After Hindlimb Ischemia
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE peripheral arterial diseases; receptors, interleukin 21
ID PERIPHERAL ARTERIAL-DISEASE; CRITICAL LIMB ISCHEMIA; INTERMITTENT
CLAUDICATION; THERAPEUTIC ANGIOGENESIS; GROWTH-FACTOR; PATHWAY; BIOLOGY;
CANCER; MICE; INTERVENTION
AB Objective-Surgical hindlimb ischemia (HLI) in mice has become a valuable preclinical model to study peripheral arterial disease. We previously identified that the different phenotypic outcomes after HLI across inbred mouse strains is related to a region on the short arm of mouse chromosome 7. The gene coding the interleukin-21 receptor (IL-21R) lies at the peak of association in this region.
Approach and Results-With quantitative real-time polymerase chain reaction, we found that a mouse strain with a greater ability to upregulate IL-21R after HLI had better perfusion recovery than a strain with no upregulation after HLI. Immunofluorescent staining of ischemic hindlimb tissue showed IL-21R expression on endothelial cells (ECs) from C57BL/6 mice. An EC-enriched fraction isolated from ischemic hindlimb muscle showed higher Il-21R levels than an EC-enriched fraction from nonischemic limbs. In vitro, human umbilical vein ECs showed elevated IL-21R expression after hypoxia and serum starvation. Under these conditions, IL-21 treatment increased cell viability, decreased cell apoptosis, and augmented tube formation. In vivo, either knockout Il21r or blocking IL-21 signaling by treating with IL-21R-Fc (fusion protein that blocks IL-21 binding to its receptor) in C57BL/6 mice resulted in less perfusion recovery after HLI. Both in vitro and in vivo modulation of the IL-21/IL-21R axis under hypoxic conditions resulted in increased signal transducer and activator of transcription 3 phosphorylation and a subsequent increase in the B-cell lymphoma leukemia-2/BCL-2-associated X protein ratio.
Conclusion-Our data indicate that IL-21R upregulation and ligand activation in hypoxic ECs may help perfusion recovery by limiting/preventing apoptosis and favoring cell survival and angiogenesis through the signal transducer and activator of transcription 3 pathway.
C1 [Wang, Tao; Cunningham, Alexis; Dokun, Ayotunde O.; Hazarika, Surovi; Houston, Kevin; Chen, Lingdan; Lye, R. John; Annex, Brian H.] Univ Virginia, Robert M Berne Cardiovasc Res Ctr, Charlottesville, VA USA.
[Hazarika, Surovi; Annex, Brian H.] Univ Virginia, Dept Med, Div Cardiovasc Med, Charlottesville, VA USA.
[Spolski, Rosanne; Leonard, Warren J.] NHLBI, Lab Mol Immunol, Bethesda, MD 20892 USA.
[Spolski, Rosanne; Leonard, Warren J.] NHLBI, Ctr Immunol, NIH, Bethesda, MD 20892 USA.
RP Annex, BH (reprint author), Div Cardiovasc Med, POB 800158, Charlottesville, VA 22908 USA.
EM annex@virginia.edu
RI WANG, TAO/B-1888-2013
FU Division of Intramural Research, National Heart, Lung, and Blood
Institute, National Institutes of Health; National Institutes of Health
[RO1HL16455, RO1HL121635]
FX W.J. Leonard and R. Spolski are supported by the Division of Intramural
Research, National Heart, Lung, and Blood Institute, National Institutes
of Health. B.H. Annex is supported by the National Institutes of Health
RO1HL16455 and RO1HL121635.
NR 41
TC 5
Z9 6
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1079-5642
EI 1524-4636
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD MAY
PY 2015
VL 35
IS 5
BP 1218
EP 1225
DI 10.1161/ATVBAHA.115.305476
PG 8
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CG5MF
UT WOS:000353335300020
PM 25838422
ER
PT J
AU Gebreab, SY
Riestra, P
Khan, RJ
Xu, RH
Musani, SK
Tekola-yele, F
Correa, A
Wilson, JG
Rotimi, CN
Davis, SK
AF Gebreab, Samson Y.
Riestra, Pia
Khan, Rumana J.
Xu, Ruihua
Musani, Solomon K.
Tekola-yele, Fasil
Correa, Adolfo
Wilson, James G.
Rotimi, Charles N.
Davis, Sharon K.
TI Genetic Ancestry Is Associated With Measures of Subclinical
Atherosclerosis in African Americans The Jackson Heart Study
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE African Americans; cardiovascular disease; epidemiology; genetic
ancestry; subclinical atherosclerosis
ID PERIPHERAL ARTERIAL-DISEASE; INTIMA-MEDIA THICKNESS; CARDIOVASCULAR
RISK-FACTORS; BEAM COMPUTED-TOMOGRAPHY; ETHNIC-DIFFERENCES; CORONARY
CALCIFICATION; CAROTID ATHEROSCLEROSIS; POPULATION; PREVALENCE;
ADMIXTURE
AB Objective-To determine whether genetic ancestry was associated with subclinical atherosclerosis measures after adjustment for traditional cardiovascular disease risk factors, inflammatory marker, socioeconomic status, and psychosocial factors in a large admixed African American population.
Approach and Results-Participants were drawn from the Jackson Heart Study. Participant's percent of European ancestry (PEA) was estimated based on 1747 genetic markers using HAPMIX. Association of PEA with peripheral arterial disease and common carotid intima-media thickness were investigated among 2168 participants and with coronary artery calcification >0 and abdominal aortic calcification >0 among 1139 participants. The associations were evaluated using multivariable regression models. Our results showed that a 1 SD increase in PEA was associated with a lower peripheral arterial disease prevalence after adjusting for age and sex (prevalence ratio=0.90 [95% CI, 0.82-0.99]; P=0.036). Adjustments for traditional cardiovascular disease risk factors, socioeconomic status, and psychosocial factors attenuated this association (prevalence ratio=0.91 [0.82-1.00]; P=0.046). There was also a nonlinear association between PEA and coronary artery calcification and abdominal aortic calcification. The lowest PEA was associated with a lower coronary artery calcification (prevalence ratio=0.75 [0.58-0.96]; P=0.022) and a lower abdominal aortic calcification [prevalence ratio=0.80 [0.67-0.96]; P=0.016) compared with the reference group (10th-90th percentile) after adjusting for traditional cardiovascular disease risk factors, inflammatory marker, socioeconomic status, and psychosocial factors. However, we found no significant association between PEA and common carotid intima-media thickness.
Conclusions-Overall, our findings indicate that genetic ancestry was associated with subclinical atherosclerosis, suggesting unmeasured risk factors and interactions with genetic factors might contribute to the distribution of subclinical atherosclerosis among African Americans.
C1 [Gebreab, Samson Y.; Riestra, Pia; Khan, Rumana J.; Xu, Ruihua; Tekola-yele, Fasil; Rotimi, Charles N.; Davis, Sharon K.] NHGRI, Metab Cardiovasc & Inflammatory Dis Genom Branch, Bethesda, MD 20892 USA.
[Musani, Solomon K.; Correa, Adolfo] Univ Mississippi, Med Ctr, Jackson Heart Study, Jackson, MS USA.
[Wilson, James G.] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS USA.
RP Gebreab, SY (reprint author), NHGRI, Metab Cardiovasc & Inflammatory Dis Genom Branch, 10 Ctr Dr,MSC 1644, Bethesda, MD 20892 USA.
EM samson.gebreab@nih.gov
OI Tekola-Ayele, Fasil/0000-0003-4194-9370
FU National Human Genomics Institute, National Institutes of Health;
National Heart, Lung, and Blood Institute [HHSN268201300046C,
HHSN268201300047C, HHSN268201300048C, HHSN268201 300049C,
HHSN268201300050C]; National Institute on Minority Health and Health
Disparities
FX This research is supported by Intermural Program of National Human
Genomics Institute, National Institutes of Health. The Jackson Heart
Study is supported by contracts HHSN268201300046C, HHSN268201300047C,
HHSN268201300048C, HHSN268201 300049C, and HHSN268201300050C from the
National Heart, Lung, and Blood Institute and the National Institute on
Minority Health and Health Disparities.
NR 43
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1079-5642
EI 1524-4636
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD MAY
PY 2015
VL 35
IS 5
BP 1271
EP 1278
DI 10.1161/ATVBAHA.114.304855
PG 8
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CG5MF
UT WOS:000353335300026
PM 25745061
ER
PT J
AU Long, MT
Wang, N
Larson, MG
Mitchell, GF
Palmisano, J
Vasan, RS
Hoffmann, U
Speliotes, EK
Vita, JA
Benjamin, EJ
Fox, CS
Hamburg, NM
AF Long, Michelle T.
Wang, Na
Larson, Martin G.
Mitchell, Gary F.
Palmisano, Joseph
Vasan, Ramachandran S.
Hoffmann, Udo
Speliotes, Elizabeth K.
Vita, Joseph A.
Benjamin, Emelia J.
Fox, Caroline S.
Hamburg, Naomi M.
TI Nonalcoholic Fatty Liver Disease and Vascular Function Cross-Sectional
Analysis in the Framingham Heart Study
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE multidetector computed tomography; obesity; risk factors; vascular
endothelium
ID INCREASED ARTERIAL STIFFNESS; FLOW-MEDIATED DILATION; ENDOTHELIAL
DYSFUNCTION; CARDIOVASCULAR-DISEASE; HEPATIC STEATOSIS; RISK-FACTORS;
SYSTEMIC INFLAMMATION; METABOLIC SYNDROME; NATURAL-HISTORY;
ATHEROSCLEROSIS
AB Objective-Patients with nonalcoholic fatty liver disease (NAFLD) have an increased risk of cardiovascular disease; however, it is not known whether NAFLD contributes to cardiovascular disease independent of established risk factors. We examined the association between NAFLD and vascular function.
Approach and Results-We conducted a cross-sectional study of 2284 Framingham Heart Study participants without overt cardiovascular disease who had liver fat attenuation measured on computed tomography and who had measurements of vascular function and covariates. We evaluated the association between NAFLD and vascular function using multivariable partial correlations adjusting for age, sex, cohort, smoking, diabetes mellitus, hyperlipidemia, hypertension, body mass index, and visceral adipose tissue. The prevalence of NAFLD in our sample (mean age, 52 +/- 12 years; 51.4% women) was 15.3%. In age-, sex-, and cohort-adjusted analyses, greater liver fat was modestly associated with lower flow-mediated dilation (r=-0.05; P=0.02), lower peripheral arterial tonometry ratio (r=-0.20; P<0.0001), higher carotid-femoral pulse wave velocity (r=0.13; P<0.0001), and higher mean arterial pressure (r=0.11; P<0.0001). In multivariable-adjusted models, NAFLD remained associated with higher mean arterial pressure (r=0.06; P=0.005) and lower peripheral arterial tonometry ratio (r=-0.12; P<0.0001). The association between NAFLD and peripheral arterial tonometry ratio persisted after further adjustment for body mass index and visceral adipose tissue.
Conclusions-For multiple measures of vascular function, the relationship with NAFLD appeared largely determined by shared cardiometabolic risk factors. The persistent relationship with reduced peripheral arterial tonometry response beyond established risk factors suggests that NAFLD may contribute to microvascular dysfunction.
C1 [Long, Michelle T.] Boston Univ, Sch Med, Boston Med Ctr, Div Gastroenterol, Boston, MA 02118 USA.
[Vasan, Ramachandran S.] Boston Univ, Sch Med, Sect Prevent Med, Dept Med, Boston, MA 02118 USA.
[Vasan, Ramachandran S.; Vita, Joseph A.; Hamburg, Naomi M.] Boston Univ, Sch Med, Evans Dept Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA.
[Vasan, Ramachandran S.; Vita, Joseph A.; Hamburg, Naomi M.] Boston Univ, Sch Med, Cardiol Sect, Boston, MA 02118 USA.
[Long, Michelle T.; Larson, Martin G.; Vasan, Ramachandran S.; Benjamin, Emelia J.; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02118 USA.
[Mitchell, Gary F.] Cardiovasc Engn Inc, Norwood, MA USA.
[Wang, Na; Palmisano, Joseph] Boston Univ, Sch Publ Hlth, Data Coordinating Ctr, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Hoffmann, Udo; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Speliotes, Elizabeth K.] Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Speliotes, Elizabeth K.] Univ Michigan, Dept Computat Med & Bioinformat, Ann Arbor, MI 48109 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol Hypertens & Metab, Boston, MA 02115 USA.
RP Hamburg, NM (reprint author), Boston Univ, Sch Med, Whitaker Cardiovasc Inst, 88 East Newton St,Suite C-818, Boston, MA 02118 USA.
EM nhamburg@bu.edu
OI Long, Michelle/0000-0001-6131-3981; Ramachandran,
Vasan/0000-0001-7357-5970; Benjamin, Emelia/0000-0003-4076-2336
FU Boston University School of Medicine; National Heart, Lung, and Blood
Institute's Framingham Heart Study [N01-HC-25195]; Division of
Intramural Research of the National Heart, Lung, and Blood Institute;
National Institutes of Health (NIH) [R01 AG047645-1, HL102299,
1R01HL60040, HL70100, HL076784, HL077447, HL107385]; Donald W. Reynolds
Foundation; Boston University Clinical and Translational Science
Institute [UL1-TR000157]; NIH [K23DK08145]; Doris Duke Foundation;
Central Society for Clinical Research; Department of Internal Medicine
at University of Michigan; BSSP program at University of Michigan
FX This work was supported by the Boston University School of Medicine and
the National Heart, Lung, and Blood Institute's Framingham Heart Study
(contract N01-HC-25195) and the Division of Intramural Research of the
National Heart, Lung, and Blood Institute. The project was supported by
National Institutes of Health (NIH) grants R01 AG047645-1, HL102299,
1R01HL60040; HL70100, HL076784, HL077447, HL107385 and the Donald W.
Reynolds Foundation. Dr Long was supported in part by the Boston
University Clinical and Translational Science Institute (grant
UL1-TR000157). E. K. Speliotes was supported by NIH K23DK08145, The
Doris Duke Foundation, Central Society for Clinical Research, and the
Department of Internal Medicine and BSSP program at University of
Michigan.
NR 40
TC 13
Z9 13
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1079-5642
EI 1524-4636
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD MAY
PY 2015
VL 35
IS 5
BP 1284
EP 1291
DI 10.1161/ATVBAHA.114.305200
PG 8
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CG5MF
UT WOS:000353335300028
PM 25745056
ER
PT J
AU Golin, J
Ambudkar, SV
AF Golin, John
Ambudkar, Suresh V.
TI The multidrug transporter Pdr5 on the 25th anniversary of its discovery:
an important model for the study of asymmetric ABC transporters
SO BIOCHEMICAL JOURNAL
LA English
DT Review
DE asymmetric ABC transporter; molecular diode; Pdr5
ID NUCLEOTIDE-BINDING DOMAINS; INWARD-FACING CONFORMATION; MULTIPLE-DRUG
RESISTANCE; P-GLYCOPROTEIN; SACCHAROMYCES-CEREVISIAE; CANDIDA-ALBICANS;
ATP HYDROLYSIS; CASSETTE TRANSPORTER; CRYSTAL-STRUCTURE; MOLECULAR DIODE
AB Asymmetric ABC (ATP-binding cassette) transporters make up a significant proportion of this important superfamily of integral membrane proteins. These proteins contain one canonical (catalytic) ATP-binding site and a second atypical site with little enzymatic capability. The baker's yeast (Saccharomyces cerevisiae) Pdr5 multidrug transporter is the founding member of the Pdr subfamily of asymmetric ABC transporters, which exist only in fungi and slime moulds. Because these organisms are of considerable medical and agricultural significance, Pdr5 has been studied extensively, as has its medically important homologue Cdr1 from Candida albicans. Genetic and biochemical analyses of Pdr5 have contributed important observations that are likely to be applicable to mammalian asymmetric ABC multidrug transporter proteins, including the basis of transporter promiscuity, the function of the non-catalytic deviant ATP-binding site, the most complete description of an in vivo transmission interface, and the recent discovery that Pdr5 is a molecular diode (one-way gate). In the present review, we discuss the observations made with Pdr5 and compare them with findings from clinically important asymmetric ABC transporters, such as CFTR (cystic fibrosis transmembrane conductance regulator), Cdr1 and Tap1/Tap2.
C1 [Golin, John] Catholic Univ Amer, Dept Biol, Washington, DC 20064 USA.
[Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Golin, J (reprint author), Catholic Univ Amer, Dept Biol, Washington, DC 20064 USA.
EM golin@cua.edu
FU National Science Foundation [MCB1048838]; National Institutes of Health
[GM077211]; National Institutes of Health National Cancer Institute's
Center for Cancer Research
FX The work described in this review that was performed in the Golin
laboratory was supported by National Science Foundation [grant number
MCB1048838] and National Institutes of Health [grant number GM077211].
The many years of funding from these agencies is deeply appreciated.
S.V.A. was supported by the Intramural Research Program of the National
Institutes of Health National Cancer Institute's Center for Cancer
Research.
NR 71
TC 4
Z9 4
U1 3
U2 23
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0264-6021
EI 1470-8728
J9 BIOCHEM J
JI Biochem. J.
PD MAY 1
PY 2015
VL 467
BP 353
EP 363
DI 10.1042/BJ20150042
PN 3
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CG3YX
UT WOS:000353217200001
PM 25886173
ER
PT J
AU Nussinov, R
Jang, H
Tsai, CJ
AF Nussinov, Ruth
Jang, Hyunbum
Tsai, Chung-Jung
TI Oligomerization and nanocluster organization render specificity
SO BIOLOGICAL REVIEWS
LA English
DT Review
DE nanoclusters; signalling; oligomerization; structure; Ras;
microclusters; cytoskeleton; allostery; conformational states;
allosteric; scaffolding; co-localization
ID RAS MEMBRANE ORIENTATION; SIGNAL-TRANSDUCTION; H-RAS; RECEPTOR
SUPERFAMILY; SPATIAL-ORGANIZATION; KINASE DOMAIN; LIPID-BILAYER; K-RAS;
N-RAS; CELL
AB Nanoclusters are anchored to membranes, either within them or in the cytoplasm latched onto the cytoskeleton, whose reorganization can regulate their activity. Nanoclusters have been viewed in terms of cooperativity and activation; here we perceive nanocluster organization from a conformational standpoint. This leads us to suggest that while single molecules encode activity, nanoclusters induce specificity, and that this is their main evolutionary aim. Distinct, isoform-specific nanocluster organization can drive the preferred effector (and ligand) interactions and thereby designate signalling pathways. The absence of detailed structural information across the nanocluster, due to size and dynamics, hinders an in-depth grasp of its mechanistic features; however, available data already capture some of the principles and their functional 'raison d'etre'. Collectively, clustering lends stability and reduces the likelihood of proteolytic cleavage; it also increases the effective local concentration and enables efficient cooperative activation. However, clustering does not determine the ability of the single molecule to function. Drugs targeting nanoclusters can attenuate activity by hampering cooperativity; however, this may not perturb activation and signalling, which originate from the molecules themselves, and as such, are likely to endure. What then is the major role of nanoclustering? Assuming that single molecules evolved first, with a subsequent increase in cellular complexity and emergence of highly similar isoform variants, evolution faced the threat of signalling promiscuity. We reason that this potential risk was thwarted by oligomerization and clustering; clustering confers higher specificity, and a concomitant extra layer of cellular control. In our Ras example, signalling will be more accurate as a dimer than as a monomer, where its isomer specificity could be compromised.
C1 [Nussinov, Ruth; Jang, Hyunbum; Tsai, Chung-Jung] NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Inst Mol Med, Sackler Sch Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab, Frederick, MD 21702 USA.
EM NussinoR@helix.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Intramural Research Program of the NIH, National
Cancer Institute, Center for Cancer Research
FX This project has been funded in whole or in part with Federal funds from
the National Cancer Institute, National Institutes of Health, under
contract number HHSN261200800001E. The content of this publication does
not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
This research was supported (in part) by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research.
NR 86
TC 9
Z9 9
U1 1
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-7931
EI 1469-185X
J9 BIOL REV
JI Biol. Rev.
PD MAY
PY 2015
VL 90
IS 2
BP 587
EP 598
DI 10.1111/brv.12124
PG 12
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA CF8NL
UT WOS:000352818700012
PM 24917483
ER
PT J
AU Kale, SS
Jedhe, GS
Meshram, SN
Santra, MK
Hamel, E
Sanjayan, GJ
AF Kale, Sangram S.
Jedhe, Ganesh S.
Meshram, Sachin N.
Santra, Manas K.
Hamel, Ernest
Sanjayan, Gangadhar J.
TI Novel hybrid nocodazole analogues as tubulin polymerization inhibitors
and their antiproliferative activity
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Tubulin binding; Nocodazole; Colchicine; Anticancer
ID COMBRETASTATIN A-4; COLCHICINE; AGENTS
AB We describe the design, synthesis and SAR profiling of a series of novel combretastatin-nocodazole conjugates as potential anticancer agents. The thiophene ring in the nocodazole moiety was replaced by a substituted phenyl ring from the combretastatin moiety to design novel hybrid analogues. The hydroxyl group at the ortho position in compounds 2, 3 and 4 was used as the conformationally locking tool by anticipated six-membered hydrogen bonding. The bioactivity profiles of all compounds as tubulin polymerization inhibitors and as antiproliferative agents against the A-549 human lung cancer cell line were investigated Compounds 1 and 4 showed mu M IC50 values in both assays. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Kale, Sangram S.; Jedhe, Ganesh S.; Sanjayan, Gangadhar J.] CSIR Natl Chem Lab, Div Organ Chem, Pune 411008, Maharashtra, India.
[Meshram, Sachin N.; Santra, Manas K.] Natl Ctr Cell Sci, Pune 411007, Maharashtra, India.
[Hamel, Ernest] NCI, Screening Technol Branch, Dev Therapeut Program,NIH, Div Canc Treatment & Diag,Frederick Natl Lab Canc, Frederick, MD 21702 USA.
RP Hamel, E (reprint author), NCI, Screening Technol Branch, Dev Therapeut Program,NIH, Div Canc Treatment & Diag,Frederick Natl Lab Canc, Frederick, MD 21702 USA.
EM gj.sanjayan@ncl.res.in
RI Jedhe, Ganesh/M-9019-2015
OI Jedhe, Ganesh/0000-0001-7404-3677
FU CSIR, New Delhi; CSIR-Biodiversity programme [BSC-0120]
FX S.S.K. and G.S.J. are thankful to CSIR, New Delhi, for a research
fellowship. G.J.S. thanks CSIR-Biodiversity programme (BSC-0120) for
funding this project.
NR 20
TC 5
Z9 5
U1 1
U2 16
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 MAY 1
PY 2015
VL 25
IS 9
BP 1982
EP 1985
DI 10.1016/j.bmcl.2015.03.019
PG 4
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA CG3UL
UT WOS:000353205000033
PM 25817588
ER
PT J
AU Jukic, AM
AF Jukic, A. M.
TI The impact of systematic errors on gestational age estimation
SO BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY
LA English
DT Editorial Material
C1 NIEHS, Durham, NC 27713 USA.
RP Jukic, AM (reprint author), NIEHS, Durham, NC 27713 USA.
FU Intramural NIH HHS
NR 4
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1470-0328
EI 1471-0528
J9 BJOG-INT J OBSTET GY
JI BJOG
PD MAY
PY 2015
VL 122
IS 6
BP 842
EP 842
DI 10.1111/1471-0528.13169
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA CG4ZV
UT WOS:000353299000013
PM 25377244
ER
PT J
AU Hong, CW
Rais-Bahrami, S
Walton-Diaz, A
Shakir, N
Su, D
George, AK
Merino, MJ
Turkbey, B
Choyke, PL
Wood, BJ
Pinto, PA
AF Hong, Cheng W.
Rais-Bahrami, Soroush
Walton-Diaz, Annerleim
Shakir, Nabeel
Su, Daniel
George, Arvin K.
Merino, Maria J.
Turkbey, Baris
Choyke, Peter L.
Wood, Bradford J.
Pinto, Peter A.
TI Comparison of magnetic resonance imaging and ultrasound (MRI-US)
fusion-guided prostate biopsies obtained from axial and sagittal
approaches
SO BJU INTERNATIONAL
LA English
DT Article
DE multiparametric MRI; fusion biopsy; prostate cancer
ID CANCER-DETECTION; GLAND VOLUME; DIAGNOSIS; GUIDANCE
AB Objective
To compare cancer detection rates and concordance between magnetic resonance imaging and ultrasound (MRI-US) fusion-guided prostate biopsy cores obtained from axial and sagittal approaches.
Patients and Methods
Institutional records of MRI-US fusion-guided biopsy were reviewed. Detection rates for all cancers, Gleason >= 3 + 4 cancers, and Gleason >= 4 + 3 cancers were computed. Agreement between axial and sagittal cores for cancer detection, and frequency where one was upgraded the other was computed on a per-target and per-patient basis.
Results
In all, 893 encounters from 791 patients that underwent MRI-US fusion-guided biopsy in 2007-2013 were reviewed, yielding 4688 biopsy cores from 2344 targets for analysis. The mean age and PSA level at each encounter was 61.8 years and 9.7 ng/mL (median 6.45 ng/mL). Detection rates for all cancers, >= 3 + 4 cancers, and >= 4 + 3 cancers were 25.9%, 17.2%, and 8.1% for axial cores, and 26.1%, 17.6%, and 8.6% for sagittal cores. Per-target agreement was 88.6%, 93.0%, and 96.5%, respectively. On a per-target basis, the rates at which one core upgraded or detected a cancer missed on the other were 8.3% and 8.6% for axial and sagittal cores, respectively. Even with the inclusion of systematic biopsies, omission of axial or sagittal cores would have resulted in missed detection or under-characterisation of cancer in 4.7% or 5.2% of patients, respectively.
Conclusion
Cancer detection rates, Gleason scores, and core involvement from axial and sagittal cores are similar, but significant cancer may be missed if only one core is obtained for each target. Discordance between axial and sagittal cores is greatest in intermediate-risk scenarios, where obtaining multiple cores may improve tissue characterisation.
C1 [Hong, Cheng W.; Wood, Bradford J.; Pinto, Peter A.] NCI, NIH, Ctr Intervent Oncol, Ctr Clin, Bethesda, MD 20892 USA.
[Rais-Bahrami, Soroush; Walton-Diaz, Annerleim; Shakir, Nabeel; Su, Daniel; George, Arvin K.; Pinto, Peter A.] NCI, NIH, Urol Oncol Branch, Bethesda, MD 20892 USA.
[Merino, Maria J.] NCI, NIH, Pathol Lab, Bethesda, MD 20892 USA.
[Turkbey, Baris; Choyke, Peter L.] NCI, NIH, Mol Imaging Program, Bethesda, MD 20892 USA.
RP Pinto, PA (reprint author), NCI, NIH, Urol Oncol Branch, CRC, 10 Ctr Dr,MSC 1210,Bldg 10,Rm 2W-5940, Bethesda, MD 20892 USA.
EM pintop@mail.nih.gov
OI Rais-Bahrami, Soroush/0000-0001-9466-9925
FU National Cancer Institute; Center for Interventional Oncology; NIH
FX NIH and Philips Healthcare have a cooperative research and development
agreement. NIH and Philips Healthcare share intellectual property in the
field. This work was supported by the National Cancer Institute, the
Center for Interventional Oncology, and the Intramural Research Program
of the NIH. This research was made possible through the NIH Medical
Research Scholars Program, a public-private partnership supported
jointly by the NIH and generous contributions to the Foundation for the
NIH from Pfizer Inc., The Leona M and Harry B. Helmsley Charitable
Trust, and the Howard Hughes Medical Institute, as well as other private
donors. For a complete list, please visit the Foundation website at (
http://www.fnih.org/work/programs-development/medical-research-scholars-
program).
NR 29
TC 22
Z9 22
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-4096
EI 1464-410X
J9 BJU INT
JI BJU Int.
PD MAY
PY 2015
VL 115
IS 5
BP 772
EP 779
DI 10.1111/bju.12871
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA CG4CT
UT WOS:000353230500018
PM 25045781
ER
PT J
AU Yamazaki, F
Moller, M
Fu, C
Clokie, SJ
Zykovich, A
Coon, SL
Klein, DC
Rath, MF
AF Yamazaki, Fumiyoshi
Moller, Morten
Fu, Cong
Clokie, Samuel J.
Zykovich, Artem
Coon, Steven L.
Klein, David C.
Rath, Martin F.
TI The Lhx9 homeobox gene controls pineal gland development and prevents
postnatal hydrocephalus
SO Brain Structure & Function
LA English
DT Article
DE Lhx9; Homeobox gene; Brain development; Pineal gland; Hydrocephalus
ID RNA-SEQ; SUBCOMMISSURAL ORGAN; EXPRESSION PATTERNS; S-ANTIGEN; RETINA;
RAT; EYE; FOREBRAIN; ADULT; BRAIN
AB Lhx9 is a member of the LIM homeobox gene family. It is expressed during mammalian embryogenesis in the brain including the pineal gland. Deletion of Lhx9 results in sterility due to failure of gonadal development. The current study was initiated to investigate Lhx9 biology in the pineal gland. Lhx9 is highly expressed in the developing pineal gland of the rat with transcript abundance peaking early in development; transcript levels decrease postnatally to nearly undetectable levels in the adult, a temporal pattern that is generally similar to that reported for Lhx9 expression in other brain regions. Studies with C57BL/6J Lhx9 (-/-) mutant mice revealed marked alterations in brain and pineal development. Specifically, the superficial pineal gland is hypoplastic, being reduced to a small cluster of pinealocytes surrounded by meningeal and vascular tissue. The deep pineal gland and the pineal stalk are also reduced in size. Although the brains of neonatal Lhx9 (-/-) mutant mice appear normal, severe hydrocephalus develops in about 70 % of the Lhx9 (-/-) mice at 5-8 weeks of age; these observations are the first to document that deletion of Lhx9 results in hydrocephalus and as such indicate that Lhx9 contributes to the maintenance of normal brain structure. Whereas hydrocephalus is absent in neonatal Lhx9 (-/-)mutant mice, the neonatal pineal gland in these animals is hypoplastic. Accordingly, it appears that Lhx9 is essential for early development of the mammalian pineal gland and that this effect is not secondary to hydrocephalus.
C1 [Yamazaki, Fumiyoshi; Fu, Cong; Clokie, Samuel J.; Zykovich, Artem; Coon, Steven L.; Klein, David C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Neuroendocrinol, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
[Moller, Morten; Rath, Martin F.] Univ Copenhagen, Fac Hlth & Med Sci, Dept Neurosci & Pharmacol, Copenhagen, Denmark.
RP Klein, DC (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Neuroendocrinol, Program Dev Endocrinol & Genet, NIH, 49 Convent Dr,Room 6A82, Bethesda, MD 20892 USA.
EM kleind@mail.nih.gov
OI Clokie, Samuel/0000-0002-0025-3652; Rath, Martin/0000-0002-4047-6324
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development of the National Institutes of Health; Lundbeck Foundation
[R108-A10301]
FX This study was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development of the National Institutes of Health and the Lundbeck
Foundation (grant number R108-A10301). We are grateful to Dr. Heiner
Westphal's (NICHD) gift of the Lhx9-/- mice and for the
support provided by Dr. Yangu Zhao (NICHD) in establishing a colony of
Lhx9 mutant mice. We recognize the full value of the willingness of Dr.
Joseph D. Dougherty, Washington University, to share unpublished
observations. The expertise and dedication of Daniel Abebe as applied to
the expansion and management of the mutant Lhx9 colony in our
facilities, which was essential to the success of this investigation, is
greatly valued. The authors declare no competing financial interests.
NR 45
TC 2
Z9 2
U1 0
U2 6
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2653
EI 1863-2661
J9 BRAIN STRUCT FUNCT
JI Brain Struct. Funct.
PD MAY
PY 2015
VL 220
IS 3
BP 1497
EP 1509
DI 10.1007/s00429-014-0740-x
PG 13
WC Anatomy & Morphology; Neurosciences
SC Anatomy & Morphology; Neurosciences & Neurology
GA CG7VX
UT WOS:000353515200018
PM 24647753
ER
PT J
AU Acs, P
Bauer, PO
Mayer, B
Bera, T
Macallister, R
Mezey, E
Pastan, I
AF Acs, Peter
Bauer, Peter O.
Mayer, Balazs
Bera, Tapan
Macallister, Rhonda
Mezey, Eva
Pastan, Ira
TI A novel form of ciliopathy underlies hyperphagia and obesity in Ankrd26
knockout mice
SO Brain Structure & Function
LA English
DT Article
DE Obesity; Neuronal cilia; Leptin receptor; ANKRD26; Melanocortin
receptor; Feeding behavior; Paraventricular nucleus; Arcuate nucleus;
CRH; Ciliary body proteins
ID BARDET-BIEDL-SYNDROME; CORTICOTROPIN-RELEASING HORMONE;
MELANOCYTE-STIMULATING HORMONE; PROTEIN-COUPLED-RECEPTORS; FOOD-INTAKE;
MELANOCORTIN-4 RECEPTOR; PARAVENTRICULAR NUCLEUS; CILIARY ROOTLET;
LEPTIN RECEPTOR; GENE-EXPRESSION
AB Human ciliopathies are genetic disorders caused by mutations in genes responsible for the formation and function of primary cilia. Some are associated with hyperphagia and obesity (e.g., Bardet-Biedl Syndrome, Alstrom Syndrome), but the mechanisms underlying these problems are not fully understood. The human gene ANKRD26 is located on 10p12, a locus that is associated with some forms of hereditary obesity. Previously, we reported that disruption of this gene causes hyperphagia, obesity and gigantism in mice. In the present study, we looked for the mechanisms that induce hyperphagia in the Ankrd26-/- mice and found defects in primary cilia in regions of the central nervous system that control appetite and energy homeostasis.
C1 [Acs, Peter; Bera, Tapan; Pastan, Ira] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Bauer, Peter O.] NCI, Neurooncol Branch, NINDS, NIH, Bethesda, MD 20892 USA.
[Mayer, Balazs; Mezey, Eva] Natl Inst Dent & Craniofacial Res, Adult Stem Cell Unit, CSDB, NIH, Bethesda, MD 20892 USA.
[Macallister, Rhonda] NCI, NIH, Bethesda, MD 20892 USA.
RP Mezey, E (reprint author), Natl Inst Dent & Craniofacial Res, Adult Stem Cell Unit, CSDB, NIH, Bethesda, MD 20892 USA.
EM mezeye@mail.nih.gov
FU Division of Intramural Research program of NCI; NIDCR in the Intramural
Research Program, NIH, DHHS
FX The authors want to acknowledge the invaluable help of Miklos Palkovits,
Harold Gainer and Michael Brownstein for their continuous support and
advice as well as help with editing the manuscript. We also thank Prof.
Ronald DeKloet (Leiden University) for his expert advice regarding
studies on adrenal function. This research was supported by the Division
of Intramural Research program of NCI and NIDCR in the Intramural
Research Program, NIH, DHHS. We dedicate this work to the memory of
Wylie Vale, who discovered CRF and who was an outstanding scientist; a
wonderful human being and a good friend.
NR 60
TC 4
Z9 4
U1 3
U2 12
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2653
EI 1863-2661
J9 BRAIN STRUCT FUNCT
JI Brain Struct. Funct.
PD MAY
PY 2015
VL 220
IS 3
BP 1511
EP 1528
DI 10.1007/s00429-014-0741-9
PG 18
WC Anatomy & Morphology; Neurosciences
SC Anatomy & Morphology; Neurosciences & Neurology
GA CG7VX
UT WOS:000353515200019
PM 24633808
ER
PT J
AU Enewold, L
Geiger, AM
Zujewski, J
Harlan, LC
AF Enewold, Lindsey
Geiger, Ann M.
Zujewski, JoAnne
Harlan, Linda C.
TI Oncotype Dx assay and breast cancer in the United States: usage and
concordance with chemotherapy
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Female; Breast cancer; Tumor markers, biological/*genetics;
Chemotherapy, adjuvant; SEER
ID GENE-EXPRESSION; RECURRENCE; RISK; TAMOXIFEN; UTILITY; WOMEN
AB The 21-gene recurrence score (RS) assay (Oncotype DX (TM)) predicts the likelihood of breast cancer recurrence and chemotherapy responsiveness. The aims of this study were to describe temporal trends in assay usage, to investigate factors associated with the receipt of the assay and to determine how the assay is associated with treatment decisions. Random samples of stage I-II female breast cancer patients diagnosed in 2004, 2005 and 2010 as reported to the National Cancer Institute's Surveillance Epidemiology and End Results program were included. Among women diagnosed in 2010 with estrogen receptor positive (ER+), lymph node-negative (LN-) tumors, factors associated with receipt of the assay were identified and the likelihood of chemotherapy by RS was estimated. Assay usage increased over time (ER+/LN-:8.0-27.0 %, p < 0.01; ER+/LN+: 2.0-15.7 %, p = 0.09; ER-: 0.2-1.7 %, p < 0.01) from 2005 to 2010. Receipt of the assay was associated with younger age, lower area income and tumor characteristics. Among women in the low (RS < 18) and high risk (RS > 30) categories, 3.3 and 95.9 % received chemotherapy, respectively. Within the intermediate risk group the receipt of chemotherapy varied: 12.8 % (RS: 18-19), 35.0 % (RS: 20-23) and 84.0 % (RS: 24-30). During the study years, assay usage increased among women for whom the assay is and is not guideline recommended. Factors such as insurance and race/ethnicity do not appear to be associated with the receipt of the assay. The RS, as determined broadly via three categories and within the intermediate risk group, does appear to influence chemotherapy decisions.
C1 [Enewold, Lindsey; Geiger, Ann M.; Zujewski, JoAnne; Harlan, Linda C.] NCI, Appl Res Program, Bethesda, MD 20892 USA.
RP Enewold, L (reprint author), NCI, Appl Res Program, 9609 Med Ctr Dr,Room 3E506, Bethesda, MD 20892 USA.
EM lindsey.enewold@nih.gov
FU National Cancer Institute [HHSN261201000024C, HHSN261201000025C,
HHSN261201000032C, HHSN261201000027C, HHSN261201000 026C,
HHSN261201000140C, HHSN261201000037C, HHSN26120 1000033C,
HHSN261201000034C, HHSN261201000035C, HHSN 261201000029C,
HHSN261201000031C, HHSN261201000028C, HHSN261201000030C]
FX This work was supported by National Cancer Institute contracts:
HHSN261201000024C; HHSN261201000025C, HHSN261201000032C,
HHSN261201000027C, HHSN261201000 026C, HHSN261201000140C,
HHSN261201000037C, HHSN26120 1000033C, HHSN261201000034C,
HHSN261201000035C, HHSN 261201000029C, HHSN261201000031C,
HHSN261201000028C, and HHSN261201000030C. The authors have disclosed
that they have no financial interests, arrangements, affiliations, or
commercial interests with the manufacturers of any products discussed in
this article or their competitors. This article was produced by
employees of the US government as part of their official duties and, as
such, is in the public domain in the United States of America. The
content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Cancer
Institute or the National Institutes of Health.
NR 31
TC 8
Z9 8
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
EI 1573-7217
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD MAY
PY 2015
VL 151
IS 1
BP 149
EP 156
DI 10.1007/s10549-015-3366-7
PG 8
WC Oncology
SC Oncology
GA CG5RU
UT WOS:000353352500014
PM 25859924
ER
PT J
AU Bonano, JS
Banks, ML
Kolanos, R
Sakloth, F
Barnier, ML
Glennon, RA
Cozzi, NV
Partilla, JS
Baumann, MH
Negus, SS
AF Bonano, J. S.
Banks, M. L.
Kolanos, R.
Sakloth, F.
Barnier, M. L.
Glennon, R. A.
Cozzi, N. V.
Partilla, J. S.
Baumann, M. H.
Negus, S. S.
TI Quantitative structure-activity relationship analysis of the
pharmacology of para-substituted methcathinone analogues
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
ID INTRACRANIAL SELF-STIMULATION; BATH SALTS; SYNTHETIC CATHINONES;
MONOAMINE TRANSPORTERS; ARRIVE GUIDELINES; ABUSE; DRUGS; MEPHEDRONE;
BRAIN; 4-METHYLMETHCATHINONE
AB Background and PurposeMethcathinone (MCAT) is a potent monoamine releaser and parent compound to emerging drugs of abuse including mephedrone (4-CH3 MCAT), the para-methyl analogue of MCAT. This study examined quantitative structure-activity relationships (QSAR) for MCAT and six para-substituted MCAT analogues on (a) in vitro potency to promote monoamine release via dopamine and serotonin transporters (DAT and SERT, respectively), and (b) in vivo modulation of intracranial self-stimulation (ICSS), a behavioural procedure used to evaluate abuse potential. Neurochemical and behavioural effects were correlated with steric (E-s), electronic (sigma(p)) and lipophilic ((p)) parameters of the para substituents.
Experimental ApproachFor neurochemical studies, drug effects on monoamine release through DAT and SERT were evaluated in rat brain synaptosomes. For behavioural studies, drug effects were tested in male Sprague-Dawley rats implanted with electrodes targeting the medial forebrain bundle and trained to lever-press for electrical brain stimulation.
Key ResultsMCAT and all six para-substituted analogues increased monoamine release via DAT and SERT and dose- and time-dependently modulated ICSS. In vitro selectivity for DAT versus SERT correlated with in vivo efficacy to produce abuse-related ICSS facilitation. In addition, the E-s values of the para substituents correlated with both selectivity for DAT versus SERT and magnitude of ICSS facilitation.
Conclusions and ImplicationsSelectivity for DAT versus SERTin vitro is a key determinant of abuse-related ICSS facilitation by these MCAT analogues, and steric aspects of the para substituent of the MCAT scaffold (indicated by E-s) are key determinants of this selectivity.
C1 [Bonano, J. S.; Banks, M. L.; Negus, S. S.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA USA.
[Kolanos, R.; Sakloth, F.; Barnier, M. L.; Glennon, R. A.] Virginia Commonwealth Univ, Dept Med Chem, Richmond, VA 23298 USA.
[Cozzi, N. V.] Univ Wisconsin, Dept Cell & Regenerat Biol, Madison, WI USA.
[Partilla, J. S.; Baumann, M. H.] NIDA, Designer Drug Res Unit, Intramural Res Program, NIH, Baltimore, MD USA.
RP Bonano, JS (reprint author), 410 North 12th St,Smith Bldg Room 760B,POB 980613, Richmond, VA 23298 USA.
EM bonanojs@vcu.edu
RI Banks, Matthew/K-4429-2014
OI Banks, Matthew/0000-0003-4949-5246
FU National Institutes of Health [F30DA037649, R01DA033930, R21DA017675];
National Institute on Drug Abuse, Intramural Research Programme
[DA000523-07]
FX This research was supported by the National Institutes of Health grants
F30DA037649 (J. S. B.), R01DA033930 (R. A. G. and S. S. N.), R21DA017675
(N. V. C.) and by the National Institute on Drug Abuse, Intramural
Research Programme Grant DA000523-07 (M. H. B.).
NR 46
TC 10
Z9 10
U1 2
U2 17
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 MAY
PY 2015
VL 172
IS 10
BP 2433
EP 2444
DI 10.1111/bph.13030
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CG6EQ
UT WOS:000353389600002
PM 25438806
ER
PT J
AU Altimari, JM
Hockey, SC
Boshoff, HI
Sajid, A
Henderson, LC
AF Altimari, Jarrad M.
Hockey, Samantha C.
Boshoff, Helena I.
Sajid, Andaleeb
Henderson, Luke C.
TI Novel 1,4-Substituted-1,2,3-Triazoles as Antitubercular Agents
SO CHEMMEDCHEM
LA English
DT Article
DE antibacterial agents; azides; click chemistry; Mycobacterium
tuberculosis; triazoles; tuberculosis
ID ANDROGEN RECEPTOR ANTAGONISTS; MYCOBACTERIUM-TUBERCULOSIS; POTENT
INHIBITORS; CLICK CHEMISTRY; BIOLOGICAL EVALUATION; TRIAZOLE
DERIVATIVES; DRUG DEVELOPMENT; DESIGN; 1,2,3-TRIAZOLES; INHA
AB Tuberculosis (TB) remains a pressing unmet medical need, particularly with the emergence of multidrug-resistant and extensively drug-resistant tuberculosis. Here, a series of 1,4-substituted-1,2,3-triazoles have been synthesized and evaluated as potential antitubercular agents. These compounds were assembled via click chemistry in high crude purity and in moderate to high yield. Of the compounds tested, 12 compounds showed promising antitubercular activity with six possessing minimum inhibitory concentration (MIC) values <10gmL(-1), and total selectivity for Mycobacterium tuberculosis (Mtb) growth inhibition. A second set of 21 compounds bearing variations on ringC were synthesized and evaluated. This second library gave an additional six compounds displaying MIC values 10gmL(-1) and total selectivity for Mtb growth inhibition. These compounds serve as an excellent starting point for further development of antitubercular therapies.
C1 [Altimari, Jarrad M.; Hockey, Samantha C.; Henderson, Luke C.] Deakin Univ, Inst Frontier Mat, Geelong, Vic 3216, Australia.
[Altimari, Jarrad M.; Hockey, Samantha C.; Henderson, Luke C.] Deakin Univ, Strateg Res Ctr Chem & Biotechnol, Geelong, Vic 3216, Australia.
[Boshoff, Helena I.; Sajid, Andaleeb] NIAID, TB Res Sect, LCID, NIH, Bethesda, MD 20892 USA.
RP Altimari, JM (reprint author), Deakin Univ, Inst Frontier Mat, Waurn Ponds Campus, Geelong, Vic 3216, Australia.
EM luke.henderson@deakin.edu.au
OI Sajid, Andaleeb/0000-0001-6248-4985; Henderson, Luke/0000-0002-4244-2056
FU Deakin University (Australia) Strategic Research Center for Chemistry
and Biotechnology; School of Life and Environmental Sciences; Faculty of
Science Engineering and Built Environment; National Institute of Allergy
and Infectious Diseases (NIAID), US National Institutes of Health (NIH);
Australian government
FX The authors thank the Deakin University (Australia) Strategic Research
Center for Chemistry and Biotechnology, the School of Life and
Environmental Sciences and the Faculty of Science Engineering and Built
Environment for financial support of this project. This work was
supported in part by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases (NIAID), US National
Institutes of Health (NIH). J.A. gratefully acknowledges the Australian
government for the Australian Postgraduate Award (APA) scholarship.
NR 30
TC 3
Z9 3
U1 3
U2 22
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA BOSCHSTRASSE 12, D-69469 WEINHEIM, GERMANY
SN 1860-7179
EI 1860-7187
J9 CHEMMEDCHEM
JI ChemMedChem
PD MAY
PY 2015
VL 10
IS 5
BP 787
EP 791
DI 10.1002/cmdc.201500051
PG 5
WC Chemistry, Medicinal; Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CG7HM
UT WOS:000353473600002
PM 25788466
ER
PT J
AU Kotlyar, DS
Lewis, JD
Beaugerie, L
Tierney, A
Brensinger, CM
Gisbert, JP
Loftus, EV
Peyrin-Biroulet, L
Blonski, WC
Van Domselaar, M
Chaparro, M
Sandilya, S
Bewtra, M
Beigel, F
Biancone, L
Lichtenstein, GR
AF Kotlyar, David S.
Lewis, James D.
Beaugerie, Laurent
Tierney, Ann
Brensinger, Colleen M.
Gisbert, Javier P.
Loftus, Edward V., Jr.
Peyrin-Biroulet, Laurent
Blonski, Wojciech C.
Van Domselaar, Manuel
Chaparro, Maria
Sandilya, Sandipani
Bewtra, Meenakshi
Beigel, Florian
Biancone, Livia
Lichtenstein, Gary R.
TI Risk of Lymphoma in Patients With Inflammatory Bowel Disease Treated
With Azathioprine and 6-Mercaptopurine: A Meta-analysis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Cancer Risk; Ulcerative Colitis; Crohn's Disease; Treatment
ID NON-HODGKINS-LYMPHOMA; SINGLE-CENTER COHORT; T-CELL LYMPHOMA;
RHEUMATOID-ARTHRITIS; ULCERATIVE-COLITIS; CROHNS-DISEASE; CANCER-RISK;
TRANSPLANTATION; ASSOCIATION; THIOPURINES
AB BACKGROUND & AIMS: Thiopurine therapy for inflammatory bowel disease (IBD) has been associated with increased risk for lymphoma. We estimated the relative risk of lymphoma in patients with IBD exposed to thiopurines and compared relative risk values derived from population-based studies with those from referral center-based studies. We investigated whether active use increased risk compared with past use, and whether sex, age, or duration of use affects risk of lymphoma.
METHODS: We searched MEDLINE, EMBASE, and Cochrane databases, as well as conference abstracts and international publications, for the terms "6-MP and lymphoma," "6-mercaptopurine and lymphoma," "thiopurines and lymphoma," "azathioprine and cancer and IBD," "azathioprine and malignancy and IBD," "azathioprine and lymphoma," and "lymphoproliferative and thiopurines." Pooled standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were estimated. The deviance statistic from Poisson models was used to calculate heterogeneity.
RESULTS: Eighteen studies (among 4383 citations) met our inclusion criteria. Overall, the SIR for lymphoma was 4.92 (95% CI, 3.10-7.78), ranging from 2.80 (95% CI, 1.82-4.32) in 8 population studies to 9.24 (95% CI, 4.69-18.2) in 10 referral studies. Population studies demonstrated an increased risk among current users (SIR = 5.71; 95% CI, 3.72-10.1) but not former users (SIR = 1.42; 95% CI, 0.86-2.34). Level of risk became significant after 1 year of exposure. Men have a greater risk than women (relative risk = 1.98; P<.05); both sexes were at increased risk for lymphoma (SIR for men = 4.50; 95% CI = 3.71-5.40 and SIR for women = 2.29; 95% CI = 1.69-3.05). Patients younger than 30 years had the highest relative risk (SIR = 6.99; 95% CI, 2.99-16.4); younger men had the highest risk. The absolute risk was highest in patients older than 50 years (1: 354 cases per patient-year, with a relative risk of 4.78).
CONCLUSIONS: Compared with studies from referral centers, population-based studies of IBD patients show a lower but significantly increased risk of lymphoma among patients taking thiopurines. The increased risk does not appear to persist after discontinuation of therapy. Patients over 50 have the highest absolute risk of lymphoma per year on thiopurines, while men under 35 may also be a high risk group. More study is needed to precisely understand groups highest at risk. The risks of lymphoma and potential benefits of therapy should be considered for all patients with IBD.
C1 [Kotlyar, David S.] NCI, Med Oncol Serv, NIH, Bethesda, MD 20892 USA.
[Kotlyar, David S.; Lewis, James D.; Blonski, Wojciech C.; Bewtra, Meenakshi; Lichtenstein, Gary R.] Univ Penn, Perelman Sch Med, Dept Med, Div Gastroenterol, Philadelphia, PA 19174 USA.
[Lewis, James D.; Tierney, Ann; Brensinger, Colleen M.; Bewtra, Meenakshi] Univ Penn, Perelman Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19174 USA.
[Beaugerie, Laurent] Univ Paris 06, Hop St Antoine, AP HP, Gastroenterol, Paris, France.
[Gisbert, Javier P.; Chaparro, Maria] La Princesa Univ Hosp, Inst Invest Sanitaria Princesa IP, Gastroenterol, Madrid, Spain.
[Gisbert, Javier P.; Chaparro, Maria] CIBERehd, Madrid, Spain.
[Loftus, Edward V., Jr.] Mayo Clin, Dept Med, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Peyrin-Biroulet, Laurent] Nancy Univ Hosp, INSERM, Dept Gastroenterol, U954, Nancy, France.
[Blonski, Wojciech C.] SUNY Upstate, Dept Med, Binghamton, NY USA.
[Blonski, Wojciech C.] Med Univ, Wroclaw, Poland.
[Van Domselaar, Manuel] Hosp Ramon & Cajal, Gastroenterol, E-28034 Madrid, Spain.
[Sandilya, Sandipani] Montefiore Med Ctr, Dept Med, Div Nephrol, Bronx, NY 10467 USA.
[Beigel, Florian] Univ Munich Grosshadern, Dept Med, Munich, Germany.
[Biancone, Livia] Univ Roma Tor Vergata, Dept Med, GI Unit, Rome, Italy.
RP Lichtenstein, GR (reprint author), Univ Penn, Perelman Sch Med, Perelman Bldg,7-South Room 753,3400 Civ Ctr Blvd, Philadelphia, PA 19174 USA.
EM grl@mail.med.upenn.edu
RI Loftus, Edward/E-8304-2011;
OI Gisbert, Javier Perez/0000-0003-2090-3445
FU Intramural Research Program at the National Institutes of Health -
United States Government
FX David S. Kotlyar is supported by the Intramural Research Program at the
National Institutes of Health, funded by the United States Government.
NR 43
TC 40
Z9 40
U1 2
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD MAY
PY 2015
VL 13
IS 5
BP 847
EP U541
DI 10.1016/j.cgh.2014.05.015
PG 16
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CG1XN
UT WOS:000353069000012
PM 24879926
ER
PT J
AU Kesarwala, AH
Ko, CJ
Ning, H
Xanthopoulos, E
Haglund, KE
O'Meara, WP
Simone, CB
Rengan, R
AF Kesarwala, Aparna H.
Ko, Christine J.
Ning, Holly
Xanthopoulos, Eric
Haglund, Karl E.
O'Meara, William P.
Simone, Charles B., II
Rengan, Ramesh
TI Intensity-Modulated Proton Therapy for Elective Nodal Irradiation and
Involved-Field Radiation in the Definitive Treatment of Locally Advanced
Non-Small-Cell Lung Cancer: A Dosimetric Study
SO CLINICAL LUNG CANCER
LA English
DT Article
DE ENI; IFRT; IMPT; NSCLC; Radiation therapy
ID POSITRON-EMISSION-TOMOGRAPHY; DOSE-ESCALATION; PHASE-III; RADIOTHERAPY;
TRIAL; TUMOR; CHEMOTHERAPY; CONCURRENT; VOLUME; NSCLC
AB In this study we examined the feasibility of intensity-modulated proton therapy for elective nodal irradiation in locally-advanced non-small-cell lung cancer. Proton involved-field and elective nodal irradiation improved target coverage and dosimetry to all evaluated organs at risk compared with photon involved-field radiation therapy, demonstrating potential for enhancement of the therapeutic window.
Background: Photon involved-field (IF) radiation therapy (IFRT), the standard for locally advanced (LA) non-small cell lung cancer (NSCLC), results in favorable outcomes without increased isolated nodal failures, perhaps from scattered dose to elective nodal stations. Because of the high conformality of intensity-modulated proton therapy (IMPT), proton IFRT could increase nodal failures. We investigated the feasibility of IMPT for elective nodal irradiation (ENI) in LA-NSCLC. Patients and Methods: IMPT IFRT plans were generated to the same total dose of 66.6-72 Gy received by 20 LA-NSCLC patients treated with photon IFRT. IMPT ENI plans were generated to 46 cobalt Gray equivalent (CGE) to elective nodal planning treatment volumes (PTV) plus 24 CGE to IF-PTVs. Results: Proton IFRT and ENI improved the IF-PTV percentage of volume receiving 95% of the prescribed dose (D95) by 4% (P < .01) compared with photon IFRT. All evaluated dosimetric parameters improved significantly with both proton plans. The lung percentage of volume receiving 20 Gy/CGE (V20) and mean lung dose decreased 18% (P < .01) and 36% (P < .01), respectively, with proton IFRT, and 11% (P = .03) and 26% (P < .01) with ENI. The mean esophagus dose decreased 16% with IFRT and 12% with ENI; heart V25 decreased 63% with both (all P < .01). Conclusion: This study demonstrates the feasibility of IMPT for LA-NSCLC ENI. Potential decreased toxicity indicates that IMPT could allow ENI while maintaining a favorable therapeutic ratio compared with photon IFRT.
C1 [Kesarwala, Aparna H.; Ning, Holly; Haglund, Karl E.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Ko, Christine J.; O'Meara, William P.] Walter Reed Natl Mil Med Ctr, Dept Radiol, Div Radiat Oncol, Bethesda, MD USA.
[Xanthopoulos, Eric; Simone, Charles B., II] Univ Penn, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
[Rengan, Ramesh] Univ Washington, Dept Radiat Oncol, Seattle, WA 98195 USA.
RP Kesarwala, AH (reprint author), NCI, Radiat Oncol Branch, NIH, Bldg 10 CRC,Room B2-3500, Bethesda, MD 20892 USA.
EM aparna.kesarwala@nih.gov
FU Intramural Research Program, Center for Cancer Research, National Cancer
Institute, National Institutes of Health
FX This research was supported in part by the Intramural Research Program,
Center for Cancer Research, National Cancer Institute, National
Institutes of Health.
NR 46
TC 5
Z9 5
U1 2
U2 4
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1525-7304
EI 1938-0690
J9 CLIN LUNG CANCER
JI Clin. Lung Cancer
PD MAY
PY 2015
VL 16
IS 3
BP 237
EP 244
DI 10.1016/j.cllc.2014.12.001
PG 8
WC Oncology
SC Oncology
GA CG5RC
UT WOS:000353350500010
PM 25604729
ER
PT J
AU Simon, R
Blumenthal, GM
Rothenberg, ML
Sommer, J
Roberts, SA
Armstrong, DK
LaVange, LM
Pazdur, R
AF Simon, R.
Blumenthal, G. M.
Rothenberg, M. L.
Sommer, J.
Roberts, S. A.
Armstrong, D. K.
LaVange, L. M.
Pazdur, R.
TI The Role of Nonrandomized Trials in the Evaluation of Oncology Drugs
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID ADMINISTRATION APPROVAL; CLINICAL-TRIALS; END-POINTS; PHASE-II;
SURVIVAL; CANCER; THERAPIES
AB Although randomized trials provide the most reliable evidence of a drug's safety and efficacy, there are situations where randomized trials are not possible or ethical. In this article we discuss when and how single-arm trials can be used to support full approval of oncology drugs. These include situations in which an unprecedented effect on tumor response is observed in a setting of high unmet medical need, clinical trial patients have been well characterized, enabling a target population to be clearly defined, experience exists in a sufficient number of patients to allow adequate assessment of the risk:benefit relationship, and a proper historical context can be provided for analysis. We also discuss how response rates might be considered predictive of long-term outcomes or clinically meaningful in and of themselves in certain contexts.
C1 [Simon, R.] NCI, Bethesda, MD 20892 USA.
[Blumenthal, G. M.; LaVange, L. M.] US FDA, Silver Spring, MD USA.
[Rothenberg, M. L.; Pazdur, R.] Pfizer Inc, New York, NY USA.
[Sommer, J.] Chordoma Fdn, Durham, NC USA.
[Roberts, S. A.] Friends Canc Res, Washington, DC 20036 USA.
[Armstrong, D. K.] Johns Hopkins Kimmel Canc Ctr, Baltimore, MD USA.
RP Roberts, SA (reprint author), Friends Canc Res, Washington, DC 20036 USA.
EM sroberts@focr.org
FU American Society of Clinical Oncology; Susan G. Komen for the Cure
FX This article was developed as an issue brief for the seventh annual
Friends of Cancer Research-Brookings Institution Conference on Clinical
Cancer Research, held on November 21, 2014. The authors thank the
American Society of Clinical Oncology and Susan G. Komen for the Cure
for their generous financial support of this conference. We also thank
staff at Friends of Cancer Research and the Brookings Institution for
their expertise and logistical support, in particular Marina Kozak at
Friends of Cancer Research for thoughtful input on the article.
NR 20
TC 11
Z9 11
U1 1
U2 5
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 MAY
PY 2015
VL 97
IS 5
BP 502
EP 507
DI 10.1002/cpt.86
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CG4DT
UT WOS:000353233900011
PM 25676488
ER
PT J
AU Kemp, TJ
Castro, FA
Gao, YT
Hildesheim, A
Nogueira, L
Wang, BS
Sun, L
Shelton, G
Pfeiffer, RM
Hsing, AW
Pinto, LA
Koshiol, J
AF Kemp, Troy J.
Castro, Felipe A.
Gao, Yu-Tang
Hildesheim, Allan
Nogueira, Leticia
Wang, Bing-Sheng
Sun, Lu
Shelton, Gloriana
Pfeiffer, Ruth M.
Hsing, Ann W.
Pinto, Ligia A.
Koshiol, Jill
TI Application of multiplex arrays for cytokine and chemokine profiling of
bile
SO CYTOKINE
LA English
DT Article
DE Bile; Gallstones; Cytokines; Chemokines
ID BILIARY-TRACT CANCER; GALLBLADDER CANCER; LIVER; RISK; INFLAMMATION;
GALLSTONES; MARKERS; IMMUNE; SERUM; CHOLANGITIS
AB Background: Gallbladder disease is highly related to inflammation, but the inflammatory processes are not well understood. Bile provides a direct substrate in assessing the local inflammatory response that develops in the gallbladder. To assess the reproducibility of measuring inflammatory markers in bile, we designed a methods study of 69 multiplexed immune-related markers measured in bile obtained from gallstone patients.
Methods: To evaluate assay performance, a total of 18 bile samples were tested twice within the same plate for each analyte, and the 18 bile samples were tested on two different days for each analyte. We used the following performance parameters: detectability, coefficient of variation (CV), intraclass correlation coefficient (ICC), and percent agreement (concordance among replicate measures above and below detection limit). Furthermore, we examined the association of analyte levels with gallstone characteristics such as type, numbers, and size.
Results: All but 3 analytes (Stem Cell Factor, SCF; Thrombopoietin, TPO; sIL-1RI) were detectable in bile. 52 of 69 (75.4%) analytes had detectable levels for at least 50% of the subjects tested. The within-plate CVs were <= 25% for 53 of 66 (80.3%) detectable analytes, and across-plate CVs were <= 25% for 32 of 66 (48.5%) detectable analytes. Moreover, 64 of 66 (97.0%) analytes had ICC values of at least 0.8. Lastly, the percent agreement was high between replicates for all of the analytes (median; within plate, 97.2%; across plate, 97.2%). In exploratory analyses, we assessed analyte levels by gallstone characteristics and found that levels for several analytes decreased with increasing size of the largest gallstone per patient.
Conclusions: Our data suggest that multiplex assays can be used to reliably measure cytokines and chemokines in bile. In addition, gallstone size was inversely related to the levels of select analytes, which may aid in identifying critical pathways and mechanisms associated with the pathogenesis of gallbladder diseases. (c) 2015 Elsevier Ltd. All rights reserved.
C1 [Kemp, Troy J.; Shelton, Gloriana; Pinto, Ligia A.] Leidos Biomed Res Inc, HPV Immunol Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Castro, Felipe A.; Hildesheim, Allan; Nogueira, Leticia; Koshiol, Jill] NCI, Infect & Immunoepidemiol Branch, DCEG, NIH, Bethesda, MD 20892 USA.
[Gao, Yu-Tang] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
[Wang, Bing-Sheng] Fudan Univ, Sch Med, Zhongshan Hosp, Dept Gen Surg, Shanghai 200433, Peoples R China.
[Sun, Lu] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
[Pfeiffer, Ruth M.] NCI, Biostat Branch, DCEG, NIH, Bethesda, MD 20892 USA.
[Hsing, Ann W.] Canc Prevent Inst Calif, Fremont, CA USA.
[Hsing, Ann W.] Stanford Canc Inst, Palo Alto, CA USA.
[Hsing, Ann W.] Stanford Univ, Sch Med, Dept Hlth Res & Policy, Palo Alto, CA 94304 USA.
RP Pinto, LA (reprint author), Leidos Biomed Res Inc, HPV Immunol Lab, Frederick Natl Lab Canc Res, Bldg 469,Room 111, Frederick, MD 21702 USA.
EM kemptj@mail.nih.gov; felipe.castro@nih.gov; ytgao@vip.sina.com;
hilde-sha@exchange.nih.gov; leticia.nogueira@nih.gov;
wang.bingsheng@zs-hospital.sh.cn; sunlush@126.com;
Glori-ana.Shelton@nih.gov; pfeiffer@mail.nih.gov; Ann.Hsing@cpic.org;
pintol@mail.nih.gov; koshiolj@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; National Institutes of Health, National Cancer
Institute, Division of Cancer Epidemiology and Genetics, USA
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract No. HHSN261200800001E. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
Furthermore, The Intramural Research Program of the National Institutes
of Health, National Cancer Institute, Division of Cancer Epidemiology
and Genetics, USA provided funds for the current study.
NR 30
TC 2
Z9 2
U1 0
U2 1
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 MAY
PY 2015
VL 73
IS 1
BP 84
EP 90
DI 10.1016/j.cyto.2015.01.033
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA CG2AY
UT WOS:000353078500013
PM 25743242
ER
PT J
AU Granzin, M
Soltenborn, S
Muller, S
Kollet, J
Berg, M
Cerwenka, A
Childs, RW
Huppert, V
AF Granzin, Markus
Soltenborn, Stephanie
Mueller, Sabine
Kollet, Jutta
Berg, Maria
Cerwenka, Adelheid
Childs, Richard W.
Huppert, Volker
TI Fully automated expansion and activation of clinical-grade natural
killer cells for adoptive immunotherapy
SO CYTOTHERAPY
LA English
DT Article
DE automation; CliniMACS Prodigy; immunotherapy; natural killer cells; NK
cell expansion; NK cell therapy
ID GENE-EXPRESSION ANALYSIS; ACUTE MYELOID-LEUKEMIA; EX-VIVO EXPANSION;
LARGE-SCALE; NK CELLS; CANCER-PATIENTS; PHASE-II; T-CELLS; THERAPY;
TRANSPLANTATION
AB Background aims. Ex vivo expansion of natural killer (NK) cells is a strategy to produce large numbers of these effector cells for immunotherapy. However, the transfer of bench-top expansion protocols to clinically applicable methods is challenging for NK cell based therapy because of regulatory aspects and scale-up issues. Therefore, we developed an automated, large-scale NK cell expansion process. Methods. Enriched NK cells were expanded with interleukin-2 and irradiated clinical-grade Epstein-Barr virus transformed lymphoblastoid feeder cells with the use of an automated system in comparison to manual expansion, and the cells were investigated for their functionality, phenotype and gene expression. Results. Automated expansion resulted in a mean 850-fold expansion of NK cells by day 14, Yielding 1.3 (+/- 0.9) x 10(9) activated NK cells. Automatically and manually produced NK cells were comparable in target cell lysis, degranulation and production of interferon-gamma and tumor necrosis factor-alpha and had similar high levels of antibody-dependent cellular cytotoxicity against rituximab-treated leukemic cells. NK cells after automated or manual expansion showed similar gene expression and marker profiles. However, expanded NK cells differed significantly from primary NK cells including upregulation of the functional relevant molecules TRAIL and FasL and NK cell activating receptors NKp30, NKG2D and DNAM-1. Neither automatically nor manually expanded NK cells showed reduced telomere length indicative of a conserved proliferative potential. Conclusions. We established an automated method to expand high numbers of clinical-grade NK cells with properties similar to their manually produced counterparts. This automated process represents a highly efficient tool to standardize NK cell processing for therapeutic applications.
C1 [Granzin, Markus; Soltenborn, Stephanie; Mueller, Sabine; Kollet, Jutta; Huppert, Volker] Miltenyi Biotec GmbH, D-51429 Bergisch Gladbach, Germany.
[Granzin, Markus; Cerwenka, Adelheid] German Canc Res Ctr, Innate Immun Grp, Heidelberg, Germany.
[Berg, Maria; Childs, Richard W.] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
RP Granzin, M (reprint author), Miltenyi Biotec GmbH, D-51429 Bergisch Gladbach, Germany.
EM markusgr@miltenyibiotec.de; volker@miltenyibiotec.de
RI Granzin, Markus/M-9226-2015
OI Granzin, Markus/0000-0002-4774-1469
NR 40
TC 8
Z9 8
U1 2
U2 15
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1465-3249
EI 1477-2566
J9 CYTOTHERAPY
JI Cytotherapy
PD MAY
PY 2015
VL 17
IS 5
BP 621
EP 632
DI 10.1016/j.jcyt.2015.03.611
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology; Hematology; Medicine, Research & Experimental
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
& Experimental Medicine
GA CG5VQ
UT WOS:000353364400011
PM 25881519
ER
PT J
AU Tseng, WL
Guyer, AE
Briggs-Gowan, MJ
Axelson, D
Birmaher, B
Egger, HL
Helm, J
Stowe, Z
Towbin, KA
Wakschlag, LS
Leibenluft, E
Brotman, MA
AF Tseng, Wan-Ling
Guyer, Amanda E.
Briggs-Gowan, Margaret J.
Axelson, David
Birmaher, Boris
Egger, Helen L.
Helm, Jonathan
Stowe, Zachary
Towbin, Kenneth A.
Wakschlag, Lauren S.
Leibenluft, Ellen
Brotman, Melissa A.
TI BEHAVIOR AND EMOTION MODULATION DEFICITS IN PRESCHOOLERS AT RISK FOR
BIPOLAR DISORDER
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE children; bipolar disorder; familial risk; irritability; inflexible
behavior; diagnostic observation
ID MANIC-DEPRESSIVE PARENT; SCHEDULE DB-DOS; DIAGNOSTIC-OBSERVATION;
PSYCHIATRIC-DISORDERS; DISRUPTIVE-BEHAVIOR; YOUNG-CHILDREN; DIMENSIONAL
PSYCHOPATHOLOGY; CHILDHOOD PSYCHOPATHOLOGY; OBSERVATIONAL ASSESSMENT;
FAMILY-HISTORY
AB BackgroundBipolar disorder (BD) is highly familial, but studies have yet to examine preschoolers at risk for BD using standardized, developmentally appropriate clinical assessment tools. We used such methods to test whether preschoolers at familial risk for BD have more observed difficulty modulating emotions and behaviors than do low-risk preschoolers. Identification of emotional and behavioral difficulties in at-risk preschoolers is crucial for developing new approaches for early intervention and prevention of BD.
MethodsUsing the standardized disruptive behavior diagnostic observation schedule (DB-DOS) protocol for preschoolers, we compared 23 preschoolers (M-age: 4.53 0.73 years; 18 males) with a first-degree relative with BD to 21 preschoolers (M-age: 4.65 0.84 years; 11 males) without a family history of BD. We characterized psychopathology in this sample using the Preschool Aged Psychiatric Assessment and behavioral and emotional problems using the Child Behavior Checklist.
ResultsHigh-risk preschoolers demonstrated significantly more intense, pervasive, and clinically concerning problems in anger modulation and behavior dysregulation on the DB-DOS than the low-risk group. High-risk relative to low-risk preschoolers, were also more likely to have maternal-reported anxiety and oppositional defiant disorders and internalizing and externalizing problems.
ConclusionsClinically concerning problems in anger modulation and behavior regulation, measured during standardized laboratory observation, differentiate preschoolers at high familial risk for BD from those at low risk. Investigation in a large longitudinal sample is critical for replication and for determining whether these observed behavioral differences can be reliably used as prodromal indicators of mood disorders. (C) 2015 Wiley Periodicals, Inc.
C1 [Tseng, Wan-Ling; Towbin, Kenneth A.; Leibenluft, Ellen; Brotman, Melissa A.] NIMH, Emot & Dev Branch, NIH, US Dept HHS, Bethesda, MD USA.
[Guyer, Amanda E.] Univ Calif Davis, Dept Human Ecol, Ctr Mind & Brain, Davis, CA 95616 USA.
[Briggs-Gowan, Margaret J.] Univ Connecticut, Ctr Hlth, Dept Psychiat, Farmington, CT 06032 USA.
[Axelson, David] Nationwide Childrens Hosp, Columbus, OH USA.
[Axelson, David] Ohio State Univ, Sch Med, Columbus, OH 43210 USA.
[Birmaher, Boris] Univ Pittsburgh, Western Psychiat Inst, Pittsburgh, PA USA.
[Egger, Helen L.] Duke Univ, Dept Psychiat, Durham, NC 27706 USA.
[Helm, Jonathan] Univ Calif Davis, Ctr Mind & Brain, Davis, CA 95616 USA.
[Stowe, Zachary] Univ Arkansas, Dept Psychiat, Fayetteville, AR 72701 USA.
[Wakschlag, Lauren S.] Northwestern Univ, Feinberg Sch Med, Dept Med Social Sci, Chicago, IL 60611 USA.
RP Tseng, WL (reprint author), Bldg 15K Room 208,MSC 2670,15K North Dr, Bethesda, MD 20892 USA.
EM wan-ling.tseng@nih.gov
RI Brotman, Melissa/H-7409-2013;
OI Egger, Helen/0000-0001-8447-5350
FU National Institute of Mental Health (NIMH); NARSAD [MH068455, MH60952];
Walden W. and Jean Young Shaw Foundation; Children's Brain Research
Foundation
FX Contract grant sponsor: National Institute of Mental Health (NIMH);
contract grant sponsor: NARSAD Young Investigator Award (to A. E. G.);
contract grant number: MH068455 (to L. W., M. B. G.); contract grant
number: MH60952 (to B. B.), contract grant sponsor: Walden W. and Jean
Young Shaw Foundation (to L. W.); contract grant sponsor: Children's
Brain Research Foundation (to L. W.).
NR 53
TC 1
Z9 1
U1 2
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1091-4269
EI 1520-6394
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD MAY
PY 2015
VL 32
IS 5
BP 325
EP 334
DI 10.1002/da.22342
PG 10
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA CG6LM
UT WOS:000353412400003
PM 25691090
ER
PT J
AU Deveney, CM
Hommer, RE
Reeves, E
Stringaris, A
Hinton, KE
Haring, CT
Vidal-Ribas, P
Towbin, K
Brotman, MA
Leibenluft, E
AF Deveney, Christen M.
Hommer, Rebecca E.
Reeves, Elizabeth
Stringaris, Argyris
Hinton, Kendra E.
Haring, Catherine T.
Vidal-Ribas, Pablo
Towbin, Kenneth
Brotman, Melissa A.
Leibenluft, Ellen
TI A PROSPECTIVE STUDY OF SEVERE IRRITABILITY IN YOUTHS: 2-AND 4-YEAR
FOLLOW-UP
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE irritability; longitudinal; DMDD; severe mood dysregulation
ID MOOD DYSREGULATION DISORDER; OF-ONSET DISTRIBUTIONS; LIFETIME
PREVALENCE; MENTAL-DISORDERS; ADULT OUTCOMES; ASSOCIATIONS; COMORBIDITY;
DEPRESSION; PREDICTORS; CHILDREN
AB BackgroundSevere, chronic irritability is receiving increased research attention, and is the cardinal symptom of a new diagnostic category, disruptive mood dysregulation disorder (DMDD). Although data from epidemiological community samples suggest that childhood chronic irritability predicts unipolar depression and anxiety in adulthood, whether these symptoms are stable and cause ongoing clinical impairment is unknown. The present study presents 4-year prospective and longitudinal diagnostic and impairment data on a clinical sample of children selected for symptoms of severe irritability (operationalized as severe mood dysregulation [SMD]).
MethodsYouth meeting criteria for SMD (n = 200) were evaluated at baseline using standard diagnostic methods. Two-year (n = 78) and 4-year (n = 46) follow-up diagnostic and clinical impairment ratings collected at 6-month intervals were completed with those youths enrolled in the study for a sufficient time.
ResultsAlthough the number of youth meeting strict categorical SMD criteria declined over time (49 and 40% at 2 and 4 years, respectively), many individuals not meeting full criteria continued to display clinically significant irritability symptoms (2 years: 42%; 4 years: 37%). Impairment due to these irritability symptoms remained consistently in the moderate range on the Clinical Global Impressions Scale.
ConclusionsBy the 4-year follow-up, only 40% of youths meet strict SMD criteria; however, most continue to display clinically impairing symptoms and significant impairment warranting psychiatric treatment. These findings provide evidence for the course of irritability, with implications for DMDD. Future research with populations meeting DMDD criteria and followed through the ages of high risk for psychiatric diagnoses is necessary. (C) 2015 Wiley Periodicals, Inc.
C1 [Deveney, Christen M.] Wellesley Coll, Dept Psychol, Wellesley, MA 02481 USA.
[Hommer, Rebecca E.] NIMH, Pediatr & Dev Neurosci Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Reeves, Elizabeth; Towbin, Kenneth; Brotman, Melissa A.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Stringaris, Argyris; Hinton, Kendra E.; Haring, Catherine T.; Vidal-Ribas, Pablo] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
RP Deveney, CM (reprint author), Wellesley Coll, Dept Psychol, 106 Cent St, Wellesley, MA 02481 USA.
EM cdeveney@wellesley.edu
RI Brotman, Melissa/H-7409-2013
FU NIMH [NCT00025935]
FX Contract grant sponsor: Intramural Research Program of the NIMH;
Contract grant number: NCT00025935.
NR 29
TC 6
Z9 6
U1 1
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1091-4269
EI 1520-6394
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD MAY
PY 2015
VL 32
IS 5
BP 364
EP 372
DI 10.1002/da.22336
PG 9
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA CG6LM
UT WOS:000353412400008
PM 25504765
ER
PT J
AU Mauras, N
Mazaika, P
Buckingham, B
Weinzimer, S
White, NH
Tsalikian, E
Hershey, T
Cato, A
Cheng, PY
Kollman, C
Beck, RW
Ruedy, K
Aye, T
Fox, L
Arbelaez, AM
Wilson, D
Tansey, M
Tamborlane, W
Peng, D
Marzelli, M
Winer, KK
Reiss, AL
AF Mauras, Nelly
Mazaika, Paul
Buckingham, Bruce
Weinzimer, Stuart
White, Neil H.
Tsalikian, Eva
Hershey, Tamara
Cato, Allison
Cheng, Peiyao
Kollman, Craig
Beck, Roy W.
Ruedy, Katrina
Aye, Tandy
Fox, Larry
Arbelaez, Ana Maria
Wilson, Darrell
Tansey, Michael
Tamborlane, William
Peng, Daniel
Marzelli, Matthew
Winer, Karen K.
Reiss, Allan L.
CA Diabet Res Children Network
TI Longitudinal Assessment of Neuroanatomical and Cognitive Differences in
Young Children With Type 1 Diabetes: Association With Hyperglycemia
SO DIABETES
LA English
DT Article
ID SEVERE HYPOGLYCEMIA; NERVOUS-SYSTEM; DISEASE ONSET; BRAIN VOLUME;
MELLITUS; RATS; ADOLESCENTS; YOUTH; LIFE; METAANALYSIS
AB Significant regional differences in gray and white matter volume and subtle cognitive differences between young diabetic and nondiabetic children have been observed. Here, we assessed whether these differences change over time and the relation with dysglycemia. Children ages 4 to <10 years with (n = 144) and without (n = 72) type 1 diabetes (T1D) had high-resolution structural MRI and comprehensive neurocognitive tests at baseline and 18 months and continuous glucose monitoring and HbA(1c) performed quarterly for 18 months. There were no differences in cognitive and executive function scores between groups at 18 months. However, children with diabetes had slower total gray and white matter growth than control subjects. Gray matter regions (left precuneus, right temporal, frontal, and parietal lobes and right medial-frontal cortex) showed lesser growth in diabetes, as did white matter areas (splenium of the corpus callosum, bilateral superior-parietal lobe, bilateral anterior forceps, and inferior-frontal fasciculus). These changes were associated with higher cumulative hyperglycemia and glucose variability but not with hypoglycemia. Young children with T1D have significant differences in total and regional gray and white matter growth in brain regions involved in complex sensorimotor processing and cognition compared with age-matched control subjects over 18 months, suggesting that chronic hyperglycemia may be detrimental to the developing brain.
C1 [Mauras, Nelly; Fox, Larry] Nemours Childrens Clin, Div Endocrinol Diabet & Metab, Jacksonville, FL 32207 USA.
[Mazaika, Paul; Peng, Daniel; Marzelli, Matthew; Reiss, Allan L.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Ctr Interdisciplinary Brain Sci Res, Stanford, CA 94305 USA.
[Buckingham, Bruce; Aye, Tandy; Wilson, Darrell; Reiss, Allan L.] Stanford Univ, Dept Pediat, Sch Med, Stanford, CA 94305 USA.
[Weinzimer, Stuart; Tamborlane, William] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06510 USA.
[White, Neil H.; Arbelaez, Ana Maria] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
[Tsalikian, Eva; Tansey, Michael] Univ Iowa, Pediat Endocrinol, Iowa City, IA USA.
[Hershey, Tamara] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
[Hershey, Tamara] Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA.
[Hershey, Tamara] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Cato, Allison] Nemours Childrens Clin, Div Neurol, Jacksonville, FL USA.
[Cheng, Peiyao; Kollman, Craig; Beck, Roy W.; Ruedy, Katrina] Jaeb Ctr Hlth Res, Tampa, FL USA.
[Marzelli, Matthew] Stanford Univ, Sch Med, Dept Bioengn, Stanford, CA 94305 USA.
[Winer, Karen K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Reiss, Allan L.] Stanford Univ, Sch Med, Dept Radiol, Stanford, CA 94305 USA.
RP Mauras, N (reprint author), Nemours Childrens Clin, Div Endocrinol Diabet & Metab, Jacksonville, FL 32207 USA.
EM nmauras@nemours.org
FU National Institutes of Health (NIH) [DIRECNET U01-HD-41890, HD-41906,
HD-41908, HD-41915, HD-41918, HD-56526, 1R01-HD-078463, UL1-RR-024992]
FX This research was supported by funding from the National Institutes of
Health (NIH) (DIRECNET U01-HD-41890, HD-41906, HD-41908, HD-41915,
HD-41918, and HD-56526), 1R01-HD-078463, and UL1-RR-024992.
NR 61
TC 17
Z9 19
U1 1
U2 7
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 MAY
PY 2015
VL 64
IS 5
BP 1770
EP 1779
DI 10.2337/db14-1445
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CG6RX
UT WOS:000353431200032
PM 25488901
ER
PT J
AU Torn, C
Hadley, D
Lee, HS
Hagopian, W
Lernmark, A
Simell, O
Rewers, M
Ziegler, A
Schatz, D
Akolkar, B
Onengut-Gumuscu, S
Chen, WM
Toppari, J
Mykkanen, J
Ilonen, J
Rich, SS
She, JX
Steck, AK
Krischer, J
AF Torn, Carina
Hadley, David
Lee, Hye-Seung
Hagopian, William
Lernmark, Ake
Simell, Olli
Rewers, Marian
Ziegler, Anette
Schatz, Desmond
Akolkar, Beena
Onengut-Gumuscu, Suna
Chen, Wei-Min
Toppari, Jorma
Mykkanen, Juha
Ilonen, Jorma
Rich, Stephen S.
She, Jin-Xiong
Steck, Andrea K.
Krischer, Jeffrey
CA TEDDY Study Grp
TI Role of Type 1 Diabetes-Associated SNPs on Risk of Autoantibody
Positivity in the TEDDY Study
SO DIABETES
LA English
DT Article
ID TYROSINE-PHOSPHATASE PTPN22; ANTIBODY STANDARDIZATION PROGRAM;
GLUTAMIC-ACID DECARBOXYLASE; GENOME-WIDE ASSOCIATION; ISLET
AUTOIMMUNITY; POPULATION; GENE; POLYMORPHISM; ASSAYS; LOCUS
AB The Environmental Determinants of Diabetes in the Young (TEDDY) study prospectively follows 8,677 children enrolled from birth who carry HLA-susceptibility genotypes for development of islet autoantibodies (IA) and type 1 diabetes (T1D). During the median follow-up time of 57 months, 350 children developed at least one persistent IA (GAD antibody, IA-2A, or micro insulin autoantibodies) and 84 of them progressed to T1D. We genotyped 5,164 Caucasian children for 41 non-HLA single nucleotide polymorphisms (SNPs) that achieved genome-wide significance for association with T1D in the genome-wide association scan meta-analysis conducted by the Type 1 Diabetes Genetics Consortium. In TEDDY participants carrying high-risk HLA genotypes, eight SNPs achieved significant association to development of IA using time-to-event analysis (P < 0.05), whereof four were significant after adjustment for multiple testing (P < 0.0012): rs2476601 in PTPN22 (hazard ratio [HR] 1.54 [95% CI 1.27-1.88]), rs2292239 in ERBB3 (HR 1.33 [95% CI 1.14-1.55]), rs3184504 in SH2B3 (HR 1.38 [95% CI 1.19-1.6]), and rs1004446 in INS (HR 0.77 [0.66-0.90]). These SNPs were also significantly associated with T1D in particular: rs2476601 (HR 2.42 [95% CI 1.70-3.44]). Although genes in the HLA region remain the most important genetic risk factors for T1D, other non-HLA genetic factors contribute to IA, a first step in the pathogenesis of T1D, and the progression of the disease.
C1 [Torn, Carina; Lernmark, Ake] Lund Univ, CRC, Dept Clin Sci, Malmo, Sweden.
[Hadley, David; Lee, Hye-Seung; Krischer, Jeffrey] Univ S Florida, Dept Pediat, Pediat Epidemiol Ctr, Tampa, FL 33620 USA.
[Hadley, David] St Georges Univ London, Div Populat Hlth Sci & Educ, London, England.
[Hagopian, William] Pacific Northwest Diabet Res Inst, Seattle, WA USA.
[Simell, Olli; Toppari, Jorma; Mykkanen, Juha] Univ Turku, Dept Pediat, Turku, Finland.
[Rewers, Marian; Steck, Andrea K.] Univ Colorado, Barbara Davis Ctr Childhood Diabet, Aurora, CO USA.
[Ziegler, Anette] Diabet Res Inst, Dept Pediat, Munich, Germany.
[Schatz, Desmond] Univ Florida, Dept Pediat, Gainesville, FL USA.
[Akolkar, Beena] NIDDK, NIH, Bethesda, MD 20892 USA.
[Onengut-Gumuscu, Suna; Chen, Wei-Min; Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Ilonen, Jorma] Univ Turku, Immunogenet Lab, Turku, Finland.
[Ilonen, Jorma] Univ Eastern Finland, Dept Clin Microbiol, Kuopio, Finland.
[She, Jin-Xiong] Georgia Regents Univ, Ctr Biotechnol & Genom Med, Augusta, GA USA.
RP Torn, C (reprint author), Lund Univ, CRC, Dept Clin Sci, Malmo, Sweden.
EM carina.torn@med.lu.se
RI Ziegler, Anette-Gabriele/M-4614-2014; Bonifacio, Ezio/E-7700-2010;
Mykkanen, Juha/Q-1663-2015
OI Ziegler, Anette-Gabriele/0000-0002-6290-5548; Bonifacio,
Ezio/0000-0002-8704-4713; Mykkanen, Juha/0000-0001-9898-2660
FU National Institute of Diabetes and Digestive and Kidney Diseases [U01
DK63829, U01 DK63861, U01 DK63821, U01 DK63865, U01 DK63863, U01
DK63836, U01 DK63790, UC4 DK63829, UC4 DK63861, UC4 DK63821, UC4
DK63865, UC4 DK63863, UC4 DK63836, UC4 DK95300, HHSN267200700014C];
National Institute of Allergy and Infectious Diseases; National
Institute of Child Health and Human Development; National Institute of
Environmental Health Sciences; JDRF; Centers for Disease Control and
Prevention; National Institutes of Health/National Center for Advancing
Translational Sciences Clinical and Translational Science Awards [UL1
TR000064, UL1 TR001082]; Royal Physiographic Society in Lund, Sweden
FX This work was funded by U01 DK63829, U01 DK63861, U01 DK63821, U01
DK63865, U01 DK63863, U01 DK63836, U01 DK63790, UC4 DK63829, UC4
DK63861, UC4 DK63821, UC4 DK63865, UC4 DK63863, UC4 DK63836, and UC4
DK95300 and contract number HHSN267200700014C from the National
Institute of Diabetes and Digestive and Kidney Diseases, the National
Institute of Allergy and Infectious Diseases, the National Institute of
Child Health and Human Development, the National Institute of
Environmental Health Sciences, JDRF, and the Centers for Disease Control
and Prevention. This work was supported in part by the National
Institutes of Health/National Center for Advancing Translational
Sciences Clinical and Translational Science Awards to the University of
Florida (UL1 TR000064) and the University of Colorado (UL1 TR001082).
The Royal Physiographic Society in Lund, Sweden, contributed with a
travel grant to C.T. for participation in the 2013 Immunology of
Diabetes Society Meeting.
NR 40
TC 15
Z9 15
U1 1
U2 4
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 MAY
PY 2015
VL 64
IS 5
BP 1818
EP 1829
DI 10.2337/db14-1497
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CG6RX
UT WOS:000353431200037
PM 25422107
ER
PT J
AU Steck, AK
Vehik, K
Bonifacio, E
Lernmark, A
Ziegler, AG
Hagopian, WA
She, JX
Simell, O
Akolkar, B
Krischer, J
Schatz, D
Rewers, MJ
AF Steck, Andrea K.
Vehik, Kendra
Bonifacio, Ezio
Lernmark, Ake
Ziegler, Anette-G.
Hagopian, William A.
She, JinXiong
Simell, Olli
Akolkar, Beena
Krischer, Jeffrey
Schatz, Desmond
Rewers, Marian J.
CA TEDDY Study Grp
TI Predictors of Progression From the Appearance of Islet Autoantibodies to
Early Childhood Diabetes: The Environmental Determinants of Diabetes in
the Young (TEDDY)
SO DIABETES CARE
LA English
DT Article
ID GLUTAMIC-ACID DECARBOXYLASE; GENERAL-POPULATION; PREVENTION
TRIAL-TYPE-1; RISK SCORE; TYPE-1; CHILDREN; INSULIN; AUTOIMMUNITY;
INDIVIDUALS; ASSOCIATION
AB OBJECTIVEWhile it is known that there is progression to diabetes in <10 years in 70% of children with two or more islet autoantibodies, predictors of the progression to diabetes are only partially defined.RESEARCH DESIGN AND METHODSThe Environmental Determinants of Diabetes in the Young (TEDDY) study has observed 8,503 children who were at increased genetic risk for autoimmune diabetes. Insulin autoantibodies (IAAs), GAD65 autoantibodies (GADAs), and insulinoma-associated protein 2 autoantibodies (IA-2As) were measured every 3 months until 4 years of age and every 6 months thereafter; if results were positive, the autoantibodies were measured every 3 months.RESULTSLife table analysis revealed that the cumulative incidence of diabetes by 5 years since the appearance of the first autoantibody differed significantly by the number of positive autoantibodies (47%, 36%, and 11%, respectively, in those with three autoantibodies, two autoantibodies, and one autoantibody, P < 0.001). In time-varying survival models adjusted for first-degree relative status, number of autoantibodies, age at first persistent confirmed autoantibodies, and HLA genotypes, higher mean IAA and IA-2A levels were associated with an increased risk of type 1 diabetes in children who were persistently autoantibody positive (IAAs: hazard ratio [HR] 8.1 [95% CI 4.6-14.2]; IA-2A: HR 7.4 [95% CI 4.3-12.6]; P < 0.0001]). The mean GADA level did not significantly affect the risk of diabetes.CONCLUSIONSIn the TEDDY study, children who have progressed to diabetes usually expressed two or more autoantibodies. Higher IAA and IA-2A levels, but not GADA levels, increased the risk of diabetes in those children who were persistently autoantibody positive.
C1 [Steck, Andrea K.; Rewers, Marian J.] Univ Colorado, Sch Med, Barbara Davis Ctr Childhood Diabet, Aurora, CO 80045 USA.
[Vehik, Kendra; Krischer, Jeffrey] Univ S Florida, Pediat Epidemiol Ctr, Tampa, FL USA.
[Bonifacio, Ezio] Tech Univ Dresden, D-01062 Dresden, Germany.
[Lernmark, Ake] Lund Univ, Skane Univ Hosp, Clin Res Ctr, Malmo, Sweden.
[Ziegler, Anette-G.] Helmholtz Zentrum Munchen, Diabet Res Inst, Neuherberg, Germany.
[Ziegler, Anette-G.] Tech Univ Munich, Klinikum Rechts Isar, D-80290 Munich, Germany.
[Ziegler, Anette-G.] Forschergrp Diabet eV, Neuherberg, Germany.
[Hagopian, William A.] Pacific Northwest Diabet Res Inst, Seattle, WA USA.
[She, JinXiong] Georgia Regents Univ, Med Coll Georgia, Augusta, GA USA.
[Simell, Olli] Univ Turku, Dept Pediat, Turku, Finland.
[Akolkar, Beena] NIDDK, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD 20892 USA.
[Schatz, Desmond] Univ Florida, Gainesville, FL USA.
RP Steck, AK (reprint author), Univ Colorado, Sch Med, Barbara Davis Ctr Childhood Diabet, Aurora, CO 80045 USA.
EM andrea.steck@ucdenver.edu
RI Ziegler, Anette-Gabriele/M-4614-2014; Bonifacio, Ezio/E-7700-2010
OI Ziegler, Anette-Gabriele/0000-0002-6290-5548; Bonifacio,
Ezio/0000-0002-8704-4713
FU National Institute of Diabetes and Digestive and Kidney Diseases
[U01-DK-63829, U01-DK-63861, U01-DK-63821, U01-DK-63865, U01-DK-63863,
U01-DK-63836, U01-DK-63790, UC4-DK-63829, UC4-DK-63861, UC4-DK-63821,
UC4-DK-63865, UC4-DK-63863, UC4-DK-63836, UC4-DK95300,
HHSN267200700014C]; National Institute of Allergy and Infectious
Diseases; Eunice Kennedy Shriver National Institute of Child Health and
Human Development; National Institute of Environmental Health Sciences;
JDRF; Centers for Disease Control and Prevention; National Institutes of
Health/National Center for Advancing Translational Sciences Clinical and
Translational Science Awards [UL1-TR-000064, UL1-TR-001082]
FX The TEDDY Study Group is funded by grants U01-DK-63829, U01-DK-63861,
U01-DK-63821, U01-DK-63865, U01-DK-63863, U01-DK-63836, U01-DK-63790,
UC4-DK-63829, UC4-DK-63861, UC4-DK-63821, UC4-DK-63865, UC4-DK-63863,
UC4-DK-63836, and UC4-DK95300 and by Contract no. HHSN267200700014C from
the National Institute of Diabetes and Digestive and Kidney Diseases,
National Institute of Allergy and Infectious Diseases, Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
National Institute of Environmental Health Sciences, JDRF, and Centers
for Disease Control and Prevention. This work was supported in part by
the National Institutes of Health/National Center for Advancing
Translational Sciences Clinical and Translational Science Awards to the
University of Florida (UL1-TR-000064) and the University of Colorado
(UL1-TR-001082).
NR 38
TC 21
Z9 22
U1 0
U2 2
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD MAY
PY 2015
VL 38
IS 5
BP 808
EP 813
DI 10.2337/dc14-2426
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CG7SP
UT WOS:000353505600020
PM 25665818
ER
PT J
AU Krischer, JP
Lynch, KF
Schatz, DA
Ilonen, J
Lernmark, A
Hagopian, WA
Rewers, MJ
She, JX
Simell, OG
Toppari, J
Ziegler, AG
Akolkar, B
Bonifacio, E
AF Krischer, Jeffrey P.
Lynch, Kristian F.
Schatz, Desmond A.
Ilonen, Jorma
Lernmark, Ake
Hagopian, William A.
Rewers, Marian J.
She, Jin-Xiong
Simell, Olli G.
Toppari, Jorma
Ziegler, Anette-G.
Akolkar, Beena
Bonifacio, Ezio
CA TEDDY Study Grp
TI The 6 year incidence of diabetes-associated autoantibodies in
genetically at-risk children: the TEDDY study
SO DIABETOLOGIA
LA English
DT Article
DE Autoimmunity; Diabetes in young children; HLA-DR-DQ genotypes;
Incidence; Islet autoantibodies; Type 1 diabetes
ID ISLET AUTOANTIBODIES; CLASSIFICATION; ANTIBODIES; ANTIGEN-2; AGE
AB Aims/hypothesis Islet autoantibodies, in addition to elevated blood glucose, define type 1 diabetes. These autoantibodies are detectable for a variable period of time before diabetes onset. Thus, the occurrence of islet autoantibodies is associated with the beginning of the disease process. The age at, and order in, which autoantibodies appear may be associated with different genetic backgrounds or environmental exposures, or both.
Methods Infants with HLA-DR high-risk genotypes (DR3/4, DR4/4, DR4/8 and DR3/3) were enrolled and prospectively followed with standardised autoantibody assessments quarterly throughout the first 4 years of life and then semi-annually thereafter.
Results Autoantibodies appeared in 549/8,503 (6.5%) children during 34,091 person-years of follow-up. Autoantibodies at 3 (0.1%) and 6 (0.2%) months of age were rare. Of the 549, 43.7% had islet autoantibodies to insulin (IAA) only, 37.7% had glutamic acid decarboxylase autoantibodies (GADA) only, 13.8% had both GADA and IAA only, 1.6% had insulinoma antigen-2 only and 3.1% had other combinations. The incidence of IAA only peaked within the first year of life and declined over the following 5 years, but GADA only increased until the second year and remained relatively constant. GADA only were more common than IAA only in HLA-DR3/3 children but less common in HLA-DR4/8 children.
Conclusions/interpretation Islet autoantibodies can occur very early in life and the order of appearance was related to HLA-DR-DQ genotype.
C1 [Krischer, Jeffrey P.; Lynch, Kristian F.] Univ S Florida, Dept Pediat, Morsani Coll Med, Tampa, FL 33612 USA.
[Schatz, Desmond A.] Univ Florida, Coll Med, Dept Pediat, Gainesville, FL USA.
[Ilonen, Jorma] Univ Eastern Finland, Dept Clin Microbiol, Kuopio, Finland.
[Ilonen, Jorma] Univ Turku, Immunogenet Lab, Turku, Finland.
[Lernmark, Ake] Lund Univ, Skane Univ Hosp SUS, Dept Clin Sci, CRC, Malmo, Sweden.
[Hagopian, William A.] Pacific NW Diabet Res Inst, Seattle, WA USA.
[Rewers, Marian J.] Univ Colorado, Barbara Davis Ctr Childhood Diabet, Aurora, CO USA.
[She, Jin-Xiong] Georgia Regents Univ, Med Coll Georgia, Ctr Biotechnol & Genom Med, Augusta, GA USA.
[Simell, Olli G.; Toppari, Jorma] Turku Univ Hosp, Dept Pediat, FIN-20520 Turku, Finland.
[Toppari, Jorma] Univ Turku, Dept Physiol, Turku, Finland.
[Ziegler, Anette-G.] Helmholtz Zentrum Munchen, Diabet Res Inst, Neuherberg, Germany.
[Ziegler, Anette-G.] Tech Univ Munich, Klinikum Rechts Isar, D-80290 Munich, Germany.
[Ziegler, Anette-G.] Helmholtz Zentrum Munchen, Forschergrp Diabet eV, Neuherberg, Germany.
[Akolkar, Beena] NIDDK, Bethesda, MD 20892 USA.
[Bonifacio, Ezio] Tech Univ Dresden, Ctr Regenerat Therapies Dresden, Dresden, Germany.
RP Krischer, JP (reprint author), Univ S Florida, Dept Pediat, Morsani Coll Med, 3650 Spectrum Blvd,Suite 100, Tampa, FL 33612 USA.
EM jeffrey.krischer@epi.usf.edu
RI Ziegler, Anette-Gabriele/M-4614-2014; Bonifacio, Ezio/E-7700-2010
OI Ziegler, Anette-Gabriele/0000-0002-6290-5548; Bonifacio,
Ezio/0000-0002-8704-4713
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[U01 DK63829, U01 DK63861, U01 DK63821, U01 DK63865, U01 DK63863, U01
DK63836, U01 DK63790, UC4 DK63829, UC4 DK63861, UC4 DK63821, UC4
DK63865, UC4 DK63863, UC4 DK63836, UC4 DK95300, HHSN267200700014C];
National Institute of Allergy and Infectious Diseases (NIAID); National
Institute of Child Health and Human Development (NICHD); National
Institute of Environmental Health Sciences (NIEHS); Juvenile Diabetes
Research Foundation (JDRF); Centers for Disease Control and Prevention
(CDC); NIH/NCATS Clinical and Translational Science [UL1 TR000064];
University of Colorado [UL1 TR001082]
FX This work was funded by U01 DK63829, U01 DK63861, U01 DK63821, U01
DK63865, U01 DK63863, U01 DK63836, U01 DK63790, UC4 DK63829, UC4
DK63861, UC4 DK63821, UC4 DK63865, UC4 DK63863, UC4 DK63836, and UC4
DK95300 and Contract No. HHSN267200700014C from the National Institute
of Diabetes and Digestive and Kidney Diseases (NIDDK), National
Institute of Allergy and Infectious Diseases (NIAID), National Institute
of Child Health and Human Development (NICHD), National Institute of
Environmental Health Sciences (NIEHS), Juvenile Diabetes Research
Foundation (JDRF), and Centers for Disease Control and Prevention (CDC).
This work supported in part by the NIH/NCATS Clinical and Translational
Science Awards to the University of Florida (UL1 TR000064) and the
University of Colorado (UL1 TR001082).
NR 18
TC 40
Z9 41
U1 1
U2 3
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 MAY
PY 2015
VL 58
IS 5
BP 980
EP 987
DI 10.1007/s00125-015-3514-y
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CF6CL
UT WOS:000352644200014
PM 25660258
ER
PT J
AU Raghavan, S
Porneala, B
McKeown, N
Fox, CS
Dupuis, J
Meigs, JB
AF Raghavan, Sridharan
Porneala, Bianca
McKeown, Nicola
Fox, Caroline S.
Dupuis, Josee
Meigs, James B.
TI Metabolic factors and genetic risk mediate familial type 2 diabetes risk
in the Framingham Heart Study
SO DIABETOLOGIA
LA English
DT Article
DE Diet; Family history; Genetic risk; Metabolic syndrome; Physical
activity; Type 2 diabetes
ID INSULIN-SECRETION; LIFE-STYLE; GLUCOSE-TOLERANCE; PHYSICAL-ACTIVITY;
YOUNG ADULTHOOD; GLYCEMIC TRAITS; MELLITUS; ASSOCIATION; PARENTS;
HERITABILITY
AB Aims/hypothesis Type 2 diabetes mellitus in parents is a strong determinant of diabetes risk in their offspring. We hypothesise that offspring diabetes risk associated with parental diabetes is mediated by metabolic risk factors.
Methods We studied initially non-diabetic participants of the Framingham Offspring Study. Metabolic risk was estimated using beta cell corrected insulin response (CIR), HOMA-IR or a count of metabolic syndrome components (metabolic syndrome score [MSS]). Dietary risk and physical activity were estimated using questionnaire responses. Genetic risk score (GRS) was estimated as the count of 62 type 2 diabetes risk alleles. The outcome of incident diabetes in offspring was examined across levels of parental diabetes exposure, accounting for sibling correlation and adjusting for age, sex and putative mediators. The proportion mediated was estimated by comparing regression coefficients for parental diabetes with (beta (adj)) and without (beta (unadj)) adjustments for CIR, HOMA-IR, MSS and GRS (percentage mediated = 1 - beta(adj)/beta(unadj)).
Results Metabolic factors mediated 11% of offspring diabetes risk associated with parental diabetes, corresponding to a reduction in OR per diabetic parent from 2.13 to 1.96. GRS mediated 9% of risk, corresponding to a reduction in OR per diabetic parent from 2.13 to 1.99.
Conclusions/interpretation Metabolic risk factors partially mediated offspring type 2 diabetes risk conferred by parental diabetes to a similar magnitude as genetic risk. However, a substantial proportion of offspring diabetes risk associated with parental diabetes remains unexplained by metabolic factors, genetic risk, diet and physical activity, suggesting that important familial influences on diabetes risk remain undiscovered.
C1 [Raghavan, Sridharan; Porneala, Bianca; Meigs, James B.] Harvard Univ, Sch Med, Dept Med, Div Gen Internal Med, Boston, MA 02114 USA.
[Raghavan, Sridharan; Porneala, Bianca; Meigs, James B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[McKeown, Nicola] Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Nutr Epidemiol Program, Boston, MA 02111 USA.
[Fox, Caroline S.] NHLBI, Lab Metab & Populat Hlth, Framingham, MA USA.
[Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
RP Meigs, JB (reprint author), Harvard Univ, Sch Med, Dept Med, Div Gen Internal Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM jmeigs@partners.org
FU National Institutes of Health National Research Service [T32HP10251];
Ryoichi Sasakawa Fellowship Fund; NIH [RO1DK78616]; National Heart, Lung
and Blood Institute's Framingham Heart Study [N01-HC-25195]; Affymetrix
for genotyping services [N02-HL-6-4278]; USDA [1950-51530-011-00D];
[K24 DK080140]
FX SR is supported by National Institutes of Health National Research
Service Award T32HP10251 and the Ryoichi Sasakawa Fellowship Fund. JBM
and JD are supported by NIH RO1DK78616, and JBM is also supported by K24
DK080140. We gratefully acknowledge the FHS study participants and staff
for their contributions. This work was partially supported by the
National Heart, Lung and Blood Institute's Framingham Heart Study
(Contract No. N01-HC-25195) and its contract with Affymetrix for
genotyping services (Contract No. N02-HL-6-4278). NM is supported by
USDA agreement number 1950-51530-011-00D.
NR 32
TC 1
Z9 1
U1 1
U2 5
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 MAY
PY 2015
VL 58
IS 5
BP 988
EP 996
DI 10.1007/s00125-015-3498-7
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CF6CL
UT WOS:000352644200015
PM 25619168
ER
PT J
AU Farooq, PD
Urrunaga, NH
Tang, DM
von Rosenvinge, EC
AF Farooq, Priya D.
Urrunaga, Nathalie H.
Tang, Derek M.
von Rosenvinge, Erik C.
TI Pseudomembranous colitis
SO DM DISEASE-A-MONTH
LA English
DT Article
ID CLOSTRIDIUM-DIFFICILE INFECTION; GASTROINTESTINAL
CYTOMEGALOVIRUS-INFECTION; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
YERSINIA-ENTEROCOLITICA INFECTIONS; FECAL MICROBIOTA TRANSPLANTATION;
RESISTANT STAPHYLOCOCCUS-AUREUS; OF-THE-LITERATURE; ISCHEMIC COLITIS;
COLLAGENOUS-COLITIS; STRONGYLOIDES-STERCORALIS
C1 [Farooq, Priya D.] Univ Maryland, Med Ctr, Dept Med, Div Gastroenterol & Hepatol, Baltimore, MD 21201 USA.
NIDDK, NIH, Bethesda, MD 20892 USA.
Vet Affairs Maryland Hlth Ctr Syst, Vet Affairs, Baltimore, MD USA.
RP Farooq, PD (reprint author), Univ Maryland, Med Ctr, Dept Med, Div Gastroenterol & Hepatol, Baltimore, MD 21201 USA.
FU National Institutes of Health (NIH), National Institute of Diabetes and
Digestive and Kidney Disease (NIDDK) [5 T32 DK067872-07]; Intramural
Research Program of the NIDDK at NIH
FX Nathalie H. Urrunaga, MD, MS was supported by Grant no. 5 T32
DK067872-07 from the National Institutes of Health (NIH), National
Institute of Diabetes and Digestive and Kidney Disease (NIDDK). This
document was also supported by the Intramural Research Program of the
NIDDK at NIH.
NR 182
TC 2
Z9 3
U1 1
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0011-5029
EI 1557-8194
J9 DM-DIS MON
JI DM-Dis.-a-Mon.
PD MAY
PY 2015
VL 61
IS 5
BP 181
EP 206
DI 10.1016/j.disamonth.2015.01.006
PG 26
WC Medicine, General & Internal
SC General & Internal Medicine
GA CG5DD
UT WOS:000353310400002
PM 25769243
ER
PT J
AU McMahen, RL
Strynar, MJ
Dagnino, S
Herr, DW
Moser, VC
Garantziotis, S
Andersen, EM
Freeborn, DL
McMillan, L
Lindstrom, AB
AF McMahen, Rebecca L.
Strynar, Mark J.
Dagnino, Sonia
Herr, David W.
Moser, Virginia C.
Garantziotis, Stavros
Andersen, Erik M.
Freeborn, Danielle L.
McMillan, Larry
Lindstrom, Andrew B.
TI Identification of fipronil metabolites by time-of-flight mass
spectrometry for application in a human exposure study
SO ENVIRONMENT INTERNATIONAL
LA English
DT Article
DE Fipronil; LC/TOF; Biomarker; Human exposure; Metabolism
ID HETEROCYCLIC AMINES; ENVIRONMENTAL FATE; FOOD; INSECTICIDE;
CYTOCHROME-P450; CHEMISTRY; FLUORINE; SULFONE; INDOOR
AB Fipronil is a phenylpyrazole insecticide commonly used in residential and agricultural applications. To understand more about the potential risks for human exposure associated with fipronil, urine and serum from dosed Long Evans adult rats (5 and 10 mg/kg bw) were analyzed to identify metabolites as potential biomarkers for use in human biomonitoring studies. Urine from treated rats was found to contain seven unique metabolites, two of which had not been previously reported-M4 and M7 which were putatively identified as a nitroso compound and an imine, respectively. Fipronil sulfone was confirmed to be the primary metabolite in rat serum. The fipronil metabolites identified in the respective matrices were then evaluated in matched human urine (n = 84) and serum (n = 96) samples from volunteers with no known pesticide exposures. Although no fipronil or metabolites were detected in human urine, fipronil sulfone was present in the serum of approximately 25% of the individuals at concentrations ranging from 0.1 to 4 ng/mL These results indicate that many fipronil metabolites are produced following exposures in rats and that fipronil sulfone is a useful biomarker in human serum. Furthermore, human exposure to fipronil may occur regularly and require more extensive characterization. Published by Elsevier Ltd.
C1 [McMahen, Rebecca L.; Strynar, Mark J.; Dagnino, Sonia; Andersen, Erik M.; Lindstrom, Andrew B.] US EPA, Natl Exposure Res Lab, Res Triangle Pk, NC 27711 USA.
[Herr, David W.; Moser, Virginia C.; Freeborn, Danielle L.] US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA.
[Garantziotis, Stavros] NIEHS, Res Triangle Pk, NC 27709 USA.
[McMillan, Larry] US EPA, Natl Caucus & Ctr Black Aged Employee, Natl Exposure Res Lab, Res Triangle Pk, NC 27711 USA.
RP Strynar, MJ (reprint author), 109 TW Alexander Dr, Durham, NC 27705 USA.
EM strynar.mark@epa.gov
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
FU National Exposure Research Laboratory; U.S. Department of Energy; U.S.
Environmental Protection Agency
FX This research was supported by an appointment to the Research
Participation Program at the National Exposure Research Laboratory
administered by the Oak Ridge Institute for Science Education through an
interagency agreement between the U.S. Department of Energy and the U.S.
Environmental Protection Agency. We thank Agilent Technologies for
providing us with the LC/TOF mass spectrometer that was used to
investigate metabolic products. We also thank Michael Hays of the US EPA
who kindly allowed the use of his LC/Q-TOF mass spectrometer for further
structure elucidation, Benny Pyke of Arizona State University for
discussions on detection of fipronil in human urine, and Matthew
Stiegel, Jon Sobus, and Peter Egeghy for help with data analysis.
NR 41
TC 6
Z9 6
U1 2
U2 30
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0160-4120
EI 1873-6750
J9 ENVIRON INT
JI Environ. Int.
PD MAY
PY 2015
VL 78
BP 16
EP 23
DI 10.1016/j.envint.2015.01.016
PG 8
WC Environmental Sciences
SC Environmental Sciences & Ecology
GA CG2GH
UT WOS:000353092400003
PM 25687022
ER
PT J
AU Kengyel, A
Becsi, B
Konya, Z
Sellers, JR
Erdodi, F
Nyitrai, M
AF Kengyel, Andras
Becsi, Balint
Konya, Zoltan
Sellers, James R.
Erdodi, Ferenc
Nyitrai, Miklos
TI Ankyrin domain of myosin 16 influences motor function and decreases
protein phosphatase catalytic activity
SO EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS
LA English
DT Article
DE Myosin; Protein phosphatase-1 (PP1); Actin; ATPases; Phosphorylation
ID SUBSTRATE-SPECIFICITY; KINETIC MECHANISM; BINDING; MUSCLE; LOCALIZATION;
SUBUNIT; REGIONS; DEFINES; FAMILY; CELLS
AB The unconventional myosin 16 (Myo16), which may have a role in regulation of cell cycle and cell proliferation, can be found in both the nucleus and the cytoplasm. It has a unique, eight ankyrin repeat containing pre-motor domain, the so-called ankyrin domain (My16Ank). Ankyrin repeats are present in several other proteins, e.g., in the regulatory subunit (MYPT1) of the myosin phosphatase holoenzyme, which binds to the protein phosphatase-1 catalytic subunit (PP1c). My16Ank shows sequence similarity to MYPT1. In this work, the interactions of recombinant and isolated My16Ank were examined in vitro. To test the effects of My16Ank on myosin motor function, we used skeletal muscle myosin or nonmuscle myosin 2B. The results showed that My16Ank bound to skeletal muscle myosin (K (D) a parts per thousand 2.4 A mu M) and the actin-activated ATPase activity of heavy meromyosin (HMM) was increased in the presence of My16Ank, suggesting that the ankyrin domain can modulate myosin motor activity. My16Ank showed no direct interaction with either globular or filamentous actin. We found, using a surface plasmon resonance-based binding technique, that My16Ank bound to PP1c alpha (K (D) a parts per thousand 540 nM) and also to PP1c delta (K (D) a parts per thousand 600 nM) and decreased its phosphatase activity towards the phosphorylated myosin regulatory light chain. Our results suggest that one function of the ankyrin domain is probably to regulate the function of Myo16. It may influence the motor activity, and in complex with the PP1c isoforms, it can play an important role in the targeted dephosphorylation of certain, as yet unidentified, intracellular proteins.
C1 [Kengyel, Andras; Nyitrai, Miklos] Univ Pecs, Sch Med, Dept Biophys, H-7624 Pecs, Hungary.
[Kengyel, Andras; Nyitrai, Miklos] Janos Szentagothai Res Ctr, Pecs, Hungary.
[Becsi, Balint; Konya, Zoltan; Erdodi, Ferenc] Univ Debrecen, Dept Med Chem, Debrecen, Hungary.
[Becsi, Balint; Erdodi, Ferenc] Univ Debrecen, MTA DE Cell Biol & Signaling Res Grp, Fac Med, Debrecen, Hungary.
[Sellers, James R.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Nyitrai, Miklos] MTA PTE Nucl Mitochondrial Interact Res Grp, Pecs, Hungary.
RP Nyitrai, M (reprint author), Univ Pecs, Sch Med, Dept Biophys, Szigeti Str 12, H-7624 Pecs, Hungary.
EM miklos.nyitrai@aok.pte.hu
FU Hungarian Scientific Research Fund (OTKA) [NN 107776, K112794, K109249];
European Union [TAMOP 4.2.4. A/2-11-1-2012-0001]; State of Hungary;
European Social Fund
FX This work was supported by grants from the Hungarian Scientific Research
Fund (OTKA grants NN 107776 and K112794 to M.N. and K109249 to F.E.) and
by the "TAMOP 4.2.4. A/2-11-1-2012-0001 National Excellence Program"
supported by the European Union and the State of Hungary, co-financed by
the European Social Fund to Z.K. and B.B. The authors thank Attila Nagy
for preparing and providing NMIIB HMM.
NR 39
TC 0
Z9 0
U1 2
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0175-7571
EI 1432-1017
J9 EUR BIOPHYS J BIOPHY
JI Eur. Biophys. J. Biophys. Lett.
PD MAY
PY 2015
VL 44
IS 4
BP 207
EP 218
DI 10.1007/s00249-015-1015-z
PG 12
WC Biophysics
SC Biophysics
GA CF9AE
UT WOS:000352853000002
PM 25775934
ER
PT J
AU Oh, SK
Baek, JI
Weigand, KM
Venselaar, H
Swarts, HGP
Park, SH
Raza, MH
Jung, DJ
Choi, SY
Lee, SH
Friedrich, T
Vriend, G
Koenderink, JB
Kim, UK
Lee, KY
AF Oh, Se-Kyung
Baek, Jeong-In
Weigand, Karl M.
Venselaar, Hanka
Swarts, Herman G. P.
Park, Seong-Hyun
Raza, Muhammad Hashim
Jung, Da Jung
Choi, Soo-Young
Lee, Sang-Heun
Friedrich, Thomas
Vriend, Gert
Koenderink, Jan B.
Kim, Un-Kyung
Lee, Kyu-Yup
TI A missense variant of the ATP1A2 gene is associated with a novel
phenotype of progressive sensorineural hearing loss associated with
migraine
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID FAMILIAL HEMIPLEGIC MIGRAINE; CATION-BINDING POCKET; GASTRIC H,K-ATPASE;
NA+/K+-ATPASE; K+-ATPASE; NA,K-ATPASE; MUTATIONS; NA+,K+-ATPASE;
OUABAIN; PUMP
AB Hereditary sensorineural hearing loss is an extremely clinical and genetic heterogeneous disorder in humans. Especially, syndromic hearing loss is subdivided by combinations of various phenotypes, and each subtype is related to different genes. We present a new form of progressive hearing loss with migraine found to be associated with a variant in the ATP1A2 gene. The ATP1A2 gene has been reported as the major genetic cause of familial migraine by several previous studies. A Korean family presenting progressive hearing loss with migraine was ascertained. The affected members did not show any aura or other neurologic symptoms during migraine attacks, indicating on a novel phenotype of syndromic hearing loss. To identify the causative gene, linkage analysis and whole-exome sequencing were performed. A novel missense variant, c.571G>A (p.(Val191Met)), was identified in the ATP1A2 gene that showed co-segregation with the phenotype in the family. In silico studies suggest that this variant causes a change in hydrophobic interactions and thereby slightly destabilize the A-domain of Na+/K+-ATPase. However, functional studies failed to show any effect of the p.(Val191Met) substitution on the catalytic rate of this enzyme. We describe a new phenotype of progressive hearing loss with migraine associated with a variant in the ATP1A2 gene. This study suggests that a variant in Na+/K+-ATPase can be involved in both migraine and hearing loss.
C1 [Oh, Se-Kyung; Baek, Jeong-In; Kim, Un-Kyung] Kyungpook Natl Univ, Coll Nat Sci, Dept Biol, Taegu 702701, South Korea.
[Oh, Se-Kyung; Kim, Un-Kyung] Kyungpook Natl Univ, Sch Life Sci, KNU Creat BioRes Grp, Plus Project BK21, Taegu 702701, South Korea.
[Baek, Jeong-In; Choi, Soo-Young] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
[Weigand, Karl M.; Swarts, Herman G. P.; Koenderink, Jan B.] Radboud Univ Nijmegen, Med Ctr, Nijmegen Ctr Mol Life Sci, Dept Pharmacol & Toxicol, NL-6525 ED Nijmegen, Netherlands.
[Venselaar, Hanka; Vriend, Gert] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Park, Seong-Hyun] Kyungpook Natl Univ Hosp, Dept Neurosurg, Daegu, South Korea.
[Raza, Muhammad Hashim] NIDCD, NIH, Bethesda, MD USA.
[Jung, Da Jung; Lee, Sang-Heun; Lee, Kyu-Yup] Kyungpook Natl Univ, Coll Med, Dept Otorhinolaryngol Head & Neck Surg, Taegu 700721, South Korea.
[Friedrich, Thomas] Tech Univ Berlin, Inst Chem, Berlin, Germany.
[Kim, Un-Kyung] Kyungpook Natl Univ, Adv Bioresource Res Ctr, Taegu 702701, South Korea.
RP Kim, UK (reprint author), Kyungpook Natl Univ, Coll Nat Sci, Dept Biol, Taegu 702701, South Korea.
EM kimuk@knu.ac.kr; kylee@knu.ac.kr
RI Vriend, G./H-8112-2014; Koenderink, Jan/N-3578-2014; Venselaar,
Hanka/D-2009-2016
FU Korea Health Technology R&D Project through Korea Health Industry
Development Institute - Ministry of Health & Welfare, Republic of Korea
[HI12C1004(A121100)]; TJ Park Science Fellowship - POSCO Foundation of
Korea
FX We are grateful to the family for their collaboration in this study. We
thank Dr Susan Spiller for electrophysiological experiments, and Dr
Drayna for critical comments on the manuscript. This research was
supported by a grant of the Korea Health Technology R&D Project through
the Korea Health Industry Development Institute, funded by the Ministry
of Health & Welfare, Republic of Korea (grant number:
HI12C1004(A121100)), and the TJ Park Science Fellowship funded by the
POSCO Foundation of Korea (S-KO).
NR 40
TC 6
Z9 6
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD MAY
PY 2015
VL 23
IS 5
BP 639
EP 645
DI 10.1038/ejhg.2014.154
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA CG1JF
UT WOS:000353028200016
PM 25138102
ER
PT J
AU Bakir-Gungor, B
Remmers, EF
Meguro, A
Mizuki, N
Kastner, DL
Gul, A
Sezerman, OU
AF Bakir-Gungor, Burcu
Remmers, Elaine F.
Meguro, Akira
Mizuki, Nobuhisa
Kastner, Daniel L.
Gul, Ahmet
Sezerman, Osman U.
TI Identification of possible pathogenic pathways in Behcet's disease using
genome-wide association study data from two different populations
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID SUSCEPTIBILITY LOCI; T-CELLS; VARIANTS; COAGULATION; ACTIVATION;
IL23R-IL12RB2; MUTATIONS; MEDICINE; RISK; IL10
AB Behcet's disease (BD) is a multi-system inflammatory disorder of unknown etiology. Two recent genome-wide association studies (GWASs) of BD confirmed a strong association with the MHC class I region and identified two non-HLA common genetic variations. In complex diseases, multiple factors may target different sets of genes in the same pathway and thus may cause the same disease phenotype. We therefore hypothesized that identification of disease-associated pathways is critical to elucidate mechanisms underlying BD, and those pathways may be conserved within and across populations. To identify the disease-associated pathways, we developed a novel methodology that combines nominally significant evidence of genetic association with current knowledge of biochemical pathways, protein-protein interaction networks, and functional information of selected SNPs. Using this methodology, we searched for the disease-related pathways in two BD GWASs in Turkish and Japanese case-control groups. We found that 6 of the top 10 identified pathways in both populations were overlapping, even though there were few significantly conserved SNPs/genes within and between populations. The probability of random occurrence of such an event was 2.24E -39. These shared pathways were focal adhesion, MAPK signaling, TGF-beta signaling, ECM-receptor interaction, complement and coagulation cascades, and proteasome pathways. Even though each individual has a unique combination of factors involved in their disease development, the targeted pathways are expected to be mostly the same. Hence, the identification of shared pathways between the Turkish and the Japanese patients using GWAS data may help further elucidate the inflammatory mechanisms in BD pathogenesis.
C1 [Bakir-Gungor, Burcu] Bahcesehir Univ, Dept Genet & Bioinformat, Fac Arts & Sci, Istanbul, Turkey.
[Bakir-Gungor, Burcu] Abdullah Gul Univ, Fac Engn & Nat Sci, Dept Comp Engn, Kayseri, Turkey.
[Remmers, Elaine F.; Kastner, Daniel L.] NHGRI, Inflammatory Dis Sect, NIH, Bethesda, MD 20892 USA.
[Meguro, Akira; Mizuki, Nobuhisa] Yokohama City Univ, Sch Med, Dept Ophthalmol, Yokohama, Kanagawa 232, Japan.
[Gul, Ahmet] Istanbul Univ, Dept Internal Med, Div Rheumatol, Istanbul, Turkey.
[Sezerman, Osman U.] Sabanci Univ, Fac Engn & Nat Sci, Biol Sci & Bioengn, Istanbul, Turkey.
RP Bakir-Gungor, B (reprint author), Abdullah Gul Univ, Fac Engn & Nat Sci, Dept Comp Engn, Kayseri, Turkey.
EM burcub@gatech.edu
FU Intensified Cooperation (IntenC): Promotion of German-Turkish Higher
Education Research Grant of The Scientific and Technological Research
Council of Turkey (TUBITAK) [109S218]; Abdullah Gul University Support
Foundation (AGUV)
FX This work was supported by the Intensified Cooperation (IntenC):
Promotion of German-Turkish Higher Education Research Grant of The
Scientific and Technological Research Council of Turkey (TUBITAK;
109S218). The Abdullah Gul University Support Foundation (AGUV)
supported the work of BB-G.
NR 55
TC 3
Z9 3
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD MAY
PY 2015
VL 23
IS 5
BP 678
EP 687
DI 10.1038/ejhg.2014.158
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA CG1JF
UT WOS:000353028200021
PM 25227143
ER
PT J
AU Kim, J
Sidransky, E
Lopez, G
AF Kim, Jenny
Sidransky, Ellen
Lopez, Grisel
TI Understanding and managing parkinsonism in patients with
glucocerebrosidase mutations
SO EXPERT OPINION ON ORPHAN DRUGS
LA English
DT Review
DE chaperones; Gaucher disease; glucocerebrosidase; parkinsonism
ID RANDOMIZED CONTROLLED-TRIAL; TYPE-1 GAUCHER-DISEASE; ENZYME REPLACEMENT
THERAPY; QUALITY-OF-LIFE; RESTLESS LEGS SYNDROME; NONMOTOR SYMPTOMS;
DOUBLE-BLIND; LEWY BODIES; EARLY-ONSET; RISK-FACTOR
AB Introduction: Identification of an association between mutations in the glucocerebrosidase gene (GBA1) and the development of parkinsonism has contributed to a greater understanding of the role of lysosomal function in neuronal degeneration. This review will discuss the phenotypic presentation of patients with GBA1-associated parkinsonism. Some treatment strategies will be discussed although treatment studies in this cohort are limited.
Areas covered: Current literature suggests that parkinsonism associated with GBA1 mutations may have specific characteristics distinct from idiopathic Parkinson's disease or parkinsonism due to other genetic mutations. In this review, we performed an electronic search in the PubMed database for papers using the terms 'Parkinson disease', 'parkinsonism', 'Gaucher disease', and 'GBA1'. Papers were selected if they discussed or described clinical presentation, treatment and current research efforts related to these terms.
Expert opinion: Although there are no studies identifying treatments specific to patients with GBA1-associated parkinsonism, careful phenotypic characterization is crucial for the elucidation of the interaction between glucocerebrosidase and alpha-synuclein as well as for proper determination of disease prognosis and appropriate clinical counseling.
C1 [Kim, Jenny; Sidransky, Ellen; Lopez, Grisel] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Sidransky, E (reprint author), NHGRI, Med Genet Branch, NIH, Bldg 35A,Room 1E623, Bethesda, MD 20892 USA.
EM sidranse@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute; Intramural Research Program of the National Institutes of
Health
FX This work was supported by the Intramural Research Programs of the
National Human Genome Research Institute and the National Institutes of
Health. 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. This includes employment, consultancies, honoraria,
stock ownership or options, expert testimony, grants or patents,
received or pending, or royalties.
NR 129
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Z9 0
U1 0
U2 3
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 2167-8707
J9 EXPERT OPIN ORPHAN D
JI Exp. Opin. Orphan Drugs
PD MAY
PY 2015
VL 3
IS 5
BP 549
EP 562
DI 10.1517/21678707.2015.1034271
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CG6LK
UT WOS:000353412200006
ER
PT J
AU Grey, MJ
James, SP
Rodgers, GP
AF Grey, Michael J.
James, Stephen P.
Rodgers, Griffin P.
TI NIDDK Programs and Emerging Opportunities for Digestive Diseases
Research
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID PANCREATITIS
C1 [Grey, Michael J.; James, Stephen P.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
[Rodgers, Griffin P.] NIDDK, Off Director, NIH, Bethesda, MD 20892 USA.
RP Grey, MJ (reprint author), NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
NR 2
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD MAY
PY 2015
VL 148
IS 5
BP 868
EP 876
DI 10.1053/j.gastro.2015.03.009
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CG5MJ
UT WOS:000353335700009
PM 25770083
ER
PT J
AU Abnet, CC
Corley, DA
Freedman, ND
Kamangar, F
AF Abnet, Christian C.
Corley, Douglas A.
Freedman, Neal D.
Kamangar, Farin
TI Diet and Upper Gastrointestinal Malignancies
SO GASTROENTEROLOGY
LA English
DT Article
DE Esophageal; Gastric; Cancer; Epidemiology
ID SQUAMOUS-CELL CARCINOMA; GREEN TEA CONSUMPTION; CIRCULATING
25-HYDROXYVITAMIN D; NUTRITION INTERVENTION TRIAL; GENOME-WIDE
ASSOCIATION; COLORECTAL-CANCER RISK; CHRONIC LIVER-DISEASE; SERVICES
TASK-FORCE; CHRONIC HEPATITIS-C; ESOPHAGEAL CANCER
AB Diet is believed to modulate cancer risk and this relationship has been widely studied in the gastrointestinal tract. Observational epidemiologic studies have provided most of the evidence about the effects of diet on cancer risk because clinical trials to determine nutritional exposures are often impossible, impractical, or unaffordable. Although a few foods or nutrients are thought to protect against specific types of cancer, it seems clear that the strength and even direction of dietary associations (increasing or decreasing risk) is organ-site and even histology-specific, along the gastrointestinal tract. Although some hypotheses are supported by a substantial body of observational data (drinking hot mate [an infusion of the herb Ilex Paraguarensis] contributes to esophageal cancer), there are not much data to support others. We discuss some highly touted hypotheses and draw interim conclusions about what is known and what could be done to improve the level of evidence. The complex nature of diet and its associations can be productively investigated with disease-specific studies. However, public health recommendations for normal-risk individuals regarding diet and gastrointestinal cancer should probably emphasize the importance of eating for overall health rather than eating specific foods to reduce risk for specific cancers.
C1 [Abnet, Christian C.; Freedman, Neal D.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Corley, Douglas A.] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
[Kamangar, Farin] Morgan State Univ, Dept Publ Hlth Anal, Sch Community Hlth & Policy, Baltimore, MD 21239 USA.
[Kamangar, Farin] Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran.
RP Abnet, CC (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6e344 MSC 9768, Bethesda, MD 20892 USA.
EM abnetc@mail.nih.gov
RI Freedman, Neal/B-9741-2015; Abnet, Christian/C-4111-2015
OI Freedman, Neal/0000-0003-0074-1098; Abnet, Christian/0000-0002-3008-7843
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute [U54 CA163262]
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health, National Cancer Institute and by
Grant U54 CA163262 (to D.A.C.).
NR 164
TC 13
Z9 14
U1 3
U2 29
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD MAY
PY 2015
VL 148
IS 6
BP 1234
EP U184
DI 10.1053/j.gastro.2015.02.007
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CG5MO
UT WOS:000353336200013
PM 25680671
ER
PT J
AU Wang, YF
Liu, AY
Mills, JL
Boehnke, M
Wilson, AF
Bailey-Wilson, JE
Xiong, MM
Wu, CO
Fan, RZ
AF Wang, Yifan
Liu, Aiyi
Mills, James L.
Boehnke, Michael
Wilson, Alexander F.
Bailey-Wilson, Joan E.
Xiong, Momiao
Wu, Colin O.
Fan, Ruzong
TI Pleiotropy Analysis of Quantitative Traits at Gene Level by Multivariate
Functional Linear Models
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE pleiotropy analysis; rare variants; common variants; association
mapping; quantitative trait loci; complex traits; functional data
analysis; multivariate linear models
ID GENOME-WIDE ASSOCIATION; COMPLEX TRAITS; SUSCEPTIBILITY LOCI; METABOLIC
SYNDROME; GLUCOSE-TOLERANCE; COMMON DISEASES; MULTIPLE TRAITS;
SEQUENCING DATA; RARE VARIANTS; TYPE-2
AB In genetics, pleiotropy describes the genetic effect of a single gene on multiple phenotypic traits. A common approach is to analyze the phenotypic traits separately using univariate analyses and combine the test results through multiple comparisons. This approach may lead to low power. Multivariate functional linear models are developed to connect genetic variant data to multiple quantitative traits adjusting for covariates for a unified analysis. Three types of approximate F-distribution tests based on Pillai-Bartlett trace, Hotelling-Lawley trace, and Wilks's Lambda are introduced to test for association between multiple quantitative traits and multiple genetic variants in one genetic region. The approximate F-distribution tests provide much more significant results than those of F-tests of univariate analysis and optimal sequence kernel association test (SKAT-O). Extensive simulations were performed to evaluate the false positive rates and power performance of the proposed models and tests. We show that the approximate F-distribution tests control the type I error rates very well. Overall, simultaneous analysis of multiple traits can increase power performance compared to an individual test of each trait. The proposed methods were applied to analyze (1) four lipid traits in eight European cohorts, and (2) three biochemical traits in the Trinity Students Study. The approximate F-distribution tests provide much more significant results than those of F-tests of univariate analysis and SKAT-O for the three biochemical traits. The approximate F-distribution tests of the proposed functional linear models are more sensitive than those of the traditional multivariate linear models that in turn are more sensitive than SKAT-O in the univariate case. The analysis of the four lipid traits and the three biochemical traits detects more association than SKAT-O in the univariate case.
C1 [Wang, Yifan; Liu, Aiyi; Fan, Ruzong] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20892 USA.
[Mills, James L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20892 USA.
[Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
[Wilson, Alexander F.; Bailey-Wilson, Joan E.] NHGRI, Computat & Stat Genom Branch, NIH, Bethesda, MD 20892 USA.
[Xiong, Momiao] Univ Texas Houston, Ctr Human Genet, Houston, TX USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP Fan, RZ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20892 USA.
EM fanr@mail.nih.gov
OI Bailey-Wilson, Joan/0000-0002-9153-2920; Liu, Aiyi/0000-0002-6618-5082
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development; Intramural Research
Program of the National Human Genome Research Institute, National
Institutes of Health, Bethesda, MD
FX Two anonymous reviewers and the editors, Dr. Shete and Dr. Cordell,
provided very good and insightful comments for us to improve the
manuscript. We greatly thank the European cohort investigators and the
Trinity Students Study (NICHD, NHGRI, Trinity College, Dublin and the
Health Research Board of Ireland) investigators for letting us analyze
the data and use them as examples. Dr. Stringham and Dr. Teslovich
kindly sent us the data of the European cohorts and patiently answered
many questions about the cohorts, and we greatly appreciated them. This
study was supported by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(Ruzong Fan, Yifan Wang, Aiyi Liu, and James L. Mills), and by the
Intramural Research Program of the National Human Genome Research
Institute (Alexander F. Wilson and Joan E. Bailey-Wilson), National
Institutes of Health, Bethesda, MD. We thank Dr. Seunggeun Lee who sent
us their simulation program of SKAT and sequence data generated by Dr.
Yun Li using program COSI. This study utilized the high-performance
computational capabilities of the Biowulf Linux cluster at the National
Institutes of Health, Bethesda, MD (http://biowulf.nih.gov).
NR 73
TC 18
Z9 18
U1 2
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD MAY
PY 2015
VL 39
IS 4
BP 259
EP 275
DI 10.1002/gepi.21895
PG 17
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA CG4EK
UT WOS:000353235900004
PM 25809955
ER
PT J
AU Mukhopadhyay, B
Schuebel, K
Mukhopadhyay, P
Cinar, R
Godlewski, G
Xiong, KM
Mackie, K
Lizak, M
Yuan, QP
Goldman, D
Kunos, G
AF Mukhopadhyay, Bani
Schuebel, Kornel
Mukhopadhyay, Partha
Cinar, Resat
Godlewski, Grzegorz
Xiong, Keming
Mackie, Ken
Lizak, Martin
Yuan, Qiaoping
Goldman, David
Kunos, George
TI Cannabinoid Receptor 1 Promotes Hepatocellular Carcinoma Initiation and
Progression Through Multiple Mechanisms
SO HEPATOLOGY
LA English
DT Article
ID ANTI-TUMORAL ACTION; INDOLEAMINE 2,3-DIOXYGENASE; ENDOCANNABINOID
SYSTEM; DEPENDENT ACTIVATION; TRANSCRIPTION FACTOR; IMMUNE ESCAPE; CB1
RECEPTORS; CANCER; LIVER; CELLS
AB Hepatocellular carcinoma (HCC) has high mortality and no adequate treatment. Endocannabinoids interact with hepatic cannabinoid 1 receptors (CB1Rs) to promote hepatocyte proliferation in liver regeneration by inducing cell cycle proteins involved in mitotic progression, including Forkhead Box M1. Because this protein is highly expressed in HCC and contributes to its genesis and progression, we analyzed the involvement of the endocannabinoid/CB1R system in murine and human HCC. Postnatal diethylnitrosamine treatment induced HCC within 8 months in wild-type mice but fewer and smaller tumors in CB1R(-/-) mice or in wild-type mice treated with the peripheral CB1R antagonist JD5037, as monitored in vivo by serial magnetic resonance imaging. Genome-wide transcriptome analysis revealed CB1R-dependent, tumor-induced up-regulation of the hepatic expression of CB1R, its endogenous ligand anandamide, and a number of tumor-promoting genes, including the GRB2 interactome as well as Forkhead Box M1 and its downstream target, the tryptophan-catalyzing enzyme indoleamine 2,3-dioxygenase. Increased indoleamine 2,3-dioxygenase activity and consequent induction of immunosuppressive T-regulatory cells in tumor tissue promote immune tolerance. Conclusion: The endocannabinoid/CB1R system is up-regulated in chemically induced HCC, resulting in the induction of various tumor-promoting genes, including indoleamine 2,3-dioxygenase; and attenuation of these changes by blockade or genetic ablation of CB1R suppresses the growth of HCC and highlights the therapeutic potential of peripheral CB1R blockade. (Hepatology 2015;61:1615-1626)
C1 [Mukhopadhyay, Bani; Mukhopadhyay, Partha; Cinar, Resat; Godlewski, Grzegorz; Xiong, Keming; Kunos, George] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Schuebel, Kornel; Yuan, Qiaoping; Goldman, David] NIAAA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Mackie, Ken] Indiana Univ, Gill Ctr Biomol Sci, Bloomington, IN USA.
[Lizak, Martin] NINDS, In Vivo NMR Ctr, NIH, Bethesda, MD 20892 USA.
RP Mukhopadhyay, B (reprint author), NIAAA, 5625 Fishers Lane,MSC-9413, Bethesda, MD 20892 USA.
EM mukhopadhyayb@mail.nih.gov; George.Kunos@nih.gov
RI Goldman, David/F-9772-2010;
OI Goldman, David/0000-0002-1724-5405; CINAR, RESAT/0000-0002-8597-7253
FU National Institute on Alcohol Abuse and Alcoholism
FX Supported by funds from the intramural research program of National
Institute on Alcohol Abuse and Alcoholism.
NR 40
TC 18
Z9 18
U1 3
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 MAY
PY 2015
VL 61
IS 5
BP 1615
EP 1626
DI 10.1002/hep.27686
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CG4DR
UT WOS:000353233500021
PM 25580584
ER
PT J
AU Zhang, GY
Yao, L
Shen, JH
Yang, YH
Zhao, XJ
AF Zhang, Gaoyan
Yao, Li
Shen, Jiahui
Yang, Yihong
Zhao, Xiaojie
TI Reorganization of Functional Brain Networks Mediates the Improvement of
Cognitive Performance Following Real-Time Neurofeedback Training of
Working Memory
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE functional reorganization; working memory network; default mode network;
mediation effect; real-time neurofeedback; working memory
ID POSTERIOR CINGULATE CORTEX; DEFAULT MODE NETWORK; PREFRONTAL CORTEX;
RESTING-STATE; TOP-DOWN; RANDOM-FIELDS; CONNECTIVITY; FMRI; ACTIVATION;
ATTENTION
AB Working memory (WM) is essential for individuals' cognitive functions. Neuroimaging studies indicated that WM fundamentally relied on a frontoparietal working memory network (WMN) and a cinguloparietal default mode network (DMN). Behavioral training studies demonstrated that the two networks can be modulated by WM training. Different from the behavioral training, our recent study used a real-time functional MRI (rtfMRI)-based neurofeedback method to conduct WM training, demonstrating that WM performance can be significantly improved after successfully upregulating the activity of the target region of interest (ROI) in the left dorsolateral prefrontal cortex (Zhang et al., [2013]: PloS One 8:e73735); however, the neural substrate of rtfMRI-based WM training remains unclear. In this work, we assessed the intranetwork and internetwork connectivity changes of WMN and DMN during the training, and their correlations with the change of brain activity in the target ROI as well as with the improvement of post-training behavior. Our analysis revealed an ROI-network-behavior correlation relationship underlying the rtfMRI training. Further mediation analysis indicated that the reorganization of functional brain networks mediated the effect of self-regulation of the target brain activity on the improvement of cognitive performance following the neurofeedback training. The results of this study enhance our understanding of the neural basis of real-time neurofeedback and suggest a new direction to improve WM performance by regulating the functional connectivity in the WM related networks. Hum Brain Mapp 36:1705-1715, 2015. (c) 2014 Wiley Periodicals, Inc.
C1 [Zhang, Gaoyan; Yao, Li; Zhao, Xiaojie] Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
[Zhang, Gaoyan] Tianjin Univ, Sch Comp Sci & Technol, Tianjin Key Lab Cognit Comp & Applicat, Tianjin 300072, Peoples R China.
[Yao, Li; Shen, Jiahui; Zhao, Xiaojie] Beijing Normal Univ, Coll Informat Sci & Technol, Beijing 100875, Peoples R China.
[Yang, Yihong] NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
RP Zhao, XJ (reprint author), Beijing Normal Univ, Coll Informat Sci & Technol, Beijing 100875, Peoples R China.
EM yihongyang@mail.nih.gov; zhaoxj86@hotmail.com
FU National Natural Science Foundation of China [61210001, 61473044];
National Program on Key Basic Research Project (973 Program)
[2013CB329301]; National Institute on Drug Abuse, National Institutes of
Health
FX Contract grant sponsor: Funds for International Cooperation and Exchange
of the National Natural Science Foundation of China; Contract grant
number: 61210001; Contract grant sponsor: National Program on Key Basic
Research Project (973 Program); Contract grant number: 2013CB329301;
Contract grant sponsor: National Natural Science Foundation of China;
Contract grant number: 61473044; Contract grant sponsor: Intramural
Research Program of the National Institute on Drug Abuse, National
Institutes of Health (to Y.Y.).
NR 44
TC 2
Z9 2
U1 3
U2 21
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD MAY
PY 2015
VL 36
IS 5
BP 1705
EP 1715
DI 10.1002/hbm.22731
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA CG1XH
UT WOS:000353068300006
PM 25545862
ER
PT J
AU Wu, T
Hou, YA
Hallett, M
Zhang, JR
Chan, P
AF Wu, Tao
Hou, Yanan
Hallett, Mark
Zhang, Jiarong
Chan, Piu
TI Lateralization of Brain Activity Pattern During Unilateral Movement in
Parkinson's Disease
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE Parkinson's disease; lateralization of brain activity; basal ganglia
circuits; transcallosal inhibition; compensation
ID TRANSCRANIAL MAGNETIC STIMULATION; SUPPLEMENTARY MOTOR AREA;
CEREBRAL-BLOOD-FLOW; EXTERNALLY TRIGGERED MOVEMENTS; SEQUENTIAL FINGER
MOVEMENTS; DORSAL PREMOTOR CORTEX; MIRROR MOVEMENTS; BASAL GANGLIA;
INTERHEMISPHERIC INHIBITION; FUNCTIONAL MRI
AB We investigated the lateralization of brain activity pattern during performance of unilateral movement in drug-naive Parkinson's disease (PD) patients with only right hemiparkinsonian symptoms. Functional MRI was obtained when the subjects performed strictly unilateral right hand movement. A laterality index was calculated to examine the lateralization. Patients had decreased activity in the left putamen and left supplementary motor area, but had increased activity in the right primary motor cortex, right premotor cortex, left postcentral gyrus, and bilateral cerebellum. The laterality index was significantly decreased in PD patients compared with controls (0.41 +/- 0.14 vs. 0.84 +/- 0.09). The connectivity from the left putamen to cortical motor regions and cerebellum was decreased, while the interactions between the cortical motor regions, cerebellum, and right putamen were increased. Our study demonstrates that in early PD, the lateralization of brain activity during unilateral movement is significantly reduced. The dysfunction of the striatum-cortical circuit, decreased transcallosal inhibition, and compensatory efforts from cortical motor regions, cerebellum, and the less affected striatum are likely reasons contributing to the reduced motor lateralization. The disruption of the lateralized brain activity pattern might be a reason underlying some motor deficits in PD, like mirror movements or impaired bilateral motor coordination. Hum Brain Mapp 36:1878-1891, 2015. (c) 2015 Wiley Periodicals, Inc.
C1 [Wu, Tao; Hou, Yanan; Zhang, Jiarong; Chan, Piu] Capital Med Univ, Beijing Inst Geriatr, Xuanwu Hosp,Minist Educ, Dept Neurobiol,Key Lab Neurodegenerat Disorders, Beijing 100053, Peoples R China.
[Wu, Tao; Hou, Yanan; Zhang, Jiarong; Chan, Piu] Beijing Inst Brain Disorders, Beijing Key Lab Parkinsons Dis, Parkinson Dis Ctr, Beijing, Peoples R China.
[Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Wu, T (reprint author), Capital Med Univ, Beijing Inst Geriatr, Xuanwu Hosp,Minist Educ, Dept Neurobiol,Key Lab Neurodegenerat Disorders, Beijing 100053, Peoples R China.
EM wutao69@gmail.com
FU National Science Foundation of China [81071012, 81271429]
FX Contract grant sponsor: The National Science Foundation of China;
Contract grant number: 81071012; 81271429
NR 118
TC 5
Z9 5
U1 3
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD MAY
PY 2015
VL 36
IS 5
BP 1878
EP 1891
DI 10.1002/hbm.22743
PG 14
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA CG1XH
UT WOS:000353068300018
PM 25644527
ER
PT J
AU Vanderbeck, S
Bockhorst, J
Kleiner, D
Komorowski, R
Chalasani, N
Gawrieh, S
AF Vanderbeck, Scott
Bockhorst, Joseph
Kleiner, David
Komorowski, Richard
Chalasani, Naga
Gawrieh, Samer
TI Automatic quantification of lobular inflammation and hepatocyte
ballooning in nonalcoholic fatty liver disease liver biopsies
SO HUMAN PATHOLOGY
LA English
DT Article
DE Fatty liver; Lobular inflammation; Hepatocyte ballooning; Machine
learning; NAFLD activity score; Digital image analysis
ID SCORING SYSTEM; HEPATITIS-C; STEATOHEPATITIS; PREVALENCE; VALIDATION;
CIRRHOSIS; OUTCOMES
AB Automatic quantification of cardinal histologic features of nonalcoholic fatty liver disease (NAFLD) may reduce human variability and allow continuous rather than semiquantitative assessment of injury. We recently developed an automated classifier that can detect and quantify macrosteatosis with greater than or equal to 95% precision and recall (sensitivity). Here, we report our early results on the classifier's performance in detecting lobular inflammation and hepatocellular ballooning. Automatic quantification of lobular inflammation and ballooning was performed on digital images of hematoxylin and eosin stained slides of liver biopsy samples from 59 individuals with normal liver histology and varying severity of NAFLD. Two expert hepatopathologists scored liver biopsies according the nonalcoholic steatohepatitis clinical research network scoring system and provided annotations of lobular inflammation and hepatocyte ballooning on the digital images. The classifier had precision and recall of 70% and 49% for lobular inflammation, and 91% and 54% for hepatocyte ballooning. In addition, the classifier had an area under the curve of 95% for lobular inflammation and 98% for hepatocyte, ballooning. The Spearman rank correlation coefficient for comparison with pathologist grades was 45.2% for lobular inflammation and 46% for hepatocyte ballooning. Our novel observations demonstrate that automatic quantification of cardinal NAFLD histologic lesions is feasible and offer promise for further development of automatic quantification as a potential aid to pathologists evaluating NAFLD biopsies in clinical practice and clinical trials. (C) 2015 Elsevier Inc. All rights reserved..
C1 [Vanderbeck, Scott; Bockhorst, Joseph] Univ Wisconsin, Dept Elect Engn & Comp Sci, Milwaukee, WI 53211 USA.
[Kleiner, David] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Komorowski, Richard] Med Coll Wisconsin, Dept Pathol, Milwaukee, WI 53226 USA.
[Chalasani, Naga; Gawrieh, Samer] Indiana Univ Sch Med, Div Gastroenterol & Hepatol, Indianapolis, IN 46202 USA.
RP Gawrieh, S (reprint author), Indiana Univ Sch Med, Div Gastroenterol & Hepatol, 702 Rotary Circle, Indianapolis, IN 46202 USA.
EM sgawrieh@iu.edu
OI Kleiner, David/0000-0003-3442-4453
FU Milwaukee Research Foundation University of Wisconsin (Milwaukee, WI)
[PRJ-391B]; Intramural Research Program of the National Cancer
Institute, National Institutes of Health; University of Wisconsin
Extension Ideadvance Seed Fund; WI Economic Development Corporation
(Madison, WI); University of Wisconsin System (Madison, WI)
FX This research was supported by the Milwaukee Research Foundation
University of Wisconsin (Milwaukee, WI) (J. B. and S. G.) grant number
PRJ-391B and in part by the Intramural Research Program of the National
Cancer Institute, National Institutes of Health (D. K.).; SV is owner
and founder of Organic Research Corporation (Milwaukee, WI), a start-up
funded in part by a grant from the University of Wisconsin Extension
Ideadvance Seed Fund through its partnership with the WI Economic
Development Corporation (Madison, WI) and the University of Wisconsin
System (Madison, WI). The work contained herein was completed in its
entirety while Vanderbeck was a student at University of Wisconsin
Milwaukee, WI, before founding Organic Research Corporation.
NR 24
TC 0
Z9 0
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 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD MAY
PY 2015
VL 46
IS 5
BP 767
EP 775
DI 10.1016/j.humpath.2015.01.019
PG 9
WC Pathology
SC Pathology
GA CG5EQ
UT WOS:000353314300017
PM 25776030
ER
PT J
AU Alonso, WJ
Guillebaud, J
Viboud, C
Razanajatovo, NH
Orelle, A
Zhou, SZ
Randrianasolo, L
Heraud, JM
AF Alonso, Wladimir Jimenez
Guillebaud, Julia
Viboud, Cecile
Razanajatovo, Norosoa Harline
Orelle, Arnaud
Zhou, Steven Zhixiang
Randrianasolo, Laurence
Heraud, Jean-Michel
TI Influenza seasonality in Madagascar: the mysterious African free-runner
SO Influenza and Other Respiratory Viruses
LA English
DT Article
DE Influenza; Madagascar; population connectivity; seasonality; time
series; viral migration
ID VIRUS SUBTYPE H1N1; A VIRUS; SENTINEL SURVEILLANCE; WEST-AFRICA;
CIRCULATION; DYNAMICS; PERSISTENCE; MORTALITY; SYNCHRONY; ILLNESS
AB BackgroundThe seasonal drivers of influenza activity remain debated in tropical settings where epidemics are not clearly phased. Antananarivo is a particularly interesting case study because it is in Madagascar, an island situated in the tropics and with quantifiable connectivity levels to other countries.
ObjectivesWe aimed at disentangling the role of environmental forcing and population fluxes on influenza seasonality in Madagascar.
MethodsWe compiled weekly counts of laboratory-confirmed influenza-positive specimens for the period 2002 to 2012 collected in Antananarivo, with data available from sub-Saharan countries and countries contributing most foreign travelers to Madagascar. Daily climate indicators were compiled for the study period.
ResultsOverall, influenza activity detected in Antananarivo predated that identified in temperate Northern Hemisphere locations. This activity presented poor temporal matching with viral activity in other countries from the African continent or countries highly connected to Madagascar excepted for A(H1N1)pdm09. Influenza detection in Antananarivo was not associated with travel activity and, although it was positively correlated with all climatic variables studied, such association was weak.
ConclusionsThe timing of influenza activity in Antananarivo is irregular, is not driven by climate, and does not align with that of countries in geographic proximity or highly connected to Madagascar. This work opens fresh questions regarding the drivers of influenza seasonality globally particularly in mid-latitude and less-connected regions to tailor vaccine strategies locally.
C1 [Alonso, Wladimir Jimenez; Viboud, Cecile] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Guillebaud, Julia; Razanajatovo, Norosoa Harline; Orelle, Arnaud; Heraud, Jean-Michel] Inst Pasteur Madagascar, Natl Influenza Ctr, Antananarivo 101, Madagascar.
[Orelle, Arnaud] Integrated Qual Lab Serv IQLS, Lyon, France.
[Zhou, Steven Zhixiang] London Sch Hyg & Trop Med, London WC1, England.
[Randrianasolo, Laurence] Inst Pasteur Madagascar, Epidemiol Unit, Antananarivo 101, Madagascar.
RP Heraud, JM (reprint author), Inst Pasteur Madagascar, Virol Unit, Natl Influenza Ctr, BP 1274, Antananarivo 101, Madagascar.
EM jmheraud@pasteur.mg
RI HERAUD, Jean-Michel/O-1464-2013
OI HERAUD, Jean-Michel/0000-0003-1107-0859
NR 40
TC 4
Z9 4
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1750-2640
EI 1750-2659
J9 INFLUENZA OTHER RESP
JI Influenza Other Respir. Viruses
PD MAY
PY 2015
VL 9
IS 3
BP 101
EP 109
DI 10.1111/irv.12308
PG 9
WC Infectious Diseases; Virology
SC Infectious Diseases; Virology
GA CG6JU
UT WOS:000353407400002
PM 25711873
ER
PT J
AU Vajda, S
Plotz, T
Fink, GA
AF Vajda, Szilard
Ploetz, Thomas
Fink, Gernot A.
TI Camera-Based Whiteboard Reading for Understanding Mind Maps
SO INTERNATIONAL JOURNAL OF PATTERN RECOGNITION AND ARTIFICIAL INTELLIGENCE
LA English
DT Article
DE Camera-based document recognition; whiteboard reading; mind map
recognition; handwriting recognition; document layout analysis
ID HANDWRITING RECOGNITION; LAYOUT ANALYSIS; SEPARATION; CHARACTER;
ALGORITHM
AB Mind maps, i.e. the spatial organization of ideas and concepts around a central topic and the visualization of their relations, represent a very powerful and thus popular means to support creative thinking and problem solving processes. Typically created on traditional whiteboards, they represent an important technique for collaborative brainstorming sessions. We describe a camera-based system to analyze hand-drawn mind maps written on a whiteboard. The goal of the presented system is to produce digital representations of such mind maps, which would enable digital asset management, i.e. storage and retrieval of manually created documents. Our system is based on image acquisition by means of a camera, followed by the segmentation of the particular whiteboard image focusing on the extraction of written context, i.e. the ideas captured by the mind map. The spatial arrangement of these ideas is recovered using layout analysis based on unsupervised clustering, which results in graph representations of mind maps. Finally, handwriting recognition derives textual transcripts of the ideas captured by the mind map. We demonstrate the capabilities of our mind map reading system by means of an experimental evaluation, where we analyze images of mind maps that have been drawn on whiteboards, without any further constraints other than the underlying topic. In addition to the promising recognition results, we also discuss training strategies, which effectively allow for system bootstrapping using out-of-domain sample data. The latter is important when addressing creative thinking processes where domain-related training data are difficult to obtain as they focus on novelty by definition.
C1 [Vajda, Szilard] NIH, Lister Hill Natl Ctr Biomed Commun, Natl Lib Med, Bethesda, MD 20892 USA.
[Ploetz, Thomas] Newcastle Univ, Sch Comp Sci, Newcastle Upon Tyne NE7 1NP, Tyne & Wear, England.
[Fink, Gernot A.] TU Dortmund Univ, Dept Comp Sci, D-44221 Dortmund, Germany.
RP Vajda, S (reprint author), NIH, Lister Hill Natl Ctr Biomed Commun, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM szilard.vajda@nih.gov; t.ploetz@ncl.ac.uk; gernot.fink@udo.edu
FU German Research Foundation (DFG) [Fi799/3]
FX This work has been supported by the German Research Foundation (DFG)
within project Fi799/3. The authors would also like to thank Leonard
Rothacker for his valuable support in the implementation of the
whiteboard reading system.
NR 55
TC 2
Z9 2
U1 1
U2 19
PU WORLD SCIENTIFIC PUBL CO PTE LTD
PI SINGAPORE
PA 5 TOH TUCK LINK, SINGAPORE 596224, SINGAPORE
SN 0218-0014
EI 1793-6381
J9 INT J PATTERN RECOGN
JI Int. J. Pattern Recognit. Artif. Intell.
PD MAY
PY 2015
VL 29
IS 3
AR 1553003
DI 10.1142/S0218001415530031
PG 26
WC Computer Science, Artificial Intelligence
SC Computer Science
GA CG8IS
UT WOS:000353551500007
ER
PT J
AU Sherman, ME
Piedmonte, M
Mai, PL
Greene, MH
AF Sherman, Mark E.
Piedmonte, Marion
Mai, Phuong L.
Greene, Mark H.
TI Pathologic Findings at Risk-Reducing Surgery Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
C1 [Sherman, Mark E.; Mai, Phuong L.; Greene, Mark H.] NCI, Rockville, MD 20850 USA.
[Piedmonte, Marion] Roswell Pk Canc Inst, NRG Oncol Stat & Data Ctr, Buffalo, NY 14263 USA.
RP Sherman, ME (reprint author), NCI, Rockville, MD 20850 USA.
NR 2
TC 0
Z9 0
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 MAY 1
PY 2015
VL 33
IS 13
BP 1515
EP 1515
DI 10.1200/JCO.2014.60.2482
PG 1
WC Oncology
SC Oncology
GA CG4CQ
UT WOS:000353230100020
PM 25732162
ER
PT J
AU Xue, Y
Wang, L
Xia, D
Li, Q
Gao, S
Dong, M
Cai, T
Shi, S
He, L
Hu, K
Mao, T
Duan, X
AF Xue, Y.
Wang, L.
Xia, D.
Li, Q.
Gao, S.
Dong, M.
Cai, T.
Shi, S.
He, L.
Hu, K.
Mao, T.
Duan, X.
TI Dental Abnormalities Caused by Novel Compound Heterozygous CTSK
Mutations
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE pycnodysostosis; cathepsin K; molecular biology; tooth; dental cementum;
alveolar bone
ID CATHEPSIN-K; PYCNODYSOSTOSIS; BONE; PYKNODYSOSTOSIS; ODONTOCLASTS;
MICROSCOPY; RESORPTION; FEATURES; CEMENTUM; PATIENT
AB Cathepsin K (CTSK) is an important protease responsible for degrading type I collagen, osteopontin, and other bone matrix proteins. The mutations in the CTSK gene can cause pycnodysostosis (OMIM 265800), a rare autosomal recessive bone dysplasia. Patients with pycnodysostosis have been reported to present specific dental abnormalities; however, whether these dental abnormalities are related to dysfunctional CTSK has never been reported. Here we investigated the histologic changes of cementum and alveolar bone in a pycnodysostosis patient, caused by novel compound heterozygous mutations in the CTSK gene (c.87 G>A p.W29X and c.848 A>G p.Y283C). The most impressive manifestations in tooth were extensive periradicular high-density clumps with unclear periodontal space by orthopantomography examination and micro-computed tomography scanning analysis. Hematoxylin/eosin and toluidine blue staining and atomic force microscopy analysis showed that the cementum became significantly thickened, softened, and full of cementocytes. The disorganized bone structure was the main character of alveolar bone. The p.W29X mutation may represent the loss-of-function allele with an earlier termination codon in the precursor CTSK polypeptide. Residue Y283 is highly conserved among papain-like cysteine proteases. Three-dimensional structure modeling analysis found that the loss of the hydroxybenzene residue in the Y283C mutation would interrupt the hydrogen network and possibly affect the self-cleavage of the CTSK enzyme. Furthermore, p.Y283C mutation did not affect the mRNA and protein levels of overexpressed CTSK in COS-7 system but did reduce CTSK enzyme activity. In conclusion, the histologic and ultrastructural changes of cementum and alveolar bone might be affected by CTSK mutation via reduction of its enzyme activity (clinical trial registration: ChiCTR-TNC-10000876).
C1 [Xue, Y.; Duan, X.] Fourth Mil Med Univ, Sch Stomatol, Clin Oral Rare & Genet Dis, State Key Lab Mil Stomatol,Dept Oral Biol, Xian 710032, Shaanxi, Peoples R China.
[Wang, L.] Fourth Mil Med Univ, Dept Mol Biol, Xian 710032, Shaanxi, Peoples R China.
[Xia, D.; Li, Q.; Gao, S.; Dong, M.] Aarhus Univ, Interdisciplinary Nanosci Ctr iNANO, Aarhus C, Denmark.
[Cai, T.] Natl Inst Dent & Craniofacial Res, Oral Infect & Immun Branch, NIH, Bethesda, MD USA.
[Shi, S.] Univ So Calif, Ctr Craniofacial Mol Biol, Sch Dent, Los Angeles, CA 90033 USA.
[He, L.; Hu, K.; Mao, T.] Fourth Mil Med Univ, Sch Stomatol, Dept Oral & Maxillofacial Surg, State Key Lab Mil Stomatol, Xian 710032, Shaanxi, Peoples R China.
RP Duan, X (reprint author), Fourth Mil Med Univ, Sch Stomatol, Clin Oral Rare & Genet Dis, State Key Lab Mil Stomatol,Dept Oral Biol, 145 West Changle Rd, Xian 710032, Shaanxi, Peoples R China.
EM xhduan@fmmu.edu.cn
RI Xia, Dan/O-9779-2014; Li, Qiang/L-7741-2013; Dong, Mingdong/B-3341-2010
OI Xia, Dan/0000-0001-7892-7381; Li, Qiang/0000-0003-1056-4152; Dong,
Mingdong/0000-0002-2025-2171
FU National Natural Science Foundation of China [NSFC 81271116, NSFC
81300861]
FX This work was supported in part by grants of the National Natural
Science Foundation of China (NSFC 81271116 for X.D., NSFC 81300861 for
Y.X.). We thank the patient, his family members, and the controls for
joining this research. We are also grateful for the technique support
from Equipment Center of PLA Institute of Stomatological Research. The
authors declare no potential conflicts of interest with respect to the
authorship and/or publication of this article.
NR 22
TC 4
Z9 5
U1 4
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
EI 1544-0591
J9 J DENT RES
JI J. Dent. Res.
PD MAY
PY 2015
VL 94
IS 5
BP 674
EP 681
DI 10.1177/0022034515573964
PG 8
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA CG3VN
UT WOS:000353207800006
PM 25731711
ER
PT J
AU Foster, BL
Sheen, CR
Hatch, NE
Liu, J
Cory, E
Narisawa, S
Kiffer-Moreira, T
Sah, RL
Whyte, MP
Somerman, MJ
Millan, JL
AF Foster, B. L.
Sheen, C. R.
Hatch, N. E.
Liu, J.
Cory, E.
Narisawa, S.
Kiffer-Moreira, T.
Sah, R. L.
Whyte, M. P.
Somerman, M. J.
Millan, J. L.
TI Periodontal Defects in the A116T Knock-in Murine Model of
Odontohypophosphatasia
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE alkaline phosphatase; hypophosphatasia; bone; cementum; dentin;
periodontium
ID INFANTILE HYPOPHOSPHATASIA; BONE; MICE; OSTEOPONTIN; PHENOTYPE;
CEMENTUM; VIVO
AB Mutations in ALPL result in hypophosphatasia (HPP), a disease causing defective skeletal mineralization. ALPL encodes tissue nonspecific alkaline phosphatase (ALP), an enzyme that promotes mineralization by reducing inorganic pyrophosphate, a mineralization inhibitor. In addition to skeletal defects, HPP causes dental defects, and a mild clinical form of HPP, odontohypophosphatasia, features only a dental phenotype. The Alpl knockout (Alpl(-/-)) mouse phenocopies severe infantile HPP, including profound skeletal and dental defects. However, the severity of disease in Alpl(-/-) mice prevents analysis at advanced ages, including studies to target rescue of dental tissues. We aimed to generate a knock-in mouse model of odontohypophosphatasia with a primarily dental phenotype, based on a mutation (c.346G>A) identified in a human kindred with autosomal dominant odontohypophosphatasia. Biochemical, skeletal, and dental analyses were performed on the resulting Alpl(+/A116T) mice to validate this model. Alpl(+/A116T) mice featured 50% reduction in plasma ALP activity compared with wild-type controls. No differences in litter size, survival, or body weight were observed in Alpl(+/A116T) versus wild-type mice. The postcranial skeleton of Alpl(+/A116T) mice was normal by radiography, with no differences in femur length, cortical/trabecular structure or mineral density, or mechanical properties. Parietal bone trabecular compartment was mildly altered. Alpl(+/A116T) mice featured alterations in the alveolar bone, including radiolucencies and resorptive lesions, osteoid accumulation on the alveolar bone crest, and significant differences in several bone properties measured by micro-computed tomography. Nonsignificant changes in acellular cementum did not appear to affect periodontal attachment or function, although circulating ALP activity was correlated significantly with incisor cementum thickness. The Alpl(+/A116T) mouse is the first model of odontohypophosphatasia, providing insights on dentoalveolar development and function under reduced ALP, bringing attention to direct effects of HPP on alveolar bone, and offering a new model for testing potential dental-targeted therapies in future studies.
C1 [Foster, B. L.; Somerman, M. J.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Sheen, C. R.; Narisawa, S.; Kiffer-Moreira, T.; Millan, J. L.] Sanford Burnham Med Res Inst, Sanford Childrens Hlth Res Ctr, La Jolla, CA 92037 USA.
[Hatch, N. E.; Liu, J.] Univ Michigan, Sch Dent, Dept Orthodont & Pediat Dent, Ann Arbor, MI 48109 USA.
[Cory, E.; Sah, R. L.] Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA.
[Whyte, M. P.] Shriners Hosp Children, Ctr Metab Bone Dis & Mol Res, St Louis, MO USA.
[Whyte, M. P.] Washington Univ, Sch Med, Div Bone & Mineral Dis, St Louis, MO USA.
RP Millan, JL (reprint author), Sanford Burnham Med Res Inst, Sanford Childrens Hlth Res Ctr, La Jolla, CA 92037 USA.
EM millan@sanfordburnham.org
RI Foster, Brian/H-8375-2015
OI Foster, Brian/0000-0003-3444-0576
FU National Institute for Dental and Craniofacial Research of the National
Institutes of Health (NIH; Bethesda, MD) [DE 12889]; National Institute
of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) /NIH [AR
066110]; Intramural Research Program of NIAMS; Shriners Hospitals for
Children
FX This research was supported by a grant (DE 12889) to J.L.M. from the
National Institute for Dental and Craniofacial Research of the National
Institutes of Health (NIH; Bethesda, MD), a grant (AR 066110) to B.L.F.
from the National Institute of Arthritis and Musculoskeletal and Skin
Diseases (NIAMS) /NIH, the Intramural Research Program of NIAMS
(M.J.S.), and support from Shriners Hospitals for Children (M.P.W.). We
thank Kenn Holmbeck (National Institute for Dental and Craniofacial
Research) and Lyudmila Lukashova (Hospital for Special Surgery, New
York, NY, USA; NIH AR 046121) for assistance with micro-computed
tomography analysis, Nasrin Kalantari Pour (NIAMS) for assistance with
histology, and Helen Wimer (Smithsonian Institute, Washington, DC) for
assistance with plastic sectioning and staining. We thank Ling Wang of
the Sanford-Burnham Medical Research Institute Animal Facility for
assistance with blastocyst injection and Greg Martin and Sergey
Kupriyanov of The Scripps Research Institute Mouse Genetics Core for
assistance with embryonic stem cell electroporation. We also thank
Carmen Huesa for assistance with 3-point bending analysis. The authors
declare no potential conflicts of interest with respect to the
authorship and/or publication of this article.
NR 28
TC 6
Z9 6
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
EI 1544-0591
J9 J DENT RES
JI J. Dent. Res.
PD MAY
PY 2015
VL 94
IS 5
BP 706
EP 714
DI 10.1177/0022034515573273
PG 9
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA CG3VN
UT WOS:000353207800010
PM 25716980
ER
PT J
AU Kondo, Y
Nakamoto, T
Jaramillo, Y
Choi, S
Catalan, MA
Melvin, JE
AF Kondo, Y.
Nakamoto, T.
Jaramillo, Y.
Choi, S.
Catalan, M. A.
Melvin, J. E.
TI Functional Differences in the Acinar Cells of the Murine Major Salivary
Glands
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE epithelia; physiology; salivary physiology; chloride channel; Na-K-Cl
transporter; calcium signaling
ID FLUID SECRETION; CL--HCO3-EXCHANGE; MOUSE; CHANNEL; TMEM16A;
COTRANSPORTERS; ELECTROLYTE; EXPRESSION; TRANSPORT; MICE
AB In humans, approximately 90% of saliva is secreted by the 3 major salivary glands: the parotid (PG), the submandibular (SMG), and the sublingual glands (SLG). Even though it is known that all 3 major salivary glands secrete saliva by a Cl--dependent mechanism, salivary secretion rates differ greatly among these glands. The goal of this study was to gain insight into the properties of the ion-transporting pathways in acinar cells that might account for the differences among the major salivary glands. Pilocarpine-induced saliva was simultaneously collected in vivo from the 3 major salivary glands of mice. When normalized by gland weight, the amount of saliva secreted by the PG was more than 2-fold larger than that obtained from the SMG and SLG. At the cellular level, carbachol induced an increase in the intracellular [Ca2+] that was more than 2-fold larger in PG and SMG than in SLG acinar cells. Carbachol-stimulated Cl- efflux and the protein levels of the Ca2+-activated Cl- channel TMEM16A, the major apical Cl- efflux pathway in salivary acinar cells, were significantly greater in PG compared with SMG and SLG. In addition, we evaluated the transporter activity of the Na+-K+-2Cl(-) cotransporters (NKCC1) and anion exchangers (AE), the 2 primary basolateral Cl- uptake mechanisms in acinar cells. The SMG NKCC1 activity was about twice that of the PG and more than 12-fold greater than that of the SLG. AE activity was similar in PG and SLG, and both PG and SLG AE activity was about 2-fold larger than that of SMG. In summary, the salivation kinetics of the 3 major glands are distinct, and these differences can be explained by the unique functional properties of each gland related to Cl- movement, including the transporter activities of the Cl- uptake and efflux pathways, and intracellular Ca2+ mobilization.
C1 [Kondo, Y.; Jaramillo, Y.; Choi, S.; Catalan, M. A.; Melvin, J. E.] Natl Inst Dent & Craniofacial Res, Secretory Mech & Dysfunct Sect, NIH, Bethesda, MD 20892 USA.
[Kondo, Y.; Nakamoto, T.] Kyushu Dent Univ, Dept Oral Reconstruct & Rehabil, Kitakyushu, Fukuoka, Japan.
RP Melvin, JE (reprint author), Natl Inst Dent & Craniofacial Res, Secretory Mech & Dysfunct Sect, NIH, 10 Ctr Dr,Bldg 10,Room 1N117B, Bethesda, MD 20892 USA.
EM james.melvin@nih.gov
OI Catalan, Marcelo/0000-0003-3544-2821
FU Intramural Research Program of the National Institutes of Health [NIH,
National Institute of Dental and Craniofacial Research (NIDCR)]
FX The Secretory Mechanisms and Dysfunction Section is supported by the
Intramural Research Program of the National Institutes of Health [NIH,
National Institute of Dental and Craniofacial Research (NIDCR)]. We are
thankful to Drs. Z. Borok, E.D. Crandall, and U.P. Flodby for providing
the ACID mice and to Dr. Natalie Porat-Shliom for helping with the data
analysis using ImageJ software. The authors declare no potential
conflicts of interest with respect to the authorship and/or publication
of this article.
NR 25
TC 3
Z9 3
U1 0
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
EI 1544-0591
J9 J DENT RES
JI J. Dent. Res.
PD MAY
PY 2015
VL 94
IS 5
BP 715
EP 721
DI 10.1177/0022034515570943
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA CG3VN
UT WOS:000353207800011
PM 25680367
ER
PT J
AU Myers, SL
Yang, CZ
Bittner, GD
Witt, KL
Tice, RR
Baird, DD
AF Myers, Sharon L.
Yang, Chun Z.
Bittner, George D.
Witt, Kristine L.
Tice, Raymond R.
Baird, Donna D.
TI Estrogenic and anti-estrogenic activity of off-the-shelf hair and skin
care products
SO Journal of Exposure Science and Environmental Epidemiology
LA English
DT Article
DE cosmetics; endocrine disruptors; estrogen receptor binding; estrogenic
activity; anti-estrogenic activity; personal care products
ID BREAST-CANCER; PREPUBERTAL GYNECOMASTIA; ENVIRONMENTAL ESTROGENS;
PHTHALATE METABOLITES; URINARY-EXCRETION; WOMEN; PARABENS; POPULATION;
CREAM; ASSAY
AB Use of personal care products is widespread in the United States but tends to be greater among African Americans than whites. Of special concern is the possible hazard of absorption of chemicals with estrogenic activity (EA) or anti-EA (AEA) in these products. Such exposure may have adverse health effects, especially when it occurs during developmental windows (e.g., prepubertally) when estrogen levels are low. We assessed the ethanol extracts of eight commonly used hair and skin products popular among African Americans for EA and AEA using a cell proliferation assay with the estrogen sensitive MCF-7: WS8 cell line derived from a human breast cancer. Four of the eight personal care products tested (Oil Hair Lotion, Extra-dry Skin Lotion, Intensive Skin Lotion, Petroleum Jelly) demonstrated detectable EA, whereas three (Placenta Hair Conditioner, Tea-Tree Hair Conditioner, Cocoa Butter Skin Cream) exhibited AEA. Our data indicate that hair and skin care products can have EA or AEA, and suggest that laboratory studies are warranted to investigate the in vivo activity of such products under chronic exposure conditions as well as epidemiologic studies to investigate potential adverse health effects that might be associated with use of such products.
C1 [Myers, Sharon L.; Baird, Donna D.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Myers, Sharon L.] Univ Calif Davis, Hlth Syst, Sacramento, CA 95817 USA.
[Yang, Chun Z.; Bittner, George D.] CertiChem, Austin, TX USA.
[Bittner, George D.] Univ Texas Austin, Neurobiol Sect, Austin, TX 78712 USA.
[Bittner, George D.] Univ Texas Austin, Sch Biol, Austin, TX 78712 USA.
[Witt, Kristine L.; Tice, Raymond R.] NIEHS, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Baird, DD (reprint author), NIEHS, Epidemiol Branch, POB 12233, Res Triangle Pk, NC 27709 USA.
EM baird@niehs.nih.gov
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU Divisions of Intramural Research and the National Toxicology Program of
the National Institute of Environmental Health Sciences at the National
Institutes of Health (NIH); NIH [1R43/44 ES014806, 01-03]
FX This work was supported by the Divisions of Intramural Research and the
National Toxicology Program of the National Institute of Environmental
Health Sciences at the National Institutes of Health (NIH), and by NIH
grant 1R43/44 ES014806, 01-03 to C.Z.Y. This article may be the work
product of an employee or group of employees of the NIH; however, the
statements, opinions or conclusions contained therein do not necessarily
represent the statements, opinions or conclusions of NIH or the United
States government. We thank Aimee D'Aloisio, Elizabeth Maull, and Kyla
Taylor who critically reviewed an earlier draft of the manuscript.
NR 57
TC 3
Z9 3
U1 9
U2 40
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1559-0631
EI 1559-064X
J9 J EXPO SCI ENV EPID
JI J. Expo. Sci. Environ. Epidemiol.
PD MAY-JUN
PY 2015
VL 25
IS 3
BP 271
EP 277
DI 10.1038/jes.2014.32
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA CG6JF
UT WOS:000353405500006
PM 24849798
ER
PT J
AU Trabert, B
Chen, Z
Kannan, K
Peterson, CM
Pollack, AZ
Sun, L
Louis, GMB
AF Trabert, Britton
Chen, Zhen
Kannan, Kurunthachalam
Peterson, C. Matthew
Pollack, Anna Z.
Sun, Liping
Louis, Germaine M. Buck
TI Persistent organic pollutants (POPs) and fibroids: results from the ENDO
study
SO Journal of Exposure Science and Environmental Epidemiology
LA English
DT Article
DE epidemiology; uterine fibroids; persistent organic pollutants; omental
fat; serum
ID POLYBROMINATED DIPHENYL ETHERS; UTERINE LEIOMYOMAS; ORGANOCHLORINE
PESTICIDES; POLYCHLORINATED-BIPHENYLS; ADIPOSE-TISSUE; SERUM;
ENDOMETRIOSIS; EXPOSURE; POPULATION; CHEMICALS
AB To evaluate the association between persistent organic pollutants (POPs) and uterine fibroids, we used previously collected data from a cohort of women aged 18-44 years undergoing laparoscopy or laparotomy at 14 participating hospital surgical centers (n = 473). POP concentrations were measured in omental fat and serum. Presence of fibroids was defined on the basis of a postoperative diagnosis (n = 99). Odds ratios (OR) and 95% confidence interval (CI) for each POP by biologic medium were estimated using unconditional logistic regression adjusted for identified covariates. Concentrations were higher in omental fat than in serum for all POPs. Serum p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) was the only POP associated with fibroids (per 1-SD increase in log-transformed p,p'-DDE OR (95% CI): 1.37 (1.05-1.80)). In analyses excluding women diagnosed with endometriosis, a number of polychlorinated biphenyls (PCBs) measured in omental fat were associated with fibroids (PCB 99: 1.64 (1.08, 2.49); PCB 138: 1.64 (1.03, 2.59); PCB 146: 1.54 (1.01, 2.37); PCB 153: 1.88 (1.12, 3.13); PCB 196: 1.60 (1.02, 2.51); PCB 206: 1.52 (1.01, 2.29)). Although exploratory, our study suggests that PCBs may be associated with fibroids in the absence of other gynecologic disorders such as endometriosis, but the associations varied by biologic media with more POPs emerging when quantified in fat.
C1 [Trabert, Britton] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Chen, Zhen; Sun, Liping; Louis, Germaine M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
[Kannan, Kurunthachalam] SUNY Albany, Wadsworth Ctr, New York State Dept Hlth, Div Environm Hlth Sci, Albany, NY 12222 USA.
[Kannan, Kurunthachalam] SUNY Albany, Dept Environm Hlth Sci, Albany, NY 12222 USA.
[Peterson, C. Matthew] Univ Utah, Dept Obstet & Gynecol, Div Reprod Endocrinol & Infertil, Salt Lake City, UT USA.
[Pollack, Anna Z.] George Mason Univ, Coll Hlth & Human Serv, Dept Global & Community Hlth, Fairfax, VA 22030 USA.
RP Trabert, B (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM britton.trabert@nih.gov
RI Trabert, Britton/F-8051-2015;
OI Pollack, Anna/0000-0002-4313-3298; Buck Louis,
Germaine/0000-0002-1774-4490
FU Intramural Research Program, Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD), National Institutes of
Health [NO1-DK-6-3428, NO1-DK-6-3427, 10001406-02]
FX This work was funded in part by the Intramural Research Program, Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD), National Institutes of Health (contracts NO1-DK-6-3428,
NO1-DK-6-3427, 10001406-02 and 10001406-02). Ethicon Endo-Surgery, LLC,
donated the HARMONIC ACE 36P shears and scalpel blades through a signed
materials transfer agreement with the University of Utah and NICHD.
NR 34
TC 3
Z9 3
U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1559-0631
EI 1559-064X
J9 J EXPO SCI ENV EPID
JI J. Expo. Sci. Environ. Epidemiol.
PD MAY-JUN
PY 2015
VL 25
IS 3
BP 278
EP 285
DI 10.1038/jes.2014.31
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA CG6JF
UT WOS:000353405500007
PM 24802554
ER
PT J
AU Spaan, S
Pronk, A
Koch, HM
Jusko, TA
Jaddoe, VWV
Shaw, PA
Tiemeier, HM
Hofman, A
Pierik, FH
Longnecker, MP
AF Spaan, Suzanne
Pronk, Anjoeka
Koch, Holger M.
Jusko, Todd A.
Jaddoe, Vincent W. V.
Shaw, Pamela A.
Tiemeier, Henning M.
Hofman, Albert
Pierik, Frank H.
Longnecker, Matthew P.
TI Reliability of concentrations of organophosphate pesticide metabolites
in serial urine specimens from pregnancy in the Generation R Study
SO Journal of Exposure Science and Environmental Epidemiology
LA English
DT Article
DE organophosphate pesticide metabolites; environmental exposure;
variability; reliability; cohort study; epidemiologic studies
ID DIALKYL PHOSPHATE METABOLITES; MEXICAN-AMERICAN CHILDREN; IN-UTERO;
AGRICULTURAL COMMUNITY; EXPOSURE; ASSOCIATION; WOMEN; NEURODEVELOPMENT;
CHLORPYRIFOS; POPULATION
AB The widespread use of organophosphate (OP) pesticides has resulted in ubiquitous exposure in humans, primarily through their diet. Exposure to OP pesticides may have adverse health effects, including neurobehavioral deficits in children. The optimal design of new studies requires data on the reliability of urinary measures of exposure. In the present study, urinary concentrations of six dialkyl phosphate (DAP) metabolites, the main urinary metabolites of OP pesticides, were determined in 120 pregnant women participating in the Generation R Study in Rotterdam. Intra-class correlation coefficients (ICCs) across serial urine specimens taken at <18, 18-25, and >25 weeks of pregnancy were determined to assess reliability. Geometric mean total DAP metabolite concentrations were 229 (GSD 2.2), 240 (GSD 2.1), and 224 (GSD 2.2) nmol/g creatinine across the three periods of gestation. Metabolite concentrations from the serial urine specimens in general correlated moderately. The ICCs for the six DAP metabolites ranged from 0.14 to 0.38 (0.30 for total DAPs), indicating weak to moderate reliability. Although the DAP metabolite levels observed in this study are slightly higher and slightly more correlated than in previous studies, the low to moderate reliability indicates a high degree of within-person variability, which presents challenges for designing well-powered epidemiological studies.
C1 [Spaan, Suzanne; Pronk, Anjoeka] TNO, Dept Risk Anal Prod Dev, NL-3700 AJ Zeist, Netherlands.
[Koch, Holger M.] Ruhr Univ Bochum, Inst Prevent & Occupat Med German Social Accid In, Bochum, Germany.
[Jusko, Todd A.] Univ Rochester, Sch Med & Dent, Dept Publ Hlth Sci, Rochester, NY USA.
[Jusko, Todd A.] Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY USA.
[Jaddoe, Vincent W. V.; Tiemeier, Henning M.; Hofman, Albert] Erasmus MC, Generat R Study Grp, Rotterdam, Netherlands.
[Jaddoe, Vincent W. V.; Hofman, Albert] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Jaddoe, Vincent W. V.] Erasmus MC, Dept Pediat, Rotterdam, Netherlands.
[Shaw, Pamela A.] Univ Penn, Perelman Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA USA.
[Tiemeier, Henning M.] Erasmus MC, Dept Child & Adolescent Psychiat, Rotterdam, Netherlands.
[Pierik, Frank H.] TNO, Dept Urban Environm & Safety, Utrecht, Netherlands.
[Longnecker, Matthew P.] NIEHS, Epidemiol Branch, NIH, DHHS, Res Triangle Pk, NC USA.
RP Spaan, S (reprint author), TNO, Dept Risk Anal Prod Dev, Utrechtseweg 48,POB 360, NL-3700 AJ Zeist, Netherlands.
EM suzanne.spaan@tno.nl
RI Koch, Holger/B-3277-2011;
OI Koch, Holger/0000-0002-8328-2837; Tiemeier, Henning/0000-0002-4395-1397;
Longnecker, Matthew/0000-0001-6073-5322
FU Erasmus MC, Rotterdam; Erasmus University Rotterdam; Netherlands
Organization for Health Research and Development (ZonMw); National
Institutes of Health, National Institute of Environmental Health
Sciences from the National Institutes of Health (NIH, USA) [K12
ES019852, P30 001247]
FX The Generation R Study is conducted by the Erasmus MC, University
Medical Center, Rotterdam, the Netherlands in close collaboration with
the School of Law and Faculty of Social Sciences of the Erasmus
University Rotterdam, the Municipal Health Service Rotterdam area, the
Rotterdam Homecare Foundation and the Stichting Trombose-dienst and
Artsenlaboratorium Rijnmond (STAR), Rotterdam. We gratefully acknowledge
the contribution of general practitioners, hospitals, midwives and
pharmacies in Rotterdam. The first phase of the Generation R Study is
made possible by financial support from the Erasmus MC, Rotterdam, the
Erasmus University Rotterdam and the Netherlands Organization for Health
Research and Development (ZonMw). We also thank Edwin van Wijngaarden
for reviewing previous versions of the manuscript. This research
received support from the Intramural Research Program of the National
Institutes of Health, National Institute of Environmental Health
Sciences and grants K12 ES019852 and P30 001247 from the National
Institutes of Health (NIH, USA). We are grateful to R. Hauser of Harvard
University for the suggestion to collect multiple urine specimens from
subjects.
NR 51
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Z9 4
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1559-0631
EI 1559-064X
J9 J EXPO SCI ENV EPID
JI J. Expo. Sci. Environ. Epidemiol.
PD MAY-JUN
PY 2015
VL 25
IS 3
BP 286
EP 294
DI 10.1038/jes.2014.81
PG 9
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA CG6JF
UT WOS:000353405500008
PM 25515376
ER
PT J
AU Persky, S
McBride, CM
Faith, MS
Wagner, LK
Ward, DS
AF Persky, Susan
McBride, Colleen M.
Faith, Myles S.
Wagner, Laura K.
Ward, Dianne S.
TI Mothers' guilt responses to children's obesity risk feedback
SO JOURNAL OF HEALTH PSYCHOLOGY
LA English
DT Article
DE family health history; guilt; obesity; parent; risk communication
ID GENETIC INFORMATION; PREDICTING OBESITY; PARENTAL OBESITY; CHILDHOOD;
INDIVIDUALS; OVERWEIGHT; BEHAVIORS; ADULTHOOD; FAMILIES
AB This study explored the influence of family health history-based obesity risk feedback for their child on 147 overweight mothers' guilt related to children's lifestyle behaviors and passing down a genetic propensity for overweight. Mothers were randomized to receive, or not, obesity risk feedback for their 4- to 5-year-old child and then made food choices for them using a virtual reality-based buffet. Receipt of risk information increased lifestyle- and genetics-related guilt. Choosing fewer unhealthful foods for the child attenuated both types of guilt. Work in this area may aid in development of obesity risk feedback strategies that enhance child feeding.
C1 [Persky, Susan; McBride, Colleen M.; Wagner, Laura K.] NHGRI, Bethesda, MD 20892 USA.
[Faith, Myles S.; Ward, Dianne S.] Univ N Carolina, Chapel Hill, NC 27515 USA.
RP Persky, S (reprint author), NHGRI, Social & Behav Res Branch, NIH, 31 Ctr Dr,Rm B1B36, Bethesda, MD 20892 USA.
EM perskys@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Human Genome Research Institute, National Institutes of Health.
NR 27
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U1 4
U2 8
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1359-1053
EI 1461-7277
J9 J HEALTH PSYCHOL
JI J. Health Psychol.
PD MAY
PY 2015
VL 20
IS 5
SI SI
BP 649
EP 658
DI 10.1177/1359105315576608
PG 10
WC Psychology, Clinical
SC Psychology
GA CG7FJ
UT WOS:000353467700018
PM 25903251
ER
PT J
AU Davis, AS
Chertow, DS
Moyer, JE
Suzich, J
Sandouk, A
Dorward, DW
Logun, C
Shelhamer, JH
Taubenberger, JK
AF Davis, A. Sally
Chertow, Daniel S.
Moyer, Jenna E.
Suzich, Jon
Sandouk, Aline
Dorward, David W.
Logun, Carolea
Shelhamer, James H.
Taubenberger, Jeffery K.
TI Validation of Normal Human Bronchial Epithelial Cells as a Model for
Influenza A Infections in Human Distal Trachea
SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
LA English
DT Article
DE confocal microscopy; electron microscopy; experimental pathology;
immunohistochemistry; respiratory tract; viruses; viral diseases
ID HUMAN AIRWAY EPITHELIUM; HUMAN RESPIRATORY-TRACT; RECEPTOR SPECIFICITY;
VIRUS HEMAGGLUTININ; HUMAN LUNG; BINDING-SPECIFICITY;
BETA-PROPIOLACTONE; SECRETORY PROTEIN; LIQUID INTERFACE; DERMAL MATRIX
AB Primary normal human bronchial/tracheal epithelial (NHBE) cells, derived from the distal-most aspect of the trachea at the bifurcation, have been used for a number of studies in respiratory disease research. Differences between the source tissue and the differentiated primary cells may impact infection studies based on this model. Therefore, we examined how well-differentiated NHBE cells compared with their source tissue, the human distal trachea, as well as the ramifications of these differences on influenza A viral pathogenesis research using this model. We employed a histological analysis including morphological measurements, electron microscopy, multi-label immunofluorescence confocal microscopy, lectin histochemistry, and microarray expression analysis to compare differentiated NHBEs to human distal tracheal epithelium. Pseudostratified epithelial height, cell type variety and distribution varied significantly. Electron microscopy confirmed differences in cellular attachment and paracellular junctions. Influenza receptor lectin histochemistry revealed that 2,3 sialic acids were rarely present on the apical aspect of the differentiated NHBE cells, but were present in low numbers in the distal trachea. We bound fluorochrome bioconjugated virus to respiratory tissue and NHBE cells and infected NHBE cells with human influenza A viruses. Both indicated that the pattern of infection progression in these cells correlated with autopsy studies of fatal cases from the 2009 pandemic.
C1 [Davis, A. Sally; Chertow, Daniel S.; Moyer, Jenna E.; Sandouk, Aline; Taubenberger, Jeffery K.] NIAID, Viral Pathogenesis & Evolut Sect, NIH, Bethesda, MD 20892 USA.
[Davis, A. Sally] Kansas State Univ, Coll Vet Med, Diagnost Med Pathobiol, Manhattan, KS 66506 USA.
[Chertow, Daniel S.; Suzich, Jon; Logun, Carolea; Shelhamer, James H.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Dorward, David W.] NIAID, Electron Microscopy Unit, Res Technol Branch, Hamilton, MT USA.
RP Taubenberger, JK (reprint author), NIAID, Viral Pathogenesis & Evolut Sect, NIH, 33 North Dr,MSC 3203, Bethesda, MD 20892 USA.
EM taubenbergerj@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institute of Health; NIH Comparative Molecular Pathology Research
Training Program
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: This work was
supported by the Intramural Research Program of the National Institute
of Allergy and Infectious Diseases, National Institute of Health. ASD
and JKT are further thankful for the support of the NIH Comparative
Molecular Pathology Research Training Program.
NR 66
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Z9 7
U1 1
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0022-1554
EI 1551-5044
J9 J HISTOCHEM CYTOCHEM
JI J. Histochem. Cytochem.
PD MAY
PY 2015
VL 63
IS 5
BP 312
EP 328
DI 10.1369/0022155415570968
PG 17
WC Cell Biology
SC Cell Biology
GA CG9KO
UT WOS:000353634100002
PM 25604814
ER
PT J
AU Kim, SYH
De Vries, R
Parnami, S
Wilson, R
Kim, HM
Frank, S
Holloway, RG
Kieburtz, K
AF Kim, Scott Y. H.
De Vries, Raymond
Parnami, Sonali
Wilson, Renee
Kim, H. Myra
Frank, Samuel
Holloway, Robert G.
Kieburtz, Karl
TI Are therapeutic motivation and having one's own doctor as researcher
sources of therapeutic misconception?
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Article
ID ADVANCED PARKINSONS-DISEASE; SHAM-SURGERY; CLINICAL-TRIALS;
DOUBLE-BLIND; ONCOLOGY
AB Background Desire for improvement in one's illness and having one's own doctor functioning as a researcher are thought to promote therapeutic misconception (TM), a phenomenon in which research subjects are said to conflate research with treatment.
Purpose To examine whether subjects' therapeutic motivation and own doctor functioning as researcher are associated with TM.
Methods We interviewed 90 persons with advanced Parkinson's disease (PD) enrolled or intending to enrol in sham surgery controlled neurosurgical trials, using qualitative interviews. Subjects were compared by motivation (primarily therapeutic vs primarily altruistic or dually motivated by altruistic and therapeutic motivation), and by doctor status (own doctor as site investigator vs not) on the following: understanding of purpose of study; understanding of research procedures; perception of chance of direct benefit; and recollection and perceptions concerning the risks.
Results 60% had primarily therapeutic motivation and 44% had their own doctor as the site investigator, but neither were generally associated with increased TM responses. Overall level of understanding of purpose and procedures of research were high. Subjects responded with generally high estimates of probability of direct benefit, but their rationales were personal and complex. The therapeutic-motivation group was more sensitive to risks. Five (5.6%) subjects provided incorrect answers to the question about purpose of research, and yet, showed excellent understanding of research procedures.
Conclusions In persons with PD involved in sham surgery clinical trials, being primarily motivated by desire for direct benefit to one's illness or having one's own doctor as the site investigator were not associated with greater TM responses.
C1 [Kim, Scott Y. H.] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Kim, Scott Y. H.; De Vries, Raymond; Parnami, Sonali] Univ Michigan, Ctr Bioeth & Social Sci Med, Ann Arbor, MI 48109 USA.
[De Vries, Raymond] Univ Michigan, Dept Med Educ, Ann Arbor, MI 48109 USA.
[Wilson, Renee; Kieburtz, Karl] Univ Rochester, Ctr Human Expt Therapeut, Rochester, NY USA.
[Kim, H. Myra] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Frank, Samuel] Boston Univ, Dept Neurol, Boston, MA 02215 USA.
[Holloway, Robert G.; Kieburtz, Karl] Univ Rochester, Dept Neurol, Rochester, NY USA.
[Holloway, Robert G.] Univ Rochester, Dept Community & Prevent Med, Rochester, NY USA.
[Kieburtz, Karl] Univ Rochester, Dept Environm Med, Rochester, NY USA.
RP Kim, SYH (reprint author), NIH, Dept Bioeth, 10 Ctr Dr,1C118, Bethesda, MD 20892 USA.
EM scott.kim@nih.gov
FU National Institute for Neurological Disorders and Stroke [R01-NS062770];
CTSA award from the National Center for Research Resources [UL1
RR024160]; National Center for Advancing Translational Sciences of the
National Institutes of Health
FX This work was supported by the National Institute for Neurological
Disorders and Stroke (R01-NS062770) and a CTSA award (UL1 RR024160) from
the National Center for Research Resources and the National Center for
Advancing Translational Sciences of the National Institutes of Health.
NR 18
TC 4
Z9 4
U1 0
U2 3
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 MAY
PY 2015
VL 41
IS 5
BP 391
EP 397
DI 10.1136/medethics-2013-101987
PG 7
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA CG6EL
UT WOS:000353388900010
PM 24855070
ER
PT J
AU DeGrazia, D
AF DeGrazia, David
TI Creation ethics: reproduction, genetics and quality of life
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Editorial Material
C1 NIH, Dept Bioeth, Bethesda, MD 20814 USA.
RP DeGrazia, D (reprint author), NIH, Dept Bioeth, Bldg 10,Rm 1C118,10 Ctr Dr, Bethesda, MD 20814 USA.
EM ddd@gwu.edu
FU National Institutes of Health Clinical Center
FX This work was supported, in part, by intramural funds from the National
Institutes of Health Clinical Center. The views expressed are the
author's own. They do not represent the position or policy of the
National Institutes of Health, the US Public Health Service or the
Department of Health and Human Services.
NR 1
TC 0
Z9 0
U1 1
U2 3
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 MAY
PY 2015
VL 41
IS 5
BP 415
EP 416
DI 10.1136/medethics-2013-101917
PG 2
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA CG6EL
UT WOS:000353388900015
PM 24368841
ER
PT J
AU DeGrazia, D
AF DeGrazia, David
TI A reply to critics of Creation Ethics
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Editorial Material
C1 NIH, Dept Bioeth, Bethesda, MD 20814 USA.
RP DeGrazia, D (reprint author), NIH, Dept Bioeth, Bldg 10,Rm 1C118,10 Ctr Dr, Bethesda, MD 20814 USA.
EM ddd@gwu.edu
FU National Institutes of Health Clinical Center
FX This work was supported, in part, by intramural funds from the National
Institutes of Health Clinical Center. The views expressed here are the
author's own. They do not represent the position or policy of NIH, the
US Public Health Service, or the Department of Health and Human
Services.
NR 4
TC 0
Z9 0
U1 0
U2 0
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 MAY
PY 2015
VL 41
IS 5
BP 423
EP 424
DI 10.1136/medethics-2014-102531
PG 2
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA CG6EL
UT WOS:000353388900020
PM 25691666
ER
PT J
AU Li, LL
Hamel, N
Baker, K
McGuffin, MJ
Couillard, M
Gologan, A
Marcus, VA
Chodirker, B
Chudley, A
Stefanovici, C
Durandy, A
Hegele, RA
Feng, BJ
Goldgar, DE
Zhu, J
De Rosa, M
Gruber, SB
Wimmer, K
Young, B
Chong, G
Tischkowitz, MD
Foulkes, WD
AF Li, Lili
Hamel, Nancy
Baker, Kristi
McGuffin, Michael J.
Couillard, Martin
Gologan, Adrian
Marcus, Victoria A.
Chodirker, Bernard
Chudley, Albert
Stefanovici, Camelia
Durandy, Anne
Hegele, Robert A.
Feng, Bing-Jian
Goldgar, David E.
Zhu, Jun
De Rosa, Marina
Gruber, Stephen B.
Wimmer, Katharina
Young, Barbara
Chong, George
Tischkowitz, Marc D.
Foulkes, William D.
TI A homozygous PMS2 founder mutation with an attenuated constitutional
mismatch repair deficiency phenotype
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
ID CANCER SYNDROME; GENE; DIAGNOSIS
AB Background Inherited mutations in DNA mismatch repair genes predispose to different cancer syndromes depending on whether they are mono-allelic or bi-allelic. This supports a causal relationship between expression level in the germline and phenotype variation. As a model to study this relationship, our study aimed to define the pathogenic characteristics of a recurrent homozygous coding variant in PMS2 displaying an attenuated phenotype identified by clinical genetic testing in seven Inuit families from Northern Quebec.
Methods Pathogenic characteristics of the PMS2 mutation NM_000535.5: c.2002A>G were studied using genotype-phenotype correlation, single-molecule expression detection and single genome microsatellite instability analysis.
Results This PMS2 mutation generates a de novo splice site that competes with the authentic site. In homozygotes, expression of the full-length protein is reduced to a level barely detectable by conventional diagnostics. Median age at primary cancer diagnosis is 22 years among 13 NM_000535.5: c.2002A>G homozygotes, versus 8 years in individuals carrying biallelic truncating mutations. Residual expression of full-length PMS2 transcript was detected in normal tissues from homozygotes with cancers in their 20s.
Conclusions Our genotype-phenotype study of c.2002A>G illustrates that an extremely low level of PMS2 expression likely delays cancer onset, a feature that could be exploited in cancer preventive intervention.
C1 [Li, Lili; Hamel, Nancy; Couillard, Martin; Tischkowitz, Marc D.; Foulkes, William D.] McGill Univ, Dept Oncol, Program Canc Genet, Montreal, PQ H3T 1E2, Canada.
[Li, Lili; Hamel, Nancy; Couillard, Martin; Tischkowitz, Marc D.; Foulkes, William D.] McGill Univ, Dept Human Genet, Program Canc Genet, Montreal, PQ H3T 1E2, Canada.
[Li, Lili; Chong, George; Tischkowitz, Marc D.; Foulkes, William D.] McGill Univ, Dept Human Genet, Montreal, PQ H3T 1E2, Canada.
[Hamel, Nancy; Foulkes, William D.] McGill Univ, Dept Med Genet, Ctr Hlth, Montreal, PQ H3T 1E2, Canada.
[Baker, Kristi] McGill Univ, Dept Pathol, Montreal, PQ H3T 1E2, Canada.
[Baker, Kristi] Brigham & Womens Hosp, Div Gastroenterol, Boston, MA 02115 USA.
[McGuffin, Michael J.] Ecole Technol Super, Dept Software & Informat Technol Engn, Montreal, PQ, Canada.
[Couillard, Martin; Tischkowitz, Marc D.; Foulkes, William D.] McGill Univ, Jewish Gen Hosp, Lady Davis Inst Med Res, Montreal, PQ H3T 1E2, Canada.
[Gologan, Adrian; Chong, George] McGill Univ, Jewish Gen Hosp, Dept Pathol, Montreal, PQ H3T 1E2, Canada.
[Marcus, Victoria A.] McGill Univ, Ctr Hlth, Dept Pathol, Montreal, PQ H3T 1E2, Canada.
[Chodirker, Bernard; Chudley, Albert] Univ Manitoba, Dept Pediat & Child Hlth, Winnipeg, MB R3T 2N2, Canada.
[Chodirker, Bernard; Chudley, Albert] Dept Biochem & Med Genet, Winnipeg, MB, Canada.
[Stefanovici, Camelia] Univ Manitoba, Fac Med, Dept Pathol, Winnipeg, MB, Canada.
[Durandy, Anne] Hop Necker Enfants Malad, INSERM, U768, Paris, France.
[Hegele, Robert A.] Univ Western Ontario, Robarts Res Inst, London, ON, Canada.
[Hegele, Robert A.] Univ Western Ontario, Schulich Sch Med & Dent, London, ON, Canada.
[Feng, Bing-Jian; Goldgar, David E.] Univ Utah, Hlth Sci Ctr, Dept Dermatol, Salt Lake City, UT USA.
[Zhu, Jun] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[De Rosa, Marina] Univ Naples Federico II, Dept Mol Med & Med Biotechnol, Naples, Italy.
[De Rosa, Marina] Univ Naples Federico II, CEINGE Biotechnol Avanzate, Naples, Italy.
[Gruber, Stephen B.] Univ So Calif, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Wimmer, Katharina] Med Univ Innsbruck, Dept Med Genet Mol & Clin Pharmacol, Div Human Genet, A-6020 Innsbruck, Austria.
[Young, Barbara] McGill Univ, Ctr Hlth, Dept Med, Montreal, PQ H3T 1E2, Canada.
[Young, Barbara] Hlth Canada Quebec Reg, Nations & Inuit Hlth Branch 1, Montreal, PQ, Canada.
[Tischkowitz, Marc D.] Univ Cambridge, Dept Med Genet, Cambridge, England.
RP Foulkes, WD (reprint author), McGill Univ, Jewish Gen Hosp, Lady Davis Inst, 3755 Cote Ste Catherine Rd, Montreal, PQ H3T 1E2, Canada.
EM william.foulkes@mcgill.ca
RI Hegele, Robert/G-3301-2011;
OI Baker, Kristi/0000-0002-2993-3889; foulkes, william/0000-0001-7427-4651
FU Canadian Gene Cure Foundation; Canadian Cancer Society Research
Institute [700252]; Systems Biology Training Program by Canadian
Institute of Health Research
FX This work was supported by grants from the Canadian Gene Cure Foundation
and the Canadian Cancer Society Research Institute (grant # 700252). LL
received fellowship funding from the Systems Biology Training Program by
the Canadian Institute of Health Research.
NR 18
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U1 0
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
EI 1468-6244
J9 J MED GENET
JI J. Med. Genet.
PD MAY
PY 2015
VL 52
IS 5
BP 348
EP 352
DI 10.1136/jmedgenet-2014-102934
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA CG1NX
UT WOS:000353041000009
PM 25691505
ER
PT J
AU Chittiboina, P
Heiss, JD
Lonser, RR
AF Chittiboina, Prashant
Heiss, John D.
Lonser, Russell R.
TI Accuracy of direct magnetic resonance imaging-guided placement of drug
infusion cannulae
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE accuracy; convection-enhanced delivery; brainstem glioma; gadolinium;
magnetic resonance imaging; targeting; surgical technique
ID CONVECTION-ENHANCED DELIVERY; GLIOBLASTOMA; BRAIN; TRIAL; MRI
AB An intraoperative MRI (iMRI)-compatible system has been developed for direct placement of convection-enhanced delivery (CED) cannulae using real-time imaging. To establish the precision and feasibility of this technology, the authors analyzed findings in patients who underwent direct iMRI CED cannula placement.
Three consecutive patients underwent iMRI-guided placement of CED infusion cannulae (6 cannulae) for treatment of diffuse intrinsic brainstem glioma (2 patients) or Parkinson's disease (1 patient). Convective infusion cannulae were guided to the target using the ClearPoint iMRI-based navigation platform (MRI Interventions, Inc.). Placement accuracy was analyzed.
Real-time iMRI during infusion cannula insertion allowed for monitoring of trajectory accuracy during placement. During cannula insertion, no reinsertions or changes due to errors in targeting were necessary. The mean radial error was 1.0 +/- 0.5 mm (+/- SD). There was no correlation between the total length of the planned trajectory and the radial error (Pearson's coefficient: -0.40; p = 0.5). The mean anteroposterior and lateral errors were 0.9 +/- 0.5 and 0.3 +/- 0.2 mm, respectively. The mean in-plane distance error was 1.0 +/- 0.4 mm. The mean tip error (scalar distance between the planned target and actual tip) was 1.9 +/- 0.9 mm. There was no correlation between the length of the planned trajectory and any of the measured errors. No complications were associated with cannula placement.
Real-time iMRI-based targeting and monitoring of infusion cannula placement is a safe, effective, and accurate technique that should enable more selective perfusion of brain regions.
C1 [Chittiboina, Prashant; Heiss, John D.; Lonser, Russell R.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Lonser, Russell R.] Ohio State Univ, Wexner Med Ctr, Dept Neurol Surg, Columbus, OH 43210 USA.
RP Lonser, RR (reprint author), Ohio State Univ, Wexner Med Ctr, Dept Neurol Surg, 410 W 10th Ave,N1047 Doan Hall, Columbus, OH 43210 USA.
EM russell.lonser@osumc.edu
OI Heiss, John/0000-0002-3890-0165
FU National Institute of Neurological Disorders and Stroke (NINDS) at the
National Institutes of Health
FX This study was funded by the intramural research program of the National
Institute of Neurological Disorders and Stroke (NINDS) at the National
Institutes of Health. IL13-PE was provided by InSys Therapeutics, Inc.,
under a cooperative research and development agreement with NINDS. The
Smart Flow cannula and Clear Point system were provided by MRI
Interventions, Inc., under a clinical trial agreement with NINDS.
NR 19
TC 5
Z9 5
U1 0
U2 9
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 MAY
PY 2015
VL 122
IS 5
BP 1173
EP 1179
DI 10.3171/2014.11.JNS131888
PG 7
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA CG5XP
UT WOS:000353369500027
PM 25594325
ER
PT J
AU Lukas, VA
Fishbein, KW
Lin, PC
Schar, M
Schneider, E
Neu, CP
Spencer, RG
Reiter, DA
AF Lukas, Vanessa A.
Fishbein, Kenneth W.
Lin, Ping-Chang
Schaer, Michael
Schneider, Erika
Neu, Corey P.
Spencer, Richard G.
Reiter, David A.
TI Classification of Histologically Scored Human Knee Osteochondral Plugs
by Quantitative Analysis of Magnetic Resonance Images at 3T
SO JOURNAL OF ORTHOPAEDIC RESEARCH
LA English
DT Article
DE osteoarthritis; imaging; cartilage matrix; quantitative MRI;
classification
ID OSTEOARTHRITIS CARTILAGE HISTOPATHOLOGY; SUPERFICIAL ZONE PROTEIN;
ARTICULAR-CARTILAGE; IN-VIVO; TIBIOFEMORAL JOINT; HYALINE CARTILAGE;
RELAXATION-TIMES; T-2 RELAXATION; MRI; T2
AB This work evaluates the ability of quantitative MRI to discriminate between normal and pathological human osteochondral plugs characterized by the Osteoarthritis Research Society International (OARSI) histological system. Normal and osteoarthritic human osteochondral plugs were scored using the OARSI histological system and imaged at 3 T using MRI sequences producing T1 and T2 contrast and measuring T-1, T-2, and T-2* relaxation times, magnetization transfer, and diffusion. The classification accuracies of quantitative MRI parameters and corresponding weighted image intensities were evaluated. Classification models based on the Mahalanobis distance metric for each MRI measurement were trained and validated using leave-one-out cross-validation with plugs grouped according to OARSI histological grade and score. MRI measurements used for classification were performed using a region-of-interest analysis which included superficial, deep, and full-thickness cartilage. The best classifiers based on OARSI grade and score were T-1- and T-2-weighted image intensities, which yielded accuracies of 0.68 and 0.75, respectively. Classification accuracies using OARSI score-based group membership were generally higher when compared with grade-based group membership. MRI-based classificationeither using quantitative MRI parameters or weighted image intensitiesis able to detect early osteoarthritic tissue changes as classified by the OARSI histological system. These findings suggest the benefit of incorporating quantitative MRI acquisitions in a comprehensive clinical evaluation of OA. (c) 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:640-650, 2015.
C1 [Lukas, Vanessa A.; Fishbein, Kenneth W.; Spencer, Richard G.; Reiter, David A.] NIA, Lab Clin Invest, NIH, Baltimore, MD 21224 USA.
[Lin, Ping-Chang] Howard Univ, Coll Med, Dept Radiol, Washington, DC USA.
[Schaer, Michael] Philips Healthcare, Highland Hts, OH USA.
[Schneider, Erika] Cleveland Clin Fdn, Imaging Inst, Cleveland, OH 44195 USA.
[Neu, Corey P.] Purdue Univ, Weldon Sch Biomed Engn, W Lafayette, IN 47907 USA.
RP Reiter, DA (reprint author), NIA, Lab Clin Invest, NIH, 3001 S Hanover St, Baltimore, MD 21224 USA.
EM reiterda@mail.nih.gov
RI Lin, Ping-Chang/C-9811-2009;
OI Lin, Ping-Chang/0000-0003-0918-4072; Schar, Michael/0000-0002-7044-9941;
Fishbein, Kenneth/0000-0002-6353-4603
FU National Institutes of Health; National Institute on Aging; NIH [R01
AR063712]
FX Grant sponsor: Intramural Research Program of the National Institutes of
Health; Grant sponsor: National Institute on Aging; Grant sponsor: NIH;
Grant number: R01 AR063712.
NR 53
TC 3
Z9 3
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0736-0266
EI 1554-527X
J9 J ORTHOP RES
JI J. Orthop. Res.
PD MAY
PY 2015
VL 33
IS 5
BP 640
EP 650
DI 10.1002/jor.22810
PG 11
WC Orthopedics
SC Orthopedics
GA CG6NB
UT WOS:000353417300005
PM 25641500
ER
PT J
AU Coelho, SG
Valencia, JC
Yin, LL
Smuda, C
Mahns, A
Kolbe, L
Miller, SA
Beer, JZ
Zhang, GF
Tuma, PL
Hearing, VJ
AF Coelho, Sergio G.
Valencia, Julio C.
Yin, Lanlan
Smuda, Christoph
Mahns, Andre
Kolbe, Ludger
Miller, Sharon A.
Beer, Janusz Z.
Zhang, Guofeng
Tuma, Pamela L.
Hearing, Vincent J.
TI UV exposure modulates hemidesmosome plasticity, contributing to
long-term pigmentation in human skin
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE hemidesmosome; skin; pigmentation; ultraviolet radiation; sunburn
ID ULTRAVIOLET-RADIATION; HUMAN KERATINOCYTES; SOX PROTEINS; IN-SITU;
MELANOMA; DIFFERENTIATION; ASSOCIATION; GENE; DNA; PROLIFERATION
AB Human skin colour, ie pigmentation, differs widely among individuals, as do their responses to various types of ultraviolet radiation (UV) and their risks of skin cancer. In some individuals, UV-induced pigmentation persists for months to years in a phenomenon termed long-lasting pigmentation (LLP). It is unclear whether LLP is an indicator of potential risk for skin cancer. LLP seems to have similar features to other forms of hyperpigmentation, eg solar lentigines or age spots, which are clinical markers of photodamage and risk factors for precancerous lesions. To investigate what UV-induced molecular changes may persist in individuals with LLP, clinical specimens from non-sunburn-inducing repeated UV exposures (UVA, UVB or UVA + UVB) at 4 months post-exposure (short-term LLP) were evaluated by microarray analysis and dataset mining. Validated targets were further evaluated in clinical specimens from six healthy individuals (three LLP+ and three LLP-) followed for more than 9 months (long-term LLP) who initially received a single sunburn-inducing UVA + UVB exposure. The results support a UV-induced hyperpigmentation model in which basal keratinocytes have an impaired ability to remove melanin that leads to a compensatory mechanism by neighbouring keratinocytes with increased proliferative capacity to maintain skin homeostasis. The attenuated expression of SOX7 and other hemidesmosomal components (integrin 64 and plectin) leads to increased melanosome uptake by keratinocytes and points to a spatial regulation within the epidermis. The reduced density of hemidesmosomes provides supporting evidence for plasticity at the epidermal-dermal junction. Altered hemidesmosome plasticity, and the sustained nature of LLP, may be mediated by the role of SOX7 in basal keratinocytes. The long-term sustained subtle changes detected are modest, but sufficient to create dramatic visual differences in skin colour. These results suggest that the hyperpigmentation phenomenon leading to increased interdigitation develops in order to maintain normal skin homeostasis in individuals with LLP. Copyright (c) 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Coelho, Sergio G.; Valencia, Julio C.; Yin, Lanlan; 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.
[Zhang, Guofeng] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Tuma, Pamela L.] Catholic Univ Amer, Dept Biol, Washington, DC 20064 USA.
RP Coelho, SG (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37,Room 2132, Bethesda, MD 20892 USA.
EM sergio.coelho@fda.hhs.gov
FU Office of Science; Center for Devices and Radiological Health, Food and
Drug Administration; National Cancer Institute, National Institutes of
Health
FX This research was supported in part by the Office of Science and the
Center for Devices and Radiological Health, Food and Drug
Administration, and in part by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health. We would like
to acknowledge Professors Ito and Wakamatsu for completing the
melanosome melanin analysis.
NR 39
TC 4
Z9 4
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD MAY
PY 2015
VL 236
IS 1
BP 17
EP 29
DI 10.1002/path.4497
PG 13
WC Oncology; Pathology
SC Oncology; Pathology
GA CG1OF
UT WOS:000353041900003
PM 25488118
ER
PT J
AU Akshintala, S
Avery, RA
Murnick, J
Verdun, N
Diab, Y
AF Akshintala, Srivandana
Avery, Robert A.
Murnick, Jonathan
Verdun, Nicole
Diab, Yaser
TI Isolated Midbrain Ischemic Infarct in Association With
Hyperlipoproteinemia (a): A Report of 2 Adolescent Patients
SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
LA English
DT Article
DE thrombophilia; acute ischemic stroke; hyperlipoproteinemia (a);
midbrain; adolescent
ID RISK-FACTORS; PEDIATRIC STROKE; CHILDHOOD; LIPOPROTEIN; CHILDREN
AB Arterial ischemic strokes (AIS) localized solely to the midbrain are extremely uncommon in the pediatric population. Elevated lipoprotein (a), which promotes atherosclerosis and a prothrombotic state, has been associated with increased risk of AIS in children and adults. Here we describe a 17-year-old boy and a 15-year-old girl who presented with internuclear ophthalmoplegia secondary to an isolated midbrain AIS. Evaluation for risk factors for AIS in these otherwise healthy adolescents identified hyperlipoproteinemia (a) in combination with other potential prothrombotic conditions suggesting that hypercoagulable states such as hyperlipoproteinemia (a) may have contributed to development of small-vessel arteriopathy and localized AIS.
C1 [Akshintala, Srivandana; Verdun, Nicole; Diab, Yaser] Childrens Natl Med Ctr, Dept Hematol, Washington, DC 20010 USA.
[Avery, Robert A.] Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
[Murnick, Jonathan] Childrens Natl Med Ctr, Dept Diagnost Imaging & Radiol, Washington, DC 20010 USA.
RP Akshintala, S (reprint author), NCI, Pediat Oncol Branch, 10 Ctr Dr,Bldg 10 CRC,Room 1-5750,MSC 1101, Bethesda, MD 20892 USA.
EM akshintalas@mail.nih.gov
OI Avery, Robert/0000-0003-1453-7282
NR 16
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1077-4114
EI 1536-3678
J9 J PEDIAT HEMATOL ONC
JI J. Pediatr. Hematol. Oncol.
PD MAY
PY 2015
VL 37
IS 4
BP 315
EP 318
PG 4
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CG5AR
UT WOS:000353301600032
PM 25739027
ER
PT J
AU Katarkar, A
Saha, A
Mukherjee, S
Kundu, D
Bandyopadhyay, P
Chaudhuri, K
AF Katarkar, Atul
Saha, Arindam
Mukherjee, Sanjit
Kundu, Debabrata
Bandyopadhyay, Prasanta
Chaudhuri, Keya
TI Telomerase Expression in Individuals With Chronic and Aggressive
Periodontitis
SO JOURNAL OF PERIODONTOLOGY
LA English
DT Article
DE Aggressive periodontitis; chronic periodontitis; gingival crevicular
fluid; gingival recession; periodontal attachment loss; telomerase
ID GINGIVAL CREVICULAR FLUID; REVERSE-TRANSCRIPTASE HTERT; MESSENGER-RNA
EXPRESSION; CATALYTIC SUBUNIT; GENE-EXPRESSION; UP-REGULATION; HUMAN
CANCER; CELLS; ACTIVATION; DISEASES
AB Background: The aim of this study is to evaluate the expression of human telomerase reverse transcription (hTERT) enzyme in chronic periodontitis (CP) and aggressive periodontitis (AgP) compared with healthy individuals.
Methods: A total of 79 individuals consented to participate in the study. The study sample comprised healthy individuals (n = 30), patients with CP (n = 30), and patients with AgP (n = 19). Gingival tissue was collected and evaluated for hTERT expression by Western blot and immunohistochemical methods. Reverse transcription polymerase chain reaction was performed using the gingival crevicular fluid (GCF) samples.
Results: The hTERT messenger RNA (mRNA) and protein expression was significantly higher in AgP compared with CP (P < 0.001). In GCF, 53.33% of patients with CP and 68.42% of patients with AgP were showing hTERT mRNA expression, but it was not detected in the control group. The AgP tissue showed higher hTERT expression compared with CP (P < 0.001). The hTERT mRNA expression did not show a correlation with gingival index (GI), plaque index (PI), probing depth (PD), and clinical attachment loss (AL) in patients with AgP, whereas hTERT protein expression was strongly correlated with GI, PI, PD, and AL in patients with AgP. The protein expression of hTERT shows significant but moderate correlation with GI and AL in patients with CP.
Conclusion: High expression of hTERT might be associated with periodontal disease progression, suggesting that hTERT could be a potential prognostic marker.
C1 [Katarkar, Atul; Mukherjee, Sanjit; Chaudhuri, Keya] Indian Inst Chem Biol, CSIR, Mol & Human Genet Div, Kolkata 700032, India.
[Saha, Arindam; Kundu, Debabrata; Bandyopadhyay, Prasanta] Dr R Ahmed Dent Coll & Hosp, Dept Periodont, Kolkata, India.
[Mukherjee, Sanjit] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
RP Chaudhuri, K (reprint author), Indian Inst Chem Biol, CSIR, Mol & Human Genet Div, 4 Raja SC Mullick Rd, Kolkata 700032, India.
EM kchaudhuri@iicb.res.in
OI MUKHERJEE, SANJIT/0000-0002-3295-9668
FU Council of Scientific and Industrial Research Grant
[21(0932)/12/EMR-II]; Indian Council of Medical Research
FX This study is supported by the Council of Scientific and Industrial
Research Grant 21(0932)/12/EMR-II. Drs. Katarkar and Saha contributed
equally to this work. Dr. Katarkar is grateful to the Indian Council of
Medical Research for providing a senior research fellowship. The authors
report no conflicts of interest related to this study.
NR 50
TC 1
Z9 1
U1 2
U2 6
PU AMER ACAD PERIODONTOLOGY
PI CHICAGO
PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 USA
SN 0022-3492
EI 1943-3670
J9 J PERIODONTOL
JI J. Periodont.
PD MAY
PY 2015
VL 86
IS 5
BP 656
EP 665
DI 10.1902/jop.2015.140540
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA CG6LE
UT WOS:000353411400009
PM 25660499
ER
PT J
AU Daikoku, E
Saito, M
Ono, F
AF Daikoku, Eriko
Saito, Masahisa
Ono, Fumihito
TI Zebrafish mutants of the neuromuscular junction: swimming in the gene
pool
SO Journal of Physiological Sciences
LA English
DT Review
DE Synapse; Zebrafish; Acetylcholine receptor; Mutant
ID MUSCLE ACETYLCHOLINE-RECEPTOR; IN-VIVO; MYASTHENIC SYNDROME; RAPSYN
CLUSTERS; BETA-SUBUNIT; IDENTIFICATION; SYNAPSES; PROTEIN; REVEALS; SLOW
AB This review provides an overview of zebrafish mutants with dysfunctional acetylcholine receptors or related proteins at the neuromuscular junction (NMJ). The NMJ, which has served as the classical model of the chemical synapse, uses acetylcholine as the neurotransmitter, and mutations of proteins involved in the signaling cascade lead to a variety of behavioral phenotypes. Mutants isolated after random chemical mutagenesis screening are summarized, and advances in the field resulting from these mutants are discussed.
C1 [Daikoku, Eriko; Saito, Masahisa; Ono, Fumihito] Osaka Med Coll, Dept Physiol, Takatsuki, Osaka 5698686, Japan.
[Ono, Fumihito] NIAAA, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
RP Ono, F (reprint author), Osaka Med Coll, Dept Physiol, Takatsuki, Osaka 5698686, Japan.
EM onof@art.osaka-med.ac.jp
FU intramural program at NIAAA
FX We thank Dr Henry Puhl for critical reading of the manuscript. We thank
Ms Kasumi Minamimoto and Ms Chika Murakami for their help with
preparation of the figures. This work was supported by the intramural
program at NIAAA.
NR 43
TC 3
Z9 3
U1 0
U2 3
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 1880-6546
EI 1880-6562
J9 J PHYSIOL SCI
JI J. Physiol. Sci.
PD MAY
PY 2015
VL 65
IS 3
BP 217
EP 221
DI 10.1007/s12576-015-0372-9
PG 5
WC Physiology
SC Physiology
GA CG6LB
UT WOS:000353411100002
PM 25782439
ER
PT J
AU Harlan, LC
Eisenstein, J
Russell, MC
Stevens, JL
Cardona, K
AF Harlan, Linda C.
Eisenstein, Jana
Russell, Maria C.
Stevens, Jennifer L.
Cardona, Kenneth
TI Gastrointestinal Stromal Tumors: Treatment Patterns of a
Population-Based Sample
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE SEER registry; sarcoma; imatinib; GIST
ID ADJUVANT THERAPY; MANAGEMENT; PATHOLOGY; PROGNOSIS; MUTATIONS;
DIAGNOSIS; STOMACH; KIT
AB ObjectivesThe National Cancer Institute (NCI) annually confirms therapy with treating physicians on a sample of patients diagnosed with a specific cancer.
MethodsUsing the NCI Patterns of Care data, treatment patterns were examined on a population-based sample of patients diagnosed with gastrointestinal stromal tumors (GIST) in 2008.
ResultsA random sample of 323 of 405 GIST patients registered in SEER was selected. Most patients had gastric GISTs, were 65years, white, had private insurance, and treated in a hospital with a residency program. Surgery was primarily performed in patients with non-metastatic disease (94%), in which: 26, 12, and 36% were at low, intermediate, and high-risk of recurrence, respectively. Amongst low-risk patients, approximate to 30% received adjuvant therapy. Amongst patients at higher risk, 26-40% did not receive adjuvant therapy. Imatinib was the most common targeted therapy administered. On multivariate analysis, age and risk-group were associated with receipt of adjuvant targeted therapy.
ConclusionsOur study shows that in 2008, the majority of patients diagnosed with GIST received appropriate surgical and adjuvant therapies. However, a considerable subset may have been overtreated and undertreated. Future studies identifying factors that impact the delivery of adjuvant therapy should be conducted. J. Surg. Oncol. 2015 111:702-707. (c) 2015 Wiley Periodicals, Inc.
C1 [Harlan, Linda C.; Eisenstein, Jana] NCI, ARP, Bethesda, MD 20892 USA.
[Russell, Maria C.; Cardona, Kenneth] Emory Univ, Winship Canc Inst, Dept Surg, Div Surg Oncol, Atlanta, GA 30322 USA.
[Stevens, Jennifer L.] Informat Management Serv Inc, Silver Spring, MD USA.
RP Harlan, LC (reprint author), NCI, ARP, 9609 Med Ctr Dr,MSC 9762,Room 3E426, Bethesda, MD 20892 USA.
EM lh50w@nih.gov
FU National Cancer Institute [HHSN261201000024C, HSN261201000025C,
HHSN261201000032C, HHSN261201000027C, HHSN261201000026C,
HHSN261201000140C, HHSN261201000037C, HHSN261201000033C,
HHSN261201000034C, HHSN261201000035C, HHSN261201000029C,
HHSN261201000031C, HHSN261201000028C, HHSN261201000030C]
FX Grant sponsor: National Cancer Institute contracts; Grant numbers:
HHSN261201000024C, HSN261201000025C, HHSN261201000032C,
HHSN261201000027C, HHSN261201000026C, HHSN261201000140C,
HHSN261201000037C, HHSN261201000033C, HHSN261201000034C,
HHSN261201000035C, HHSN261201000029C, HHSN261201000031C,
HHSN261201000028C, HHSN261201000030C.
NR 20
TC 2
Z9 3
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD MAY 1
PY 2015
VL 111
IS 6
BP 702
EP 707
DI 10.1002/jso.23879
PG 6
WC Oncology; Surgery
SC Oncology; Surgery
GA CG6ND
UT WOS:000353417700007
PM 25900896
ER
PT J
AU Teranishi, Y
Matsubara, T
Krausz, KW
Le, TTT
Gonzalez, FJ
Yoshizato, K
Ikeda, K
Kawada, N
AF Teranishi, Yuga
Matsubara, Tsutomu
Krausz, Kristopher W.
Le, Thi T. T.
Gonzalez, Frank J.
Yoshizato, Katsutoshi
Ikeda, Kazuo
Kawada, Norifumi
TI Involvement of hepatic stellate cell cytoglobin in acute hepatocyte
damage through the regulation of CYP2E1-mediated xenobiotic metabolism
SO LABORATORY INVESTIGATION
LA English
DT Article
ID LIVER-INJURY; ACETAMINOPHEN; HYPOXIA; MICE; ACTIVATION; RAT;
MICROCIRCULATION; REGENERATION; NEUROGLOBIN; PROTEIN
AB Oxygen (O-2) is required for cytochrome P450 (CYP)-dependent drug metabolism. Cytoglobin (CYGB) is a unique globin expressed exclusively in hepatic stellate cells (HSCs). However, its role in O-2-dependent metabolism in neighboring hepatocytes remains unknown. This study provides evidence that CYGB in HSCs is involved in acetaminophen (N-acetyl-p-aminophenol; APAP)-induced hepatotoxicity. Serum alanine aminotransferase levels were higher in wild-type mice than in Cygb-null mice. Wild-type mice exhibited more severe hepatocyte necrosis around the central vein area compared with Cygb-null mice, thus indicating that CYGB deficiency protects against APAP-induced liver damage. Although no difference in the hepatic expression of CYP2E1, a key enzyme involved in APAP toxicity, was observed between wild-type and Cygb-null mice, the serum levels of the APAP metabolites cysteinyl-APAP and N-acetyl-cysteinyl-APAP were decreased in Cygb-null mice, suggesting reduced APAP metabolism in the livers of Cygb-null mice. In primary cultures, APAP-induced hepatocyte damage was increased by co-culturing with wild-type HSCs but not with Cygb-null HSCs. In addition, cell damage was markedly alleviated under low O-2 condition (5% O2), suggesting the requirement of O-2 for APAP toxicity. Carbon tetrachloride-induced liver injury (CYP2E1-dependent), but not lipopolysaccharide/ D-galactosamine-induced injury (CYP2E1-independent), was similarly alleviated in Cygb-null mice. Considering the function of CYGB as O-2 carrier, these results strongly support the hypothesis that HSCs are involved in the CYP2E1-mediated xenobiotic activation by augmenting O-2 supply to hepatocytes. In conclusion, CYGB in HSCs contributes to the CYP-mediated metabolism of xenobiotics in hepatocytes by supplying O-2 for enzymatic oxidation.
C1 [Teranishi, Yuga; Le, Thi T. T.; Yoshizato, Katsutoshi; Kawada, Norifumi] Osaka City Univ, Grad Sch Med, Dept Hepatol, Osaka 5458585, Japan.
[Matsubara, Tsutomu; Ikeda, Kazuo] Osaka City Univ, Grad Sch Med, Dept Anat & Regenerat Biol, Osaka 5458585, Japan.
[Krausz, Kristopher W.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Yoshizato, Katsutoshi] Phoenixbio Co Ltd, Hiroshima, Japan.
RP Kawada, N (reprint author), Osaka City Univ, Grad Sch Med, Dept Hepatol, Abeno Ku, 1-4-3 Asahimachi, Osaka 5458585, Japan.
EM kawadanori@med.osaka-cu.ac.jp
FU Japan Society for the Promotion of Science (JSPS) [25293177, 20132016];
Mochida Memorial Foundation; National Cancer Institute Intramural
Research Program
FX We thank Ms Chiho Kadono for animal care, and Dr Wenhao Cui, Dr Keiko
Iwaisako, and Dr Kazuki Nakatani (Osaka City University) for their
valuable discussion and comments on this study. This investigation was
supported in part by a Grant-in-Aid for Scientific Research (B) from the
Japan Society for the Promotion of Science (JSPS) through grant 25293177
(to NK) (20132016), the Mochida Memorial Foundation (to TM), and the
National Cancer Institute Intramural Research Program (to FJG).
NR 27
TC 4
Z9 4
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD MAY
PY 2015
VL 95
IS 5
BP 515
EP 524
DI 10.1038/labinvest.2015.29
PG 10
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA CG8SR
UT WOS:000353583300006
PM 25686096
ER
PT J
AU Hayashi, PH
Barnhart, HX
Fontana, RJ
Chalasani, N
Davern, TJ
Talwalkar, JA
Reddy, KR
Stolz, AA
Hoofnagle, JH
Rockey, DC
AF Hayashi, Paul H.
Barnhart, Huiman X.
Fontana, Robert J.
Chalasani, Naga
Davern, Timothy J.
Talwalkar, Jayant A.
Reddy, K. Rajender
Stolz, Andrew A.
Hoofnagle, Jay H.
Rockey, Don C.
TI Reliability of causality assessment for drug, herbal and dietary
supplement hepatotoxicity in the Drug-Induced Liver Injury Network
(DILIN)
SO LIVER INTERNATIONAL
LA English
DT Article
DE adverse reaction; diagnosis; drug-induced liver injury; hepatotoxicity;
toxicity
ID ADVERSE REACTIONS; HEPATITIS; VALIDATION; DIAGNOSIS; DESIGN
AB Background & AimsBecause of the lack of objective tests to diagnose drug-induced liver injury (DILI), causality assessment is a matter of debate. Expert opinion is often used in research and industry, but its test-retest reliability is unknown. To determine the test-retest reliability of the expert opinion process used by the Drug-Induced Liver Injury Network (DILIN).
MethodsThree DILIN hepatologists adjudicate suspected hepatotoxicity cases to one of five categories representing levels of likelihood of DILI. Adjudication is based on retrospective assessment of gathered case data that include prospective follow-up information. One hundred randomly selected DILIN cases were re-assessed using the same processes for initial assessment but by three different reviewers in 92% of cases.
ResultsThe median time between assessments was 938days (range 140-2352). Thirty-one cases involved >1 agent. Weighted kappa statistics for overall case and individual agent category agreement were 0.60 (95% CI: 0.50-0.71) and 0.60 (0.52-0.68) respectively. Overall case adjudications were within one category of each other 93% of the time, while 5% differed by two categories and 2% differed by three categories. Fourteen per cent crossed the 50% threshold of likelihood owing to competing diagnoses or atypical timing between drug exposure and injury.
ConclusionsThe DILIN expert opinion causality assessment method has moderate interobserver reliability but very good agreement within one category. A small but important proportion of cases could not be reliably diagnosed as 50% likely to be DILI.
C1 [Hayashi, Paul H.] Univ N Carolina, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Barnhart, Huiman X.] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
[Barnhart, Huiman X.] Duke Univ, Dept Biostat, Durham, NC USA.
[Fontana, Robert J.] Univ Michigan, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Chalasani, Naga] Indiana Univ Sch Med, Div Gastroenterol & Hepatol, Indianapolis, IN 46202 USA.
[Davern, Timothy J.] Calif Pacific Med Ctr, Div Gastroenterol, San Francisco, CA USA.
[Talwalkar, Jayant A.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Reddy, K. Rajender] Univ Penn, Div Gastroenterol, Philadelphia, PA 19104 USA.
[Stolz, Andrew A.] Univ So Calif, Div Gastrointestinal & Liver Dis, Los Angeles, CA USA.
[Hoofnagle, Jay H.] NIDDK, Liver Dis Res Branch, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
[Rockey, Don C.] Univ Texas Southwestern, Div Gastroenterol, Dallas, TX USA.
RP Hayashi, PH (reprint author), UNC Liver Program, Div Gastroenterol & Hepatol, CB 7584 Burnett Womack Bldg,Room 8011, Chapel Hill, NC 27599 USA.
EM paul_hayashi@med.unc.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[2U01-DK065176-06, 2U01-DK065201-06, 2U01-DK065184-06, 2U01-DK065211-06,
5U01DK065 193-04, 5U01-DK065238-08, 1U01-DK083023-01, 1U01-DK083027-01,
1U01-DK082992-01, 1U01-DK083020-01]; CTSA [UL1 RR025761, UL1 RR025747,
UL1 RR024134, UL1 RR024986, UL1 RR024982, UL1 RR024150]; Intramural
Research Program of the NIH, National Cancer Institute
FX The DILIN Network is structured as a U01 cooperative agreement with
funds provided by the National Institute of Diabetes and Digestive and
Kidney Diseases (NIDDK) under grants: 2U01-DK065176-06 (Duke),
2U01-DK065201-06 (UNC), 2U01-DK065184-06 (Michigan), 2U01-DK065211-06
(Indiana), 5U01DK065 193-04 (UConn), 5U01-DK065238-08 (UCSF/CPMC),
1U01-DK083023-01 (UTSW), 1U01-DK083027-01 (TJH/UPenn), 1U01-DK082992-01
(Mayo), 1U01-DK083020-01 (USC). Additional funding is provided by CTSA
grants: UL1 RR025761 (Indiana), UL1 RR025747 (UNC), UL1 RR024134
(UPenn), UL1 RR024986 (Michigan), UL1 RR024982 (UTSW), UL1 RR024150
(Mayo) and in part by the Intramural Research Program of the NIH,
National Cancer Institute.
NR 20
TC 10
Z9 10
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD MAY
PY 2015
VL 35
IS 5
BP 1623
EP 1632
DI 10.1111/liv.12540
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CG9OM
UT WOS:000353645900018
PM 24661785
ER
PT J
AU Habermann, N
Makar, KW
Abbenhardt, C
Xiao, LR
Wang, CY
Utsugi, HK
Alfano, CM
Campbell, KL
Duggan, C
Foster-Schubert, KE
Mason, CE
Imayama, I
Blackburn, GL
Potter, JD
Mctiernan, A
Ulrich, CM
AF Habermann, Nina
Makar, Karen W.
Abbenhardt, Clare
Xiao, Liren
Wang, Ching-Yun
Utsugi, Heidi K.
Alfano, Catherine M.
Campbell, Kristin L.
Duggan, Catherine
Foster-Schubert, Karen E.
Mason, Caitlin E.
Imayama, Ikuyo
Blackburn, George L.
Potter, John D.
Mctiernan, Anne
Ulrich, Cornelia M.
TI No Effect of Caloric Restriction or Exercise on Radiation Repair
Capacity
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE DNA REPAIR; COMET ASSAY; RANDOMIZED CONTROLLED TRIAL; EXERCISE; CALORIC
RESTRICTION; WOMEN
ID OXIDATIVE DNA-DAMAGE; ALKALINE COMET ASSAY; WEIGHT-LOSS; BREAST-CANCER;
POSTMENOPAUSAL WOMEN; PHYSICAL-ACTIVITY; SKELETAL-MUSCLE; STRESS;
INTERVENTION; LYMPHOCYTES
AB Introduction: Maintenance of normal weight and higher levels of physical activity are associated with a reduced risk of several types of cancer. Because genomic instability is regarded as a hallmark of cancer development, one proposed mechanism is improvement of DNA repair function. We investigated links between dietary weight loss, exercise, and strand break rejoining in an ancillary study to a randomized-controlled trial. Methods: Overweight/obese postmenopausal women (n = 439) were randomized to the following: a) reduced calorie weight loss diet ("diet,'' n = 118), b) moderate-to vigorous-intensity aerobic exercise ("exercise,'' n = 117), c) a combination ("diet + exercise,'' n = 117), or d) control (n = 87). The reduced calorie diet had a 10% weight loss goal. The exercise intervention consisted of 45 min of moderate to vigorous aerobic activity 5 d.wk(-1) for 12 months. DNA repair capacity was measured in a subset of 226 women at baseline and 12 months from cryopreserved peripheral mononuclear cells using the comet assay. Anthropometric and body composition measures were performed at baseline and 12 months. Results: DNA repair capacity did not change significantly with any of the 12-month interventions compared with control; there were also no significant changes when stratified by changes in body composition or aerobic fitness ((V) over dotO(2max)). At baseline, DNA repair capacity was positively associated with weight, body mass index, and fat mass (r = 0.20, P = 0.003; r = 0.19, P = 0.004; r = 0.13, P = 0.04, respectively) and inversely with lean body mass (r = -0.14, P = 0.04). Conclusion: In conclusion, DNA repair capacity in cryopreserved PBMCs (Comet Assay) did not change with dietary weight loss or exercise interventions in postmenopausal women within a period of 12 months. Other assays that capture different facets of DNA repair function may be needed.
C1 [Habermann, Nina; Abbenhardt, Clare; Ulrich, Cornelia M.] German Canc Res Ctr, Div Prevent Oncol, Heidelberg, Germany.
[Habermann, Nina; Abbenhardt, Clare; Ulrich, Cornelia M.] Natl Ctr Tumor Dis, D-69120 Heidelberg, Germany.
[Makar, Karen W.; Xiao, Liren; Wang, Ching-Yun; Utsugi, Heidi K.; Duggan, Catherine; Mason, Caitlin E.; Imayama, Ikuyo; Mctiernan, Anne] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Alfano, Catherine M.] NCI, Off Canc Survivorship, NIH, Bethesda, MD 20892 USA.
[Campbell, Kristin L.] Univ British Columbia, Fac Med, Vancouver, BC, Canada.
[Foster-Schubert, Karen E.; Mctiernan, Anne] Univ Washington, Sch Med, Seattle, WA USA.
[Blackburn, George L.] Harvard Univ, Sch Med, Div Nutr, Boston, MA USA.
[Potter, John D.; Ulrich, Cornelia M.] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98104 USA.
[Potter, John D.; Mctiernan, Anne] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
[Potter, John D.] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
RP Ulrich, CM (reprint author), Natl Ctr Tumor Dis, Div Prevent Oncol, Neuenheimer Feld 460, D-69120 Heidelberg, Germany.
EM neli.ulrich@nct-heidelberg.de
RI Duggan, Catherine/F-9414-2015; Biguzzi, Felipe/E-4724-2015;
OI Duggan, Catherine/0000-0001-7369-4021; Potter, John/0000-0001-5439-1500
FU National Cancer Institute at the National Institutes of Health
[U54-CA116847, R01 CA102504, 5KL2RR025015-03, R25 CA94880]; Canadian
Institutes of Health Research
FX This work was supported by the National Cancer Institute at the National
Institutes of Health (grants U54-CA116847, R01 CA102504; 5KL2RR025015-03
to K.F.S; R25 CA94880 to A.K.) and Canadian Institutes of Health
Research (fellowships to K.L.C and C.M.). None of the funding agencies
were involved in the trial design or conduct. During the trial, Dr.
Alfano was a faculty member at The Ohio State University and relocated
to NCI after completion of her efforts on the NEW trial.
NR 48
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2015
VL 47
IS 5
BP 896
EP 904
DI 10.1249/MSS.0000000000000480
PG 9
WC Sport Sciences
SC Sport Sciences
GA CG3CS
UT WOS:000353155400002
PM 25160845
ER
PT J
AU Steeves, JA
Bowles, HR
Mcclain, JJ
Dodd, KW
Brychta, RJ
Wang, J
Chen, KY
AF Steeves, Jeremy A.
Bowles, Heather R.
Mcclain, James J.
Dodd, Kevin W.
Brychta, Robert J.
Wang, Juan
Chen, Kong Y.
TI Ability of Thigh-Worn ActiGraph and activPAL Monitors to Classify
Posture and Motion
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE SITTING; STANDING; STEPPING; TRANSITIONS; ACTIVITIES; INCLINATION
ID PHYSICAL-ACTIVITY; TIME SPENT; US ADULTS; OBESITY; VALIDATION;
MORTALITY; CHILDREN; VALIDITY; DISEASE
AB Purpose: This study compared sitting, standing, and stepping classifications from thigh-worn ActiGraph and activPAL monitors under laboratory and free-living conditions. Methods: Adults wore both monitors on the right thigh while performing activities (six sitting, two standing, nine stepping, and one cycling) and writing on a whiteboard with intermittent stepping under laboratory conditions (n = 21) and under free-living conditions for 3 d (n = 18). Percent time correctly classified was calculated under laboratory conditions. Between-monitor agreement and weighted kappa were calculated under free-living conditions. Results: In the laboratory, both monitors correctly classified 100% of standing time and >95% of the time spent in four of six sitting postures. Both monitors demonstrated misclassification of laboratory stool sitting time (ActiGraph 14% vs activPAL 95%). ActivPAL misclassified 14% of the time spent sitting with legs outstretched; ActiGraph was 100% accurate. Monitors were >95% accurate for stepping, although ActiGraph was less so for descending stairs (86%), ascending stairs (92%), and running at 2.91 m.s(-1) (93%). Monitors classified whiteboard writing differently (ActiGraph 83% standing/15% stepping vs activPAL 98% standing/2% stepping). ActivPAL classified 93% of cycling time as stepping, whereas ActiGraph classified <1% of cycling time as stepping. During free-living wear, monitors had substantial agreement (86% observed; weighted kappa = 0.77). Monitors classified similar amounts of time as sitting (ActiGraph 64% vs activPAL 62%). There were differences in time recorded as standing (ActiGraph 21% vs activPAL 27%) and stepping (ActiGraph 15% vs activPAL 11%). Conclusions: Differences in data processing algorithms may have resulted in the observed disagreement in posture and activity classification between thigh-worn ActiGraph and activPAL. Despite between-monitor agreement in classifying sitting time under free-living conditions, ActiGraph appears to be more sensitive to free-living upright walking motions than activPAL.
C1 [Steeves, Jeremy A.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD 20892 USA.
[Bowles, Heather R.; Mcclain, James J.] NCI, Risk Factor Monitoring & Methods Branch, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[Dodd, Kevin W.] NCI, Biometry Res Grp, Canc Prevent Div, Rockville, MD 20892 USA.
[Brychta, Robert J.; Wang, Juan; Chen, Kong Y.] NIDDKD, Diabet Endocrinol & Obes Branch, Bethesda, MD USA.
RP Steeves, JA (reprint author), NCI, Canc Prevent Fellowship Program, Canc Prevent Div, 9609 Med Ctr Dr,MSC 9762, Rockville, MD 20892 USA.
EM steevesja@mail.nih.gov
OI Chen, Kong/0000-0002-0306-1904
FU National Institutes of Diabetes, Digestive, and Kidney Diseases,
National Institutes of Health [Z01 DK07013, Z01 DK07014]
FX This project was supported by the Intramural Research Program of the
National Institutes of Diabetes, Digestive, and Kidney Diseases,
National Institutes of Health (grants Z01 DK07013 and Z01 DK07014).
NR 32
TC 14
Z9 14
U1 2
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2015
VL 47
IS 5
BP 952
EP 959
DI 10.1249/MSS.0000000000000497
PG 8
WC Sport Sciences
SC Sport Sciences
GA CG3CS
UT WOS:000353155400009
PM 25202847
ER
PT J
AU Rosales, T
Sackett, DL
Xu, JH
Shi, ZD
Xu, BY
Li, HT
Kaur, G
Frohart, E
Shenoy, N
Cheal, SM
Wu, HT
Dulcey, AE
Hu, YL
Li, CH
Lane, K
Griffiths, GL
Knutson, JR
AF Rosales, Tilman
Sackett, Dan L.
Xu, Jianhua
Shi, Zhen-Dan
Xu, Biying
Li, Haitao
Kaur, Gurpreet
Frohart, Erin
Shenoy, Nalini
Cheal, Sarah M.
Wu, Haitao
Dulcey, Andres E.
Hu, Yulin
Li, Changhui
Lane, Kelly
Griffiths, Gary L.
Knutson, Jay R.
TI STAQ: A Route Toward Low Power, Multicolor Nanoscopy
SO MICROSCOPY RESEARCH AND TECHNIQUE
LA English
DT Article
DE super resolution; STED; microscopy; imaging
ID RESONANCE ENERGY-TRANSFER; STED MICROSCOPY; IN-VIVO; FLUORESCENCE
MICROSCOPY; TUBULIN POLYMERIZATION; STIMULATED-EMISSION; RESOLUTION
LIMIT; GFP; BEAM
AB Nanoscopy has now become a real procedure in fluorescence microscopy of living cells. The STED/RESOLFT family of nanoscopy approaches has the best prospects for delivering high speed imaging, but the history of STED includes a continuing struggle to reduce the deactivation power applied, along with difficulties in achieving simultaneous multicolor images. In this manuscript, we present a concept for a similar real-time nanoscopy, using a new class of bipartite probes that separate the luminescent and quenching functions into two coupled molecules. In particular, the STAQ (Superresolution via Transiently Activated Quencher) example we show herein employs the excited state absorbance (not ground state) of the partner to accept energy from and quench the luminescent dye. The result is that much less deactivation power is needed for superresolved (approximate to 50 nm) imaging. Moreover, the TAQ partner excited by the donut beam is shown to quench several different visible dyes via the same mechanism, opening the door to easier multicolor imaging. We demonstrate three dyes sharing the same deactivation and show examples of superresolved multicolor images. We suggest STAQ will facilitate the growth of real-time nanoscopy by reducing confounding photodamage within living cells while expanding the nanoscopist's palette. Microsc. Res. Tech. 78:343-355, 2015. Published 2015. This article is a U.S. Government work and is in the public domain in the USA
C1 [Rosales, Tilman; Xu, Jianhua; Knutson, Jay R.] NHLBI, Opt Spect Sect, Lab Mol Biophys, NIH, Bethesda, MD 20892 USA.
[Sackett, Dan L.] NICHHD, Lab Integrat & Med Biophys, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Shi, Zhen-Dan; Xu, Biying; Li, Haitao; Kaur, Gurpreet; Frohart, Erin; Shenoy, Nalini; Cheal, Sarah M.; Wu, Haitao; Dulcey, Andres E.; Hu, Yulin; Li, Changhui; Lane, Kelly; Griffiths, Gary L.] NHLBI, Imaging Probe Dev Ctr, NIH, Rockville, MD 20850 USA.
RP Knutson, JR (reprint author), 10 Ctr Dr,Bldg 10,Rm 5D14, Bethesda, MD 20892 USA.
EM knutsonj@nhlbi.nih.gov
FU NIH; NHLBI; NICHD
FX Contract grant sponsors: Intramural Research Programs of the NIH, NHLBI,
NICHD.
NR 43
TC 0
Z9 0
U1 4
U2 27
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1059-910X
EI 1097-0029
J9 MICROSC RES TECHNIQ
JI Microsc. Res. Tech.
PD MAY
PY 2015
VL 78
IS 5
BP 343
EP 355
DI 10.1002/jemt.22478
PG 13
WC Anatomy & Morphology; Biology; Microscopy
SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics;
Microscopy
GA CG5PF
UT WOS:000353344300003
PM 25762506
ER
PT J
AU Pobezinsky, LA
Etzensperger, R
Jeurling, S
Alag, A
Kadakia, T
McCaughtry, TM
Kimura, MY
Sharrow, SO
Guinter, TI
Feigenbaum, L
Singer, A
AF Pobezinsky, Leonid A.
Etzensperger, Ruth
Jeurling, Susanna
Alag, Amala
Kadakia, Tejas
McCaughtry, Tom M.
Kimura, Motoko Y.
Sharrow, Susan O.
Guinter, Terry I.
Feigenbaum, Lionel
Singer, Alfred
TI Let-7 microRNAs target the lineage-specific transcription factor PLZF to
regulate terminal NKT cell differentiation and effector function
SO NATURE IMMUNOLOGY
LA English
DT Article
ID VITAMIN-D-RECEPTOR; T-CELLS; CAENORHABDITIS-ELEGANS; MESSENGER-RNAS;
ENZYME DICER; LIN28; RECOGNITION; PATHWAY; PROTEIN; FAMILY
AB Lethal-7 (let-7) microRNAs (miRNAs) are the most abundant miRNAs in the genome, but their role in developing thymocytes is unclear. We found that let-7 miRNAs targeted Zbtb16 mRNA, which encodes the lineage-specific transcription factor PLZF, to post-transcriptionally regulate PLZF expression and thereby the effector functions of natural killer T cells (NKT cells). Dynamic upregulation of let-7 miRNAs during the development of NKT thymocytes downregulated PLZF expression and directed their terminal differentiation into interferon-gamma (IFN-gamma)-producing NKT1 cells. Without upregulation of let-7 miRNAs, NKT thymocytes maintained high PLZF expression and terminally differentiated into interleukin 4 (IL-4)-producing NKT2 cells or IL-17-producing NKT17 cells. Upregulation of let-7 miRNAs in developing NKT thymocytes was signaled by IL-15, vitamin D and retinoic acid. Such targeting of a lineage-specific transcription factor by miRNA represents a previously unknown level of developmental regulation in the thymus.
C1 [Pobezinsky, Leonid A.; Etzensperger, Ruth; Jeurling, Susanna; Alag, Amala; Kadakia, Tejas; McCaughtry, Tom M.; Kimura, Motoko Y.; Sharrow, Susan O.; Guinter, Terry I.; Singer, Alfred] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel] NCI Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD USA.
RP Singer, A (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM singera@nih.gov
FU Intramural Research Program of the US National Institutes of Health;
National Cancer Institute, Center for Cancer Research
FX We thank N. Taylor and J.-H. Park for critical reading of the
manuscript; G.Q. Daley (Harvard Medical School) for iLet7Delta
LIN28 and M2rtTA double-transgenic mice; A. Bendelac (University
of Chicago) for Zbtb16+/LU mice; the Tetramer Core Facility
of the US National Institutes of Health for tetramer reagents; A. Adams
and L. Granger for flow cytometry; and J.A. Williams (National Cancer
Institute) for cDNA reagents. Supported by the Intramural Research
Program of the US National Institutes of Health, the National Cancer
Institute, Center for Cancer Research.
NR 46
TC 20
Z9 20
U1 3
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
EI 1529-2916
J9 NAT IMMUNOL
JI Nat. Immunol.
PD MAY
PY 2015
VL 16
IS 5
BP 517
EP U234
DI 10.1038/ni.3146
PG 9
WC Immunology
SC Immunology
GA CG5BN
UT WOS:000353305200014
PM 25848867
ER
PT J
AU Wynn, TA
AF Wynn, Thomas A.
TI Type 2 cytokines: mechanisms and therapeutic strategies
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID ALTERNATIVELY ACTIVATED MACROPHAGES; ALLERGIC AIRWAY INFLAMMATION;
REGULATORY T-CELLS; TUMOR-ASSOCIATED MACROPHAGES; IL-13 RECEPTOR
ALPHA-2; MONOCYTE CHEMOATTRACTANT PROTEIN-1; HELMINTH INFECTION
PROTECTS; BRONCHIAL EPITHELIAL-CELLS; INNATE LYMPHOID-CELLS; HOUSE-DUST
MITE
AB Type 2 immune responses are defined by the cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13, which can either be host protective or have pathogenic activity. Type 2 immunity promotes antihelminth immunity, suppresses type 1-driven autoimmune disease, neutralizes toxins, maintains metabolic homeostasis, and regulates wound repair and tissue regeneration pathways following infection or injury. Nevertheless, when type 2 responses are dysregulated, they can become important drivers of disease. Type 2 immunity induces a complex inflammatory response characterized by eosinophils, mast cells, basophils, type 2 innate lymphoid cells, IL-4-and/or IL-13-conditioned macrophages and T helper 2 (TH2) cells, which are crucial to the pathogenesis of many allergic and fibrotic disorders. As chronic type 2 immune responses promote disease, the mechanisms that regulate their maintenance are thought to function as crucial disease modifiers. This Review discusses the many endogenous negative regulatory mechanisms that antagonize type 2 immunity and highlights how therapies that target some of these pathways are being developed to treat type 2-mediated disease.
C1 NIAID, Immunopathogenesis Sect, Program Barrier Immun & Repair, Parasit Dis Lab,NIH, Bethesda, MD 20892 USA.
RP Wynn, TA (reprint author), NIAID, Immunopathogenesis Sect, Program Barrier Immun & Repair, Parasit Dis Lab,NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM twynn@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, US National
Institutes of Health, Bethesda, Maryland, USA
FX The author is supported by the intramural research programme of the
National Institute of Allergy and Infectious Diseases, US National
Institutes of Health, Bethesda, Maryland, USA.
NR 186
TC 66
Z9 68
U1 11
U2 41
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 MAY
PY 2015
VL 15
IS 5
BP 271
EP 282
DI 10.1038/nri3831
PG 12
WC Immunology
SC Immunology
GA CG6YV
UT WOS:000353449800008
PM 25882242
ER
PT J
AU Soltesz, I
Alger, BE
Kano, M
Lee, SH
Lovinger, DM
Ohno-Shosaku, T
Watanabe, M
AF Soltesz, Ivan
Alger, Bradley E.
Kano, Masanobu
Lee, Sang-Hun
Lovinger, David M.
Ohno-Shosaku, Takako
Watanabe, Masahiko
TI Weeding out bad waves: towards selective cannabinoid circuit control in
epilepsy
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Review
ID LONG-TERM DEPRESSION; TEMPORAL-LOBE EPILEPSY; FRAGILE-X-SYNDROME;
DIACYLGLYCEROL LIPASE-ALPHA; HIPPOCAMPAL PYRAMIDAL CELLS;
PHOSPHOLIPASE-C-BETA; SPIKING BASKET CELLS; IN-VIVO EXPOSURE;
ENDOCANNABINOID SYSTEM; ENDOGENOUS CANNABINOIDS
AB Endocannabinoids are lipid-derived messengers, and both their synthesis and breakdown are under tight spatiotemporal regulation. As retrograde signalling molecules, endocannabinoids are synthesized postsynaptically but activate presynaptic cannabinoid receptor 1 (CB1) receptors to inhibit neurotransmitter release. In turn, CB1-expressing inhibitory and excitatory synapses act as strategically placed control points for activity-dependent regulation of dynamically changing normal and pathological oscillatory network activity. Here, we highlight emerging principles of cannabinoid circuit control and plasticity, and discuss their relevance for epilepsy and related comorbidities. New insights into cannabinoid signalling may facilitate the translation of the recent interest in cannabis-related substances as antiseizure medications to evidence-based treatment strategies.
C1 [Soltesz, Ivan; Lee, Sang-Hun] Univ Calif Irvine, Dept Anat & Neurobiol, Irvine, CA 92697 USA.
[Alger, Bradley E.] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
[Kano, Masanobu] Univ Tokyo, Grad Sch Med, Dept Neurophysiol, Tokyo 1130033, Japan.
[Lovinger, David M.] NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Ohno-Shosaku, Takako] Kanazawa Univ, Grad Sch Med Sci, Dept Impairment Study, Kanazawa, Ishikawa 9200942, Japan.
[Watanabe, Masahiko] Hokkaido Univ, Grad Sch Med, Dept Anat, Sapporo, Hokkaido 0608638, Japan.
RP Soltesz, I (reprint author), Univ Calif Irvine, Dept Anat & Neurobiol, Irvine, CA 92697 USA.
EM isoltesz@uci.edu
RI WATANABE, Masahiko/A-4055-2012; Ohno-Shosaku, Takako/C-3250-2015;
OI Soltesz, Ivan/0000-0003-1493-3744
FU US National Institutes of Health grant [NS74432]; Ministry of Education,
Culture, Sports, Science and Technology of Japan [23500466, 25000015]
FX The authors thank J. G. Malpeli for comments on the manuscript and M.
Uchigashima for Figure 1c. This work was supported by a US National
Institutes of Health grant (NS74432 to I.S.) and Grants-in-Aid for
Scientific Research (23500466 to T.O.-S. and 25000015 to M.K.) from the
Ministry of Education, Culture, Sports, Science and Technology of Japan.
NR 153
TC 24
Z9 24
U1 5
U2 37
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-003X
EI 1471-0048
J9 NAT REV NEUROSCI
JI Nat. Rev. Neurosci.
PD MAY
PY 2015
VL 16
IS 5
BP 264
EP 277
DI 10.1038/nrn3937
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA CG4CO
UT WOS:000353229800006
PM 25891509
ER
PT J
AU Xie, LK
Qi, Y
Subashi, E
Liao, G
Miller-DeGraff, L
Jetten, AM
Johnson, GA
AF Xie, Luke
Qi, Yi
Subashi, Ergys
Liao, Grace
Miller-DeGraff, Laura
Jetten, Anton M.
Johnson, G. Allan
TI 4D MRI of polycystic kidneys from rapamycin-treated Glis3-deficient mice
SO NMR IN BIOMEDICINE
LA English
DT Article
DE small animal preclinical imaging; MRI; MR microscopy; three-dimensional
dynamic contrast-enhanced; polycystic kidney disease; Glis3 protein
ID GLOMERULAR-FILTRATION-RATE; NEONATAL DIABETES-MELLITUS; VOLUME
PROGRESSION; MOUSE MODEL; DISEASE; BIOMARKERS; PERFUSION; INSIGHTS;
INJURY; GLIS3
AB Polycystic kidney disease (PKD) is a life-threatening disease that leads to a grotesque enlargement of the kidney and significant loss of function. Several imaging studies with MRI have demonstrated that cyst size in polycystic kidneys can determine disease severity and progression. In the present study, we found that, although kidney volume and cyst volume decreased with drug treatment, renal function did not improve with treatment. Here, we applied dynamic contrast-enhanced MRI to study PKD in a Glis3 (GLI-similar 3)-deficient mouse model. Cysts from this model have a wide range of sizes and develop at an early age. To capture this crucial stage and assess cysts in detail, we imaged during early development (3-17 weeks) and applied high spatiotemporal resolution MRI (125x125x125cubic microns every 7.7s). A drug treatment with rapamycin (also known as sirolimus) was applied to determine whether disease progression could be halted. The effect and synergy (interaction) of aging and treatment were evaluated using an analysis of variance (ANOVA). Structural measurements, including kidney volume, cyst volume and cyst-to-kidney volume ratio, changed significantly with age. Drug treatment significantly decreased these metrics. Functional measurements of time-to-peak (TTP) mean and TTP variance were determined. TTP mean did not change with age, whereas TTP variance increased with age. Treatment with rapamycin generally did not affect these functional metrics. Synergistic effects of treatment and age were not found for any measurements. Together, the size and volume ratio of cysts decreased with drug treatment, whereas renal function remained the same. The quantification of renal structure and function with MRI can comprehensively assess the pathophysiology of PKD and response to treatment. Copyright (c) 2015 John Wiley & Sons, Ltd.
C1 [Xie, Luke; Qi, Yi; Subashi, Ergys; Johnson, G. Allan] Duke Univ, Med Ctr, Dept Radiol, Ctr Vivo Microscopy, Durham, NC 27710 USA.
[Xie, Luke; Johnson, G. Allan] Duke Univ, Dept Biomed Engn, Durham, NC 27710 USA.
[Subashi, Ergys] Duke Univ, Med Ctr, Med Phys Grad Program, Durham, NC 27710 USA.
[Liao, Grace; Miller-DeGraff, Laura; Jetten, Anton M.] NIEHS, Cell Biol Sect, Immun Inflammat & Dis Lab, Div Intramural Res,NIH, Res Triangle Pk, NC 27709 USA.
RP Johnson, GA (reprint author), Duke Univ, Med Ctr, Dept Radiol, Ctr Vivo Microscopy, Box 3302, Durham, NC 27710 USA.
EM gjohnson@duke.edu
OI Jetten, Anton/0000-0003-0954-4445
FU National Institutes of Health/National Institute of Biomedical Imaging
and Bioengineering Biomedical Technology Resource Center [P41 EB015897];
National Institutes of Health/National Institute of Environmental Health
Sciences Intramural Research Program [Z01 ES100485]
FX This work was supported by the National Institutes of Health/National
Institute of Biomedical Imaging and Bioengineering Biomedical Technology
Resource Center (P41 EB015897 to G.A.J.), and by the National Institutes
of Health/National Institute of Environmental Health Sciences Intramural
Research Program (Z01 ES100485 to A.M.J.).
NR 43
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0952-3480
EI 1099-1492
J9 NMR BIOMED
JI NMR Biomed.
PD MAY
PY 2015
VL 28
IS 5
BP 546
EP 554
DI 10.1002/nbm.3281
PG 9
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA CG9PX
UT WOS:000353650100004
PM 25810360
ER
PT J
AU Indaram, M
Agron, E
Clemons, TE
Sperduto, RD
Wong, WT
Ferris, FL
Chew, EY
AF Indaram, Maanasa
Agron, Elvira
Clemons, Traci E.
Sperduto, Robert D.
Wong, Wai T.
Ferris, Frederick L., III
Chew, Emily Y.
CA Age Related Eye Dis Study Res Grp
TI Changes in Lens Opacities on the Age-Related Eye Disease Study Grading
Scale Predict Progression to Cataract Surgery and Vision Loss
SO OPHTHALMOLOGY
LA English
DT Article
ID BLUE MOUNTAINS EYE; II LOCS-II; REGRESSION; AREDS
AB Purpose: To investigate whether the 2-year change in lens opacity severity on the Age-Related Eye Disease Study (AREDS) lens grading scale predicts progression to cataract surgery or loss of visual acuity by 5 years.
Design: Prospective cohort study within a randomized clinical trial of oral supplements. Participants: The AREDS participants whose eyes were phakic at baseline and free of late age-related macular degeneration throughout the study.
Methods: Baseline and annual lens photographs of AREDS participants (n = 3466/4757; 73%) were graded for severity of cataracts using the AREDS system for classifying cataracts from photographs. Clinical examinations conducted semiannually collected data on cataract surgery and visual acuity. Association of the change in lens opacities at 2 years with these outcomes at 5 years was analyzed with adjusted Cox proportional hazard models.
Main Outcome Measurements: Progression of lens opacities on stereoscopic lens photographs at 2 years, cataract surgery, and visual acuity loss of 2 lines or more at 5 years.
Results: The adjusted hazard ratios (HRs) for association of progression to cataract surgery at 5 years were: nuclear cataract increase of 1.0 unit or more compared with less than 1.0-unit change at 2 years, 2.77 (95% confidence interval [CI], 2.07-3.70; P < 0.001); cortical cataract increase of 5% or more in lens opacity in the central 5 mm of the lens compared with less than 5% increase at 2 years, 1.91 (95% CI, 1.27-2.87; P = 0.002); and posterior subcapsular cataract increase of 5% or more versus less than 5% in the central 5 mm of the lens, 8.25 (95% CI, 5.55-12.29; P < 0.001). Similarly, HRs of vision loss of 2 lines or more at 5 years for this degree of lens changes at 2 years were the following: nuclear, 1.83 (95% CI, 1.49-2.25; P < 0.001); cortical, 1.13 (95% CI, 0.78-1.65; P = 0.519); and posterior subcapsular cataract, 3.05 (95% CI, 1.79-5.19; P < 0.001).
Conclusions: Two-year changes in severity of lens opacities on the AREDS lens grading scale are predictive of long-term clinically relevant outcomes, making them potential surrogate end points in follow-up studies. (C) 2015 by the American Academy of Ophthalmology.
C1 [Indaram, Maanasa; Agron, Elvira; Ferris, Frederick L., III; Chew, Emily Y.] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Clemons, Traci E.; Sperduto, Robert D.] EMMES Corp, Rockville, MD USA.
[Wong, Wai T.] NEI, Unit Neuron Glia Interact Retinal Dis, NIH, Bethesda, MD 20892 USA.
RP Chew, EY (reprint author), NEI, NIH, Bldg 10,CRC Room 3-2531,10 Ctr Dr,MSC 1204, Bethesda, MD 20892 USA.
EM echew@nei.nih.gov
RI Wong, Wai/B-6118-2017;
OI Wong, Wai/0000-0003-0681-4016; Indaram, Maanasa/0000-0001-6228-3307
FU National Eye Institute, National Institutes of Health, Bethesda,
Maryland [NOI-EY-0-2127]
FX Supported by the National Eye Institute, National Institutes of Health,
Bethesda, Maryland (grant no.: NOI-EY-0-2127). Maanasa Indaram performed
this work as part of the Howard Hughes Scholars Program at the National
Institutes of Health.
NR 18
TC 1
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
EI 1549-4713
J9 OPHTHALMOLOGY
JI Ophthalmology
PD MAY
PY 2015
VL 122
IS 5
BP 888
EP 896
DI 10.1016/j.ophtha.2014.12.037
PG 9
WC Ophthalmology
SC Ophthalmology
GA CG5NB
UT WOS:000353337600013
PM 25682177
ER
PT J
AU Muterko, A
Kalendar, R
Cockram, J
Balashova, I
AF Muterko, Alexandr
Kalendar, Ruslan
Cockram, James
Balashova, Irina
TI Discovery, evaluation and distribution of haplotypes and new alleles of
the Photoperiod-A1 gene in wheat
SO PLANT MOLECULAR BIOLOGY
LA English
DT Article
DE Cereal; Flowering time; Genetic variation; Heteroduplex mobility assay;
Molecular evolution; Photoperiod response; Ppd-A1 haplotype; Wheat
ID HETERODUPLEX MOBILITY ASSAY; PSEUDO-RESPONSE-REGULATOR;
TRITICUM-AESTIVUM L.; FLOWERING TIME; DNA HETERODUPLEXES; GENOME
EVOLUTION; FERTILE CRESCENT; CONSTANS; DOMESTICATION; BARLEY
AB Photoperiod response in wheat is determined to a large extent by the homoeologous series of Photoperiod 1 (Ppd1) genes. In this study, Ppd-A1 genomic sequences from the 5' UTR and promoter region were analysed in 104 accessions of six tetraploid wheat species (Triticum dicoccoides, T. dicoccum, T. turgidum, T. polonicum, T. carthlicum, T. durum) and 102 accessions of six hexaploid wheat species (T. aestivum, T. compactum, T. sphaerococcum, T. spelta, T. macha, T. vavilovii). This data was supplemented with in silico analysis of publicly available sequences from 46 to 193 accessions of diploid and tetraploid wheat, respectively. Analysis of a region of the Ppd-A1 promoter identified thirteen haplotypes, which were divided in two haplogroups. Distribution of the Ppd-A1 haplogroups and haplotypes in wheat species, and their geographical distributions were analysed. Polymerase chain reaction combined with a heteroduplex mobility assay was subsequently used to efficiently discriminate between Ppd-A1 alleles, allowing identification of the Ppd-A1b haplotypes and haplogroups. The causes of anomalous migration of Ppd-A1 heteroduplexes in gels were found to be the localization of mismatches relative to the center of fragment, the cumulative effect of neighbouring polymorphic sites, and the location of mismatches within A/T-tracts. Analysis of the Ppd-A1 5' UTR in hexaploid wheat revealed a novel mutation within the "photoperiod critical" region in a subset of T. compactum accessions. This putative photoperiod insensitive allele (designated Ppd-A1a.4) includes a 684 bp deletion which spans region in common with deletions previously identified in other photoperiod insensitive Ppd1 alleles.
C1 [Muterko, Alexandr; Balashova, Irina] Breeding & Genet Inst Natl Ctr Seed & Cultivar In, Dept Genom & Biotechnol, UA-65036 Odessa, Ukraine.
[Kalendar, Ruslan] RSE Natl Ctr Biotechnol, Lab Plant Genom & Bioinformat, Astana 010000, Kazakhstan.
[Cockram, James] NIAB, Cambridge CB3 0LE, England.
RP Muterko, A (reprint author), Breeding & Genet Inst Natl Ctr Seed & Cultivar In, Dept Genom & Biotechnol, Ovidiopolskaya Rd 3, UA-65036 Odessa, Ukraine.
EM muterko@gmail.com
RI Kalendar, Ruslan/D-9751-2012;
OI Kalendar, Ruslan/0000-0003-3986-2460; Muterko,
Alexandr/0000-0002-9083-9162
NR 55
TC 3
Z9 3
U1 4
U2 25
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-4412
EI 1573-5028
J9 PLANT MOL BIOL
JI Plant Mol.Biol.
PD MAY
PY 2015
VL 88
IS 1-2
BP 149
EP 164
DI 10.1007/s11103-015-0313-2
PG 16
WC Biochemistry & Molecular Biology; Plant Sciences
SC Biochemistry & Molecular Biology; Plant Sciences
GA CG6IQ
UT WOS:000353403600011
PM 25851614
ER
PT J
AU Mashalidis, EH
Gittis, AG
Tomczak, A
Abell, C
Barry, CE
Garboczi, DN
AF Mashalidis, Ellene H.
Gittis, Apostolos G.
Tomczak, Aurelie
Abell, Chris
Barry, Clifton E., III
Garboczi, David N.
TI Molecular insights into the binding of coenzyme F-420 to the conserved
protein Rv1155 from Mycobacterium tuberculosis
SO PROTEIN SCIENCE
LA English
DT Article
DE Mycobacterium tuberculosis; Rv1155; coenzyme F-420; conserved
hypothetical protein
ID PYRIDOXINE 5'-PHOSPHATE OXIDASE; BACTERIAL LUCIFERASE FAMILY;
F-420-DEPENDENT GLUCOSE-6-PHOSPHATE-DEHYDROGENASE; CRYSTAL-STRUCTURE;
DRUG DISCOVERY; SYSTEM; PA-824; SMEGMATIS; FLAVIN; IDENTIFICATION
AB Coenzyme F-420 is a deazaflavin hydride carrier with a lower reduction potential than most flavins. In Mycobacterium tuberculosis (Mtb), F-420 plays an important role in activating PA-824, an antituberculosis drug currently used in clinical trials. Although F-420 is important to Mtb redox metabolism, little is known about the enzymes that bind F-420 and the reactions that they catalyze. We have identified a novel F-420-binding protein, Rv1155, which is annotated in the Mtb genome sequence as a putative flavin mononucleotide (FMN)-binding protein. Using biophysical techniques, we have demonstrated that instead of binding FMN or other flavins, Rv1155 binds coenzyme F-420. The crystal structure of the complex of Rv1155 and F-420 reveals one F-420 molecule bound to each monomer of the Rv1155 dimer. Structural, biophysical, and bioinformatic analyses of the Rv1155-F-420 complex provide clues about its role in the bacterium.
C1 [Mashalidis, Ellene H.] NIAID, TB Res Sect, Bethesda, MD 20892 USA.
[Mashalidis, Ellene H.; Abell, Chris] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
[Gittis, Apostolos G.; Garboczi, David N.] NIAID, Struct Biol Sect, Res Technol Branch, Rockville, MD 20852 USA.
[Tomczak, Aurelie] NIAID, Mol Signaling Sect, Lab Mol Immunol, Bethesda, MD 20892 USA.
RP Garboczi, DN (reprint author), Twinbrook 2 Rm 110,12441 Parklawn Dr, Rockville, MD 20852 USA.
EM dgarboczi@niaid.nih.gov
RI Barry, III, Clifton/H-3839-2012
FU NIH, NIAID
FX Grant sponsor: Intramural Research Program of the NIH, NIAID.
NR 52
TC 5
Z9 5
U1 2
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0961-8368
EI 1469-896X
J9 PROTEIN SCI
JI Protein Sci.
PD MAY
PY 2015
VL 24
IS 5
BP 729
EP 740
DI 10.1002/pro.2645
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CG7YV
UT WOS:000353524700015
PM 25644473
ER
PT J
AU Leggio, L
Zywiak, WH
Edwards, SM
Tidey, JW
Swift, RM
Kenna, GA
AF Leggio, Lorenzo
Zywiak, William H.
Edwards, Steven M.
Tidey, Jennifer W.
Swift, Robert M.
Kenna, George A.
TI A preliminary double-blind, placebo-controlled randomized study of
baclofen effects in alcoholic smokers (vol 232, pg 233, 2015)
SO PSYCHOPHARMACOLOGY
LA English
DT Correction
C1 [Leggio, Lorenzo] NIAAA, Sect Clin Psychoneuroendocrinol & Neuropsychophar, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
[Leggio, Lorenzo] NIDA, Intramural Res Program, NIH, Baltimore, MD USA.
[Leggio, Lorenzo] Brown Univ, Dept Behav & Social Sci, Ctr Alcohol & Addict Studies, Providence, RI 02912 USA.
[Zywiak, William H.] PIRE, Decis Sci Inst, Pawtucket, RI USA.
[Zywiak, William H.] Butler Hosp, Providence, RI 02906 USA.
[Zywiak, William H.; Tidey, Jennifer W.; Swift, Robert M.; Kenna, George A.] Brown Univ, Dept Psychiat & Human Behav, Ctr Alcohol & Addict Studies, Providence, RI 02912 USA.
[Edwards, Steven M.] Univ Nebraska, Dept Psychol, Lincoln, NE 68588 USA.
[Swift, Robert M.] Vet Affairs Med Ctr, Providence, RI USA.
[Swift, Robert M.] Roger Williams Med Ctr, Providence, RI USA.
RP Leggio, L (reprint author), NIAAA, Sect Clin Psychoneuroendocrinol & Neuropsychophar, Lab Clin & Translat Studies, NIH, 10 Ctr Dr,10CRC 15330,MSC 1108,Room 1-5429, Bethesda, MD 20892 USA.
EM lorenzo.leggio@nih.gov
RI Leggio, Lorenzo/M-2972-2016
NR 1
TC 0
Z9 0
U1 0
U2 0
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 MAY
PY 2015
VL 232
IS 9
BP 1667
EP 1667
DI 10.1007/s00213-015-3916-z
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CF8DW
UT WOS:000352786900015
PM 25804430
ER
PT J
AU Soto, PL
Grandy, DK
Hursh, SR
Katz, JL
AF Soto, Paul L.
Grandy, David K.
Hursh, Steven R.
Katz, Jonathan L.
TI Behavioral economics of food reinforcement and the effects of
prefeeding, extinction, and eticlopride in dopamine D-2 receptor mutant
mice (vol 215, pg 775, 2015)
SO PSYCHOPHARMACOLOGY
LA English
DT Correction
C1 [Soto, Paul L.; Hursh, Steven R.] Johns Hopkins Univ, Div Behav Biol, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.
[Grandy, David K.] Oregon Hlth & Sci Univ, Portland, OR USA.
[Katz, Jonathan L.] NIDA, Baltimore, MD USA.
RP Soto, PL (reprint author), Johns Hopkins Univ, Div Behav Biol, Dept Psychiat & Behav Sci, Ross 469,720 Rutland Ave, Baltimore, MD 21205 USA.
EM psoto@jhmi.edu
NR 1
TC 0
Z9 0
U1 1
U2 2
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 MAY
PY 2015
VL 232
IS 9
BP 1669
EP 1669
DI 10.1007/s00213-015-3918-x
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CF8DW
UT WOS:000352786900016
PM 25814138
ER
PT J
AU Kahn, JA
Rudy, BJ
Xu, JH
Secord, EA
Kapogiannis, BG
Thornton, S
Gillison, ML
AF Kahn, Jessica A.
Rudy, Bret J.
Xu, Jiahong
Secord, Elizabeth A.
Kapogiannis, Bill G.
Thornton, Sarah
Gillison, Maura L.
TI Behavioral, Immunologic, and Virologic Correlates of Oral Human
Papillomavirus Infection in HIV-Infected Youth
SO SEXUALLY TRANSMITTED DISEASES
LA English
DT Article
ID HPV INFECTION; UNITED-STATES; NECK CANCERS; PREVALENCE; POPULATION;
WOMEN; RISK; ADOLESCENTS; HEAD; CHILDREN
AB Background: Little is known about the epidemiology or risk factors for oral human papillomavirus (HPV) in HIV-infected youth. The objectives of this study were to determine the prevalence and correlates of oral HPV infection and to explore the association between HPV vaccination and oral infection in HIV-infected youth.
Methods: Youth 12 to 24 years of age with behaviorally acquired HIV were recruited for this cross-sectional study. Procedures involved medical chart review, survey, and collection of an oral rinse sample. Univariable and multivariable logistic regression models were used to determine whether demographic, behavioral, immunologic, and virologic factors and history of vaccination were significantly associated with oral HPV infection.
Results: Mean age of the 272 participants was 21.5 years; 64% were non-Hispanic black and 20.2% were Hispanic; and 10.8% of men compared with 20.3% of women were fully vaccinated. Human papillomavirus prevalence was 19.7% in men and 18.6% in women (P = 1.0). Only men were positive for vaccine-type HPV: 5.6% were positive for HPV-6, HPV-11, HPV-16, and/or HPV-18, and 4.2% were positive for HPV-16 and/or HPV-18. Among men who were fully vaccinated, none were positive for HPV-6, HPV-11, HPV-16, and/or HPV-18, compared with 12 (6.3%) of men who were not fully vaccinated (P = 0.37). Two variables were marginally associated with oral HPV (P < 0.10): marijuana use in the previous 3 months and lower CD4+ T-cell count.
Conclusions: Prevalence rates of oral HPV were relatively high in this population of HIV-infected youth and were similar in male and female youth. No fully vaccinated men were infected with vaccine-type HPV.
C1 [Kahn, Jessica A.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Kahn, Jessica A.] Univ Cincinnati, Coll Med, Cincinnati, OH USA.
[Rudy, Bret J.] NYU, Sch Med, New York, NY USA.
[Xu, Jiahong; Thornton, Sarah] WESTAT Corp, Rockville, MD 20850 USA.
[Secord, Elizabeth A.] Wayne State Univ, Detroit, MI USA.
[Kapogiannis, Bill G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, NIH, Rockville, MD USA.
[Gillison, Maura L.] Ohio State Univ, Columbus, OH 43210 USA.
RP Kahn, JA (reprint author), Cincinnati Childrens Hosp Med Ctr, Div Adolescent Med, MLC 4000,3333 Burnet Ave, Cincinnati, OH 45229 USA.
EM jessica.kahn@cchmc.org
FU NCATS NIH HHS [UL1 TR001082]; NICHD NIH HHS [5 U01HD 40474, U01
HD040474, U01 HD040533, U01 HD068030, U01-HD040533]
NR 36
TC 3
Z9 3
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0148-5717
EI 1537-4521
J9 SEX TRANSM DIS
JI Sex. Transm. Dis.
PD MAY
PY 2015
VL 42
IS 5
BP 246
EP 252
DI 10.1097/OLQ.0000000000000264
PG 7
WC Infectious Diseases
SC Infectious Diseases
GA CG1QY
UT WOS:000353049700004
PM 25868136
ER
PT J
AU Rosenberg, M
Pettifor, A
Lippman, SA
Thirumurthy, H
Emch, M
Miller, WC
Selin, A
Gomez-Olive, FX
Hughes, JP
Laeyendecker, O
Tollman, S
Kahn, K
AF Rosenberg, Molly
Pettifor, Audrey
Lippman, Sheri A.
Thirumurthy, Harsha
Emch, Michael
Miller, William C.
Selin, Amanda
Gomez-Olive, Francesc Xavier
Hughes, James P.
Laeyendecker, Oliver
Tollman, Stephen
Kahn, Kathleen
TI Relationship Between Community-Level Alcohol Outlet Accessibility and
Individual-Level Herpes Simplex Virus Type 2 Infection Among Young Women
in South Africa
SO SEXUALLY TRANSMITTED DISEASES
LA English
DT Article
ID INTIMATE PARTNER VIOLENCE; HIV PREVALENCE; PUBLIC-HEALTH; CONSUMPTION;
DRINKING; DENSITY; AVAILABILITY; ASSOCIATION; METAANALYSIS; POPULATION
AB Background: Exposure to alcohol outlets may influence sexual health outcomes at the individual and community levels. Visiting alcohol outlets facilitates alcohol consumption and exposes patrons to a risky environment and network of potential partners, whereas the presence of alcohol outlets in the community may shift social acceptance of riskier behavior. We hypothesize that living in communities with more alcohol outlets is associated with increased sexual risk.
Methods: We performed a cross-sectional analysis in a sample of 2174 South African schoolgirls (ages 13-21 years) living across 24 villages in the rural Agincourt subdistrict, underpinned by long-term health and sociodemographic surveillance. To examine the association between number of alcohol outlets in village of residence and individual-level prevalent herpes simplex virus type 2 (HSV-2) infection, we used generalized estimating equations with logit links, adjusting for individual-and villagelevel covariates.
Results: The median number of alcohol outlets per village was 3 (range, 0-7). Herpes simplex virus type 2 prevalence increased from villages with no outlets (1.4%[95% confidence interval, 0.2-12.1]), to villages with 1 to 4 outlets (4.5% [3.7-5.5]), and to villages with more than 4 outlets (6.3% [5.6, 7.1]). An increase of 1 alcohol outlet per village was associated with an 11% increase in the odds of HSV-2 infection (adjusted odds ratio [95% confidence interval], 1.11 [0.98-1.25]).
Conclusions: Living in villages with more alcohol outlets was associated with increased prevalence of HSV-2 infection in young women. Structural interventions and sexual health screenings targeting villages with extensive alcohol outlet environments could help prevent the spread of sexually transmitted infections.
C1 [Rosenberg, Molly] Harvard Univ, Ctr Populat & Dev Studies, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Rosenberg, Molly; Pettifor, Audrey; Emch, Michael; Miller, William C.] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Rosenberg, Molly; Pettifor, Audrey; Thirumurthy, Harsha; Emch, Michael; Selin, Amanda] Univ N Carolina, Carolina Populat Ctr, Chapel Hill, NC USA.
[Pettifor, Audrey; Lippman, Sheri A.; Tollman, Stephen; Kahn, Kathleen] Univ Witwatersrand, Sch Publ Hlth, MRC Wits Rural Publ Hlth & Hlth Transit Res Unit, Fac Hlth Sci, Johannesburg, South Africa.
[Lippman, Sheri A.] Univ Calif San Francisco, Ctr AIDS Prevent Studies, Dept Med, San Francisco, CA USA.
[Thirumurthy, Harsha] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Hlth Policy & Management, Chapel Hill, NC USA.
[Emch, Michael] Univ N Carolina, Sch Med, Dept Geog, Chapel Hill, NC USA.
[Miller, William C.] Univ N Carolina, Sch Med, Div Infect Dis, Dept Med, Chapel Hill, NC USA.
[Tollman, Stephen; Kahn, Kathleen] INDEPTH Network, Accra, Ghana.
[Hughes, James P.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Laeyendecker, Oliver] NIAID, Immunoregulat Lab, NIH, Baltimore, MD USA.
[Laeyendecker, Oliver] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[Tollman, Stephen; Kahn, Kathleen] Umea Univ, Ctr Global Hlth Res, Umea, Sweden.
RP Rosenberg, M (reprint author), Harvard Univ, Ctr Populat & Dev Studies, 9 Bow St, Cambridge, MA 02138 USA.
EM mrosenb@hsph.harvard.edu
OI Laeyendecker, Oliver/0000-0002-6429-4760
FU NIAID NIH HHS [U01 AI069423, 5U01AI069423-04, UM1 AI068617, UM1
AI068613, UM1 AI068619]; NICHD NIH HHS [P2C HD050924, T32 HD007168, R24
HD050924]; NIMH NIH HHS [R01 MH087118, R21 MH090887, 1R21MH090887-01,
5R01MH087118-02]; Wellcome Trust [058893/Z/99/A, 069683/Z/02/Z,
085477/Z/08/Z]
NR 34
TC 0
Z9 0
U1 3
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0148-5717
EI 1537-4521
J9 SEX TRANSM DIS
JI Sex. Transm. Dis.
PD MAY
PY 2015
VL 42
IS 5
BP 259
EP 265
DI 10.1097/OLQ.0000000000000263
PG 7
WC Infectious Diseases
SC Infectious Diseases
GA CG1QY
UT WOS:000353049700006
PM 25868138
ER
PT J
AU Huang, XS
Wang, Y
Yan, W
Smith, C
Ye, ZH
Wang, J
Gao, YX
Mendelsohn, L
Cheng, LZ
AF Huang, Xiaosong
Wang, Ying
Yan, Wei
Smith, Cory
Ye, Zhaohui
Wang, Jing
Gao, Yongxing
Mendelsohn, Laurel
Cheng, Linzhao
TI Production of Gene-Corrected Adult Beta Globin Protein in Human
Erythrocytes Differentiated From Patient iPSCs After Genome Editing of
the Sickle Point Mutation
SO STEM CELLS
LA English
DT Article
DE Human iPSCs; Genome editing; Erythroid cells; Globin switching
ID PLURIPOTENT STEM-CELLS; ZINC-FINGER NUCLEASES; RED-BLOOD-CELLS;
HOMOLOGOUS RECOMBINATION; HUMAN ERYTHROBLASTS; IN-VIVO; GENERATION;
ERYTHROPOIESIS; CRISPR/CAS9; TALEN
AB Human induced pluripotent stem cells (iPSCs) and genome editing provide a precise way to generate gene-corrected cells for disease modeling and cell therapies. Human iPSCs generated from sickle cell disease ( SCD) patients have a homozygous missense point mutation in the HBB gene encoding adult beta-globin proteins, and are used as a model system to improve strategies of human gene therapy. We demonstrate that the CRISPR/Cas9 system designer nuclease is much more efficient in stimulating gene targeting of the endogenous HBB locus near the SCD point mutation in human iPSCs than zinc finger nucleases and TALENs. Using a specific guide RNA and Cas9, we readily corrected one allele of the SCD HBB gene in human iPSCs by homologous recombination with a donor DNA template containing the wild-type HBB DNA and a selection cassette that was subsequently removed to avoid possible interference of HBB transcription and translation. We chose targeted iPSC clones that have one corrected and one disrupted SCD allele for erythroid differentiation assays, using an improved xeno-free and feeder-free culture condition we recently established. Erythrocytes from either the corrected or its parental ( uncorrected) iPSC line were generated with similar efficiencies. Currently similar to 6%-10% of these differentiated erythrocytes indeed lacked nuclei, characteristic of further matured erythrocytes called reticulocytes. We also detected the 16-kDa beta-globin protein expressed from the corrected HBB allele in the erythrocytes differentiated from genome-edited iPSCs. Our results represent a significant step toward the clinical applications of genome editing using patient-derived iPSCs to generate disease-free cells for cell and gene therapies.
C1 [Huang, Xiaosong; Yan, Wei; Smith, Cory; Ye, Zhaohui; Wang, Jing; Gao, Yongxing; Cheng, Linzhao] Johns Hopkins Univ, Sch Med, Dept Med, Div Hematol, Baltimore, MD 21205 USA.
[Huang, Xiaosong; Wang, Ying; Yan, Wei; Smith, Cory; Ye, Zhaohui; Wang, Jing; Gao, Yongxing; Cheng, Linzhao] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD USA.
[Smith, Cory; Cheng, Linzhao] Johns Hopkins Univ, Sch Med, Predoctoral Training Program Human Genet, Baltimore, MD USA.
[Wang, Ying] Johns Hopkins Univ, Dept Chem & Biomol Engn, Baltimore, MD USA.
[Mendelsohn, Laurel] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Cheng, LZ (reprint author), Miller Res Bldg 747,733 North Broadway, Baltimore, MD 21205 USA.
EM lcheng2@jhmi.edu
FU Maryland State Stem Cell Research Fund [2011-MSCRFII-0088,
2011-MSCRFE-0087]; NIH [2R01 HL-073781, U01 HL107446, T32HL007525-31];
Edythe Harris Lucas and Clara Lucas Lynn Chair in Hematology of Johns
Hopkins University
FX We thank Dr. Xiuli An at NYBC for providing Band 3 antibodies, Dr. J.
Keith Joung in MGH for providing the MGH donor vector, and Drs. Evan
Braunstein and Robert Brodsky for discussions and critical reading. This
work was supported in part by grants from Maryland State Stem Cell
Research Fund (2011-MSCRFII-0088 and 2011-MSCRFE-0087) and from NIH
(2R01 HL-073781, U01 HL107446, and T32HL007525-31). L.C. is also
supported by Edythe Harris Lucas and Clara Lucas Lynn Chair in
Hematology of Johns Hopkins University.
NR 47
TC 36
Z9 38
U1 6
U2 37
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD MAY
PY 2015
VL 33
IS 5
BP 1470
EP 1479
DI 10.1002/stem.1969
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA CG4XM
UT WOS:000353292600009
PM 25702619
ER
PT J
AU Chen, P
Denniston, AK
Hirani, S
Hannes, S
Nussenblatt, RB
AF Chen, Ping
Denniston, Alastair K.
Hirani, Sima
Hannes, Susan
Nussenblatt, Robert B.
TI Role of dendritic cell subsets in immunity and their contribution to
noninfectious uveitis
SO SURVEY OF OPHTHALMOLOGY
LA English
DT Review
DE conventional dendritic cells; myeloid dendritic cells; plasmacytoid
dendritic cells; noninfectious uveitis; experimental autoimmune uveitis
ID EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; COLONY-STIMULATING FACTOR; MOUSE
BONE-MARROW; T-CELLS; PERIPHERAL-BLOOD; RETINAL ANTIGENS;
INTERFERON-ALPHA; LYMPHOID ORGANS; AQUEOUS-HUMOR; FLT3 LIGAND
AB Dendritic cells (DCs) are a heterogeneous population. Murine DCs consist of conventional DCs (cDCs) and plasmacytoid DCs (pDCs). In humans, the analogous populations are myeloid DCs (mDCs) and pDCs. Though distinct in phenotypes and functions, studies have shown that these DC subsets may interact or "crosstalk" during immune responses. For example, cDCs may facilitate pDC maturation, and pDCs may enhance antigen presentation of cDCs in certain pathogenic conditions or even take on a cDC phenotype themselves. The role of DCs in noninfectious uveitis has been studied primarily in the experimental autoimmune uveitis mouse model and to a more limited extent in patients. Recent evidence shows that the number, phenotype, and function of DC subsets are altered in this disease. We provide an overview of selected recent developments of pDCs and cDCs/mDCs, with special attention to their interaction and the dual roles of DC subsets in noninfectious uveitis. Published by Elsevier Inc.
C1 [Chen, Ping; Hirani, Sima; Hannes, Susan; Nussenblatt, Robert B.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Denniston, Alastair K.] Univ Hosp Birmingham NHS Fdn Trust, Queen Elizabeth Hosp Birmingham, Dept Ophthalmol, Birmingham, W Midlands, England.
RP Nussenblatt, RB (reprint author), NEI, NIH, 9000 Rockville Pike,Bldg 10-10N109, Rockville, MD 20892 USA.
EM nussenblattr@nei.nih.gov
OI Denniston, Alastair/0000-0001-7849-0087
FU Intramural Research Program of the National Institute of Eye, NIH
FX The research was supported by the Intramural Research Program of the
National Institute of Eye, NIH. We thank Drs. Igal Gery, William Tucker,
and Carlos Blades for critical reading of the manuscript.
NR 71
TC 3
Z9 3
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6257
EI 1879-3304
J9 SURV OPHTHALMOL
JI Surv. Ophthalmol.
PD MAY-JUN
PY 2015
VL 60
IS 3
BP 242
EP 249
DI 10.1016/j.survophthal.2015.01.003
PG 8
WC Ophthalmology
SC Ophthalmology
GA CG6SP
UT WOS:000353433000006
PM 25749202
ER
PT J
AU Tana, MM
Zhao, XC
Bradshaw, A
Moon, MS
Page, S
Turner, T
Rivera, E
Kleiner, DE
Heller, T
AF Tana, Michele M.
Zhao, Xiongce
Bradshaw, Alyson
Moon, Mi Sun
Page, Sandy
Turner, Tiffany
Rivera, Elenita
Kleiner, David E.
Heller, Theo
TI Factors associated with the platelet count in patients with chronic
hepatitis C
SO THROMBOSIS RESEARCH
LA English
DT Article
DE Platelet biology; Non-invasive markers; Conceptual model
ID COUNT/SPLEEN DIAMETER RATIO; CHRONIC LIVER-DISEASE; VIRUS-INFECTION;
COMPENSATED CIRRHOSIS; ESOPHAGEAL-VARICES; THROMBOCYTOPENIA;
THROMBOPOIETIN; FIBROSIS; DIAGNOSIS; FRACTION
AB Background: There are many potential causes of thrombocytopenia in patients with chronic hepatitis C (CHC).
Aims: We sought to determine the association between thrombopoietin (TPO) level, immature platelet fraction (IPF), immunoglobulin G (IgG) level, spleen size, and the platelet count in CHC.
Methods: We studied a consecutive sample of patients enrolled in an observational study at a referral-based research center, excluding subjects based on eligibility criteria. TPO, glycocalicin, and von Willebrand Factor (vWF) levels were determined using stored sera. Hepatic fibrosis was assessed via transient elastography (TE) when available, and clinical laboratory values and radiologic data were obtained from the medical record. We performed analyses of the relationships between independent variables and the platelet count.
Results: On univariate analysis, the following variables were significantly associated with the platelet count: age, alanine aminotransferase (ALT), direct bilirubin, total bilirubin, IPF, international normalized ratio (INR), spleen size, vWF, glycocalicin, fibrosis stage on liver biopsy, and TE (P-values all < 0.05). A multivariable model determined that imputed TE score, TPO, IPF, and spleen size were independently associated with the platelet count (P-values all < 0.05).
Conclusions: The platelet count in CHC is significantly associated with fibrosis, TPO level, IPF, and spleen size. Our findings challenge the proposed mechanism of decreased TPO levels or decreased bone marrow production of platelets as a cause of thrombocytopenia in CHC. Future studies focusing on the effects of fibrosis and splenomegaly on platelets may shed more light on the pathophysiology of thrombocytopenia in patients with CHC. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Tana, Michele M.; Zhao, Xiongce; Bradshaw, Alyson; Moon, Mi Sun; Page, Sandy; Turner, Tiffany; Rivera, Elenita; Heller, Theo] NIDDKD, Liver Dis Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Tana, Michele M.] Univ Calif San Francisco, Div Gastroenterol, UCSF Liver Ctr, San Francisco, CA 94143 USA.
[Kleiner, David E.] NCI, NIH, Bethesda, MD 20892 USA.
RP Tana, MM (reprint author), NIDDKD, Liver Dis Branch, Div Intramural Res, NIH, 9000 Rockville Pike,Bldg 10,Rm 9B16, Bethesda, MD 20892 USA.
EM tanam@medsfgh.ucsf.edu
FU Intramural Division of the National Institute of Diabetes and Digestive
and Kidney Diseases; National Cancer Institute, National Institutes of
Health
FX This work was funded by the Intramural Division of the National
Institute of Diabetes and Digestive and Kidney Diseases and the National
Cancer Institute, National Institutes of Health.
NR 26
TC 5
Z9 5
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0049-3848
J9 THROMB RES
JI Thromb. Res.
PD MAY
PY 2015
VL 135
IS 5
BP 823
EP 828
DI 10.1016/j.thromres.2015.02.010
PG 6
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA CG7NP
UT WOS:000353490800009
PM 25728497
ER
PT J
AU Singh, SK
Lupo, PJ
Scheurer, ME
Kennedy, AE
Okcu, MF
Dorak, MT
AF Singh, Sandeep K.
Lupo, Philip J.
Scheurer, Michael E.
Kennedy, Amy E.
Okcu, M. Fatih
Dorak, Mehmet Tevfik
TI HLA REGION CONTRIBUTES TO THE GENDER DIFFERENTIAL IN CHILDHOOD LEUKAEMIA
RISK
SO TISSUE ANTIGENS
LA English
DT Meeting Abstract
CT European-Federation-for-Immunogenetics Conference
CY APR 26-29, 2015
CL Geneva, SWITZERLAND
SP European Federat Immunogenet
C1 [Singh, Sandeep K.] Florida Int Univ, Miami, FL 33199 USA.
[Lupo, Philip J.; Scheurer, Michael E.; Okcu, M. Fatih] Baylor Coll Med, Houston, TX 77030 USA.
[Kennedy, Amy E.] NCI, Bethesda, MD 20892 USA.
[Dorak, Mehmet Tevfik] Liverpool Hope Univ, Liverpool, Merseyside, England.
EM mtd3053@gmail.com
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0001-2815
EI 1399-0039
J9 TISSUE ANTIGENS
JI Tissue Antigens
PD MAY
PY 2015
VL 85
IS 5
MA P26
BP 339
EP 339
PG 1
WC Cell Biology; Immunology; Pathology
SC Cell Biology; Immunology; Pathology
GA CF9SN
UT WOS:000352907000103
ER
PT J
AU Chaloupka, FJ
Tauras, JA
Strasser, JH
Willis, G
Gibson, JT
Hartman, AM
AF Chaloupka, Frank J.
Tauras, John A.
Strasser, Julia H.
Willis, Gordon
Gibson, James T.
Hartman, Anne M.
TI A comparison of alternative methods for measuring cigarette prices
SO TOBACCO CONTROL
LA English
DT Article
AB Background Government agencies, public health organisations and tobacco control researchers rely on accurate estimates of cigarette prices for a variety of purposes. Since the 1950s, the Tax Burden on Tobacco (TBOT) has served as the most widely used source of this price data despite its limitations.
Purpose This paper compares the prices and collection methods of the TBOT retail-based data and the 2003 and 2006/2007 waves of the population-based Tobacco Use Supplement to the Current Population Survey (TUS-CPS).
Methods From the TUS-CPS, we constructed multiple state-level measures of cigarette prices, including weighted average prices per pack (based on average prices for single-pack purchases and average prices for carton purchases) and compared these with the weighted average price data reported in the TBOT. We also constructed several measures of tax avoidance from the TUS-CPS self-reported data.
Results For the 2003 wave, the average TUS-CPS price was 71 cents per pack less than the average TBOT price; for the 2006/2007 wave, the difference was 47 cents. TUS-CPS and TBOT prices were also significantly different at the state level. However, these differences varied widely by state due to tax avoidance opportunities, such as cross-border purchasing.
Conclusions The TUS-CPS can be used to construct valid measures of cigarette prices. Unlike the TBOT, the TUS-CPS captures the effect of price-reducing marketing strategies, as well as tax avoidance practices and non-traditional types of purchasing. Thus, self-reported data like TUS-CPS appear to have advantages over TBOT in estimating the 'real' price that smokers face.
C1 [Chaloupka, Frank J.] Univ Illinois, Inst Hlth Res & Policy, Dept Econ, Chicago, IL 60608 USA.
[Tauras, John A.] Univ Illinois, Dept Econ, Chicago, IL 60608 USA.
[Strasser, Julia H.; Willis, Gordon; Hartman, Anne M.] NCI, Div Canc Control & Populat Sci, Rockville, MD 20850 USA.
[Gibson, James T.] Informat Management Serv Inc, Calverton, MD USA.
RP Chaloupka, FJ (reprint author), Univ Illinois, Inst Hlth Res & Policy, 1747 W Roosevelt,Room 558, Chicago, IL 60608 USA.
EM hartmana@mail.nih.gov
FU National Cancer Institute [HHSN21200800697P]
FX Funding support provided by the National Cancer Institute Contract #:
HHSN21200800697P.
NR 14
TC 1
Z9 1
U1 2
U2 8
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0964-4563
EI 1468-3318
J9 TOB CONTROL
JI Tob. Control
PD MAY
PY 2015
VL 24
IS 3
BP 269
EP 274
DI 10.1136/tobaccocontrol-2013-051320
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CG5NA
UT WOS:000353337500016
PM 24365701
ER
PT J
AU Gilman, JM
Smith, AR
Bjork, JM
Ramchandani, VA
Momenan, R
Hommer, DW
AF Gilman, Jodi M.
Smith, Ashley R.
Bjork, James M.
Ramchandani, Vijay A.
Momenan, Reza
Hommer, Daniel W.
TI Cumulative gains enhance striatal response to reward opportunities in
alcohol-dependent patients
SO ADDICTION BIOLOGY
LA English
DT Article
DE Alcoholism; reward; ventral striatum
ID DECISION-MAKING DEFICITS; RISK-TAKING; DETOXIFIED ALCOHOLICS; FUTURE
CONSEQUENCES; ANTERIOR CINGULATE; PREFRONTAL CORTEX; DOPAMINE NEURONS;
WORKING-MEMORY; GAMBLING TASK; NEURAL BASIS
AB Substance use disorder is characterized by a transition from volitional to compulsive responding for drug reward. A possible explanation for this transition may be that alcohol-dependent patients (ADP) show a general propensity for a history of rewarded instrumental responses, and these rewarded responses may boost the activation of motivational neurocircuitry for additional reward. Brain imaging studies of decision-making have demonstrated that ADP relative to controls (CON) often show altered neural activation in response to anticipating and receiving rewards, but the majority of studies have not investigated how past performance affects activation. A potential exists for ADP to show increased sensitivity to reward as a function of reward delivery history. In the current study, we used functional magnetic resonance imaging to investigate the neural correlates of risky decision-making in ADP (n=18) and CON (n=18) while they played a two-choice monetary risk-taking game. In addition to investigating general neural recruitment by risky decision-making, we also modeled each participant's running total of monetary earnings in order to determine areas of activation that correlated with cumulative reward. We found that ADP and CON showed few differences in behavior or in mesolimbic activation by choice for, and receipt of, risky gains. However, when including a cumulative-earnings covariate, ADP exhibited heightened striatal activation that correlated with total earnings during the choice event in the task. The heightened contextual sensitivity of striatal responses to cumulative earnings in ADP may represent a general neurobiological affective substrate for development of automatized instrumental behavior.
C1 [Gilman, Jodi M.] Massachusetts Gen Hosp, Ctr Addict Med, Boston, MA 02114 USA.
[Smith, Ashley R.] Temple Univ, Dept Psychol, Neurocognit Lab, Philadelphia, PA 19122 USA.
[Bjork, James M.] NIDA, Clin Neurosci Branch, Div Clin Neurosci & Behav Res, Bethesda, MD 20892 USA.
[Ramchandani, Vijay A.] NIAAA, Sect Human Psychopharmacol, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Momenan, Reza; Hommer, Daniel W.] NIAAA, Sect Brain Electrophysiol & Imaging, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
RP Gilman, JM (reprint author), Massachusetts Gen Hosp, MGH Ctr Addict Med, 60 Staniford St, Boston, MA 02114 USA.
EM jgilman1@partners.org
OI Bjork, James/0000-0003-0593-3291
FU NIDA NIH HHS [K01 DA034093, L30 DA034327]
NR 65
TC 3
Z9 3
U1 3
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1355-6215
EI 1369-1600
J9 ADDICT BIOL
JI Addict. Biol.
PD MAY
PY 2015
VL 20
IS 3
BP 580
EP 593
DI 10.1111/adb.12147
PG 14
WC Biochemistry & Molecular Biology; Substance Abuse
SC Biochemistry & Molecular Biology; Substance Abuse
GA CF6FK
UT WOS:000352652200015
PM 24754451
ER
PT J
AU Papadopoulos, NG
Bernstein, JA
Demoly, P
Dykewicz, M
Fokkens, W
Hellings, PW
Peters, AT
Rondon, C
Togias, A
Cox, LS
AF Papadopoulos, N. G.
Bernstein, J. A.
Demoly, P.
Dykewicz, M.
Fokkens, W.
Hellings, P. W.
Peters, A. T.
Rondon, C.
Togias, A.
Cox, L. S.
TI Phenotypes and endotypes of rhinitis and their impact on management: a
PRACTALL report
SO ALLERGY
LA English
DT Article
DE classification; endotypes; phenotypes; rhinitis; treatment
ID SEASONAL ALLERGIC RHINITIS; AQUEOUS NASAL SPRAY; PLACEBO-CONTROLLED
TRIAL; IMMUNOLOGY/PRACTALL CONSENSUS REPORT; INTRANASAL
CORTICOSTEROID-THERAPY; NONINFECTIOUS PERENNIAL RHINITIS; LEUKOTRIENE
RECEPTOR ANTAGONISTS; EXACERBATED RESPIRATORY-DISEASE; NONALLERGIC
VASOMOTOR RHINITIS; ENVIRONMENTAL EXPOSURE CHAMBER
AB Rhinitis is an umbrella term that encompasses many different subtypes, several of which still elude complete characterization. The concept of phenotyping, being the definition of disease subtypes on the basis of clinical presentation, has been well established in the last decade. Classification of rhinitis entities on the basis of phenotypes has facilitated their characterization and has helped practicing clinicians to efficiently approach rhinitis patients. Recently, the concept of endotypes, that is, the definition of disease subtypes on the basis of underlying pathophysiology, has emerged. Phenotypes/endotypes are dynamic, overlapping, and may evolve into one another, thus rendering clear-cut definitions difficult. Nevertheless, a phenotype-/endotype-based classification approach could lead toward the application of stratified and personalized medicine in the rhinitis field. In this PRACTALL document, rhinitis phenotypes and endotypes are described, and rhinitis diagnosis and management approaches focusing on those phenotypes/endotypes are presented and discussed. We emphasize the concept of control-based management, which transcends all rhinitis subtypes.
C1 [Papadopoulos, N. G.] Univ Manchester, Inst Human Dev, Ctr Paediat & Child Hlth, Manchester, Lancs, England.
[Papadopoulos, N. G.] Univ Athens, Dept Allergy, Paediat Clin 2, Athens, Greece.
[Bernstein, J. A.] Univ Cincinnati, Dept Internal Med, Cincinnati, OH USA.
[Demoly, P.] Univ Hosp Montpellier, Dept Allergy, Montpellier, France.
[Dykewicz, M.] St Louis Univ, Sch Med, Sect Allergy & Clin Immunol, St Louis, MO USA.
[Fokkens, W.] Univ Amsterdam, Acad Med Ctr, Dept Otorhinolaryngol, NL-1105 AZ Amsterdam, Netherlands.
[Hellings, P. W.] Univ Hosp Leuven, Dept Otorhinolaryngol, Leuven, Belgium.
[Peters, A. T.] Northwestern Univ, Dept Med, Div Allergy Immunol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Rondon, C.] Hosp Carlos Haya, Serv Alergol, Malaga, Spain.
[Togias, A.] NIAID, NIH, Bethesda, MD 20892 USA.
[Cox, L. S.] Nova SE Univ, Davie, FL USA.
RP Papadopoulos, NG (reprint author), Royal Manchester Childrens Hosp, 5th Floor Res, Manchester M13 9WL, Lancs, England.
EM Nikolaos.Papadopoulos@manchester.ac.uk
FU European Academy of Allergy and Clinical Immunology; American Academy of
Allergy, Asthma and Immunology
FX This work has been funded by the European Academy of Allergy and
Clinical Immunology and the American Academy of Allergy, Asthma and
Immunology.
NR 305
TC 23
Z9 25
U1 1
U2 9
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 MAY
PY 2015
VL 70
IS 5
BP 474
EP 494
DI 10.1111/all.12573
PG 21
WC Allergy; Immunology
SC Allergy; Immunology
GA CF4RJ
UT WOS:000352538200002
PM 25620381
ER
PT J
AU Schindler-Ruwisch, J
Augustson, E
Lynch, K
Patrick, H
AF Schindler-Ruwisch, Jennifer
Augustson, Erik
Lynch, Krystal
Patrick, Heather
TI BMI and Smoking: Interrelated Factors among Cessation Website Users
SO AMERICAN JOURNAL OF HEALTH BEHAVIOR
LA English
DT Article
DE body mass index; obesity; cigarette smoking
ID BODY-WEIGHT; METABOLIC SYNDROME; UNITED-STATES; OBESITY; POPULATION;
MORTALITY; ADULTS; RISK
AB Objective: To investigate the relationship between body mass index (BMI) and smoking. Methods: Participants (N = 2243) provided demographic, height, weight, smoking information through a survey conducted on smokefree.gov and women. smokefree.gov websites. Analysis assessed associations among BMI, smoking status, and cigarettes smoked per day (CPD). Results: The average (SD) BMI of never, former, intermittent, and daily smokers was 26.3 (6.2), 27.9 (6.5), 27.4 (6.7) and 28.1 (6.8) respectively. Daily (31.2%) and former (32.3%) were more likely to be to be obese compared to never (22.0%) and intermittent (26.1%) smokers. Odds of being obese increased with number of CPD adjusting for potential confounders. Conclusions: Smokers may currently have BMIs similar to the general population. BMI and CPD were positively correlated.
C1 [Schindler-Ruwisch, Jennifer; Lynch, Krystal] BLH Technol Inc, Rockville, MD USA.
[Augustson, Erik] NCI, Tobacco Control Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20852 USA.
[Patrick, Heather] LiveHealthier Inc, Prod Dev, Bethesda, MD USA.
RP Augustson, E (reprint author), NCI, Tobacco Control Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20852 USA.
EM augustse@mail.nih.gov
FU Federal funds from the National Cancer Institute, National Institutes of
Health, US Department of Health and Human Services; [HHSN261201000043C]
FX This project has been funded in part with Federal funds from the
National Cancer Institute, National Institutes of Health, US Department
of Health and Human Services; this analysis was funded partially under
Contract No. HHSN261201000043C.
NR 22
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U1 3
U2 3
PU PNG PUBLICATIONS
PI OAK RIDGE
PA 2205-K OAK RIDGE RD, #115, OAK RIDGE, NC 27310 USA
SN 1945-7359
J9 AM J HEALTH BEHAV
JI Am. J. Health Behav.
PD MAY
PY 2015
VL 39
IS 3
BP 330
EP 337
DI 10.5993/AJHB.39.3.5
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CF5UD
UT WOS:000352621700005
PM 25898436
ER
PT J
AU Hesse, BW
Moser, RP
Riley, WT
AF Hesse, Bradford W.
Moser, Richard P.
Riley, William T.
TI From Big Data to Knowledge in the Social Sciences
SO ANNALS OF THE AMERICAN ACADEMY OF POLITICAL AND SOCIAL SCIENCE
LA English
DT Article
DE big data; data visualization; integrative data analysis; informatics
ID HEALTH; COMMUNICATION; NETWORKS; PROMISE; SYSTEM
AB One of the challenges associated with high-volume, diverse datasets is whether synthesis of open data streams can translate into actionable knowledge. Recognizing that challenge and other issues related to these types of data, the National Institutes of Health developed the Big Data to Knowledge or BD2K initiative. The concept of translating big data to knowledge is important to the social and behavioral sciences in several respects. First, a general shift to data-intensive science will exert an influence on all scientific disciplines, but particularly on the behavioral and social sciences given the wealth of behavior and related constructs captured by big data sources. Second, science is itself a social enterprise; by applying principles from the social sciences to the conduct of research, it should be possible to ameliorate some of the systemic problems that plague the scientific enterprise in the age of big data. We explore the feasibility of recalibrating the basic mechanisms of the scientific enterprise so that they are more transparent and cumulative; more integrative and cohesive; and more rapid, relevant, and responsive.
C1 [Hesse, Bradford W.] Natl Canc Inst, Training, Bethesda, MD 20892 USA.
[Hesse, Bradford W.] Natl Canc Inst, Hlth Commun & Informat Res Branch, Behav Res Program, Bethesda, MD USA.
[Moser, Richard P.] Natl Canc Inst, Sci Res & Technol Branch, Behav Res Program, Bethesda, MD USA.
[Riley, William T.] Natl Inst Hlth, Off Behav & Social Sci Res, Bethesda, MD USA.
[Riley, William T.] Natl Canc Inst, Sci Res & Technol Branch, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD USA.
RP Hesse, BW (reprint author), Natl Canc Inst, Training, Bethesda, MD 20892 USA.
RI Trivedi, Kruti/E-7558-2015;
OI Hesse, Bradford/0000-0003-1142-1161
FU Intramural NIH HHS [Z99 CA999999]
NR 54
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U1 13
U2 51
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0002-7162
EI 1552-3349
J9 ANN AM ACAD POLIT SS
JI Ann. Am. Acad. Polit. Soc. Sci.
PD MAY
PY 2015
VL 659
IS 1
BP 16
EP 32
DI 10.1177/0002716215570007
PG 17
WC Political Science; Social Sciences, Interdisciplinary
SC Government & Law; Social Sciences - Other Topics
GA CF8EV
UT WOS:000352789600002
PM 26294799
ER
PT J
AU Jin, XT
Xu, Q
Champion, K
Kruth, HS
AF Jin, Xueting
Xu, Qing
Champion, Keith
Kruth, Howard S.
TI Endotoxin contamination of apolipoprotein A-I: Effect on macrophage
proliferation - A cautionary tale
SO ATHEROSCLEROSIS
LA English
DT Article
DE Endotoxin; Macrophages; Cell proliferation; Apolipoproteins;
Atherosclerosis
ID LIPOPOLYSACCHARIDE-BINDING PROTEIN; HIGH-DENSITY-LIPOPROTEINS;
NEUTRALIZATION; PEPTIDES; INACTIVATION; INHIBITION; EXPRESSION;
INDUCTION; CYTOKINE; CAPACITY
AB This technical report addresses the problem of endotoxin contamination of apolipoprotein reagents. Using a bromodeoxyuridine incorporation cell proliferation assay, we observed that human plasma ApoA-I as low as 1 mu g/ml resulted in a >90% inhibition in macrophage proliferation. However, not all ApoA-I from different sources showed this effect. We considered the possibility that endotoxin contamination of the apolipoproteins contributed to the differential inhibition of macrophage cell proliferation. Endotoxin alone very potently inhibited macrophage proliferation (0.1 ng/ml inhibited macrophage proliferation >90%). Measurement of endotoxin levels in the apolipoprotein products, including an analysis of free versus total endotoxin, the latter which included endotoxin that was masked due to binding to protein, suggested that free endotoxin mediated inhibition of macrophage proliferation. Despite the use of an advanced endotoxin removal procedure and agents commonly used to inhibit endotoxin action, the potency of endotoxin precluded successful elimination of endotoxin effect. Our findings show that endotoxin contamination can significantly influence apparent apolipoprotein-mediated cell effects (or effects of any other biological products), especially when these products are tested on highly endotoxin-sensitive cells, such as macrophages. Published by Elsevier Ireland Ltd.
C1 [Jin, Xueting; Xu, Qing; Kruth, Howard S.] NHLBI, Sect Expt Atherosclerosis, NIH, Bethesda, MD 20892 USA.
[Champion, Keith] BioDtech Inc, Birmingham, AL 35209 USA.
RP Kruth, HS (reprint author), NHLBI, Sect Expt Atherosclerosis, NIH, Bldg 10,Room 5N-113,10 Ctr Dr MSC 1422, Bethesda, MD 20892 USA.
EM kruthh@nhlbi.nih.gov
FU Intramural Research Program, National Heart, Lung, and Blood Institute,
National Institutes of Health
FX We thank the Department of Transfusion Medicine, Clinical Center,
National Institutes of Health, for providing elutriated monocytes. The
Intramural Research Program, National Heart, Lung, and Blood Institute,
National Institutes of Health supported this work.
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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 MAY
PY 2015
VL 240
IS 1
BP 121
EP 124
DI 10.1016/j.atherosclerosis.2015.03.007
PG 4
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA CF6YR
UT WOS:000352703400019
PM 25778625
ER
PT J
AU Kim, CHJ
Mitchell, JB
Bursill, CA
Sowers, AL
Thetford, A
Cook, JA
van Reyk, DM
Davies, MJ
AF Kim, Christine H. J.
Mitchell, James B.
Bursill, Christina A.
Sowers, Anastasia L.
Thetford, Angela
Cook, John A.
van Reyk, David M.
Davies, Michael J.
TI The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia,
elevation of inflammatory cytokines, and modulates atherosclerotic
plaque composition in apoE(-/-) mice
SO ATHEROSCLEROSIS
LA English
DT Article
DE TEMPOL; Nitroxide; Atherosclerosis; Cardiovascular disease; Lipid;
Inflammatory cytokines; Adipokines
ID NECROSIS-FACTOR-ALPHA; CARDIOVASCULAR-DISEASE; INSULIN-RESISTANCE;
MESSENGER-RNA; NITRIC-OXIDE; MYELOPEROXIDASE; INHIBITION; EXPRESSION;
CELLS; RATS
AB Objective: The nitroxide compound TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl radical) has been shown to prevent obesity-induced changes in adipokines in cell and animal systems. In this study we investigated whether supplementation with TEMPOL inhibits inflammation and atherosclerosis in apoE(-/-) mice fed a high fat diet (HFD).
Methods: ApoE(-/-) mice were fed for 12 weeks on standard chow diet or a high-fat diet. Half the mice were supplemented with 10 mg/g TEMPOL in their food. Plasma samples were analysed for triglycerides, cholesterol, low-and high-density lipoprotein cholesterol, inflammatory cytokines and markers (inter-leukin- 6, IL-6; monocyte-chemotactic protein, MCP-1; myeloperoxidase, MPO; serum amyloid A, SAA; adiponectin; leptin). Plaques in the aortic sinus were analysed for area, and content of collagen, lipid, macrophages and smooth muscle cells.
Results: High fat feeding resulted in marked increases in body mass and plasma lipid levels. Dietary TEMPOL decreased both parameters. In the high-fat-fed mice significant elevations in plasma lipid levels and the inflammatory markers IL-6, MCP-1, MPO, SAA were detected, along with an increase in leptin and a decrease in adiponectin. TEMPOL supplementation reversed these effects. When compared to HFD-fed mice, TEMPOL supplementation increased plaque collagen content, decreased lipid content and increased macrophage numbers.
Conclusions: These data indicate that in a well-established model of obesity-associated hyperlipidaemia and atherosclerosis, TEMPOL had a significant impact on body mass, atherosclerosis, hyperlipidaemia and inflammation. TEMPOL may therefore be of value in suppressing obesity, metabolic disorders and increasing atherosclerotic plaque stability. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Kim, Christine H. J.; Davies, Michael J.] Heart Res Inst, Free Radical Grp, Newtown, NSW 2042, Australia.
[Kim, Christine H. J.; Bursill, Christina A.; Davies, Michael J.] Univ Sydney, Fac Med, Sydney, NSW 2006, Australia.
[Mitchell, James B.; Sowers, Anastasia L.; Thetford, Angela; Cook, John A.] NCI, Radiat Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Bursill, Christina A.] Heart Res Inst, Immunobiol Grp, Newtown, NSW 2042, Australia.
[van Reyk, David M.] Univ Technol Sydney, Fac Sci, Broadway, NSW 2007, Australia.
[Davies, Michael J.] Univ Copenhagen, Panum Inst, Dept Biomed Sci, DK-2200 Copenhagen N, Denmark.
RP Davies, MJ (reprint author), Univ Copenhagen, Panum Inst, Dept Biomed Sci, Bldg 4-5,Blegdamsvej 3, DK-2200 Copenhagen N, Denmark.
EM christinehjkim@gmail.com; jbm@helix.nih.gov; bursillc@hri.org.au;
stasia@mail.nih.gov; thetforda@mail.nih.gov; cook@helix.nih.gov;
david.vanreyk@uts.edu.au; davies@sund.ku.dk
RI Davies, Michael/H-4939-2011
OI Davies, Michael/0000-0002-5196-6919
FU Australian Research Council (ARC Centres of Excellence and Discovery
Programs) [CE0561607, DP0988311]; Community Grant; University
Postgraduate Award from the University of Sydney
FX This work was supported by grants from the Australian Research Council
(ARC Centres of Excellence and Discovery Programs, CE0561607 and
DP0988311 respectively) and a JB Were Community Grant. Christine HJ Kim
was a recipient of a University Postgraduate Award from the University
of Sydney.
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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 MAY
PY 2015
VL 240
IS 1
BP 234
EP 241
DI 10.1016/j.atherosclerosis.2015.03.012
PG 8
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA CF6YR
UT WOS:000352703400037
PM 25818249
ER
PT J
AU Tian, Q
Glynn, NW
Erickson, KI
Aizenstein, HJ
Simonsick, EM
Yaffe, K
Harris, TB
Kritchevsky, SB
Boudreau, RM
Newman, AB
Lopez, OL
Saxton, J
Rosano, C
AF Tian, Qu
Glynn, Nancy W.
Erickson, Kirk I.
Aizenstein, Howard J.
Simonsick, Eleanor M.
Yaffe, Kristine
Harris, Tamara B.
Kritchevsky, Stephen B.
Boudreau, Robert M.
Newman, Anne B.
Lopez, Oscar L.
Saxton, Judith
Rosano, Caterina
CA Hlth ABC Study
TI Objective measures of physical activity, white matter integrity and
cognitive status in adults over age 80
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE White matter integrity; Diffusion tensor imaging; SenseWear Armband;
Very old adults
ID LIFE-STYLE INTERVENTIONS; OLDER-ADULTS; CARDIORESPIRATORY FITNESS;
SUBSEQUENT DISABILITY; ENERGY-EXPENDITURE; HEALTHY SENIORS; AEROBIC
FITNESS; AGING BRAIN; GAIT SPEED; MR-IMAGES
AB The neuroprotective effects of physical activity (PA) are consistently shown in older adults, but the neural substrates, particularly in white matter (WM), are understudied, especially in very old adults with the fastest growth rate and the highest risk of dementia. This study quantified the association between PA and WM integrity in adults over SO. The moderating effects of cardiometabolic conditions, physical functional limitations and WM hyperintensities were also examined, as they can affect PA and brain integrity. Fractional anisotropy (FA) from normal-appearing WM via diffusion tensor imaging and WM hyperintensities were obtained in 90 participants (mean age =87.4,51.1% female, 55.6% white) with concurrent objective measures of steps, active energy expenditure (AEE in kcal), duration (min), and intensity (metabolic equivalents, METs) via SenseWear Armband. Clinical adjudication of cognitive status, prevalence of stroke and diabetes, systolic blood pressure, and gait speed were assessed at time of neuroimaging. Participants were on average sedentary (mean +/- SD/day: 1766 +/- 1345 steps, 202 +/- 311 kcal, 211 +/- 39 min, 1.8 +/- 1.1 METs). Higher steps, AEE and duration, but not intensity, were significantly associated with higher FA. Associations were localized in frontal and temporal areas. Moderating effects of cardiometabolic conditions, physical functional limitations, and WM hyperintensities were not significant. Neither FA nor PA was related to cognitive status. Older adults with a sedentary lifestyle and a wide range of cardiometabolic conditions and physical functional limitations, displayed higher WM integrity in relation to higher PA. Studies of very old adults to quantify the role of PA in reducing dementia burden via WM integrity are warranted. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Tian, Qu; Glynn, Nancy W.; Boudreau, Robert M.; 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.
[Aizenstein, Howard J.; Saxton, Judith] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Simonsick, Eleanor M.] NIA, Intramural Res Program, Baltimore, MD 21224 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] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
[Harris, Tamara B.] NIA, Intramural Res Program, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Wake Forest Sch Med, Sticht Ctr Aging, Sect Gerontol & Geriatr, Med, Winston Salem, NC USA.
[Lopez, Oscar L.; Saxton, Judith] Univ Pittsburgh, Dept Neurol, Pittsburgh, PA 15260 USA.
RP Tian, Q (reprint author), 251 Bayview Blvd,Suite 100,Rm 04B316, Baltimore, MD 21224 USA.
EM qu.tian@nih.gov
RI Newman, Anne/C-6408-2013; Dey, Kamalesh/E-6568-2017;
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,
NO1-AG-6-2106, K23-AG028966-01]; NIA [R01-AG028050, R01-AG029232,
P30-AG024827]; NINR [R01-NR012459]; 8th Annual Department of
Epidemiology Small Grant program, University of Pittsburgh; Intramural
Research Program of the 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, NO1-AG-6-2106, K23-AG028966-01;
NIA grants R01-AG028050, R01-AG029232, P30-AG024827, and NINR grant
R01-NR012459, and supported by 8th Annual Department of Epidemiology
Small Grant program, University of Pittsburgh. This research was
supported in part by the Intramural Research Program of the NIH National
Institute on Aging.
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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 MAY 1
PY 2015
VL 284
BP 51
EP 57
DI 10.1016/j.bbr.2015.01.045
PG 7
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA CF6NB
UT WOS:000352672300007
PM 25655514
ER
PT J
AU Radulescu, E
Chen, Q
Mattay, VS
Callicott, JH
Zink, CF
Goldberg, TE
Ursini, G
Kleinman, JE
Weinberger, DR
AF Radulescu, Eugenia
Chen, Qiang
Mattay, Venkata S.
Callicott, Joseph H.
Zink, Caroline F.
Goldberg, Terry E.
Ursini, Gianluca
Kleinman, Joel E.
Weinberger, Daniel R.
TI Selective Effects of the GWAS DRD2 Locus Associated with Schizophrenia
on the Prefrontal-nigro-striatal Circuits Supporting the Executive
Functions
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE DRD2; fMRI; cortico-nigro-striatal circuits; working memory;
connectivity
C1 [Radulescu, Eugenia; Chen, Qiang; Mattay, Venkata S.; Zink, Caroline F.; Ursini, Gianluca; Kleinman, Joel E.; Weinberger, Daniel R.] Lieber Inst Brain Dev, Clin Sci Div, Baltimore, MD USA.
[Callicott, Joseph H.] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
[Goldberg, Terry E.] Feinstein Inst Med Res, Litwin Zucker Res Ctr, Manhasset, NY USA.
NR 0
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 9
BP 3S
EP 4S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500010
ER
PT J
AU Ursini, G
Marenco, S
Chen, Q
Straub, RE
Punzi, G
Weinberger, DR
AF Ursini, Gianluca
Marenco, Stefano
Chen, Qiang
Straub, Richard E.
Punzi, Giovanna
Weinberger, Daniel R.
TI GWAS Derived Risk Profile Score Is Associated with Schizophrenia Only in
Individuals Exposed to Obstetric Complications
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE schizophrenia; obstetric complications; GWAS derived Risk Profile
Scores; neurodevelopment; gene-environment interaction
C1 [Ursini, Gianluca; Chen, Qiang; Straub, Richard E.; Punzi, Giovanna; Weinberger, Daniel R.] Lieber Inst Brain Dev, Div Clin Sci, Baltimore, MD USA.
[Ursini, Gianluca; Punzi, Giovanna] Aldo Moro Univ, Dept Basic Med Sci Neurosci & Sense Organs, Grp Psychiat Neurosci, Bari, Italy.
[Marenco, Stefano] NIMH, Clin Brain Disorders Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RI Marenco, Stefano/A-2409-2008
OI Marenco, Stefano/0000-0002-2488-2365
NR 0
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U1 2
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 10
BP 4S
EP 4S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500011
ER
PT J
AU Tseng, WL
Brotman, MA
Deveney, CM
Moroney, E
Machlin, L
Towbin, K
Pine, DS
Leibenluft, E
AF Tseng, Wan-Ling
Brotman, Melissa A.
Deveney, Christen M.
Moroney, Elizabeth
Machlin, Laura
Towbin, Kenneth
Pine, Daniel S.
Leibenluft, Ellen
TI Neural Correlates of Irritability across Diagnoses: Categorical and
Dimensional Approaches
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE irritability; DMDD; fMRI; categorical; dimensional
C1 [Tseng, Wan-Ling; Brotman, Melissa A.; Moroney, Elizabeth; Machlin, Laura; Towbin, Kenneth; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, Bethesda, MD 20892 USA.
[Deveney, Christen M.] Wellesley Coll, Dept Psychol, Wellesley, MA 02181 USA.
RI Brotman, Melissa/H-7409-2013
NR 0
TC 0
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U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 31
BP 11S
EP 12S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500032
ER
PT J
AU Ahn, K
Mentch, FD
Kao, C
Hakonarson, H
Rapoport, JL
AF Ahn, Kwangmi
Mentch, Frank D.
Kao, Chally
Hakonarson, Hakon
Rapoport, Judith L.
TI Overall Clinical Impairment Associated with Rare Copy Number Variants
(CNVs) Associated with Neurodevelopmental Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE copy number variants; neurodevelopmental disorders
C1 [Ahn, Kwangmi; Rapoport, Judith L.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Mentch, Frank D.; Kao, Chally; Hakonarson, Hakon] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
NR 0
TC 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 49
BP 19S
EP 19S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500050
ER
PT J
AU Perez-Rodriguez, MM
New, AS
Goldstein, KE
Yuan, QP
Zhou, ZF
Chowdhury, S
Shen, PH
Rothstein, E
Rimsky, LS
Koenigsberg, HW
Goodman, M
Hodgkinson, C
Goldman, D
Hazlett, E
Siever, LJ
AF Perez-Rodriguez, M. Mercedes
New, Antonia S.
Goldstein, Kim E.
Yuan, Qiaoping
Zhou, Zhifeng
Chowdhury, Salwa
Shen, Pei-Hong
Rothstein, Ethan
Rimsky, Liza S.
Koenigsberg, Harold W.
Goodman, Marianne
Hodgkinson, Colin
Goldman, David
Hazlett, Erin
Siever, Larry J.
TI Converging Multimodal Evidence for Social Cognitive Abnormalities in
Borderline Personality Disorder: Models, Mechanisms and Novel Therapies
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Borderline Personality Disorder; Social Cognition; Oxytocin; fMRI; BDNF
C1 [Perez-Rodriguez, M. Mercedes; New, Antonia S.; Goldstein, Kim E.; Chowdhury, Salwa; Rothstein, Ethan; Rimsky, Liza S.; Koenigsberg, Harold W.; Goodman, Marianne; Hazlett, Erin; Siever, Larry J.] Icahn Sch Med Mt Sinai, Psychiat, New York, NY 10029 USA.
[Yuan, Qiaoping; Zhou, Zhifeng; Shen, Pei-Hong; Hodgkinson, Colin; Goldman, David] NIAAA, Lab Neurogenet, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 75
BP 29S
EP 29S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500076
ER
PT J
AU Michalska, KJ
Ivie, EJ
Shechner, T
Pine, DS
AF Michalska, Kalina J.
Ivie, Elizabeth J.
Shechner, Tomer
Pine, Daniel S.
TI Autonomic Modulation of Neural Responses During Fear Extinction Recall
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE fear conditioning; functional magnetic resonance imaging; skin
conductance; extinction recall
C1 [Michalska, Kalina J.; Ivie, Elizabeth J.; Pine, Daniel S.] NIH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
[Shechner, Tomer] Univ Haifa, Dept Psychol, IL-31999 Haifa, Israel.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 124
BP 45S
EP 45S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500117
ER
PT J
AU Szczepanik, J
Nugent, A
Zarate, C
Furey, M
AF Szczepanik, Joanna
Nugent, Allison
Zarate, Carlos
Furey, Maura
TI Amygdala Response to Selective Emotion Processing Conditions at Baseline
Predicts Antidepressant Treatment Response to Scopolamine in Major
Depressive Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE major depression; amygdala; fMRI; scopolamine; emotional processing
C1 [Szczepanik, Joanna; Nugent, Allison; Zarate, Carlos] NIMH, Expt Therapeut & Pathophysiol Branch, Bethesda, MD 20892 USA.
[Szczepanik, Joanna] Univ Maryland, Neurosci & Cognit Sci Program, College Pk, MD 20742 USA.
[Furey, Maura] Johnson & Johnson, Neurosci Biomarkers, San Diego, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 194
BP 73S
EP 73S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500187
ER
PT J
AU Brouwer, RM
Glahn, DC
Hibar, DP
Hua, X
Jahanshad, N
Franz, CE
Koenis, MMG
Mather, K
Swagerman, S
Thalamuthu, A
Wen, W
Boomsma, DI
Gilmore, JH
Gogtay, N
Kahn, RS
Kremen, WS
Sachdev, PS
Wright, MJ
Thompson, PM
Pol, HEH
AF Brouwer, Rachel M.
Glahn, David C.
Hibar, Derrek P.
Hua, Xue
Jahanshad, Neda
Franz, Carol E.
Koenis, Marinka M. G.
Mather, Karen
Swagerman, Suzanne
Thalamuthu, Anbupalam
Wen, Wei
Boomsma, Dorret I.
Gilmore, John H.
Gogtay, Nitin
Kahn, Rene S.
Kremen, William S.
Sachdev, Perminder S.
Wright, Margie J.
Thompson, Paul M.
Pol, Hilleke E. Hulshoff
TI Genetic Influences on Brain Plasticity: First Results of the ENIGMA
Plasticity Working Group
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Imaging; Genetics; Plasticity; heritability
C1 [Brouwer, Rachel M.; Koenis, Marinka M. G.; Kahn, Rene S.; Pol, Hilleke E. Hulshoff] Univ Med Ctr Utrecht, Dept Psychiat, Brain Ctr Rudolf Magnus, Utrecht, Netherlands.
[Glahn, David C.] Yale Univ Med, Dept Psychiat, New Haven, CT USA.
[Hibar, Derrek P.; Hua, Xue; Jahanshad, Neda; Thompson, Paul M.] USC Keck Sch Med, Inst Neuroimaging & Informat, Imaging Genet Ctr, Los Angeles, CA USA.
[Franz, Carol E.; Kremen, William S.] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
[Mather, Karen; Thalamuthu, Anbupalam; Wen, Wei; Sachdev, Perminder S.] Univ New S Wales, Dept Psychiat, Ctr Hlth Brain Ageing, Sydney, NSW, Australia.
[Swagerman, Suzanne; Boomsma, Dorret I.] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
[Gilmore, John H.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
[Gogtay, Nitin] NIMH, Dept Psychiat, NIH, Bethesda, MD 20892 USA.
[Wright, Margie J.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.
RI Karen, Mather/O-9795-2016
OI Karen, Mather/0000-0003-4143-8941
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 223
BP 84S
EP 84S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500216
ER
PT J
AU Friedman, LA
Anvari, AA
Kasoff, L
Ahn, K
Rapoport, JL
AF Friedman, Lisa A.
Anvari, Afsoon A.
Kasoff, Lauren
Ahn, Kwangmi
Rapoport, Judith L.
TI 1q21 Microduplications in Two Pediatric Patients with Neurodevelopmental
Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Copy number variation; Neurodevelopmental disorders; Genetics
C1 [Friedman, Lisa A.; Anvari, Afsoon A.; Kasoff, Lauren; Ahn, Kwangmi; Rapoport, Judith L.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 232
BP 88S
EP 88S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500225
ER
PT J
AU Bonne, O
Gill, J
Lerner, A
Nugent, AC
Vythilingam, M
Neumeister, A
Drevets, WC
AF Bonne, Omer
Gill, Jessica
Lerner, Alicja
Nugent, Allison C.
Vythilingam, Meena
Neumeister, Alexander
Drevets, Wayne C.
TI Altered Cerebral gamma-Amniobutyric Acid Type A-Benzodiazapine Receptor
Binding in PTSD Determined by [11C] Flumazenil Positron Emission
Tomography
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE PTSD; PET; GABA-A; DMN
C1 [Bonne, Omer] Hadassah Univ Hosp, Psychiat, IL-91120 Jerusalem, Israel.
[Gill, Jessica] NINR, NIH, Bethesda, MD 20892 USA.
[Lerner, Alicja] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Nugent, Allison C.] NIH, Branch Experiemental Therapeut, Bethesda, MD 20892 USA.
[Vythilingam, Meena] Deployment Hlth Clin Ctr, Clin Sci & Translat, Chevy Chase, MD USA.
[Neumeister, Alexander] NYU, Langone Med Ctr, Psychiat & Radiol, New York, NY USA.
[Drevets, Wayne C.] Johnson & Johnson Inc, Janssen Res & Dev, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 258
BP 99S
EP 99S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500251
ER
PT J
AU Park, MTM
Raznahan, A
Shaw, P
Gogtay, N
Chakravarty, MM
AF Park, Min Tae M.
Raznahan, Armin
Shaw, Philip
Gogtay, Nitin
Chakravarty, M. Mallar
TI Shared Cerebellar Phenotypes in Autism Spectrum Disorders and
Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Cerebellum; Autism; Schizophrenia; MRI
C1 [Park, Min Tae M.; Chakravarty, M. Mallar] Douglas Mental Hlth Univ Inst, Cerebral Imaging Ctr, Montreal, PQ, Canada.
[Raznahan, Armin; Gogtay, Nitin] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
[Shaw, Philip] NHGRI, Sect Neurobehav Clin Res, Social & Behav Res Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 268
BP 103S
EP 104S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500261
ER
PT J
AU Saha, D
Yan, H
Zhang, LL
Muse, T
Chen, Q
Zhang, FY
Mattay, VS
Yue, WH
Zhang, D
Weinberger, DR
Tan, HY
AF Saha, Debjani
Yan, Hao
Zhang, Lanlan
Muse, Tim
Chen, Qiang
Zhang, Fengyu
Mattay, Venkata S.
Yue, Weihua
Zhang, Dai
Weinberger, Daniel R.
Tan, Hao Yang
TI Genetic Risk for Schizophrenia During Working Memory Computation
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE schizophrenia; computational working memory; siblings; dlpfc
C1 [Saha, Debjani; Muse, Tim; Chen, Qiang; Zhang, Fengyu; Mattay, Venkata S.; Weinberger, Daniel R.; Tan, Hao Yang] Lieber Inst Brain Dev, Clin Sci, Baltimore, MD USA.
[Yan, Hao; Zhang, Lanlan; Yue, Weihua; Zhang, Dai] Peking Univ, Inst Mental Hlth, Beijing 100871, Peoples R China.
[Chen, Qiang; Mattay, Venkata S.; Weinberger, Daniel R.; Tan, Hao Yang] NIMH, Clin Brain Disorders Branch, NIH, Baltimore, MD USA.
[Weinberger, Daniel R.; Tan, Hao Yang] Johns Hopkins Sch Med, Psychiat & Behav Sci, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 312
BP 122S
EP 122S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500305
ER
PT J
AU Sastry, NV
Ordonez, AE
Moran, ME
Greenstein, D
Watsky, RE
Luscher, ZI
Shora, L
Dillard-Broadnax, D
Dillard-Broadnax, D
Clasen, L
Rapoport, J
Gogtay, N
AF Sastry, Nevin V.
Ordonez, Anna E.
Moran, Marcel E.
Greenstein, Deanna
Watsky, Rebecca E.
Luscher, Zoe I.
Shora, Lorie
Dillard-Broadnax, Diane
Dillard-Broadnax, Diane
Clasen, Liv
Rapoport, Judith
Gogtay, Nitin
TI Magnetic Resonance Imaging of the Fusiform Gyrus in Patients with
Childhood-Onset Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE COS; Schizophrenia; Fusiform; MRI; Neuroimaging
C1 [Sastry, Nevin V.; Ordonez, Anna E.; Moran, Marcel E.; Greenstein, Deanna; Watsky, Rebecca E.; Luscher, Zoe I.; Shora, Lorie; Dillard-Broadnax, Diane; Dillard-Broadnax, Diane; Clasen, Liv; Rapoport, Judith; Gogtay, Nitin] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 314
BP 122S
EP 123S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500307
ER
PT J
AU Niciu, MJ
Xu, AJ
Lundin, NB
Luckenbaugh, DA
Ionescu, DF
Richards, EM
Voort, JLV
Ballard, ED
Brutsche, NE
Machado-Vieira, R
Zarate, CA
AF Niciu, Mark J.
Xu, Annie J.
Lundin, Nancy B.
Luckenbaugh, David A.
Ionescu, Dawn F.
Richards, Erica M.
Voort, Jennifer L. Vande
Ballard, Elizabeth D.
Brutsche, Nancy E.
Machado-Vieira, Rodrigo
Zarate, Carlos A.
TI Lithium and Valproate Levels Do Not Correlate with Ketamine's
Antidepressant Efficacy in Treatment-Resistant Bipolar Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE ketamine; bipolar disorder; lithium; valproate; treatment-resistant
depression
C1 [Niciu, Mark J.; Lundin, Nancy B.; Luckenbaugh, David A.; Richards, Erica M.; Ballard, Elizabeth D.; Brutsche, Nancy E.; Machado-Vieira, Rodrigo; Zarate, Carlos A.] NIMH, Expt Therapeut & Pathophysiol Branch, NIH, Bethesda, MD 20892 USA.
[Xu, Annie J.] New York Med Coll, Valhalla, NY 10595 USA.
[Ionescu, Dawn F.] Harvard Univ, Dept Psychiat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Voort, Jennifer L. Vande] Mayo Clin, Dept Psychiat & Psychol, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 334
BP 130S
EP 130S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500327
ER
PT J
AU Voort, JLV
Ballard, ED
Duncan, WC
Luckenbaugh, DA
Richards, EM
Niciu, MJ
Zarate, CA
AF Voort, Jennifer L. Vande
Ballard, Elizabeth D.
Duncan, Wallace C.
Luckenbaugh, David A.
Richards, Erica M.
Niciu, Mark J.
Zarate, Carlos A.
TI Antisuicidal Response after Ketamine Infusion Is Associated with Reduced
Wakefulness in Treatment Resistant Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Ketamine; Suicide; Sleep; Treatment-Resistant Depression
C1 [Voort, Jennifer L. Vande; Ballard, Elizabeth D.; Duncan, Wallace C.; Luckenbaugh, David A.; Richards, Erica M.; Niciu, Mark J.; Zarate, Carlos A.] NIMH, NIH, Bethesda, MD 20892 USA.
[Voort, Jennifer L. Vande] Mayo Clin, Dept Psychiat & Psychol, Rochester, MN USA.
RI Niciu, Mark/J-1766-2014
OI Niciu, Mark/0000-0002-5612-3021
NR 0
TC 0
Z9 0
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 333
BP 130S
EP 130S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207500326
ER
PT J
AU Calkins, ME
Merikangas, KR
Burstein, M
Satterthwaite, T
Wolf, D
Moore, TM
Ruparel, K
Hakonarson, H
Gur, RC
Gur, RE
AF Calkins, Monica E.
Merikangas, Kathleen R.
Burstein, Marcy
Satterthwaite, Theodore
Wolf, Daniel
Moore, Tyler M.
Ruparel, Kosha
Hakonarson, Hakon
Gur, Ruben C.
Gur, Raquel E.
TI Clinical Phenotypic Characterization of the Philadelphia
Neurodevelopmental Cohort: Foundations for Integrative Investigations of
Psychiatric Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE psychopathology; neurodevelopment; prospective
C1 [Calkins, Monica E.] Univ Penn, Sch Med, Bethesda, MD USA.
[Merikangas, Kathleen R.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
[Burstein, Marcy] NIMH, Bethesda, MD 20892 USA.
[Satterthwaite, Theodore; Wolf, Daniel; Moore, Tyler M.; Ruparel, Kosha; Gur, Ruben C.; Gur, Raquel E.] Univ Penn, Sch Med, Psychiat, Philadelphia, PA 19104 USA.
[Hakonarson, Hakon] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 805
BP 288S
EP 289S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502006
ER
PT J
AU Pine, DS
AF Pine, Daniel S.
TI Development and Cognitive Neuroscience: Why Should I Care?
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
C1 [Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 844
BP 303S
EP 303S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502045
ER
PT J
AU Maynard, KR
Sukumar, M
Lu, B
Tessarollo, L
Schloesser, RJ
Martinowich, K
AF Maynard, Kristen R.
Sukumar, Mahima
Lu, Bai
Tessarollo, Lino
Schloesser, Robert J.
Martinowich, Keri
TI Promoter-Specific Production of BDNF Regulates Social Behaviors in Mice
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE BDNF; aggression; hypothalamus; social behavior; maternal care
C1 [Maynard, Kristen R.; Sukumar, Mahima; Schloesser, Robert J.; Martinowich, Keri] Lieber Inst Brain Dev, Basic Sci, Baltimore, MD USA.
[Lu, Bai] Tsingua Univ, Sch Med, Beijing, Peoples R China.
[Tessarollo, Lino] NCI, Unit Mouse Genet, Frederick, MD 21701 USA.
[Schloesser, Robert J.] Univ Maryland, Psychiat, Baltimore, MD 21201 USA.
[Martinowich, Keri] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.
[Martinowich, Keri] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 858
BP 308S
EP 308S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502059
ER
PT J
AU Shaw, P
AF Shaw, Philip
TI Towards an Understanding of the Neural Processes Underpinning
Persistence and Remission In ADHD
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE ADHD; Neuroimaging; Remission
C1 [Shaw, Philip] NHGRI, NIH, Betehsda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 875
BP 314S
EP 315S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502076
ER
PT J
AU Balderston, N
Hale, E
Ernst, M
Grillon, C
AF Balderston, Nicholas
Hale, Elizabeth
Ernst, Monique
Grillon, Christian
TI Resting State Alpha Oscillations in the Expression of
Anxiety-potentiated Startle
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE anxiety potentiated startle; magnetoencephalography; alpha
C1 [Balderston, Nicholas; Hale, Elizabeth; Ernst, Monique; Grillon, Christian] NIMH, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 933
BP 335S
EP 335S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502126
ER
PT J
AU Ernst, M
Patel, N
Grillon, C
Pine, D
AF Ernst, Monique
Patel, Nilam
Grillon, Christian
Pine, Daniel
TI Interaction Between Anxiety and Cognition in Adolescents and Adults
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE startle; load; workingmemory; fear; threat
C1 [Ernst, Monique; Patel, Nilam; Grillon, Christian; Pine, Daniel] NIMH, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 934
BP 335S
EP 335S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502127
ER
PT J
AU Murray, SK
Wei, SM
Nash, TA
Nguyen, TV
Reding, KM
Martinez, PE
Boyle, DE
Reuter, JM
Raab, HA
Brady, SM
Nieman, LK
Soldin, SJ
Zink, CF
Kippenhan, JS
Kohn, PD
Yanovski, JA
Schmidt, PJ
Berman, KF
AF Murray, Shanna K.
Wei, Shau-Ming
Nash, Tiffany A.
Tuong-Vi Nguyen
Reding, Katherine M.
Martinez, Pedro E.
Boyle, D. Ellen
Reuter, John M.
Raab, Hillary A.
Brady, Sheila M.
Nieman, Lynnette K.
Soldin, Steven J.
Zink, Caroline F.
Kippenhan, J. Shane
Kohn, Philip D.
Yanovski, Jack A.
Schmidt, Peter J.
Berman, Karen F.
TI Differential Recruitment of and Relationship between Ventral Striatum
and Prefrontal Cortex during Reward Outcome Processing in Children and
Adolescents
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Adolescence; Reward; Ventral Striatum; Prefrontal Cortex; Development
C1 [Murray, Shanna K.; Wei, Shau-Ming; Nash, Tiffany A.; Tuong-Vi Nguyen; Reding, Katherine M.; Raab, Hillary A.; Kippenhan, J. Shane; Kohn, Philip D.; Berman, Karen F.] NIMH, Sect Integrat Neuroimaging, Clin & Translat Neurosci Branch, Bethesda, MD 20892 USA.
[Martinez, Pedro E.; Reuter, John M.; Schmidt, Peter J.] NIMH, Behav Endocrinol Branch, Bethesda, MD 20892 USA.
[Boyle, D. Ellen; Soldin, Steven J.] NIH, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Brady, Sheila M.; Nieman, Lynnette K.; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Endocrinol & Genet, Bethesda, MD USA.
[Zink, Caroline F.] Lieber Inst Brain Dev, Clin Sci Div, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 960
BP 345S
EP 345S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502153
ER
PT J
AU Satterthwaite, TD
Shanmugan, S
Wolf, DH
Calkins, ME
Moore, TM
Hopson, R
Ruparel, K
Roalf, DR
Jackson, C
Gennatas, ED
Leibenluft, E
Pine, DS
Gur, RC
Gur, RE
AF Satterthwaite, Theodore D.
Shanmugan, Sheila
Wolf, Daniel H.
Calkins, Monica E.
Moore, Tyler M.
Hopson, Ryan
Ruparel, Kosha
Roalf, David R.
Jackson, Chad
Gennatas, Efstathios D.
Leibenluft, Ellen
Pine, Daniel S.
Gur, Ruben C.
Gur, Raquel E.
TI Common and Dissociable Mechanisms of Executive System Dysfunction Across
Psychiatric Disorders in Youth
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE working memory; adolescence; fMRI; executive
C1 [Satterthwaite, Theodore D.; Shanmugan, Sheila; Wolf, Daniel H.; Calkins, Monica E.; Moore, Tyler M.; Hopson, Ryan; Ruparel, Kosha; Roalf, David R.; Jackson, Chad; Gennatas, Efstathios D.; Gur, Ruben C.; Gur, Raquel E.] UPenn, Psychiat, Philadelphia, PA USA.
[Leibenluft, Ellen; Pine, Daniel S.] NIMH, Emot & Dev Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 964
BP 347S
EP 347S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502157
ER
PT J
AU Hantsoo, L
Golden, C
Appleby, D
Grillon, C
Epperson, CN
AF Hantsoo, Liisa
Golden, Carla
Appleby, Dina
Grillon, Christian
Epperson, C. Neill
TI Anxiety-Potentiated Acoustic Startle Response Is Elevated in the Luteal
Phase in Women with Premenstrual Dysphoric Disorder (PMDD) Compared to
Controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE premenstrual; PMS; acoustic startle; psychophysiology; allopregnanolone
C1 [Hantsoo, Liisa; Golden, Carla; Appleby, Dina; Epperson, C. Neill] Univ Penn, Psychiat, Philadelphia, PA 19104 USA.
[Grillon, Christian] NIH, Sect Neurobiol Fear & Anxiety, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1017
BP 368S
EP 368S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502210
ER
PT J
AU Deligiannidis, KM
Kroll-Desrosiers, AR
Mo, S
Nguyen, HP
Svenson, A
Jaitly, N
Hall, JE
Barton, BA
Rothschild, AJ
Shaffer, SA
AF Deligiannidis, Kristina M.
Kroll-Desrosiers, Aimee R.
Mo, Shunyan
Nguyen, Hien P.
Svenson, Abby
Jaitly, Nina
Hall, Janet E.
Barton, Bruce A.
Rothschild, Anthony J.
Shaffer, Scott A.
TI Plasma Neuroactive Steroid and GABA Concentrations in Peripartum Women
At-risk for Postpartum Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE neuroactive steroid; gamma-aminobutryic acid; postpartum; depression;
peripartum
C1 [Deligiannidis, Kristina M.; Svenson, Abby; Jaitly, Nina; Rothschild, Anthony J.] Univ Massachusetts, Sch Med, Dept Psychiat, Worcester, MA 01655 USA.
[Kroll-Desrosiers, Aimee R.; Barton, Bruce A.] Univ Massachusetts, Sch Med, Quantitat Hlth Sci, Worcester, MA USA.
[Mo, Shunyan; Nguyen, Hien P.; Shaffer, Scott A.] Univ Massachusetts, Sch Med, Proteom & Mass Spectrometry Facil, Worcester, MA USA.
[Mo, Shunyan; Nguyen, Hien P.; Shaffer, Scott A.] Univ Massachusetts, Sch Med, Dept Biochem & Mol Pharmacol, Worcester, MA USA.
[Jaitly, Nina; Hall, Janet E.] NIEHS, NIH, Res Triangle Pk, NC USA.
[Hall, Janet E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Reprod Endocrine Unit, Boston, MA USA.
RI Deligiannidis, Kristina/C-3654-2014
OI Deligiannidis, Kristina/0000-0001-7439-2236
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1018
BP 369S
EP 369S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502211
ER
PT J
AU Schiller, CE
Belger, A
Bizzell, J
Johnson, SL
Schmidt, P
Rubinow, D
AF Schiller, Crystal E.
Belger, Aysenil
Bizzell, Joshua
Johnson, Sarah L.
Schmidt, Peter
Rubinow, David
TI Effects of Gonadal Steroids on Mood and Emotion Processing in Women with
a History of Postpartum Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Estrogen; Progesterone; Postpartum Depression; Women; Neuroimaging
C1 [Schiller, Crystal E.; Belger, Aysenil; Bizzell, Joshua; Johnson, Sarah L.; Rubinow, David] Univ N Carolina, Psychiat, Chapel Hill, NC USA.
[Schmidt, Peter] NIMH, Sect Behav Endocrinol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1020
BP 369S
EP 370S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502213
ER
PT J
AU Simon, TJ
Antshel, KM
Stoddard, J
Fremont, W
Kates, WR
AF Simon, Tony J.
Antshel, Kevin M.
Stoddard, Joel
Fremont, Wanda
Kates, Wendy R.
TI A Potentially Efficient Screening Tool for Psychotic Thinking in Youth
with Chromosome 22q11.2 Deletion Syndrome
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; Psychosis-Proneness; Screening; 22q11.2 deletion
syndrome; Prodrome
C1 [Simon, Tony J.] Univ Calif Davis, Psychiat & Behav Sci, Sacramento, CA 95817 USA.
[Antshel, Kevin M.] Syracuse Univ, Psychol, Syracuse, NY USA.
[Stoddard, Joel] NIMH, NIH, Bethesday, MD USA.
[Fremont, Wanda; Kates, Wendy R.] Syracuse Univ, Psychiat, Syracuse, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1035
BP 376S
EP 376S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502228
ER
PT J
AU Hoffmann, MS
Stringaris, A
Leibenluft, E
Laporte, PP
Pan, PM
Gadelha, A
Miguel, EC
Manfro, GG
Rohde, LA
Salum, GA
AF Hoffmann, Mauricio S.
Stringaris, Argyris
Leibenluft, Ellen
Laporte, Paola P.
Pan, Pedro M.
Gadelha, Ary
Miguel, Euripedes C.
Manfro, Gisele G.
Rohde, Luis A.
Salum, Giovanni A.
TI The Validity of Positive Attributes Construct and its Interactions with
Cognition and Psychopathology: A Developmental Economics Approach
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Noncognitive skills; Cognitive skills; Mental health; School; Friendship
C1 [Hoffmann, Mauricio S.; Laporte, Paola P.] Hosp Clin Porto Alegre, Psychiat, Porto Alegre, RS, Brazil.
[Stringaris, Argyris] Inst Psychiat, Dept Child & Adolescent Psychiat, London, England.
[Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, Bethesda, MD 20892 USA.
[Pan, Pedro M.; Gadelha, Ary] Univ Fed Sao Paulo, Psychiat, Sao Paulo, Brazil.
[Miguel, Euripedes C.] Univ Sao Paulo, Inst Psychiat, Sao Paulo, Brazil.
[Manfro, Gisele G.; Rohde, Luis A.; Salum, Giovanni A.] Univ Fed Rio Grande do Sul, Psychiat, Porto Alegre, RS, Brazil.
RI Salum, Giovanni/A-7849-2010; Pan, Pedro/I-5167-2013
OI Salum, Giovanni/0000-0002-7537-7289; Pan, Pedro/0000-0002-1943-6520
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1039
BP 377S
EP 377S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502232
ER
PT J
AU Swedo, SE
AF Swedo, Susan E.
TI Treatment of PANDAS/PANS with Therapeutic Plasma Apheresis (TPA),
Intravenous Immunoglobulin (IVIG) and other Immunomodulatory Therapies
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE PANDAS; PANS; Obsessive Compulsive Disorder (OCD); Intravenous
immunoglobulin (IVIG); Therapeutic plasma apheresis (TPA)
C1 [Swedo, Susan E.] NIMH, Pediat & Dev Neurosci Branch, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1041
BP 378S
EP 378S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502234
ER
PT J
AU Hyusyan, AA
Zhang, FY
Adams, S
Khoyetsyan, AG
Straub, R
Avagyan, S
Jordan, F
Mayilyan, KR
Weinberger, DR
AF Hyusyan, Armenuhi A.
Zhang, Fengyu
Adams, Sharon
Khoyetsyan, Aren G.
Straub, Richard
Avagyan, Sevak
Jordan, Frieda
Mayilyan, Karine R.
Weinberger, Daniel R.
TI Multiallelic Association of the HLA-C Locus with Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE MHC; HLA class I; HLA class II; HLA imputation; FBAT
C1 [Hyusyan, Armenuhi A.; Khoyetsyan, Aren G.; Mayilyan, Karine R.] Armenian NAS, Inst Mol Biol, Yerevan, Armenia.
[Hyusyan, Armenuhi A.; Avagyan, Sevak; Jordan, Frieda] Armenian Bone Marrow Donor Registry Charitable Tr, Yerevan, Armenia.
[Zhang, Fengyu; Straub, Richard; Mayilyan, Karine R.; Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
[Adams, Sharon] NIH, HLA Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1099
BP 402S
EP 402S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502292
ER
PT J
AU Dutta, N
Helton, S
Hall, S
Schwandt, M
Lohoff, FW
AF Dutta, Nisha
Helton, Sarah
Hall, Sam
Schwandt, Melanie
Lohoff, Falk W.
TI The Functional VMAT1 Variant Thr136Ile Moderates Alcohol Withdrawal
Severity
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE alcohol withdrawal; VMAT1
C1 [Dutta, Nisha; Helton, Sarah; Hall, Sam; Schwandt, Melanie; Lohoff, Falk W.] NIAAA, NIH, Lab Clin Genom & Expt Therapeut, Bethesda, MD USA.
RI Lohoff, Falk/M-7951-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1116
BP 409S
EP 409S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502309
ER
PT J
AU Helton, S
Dutta, N
Hall, S
Schwandt, M
Lohoff, FW
AF Helton, Sarah
Dutta, Nisha
Hall, Sam
Schwandt, Melanie
Lohoff, Falk W.
TI Association Analysis between Genetic Variation in the GATA4 Gene and
Alcohol Dependence
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE GATA4; alcohol dependence; gene variants; case-control
C1 [Helton, Sarah; Dutta, Nisha; Hall, Sam; Schwandt, Melanie; Lohoff, Falk W.] NIAAA, NIH, Bethesda, MD USA.
RI Lohoff, Falk/M-7951-2016
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1117
BP 409S
EP 409S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502310
ER
PT J
AU Huang, MC
Schwandt, ML
Heilig, M
AF Huang, Ming-Chyi
Schwandt, Melanie L.
Heilig, Markus
TI Association of FKBP5 Genetic Variants with Benzodiazepine Use in
Patients Receiving Alcohol Withdrawal Treatment
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE FKBP5; Alcohol Withdrawal; Benzodiazepine; Genetic Association
C1 [Huang, Ming-Chyi] Taipei City Hosp, Psychiat, Taipei City Psychiat Ctr, Taipei, Taiwan.
[Schwandt, Melanie L.; Heilig, Markus] NIAAA, Lab Clin & Translat Studies, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1118
BP 409S
EP 409S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502311
ER
PT J
AU Kramer, R
Mistry, M
Fromer, M
Elkahloun, A
Lipska, BK
AF Kramer, Robin
Mistry, Meeta
Fromer, Menachem
Elkahloun, Abdel
Lipska, Barbara K.
TI Whole Genome Expression Patterns in Dorsolateral Prefrontal Cortex and
Hippocampus in Schizophrenia, Bipolar Disorder and Major Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; Bipolar; MDD; DLPFC; Hippocampus
C1 [Kramer, Robin; Lipska, Barbara K.] NIMH, Human Brain Collect Core, Bethesda, MD 20892 USA.
[Mistry, Meeta] Harvard Univ, Sch Publ Hlth, HSPH Bioinformat Core, Boston, MA 02115 USA.
[Fromer, Menachem] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
[Elkahloun, Abdel] NHGRI, Microarray Core, Bethesda, MD 20892 USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1137
BP 416S
EP 416S
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502329
ER
PT J
AU Lipska, BK
Kunii, Y
Zhang, WY
Xu, Q
Feng, NP
Wang, KH
AF Lipska, Barbara K.
Kunii, Yasuto
Zhang, Wenyu
Xu, Qing
Feng, Ningping
Wang, Kuan Hong
TI Co-Localization of CHRNA7 and CHRFAM7A mRNA and Their Altered Expression
in the Postmortem Dorsolateral Prefrontal Cortex of Patients with Major
Psychiatric Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE schizophrenia; nicotinic receptor; bipolar disorder; prefrontal cortex;
major depression
C1 [Lipska, Barbara K.; Kunii, Yasuto; Xu, Qing; Feng, Ningping] NIMH, HBCC, Bethesda, MD 20892 USA.
[Zhang, Wenyu; Wang, Kuan Hong] NIMH, DIRP, Bethesda, MD 20892 USA.
RI Lipska, Barbara/E-4569-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1138
BP 416S
EP 417S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502330
ER
PT J
AU Zhang, L
Raheja, UK
Shuldiner, AR
Amritwar, A
Sleemi, A
Stiller, JW
Evans, DS
Hsueh, WC
Snitker, S
Mitchell, BD
Postolache, TT
AF Zhang, Layan
Raheja, Uttam K.
Shuldiner, Alan R.
Amritwar, Ameya
Sleemi, Aamar
Stiller, John W.
Evans, Daniel S.
Hsueh, Wen-Chi
Snitker, Soren
Mitchell, Braxton D.
Postolache, Teodor T.
TI Chronotype Is Associated with Seasonal Weight and Sleep Duration Changes
in the Old Order Amish
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Seasonal Pattern Assessment Questionnaire (SPAQ); Seasonal Sleep
Duration Changes; Seasonal Weight Changes; Morningness-Eveningness
Questionnaire (MEQ); Amish
C1 [Zhang, Layan; Raheja, Uttam K.; Amritwar, Ameya; Sleemi, Aamar; Stiller, John W.] St Elizabeth Hosp, Dept Psychiat, Washington, DC USA.
[Zhang, Layan; Raheja, Uttam K.; Amritwar, Ameya; Sleemi, Aamar; Postolache, Teodor T.] Univ Maryland, Sch Med, Mood & Anxiety Program, Baltimore, MD USA.
[Shuldiner, Alan R.; Snitker, Soren; Mitchell, Braxton D.] Univ Maryland, Sch Med, Dept Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[Evans, Daniel S.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Hsueh, Wen-Chi] NIDDK, Phoenix Epidemiol & Clin Res Branch, NIH, Phoenix, AZ USA.
[Postolache, Teodor T.] Mental Illness Res Educ & Clin Ctr MIRECC, Capitol Hlth Care Network, Baltimore, MD USA.
Mental Illness Res Educ & Clin Ctr MIRECC, Capitol Hlth Care Network, Denver, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 1150
BP 421S
EP 422S
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207502342
ER
PT J
AU Bartholomew, ME
Ihne, JL
Berman, KF
Weinberger, DR
Callicott, JH
AF Bartholomew, Morgan E.
Ihne, Jessica L.
Berman, Karen F.
Weinberger, Daniel R.
Callicott, Joseph H.
TI Gene-environment Interaction Between COMT Genotype and Childhood
Urbanicity on Prefrontal Efficiency in Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; Urbanicity; COMT
C1 [Bartholomew, Morgan E.; Ihne, Jessica L.; Berman, Karen F.; Callicott, Joseph H.] NIH, Clin & Translat Neurosci Branch, Bethesda, MD 20892 USA.
[Weinberger, Daniel R.] Lieber Inst Brain Dev, Clin Sci, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 572
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501166
ER
PT J
AU Cadet, JL
AF Cadet, Jean Lud
TI Transcriptional and Epigenetic Substrates of Methamphetamine
Self-administration
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Methamphetamine Addiction; gene networks; epigenetics; transcription
factors; self-administration
C1 [Cadet, Jean Lud] NIDA, Mol Neuropsychiat Res Branch, NIH, DHHS, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 440
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501042
ER
PT J
AU Callicott, JH
Dickinson, D
Berman, KF
Weinberger, DR
AF Callicott, Joseph H.
Dickinson, Dwight
Berman, Karen F.
Weinberger, Daniel R.
TI General Intelligence and Associated fMRI Networks in Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE intelligence; prefrontal; schizophrenia; fMRI; working memory
C1 [Callicott, Joseph H.; Dickinson, Dwight; Berman, Karen F.] NIMH, Clin & Translat Neurosci Branch, NIH, Bethesda, MD 20892 USA.
[Weinberger, Daniel R.] Lieber Inst Bran Dev, Clin Sci, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 574
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501168
ER
PT J
AU Davis, A
Torrisi, S
Reynolds, R
O'Connell, K
Balderston, N
Grillon, C
Ernst, M
AF Davis, Andrew
Torrisi, Salvatore
Reynolds, Rick
O'Connell, Katherine
Balderston, Nicholas
Grillon, Christian
Ernst, Monique
TI Functional Connectivity of the Human Bed Nucleus of the Stria Terminalis
at Ultra High Field fMRI
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE BNST; Anxiety; fMRI; Connectivity; Subcortical
C1 [Davis, Andrew; Torrisi, Salvatore; O'Connell, Katherine; Balderston, Nicholas; Grillon, Christian; Ernst, Monique] NIMH, Div Intramural Res Programs, Bethesda, MD 20892 USA.
[Reynolds, Rick] NIMH, Sci & Stat Comp Core, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 631
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501225
ER
PT J
AU Dickinson, D
Giangrande, E
Pratt, D
Weinberger, DR
Berman, KF
AF Dickinson, Dwight
Giangrande, Evan
Pratt, Danielle
Weinberger, Daniel R.
Berman, Karen F.
TI Cognitive Subgrouping in People with Schizophrenia and Their Siblings: A
Focus on "Neuropsychologically Normal" Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; Cognition; Cluster Analysis; Subgrouping; Unaffected
Siblings
C1 [Dickinson, Dwight; Giangrande, Evan; Pratt, Danielle; Berman, Karen F.] NIMH, Clin & Translat Neurosci Branch, Bethesda, MD 20892 USA.
[Weinberger, Daniel R.] Lieber Inst Brain Dev, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 573
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501167
ER
PT J
AU Diehl, C
Cho, YST
Yang, G
Repovs, G
Murray, JD
Pearlson, GD
Glahn, DC
Anticevic, A
AF Diehl, Caroline
Cho, Youngsun T.
Yang, Genevieve
Repovs, Grega
Murray, John D.
Pearlson, Godfrey D.
Glahn, David C.
Anticevic, Alan
TI Characterizing Striatal Connectivity Disturbances in Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE schizophrenia; connectivity; striatum
C1 [Diehl, Caroline; Cho, Youngsun T.; Yang, Genevieve; Pearlson, Godfrey D.; Glahn, David C.; Anticevic, Alan] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Diehl, Caroline; Anticevic, Alan] Yale Univ, Dept Psychol, New Haven, CT 06520 USA.
[Yang, Genevieve; Anticevic, Alan] Connecticut Mental Hlth Ctr, Abraham Ribicoff Res Facil, New Haven, CT USA.
[Yang, Genevieve; Anticevic, Alan] Yale Univ, Interdept Neurosci Program, New Haven, CT USA.
[Repovs, Grega] Univ Ljubljana, Dept Psychol, Ljubljana, Slovenia.
[Murray, John D.; Pearlson, Godfrey D.] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT USA.
[Murray, John D.] Yale Univ, Dept Phys, New Haven, CT USA.
[Pearlson, Godfrey D.; Glahn, David C.; Anticevic, Alan] NIAAA, Ctr Translat Neurosci Alcoholism, New Haven, CT USA.
[Pearlson, Godfrey D.] Hartford Hosp, Olin Neuropsychiat Res Ctr, Hartford, CT 06115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 685
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501279
ER
PT J
AU Farokhnia, M
Haass-Koffler, C
Zywiak, W
Swift, RM
Kenna, GA
Leggio, L
AF Farokhnia, Mehdi
Haass-Koffler, Carolina
Zywiak, William
Swift, Robert M.
Kenna, George A.
Leggio, Lorenzo
TI Noradrenergic System as a Pharmacological Target for Alcoholism: A
Randomized, Double-Blind, Placebo-Controlled, Proof-of-Concept, Clinical
Trial with Doxazosin
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Doxazosin; Noradrenergic System; Alcohol Dependence; Alcohol Use
Disorder; Clinical Trial
C1 [Farokhnia, Mehdi; Leggio, Lorenzo] NIAAA, Sect Clin Psychoneuroendocrinol & Neuropsychophar, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Farokhnia, Mehdi; Leggio, Lorenzo] NIDA, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Haass-Koffler, Carolina; Zywiak, William; Swift, Robert M.; Kenna, George A.] Brown Univ, Ctr Alcohol & Addict Studies, Providence, RI 02912 USA.
RI Leggio, Lorenzo/M-2972-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 500
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501094
ER
PT J
AU Grannan, MD
Bubser, M
Bridges, TM
Gould, RW
Dencker, D
Daniels, JS
Noetzel, MJ
Niswender, CM
Duggan, ME
Brandon, NJ
Dunlop, J
Wood, MW
Wess, J
Wood, MR
Lindsley, CW
Conn, PJ
Jones, CK
AF Grannan, Michael D.
Bubser, Michael
Bridges, Thomas M.
Gould, Robert W.
Dencker, Ditte
Daniels, J. Scott
Noetzel, Meredith J.
Niswender, Colleen M.
Duggan, Mark E.
Brandon, Nicholas J.
Dunlop, John
Wood, Michael W.
Wess, Jurgen
Wood, Michael R.
Lindsley, Craig W.
Conn, P. Jeffrey
Jones, Carrie K.
TI Effects of the M4 Positive Allosteric Modulator VU0467154 on Cognition
and Electrophysiological Properties in the mPFC
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; Cognition; PAM; electrophysiology
C1 [Grannan, Michael D.; Bubser, Michael; Bridges, Thomas M.; Gould, Robert W.; Daniels, J. Scott; Noetzel, Meredith J.; Niswender, Colleen M.; Wood, Michael R.; Lindsley, Craig W.; Conn, P. Jeffrey; Jones, Carrie K.] Vanderbilt Univ, Pharmacol, Nashville, TN 37235 USA.
[Grannan, Michael D.; Bubser, Michael; Bridges, Thomas M.; Gould, Robert W.; Daniels, J. Scott; Noetzel, Meredith J.; Niswender, Colleen M.; Wood, Michael R.; Lindsley, Craig W.; Conn, P. Jeffrey; Jones, Carrie K.] Vanderbilt Univ, Vanderbilt Ctr Neurosci Drug Discovery, Nashville, TN 37235 USA.
[Dencker, Ditte] Copenhagen Univ Hosp, Lab Neuropsychiat, Copenhagen, Denmark.
[Duggan, Mark E.; Brandon, Nicholas J.; Dunlop, John; Wood, Michael W.] AstraZeneca, Neurosci Innovat Med, Cambridge, MA USA.
[Wess, Jurgen] NIH, Lab Bioorgan Chem, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 740
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501333
ER
PT J
AU Holmes, A
AF Holmes, Andrew
TI Amygdala Circuit Mechanisms Moderating Pharmacological Rescue of Fear
Extinction Impairments
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE cannabinoid; fluoxetine; amygdala; fear; plasticity
C1 [Holmes, Andrew] NIAAA, LBGN, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 6
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 416
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501018
ER
PT J
AU Hsu, DT
Mickey, BJ
Langenecker, SA
Heitzeg, MM
Love, TM
Wang, H
Kennedy, SE
Pecina, M
Shafir, T
Hodgkinson, CA
Enoch, MA
Goldman, D
Zubieta, JK
AF Hsu, David T.
Mickey, Brian J.
Langenecker, Scott A.
Heitzeg, Mary M.
Love, Tiffany M.
Wang, Heng
Kennedy, Susan E.
Pecina, Marta
Shafir, Tal
Hodgkinson, Colin A.
Enoch, Mary-Anne
Goldman, David
Zubieta, Jon-Kar
TI Allelic Variation in the Corticotropin-Releasing Hormone Receptor 1
(CRHR1) Gene Influences fMRI Signal Responses to Emotional Stimuli
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE corticotropin-releasing; CRH; stress; fMRI; CRHR1
C1 [Hsu, David T.] SUNY Stony Brook, Psychiat, Stony Brook, NY 11794 USA.
[Mickey, Brian J.; Heitzeg, Mary M.; Love, Tiffany M.; Wang, Heng; Pecina, Marta; Zubieta, Jon-Kar] Univ Michigan, Psychiat, Ann Arbor, MI 48109 USA.
[Langenecker, Scott A.] Univ Illinois, Psychiat, Chicago, IL USA.
[Kennedy, Susan E.] Univ Alabama, Biol Sci, Tuscaloosa, AL USA.
[Shafir, Tal] Univ Haifa, Social Welf & Hlth Sci, IL-31999 Haifa, Israel.
[Hodgkinson, Colin A.; Enoch, Mary-Anne; Goldman, David] NIAAA, Neurogenet Lab, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 434
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501036
ER
PT J
AU Koob, GF
AF Koob, George F.
TI Addiction as a Stress Surfeit Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
ID ANTAGONISM; HEROIN; RATS
C1 [Koob, George F.] NIAAA, NIH, Washington, DC USA.
RI koob, george/P-8791-2016
NR 5
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 401
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501003
ER
PT J
AU Krasnova, IN
AF Krasnova, Irina N.
TI Molecular Mechanisms Underlying Incubation of Methamphetamine Craving
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE methamphetamine; self-administration; punishment; craving; histone
diacetylase
C1 [Krasnova, Irina N.] NIDA, Mol Neuropsychiat Res Branch, NIH, DHHS, Baltimore, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 441
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501043
ER
PT J
AU Kwako, LE
Warmingham, JM
Goldman, D
George, DT
Heilig, M
Ramchandani, VA
Schwandt, ML
AF Kwako, Laura E.
Warmingham, Jennifer M.
Goldman, David
George, David T.
Heilig, Markus
Ramchandani, Vijay A.
Schwandt, Melanie L.
TI Early Life Stress and Suicide in Treatment-Seeking Alcoholics
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Alcoholism; Suicide; Posttraumatic stress disorder; Trauma; Addiction
C1 [Kwako, Laura E.; Goldman, David; George, David T.] NIAAA, Off Clin Director, NIH, Bethesda, MD USA.
[Warmingham, Jennifer M.; Heilig, Markus; Ramchandani, Vijay A.; Schwandt, Melanie L.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 3
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 604
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501198
ER
PT J
AU Luscher, ZI
Ordonez, AE
Sastry, NV
Watsky, RE
Greenstein, D
Clasen, L
Rapoport, J
Gogtay, N
AF Luscher, Zoe I.
Ordonez, Anna E.
Sastry, Nevin V.
Watsky, Rebecca E.
Greenstein, Deanna
Clasen, Liv
Rapoport, Judith
Gogtay, Nitin
TI Structural Magnetic Resonance Imaging of the Amygdala in Patients with
Childhood-Onset Schizophrenia, their Non-Psychotic Siblings, and Healthy
Volunteers
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; amygdala; childhood; siblings; MRI
C1 [Luscher, Zoe I.; Ordonez, Anna E.; Sastry, Nevin V.; Watsky, Rebecca E.; Greenstein, Deanna; Clasen, Liv; Rapoport, Judith; Gogtay, Nitin] NIMH, 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 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 674
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501268
ER
PT J
AU McMahon, FJ
AF McMahon, Francis J.
CA Consortium Lithium Genetics
TI Genomewide Association Study Implicates a Long Noncoding (lnc) RNA in
the Response to Lithium for Bipolar Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE pharmacogenomics; bipolar; mood stabilizers
C1 [McMahon, Francis J.; Consortium Lithium Genetics] NIMH, Human Genet Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 612
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501206
ER
PT J
AU Pine, DS
AF Pine, Daniel S.
TI Shared and Specific Neural Correlates of Pediatric Anxiety Phenotypes
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE anxiety; fMRI
C1 [Pine, Daniel S.] NIMH, IRP, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 405
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501007
ER
PT J
AU Richards, EM
Zanotti-Fregonara, P
Fujita, M
Walls, T
Niciu, MJ
Machado-Vieira, R
Salvadore, G
Kolb, H
Zarate, CA
Innis, RB
AF Richards, Erica M.
Zanotti-Fregonara, Paolo
Fujita, Masahiro
Walls, Tessa
Niciu, Mark J.
Machado-Vieira, Rodrigo
Salvadore, Giacomo
Kolb, Hartmuth
Zarate, Carlos A.
Innis, Robert B.
TI Increased PET Radioligand Binding to Translocator Protein Suggests that
Major Depressive Disorder Is Associated with Neuroinflammation
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE PET; Inflammation; TSPO; Depression
C1 [Richards, Erica M.; Walls, Tessa; Niciu, Mark J.; Machado-Vieira, Rodrigo; Zarate, Carlos A.] NIMH, Expt Therapeut & Pathophysiol Branch, Bethesda, MD 20892 USA.
[Zanotti-Fregonara, Paolo; Fujita, Masahiro; Innis, Robert B.] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Salvadore, Giacomo] Janssen Res & Dev LLC, Neurosci Expt Med, Titusville, NJ USA.
[Kolb, Hartmuth] Janssen Res & Dev LLC, Neurosci Biomakers, San Diego, CA USA.
RI MACHADO-VIEIRA, RODRIGO/D-8293-2012
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 652
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501246
ER
PT J
AU Schuebel, KE
AF Schuebel, Kornel E.
TI Epigenomic Responses to Alcohol in a Rat Model of Fetal Alcohol Spectrum
Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Epigenetics; Fetal alcohol spectrum disorders; Alcohol; Choline; Gene
expression
C1 [Schuebel, Kornel E.] NIAAA, Neurogenet Lab, NIH, DHHS, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 443
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501045
ER
PT J
AU Stangl, BL
Hendershot, CS
Ramchandani, VA
AF Stangl, Bethany L.
Hendershot, Christian S.
Ramchandani, Vijay A.
TI Determinants of Intravenous Self-administration of Alcohol in Humans:
Impulsivity and Attention
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE IV Alcohol; Self-administration; Impulsivity; Attention; Social Drinkers
C1 [Stangl, Bethany L.; Ramchandani, Vijay A.] NIAAA, NIH, Sect Human Psychopharmacol, Bethesda, MD USA.
[Hendershot, Christian S.] Campbell Family Mental Hlth Res Inst, Ctr Addict & Mental Hlth, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 504
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501098
ER
PT J
AU Steuber, ER
Gold, AL
Pacheco, J
Leibenluft, E
Pine, DS
AF Steuber, Elizabeth R.
Gold, Andrea L.
Pacheco, Jennifer
Leibenluft, Ellen
Pine, Daniel S.
TI Brain Morphometry in Pediatric Anxiety Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Anxiety Disorders; Pediatrics; Freesurfer; Cortical Thickness; Gray
Matter Volume
C1 [Steuber, Elizabeth R.; Gold, Andrea L.; Leibenluft, Ellen; Pine, Daniel S.] NIMH, Emot & Dev Branch, Bethesda, MD 20892 USA.
[Pacheco, Jennifer] Natl Intrepid Ctr Excellence, Walter Reed Natl Mil Med Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 632
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501226
ER
PT J
AU Tromp, DPM
Williams, LE
Fox, AS
Oler, JA
Rogers, GR
Pine, DS
Kalin, NH
AF Tromp, Do P. M.
Williams, Lisa E.
Fox, Andrew S.
Oler, Jonathan A.
Rogers, Gregory R.
Pine, Daniel S.
Kalin, Ned H.
TI White Matter Alterations in Pre-Adolescent Children with Anxiety
Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Anxiety Disorders; Pre-adolescents; Diffusion Tensor Imaging; White
Matter
C1 [Tromp, Do P. M.; Williams, Lisa E.; Fox, Andrew S.; Oler, Jonathan A.; Rogers, Gregory R.; Kalin, Ned H.] Univ Wisconsin, Psychiat, Madison, WI USA.
[Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 642
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501236
ER
PT J
AU Tseng, WL
Tseng, MB
Deveney, C
Machlin, L
Moroney, E
Towbin, K
Pine, D
Leibenluft, E
AF Tseng, Wan-Ling
Tseng, Melissa Brotman
Deveney, Christen
Machlin, Laura
Moroney, Elizabeth
Towbin, Kenneth
Pine, Daniel
Leibenluft, Ellen
TI Neural Correlates of Irritability across Diagnoses: Categorical and
Dimensional Approaches
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE irritability; DMDD; fMRI; categorical; dimensional
C1 [Tseng, Wan-Ling; Tseng, Melissa Brotman; Machlin, Laura; Moroney, Elizabeth; Towbin, Kenneth; Pine, Daniel; Leibenluft, Ellen] NIMH, Emot & Dev Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Deveney, Christen] Wellesley Coll, Dept Psychol, Wellesley, MA 02181 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 653
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501247
ER
PT J
AU Warner, V
Xu, DR
Liu, J
Xao, XJ
Jiang, YW
Durken, K
Grillon, C
AF Warner, Virginia
Xu, Dongrong
Liu, Jun
Xao, Xuejun
Jiang, Yuwei
Durken, Kathleen
Grillon, Christian
TI White Matter Integrity and Its Association with Overactive Defense
Survival Circuitry: Three Generation Study
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE startle; diffusion imaging; depression; 3 generations
C1 [Warner, Virginia; Xu, Dongrong; Liu, Jun; Xao, Xuejun; Jiang, Yuwei] New York State Psychiat Inst & Hosp, Epidemiol, New York, NY 10032 USA.
[Durken, Kathleen] New York State Psychiat Inst & Hosp, MRI Unit, New York, NY 10032 USA.
[Grillon, Christian] NIMH, Neurobiol Fear & Anxiety, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 743
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501336
ER
PT J
AU Watsky, RE
Gotts, SJ
Berman, RA
Sastry, NV
Luscher, ZI
McAdams, HM
Greenstein, D
Lalonde, F
Martin, A
Ordonez, AE
Gogtay, N
Rapoport, JL
AF Watsky, Rebecca E.
Gotts, Stephen J.
Berman, Rebecca A.
Sastry, Nevin V.
Luscher, Zoe I.
McAdams, Harrison M.
Greenstein, Dede
Lalonde, Francois
Martin, Alex
Ordonez, Anna E.
Gogtay, Nitin
Rapoport, Judith L.
TI Resting State Networks in the Non-Psychotic Siblings of Patients with
Childhood-Onset Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE Schizophrenia; Neuroimaging; Functional MRI; Childhood psychosis
C1 [Watsky, Rebecca E.; Berman, Rebecca A.; Sastry, Nevin V.; Luscher, Zoe I.; McAdams, Harrison M.; Greenstein, Dede; Lalonde, Francois; Ordonez, Anna E.; Gogtay, Nitin; Rapoport, Judith L.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
[Gotts, Stephen J.; Martin, Alex] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 672
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501266
ER
PT J
AU Williams, LE
Oler, JA
Fox, AS
McFarlin, DR
Rogers, GM
Jesson, MAL
Davidson, RJ
Pine, DS
Kalin, NH
AF Williams, Lisa E.
Oler, Jonathan A.
Fox, Andrew S.
McFarlin, Daniel R.
Rogers, Gregory M.
Jesson, Maria A. L.
Davidson, Richard J.
Pine, Daniel S.
Kalin, Ned H.
TI Fear of the Unknown: Increased Neural Activation During Uncertain
Anticipation in Childhood Anxiety Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
CT 70th Annual Scientific Meeting of the Society-of-Biological-Psychiatry
on Stress, Emotion, Neurodevelopment and Psychopathology
CY MAY 14-16, 2015
CL Toronto, CANADA
SP Soc Biol Psychiat
DE anxiety disorders; childhood; amygdala; uncertainty; anticipation
C1 [Williams, Lisa E.; Oler, Jonathan A.; Fox, Andrew S.; McFarlin, Daniel R.; Rogers, Gregory M.; Jesson, Maria A. L.; Kalin, Ned H.] Univ Wisconsin, Psychiat, Madison, WI USA.
[Davidson, Richard J.] Univ Wisconsin, Psychol, Madison, WI USA.
[Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
SU S
MA 643
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CF0BM
UT WOS:000352207501237
ER
PT J
AU Sakloth, F
Kolanos, R
Mosier, PD
Bonano, JS
Banks, ML
Partilla, JS
Baumann, MH
Negus, SS
Glennon, RA
AF Sakloth, F.
Kolanos, R.
Mosier, P. D.
Bonano, J. S.
Banks, M. L.
Partilla, J. S.
Baumann, M. H.
Negus, S. S.
Glennon, R. A.
TI Steric parameters, molecular modeling and hydropathic interaction
analysis of the pharmacology of para-substituted methcathinone analogues
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
ID HUMAN SEROTONIN TRANSPORTER; DOPAMINE TRANSPORTER; MONOAMINE
TRANSPORTERS; SUBSTRATE TRANSPORT; CONCISE GUIDE; BINDING-SITE; BATH
SALTS; COCAINE; VALIDATION; MEPHEDRONE
AB Background and PurposeThere is growing concern over the abuse of certain psychostimulant methcathinone (MCAT) analogues. This study extends an initial quantitative structure-activity relationship (QSAR) investigation that demonstrated important steric considerations of seven 4- (or para-)substituted analogues of MCAT. Specifically, the steric character (Taft's steric E-S) of the 4-position substituent affected in vitro potency to induce monoamine release via dopamine and 5-HT transporters (DAT and SERT) and in vivo modulation of intracranial self-stimulation (ICSS). Here, we have assessed the effects of other steric properties of the 4-position substituents.
Experimental ApproachDefinitive steric parameters that more explicitly focus on the volume, width and length of the MCAT 4-position substituents were assessed. In addition, homology models of human DAT and human SERT based upon the crystallized DrosophilaDAT were constructed and docking studies were performed, followed by hydropathic interaction (HINT) analysis of the docking results.
Key ResultsThe potency of seven MCAT analogues at DAT was negatively correlated with the volume and maximal width of their 4-position substituents, whereas potency at SERT increased as substituent volume and length increased. SERT/DAT selectivity, as well as abuse-related drug effects in the ICSS procedure, also correlated with the same parameters. Docking solutions offered a means of visualizing these findings.
Conclusions and ImplicationsThese results suggest that steric aspects of the 4-position substituents of MCAT analogues are key determinants of their action and selectivity, and that the hydrophobic nature of these substituents is involved in their potency at SERT.
C1 [Sakloth, F.; Kolanos, R.; Mosier, P. D.; Glennon, R. A.] Virginia Commonwealth Univ, Sch Pharm, Dept Med Chem, Richmond, VA 23298 USA.
[Bonano, J. S.; Banks, M. L.; Negus, S. S.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
[Partilla, J. S.; Baumann, M. H.] NIDA, Designer Drug Res Unit, Intramural Res Program, NIH, Baltimore, MD USA.
RP Glennon, RA (reprint author), Virginia Commonwealth Univ, Box 980540, Richmond, VA 23298 USA.
EM glennon@vcu.edu
RI Banks, Matthew/K-4429-2014
OI Banks, Matthew/0000-0003-4949-5246
FU National Institutes of Health [R01DA033930]
FX This research was supported by National Institutes of Health (Grant No.
R01DA033930).
NR 36
TC 6
Z9 6
U1 2
U2 12
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 MAY
PY 2015
VL 172
IS 9
BP 2210
EP 2218
DI 10.1111/bph.13043
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CF8LB
UT WOS:000352809900003
PM 25522019
ER
PT J
AU Graham, BS
Ambrosino, DM
AF Graham, Barney S.
Ambrosino, Donna M.
TI History of passive antibody administration for prevention and treatment
of infectious diseases
SO CURRENT OPINION IN HIV AND AIDS
LA English
DT Review
DE antibody; history; immunoglobulin; passive immunization; serum therapy
ID ARGENTINE HEMORRHAGIC-FEVER; SOLUBLE SPECIFIC SUBSTANCE; B-CELLS;
NEUTRALIZING ANTIBODIES; MONOCLONAL-ANTIBODIES; IMMUNE PLASMA; SERUM
THERAPY; PNEUMOCOCCUS; VIRUS; ANTIGEN
AB Purpose of review
We describe the history of passive immunization to provide context for the series of articles to follow. The history of passive immunization with antibodies to prevent or treat infectious diseases is a story of different eras. There was an extraordinary era of discovery and clinical implementation before the chemical nature of antibodies was even known. This empirical process provided the resources and reagents used to describe and characterize humoral immunity, better define the chemical properties and structure of antibodies, and extend the clinical use of immunoglobulin products to treat or prevent multiple viral and bacterial diseases over the ensuing several decades. The next distinct era came with the discovery of processes to produce monoclonal antibodies (mAbs), and development of more specific therapies. Interestingly, mAb technology resulted in many products to treat autoimmune and allergic diseases, but only one common infectious disease, respiratory syncytial virus, and only in a restricted population of high-risk infants.
Recent findings
The current era began in 2003 with a series of publications demonstrating processes for rapidly producing human mAbs.
Summary
This technology combined with new sequencing technology, advances in structural biology, atomic-level molecular design, and increased capacity for synthetic biology, promises new opportunities to apply passive immunization to the prevention and treatment of infectious diseases.
C1 [Graham, Barney S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Ambrosino, Donna M.] CVC, Rockville, MD USA.
RP Graham, BS (reprint author), NIAID, Vaccine Res Ctr, NIH, 40 Convent Dr,Bldg 40,Room 2502, Bethesda, MD 20892 USA.
EM bgraham@nih.gov
FU National Institute of Allergy and Infectious Diseases
FX This work was supported by intramural funding from the National
Institute of Allergy and Infectious Diseases.
NR 29
TC 8
Z9 8
U1 2
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1746-630X
EI 1746-6318
J9 CURR OPIN HIV AIDS
JI Curr. Opin. HIV AIDS
PD MAY
PY 2015
VL 10
IS 3
BP 129
EP 134
DI 10.1097/COH.0000000000000154
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CF8GG
UT WOS:000352793600001
PM 25760933
ER
PT J
AU Dey, B
Berger, EA
AF Dey, Barna
Berger, Edward A.
TI Towards an HIV cure based on targeted killing of infected cells:
different approaches against acute versus chronic infection
SO CURRENT OPINION IN HIV AND AIDS
LA English
DT Review
DE chimeric antigen receptor; Fc-mediated effector functions; genetically
modified T cells; HIV cure; recombinant immunotoxins; T cell receptor;
targeted cytotoxic therapy
ID COMBINATION ANTIRETROVIRAL THERAPY; CD8(+) T-CELLS;
IMMUNODEFICIENCY-VIRUS-INFECTION; BROADLY NEUTRALIZING ANTIBODIES;
CANCER-THERAPY; IN-VIVO; RECOMBINANT IMMUNOTOXIN; LOW IMMUNOGENICITY;
FOLLICULAR HELPER; GENE-THERAPY
AB Purpose of review
Current regimens of combination antiretroviral therapy (cART) offer effective control of HIV infection, with maintenance of immune health and near-normal life expectancy. What will it take to progress beyond the status quo, whereby infectious virus can be eradicated (a 'sterilizing cure') or fully controlled without the need for ongoing cART (a 'functional cure')?
Recent findings
On the basis of therapeutic advances in the cancer field, we propose that targeted cytotoxic therapy to kill HIV-infected cells represents a logical complement to cART for achieving an HIV cure. This concept is based on the fact that cART effectively blocks replication of the virus, but does not eliminate cells that are already infected; targeted cytotoxic therapy would contribute precisely this missing component. We suggest that different modalities are suited for curing primary acute versus established chronic infection. For acute infection, relatively short-acting potent agents such as recombinant immunotoxins might prove sufficient for HIV eradication, whereas for chronic infection, a long-lasting (lifelong?) modality is required to maintain full virus control, as might be achieved with genetically modified autologous T cells.
Summary
We present perspectives for complementing cART with targeted cytotoxic therapy, whereby HIV infection is either eradicated or fully controlled, thereby eliminating the need for lifelong cART.
C1 [Dey, Barna; Berger, Edward A.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Berger, EA (reprint author), NIH, 33 North Dr,Room 1E19A, Bethesda, MD 20892 USA.
EM edward_berger@nih.gov
FU Division of Intramural Research of NIAID; NIH Intramural AIDS Targeted
Antiviral Program
FX Authors were supported by the Division of Intramural Research of NIAID
and by the NIH Intramural AIDS Targeted Antiviral Program.
NR 68
TC 4
Z9 4
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1746-630X
EI 1746-6318
J9 CURR OPIN HIV AIDS
JI Curr. Opin. HIV AIDS
PD MAY
PY 2015
VL 10
IS 3
BP 207
EP 213
DI 10.1097/COH.0000000000000151
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CF8GG
UT WOS:000352793600011
PM 25710815
ER
PT J
AU Kim, JW
Tomita, Y
Trepel, J
Apolo, AB
AF Kim, Joseph W.
Tomita, Yusuke
Trepel, Jane
Apolo, Andrea B.
TI Emerging immunotherapies for bladder cancer
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE adoptive T-cell therapy; B7-H3; bladder cancer; immune escape;
immunotherapy; NY-ESO-1; OX40; programmed death-ligand 1; urothelial
carcinoma
ID RESISTANT PROSTATE-CANCER; METASTATIC UROTHELIAL CARCINOMA; PHASE-III
TRIAL; NEOADJUVANT CHEMOTHERAPY; IMMUNE-RESPONSES; COSTIMULATORY
MOLECULE; ANTI-PD-L1 ANTIBODY; CLINICAL ACTIVITY; CELL-CARCINOMA;
T-CELLS
AB Purpose of review
Inhibition of immune escape mechanisms, such as the programed death-ligand 1 pathway, has demonstrated rapid, durable responses in multiple tumor types, including advanced urothelial carcinoma. This review discusses emerging immunotherapies for urothelial carcinoma in various stages of clinical development.
Recent findings
Urothelial carcinoma has a high mutational burden, which may increase the number of tumor antigens and potentially enhance the ability of the immune system to recognize tumor cells as foreign. However, urothelial carcinoma can evade the immune system by downregulating tumor-antigen presentation, upregulating various immune checkpoints, and inactivating cytotoxic T cells. Immunotherapies for urothelial carcinoma target each of these steps to restore immune-mediated cytotoxicity. Many of these agents are in clinical trials for urothelial carcinoma.
Summary
Immunotherapies are active in urothelial carcinoma, but only in a fraction of patients, implying the presence of persistent immune escape. Identifying the mechanisms of immune escape and developing rational combinatorial regimens may make the benefit of immunotherapy accessible to a broader population.
C1 [Kim, Joseph W.] Yale Univ, Sch Med, Yale Canc Ctr, Prostate & Urol Canc Program, New Haven, CT USA.
[Tomita, Yusuke; Trepel, Jane] NCI, NIH, Dev Therapeut Branch, Bethesda, MD 20892 USA.
[Apolo, Andrea B.] NCI, NIH, Ctr Canc Res, Genitourinary Malignancies Branch, Bethesda, MD 20892 USA.
RP Apolo, AB (reprint author), 10 Ctr Dr,Rm 12N226,MSC 1906, Bethesda, MD 20892 USA.
EM andrea.apolo@nih.gov
FU National Institutes of Health; Intramural Research Program of the Center
for Cancer Research, National Cancer Institute
FX The authors from National Institutes of Health are supported by funds
from the Intramural Research Program of the Center for Cancer Research,
National Cancer Institute, and National Institutes of Health.
NR 89
TC 8
Z9 8
U1 1
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8746
EI 1531-703X
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD MAY
PY 2015
VL 27
IS 3
BP 191
EP 200
DI 10.1097/CCO.0000000000000177
PG 10
WC Oncology
SC Oncology
GA CF6ES
UT WOS:000352650300007
PM 25811346
ER
PT J
AU Su, D
Singer, EA
Srinivasan, R
AF Su, Daniel
Singer, Eric A.
Srinivasan, Ramaprasad
TI Molecular pathways in renal cell carcinoma: recent advances in genetics
and molecular biology
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE molecular pathways; renal cell carcinoma; targeted therapy
ID FUMARATE HYDRATASE; SIGNALING PATHWAY; CANCER-THERAPY; KIDNEY CANCER;
GROWTH-FACTOR; C-MET; BAP1; NRF2; MUTATIONS; SURVIVAL
AB Purpose of review
Advanced renal cell carcinoma (RCC) remains a largely incurable disease with a grave prognosis despite the availability of a multiplicity of systemic therapies targeted against vascular endothelial growth factor, its receptors, and the mammalian target of rapamycin. Although immune 'checkpoint inhibitors' appear to have activity in clear cell RCC based on recent early phase trials, the true magnitude of the benefit conferred by these agents remains to be fully understood. Given the limitations of existing treatment paradigms, ongoing research into new targetable pathways is critical. This review will highlight some of the more promising avenues of investigation into the molecular biology of RCC.
Recent findings
The hypoxia-inducible factor and mammalian target of rapamycin pathways remain critical targets in clear cell RCC. In addition, genes involved in chromatin remodeling such as polybromo 1 (PBRM1), SET domain containing 2 (SETD2), and BRCA-1-associated protein-1 (BAP1) have been shown to influence tumor biology and predict survival. MET alterations and the Krebs cycle enzyme fumarate hydratase are associated with familial type 1 and type 2 papillary RCC (PRCC), respectively. Alterations in nuclear factor (erythroid-derived 2)-like 2, Kelch-like erythroid-derived cap-n-collar homology-associated protein 1, and cullin 3, components of an oxidative stress response pathway, have been recently recognized in some sporadic papillary tumors as well as in fumarate hydratase-deficient tumor and may serve as additional therapeutic targets. In addition, whole-genome sequencing and integrated genomic analysis strategies are beginning to uncover unique molecular signatures associated with distinct subtypes of RCC, laying the foundation for a molecular classification of RCC and more precise, mechanism-based therapeutic intervention.
Summary
The complex molecular changes underlying individual RCC variants are yet to be fully elucidated and remain the subject of ongoing investigation. The findings summarized here further exemplify the diversity of RCC and the need to tailor our therapeutic approaches to the unique genetic alterations specific to individual subtypes of RCC.
C1 [Su, Daniel; Srinivasan, Ramaprasad] NCI, Ctr Canc Res, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Singer, Eric A.] Rutgers Canc Inst New Jersey, Sect Urol Oncol, New Brunswick, NJ USA.
[Singer, Eric A.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
RP Srinivasan, R (reprint author), NCI, Ctr Canc Res, Urol Oncol Branch, Mol Canc Sect, 10 Ctr Dr,CRC2-5950, Bethesda, MD 20892 USA.
EM ramasrin@mail.nih.gov
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research, Bethesda, Maryland, USA; National Cancer Institute
[P30CA072720]
FX This research was funded by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research, Bethesda, Maryland, USA, and by a grant from the
National Cancer Institute (P30CA072720).
NR 56
TC 6
Z9 8
U1 0
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8746
EI 1531-703X
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD MAY
PY 2015
VL 27
IS 3
BP 217
EP 223
DI 10.1097/CCO.0000000000000186
PG 7
WC Oncology
SC Oncology
GA CF6ES
UT WOS:000352650300010
PM 25811348
ER
PT J
AU Bouchelouche, K
Turkbey, B
Choyke, PL
AF Bouchelouche, Kirsten
Turkbey, Baris
Choyke, Peter L.
TI Advances in imaging modalities in prostate cancer
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE MRI; PET/CT; PET/MRI; prostate cancer; transrectal ultrasound
ID LYMPH-NODE DISSECTION; EMISSION TOMOGRAPHY/COMPUTED TOMOGRAPHY;
ANDROGEN-DEPRIVATION THERAPY; GA-68-LABELED PSMA LIGAND; FUSION-GUIDED
BIOPSY; C-11-CHOLINE PET/CT; RADICAL PROSTATECTOMY; F-18-FLUOROCHOLINE
PET/CT; BIOCHEMICAL RELAPSE; BONE-SCINTIGRAPHY
AB Purpose of review
Imaging plays an important role in the clinical management of prostate cancer (PCa). Thus, much effort has gone into improving imaging modalities in PCa. This review focuses on the recent advancements in transrectal ultrasound, MRI and PET during the past year.
Recent findings
Contrast-enhanced transrectal ultrasound with microbubbles may be useful in PCa, but needs further evaluation before more widespread use. Multiparametric MRI has emerged as a valuable tool to assist clinical management of PCa, and great progress has been made in the past year. Several radionuclides for PET/computed tomography have been tested in clinical trials; most of the studies have used radiolabeled choline. However, new PET tracers such as F-18-1-amino-3-fluorine 18-fluorocyclobutane-1-carboxylic acid and Ga-68-labeled prostate-specific membrane antigen ligands are demonstrating promising results. PET/MRI may further improve imaging in PCa, but this imaging modality needs to be evaluated further.
Summary
Several advances in the imaging of PCa have been made during the past year. In particular, important clinical developments have been reported in multiparametric MRI, PET/computed tomography, and PET/MRI. The continuing development of imaging techniques in PCa has the potential to optimize treatment of PCa. However, the optimal imaging strategies for each of the major clinical scenarios in PCa have not yet been identified.
C1 [Bouchelouche, Kirsten] Aarhus Univ Hosp, Dept Nucl Med, DK-8200 Aarhus, Denmark.
[Bouchelouche, Kirsten] Aarhus Univ Hosp, PET Ctr, DK-8200 Aarhus, Denmark.
[Turkbey, Baris; Choyke, Peter L.] NCI, Ctr Canc Res, Mol Imaging Program, Bethesda, MD 20892 USA.
RP Bouchelouche, K (reprint author), Aarhus Univ Hosp, Dept Nucl Med, Palle Juul Jensens Blvd 99, DK-8200 Aarhus, Denmark.
EM kirsbouc@rm.dk
NR 88
TC 2
Z9 2
U1 0
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8746
EI 1531-703X
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD MAY
PY 2015
VL 27
IS 3
BP 224
EP 231
DI 10.1097/CCO.0000000000000174
PG 8
WC Oncology
SC Oncology
GA CF6ES
UT WOS:000352650300011
PM 25715326
ER
PT J
AU Hallett, M
AF Hallett, M.
TI The dystonias: a heterogeneous collection
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Editorial Material
ID CEREBELLUM
AB Click to view the accompanying paper in this issue.
C1 NINDS, Human Motor Control Sect, Bethesda, MD 20892 USA.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
FU Intramural NIH HHS
NR 4
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1351-5101
EI 1468-1331
J9 EUR J NEUROL
JI Eur. J. Neurol.
PD MAY
PY 2015
VL 22
IS 5
BP 741
EP 742
DI 10.1111/ene.12526
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CF5BC
UT WOS:000352568600003
PM 25065529
ER
PT J
AU Khan, BA
Yeh, AJ
Cheung, GYC
Otto, M
AF Khan, Burhan A.
Yeh, Anthony J.
Cheung, Gordon Y. C.
Otto, Michael
TI Investigational therapies targeting quorum-sensing for the treatment of
Staphylococcus aureus infections
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE quorum-sensing; quorum-sensing blockers; Staphylococcus aureus;
Staphylococcus epidermidis
ID VIRULENCE-GENE-EXPRESSION; 2-COMPONENT REGULATORY SYSTEM; BIOFILM
FORMATION; PSEUDOMONAS-AERUGINOSA; AUTOINDUCING PEPTIDE; CYCLIC
DIPEPTIDES; ALPHA-HEMOLYSIN; CROSS-TALK; IN-VITRO; MARINE PHOTOBACTERIUM
AB Introduction: Antibiotic resistance is a serious global health concern for developed and developing nations. MRSA represents a particularly severe public health threat that is associated with high morbidity and mortality. The lack of novel antibiotics has led scientists to explore therapies targeting bacterial virulence mechanisms and virulence regulators, including those controlling cell-cell communication.
Areas covered: The authors discuss the role of quorum-sensing in Staphylococcus aureus infections and components of the system that are being targeted using novel investigational drugs. In particular, the authors examine the role of the accessory gene regulator (Agr) system in virulence regulation of S. aureus pathogenesis. Finally, the authors present and compare natural and synthetic compounds that have been found to interfere with Agr functionality.
Expert opinion: There is a great need to develop new therapeutic methods to combat S. aureus infections. These include anti-virulence therapies that target key global regulators involved with the establishment and propagation of infection. Several molecules have been found to interfere with S. aureus virulence regulation, especially those targeting the Agr quorum-sensing signaling molecule. These preliminary findings warrant further investigation and validation, with the goal of refining a compound that has broadspectrum inhibitory effects on most S. aureus strains and Agr subtypes.
C1 [Khan, Burhan A.] NIAID, NIH, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT 59840 USA.
[Yeh, Anthony J.; Cheung, Gordon Y. C.; Otto, Michael] NIAID, NIH, Lab Human Bacterial Pathogenesis, Bethesda, MD 20892 USA.
RP Otto, M (reprint author), NIAID, NIH, Lab Human Bacterial Pathogenesis, Bldg 33,1W10,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM motto@niaid.nih.gov
OI Otto, Michael/0000-0002-2222-4115
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases (NIAID), The National Institutes of Health (NIH);
NIAID
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases (NIAID), The
National Institutes of Health (NIH). BA Khan and AJ Yeh have post
baccalaureate fellowships from the NIAID. 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 133
TC 13
Z9 13
U1 3
U2 40
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD MAY
PY 2015
VL 24
IS 5
BP 689
EP 704
DI 10.1517/13543784.2015.1019062
PG 16
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CF6EF
UT WOS:000352648800008
PM 25704585
ER
PT J
AU Nikolaeva, D
Draper, SJ
Biswas, S
AF Nikolaeva, Daria
Draper, Simon J.
Biswas, Sumi
TI Toward the development of effective transmission-blocking vaccines for
malaria
SO EXPERT REVIEW OF VACCINES
LA English
DT Review
DE genome; malaria; membrane feeding assay; Plasmodium falciparum;
transmission-blocking vaccine
ID PARASITE PLASMODIUM-FALCIPARUM; GAMETE-SURFACE PROTEIN; CELL-FREE
SYSTEM; MOSQUITO MIDGUT INVASION; IN-VIVO ELECTROPORATION; AERUGINOSA
EXOPROTEIN-A; MEMBRANE-FEEDING ASSAY; SEXUAL-STAGE ANTIGEN;
ANOPHELES-GAMBIAE; RECOMBINANT PROTEINS
AB The continued global burden of malaria can in part be attributed to a complex lifecycle, with both human hosts and mosquito vectors serving as transmission reservoirs. In preclinical models of vaccine-induced immunity, antibodies to parasite sexual-stage antigens, ingested in the mosquito blood meal, can inhibit parasite survival in the insect midgut as judged by ex vivo functional studies such as the membrane feeding assay. In an era of renewed political momentum for malaria elimination and eradication campaigns, such observations have fueled support for the development and implementation of so-called transmission-blocking vaccines. While leading candidates are being evaluated using a variety of promising vaccine platforms, the field is also beginning to capitalize on global '-omics' data for the rational genome-based selection and unbiased characterization of parasite and mosquito proteins to expand the candidate list. This review covers the progress and prospects of these recent developments.
C1 [Nikolaeva, Daria; Draper, Simon J.; Biswas, Sumi] Univ Oxford, Jenner Inst, Oxford OX3 7DQ, England.
[Nikolaeva, Daria] NIAID, Malaria Immunol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP Nikolaeva, D (reprint author), Univ Oxford, Jenner Inst, Old Rd Campus Res Bldg,Roosevelt Dr, Oxford OX3 7DQ, England.
EM daria.nikolaeva@ndm.ox.ac.uk
OI Draper, Simon/0000-0002-9415-1357
FU Intramural Research Program of the NIAID/NIH; UK Medical Research
Council Career Development Fellow [G1000527]; Jenner Investigator;
Lister Institute Research Prize Fellow
FX D Nikolaeva is a student of the NIH-Oxford/Cambridge Scholars Program;
this publication was supported in part by the Intramural Research
Program of the NIAID/NIH. SJ Draper is a UK Medical Research Council
Career Development Fellow (Grant G1000527), Jenner Investigator and
Lister Institute Research Prize Fellow. He is a named inventor on patent
applications covering malaria vaccines and immunization regimes. S
Biswas is a NDM Leadership Fellow and Junior Research Fellow of St
Catherine's College, Oxford University. The authors have no 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 214
TC 12
Z9 12
U1 3
U2 25
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1476-0584
EI 1744-8395
J9 EXPERT REV VACCINES
JI Expert Rev. Vaccines
PD MAY
PY 2015
VL 14
IS 5
BP 653
EP 680
DI 10.1586/14760584.2015.993383
PG 28
WC Immunology
SC Immunology
GA CF8JJ
UT WOS:000352804000004
PM 25597923
ER
PT J
AU Wang, LH
Lingappan, K
Jiang, WW
Couroucli, XI
Welty, SE
Shivanna, B
Barrios, R
Wang, GD
Khan, MF
Gonzalez, FJ
Roberts, LJ
Moorthy, B
AF Wang, Lihua
Lingappan, Krithika
Jiang, Weiwu
Couroucli, Xanthi I.
Welty, Stephen E.
Shivanna, Binoy
Barrios, Roberto
Wang, Gangduo
Khan, M. Firoze
Gonzalez, Frank J.
Roberts, L. Jackson
Moorthy, Bhagavatula
TI Disruption of cytochrome P4501A2 in mice leads to increased
susceptibility to hyperoxic lung injury
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Acute lung injury; CYP1A2; ARDS; Oxidative stress; Free radicals
ID RESPIRATORY-DISTRESS-SYNDROME; POLYCYCLIC AROMATIC-HYDROCARBONS;
OXIDATIVE STRESS; OXYGEN-TOXICITY; PREMATURE-INFANTS; GENE-EXPRESSION;
NEWBORN MICE; IN-VIVO; INDUCTION; PULMONARY
AB Hyperoxia contributes to acute lung injury in diseases such as acute respiratory distress syndrome. Cytochrome P450 (CYP) lA enzymes have been implicated in hyperoxic lung injury, but the mechanistic role of CYP1A2 in pulmonary injury is not known. We hypothesized that mice lacking the gene Cypl a2 (which is predominantly expressed in the liver) will be more sensitive to lung injury and inflammation mediated by hyperoxia and that CYP1A2 will play a protective role by attenuating lipid peroxidation and oxidative stress in the lung. Eight- to ten-week-old WT (C57BL/6) or Cyp1a2(-/-) mice were exposed to hyperoxia ( > 95% O-2) or maintained in room air for 24-72 h. Lung injury was assessed by determining the ratio of lung weight/body weight (LW/BW) and by histology. Extent of inflammation was determined by measuring the number of neutrophils in the lung as well as cytokine expression. The Cyp1a2(-/-) mice under hyperoxic conditions showed increased LW/BW ratios, lung injury, neutrophil infiltration, and IL-6 and TNF-alpha levels and augmented lipid peroxidation, as evidenced by increased formation of malondialdehyde- and 4-hydroxynonenal-protein adducts and pulmonary isofurans compared to WT mice. In vitro experiments showed that the F-2-isoprostane PGF(2)-alpha is metabolized by CYP1A2 to a dinor metabolite, providing evidence for a catalytic role for CYP1A2 in the metabolism of F-2-isoprostanes. In summary, our results support the hypothesis that hepatic CYP1A2 plays a critical role in the attenuation of hyperoxic lung injury by decreasing lipid peroxidation and oxidative stress in vivo. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Wang, Lihua; Lingappan, Krithika; Jiang, Weiwu; Couroucli, Xanthi I.; Welty, Stephen E.; Shivanna, Binoy; Moorthy, Bhagavatula] Texas Childrens Hosp, Baylor Coll Med, Dept Pediat, Div Neonatal Perinatal Med, Houston, TX 77030 USA.
[Barrios, Roberto] Houston Methodist Res Inst, Dept Pathol, Houston, TX 77030 USA.
[Wang, Gangduo; Khan, M. Firoze] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
[Gonzalez, Frank J.] NCI, Mol Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Roberts, L. Jackson] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37240 USA.
RP Moorthy, B (reprint author), Texas Childrens Hosp, Baylor Coll Med, Dept Pediat, Div Neonatal Perinatal Med, Houston, TX 77030 USA.
EM bmoorthy@bcm.edu
FU National Institutes of Health [ES-009132, HL-112516, HL-087174,
ES-019689, HL-088343]; Center for Translational Environmental Health
Research [P30ES023512]
FX This work was supported in part by funds from RO1 grants from the
National Institutes of Health (ES-009132, HL-112516, HL-087174, and
ES-019689) to B.M., HL-088343 to X.I.C., and the Center for
Translational Environmental Health Research, P30ES023512.
NR 65
TC 5
Z9 6
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD MAY
PY 2015
VL 82
BP 147
EP 159
DI 10.1016/j.freeradbiomed.2015.01.019
PG 13
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA CF8PF
UT WOS:000352823700013
PM 25680282
ER
PT J
AU Liu, CY
Chen, D
Bluemke, DA
Wu, CO
Teixido-Tura, G
Chugh, A
Vasu, S
Lima, JAC
Hundley, WG
AF Liu, Chia-Ying
Chen, Doris
Bluemke, David A.
Wu, Colin O.
Teixido-Tura, Gisela
Chugh, Atul
Vasu, Sujethra
Lima, Joao A. C.
Hundley, W. Gregory
TI Evolution of Aortic Wall Thickness and Stiffness With Atherosclerosis
Long-Term Follow Up From the Multi-Ethnic Study of Atherosclerosis
SO HYPERTENSION
LA English
DT Article
DE hypertension; magnetic resonance imaging; vascular stiffness
ID INTIMA-MEDIA THICKNESS; CAROTID ARTERIES; RISK; AGE; DISTENSIBILITY;
DISEASE; ADULTS; RACE; MRI; SEX
AB The study was performed to determine age, sex, and time-dependent changes in aortic wall thickness (AWT) and to evaluate cross-sectional associations between AWT and arterial stiffness in older adults. Three hundred seventy-one longitudinal and 426 cross-sectional measurements of AWT from cardiovascular magnetic resonance imaging studies conducted within the Multi-Ethnic Study of Atherosclerosis were analyzed at 2 points in time, in 2000 to 2002 and then again from follow-up examinations in 2010 to 2012. Aortic wall thickness was determined from a double inversion recovery black-blood fast spin-echo sequence, and aortic stiffness was measured from a phase-contrast cine gradient echo sequence. The thickness of the midthoracic descending aortic wall was measured and correlated to distensibility of the ascending aorta and aortic pulse wave velocity. The average rate of AWT change was 0.032 mm/y. The increase in AWT was greater for those aged 45 to 54 years relative to individuals older than 55 years (P trend<0.001). Ascending aortic distensibility was lower (P<0.001) and pulse wave velocity was higher (P=0.012) for hypertensive subjects. After adjustment for traditional risk factors, distensibility of the ascending aorta was significantly related to AWT in participants without hypertension. Hypertension was associated with increased aortic stiffness independent of aortic wall thickness.
C1 [Liu, Chia-Ying; Bluemke, David A.] NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Chen, Doris; Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Univ Hosp, Dept Radiol, Baltimore, MD 21287 USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Teixido-Tura, Gisela] Univ Autonoma Barcelona, Dept Cardiol, Hosp Gen Univ Vall dHebron, E-08193 Barcelona, Spain.
[Chugh, Atul] Univ Louisville, Sch Med, Div Cardiovasc Med, Louisville, KY 40292 USA.
[Vasu, Sujethra; Hundley, W. Gregory] Wake Forest Univ, Dept Internal Med, Div Cardiovasc Med, Winston Salem, NC 27109 USA.
RP Hundley, WG (reprint author), Wake Forest Hlth Sci, Div Cardiovasc Med, 1 Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM ghundley@wakehealth.edu
OI Teixido-Tura, Gisela/0000-0003-4714-2420; Bluemke,
David/0000-0002-8323-8086
FU National Heart, Lung, and Blood Institute [N01-HC-95165, N01-HC-95168];
[R01 HL076438]
FX This research was supported by contracts N01-HC-95165, N01-HC-95168,
from the National Heart, Lung, and Blood Institute and by grant R01
HL076438.
NR 15
TC 3
Z9 3
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0194-911X
EI 1524-4563
J9 HYPERTENSION
JI Hypertension
PD MAY
PY 2015
VL 65
IS 5
BP 1015
EP 1019
DI 10.1161/HYPERTENSIONAHA.114.05080
PG 5
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA CF4AJ
UT WOS:000352490400095
PM 25776078
ER
PT J
AU Morris, BJ
Willcox, BJ
Tranah, GJ
Chen, R
Masaki, KH
He, Q
Willcox, DC
Allsopp, R
Moisyad, S
Poon, LW
Newman, AB
Harris, TB
Cummings, SR
Liu, Y
Parimi, N
Evans, DS
Donlon, TA
AF Morris, B. J.
Willcox, B. J.
Tranah, G. J.
Chen, R.
Masaki, K. H.
He, Q.
Willcox, D. C.
Allsopp, R.
Moisyad, S.
Poon, L. W.
Newman, A. B.
Harris, T. B.
Cummings, S. R.
Liu, Y.
Parimi, N.
Evans, D. S.
Donlon, T. A.
TI FOXO3 GENOTYPE INCREASES LIFESPAN BY A MAJOR EFFECT ON CARDIOVASCULAR
MORTALITY
SO HYPERTENSION
LA English
DT Meeting Abstract
CT 36th Annual Scientific Meeting of the
High-Blood-Pressure-Research-Council-of-Australia (HBPRCA)
CY NOV 26-28, 2014
CL Adelaide, AUSTRALIA
SP High Blood Pressure Res Council Australia
C1 [Morris, B. J.; Chen, R.; Masaki, K. H.; He, Q.; Donlon, T. A.] Kuakini Med Ctr, Dept Res, Honolulu, HI USA.
[Morris, B. J.; Masaki, K. H.] Univ Hawaii, John A Burns Sch Med, Dept Geriatr, Honolulu, HI 96822 USA.
[Morris, B. J.] Univ Sydney, Sch Med Sci & Bosch Inst, Basic & Clin Genom Lab, Sydney, NSW 2006, Australia.
[Tranah, G. J.; Cummings, S. R.; Parimi, N.; Evans, D. S.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Willcox, D. C.] Okinawa Int Univ, Dept Human Welf, Okinawa, Japan.
[Allsopp, R.; Moisyad, S.] Univ Hawaii, Inst Biogenesis Res, Honolulu, HI 96822 USA.
[Poon, L. W.] Univ Georgia, Inst Gerontol, Athens, GA 30602 USA.
[Newman, A. B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Harris, T. B.] NIA, Neurogenet Lab, Intramural Res Program, Bethesda, MD 20892 USA.
[Liu, Y.] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0194-911X
EI 1524-4563
J9 HYPERTENSION
JI Hypertension
PD MAY
PY 2015
VL 65
IS 5
BP E29
EP E30
PG 2
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA CF4AJ
UT WOS:000352490400018
ER
PT J
AU Rudy, BJ
Kapogiannis, BG
Worrell, C
Squires, K
Bethel, J
Li, S
Wilson, CM
Agwu, A
Emmanuel, P
Price, G
Hudey, S
Goodenow, MM
Sleasman, JW
AF Rudy, Bret J.
Kapogiannis, Bill G.
Worrell, Carol
Squires, Kathleen
Bethel, James
Li, Su
Wilson, Craig M.
Agwu, Allison
Emmanuel, Patricia
Price, Georgine
Hudey, Stephanie
Goodenow, Maureen M.
Sleasman, John W.
CA Adolescent Trials Network HIV AIDS
TI Immune Reconstitution but Persistent Activation After 48 Weeks of
Antiretroviral Therapy in Youth With Pre-Therapy CD4 > 350 in ATN 061
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE adolescents; antiretroviral therapy; immune reconstitution; inflammation
ID T-CELL-ACTIVATION; VIRUS-INFECTED PATIENTS; PATIENT-RELATED RISKS;
HIV-INFECTION; MICROBIAL TRANSLOCATION; UNITED-STATES; VIRAL LOAD;
THYMIC OUTPUT; ADOLESCENTS; RNA
AB Background: Measures of immune outcomes in youth who initiate combination antiretroviral therapy (cART) early in HIV infection are limited.
Design: Adolescent Trials Network 061 examined changes over 48 weeks of cART in T-cell subsets and markers of T-cell and macrophage activation in subjects with pre-therapy CD4. 350 cells/mm(3). All subjects had optimal viral suppression from weeks 24 through 48.
Methods: Subjects (n = 48) initiated cART with tenofovir/emtricitabine plus ritonavir-boosted atazanavir. Data were collected at baseline and weeks 12, 24, and 48. Trends were compared to uninfected controls.
Results: Significant increases over 48 weeks were noted in all CD4 populations, including total, naive, central memory (CM), and effector memory RO (EM RO) and effector memory RA (EM RA), whereas numbers of CM and EM RO CD8 cells declined significantly. By week 48, CD4 naive cells were similar to controls, whereas CM CD4 cells remained significantly lower and EM RO and EM RA subsets were significantly higher. CD38 and HLA DR expression, both individually and when co-expressed, decreased over 48 weeks of cART on CD8 cells but remained significantly higher than controls at week 48. In contrast, markers of macrophage activation measured by sCD14 and sCD163 in plasma did not change with cART and were significantly higher than controls.
Conclusions: In youth initiating early cART, CD4 cell reconstitution is robust with decreases in CD8 cells. However, CD8 T-cell and macrophage activation persists at higher levels than uninfected controls.
C1 [Rudy, Bret J.] NYU, Sch Med, New York, NY USA.
[Kapogiannis, Bill G.; Worrell, Carol] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Squires, Kathleen] Thomas Jefferson Univ, Sidney Kimmel Med Coll, Philadelphia, PA 19107 USA.
[Bethel, James; Li, Su; Price, Georgine] Westat Corp, Rockville, MD USA.
[Wilson, Craig M.] Univ Alabama Birmingham, Birmingham, AL USA.
[Agwu, Allison] Johns Hopkins Sch Med, Baltimore, MD USA.
[Emmanuel, Patricia; Hudey, Stephanie] Univ S Florida, Sch Med, Tampa, FL 33620 USA.
[Goodenow, Maureen M.] Univ Florida, Hlth Sci Ctr, Gainesville, FL USA.
[Sleasman, John W.] Duke Univ, Sch Med, Durham, NC USA.
RP Rudy, BJ (reprint author), NYULMC Pediat, 145 E 32nd St,Room 1408, New York, NY 10016 USA.
EM bret.rudy@nyumc.org
FU PHS National Institute of Drug Abuse [DA031017]; Adolescent Trials
Network for HIV/AIDS Interventions (ATN) from the National Institutes of
Health through the Eunice Kennedy Shriver National Institute of Child
Health and Human Development [U01 HD 040533, U01 HD 040474]; National
Institute on Drug Abuse; National Institute on Mental Health; National
Institute of Allergy and Infectious Diseases; Eunice Kennedy Shriver
National Institute of Child Health and Human Development; National
Institute of Mental Health [U01 A1068632]; [R01 DA DA031017]
FX Supported in part by PHS National Institute of Drug Abuse DA031017 and
by The Adolescent Trials Network for HIV/AIDS Interventions (ATN) from
the National Institutes of Health (U01 HD 040533 and U01 HD 040474)
through the Eunice Kennedy Shriver National Institute of Child Health
and Human Development (B.G.K.), with supplemental funding from the
National Institutes on Drug Abuse (K. Davenny) and Mental Health (P.
Brouwers and S. Allison). It was also supported by R01 DA DA031017
(M.M.G. and J.W.S.). The protocol was co-endorsed by the International
Maternal Pediatric Adolescent AIDS Clinical Trials Group. Support for
the International Maternal Pediatric Adolescent AIDS Clinical Trials
Group (IMPAACT) was provided by the National Institute of Allergy and
Infectious Diseases, the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, and the National Institute of Mental
Health (U01 A1068632). The study was scientifically reviewed by the
ATN's Therapeutic Leadership Group. Network, scientific, and logistical
support was provided by the ATN Coordinating Center (C.M.W. and C.
Partlow) at The University of Alabama at Birmingham. Network operations
and analytic support was provided by the ATN Data and Operations Center
at Westat, Inc. (J. Korelitz, B. Driver, and G.P.).
NR 53
TC 6
Z9 6
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD MAY 1
PY 2015
VL 69
IS 1
BP 52
EP 60
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA CG1LE
UT WOS:000353033300015
PM 25942459
ER
PT J
AU Raine, A
Portnoy, J
Liu, JH
Mahoomed, T
Hibbeln, JR
AF Raine, Adrian
Portnoy, Jill
Liu, Jianghong
Mahoomed, Tashneem
Hibbeln, Joseph R.
TI Reduction in behavior problems with omega-3 supplementation in children
aged 8-16 years: a randomized, double-blind, placebo-controlled,
stratified, parallel-group trial
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Omega-3; externalizing; internalizing; aggression; randomized trial
ID PROACTIVE AGGRESSION QUESTIONNAIRE; ATTENTION-DEFICIT/HYPERACTIVITY
DISORDER; BRAIN STRUCTURE ABNORMALITIES; YOUNG-ADULT PRISONERS; CONDUCT
PROBLEMS; ANTISOCIAL-BEHAVIOR; UNEMOTIONAL TRAITS; ADOLESCENT BOYS;
OMEGA-3-FATTY-ACIDS; PSYCHOPATHOLOGY
AB BackgroundWhile limited evidence suggests that omega-3 supplementation may reduce antisocial behavior in children, studies have not reported on posttreatment follow-up and most treatment periods have been of short duration. This study tests the hypothesis that omega-3 supplementation over 6months will reduce behavior problems in children both at the end of treatment and at 6months post treatment.
MethodsIn this randomized, double-blind, placebo-controlled, stratified, parallel-group trial, a community sample of 8-16year old children were randomized into a treatment group (N=100) and a placebo-control group (N=100). The supplementation consisted of a fruit drink containing 1g/day of omega-3 or a placebo consisting of the same fruit drink without omega-3. Participants, caregivers, and research assistants were blinded to group assignment. The primary outcome measures of externalizing and internalizing behavior problems were reported by both caregivers and their children in a laboratory setting at 0months (baseline), 6months (end of treatment) and 12months (6months post treatment), together with the secondary outcome measures of parental antisocial behavior. Data were analyzed on an intention-to-treat basis including all participants. Trial registration: ClinicalTrials.gov:
ResultsSignificant groupxtime interactions were observed with the treatment group showing long-term improvements in child behavior problems. The average posttreatment effect size was d=-.59. Effects were documented for parent reports, but with the exception of proactive and reactive aggression, child-report data were nonsignificant. Parents whose children took omega-3 showed significant posttreatment reductions in their own antisocial and aggressive behavior. This improvement in caregiver behavior partly mediated the improvements observed in child behavior.
ConclusionsFindings provide initial evidence that omega-3 supplementation can produce sustained reductions in externalizing and internalizing behavior problems. Results are the first to report improvements in caregiver behavior, and to establish this improvement as a part-mechanism for the efficacy of omega-3.
C1 [Raine, Adrian; Portnoy, Jill] Univ Penn, Dept Criminol, Philadelphia, PA 19104 USA.
[Raine, Adrian; Portnoy, Jill] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Raine, Adrian; Portnoy, Jill] Univ Penn, Dept Psychol, Philadelphia, PA 19104 USA.
[Liu, Jianghong] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
[Mahoomed, Tashneem] Joint Child Hlth Project, Quatre Bornes, Quatre Bornes, Mauritius.
[Hibbeln, Joseph R.] NIAAA, Sect Nutr Neurosci, Bethesda, MD USA.
RP Raine, A (reprint author), Univ Penn, Dept Criminol, 3809 Walnut St, Philadelphia, PA 19104 USA.
EM araine@sas.upenn.edu
FU Smartfish AA, Oslo, Norway; Intramural Research Program of the National
Institute on Alcohol Abuse and Alcoholism, Rockville, MD; University of
Pennsylvania
FX This study was made possible in part by funding from Smartfish AA, Oslo,
Norway, who produced the omega-3 supplement and placebo drink used in
this study. It was also supported in part by the Intramural Research
Program of the National Institute on Alcohol Abuse and Alcoholism,
Rockville, MD, and the University of Pennsylvania. The authors wish to
thank Shameem Oomur, Shameemah Golamnobee, and Joelle Rawoteea for their
assistance in data collection. The authors have declared that they have
no competing or potential conflicts of interest.
NR 48
TC 13
Z9 13
U1 5
U2 30
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
EI 1469-7610
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD MAY
PY 2015
VL 56
IS 5
BP 509
EP 520
DI 10.1111/jcpp.12314
PG 12
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA CF4YQ
UT WOS:000352560900003
PM 25146492
ER
PT J
AU Shinomiya, K
Tokura, K
Kimura, E
Takai, M
Harikai, N
Yoshida, K
Yanagidaira, K
Ito, Y
AF Shinomiya, Kazufusa
Tokura, Koji
Kimura, Emiru
Takai, Midori
Harikai, Naoki
Yoshida, Kazunori
Yanagidaira, Kazuhiro
Ito, Yoichiro
TI Design of a coil satellite centrifuge and its performance on
counter-current chromatographic separation of 4-methylumbelliferyl sugar
derivatives with polar organic-aqueous two-phase solvent systems
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article; Proceedings Paper
CT 8th International Conference on Countercurrent Chromatography (CCC)
CY JUL 23-25, 2014
CL Uxbridge, ENGLAND
DE Counter-current chromatography; Instrumentation; Coil satellite
centrifuge; Partition efficiency; Separation of sugar derivatives
ID PLANET CENTRIFUGE; ROTARY SEALS; APPARATUS; PROTEINS
AB A new high-speed counter-current chromatograph, named coil satellite centrifuge (CSC), was designed and fabricated in our laboratory. The CSC apparatus produces the satellite motion such that the coiled column simultaneously rotates around the sun axis (the angular velocity, omega(1)), the planet axis (omega(2)) and the satellite axis (the central axis of the column) (omega(3)). In order to achieve this triplicate rotary motion without twisting of the flow tube, the rotation of each axis was determined by the following formula: omega(1) = omega(2) + omega(3). This relation enabled to lay out the flow tube without twisting by the simultaneous rotation of three axes. The flow tube was introduced from the bottom side of the apparatus into the sun axis of the first rotary frame reaching the upper side of the planet axis and connected to the column in the satellite axis. The performance of the apparatus was examined on separation of 4-methylumbelliferyl (MU) sugar derivatives as test samples with organic-aqueous two-phase solvent systems composed of ethyl acetate/1-butanol/water (3:2:5, v/v) for lower phase mobile and (1:4:5, v/v) for upper phase mobile. With lower phase mobile, five 4-MU sugar derivatives including beta-D-cellobioside (Cel), beta-D-glucopyranoside, alpha-D-mannopyranoside, beta-D-fucopyranoside and alpha-L-fucopyranoside (alpha-L-Fuc) were separated with the combined rotation around each axis at counterclockwise (CCW) (omega(1)) - CCW (omega(2)) - CCW (omega(3)) by the flow tube distribution. With upper phase mobile, three 4-MU sugar derivatives including alpha-L-Fuc, beta-D-galactopyranoside and Cel were separated with the combined rotation around each axis at clockwise (CW) (omega(1)) - CW (omega(2)) - CW (omega(3)) by the flow tube distribution. A series of experiments on peak resolution and stationary phase retention revealed that better partition efficiencies were obtained at the flow rate of 0.5 mL/min (column 1) and 0.8 mL/min (column 2) for lower phase mobile and 0.2 mL/min (column 1) and 0.4 mL/min (column 2) for upper phase mobile when using the left-handed multilayer coil (total capacity: 57.0 mL for column 1 and 75.0 mL for column 2) under the rotation speeds of approximately omega(1) =300 rpm, omega(2) = 150 rpm and omega(3) = 150 rpm. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Shinomiya, Kazufusa; Kimura, Emiru; Takai, Midori; Harikai, Naoki] Nihon Univ, Sch Pharm, Funabashi, Chiba 2748555, Japan.
[Tokura, Koji; Yoshida, Kazunori; Yanagidaira, Kazuhiro] Nihon Univ, Coll Sci & Technol, Funabashi, Chiba 2748501, Japan.
[Ito, Yoichiro] NHLBI, Lab Bioseparat Technol, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Shinomiya, K (reprint author), Nihon Univ, Sch Pharm, 7-7-1 Narashinodai, Funabashi, Chiba 2748555, Japan.
EM shinomiya.kazufusa@nihon-u.ac.jp
FU Intramural NIH HHS [ZIA HL006022-04]
NR 17
TC 3
Z9 3
U1 4
U2 17
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
EI 1873-3778
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD MAY 1
PY 2015
VL 1392
BP 48
EP 55
DI 10.1016/j.chroma.2015.03.011
PG 8
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA CG2CG
UT WOS:000353081900006
PM 25805719
ER
PT J
AU Jahangir, E
Lipworth, L
Edwards, TL
Kabagambe, EK
Mumma, MT
Mensah, GA
Fazio, S
Blot, WJ
Sampson, UKA
AF Jahangir, Eiman
Lipworth, Loren
Edwards, Todd L.
Kabagambe, Edmond K.
Mumma, Michael T.
Mensah, George A.
Fazio, Sergio
Blot, William J.
Sampson, Uchechukwu K. A.
TI Smoking, sex, risk factors and abdominal aortic aneurysms: a prospective
study of 18 782 persons aged above 65 years in the Southern Community
Cohort Study
SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH
LA English
DT Article
ID COST-EFFECTIVENESS; OLDER-ADULTS; WOMEN; PREVALENCE; HEALTH; MORTALITY;
MEN; PROGRAM; TROMSO; TRIAL
AB Background Abdominal aortic aneurysm (AAA) is a leading cause of death in the USA. We evaluated the incidence and predictors of AAA in a prospectively followed cohort.
Methods We calculated age-adjusted AAA incidence rates (IR) among 18 782 participants aged >= 65 years in the Southern Community Cohort Study who received Medicare coverage from 1999-2012, and assessed predictors of AAA using multivariable Cox proportional hazards models, overall and stratified by sex, adjusting for demographic, lifestyle, socioeconomic, medical and other factors. HRs and 95% CIs were calculated for AAA in relation to factors ascertained at enrolment.
Results Over a median follow-up of 4.94 years, 281 cases were identified. Annual IR was 153/100 000, 401, 354 and 174 among blacks, whites, men and women, respectively. AAA risk was lower among women (HR 0.48, 95% CI 0.36 to 0.65) and blacks (HR 0.51, 95% CI 0.37 to 0.69). Smoking was the strongest risk factor (former: HR 1.91, 95% CI 1.27 to 2.87; current: HR 5.55, 95% CI 3.67 to 8.40), and pronounced in women (former: HR 3.4, 95% CI 1.83 to 6.31; current: HR 9.17, 95% CI 4.95 to 17). A history of hypertension (HR 1.44, 95% CI 1.04 to 2.01) and myocardial infarction or coronary artery bypass surgery (HR 1.9, 95% CI 1.37 to 2.63) was negatively associated, whereas a body mass index > 25 kg/m(2) (HR 0.72; 95% CI 0.53 to 0.98) was protective. College education (HR 0.6, 95% CI 0.37 to 0.97) and black race (HR 0.44, 95% CI 0.28 to 0.67) were protective among men.
Conclusions Smoking is a major risk factor for incident AAA, with a strong and similar association between men and women. Further studies are needed to evaluate benefits of ultrasound screening for AAA among women smokers.
C1 [Jahangir, Eiman; Lipworth, Loren; Edwards, Todd L.; Kabagambe, Edmond K.; Blot, William J.; Sampson, Uchechukwu K. A.] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN USA.
[Jahangir, Eiman] Univ Queensland, Sch Med, Ochsner Clin Sch, John Ochsner Heart & Vasc Inst, New Orleans, LA 70121 USA.
[Mumma, Michael T.; Blot, William J.] Int Epidemiol Inst, Rockville, MD USA.
[Mensah, George A.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Fazio, Sergio] Oregon Hlth & Sci Univ, Knight Cardiovasc Inst, Ctr Prevent Cardiol, Portland, OR 97201 USA.
[Sampson, Uchechukwu K. A.] Vanderbilt Univ, Med Ctr, Dept Pathol Microbiol & Immunol, Nashville, TN USA.
[Sampson, Uchechukwu K. A.] Vanderbilt Univ, Med Ctr, Dept Radiol & Radiol Sci, Nashville, TN 37232 USA.
RP Jahangir, E (reprint author), Univ Queensland, Sch Med, Ochsner Clin Sch, John Ochsner Heart & Vasc Inst, 1514 Jefferson Highway, New Orleans, LA 70121 USA.
EM ejahangir@ochsner.org
RI Jahangir, Eiman/P-1053-2015
OI Jahangir, Eiman/0000-0001-6944-5321
FU Foundation for the National Institutes of Health [2T32HL007411-31];
National Institute of Health [HL106845, HL57986]; Pepsi Co [R01
CA092447]
FX Funding Institution: Foundation for the National Institutes of Health.
2T32HL007411-31. National Institute of Health. HL106845 and HL57986. R01
CA092447. Pepsi Co
NR 41
TC 9
Z9 9
U1 3
U2 10
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0143-005X
EI 1470-2738
J9 J EPIDEMIOL COMMUN H
JI J. Epidemiol. Community Health
PD MAY
PY 2015
VL 69
IS 5
BP 481
EP 488
DI 10.1136/jech-2014-204920
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CF4TR
UT WOS:000352545300012
PM 25563744
ER
PT J
AU Margolis, KL
Evans, GW
Schwartz, AV
Fleg, J
AF Margolis, Karen L.
Evans, Gregory W.
Schwartz, Ann V.
Fleg, Jerome
TI Intensive BP Control, Falls, and Fractures: Response to Jolobe (MS
#17620)
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Letter
C1 [Margolis, Karen L.] HealthPartners Inst Educ & Res, Minneapolis, MN 55440 USA.
[Evans, Gregory W.] Wake Forest Sch Med, Winston Salem, NC USA.
[Schwartz, Ann V.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Fleg, Jerome] NHLBI, Bethesda, MD 20892 USA.
RP Margolis, KL (reprint author), HealthPartners Inst Educ & Res, Box 1524,Mailstop 23301A, Minneapolis, MN 55440 USA.
EM karen.l.margolis@healthpartners.com
NR 1
TC 0
Z9 0
U1 0
U2 0
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 MAY
PY 2015
VL 30
IS 5
BP 547
EP 547
DI 10.1007/s11606-015-3191-z
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA CF7CJ
UT WOS:000352713400007
PM 25650261
ER
PT J
AU Chawla, N
Urato, M
Ambs, A
Schussler, N
Hays, RD
Clauser, SB
Zaslavsky, AM
Walsh, K
Schwartz, M
Halpern, M
Gaillot, S
Goldstein, EH
Arora, NK
AF Chawla, Neetu
Urato, Matthew
Ambs, Anita
Schussler, Nicola
Hays, Ron D.
Clauser, Steven B.
Zaslavsky, Alan M.
Walsh, Kayo
Schwartz, Margot
Halpern, Michael
Gaillot, Sarah
Goldstein, Elizabeth H.
Arora, Neeraj K.
TI Unveiling SEER-CAHPSA (R): A New Data Resource for Quality of Care
Research
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE patient experiences; cancer; chronic disease; data linkage; Medicare
claims; quality of care; CAHPS; SEER registry
ID MEDICARE CONSUMER ASSESSMENT; HEALTH-CARE; PATIENT EXPERIENCES;
MULTILEVEL FACTORS; BENEFICIARIES; CONTINUUM; PROVIDERS
AB Since 1990, the National Cancer Institute (NCI) and Centers for Medicare and Medicaid Services (CMS) have collaborated to create linked data resources to improve our understanding of patterns of care, health care costs, and trends in utilization. However, existing data linkages have not included measures of patient experiences with care.
To describe a new resource for quality of care research based on a linkage between the Medicare Consumer Assessment of Healthcare Providers and Systems (CAHPSA (R)) patient surveys and the NCI's Surveillance, Epidemiology and End Results (SEER) data.
This is an observational study of CAHPS respondents and includes both fee-for-service and Medicare Advantage beneficiaries with and without cancer. The data linkage includes: CAHPS survey data collected between 1998 and 2010 to assess patient reports on multiple aspects of their care, such as access to needed and timely care, doctor communication, as well as patients' global ratings of their personal doctor, specialists, overall health care, and their health plan; SEER registry data (1973-2007) on cancer site, stage, treatment, death information, and patient demographics; and longitudinal Medicare claims data (2002-2011) for fee-for-service beneficiaries on utilization and costs of care.
In total, 150,750 respondents were in the cancer cohort and 571,318 were in the non-cancer cohort.
The data linkage includes SEER data on cancer site, stage, treatment, death information, and patient demographics, in addition to longitudinal data from Medicare claims and information on patient experiences from CAHPS surveys.
Sizable proportions of cases from common cancers (e.g., breast, colorectal, prostate) and short-term survival cancers (e.g., pancreas) by time since diagnosis enable comparisons across the cancer care trajectory by MA vs. FFS coverage.
SEER-CAHPS is a valuable resource for information about Medicare beneficiaries' experiences of care across different diagnoses and treatment modalities, and enables comparisons by type of insurance.
C1 [Chawla, Neetu; Ambs, Anita; Arora, Neeraj K.] NCI, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[Urato, Matthew; Schwartz, Margot; Halpern, Michael] RTI Int, Res Triangle Pk, NC USA.
[Schussler, Nicola] Informat Management Serv Inc, Calverton, MD USA.
[Hays, Ron D.] Univ Calif Los Angeles, Dept Med, Div Gen Internal Med & Hlth Serv Res, Los Angeles, CA 90024 USA.
[Clauser, Steven B.] Patient Ctr Outcomes Res Inst, Washington, DC USA.
[Zaslavsky, Alan M.; Walsh, Kayo] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Gaillot, Sarah; Goldstein, Elizabeth H.] Ctr Medicare & Medicaid Serv, Baltimore, MD USA.
RP Chawla, N (reprint author), NCI, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,3E450, Rockville, MD 20892 USA.
EM neetu.chawla@nih.gov
FU Indian Health Service in Alaska [Y1-PC-0064]; Connecticut Department of
Public Health [HHSN261201000024C]; Emory University [HSN261201000025C];
University of Iowa [HHSN261201000032C]; University of Medicine and
Dentistry of New Jersey [HHSN261201000027C]; University of Utah
[HHSN261201000026C]; Cancer Prevention Institute of California
[HHSN261201000140C]; University of Hawaii [HHSN261201000037C];
University of New Mexico [HHSN261201000033C]; Public Health Institute
[HHSN261201000034C]; University of Southern California
[HHSN261201000035C]; Fred Hutchinson Cancer Research Center
[HHSN261201000029C]; University of Kentucky Research Foundation
[HHSN261201000031C]; Wayne State University [HHSN261201000028C];
Louisiana State University Health Sciences Center [HHSN261201000030C]
FX SEER is supported by an interagency agreement with Indian Health Service
in Alaska (No. Y1-PC-0064) and the following contract agreements:
Connecticut Department of Public Health (No. HHSN261201000024C); Emory
University (No. HSN261201000025C); University of Iowa (No.
HHSN261201000032C); University of Medicine and Dentistry of New Jersey
(No. HHSN261201000027C); University of Utah (No. HHSN261201000026C);
Cancer Prevention Institute of California (No. HHSN261201000140C);
University of Hawaii (No. HHSN261201000037C); University of New Mexico
(No. HHSN261201000033C); Public Health Institute (No.
HHSN261201000034C); University of Southern California (No.
HHSN261201000035C); Fred Hutchinson Cancer Research Center (No.
HHSN261201000029C); University of Kentucky Research Foundation (No.
HHSN261201000031C); Wayne State University (No. HHSN261201000028C); and
Louisiana State University Health Sciences Center (No.
HHSN261201000030C). Data from this paper was presented at the Academy
Health Annual Research Meeting on June 8-10, 2014.
NR 25
TC 5
Z9 5
U1 0
U2 0
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 MAY
PY 2015
VL 30
IS 5
BP 641
EP 650
DI 10.1007/s11606-014-3162-9
PG 10
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA CF7CJ
UT WOS:000352713400020
PM 25586868
ER
PT J
AU Wendler, D
AF Wendler, David
TI "Targeted" Consent for Pragmatic Clinical Trials
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE informed consent; pragmatic trials; research; standard care
ID CHOICE
AB Research on interventions within the standard of care has enormous potential, yet it also raises several ethical and regulatory challenges. Perhaps the most important is determining what consent process is needed for these "pragmatic" clinical trials. Some argue that pragmatic clinical trials need to obtain in-depth research consent. This approach ensures that patients are informed, but may introduce substantial selection bias and disruption of clinical care. Others argue that trials limited to interventions within the standard of care do not need to obtain research consent at all. While this approach avoids the problems with in-depth consent, it results in patients not knowing whether they are in research. The present manuscript proposes a way to avoid both sets of concerns. It argues that consent for research needs to supplement appropriate consent for standard care only to the extent that the research differs from standard care. Hence, pragmatic trials designed to mirror clinical care can obtain consent with only minimal additions to consent for standard care. This conclusion suggests that it may be possible for many pragmatic trials to obtain consent that is ethically appropriate, satisfies research regulations, and does not introduce substantial selection bias or clinical disruption.
C1 NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Wendler, D (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM dwendler@nih.gov
FU NIH Clinical Center intramural funds
FX This work was supported by NIH Clinical Center intramural funds. The
views expressed herein are solely those of the author, and do not
represent the position or policy of the NIH or the U.S. government.
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PT J
AU Cataisson, C
Kitagawa, H
Hollander, C
Dennis, PA
Yuspa, SH
AF Cataisson, C.
Kitagawa, H.
Hollander, C.
Dennis, P. A.
Yuspa, S. H.
TI Rapamycin is a chemopreventive and chemotherapeutic agent for RAS-driven
epidermal squamous cell carcinoma: Evidence from mouse models
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Cataisson, C.; Hollander, C.; Yuspa, S. H.] NCI, Bethesda, MD 20892 USA.
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AU DiGiovanna, JJ
Tamura, D
Merideth, M
Khan, SG
Angra, D
Kraemer, KH
AF DiGiovanna, J. J.
Tamura, D.
Merideth, M.
Khan, S. G.
Angra, D.
Kraemer, K. H.
TI Premature menopause and hematologic neoplasms further characterize
xeroderma pigmentosum as a disorder of accelerated aging
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
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CL Atlanta, GA
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[Merideth, M.] NHGRI, Bethesda, MD 20892 USA.
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PT J
AU Elder, JT
Tsoi, LC
Iyer, MK
Stuart, PE
Swindell, WR
Gudjonsson, JE
Tejasvi, T
Sarkar, MK
Li, B
Ding, J
Voorhees, JJ
Kang, HM
Nair, RP
Chinnaiyan, AM
Abecasis, G
AF Elder, J. T.
Tsoi, L. C.
Iyer, M. K.
Stuart, P. E.
Swindell, W. R.
Gudjonsson, J. E.
Tejasvi, T.
Sarkar, M. K.
Li, B.
Ding, J.
Voorhees, J. J.
Kang, H. M.
Nair, R. P.
Chinnaiyan, A. M.
Abecasis, G.
TI Analysis of long non-coding RNAs highlights tissue-specific expression
patterns and epigenetic profiles in normal and psoriatic skin
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
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C1 [Elder, J. T.; Stuart, P. E.; Swindell, W. R.; Gudjonsson, J. E.; Tejasvi, T.; Sarkar, M. K.; Voorhees, J. J.; Nair, R. P.] Univ Michigan, Dermatol, Ann Arbor, MI 48109 USA.
[Elder, J. T.; Tejasvi, T.] Ann Arbor VA Hosp, Ann Arbor, MI USA.
[Tsoi, L. C.; Kang, H. M.; Abecasis, G.] Univ Michigan, Biostat, Ann Arbor, MI 48109 USA.
[Iyer, M. K.] Univ Michigan, Bioinformat, Ann Arbor, MI 48109 USA.
[Li, B.] Vanderbilt Univ, Nashville, TN 37235 USA.
[Ding, J.] NIH, Bethesda, MD 20892 USA.
[Chinnaiyan, A. M.] Univ Michigan, Pathol, Ann Arbor, MI 48109 USA.
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PU NATURE PUBLISHING GROUP
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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J9 J INVEST DERMATOL
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VL 135
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PT J
AU Gaiser, MR
Daily, K
Brownell, I
AF Gaiser, M. R.
Daily, K.
Brownell, I.
TI Blood levels of neuron specific enolase, chromogranin A, and circulating
tumor cells as Merkel cell carcinoma biomarkers
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
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[Gaiser, M. R.] Heidelberg Univ, Dept Dermatol, Heidelberg, Germany.
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Z9 0
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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VL 135
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MA 241
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UT WOS:000352783200242
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PT J
AU Glatz, M
Polley, EC
Simpson, EL
Kong, HH
AF Glatz, M.
Polley, E. C.
Simpson, E. L.
Kong, H. H.
TI Emollient therapy alters skin barrier and microbes in infants at risk
for developing atopic dermatitis
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Glatz, M.; Kong, H. H.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Polley, E. C.] NCI, Biometr Res Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Simpson, E. L.] Oregon Hlth & Sci Univ, Dermatol, Portland, OR 97201 USA.
NR 0
TC 1
Z9 1
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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J9 J INVEST DERMATOL
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VL 135
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MA 180
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UT WOS:000352783200181
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PT J
AU Kim, J
Nagato, G
Ogawa, Y
Udey, MC
Morasso, M
AF Kim, J.
Nagato, G.
Ogawa, Y.
Udey, M. C.
Morasso, M.
TI Keratinocytes devoid of DLX3 initiate psoriasis-like inflammation in
mice
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Kim, J.; Morasso, M.] NIAMS, NIH, Bethesda, MD USA.
[Nagato, G.; Ogawa, Y.; Udey, M. C.] NCI, NIH, Bethesda, MD 20892 USA.
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PU NATURE PUBLISHING GROUP
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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VL 135
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MA 669
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UT WOS:000352783200669
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PT J
AU Kobayashi, T
Glatz, M
Horiuchi, K
Doebel, T
Kaplan, D
Kong, HH
Amagai, M
Nagao, K
AF Kobayashi, T.
Glatz, M.
Horiuchi, K.
Doebel, T.
Kaplan, D.
Kong, H. H.
Amagai, M.
Nagao, K.
TI Dysbiotic microbiota drives atopic inflammation in Adam17(fl/fl)Sox9-Cre
mice
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Kobayashi, T.; Amagai, M.; Nagao, K.] Keio Univ, Sch Med, Dermatol, Tokyo, Japan.
[Kobayashi, T.; Glatz, M.; Doebel, T.; Kong, H. H.; Nagao, K.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Horiuchi, K.] Keio Univ, Sch Med, Orthoped Surg, Tokyo, Japan.
[Kaplan, D.] Univ Minnesota, Ctr Immunol, Dermatol, Minneapolis, MN USA.
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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J9 J INVEST DERMATOL
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PT J
AU Li, L
Cataisson, C
Flowers, B
Michalowski, A
Yuspa, SH
AF Li, L.
Cataisson, C.
Flowers, B.
Michalowski, A.
Yuspa, S. H.
TI Comparative evaluation of gene expression induced by RAS oncogenic
alleles in mouse and human keratinocytes
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
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PU NATURE PUBLISHING GROUP
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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J9 J INVEST DERMATOL
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PT J
AU Li, S
Klover, P
Thangapazham, RL
Wang, J
Moss, J
Darling, TN
AF Li, S.
Klover, P.
Thangapazham, R. L.
Wang, J.
Moss, J.
Darling, T. N.
TI MCP-1 is overexpressed by Tsc2-null skin fibroblasts in a mouse model of
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SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Li, S.; Klover, P.; Thangapazham, R. L.; Wang, J.; Darling, T. N.] Uniformed Serv Univ Hlth Sci, Dermatol, Bethesda, MD 20814 USA.
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PT J
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Natarajan, B
Salahuddin, T
Ng, Q
Doveikis, J
Playford, M
Lockshin, B
Kaplan, M
Gelfand, J
Mehta, NN
AF Naik, H. B.
Natarajan, B.
Salahuddin, T.
Ng, Q.
Doveikis, J.
Playford, M.
Lockshin, B.
Kaplan, M.
Gelfand, J.
Mehta, N. N.
TI Psoriasis area severity index score positively associates with vascular
inflammation by FDG PET/CT
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CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Naik, H. B.] NCI, Dermatol Branch, Bethesda, MD 20892 USA.
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[Playford, M.; Lockshin, B.] DermAssociates, Silver Spring, MD USA.
[Kaplan, M.] NIAMSD, Syst Autoimmun Branch, Bethesda, MD 20892 USA.
[Gelfand, J.] Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
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J9 J INVEST DERMATOL
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PT J
AU Nathan, N
Wang, J
Li, S
Cowen, EW
Haughey, M
Moss, J
Darling, TN
AF Nathan, N.
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Haughey, M.
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Darling, T. N.
TI Oral sirolimus improves tuberous sclerosis complex skin tumors without
evidence of resistance
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Nathan, N.; Wang, J.; Li, S.; Darling, T. N.] Uniformed Serv Univ Hlth Sci, Dept Dermatol, Bethesda, MD 20814 USA.
[Nathan, N.; Haughey, M.; Moss, J.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Cowen, E. W.] NIH, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
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J9 J INVEST DERMATOL
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PT J
AU Palazzo, E
Kellett, MD
Cataisson, C
Gormley, A
Bible, P
Pietroni, V
Radoja, N
Hwang, J
Blumenberg, M
Yuspa, SH
Morasso, M
AF Palazzo, E.
Kellett, M. D.
Cataisson, C.
Gormley, A.
Bible, P.
Pietroni, V.
Radoja, N.
Hwang, J.
Blumenberg, M.
Yuspa, S. H.
Morasso, M.
TI DLX3-dependent p53 signaling network controls keratinocyte cell cycle
and squamous tumor growth
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Palazzo, E.; Kellett, M. D.; Gormley, A.; Bible, P.; Pietroni, V.; Radoja, N.; Hwang, J.; Morasso, M.] NIH, Skin Biol Lab, Bethesda, MD 20892 USA.
[Cataisson, C.; Yuspa, S. H.] NIH, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Blumenberg, M.] NYU, Dept Dermatol, New York, NY 10016 USA.
RI Palazzo, Elisabetta/J-5287-2016
OI Palazzo, Elisabetta/0000-0002-0812-5524
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J9 J INVEST DERMATOL
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PT J
AU Pichard, D
Cardones, A
Chu, E
Kong, HH
AF Pichard, D.
Cardones, A.
Chu, E.
Kong, H. H.
TI Patients with sorafenib induced drug eruptions can be successfully
re-challenged
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Pichard, D.; Kong, H. H.] NCI, Dermatol Branch, CCR, NIH, Bethesda, MD 20892 USA.
[Cardones, A.] Duke Univ, Dermatol, Durham, NC USA.
[Chu, E.] Univ Penn, Dermatol, Philadelphia, PA 19104 USA.
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Z9 0
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
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J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2015
VL 135
SU 1
MA 240
BP S41
EP S41
PG 1
WC Dermatology
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GA CF8CO
UT WOS:000352783200241
ER
PT J
AU Scharschmidt, TC
Vasquez, KS
Truong, H
Gearty, SV
Pauli, ML
Nosbaum, A
Otto, M
Moon, JJ
Abbas, AK
Fischbach, MA
Rosenblum, MD
AF Scharschmidt, T. C.
Vasquez, K. S.
Truong, H.
Gearty, S. V.
Pauli, M. L.
Nosbaum, A.
Otto, M.
Moon, J. J.
Abbas, A. K.
Fischbach, M. A.
Rosenblum, M. D.
TI A wave of regulatory T cells into neonatal skin mediates tolerance to
commensal microbes
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Scharschmidt, T. C.; Vasquez, K. S.; Truong, H.; Gearty, S. V.; Pauli, M. L.; Nosbaum, A.; Rosenblum, M. D.] UCSF, Dermatol, San Francisco, CA USA.
[Abbas, A. K.] UCSF, Pathol, San Francisco, CA USA.
[Fischbach, M. A.] UCSF, Bioengn, San Francisco, CA USA.
[Otto, M.] NIAID, Bethesda, MD 20892 USA.
[Moon, J. J.] MGH, Ctr Immunol & Inflammatory Dis, Charlestown, MA USA.
NR 0
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Z9 0
U1 1
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
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J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2015
VL 135
SU 1
MA 011
BP S2
EP S2
PG 1
WC Dermatology
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GA CF8CO
UT WOS:000352783200012
ER
PT J
AU Tom, W
Eichenfield, LF
Playford, M
Admani, S
Natarajan, B
Mehta, NN
AF Tom, W.
Eichenfield, L. F.
Playford, M.
Admani, S.
Natarajan, B.
Mehta, N. N.
TI Characterization of lipoprotein composition and function in pediatric
psoriasis reveals a more atherogenic profile
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Tom, W.; Eichenfield, L. F.; Admani, S.] Univ Calif San Diego, Pediat & Med Dermatol, San Diego, CA 92103 USA.
[Tom, W.; Eichenfield, L. F.; Admani, S.] Rady Childrens Hosp, San Diego, CA USA.
[Playford, M.; Natarajan, B.; Mehta, N. N.] NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
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J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2015
VL 135
SU 1
MA 219
BP S38
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PG 1
WC Dermatology
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GA CF8CO
UT WOS:000352783200220
ER
PT J
AU Yang, C
Pomerantz, H
Corwin, J
Weinstock, MA
Fleckman, P
DiGiovanna, JJ
Robinson-Bostom, L
AF Yang, C.
Pomerantz, H.
Corwin, J.
Weinstock, M. A.
Fleckman, P.
DiGiovanna, J. J.
Robinson-Bostom, L.
TI Skin histopathology from patients with X-linked recessive ichthyosis and
autosomal recessive congenital ichthyosis with transglutaminase 1
mutation
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
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DT Meeting Abstract
CT Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 06-09, 2015
CL Atlanta, GA
SP Soc Investigat Dermatol
C1 [Yang, C.; Robinson-Bostom, L.] Brown Univ, Alpert Med Sch, Dermatol, Providence, RI 02912 USA.
[Pomerantz, H.; Weinstock, M. A.] VA Med Ctr, Dermatoepidemiol, Providence, RI USA.
[Corwin, J.] Vacaville Med Ctr, Dermatol, Vacaville, CA USA.
[Fleckman, P.] Univ Washington, Dermatol, Seattle, WA 98195 USA.
[DiGiovanna, J. J.] NCI NIH, Dermatol, CCR, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD MAY
PY 2015
VL 135
SU 1
MA 195
BP S34
EP S34
PG 1
WC Dermatology
SC Dermatology
GA CF8CO
UT WOS:000352783200196
ER
PT J
AU Butcher, M
Fwu, C
Kirkali, Z
Kohler, T
Burrows, P
Eggers, P
Kusek, J
McVary, K
AF Butcher, M.
Fwu, C.
Kirkali, Z.
Kohler, T.
Burrows, P.
Eggers, P.
Kusek, J.
McVary, K.
TI SEXUAL FUNCTION ASSOCIATED WITH LOWER URINARY TRACT SYMPTOMS IN MEN WITH
BENIGN PROSTATIC HYPERPLASIA: MTOPS COHORT OF CROSS-SECTIONAL AND
LONGITUDINAL DATA
SO JOURNAL OF SEXUAL MEDICINE
LA English
DT Meeting Abstract
C1 [Butcher, M.] So Illinois Univ, Carbondale, IL 62901 USA.
[Fwu, C.] Social & Sci Syst Inc, Silver Spring, MD USA.
[Kirkali, Z.; Eggers, P.; Kusek, J.] NIDDK, Div Kideny Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
[Kohler, T.; McVary, K.] So Illinois Univ, Dept Urol, Springfield, IL USA.
[Burrows, P.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-6095
EI 1743-6109
J9 J SEX MED
JI J. Sex. Med.
PD MAY
PY 2015
VL 12
SU 2
SI SI
MA 042
BP 116
EP 116
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA CF8EQ
UT WOS:000352789100043
ER
PT J
AU Clemens, JQ
Clauw, DJ
Kreder, K
Krieger, JN
Kusek, JW
Lai, HH
Rodriguez, L
Williams, DA
Hou, XL
Stephens, A
Landis, JR
AF Clemens, J. Quentin
Clauw, Daniel J.
Kreder, Karl
Krieger, John N.
Kusek, John W.
Lai, H. Henry
Rodriguez, Larissa
Williams, David A.
Hou, Xiaoling
Stephens, Alisa
Landis, J. Richard
CA MAPP Res Network
TI Comparison of Baseline Urological Symptoms in Men and Women in the MAPP
Research Cohort
SO JOURNAL OF UROLOGY
LA English
DT Article
DE cystitis; interstitial; prostatitis; pelvic pain; chronic pain
ID PELVIC PAIN SYNDROME; INTERSTITIAL CYSTITIS EPIDEMIOLOGY;
RANDOMIZED-CONTROLLED-TRIAL; CHRONIC PROSTATITIS; RESEARCH NETWORK;
INDEX; PREVALENCE; CLASSIFICATION; PREDICTORS; SEVERITY
AB Purpose: The clinical features of the interstitial cystitis/bladder pain syndrome are similar to those of the chronic prostatitis/chronic pelvic pain syndrome. However, to our knowledge no studies have directly compared the characteristics of these syndromes in men and women.
Materials and Methods: The MAPP Research Network recruited 191 men and 233 women with IC/BPS or CP/CPPS. Baseline data included demographics, Interstitial Cystitis Symptom Index and Problem Index scores; Genitourinary Pain Index score; American Urological Association Symptom Index score; Likert scales to assess urinary urgency, frequency, pain and overall symptom severity; and a single question about the most bothersome pelvic symptom.
Results: After adjustment for age, income and symptom duration, measures of pain severity were similar across genders. Mean scores for the ICSI, ICPI and AUASI were significantly higher in women than in men, reflecting more bladder focused symptoms in women. The most bothersome single symptom in men as well as in women was pain in the pubic/bladder area (men 34%, women 58%). The characteristics of the men and women in the MAPP cohort were similar to those reported in other research cohorts for IC/BPS and CP/CPPS.
Conclusions: Our findings indicate that pain severity is similar for both genders and that bladder focused symptoms (urgency, suprapubic pain, frequency) are more common in women. However, a substantial proportion of men also reported these types of bladder symptoms.
C1 [Clemens, J. Quentin; Clauw, Daniel J.; Williams, David A.] Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA.
[Kreder, Karl] Univ Iowa, Iowa City, IA USA.
[Krieger, John N.] Univ Washington, Seattle, WA 98195 USA.
[Kusek, John W.] NIDDK, Bethesda, MD 20892 USA.
[Lai, H. Henry] Washington Univ, St Louis, MO USA.
[Rodriguez, Larissa] Univ Calif Los Angeles, Los Angeles, CA USA.
[Hou, Xiaoling; Stephens, Alisa; Landis, J. Richard] Univ Penn, Philadelphia, PA 19104 USA.
RP Clauw, DJ (reprint author), Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA.
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health [DK82370, DK82342, DK82315, DK82344,
DK82325, DK82345, DK82333, DK82316]; Pfizer; Forest; Eli Lilly; Pierre
Fabre; Cypress Bioscience; Wyeth; UCB; Astra Zeneca; Merck; J J; Nuvo;
Jazz; Abbott; Cerephex; Iroko; Tonix; Theravance; IMC; Zynerba; Samumed;
Medtronic; Tengion; Symptelligence; Health Focus
FX Funding for the MAPP Research Network was obtained under a cooperative
agreement from the National Institute of Diabetes and Digestive and
Kidney Diseases, National Institutes of Health (DK82370, DK82342,
DK82315, DK82344, DK82325, DK82345, DK82333 and DK82316.); Financial
interest and/or other relationship with Pfizer, Forest, Eli Lilly,
Pierre Fabre, Cypress Bioscience, Wyeth, UCB, Astra Zeneca, Merck, J &
J, Nuvo, Jazz, Abbott, Cerephex, Iroko, Tonix, Theravance, IMC, Zynerba
and Samumed.; Financial interest and/or other relationship with
Medtronic, Tengion and Symptelligence.; Financial interest and/or other
relationship with Medtronic.; Financial interest and/or other
relationship with Health Focus.
NR 25
TC 3
Z9 3
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD MAY
PY 2015
VL 193
IS 5
BP 1554
EP 1558
DI 10.1016/j.juro.2014.11.016
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA CG2OD
UT WOS:000353113200032
PM 25463989
ER
PT J
AU Reinartz, MT
Kalble, S
Wainer, IW
Seifert, R
AF Reinartz, Michael T.
Kaelble, Solveig
Wainer, Irving W.
Seifert, Roland
TI Interaction of fenoterol stereoisomers with
beta(2)-adrenoceptor-G(s)alpha fusion proteins: antagonist and agonist
competition binding
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Article
DE beta(2)-adrenergic receptor; Structure-bias relationships; Functional
selectivity; Fenoterol
ID MOLECULAR-FIELD ANALYSIS; BETA(2)-ADRENERGIC RECEPTOR; STEREOCHEMISTRY;
DERIVATIVES; LIGAND; CELLS; MODEL; CONFORMATIONS; EFFICIENCY; DOPAMINE
AB The specific interaction between G-protein-coupled receptors and ligand is the starting point for downstream signaling. Fenoterol stereoisomers were successfully used to probe ligand-specific activation (functional selectivity) of the beta(2)-adrenoceptor (beta(2)AR) (Reinartz et al. 2015). In the present study, we extended the pharmacological profile of fenoterol stereoisomers using beta(2)AR-G(s)alpha fusion proteins in agonist and antagonist competition binding assays. Dissociations between binding affinities and effector potencies were found for (R,S')- and (S,S')-isomers of 4'-methoxy-1-naphthyl-fenoterol. Our data corroborate former studies on the importance of the aminoalkyl moiety of fenoterol derivatives for functional selectivity.
C1 [Reinartz, Michael T.; Kaelble, Solveig; Seifert, Roland] Hannover Med Sch, Inst Pharmacol, D-30625 Hannover, Germany.
[Wainer, Irving W.] NIA, Lab Clin Invest, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Seifert, R (reprint author), Hannover Med Sch, Inst Pharmacol, Carl Neuberg Str 1, D-30625 Hannover, Germany.
EM seifert.roland@mh-hannover.de
OI Reinartz, Michael/0000-0002-4211-4562
NR 27
TC 2
Z9 2
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD MAY
PY 2015
VL 388
IS 5
BP 517
EP 524
DI 10.1007/s00210-015-1086-5
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CF8XU
UT WOS:000352846200005
PM 25637582
ER
PT J
AU Baeck, A
Kravitz, D
Baker, C
Op de Beeck, HP
AF Baeck, Annelies
Kravitz, Dwight
Baker, Chris
Op de Beeck, Hans P.
TI Influence of lexical status and orthographic similarity on the
multi-voxel response of the visual word form area
SO NEUROIMAGE
LA English
DT Article
DE Visual word form area; fMRI; Orthography; Lexicality
ID HUMAN EXTRASTRIATE CORTEX; LEFT FUSIFORM GYRUS; VENTRAL STREAM;
OCCIPITOTEMPORAL CORTEX; NEURAL BASIS; FMRI; PSEUDOWORDS; RECOGNITION;
REPRESENTATIONS; ORGANIZATION
AB Previous studies demonstrated that a region in the left fusiform gyrus, often referred to as the 'visual word form area' (VWFA), is responsive to written words, but the precise functional role of VWFA remains unclear. In the present study, we investigated the influence of orthographic similarity, and lexical factors on the multivoxel response patterns to written stimuli. Using high-resolution fMRI at 7 T, we compared the organization of visual word representations in VWFA to the organization in early visual cortex and a language region in the superior temporal gyrus. Sets of four letter words and pseudowords were presented, in which orthographic similarity was parametrically manipulated. We found that during a lexical decision task VWFA is responsive to the lexical status of a stimulus, but both real words and pseudowords were further processed in terms of orthographic similarity. In contrast, early visual cortex was only responsive to the visual aspects of the stimuli and in the left superior temporal gyrus there was an interaction between lexical status and orthography such that only real words were processed in terms of orthographic similarity. These findings indicate that VWFA represents the word/non-word status of letter strings as well as their orthographic similarity. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Baeck, Annelies; Op de Beeck, Hans P.] KULeuven, Univ Leuven, Lab Biol Psychol, B-3000 Leuven, Belgium.
[Baeck, Annelies] KULeuven, Univ Leuven, Expt Psychol Lab, B-3000 Leuven, Belgium.
[Baeck, Annelies; Kravitz, Dwight; Baker, Chris] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD USA.
RP Baeck, A (reprint author), KULeuven, Univ Leuven, Lab Biol Psychol, Tiensestr 102, B-3000 Leuven, Belgium.
EM Annelies.baeck@ppw.kuleuven.be; kravitzd@email.gwu.edu;
bakerchris@mail.nih.gov; Hans.opdebeeck@ppw.kuleuven.be
OI Baker, Chris/0000-0001-6861-8964
FU European Research Council [284101]; Intramural NIH HHS [Z01
MH002909-01]; NIMH NIH HHS [MH002909-07]
NR 65
TC 1
Z9 1
U1 1
U2 11
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 MAY 1
PY 2015
VL 111
BP 321
EP 328
DI 10.1016/j.neuroimage.2015.01.060
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA CF0HO
UT WOS:000352224100030
PM 25665965
ER
PT J
AU Chen, JE
Chang, C
Greicius, MD
Glover, GH
AF Chen, Jingyuan E.
Chang, Catie
Greicius, Michael D.
Glover, Gary H.
TI Introducing co-activation pattern metrics to quantify spontaneous brain
network dynamics
SO NEUROIMAGE
LA English
DT Article
DE Brain dynamics; Resting state networks; Co-activation patterns; Point
process analysis; Working memory
ID FUNCTIONAL CONNECTIVITY; RESTING STATE; FMRI
AB Recently, fMRI researchers have begun to realize that the brain's intrinsic network patterns may undergo substantial changes during a single resting state (RS) scan. However, despite the growing interest in brain dynamics, metrics that can quantify the variability of network patterns are still quite limited. Here, we first introduce various quantification metrics based on the extension of co-activation pattern (CAP) analysis, a recently proposed point-process analysis that tracks state alternations at each individual time frame and relies on very fewassumptions; then apply these proposed metrics to quantify changes of brain dynamics during a sustained 2-backworking memory (WM) task compared to rest. We focus on the functional connectivity of two prominent RS networks, the default-mode network (DMN) and executive control network (ECN). We first demonstrate less variability of global Pearson correlations with respect to the two chosen networks using a sliding-window approach duringWMtask compared to rest; then we show that the macroscopic decrease in variations in correlations during a WM task is also well characterized by the combined effect of a reduced number of dominant CAPs, increased spatial consistency across CAPs, and increased fractional contributions of a few dominant CAPs. These CAP metrics may provide alternative and more straightforward quantitative means of characterizing brain network dynamics than time-windowed correlation analyses. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Chen, Jingyuan E.; Glover, Gary H.] Stanford Univ, Dept Radiol, Stanford, CA 94305 USA.
[Chen, Jingyuan E.] Stanford Univ, Dept Elect Engn, Stanford, CA 94305 USA.
[Chang, Catie] NINDS, Adv MRI Sect, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
[Greicius, Michael D.] Stanford Sch Med, Dept Neurol & Neurol Sci, Funct Imaging Neuropsychiat Disorders Lab, Stanford, CA 94305 USA.
RP Chen, JE (reprint author), Lucas MRI S Ctr, MC 5488,1201 Welch Rd, Stanford, CA 94305 USA.
EM cjy2010@stanford.edu
FU NIH [P41 EB015891]
FX The authors gratefully acknowledge Bernard Ng and William Shirer for
providing the brain functional atlas (ROI499w), the NIH for funding
support (P41 EB015891), and three anonymous reviewers for their
constructive comments, which have substantially improved the quality of
the manuscript.
NR 30
TC 10
Z9 10
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD MAY 1
PY 2015
VL 111
BP 476
EP 488
DI 10.1016/j.neuroimage.2015.01.057
PG 13
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA CF0HO
UT WOS:000352224100042
PM 25662866
ER
PT J
AU Saha, K
Partilla, JS
Lehner, KR
Seddik, A
Stockner, T
Holy, M
Sandtner, W
Ecker, GF
Sitte, HH
Baumann, MH
AF Saha, Kusumika
Partilla, John S.
Lehner, Kurt R.
Seddik, Amir
Stockner, Thomas
Holy, Marion
Sandtner, Walter
Ecker, Gerhard F.
Sitte, Harald H.
Baumann, Michael H.
TI 'Second-Generation' Mephedrone Analogs, 4-MEC and 4-MePPP,
Differentially Affect Monoamine Transporter Function
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
ID HUMAN DOPAMINE TRANSPORTER; HUMAN SEROTONIN TRANSPORTER; CONSTITUENT
3,4-METHYLENEDIOXYPYROVALERONE MDPV; CHROMATOGRAPHY-MASS-SPECTROMETRY;
BIOGENIC-AMINE TRANSPORTERS; PSYCHOACTIVE BATH SALTS; SYNTHETIC
CATHINONES; METHYLENEDIOXYPYROVALERONE MDPV; NEUROTRANSMITTER
TRANSPORTERS; TOXICOLOGICAL DETECTION
AB The nonmedical use of synthetic cathinones is increasing on a global scale. 4-Methyl-N-methylcathinone (mephedrone) is a popular synthetic cathinone that is now illegal in the United States and other countries. Since the legislative ban on mephedrone, a number of 'second-generation' analogs have appeared in the street drug marketplace, including 4-methyl-N-ethylcathinone (4-MEC) and 4'-methyl-alpha-pyrrolidinopropiophenone (4-MePPP). Here we characterized the interactions of 4-MEC and 4-MePPP with transporters for 5-HT (SERT) and dopamine (DAT) using molecular, cellular, and whole-animal methods. In vitro transporter assays revealed that 4-MEC displays unusual 'hybrid' activity as a SERT substrate (ie, 5-HT releaser) and DAT blocker, whereas 4-MePPP is a blocker at both transporters but more potent at DAT. In vivo microdialysis experiments in rat brain demonstrated that 4-MEC (1-3 mg/kg, i.v.) produced large increases in extracellular 5-HT, small increases in dopamine, and minimal motor stimulation. In contrast, 4-MePPP (1-3 mg/kg, i.v.) produced selective increases in dopamine and robust motor stimulation. Consistent with its activity as a SERT substrate, 4-MEC evoked inward current in SERT-expressing Xenopus oocytes, whereas 4-MePPP was inactive in this regard. To examine drug-transporter interactions at the molecular level, we modeled the fit of 4-MEC and 4-MePPP into the binding pockets for DAT and SERT. Subtle distinctions in ligand-transporter binding were found that account for the differential effects of 4-MEC and 4-MePPP at SERT. Collectively, our results provide key information about the pharmacology of newly emerging mephedrone analogs, and give clues to structural requirements that govern drug selectivity at DAT vs SERT.
C1 [Saha, Kusumika; Stockner, Thomas; Holy, Marion; Sandtner, Walter; Sitte, Harald H.] Med Univ Vienna, Ctr Physiol & Pharmacol, Inst Pharmacol, Vienna, Austria.
[Partilla, John S.; Lehner, Kurt R.; Baumann, Michael H.] NIDA, Designer Drug Res Unit, IRP, NIH, Baltimore, MD 21224 USA.
[Seddik, Amir; Ecker, Gerhard F.] Univ Vienna, Dept Pharmaceut Sci, Vienna, Austria.
[Sitte, Harald H.] Med Univ Vienna, Ctr Addict Res & Sci, Vienna, Austria.
RP Baumann, MH (reprint author), NIDA, Designer Drug Res Unit, IRP, NIH,DHHS, 333 Cassell Dr,Suite 4400, Baltimore, MD 21224 USA.
EM mbaumann@mail.nih.gov
RI Stockner, Thomas/A-9509-2014;
OI Stockner, Thomas/0000-0002-7071-8283; Sitte, Harald/0000-0002-1339-7444
FU Austrian Research Fund/FWF [F3506, W1232]; NIDA, NIH [DA000523-07]
FX This research was supported by the Austrian Research Fund/FWF grants
F3506 and W1232 to HHS and the Intramural Research Program of the NIDA,
NIH, grant DA000523-07 to MHB.
NR 63
TC 13
Z9 13
U1 0
U2 18
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD MAY
PY 2015
VL 40
IS 6
BP 1321
EP 1331
DI 10.1038/npp.2014.325
PG 11
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CG0PI
UT WOS:000352968100003
PM 25502630
ER
PT J
AU Williams, LE
Oler, JA
Fox, AS
McFarlin, DR
Rogers, GM
Jesson, MAL
Davidson, RJ
Pine, DS
Kalin, NH
AF Williams, Lisa E.
Oler, Jonathan A.
Fox, Andrew S.
McFarlin, Daniel R.
Rogers, Gregory M.
Jesson, Maria A. L.
Davidson, Richard J.
Pine, Daniel S.
Kalin, Ned H.
TI Fear of the Unknown: Uncertain Anticipation Reveals Amygdala Alterations
in Childhood Anxiety Disorders
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
ID FACIAL EXPRESSIONS; BRAIN ACTIVATION; NEURAL RESPONSES; FUNCTIONAL MRI;
CHILDREN; ADOLESCENTS; METAANALYSIS; DEPRESSION; REACTIVITY; AVERSION
AB Children with anxiety disorders (ADs) experience persistent fear and worries that are highly debilitating, conferring risk for lifelong psychopathology. Anticipatory anxiety is a core clinical feature of childhood ADs, often leading to avoidance of uncertain and novel situations. Extensive studies in non-human animals implicate amygdala dysfunction as a critical substrate for early life anxiety. To test specific amygdala-focused hypotheses in preadolescent children with ADs, we used fMRI to characterize amygdala activation during uncertain anticipation and in response to unexpected stimuli. Forty preadolescent (age 8-12 years) children, 20 unmedicated AD patients and 20 matched controls completed an anticipation task during an fMRI scan. In the task, symbolic cues preceded fear or neutral faces, such that 'certain' cues always predicted the presentation of fear or neutral faces, whereas 'uncertain' cues were equally likely to be followed by fear or neutral faces. Both AD children and controls showed robust amygdala response to faces. In response to the uncertain cues, AD children had increased amygdala activation relative to controls. Moreover, in the AD children, faces preceded by an 'uncertain' cue elicited increased amygdala activation, as compared with the same faces following a 'certain' cue. Children with ADs experience distress both in anticipation of and during novel and surprising events. Our findings suggest that increased amygdala activation may have an important role in the generation of uncertainty-related anxiety. These findings may guide the development of neuroscientifically informed treatments aimed at relieving the suffering and preventing the lifelong disability associated with pediatric ADs.
C1 [Williams, Lisa E.; Oler, Jonathan A.; Fox, Andrew S.; McFarlin, Daniel R.; Rogers, Gregory M.; Jesson, Maria A. L.; Davidson, Richard J.; Kalin, Ned H.] Univ Wisconsin, Dept Psychiat, Wisconsin Psychiat Inst & Clin, Madison, WI 53719 USA.
[Williams, Lisa E.; Oler, Jonathan A.; Fox, Andrew S.; McFarlin, Daniel R.; Jesson, Maria A. L.; Davidson, Richard J.; Kalin, Ned H.] Univ Wisconsin, HealthEmot Res Inst, Madison, WI 53719 USA.
[Williams, Lisa E.; Oler, Jonathan A.; Fox, Andrew S.; McFarlin, Daniel R.; Jesson, Maria A. L.; Kalin, Ned H.] Univ Wisconsin, Lane Neuroimaging Lab, Madison, WI 53719 USA.
[Fox, Andrew S.; Davidson, Richard J.; Kalin, Ned H.] Univ Wisconsin, Ctr Investigating Hlth Minds, Madison, WI 53719 USA.
[Fox, Andrew S.; Davidson, Richard J.; Kalin, Ned H.] Univ Wisconsin, Waisman Lab Brain Imaging & Behav, Madison, WI 53719 USA.
[Davidson, Richard J.] Univ Wisconsin, Dept Psychol, Madison, WI 53719 USA.
[Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
RP Williams, LE (reprint author), Univ Wisconsin, Dept Psychiat, Wisconsin Psychiat Inst & Clin, 6001 Res Pk Blvd, Madison, WI 53719 USA.
EM lewilliams1@gmail.com
FU National Institutes of Health [R21 MH092581]
FX We acknowledge the assistance of Anna White and Travis Doran, and the
staffs of the HealthEmotions Research Institute (HERI) and Lane
Neuroimaging Laboratory. This work was supported by the National
Institutes of Health grant R21 MH092581 (NHK and JAO).
NR 50
TC 9
Z9 9
U1 3
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD MAY
PY 2015
VL 40
IS 6
BP 1428
EP 1435
DI 10.1038/npp.2014.328
PG 8
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CG0PI
UT WOS:000352968100013
PM 25502633
ER
PT J
AU Holroyd, KB
Adrover, MF
Fuino, RL
Bock, R
Kaplan, AR
Gremel, CM
Rubinstein, M
Alvarez, VA
AF Holroyd, Kathryn B.
Adrover, Martin F.
Fuino, Robert L.
Bock, Roland
Kaplan, Alanna R.
Gremel, Christina M.
Rubinstein, Marcelo
Alvarez, Veronica A.
TI Loss of Feedback Inhibition via D2 Autoreceptors Enhances Acquisition of
Cocaine Taking and Reactivity to Drug-Paired Cues
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
ID KNOCK-OUT MICE; STRIATAL DOPAMINE RELEASE; CHOLINERGIC INTERNEURONS;
NUCLEUS-ACCUMBENS; DORSAL STRIATUM; RECEPTORS; IMPULSIVITY; ADDICTION;
RATS; RESPONSES
AB A prominent aspect of drug addiction is the ability of drug-associated cues to elicit craving and facilitate relapse. Understanding the factors that regulate cue reactivity will be vital for improving treatment of addictive disorders. Low availability of dopamine (DA) D2 receptors (D2Rs) in the striatum is associated with high cocaine intake and compulsive use. However, the role of D2Rs of nonstriatal origin in cocaine seeking and taking behavior and cue reactivity is less understood and possibly underestimated. D2Rs expressed by midbrain DA neurons function as autoreceptors, exerting inhibitory feedback on DA synthesis and release. Here, we show that selective loss of D2 autoreceptors impairs the feedback inhibition of DA release and amplifies the effect of cocaine on DA transmission in the nucleus accumbens (NAc) in vitro. Mice lacking D2 autoreceptors acquire a cued-operant self-administration task for cocaine faster than littermate control mice but acquire similarly for a natural reward. Furthermore, although mice lacking D2 autoreceptors were able to extinguish self-administration behavior in the absence of cocaine and paired cues, they exhibited perseverative responding when cocaine-paired cues were present. This enhanced cue reactivity was selective for cocaine and was not seen during extinction of sucrose self-administration. We conclude that low levels of D2 autoreceptors enhance the salience of cocaine-paired cues and can contribute to the vulnerability for cocaine use and relapse.
C1 [Holroyd, Kathryn B.; Adrover, Martin F.; Fuino, Robert L.; Bock, Roland; Alvarez, Veronica A.] NIAAA, Sect Neuronal Struct, NIH, Bethesda, MD 20892 USA.
[Gremel, Christina M.] NIAAA, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA.
[Rubinstein, Marcelo] Consejo Nacl Invest Cient & Tecn, Inst Invest Ingn Genet & Biol Mol, Buenos Aires, DF, Argentina.
[Rubinstein, Marcelo] Univ Buenos Aires, Fac Ciencias Exactas & Nat, Buenos Aires, DF, Argentina.
RP Alvarez, VA (reprint author), NIAAA, Sect Neuronal Struct, NIH, 5625 Fishers Lane,MSC 9411, Bethesda, MD 20892 USA.
EM alvarezva@mail.nih.gov
RI Alvarez, Veronica /E-9745-2015; Bock, Roland/G-2982-2016;
OI Alvarez, Veronica /0000-0003-2611-8675; Bock,
Roland/0000-0002-8654-1080; Kaplan, Alanna/0000-0002-2612-4736; Holroyd,
Kathryn/0000-0001-5884-9734
FU NIAAA; NINDS [ZIA-AA000421]; ANPCYT-Mincyt of Argentina; Universidad de
Buenos Aires; Tourette Syndrome Association
FX The authors declare no conflict of interest. This study was funded by
the Intramural Programs of NIAAA (VAA) and NINDS ZIA-AA000421 (to VAA),
and by the ANPCYT-Mincyt of Argentina (to MR), Universidad de Buenos
Aires (to MR), and Tourette Syndrome Association (to MR).
NR 39
TC 10
Z9 10
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD MAY
PY 2015
VL 40
IS 6
BP 1495
EP 1509
DI 10.1038/npp.2014.336
PG 15
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA CG0PI
UT WOS:000352968100019
PM 25547712
ER
PT J
AU Kiris, E
Burnett, JC
Nuss, JE
Wanner, LM
Peyser, BD
Du, HT
Gomba, GY
Kota, KP
Panchal, RG
Gussio, R
Kane, CD
Tessarollo, L
Bavari, S
AF Kiris, Erkan
Burnett, James C.
Nuss, Jonathan E.
Wanner, Laura M.
Peyser, Brian D.
Du, Hao T.
Gomba, Glenn Y.
Kota, Krishna P.
Panchal, Rekha G.
Gussio, Rick
Kane, Christopher D.
Tessarollo, Lino
Bavari, Sina
TI Src Family Kinase Inhibitors Antagonize the Toxicity of Multiple
Serotypes of Botulinum Neurotoxin in Human Embryonic Stem Cell-Derived
Motor Neurons
SO NEUROTOXICITY RESEARCH
LA English
DT Article
DE Motor neurons; Human embryonic stem cells; Src inhibitors; Botulinum
neurotoxins; Cell-based assay; Drug discovery
ID TYROSINE PHOSPHORYLATION; SYNAPTIC-VESICLE; DIRECTED DIFFERENTIATION;
CLOSTRIDIAL NEUROTOXINS; CATALYTIC DOMAIN; RECEPTOR; SNAP-25; BINDING;
METALLOPROTEASE; STABILIZATION
AB Botulinum neurotoxins (BoNTs), the causative agents of botulism, are potent inhibitors of neurotransmitter release from motor neurons. There are currently no drugs to treat BoNT intoxication after the onset of the disease symptoms. In this study, we explored how modulation of key host pathways affects the process of BoNT intoxication in human motor neurons, focusing on Src family kinase (SFK) signaling. Motor neurons derived from human embryonic stem (hES) cells were treated with a panel of SFK inhibitors and intoxicated with BoNT serotypes A, B, or E (which are responsible for > 95 % of human botulism cases). Subsequently, it was found that bosutinib, dasatinib, KX2-391, PP1, PP2, Src inhibitor-1, and SU6656 significantly antagonized all three of the serotypes. Furthermore, the data indicated that the treatment of hES-derived motor neurons with multiple SFK inhibitors increased the antagonistic effect synergistically. Mechanistically, the small molecules appear to inhibit BoNTs by targeting host pathways necessary for intoxication and not by directly inhibiting the toxins' proteolytic activity. Importantly, the identified inhibitors are all well-studied with some in clinical trials while others are FDA-approved drugs. Overall, this study emphasizes the importance of targeting host neuronal pathways, rather than the toxin's enzymatic components, to antagonize multiple BoNT serotypes in motor neurons.
C1 [Kiris, Erkan] Geneva Fdn, Tacoma, WA 98402 USA.
[Kiris, Erkan; Nuss, Jonathan E.; Wanner, Laura M.; Gomba, Glenn Y.; Kota, Krishna P.; Panchal, Rekha G.; Kane, Christopher D.; Bavari, Sina] US Army Med Res Inst Infect Dis, Dept Mol & Translat Sci, Frederick, MD 21702 USA.
[Kiris, Erkan; Du, Hao T.; Tessarollo, Lino] NCI, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Burnett, James C.] NCI, Leidos Biomed Res Inc, CDDG, Frederick, MD 21702 USA.
[Burnett, James C.; Peyser, Brian D.; Gussio, Rick] NCI, CDDG, Dev Therapeut Program, Frederick, MD 21702 USA.
[Kane, Christopher D.] Henry M Jackson Fdn, Bethesda, MD USA.
[Kane, Christopher D.] USAMRMC, DoD Biotechnol High Performance Comp Software App, TATRC, Frederick, MD USA.
RP Kiris, E (reprint author), Geneva Fdn, Tacoma, WA 98402 USA.
EM erkan.kiris@nih.gov; sina.bavari.civ@mail.mil
OI Peyser, Brian/0000-0002-3455-5181
FU Defense Threat Reduction Agency; National Institutes of Health
[4R33AI101387 - 03]; National Cancer Institute (NCI), National
Institutes of Health (NIH) [HHSN261200800001E]; Intramural Research
Program of the NCI, Center for Cancer Research, NIH
FX We are indebted to Drs. Esta Sterneck and Balamurugan Kuppusamy for
their insightful discussion concerning SFK inhibitors. Also, we thank
Rajarshi Guha for R functions to optimize beta for synergy calculations,
and Veronica Soloveva for helpful discussion. This research was
supported by grants from the Defense Threat Reduction Agency and
National Institutes of Health (4R33AI101387 - 03). For JCB, this project
has been funded in whole or in part with federal funds from the National
Cancer Institute (NCI), National Institutes of Health (NIH), under
contract no. HHSN261200800001E. LT has been supported by the Intramural
Research Program of the NCI, Center for Cancer Research, NIH.
NR 81
TC 5
Z9 5
U1 1
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1029-8428
EI 1476-3524
J9 NEUROTOX RES
JI Neurotox. Res.
PD MAY
PY 2015
VL 27
IS 4
BP 384
EP 398
DI 10.1007/s12640-015-9526-z
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA CF1IR
UT WOS:000352298900003
PM 25782580
ER
PT J
AU Lan, Q
Vermeulen, R
Dai, YF
Ren, DZ
Hu, W
Duan, HW
Niu, Y
Xu, J
Fu, W
Meliefste, K
Zhou, BS
Yang, JF
Ye, M
Jia, XW
Meng, T
Bin, P
Kim, C
Bassig, BA
Hosgood, HD
Silverman, D
Zheng, YX
Rothman, N
AF Lan, Qing
Vermeulen, Roel
Dai, Yufei
Ren, Dianzhi
Hu, Wei
Duan, Huawei
Niu, Yong
Xu, Jun
Fu, Wei
Meliefste, Kees
Zhou, Baosen
Yang, Jufang
Ye, Meng
Jia, Xiaowei
Meng, Tao
Bin, Ping
Kim, Christopher
Bassig, Bryan A.
Hosgood, H. Dean, III
Silverman, Debra
Zheng, Yuxin
Rothman, Nathaniel
TI Occupational exposure to diesel engine exhaust and alterations in
lymphocyte subsets
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID INFLAMMATORY RESPONSES; LUNG-CANCER; PERIPHERAL-BLOOD; HEALTHY HUMANS;
AIRWAY; VOLUNTEERS; BIOMARKERS; MARKERS; MINERS
AB Background The International Agency for Research on Cancer recently classified diesel engine exhaust (DEE) as a Group I carcinogen based largely on its association with lung cancer. However, the exposure-response relationship is still a subject of debate and the underlying mechanism by which DEE causes lung cancer in humans is not well understood.
Methods We conducted a cross-sectional molecular epidemiology study in a diesel engine truck testing facility of 54 workers exposed to a wide range of DEE (ie, elemental carbon air levels, median range: 49.7, 6.1-107.7 mu g/m(3)) and 55 unexposed comparable controls.
Results The total lymphocyte count (p=0.00044) and three of the four major lymphocyte subsets (ie, CD4+ T cells (p=0.00019), CD8+ T cells (p=0.0058) and B cells (p=0.017)) were higher in exposed versus control workers and findings were highly consistent when stratified by smoking status. In addition, there was evidence of an exposure-response relationship between elemental carbon and these end points (p(trends)<0.05), and CD4+ T cell levels were significantly higher in the lowest tertile of DEE exposed workers compared to controls (p=0.012).
Conclusions Our results suggest that DEE exposure is associated with higher levels of cells that play a key role in the inflammatory process, which is increasingly being recognised as contributing to the aetiology of lung cancer.
Impact This study provides new insights into the underlying mechanism of DEE carcinogenicity.
C1 [Lan, Qing; Hu, Wei; Kim, Christopher; Bassig, Bryan A.; Hosgood, H. Dean, III; Silverman, Debra; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
[Vermeulen, Roel; Meliefste, Kees] Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands.
[Dai, Yufei; Duan, Huawei; Niu, Yong; Ye, Meng; Jia, Xiaowei; Meng, Tao; Bin, Ping; Zheng, Yuxin] Chinese Ctr Dis Control & Prevent, Natl Inst Occupat Hlth & Poison Control, Key Lab Chem Safety & Hlth, Beijing, Peoples R China.
[Ren, Dianzhi; Fu, Wei; Yang, Jufang] Chaoyang Ctr Dis Control & Prevent, Chaoyang, Peoples R China.
[Xu, Jun] Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
[Zhou, Baosen] China Med Univ, Shenyang 110001, Peoples R China.
[Hosgood, H. Dean, III] Albert Einstein Coll Med, Div Epidemiol, New York, NY USA.
RP Lan, Q (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,Room 6E138, Rockville, MD 20850 USA.
EM qingl@mail.nih.gov
RI Vermeulen, Roel/F-8037-2011
OI Vermeulen, Roel/0000-0003-4082-8163
FU National Cancer Institute; National Institutes of Health
FX This work was supported by intramural funds from the National Cancer
Institute and the National Institutes of Health.
NR 16
TC 4
Z9 4
U1 1
U2 4
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 MAY
PY 2015
VL 72
IS 5
BP 354
EP 359
DI 10.1136/oemed-2014-102556
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CG0UV
UT WOS:000352987900007
PM 25673341
ER
PT J
AU Moseley, KF
Chia, CW
Simonsick, EM
Egan, JM
Ferrucci, L
Sellmeyer, DE
AF Moseley, K. F.
Chia, C. W.
Simonsick, E. M.
Egan, J. M.
Ferrucci, L.
Sellmeyer, D. E.
TI Sex-specific differences in progressive glucose intolerance and hip
geometry: the Baltimore Longitudinal Study of Aging
SO OSTEOPOROSIS INTERNATIONAL
LA English
DT Article
DE Bone architecture; Bone quality; Hip geometry; Type 2 diabetes
ID TYPE-2 DIABETES-MELLITUS; BONE-MINERAL DENSITY; IMPAIRED FASTING
GLUCOSE; FEMORAL-NECK STRENGTH; FRACTURE RISK; POSTMENOPAUSAL WOMEN;
HEALTH; POPULATION; MORTALITY; BMD
AB A Summary Fracture risk is increased in type 2 diabetes mellitus (T2DM). The effect of pre-diabetes and T2DM on bone macroarchitecture and strength has not been well investigated. In this study, we show that in women only, both pre-diabetes and T2DM are associated with decreased hip bending strength and mineralization which might lead to skeletal weakness.
Introduction Older men and women with T2DM are at increased risk for fracture despite normal bone mineral density (BMD). The discordance between bone quantity and skeletal fragility has driven investigation into additional determinants of fracture resistance in T2DM. Additionally, the effect of pre-diabetes on bone strength has not been well described. The aim of this study was to determine differences in bone macroarchitecture and strength, measured by hip geometry, in persons with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and T2DM.
Methods We performed cross-sectional analyses of older (age > 55 years) men (n = 472) and women (n = 473) participating in the Baltimore Longitudinal Study of Aging (BLSA) classified as NGT, IGT, or T2DM based on oral glucose tolerance testing. Bone strength measures included the hip geometry parameters of section modulus (Z), cross-sectional area (CSA), and buckling ratio (BR). Sex-stratified analyses were conducted using adjusted stepwise regression models.
Results In women, IGT and T2DM were negatively associated with hip geometry parameters including mineralization in cross section (CSA, -0.076 and -0.073, respectively; both p < 0.05) and hip bending strength (Z, -0.097 and -0.09, respectively; both p < 0.05); conversely, IGT and T2DM were associated with improved compressive strength (BR, -0.31 and -0.29, respectively; both p < 0.05). There was no significant association between glycemic status and hip geometry in men.
Conclusions In women only, both IGT and T2DM were inversely associated with bone macroarchitecture and measures of bone mineralization and bending strength. The same association between worsening glycemic status and bone strength was not observed in men. These data suggest a differential effect of sex on hip geometry with evolving glucose intolerance.
C1 [Moseley, K. F.; Sellmeyer, D. E.] Johns Hopkins Sch Med, Div Endocrinol Diabet & Metab, Baltimore, MD USA.
[Chia, C. W.; Simonsick, E. M.; Egan, J. M.; Ferrucci, L.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Moseley, K. F.] Johns Hopkins Bayview Med Ctr, Div Endocrinol Diabet & Metab, Baltimore, MD 21224 USA.
RP Moseley, KF (reprint author), Johns Hopkins Bayview Med Ctr, Div Endocrinol Diabet & Metab, Mason Lord Ctr Tower,Suite 4300,5200 Eastern Ave, Baltimore, MD 21224 USA.
EM kmosele4@jhmi.edu
FU Intramural Research Program of the National Institutes of Health;
National Institute of Diabetes and Digestive and Kidney Diseases
[K23DK093720]; Legato Research Scholar Awards in Gender-Specific
Medicine; Foundation for Gender-Specific Medicine, Inc.; National
Institute on Aging
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute on Aging, and
the National Institute of Diabetes and Digestive and Kidney Diseases,
K23DK093720. It was also supported by the Legato Research Scholar Awards
in Gender-Specific Medicine, Foundation for Gender-Specific Medicine,
Inc.
NR 38
TC 2
Z9 2
U1 1
U2 1
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0937-941X
EI 1433-2965
J9 OSTEOPOROSIS INT
JI Osteoporosis Int.
PD MAY
PY 2015
VL 26
IS 5
BP 1555
EP 1562
DI 10.1007/s00198-015-3027-z
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA CF9RP
UT WOS:000352904000011
PM 25619633
ER
PT J
AU Singewald, N
Schmuckermair, C
Whittle, N
Holmes, A
Ressler, KJ
AF Singewald, N.
Schmuckermair, C.
Whittle, N.
Holmes, A.
Ressler, K. J.
TI Pharmacology of cognitive enhancers for exposure-based therapy of fear,
anxiety and trauma-related disorders
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Fear extinction; Exposure therapy; Augmented relearning;
Reconsolidation; Drug development; Cognitive enhancer
ID POSTTRAUMATIC-STRESS-DISORDER; OBSESSIVE-COMPULSIVE DISORDER;
FIBROBLAST-GROWTH-FACTOR; MEDIAL PREFRONTAL CORTEX; RANDOMIZED
CONTROLLED-TRIAL; D-CYCLOSERINE AUGMENTATION; ACTIVATED PROTEIN-KINASE;
PLACEBO-CONTROLLED TRIAL; RECEPTOR MESSENGER-RNA; GATED CALCIUM-CHANNELS
AB Pathological fear and anxiety are highly debilitating and, despite considerable advances in psychotherapy and pharmacotherapy they remain insufficiently treated in many patients with PTSD, phobias, panic and other anxiety disorders. Increasing preclinical and clinical evidence indicates that pharmacological treatments including cognitive enhancers, when given as adjuncts to psychotherapeutic approaches [cognitive behavioral therapy including extinction-based exposure therapy] enhance treatment efficacy, while using anxiolytics such as benzodiazepines as adjuncts can undermine long-term treatment success. The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, cannabinoids, neuropeptides (oxytocin, neuropeptides Y and S, opioids) and other targets (neurotrophins BDNF and FGF2, glucocorticoids, L-type-calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models. Particularly promising approaches are discussed in regard to their effects on specific aspects of fear extinction namely, acquisition, consolidation and retrieval, including long-term protection from return of fear (relapse) phenomena like spontaneous recovery, reinstatement and renewal of fear. We also highlight the promising translational value of the preclinial research and the clinical potential of targeting certain neurochemical systems with, for example D-cycloserine, yohimbine, cortisol, and L-DOPA. The current body of research reveals important new insights into the neurobiology and neurochemistry of fear extinction and holds significant promise for pharmacologically-augmented psychotherapy as an improved approach to treat trauma and anxiety-related disorders in a more efficient and persistent way promoting enhanced symptom remission and recovery. (C) 2014 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license.
C1 [Singewald, N.; Schmuckermair, C.; Whittle, N.] Univ Innsbruck, Inst Pharm, Dept Pharmacol & Toxicol, A-6020 Innsbruck, Austria.
[Singewald, N.; Schmuckermair, C.; Whittle, N.] Univ Innsbruck, CMBI, A-6020 Innsbruck, Austria.
[Holmes, A.] NIAAA, Lab Behav & Genom Neurosci, NIH, Bethesda, MD USA.
[Ressler, K. J.] Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA USA.
RP Singewald, N (reprint author), Univ Innsbruck, Ctr Mol Biosci Innsbruck, Dept Pharmacol & Toxicol, Innrain 80-82, A-6020 Innsbruck, Austria.
EM nicolas.singewald@uibk.ac.at
OI Ressler, Kerry/0000-0002-5158-1103
FU Austrian Science Fund [FWF] [SFB F4410, P25375-B24]
FX We acknowledge the Austrian Science Fund [FWF grant numbers SFB F4410
and P25375-B24] for funding our research related to this review (NS).
NR 567
TC 45
Z9 46
U1 22
U2 83
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD MAY
PY 2015
VL 149
BP 150
EP 190
DI 10.1016/j.pharmthera.2014.12.004
PG 41
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA CG1BS
UT WOS:000353008600004
PM 25550231
ER
PT J
AU Bruce, N
Dherani, M
Liu, R
Hosgood, HD
Sapkota, A
Smith, KR
Straif, K
Lan, Q
Pope, D
AF Bruce, Nigel
Dherani, Mukesh
Liu, Rui
Hosgood, H. Dean, III
Sapkota, Amir
Smith, Kirk R.
Straif, Kurt
Lan, Qing
Pope, Daniel
TI Does household use of biomass fuel cause lung cancer? A systematic
review and evaluation of the evidence for the GBD 2010 study
SO THORAX
LA English
DT Article
ID INDOOR AIR-POLLUTION; SMOKE PARTICLE EXTRACTS; RISK-FACTORS; GLOBAL
BURDEN; SOLID FUELS; WOMEN; METAANALYSIS; EXPOSURE; DISEASE; INDIA
AB Background Around 2.4 billion people use traditional biomass fuels for household cooking or heating. In 2006, the International Agency for Research on Cancer (IARC) concluded emissions from household coal combustion are a Group 1 carcinogen, while those from biomass were categorised as 2A due to epidemiologic limitations. This review updates the epidemiologic evidence and provides risk estimates for the 2010 Global Burden of Disease study.
Methods Searches were conducted of 10 databases to July 2012 for studies of clinically diagnosed or pathologically confirmed lung cancer associated with household biomass use for cooking and/or heating.
Findings Fourteen eligible studies of biomass cooking or heating were identified: 13 had independent estimates (12 cooking only), all were case-control designs and provided 8221 cases and 11 342 controls. The ORs for lung cancer risk with biomass for cooking and/or heating were OR 1.17 (95% CI 1.01 to 1.37) overall, and 1.15 (95% CI 0.97 to 1.37) for cooking only. Publication bias was not detected, but more than half the studies did not explicitly describe a clean reference category. Sensitivity analyses restricted to studies with adequate adjustment and a clean reference category found ORs of 1.21 (95% CI 1.05 to 1.39) for men (two reports, compiling five studies) and 1.95 (95% CI 1.16 to 3.27) for women (five reports, compiling eight studies). Exposure-response evidence was seen for men, and higher risk for women in developing compared with developed countries, consistent with higher exposures in the former.
Conclusions There is now stronger evidence for biomass fuel use causing lung cancer, but future studies need better exposure assessment to strengthen exposure-response evidence.
C1 [Bruce, Nigel; Dherani, Mukesh; Pope, Daniel] Univ Liverpool, Dept Publ Hlth & Policy, Liverpool L69 3GB, Merseyside, England.
[Liu, Rui; Smith, Kirk R.] Univ Calif Berkeley, Sch Publ Hlth, Environm Hlth Sci, Berkeley, CA 94720 USA.
[Hosgood, H. Dean, III; Lan, Qing] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Hosgood, H. Dean, III] Albert Einstein Coll Med, Div Epidemiol, Bronx, NY 10467 USA.
[Sapkota, Amir] Univ Maryland, Maryland Inst Appl Environm Hlth, Sch Publ Hlth, College Pk, MD 20742 USA.
[Straif, Kurt] Int Agcy Res Canc, F-69372 Lyon, France.
RP Bruce, N (reprint author), Univ Liverpool, Dept Publ Hlth & Policy, Whelan Bldg, Liverpool L69 3GB, Merseyside, England.
EM ngb@liv.ac.uk
RI Sapkota, Amir/A-5968-2011
FU Bill and Melinda Gates Foundation
FX A grant from the Bill and Melinda Gates Foundation partially supported
the collaboration between some of the authors of this review.
NR 33
TC 5
Z9 6
U1 4
U2 10
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0040-6376
EI 1468-3296
J9 THORAX
JI Thorax
PD MAY
PY 2015
VL 70
IS 5
BP 433
EP 441
DI 10.1136/thoraxjnl-2014-206625
PG 9
WC Respiratory System
SC Respiratory System
GA CF8XY
UT WOS:000352846600008
PM 25758120
ER
PT J
AU Dickherber, A
Morris, SA
Grodzinski, P
AF Dickherber, Anthony
Morris, Stephanie A.
Grodzinski, Piotr
TI NCI investment in nanotechnology: achievements and challenges for the
future
SO WILEY INTERDISCIPLINARY REVIEWS-NANOMEDICINE AND NANOBIOTECHNOLOGY
LA English
DT Review
ID IN-VIVO; CANCER NANOTECHNOLOGY; PRECISION MEDICINE; QUANTUM DOTS;
DELIVERY; NANOPARTICLE; CELLS; NANOMEDICINE; ONCOLOGY; TUMORS
AB Nanotechnology offers an exceptional and unique opportunity for developing a new generation of tools addressing persistent challenges to progress in cancer research and clinical care. The National Cancer Institute (NCI) recognizes this potential, which is why it invests roughly $150 M per year in nanobiotechnology training, research and development. By exploiting the various capacities of nanomaterials, the range of nanoscale vectors and probes potentially available suggests much is possible for precisely investigating, manipulating, and targeting the mechanisms of cancer across the full spectrum of research and clinical care. NCI has played a key role among federal R&D agencies in recognizing early the value of nanobiotechnology in medicine and committing to its development as well as providing training support for new investigators in the field. These investments have allowed many in the research community to pursue breakthrough capabilities that have already yielded broad benefits. Presented here is an overview of how NCI has made these investments with some consideration of how it will continue to work with this research community to pursue paradigm-changing innovations that offer relief from the burdens of cancer.Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Dickherber, Anthony] NCI, Off Director, Ctr Strateg Sci Initiat, NIH, Bethesda, MD 20892 USA.
[Morris, Stephanie A.; Grodzinski, Piotr] NCI, Office Canc Nanotechnol Res, Ctr Strateg Sci Initiat, NIH, Bethesda, MD 20892 USA.
RP Dickherber, A (reprint author), NCI, Off Director, Ctr Strateg Sci Initiat, NIH, Bethesda, MD 20892 USA.
EM anthony.dickherber@nih.gov
FU NIH
FX Data obtained using NIH RePORTer (http://projectreporter.nih.gov) for
all SBIR/STTR contract and grant awards between FY09-13.
NR 72
TC 3
Z9 3
U1 4
U2 27
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-5116
EI 1939-0041
J9 WIRES NANOMED NANOBI
JI Wiley Interdiscip. Rev.-Nanomed. Nanobiotechnol.
PD MAY-JUN
PY 2015
VL 7
IS 3
BP 251
EP 265
DI 10.1002/wnan.1318
PG 15
WC Nanoscience & Nanotechnology; Medicine, Research & Experimental
SC Science & Technology - Other Topics; Research & Experimental Medicine
GA CF8LK
UT WOS:000352811000001
PM 25429991
ER
PT J
AU Sigurdardottir, EE
Turesson, I
Lund, SH
Lindqvist, EK
Mailankody, S
Korde, N
Bjorkholm, M
Landgren, O
Kristinsson, SY
AF Sigurdardottir, Elin Edda
Turesson, Ingemar
Lund, Sigrun Helga
Lindqvist, Ebba K.
Mailankody, Sham
Korde, Neha
Bjorkholm, Magnus
Landgren, Ola
Kristinsson, Sigurdur Y.
TI The Role of Diagnosis and Clinical Follow-up of Monoclonal Gammopathy of
Undetermined Significance on Survival in Multiple Myeloma
SO JAMA ONCOLOGY
LA English
DT Article
ID SIGNIFICANCE MGUS; WORKING GROUP; LONG-TERM; RISK; POPULATION; SWEDEN;
MALIGNANCIES; PROGRESSION; PREVALENCE; VALIDATION
AB IMPORTANCE Multiple myeloma (MM) is consistently preceded by the precursor state, monoclonal gammopathy of undetermined significance (MGUS). The average annual risk of progression from MGUS to multiple myeloma is 0.5% to 1.0%. Current guidelines suggest life-long clinical follow-up of individuals diagnosed as having MGUS depending on risk stratification. The impact of diagnosing and conducting clinical follow-up of MGUS on MM survival is unclear.
OBJECTIVE To estimate the impact of prior knowledge of MGUS diagnosis and comorbidities on MM survival.
DESIGN, SETTING, AND PARTICIPANTS We conducted a population-based study including all patients with MM(MM patients) diagnosed in Sweden (n = 14 798) from 1976 to 2005 (with follow-up until 2007); 394 (2.7%) had previously been diagnosed as having MGUS. Information on comorbidities was gathered for all patients. We calculated survival rates from the time of MM diagnosis, comparing patients with vs those without prior knowledge of MGUS. Using Cox proportional hazards models, we calculated hazard ratios (HRs) and 95% CIs for risk factors for death. chi(2) Tests were used to evaluate differences in comorbidities.
EXPOSURES Prior knowledge of MGUS among MM patients. In a subanalysis, monoclonal (M)-protein concentration and type were used as exposure.
MAIN OUTCOMES AND MEASURES Risk of death and comorbidities.
RESULTS Patients with MM with prior knowledge of MGUS had significantly (HR, 0.86; 95% CI, 0.77-0.96; P<.01) better overall survival (median survival, 2.8 years) than MM patients without prior knowledge of MGUS (median survival, 2.1 years), although MM patients with (vs without) prior knowledge of MGUS had more comorbidities (P<.001). Among MM patients with prior knowledge of MGUS, low M-protein concentration (<0.5 g/dL) at MGUS diagnosis was associated with poorer MM survival (HR, 1.86; 95% CI, 1.13-3.04; P=.01).
CONCLUSIONS AND RELEVANCE Patients with MM with prior knowledge of MGUS had better MM survival, suggesting that earlier treatment of MM leads to better survival. The observation that a low M-protein concentration at MGUS diagnosis was associated with poorer MM survival may reflect less frequent clinical follow-up. Our observations stress the importance of clinical follow-up in patients with MGUS, regardless of risk stratification.
C1 [Sigurdardottir, Elin Edda; Lund, Sigrun Helga; Kristinsson, Sigurdur Y.] Univ Iceland, Fac Med, Stapi 5, Reykjavik 101, Iceland.
[Turesson, Ingemar] Skane Univ Hosp, Dept Hematol & Coagulat Disorders, Malmo, Sweden.
[Lindqvist, Ebba K.; Bjorkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
[Lindqvist, Ebba K.; Bjorkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Mailankody, Sham; Korde, Neha] NCI, Multiple Myeloma Sect, Lymphoid Malignancies Branch, Bethesda, MD 20892 USA.
[Landgren, Ola] Mem Sloan Kettering Canc Ctr, Myeloma Serv, New York, NY 10021 USA.
RP Kristinsson, SY (reprint author), Univ Iceland, Fac Med, Stapi 5, Reykjavik 101, Iceland.
EM sigyngvi@hi.is
RI Kristinsson, Sigurdur /M-2910-2015; Lund, Sigrun Helga/K-9144-2015;
OI Kristinsson, Sigurdur /0000-0002-4964-7476; Lund, Sigrun
Helga/0000-0002-3806-2296; Lindqvist, Ebba K/0000-0001-7662-1338
FU Swedish Cancer Society; Karolinska Institutet Foundations; Marie-Curie
CIG; University of Iceland Research Fund; Icelandic Centre for Research
(RANNIS); Landspitali University Hospital Research Fund
FX This research was supported by grants from the Swedish Cancer Society,
the Karolinska Institutet Foundations, Marie-Curie CIG, the University
of Iceland Research Fund, Icelandic Centre for Research (RANNIS), and
Landspitali University Hospital Research Fund.
NR 26
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PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD MAY
PY 2015
VL 1
IS 2
BP 168
EP 174
DI 10.1001/jamaoncol.2015.23
PG 7
WC Oncology
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GA DW5FK
UT WOS:000383668400008
PM 26181017
ER
PT J
AU Adkins, E
Wang, XL
Sproule, T
Christianson, G
Park, G
Lane-Reticker, SK
Carter, G
Morse, H
Roopenian, D
AF Adkins, Elisabeth
Wang, Xulong
Sproule, Thomas
Christianson, Gregory
Park, Giljun
Lane-Reticker, Sarah Kate
Carter, Gregory
Morse, Herbert
Roopenian, Derry
TI An IL21 reporter mouse reveals a novel population of T-FH precursors in
young mice.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Adkins, Elisabeth; Wang, Xulong; Sproule, Thomas; Christianson, Gregory; Park, Giljun; Lane-Reticker, Sarah Kate; Carter, Gregory; Roopenian, Derry] Jackson Lab, Bar Harbor, ME 04609 USA.
[Adkins, Elisabeth; Carter, Gregory; Roopenian, Derry] Tufts Univ, Sackler Sch Grad Biomed Sci, Boston, MA 02111 USA.
[Morse, Herbert] NIAID, Virol & Cellular Immunol, NIH, Rockville, MD USA.
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VL 194
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PT J
AU Alam, M
Gaida, M
Bergmann, F
Lasitschka, F
Giese, T
Giese, N
Hackert, T
Hinz, U
Hossain, S
Kozlov, S
Ashwell, J
AF Alam, Muhammad
Gaida, Matthias
Bergmann, Frank
Lasitschka, Felix
Giese, Thomas
Giese, Nathalia
Hackert, Thilo
Hinz, Ulf
Hossain, S.
Kozlov, Serguei
Ashwell, Jonathan
TI Selective inhibition of the T cell p38 alternative activation pathway
and pancreatic cancer
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Alam, Muhammad; Ashwell, Jonathan] NCI, Lab Immune Cell Biol, NIH, Bethesda, MD 20892 USA.
[Gaida, Matthias; Bergmann, Frank; Lasitschka, Felix] Univ Heidelberg Hosp, Inst Pathol, Heidelberg, Germany.
[Kozlov, Serguei] NCI, Canc & Dev Biol, NIH, Frederick, MD 21701 USA.
[Hossain, S.] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Giese, Thomas] Heidelberg Univ, Inst Immunol, Heidelberg, Germany.
[Giese, Nathalia; Hackert, Thilo; Hinz, Ulf] Heidelberg Univ, Dept Surg, Heidelberg, Germany.
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VL 194
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GA DQ7RG
UT WOS:000379404502163
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PT J
AU Azzam, K
Madenspacher, J
Lai, LH
Gowdy, K
Cain, D
Clayton, N
Cunningham, W
Janardhan, K
Taylor, G
Fessler, M
AF Azzam, Kathleen
Madenspacher, Jennifer
Lai, Lihua
Gowdy, Kimberly
Cain, Derek
Clayton, Natasha
Cunningham, Willie
Janardhan, Kyathanahalli
Taylor, Gregory
Fessler, Michael
TI A novel role for Irgm1 in immune homeostasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Azzam, Kathleen; Madenspacher, Jennifer; Fessler, Michael] NIEHS, LRB, NIH, Durham, NC USA.
[Lai, Lihua] Zhejiang Univ, Sch Med, Hangzhou, Zhejiang, Peoples R China.
[Gowdy, Kimberly] ECU, Greenville, NC USA.
[Cain, Derek; Clayton, Natasha; Cunningham, Willie; Janardhan, Kyathanahalli] NIEHS, Durham, NC USA.
[Taylor, Gregory] Duke Univ, Durham, NC USA.
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VL 194
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PT J
AU Bayik, D
Wang, J
Gursel, I
Klinman, D
AF Bayik, Defne
Wang, Jing
Gursel, Ihsan
Klinman, Dennis
TI Defined combinations of cytokines plus survival factors drive the
differentiation of human monocytic myeloid derived suppressor cells into
M1-or M2-like macrophages
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Gursel, Ihsan] Bilkent Univ, Ankara, Turkey.
[Bayik, Defne; Wang, Jing; Klinman, Dennis] NCI, Canc & Inflammat Program, NIH, Frederick, MD 21701 USA.
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J9 J IMMUNOL
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VL 194
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GA DQ7RG
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PT J
AU Bhattacharya, P
Dey, R
Dagur, P
Kruhlak, M
Debrabant, A
Okeeffe, NI
McCoy, J
Nakhasi, H
AF Bhattacharya, Parna
Dey, Ranadhir
Dagur, Pradeep
Kruhlak, Michael
Debrabant, Alain
Okeeffe, Nevien Ismail
McCoy, John
Nakhasi, Hira
TI Genetically modified live attenuated L. donovani parasite induces
classical activation of macrophages (M1 phenotype) leading to generation
of Th1 response in BALB/c mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Dagur, Pradeep; McCoy, John] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kruhlak, Michael] NCI, NIH, Bethesda, MD 20892 USA.
[Bhattacharya, Parna; Dey, Ranadhir; Debrabant, Alain; Okeeffe, Nevien Ismail; Nakhasi, Hira] US FDA, DETTD, CBER, Silver Spring, MD USA.
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J9 J IMMUNOL
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PD MAY 1
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VL 194
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PT J
AU Bolland, S
Voynova, E
Skinner, J
Scott, B
Qi, CF
AF Bolland, Silvia
Voynova, Elisaveta
Skinner, Jeffrey
Scott, Bethany
Qi, Chen-Feng
TI Induction of autoimmune disease by adoptive transfer of an atypical NK
cell subset
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Bolland, Silvia; Voynova, Elisaveta; Skinner, Jeffrey; Scott, Bethany; Qi, Chen-Feng] NIAID, NIH, Rockville, MD USA.
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J9 J IMMUNOL
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PD MAY 1
PY 2015
VL 194
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GA DQ7RG
UT WOS:000379404501264
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PT J
AU Caspi, R
Mattapallil, M
Rigden, R
Zarate-Blades, C
Silver, P
Luger, D
Chan, CC
AF Caspi, Rachel
Mattapallil, Mary
Rigden, Rachael
Zarate-Blades, Carlos
Silver, Phyllis
Luger, Dror
Chan, Chi Chao
TI Neuroprotective effects of IL-22 during CNS inflammation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Caspi, Rachel; Mattapallil, Mary; Rigden, Rachael; Zarate-Blades, Carlos; Silver, Phyllis; Luger, Dror; Chan, Chi Chao] NEI, NIH, Bethesda, MD 20892 USA.
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J9 J IMMUNOL
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PD MAY 1
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VL 194
SU 1
MA CCR4P.203
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GA DQ7RG
UT WOS:000379404501035
ER
PT J
AU Chen, GB
Subedi, K
Mi, J
Shi, A
Weng, NP
AF Chen, Guobing
Subedi, Kalpana
Mi, Jenny
Shi, Alvin
Weng, Nan-Ping
TI Histone methyltransferase Ezh2 is critical for activation-induced CD8 T
cell proliferation and survival
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Chen, Guobing; Subedi, Kalpana; Mi, Jenny; Shi, Alvin; Weng, Nan-Ping] NIA, NIH, Baltimore, MD 21224 USA.
RI Chen, Guobing/D-9572-2012
OI Chen, Guobing/0000-0002-2401-6168
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VL 194
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GA DQ7RG
UT WOS:000379404502229
ER
PT J
AU Chen, P
Denniston, A
Hannes, S
Tucker, W
Wei, L
Liu, BY
Hirani, S
Li, ZY
Lee, R
Sen, H
Nussenblatt, R
AF Chen, Ping
Denniston, Alastair
Hannes, Susan
Tucker, William
Wei, Lai
Liu, Baoying
Hirani, Sima
Li, Zhiyu
Lee, Richard
Sen, H.
Nussenblatt, Robert
TI Myeloid dendritic cells with elevated CD1c expression in non-infectious
uveitis patients exhibited mature phenotype through the regulation of
TNFa-p38 MAPK pathway
SO JOURNAL OF IMMUNOLOGY
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CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
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C1 [Chen, Ping; Hannes, Susan; Tucker, William; Wei, Lai; Liu, Baoying; Hirani, Sima; Li, Zhiyu; Sen, H.; Nussenblatt, Robert] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Denniston, Alastair] Queen Elizabeth Hosp Birmingham, Edgbaston, England.
[Lee, Richard] Univ Bristol, Bristol, Avon, England.
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Hodes, R
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TI T cell development is regulated by the coordinated function of two Lck
promoters
SO JOURNAL OF IMMUNOLOGY
LA English
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CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Chiang, Jeffrey] NCI, EIB, NIH, Bethesda, MD 20892 USA.
[Hodes, Richard] NIA, NIH, Bethesda, MD 20892 USA.
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VL 194
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UT WOS:000379404504330
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PT J
AU Cunningham, M
Myers, J
Cooper, L
Kem, D
Stavrakis, S
Shevach, E
Fairweather, D
Stoner, J
Cox, C
AF Cunningham, Madeleine
Myers, Jennifer
Cooper, Leslie
Kem, David
Stavrakis, Stavros
Shevach, Ethan
Fairweather, DeLisa
Stoner, Julie
Cox, Carol
TI Cardiac myosin and the Th17 immunophenotype in human autoimmune
myocarditis
SO JOURNAL OF IMMUNOLOGY
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CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Cunningham, Madeleine; Myers, Jennifer; Kem, David; Stavrakis, Stavros; Stoner, Julie; Cox, Carol] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA.
[Cooper, Leslie] Mayo Clin, Rochester, MN USA.
[Shevach, Ethan] Natl Inst Allergy & Immunol, Bethesda, MD USA.
[Fairweather, DeLisa] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
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VL 194
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PT J
AU Dileepan, T
Linehan, J
Cleary, P
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Linehan, Jonathan
Cleary, P.
Jenkins, Marc
TI Robust Th17 response to intranasal group A streptococcal infection
requires IL-6 produced by CD301b(+)CD11b(+)CD103(-) migratory dendritic
cells
SO JOURNAL OF IMMUNOLOGY
LA English
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CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Dileepan, Thamotharampillai; Cleary, P.; Jenkins, Marc] Univ Minnesota, Minneapolis, MN USA.
[Linehan, Jonathan] NIAID, Bethesda, MD 20892 USA.
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PU AMER ASSOC IMMUNOLOGISTS
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PY 2015
VL 194
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GA DQ7RG
UT WOS:000379404504052
ER
PT J
AU Felber, B
Bergamaschi, C
Ng, SM
Chen, S
Bear, J
Alicea, C
Beach, RK
Chertova, E
Sowder, R
Pavlakis, G
AF Felber, Barbara
Bergamaschi, Cristina
Ng, Sin Man
Chen, Stephanie
Bear, Jenifer
Alicea, Candido
Beach, Rachel Kelly
Chertova, Elena
Sowder, Raymond
Pavlakis, George
TI Heterodimeric IL-15 regulates the balance of effector and regulatory
cells, promoting anti-cancer tumor effects
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Felber, Barbara; Bergamaschi, Cristina; Ng, Sin Man; Chen, Stephanie; Bear, Jenifer; Alicea, Candido; Beach, Rachel Kelly; Pavlakis, George] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
[Chertova, Elena; Sowder, Raymond] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD USA.
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J9 J IMMUNOL
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PD MAY 1
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VL 194
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MA CCR4P.213
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GA DQ7RG
UT WOS:000379404501030
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PT J
AU Golding, A
Darko, S
Wylie, W
Douek, D
Shevach, E
AF Golding, Amit
Darko, Samuel
Wylie, William
Douek, Daniel
Shevach, Ethan
TI Deep sequencing of the TCRB repertoire of human Foxp3(+) and Foxp3(-) T
cells demonstrates that they are completely distinct and non-overlapping
SO JOURNAL OF IMMUNOLOGY
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CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Golding, Amit] Univ Maryland, Dept Rheumatol, Baltimore, MD 21201 USA.
[Golding, Amit] VA Maryland Hlth Care Syst, Med Res, Baltimore, MD USA.
[Darko, Samuel; Wylie, William; Douek, Daniel] NIAID, VRC, NIH, Bethesda, MD 20892 USA.
[Shevach, Ethan] NIAID, LI, NIH, Bethesda, MD 20892 USA.
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PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
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J9 J IMMUNOL
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PD MAY 1
PY 2015
VL 194
SU 1
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GA DQ7RG
UT WOS:000379404503275
ER
PT J
AU Gomez-Rodriguez, J
Meylan, F
Handon, R
Hayes, E
Siegel, R
Schwartzberg, P
AF Gomez-Rodriguez, Julio
Meylan, Francoise
Handon, Robin
Hayes, Erika
Siegel, Richard
Schwartzberg, Pamela
TI The Tec family kinase Itk is required for Th9 cell differentiation
SO JOURNAL OF IMMUNOLOGY
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CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Gomez-Rodriguez, Julio; Meylan, Francoise; Handon, Robin; Hayes, Erika; Siegel, Richard; Schwartzberg, Pamela] NIH, Bethesda, MD 20892 USA.
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J9 J IMMUNOL
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PD MAY 1
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VL 194
SU 1
MA LYM8P.642
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GA DQ7RG
UT WOS:000379404503271
ER
PT J
AU Gowdy, K
Madenspacher, J
Thomas, S
Nakano, H
Cook, D
Fessler, M
AF Gowdy, Kymberly
Madenspacher, Jennifer
Thomas, Seddon
Nakano, Hideki
Cook, Donald
Fessler, Michael
TI Novel role for scavenger receptor B-I in neutrophilic asthma
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Madenspacher, Jennifer; Thomas, Seddon; Nakano, Hideki; Cook, Donald; Fessler, Michael] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
[Gowdy, Kymberly] East Carolina Univ, Pharmacol & Toxicol, Greenville, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRC10P.419
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503248
ER
PT J
AU Green, S
Smith, M
Hasley, R
Stephany, D
Harned, A
Nagashima, K
Imamichi, T
Qin, J
Rupert, A
Ober, A
Lane, H
Catalfamo, M
AF Green, Samantha
Smith, Mindy
Hasley, Rebecca
Stephany, David
Harned, Adam
Nagashima, Kunio
Imamichi, Tomozumi
Qin, Jing
Rupert, Adam
Ober, Alexander
Lane, H.
Catalfamo, Marta
TI Increased activated platelet-T cell conjugates in patients with HIV
infection: relationship between coagulation/inflammation and T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Green, Samantha; Smith, Mindy; Hasley, Rebecca; Ober, Alexander; Lane, H.; Catalfamo, Marta] NIAID, CMRS LIR, NIH, Bethesda, MD 20892 USA.
[Stephany, David] NIAID, NIH, Bethesda, MD 20892 USA.
[Harned, Adam; Nagashima, Kunio] Leidos Biomed Res Inc, Electron Microscopy Lab, Canc Res Technol Program, Frederick, MD USA.
[Imamichi, Tomozumi] Leidos Biomed Res Inc, Collaborat Clin Res Branch, Frederick, MD USA.
[Qin, Jing] NIAID, DCR BRB, NIH, Rockville, MD USA.
[Rupert, Adam] Leidos Biomed Res Inc, AIDS Monitoring Labs, Frederick, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504064
ER
PT J
AU Gros, A
Tran, E
Pasetto, A
Parkhurst, MR
Prickett, T
Gartner, J
Yu, ZY
Wunderlich, J
Robbins, P
Yang, J
Rosenberg, S
AF Gros, Alena
Tran, Eric
Pasetto, Anna
Parkhurst, Maria R.
Prickett, Todd
Gartner, Jared
Yu, Zhiya
Wunderlich, John
Robbins, Paul
Yang, James
Rosenberg, Steve
TI PD-1 expression on peripheral blood lymphocytes enables direct
enrichment of mutation-specific lymphocytes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Gros, Alena; Tran, Eric; Pasetto, Anna; Parkhurst, Maria R.; Prickett, Todd; Gartner, Jared; Yu, Zhiya; Wunderlich, John; Robbins, Paul; Yang, James; Rosenberg, Steve] NCI, Surg Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC12P1117
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501021
ER
PT J
AU Guenther, G
Telford, W
AF Guenther, Garret
Telford, William
TI Comparison of flow cytometers using the side population technique to
identify stem cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Guenther, Garret] ACEA Biosci, San Diego, CA USA.
[Telford, William] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA TECH2P.900
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504164
ER
PT J
AU Gurusamy, D
Shoe, J
Hocker, J
Hurwitz, A
AF Gurusamy, Devikala
Shoe, Jennifer
Hocker, James
Hurwitz, Arthur
TI A role for IL-13 in the progression of prostate tumors
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Gurusamy, Devikala; Shoe, Jennifer; Hocker, James; Hurwitz, Arthur] NCI, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504297
ER
PT J
AU Hajduczki, A
Bundoc, V
Berger, E
AF Hajduczki, Agnes
Bundoc, Virgilio
Berger, Edward
TI Developing soluble mimetics of the chemokine receptor CCR5 for the study
of HIV Env/receptor interactions
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Hajduczki, Agnes; Bundoc, Virgilio; Berger, Edward] NIAID, Lab Viral Dis, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA CCR6P.216
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502025
ER
PT J
AU Hart, G
Gordon, E
Waisberg, M
Tran, T
Akkaya, M
Skinner, J
Zinocker, S
Pena, M
Yazew, T
Qi, CF
Miller, L
Pierce, S
AF Hart, Geoffrey
Gordon, Emile
Waisberg, Michael
Tran, Tuan
Akkaya, Munir
Skinner, Jeffrey
Zinocker, Severin
Pena, Mirna
Yazew, Takele
Qi, Chenfeng
Miller, Louis
Pierce, Susan
TI Inhibiting the mammalian target of rapamycin as an adjunctive therapy
for cerebral malaria
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Hart, Geoffrey; Gordon, Emile; Waisberg, Michael; Tran, Tuan; Akkaya, Munir; Skinner, Jeffrey; Zinocker, Severin; Pena, Mirna; Yazew, Takele; Qi, Chenfeng; Miller, Louis; Pierce, Susan] NIAID, NIH, Rockville, MD USA.
[Gordon, Emile] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Waisberg, Michael] Univ Virginia, Sch Med, Dept Pathol, Charlottesville, VA 22908 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA MPF7P.714
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503045
ER
PT J
AU Hayes, E
Villarreal, S
Ferdinand, J
Engel, O
Meylan, F
Siegel, R
AF Hayes, Erika
Villarreal, Sarah
Ferdinand, John
Engel, Odile
Meylan, Francoise
Siegel, Richard
TI The TNF-family cytokine receptor death-receptor 3 (TNFRSF25) is required
for nephritis but not systemic autoimmunity in the Ipr murine model of
lupus
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Hayes, Erika; Villarreal, Sarah; Ferdinand, John; Engel, Odile; Meylan, Francoise; Siegel, Richard] NIAMS, Immunoregulat Sect, Autoimmun Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA CCR5P.209
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501055
ER
PT J
AU Hessell, A
Sacha, J
Kahl, C
Graham, B
Mascola, J
Haigwood, N
AF Hessell, Ann
Sacha, Jonah
Kahl, Christoph
Graham, Barney
Mascola, John
Haigwood, Nancy
TI Post-exposure treatment with neutralizing monoclonal antibodies prevents
SHIV infection in infant rhesus macaques and limits establishment of
latent viral reservoirs
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Hessell, Ann; Sacha, Jonah; Kahl, Christoph; Haigwood, Nancy] Oregon Hlth & Sci Univ, Beaverton, OR USA.
[Graham, Barney; Mascola, John] NIAID, Vaccine Res Ctr, NIH, Bethesday, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500212
ER
PT J
AU Jain, S
Adkins, E
Christianson, G
Sproule, T
Roopenian, D
Morse, H
AF Jain, Shweta
Adkins, Elisabeth
Christianson, Gregory
Sproule, Thomas
Roopenian, Derry
Morse, Herbert
TI Interleukin 6 (IL6) is an important upstream contributor towards the
progression of SLE-like disease in BXSB.Yaa mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Jain, Shweta; Morse, Herbert] NIAID, NIH, Rockville, MD USA.
[Adkins, Elisabeth; Christianson, Gregory; Sproule, Thomas; Roopenian, Derry] Jackson Labs, Bar Harbor, ME USA.
[Adkins, Elisabeth] Tufts Univ, Sackler Sch Grad Biomed Sci, Genet Program, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA BA11P.134
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504141
ER
PT J
AU Jain, S
Trivett, M
Ayala, V
Coren, L
Barsov, E
Ohlen, C
Ott, D
AF Jain, Sumiti
Trivett, Matthew
Ayala, Victor
Coren, Lori
Barsov, Eugene
Ohlen, Claes
Ott, David
TI SIV-specific rhesus CD4 T cells expressing African green monkey TRIM5
alpha exhibit prolonged persistence and enhanced antiviral function.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Jain, Sumiti; Trivett, Matthew; Ayala, Victor; Coren, Lori; Barsov, Eugene; Ohlen, Claes; Ott, David] Frederick Natl Lab Canc Res, AIDS & Canc Virus Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VIR1P.1153
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500033
ER
PT J
AU Janosko, K
Cohen, M
Josleyn, N
Zhang, TF
Cong, Y
Jahrling, P
Johnson, R
AF Janosko, Krisztina
Cohen, Melanie
Josleyn, Nicole
Zhang, Tengfei
Cong, Yu
Jahrling, Peter
Johnson, Reed
TI Pro-inflammatory cytokine production by activated monocytes and
macrophages in response to cowpox virus infection in cynomologus
macaques
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Janosko, Krisztina; Cohen, Melanie; Josleyn, Nicole; Zhang, Tengfei; Cong, Yu; Jahrling, Peter] NIAID, Integrated Res Facil, Frederick, MD USA.
[Jahrling, Peter; Johnson, Reed] NIAID, Emerging Viral Pathogens Sect, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VIR9P.1144
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502002
ER
PT J
AU Jeon, H
Williams, J
Hodes, R
AF Jeon, Hyein
Williams, Joy
Hodes, Richard
TI Cell types and cell signals important for normal thymic medullary
epithelial cell development
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Jeon, Hyein; Williams, Joy] NCI, NIH, Bethesda, MD 20892 USA.
[Hodes, Richard] NIH, NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HEM7P.231
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504211
ER
PT J
AU Josleyn, N
Yellayi, S
Martinez, M
Janosko, K
Adams, R
Burdette, T
Cohen, M
Zhang, TF
Jahrling, P
Johnson, R
AF Josleyn, Nicole
Yellayi, Srikanth
Martinez, Mark
Janosko, Krisztina
Adams, Ricky
Burdette, Tracey
Cohen, Melanie
Zhang, Tengfei
Jahrling, Peter
Johnson, Reed
TI Evaluation of bone marrow in cowpox virus infection in cynomolgus
macaques
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Josleyn, Nicole; Yellayi, Srikanth; Martinez, Mark; Janosko, Krisztina; Adams, Ricky; Burdette, Tracey; Cohen, Melanie; Zhang, Tengfei; Jahrling, Peter] NIAID, Integrated Res Facil, NIH, Frederick, MD USA.
[Jahrling, Peter; Johnson, Reed] NIAID, Emerging Viral Pathogens Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VIR1P.1127
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500041
ER
PT J
AU Kamphorst, A
Watanabe, M
Araki, K
Rasheed, MAU
Davis, C
Yang, S
Konieczny, B
Hodes, R
Ahmed, R
AF Kamphorst, Alice
Watanabe, Masashi
Araki, Koichi
Rasheed, Mohammed Ata Ur
Davis, Carl
Yang, Shu
Konieczny, Bogumila
Hodes, Richard
Ahmed, Rafi
TI Differential role of B7 co-stimulation on B cells and dendritic cells
for Th1 and Tfh differentiation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kamphorst, Alice; Araki, Koichi; Rasheed, Mohammed Ata Ur; Davis, Carl; Yang, Shu; Konieczny, Bogumila; Ahmed, Rafi] Emory Univ, Sch Med, Emory Vaccine Ctr, Microbiol & Immunol, Atlanta, GA USA.
[Watanabe, Masashi; Hodes, Richard] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA LYM8P.631
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503259
ER
PT J
AU Kang, JG
Sung, HJ
Amar, M
Remaley, A
Springer, D
Kwon, J
Chen, JC
Wang, PY
Hwang, P
AF Kang, Ju-Gyeong
Sung, Ho Joong
Amar, Marcelo
Remaley, Alan
Springer, Danielle
Kwon, Jaeyul
Chen, Jichun
Wang, Pingyuan
Hwang, Paul
TI Low ambient oxygen prevents atherosclerosis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kang, Ju-Gyeong; Amar, Marcelo; Remaley, Alan; Springer, Danielle; Chen, Jichun; Wang, Pingyuan; Hwang, Paul] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Sung, Ho Joong] Eulji Univ, Gyeonggi Do, South Korea.
[Kwon, Jaeyul] Chungnam Natl Univ, Daejeon, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HUM1P.254
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500317
ER
PT J
AU Karauzum, H
Datta, S
AF Karauzum, Hatice
Datta, Sandip
TI Immunization with superantigen-derived oligopeptides protect against
S-aureus bacteremia
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Datta, Sandip] NIAID, NIH, Bethesda, MD 20892 USA.
[Karauzum, Hatice] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC8P.1058
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503175
ER
PT J
AU Kenyon, E
Nayak, D
Moseman, E
McGavern, D
AF Kenyon, Elizabeth
Nayak, Debasis
Moseman, E.
McGavern, Dorian
TI Tetherin (BST-2) promotes control of a persistent infection by reducing
viral spread and T cell exhaustion
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kenyon, Elizabeth; Nayak, Debasis; Moseman, E.; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504055
ER
PT J
AU Khan, B
Mukherjee, P
Taylor, K
Woods, T
Winkler, C
Peterson, K
AF Khan, Burhan
Mukherjee, Piyali
Taylor, Katherine
Woods, Tyson
Winkler, Clayton
Peterson, Karin
TI The role of SARM1 in Toll-like receptor and viral-induced neuronal
apoptosis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Khan, Burhan; Mukherjee, Piyali; Taylor, Katherine; Woods, Tyson; Winkler, Clayton; Peterson, Karin] NIAID, Persistent Viral Dis Lab, NIH, Hamilton, MT USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INM7P.347
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504224
ER
PT J
AU Kielczewski, J
Horai, R
Caspi, R
AF Kielczewski, Jennifer
Horai, Reiko
Caspi, Rachel
TI Retina-specific T cells provide neuroprotection in a mouse model of
glaucoma
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kielczewski, Jennifer; Horai, Reiko; Caspi, Rachel] NEI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA BA6P.140
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500199
ER
PT J
AU Kim, HK
Castro, E
Voong, N
Telford, W
Gress, R
AF Kim, Hye Kyung
Castro, Ehydel
Voong, Nga
Telford, William
Gress, Ronald
TI Enhanced IL-7 responsiveness provides competitive advantage to recent
thymic emigrants in peripheral T cell survival and homeostasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kim, Hye Kyung; Castro, Ehydel; Voong, Nga; Telford, William; Gress, Ronald] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRC8P.451
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504085
ER
PT J
AU Kimura, M
Nakayama, T
Singer, A
AF Kimura, Motoko
Nakayama, Toshinori
Singer, Alfred
TI Strong TCR signaling prolongs lineage uncertainty during MHC-1 specific
positive selection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kimura, Motoko; Nakayama, Toshinori] Chiba Univ, Dept Immunol, Chiba, Japan.
[Singer, Alfred] NCI, NIH, Bethesda, MD 20892 USA.
RI Nakayama, Toshinori/E-1067-2017
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HEM8P.241
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502029
ER
PT J
AU Kiwanuka, K
Lin, JX
Leonard, W
Ryan, J
AF Kiwanuka, Kasalina
Lin, Jian-Xin
Leonard, Warren
Ryan, John
TI STAT5 tetramer formation is critical for mast cell function
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Kiwanuka, Kasalina; Ryan, John] Virginia Commonwealth Univ, Richmond, VA USA.
[Lin, Jian-Xin; Leonard, Warren] NHLBI, NIH, Lab Mol Immunol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HYP4P.312
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502251
ER
PT J
AU Laky, K
Evans, S
Fowlkes, B
AF Laky, Karen
Evans, Sharron
Fowlkes, B.
TI Notch signaling regulates antigen sensitivity of naive CD4(+) T cells by
tuning co-stimulation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Laky, Karen] NIH, Bethesda, MD 20892 USA.
[Laky, Karen; Evans, Sharron; Fowlkes, B.] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA LYM7P.613
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502231
ER
PT J
AU Lalani, A
Luo, C
Morse, H
Xie, P
AF Lalani, Almin
Luo, Chang
Morse, Herbert
Xie, Ping
TI Specific deletion of TRAF3 in myeloid cells leads to spontaneous
inflammation and tumor development in mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Lalani, Almin; Luo, Chang; Xie, Ping] Rutgers State Univ, Dept Cell Biol & Neurosci, Piscataway, NJ USA.
[Morse, Herbert] NIAID, Immunopathol Lab, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INC6P.304
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501326
ER
PT J
AU Le Saout, C
Hasley, R
Imamichi, H
Tcheung, L
Hu, ZH
Smith, M
Rupert, A
Sneller, M
Lane, H
Catalfamo, M
AF Le Saout, Cecile
Hasley, Rebecca
Imamichi, Hiromi
Tcheung, Lueng
Hu, Zonghui
Smith, Mindy
Rupert, Adam
Sneller, Michael
Lane, H.
Catalfamo, Marta
TI Role of IFN-alpha signaling in T cell pool dysregulation during chronic
exposure to type-I IFN under lymphopenic conditions: impact on HIV
pathogenesis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Le Saout, Cecile; Hasley, Rebecca; Imamichi, Hiromi; Tcheung, Lueng; Smith, Mindy; Sneller, Michael; Lane, H.; Catalfamo, Marta] NIAID, CMRS, LIR, Bethesda, MD 20892 USA.
[Hu, Zonghui] NIAID, Biostat Res Branch, DCR, Bethesda, MD 20892 USA.
[Rupert, Adam] SAIC Frederick Inc, AIDS Monitoring Labs, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VIR9P.1145
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501340
ER
PT J
AU Lowe, J
Menendez, D
Nguyen, TA
Grim, S
Resnick, M
Fessler, M
AF Lowe, Julie
Menendez, Daniel
Thuy-Ai Nguyen
Grim, Sara
Resnick, Michael
Fessler, Michael
TI p53 regulates expression of the early response gene tumor necrosis
factor-alpha-induced protein 8 in macrophage
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Lowe, Julie; Menendez, Daniel; Thuy-Ai Nguyen; Grim, Sara; Resnick, Michael; Fessler, Michael] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRM6P.660
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501098
ER
PT J
AU Lu, W
Zhang, Y
Hambleton, S
Lenardo, M
AF Lu, Wei
Zhang, Yu
Hambleton, Sophie
Lenardo, Michael
TI Tripeptidyl peptidase II links intracellular amino acids homeostasis
with immune response through glycolytic pathway
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Lu, Wei; Lenardo, Michael] NIAID, Immunol Lab, MDISS, Bethesda, MD 20892 USA.
[Hambleton, Sophie] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Zhang, Yu] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRM9P.463
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502312
ER
PT J
AU Marrero, B
Liu, Y
Huang, Y
De Jesus, AA
Goldbach-Mansky, R
AF Marrero, Bernadette
Liu, Yin
Huang, Yan
De Jesus, Adriana Almeida
Goldbach-Mansky, Raphaela
TI Comparative studies connecting IFN dysregulation with pathway
dysregulation in 2 autoinflammatory diseases, SAVI and CANDLE
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Marrero, Bernadette; Liu, Yin; Huang, Yan; De Jesus, Adriana Almeida; Goldbach-Mansky, Raphaela] Natl Inst Arthrit Musculoskeletal & Skin, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HUM1P.274
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500313
ER
PT J
AU McBerry, C
Sakai, S
Kauffman, K
Barber, D
AF McBerry, Cortez
Sakai, Shunsuke
Kauffman, Keith
Barber, Daniel
TI Supraphysiological myeloid cell activation during mycobacterial immune
reconstitution inflammatory syndrome
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [McBerry, Cortez; Sakai, Shunsuke; Kauffman, Keith; Barber, Daniel] NIAID, LPD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRC4P.456
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501283
ER
PT J
AU Mehta, G
Sukumar, M
McGavern, D
Restifo, N
AF Mehta, Gautam
Sukumar, Madhuhasan
McGavern, Dorian
Restifo, Nicholas
TI PD-1 blockade reverts motility arrest of transferred tumor-infiltrating
CD8+T cells in adoptive cell transfer immunotherapy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Mehta, Gautam] NINDS, Surg Neurol Branch, Bethesda, MD 20892 USA.
[Mehta, Gautam; Sukumar, Madhuhasan; Restifo, Nicholas] NCI, Surg Branch, Bethesda, MD 20892 USA.
[McGavern, Dorian] NINDS, Viral Immunol & Intravital Imaging Sect, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA TUM7P.1014
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504110
ER
PT J
AU Meylan, F
Richard, A
Tan, C
Hawley, E
Gomez-Rodriguez, J
Goswami, R
Yang, XP
Cruz, A
Penumetcha, P
Hayes, E
Pelletier, M
Gabay, O
Walsh, M
Ferdinand, J
Keane-Myers, A
Choi, YW
O'Shea, J
Al-Shamkhani, A
Kaplan, M
Gery, I
Siegel, R
AF Meylan, Francoise
Richard, Arianne
Tan, Cuiyan
Hawley, Eric
Gomez-Rodriguez, Julio
Goswami, Ritobrata
Yang, Xiangping
Cruz, Anthony
Penumetcha, Pallavi
Hayes, Erika
Pelletier, Martin
Gabay, Odile
Walsh, Matthew
Ferdinand, John
Keane-Myers, Andrea
Choi, Yongwon
O'Shea, John
Al-Shamkhani, Aymen
Kaplan, Mark
Gery, Igal
Siegel, Richard
TI The TNF-family ligand TL1A and its receptor DR3 promote T cell mediated
allergic immunopathology by enhancing differentiation and pathogenicity
of IL-9 producing T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Meylan, Francoise; Richard, Arianne; Hawley, Eric; Yang, Xiangping; Cruz, Anthony; Penumetcha, Pallavi; Hayes, Erika; Pelletier, Martin; Gabay, Odile; Ferdinand, John; O'Shea, John; Siegel, Richard] NIAMS, NIH, Bethesda, MD USA.
[Tan, Cuiyan; Gery, Igal] NEI, NIH, Bethesda, MD 20892 USA.
[Gomez-Rodriguez, Julio] NHGRI, NIH, Bethesda, MD 20892 USA.
[Goswami, Ritobrata; Kaplan, Mark] Indiana Univ Sch Med, Bethesda, IN USA.
[Keane-Myers, Andrea] Biol Naval Med Res Ctr, Ft Detrick, MD USA.
[Al-Shamkhani, Aymen] Univ Southampton, Fac Med, Southhsmpton, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HYP2P.333
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500101
ER
PT J
AU Morozov, G
Zhao, HY
Mage, M
Boyd, L
Venna, R
Norcross, M
McMurtrey, C
Hildebrand, W
Schuck, P
Jiang, JS
Natarajan, K
Margulies, D
AF Morozov, Giora
Zhao, Huaying
Mage, Michael
Boyd, Lisa
Venna, Ramesh
Norcross, Michael
McMurtrey, Curtis
Hildebrand, William
Schuck, Peter
Jiang, Jiansheng
Natarajan, Kannan
Margulies, David
TI Direct interaction of recombinant TAPBPR with MHC-I molecules:
stabilization of peptide-free MHC-I promotes high affinity peptide
loading
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Morozov, Giora; Mage, Michael; Boyd, Lisa; Jiang, Jiansheng; Natarajan, Kannan; Margulies, David] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Zhao, Huaying; Schuck, Peter] NIBIB, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD USA.
[Venna, Ramesh; Norcross, Michael] US FDA, Lab Immunol, Div Therapeut Prot, CDER, Bethesda, MD 20014 USA.
[McMurtrey, Curtis; Hildebrand, William] Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Oklahoma City, OK 73190 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA APP5P.102
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500132
ER
PT J
AU Munitic, I
Giardino-Torchia, ML
Ashwell, J
AF Munitic, Ivana
Giardino-Torchia, Maria Letizia
Ashwell, Jonathan
TI Optineurin is dispensable for LPS- and Salmonella typhimurium-induced
autophagy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Munitic, Ivana] Univ Rijeka, Dept Biotechnol, Rijeka, Croatia.
[Munitic, Ivana; Giardino-Torchia, Maria Letizia; Ashwell, Jonathan] NCI, LICB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INM3P.412
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503223
ER
PT J
AU Myers, L
Joedicke, J
Carmody, A
Messer, R
Dittmer, U
Kim, H
AF Myers, Lara
Joedicke, Jara
Carmody, Aaron
Messer, Ron
Dittmer, Ulf
Kim, Hasenkrug
TI Mechanisms of regulatory T cell activation and expansion utilizing
virus-specific CD8+T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Myers, Lara; Carmody, Aaron; Messer, Ron; Kim, Hasenkrug] NIH, Rocky Mt Labs, Hamilton, MT USA.
[Joedicke, Jara; Dittmer, Ulf] Univ Duisburg Essen, Essen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504060
ER
PT J
AU Myles, I
Datta, S
AF Myles, Ian
Datta, Sandip
TI Transfer factor: forgotten, but not gone
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Myles, Ian; Datta, Sandip] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA MUC2P.934
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504035
ER
PT J
AU Nair, M
Jang, J
Barnes, M
Le Gros, G
Cooper, P
Steel, C
Nutman, T
Lazar, M
AF Nair, Meera
Jang, Jessica
Barnes, Mark
Le Gros, Graham
Cooper, Philip
Steel, Cathy
Nutman, Thomas
Lazar, Mitchell
TI The human protein resistin drives detrimental inflammatory monocyte
responses in helminth infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Nair, Meera; Jang, Jessica; Barnes, Mark] Univ Calif Riverside, Riverside, CA 92521 USA.
[Le Gros, Graham] Malaghan Inst, Wellington, New Zealand.
[Cooper, Philip] Lab Invest Ecuador, Quito, Ecuador.
[Steel, Cathy; Nutman, Thomas] NIH, Bethesda, MD 20892 USA.
[Lazar, Mitchell] Univ Penn, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA MPF7P.710
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503046
ER
PT J
AU Nakano, H
Moran, T
Nakano, K
Whitehead, G
Thomas, S
Cook, D
AF Nakano, Hideki
Moran, Timothy
Nakano, Keiko
Whitehead, Gregory
Thomas, Seddon
Cook, Donald
TI CCR2 promotes accumulation of conventional dendritic cells in the lung
during inflammation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Nakano, Hideki; Moran, Timothy; Nakano, Keiko; Whitehead, Gregory; Thomas, Seddon; Cook, Donald] NIEHS, Res Triangle Pk, NC 27709 USA.
[Moran, Timothy] Univ N Carolina, Sch Med, Pediat, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA CAM4P.149
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502207
ER
PT J
AU Navid, F
Layh-Schmitt, G
Colbert, R
AF Navid, Fatemeh
Layh-Schmitt, Gerlinde
Colbert, Robert
TI Autophagy reduces the accumulation of misfolded HLA-B27 in a rat model
of spondyloarthritis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Navid, Fatemeh; Layh-Schmitt, Gerlinde; Colbert, Robert] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA THER2P.951
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500014
ER
PT J
AU Ong, S
Ligons, D
Barin, J
Wu, L
Talor, M
Diny, N
Fontes, J
Gebremariam, E
Rose, N
Cihakova, D
AF Ong, SuFey
Ligons, Davinna
Barin, Jobert
Wu, Lei
Talor, Monica
Diny, Nicola
Fontes, Jillian
Gebremariam, Elizabeth
Rose, Noel
Cihakova, Daniela
TI Natural killer cells protect against cardiac inflammation and fibrosis
by directly limiting eosinophilic accumulation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Ong, SuFey; Wu, Lei; Diny, Nicola; Fontes, Jillian] Johns Hopkins Bloomberg Sch Publ Hlth, Mol Microbiol & Immunol, Baltimore, MD USA.
[Ong, SuFey] Benaroya Res Inst, Immunol Grp, Seattle, WA USA.
[Barin, Jobert; Talor, Monica; Gebremariam, Elizabeth; Rose, Noel; Cihakova, Daniela] Johns Hopkins Univ, Sch Med, Pathol, Baltimore, MD USA.
[Ligons, Davinna] NCI, NIH, Bethesda, MD 20892 USA.
RI Cihakova, Daniela /A-9821-2017
OI Cihakova, Daniela /0000-0002-8713-2860
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA BA7P.144
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501263
ER
PT J
AU Park, JH
Luckey, M
Liu, Y
Shaw, S
AF Park, Jung-Hyun
Luckey, Megan
Liu, Yin
Shaw, Stephen
TI Constitutively active ezrin desensitizes IL-7 signaling and impairs T
cell homeostasis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Park, Jung-Hyun; Luckey, Megan; Shaw, Stephen] NCI, Bethesda, MD 20892 USA.
[Liu, Yin] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA LYM2P.735
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503231
ER
PT J
AU Paschall, A
Zhang, RH
Qi, CF
Bardhan, K
Peng, L
Lu, GM
Yang, JJ
Merad, M
McGaha, T
Zhou, G
Mellor, A
Abrams, S
Morse, H
Ozato, K
Xiong, HB
Liu, KB
AF Paschall, Amy
Zhang, Rui-hua
Qi, Chen-Feng
Bardhan, Kankana
Peng, Liang
Lu, Geming
Yang, Jianjun
Merad, Miriam
McGaha, Tracy
Zhou, Gang
Mellor, Andrew
Abrams, Scott
Morse, Herbert
Ozato, Keiko
Xiong, Huabao
Liu, Kebin
TI IRF8 expressed in T cells regulates GM-CSF expression to control myeloid
derived suppressor cell differentiation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Paschall, Amy; Bardhan, Kankana; Liu, Kebin] Georgia Regents Univ, Biochem & Mol Biol, Augusta, GA USA.
[Paschall, Amy; Liu, Kebin] Charlie Norwood VA Med Ctr, Augusta, GA USA.
[Paschall, Amy; McGaha, Tracy; Zhou, Gang; Mellor, Andrew; Liu, Kebin] Georgia Regents Univ, Canc Immunol Inflammat & Tolerance, Augusta, GA USA.
[Zhang, Rui-hua; Peng, Liang; Lu, Geming; Yang, Jianjun; Merad, Miriam; Xiong, Huabao] Icahn Sch Med Mt Sinai, Immunol Inst, New York, NY 10029 USA.
[Qi, Chen-Feng; Morse, Herbert] NIAID, Immunogenet Lab, NIH, Bethesda, MD 20892 USA.
[Abrams, Scott] Roswell Pk Canc Inst, Immunol, Buffalo, NY 14263 USA.
[Ozato, Keiko] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, Programs Genom Differentiat, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA TUM6P.955
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503112
ER
PT J
AU Patial, S
Stumpo, D
Huang, W
Flake, G
Blackshear, P
AF Patial, Sonika
Stumpo, Deborah
Huang, Weichun
Flake, Gordon
Blackshear, Perry
TI Genetic deletion of AU-rich region in the tristetraprolin (TTP)
transcript increases TTP stability and expression and provides
protection against inflammatory diseases
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Patial, Sonika; Stumpo, Deborah; Blackshear, Perry] NIEHS, Lab Signal Transduct, Durham, NC USA.
[Huang, Weichun] NIEHS, Biostat Branch, Durham, NC USA.
[Flake, Gordon] NIEHS, Lab Expt Pathol, Durham, NC USA.
[Blackshear, Perry] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Blackshear, Perry] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INM1P.433
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503295
ER
PT J
AU Paylakis, G
Bergamaschi, C
Valentin, A
Kulkarni, V
Jalah, R
Rosati, M
Alicea, C
Sowder, R
Chertova, E
Felber, B
AF Paylakis, George
Bergamaschi, Cristina
Valentin, Antonio
Kulkarni, Viraj
Jalah, Rashmi
Rosati, Margherita
Alicea, Candido
Sowder, Raymond
Chertova, Elena
Felber, Barbara
TI Use of heterodimeric IL-15 in immune therapeutic regimens against HIV-1
or SIV infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Paylakis, George; Bergamaschi, Cristina; Valentin, Antonio; Kulkarni, Viraj; Jalah, Rashmi; Rosati, Margherita; Alicea, Candido; Felber, Barbara] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
[Sowder, Raymond; Chertova, Elena] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC8P.1048
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503169
ER
PT J
AU Penaloza-MacMaster, P
Barber, D
Wherry, E
Provine, N
Teigler, JE
Parenteau, L
Blackmore, S
Borducchi, E
Larocca, R
Yates, K
Shen, H
Haining, W
Sommerstein, R
Pinschewer, D
Ahmed, R
Barouch, D
AF Penaloza-MacMaster, Pablo
Barber, Daniel
Wherry, E.
Provine, Nicholas
Teigler, Jeffrey E.
Parenteau, Lily
Blackmore, Stephen
Borducchi, Erica
Larocca, Rafael
Yates, Kathleen
Shen, Hao
Haining, W.
Sommerstein, Rami
Pinschewer, Daniel
Ahmed, Rafi
Barouch, Dan
TI LCMV-specific CD4 T cells induce immunopathology and impair immune
protection following chronic LCMV infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Penaloza-MacMaster, Pablo; Provine, Nicholas; Teigler, Jeffrey E.; Parenteau, Lily; Blackmore, Stephen; Borducchi, Erica; Larocca, Rafael; Barouch, Dan] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Ctr Virol & Vaccine Res, Boston, MA USA.
[Barber, Daniel] NIAID, Parasit Dis Lab, Bethesda, MD USA.
[Wherry, E.; Shen, Hao] Univ Penn, Dept Microbiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Wherry, E.; Shen, Hao] Univ Penn, Inst Immunol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Yates, Kathleen; Haining, W.] Harvard Med Sch, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA USA.
[Sommerstein, Rami; Pinschewer, Daniel] Univ Geneva, Dept Pathol & Immunol, Geneva, Switzerland.
[Sommerstein, Rami; Pinschewer, Daniel] Univ Geneva, WHO Collaborating Ctr Vaccine Immunol, Geneva, Switzerland.
[Pinschewer, Daniel] Univ Basel, Dept Biomed Haus Peterspl, Div Expt Virol, Basel, Switzerland.
[Ahmed, Rafi] Emory Univ, Sch Med, Emory Vaccine Ctr, Atlanta, GA USA.
[Ahmed, Rafi] Emory Univ, Sch Med, Dept Microbiol & Immunol, Atlanta, GA 30322 USA.
[Barouch, Dan] Ragon Inst MGH MIT & Harvard, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VIR1P.1132
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500022
ER
PT J
AU Placek, K
Cui, KR
Hu, GQ
Lee, JE
Wang, CC
Konkel, J
Zhang, DF
Chen, WJ
Ge, K
Zhao, KJ
AF Placek, Katarzyna
Cui, Kairong
Hu, Gangqing
Lee, Ji-Eun
Wang, Chaochen
Konkel, Joanne
Zhang, Dunfang
Chen, WanJun
Ge, Kai
Zhao, Keji
TI KMT2D histone methyltransferase modulates chromatin accessibility during
regulatory T cell development
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Placek, Katarzyna; Cui, Kairong; Hu, Gangqing; Zhao, Keji] NHLBI, NIH, Bethesda, MD 20892 USA.
[Lee, Ji-Eun; Wang, Chaochen; Ge, Kai] NIDDK, NIH, Bethesda, MD 20892 USA.
[Konkel, Joanne] Univ Manchester, Manchester, Lancs, England.
[Zhang, Dunfang; Chen, WanJun] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA LYM6P.714
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502109
ER
PT J
AU Rajagopalan, S
Lee, E
DuPrie, M
Long, E
AF Rajagopalan, Sumati
Lee, Elizabeth
DuPrie, Matthew
Long, Eric
TI TRAF6 and TAK1 control signals for a senescence response by an endosomal
NK cell receptor
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Rajagopalan, Sumati; Lee, Elizabeth; DuPrie, Matthew; Long, Eric] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INC2P.414
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502088
ER
PT J
AU Rua, R
McGavern, D
AF Rua, Rejane
McGavern, Dorian
TI Alternatively activated brain-resident macrophages rapidly acquire
inflammatory properties following CNS infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Rua, Rejane; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INC6P.301
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501308
ER
PT J
AU Rus, H
Tegla, C
Cudrici, C
Nguyen, V
Kruszewski, A
Mekala, A
Rus, V
Badea, T
AF Rus, Horea
Tegla, Cosmin
Cudrici, Cornelia
Vinh Nguyen
Kruszewski, Adam
Mekala, Amurgam
Rus, Violeta
Badea, Tudor
TI RGC-32 regulates T lymphocyte cell cycle activation in a
phosphatidylinositol 3-kinase and IL-2-dependent manner
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Rus, Horea; Tegla, Cosmin; Cudrici, Cornelia; Vinh Nguyen; Kruszewski, Adam; Mekala, Amurgam; Rus, Violeta] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Rus, Horea; Tegla, Cosmin] Vet Adm Maryland Hlth Care Sysytem, Baltimore, MD USA.
[Badea, Tudor] NEI, Retinal Circuit Dev & Genet Unit, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRC8P.442
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504092
ER
PT J
AU Rus, V
Nguyen, V
Badea, T
Cudrici, C
Tegla, C
Mekala, A
Rus, H
AF Rus, Violeta
Vinh Nguyen
Badea, Tudor
Cudrici, Cornelia
Tegla, Cosmin
Mekala, Armugam
Rus, Horea
TI RGC-32 enhances suboptimal CD8 cytotoxic T cell effector function in
acute graft versus host disease and promotes lupus-like disease in
chronic graft versus host disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Rus, Violeta; Vinh Nguyen; Tegla, Cosmin; Mekala, Armugam; Rus, Horea] VAMHCS, Res Serv, Baltimore, MD USA.
[Badea, Tudor] NEI, Retinal Circuit Dev & Genet Unit, N NRL, NIH, Bethesda, MD 20892 USA.
[Cudrici, Cornelia] NIAMS, NIH, Bethesda, MD USA.
[Rus, Violeta; Vinh Nguyen; Tegla, Cosmin; Mekala, Armugam; Rus, Horea] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA THER2P.965
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500009
ER
PT J
AU Saxena, A
Xiao, ZX
Yagita, H
Larman, B
Donner, T
Hamad, AR
AF Saxena, Ankit
Xiao, Zuoxiang
Yagita, Hideo
Larman, Ben
Donner, Thomas
Hamad, Abdel Rahim
TI FasL-expressing B cells are major players in type 1 diabetes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Saxena, Ankit; Larman, Ben; Donner, Thomas; Hamad, Abdel Rahim] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Xiao, Zuoxiang] NCI Frederick, Ctr Canc Res, Frederick, MD USA.
[Yagita, Hideo] Juntendo Univ, Sch Med, Tokyo, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA BA6P.129
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500180
ER
PT J
AU Sckisel, G
Mirsoian, A
Tietze, J
Monjazeb, A
Blazar, B
Wiltrout, R
Murphy, W
AF Sckisel, Gail
Mirsoian, Annie
Tietze, Julia
Monjazeb, Arta
Blazar, Bruce
Wiltrout, Robert
Murphy, William
TI Strong systemic cancer immunostimulatory therapies cause stress-induced
acute thymic involution
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Sckisel, Gail; Mirsoian, Annie; Tietze, Julia; Monjazeb, Arta; Murphy, William] UC Davis Sch Med, Dermatol, Sacramento, CA USA.
[Blazar, Bruce] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA.
[Wiltrout, Robert] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC12P1114
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501018
ER
PT J
AU Seedhom, M
David, A
Hickman, H
Bennink, J
Yewdell, J
AF Seedhom, Mina
David, Alexandre
Hickman, Heather
Bennink, Jack
Yewdell, Jonathan
TI The RiboPuromycylation Method Reveals Rapid IL12-Dependent
Antigen-Independent Activation of Bone Marrow Virtual Memory T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Seedhom, Mina; Hickman, Heather; Bennink, Jack; Yewdell, Jonathan] NIAID, Rockville, MD USA.
[David, Alexandre] Inst Genom Fonct, Oncol, Montpellier, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INC1P.403
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503168
ER
PT J
AU Sgourakis, N
AF Sgourakis, Nikolaos
TI Mapping the interaction footprint of Viral Immunoevasins on a "platform"
MHC-1 molecule using solution NMR spectroscopy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Sgourakis, Nikolaos] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA APP2P.102
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502014
ER
PT J
AU Siebenlist, U
Claudio, E
Tassi, I
Wang, HS
AF Siebenlist, Ulrich
Claudio, Estefania
Tassi, Ilaria
Wang, Hongshan
TI Dendritic cells are functionally relevant targets of IL-25 in allergic
lung inflammation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Siebenlist, Ulrich; Claudio, Estefania; Tassi, Ilaria; Wang, Hongshan] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HYP2P.320
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500110
ER
PT J
AU Silvestre, I
Peterson, D
Redelman, D
Anderson, S
Hudig, D
AF Silvestre, Isabel
Peterson, Daniel
Redelman, Douglas
Anderson, Stephen
Hudig, Dorothy
TI Assessment of the Fc receptor CD16A of NK cells of CFS patients for
potential to mediate ADCC activity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Silvestre, Isabel; Hudig, Dorothy] Univ Nevada, Sch Med, Microbiol & Immunol, Reno, NV 89557 USA.
[Peterson, Daniel] Sierra Internal Med, Incline, NV USA.
[Redelman, Douglas] Univ Nevada, Sch Med, Physiol, Reno, NV 89557 USA.
[Anderson, Stephen] NCI, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HUM1P.303
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500333
ER
PT J
AU Skarzynski, M
Butera, V
Lindorfer, M
Vire, B
Farooqui, M
Rader, C
Taylor, R
Wiestner, A
AF Skarzynski, Martin
Butera, Vicent
Lindorfer, Margaret
Vire, Berengere
Farooqui, Mohammed
Rader, Christoph
Taylor, Ronald
Wiestner, Adrian
TI Targeting deposited complement component C3d to potentiate monoclonal
antibody cancer therapy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Skarzynski, Martin; Butera, Vicent; Vire, Berengere; Farooqui, Mohammed; Wiestner, Adrian] NHLBI, North Bethesda, MD USA.
[Lindorfer, Margaret; Taylor, Ronald] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Rader, Christoph] Scripps Res Inst, Jupiter, FL USA.
[Rader, Christoph] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC3P.1057
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501170
ER
PT J
AU Smith, C
Vivekanandan-Giri, A
Playford, M
Berthier, C
Kretzler, M
Mehta, N
Pennathur, S
Kaplan, M
AF Smith, Carolyne
Vivekanandan-Giri, Anuradha
Playford, Martin
Berthier, Celine
Kretzler, Matthias
Mehta, Nehal
Pennathur, Subramaniam
Kaplan, Mariana
TI Modulation of macrophage responses by aberrant lipoproteins in chronic
inflammatory diseases.
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Smith, Carolyne] Univ Michigan, Gaithersburg, MD USA.
[Kaplan, Mariana] NIH, Syst Autoimmun Branch, Bethesda, MD 20892 USA.
[Vivekanandan-Giri, Anuradha; Berthier, Celine; Kretzler, Matthias; Pennathur, Subramaniam] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Playford, Martin; Mehta, Nehal] NHLBI, Sect Inflammat & Cardiometab Dis, NIH, Bethesda, MD 20892 USA.
[Smith, Carolyne] NIAMS, Syst Autoimmun Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HUM3P.241
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500155
ER
PT J
AU Srivastava, A
Paria, B
Chandran, S
Kammula, U
AF Srivastava, Abhishek
Paria, Biman
Chandran, Smita
Kammula, Udai
TI Ex vivo co-stimulatory 4-1BBL enhances the antitumor capacity of antigen
specific CD8+T cells after adoptive transfer in NSG mice
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Srivastava, Abhishek; Paria, Biman; Chandran, Smita; Kammula, Udai] NCI, Surg Branch, NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC7P.1042
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500289
ER
PT J
AU St Leger, A
Caspi, R
AF St Leger, Anthony
Caspi, Rachel
TI Ocular microflora modulates IL-17 and neutrophil recruitment within the
conjunctiva associated lymphoid tissue
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [St Leger, Anthony; Caspi, Rachel] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA MUC9P.739
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502319
ER
PT J
AU Stevanovic, S
Campbell, T
Draper, L
Langhan, M
Somerville, R
Wunderlich, J
Kwong, ML
Kerkar, S
Yang, J
Sherry, R
Kammula, U
Rosenberg, S
Hinrichs, C
AF Stevanovic, Sanja
Campbell, Tracy
Draper, Lindsey
Langhan, Michelle
Somerville, Robert
Wunderlich, John
Kwong, Mei Li
Kerkar, Sid
Yang, James
Sherry, Richard
Kammula, Udai
Rosenberg, Steven
Hinrichs, Christian
TI Adoptive transfer of autologous tumor infiltrating lymphocytes in
metastatic human papilloma virus-induced carcinoma
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Stevanovic, Sanja; Campbell, Tracy; Draper, Lindsey; Langhan, Michelle; Somerville, Robert; Wunderlich, John; Kwong, Mei Li; Yang, James; Sherry, Richard; Kammula, Udai; Rosenberg, Steven; Hinrichs, Christian] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Kerkar, Sid] NCI, Pathol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VAC7P.1040
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500285
ER
PT J
AU Su, XL
Zhang, JL
Yu, L
Xing, ZW
Liang, JQ
Nanda, A
AF Su, Xiulan
Zhang, Jialing
Yu, Lan
Xing, Zhiwei
Liang, Junqing
Nanda, A.
TI Identification of miRNA-338-5P as an effector of the tumor suppressor
activity of immunized anticancer bioactive peptide-3
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Su, Xiulan; Zhang, Jialing; Yu, Lan; Liang, Junqing] Inner Mongolia Peoples Hosp, Clin Med Res Ctr, Hohhot, Peoples R China.
[Zhang, Jialing] NIDCD, Head & Neck Surg Branch, NIH, Betheda, MD USA.
[Xing, Zhiwei] Inner Mongolia Med Univ, Affiliated Hosp, Clin Med Res Ctr, Hohhot, Peoples R China.
[Nanda, A.] Inner Mongolia Med Univ, Affiliated Hosp, Clin Med Res Ctr, Hohhot, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA TUM2P.1036
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500248
ER
PT J
AU Sun, C
Lee, YS
Lipsky, A
Farooqui, M
Herman, S
Salem, D
Stetler-Stevenson, M
Yuan, C
Aue, G
Wiestner, A
AF Sun, Clare
Lee, Yuh Shan
Lipsky, Andrew
Farooqui, Mohammed
Herman, Sarah
Salem, Dalia
Stetler-Stevenson, Maryalice
Yuan, Constance
Aue, Georg
Wiestner, Adrian
TI Effects of the Bruton's tyrosine kinase inhibitor ibrutinib on humoral
immunity in patients with chronic lymphocytic leukemia
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Sun, Clare; Lee, Yuh Shan; Farooqui, Mohammed; Herman, Sarah; Aue, Georg; Wiestner, Adrian] NHLBI, Hematol, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Lipsky, Andrew] Montefiore Med Ctr, Internal Med, 111 E 210th St, Bronx, NY 10467 USA.
[Salem, Dalia; Stetler-Stevenson, Maryalice; Yuan, Constance] NCI, Pathol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
RI Salem, Dalia/R-9314-2016
OI Salem, Dalia/0000-0002-4209-2260
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HUM1P.258
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500304
ER
PT J
AU Tajima, M
Fuss, I
Kitani, A
Strober, W
AF Tajima, Masaki
Fuss, Ivan
Kitani, Atsushi
Strober, Warren
TI Fungal recognition by Dectin-1 on dendritic cells induces IL-10
producing CD4(+) T cells by GATA3 / C/EBP-beta pathway
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Tajima, Masaki; Fuss, Ivan; Kitani, Atsushi; Strober, Warren] NIAID, Lab Host Def, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA MPF4P.733
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503012
ER
PT J
AU Thornton, A
Sebastian, M
Korty, P
Lopez-Ocasio, M
Shevach, E
AF Thornton, Angela
Sebastian, Mathew
Korty, Patricia
Lopez-Ocasio, Maria
Shevach, Ethan
TI Expression of Helios is required for the differentiation of
activated/effector T regulatory cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Thornton, Angela; Sebastian, Mathew; Korty, Patricia; Lopez-Ocasio, Maria; Shevach, Ethan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRC11P.438
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504003
ER
PT J
AU Tosh, K
Singer, S
Sher, A
Jankovic, D
AF Tosh, Kevin
Singer, Steven
Sher, Alan
Jankovic, Dragana
TI Toxoplasma gondii elicits a phagocytosis dependent pro-inflammatory
cytokine response in human primary myeloid cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Tosh, Kevin; Singer, Steven] Georgetown Univ, Microbiol & Immunol, Washington, DC USA.
[Tosh, Kevin; Sher, Alan; Jankovic, Dragana] NIAID, Parasit Dis Lab, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INC4P.327
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404500340
ER
PT J
AU Tse, H
Anderson, B
Ganini, D
Mason, R
AF Tse, Hubert
Anderson, Brian
Ganini, Douglas
Mason, Ron
TI Immuno-spin trapping to detect immune derived free radicals in type 1
diabetes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Tse, Hubert; Anderson, Brian] Univ Alabama Birmingham, Birmingham, AL USA.
[Ganini, Douglas; Mason, Ron] NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA TECH2P.903
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504174
ER
PT J
AU Watanabe, M
Hodes, R
AF Watanabe, Masashi
Hodes, Richard
TI Cellular and molecular basis of Ag-specific and Ag-nonspecific
T-dependent antibody responses in vivo
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Watanabe, Masashi; Hodes, Richard] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA IRC8P.447
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504093
ER
PT J
AU Williams, J
Jeon, H
Hodes, R
AF Williams, Joy
Jeon, Hyein
Hodes, Richard
TI Thymocyte requirements for normal thymic medullary epithelial cell
development
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Williams, Joy; Jeon, Hyein; Hodes, Richard] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HEM7P.227
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504208
ER
PT J
AU Witter, A
Break, T
Indramohan, M
Mummert, M
Berg, R
AF Witter, Alexandra
Break, Timothy
Indramohan, Mohanalaxmi
Mummert, Mark
Berg, Rance
TI Extracellular superoxide dismutase promotes immature neutrophil egress
from the bone marrow
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Witter, Alexandra; Berg, Rance] Univ North Texas, Hlth Sci Ctr, Cell Biol & Immunol, Ft Worth, TX USA.
[Mummert, Mark] Univ North Texas, Hlth Sci Ctr, Psychiat & Behav Hlth, Ft Worth, TX USA.
[Break, Timothy] NIAID, NIH, Bethesda, MD 20892 USA.
[Indramohan, Mohanalaxmi] Northwestern Univ, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA INC6P.303
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501316
ER
PT J
AU Yang, Q
Xue, HHH
Bhandoola, A
AF Yang, Qi
Xue, Hai-Hui Howard
Bhandoola, Avinash
TI a conversed gene regulatory pathway underwrites the development of
innate lymphoid cells and adaptive T cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Yang, Qi] Univ Penn, Philadelphia, PA 19104 USA.
[Bhandoola, Avinash] NCI, NIH, Bethesda, MD 20892 USA.
[Xue, Hai-Hui Howard] Univ Iowa, Iowa City, IA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA HEM8P.239
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502031
ER
PT J
AU Yen, JH
Kong, W
Hooper, K
Emig, F
Rahbari, K
Kuo, PC
Scofield, B
Ganea, D
AF Yen, Jui-Hung
Kong, Weimin
Hooper, Kirsten
Emig, Fran
Rahbari, Kate
Kuo, Ping-Chang
Scofield, Barbara
Ganea, Doina
TI Differential effects of IFN beta on IL-12, IL-23, and IL-10 expression
in TLR-stimulated dendritic cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Yen, Jui-Hung; Kuo, Ping-Chang; Scofield, Barbara] Indiana Univ Sch Med, Microbiol & Immunol, Ft Wayne, IN USA.
[Kong, Weimin; Hooper, Kirsten; Emig, Fran; Ganea, Doina] Temple Univ, Sch Med, Microbiol & Immunol, Philadelphia, PA 19122 USA.
[Rahbari, Kate] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA BA7P.157
PG 2
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404501266
ER
PT J
AU Younes, S
Shive, C
Reynaldi, A
Freeman, M
Panigrahi, S
Estes, J
Anderson, J
Schacker, T
Davenport, M
McCune, J
Hunt, P
Lee, S
Serrano-Villar, S
Canaday, D
Cameron, C
Sekaly, RP
Rodriguez, B
Sieg, S
Lederman, M
AF Younes, Souheil
Shive, Carey
Reynaldi, Arnold
Freeman, Michael
Panigrahi, Soumya
Estes, Jacob
Anderson, Jodi
Schacker, Timothy
Davenport, Miles
McCune, Joseph
Hunt, Peter
Lee, Sulggi
Serrano-Villar, Sergio
Canaday, David
Cameron, Cheryl
Sekaly, Rafick-Pierre
Rodriguez, Benigno
Sieg, Scott
Lederman, Michael
TI IL-15 drives CD8 T cell cycling and differentiation in chronic HIV-1
infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Younes, Souheil; Shive, Carey; Panigrahi, Soumya; Cameron, Cheryl; Sekaly, Rafick-Pierre; Rodriguez, Benigno; Sieg, Scott; Lederman, Michael] Case Western Reserve Univ, Infect Dis, Cleveland, OH 44106 USA.
[Freeman, Michael] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Canaday, David] Cleveland VA, Cleveland, OH USA.
[McCune, Joseph] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Estes, Jacob] Frederick Natl Lab Canc Res, AIDS & Canc Virus Program, Frederick, MD USA.
[Anderson, Jodi; Schacker, Timothy] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
[Reynaldi, Arnold; Davenport, Miles] Univ New S Wales, Ctr Vasc Res, Sydney, NSW, Australia.
[Hunt, Peter; Lee, Sulggi] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Serrano-Villar, Sergio] Univ Hosp Ramon y Cajal, Dept Infect Dis, Madrid, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA VIR6P.1162
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404505004
ER
PT J
AU Zander, R
Obeng-Adjei, N
Guthmiller, J
Kulu, D
Li, J
Ongoiba, A
Traore, B
Crompton, P
Butler, N
AF Zander, Ryan
Obeng-Adjei, Nyamekye
Guthmiller, Jenna
Kulu, Divine
Li, Jun
Ongoiba, Aissata
Traore, Boubacar
Crompton, Peter
Butler, Noah
TI Co-inhibitory and co-stimulatory crosstalk regulates helper T cell
differentiation and humoral immunity during Plasmodium infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Zander, Ryan; Guthmiller, Jenna; Kulu, Divine; Butler, Noah] OUHSC, Microbiol & Immunol, Oklahoma City, OK USA.
[Obeng-Adjei, Nyamekye; Crompton, Peter] NIAID, Lab Immunogenet, NIH, Rockville, MD USA.
[Li, Jun] Univ Oklahoma, Dept Chem & Biochem, Norman, OK 73019 USA.
[Ongoiba, Aissata; Traore, Boubacar] Univ Sci Tech & Technol Bamako, Mali Int Ctr Excellence Res, Bamako, Mali.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA MPF5P.742
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502121
ER
PT J
AU Zanin-Zhorov, A
Flynn, R
Luznik, L
Nyuydzefe, M
Panoskaltsis-Mortari, A
Du, J
Goodman, K
Weiss, J
Chen, W
Serody, J
MacDonald, K
Hill, G
O'Shea, J
Waksal, S
Blazar, B
AF Zanin-Zhorov, Alexandra
Flynn, Ryan
Luznik, Leo
Nyuydzefe, Melanie
Panoskaltsis-Mortari, Angela
Du, Jing
Goodman, Katelyn
Weiss, Jonathan
Chen, Wei
Serody, Jonathan
MacDonald, Kelli
Hill, Geoffrey
O'Shea, John
Waksal, Samuel
Blazar, Bruce
TI Selective ROCK2 inhibitor reverses experimental chronic
graft-versus-host disease via concurrent regulation of STAT3/STAT5
phosphorylation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Zanin-Zhorov, Alexandra; Nyuydzefe, Melanie; Weiss, Jonathan; Chen, Wei; Waksal, Samuel] Kadmon Res Inst, New York, NY USA.
[Flynn, Ryan; Panoskaltsis-Mortari, Angela; Du, Jing; Goodman, Katelyn; Blazar, Bruce] Univ Minnesota, Div Blood & Marrow Transplantat, Minneapolis, MN USA.
[Luznik, Leo] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
[Serody, Jonathan] Univ N Carolina, Canc Ctr, Chapel Hill, NC USA.
[MacDonald, Kelli; Hill, Geoffrey] Queensland Inst Med Res, Brisbane, ACT, Australia.
[O'Shea, John] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504239
ER
PT J
AU Zhang, H
Robins, H
Mackall, C
AF Zhang, Hua
Robins, Harlan
Mackall, Crystal
TI Recombinant human IL7 enhances naive and T stem cell memory
reconstitution and enhances repertoire diversity following cytotoxic
chemotherapy
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Robins, Harlan] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Mackall, Crystal] NCI, Bethesda, MD 20892 USA.
[Zhang, Hua] NCI, POB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA LYM5P.705
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404502244
ER
PT J
AU Zhang, JL
Chen, H
Yang, XP
Guven, E
Nussinov, R
Chen, Z
VanWaes, C
AF Zhang, Jialing
Chen, Hui
Yang, Xinping
Guven, Emine
Nussinov, Ruth
Chen, Zhong
VanWaes, Carter
TI Defective TRAF3 modulates alternative NF-kB signaling and cytokine
expression to promote cancer cell survival in HPV positive head and neck
cancer
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Guven, Emine] Koc Univ, Dept Chem & Biol Engn, Istanbul, Turkey.
[Zhang, Jialing; Chen, Hui; Yang, Xinping; Chen, Zhong; VanWaes, Carter] NIDCD, Head & Neck Surg Branch, NIH, Bethesda, MD USA.
[Nussinov, Ruth] NCI, Nanobiol Program, Computat Struct Biol Grp, Ctr Canc Res,NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404504309
ER
PT J
AU Zhong, C
Hu, GQ
Zhao, KJ
AF Zhong, Chao
Hu, Gangqing
Zhao, Keji
TI GATA-3 regulates the development of ILC3 subsets at multiple stages
SO JOURNAL OF IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Association-of-Immunologists (IMMUNOLOGY)
CY MAY 08-12, 2015
CL New Orleans, LA
SP Amer Assoc Immunologists
C1 [Zhong, Chao] NIAID, Mol & Cellular Immunoregulat Unit, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Hu, Gangqing; Zhao, Keji] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD MAY 1
PY 2015
VL 194
SU 1
MA LYM2P.721
PG 1
WC Immunology
SC Immunology
GA DQ7RG
UT WOS:000379404503236
ER
PT J
AU Dye, BA
Hsu, KLC
Afful, J
AF Dye, Bruce A.
Hsu, Kuei-Ling C.
Afful, Joseph
TI Prevalence and Measurement of Dental Caries in Young Children
SO PEDIATRIC DENTISTRY
LA English
DT Article
DE EARLY CHILDHOOD CARIES; NURSING BOTTLE CARIES; TOOTH DECAY; NHANES;
EPIDEMIOLOGY
ID EARLY-CHILDHOOD CARIES; ORAL-HEALTH COMPONENT; RANDOMIZED
CONTROLLED-TRIAL; EXAMINATION SURVEY NHANES; PRESCHOOL-CHILDREN;
RISK-FACTORS; NATIONAL-HEALTH; UNITED-STATES; BEHAVIORAL DETERMINANTS;
SOCIOECONOMIC-STATUS
AB Purpose: Dental caries in preschool children was historically considered to have a unique and more intense pattern of decoy and was known by a variety of terms. In 1999, the term early childhood caries (ECC), along with a classification system, was proposed to facilitate epidemiologic research of dental caries in young children. The purpose of this study was to assess the impact of those early childhood caries recommendations on the prevalence and measurement of caries in preschool children. Methods: A systematic search of the MEDLINE database was performed. Key search words included: ECC, dental decay, dental caries, carious dentin, baby bottle tooth decay, nursing caries, maxillary anterior caries, and labial caries. English language studies and studies on more than 100 children younger than six years old were eligible for selection. National Health and Nutrition Examination Survey data collected from 1988 to 1994, 1999 to 2004, and 2011 to 2072 were used to assess ECC prevalence using different operational definitions. Results: There were 87 articles selected for this review. The term ECC was used in 55 percent of the selected articles as the primary outcome measure. The majority of studies used a cross-section study design, but diagnostic criteria varied greatly. Caries experience in young children may be shifting away from majority of untreated surfaces to a majority of restored surfaces. Little difference was observed by dental surface type in the distribution of decayed and filled surfaces in primary teeth. Conclusions: Although the term early childhood caries is widely used, varied use of diagnostic criteria and operational definitions continue to limit comparability across studies. Emerging changes in the proportion of decayed and filled surfaces in the United States also raises questions regarding the ECC case definition limiting our ability to understand the epidemiology of dental caries in preschool children.
C1 [Dye, Bruce A.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
[Hsu, Kuei-Ling C.] Univ Maryland, Sch Dent, Div Pediat Dent, Baltimore, MD 21201 USA.
[Afful, Joseph] Ctr Dis Control & Prevent, Harris Corp, Natl Ctr Hlth Stat, Hyattsville, MD USA.
RP Dye, BA (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
EM bruce.dye@nih.gov
NR 108
TC 11
Z9 11
U1 4
U2 9
PU AMER ACAD PEDIATRIC DENTISTRY
PI CHICAGO
PA 211 E CHICAGO AVENUE SUITE 1036, CHICAGO, IL 60611-2616 USA
SN 0164-1263
EI 1942-5473
J9 PEDIATR DENT
JI Pediatr. Dent.
PD MAY-JUN
PY 2015
VL 37
IS 3
BP 200
EP 216
PG 17
WC Dentistry, Oral Surgery & Medicine; Pediatrics
SC Dentistry, Oral Surgery & Medicine; Pediatrics
GA DL6DO
UT WOS:000375729600002
PM 26063550
ER
PT J
AU Dagur, PK
Mccoy, JP
AF Dagur, Pradeep K.
Mccoy, J. Philip, Jr.
TI Endothelial-binding, proinflammatory T cells identified by MCAM (CD146)
expression: Characterization and role in human autoimmune diseases
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE CD146; MCAM Th17; Tc17; Rheumatoid arthritis; Psoriasis; Multiple
sclerosis; EPIC T cell; lymphocyte
ID MESENCHYMAL STEM-CELLS; HELPER 17 CELLS; PSORIATIC-ARTHRITIS; ADHESION
MOLECULE; SIGNALING PATHWAY; PERIPHERAL-BLOOD; PROGENITOR CELLS; CD8+T
CELLS; LYMPHOCYTES; ACTIVATION
AB A subset of T cells defined by the cell surface expression of MCAM (CD146) has been identified in the peripheral circulation of healthy individuals. These cells comprise approximately 3% of the pool of circulating T cells, have an effector memory phenotype, and are capable of producing several cytokines. Notably, the MCAM positive cells are enhanced for IL-17 production compared to MCAM negative effector memory T cells. These cells are committed to IL-17 production and do not require in vitro polarization with exogenous cytoldnes. MCAM positive T cells also demonstrate an increased ability to bind to endothelial monolayers. In numerous autoimmune diseases these cells are found at increased proportions in the peripheral circulation, and at the sites of active inflammation in patients with autoimmune disease, these cells appear in large numbers and are major contributors to IL-17 production. Studies to date have been performed with human subjects and it is uncertain if appropriate mouse models exist for this cell type. These cells could represent early components of the adaptive immune response and serve as targets of therapy in these diseases, although much work remains to be performed in order to discern the exact nature and function of these cells. Published by Elsevier B.V.
C1 [Dagur, Pradeep K.; Mccoy, J. Philip, Jr.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Mccoy, JP (reprint author), NHLBI, Hematol Branch, NIH, 10 Ctr Dr,MSC 1357, Bethesda, MD 20892 USA.
EM mccoyjp@mail.nih.gov
FU intramural reserch program of the National Heart, Lung, and Blood
Institute of NIH
FX This work was supported by the intramural reserch program of the
National Heart, Lung, and Blood Institute of NIH. The authors would like
to thank numerous collaborators for providing their clinical samples as
well as valuable advice and insight: Robert S Nussenblatt, H Nida Sen,
Warren Strober, Michael Yao, Bibi Bielekova, Mark Gourley, Nehal N
Mehta, Angelique Biancotto, and Shawn Rose.
NR 53
TC 2
Z9 4
U1 3
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD MAY
PY 2015
VL 14
IS 5
BP 415
EP 422
DI 10.1016/j.autrev.2015.01.003
PG 8
WC Immunology
SC Immunology
GA CF6JS
UT WOS:000352663600007
PM 25595133
ER
PT J
AU Aceti, M
Creson, TK
Vaissiere, T
Rojas, C
Huang, WC
Wang, YX
Petralia, RS
Page, DT
Miller, CA
Rumbaugh, G
AF Aceti, Massimiliano
Creson, Thomas K.
Vaissiere, Thomas
Rojas, Camilo
Huang, Wen-Chin
Wang, Ya-Xian
Petralia, Ronald S.
Page, Damon T.
Miller, Courtney A.
Rumbaugh, Gavin
TI Syngap1 Haploinsufficiency Damages a Postnatal Critical Period of
Pyramidal Cell Structural Maturation Linked to Cortical Circuit Assembly
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Autism spectrum disorder; Development; Epilepsy; Intellectual
disability; Mouse model; Synapse; Syngap1
ID DE-NOVO MUTATIONS; AUTISM SPECTRUM DISORDERS; GTPASE-ACTIVATING PROTEIN;
INTELLECTUAL DISABILITY; SYNAPTIC PLASTICITY; NEUROPSYCHIATRIC
DISORDERS; MENTAL-RETARDATION; NEURONS; CORTEX; SCHIZOPHRENIA
AB BACKGROUND: Genetic haploinsufficiency of SYNGAP1/Syngap1 commonly occurs in developmental brain disorders, such as intellectual disability, epilepsy, schizophrenia, and autism spectrum disorder. Thus, studying mouse models of Syngap1 haploinsufficiency may uncover pathologic developmental processes common among distinct brain disorders.
METHODS: A Syngap1 haploinsufficiency model was used to explore the relationship between critical period dendritic spine abnormalities, cortical circuit assembly, and the window for genetic rescue to understand how damaging mutations disrupt key substrates of mouse brain development.
RESULTS: Syngap1 mutations broadly disrupted a developmentally sensitive period that corresponded to the period of heightened postnatal cortical synaptogenesis. Pathogenic Syngap1 mutations caused a coordinated acceleration of dendrite elongation and spine morphogenesis and pruning of these structures in neonatal cortical pyramidal neurons. These mutations also prevented a form of developmental structural plasticity associated with experience-dependent reorganization of brain circuits. Consistent with these findings, Syngap1 mutant mice displayed an altered pattern of long-distance synaptic inputs into a cortical area important for cognition. Interestingly, the ability to genetically improve the behavioral endophenotype of Syngap1 mice decreased slowly over postnatal development and mapped onto the developmental period of coordinated dendritic insults.
CONCLUSIONS: Pathogenic Syngap1 mutations have a profound impact on the dynamics and structural integrity of pyramidal cell postsynaptic structures known to guide the de novo wiring of nascent cortical circuits. These findings support the idea that disrupted critical periods of dendritic growth and spine plasticity may be a common pathologic process in developmental brain disorders.
C1 [Aceti, Massimiliano; Creson, Thomas K.; Vaissiere, Thomas; Rojas, Camilo; Huang, Wen-Chin; Page, Damon T.; Miller, Courtney A.; Rumbaugh, Gavin] Scripps Res Inst, Dept Neurosci, Jupiter, FL USA.
[Vaissiere, Thomas; Miller, Courtney A.] Scripps Res Inst, Dept Metab & Aging, Jupiter, FL USA.
[Wang, Ya-Xian; Petralia, Ronald S.] NIDCD, Adv Imaging Core, NIH, Bethesda, MD USA.
RP Rumbaugh, G (reprint author), Scripps Florida, 130 Scripps Way, Jupiter, FL 33458 USA.
EM grumbaug@scripps.edu
OI Aceti, Massimiliano/0000-0002-6632-1398
FU National Institute for Neurological Disorders and Stroke [R01NS064079];
National Institute for Mental Health [R01MH096847]; National Institute
for Drug Abuse [R01 DA034116, R03 DA033499]; National Institute on
Deafness and Other Communication Disorders/National Institutes of Health
Intramural Research Program; State of Florida
FX This work was supported by grants to GR from The National Institute for
Neurological Disorders and Stroke (R01NS064079) andThe National
Institute for Mental Health (R01MH096847). CAM was supported by grants
from the National Institute for Drug Abuse (R01 DA034116; R03 DA033499).
Y-XW and RSP were supported by the National Institute on Deafness and
Other Communication Disorders/National Institutes of Health Intramural
Research Program. W-CH and DTP were supported by gift funds from Mrs.
Nancy Lurie Marks. GR, CAM, and DTP were supported by the State of
Florida.
NR 43
TC 5
Z9 5
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD MAY 1
PY 2015
VL 77
IS 9
BP 805
EP 815
DI 10.1016/j.biopsych.2014.08.001
PG 11
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA CE8LM
UT WOS:000352093800007
PM 25444158
ER
PT J
AU Wnorowski, A
Sadowska, M
Paul, RK
Singh, NS
Boguszewska-Czubara, A
Jimenez, L
Abdelmohsen, K
Toll, L
Jozwiak, K
Bernier, M
Wainer, IW
AF Wnorowski, Artur
Sadowska, Mariola
Paul, Rajib K.
Singh, Nagendra S.
Boguszewska-Czubara, Anna
Jimenez, Lucita
Abdelmohsen, Kotb
Toll, Lawrence
Jozwiak, Krzysztof
Bernier, Michel
Wainer, Irving W.
TI Activation of beta 2-adrenergic receptor by (R,R ')-4
'-methoxy-1-naphthylfenoterol inhibits proliferation and motility of
melanoma cells
SO CELLULAR SIGNALLING
LA English
DT Article
DE Beta2 adrenoreceptor selective agonist; Melanocyte; Metastasis; Beta
blocker; Migration; Melanocortin 1 receptor
ID MOLECULAR-FIELD ANALYSIS; DEPENDENT PROTEIN-KINASE; FENOTEROL
DERIVATIVES; STIMULATING HORMONE; BETA(2)-ADRENERGIC RECEPTOR;
KERATINOCYTE MIGRATION; METASTATIC MELANOMA; MALIGNANT-MELANOMA; CAMP;
PHOSPHORYLATION
AB (R,R')-4'-methoxy-1-naphthylfenoterol [(R,R')-MNF] is a highly-selective beta(2) adrenergic receptor (beta(2)-AR) agonist. Incubation of a panel of human-derived melanoma cell lines with (R,R')-MNF resulted in a dose- and time-dependent inhibition of motility as assessed by in vitro wound healing and xCELLigence migration and invasion assays. Activity of (R,R')-MNF positively correlated with the beta(2)-AR expression levels across tested cell lines. The anti-motility activity of (R,R')-MNF was inhibited by the beta(2)-AR antagonist ICI-118,551 and the protein kinase A inhibitor H-89. The adenylyl cyclase activator forskolin and the phosphodiesterase 4 inhibitor Ro 20-1724 mimicked the ability of (R,R')-MNF to inhibit migration of melanoma cell lines in culture, highlighting the importance of cAMP for this phenomenon. (R,R')-MNF caused significant inhibition of cell growth in beta(2)-AR-expressing cells as monitored by radiolabeled thymidine incorporation and xCELLigence system. The MEK/ERK cascade functions in cellular proliferation, and constitutive phosphorylation of MEK and ERK at their active sites was significantly reduced upon beta(2)-AR activation with (R,R')-MNF. Protein synthesis was inhibited concomitantly both with increased eEF2 phosphorylation and lower expression of tumor cell regulators, EGF receptors, cyclin A and MMP-9. Taken together, these results identified beta(2)-AR as a novel potential target for melanoma management, and (R,R')-MNF as an efficient trigger of anti-tumorigenic cAMP/PKA-dependent signaling in beta(2)-AR-expressing lesions. Published by Elsevier Inc.
C1 [Wnorowski, Artur; Jozwiak, Krzysztof] Med Univ Lublin, Dept Chem, PL-20093 Lublin, Poland.
[Wnorowski, Artur; Paul, Rajib K.; Singh, Nagendra S.; Wainer, Irving W.] NIA, Lab Clin Invest, NIH, Baltimore, MD 21224 USA.
[Sadowska, Mariola] Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Boguszewska-Czubara, Anna] Med Univ Lublin, Dept Med Chem, PL-20093 Lublin, Poland.
[Jimenez, Lucita] SRI Int, Menlo Pk, CA 94025 USA.
[Abdelmohsen, Kotb] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
[Toll, Lawrence] Torrey Pines Inst Mol Studies, Port St Lucie, FL 34987 USA.
[Bernier, Michel] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
RP Bernier, M (reprint author), NIA, Translat Gerontol Branch, NIH, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM artur.wnorowski@gmail.com; mariolas349@gmail.com; rajibkpaul@gmail.com;
nagendra.singh@nih.gov; anna.boguszewska-czubara@am.lublin.pl;
lucita.jimenez@sri.com; abdelmohsenk@grc.nia.nih.gov; ltoll@tpims.org;
krzysztof.jozwiak@umlub.pl; Bernierm@mail.nih.gov;
iwwainer@mitchellwoods.com
RI Singh, Nagendra/K-8966-2015
FU Intramural Research Program of the National Institute on Aging/NIH;
NIA/NIH [N01-AG-3-1009]; Foundation for Polish Science [TEAM 2009-4/5]
FX This work was supported by funds from the Intramural Research Program of
the National Institute on Aging/NIH, NIA/NIH (contract N01-AG-3-1009)
and the Foundation for Polish Science (TEAM 2009-4/5 programme).
NR 60
TC 2
Z9 2
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0898-6568
EI 1873-3913
J9 CELL SIGNAL
JI Cell. Signal.
PD MAY
PY 2015
VL 27
IS 5
BP 997
EP 1007
DI 10.1016/j.cellsig.2015.02.012
PG 11
WC Cell Biology
SC Cell Biology
GA CE7RG
UT WOS:000352038900012
PM 25703025
ER
PT J
AU Harpaz, Y
Robinson, SE
Medvedovsky, M
Goldstein, A
AF Harpaz, Yuval
Robinson, Stephen E.
Medvedovsky, Mordekhay
Goldstein, Abraham
TI Improving the excess kurtosis (g(2)) method for localizing epileptic
sources in magnetoencephalographic recordings
SO CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE Epilepsy; Beamforming; Kurtosis; Spike; Source localization
ID SYNTHETIC-APERTURE MAGNETOMETRY; INTRACTABLE EPILEPSY; INTERICTAL
SPIKES; MEG; LOCALIZATION; CHILDREN; FOCI; EEG
AB Objective: To suggest ways to apply the excess kurtosis estimator g(2), in the detection of epileptic activity with magnetoencephalography, while avoiding its bias towards detecting high-amplitude, infrequent events.
Methods: Synthetic aperture magnetometry (SAM), combined with g2, was applied using window lengths ranging from 0.125 s to 32 s and with sum and maximum metrics on simulated data and recordings of two focal epilepsy patients.
Results: Comparing sources with different spike rates (two per second and one per 2 s), the sum metric was most efficient when using a window of 0.25 s. Simulations showed that the sum metric is insensitive to spike frequency when the window includes more than one spike. SAM(g2) images from long segments with maximum metric resulted in misleading images, showing the strongest activity away from the lesions.
Conclusions: Using a sliding window and the sum metric is beneficial when imaging interictal spikes and status epilepticus. Windows should be short enough not to include more than one interictal event. For continuous events such as electrographic seizures windows should contain baseline data and the epileptic event. Significance: The sliding window and metric should be set according to the suggested guidelines when using SAM(g2) for presurgical evaluation. (C) 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
C1 [Harpaz, Yuval; Goldstein, Abraham] Bar Ilan Univ, Gonda Brain Res Ctr, Ramat Gan, Israel.
[Robinson, Stephen E.] NIMH, MEG Core Facil, NIH, Bethesda, MD 20892 USA.
[Medvedovsky, Mordekhay] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Brain Funct Imaging Unit, IL-69978 Tel Aviv, Israel.
[Goldstein, Abraham] Bar Ilan Univ, Dept Psychol, Ramat Gan, Israel.
[Medvedovsky, Mordekhay] Univ Helsinki, Cent Hosp, BioMag Lab, Helsinki, Finland.
RP Harpaz, Y (reprint author), Bar Ilan Univ, Gonda Multidisciplinary Brain Res Inst, Max & Anna Webb St, Ramat Gan, Israel.
EM Yuval.Harpaz@biu.ac.il
OI Harpaz, Yuval/0000-0002-3372-3630; Goldstein,
Abraham/0000-0002-9349-0621
NR 19
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1388-2457
EI 1872-8952
J9 CLIN NEUROPHYSIOL
JI Clin. Neurophysiol.
PD MAY
PY 2015
VL 126
IS 5
BP 889
EP 897
DI 10.1016/j.clinph.2014.09.002
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CF0KT
UT WOS:000352233500008
PM 25281474
ER
PT J
AU Ewen, JB
Lakshmanan, BM
Hallett, M
Mostofsky, SH
Crone, NE
Korzeniewska, A
AF Ewen, Joshua B.
Lakshmanan, Balaji M.
Hallett, Mark
Mostofsky, Stewart H.
Crone, Nathan E.
Korzeniewska, Anna
TI Dynamics of functional and effective connectivity within human cortical
motor control networks
SO CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE EEG; Effective connectivity; Efference copy; Praxis
ID CENTRAL EXECUTIVE FUNCTIONS; EVENT-RELATED CAUSALITY; PRAXIS HAND
MOVEMENTS; THETA-OSCILLATIONS; WORKING-MEMORY; GAMMA OSCILLATIONS;
IDEOMOTOR APRAXIA; INFORMATION-FLOW; BRAIN STRUCTURES; PREMOTOR AREAS
AB Objective: Praxis, the performance of complex motor gestures, is crucial to the development of motor and social/communicative capacities. Praxis relies on a network consisting of inferior parietal and premotor regions, particularly on the left, and is thought to require transformation of spatio-temporal representations (parietal) into movement sequences (premotor).
Method: We examined praxis network dynamics by measuring EEG effective connectivity while healthy subjects performed a praxis task.
Results: Propagation from parietal to frontal regions was not statistically greater on the left than the right. However, propagation from left parietal regions to all other regions was significantly greater during gesture preparation than execution. Moreover, during gesture preparation only, propagation from the left parietal region to bilateral frontal regions was greater than reciprocal propagations to the left parietal region. This directional specificity was not observed for the right parietal region.
Conclusions: These findings represent direct electrophysiological evidence for directionally predominant propagation in left frontal-parietal networks during praxis behavior, which may reflect neural mechanisms by which representations in the human brain select appropriate motor sequences for subsequent execution.
Significance: In addition to bolstering the classic view of praxis network function, these results also demonstrate the relevance of additional information provided by directed connectivity measures. (C) 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
C1 [Ewen, Joshua B.; Lakshmanan, Balaji M.] Kennedy Krieger Inst, Dept Neurol & Dev Med, Baltimore, MD 21205 USA.
[Ewen, Joshua B.; Mostofsky, Stewart H.; Crone, Nathan E.; Korzeniewska, Anna] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA.
[Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Mostofsky, Stewart H.] Kennedy Krieger Inst, Lab Neurocognit & Imaging Res, Baltimore, MD 21205 USA.
[Mostofsky, Stewart H.] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21287 USA.
RP Ewen, JB (reprint author), Kennedy Krieger Inst, Dept Neurol & Dev Med, 707 N Broadway, Baltimore, MD 21205 USA.
EM ewen@kennedykrieger.org; lakshmanan@kennedykrieger.org;
hallettm@ninds.nih.gov; mostofsky@kennedykrieger.org; ncrone@jhmi.edu;
akorzen@jhmi.edu
OI Ewen, Joshua/0000-0002-9203-9564
FU National Institutes of Neurological Disorders and Stroke at the National
Institutes of Health [K23 NS073626, R01 NS048527, R01 NS40596]; Autism
Speaks; NINDS
FX This work was supported by the National Institutes of Neurological
Disorders and Stroke at the National Institutes of Health (grant numbers
K23 NS073626 to J.B.E., R01 NS048527 to S.H.M., and R01 NS40596 to
N.E.C.; Intramural Program to M.H.) and Autism Speaks (to S.H.M.). Dr.
Hallett is supported by the NINDS Intramural Program. The study sponsors
had no role in collection, analysis or interpretation, or in the
preparation of the manuscript.
NR 54
TC 3
Z9 3
U1 1
U2 12
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1388-2457
EI 1872-8952
J9 CLIN NEUROPHYSIOL
JI Clin. Neurophysiol.
PD MAY
PY 2015
VL 126
IS 5
BP 987
EP 996
DI 10.1016/j.clinph.2014.09.006
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA CF0KT
UT WOS:000352233500020
PM 25270239
ER
PT J
AU Whitworth, KW
Baird, DD
Steiner, AZ
Bornman, RMS
Travlos, GS
Wilson, RE
Longnecker, MP
AF Whitworth, Kristina W.
Baird, Donna D.
Steiner, Anne Z.
Bornman, Riana M. S.
Travlos, Gregory S.
Wilson, Ralph E.
Longnecker, Matthew P.
TI Anti-Mullerian Hormone and Lifestyle, Reproductive, and Environmental
Factors Among Women in Rural South Africa
SO EPIDEMIOLOGY
LA English
DT Article
ID INHIBITING SUBSTANCE; OVARIAN RESERVE; SERUM-LEVELS; MARKER; HEALTH;
ORGANOPHOSPHORUS; INSECTICIDES; FOLLICLES; ADULTHOOD; HISTORY
AB Background: Few data exist regarding anti-Mullerian hormone, a marker of ovarian reserve, in relation to environmental factors with potential ovarian toxicity.
Methods: This analysis included 420 women from Limpopo, South Africa studied in 2010-2011. Women were administered comprehensive questionnaires, and plasma concentrations of anti-Mullerian hormone and dichlorodiphenyltrichloroethane were determined. We used separate multivariable models to examine the associations between natural log-transformed anti-Mullerian hormone concentration (ng/ml) and each of the lifestyle, reproductive, and environmental factors of interest, adjusted for age, body mass index, education, and parity.
Results: The median age of women was 24 years (interquartile range [IQR] - 22 to 26); the median anti-Mullerian hormone concentration was 3.1 ng/ml (IQR - 2.0 to 6.0). Women who reported indoor residual spraying in homes with painted walls (indicative of exposure to pyrethroids) had 25% lower (95% confidence interval [CI] = -39%, -8%) anti-Mullerian hormone concentrations compared with women who reported no spraying. Little evidence of decreased anti-Mullerian hormone concentrations was observed among women with the highest dichlorodiphenyltrichloroethane levels. Compared with women who used an electric stove, no association was observed among women who cooked indoors over open wood fires. The findings also suggested lower anti-Mullerian hormone concentrations among women who drank coffee (-19% [95% CI = -31%, -5%]) or alcohol (-21% [95% CI = -36%, -3%]).
Conclusions: These are among the first data regarding anti-Mullerian hormone concentrations relative to pesticides and indoor air pollution. Our results are suggestive of decreased ovarian reserve associated with exposure to pyrethroid pesticides, which is consistent with laboratory animal data.
C1 [Whitworth, Kristina W.] Univ Texas Sch Publ Hlth, San Antonio, TX 77030 USA.
[Baird, Donna D.; Longnecker, Matthew P.] NIEHS, Epidemiol Branch, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Travlos, Gregory S.; Wilson, Ralph E.] NIEHS, Cellular & Mol Pathol Branch, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Steiner, Anne Z.] Univ N Carolina, Dept Obstet & Gynecol, Div Reprod Endocrinol & Infertil, Chapel Hill, NC USA.
[Bornman, Riana M. S.] Univ Pretoria, Dept Urol, Pretoria, South Africa.
[Bornman, Riana M. S.] Univ Pretoria, Ctr Sustainable Malaria Control, ZA-0002 Pretoria, South Africa.
RP Whitworth, KW (reprint author), Univ Texas Sch Publ Hlth, San Antonio Reg Campus, San Antonio, TX 77030 USA.
EM Kristina.W.Whitworth@uth.tmc.edu
RI Baird, Donna/D-5214-2017;
OI Baird, Donna/0000-0002-5544-2653; Longnecker,
Matthew/0000-0001-6073-5322
FU National Institutes of Health (NIH), National Institute of Environmental
Health Sciences (NIEHS)
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health (NIH), National Institute of
Environmental Health Sciences (NIEHS).
NR 38
TC 8
Z9 8
U1 3
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1044-3983
EI 1531-5487
J9 EPIDEMIOLOGY
JI Epidemiology
PD MAY
PY 2015
VL 26
IS 3
BP 429
EP 435
DI 10.1097/EDE.0000000000000265
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CF4BA
UT WOS:000352492200025
PM 25710247
ER
PT J
AU Metcalf, CJE
Tatem, A
Bjornstad, ON
Lessler, J
O'Reilly, K
Takahashi, S
Cutts, F
Grenfell, BT
AF Metcalf, C. J. E.
Tatem, A.
Bjornstad, O. N.
Lessler, J.
O'Reilly, K.
Takahashi, S.
Cutts, F.
Grenfell, B. T.
TI Transport networks and inequities in vaccination: remoteness shapes
measles vaccine coverage and prospects for elimination across Africa
SO EPIDEMIOLOGY AND INFECTION
LA English
DT Article
DE Epidemiology; modelling; measles (rubeola); rubella; vaccine policy
development
ID RUBELLA VACCINATION; UNITED-STATES; COUNTRIES; IMPACT; IMMUNIZATION;
NIGERIA; EQUITY; RISK; SIZE; CHAD
AB Measles vaccination is estimated to have averted 13.8 million deaths between 2000 and 2012. Persisting heterogeneity in coverage is a major contributor to continued measles mortality, and a barrier to measles elimination and introduction of rubella-containing vaccine. Our objective is to identify determinants of inequities in coverage, and how vaccine delivery must change to achieve elimination goals, which is a focus of the WHO Decade of Vaccines. We combined estimates of travel time to the nearest urban centre (>= 50 000 people) with vaccination data from Demographic Health Surveys to assess how remoteness affects coverage in 26 African countries. Building on a statistical mapping of coverage against age and geographical isolation, we quantified how modifying the rate and age range of vaccine delivery affects national coverage. Our scenario analysis considers increasing the rate of delivery of routine vaccination, increasing the target age range of routine vaccination, and enhanced delivery to remote areas. Geographical isolation plays a key role in defining vaccine inequity, with greater inequity in countries with lower measles vaccine coverage. Eliminating geographical inequities alone will not achieve thresholds for herd immunity, indicating that changes in delivery rate or age range of routine vaccination will be required. Measles vaccine coverage remains far below targets for herd immunity in many countries on the African continent and is likely to be inadequate for achieving rubella elimination. The impact of strategies such as increasing the upper age range eligible for routine vaccination should be considered.
C1 [Metcalf, C. J. E.] Univ Oxford, Dept Zool, Oxford, England.
[Metcalf, C. J. E.; Tatem, A.; Grenfell, B. T.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Metcalf, C. J. E.; Takahashi, S.; Grenfell, B. T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Tatem, A.] Univ Southampton, Dept Geog & Environm, Southampton, Hants, England.
[Tatem, A.] Flowminder Fdn, Stockholm, Sweden.
[Bjornstad, O. N.] Penn State Univ, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Lessler, J.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[O'Reilly, K.] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Infect Dis Epidemiol, Med Res Council Ctr Outbreak Anal & Modelling, London, England.
[Cutts, F.] London Sch Hyg & Trop Med, London WC1, England.
RP Metcalf, CJE (reprint author), Princeton Univ, Dept Ecol & Evolutionary Biol, Eno Hall, Princeton, NJ 08544 USA.
EM cmetcalf@princeton.edu
OI Lessler, Justin/0000-0002-9741-8109; O'Reilly,
Kathleen/0000-0002-4892-8022
FU Royal Society; Oxford University; Bill and Melinda Gates Foundation;
Science and Technology Directorate, Department of Homeland Security
[HSHQDC-12-C-00058]; RAPIDD program of the Science & Technology
Directorate, Department of Homeland Security; Fogarty International
Center, National Institutes of Health; Medical Research Council, UK
FX This work is funded by the Royal Society and Oxford University
(C.J.E.M.), the Bill and Melinda Gates Foundation, the Science and
Technology Directorate, Department of Homeland Security contract
HSHQDC-12-C-00058 (B.T.G.), and the RAPIDD program of the Science &
Technology Directorate, Department of Homeland Security and the Fogarty
International Center, National Institutes of Health (C.J.E.M., B.T.G.,
O.N.B., A.J.T.), and the Medical Research Council, UK (K.O'R.). The
funding sources played no role in developing this paper and preparing it
for submission.
NR 47
TC 4
Z9 4
U1 3
U2 13
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0950-2688
EI 1469-4409
J9 EPIDEMIOL INFECT
JI Epidemiol. Infect.
PD MAY
PY 2015
VL 143
IS 7
BP 1457
EP 1466
DI 10.1017/S0950268814001988
PG 10
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA CF6ZW
UT WOS:000352706700014
PM 25119237
ER
PT J
AU Greten, TF
Wang, XW
Korangy, F
AF Greten, Tim F.
Wang, Xin W.
Korangy, Firouzeh
TI Current concepts of immune based treatments for patients with HCC: from
basic science to novel treatment approaches
SO GUT
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA PATIENTS; REGULATORY T-CELLS; LIVER-CANCER;
RADIOFREQUENCY ABLATION; ANTITUMOR IMMUNITY; SUPPRESSOR-CELLS; DENDRITIC
CELLS; CLINICAL-TRIAL; RESPONSES; SORAFENIB
AB The recent approval of two immune checkpoint inhibitors for the treatment of malignant melanoma has sparked great interest by physicians and basic scientists searching for novel therapeutics for GI cancer. Chronic inflammation is recognised as a major risk factor for the development of hepatocellular carcinoma (HCC) and makes this type of cancer a potentially ideal target for an immune based treatment approach. Further evidence for a critical role of immune responses in patients with HCC is derived from the fact that immune signatures and profiles predict patients' outcome as well as the fact that tumour-induced spontaneous antitumour immunity can be detected. In addition ablative therapies can lead to changes in the number, phenotype and function of different immune cell subsets, which correlate with patients' survival. Various HCC-specific mouse models have been developed, which improve our understanding of hepatocarcinogenesis and tumour-immune cell interactions, and lead to the development of novel immune based treatment approaches, which are currently being evaluated in preclinical and in early clinical settings. Immune checkpoint blockade along with adoptive immune cell therapy and vaccine approaches are currently being evaluated either alone or in combination with other treatments. Here, we provide an overview for the rationale of immunotherapy in HCC, summarise ongoing studies and provide a perspective for immune based approaches in patients with HCC.
C1 [Greten, Tim F.; Korangy, Firouzeh] NCI, Gastrointestinal Malignancy Sect, Thorac & Gastrointestinal Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Wang, Xin W.] NCI, Liver Carcinogenesis Sect, Human Carcinogenesis Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Greten, TF (reprint author), NCI, Gastrointestinal Malignancy Sect, Thorac & Gastrointestinal Oncol Branch, Ctr Canc Res, NIH NCI CCR Bldg 10 Rm 12N226, Bethesda, MD 20892 USA.
EM tim.greten@nih.gov
RI Wang, Xin/B-6162-2009
FU Intramural Research Program of the NCI, NIH
FX This work was supported by the Intramural Research Program of the NCI,
NIH.
NR 111
TC 14
Z9 17
U1 1
U2 18
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD MAY
PY 2015
VL 64
IS 5
BP 842
EP 848
DI 10.1136/gutjnl-2014-307990
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA CF1GD
UT WOS:000352291200019
PM 25666193
ER
PT J
AU Wall, AM
Mukandala, G
Greig, NH
O'Connor, JJ
AF Wall, Audrey M.
Mukandala, Gatambwa
Greig, Nigel H.
O'Connor, John J.
TI Tumor Necrosis Factor-alpha Potentiates Long-Term Potentiation in the
Rat Dentate Gyrus After Acute Hypoxia
SO JOURNAL OF NEUROSCIENCE RESEARCH
LA English
DT Article
DE tumor necrosis factor-alpha; interleukin-1 beta; long-term potentiation;
dentate gyrus; hypoxia; high-frequency stimulation; theta burst
stimulation; 3,6 '-dithiothalidomide; 1,6 '-dithiorevlimid; CNTO1081;
prolyl hydroxylase inhibition
ID ELEMENT-BINDING PROTEIN; GLIAL TNF-ALPHA; IN-VITRO;
SYNAPTIC-TRANSMISSION; INTERMITTENT HYPOXIA; HIPPOCAMPAL SLICES;
RECEPTOR TRAFFICKING; SYNTHESIS INHIBITOR; GLUTAMATE-RECEPTOR;
INTERLEUKIN-1-BETA
AB An inadequate supply of oxygen in the brain may lead to an inflammatory response through neuronal and glial cells that can result in neuronal damage. Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that is released during acute hypoxia and can have neurotoxic or neuroprotective effects in the brain. Both TNF-alpha and interleukin-1 beta (IL-1 beta) have been shown by a number of research groups to alter synaptic scaling and also to inhibit long-term potentiation (LTP) in the hippocampus when induced by specific high-frequency stimulation (HFS) protocols. This study examines the effects of TNFa on synaptic transmission and plasticity in hippocampal slices after acute hypoxia using two HFS protocols. Field excitatory postsynaptic potentials were elicited in the medial perforant pathway of the dentate gyrus. Exogenous TNF-alpha (5 ng/ml) attenuated LTP induced by theta burst stimulation but had no effect on LTP induced by a more prolonged HFS. Pretreatment with lipopolysaccharide (100 ng/ml) or TNF-alpha but not IL-1 beta (4 ng/ml) prior to a 30-min hypoxic insult resulted in a significant enhancement of LTP post hypoxia when induced by the HFS. Anti-TNF, 3,60-dithiothalidomide (a TNF-alpha synthesis inhibitor), and SB203580 (a p38 MAPK inhibitor) significantly reduced this effect. These results indicate an important modulatory role for elevated TNF-alpha levels on LTP in the hippocampus after an acute hypoxic event. VC 2015 Wiley Periodicals, Inc.
C1 [Wall, Audrey M.; Mukandala, Gatambwa; O'Connor, John J.] Univ Coll Dublin, UCD Sch Biomol & Biomed Sci, UCD Conway Inst Biomol & Biomed Res, Dublin 4, Ireland.
[Greig, Nigel H.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP O'Connor, JJ (reprint author), Univ Coll Dublin, UCD Sch Biomol & Biomed Sci, UCD Conway Inst Biomol & Biomed Res, Dublin 4, Ireland.
EM john.connor@ucd.ie
FU Science Foundation Ireland (SFI) [09/RFP/NES2450]; Intramural Research
Program, National Institute on Aging
FX Contract grant sponsor: Science Foundation Ireland (SFI); Contract grant
number: 09/RFP/NES2450 (to J.J.O.); Contract grant sponsor: Intramural
Research Program, National Institute on Aging (to N.H.G.)
NR 56
TC 6
Z9 6
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0360-4012
EI 1097-4547
J9 J NEUROSCI RES
JI J. Neurosci. Res.
PD MAY
PY 2015
VL 93
IS 5
BP 815
EP 829
DI 10.1002/jnr.23540
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA CE9FE
UT WOS:000352148600014
PM 25641742
ER
PT J
AU Nalwoga, A
Cose, S
Wakeham, K
Miley, W
Ndibazza, J
Drakeley, C
Elliott, A
Whitby, D
Newton, R
AF Nalwoga, Angela
Cose, Stephen
Wakeham, Katie
Miley, Wendell
Ndibazza, Juliet
Drakeley, Christopher
Elliott, Alison
Whitby, Denise
Newton, Robert
TI Association between malaria exposure and Kaposi's sarcoma-associated
herpes virus seropositivity in Uganda
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Article
DE Kaposi's sarcoma-associated herpes virus; malaria; Uganda
ID PLASMODIUM-FALCIPARUM; DOUBLE-BLIND; CHILDREN; RISK;
HUMAN-HERPESVIRUS-8; EPIDEMIOLOGY; TRANSMISSION; IMMUNIZATION;
ANTIBODIES; INFECTION
AB ObjectiveUnlike other herpes viruses, Kaposi's sarcoma-associated herpes virus (KSHV) is not ubiquitous worldwide and is most prevalent in sub-Saharan Africa. The reasons for this are unclear. As part of a wider investigation of factors that facilitate transmission in Uganda, a high prevalence country, we examined the association between antimalaria antibodies and seropositivity against KSHV.
MethodsAntibodies against P.falciparum merozoite surface protein (PfMSP)-1, P.falciparum apical membrane antigen (PfAMA)-1 and KSHV antigens (ORF73 and K8.1) were measured in samples from 1164 mothers and 1227 children.
ResultsKaposi's sarcoma-associated herpes virus seroprevalence was 69% among mothers and 15% children. Among mothers, KSHV seroprevalence increased with malaria antibody titres: from 60% to 82% and from 54% to 77%, comparing those with the lowest and highest titres for PfMSP-1 and PfAMA-1, respectively (P<0.0001). Among children, only antibodies to PfAMA-1 were significantly associated with KSHV seropositivity, (P<0.0001). In both mothers and children, anti-ORF73 antibodies were more strongly associated with malaria antibodies than anti-K8.1 antibodies.
ConclusionThe association between malaria exposure and KSHV seropositivity suggests that malaria is a cofactor for KSHV infection or reactivation.
C1 [Nalwoga, Angela; Cose, Stephen; Wakeham, Katie; Ndibazza, Juliet; Elliott, Alison; Newton, Robert] Uganda Virus Res Inst, Med Res Council, Entebbe, Uganda.
[Cose, Stephen; Drakeley, Christopher; Elliott, Alison] London Sch Hyg & Trop Med, London WC1, England.
[Wakeham, Katie] Univ Glasgow, Inst Canc Sci, Glasgow, Lanark, Scotland.
[Miley, Wendell; Whitby, Denise] Frederick Natl Lab Canc Res, Viral Oncol Sect, Frederick, MD USA.
[Newton, Robert] Univ York, York YO10 5DD, N Yorkshire, England.
[Newton, Robert] Int Agcy Res Canc, F-69372 Lyon, France.
RP Nalwoga, A (reprint author), MRC UVRI Uganda Res Unit AIDS, POB 49, Entebbe, Uganda.
EM Angela.nalwoga@mrcuganda.org
OI Elliott, Alison/0000-0003-2818-9549; Cose, Stephen/0000-0002-5156-037X
FU National Institute of Health; Wellcome Trust, United Kingdom
FX We thank the Entebbe Mother and Baby Study participants for their
cooperation and providing us with their samples to make this project
possible. We would like to acknowledge the Co-Infection Studies Program
team of MRC/UVRI Uganda Research Unit on AIDS, for their support in
carrying out this project, and thank Prof. Jonathan Levin for his
statistical support. We would like to acknowledge Ismail Sebina and
Alison Rand for their support in carrying out KSHV serological assays
and malaria serological assays respectively. This project was funded
with federal funds from the National Institute of Health and the
Wellcome Trust, United Kingdom.
NR 35
TC 4
Z9 4
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1360-2276
EI 1365-3156
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD MAY
PY 2015
VL 20
IS 5
BP 665
EP 672
DI 10.1111/tmi.12464
PG 8
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA CF4QG
UT WOS:000352534600012
PM 25611008
ER
PT J
AU Pongpiachan, S
Hattayanone, M
Choochuay, C
Mekmok, R
Wuttijak, N
Ketratanakul, A
AF Pongpiachan, S.
Hattayanone, M.
Choochuay, C.
Mekmok, R.
Wuttijak, N.
Ketratanakul, A.
TI Enhanced PM10 bounded PAHs from shipping emissions
SO ATMOSPHERIC ENVIRONMENT
LA English
DT Article
DE Industrial estate; Mutagenicity; Polycyclic aromatic compounds; Vehicle
emissions; Thailand
ID POLYCYCLIC AROMATIC-HYDROCARBONS; AIRBORNE PARTICULATE MATTER; SOURCE
IDENTIFICATION; VERTICAL-DISTRIBUTION; SOURCE APPORTIONMENT;
MUTAGENIC-ACTIVITY; WOOD COMBUSTION; RISK-ASSESSMENT; CHINESE COAL;
URBAN AIR
AB Earlier studies have highlighted the importance of maritime transport as a main contributor of air pollutants in port area. The authors intended to investigate the effects of shipping emissions on the enhancement of PM10 bounded polycyclic aromatic hydrocarbons (PAHs) and mutagenic substances in an industrial area of Rayong province, Thailand. Daily PM10 speciation data across two air quality observatory sites in Thailand during 2010-2013 were collected. Diagnostic binary ratios of PAH congeners, analysis of variances (ANOVA), and principal component analysis (PCA) were employed to evaluate the enhanced genotoxicity of PM10 during the docking period. Significant increase of PAHs and mutagenic index (MI) of PM10 were observed during the docking period in both sampling sites. Although stationary sources like coal combustions from power plants and vehicular exhausts from motorway can play a great role in enhancing PAH concentrations, regulating shipping emissions from diesel engine in the port area like Rayong is predominantly crucial. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Pongpiachan, S.; Choochuay, C.] NIDA, Sch Social & Environm Dev, Ctr Res & Dev Disaster Prevent & Management, Bangkok 10240, Thailand.
[Hattayanone, M.] Songkhla Rajabhat Univ, Fac Humanities & Social Sci, Songkhla 90000, Thailand.
[Mekmok, R.; Wuttijak, N.; Ketratanakul, A.] IRPC PCL, Bangkok 10900, Thailand.
RP Pongpiachan, S (reprint author), NIDA, Sch Social & Environm Dev, Ctr Res & Dev Disaster Prevent & Management, 118 Moo 3,Sereethai Rd, Bangkok 10240, Thailand.
EM pongpiajun@gmail.com
FU IRPC
FX This work was performed with the approval of the National Institute of
Development Administration (NIDA) and financial support from IRPC. The
authors acknowledge the staff of the Faculty of Environmental
Management, Prince of Songkla University, and Bara Scientific Co., Ltd.
for their contributions to the laboratory work.
NR 58
TC 6
Z9 6
U1 4
U2 33
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1352-2310
EI 1873-2844
J9 ATMOS ENVIRON
JI Atmos. Environ.
PD MAY
PY 2015
VL 108
BP 13
EP 19
DI 10.1016/j.atmosenv.2015.02.072
PG 7
WC Environmental Sciences; Meteorology & Atmospheric Sciences
SC Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences
GA CE4OB
UT WOS:000351808800002
ER
PT J
AU Lee, W
Mun, S
Kang, K
Hennighausen, L
Han, K
AF Lee, Wooseok
Mun, Seyoung
Kang, Keunsoo
Hennighausen, Lothar
Han, Kyudong
TI Genome-wide target site triplication of Alu elements in the human genome
SO GENE
LA English
DT Article
DE Target site; Alu; Mobile element; Retrotransposon; TSD-TSD recombination
ID MEDIATED DELETION; INSERTION; EVOLUTION; DNA; RETROPOSONS; LINEAGE
AB Alu elements are the most successful short interspersed elements in primate genomes and their retrotransposition is a major source of genomic expansion. Alu elements integrate into genomic regions through target-site primed reverse transcription, which generates target site duplications (TSDs). Unexpectedly, we have identified target site triplications (TSTs) at some lad, where two Alu elements in tandem share one direct repeat. Thus, the three copies of the repeat are present. We located 212 TST loci in the human genome and examined 25 putative human-specific TST loci using PCR validation. As a result, 12 human-specific TST loci were identified. These findings suggest that unequal homologous recombination between TSDs can lead to TST. Through this mechanism, the copy number of Alu elements could have increased in primate genomes without new Alu retrotransposition events. This study provides new insight into the augmentation of Alu elements in the primate genome. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Lee, Wooseok; Mun, Seyoung; Han, Kyudong] Dankook Univ, Dept Nanobiomed Sci, Cheonan 330714, South Korea.
[Lee, Wooseok; Mun, Seyoung; Han, Kyudong] Dankook Univ, PLUS NBM Global Res Ctr Regenerat Med BK21, Cheonan 330714, South Korea.
[Mun, Seyoung; Hennighausen, Lothar] NIDDK, NIH, Lab Genet & Physiol, Bethesda, MD 20892 USA.
[Kang, Keunsoo] Dankook Univ, Dept Microbiol, Cheonan 330714, South Korea.
[Han, Kyudong] DKU Theragen Inst NGS Anal DTiNa, Cheonan 330714, South Korea.
RP Han, K (reprint author), Dankook Univ, Dept Nanobiomed Sci, Cheonan 330714, South Korea.
EM jim97@dankook.ac.kr
FU Dankook University
FX The present research was conducted by the research fund of Dankook
University (BK21 Plus) in 2014.
NR 25
TC 1
Z9 1
U1 2
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
EI 1879-0038
J9 GENE
JI Gene
PD MAY 1
PY 2015
VL 561
IS 2
BP 283
EP 291
DI 10.1016/j.gene.2015.02.052
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA CE4LM
UT WOS:000351802100014
PM 25701601
ER
PT J
AU Drozdovitch, V
Brill, AB
Callahan, RJ
Clanton, JA
DePietro, A
Goldsmith, SJ
Greenspan, BS
Gross, MD
Hays, MT
Moore, SC
Ponto, JA
Shreeve, WW
Melo, DR
Linet, MS
Simon, SL
AF Drozdovitch, Vladimir
Brill, Aaron B.
Callahan, Ronald J.
Clanton, Jeffrey A.
DePietro, Allegra
Goldsmith, Stanley J.
Greenspan, Bennett S.
Gross, Milton D.
Hays, Marguerite T.
Moore, Stephen C.
Ponto, James A.
Shreeve, Walton W.
Melo, Dunstana R.
Linet, Martha S.
Simon, Steven L.
TI USE OF RADIOPHARMACEUTICALS IN DIAGNOSTIC NUCLEAR MEDICINE IN THE UNITED
STATES: 1960-2010
SO HEALTH PHYSICS
LA English
DT Article
DE diagnostic imaging; nuclear medicine; radiation, medical;
radiopharmaceuticals
ID LOWER GASTROINTESTINAL HEMORRHAGE; RED-BLOOD-CELLS; IN-111 CAPROMAB
PENDETIDE; RADIOLOGIC TECHNOLOGISTS; TC-99M PYROPHOSPHATE;
COMPUTED-TOMOGRAPHY; PULMONARY EMBOLISM; TECHNETIUM TC-99M;
PROSTATE-CANCER; SCANNING AGENT
AB To reconstruct reliable nuclear medicine-related occupational radiation doses or doses received as patients from radiopharmaceuticals over the last five decades, the authors assessed which radiopharmaceuticals were used in different time periods, their relative frequency of use, and typical values of the administered activity. This paper presents data on the changing patterns of clinical use of radiopharmaceuticals and documents the range of activity administered to adult patients undergoing diagnostic nuclear medicine procedures in the U.S. between 1960 and 2010. Data are presented for 15 diagnostic imaging procedures that include thyroid scan and thyroid uptake; brain scan; brain blood flow; lung perfusion and ventilation; bone, liver, hepatobiliary, bone marrow, pancreas, and kidney scans; cardiac imaging procedures; tumor localization studies; localization of gastrointestinal bleeding; and non-imaging studies of blood volume and iron metabolism. Data on the relative use of radiopharmaceuticals were collected using key informant interviews and comprehensive literature reviews of typical administered activities of these diagnostic nuclear medicine studies. Responses of key informants on relative use of radiopharmaceuticals are in agreement with published literature. Results of this study will be used for retrospective reconstruction of occupational and personal medical radiation doses from diagnostic radiopharmaceuticals to members of the U.S. radiologic technologists' cohort and in reconstructing radiation doses from occupational or patient radiation exposures to other U.S. workers or patient populations.
C1 [Drozdovitch, Vladimir; Linet, Martha S.; Simon, Steven L.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Brill, Aaron B.] Vanderbilt Univ, Radiol & Radiol Sci, Nashville, TN 37235 USA.
[Callahan, Ronald J.; DePietro, Allegra] Massachusetts Gen Hosp, Boston, MA USA.
[Clanton, Jeffrey A.] Vanderbilt Univ, Nashville, TN 37235 USA.
[Goldsmith, Stanley J.] New York Presbyterian Hosp, Weill Cornell Med Ctr, New York, NY USA.
[Greenspan, Bennett S.] Univ Missouri, Columbia Nucl Med Program, Columbia, MO USA.
[Gross, Milton D.] Dept Vet Affairs Hlth Syst, Nucl Med & Radiat Serv, Ann Arbor, MI USA.
[Hays, Marguerite T.] Dept Vet Affairs Hlth Syst, Palo Alto, CA USA.
[Moore, Stephen C.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Ponto, James A.] Univ Iowa Hosp & Clin, Iowa City, IA 52242 USA.
[Shreeve, Walton W.] Vet Affairs Northport, Long Isl City, NY USA.
[Melo, Dunstana R.] Lovelace Resp Res Inst, Ctr Countermeasures Radiat, Albuquerque, NM USA.
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
FU Intramural Research Program of the 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. Special thanks
to Fred A. Mettler Jr. (New Mexico VA Health Care System, Albuquerque,
NM) for his participation in the survey and for comments on our
manuscript.
NR 126
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U1 1
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0017-9078
EI 1538-5159
J9 HEALTH PHYS
JI Health Phys.
PD MAY
PY 2015
VL 108
IS 5
BP 520
EP 537
DI 10.1097/HP.0000000000000261
PG 18
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 CE5PP
UT WOS:000351887900005
PM 25811150
ER
PT J
AU Grant, EJ
Ozasa, K
Ban, N
Gonzalez, AB
Cologne, J
Cullings, HM
Doi, K
Furukawa, K
Imaoka, T
Kodama, K
Nakamura, N
Niwa, O
Preston, DL
Rajaraman, P
Sadakane, A
Saigusa, S
Sakata, R
Sobue, T
Sugiyama, H
Ullrich, R
Wakeford, R
Yasumura, S
Milder, CM
Shore, RE
AF Grant, E. J.
Ozasa, K.
Ban, N.
de Gonzalez, A. Berrington
Cologne, J.
Cullings, H. M.
Doi, K.
Furukawa, K.
Imaoka, T.
Kodama, K.
Nakamura, N.
Niwa, O.
Preston, D. L.
Rajaraman, P.
Sadakane, A.
Saigusa, S.
Sakata, R.
Sobue, T.
Sugiyama, H.
Ullrich, R.
Wakeford, R.
Yasumura, S.
Milder, C. M.
Shore, R. E.
TI A REPORT FROM THE 2013 INTERNATIONAL SYMPOSIUM: THE EVALUATION OF THE
EFFECTS OF LOW-DOSE RADIATION EXPOSURE IN THE LIFE SPAN STUDY OF ATOMIC
BOMB SURVIVORS AND OTHER SIMILAR STUDIES
SO HEALTH PHYSICS
LA English
DT Article
DE cancer; epidemiology; radiation damage; radiation risk
ID NATURAL BACKGROUND-RADIATION; GENERALIZED LINEAR-MODELS; CHILDHOOD
LEUKEMIA; CANCER
AB The RERF International Low-Dose Symposium was held on 5-6 December 2013 at the RERF campus in Hiroshima, Japan, to discuss the issues facing the Life Span Study (LSS) and other low-dose studies. Topics included the current status of low-dose risk detection, strategies for low-dose epidemiological and statistical research, methods to improve communication between epidemiologists and biologists, and the current status of radiological studies and tools. Key points made by the participants included the necessity of pooling materials over multiple studies to gain greater insight where data from single studies are insufficient; generating models that reflect epidemiological, statistical, and biological principles simultaneously; understanding confounders and effect modifiers in the current data; and taking into consideration less studied factors such as the impact of dose rate. It is the hope of all participants that this symposium be used as a trigger for further studies, especially those using pooled data, in order to reach a greater understanding of the health effects of low-dose radiation.
C1 [Grant, E. J.; Ozasa, K.; Cologne, J.; Cullings, H. M.; Furukawa, K.; Kodama, K.; Nakamura, N.; Niwa, O.; Sadakane, A.; Saigusa, S.; Sakata, R.; Sugiyama, H.; Ullrich, R.; Milder, C. M.; Shore, R. E.] Radiat Effects Res Fdn, Hiroshima 7320815, Japan.
[Ban, N.] Tokyo Healthcare Univ, Tokyo, Japan.
[de Gonzalez, A. Berrington; Rajaraman, P.] US Natl Canc Inst, Bethesda, MD USA.
[Doi, K.; Imaoka, T.; Saigusa, S.] Natl Inst Radiol Sci, Chiba 260, Japan.
[Niwa, O.; Yasumura, S.] Fukushima Med Univ, Fukushima, Japan.
[Preston, D. L.] Hirosoft, Eureka, CA USA.
[Sobue, T.] Osaka Univ, Osaka, Japan.
[Wakeford, R.] Univ Manchester, Manchester, Lancs, England.
RP Grant, EJ (reprint author), Radiat Effects Res Fdn, Minami Ku, 5-2 Hijiyama Koen, Hiroshima 7320815, Japan.
EM egrant@rerf.or.jp
RI Imaoka, Tatsuhiko/E-5134-2012;
OI Imaoka, Tatsuhiko/0000-0003-1507-585X; Wakeford,
Richard/0000-0002-2934-0987
FU Japanese Ministry of Health, Labour and Welfare (MHLW); MHLW; U.S.
Department of Energy (USDOE); USDOE [DE-HS0000031]; RERF Research
Protocol [1-75]
FX This symposium was funded through a grant for international
collaboration from the Japanese Ministry of Health, Labour and Welfare
(MHLW). The Radiation Effects Research Foundation (RERF), Hiroshima and
Nagasaki, Japan, is a public interest foundation funded by the MHLW and
the U.S. Department of Energy (USDOE). RERF research is also funded in
part through USDOE award DE-HS0000031 to the National Academy of
Sciences. This publication was supported by RERF Research Protocol 1-75.
The views of the authors do not necessarily reflect those of the two
governments.
NR 6
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U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0017-9078
EI 1538-5159
J9 HEALTH PHYS
JI Health Phys.
PD MAY
PY 2015
VL 108
IS 5
BP 551
EP 556
DI 10.1097/HP.0000000000000262
PG 6
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 CE5PP
UT WOS:000351887900008
PM 25811153
ER
PT J
AU Lindsey, EW
MacKinnon-Lewis, C
Frabutt, JM
Chambers, JC
AF Lindsey, Eric W.
MacKinnon-Lewis, Carol
Frabutt, James M.
Chambers, Jessica Campbell
TI Cognitive Attributions and Emotional Expectancies Predict Emotions in
Mother-Adolescent Interactions
SO JOURNAL OF EARLY ADOLESCENCE
LA English
DT Article
DE mother-adolescent; emotional expectancies; hostile attributions;
expression of emotion
ID LONGITUDINAL EXAMINATION; AGGRESSIVE-BEHAVIOR; CHILD RELATIONSHIPS;
FAMILY; CONFLICT; INTERVENTION; ASSOCIATIONS; ADJUSTMENT; FATHERS
AB The purpose of this study was to examine adolescent's hostile attributions of mother's intent and emotional self-expectancies as contributors to expression of emotion between mothers and adolescents. Data were collected from 268 10- to 12-year-olds (133 girls, 135 boys) and their mothers. Each dyad was observed in a conversational activity that was coded for both partners' expressions of four discrete emotions: happiness, anger, sadness, and fear. Adolescents responded to hypothetical stories to assess their emotional expectancies and attributions. Regression analysis revealed that adolescents' hostile attributions and emotional expectancies made independent contributions to the expression of happiness and anger with their mother. Adolescents who interpreted their mother's hypothetical behavior as hostile, and who expected to feel less happiness and more anger in response to their mother's hypothetical behavior, expressed less happiness and more anger with their mother. The findings support the conceptual distinction between hostile attributions and emotional expectancies.
C1 [Lindsey, Eric W.] Penn State Univ, Appl Psychol, Reading, PA 19610 USA.
[MacKinnon-Lewis, Carol] Univ S Florida, Dept Child & Family Studies, Tampa, FL USA.
[Frabutt, James M.] Univ Notre Dame, Notre Dame, IN 46556 USA.
[Chambers, Jessica Campbell] NIDA, Div Clin Neurosci Dev & Behav Res, Bethesda, MD 20892 USA.
RP Lindsey, EW (reprint author), Penn State Univ, Dept Appl Psychol, Berks Campus,Tulpehocken Rd,POB 7009, Reading, PA 19610 USA.
EM EWL10@psu.edu
FU William T. Grant Foundation [017396218]
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 William T. Grant Foundation Grant 017396218.
NR 37
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U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0272-4316
EI 1552-5449
J9 J EARLY ADOLESCENCE
JI J. Early Adolesc.
PD MAY
PY 2015
VL 35
IS 4
BP 484
EP 510
DI 10.1177/0272431614540525
PG 27
WC Family Studies; Psychology, Developmental
SC Family Studies; Psychology
GA CE5DG
UT WOS:000351849900003
ER
PT J
AU Jager, J
Yuen, CX
Putnick, DL
Hendricks, C
Bornstein, MH
AF Jager, Justin
Yuen, Cynthia X.
Putnick, Diane L.
Hendricks, Charlene
Bornstein, Marc H.
TI Adolescent-Peer Relationships, Separation and Detachment From Parents,
and Internalizing and Externalizing Behaviors: Linkages and Interactions
SO JOURNAL OF EARLY ADOLESCENCE
LA English
DT Article
DE separation; detachment; internalizing; externalizing; latent variable
interactions
ID EMOTIONAL AUTONOMY SCALE; PSYCHOLOGICAL SEPARATION; PSYCHOSOCIAL
ADJUSTMENT; SOCIOECONOMIC-STATUS; LATENT-VARIABLES; YOUNG ADULTHOOD;
FAMILY-MEMBERS; WORKING MODELS; FIT INDEXES; ALCOHOL-USE
AB Most research exploring the interplay between context and adolescent separation and detachment has focused on the family; in contrast, this investigation directs its attention outside of the family to peers. Utilizing a latent variable approach for modeling interactions and incorporating reports of behavioral adjustment from 14-year-old adolescents (N = 190) and their mothers, we examine how separation and detachment relate to adolescent-peer relationships, and whether peer relationships moderate how separation and detachment relate to adolescent internalizing and externalizing behaviors. Positive peer relationships were both associated with lower detachment and sharply attenuated relations between detachment and higher adolescent internalizing and externalizing. Separation from parents was unrelated to peer relationships, and regardless of whether peer relationships were positive, separation was not related to adolescent internalizing and externalizing. We integrate these findings with those from family-focused investigations and discuss their substantive and clinical implications.
C1 [Jager, Justin] Arizona State Univ, T Denny Sanford Sch Social & Family Dynam, Tempe, AZ 85287 USA.
[Yuen, Cynthia X.] Univ Illinois, Urbana, IL 61801 USA.
[Putnick, Diane L.; Hendricks, Charlene] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Child & Family Res Sect, Bethesda, MD USA.
[Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Child & Family Res, Bethesda, MD USA.
RP Jager, J (reprint author), Arizona State Univ, T Denny Sanford Sch Social & Family Dynam, POB 873701, Tempe, AZ 85287 USA.
EM justin.jager@asu.edu
OI Putnick, Diane/0000-0002-6323-749X
FU Intramural Research Program of the NIH, NICHD
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This
research was supported by the Intramural Research Program of the NIH,
NICHD.
NR 72
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Z9 1
U1 6
U2 33
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0272-4316
EI 1552-5449
J9 J EARLY ADOLESCENCE
JI J. Early Adolesc.
PD MAY
PY 2015
VL 35
IS 4
BP 511
EP 537
DI 10.1177/0272431614537116
PG 27
WC Family Studies; Psychology, Developmental
SC Family Studies; Psychology
GA CE5DG
UT WOS:000351849900004
ER
PT J
AU Farhat, T
Haynie, D
Summersett-Ringgold, F
Brooks-Russell, A
Iannotti, RJ
AF Farhat, Tilda
Haynie, Denise
Summersett-Ringgold, Faith
Brooks-Russell, Ashley
Iannotti, Ronald J.
TI Weight Perceptions, Misperceptions, and Dating Violence Victimization
Among US Adolescents
SO JOURNAL OF INTERPERSONAL VIOLENCE
LA English
DT Article
DE dating violence; adolescents; obesity; weight perceptions; gender
ID HEALTH-RISK BEHAVIORS; BODY-MASS INDEX; ROMANTIC RELATIONSHIPS;
RELATIONAL AGGRESSION; SEXUAL RELATIONSHIPS; PARTNER VIOLENCE; SUBSTANCE
USE; OBESITY; PREVALENCE; CHILDREN
AB Dating violence is a major public health issue among youth. Overweight/obese adolescents experience peer victimization and discrimination and may be at increased risk of dating violence victimization. Furthermore, given the stigma associated with overweight/obesity, perceptions and misperceptions of overweight may be more important than actual weight status for dating violence victimization. This study examines the association of three weight indices (weight status, perceived weight, and weight perception accuracy) with psychological and physical dating violence victimization. The 2010 baseline survey of the 7-year NEXT Generation Health Study used a three-stage stratified clustered sampling design to select a nationally representative sample of U.S. 10th-grade students (n = 1,983). Participants who have had a boyfriend/girlfriend reported dating violence victimization and perceived weight. Weight status was computed from measured height/weight. Weight perception accuracy (accurate/underestimate/overestimate) was calculated by comparing weight status and perceived weight. Gender-stratified regressions examined the association of weight indices and dating violence victimization. Racial/ethnic differences were also examined. The association of weight indices with dating violence victimization significantly differed by gender. Overall, among boys, no associations were observed. Among girls, weight status was not associated with dating violence victimization, nor with number of dating violence victimization acts; however, perceived weight and weight perception accuracy were significantly associated with dating violence victimization, type of victimization, and number of victimization acts. Post hoc analyses revealed significant racial/ethnic differences. White girls who perceive themselves (accurately or not) to be overweight, and Hispanic girls who are overweight, may be at increased risk of dating violence victimization. These findings suggest a targeted approach to dating violence victimization prevention.
C1 [Farhat, Tilda] NCI, Ctr Reduce Canc Hlth Dispar, NIH, Bethesda, MD 20892 USA.
[Haynie, Denise] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, NIH, Bethesda, MD USA.
[Summersett-Ringgold, Faith; Brooks-Russell, Ashley; Iannotti, Ronald J.] NIH, Bethesda, MD 20892 USA.
RP Farhat, T (reprint author), NCI, Dispar Res Branch, Ctr Reduce Canc Hlth Dispar, NIH, 9609 Med Ctr Dr,MSC 9746,Room 6W246, Bethesda, MD 20892 USA.
EM Tilda.Farhat@nih.gov
OI Haynie, Denise/0000-0002-8270-6079
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD)
[HHSN267200800009C]; National Heart, Lung and Blood Institute (NHLBI);
National Institute on Alcohol Abuse and Alcoholism (NIAAA); Maternal and
Child Health Bureau (MCHB) of the Health Resources and Services
Administration (HRSA)
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This
project (contract number HHSN267200800009C) was supported in part by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD), and the
National Heart, Lung and Blood Institute (NHLBI); the National Institute
on Alcohol Abuse and Alcoholism (NIAAA); and Maternal and Child Health
Bureau (MCHB) of the Health Resources and Services Administration
(HRSA), with supplemental support from the National Institute on Drug
Abuse (NIDA).
NR 37
TC 3
Z9 3
U1 4
U2 9
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0886-2605
EI 1552-6518
J9 J INTERPERS VIOLENCE
JI J. Interpers. Violence
PD MAY
PY 2015
VL 30
IS 9
BP 1511
EP 1532
DI 10.1177/0886260514540804
PG 22
WC Criminology & Penology; Family Studies; Psychology, Applied
SC Criminology & Penology; Family Studies; Psychology
GA CE7FR
UT WOS:000352003900004
PM 25001616
ER
PT J
AU John, WS
Newman, AH
Nader, MA
AF John, William S.
Newman, Amy Hauck
Nader, Michael A.
TI Differential effects of the dopamine D-3 receptor antagonist PG01037 on
cocaine and methamphetamine self-administration in rhesus monkeys
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Cocaine; Methamphetamine; Dopamine D-3 receptors; PG01037;
Self-administration; Rhesus monkeys
ID CUE-INDUCED REINSTATEMENT; DRUG-SEEKING BEHAVIOR; D3 RECEPTOR;
DISCRIMINATIVE-STIMULUS; SQUIRREL-MONKEYS; AGONIST 7-OH-DPAT;
NICOTINE-SEEKING; UP-REGULATION; MICE LACKING; RATS
AB The dopamine D-3 receptor (D3R) has been shown to mediate many of the behavioral effects of psychostimulants associated with high abuse potential. This study extended the assessment of the highly selective D3R antagonist PG01037 on cocaine and methamphetamine (MA) self-administration to include a food-drug choice procedure. Eight male rhesus monkeys (n = 4/group) served as subjects in which complete cocaine and MA dose response curves were determined daily in each session. When choice was stable, monkeys received acute and five-day treatment of PG01037 (1.0-5.6 mg/kg, i.v.). Acute administration of PG01037 was effective in reallocating choice from cocaine to food and decreasing cocaine intake, however, tolerance developed by day 5 of treatment. Up to doses that disrupted responding, MA choice and intake were not affected by PG01037 treatment. PG01037 decreased total reinforcers earned per session and the behavioral potency was significantly greater on MA-food choice compared to cocaine-food choice. Furthermore, the acute efficacy of PG01037 was correlated with the sensitivity of the D-3/D2R agonist quinpirole to elicit yawning. These data suggest (1) that efficacy of D3R compounds in decreasing drug choice is greater in subjects with lower D3R, perhaps suggesting that it is percent occupancy that is the critical variable in determining efficacy and (2) differences in D3R activity in chronic cocaine vs. MA users. Although tolerance developed to the effects of PG01037 treatment on cocaine choice, tolerance did not develop to the disruptive effects on food-maintained responding. These findings suggest that combination treatments that decrease cocaine-induced elevations in DA may enhance the efficacy of D3R antagonists on cocaine self-administration. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [John, William S.; Nader, Michael A.] Wake Forest Univ, Bowman Gray Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27157 USA.
[Newman, Amy Hauck] NIDA, Med Chem Sect, Mol Targets & Medicat Discovery Branch, Intramural Res Program,NIH, Baltimore, MD USA.
RP Nader, MA (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Dept Physiol & Pharmacol, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM wjohn@wakehealth.edu; anewman@intra.nida.nih.gov; mnader@wakehealth.edu
FU National Institute on Drug Abuse [DA012460]; NIDA-IRP; [T32 AA-007565]
FX We would like to thank Michelle Bell for excellent technical assistance
working with the monkeys, J. Cao for the synthesis of PG01037 and Dr.
Paul Czoty for statistical consultation. This research was supported by
the National Institute on Drug Abuse grant DA012460 and NIDA-IRP. WS
John is supported by T32 AA-007565.
NR 73
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U1 0
U2 8
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 MAY
PY 2015
VL 92
BP 34
EP 43
DI 10.1016/j.neuropharm.2014.12.024
PG 10
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA CE4IG
UT WOS:000351793700005
PM 25576373
ER
PT J
AU Kolb, EA
Sampson, V
Stabley, D
Walter, A
Sol-Church, K
Cripe, T
Hingorani, P
Ahern, CH
Weigel, BJ
Zwiebel, J
Blaney, SM
AF Kolb, E. . Anders
Sampson, Valerie
Stabley, Deborah
Walter, Alexa
Sol-Church, Katia
Cripe, Timothy
Hingorani, Pooja
Ahern, Charlotte Hsieh
Weigel, Brenda J.
Zwiebel, James
Blaney, Susan M.
TI A Phase I Trial and Viral Clearance Study of Reovirus (Reolysin) in
Children With Relapsed or Refractory Extracranial Solid Tumors: A
Children's Oncology Group Phase I Consortium Report
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE phase 1; pediatric cancer; pirotherapy
ID INTRAVENOUS ONCOLYTIC REOVIRUS; RECURRENT MALIGNANT GLIOMAS; ADVANCED
CANCER; NEONATAL MICE; THERAPY; TYPE-3; INFECTION; CELLS; PREVALENCE;
ANTIBODIES
AB BackgroundReovirus is a naturally occurring human virus that is cytopathic to malignant cells possessing an activated Ras signaling pathway. We conducted a phase I trial of Reolysin, a manufactured, proprietary isolate of purified reovirus, in children with relapsed/refractory extracranial solid tumors to define the recommended phase 2 dose (RP2D), toxicities, and pharmacokinetic properties when administered as a single agent or in combination with cyclophosphamide.
ProceduresReolysin was administered intravenously for 5 consecutive days, every 28 days. Using a 3+3 design, the following dose levels were evaluated: 3x10(8) Tissue Culture Inhibitory Dose 50% (TCID50)/kg; 5x10(8) TCID50/kg (maximum dose was 3x10(10) TCID50); and 5x10(8) TCID50/kg plus oral cyclophosphamide (50mg/m(2)/day x 21 days).
ResultsTwenty-nine patients were enrolled; 28 were eligible and 24 were evaluable for toxicity and response. There were no hematologic dose-limiting toxicities. Grade 5 respiratory failure and a Grade 5 thromboembolic event were reported, both in the setting of progressive disease. The median time to clear the reovirus viremia was 6.5 days. Eight of 24 patients were viremic beyond the 5 days of therapy, all were negative by day 17. No patient had detectable viral RNA in saliva or stool. There were no objective responses.
ConclusionsReolysin at a dose of 5x10(8) TCID50/kg daily for 5 days was well tolerated in children alone and in combination with oral cyclophosphamide. Virus was cleared rapidly from the serum and shedding in stool and saliva was not detectable. Pediatr Blood Cancer 2015;62:751-758. (c) 2015 Wiley Periodicals, Inc.
C1 [Kolb, E. . Anders; Sampson, Valerie; Walter, Alexa] Nemours AI duPont Jospital Children, Nemours Ctr Canc & Blood Disorders, Wilmington, DE USA.
[Stabley, Deborah; Sol-Church, Katia] Nemours AI duPont Jospital Children, Nemours Biomol Core Lab, Wilmington, DE USA.
[Cripe, Timothy] Ohio State Univ, Nationwide Childrens Hosp, Div Hematol Oncol BMT, Columbus, OH 43210 USA.
[Hingorani, Pooja] Phoenix Childrens Hosp, Div Hematol & Oncol, Phoenix, AZ USA.
[Ahern, Charlotte Hsieh] Baylor Coll Med, Dept Med, Div Biostat, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
[Weigel, Brenda J.] Univ Minnesota, Amplatz Childrens Hosp, Div Hematol & Oncol, Minneapolis, MN USA.
[Zwiebel, James] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Blaney, Susan M.] Baylor Coll Med, Texas Childrens Canc Ctr, Div Hematol Oncol, Dept Med, Houston, TX 77030 USA.
RP Kolb, EA (reprint author), Alfred I DuPont Hosp Children, Nemours Ctr Canc & Blood Disorders, 1600 Rockland Rd, Wilmington, DE 19803 USA.
EM eakolb@nemours.org
FU National Institute of General Medical Sciences of the National
Institutes of Health [P20GM103464, P20GM103446]; NIH Pediatric Phase
1/Pilot Consortium [5UM1 CA097452-12]
FX Grant sponsor: National Institute of General Medical Sciences of the
National Institutes of Health; Grant numbers: P20GM103464; P20GM103446;
Grant sponsor: NIH Pediatric Phase 1/Pilot Consortium; Grant number:
5UM1 CA097452-12
NR 39
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Z9 6
U1 1
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 MAY
PY 2015
VL 62
IS 5
BP 751
EP 758
DI 10.1002/pbc.25464
PG 8
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CE2WC
UT WOS:000351680400005
PM 25728527
ER
PT J
AU Estrada-Veras, J
Alvarado-Enriquez, J
O'Brien, K
Gahl, W
AF Estrada-Veras, Juvianee
Alvarado-Enriquez, Jhonell
O'Brien, Kevin
Gahl, William
TI ERDHEIM CHESTER DISEASE: CLINICAL CHARACTERISTICS OF 40 CASES SEEN AT
THE NIH CLINICAL CENTER
SO PEDIATRIC BLOOD & CANCER
LA English
DT Meeting Abstract
C1 [Estrada-Veras, Juvianee; Alvarado-Enriquez, Jhonell; O'Brien, Kevin; Gahl, William] NHGRI, 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 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD MAY
PY 2015
VL 62
SU 1
BP S8
EP S8
PG 1
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CE2VZ
UT WOS:000351680100034
ER
PT J
AU Sieni, E
Tesi, B
Romano, F
Ciambotti, B
Neves, C
Chiang, S
Galli, L
Avenali, S
Tondo, A
Cordeiro, AI
Schlums, H
Jan-Inge-Henter
Canessa, C
Lippi, F
Nordenskjold, M
Hsu, A
Holland, SM
Neves, JF
Azzari, C
Bryceson, Y
AF Sieni, Elena
Tesi, Bianca
Romano, Francesca
Ciambotti, Benedetta
Neves, Conceicao
Chiang, Samuel
Galli, Luisa
Avenali, Stefano
Tondo, Annalisa
Cordeiro, Ana Isabel
Schlums, Heinrich
Jan-Inge-Henter
Canessa, Clementina
Lippi, Francesca
Nordenskjold, Magnus
Hsu, Amy
Holland, Steven M.
Neves, Joao Farelas
Azzari, Chiara
Bryceson, Yenan
TI INTERFERON (IFN)-gamma RECEPTOR DEFICIENCY PRESENTING AS FATAL
HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS (HLH): REPORT OF TWO CASES
SO PEDIATRIC BLOOD & CANCER
LA English
DT Meeting Abstract
C1 [Sieni, Elena; Ciambotti, Benedetta; Tondo, Annalisa] Anna Meyer Childrens Univ Hosp, Dept Pediat Hematol Oncol, Florence, Italy.
[Tesi, Bianca; Jan-Inge-Henter] Karolinska Inst, Dept Womens & Childrens Hlth, Childhood Canc Res Unit, Karolinska Univ Hosp Solna, Stockholm, Sweden.
[Tesi, Bianca; Nordenskjold, Magnus] Karolinska Inst, Clin Genet Unit, Dept Mol Med & Surg, Karolinska Univ Hosp, Stockholm, Sweden.
[Tesi, Bianca; Nordenskjold, Magnus] Karolinska Inst, Ctr Mol Med, Karolinska Univ Hosp, Stockholm, Sweden.
[Romano, Francesca; Canessa, Clementina; Lippi, Francesca; Azzari, Chiara] Univ Florence, Dept Hlth Sci, Div Pediat Immunol, Florence, Italy.
[Romano, Francesca; Galli, Luisa; Canessa, Clementina; Lippi, Francesca; Azzari, Chiara] Anna Meyer Childrens Hosp, Florence, Italy.
[Neves, Conceicao; Cordeiro, Ana Isabel; Neves, Joao Farelas] Pediat Univ Hosp, Hosp Dona Estefania, Primary Immunodeficiencies Unit, Lisbon, Portugal.
[Chiang, Samuel; Schlums, Heinrich; Bryceson, Yenan] Karolinska Inst, Karolinska Univ Hosp Huddinge, Dept Med, Ctr Infect Med, Stockholm, Sweden.
[Galli, Luisa] Univ Florence, Dept Hlth Sci, Div Pediat Infect Dis, Florence, Italy.
[Avenali, Stefano] Anna Meyer Childrens Univ Hosp, Dept Pediat Anesthesia & Intens Care, Florence, Italy.
[Hsu, Amy; Holland, Steven M.] NIAID, 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 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD MAY
PY 2015
VL 62
SU 1
BP S15
EP S15
PG 1
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA CE2VZ
UT WOS:000351680100062
ER
PT J
AU Mattoo, TK
Carpenter, MA
Moxey-Mims, M
Chesney, RW
AF Mattoo, Tej K.
Carpenter, Myra A.
Moxey-Mims, Marva
Chesney, Russell W.
CA RIVUR Trial Investigators
TI The RIVUR trial: a factual interpretation of our data
SO PEDIATRIC NEPHROLOGY
LA English
DT Editorial Material
DE Vesicoureteral reflux; Urinary tract infection; Children; Antimicrobial
prophylaxis; Prospective trials; Renal scarring
ID URINARY-TRACT-INFECTION; VESICOURETERAL REFLUX; ANTIBIOTIC-PROPHYLAXIS;
CHILDREN; PYELONEPHRITIS; MULTICENTER; GUIDELINES
AB Vesicoureteral reflux (VUR) increases the risk of urinary tract infection (UTI) and renal scarring. Many prospective studies have evaluated the role of antimicrobial prophylaxis in the prevention of recurrent UTI and renal scarring in children with VUR. Of these, the RIVUR trial was the largest, randomized, placebo-controlled, double blind, multicenter study, involving 607 children aged 2-72 months with grade I-IV VUR and a first or second symptomatic UTI. The median age of children in the RIVUR trial was 12 months, 92 % were female, 91 % were randomized after a first UTI, 86 % had a febrile index UTI, and 71 (56 %) of 126 toilet-trained children had bladder bowel dysfunction. Trimethoprim/sulfamethoxazole reduced the risk of UTI recurrences by 50 % (hazard ratio 0.50; 95 % confidence interval 0.34-0.74) as compared to placebo. No significant difference was seen in renal scarring between the two groups. However, this does not invalidate the role of prophylaxis in preventing renal scars because RIVUR and other recent prospective studies were not designed to address renal scarring as a primary study endpoint. In view of the RIVUR Trial and other studies that showed similar results, albeit in selected groups of patients, the debate on antimicrobial prophylaxis should shift from "no prophylaxis" to "selective prophylaxis" in children with VUR.
C1 [Mattoo, Tej K.] Wayne State Univ, Sch Med, Childrens Hosp Michigan, Div Pediat Nephrol & Hypertens, Detroit, MI 48201 USA.
[Carpenter, Myra A.] Univ N Carolina, Chapel Hill, NC USA.
[Moxey-Mims, Marva] NIDDK, Bethesda, MD 20892 USA.
[Chesney, Russell W.] Le Bonheur Childrens Hosp, Memphis, TN USA.
RP Mattoo, TK (reprint author), Wayne State Univ, Sch Med, Childrens Hosp Michigan, Div Pediat Nephrol & Hypertens, 3901 Beaubien Blvd, Detroit, MI 48201 USA.
EM tmattoo@med.wayne.edu
FU NIDDK NIH HHS [U01 DK074062]
NR 17
TC 5
Z9 5
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0931-041X
EI 1432-198X
J9 PEDIATR NEPHROL
JI Pediatr. Nephrol.
PD MAY
PY 2015
VL 30
IS 5
BP 707
EP 712
DI 10.1007/s00467-014-3022-1
PG 6
WC Pediatrics; Urology & Nephrology
SC Pediatrics; Urology & Nephrology
GA CE3DY
UT WOS:000351706700003
PM 25558811
ER
PT J
AU Lee, JW
Huang, JD
Rodriguez, IR
AF Lee, Jung Wha
Huang, Jiahn-Dar
Rodriguez, Ignacio R.
TI Extra-hepatic metabolism of 7-ketocholesterol occurs by esterification
to fatty acids via cPLA2 alpha and SOAT1 followed by selective efflux to
HDL
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
LA English
DT Article
DE 7-Ketocholesterol; 7-Ketocholesterol fatty acid ester; SOAT1; cPLA2
alpha; HDL; Cultured RPE cell
ID CHOLESTEROL 7-ALPHA-HYDROXYLASE; HEPATIC-METABOLISM; OXYSTEROL; MICE;
SULFOTRANSFERASE; EXPRESSION; CELLS; LIVER; ACYLTRANSFERASE;
LOCALIZATION
AB Accumulation of 7-ketocholesterol (7KCh) in tissues has been previously associated with various chronic aging diseases. Orally ingested 7KCh is readily metabolized by the liver and does not pose a toxicity threat. However, 7KCh formed in situ, usually associated with lipoprotein deposits, can adversely affect surrounding tissues by causing inflammation and cytotoxicity. In this study we have investigated various mechanisms for extrahepatic metabolism of 7KCh (e.g. hydroxylation, sulfation) and found only esterification to fatty acids. The esterification of 7KCh to fatty acids involves the combined action of cytosolic phospholipase A2 alpha (cPLA2 alpha) and sterol O-acyltransferase (SOAT1). Inhibition of either one of these enzymes ablates 7KCh-fatty acid ester (7KFAE) formation. The 7KFAEs are not toxic and do not induce inflammatory responses. However, they can be unstable and re-release 7KCh. The higher the degree of unsaturation, the more unstable the 7KFAE (e.g. 18:0 > 18:1 > 18:2 >> 18:3 20:4). Biochemical inhibition and siRNA knockdown of SOAT1 and cPLA2a ablated the 7KFAE synthesis in cultured ARPE19 cells, but had little effect on the 7KCh-induced inflammatory response. Overexpression of SOAT1 reduced the 7KCh-induced inflammatory response and provided some protection from cell death. This effect is likely due to the increased conversion of 7KCh to 7KFAEs, which reduced the intracellular 7KCh levels. Addition of HDL selectively increased the efflux of 7KFAEs and enhanced the effect of SOAT1 overexpression. Our data suggests an additional function for HDL in aiding extra-hepatic tissues to eliminate 7KCh by returning 7KFAEs to the liver for bile acid formation. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Lee, Jung Wha; Huang, Jiahn-Dar; Rodriguez, Ignacio R.] NEI, NIH, LRCMB, Mech Retinal Dis Sect, Bethesda, MD 20892 USA.
RP Lee, JW (reprint author), NEI, NIH, LRCMB, Mech Retinal Dis Sect, 6 Ctr Dr,MSC0608,Bldg 6 Rm 131, Bethesda, MD 20892 USA.
EM leej@nei.nih.gov
FU National Eye Institute Intramural Research Program
FX This work was supported by the National Eye Institute Intramural
Research Program.
NR 33
TC 0
Z9 0
U1 1
U2 28
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1388-1981
EI 0006-3002
J9 BBA-MOL CELL BIOL L
JI Biochim. Biophys. Acta Mol. Cell Biol. Lipids
PD MAY
PY 2015
VL 1851
IS 5
BP 605
EP 619
DI 10.1016/j.bbalip.2015.01.007
PG 15
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA CE4LF
UT WOS:000351801400009
PM 25617738
ER
PT J
AU Konig, G
Brooks, BR
AF Koenig, Gerhard
Brooks, Bernard R.
TI Correcting for the free energy costs of bond or angle constraints in
molecular dynamics simulations
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
LA English
DT Article
DE Free energy calculation; Constraint correction; Molecular dynamics
simulation; Normal mode analysis; Bennett's acceptance ratio
ID BENNETTS ACCEPTANCE RATIO; AQUEOUS-SOLUTION; STATISTICAL-MECHANICS;
FORCE-FIELD; CHARMM; TERMS; MACROMOLECULES; SOLVATION; HYDRATION; MODELS
AB Background: Free energy simulations are an important tool in the arsenal of computational biophysics, allowing the calculation of thermodynamic properties of binding or enzymatic reactions. This paper introduces methods to increase the accuracy and precision of free energy calculations by calculating the free energy costs of constraints during post-processing. The primary purpose of employing constraints for these free energy methods is to increase the phase space overlap between ensembles, which is required for accuracy and convergence.
Methods: The free energy costs of applying or removing constraints are calculated as additional explicit steps in the free energy cycle. The new techniques focus on hard degrees of freedom and use both gradients and Hessian estimation. Enthalpy, vibrational entropy, and Jacobian free energy terms are considered.
Results: We demonstrate the utility of this method with simple classical systems involving harmonic and anharmonic oscillators, four-atomic benchmark systems, an alchemical mutation of ethane to methanol, and free energy simulations between alanine and serine. The errors for the analytical test cases are all below 0.0007 kcal/mol, and the accuracy of the free energy results of ethane to methanol is improved from 0.15 to 0.04 kcal/mol. For the alanine to serine case, the phase space overlaps of the unconstrained simulations range between 0.15 and 0.9%. The introduction of constraints increases the overlap up to 2.05%. On average, the overlap increases by 94% relative to the unconstrained value and precision is doubled.
Conclusions: The approach reduces errors arising from constraints by about an order of magnitude. Free energy simulations benefit from the use of constraints through enhanced convergence and higher precision.
General significance: The primary utility of this approach is to calculate free energies for systems with disparate energy surfaces and bonded terms, especially in multi-scale molecular mechanics/quantum mechanics simulations. This article is part of a Special Issue entitled Recent developments of molecular dynamics. Published by Elsevier B.V.
C1 [Koenig, Gerhard; Brooks, Bernard R.] NHLBI, NIH, Lab Computat Biol, Rockville, MD 20852 USA.
RP Konig, G (reprint author), NHLBI, NIH, Lab Computat Biol, 5635 Fishers Lane T-900 Suite, Rockville, MD 20852 USA.
EM gerhard.koenig@nih.gov
FU National Heart, Lung and Blood Institute of the National Institutes of
Health
FX The authors would like to thank Tim Miller, Stefan Boresch, Yihan Shao,
Alex Sodt and Lee Woodcock for insightful discussions, as well as Frank
Pickard and Noreen Gervasi for critically reading the manuscript. This
work was supported by the intramural research program of the National
Heart, Lung and Blood Institute of the National Institutes of Health and
utilized the high-performance computational capabilities of the LoBoS
and Biowulf Linux clusters at the National Institutes of Health.
(http://www.lobos.nih.gov/ and http://biowulf.nih.gov).
NR 70
TC 14
Z9 14
U1 3
U2 41
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-4165
EI 1872-8006
J9 BBA-GEN SUBJECTS
JI Biochim. Biophys. Acta-Gen. Subj.
PD MAY
PY 2015
VL 1850
IS 5
SI SI
BP 932
EP 943
DI 10.1016/j.bbagen.2014.09.001
PG 12
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA CC9QW
UT WOS:000350706700009
PM 25218695
ER
PT J
AU Karyadi, DM
Zhao, SS
He, QC
McIntosh, L
Wright, JL
Ostrander, EA
Feng, ZD
Stanford, JL
AF Karyadi, Danielle M.
Zhao, Shanshan
He, Qianchuan
McIntosh, Laura
Wright, Jonathan L.
Ostrander, Elaine A.
Feng, Ziding
Stanford, Janet L.
TI Confirmation of genetic variants associated with lethal prostate cancer
in a cohort of men from hereditary prostate cancer families
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE AKT1; hereditary prostate cancer; mortality; SNPs; XRCC1; RNASEL
ID RNASEL; MECHANISMS; PATHWAYS; LINKAGE; TRENDS; RISK
AB Germline genetic variants have been suggested as prognostic biomarkers for identifying patients at high risk for lethal prostate cancer (PCa). Validation studies have confirmed the association of several single nucleotide polymorphisms (SNPs) with fatal PCa, but whether these variants affect PCa-specific mortality (PCSM) in patients with an inherited predisposition to PCa, based on familial history, is unknown. For this study, a cohort of 957 PCa patients from 270 hereditary prostate cancer families of European ancestry was genotyped for a panel of 22 PCSM-associated SNPs. Death certificates were reviewed to confirm cause of death. Mixed-effect Cox proportional hazards models were used to assess survival according to genotypes, accounting for relatedness and clinicopathological factors. Within this cohort, 98 PCa deaths were confirmed over an average follow-up period of 12.7 years after diagnosis. Variant allele carriers for three SNPs had significantly altered risk for PCSM [rs635261 at RNASEL, hazard ratio (HR), 0.35, 95% CI, 0.18-0.66; p=0.002; rs915927 in XRCC1, HR, 1.91, 95% CI, 1.21-3.02; p=0.009; and rs2494750 at AKT1, HR, 0.45, 95% CI, 0.23-0.90; p=0.016). These results confirm the association of genetic variation in three genes with PCa lethality in a cohort of men with an inherited susceptibility to the disease and provide validation evidence that germline SNPs provide prognostic information for PCa patients. Development of a panel of germline biomarkers with clinical utility for distinguishing patients at detection who have an increased risk for fatal PCa is warranted.
What's new? Genetic variants involved in prostate cancer are promising candidate biomarkers of clinical outcome, particularly mortality. Previous investigation identified 22 germline variants associated with lethal prostate cancer. Here, analysis of those variants in high-risk patients from families with hereditary prostate cancer validates the association of three single nucleotide polymorphisms (SNPs) with lethal disease. The validated SNPs were located in the genes RNASEL, XRCC1, and AKT1. The findings indicate that germline SNPs may provide prognostic information for distinguishing patients who are at increased risk for progression to fatal prostate cancer.
C1 [Karyadi, Danielle M.; Ostrander, Elaine A.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Zhao, Shanshan; He, Qianchuan; McIntosh, Laura; Wright, Jonathan L.; Stanford, Janet L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Wright, Jonathan L.] Univ Washington, Sch Med, Dept Urol, Seattle, WA 98195 USA.
[Feng, Ziding] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
[Stanford, Janet L.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
RP Stanford, JL (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1100 Fairview Ave N,M4-B874, Seattle, WA 98109 USA.
EM jstanfor@fhcrc.org
OI Ostrander, Elaine/0000-0001-6075-9738
FU National Cancer Institute [R01 CA080122]; Fred Hutchinson Cancer
Research Center; Intramural Program of the National Human Genome
Research Institute; Prostate Cancer Foundation
FX Grant sponsor: National Cancer Institute; Grant number: R01 CA080122;
Grant sponsor: Fred Hutchinson Cancer Research Center; Grant sponsor:
Intramural Program of the National Human Genome Research Institute;
Grant sponsor: Prostate Cancer Foundation
NR 28
TC 3
Z9 3
U1 0
U2 15
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 MAY 1
PY 2015
VL 136
IS 9
BP 2166
EP 2171
DI 10.1002/ijc.29241
PG 6
WC Oncology
SC Oncology
GA CB9SI
UT WOS:000349972300017
PM 25273821
ER
PT J
AU Lee, MS
Lee, B
Park, KE
Utsuki, T
Shin, T
Oh, CW
Kim, HR
AF Lee, Min-Sup
Lee, Bonggi
Park, Kyoung-Eun
Utsuki, Tadanobu
Shin, Taisun
Oh, Chul Woong
Kim, Hyeung-Rak
TI Dieckol enhances the expression of antioxidant and detoxifying enzymes
by the activation of Nrf2-MAPK signalling pathway in HepG2 cells
SO FOOD CHEMISTRY
LA English
DT Article
DE Dieckol; Hemeoxygenase-1; NAD(P)H:quinine oxidoreductase 1; Glutathione
S-transferase; Nrf2; MAPK
ID MEDIATED GENE-EXPRESSION; RESPONSE ELEMENT; ECKLONIA-STOLONIFERA;
CYTOPROTECTIVE GENES; NRF2; INDUCTION; MECHANISM; PROTEIN; STRESS; MICE
AB Dieckol was previously reported to exhibit antioxidant and anticancer activities in vitro studies. In this study, we characterised the mechanism underlying the dieckol-mediated expression of antioxidant and detoxifying enzymes. Dieckol suppressed the production of intracellular reactive oxygen species in the presence or absence of H2O2 and increased glutathione level in HepG2 cells. Dieckol enhanced the activities of antioxidant enzymes, and the expression of detoxifying enzymes including heme oxygenase-1 (HO-1), NAD(P)H:quinine oxidoreductase 1 (NQO1), and glutathione S-transferase (GST) in HepG2 cells. Enhanced expression of antioxidant and detoxifying enzymes by dieckol was presumed to be the activation of the nuclear factor erythroid-derived 2-like 2 (Nrf2) demonstrated by its nuclear translocation and transcriptional activity via activation of mitogen-activated protein kinases in HepG2 cells. Furthermore, we demonstrated dieckol induced the expression of HO-1 in mouse liver. These results demonstrate that the dieckol-mediated cytoprotection in HepG2 cells is mediated through a ROS-independent up-regulation of antioxidant and detoxifying enzymes via Nrf2 activation as well as its intrinsic antioxidant activity, suggesting that dieckol may be used as a natural cytoprotective agent. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Lee, Min-Sup; Park, Kyoung-Eun; Kim, Hyeung-Rak] Pukyong Natl Univ, Dept Food Sci & Nutr, Pusan 608737, South Korea.
[Lee, Bonggi] NICHHD, NIH, Bethesda, MD 20892 USA.
[Utsuki, Tadanobu] Louisiana State Univ, Sch Vet Med, Dept Pathobiol Sci, Baton Rouge, LA 70803 USA.
[Shin, Taisun] Chonnam Natl Univ, Dept Food Sci & Nutr, Yeosu 550749, South Korea.
[Oh, Chul Woong] Pukyong Natl Univ, Dept Marine Biol, Pusan 608737, South Korea.
RP Kim, HR (reprint author), Pukyong Natl Univ, Dept Food Sci & Nutr, Pusan 608737, South Korea.
EM hrkim@pknu.ac.kr
FU Basic Science Research Program through the National Research Foundation
of Korea (NRF) - Ministry of Education [2013R1A1A2009588]
FX This research was supported by Basic Science Research Program through
the National Research Foundation of Korea (NRF) funded by the Ministry
of Education (2013R1A1A2009588).
NR 32
TC 14
Z9 15
U1 0
U2 31
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0308-8146
EI 1873-7072
J9 FOOD CHEM
JI Food Chem.
PD MAY 1
PY 2015
VL 174
BP 538
EP 546
DI 10.1016/j.foodchem.2014.11.090
PG 9
WC Chemistry, Applied; Food Science & Technology; Nutrition & Dietetics
SC Chemistry; Food Science & Technology; Nutrition & Dietetics
GA AZ2UP
UT WOS:000348088000073
PM 25529716
ER
PT J
AU Livingston, WS
Rusch, HL
Nersesian, PV
Baxter, T
Mysliwiec, V
Gill, JM
AF Livingston, Whitney S.
Rusch, Heather L.
Nersesian, Paula V.
Baxter, Tristin
Mysliwiec, Vincent
Gill, Jessica M.
TI Improved sleep in military personnel is associated with changes in the
expression of inflammatory genes and improvement in depression symptoms
SO FRONTIERS IN PSYCHIATRY
LA English
DT Article
DE gene expression; insomnia; inflammation; depression; military personnel
ID POSTTRAUMATIC-STRESS-DISORDER; C-REACTIVE PROTEIN; SERVICE MEMBERS;
COMBAT VETERANS; MOOD DISORDERS; MENTAL-HEALTH; CANCER CELLS; PTSD;
INSOMNIA; DISTURBANCE
AB Study objectives: Sleep disturbances are common in military personnel and are associated with increased risk for psychiatric morbidity, including posttraumatic stress disorder (PTSD) and depression, as well as inflammation. Improved sleep quality is linked to reductions in inflammatory bio-markers; however, the underlying mechanisms remain elusive.
Methods: In this study, we examine whole genome expression changes related to improved sleep in 68 military personnel diagnosed with insomnia. Subjects were classified into the following groups and then compared: improved sleep (n = 46), or non-improved sleep (n = 22) following three months of standard of care treatment for insomnia. Within subject differential expression was determined from microarray data using the Partek Genomics Suite analysis program and the ingenuity pathway analysis (IPA) was used to determine key regulators of observed expression changes. Changes in symptoms of depression and PTSD were also compared.
Results: At baseline, both groups were similar in demographics, clinical characteristics, and gene-expression profiles. The microarray data revealed that 217 coding genes were differentially expressed at the follow-up-period compared to baseline in the participants with improved sleep. Expression of inflammatory cytokines were reduced including IL1f3, IL-6, IL-8, and IL-13, with fold changes ranging from 3.19 to 2.1, and there were increases in the expression of inflammatory regulatory genes including toll-like receptors 1, 4, 7, and 8 in the improved sleep group. IPA revealed six gene networks, including ubiquitin, which was a major regulator in these gene-expression changes. The improved sleep group also had a significant reduction in the severity of depressive symptoms.
Conclusion: Interventions that restore sleep likely reduce the expression of inflammatory genes, which relate to ubiquitin genes and relate to reductions in depressive symptoms.
C1 [Livingston, Whitney S.; Rusch, Heather L.; Nersesian, Paula V.; Gill, Jessica M.] NINR, NIH, Bethesda, MD 20892 USA.
[Nersesian, Paula V.] Johns Hopkins Univ, Sch Nursing, Baltimore, MD USA.
[Baxter, Tristin; Mysliwiec, Vincent] Madigan Army Med Ctr, Tacoma, WA 98431 USA.
RP Livingston, WS (reprint author), NINR, 1 Cloister Court,Room 259, Bethesda, MD 20892 USA.
EM whitney.livingston@nih.gov
NR 60
TC 5
Z9 5
U1 3
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
SWITZERLAND
SN 1664-0640
J9 FRONT PSYCHIATRY
JI Front. Psychiatry
PD APR 30
PY 2015
VL 6
AR 59
DI 10.3389/fpsyt.2015.00059
PG 15
WC Psychiatry
SC Psychiatry
GA CV5YN
UT WOS:000364347500001
PM 25983695
ER
PT J
AU Liu, HX
Hu, Y
French, SW
Gonzalez, FJ
Wan, YJY
AF Liu, Hui-Xin
Hu, Ying
French, Samuel W.
Gonzalez, Frank J.
Wan, Yu-Jui Yvonne
TI Forced expression of fibroblast growth factor 21 reverses the sustained
impairment of liver regeneration in hPPAR alpha(PAC) mice due to
dysregulated bile acid synthesis
SO ONCOTARGET
LA English
DT Article
DE nuclear receptor; metabolism; proliferation; bile acid; species
differences
ID FARNESOID X RECEPTOR; PPAR-ALPHA; PARTIAL-HEPATECTOMY; NUCLEAR RECEPTOR;
OB/OB MICE; MOUSE; METABOLISM; PROTECTS; INJURY; FGF21
AB Peroxisome proliferator activated receptor alpha (PPAR alpha) stimulates hepatocellular proliferation is species-specific. Activation of mouse, but not human, PPAR alpha induces hepatocellular proliferation, hepatomegaly, and liver cancer. Here we tested the hypothesis that human and mouse PPAR alpha affects liver regeneration differentially. PPAR alpha-humanized mice (hPPAR alpha(PAC)) were similar to wild type mice in responding to fasting-induced PPAR alpha signaling. However, these mouse livers failed to regenerate in response to partial hepatectomy (PH). The liver-to-body weight ratios did not recover even 3 months after PH in hPPAR alpha(PAC). The mouse PPAR alpha-mediated down-regulation of let-7c was absent in hPPAR alpha(PAC), which might partially be responsible for impaired proliferation. After PH, hPPAR alpha(PAC) displayed steatosis, necrosis, and inflammation mainly in periportal zone 1, which suggested bile-induced toxicity. Quantification of hepatic bile acids (BA) revealed BA overload with increased hydrophobic BA in hPPAR alpha(PAC). Forced FGF21 expression in partial hepatectomized hPPAR alpha(PAC) reduced hepatic steatosis, prevented focal necrosis, and restored liver mass. Compared to mouse PPAR alpha, human PPAR alpha has a reduced capacity to regulate metabolic pathways required for liver regeneration. In addition, FGF21 can compensate for the reduced ability of human PPAR alpha in stimulating liver regeneration, which suggests the potential application of FGF21 in promoting hepatic growth in injured and steatotic livers in humans.
C1 [Liu, Hui-Xin; Hu, Ying; Wan, Yu-Jui Yvonne] Univ Calif Davis, Dept Med Pathol & Lab Med, Sacramento, CA 95817 USA.
[French, Samuel W.] Harbor UCLA Med Ctr, Dept Pathol & Lab Med, Torrance, CA 90509 USA.
[Gonzalez, Frank J.] NCI, NIH, Lab Metab, Bethesda, MD 20892 USA.
RP Wan, YJY (reprint author), Univ Calif Davis, Dept Med Pathol & Lab Med, Sacramento, CA 95817 USA.
EM yjywan@ucdavis.edu
FU National Institutes of Health [CA53596, DK092100]
FX The authors thank Ms. Irene Ly for technical assistance and Ms. Lisa
Teixeira for editing the manuscript. This study is supported by grants
funded by National Institutes of Health CA53596 and DK092100.
NR 48
TC 2
Z9 2
U1 1
U2 3
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD APR 30
PY 2015
VL 6
IS 12
BP 9686
EP 9700
PG 15
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA CO0WO
UT WOS:000358874600007
PM 25991671
ER
PT J
AU Hoots, WK
Abkowitz, JL
Coller, BS
DiMichele, DM
AF Hoots, W. Keith
Abkowitz, Janis L.
Coller, Barry S.
DiMichele, Donna M.
TI Planning for the future workforce in hematology research
SO BLOOD
LA English
DT Article
AB The medical research and training enterprise in the United States is complex in both its scope and implementation. Accordingly, adaptations to the associated workforce needs present particular challenges. This is particularly true for maintaining or expanding national needs for physician-scientists where training resource requirements and competitive transitional milestones are substantial. For the individual, these phenomena can produce financial burden, prolong the career trajectory, and significantly influence career pathways. Hence, when national data suggest that future medical research needs in a scientific area may be met in a less than optimal manner, strategies to expand research and training capacity must follow. This article defines such an exigency for research and training in nonneoplastic hematology and presents potential strategies for addressing these critical workforce needs. The considerations presented herein reflect a summary of the discussions presented at 2 workshops cosponsored by the National Heart, Lung, and Blood Institute and the American Society of Hematology.
C1 [Hoots, W. Keith; DiMichele, Donna M.] NHLBI, Div Blood Dis & Resources, NIH, Bethesda, MD 20892 USA.
[Abkowitz, Janis L.] Univ Washington, Dept Med, Div Hematol, Seattle, WA 98195 USA.
[Coller, Barry S.] Rockefeller Univ Hosp, Allen & Francis Adler Lab Blood & Vasc Biol, New York, NY 10021 USA.
RP Hoots, WK (reprint author), NHLBI, Div Blood Dis & Resources, NIH, 6701 Rockledge Dr,Room 9136, Bethesda, MD 20892 USA.
EM hootswk@nhlbi.nih.gov
FU NHLBI NIH HHS [K12 HL087165]
NR 9
TC 1
Z9 1
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 30
PY 2015
VL 125
IS 18
BP 2745
EP 2752
DI 10.1182/blood-201501-617811
PG 8
WC Hematology
SC Hematology
GA CJ7OR
UT WOS:000355686600006
PM 25758827
ER
PT J
AU Calvo, KR
Price, S
Braylan, RC
Oliveira, JB
Lenardo, M
Fleisher, TA
Rao, VK
AF Calvo, Katherine R.
Price, Susan
Braylan, Raul C.
Oliveira, Joao Bosco
Lenardo, Michael
Fleisher, Thomas A.
Rao, V. Koneti
TI JMML and RALD (Ras-associated autoimmune leukoproliferative disorder):
common genetic etiology yet clinically distinct entities
SO BLOOD
LA English
DT Article
ID JUVENILE MYELOMONOCYTIC LEUKEMIA; MYELODYSPLASTIC SYNDROMES;
LYMPHOPROLIFERATIVE SYNDROME; BLOOD MONOCYTES; FLOW-CYTOMETRY;
MUTATIONS; CLASSIFICATION; LEUKEMOGENESIS; IMPROVEMENT; CHILDHOOD
AB Ras-associated autoimmune leukoproliferative disorder (RALD) is a chronic, nonmalignant condition that presents with persistent monocytosis and is often associated with leukocytosis, lymphoproliferation, and autoimmune phenomena. RALD has clinical and laboratory features that overlap with those of juvenile myelomonocytic leukemia (JMML) and chronicmyelomonocytic leukemia (CMML), including identical somatic mutations in KRAS or NRAS genes noted in peripheral blood mononuclear cells. Long-term follow-up of these patients suggests that RALD has an indolent clinical course whereas JMML is fatal if left untreated. Immunophenotyping peripheral blood from RALD patients shows characteristic circulating activated monocytes and polyclonal CD10(+) B cells. Distinguishing RALD from JMML and CMML has implications for clinical care and prognosis.
C1 [Calvo, Katherine R.; Braylan, Raul C.; Fleisher, Thomas A.] Ctr Clin, Dept Lab Med, Bethesda, MD USA.
[Price, Susan; Lenardo, Michael; Rao, V. Koneti] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
[Price, Susan; Lenardo, Michael; Rao, V. Koneti] NIAID, Clin Genom Program, NIH, Bethesda, MD 20892 USA.
[Oliveira, Joao Bosco] Inst Med Integral Prof Fernando Figueira, Recife, PE, Brazil.
RP Rao, VK (reprint author), NIAID, NIH, 10 Ctr Dr,Bldg 10,Room 12C106,MSC 1899, Bethesda, MD 20892 USA.
EM koneti@nih.gov
FU National Institute of Allergy and Infectious Diseases; National
Institutes of Health Clinical Center
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases and the National
Institutes of Health Clinical Center.
NR 39
TC 7
Z9 7
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 30
PY 2015
VL 125
IS 18
BP 2753
EP 2758
DI 10.1182/blood2014-11-567917
PG 6
WC Hematology
SC Hematology
GA CJ7OR
UT WOS:000355686600007
PM 25691160
ER
PT J
AU Roberto, A
Castagna, L
Zanon, V
Bramanti, S
Crocchiolo, R
McLaren, JE
Gandolfi, S
Tentorio, P
Sarina, B
Timofeeva, I
Santoro, A
Carlo-Stella, C
Bruno, B
Carniti, C
Corradini, P
Gostick, E
Ladell, K
Price, DA
Roederer, M
Mavilio, D
Lugli, E
AF Roberto, Alessandra
Castagna, Luca
Zanon, Veronica
Bramanti, Stefania
Crocchiolo, Roberto
McLaren, James E.
Gandolfi, Sara
Tentorio, Paolo
Sarina, Barbara
Timofeeva, Inna
Santoro, Armando
Carlo-Stella, Carmelo
Bruno, Benedetto
Carniti, Cristiana
Corradini, Paolo
Gostick, Emma
Ladell, Kristin
Price, David A.
Roederer, Mario
Mavilio, Domenico
Lugli, Enrico
TI Role of naive-derived T memory stem cells in T-cell reconstitution
following allogeneic transplantation
SO BLOOD
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; RECEPTOR EXCISION CIRCLE;
POSTTRANSPLANTATION CYCLOPHOSPHAMIDE; IMMUNE RECONSTITUTION; ADOPTIVE
IMMUNOTHERAPY; CLONAL COMPOSITION; PERIPHERAL-BLOOD; ANTIGEN; PHENOTYPE;
PROLIFERATION
AB Early T-cell reconstitution following allogeneic transplantation depends on the persistence and function of T cells that are adoptively transferred with the graft. Posttransplant cyclophosphamide (pt-Cy) effectively prevents alloreactive responses from unmanipulated grafts, but its effect on subsequent immune reconstitution remains undetermined. Here, we show that T memory stem cells (TSCM), which demonstrated superior reconstitution capacity in preclinical models, are the most abundant circulating T-cell population in the early days following haploidentical transplantation combined with pt-Cy and precede the expansion of effector cells. Transferred naive, but not TSCM or conventional memory cells preferentially survive cyclophosphamide, thus suggesting that posttransplant TSCM originate from naive precursors. Moreover, donor naive T cells specific for exogenous and self/tumor antigens persist in the host and contribute to peripheral reconstitution by differentiating into effectors. Similarly, pathogen-specific memory T cells generate detectable recall responses, but only in the presence of the cognate antigen. We thus define the cellular basis of T-cell reconstitution following pt-Cy at the antigen-specific level and propose to explore naive-derived TSCM in the clinical setting to overcome immunodeficiency.
C1 [Roberto, Alessandra; Zanon, Veronica; Tentorio, Paolo; Mavilio, Domenico; Lugli, Enrico] Humanitas Clin & Res Ctr, Unit Clin & Expt Immunol, I-20089 Milan, Italy.
[Castagna, Luca; Bramanti, Stefania; Crocchiolo, Roberto; Gandolfi, Sara; Sarina, Barbara; Timofeeva, Inna; Santoro, Armando; Carlo-Stella, Carmelo] Humanitas Canc Ctr, Hematol & Bone Marrow Transplant Unit, Milan, Italy.
[McLaren, James E.; Gostick, Emma; Ladell, Kristin; Price, David A.] Cardiff Univ, Sch Med, Inst Infect & Immun, Cardiff CF10 3AX, S Glam, Wales.
[Carlo-Stella, Carmelo; Mavilio, Domenico] Univ Milan, Dept Med Biotechnol & Translat Med BioMeTra, Milan, Italy.
[Bruno, Benedetto] Univ Turin, Dept Mol Biotechnol & Hlth Sci, Turin, Italy.
[Carniti, Cristiana; Corradini, Paolo] Ist Nazl Tumori, Dept Haematol & Pediat Oncohaematol, I-20133 Milan, Italy.
[Roederer, Mario] NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Mavilio, D (reprint author), Humanitas Clin & Res Ctr, Unit Clin & Expt Immunol, Via Alessandro Manzoni 113, I-20089 Milan, Italy.
EM domenico.mavilio@humanitas.it; enrico.lugli@humanitasresearch.it
RI Price, David/C-7876-2013; Ladell, Kristin/C-8301-2013; Carniti,
Cristiana/B-8665-2017;
OI Price, David/0000-0001-9416-2737; Ladell, Kristin/0000-0002-9856-2938;
Carniti, Cristiana/0000-0003-1039-1757; Carlo-Stella,
Carmelo/0000-0003-3144-0124; Mavilio, Domenico/0000-0001-6147-0952;
Corradini, Paolo/0000-0002-9186-1353; Castagna, Luca/0000-0002-6239-7387
FU Fondazione Cariplo [Ricerca Biomedica 2012/0683]; European Union
[322093]; Associazione Italiana per la Ricerca sul Cancro [MFAG 10607,
IG 14687]; Italian Ministry of Health [GR-2008-1135082,
GR-2011-02347324]; National Institutes of Allergy and Infectious
Diseases; Humanitas Intramural Research and Clinical Funding Programs;
Fondazione Italiana per la Ricerca sul Cancro
FX This work was supported by grants from the Fondazione Cariplo (Grant
Ricerca Biomedica 2012/0683 to E.L.), the European Union (Marie Curie
Career Integration Grant 322093 to E.L.), and the Associazione Italiana
per la Ricerca sul Cancro (MFAG 10607 to E.L. and IG 14687 to D.M), by
the Italian Ministry of Health (Bando Giovani Ricercatori
GR-2008-1135082 to D.M. and GR-2011-02347324 to E.L.), as well as funds
provided by the Intramural Program of the National Institutes of Allergy
and Infectious Diseases (to M.R.) and Humanitas Intramural Research and
Clinical Funding Programs (to D.M. and L.C.). A.R. is a recipient of the
Guglielmina Lucatello e Gino Mazzega Fellowship from the Fondazione
Italiana per la Ricerca sul Cancro. D.A.P. is a Wellcome Trust Senior
Investigator.
NR 46
TC 20
Z9 20
U1 1
U2 6
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 30
PY 2015
VL 125
IS 18
BP 2855
EP 2864
DI 10.1182/blood-2014-11-608406
PG 10
WC Hematology
SC Hematology
GA CJ7OR
UT WOS:000355686600018
PM 25742699
ER
PT J
AU Maxwell, EK
Campbell, JD
Spira, A
Baxevanis, AD
AF Maxwell, Evan K.
Campbell, Joshua D.
Spira, Avrum
Baxevanis, Andreas D.
TI SubmiRine: assessing variants in microRNA targets using clinical genomic
data sets
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID GENETIC-VARIATION; COMPLEX TRAITS; SITES; EXPRESSION; DISEASE; BINDING;
SNP; ASSOCIATION; POLYMORPHISMS; RECOGNITION
AB MicroRNAs (miRNAs) regulate gene expression by binding to partially complementary sequences on target mRNA transcripts, thereby causing their degradation, deadenylation, or inhibiting their translation. Genomic variants can alter miRNA regulation by modifying miRNA target sites, and multiple human disease phenotypes have been linked to such miRNA target site variants (miR-TSVs). However, systematic genome-wide identification of functional miR-TSVs is difficult due to high false positive rates; functional miRNA recognition sequences can be as short as six nucleotides, with the human genome encoding thousands of miRNAs. Furthermore, while large-scale clinical genomic data sets are becoming increasingly commonplace, existing miR-TSV prediction methods are not designed to analyze these data. Here, we present an open-source tool called SubmiRine that is designed to perform efficient miR-TSV prediction systematically on variants identified in novel clinical genomic data sets. Most importantly, SubmiRine allows for the prioritization of predicted miR-TSVs according to their relative probability of being functional. We present the results of SubmiRine using integrated clinical genomic data from a large-scale cohort study on chronic obstructive pulmonary disease (COPD), making a number of high-scoring, novel miR-TSV predictions. We also demonstrate SubmiRine's ability to predict and prioritize known miR-TSVs that have undergone experimental validation in previous studies.
C1 [Maxwell, Evan K.; Campbell, Joshua D.; Spira, Avrum; Baxevanis, Andreas D.] NHGRI, Computat & Stat Genom Branch, NIH, Bethesda, MD 20892 USA.
[Maxwell, Evan K.; Campbell, Joshua D.; Spira, Avrum] Boston Univ, Bioinformat Program, Boston, MA 02215 USA.
[Campbell, Joshua D.; Spira, Avrum] Boston Univ, Div Computat Biomed, Dept Med, Sch Med, Boston, MA 02215 USA.
RP Baxevanis, AD (reprint author), NHGRI, Computat & Stat Genom Branch, NIH, Bethesda, MD 20892 USA.
EM andy@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health. Funding for open access
charge: Intramural Research Program of the National Human Genome
Research Institute, National Institutes of Health.
NR 44
TC 3
Z9 3
U1 0
U2 2
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 APR 30
PY 2015
VL 43
IS 8
BP 3886
EP 3898
DI 10.1093/nar/gkv256
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CJ2LV
UT WOS:000355317200009
PM 25813044
ER
PT J
AU Blatti, C
Kazemian, M
Wolfe, S
Brodsky, M
Sinha, S
AF Blatti, Charles
Kazemian, Majid
Wolfe, Scot
Brodsky, Michael
Sinha, Saurabh
TI Integrating motif, DNA accessibility and gene expression data to build
regulatory maps in an organism
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID TRANSCRIPTION FACTOR-BINDING; OPEN CHROMATIN; DROSOPHILA; GENOME;
ELEMENTS; PREDICTION; ENHANCERS; REGIONS; SITES; POLYCOMB
AB Characterization of cell type specific regulatory networks and elements is a major challenge in genomics, and emerging strategies frequently employ high-throughput genome-wide assays of transcription factor (TF) to DNA binding, histone modifications or chromatin state. However, these experiments remain too difficult/expensive for many laboratories to apply comprehensively to their system of interest. Here, we explore the potential of elucidating regulatory systems in varied cell types using computational techniques that rely on only data of gene expression, low-resolution chromatin accessibility, and TF-DNA binding specificities ('motifs'). We show that static computational motif scans overlaid with chromatin accessibility data reasonably approximate experimentally measured TF-DNA binding. We demonstrate that predicted binding profiles and expression patterns of hundreds of TFs are sufficient to identify major regulators of similar to 200 spatiotemporal expression domains in the Drosophila embryo. We are then able to learn reliable statistical models of enhancer activity for over 70 expression domains and apply those models to annotate domain specific enhancers genome-wide. Throughout this work, we apply our motif and accessibility based approach to comprehensively characterize the regulatory network of fruitfly embryonic development and show that the accuracy of our computational method compares favorably to approaches that rely on data from many experimental assays.
C1 [Blatti, Charles; Sinha, Saurabh] Univ Illinois, Dept Comp Sci, Urbana, IL 61801 USA.
[Kazemian, Majid] NHLBI, NIH, Bethesda, MD 20892 USA.
[Wolfe, Scot; Brodsky, Michael] Univ Massachusetts, Sch Med, Program Gene Funct & Express, Worcester, MA 01655 USA.
[Wolfe, Scot] Univ Massachusetts, Sch Med, Dept Mol Med, Worcester, MA 01655 USA.
[Brodsky, Michael] Univ Massachusetts, Sch Med, Dept Biochem & Mol Pharmacol, Worcester, MA 01655 USA.
[Sinha, Saurabh] Univ Illinois, Inst Genom Biol, Urbana, IL 61801 USA.
RP Sinha, S (reprint author), Univ Illinois, Dept Comp Sci, 1304 W Springfield Ave, Urbana, IL 61801 USA.
EM sinhas@illinois.edu
OI Kazemian, Majid/0000-0001-7080-8820
FU National Institutes of Health [1R01GM085233-01]; National Science
Foundation [EFRI-1136913]; Cohen Graduate Fellowship
FX This work was supported by the National Institutes of Health
[1R01GM085233-01 to S.S.]; National Science Foundation [EFRI-1136913 to
S.S.]; and Cohen Graduate Fellowship (awarded to C.B.).
NR 66
TC 6
Z9 6
U1 3
U2 13
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 APR 30
PY 2015
VL 43
IS 8
BP 3998
EP 4012
DI 10.1093/nar/gkv195
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CJ2LV
UT WOS:000355317200018
PM 25791631
ER
PT J
AU Lujan, SA
Clark, AB
Kunkel, TA
AF Lujan, Scott A.
Clark, Alan B.
Kunkel, Thomas A.
TI Differences in genome-wide repeat sequence instability conferred by
proofreading and mismatch repair defects
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID DNA-POLYMERASE-EPSILON; REPLICATION FORK; SYNTHESIS ERRORS; STRUCTURAL
BASIS; YEAST; MUTATIONS; CANCER; DELTA; FIDELITY; ROLES
AB Mutation rates are used to calibrate molecular clocks and to link genetic variants with human disease. However, mutation rates are not uniform across each eukaryotic genome. Rates for insertion/deletion (indel) mutations have been found to vary widely when examined in vitro and at specific loci in vivo. Here, we report the genome-wide rates of formation and repair of indels made during replication of yeast nuclear DNA. Using over 6000 indels accumulated in four mismatch repair (MMR) defective strains, and statistical corrections for false negatives, we find that indel rates increase by 100 000-fold with increasing homonucleotide run length, representing the greatest effect on replication fidelity of any known genomic parameter. Nonetheless, long genomic homopolymer runs are overrepresented relative to random chance, implying positive selection. Proofreading defects in the replicative polymerases selectively increase indel rates in short repetitive tracts, likely reflecting the distance over which Pols delta and I mu interact with duplex DNA upstream of the polymerase active site. In contrast, MMR defects hugely increase indel mutagenesis in long repetitive sequences. Because repetitive sequences are not uniformly distributed among genomic functional elements, the quantitatively different consequences on genome-wide repeat sequence instability conferred by defects in proofreading and MMR have important biological implications.
C1 [Lujan, Scott A.; Clark, Alan B.; Kunkel, Thomas A.] NIEHS, Genome Instabil & Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Kunkel, TA (reprint author), NIEHS, Genome Instabil & Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
EM kunkel@niehs.nih.gov
FU Division of Intramural Research of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01 ES065070];
National Institutes of Health
FX Division of Intramural Research of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01 ES065070 to
T.K.]. Funding for open access charge: National Institutes of Health.
NR 41
TC 4
Z9 4
U1 2
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 APR 30
PY 2015
VL 43
IS 8
BP 4067
EP 4074
DI 10.1093/nar/gkv271
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CJ2LV
UT WOS:000355317200023
PM 25824945
ER
PT J
AU Maslowska, KH
Makiela-Dzbenska, K
Fijalkowska, IJ
Schaaper, RM
AF Maslowska, Katarzyna H.
Makiela-Dzbenska, Karolina
Fijalkowska, Iwona J.
Schaaper, Roel M.
TI Suppression of the E-coli SOS response by dNTP pool changes
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID DNA-POLYMERASE-V; RECA PROTEIN; CONSTITUTIVE EXPRESSION;
INDUCED-MUTAGENESIS; MUTATOR ACTIVITY; RIBONUCLEOTIDE REDUCTASE;
NUCLEOSIDE TRIPHOSPHATES; PROPHAGE INDUCTION; REPLICATION FORKS; LAMBDA
REPRESSOR
AB The Escherichia coli SOS system is a well-established model for the cellular response to DNA damage. Control of SOS depends largely on the RecA protein. When RecA is activated by single-stranded DNA in the presence of a nucleotide triphosphate cofactor, it mediates cleavage of the LexA repressor, leading to expression of the 30(+)-member SOS regulon. RecA activation generally requires the introduction of DNA damage. However, certain recA mutants, like recA730, bypass this requirement and display constitutive SOS expression as well as a spontaneous (SOS) mutator effect. Presently, we investigated the possible interaction between SOS and the cellular deoxynucleoside triphosphate (dNTP) pools. We found that dNTP pool changes caused by deficiencies in the ndk or dcd genes, encoding nucleoside diphosphate kinase and dCTP deaminase, respectively, had a strongly suppressive effect on constitutive SOS expression in recA730 strains. The suppression of the recA730 mutator effect was alleviated in a lexA-deficient background. Overall, the findings suggest a model in which the dNTP alterations in the ndk and dcd strains interfere with the activation of RecA, thereby preventing LexA cleavage and SOS induction.
C1 [Maslowska, Katarzyna H.; Schaaper, Roel M.] NIEHS, Genome Integr & Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Maslowska, Katarzyna H.; Makiela-Dzbenska, Karolina; Fijalkowska, Iwona J.] Polish Acad Sci, Inst Biochem & Biophys, PL-02106 Warsaw, Poland.
RP Schaaper, RM (reprint author), NIEHS, Genome Integr & Struct Biol Lab, POB 12233, Res Triangle Pk, NC 27709 USA.
EM iwonaf@ibb.waw.pl; schaaper@niehs.nih.gov
RI Makiela-Dzbenska, Karolina/E-6751-2016; Fijalkowska, Iwona/I-7796-2016;
OI Maslowska, Katarzyna/0000-0003-3393-8225
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01 ES065086];
International PhD Projects Program of the Foundation for Polish Science
[MPD/2009-3/2]; European Union Regional Development Fund; National
Institute of Environmental Health Sciences
FX The Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [project number Z01
ES065086]; International PhD Projects Program of the Foundation for
Polish Science [project number MPD/2009-3/2] "Studies of Nucleic Acids
and Proteins - from Basic to Applied Research" and European Union
Regional Development Fund. Funding for the open access charge: the
National Institute of Environmental Health Sciences.
NR 75
TC 3
Z9 3
U1 2
U2 9
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 APR 30
PY 2015
VL 43
IS 8
BP 4109
EP 4120
DI 10.1093/nar/gkv217
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CJ2LV
UT WOS:000355317200027
PM 25824947
ER
PT J
AU Perez-Berna, AJ
Marion, S
Chichon, FJ
Fernandez, JJ
Winkler, DC
Carrascosa, JL
Steven, AC
Siber, A
San Martin, C
AF Perez-Berna, Ana J.
Marion, Sanjin
Javier Chichon, F.
Fernandez, Jose J.
Winkler, Dennis C.
Carrascosa, Jose L.
Steven, Alasdair C.
Siber, Antonio
San Martin, Carmen
TI Distribution of DNA-condensing protein complexes in the adenovirus core
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CRYOELECTRON TOMOGRAPHY; NUCLEOPROTEIN CORES; CHROMATIN-STRUCTURE;
MOLECULAR-DYNAMICS; GENOME PACKING; CROSS-LINKING; VIRUS; TYPE-2;
ORGANIZATION; VIRION
AB Genome packing in adenovirus has long evaded precise description, since the viral dsDNA molecule condensed by proteins (core) lacks icosahedral order characteristic of the virus protein coating (capsid). We show that useful insights regarding the organization of the core can be inferred from the analysis of spatial distributions of the DNA and condensing protein units (adenosomes). These were obtained from the inspection of cryo-electron tomography reconstructions of individual human adenovirus particles. Our analysis shows that the core lacks symmetry and strict order, yet the adenosome distribution is not entirely random. The features of the distribution can be explained by modeling the condensing proteins and the part of the genome in each adenosome as very soft spheres, interacting repulsively with each other and with the capsid, producing a minimum outward pressure of similar to 0.06 atm. Although the condensing proteins are connected by DNA in disrupted virion cores, in our models a backbone of DNA linking the adenosomes is not required to explain the experimental results in the confined state. In conclusion, the interior of an adenovirus infectious particle is a strongly confined and dense phase of soft particles (adenosomes) without a strictly defined DNA backbone.
C1 [Perez-Berna, Ana J.; Javier Chichon, F.; Fernandez, Jose J.; Carrascosa, Jose L.; San Martin, Carmen] CSIC, Ctr Nacl Biotecnol, Dept Macromol Struct, E-28049 Madrid, Spain.
[Perez-Berna, Ana J.; Javier Chichon, F.; Carrascosa, Jose L.; San Martin, Carmen] CSIC, Ctr Nacl Biotecnol, NanoBiomed Initiat, E-28049 Madrid, Spain.
[Marion, Sanjin; Siber, Antonio] Inst Phys, HR-10000 Zagreb, Croatia.
[Winkler, Dennis C.; Steven, Alasdair C.] Natl Inst Arthrit & Musculoskeletal & Skin Dis NI, Struct Biol Lab, NIH, Bethesda, MD 20892 USA.
[Siber, Antonio] Jozef Stefan Inst, SI-1000 Ljubljana, Slovenia.
RP San Martin, C (reprint author), CSIC, Ctr Nacl Biotecnol, Dept Macromol Struct, Plaza Murillo 2, E-28049 Madrid, Spain.
EM asiber@ifs.hr; carmen@cnb.csic.es
RI Siber, Antonio/B-8881-2008; Fernandez, Jose-Jesus/A-5084-2008; Chichon
Garcia, Francisco Javier/K-5117-2012; San Martin, Carmen/A-4074-2010;
Chichon Garcia, Francisco Javier/B-6029-2011; Perez-Berna,
Ana/G-2789-2016;
OI Siber, Antonio/0000-0003-1665-6541; Fernandez,
Jose-Jesus/0000-0003-2222-3355; Chichon Garcia, Francisco
Javier/0000-0003-2766-0327; San Martin, Carmen/0000-0001-9799-175X;
Chichon Garcia, Francisco Javier/0000-0003-2766-0327; Marion,
Sanjin/0000-0002-9892-7378
FU Ministerio de Economia y Competitividad of Spain [BFU2010-16382,
BFU2013-41249-P, TIN2012-37483-C03-02, BFU2011-29038]; Spanish
Interdisciplinary Network on the Biophysics of Viruses (Biofivinet)
[FIS2011-16090-E]; Intramural Research Program of NIAMS; Ministerio de
Ciencia e Innovacion of Spain; CSIC Travel Grant [PA1002892]
FX Grants from the Ministerio de Economia y Competitividad of Spain
[BFU2010-16382, BFU2013-41249-P (to C.S.M.), TIN2012-37483-C03-02 (to
J.J.F.), BFU2011-29038 (to J.L.C.), and Spanish Interdisciplinary
Network on the Biophysics of Viruses (Biofivinet, FIS2011-16090-E)];
Intramural Research Program of NIAMS (to A.C.S.). A.J.P.-B. was a
recipient of a Juan de la Cierva postdoctoral contract from the
Ministerio de Ciencia e Innovacion of Spain and was additionally
supported by a CSIC Travel Grant PA1002892. Funding for open access
charge: BFU2013-41249-P from the Ministerio de Economia y Competitividad
of Spain.
NR 73
TC 7
Z9 7
U1 0
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 APR 30
PY 2015
VL 43
IS 8
BP 4274
EP 4283
DI 10.1093/nar/gkv187
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CJ2LV
UT WOS:000355317200039
PM 25820430
ER
PT J
AU Lee, NCO
Larionov, V
Kouprina, N
AF Lee, Nicholas C. O.
Larionov, Vladimir
Kouprina, Natalay
TI Highly efficient CRISPR/Cas9-mediated TAR cloning of genes and
chromosomal loci from complex genomes in yeast
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID TRANSFORMATION-ASSOCIATED RECOMBINATION; HUMAN ARTIFICIAL CHROMOSOMES;
CONDITIONAL CENTROMERE; FUNCTIONAL GENOMICS; SELECTIVE ISOLATION;
DELIVERY; CRISPR-CAS9; HAPLOTYPES; REGIONS; BIOLOGY
AB Transformation-associated recombination (TAR) protocol allowing the selective isolation of full-length genes complete with their distal enhancer regions and entire genomic loci with sizes up to 250 kb from complex genomes in yeast S. cerevisiae has been developed more than a decade ago. However, its wide spread usage has been impeded by a low efficiency (0.5-2%) of chromosomal region capture during yeast transformants which in turn requires a time-consuming screen of hundreds of colonies. Here, we demonstrate that pre-treatment of genomic DNA with CRISPR-Cas9 nucleases to generate double-strand breaks near the targeted genomic region results in a dramatic increase in the fraction of gene-positive colonies (up to 32%). As only a dozen or less yeast transformants need to be screened to obtain a clone with the desired chromosomal region, extensive experience with yeast is no longer required. A TAR-CRISPR protocol may help to create a bank of human genes, each represented by a genomic copy containing its native regulatory elements, that would lead to a significant advance in functional, structural and comparative genomics, in diagnostics, gene replacement, generation of animal models for human diseases and has a potential for gene therapy.
C1 [Lee, Nicholas C. O.; Larionov, Vladimir; Kouprina, Natalay] NCI, Dev Therapeut Branch, Bethesda, MD 20892 USA.
RP Kouprina, N (reprint author), NCI, Dev Therapeut Branch, Bethesda, MD 20892 USA.
EM kouprinn@mail.nih.gov
RI Lee, Nicholas/F-3668-2015;
OI lee, nicholas/0000-0003-2628-6599
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, USA
FX Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, USA (V.L. and N.K). Funding for open access
charge: Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research, USA.
NR 24
TC 9
Z9 13
U1 4
U2 51
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 APR 30
PY 2015
VL 43
IS 8
AR e55
DI 10.1093/nar/gkv112
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CJ2LV
UT WOS:000355317200006
PM 25690893
ER
PT J
AU Nunes, MRT
Faria, NR
de Vasconcelos, JM
Golding, N
Kraemer, MUG
de Oliveira, LF
Azevedo, RDD
da Silva, DEA
da Silva, EVP
da Silva, SP
Carvalho, VL
Coelho, GE
Cruz, ACR
Rodrigues, SG
Vianez, JLDG
Nunes, BTD
Cardoso, JF
Tesh, RB
Hay, SI
Pybus, OG
Vasconcelos, PFD
AF Teixeira Nunes, Marcio Roberto
Faria, Nuno Rodrigues
de Vasconcelos, Janaina Mota
Golding, Nick
Kraemer, Moritz U. G.
de Oliveira, Layanna Freitas
da Silva Azevedo, Raimunda do Socorro
Andrade da Silva, Daisy Elaine
Pinto da Silva, Eliana Vieira
da Silva, Sandro Patroca
Carvalho, Valeria Lima
Coelho, Giovanini Evelim
Ribeiro Cruz, Ana Cecilia
Rodrigues, Sueli Guerreiro
da Silva Goncalves Vianez, Joao Lidio, Jr.
Diniz Nunes, Bruno Tardelli
Cardoso, Jedson Ferreira
Tesh, Robert B.
Hay, Simon I.
Pybus, Oliver G.
da Costa Vasconcelos, Pedro Fernando
TI Emergence and potential for spread of Chikungunya virus in Brazil
SO BMC MEDICINE
LA English
DT Article
DE Chikungunya virus; National surveillance; Public health; Spatial
prediction; Statistical methods
ID AEDES-ALBOPICTUS; POPULATION-DYNAMICS; AMERICA; INFERENCE; AEGYPTI;
IMPACT
AB Background: In December 2013, an outbreak of Chikungunya virus (CHIKV) caused by the Asian genotype was notified in the Caribbean. The outbreak has since spread to 38 regions in the Americas. By September 2014, the first autochthonous CHIKV infections were confirmed in Oiapoque, North Brazil, and in Feira de Santana, Northeast Brazil.
Methods: We compiled epidemiological and clinical data on suspected CHIKV cases in Brazil and polymerase-chain-reaction-based diagnostic was conducted on 68 serum samples from patients with symptom onset between April and September 2014. Two imported and four autochthonous cases were selected for virus propagation, RNA isolation, full-length genome sequencing, and phylogenetic analysis. We then followed CDC/PAHO guidelines to estimate the risk of establishment of CHIKV in Brazilian municipalities.
Results: We detected 41 CHIKV importations and 27 autochthonous cases in Brazil. Epidemiological and phylogenetic analyses indicated local transmission of the Asian CHIKV genotype in Oiapoque. Unexpectedly, we also discovered that the ECSA genotype is circulating in Feira de Santana. The presumed index case of the ECSA genotype was an individual who had recently returned from Angola and developed symptoms in Feira de Santana. We estimate that, if CHIKV becomes established in Brazil, transmission could occur in 94% of municipalities in the country and provide maps of the risk of importation of each strain of CHIKV in Brazil.
Conclusions: The etiological strains associated with the early-phase CHIKV outbreaks in Brazil belong to the Asian and ECSA genotypes. Continued surveillance and vector mitigation strategies are needed to reduce the future public health impact of CHIKV in the Americas.
C1 [Teixeira Nunes, Marcio Roberto; de Vasconcelos, Janaina Mota; de Oliveira, Layanna Freitas; Andrade da Silva, Daisy Elaine; da Silva, Sandro Patroca; da Silva Goncalves Vianez, Joao Lidio, Jr.; Cardoso, Jedson Ferreira] Minist Hlth, Evandro Chagas Inst, Ctr Technol Innovat, BR-67030000 Ananindeua, PA, Brazil.
[Faria, Nuno Rodrigues; Pybus, Oliver G.] Univ Oxford, Dept Zool, Oxford OX1 3PS, England.
[Golding, Nick; Kraemer, Moritz U. G.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford OX1 3PS, England.
[da Silva Azevedo, Raimunda do Socorro; Pinto da Silva, Eliana Vieira; Carvalho, Valeria Lima; Ribeiro Cruz, Ana Cecilia; Rodrigues, Sueli Guerreiro; Diniz Nunes, Bruno Tardelli; da Costa Vasconcelos, Pedro Fernando] Minist Hlth, Evandro Chagas Inst, Dept Arbovirol & Hemorrhag Fevers, BR-67030000 Ananindeua, PA, Brazil.
[Coelho, Giovanini Evelim] Brazilian Minist Hlth, Natl Dengue Control Program, BR-70058900 Brasilia, DF, Brazil.
[Tesh, Robert B.] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
[Hay, Simon I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[da Costa Vasconcelos, Pedro Fernando] Para State Univ, Dept Pathol, BR-66087670 Belem, Para, Brazil.
RP Nunes, MRT (reprint author), Minist Hlth, Evandro Chagas Inst, Ctr Technol Innovat, BR-67030000 Ananindeua, PA, Brazil.
EM marcionunesbrasil@yahoo.com.br
RI Hay, Simon/F-8967-2015; Nunes, Marcio Roberto/B-2238-2016;
OI Hay, Simon/0000-0002-0611-7272; Pybus, Oliver/0000-0002-8797-2667;
Nunes, Marcio Roberto/0000-0001-9739-5499; Faria,
Nuno/0000-0001-8839-2798; Golding, Nick/0000-0001-8916-5570
FU Brazilian National Council of Scientific and Technological Development
(CNPq) [302032/2011-8]; CNPq [573.739/2008-0, 240/2008/FAPESPA/INCT,
142492/2011-6]; Bill & Melinda Gates Foundation [OPP1053338]; German
Academic Exchange Service (DAAD); Wellcome Trust [095066]; Li Ka Shing
Foundation; RAPIDD program of the Science & Technology Directorate,
Department of Homeland Security; Fogarty International Center (FIC),
National Institutes of Health (NIH); European Research Council under the
European Union [614725]
FX We are grateful to the Brazilian Dengue and Chikungunya network composed
by 17 national laboratories for their assistance on preliminary
screening diagnostics. We thank Oliver Brady for useful discussions and
Thessika Hialla Araujo, Luiz Carlos Jr. Alcantara, and Daniele Barbosa
Medeiros for providing epidemiological information. MRTN is supported by
the Brazilian National Council of Scientific and Technological
Development (CNPq) grant no. 302032/2011-8. PFCV is supported by CNPq
grant no. 573.739/2008-0 and 240/2008/FAPESPA/INCT. JMV is a PhD student
supported by CNPq grant no. 142492/2011-6. NG is funded by a grant from
the Bill & Melinda Gates Foundation (#OPP1053338). MUGK is funded by the
German Academic Exchange Service (DAAD) graduate scholarship. SIH is
funded by a Senior Research Fellowship from the Wellcome Trust (#095066)
and receives support from the Li Ka Shing Foundation and also
acknowledges funding support from the RAPIDD program of the Science &
Technology Directorate, Department of Homeland Security, and the Fogarty
International Center (FIC), National Institutes of Health (NIH). This
research has received funding from the European Research Council under
the European Union's Seventh Framework Programme (FP7/2007-2013)/ERC
grant agreement no. 614725.
NR 42
TC 56
Z9 57
U1 3
U2 15
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1741-7015
J9 BMC MED
JI BMC Med.
PD APR 30
PY 2015
VL 13
AR 102
DI 10.1186/s12916-015-0348-x
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA CI0KC
UT WOS:000354425000001
ER
PT J
AU Bullard, KM
Ali, MK
Imperatore, G
Geiss, LS
Saydah, SH
Albu, JB
Cowie, CC
Sohler, N
Albright, A
Gregg, EW
AF Bullard, Kai McKeever
Ali, Mohammed K.
Imperatore, Giuseppina
Geiss, Linda S.
Saydah, Sharon H.
Albu, Jeanine B.
Cowie, Catherine C.
Sohler, Nancy
Albright, Ann
Gregg, Edward W.
TI Receipt of Glucose Testing and Performance of Two US Diabetes Screening
Guidelines, 2007-2012
SO PLOS ONE
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; COST-EFFECTIVENESS; PREVENTION PROGRAM;
NATIONAL-HEALTH; SECULAR CHANGES; UNITED-STATES; LIFE-STYLE; FOLLOW-UP;
PREVALENCE; ADULTS
AB Background
Screening guidelines are used to help identify prediabetes and diabetes before implementing evidence-based prevention and treatment interventions. We examined screening practices benchmarking against two US guidelines, and the capacity of each guideline to identify dysglycemia.
Methods
Using 2007-2012 National Health and Nutrition Examination Surveys, we analyzed nationally-representative, cross-sectional data from 5,813 fasting non-pregnant adults aged >= 20 years without self-reported diabetes. We examined proportions of adults eligible for diagnostic glucose testing and those who self-reported receiving testing in the past three years, as recommended by the American Diabetes Association (ADA) and the US Preventive Services Task Force (USPSTF-2008) guidelines. For each screening guideline, we also assessed sensitivity, specificity, and positive (PPV) and negative predictive values in identifying dysglycemia (defined as fasting plasma glucose >= 100 mg/dl or hemoglobin A1c >= 5.7%).
Results
In 2007-2012, 73.0% and 23.7% of US adults without diagnosed diabetes met ADA and USPSTF-2008 criteria for screening, respectively; and 91.5% had at least one major risk factor for diabetes. Of those ADA- or USPSTF-eligible adults, about 51% reported being tested within the past three years. Eligible individuals not tested were more likely to be lower educated, poorer, uninsured, or have no usual place of care compared to tested eligible adults. Among adults with >= 1 major risk factor, 45.7% reported being tested, and dysglycemia yields (i.e., PPV) ranged from 45.8% (high-risk ethnicity) to 72.6% (self-reported prediabetes). ADA criteria and having any risk factor were more sensitive than the USPSTF-2008 guideline (88.8-97.7% vs. 31.0%) but less specific (13.5-39.7% vs. 82.1%) in recommending glucose testing, resulting in lower PPVs (47.7-54.4% vs. 58.4%).
Conclusion
Diverging recommendations and variable performance of different guidelines may be impeding national diabetes prevention and treatment efforts. Efforts to align screening recommendations may result in earlier identification of adults at high risk for prediabetes and diabetes.
C1 [Bullard, Kai McKeever; Ali, Mohammed K.; Imperatore, Giuseppina; Geiss, Linda S.; Saydah, Sharon H.; Albright, Ann; Gregg, Edward W.] Ctr Dis Control & Prevent, Div Diabet Translat, Atlanta, GA 30333 USA.
[Albu, Jeanine B.] Columbia Univ, St Lukes Roosevelt Hosp Ctr, Dept Med, New York, NY USA.
[Cowie, Catherine C.] NIH, NIDDK, Bethesda, MD 20892 USA.
[Sohler, Nancy] CUNY City Coll, Sophie Davis Sch Biomed Educ, New York, NY 10031 USA.
RP Bullard, KM (reprint author), Ctr Dis Control & Prevent, Div Diabet Translat, Atlanta, GA 30333 USA.
EM kbullard@cdc.gov
FU NIDDK NIH HHS [P30 DK020541, P60 DK020541]
NR 34
TC 4
Z9 4
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 APR 30
PY 2015
VL 10
IS 4
AR e0125249
DI 10.1371/journal.pone.0125249
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CH0MA
UT WOS:000353713100073
PM 25928306
ER
PT J
AU Subramaniam, KS
Skinner, J
Ivan, E
Mutimura, E
Kim, RS
Feintuch, CM
Portugal, S
Anastos, K
Crompton, PD
Daily, JP
AF Subramaniam, Krishanthi S.
Skinner, Jeff
Ivan, Emil
Mutimura, Eugene
Kim, Ryung S.
Feintuch, Catherine M.
Portugal, Silvia
Anastos, Kathryn
Crompton, Peter D.
Daily, Johanna P.
TI HIV Malaria Co-Infection Is Associated with Atypical Memory B Cell
Expansion and a Reduced Antibody Response to a Broad Array of Plasmodium
falciparum Antigens in Rwandan Adults
SO PLOS ONE
LA English
DT Article
ID INFECTED INDIVIDUALS; CLINICAL MALARIA; COTRIMOXAZOLE PROPHYLAXIS;
ANTIRETROVIRAL THERAPY; IMMUNE-RESPONSES; UNSTABLE MALARIA;
PREGNANT-WOMEN; UGANDAN ADULTS; IMMUNOSUPPRESSION; PARASITEMIA
AB HIV infected individuals in malaria endemic areas experience more frequent and severe malaria episodes compared to non HIV infected. This clinical observation has been linked to a deficiency in antibody responses to Plasmodium falciparum antigens; however, prior studies have only focused on the antibody response to <0.5% of P. falciparum proteins. To obtain a broader and less-biased view of the effect of HIV on antibody responses to malaria we compared antibody profiles of HIV positive (HIV+) and negative (HIV-) Rwandan adults with symptomatic malaria using a microarray containing 824 P. falciparum proteins. We also investigated the cellular basis of the antibody response in the two groups by analyzing B and T cell subsets by flow cytometry. Although HIV malaria co-infected individuals generated antibodies to a large number of P. falciparum antigens, including potential vaccine candidates, the breadth and magnitude of their response was reduced compared to HIV-individuals. HIV malaria co-infection was also associated with a higher percentage of atypical memory B cells (MBC) (CD19+CD10-CD21-CD27-) compared to malaria infection alone. Among HIV+ individuals the CD4(+) T cell count and HIV viral load only partially explained variability in the breadth of P. falciparum-specific antibody responses. Taken together, these data indicate that HIV malaria co-infection is associated with an expansion of atypical MBCs and a diminished antibody response to a diverse array of P. falciparum antigens, thus offering mechanistic insight into the higher risk of malaria in HIV+ individuals.
C1 [Subramaniam, Krishanthi S.] Univ Liverpool, Liverpool Sch Trop Med, Vector Biol Dept, Liverpool L3 5QA, Merseyside, England.
[Skinner, Jeff; Portugal, Silvia; Crompton, Peter D.] NIAID, Malaria Infect Biol & Immun Unit, Immunogenet Lab, NIH, Bethesda, MD 20892 USA.
[Ivan, Emil] Univ Rwanda, Dept Biomed Lab Sci, Coll Med & Hlth Sci, Kigali, Rwanda.
[Mutimura, Eugene] Reg Alliance Sustainable Dev, Kigali, Rwanda.
[Kim, Ryung S.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Feintuch, Catherine M.; Daily, Johanna P.] Albert Einstein Coll Med, Dept Microbiol & Immunol, Bronx, NY 10467 USA.
[Anastos, Kathryn; Daily, Johanna P.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
RP Daily, JP (reprint author), Albert Einstein Coll Med, Dept Microbiol & Immunol, Bronx, NY 10467 USA.
EM jdaily@einstein.yu.edu
RI Crompton, Peter/N-1130-2016;
OI Skinner, Jeff/0000-0001-5697-0442
FU Albert Einstein College of Medicine Global Health Pilot Grant; Division
of Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health; [NIAID: 1RC1AI086224]
FX This study was supported by A. JPD supported by NIAID: 1RC1AI086224 and
an Albert Einstein College of Medicine Global Health Pilot Grant. B. JS,
SP and PDC are supported by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 56
TC 2
Z9 2
U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 30
PY 2015
VL 10
IS 4
AR e0124412
DI 10.1371/journal.pone.0124412
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CH0MA
UT WOS:000353713100032
PM 25928218
ER
PT J
AU Kahn, K
Saxena, S
Eskandar, E
Thakor, N
Schieber, M
Gale, JT
Averbeck, B
Eden, U
Sarma, SV
AF Kahn, Kevin
Saxena, Shreya
Eskandar, Emad
Thakor, Nitish
Schieber, Marc
Gale, John T.
Averbeck, Bruno
Eden, Uri
Sarma, Sridevi V.
TI A systematic approach to selecting task relevant neurons
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE Task-related neurons; Neuron selection; Model based; Point processes
ID NEURAL SPIKING ACTIVITY; PRIMARY MOTOR CORTEX; FINGER MOVEMENTS; CELLS
AB Background: Since task related neurons cannot be specifically targeted during surgery, a critical decision to make is to select which neurons are task-related when performing data analysis. Including neurons unrelated to the task degrade decoding accuracy and confound neurophysiological results. Traditionally, task-related neurons are selected as those with significant changes in firing rate when a stimulus is applied. However, this assumes that neurons' encoding of stimuli are dominated by their firing rate with little regard to temporal dynamics.
New method: This paper proposes a systematic approach for neuron selection, which uses a likelihood ratio test to capture the contribution of stimulus to spiking activity while taking into account task-irrelevant intrinsic dynamics that affect firing rates. This approach is denoted as the model deterioration excluding stimulus (MDES) test.
Results: MDES is compared to firing rate selection in four case studies: a simulation, a decoding example, and two neurophysiology examples.
Comparison with existing methods: The MDES rankings in the simulation match closely with ideal rankings, while firing rate rankings are skewed by task-irrelevant parameters. For decoding, 95% accuracy is achieved using the top 8 MDES-ranked neurons, while the top 12 firing-rate ranked neurons are needed. In the neurophysiological examples, MDES matches published results when firing rates do encode salient stimulus information, and uncovers oscillatory modulations in task-related neurons that are not captured when neurons are selected using firing rates.
Conclusions: These case studies illustrate the importance of accounting for intrinsic dynamics when selecting task-related neurons and following the MDES approach accomplishes that. MDES selects neurons that encode task-related information irrespective of these intrinsic dynamics which can bias firing rate based selection. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Kahn, Kevin; Thakor, Nitish; Sarma, Sridevi V.] Johns Hopkins Univ, Dept Biomed Engn, Baltimore, MD 21218 USA.
[Saxena, Shreya] MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA.
[Eskandar, Emad] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Schieber, Marc] Univ Rochester, Med Ctr, Sch Med & Dent, Rochester, NY 14642 USA.
[Gale, John T.] Cleveland Clin, Dept Neurosci, Cleveland, OH 44195 USA.
[Gale, John T.] Cleveland Clin, Ctr Neurol Restorat, Cleveland, OH 44195 USA.
[Averbeck, Bruno] NIH, Neuropsychol Lab, Bethesda, MD 20892 USA.
[Eden, Uri] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
RP Kahn, K (reprint author), Johns Hopkins Univ, Inst Computat Med, 3400 N Charles St,Hackerman Hall,Room 318, Baltimore, MD 21218 USA.
EM kkahn6@jhmi.edu
RI Thakor, Nitish/G-9110-2015
OI Thakor, Nitish/0000-0002-9981-9395
FU Burroughs Wellcome Fund [100727401]; National Science Foundation
[1137237]
FX K Kahn and SV Sarma were supported by the Burroughs Wellcome Fund
(100727401) and the National Science Foundation (1137237).
NR 31
TC 0
Z9 0
U1 0
U2 2
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 APR 30
PY 2015
VL 245
BP 156
EP 168
DI 10.1016/j.jneumeth.2015.02.020
PG 13
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CG8XN
UT WOS:000353599100015
PM 25746150
ER
PT J
AU Fukushima, M
Saunders, RC
Mullarkey, M
Doyle, AM
Mishkin, M
Fujii, N
AF Fukushima, Makoto
Saunders, Richard C.
Mullarkey, Matthew
Doyle, Alexandra M.
Mishkin, Mortimer
Fujii, Naotaka
TI An electrocorticographic electrode array for simultaneous recording from
medial, lateral, and intrasulcal surface of the cortex in macaque
monkeys (vol 233, pg 155, 2014)
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Correction
C1 [Fukushima, Makoto; Saunders, Richard C.; Mullarkey, Matthew; Doyle, Alexandra M.; Mishkin, Mortimer] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
[Fujii, Naotaka] RIKEN, Lab Adapt Intelligence, Brain Sci Inst, Wako, Saitama 3510198, Japan.
RP Fukushima, M (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Room 1B80,49 Convent Dr, Bethesda, MD 20892 USA.
EM makoto_fukushima@me.com
OI Fukushima, Makoto/0000-0002-8809-7892
NR 1
TC 0
Z9 0
U1 1
U2 2
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 APR 30
PY 2015
VL 245
BP 205
EP 206
DI 10.1016/j.jneumeth.2015.01.007
PG 2
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CG8XN
UT WOS:000353599100019
ER
PT J
AU Lardinois, O
Kirby, PJ
Morgan, DL
Sills, RC
Tomer, KB
Deterding, LJ
AF Lardinois, O.
Kirby, P. J.
Morgan, D. L.
Sills, R. C.
Tomer, K. B.
Deterding, L. J.
TI Mass spectrometric analysis of rat cerebrospinal fluid proteins
following exposure to the neurotoxicant carbonyl sulfide (vol 28, pg
2531, 2014)
SO RAPID COMMUNICATIONS IN MASS SPECTROMETRY
LA English
DT Correction
C1 [Lardinois, O.; Tomer, K. B.; Deterding, L. J.] NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Kirby, P. J.; Morgan, D. L.] NIEHS, Lab Toxicol & Pharmacol, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Sills, R. C.] NIEHS, Cellular & Mol Pathol, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Deterding, LJ (reprint author), NIEHS, Struct Biol Lab, NIH, DHHS, 111 TW Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
NR 1
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0951-4198
EI 1097-0231
J9 RAPID COMMUN MASS SP
JI Rapid Commun. Mass Spectrom.
PD APR 30
PY 2015
VL 29
IS 8
BP 782
EP 782
DI 10.1002/rcm.7166
PG 1
WC Biochemical Research Methods; Chemistry, Analytical; Spectroscopy
SC Biochemistry & Molecular Biology; Chemistry; Spectroscopy
GA CF4ZK
UT WOS:000352563200010
PM 26406493
ER
PT J
AU Zhang, ZW
Wang, CG
Troendle, JF
AF Zhang, Zhiwei
Wang, Chenguang
Troendle, James F.
TI Optimizing the order of hypotheses in serial testing of multiple
endpoints in clinical trials
SO STATISTICS IN MEDICINE
LA English
DT Article
DE chain procedure; fixed sequence; hierarchical testing; multiple
comparisons; multiplicity; secondary endpoint
ID BONFERRONI PROCEDURE; FIXED-SEQUENCE; GATEKEEPING STRATEGIES; ADJUSTMENT
METHODS; SELECTION; EFFICACY; WEIGHTS
AB Clinical trials usually collect information on a large number of variables or endpoints, including one or more primary endpoints as well as a number of secondary endpoints representing different aspects of treatment effectiveness and safety. In this article, we focus on serial testing procedures that test multiple endpoints in a pre-specified order, and consider how to optimize the order of endpoints subject to any clinical constraints, with respect to the expected number of successes (i.e., endpoints that reach statistical significance) or the expected gain (if endpoints are associated with numerical utilities). We consider some common approaches to this problem and propose two new approaches: a greedy algorithm based on conditional power and a simulated annealing algorithm that attempts to improve a given sequence in a random and iterative fashion. Simulation results indicate that the proposed algorithms are useful for finding a high-performing sequence, and that optimized fixed sequence procedures can be competitive against traditional multiple testing procedures such as Holm's. The methods and findings are illustrated with two examples concerning migraine and asthma. Copyright (c) 2015 John Wiley & Sons, Ltd.
C1 [Zhang, Zhiwei] US FDA, Div Biostat, Off Surveillance & Biometr, Ctr Devices & Radiol Hlth, Silver Spring, MD USA.
[Wang, Chenguang] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Div Biostat & Bioinformat, Baltimore, MD USA.
[Troendle, James F.] NHLBI, Off Biostat Res, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
RP Zhang, ZW (reprint author), DBS OSB CDRH FDA, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM zhiwei.zhang@fda.hhs.gov
NR 33
TC 0
Z9 0
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD APR 30
PY 2015
VL 34
IS 9
BP 1467
EP 1482
DI 10.1002/sim.6425
PG 16
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 CF4MV
UT WOS:000352524100003
PM 25620627
ER
PT J
AU Schiffman, M
Wentzensen, N
AF Schiffman, Mark
Wentzensen, Nicolas
TI Issues in optimising and standardising the accuracy and utility of the
colposcopic examination in the HPV era
SO ECANCERMEDICALSCIENCE
LA English
DT Review
DE cervix; screening; colposcopy; HPV
ID CERVICAL INTRAEPITHELIAL NEOPLASIA; QUALITY-ASSURANCE PROGRAM;
HUMAN-PAPILLOMAVIRUS; POSITIVE WOMEN; CANCER PRECURSORS; DIRECTED
BIOPSY; UTERINE CERVIX; SCORING SYSTEM; PERFORMANCE; PREVENTION
AB For this tribute to Mario Sideri, we reviewed some of the current issues in colposcopy, many of which we were researching with him. The review concentrates on the impact of HPV testing on cervical screening, specifically on the practice of colposcopy as the major diagnostic procedure in cervical screening programmes. Topics include the changing population of women referred to colposcopy, evolving views of the colposcopic impression, differing approaches to directed and random biopsy, issues in teaching colposcopy using static images, and the development of colposcopy aids, and simplified visual assessment techniques.
C1 [Schiffman, Mark; Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
RP Schiffman, M (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, USA 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM schiffmm@mail.nih.gov
NR 29
TC 1
Z9 1
U1 0
U2 0
PU CANCER INTELLIGENCE LTD
PI BRISTOL
PA 11 ALMA VALE RD,, BRISTOL, BS8 2HL, ENGLAND
SN 1754-6605
J9 ECANCERMEDICALSCIENC
JI eCancerMedicalScience
PD APR 29
PY 2015
VL 9
SI SI
AR 530
DI 10.3332/ecancer.2015.530
PG 6
WC Oncology
SC Oncology
GA CQ4YY
UT WOS:000360611700005
PM 25987899
ER
PT J
AU Jankovic, D
Feng, CG
AF Jankovic, Dragana
Feng, Carl G.
TI CD4(+) T cell differentiation in infection: amendments to the Th1/Th2
axiom
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Editorial Material
DE Thlymphocytes; cytokines; infection; dendriticcells; macrophages;
immunoregulation; metabolism; memory; Inc-RNA
ID PLASTICITY; POLARIZATION; PROTEINS; SUBSETS
C1 [Jankovic, Dragana] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Feng, Carl G.] Univ Sydney, Sydney Med Sch, Dept Infect Dis & Immunol, Sydney, NSW 2006, Australia.
RP Jankovic, D (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM djankovic@niaid.nih.gov
NR 18
TC 3
Z9 3
U1 2
U2 8
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD APR 29
PY 2015
VL 6
AR 198
DI 10.3389/fimmu.2015.00198
PG 3
WC Immunology
SC Immunology
GA CI7JK
UT WOS:000354939200001
PM 25972870
ER
PT J
AU Cardoso, FL
Herz, J
Fernandes, A
Rocha, J
Sepodes, B
Brito, MA
McGavern, DB
Brites, D
AF Cardoso, Filipa L.
Herz, Jasmin
Fernandes, Adelaide
Rocha, Joao
Sepodes, Bruno
Brito, Maria A.
McGavern, Dorian B.
Brites, Dora
TI Systemic inflammation in early neonatal mice induces transient and
lasting neurodegenerative effects
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
DE Astrocytes; Microglia; Myelination; Neurons; Autotaxin; HMGB1;
Neurodevelopment; LPS
ID BLOOD-BRAIN-BARRIER; WHITE-MATTER INJURY; LOW-BIRTH-WEIGHT; GROUP BOX 1;
PRETERM INFANTS; SEPTIC SHOCK; MATRIX METALLOPROTEINASES; MATERNAL
EXPOSURE; SOCIAL-BEHAVIOR; CEREBRAL-CORTEX
AB Background: The inflammatory mediator lipopolysaccharide (LPS) has been shown to induce acute gliosis in neonatal mice. However, the progressive effects on the murine neurodevelopmental program over the week that follows systemic inflammation are not known. Thus, we investigated the effects of repeated LPS administration in the first postnatal week in mice, a condition mimicking sepsis in late preterm infants, on the developing central nervous system (CNS).
Methods: Systemic inflammation was induced by daily intraperitoneal administration (i.p.) of LPS (6 mg/kg) in newborn mice from postnatal day (PND) 4 to PND6. The effects on neurodevelopment were examined by staining the white matter and neurons with Luxol Fast Blue and Cresyl Violet, respectively. The inflammatory response was assessed by quantifying the expression/activity of matrix metalloproteinases (MMP), toll-like receptor (TLR)-4, high mobility group box (HMGB)-1, and autotaxin (ATX). In addition, B6 CX3CR1(gfp/+) mice combined with cryo-immunofluorescence were used to determine the acute, delayed, and lasting effects on myelination, microglia, and astrocytes.
Results: LPS administration led to acute body and brain weight loss as well as overt structural changes in the brain such as cerebellar hypoplasia, neuronal loss/shrinkage, and delayed myelination. The impaired myelination was associated with alterations in the proliferation and differentiation of NG2 progenitor cells early after LPS administration, rather than with excessive phagocytosis by CNS myeloid cells. In addition to disruptions in brain architecture, a robust inflammatory response to LPS was observed. Quantification of inflammatory biomarkers revealed decreased expression of ATX with concurrent increases in HMGB1, TLR-4, and MMP-9 expression levels. Acute astrogliosis (GFAP(+) cells) in the brain parenchyma and at the microvasculature interface together with parenchymal microgliosis (CX3CR1(+) cells) were also observed. These changes preceded the migration/proliferation of CX3CR1(+) cells around the vessels at later time points and the subsequent loss of GFAP(+) astrocytes.
Conclusion: Collectively, our study has uncovered a complex innate inflammatory reaction and associated structural changes in the brains of neonatal mice challenged peripherally with LPS. These findings may explain some of the neurobehavioral abnormalities that develop following neonatal sepsis.
C1 [Cardoso, Filipa L.; Fernandes, Adelaide; Rocha, Joao; Sepodes, Bruno; Brito, Maria A.; Brites, Dora] Univ Lisbon, Fac Farm, Res Inst Med iMed ULisboa, P-1649003 Lisbon, Portugal.
[McGavern, Dorian B.] NINDS, NIH, Bethesda, MD 20892 USA.
[Fernandes, Adelaide; Brito, Maria A.; Brites, Dora] Univ Lisbon, Fac Farm, Dept Biochem & Human Biol, P-1649003 Lisbon, Portugal.
RP McGavern, DB (reprint author), NINDS, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM mcgavernd@ninds.nih.gov; dbrites@ff.ulisboa.pt
RI Fernandes, Adelaide/A-4787-2011; Brites, Dora/M-8293-2013; brito,
maria/M-8278-2013; Rocha, Joao/K-1102-2014; Sepodes, Bruno/A-4838-2014;
iMed.ULisboa, iMed.ULisboa/C-6292-2014; iMed.ULisboa, NeuronGliaBiol
/B-5403-2014;
OI Fernandes, Adelaide/0000-0002-2782-9519; Brites,
Dora/0000-0002-3024-9777; brito, maria/0000-0002-8493-4649; Rocha,
Joao/0000-0002-0303-8085; Sepodes, Bruno/0000-0002-2761-0955; McGavern,
Dorian/0000-0001-9568-545X
FU National Institutes of Health (NIH) intramural program; FEDER (COMPETE
Program); National Portuguese funds (Fundacao para a Ciencia e a
Tecnologia - FCT) [PTDC/SAU-FAR/118787/2010,
PEst-OE/SAU/UI4013/2011-2013]; FCT [SFRH/BD/62959/2009]; FLAD
[2014/CON3/CAN30]; EMBO [ASTF 31-2014]
FX This study was supported by the National Institutes of Health (NIH)
intramural program (to DBM), by FEDER (COMPETE Program), and by National
Portuguese funds (Fundacao para a Ciencia e a Tecnologia - FCT) through
the projects PTDC/SAU-FAR/118787/2010 (to DB) and
PEst-OE/SAU/UI4013/2011-2013 (to iMed. ULisboa). FLC is a recipient of a
PhD fellowship (SFRH/BD/62959/2009) from FCT, a fellowship
(2014/CON3/CAN30) from FLAD and a short-term fellowship (ASTF 31-2014)
from EMBO. The funding organizations had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 117
TC 10
Z9 11
U1 2
U2 13
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD APR 29
PY 2015
VL 12
AR UNSP 82
DI 10.1186/s12974-015-0299-3
PG 18
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA CI6CP
UT WOS:000354846600001
PM 25924675
ER
PT J
AU Chan, STS
Patel, PR
Ransom, TR
Henrich, CJ
Mckee, TC
Goey, AKL
Cook, KM
Figg, WD
McMahon, JB
Schnermann, MJ
Gustafson, KR
AF Chan, Susanna T. S.
Patel, Paresma R.
Ransom, Tanya R.
Henrich, Curtis J.
Mckee, Tawnya C.
Goey, Andrew K. L.
Cook, Kristina M.
Figg, William D.
McMahon, James B.
Schnermann, Martin J.
Gustafson, Kirk R.
TI Structural Elucidation and Synthesis of Eudistidine A: An Unusual
Polycyclic Marine Alkaloid that Blocks Interaction of the Protein
Binding Domains of p300 and HIF-1 alpha
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID EUDISTOMA CF RIGIDA; SMALL-MOLECULE; ANTICANCER AGENTS; DRUG DISCOVERY;
ARYL KETONES; TUMOR-GROWTH; HYPOXIA; INHIBITORS; TRANSCRIPTION; PATHWAY
AB Low oxygen environments are a hallmark of solid tumors, and transcription of many hypoxia-responsive genes needed for survival under these conditions is regulated by the transcription factor HIF-1 (hypoxia-inducible factor 1). Activation of HIF-1 requires binding of its a-subunit (HIF-1 alpha) to the transcriptional coactivator protein p300. Inhibition of the p300/HIF-1 alpha interaction can suppress HIF-I activity. A screen for inhibitors of the protein binding domains of p300 (CHI) and HIF-1 alpha (C-TAD) identified an extract of the marine ascidian Eudistoma sp. as active. Novel heterocyclic alkaloids eudistidines A (1) and B (2) were isolated from the extract, and their structures assigned by spectroscopic analyses. They contain an unprecedented tetracyclic core composed of two pyrimidine rings fused with an imidazole ring. Eudistidine A (I) was synthesized in a concise four-step sequence featuring a condensation/cyclization reaction cascade between 4-(2-aminophenyl)pyrimidin-2-amine (3) and 4-methoxy-phenylglyoxal (4), while eudistidine B (2) was synthesized in a similar fashion with glyoxylic acid (5) in place of 4. Naturally occurring eudistidine A (1) effectively inhibited CH1/C-TAD binding with an IC50 of 75 mu M, and synthetic 1 had similar activity. The eudistidine A (1) scaffold, which can be synthesized in a concise, scalable manner, May provide potential therapeutic lead compounds or molecular probes to study p300/HIP-1 alpha interactions and the role these proteins play in tumor response to low oxygen conditions. The unique structural scaffolds and functional group arrays often found in natural products make these secondary metabolites a rich source of new compounds that can disrupt critical protein protein binding events.
C1 [Chan, Susanna T. S.; Ransom, Tanya R.; Henrich, Curtis J.; Mckee, Tawnya C.; McMahon, James B.; Gustafson, Kirk R.] NCI, Mol Targets Lab, Ctr Canc Res, Ft Detrick, MD 21702 USA.
[Patel, Paresma R.; Schnermann, Martin J.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Patel, Paresma R.] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD 20892 USA.
[Henrich, Curtis J.] Frederick Natl Lab Canc Res, Basic Sci Program, Leidos Biomed Res Inc, Frederick, MD 21702 USA.
[Goey, Andrew K. L.; Cook, Kristina M.; Figg, William D.] NCI, Genitourinary Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Schnermann, MJ (reprint author), NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
EM martin.schnermann@nih.gov; gustafki@mail.nih.gov
RI Figg Sr, William/M-2411-2016
FU NCI-Frederick for extraction; Intramural Research Program of the NIH;
National Cancer Institute; Center for Cancer Research; Federal funds
from the National Cancer Institute; National Institutes of Health
[HHSN261200800001E]
FX We gratefully acknowledge D. Newman (NCI) for organizing and documenting
the collection, the Natural Products Support Group at NCI-Frederick for
extraction, and S. Tarasov and M. Dyba (Biophysics Resource Core,
Structural Biophysics Laboratory, CCR) and H. Bokesch (MTL) for
assistance with high-resolution mass spectrometry. This research was
supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research. This project was
also funded in part with Federal funds from the National Cancer
Institute, National Institutes of Health, under contract
HHSN261200800001E. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U.S. Government.
NR 42
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Z9 8
U1 6
U2 43
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 APR 29
PY 2015
VL 137
IS 16
BP 5569
EP 5575
DI 10.1021/jacs.5b02156
PG 7
WC Chemistry, Multidisciplinary
SC Chemistry
GA CH3LF
UT WOS:000353931500051
PM 25892103
ER
PT J
AU Cheng, Y
Li, J
Ito, D
Kong, DH
Ha, KS
Lu, F
Wang, B
Sattabongkot, J
Lim, CS
Tsuboi, T
Han, ET
AF Cheng, Yang
Li, Jian
Ito, Daisuke
Kong, Deok-Hoon
Ha, Kwon-Soo
Lu, Feng
Wang, Bo
Sattabongkot, Jetsumon
Lim, Chae Seung
Tsuboi, Takafumi
Han, Eun-Taek
TI Antigenicity and immunogenicity of PvRALP1, a novel Plasmodium vivax
rhoptry neck protein
SO MALARIA JOURNAL
LA English
DT Article
DE Plasmodium vivax; RALP1; Rhoptry neck protein; Antigenicity;
Immunogenicity
ID MEROZOITE SURFACE PROTEIN-1; VACCINE CANDIDATE ANTIGEN; GLUTAMATE-RICH
PROTEIN; G SUBCLASS RESPONSES; FALCIPARUM ANTIGENS; MOVING JUNCTION;
BURKINA-FASO; MALARIA; IDENTIFICATION; ANTIBODIES
AB Background: Proteins secreted from the rhoptry in Plasmodium merozoites are associated with the formation of tight junctions and parasitophorous vacuoles during invasion of erythrocytes and are sorted within the rhoptry neck or bulb. Very little information has been obtained to date about Plasmodium vivax rhoptry-associated leucine (Leu) zipper-like protein 1 (PvRALP1;PVX_096245), a putative rhoptry protein. PvRALP1 contains a signal peptide, a glycine (Gly)/glutamate (Glu)-rich domain, and a Leu-rich domain, all of which are conserved in other Plasmodium species.
Methods: Recombinant PvRALP1s were expressed as full-length protein without the signal peptide (PvRALP1-Ecto) and as truncated protein consisting of the Gly/Glu- and Leu-rich domains (PvRALP1-Tr) using the wheat germ cell-free expression system. The immunoreactivity to these two fragments of recombinant PvRALP1 protein in serum samples from P. vivax-infected patients and immunized mice, including analysis of immunoglobulin G (IgG) subclasses, was evaluated by enzyme-linked immunosorbent assay or protein microarray technology. The subcellular localization of PvRALP1 in blood stage parasites was also determined.
Results: Recombinant PvRALP1-Ecto and PvRALP1-Tr proteins were successfully expressed, and in serum samples from P. vivax patients from the Republic of Korea, the observed immunoreactivities to these proteins had 58.9% and 55.4% sensitivity and 95.0% and 92.5% specificity, respectively. The response to PvRALP1 in humans was predominantly cytophilic antibodies (IgG1 and IgG3), but a balanced Th1/Th2 response was observed in mice. Unexpectedly, there was no significant inverse correlation between levels of parasitaemia and levels of antibody against either PvRALP1-Ecto (R-2 = 0.11) or PvRALP1-Tr (R-2 = 0.14) antigens. PvRALP1 was localized in the rhoptry neck of merozoites, and this was the first demonstration of the localization of this protein in P. vivax.
Conclusions: This study analysed the antigenicity and immunogenicity of PvRALP1 and suggested that PvRALP1 may be immunogenic in humans during parasite infection and might play an important role during invasion of P. vivax parasites.
C1 [Cheng, Yang; Li, Jian; Lu, Feng; Wang, Bo; Han, Eun-Taek] Kangwon Natl Univ, Sch Med, Dept Med Environm Biol & Trop Med, Chunchon 200701, Gangwon Do, South Korea.
[Cheng, Yang; Ito, Daisuke] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Li, Jian] Hubei Univ Med, Coll Basic Med, Dept Parasitol, Wuhan 442000, Hubei, Peoples R China.
[Ito, Daisuke; Tsuboi, Takafumi] Ehime Univ, Proteo Sci Ctr, Div Malaria Res, Matsuyama, Ehime 7908577, Japan.
[Kong, Deok-Hoon; Ha, Kwon-Soo] Kangwon Natl Univ, Sch Med, Dept Mol & Cellular Biochem, Chunchon 200701, Gangwon Do, South Korea.
[Lu, Feng] Jiangsu Inst Parasit Dis, Key Lab Parasit Dis Control & Prevent, Minist Hlth, Wuxi, Jiangsu, Peoples R China.
[Lu, Feng] Jiangsu Inst Parasit Dis, Jiangsu Prov Key Lab Parasite Mol Biol, Wuxi, Jiangsu, Peoples R China.
[Wang, Bo] Anhui Med Univ, Affiliated Hosp 1, Dept Clin Lab, Hefei, Anhui, Peoples R China.
[Sattabongkot, Jetsumon] Mahidol Univ, Fac Trop Med, Mahidol Vivax Res Unit, Bangkok 10400, Thailand.
[Lim, Chae Seung] Korea Univ, Guru Teg Bahadur Hosp, Coll Med, Dept Lab Med, Seoul 152703, South Korea.
RP Tsuboi, T (reprint author), Ehime Univ, Proteo Sci Ctr, Div Malaria Res, Matsuyama, Ehime 7908577, Japan.
EM tsuboi.takafumi.mb@ehime-u.ac.jp; ethan@kangwon.ac.kr
FU National Research Foundation (NRF) of Korea Grant - Korea government
(MEST) [2011-0016401]; Korea Health technology R&D Project, Ministry of
Health & Welfare, Republic of Korea [A121180]; MEXT KAKENHI [23117008];
JSPS KAKENHI in japan [23406007]
FX This work was supported by National Research Foundation (NRF) of Korea
Grant funded by the Korea government (MEST) (2011-0016401) and a grant
from the Korea Health technology R&D Project, Ministry of Health &
Welfare, Republic of Korea (A121180). This work was also supported in
part by MEXT KAKENHI (23117008) and JSPS KAKENHI (23406007) in Japan.
NR 46
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Z9 2
U1 2
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1475-2875
J9 MALARIA J
JI Malar. J.
PD APR 29
PY 2015
VL 14
AR 186
DI 10.1186/s12936-015-0698-z
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA CI6DA
UT WOS:000354847700002
PM 25925592
ER
PT J
AU Richardson, SP
Tinaz, S
Chen, R
AF Richardson, Sarah Pirio
Tinaz, Sule
Chen, Robert
TI Repetitive Transcranial Magnetic Stimulation in Cervical Dystonia:
Effect of Site and Repetition in a Randomized Pilot Trial
SO PLOS ONE
LA English
DT Article
ID FOCAL HAND DYSTONIA; PREMOTOR CORTEX; WRITERS CRAMP; BOTULINUM TOXIN;
RTMS; TMS
AB Dystonia is characterized by abnormal posturing due to sustained muscle contraction, which leads to pain and significant disability. New therapeutic targets are needed in this disorder. The objective of this randomized, sham-controlled, blinded exploratory study is to identify a specific motor system target for non-invasive neuromodulation and to evaluate this target in terms of safety and tolerability in the cervical dystonia (CD) population. Eight CD subjects were given 15-minute sessions of low-frequency (0.2 Hz) repetitive transcranial magnetic stimulation (rTMS) over the primary motor cortex (MC), dorsal premotor cortex (dPM), supplementary motor area (SMA), anterior cingulate cortex (ACC) and a sham condition with each session separated by at least two days. The Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) score was rated in a blinded fashion immediately pre- and post-intervention. Secondary outcomes included physiology and tolerability ratings. The mean change in TWSTRS severity score by site was 0.25 +/- 1.7 (ACC), -2.9 +/- 3.4 (dPM), -3.0 +/- 4.8 (MC), -0.5 +/- 1.1 (SHAM), and -1.5 +/- 3.2 (SMA) with negative numbers indicating improvement in symptom control. TWSTRS scores decreased from Session 1 (15.1 +/- 5.1) to Session 5 (11.0 +/- 7.6). The treatment was tolerable and safe. Physiology data were acquired on 6 of 8 subjects and showed no change over time. These results suggest rTMS can modulate CD symptoms. Both dPM and MC are areas to be targeted in further rTMS studies. The improvement in TWSTRS scores over time with multiple rTMS sessions deserves further evaluation.
C1 [Richardson, Sarah Pirio] Univ New Mexico, Hlth Sci Ctr, Dept Neurol, Albuquerque, NM 87131 USA.
[Tinaz, Sule] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
[Chen, Robert] Univ Toronto, Toronto Western Res Inst, Toronto, ON, Canada.
RP Richardson, SP (reprint author), Univ New Mexico, Hlth Sci Ctr, Dept Neurol, Albuquerque, NM 87131 USA.
EM spiriorichardson@salud.unm.edu
FU Dystonia Coalition part of the National Institutes of Health (NIH) Rare
Disease Clinical Research Network (RDCRN); National Center for Research
Resources and National Center for Advancing Translational Science
(NCATS) [KL2TR000089, 8UL1TR000041]
FX The research was supported by the Dystonia Coalition (Grant Number
U54NS065701) which is a part of the National Institutes of Health (NIH)
Rare Disease Clinical Research Network (RDCRN), supported through a
collaboration between the Office of Rare Diseases Research (ORDR),
National Center for Advancing Translational Sciences (NCATS), and the
National Institute of Neurological Diseases and Stroke (NINDS). This
research was also supported (in part or in full) by the National Center
for Research Resources and National Center for Advancing Translational
Science (NCATS) through Grant Number KL2TR000089 and Grant Number
8UL1TR000041. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 17
TC 1
Z9 1
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2015
VL 10
IS 4
AR e0124937
DI 10.1371/journal.pone.0124937
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CH0LO
UT WOS:000353711600114
ER
PT J
AU Hanley, PJ
Melenhorst, JJ
Nikiforow, S
Scheinberg, P
Blaney, JW
Demmler-Harrison, G
Cruz, CR
Lam, S
Krance, RA
Leung, KS
Martinez, CA
Liu, H
Douelc, DC
Heslop, HE
Rooney, CM
Shpall, EJ
Barrett, AJ
Rodgers, JR
Bollard, CM
AF Hanley, Patrick J
Melenhorst, Jan J
Nikiforow, Sarah N
Scheinberg, Phillip S
Blaney, James W
Demmler-Harrison, Gail D
Cruz, C. Russell
Lam, Sharon
Krance, Robert A.
Leung, Kathryn S.
Martinez, Caridad A.
Liu, Hao
Douelc, Daniel C.
Heslop, Helen E.
Rooney, Cliona M.
Shpall, Elizabeth J.
Barrett, A. John
Rodgers, John R.
Bollard, Catherine M.
TI CMV-specific T cells generated from naive T cells recognize atypical
epitopes and may be protective in vivo
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID EPSTEIN-BARR-VIRUS; CELLULAR IMMUNE-RESPONSES; UMBILICAL-CORD BLOOD;
VERSUS-HOST-DISEASE; PROPHYLACTIC INFUSION; ADOPTIVE TRANSFER;
VIRAL-INFECTIONS; PROTEIN PP65; CYTOMEGALOVIRUS; TRANSPLANTATION
AB Adoptive transfer of cytomegalovirus (CMV)-specific T cells derived from adult seropositive donors can effectively restore antiviral immunity after transplantation. However, CMV-seronegative donors lack CMV-specific memory T cells, which restricts the availability of virus-specific T cells for immunoprophylaxis. We demonstrate the feasibility of deriving CMV-specific T cells from naive cells for T cell therapy. Naive T cells primed to recognize CMV were restricted to different, atypical epitopes than T cells derived from CMV-seropositive individuals; however, these two cell populations had similar avidities. CMV-seropositive individuals also had T cells recognizing these atypical epitopes, but these cells had a lower avidity than those derived from the seronegative subjects, which suggests that high-avidity T cells to these epitopes may be lost over time. Indeed, recipients of cord blood (CB) grafts who did not develop CMV were found by clonotypic analysis to have T cells recognizing atypical CMVpp65 epitopes. Therefore, we examined unmanipulated CB units and found that T cells with T cell receptors restricted by atypical epitopes were the most common, which may explain why these T cells expanded. When infused to recipients, naive donor-derived virus-specific T cells that recognized atypical epitopes were associated with prolonged periods of CMV-free survival and complete remission. These data suggest that naive-derived T cells from seronegative patients may be an additional source of cells for CMV immunoprophylaxis.
C1 [Hanley, Patrick J; Blaney, James W; Cruz, C. Russell; Lam, Sharon; Krance, Robert A.; Leung, Kathryn S.; Martinez, Caridad A.; Liu, Hao; Heslop, Helen E.; Rooney, Cliona M.; Bollard, Catherine M.] Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Hanley, Patrick J; Blaney, James W; Cruz, C. Russell; Lam, Sharon; Krance, Robert A.; Leung, Kathryn S.; Martinez, Caridad A.; Liu, Hao; Heslop, Helen E.; Rooney, Cliona M.; Bollard, Catherine M.] Houston Methodist Hosp, Houston, TX USA.
[Hanley, Patrick J; Lam, Sharon; Rooney, Cliona M.; Rodgers, John R.; Bollard, Catherine M.] Baylor Coll Med, Dept Pathol & Immunol, Houston, TX 77030 USA.
[Hanley, Patrick J; Cruz, C. Russell; Lam, Sharon; Bollard, Catherine M.] George Washington Univ, Program Cell Enhancement & Technol Immunotherapy, Sheikh Zayed Inst Pediat Surg Innovat, Ctr Canc & Immunol Res, Washington, DC 20052 USA.
[Hanley, Patrick J; Lam, Sharon; Bollard, Catherine M.] George Washington Univ, Div Blood & Marrow Transplantat, Childrens Natl Hlth Syst, Washington, DC 20052 USA.
[Melenhorst, Jan J; Scheinberg, Phillip S; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Nikiforow, Sarah N] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Demmler-Harrison, Gail D; Heslop, Helen E.; Rooney, Cliona M.; Bollard, Catherine M.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Krance, Robert A.; Heslop, Helen E.; Rooney, Cliona M.; Bollard, Catherine M.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Douelc, Daniel C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Rooney, Cliona M.] Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA.
[Shpall, Elizabeth J.] Univ Texas Houston, MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
RP Bollard, CM (reprint author), Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
EM cbollard@cnmc.org
FU American Cancer Society [PF-13e046e01-LIB]; Cancer Prevention Research
Institute of Texas [RO1 RP100469]; National Cancer Institute [PO1
CA148600e02]
FX Funding: This work was supported by a postdoctoral fellowship,
PF-13e046e01-LIB, from the American Cancer Society awarded to P.J.H.,
Cancer Prevention Research Institute of Texas RO1 RP100469 (to C.M.B.),
and National Cancer Institute PO1 CA148600e02 (to C.M.B. and E.J.S.)
awards.
NR 50
TC 8
Z9 8
U1 0
U2 3
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD APR 29
PY 2015
VL 7
IS 285
AR 285ra63
DI 10.1126/scitranslmed.aaa2546
PG 12
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA CH1MB
UT WOS:000353784700006
PM 25925682
ER
PT J
AU Navarro, G
Quiroz, C
Moreno-Delgado, D
Sierakowiak, A
McDowell, K
Moreno, E
Rea, W
Cai, NS
Aguinaga, D
Howell, LA
Hausch, F
Cortes, A
Mallol, J
Casado, V
Lluis, C
Canela, EI
Ferre, S
McCormick, PJ
AF Navarro, Gemma
Quiroz, Cesar
Moreno-Delgado, David
Sierakowiak, Adam
McDowell, Kimberly
Moreno, Estefania
Rea, William
Cai, Ning-Sheng
Aguinaga, David
Howell, Lesley A.
Hausch, Felix
Cortes, Antonio
Mallol, Josefa
Casado, Vicent
Lluis, Carme
Canela, Enric I.
Ferre, Sergi
McCormick, Peter J.
TI Orexin-Corticotropin-Releasing Factor Receptor Heteromers in the Ventral
Tegmental Area as Targets for Cocaine
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE cocaine; CRF receptor; GPCR heteromer; orexin receptor; sigma receptor
ID STRESS-INDUCED RELAPSE; PROTEIN-COUPLED RECEPTORS; CRF-BINDING-PROTEIN;
SIGMA-1 RECEPTORS; DOPAMINE NEURONS; INDUCED REINSTATEMENT; DRUG
SEEKING; OREXIN/HYPOCRETIN; HYPOTHALAMUS; PHARMACOLOGY
AB Release of the neuropeptides corticotropin-releasing factor (CRF) and orexin-A in the ventral tegmental area (VTA) play an important role in stress-induced cocaine-seeking behavior. We provide evidence for pharmacologically significant interactions between CRF and orexin-A that depend on oligomerization of CRF1 receptor (CRF1R) and orexin OX1 receptors (OX1R). CRF1R-OX1R heteromers are the conduits of a negative crosstalk between orexin-A and CRF as demonstrated in transfected cells and rat VTA, in which they significantly modulate dendritic dopamine release. The cocaine target sigma(1) receptor (sigma R-1) also associates with the CRF1R-OX1R heteromer. Cocaine binding to the sigma R-1-CRF1R-OX1R complex promotes a long-term disruption of the orexin-A-CRF negative crosstalk. Through this mechanism, cocaine sensitizes VTA cells to the excitatory effects of both CRF and orexin-A, thus providing a mechanism by which stress induces cocaine seeking.
C1 [Navarro, Gemma; Moreno-Delgado, David; Moreno, Estefania; Aguinaga, David; Cortes, Antonio; Mallol, Josefa; Casado, Vicent; Lluis, Carme; Canela, Enric I.; McCormick, Peter J.] Univ Barcelona, Fac Biol, Ctr Biomed Res Neurodegenerat Dis Network, Dept Biochem & Mol Biol, E-08028 Barcelona, Spain.
[Navarro, Gemma; Moreno-Delgado, David; Moreno, Estefania; Aguinaga, David; Cortes, Antonio; Mallol, Josefa; Casado, Vicent; Lluis, Carme; Canela, Enric I.; McCormick, Peter J.] Univ Barcelona, Inst Biomed, E-08028 Barcelona, Spain.
[Quiroz, Cesar; Sierakowiak, Adam; McDowell, Kimberly; Rea, William; Cai, Ning-Sheng; Ferre, Sergi] Natl Inst Drug Abuse, Integrat Neurobiol Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Howell, Lesley A.; McCormick, Peter J.] Univ E Anglia, Sch Pharm, Norwich NR4 7TJ, Norfolk, England.
[Hausch, Felix] Max Planck Inst Psychiat, D-80804 Munich, Germany.
RP Ferre, S (reprint author), NIDA, Integrat Neurobiol Sect, Intramural Res Program, Triad Technol Bldg,333 Cassell Dr, Baltimore, MD 21224 USA.
EM sferre@intra.nida.nih.gov; p.mccormick@uea.ac.uk
RI Casado, Vicent/K-1660-2014; Ferre, Sergi/K-6115-2014; Canela, Enric
I./M-8726-2013; McCormick, Peter/E-7387-2012;
OI Ferre, Sergi/0000-0002-1747-1779; Canela, Enric I./0000-0003-4992-7440;
McCormick, Peter/0000-0002-2225-5181; Sierakowiak,
Adam/0000-0003-2273-2133
FU intramural funds of the National Institute on Drug Abuse; Spanish
Ministry of Science and Technology [SAF2011-23813, SAF2009-07276];
Government of Catalonia Grant [2009-SGR-12]; Center for Biomedical
Research in Neurodegenerative Diseases Network Grant [CB06/05/0064];
Ramon y Cajal Fellowship
FX This work was supported by intramural funds of the National Institute on
Drug Abuse, from Spanish Ministry of Science and Technology Grants
SAF2011-23813 and SAF2009-07276, Government of Catalonia Grant
2009-SGR-12, and Center for Biomedical Research in Neurodegenerative
Diseases Network Grant CB06/05/0064. P.J.M. was supported through a
Ramon y Cajal Fellowship. We thank Jasmina Jimenez for technical
assistance.
NR 43
TC 11
Z9 11
U1 2
U2 8
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 29
PY 2015
VL 35
IS 17
BP 6639
EP 6653
DI 10.1523/JNEUROSCI.4364-14.2015
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA CG9PC
UT WOS:000353647600003
PM 25926444
ER
PT J
AU Delaville, C
Mccoy, AJ
Gerber, CM
Cruz, AV
Walters, JR
AF Delaville, Claire
Mccoy, Alex J.
Gerber, Colin M.
Cruz, Ana V.
Walters, Judith R.
TI Subthalamic Nucleus Activity in the Awake Hemiparkinsonian Rat:
Relationships with Motor and Cognitive Networks
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE beta oscillation; dopamine; gamma oscillations; medial prefrontal
cortex; Parkinson's disease; subthalamic nucleus
ID DEEP BRAIN-STIMULATION; HUMAN BASAL GANGLIA; MOVEMENT-RELATED CHANGES;
HIGH-FREQUENCY ACTIVITY; LOCAL-FIELD POTENTIALS; PARKINSONS-DISEASE;
OSCILLATORY ACTIVITY; GAMMA-ACTIVITY; BETA-OSCILLATIONS; CEREBRAL-CORTEX
AB Oscillatory activity in both beta and gamma ranges has been recorded in the subthalamic nucleus (STN) of Parkinson's disease (PD) patients and linked to motor function, with beta activity considered antikinetic, and gamma activity, prokinetic. However, the extent to which nonmotor networks contribute to this activity is unclear. This study uses hemiparkinsonian rats performing a treadmill walking task to compare synchronized STN local field potential (LFP) activity with activity in motor cortex (MCx) and medial prefrontal cortex (mPFC), areas involved in motor and cognitive processes, respectively. Data show increases in STN and MCx 29-36 Hz LFP spectral power and coherence after dopamine depletion, which are reduced by apomorphine and levodopa treatments. In contrast, recordings from mPFC3 weeks after dopamine depletion failed to show peaks in 29-36 Hz LFP power. However, mPFC and STN both showed peaks in the 45-55 Hz frequency range in LFP power and coherence during walking before and 21 days after dopamine depletion. Interestingly, power in this low gamma range was transiently reduced in both mPFC and STN after dopamine depletion but recovered by day 21. In contrast to the 45-55 Hz activity, the amplitude of the exaggerated 29-36 Hz rhythm in the STN was modulated by paw movement. Furthermore, as in PD patients, after dopamine treatment a third band (high gamma) emerged in the lesioned hemisphere. The results suggest that STN integrates activity from both motor and cognitive networks in a manner that varies with frequency, behavioral state, and the integrity of the dopamine system.
C1 [Delaville, Claire; Mccoy, Alex J.; Gerber, Colin M.; Cruz, Ana V.; Walters, Judith R.] NINDS, Neurophysiol Pharmacol Sect, NIH, Bethesda, MD 20892 USA.
RP Walters, JR (reprint author), NINDS, Neurophysiol Pharmacol Sect, NIH, 35 Convent Dr,Bldg 35,Room 1C905, Bethesda, MD 20892 USA.
EM waltersj@ninds.nih.gov
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke, National Institutes of Health (NIH)
FX This work was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, National
Institutes of Health (NIH). We thank Tom Talbot, Daryl Bandy, and Newlin
Morgan in the section of Instrumentation, National Institute of Mental
Health-National Institute of Neurological Disorders and Stroke for
design and fabrication of the rotary treadmill.
NR 64
TC 4
Z9 4
U1 0
U2 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 29
PY 2015
VL 35
IS 17
BP 6918
EP 6930
DI 10.1523/JNEUROSCI.0587-15.2015
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA CG9PC
UT WOS:000353647600025
PM 25926466
ER
PT J
AU Manzourolajdad, A
Arnold, J
AF Manzourolajdad, Amirhossein
Arnold, Jonathan
TI Secondary structural entropy in RNA switch (Riboswitch) identification
SO BMC BIOINFORMATICS
LA English
DT Article
DE Riboswitch; Entropy; RNA secondary structure; cotH; sucC
ID CONTEXT-FREE GRAMMARS; MICROBIAL GENE IDENTIFICATION; MESSENGER-RNA;
STRUCTURE PREDICTION; BACILLUS-SUBTILIS; S-ADENOSYLMETHIONINE;
LIGAND-BINDING; NONCODING RNA; TRANSCRIPTION TERMINATION; CONFORMATIONAL
SELECTION
AB Background: RNA regulatory elements play a significant role in gene regulation. Riboswitches, a widespread group of regulatory RNAs, are vital components of many bacterial genomes. These regulatory elements generally function by forming a ligand-induced alternative fold that controls access to ribosome binding sites or other regulatory sites in RNA. Riboswitch-mediated mechanisms are ubiquitous across bacterial genomes. A typical class of riboswitch has its own unique structural and biological complexity, making de novo riboswitch identification a formidable task. Traditionally, riboswitches have been identified through comparative genomics based on sequence and structural homology. The limitations of structural-homology-based approaches, coupled with the assumption that there is a great diversity of undiscovered riboswitches, suggests the need for alternative methods for riboswitch identification, possibly based on features intrinsic to their structure. As of yet, no such reliable method has been proposed.
Results: We used structural entropy of riboswitch sequences as a measure of their secondary structural dynamics. Entropy values of a diverse set of riboswitches were compared to that of their mutants, their dinucleotide shuffles, and their reverse complement sequences under different stochastic context-free grammar folding models. Significance of our results was evaluated by comparison to other approaches, such as the base-pairing entropy and energy landscapes dynamics. Classifiers based on structural entropy optimized via sequence and structural features were devised as riboswitch identifiers and tested on Bacillus subtilis, Escherichia coli, and Synechococcus elongatus as an exploration of structural entropy based approaches. The unusually long untranslated region of the cotH in Bacillus subtilis, as well as upstream regions of certain genes, such as the sucC genes were associated with significant structural entropy values in genome-wide examinations.
Conclusions: Various tests show that there is in fact a relationship between higher structural entropy and the potential for the RNA sequence to have alternative structures, within the limitations of our methodology. This relationship, though modest, is consistent across various tests. Understanding the behavior of structural entropy as a fairly new feature for RNA conformational dynamics, however, may require extensive exploratory investigation both across RNA sequences and folding models.
C1 [Manzourolajdad, Amirhossein; Arnold, Jonathan] Univ Georgia, Inst Bioinformat, Athens, GA 30602 USA.
[Manzourolajdad, Amirhossein] NIH, NCBI, Bethesda, MD 20894 USA.
[Arnold, Jonathan] Univ Georgia, Dept Genet, Athens, GA 30602 USA.
RP Manzourolajdad, A (reprint author), Univ Georgia, Inst Bioinformat, Davison Life Sci Bldg,Room B118B,120 Green St, Athens, GA 30602 USA.
EM amanzour@uga.edu
FU Georgia Advanced Computing Resource Center (GACRC); NSF [MRI - DBI
0821263]; Intramural Research Program of the NIH, National Library of
Medicine
FX This work was done under the research assistantship received from the
institute of bioinformatics at the University of Georgia. We also would
like to acknowledge the The Georgia Advanced Computing Resource Center
(GACRC) and the NSF MRI - DBI 0821263 award for the cluster for
supporting the work. This research was supported in part by the
Intramural Research Program of the NIH, National Library of Medicine. We
thank Dr. John L. Spouge for his support. We also thank anonymous
reviewers for their time and critical suggestions which were
subsequently incorporated in this work.
NR 133
TC 6
Z9 6
U1 0
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD APR 28
PY 2015
VL 16
AR 133
DI 10.1186/s12859-015-0523-2
PG 77
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
GA CJ2BS
UT WOS:000355289800001
PM 25928324
ER
PT J
AU Monaco, MCG
Major, EO
AF Monaco, Maria Chiara G.
Major, Eugene O.
TI Immune system involvement in the pathogenesis of JC virus induced PML:
what is learned from studies of patients with underlying diseases and
therapies as risk factors
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE progressive multifocal leukoencephalopathy; JCV; immunomodulatory
therapy,T cell immune response; multiple sclerosis; natalizumab
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; NATALIZUMAB-TREATED
PATIENTS; T-CELL RESPONSES; MULTIPLE-SCLEROSIS; IMMUNOMODULATORY
THERAPIES; MAINTENANCE THERAPY; GENE-EXPRESSION; BONE-MARROW; BK VIRUS;
REACTIVATION
AB The human polyomavirus JC PyV lytic infection of oligodendrocytes in the human brain results in the demyelinating disease progressive multifocal leukoencephalopathy, PML. JCV is a common virus infection in the population that leads to PML in patients with underlying diseases and therapies that cause immune deficiencies or modulate immune system functions. Patients may have high levels of antibody to JCV that neither protect them from PML nor clear the infection once PML is established. Cell-mediated immunity plays a more effective role in clearing initial or reactivated JCV infection before PML occurs. However, patients with underlying diseases and therapies for treatment are at high risk for PML. MS patients on natalizumab are one of the categories with the highest incidence of PML. Natalizumab is a humanized monoclonal antibody targeting alpha 4 integrins that prevents inflammatory cells from entering the brain and it has been used as a treatment for MS. A number of studies have investigated the occurrence of PML in these patients and their cell-mediated immune profile that might gain insight into the mechanism that ties natalizumab with a high risk of developing PML. It seems that cells of the immune system participate in the pathogenesis of PML as well as clearance of JCV infection.
C1 [Monaco, Maria Chiara G.; Major, Eugene O.] Natl Inst Neurol Disorders & Stroke, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
RP Major, EO (reprint author), Natl Inst Neurol Disorders & Stroke, Lab Mol Med & Neurosci, NIH, 10 Ctr Dr,Bldg 10,Room 3B14, Bethesda, MD 20892 USA.
EM majorg@ninds.nih.gov
NR 44
TC 15
Z9 15
U1 1
U2 1
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD APR 28
PY 2015
VL 6
AR 159
DI 10.3389/fimmu.2015.00159
PG 5
WC Immunology
SC Immunology
GA CI7IU
UT WOS:000354937400001
PM 25972864
ER
PT J
AU Lai, SJ
Huang, ZJ
Zhou, H
Anders, KL
Perkins, TA
Yin, WW
Li, Y
Mu, D
Chen, QL
Zhang, ZK
Qiu, YZ
Wang, LP
Zhang, HL
Zeng, LJ
Ren, X
Geng, MJ
Li, ZJ
Tatem, AJ
Hay, SI
Yu, HJ
AF Lai, Shengjie
Huang, Zhuojie
Zhou, Hang
Anders, Katherine L.
Perkins, T. Alex
Yin, Wenwu
Li, Yu
Mu, Di
Chen, Qiulan
Zhang, Zike
Qiu, Yanzi
Wang, Liping
Zhang, Honglong
Zeng, Linjia
Ren, Xiang
Geng, Mengjie
Li, Zhongjie
Tatem, Andrew J.
Hay, Simon I.
Yu, Hongjie
TI The changing epidemiology of dengue in China, 1990-2014: a descriptive
analysis of 25 years of nationwide surveillance data
SO BMC MEDICINE
LA English
DT Article
DE Dengue; China; Import; Indigenous; Epidemiology; Outbreak
ID REPUBLIC-OF-CHINA; AEDES-ALBOPICTUS; GUANGDONG PROVINCE;
VIRUS-INFECTIONS; OUTBREAK; FEVER; TRANSMISSION; REEMERGENCE; EMERGENCE;
GUANGZHOU
AB Background: Dengue has been a notifiable disease in China since 1 September 1989. Cases have been reported each year during the past 25 years of dramatic socio-economic changes in China, and reached a historical high in 2014. This study describes the changing epidemiology of dengue in China during this period, to identify high-risk areas and seasons and to inform dengue prevention and control activities.
Methods: We describe the incidence and distribution of dengue in mainland China using notifiable surveillance data from 1990-2014, which includes classification of imported and indigenous cases from 2005-2014.
Results: From 1990-2014, 69,321 cases of dengue including 11 deaths were reported in mainland China, equating to 2.2 cases per one million residents. The highest number was recorded in 2014 (47,056 cases). The number of provinces affected has increased, from a median of three provinces per year (range: 1 to 5 provinces) during 1990-2000 to a median of 14.5 provinces per year (range: 5 to 26 provinces) during 2001-2014. During 2005-2014, imported cases were reported almost every month and 28 provinces (90.3%) were affected. However, 99.8% of indigenous cases occurred between July and November. The regions reporting indigenous cases have expanded from the coastal provinces of southern China and provinces adjacent to Southeast Asia to the central part of China. Dengue virus serotypes 1, 2, 3, and 4 were all detected from 2009-2014.
Conclusions: In China, the area affected by dengue has expanded since 2000 and the incidence has increased steadily since 2012, for both imported and indigenous dengue. Surveillance and control strategies should be adjusted to account for these changes, and further research should explore the drivers of these trends.
C1 [Lai, Shengjie; Huang, Zhuojie; Zhou, Hang; Yin, Wenwu; Li, Yu; Mu, Di; Chen, Qiulan; Zhang, Zike; Qiu, Yanzi; Wang, Liping; Zhang, Honglong; Zeng, Linjia; Ren, Xiang; Geng, Mengjie; Li, Zhongjie; Yu, Hongjie] Chinese Ctr Dis Control & Prevent, Key Lab Surveillance & Early Warning Infect Dis, Div Infect Dis, Beijing 102206, Peoples R China.
[Lai, Shengjie; Tatem, Andrew J.] Univ Southampton, Dept Geog & Environm, Southampton SO17 1BJ, Hants, England.
[Anders, Katherine L.] Univ Oxford, Clin Res Unit, Wellcome Trust Major Overseas Programme, Ho Chi Minh City, Vietnam.
[Anders, Katherine L.] Univ Oxford, Ctr Trop Med, Oxford OX3 7FZ, England.
[Anders, Katherine L.] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[Perkins, T. Alex] Univ Notre Dame, Dept Biol Sci, Notre Dame, IN 46556 USA.
[Perkins, T. Alex] Univ Notre Dame, Eck Inst Global Hlth, Notre Dame, IN 46556 USA.
[Perkins, T. Alex; Tatem, Andrew J.; Hay, Simon I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Tatem, Andrew J.] Flowminder Fdn, SE-11355 Stockholm, Sweden.
[Hay, Simon I.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford OX1 3PS, England.
RP Yu, HJ (reprint author), Chinese Ctr Dis Control & Prevent, Key Lab Surveillance & Early Warning Infect Dis, Div Infect Dis, 155 Changbai Rd, Beijing 102206, Peoples R China.
EM yuhj@chinacdc.cn
RI Hay, Simon/F-8967-2015;
OI Hay, Simon/0000-0002-0611-7272; ren, xiang/0000-0001-5020-5838
FU Ministry of Science and Technology of China [ZX10004-201, 2014BAI13B05];
Ministry of Health of China [201202006]; China CDC's Key Laboratory of
Surveillance and Early-warning on Infectious Disease; National Health
and Medical Research Council, Australia [1002608]; Wellcome Trust
[084368/Z/07/Z]; NIH/NIAID [U19AI089674]; Bill & Melinda Gates
Foundation [OPP110642749446, 1032350]; RAPIDD program of the Science and
Technology Directorate, Department of Homeland Security; Fogarty
International Center, National Institutes of Health
FX We thank the staff members at the hospitals, local health departments,
and county-, district-, prefecture-, and provincial-level CDCs for their
valuable assistance in coordinating data collection.; This work was
supported by grants from the Ministry of Science and Technology of China
(2012 ZX10004-201, 2014BAI13B05); the Ministry of Health of China
(201202006); China CDC's Key Laboratory of Surveillance and
Early-warning on Infectious Disease; and the National Health and Medical
Research Council, Australia (1002608). KA is supported by the Wellcome
Trust (084368/Z/07/Z). AT is supported by funding from NIH/NIAID
(U19AI089674) and the Bill & Melinda Gates Foundation (OPP110642749446,
1032350). TP, AT, and SH are supported by the RAPIDD program of the
Science and Technology Directorate, Department of Homeland Security, and
the Fogarty International Center, National Institutes of Health.; The
sponsor of the study had no role in the study design, data collection,
analysis, and interpretation, preparation of the manuscript, or the
decision to publish. Dr. Hongjie Yu had full access to all the data in
the study and had final responsibility for the decision to submit the
manuscript for publication. The views expressed are those of the authors
and do not necessarily represent the policy of the China CDC.
NR 54
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Z9 28
U1 0
U2 14
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1741-7015
J9 BMC MED
JI BMC Med.
PD APR 28
PY 2015
VL 13
AR 100
DI 10.1186/s12916-015-0336-1
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA CI0KA
UT WOS:000354424800001
PM 25925417
ER
PT J
AU Banga, S
Coursen, JD
Portugal, S
Tran, TM
Hancox, L
Ongoiba, A
Traore, B
Doumbo, OK
Huang, CY
Harty, JT
Crompton, PD
AF Banga, Simran
Coursen, Jill D.
Portugal, Silvia
Tran, Tuan M.
Hancox, Lisa
Ongoiba, Aissata
Traore, Boubacar
Doumbo, Ogobara K.
Huang, Chiung-Yu
Harty, John T.
Crompton, Peter D.
TI Impact of Acute Malaria on Pre-Existing Antibodies to Viral and Vaccine
Antigens in Mice and Humans
SO PLOS ONE
LA English
DT Article
ID MEMORY B-CELLS; PLASMODIUM-FALCIPARUM; SEROLOGICAL MEMORY; HUMORAL
IMMUNITY; CHILDREN; ACTIVATION; INFECTION; RESPONSES; DURATION; LIFE
AB Vaccine-induced immunity depends on long-lived plasma cells (LLPCs) that maintain antibody levels. A recent mouse study showed that Plasmodium chaubaudi infection reduced pre-existing influenza-specific antibodies-raising concerns that malaria may compromise pre-existing vaccine responses. We extended these findings to P. yoelii infection, observing decreases in antibodies to model antigens in inbred mice and to influenza in outbred mice, associated with LLPC depletion and increased susceptibility to influenza rechallenge. We investigated the implications of these findings in Malian children by measuring vaccine-specific IgG (tetanus, measles, hepatitis B) before and after the malaria-free 6-month dry season, 10 days after the first malaria episode of the malaria season, and after the subsequent dry season. On average, vaccine-specific IgG did not decrease following acute malaria. However, in some children malaria was associated with an accelerated decline in vaccine-specific IgG, underscoring the need to further investigate the impact of malaria on pre-existing vaccine-specific antibodies.
C1 [Banga, Simran; Hancox, Lisa; Harty, John T.] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA.
[Coursen, Jill D.; Portugal, Silvia; Tran, Tuan M.; Crompton, Peter D.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Ongoiba, Aissata; Traore, Boubacar; Doumbo, Ogobara K.] Univ Sci Tech & Technol Bamako, Mali Int Ctr Excellence Res, Bamako, Mali.
[Huang, Chiung-Yu] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Div Biostat & Bioinformat, Baltimore, MD USA.
[Harty, John T.] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA.
[Harty, John T.] Univ Iowa, Interdisciplinary Grad Program Immunol, Iowa City, IA 52242 USA.
RP Harty, JT (reprint author), Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA.
EM john-harty@uiowa.edu; pcrompton@niaid.nih.gov
RI Banga, Simran/L-8806-2013; Crompton, Peter/N-1130-2016
FU National Institutes of Health (NIH) [AI085515, AI095178, AI100527];
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, NIH
FX Malaria work in the JTH laboratory is supported by National Institutes
of Health (NIH) grants (AI085515, AI095178, AI100527). The PDC
laboratory and study in Mali is supported by the Division of Intramural
Research, National Institute of Allergy and Infectious Diseases, NIH.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 35
TC 3
Z9 3
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 28
PY 2015
VL 10
IS 4
AR e0125090
DI 10.1371/journal.pone.0125090
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CG9SE
UT WOS:000353659400072
PM 25919588
ER
PT J
AU Steck, SE
Arab, L
Zhang, HM
Bensen, JT
Fontham, ETH
Johnson, CS
Mohler, JL
Smith, GJ
Su, JL
Trump, DL
Woloszynska-Read, A
AF Steck, Susan E.
Arab, Lenore
Zhang, Hongmei
Bensen, Jeannette T.
Fontham, Elizabeth T. H.
Johnson, Candace S.
Mohler, James L.
Smith, Gary J.
Su, Joseph L.
Trump, Donald L.
Woloszynska-Read, Anna
TI Association between Plasma 25-Hydroxyvitamin D, Ancestry and Aggressive
Prostate Cancer among African Americans and European Americans in PCaP
SO PLOS ONE
LA English
DT Article
ID D-BINDING-PROTEIN; SERUM VITAMIN-D; UNITED-STATES; PROSPECTIVE COHORT;
RACIAL-DIFFERENCES; PREVENTION TRIAL; SUBSEQUENT RISK; D INSUFFICIENCY;
BREAST-CANCER; MEN
AB Background
African Americans (AAs) have lower circulating 25-hydroxyvitamin D3 [25(OH) D3] concentrations and higher prostate cancer (CaP) aggressiveness than other racial/ethnic groups. The purpose of the current study was to examine the relationship between plasma 25(OH) D3, African ancestry and CaP aggressiveness among AAs and European Americans (EAs).
Methods Plasma 25(OH) D3 was measured using LC-MS/MS (Liquid Chromatography Tandem Mass Spectrometry) in 537 AA and 663 EA newly-diagnosed CaP patients from the North Carolina-Louisiana Prostate Cancer Project (PCaP) classified as having either 'high' or 'low' aggressive disease based on clinical stage, Gleason grade and prostate specific antigen at diagnosis. Mean plasma 25(OH) D3 concentrations were compared by proportion of African ancestry. Logistic regression was used to calculate multivariable adjusted odds ratios (OR) and 95% confidence intervals (95% CI) for high aggressive CaP by tertile of plasma 25(OH) D3.
Results
AAs with highest percent African ancestry (>95%) had the lowest mean plasma 25(OH)D3 concentrations. Overall, plasma 25(OH) D3 was associated positively with aggressiveness among AA men, an association that was modified by calcium intake (ORT3vs.T1: 2.23, 95% CI: 1.26-3.95 among men with low calcium intake, and ORT3vs.T1: 0.19, 95% CI: 0.05-0.70 among men with high calcium intake). Among EAs, the point estimates of the ORs were <1.0 for the upper tertiles with CIs that included the null.
Conclusions
Among AAs, plasma 25(OH)D3 was associated positively with CaP aggressiveness among men with low calcium intake and inversely among men with high calcium intake. The clinical significance of circulating concentrations of 25(OH)D3 and interactions with calcium intake in the AA population warrants further study.
C1 [Steck, Susan E.] Univ S Carolina, Arnold Sch Publ Hlth, Canc Prevent & Control Program, Ctr Res Nutr & Hlth Dispar,Dept Epidemiol & Biost, Columbia, SC 29208 USA.
[Arab, Lenore] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Zhang, Hongmei] Univ Memphis, Memphis, TN 38152 USA.
[Bensen, Jeannette T.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Fontham, Elizabeth T. H.] Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, New Orleans, LA USA.
[Johnson, Candace S.; Mohler, James L.; Smith, Gary J.; Trump, Donald L.; Woloszynska-Read, Anna] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Su, Joseph L.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Woloszynska-Read, A (reprint author), Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
EM anna.woloszynska-read@roswellpark.org
FU United States Department of Defense [11-1-0568, W81WH11-1-0308PCa];
National Institutes of Health [CA067267, CA137650, CA016056]
FX United States Department of Defense 11-1-0568
http://cdmrp.army.mil/default.shtml SES, CSJ; United States Department
of Defense W81WH11-1-0308PCa http://cdmrp.army.mil/default.shtml AWR;
National Institutes of Health CA067267, CA137650 and CA016056
http://www.nih.gov DLT and CSJ. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 64
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U1 1
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 APR 28
PY 2015
VL 10
IS 4
AR e0125151
DI 10.1371/journal.pone.0125151
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CG9SE
UT WOS:000353659400074
PM 25919866
ER
PT J
AU Stenehjem, JS
Kjaerheim, K
Bratveit, M
Samuelsen, SO
Barone-Adesi, F
Rothman, N
Lan, Q
Grimsrud, TK
AF Stenehjem, J. S.
Kjaerheim, K.
Bratveit, M.
Samuelsen, S. O.
Barone-Adesi, F.
Rothman, N.
Lan, Q.
Grimsrud, T. K.
TI Benzene exposure and risk of lymphohaematopoietic cancers in 25 000
offshore oil industry workers
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE benzene; case-cohort; cancer incidence; lymphohaematopoietic; offshore
workers; petroleum industry
ID LOW-LEVEL BENZENE; AUSTRALIAN PETROLEUM-INDUSTRY; MULTIPLE-MYELOMA;
OCCUPATIONAL-EXPOSURE; LYMPHOMA SUBTYPES; FOLLOW-UP; LEUKEMIA; COHORT;
MORTALITY; NORWAY
AB Background: The aim of this work was to examine the risk of lymphohaematopoietic (LH) cancer according to benzene exposure among offshore workers.
Methods: Cancer registry data were used to identify 112 cancer cases diagnosed during 1999-2011 in a cohort of 24 917 Norwegian men reporting offshore work between 1965 and 1999. Analyses were conducted according to a stratified case-cohort design with a reference subcohort of 1661 workers. Cox regression was used to estimate hazard ratios with 95% confidence intervals, adjusted for other benzene exposure and smoking.
Results: Most workers were exposed to benzene for <15 years. The upper range values of average intensity and cumulative exposure were estimated to 0.040 p.p.m. and 0.948 p.p.m.-years, respectively. Risks were consistently elevated among exposed workers for all LH cancers combined and for most subgroups, although case numbers were small and yielded imprecise risk estimates. There was evidence of dose-related risk patterns according to cumulative exposure for acute myeloid leukaemia (AML), multiple myeloma (MM) (P trends 0.052 and 0.024, respectively), and suggestively so for chronic lymphocytic leukaemia (CLL) according to average intensity (P trend 0.094).
Conclusions: Our results support an association between cumulative and intensity metrics of low-level benzene exposure and risk for AML, MM, and suggestively for CLL.
C1 [Stenehjem, J. S.; Kjaerheim, K.; Grimsrud, T. K.] Canc Registry Norway, Dept Res, N-0304 Oslo, Norway.
[Bratveit, M.] Univ Bergen, Dept Global Publ Hlth & Primary Care, N-5020 Bergen, Norway.
[Samuelsen, S. O.] Univ Oslo, Dept Math, N-0316 Oslo, Norway.
[Barone-Adesi, F.] St George Hosp, Populat Hlth Res Inst, London SW17 0RE, England.
[Barone-Adesi, F.] Univ Piemonte Orientale, Dept Pharmaceut Sci, I-28100 Novara, Italy.
[Rothman, N.; Lan, Q.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Grimsrud, TK (reprint author), Canc Registry Norway, Dept Res, POB 5313 Majorstuen, N-0304 Oslo, Norway.
EM tom.k.grimsrud@kreftregisteret.no
OI Kjaerheim, Kristina/0000-0003-0691-3735
FU Research Council of Norway's PETROMAKS program [189612]
FX We wish to thank our former Head of Department, Aage Andersen, without
whose efforts the establishment of the cohort and the conduct of the
subsequent studies would not have been possible, Researcher Leif Age
strand for conducting the offshore survey, Senior Consultant Tone Eggen
for cleaning the work history data, Data Manager Jan Ivar Martinsen for
sampling of the subcohort and linking cancer and exposure estimates to
the cohort, and MD Svein Hansen for advice on grouping of LH cancer
(Department of Research, Cancer Registry of Norway). We also thank
Industrial Hygienists Jorunn Kirkeleit and Bjorg Eli Hollund (Department
of Occupational Medicine, Haukeland University Hospital, Norway) and
Research Director John Cherrie (Institute of Occupational Medicine,
Edinburgh, UK) for assisting with the JEM development. This work was
funded by the Research Council of Norway's PETROMAKS program (grant no.
189612).
NR 45
TC 3
Z9 3
U1 1
U2 15
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 28
PY 2015
VL 112
IS 9
BP 1603
EP 1612
DI 10.1038/bjc.2015.108
PG 10
WC Oncology
SC Oncology
GA CG9SG
UT WOS:000353659800023
PM 25867262
ER
PT J
AU Kapitonov, VV
Koonin, EV
AF Kapitonov, Vladimir V.
Koonin, Eugene V.
TI Evolution of the RAG1-RAG2 locus: both proteins came from the same
transposon
SO BIOLOGY DIRECT
LA English
DT Article
DE Molecular evolution; genetics; immune system; V(D)J recombination; RAG1
and RAG2 proteins; Transib DNA transposons; Transib transposase
ID V(D)J RECOMBINATION; RAG2 PROTEINS; GENES; DATABASE; PERFORMANCE;
ELEMENTS; DOMAIN; DNA
AB The RAG1 and RAG2 proteins are essential subunits of the V(D)J recombinase that is required for the generation of the enormous variability of antibodies and T-cell receptors in jawed vertebrates. It was demonstrated previously that the 600-aa catalytic core of RAG1 evolved from the transposase of the Transib superfamily transposons. However, although homologs of RAG1 and RAG2 genes are adjacent in the purple sea urchin genome, a transposon encoding both proteins so far has not been reported. Here we describe such transposons in the genomes of green sea urchin, a starfish and an oyster. Comparison of the domain architectures of the RAG1 homologs in these transposons, denoted TransibSU, and other Transib superfamily transposases provides for reconstruction of the structure of the hypothetical TransibVDJ transposon that gave rise to the VDJ recombinases at the onset of vertebrate evolution some 500 million years ago.
C1 [Kapitonov, Vladimir V.; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20892 USA.
RP Kapitonov, VV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20892 USA.
EM kvladimirv@gmail.com
FU US Department of Health and Human Services
FX The authors' research is supported by intramural funds of the US
Department of Health and Human Services (to the National Library of
Medicine).
NR 28
TC 16
Z9 16
U1 0
U2 12
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD APR 28
PY 2015
VL 10
AR 20
DI 10.1186/s13062-015-0055-8
PG 8
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA CG8EJ
UT WOS:000353539700001
PM 25928409
ER
PT J
AU Chung, YW
Lagranha, C
Chen, Y
Sun, JH
Tong, G
Hockman, SC
Ahmad, F
Esfahani, SG
Bae, DH
Polidovitch, N
Wu, J
Rhee, DK
Lee, BS
Gucek, M
Daniels, MP
Brantner, CA
Backx, PH
Murphy, E
Manganiello, VC
AF Chung, Youn Wook
Lagranha, Claudia
Chen, Yong
Sun, Junhui
Tong, Guang
Hockman, Steven C.
Ahmad, Faiyaz
Esfahani, Shervin G.
Bae, Dahae H.
Polidovitch, Nazari
Wu, Jian
Rhee, Dong Keun
Lee, Beom Seob
Gucek, Marjan
Daniels, Mathew P.
Brantner, Christine A.
Backx, Peter H.
Murphy, Elizabeth
Manganiello, Vincent C.
TI Targeted disruption of PDE3B, but not PDE3A, protects murine heart from
ischemia/reperfusion injury
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE PDE3B(-/-) mice; protein kinase A; ischemia/reperfusion injury;
signalosome; membrane repair
ID GLYCOGEN-SYNTHASE KINASE-3-BETA; CA2+-ACTIVATED K+ CHANNELS;
CYCLIC-NUCLEOTIDE PHOSPHODIESTERASES; INNER MITOCHONDRIAL-MEMBRANE;
PERMEABILITY TRANSITION PORE; ISCHEMIA-REPERFUSION INJURY;
SMOOTH-MUSCLE-CELLS; CARDIAC MYOCYTES; KINASE-A; SIGNAL-TRANSDUCTION
AB Although inhibition of cyclic nucleotide phosphodiesterase type 3 (PDE3) has been reported to protect rodent heart against ischemia/reperfusion (I/R) injury, neither the specific PDE3 isoform involved nor the underlying mechanisms have been identified. Targeted disruption of PDE3 subfamily B (PDE3B), but not of PDE3 subfamily A (PDE3A), protected mouse heart from I/R injury in vivo and in vitro, with reduced infarct size and improved cardiac function. The cardioprotective effect in PDE3B(-/-) heart was reversed by blocking cAMP-dependent PKA and by paxilline, an inhibitor of mitochondrial calcium-activated K channels, the opening of which is potentiated by cAMP/PKA signaling. Compared with WT mitochondria, PDE3B(-/-) mitochondria were enriched in antiapoptotic Bcl-2, produced less reactive oxygen species, and more frequently contacted transverse tubules where PDE3B was localized with caveolin-3. Moreover, a PDE3B(-/-) mitochondrial fraction containing connexin-43 and caveolin-3 was more resistant to Ca2+ induced opening of the mitochondrial permeability transition pore. Proteomics analyses indicated that PDE3B(-/-) heart mitochondria fractions were enriched in buoyant ischemia-induced caveolin-3-enriched fractions (ICEFs) containing cardioprotective proteins. Accumulation of proteins into ICEFs was PKA dependent and was achieved by ischemic preconditioning or treatment of WT heart with the PDE3 inhibitor cilostamide. Taken together, these findings indicate that PDE3B deletion confers cardioprotective effects because of cAMP/PKA-induced preconditioning, which is associated with the accumulation of proteins with cardioprotective function in ICEFs. To our knowledge, our study is the first to define a role for PDE3B in cardioprotection against I/R injury and suggests PDE3B as a target for cardiovascular therapies.
C1 [Chung, Youn Wook; Hockman, Steven C.; Ahmad, Faiyaz; Rhee, Dong Keun; Manganiello, Vincent C.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Lagranha, Claudia; Sun, Junhui; Tong, Guang; Murphy, Elizabeth] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Chen, Yong; Gucek, Marjan] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
[Esfahani, Shervin G.; Bae, Dahae H.; Daniels, Mathew P.; Brantner, Christine A.] NHLBI, Electron Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
[Chung, Youn Wook; Lee, Beom Seob] Yonsei Univ, Coll Med, Yonsei Cardiovasc Res Inst, Seoul 120752, South Korea.
[Tong, Guang] Guangzhou Mil Command, Guangzhou Gen Hosp, Dept Cardiovasc Surg, Guangzhou 510010, Guangdong, Peoples R China.
[Polidovitch, Nazari; Wu, Jian; Backx, Peter H.] Univ Toronto, Dept Physiol, Toronto, ON M5S 3A8, Canada.
[Polidovitch, Nazari; Wu, Jian; Backx, Peter H.] Univ Toronto, Dept Med, Toronto, ON M5S 3A8, Canada.
[Lee, Beom Seob] Yonsei Univ, Grad Program Sci Aging, Seoul 120752, South Korea.
[Backx, Peter H.] Univ Hlth Network, Div Cardiol, Toronto, ON M5S 3E2, Canada.
RP Chung, YW (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM chungyw@yuhs.ac; manganiv@nhlbi.nih.gov
OI Brantner, Christine/0000-0001-8172-901X
FU National Heart, Lung, and Blood Institute; Canadian Institutes for
Health Research [MOP62954]
FX We thank Dr. M. Movsesian of the University of Utah School of Medicine
for helpful discussions. Y.W.C., C.L., Y.C., J.S., G.T., S.C.H., F.A.,
S.G.E., D.H.B., D.K.R., M.G., M.P.D., E.M., and V.C.M. were supported by
the National Heart, Lung, and Blood Institute Intramural Research
Program. N.P., J.W., and P.H.B. were supported by Canadian Institutes
for Health Research Grant MOP62954.
NR 73
TC 15
Z9 16
U1 3
U2 11
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 28
PY 2015
VL 112
IS 17
BP E2253
EP E2262
DI 10.1073/pnas.1416230112
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CG8JR
UT WOS:000353554000020
PM 25877153
ER
PT J
AU Smedlund, KB
Birnbaumer, L
Vazquez, G
AF Smedlund, Kathryn B.
Birnbaumer, Lutz
Vazquez, Guillermo
TI Increased size and cellularity of advanced atherosclerotic lesions in
mice with endothelial overexpression of the human TRPC3 channel
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE TRPC3 channels; atherosclerosis; endothelial inflammation
ID ENDOPLASMIC-RETICULUM STRESS; CATION CHANNELS; PLAQUE PROGRESSION;
MONOCYTE ADHERENCE; GENE-EXPRESSION; CELLS; VCAM-1; INFLAMMATION;
MACROPHAGES; MECHANISMS
AB In previous in vitro studies, we showed that Transient Receptor Potential Canonical 3 (TRPC3), a calcium-permeable, nonselective cation channel endowed with high constitutive function, is an obligatory component of the inflammatory signaling that controls expression of the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion to coronary artery endothelial cells. Also, TRPC3 expression in these cells was found to be up-regulated by proatherogenic factors, which enhanced inflammation and VCAM-1 expression. However, it remained to be determined whether these in vitro findings were of relevance to atherosclerotic lesion development in vivo. To answer this important question in the present work, we generated mice with endothelial-specific overexpression of human TRPC3 in an Apoe knockout background (TgEST3ApoeKO) and examined lesions in the aortic sinus following 10 and 16 wk on a high-fat diet. No significant differences were found in size or complexity of early stage lesions (10 wk). However, advanced plaques (16 wk) from TgEST3ApoeKO mice exhibited a significant increase in size and macrophage content compared with nontransgenic littermate controls. Remarkably, this change was correlated with increased VCAM-1 and phospho-IkB alpha immunoreactivity along the endothelial lining of lesions from transgenic animals compared with controls. These findings validate the in vivo relevance of previous in vitro findings and represent, to our knowledge, the first in vivo evidence for a proatherogenic role of endothelial TRPC3.
C1 [Smedlund, Kathryn B.; Vazquez, Guillermo] Univ Toledo, Coll Med, Dept Physiol & Pharmacol, Ctr Diabet & Endocrine Res, Toledo, OH 43614 USA.
[Birnbaumer, Lutz] NIEHS, Neurobiol Lab, Res Triangle Pk, NC 27709 USA.
RP Birnbaumer, L (reprint author), NIEHS, Neurobiol Lab, POB 12233, Res Triangle Pk, NC 27709 USA.
EM birnbau1@niehs.nih.gov; Guillermo.Vazquez@utoledo.edu
OI Smedlund, Kathryn/0000-0002-5746-8419
FU NIH [R01HL111877-03, Z01-ES-101864]
FX This work was supported by NIH Grant R01HL111877-03 (to G.V.) and in
part by the Intramural Research Program of the NIH (Project
Z01-ES-101864 to L.B.).
NR 37
TC 6
Z9 7
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 28
PY 2015
VL 112
IS 17
BP E2201
EP E2206
DI 10.1073/pnas.1505410112
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CG8JR
UT WOS:000353554000014
PM 25870279
ER
PT J
AU Baber, JL
Louis, JM
Clore, GM
AF Baber, James L.
Louis, John M.
Clore, G. Marius
TI Dependence of Distance Distributions Derived from Double
Electron-Electron Resonance Pulsed EPR Spectroscopy on Pulse-Sequence
Time
SO ANGEWANDTE CHEMIE-INTERNATIONAL EDITION
LA English
DT Article
DE deuteration; distance distributions; EPR spectroscopy; phase memory
time; proteins
ID SPIN-ECHO; PROTEINS; DYNAMICS; BINDING; SOLIDS; DOMAIN
AB Pulsed double electron-electron resonance (DEER) provides pairwise P(r) distance distributions in doubly spin labeled proteins. We report that in protonated proteins, P(r) is dependent on the length of the second echo period T owing to local environmental effects on the spin-label phase memory relaxation time T-m. For the protein ABD, this effect results in a 1.4 a increase in the P(r) maximum from T=6 to 20 mu s. ProteinA has a bimodal P(r) distribution, and the relative height of the shorter distance peak at T=10 mu s, the shortest value required to obtain a reliable P(r), is reduced by 40% relative to that found by extrapolation to T=0. Our results indicate that data at a series of T values are essential for quantitative interpretation of DEER to determine the extent of the T dependence and to extrapolate the results to T=0. Complete deuteration (99%) of the protein was accompanied by a significant increase in T-m and effectively abolished the P(r) dependence on T.
C1 [Baber, James L.; Louis, John M.; Clore, G. Marius] Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD 20892 USA.
RP Baber, JL (reprint author), Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD 20892 USA.
EM jamesbaber@niddk.nih.gov; mariusc@mail.nih.gov
FU NIDDK, NIH; AIDS Targeted Antiviral Program of the Office of the
Director of the NIH
FX We thank Alexey Potapov, Ad Bax, and Lalit Deshmukh for useful
discussions, and Annie Aniana for technical assistance. This work was
supported by the Intramural Program of NIDDK, NIH and by the AIDS
Targeted Antiviral Program of the Office of the Director of the NIH (to
G.M.C.)
NR 20
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U1 3
U2 18
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1433-7851
EI 1521-3773
J9 ANGEW CHEM INT EDIT
JI Angew. Chem.-Int. Edit.
PD APR 27
PY 2015
VL 54
IS 18
BP 5336
EP 5339
DI 10.1002/anie.201500640
PG 4
WC Chemistry, Multidisciplinary
SC Chemistry
GA CH7BW
UT WOS:000354191600009
PM 25757985
ER
PT J
AU Yamada, KM
Hall, A
AF Yamada, Kenneth M.
Hall, Alan
TI Reproducibility and cell biology
SO JOURNAL OF CELL BIOLOGY
LA English
DT Editorial Material
AB Growing concerns about the reproducibility of published research threaten to undermine the scientific enterprise and erode public trust. Conscientious application of "best practices" for the generation and reporting of research, along with post-publication access to raw data and other research materials, will protect the integrity of the research literature.
C1 [Yamada, Kenneth M.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, NIH, Bethesda, MD 20892 USA.
[Hall, Alan] Mem Sloan Kettering Canc Ctr, Cell Biol Program, New York, NY 10065 USA.
RP Yamada, KM (reprint author), Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, NIH, Bethesda, MD 20892 USA.
EM kenneth.yamada@nih.gov; halla@mskcc.org
NR 14
TC 3
Z9 3
U1 1
U2 5
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD APR 27
PY 2015
VL 209
IS 2
BP 191
EP 193
DI 10.1083/jcb.201503036
PG 3
WC Cell Biology
SC Cell Biology
GA CH4OM
UT WOS:000354012800004
PM 25918221
ER
PT J
AU Madsen, DH
Bugge, TH
AF Madsen, Daniel H.
Bugge, Thomas H.
TI The source of matrix-degrading enzymes in human cancer: Problems of
research reproducibility and possible solutions
SO JOURNAL OF CELL BIOLOGY
LA English
DT Editorial Material
ID TUMOR-ASSOCIATED MACROPHAGES; EXTRACELLULAR-MATRIX; BREAST-CANCER;
DEGRADATION; PROGRESSION; STROMA; CELLS; METALLOPROTEINASES; ANTIBODIES;
UROKINASE
AB Matrix degradation is central to tumor pathogenesis. Enzymes that degrade extracellular matrix are abundant in tumors. But which out of the complex mixture of cells that form a tumor produces them? Surprisingly, several hundred studies devoted to this question have provided confusion rather than clarity. Our analysis of these studies identifies likely reasons as to why this may be the case, which has implications for the broader issue of research reproducibility.
C1 [Madsen, Daniel H.; Bugge, Thomas H.] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Bugge, TH (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
EM thomas.bugge@nih.gov
OI Madsen, Daniel Hargboel/0000-0002-3183-6201
FU Intramural NIH HHS
NR 32
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U1 0
U2 4
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD APR 27
PY 2015
VL 209
IS 2
BP 195
EP 198
DI 10.1083/jcb.201501034
PG 4
WC Cell Biology
SC Cell Biology
GA CH4OM
UT WOS:000354012800005
PM 25918222
ER
PT J
AU Zhu, BP
Zhang, ZQ
Ma, T
Yang, XF
Li, YX
Shung, KK
Zhou, QF
AF Zhu, Benpeng
Zhang, Zhiqiang
Ma, Teng
Yang, Xiaofei
Li, Yongxiang
Shung, K. Kirk
Zhou, Qifa
TI (100)-Textured KNN-based thick film with enhanced piezoelectric property
for intravascular ultrasound imaging
SO APPLIED PHYSICS LETTERS
LA English
DT Article
ID ELECTRICAL-PROPERTIES; TRANSDUCER
AB Using tape-casting technology, 35 mu m free-standing (100)-textured Li doped KNN (KNLN) thick film was prepared by employing NaNbO3 (NN) as template. It exhibited similar piezoelectric behavior to lead containing materials: a longitudinal piezoelectric coefficient (d(33)) of similar to 150 pm/V and an electromechanical coupling coefficient (k(t)) of 0.44. Based on this thick film, a 52 MHz side-looking miniature transducer with a bandwidth of 61.5% at -6 dB was built for Intravascular ultrasound (IVUS) imaging. In comparison with 40 MHz PMN-PT single crystal transducer, the rabbit aorta image had better resolution and higher noise-to-signal ratio, indicating that lead-free (100)-textured KNLN thick film may be suitable for IVUS (>50 MHz) imaging. (C) 2015 AIP Publishing LLC.
C1 [Zhu, Benpeng; Yang, Xiaofei] Huazhong Univ Sci & Technol, Sch Opt & Elect Informat, Wuhan 430074, Peoples R China.
[Zhang, Zhiqiang; Li, Yongxiang] Chinese Acad Sci, Key Lab Inorgan Funct Mat & Devices, Shanghai 200050, Peoples R China.
[Zhu, Benpeng; Ma, Teng; Shung, K. Kirk; Zhou, Qifa] Univ So Calif, Dept Biomed Engn, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
[Zhu, Benpeng] Chinese Acad Sci, State Key Lab Transducer Technol, Shanghai 200050, Peoples R China.
RP Zhu, BP (reprint author), Huazhong Univ Sci & Technol, Sch Opt & Elect Informat, Wuhan 430074, Peoples R China.
EM benpengzhu@hust.edu.cn; qifazhou@usc.edu
FU National Natural Science Foundation of China [61371016, 51172257];
CAS/SAFEA International Partnership Program for Creative Research Teams;
Science and Technology Project of Shenzhen [JCYJ20140419131733976]; NIH
[R01-EB12058, P41-EB002182]
FX This work was supported by National Natural Science Foundation of China
(Grant Nos. 61371016 and 51172257), the CAS/SAFEA International
Partnership Program for Creative Research Teams, and the Science and
Technology Project of Shenzhen (JCYJ20140419131733976), and it was also
partially supported by NIH Grant Nos. R01-EB12058 and P41-EB002182. We
thank Analytical and Testing Center of Huazhong University of Science &
Technology.
NR 20
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U1 5
U2 41
PU AMER INST PHYSICS
PI MELVILLE
PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA
SN 0003-6951
EI 1077-3118
J9 APPL PHYS LETT
JI Appl. Phys. Lett.
PD APR 27
PY 2015
VL 106
IS 17
AR 173504
DI 10.1063/1.4919387
PG 4
WC Physics, Applied
SC Physics
GA CH2ES
UT WOS:000353839100060
PM 25991874
ER
PT J
AU Gonzalez, P
Hildesheim, A
Herrero, R
Katki, H
Wacholder, S
Porras, C
Safaeian, M
Jimenez, S
Darragh, TM
Cortes, B
Befano, B
Schiffman, M
Carvajal, L
Palefsky, J
Schiller, J
Ocampo, R
Schussler, J
Lowy, D
Guillen, D
Stoler, MH
Quint, W
Morales, J
Avila, C
Rodriguez, AC
Kreimer, AR
AF Gonzalez, Paula
Hildesheim, Allan
Herrero, Rolando
Katki, Hormuzd
Wacholder, Sholom
Porras, Carolina
Safaeian, Mahboobeh
Jimenez, Silvia
Darragh, Teresa M.
Cortes, Bernal
Befano, Brian
Schiffman, Mark
Carvajal, Loreto
Palefsky, Joel
Schiller, John
Ocampo, Rebeca
Schussler, John
Lowy, Douglas
Guillen, Diego
Stoler, Mark H.
Quint, Wim
Morales, Jorge
Avila, Carlos
Rodriguez, Ana Cecilia
Kreimer, Aimee R.
CA Costa Rica HPV Vaccine Trial CVT
TI Rationale and design of a long term follow-up study of women who did and
did not receive HPV 16/18 vaccination in Guanacaste, Costa Rica
SO VACCINE
LA English
DT Article
DE Human papillomavirus; Vaccines; Methods; Long term follow-up
ID HPV-16/18 AS04-ADJUVANTED VACCINE; HUMAN-PAPILLOMAVIRUS VACCINATION;
BLIND PATRICIA TRIAL; OF-STUDY ANALYSIS; PARTICLE VACCINE; YOUNG-WOMEN;
RANDOMIZED-TRIAL; EFFICACY; INFECTION; IMMUNOGENICITY
AB The Costa Rica Vaccine Trial (CVT) was a randomized clinical trial conducted between 2004 and 2010, which randomized 7466 women aged 18 to 25 to receive the bivalent HPV-16/18 vaccine or control Hepatitis-A vaccine. Participants were followed for 4 years with cross-over vaccination at the study end. In 2010 the long term follow-up (LTFU) study was initiated to evaluate the 10-year impact of HPV-16/18 vaccination, determinants of the immune response, and HPV natural history in a vaccinated population. Herein, the rationale, design and methods of the LTFU study are described, which actively follows CVT participants in the HPV-arm 6 additional years at biennial intervals (3 additional study visits for 10 years of total follow-up), or more often if clinically indicated. According to the initial commitment, women in the Hepatitis-A arm were offered HPV vaccination at cross-over; they were followed 2 additional years and exited from the study. 92% of eligible CVT women accepted participation in LTFU. To provide underlying rates of HPV acquisition and cervical disease among unvaccinated women to compare with the HPV-arm during LTFU, a new unvaccinated control group (UCG) of women who are beyond the age generally recommended for routine vaccination was enrolled, and will be followed by cervical cancer screening over 6 years. To form the UCG, 5000 women were selected from a local census, of whom 2836 women (61% of eligible women) agreed to participate. Over 90% of participants complied with an interview, blood and cervical specimen collection. Evaluation of comparability between the original (Hepatitis-A arm of CVT) and new (UCG) control groups showed that women's characteristics, as well as their predicted future risk for cervical HPV acquisition, were similar, thus validating use of the UCG. LTFU is poised to comprehensively address many important questions related to long-term effects of prophylactic HPV vaccines. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Gonzalez, Paula; Porras, Carolina; Cortes, Bernal; Carvajal, Loreto; Ocampo, Rebeca; Guillen, Diego; Morales, Jorge; Avila, Carlos; Rodriguez, Ana Cecilia] Proyecto Epidemiol Guanacaste, Fdn INCIENSA, Liberia, Guanacaste, Costa Rica.
[Gonzalez, Paula; Herrero, Rolando; Jimenez, Silvia] Int Agcy Res Canc, F-69372 Lyon, France.
[Hildesheim, Allan; Katki, Hormuzd; Wacholder, Sholom; Safaeian, Mahboobeh; Schiffman, Mark; Kreimer, Aimee R.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Darragh, Teresa M.; Palefsky, Joel] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Befano, Brian; Schussler, John] Informat Management Serv Inc, Calverton, MD USA.
[Schiller, John; Lowy, Douglas] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Stoler, Mark H.] Univ Virginia, Dept Pathol, Charlottesville, VA 22903 USA.
[Quint, Wim] DDL Diagnost Lab, Rijswijk, Netherlands.
RP Gonzalez, P (reprint author), Proyecto Epidemiol Guanacaste, Fdn INCIENSA, Solarium 8 C, Liberia, Guanacaste, Costa Rica.
EM pgonzalez@proyectoguanacaste.org
RI Hildesheim, Allan/B-9760-2015; Kreimer, Aimee/H-1687-2015
OI Hildesheim, Allan/0000-0003-0257-2363;
FU NCI [N01-CP-11005]; National Institutes of Health Office of Research on
Women's Health
FX The Costa Rica HPV Vaccine Trial is a long-standing collaboration
between investigators in Costa Rica and the NCI. The trial is sponsored
and funded by the NCI (contract N01-CP-11005), with funding support from
the National Institutes of Health Office of Research on Women's Health.
GlaxoSmithKline Biologicals (GSK) provided vaccine and support for
aspects of the trial associated with regulatory submission needs of the
company under a Clinical Trials Agreement (FDA BB-IND 7920) during the
four-year, randomized blinded phase of our study. The NCI and Costa Rica
investigators are responsible for the design and conduct of the study;
collection, management, analysis, and interpretation of the data; and
preparation of the manuscript. On efficacy-related manuscripts, GSK has
the right to review and comment. Registered with Clinicaltrials.gov
NCT00128661
NR 35
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U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD APR 27
PY 2015
VL 33
IS 18
BP 2141
EP 2151
DI 10.1016/j.vaccine.2015.03.015
PG 11
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA CH0XQ
UT WOS:000353746100006
PM 25796338
ER
PT J
AU Rosati, M
Alicea, C
Kulkarni, V
Virnik, K
Hockenbury, M
Sardesai, NY
Pavlakis, GN
Valentin, A
Berkower, I
Felber, BK
AF Rosati, Margherita
Alicea, Candido
Kulkarni, Viraj
Virnik, Konstantin
Hockenbury, Max
Sardesai, Niranjan Y.
Pavlakis, George N.
Valentin, Antonio
Berkower, Ira
Felber, Barbara K.
TI Recombinant rubella vectors elicit SIV Gag-specific T cell responses
with cytotoxic potential in rhesus macaques
SO VACCINE
LA English
DT Article
DE Live attenuated viral vector; Rubella vaccine strain RA27/3; Rhesus
macaque; SIV Gag; De nova cellular responses; Recall cellular responses;
Memory T cells; Cytotoxic T cells; DNA vaccine; CM9 tetramer response;
IFN-gamma response; HIV vaccine; DNA prime rubella boost; Rubella prime
boost
ID IMMUNODEFICIENCY VIRUS CHALLENGE; HUMORAL IMMUNE-RESPONSES;
MEASLES-VACCINE VECTOR; NEUTRALIZING ANTIBODIES; ANKARA RECOMBINANTS;
SIVMAC251 CHALLENGE; VIRAL VECTORS; HIV; DNA; ANTIGENS
AB Live-attenuated rubella vaccine strain RA27/3 has been demonstrated to be safe and immunogenic in millions of children. The vaccine strain was used to insert SIV gag sequences and the resulting rubella vectors were tested in rhesus macaques alone and together with SIV gag DNA in different vaccine prime-boost combinations. We previously reported that such rubella vectors induce robust and durable SIV-specific humoral immune responses in macaques. Here, we report that recombinant rubella vectors elicit robust de novo SIV-specific cellular immune responses detectable for >10 months even after a single vaccination. The antigen-specific responses induced by the rubella vector include central and effector memory CD4(+) and CD8(+) T cells with cytotoxic potential. Rubella vectors can be administered repeatedly even after vaccination with the rubella vaccine strain RA27/3. Vaccine regimens including rubella vector and Sly gag DNA in different prime-boost combinations resulted in robust long-lasting cellular responses with significant increase of cellular responses upon boost. Rubella vectors provide a potent platform for inducing HIV-specific immunity that can be combined with DNA in a prime-boost regimen to elicit durable cellular immunity. Published by Elsevier Ltd.
C1 [Rosati, Margherita; Pavlakis, George N.; Valentin, Antonio] NCI, Human Retrovirus Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21702 USA.
[Alicea, Candido; Kulkarni, Viraj; Felber, Barbara K.] NCI, Human Retrovirus Pathogenesis Sect, Vaccine Branch, Ctr Canc Res, Frederick, MD 21702 USA.
[Virnik, Konstantin; Hockenbury, Max; Berkower, Ira] US FDA, Immunoregulat Lab, Div Viral Prod, Off Vaccines,Ctr Biol, Silver Spring, MD USA.
[Sardesai, Niranjan Y.] Inovio Pharmaceut, Plymouth Meeting, PA USA.
RP Berkower, I (reprint author), NCI, Ctr Canc Res, 1050 Boyles St,Bldg 535,Room 209, Frederick, MD 21702 USA.
EM ira.berkower@fda.hhs.gov; barbara.felber@nih.gov
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health (NCI/NIH)
FX This work was supported in part by the Intramural Research Program of
the National Cancer Institute, National Institutes of Health (NCI/NIH)
(BKF, GNP).
NR 49
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U1 1
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD APR 27
PY 2015
VL 33
IS 18
BP 2167
EP 2174
DI 10.1016/j.vaccine.2015.02.067
PG 8
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA CH0XQ
UT WOS:000353746100009
PM 25802183
ER
PT J
AU Blein, S
Bardel, C
Danjean, V
McGuffog, L
Healey, S
Barrowdale, D
Lee, A
Dennis, J
Kuchenbaecker, KB
Soucy, P
Terry, MB
Chung, WK
Goldgar, DE
Buys, SS
Janavicius, R
Tihomirova, L
Tung, N
Dorfling, CM
van Rensburg, EJ
Neuhausen, SL
Ding, YC
Gerdes, AM
Ejlertsen, B
Nielsen, FC
Hansen, TVO
Osorio, A
Benitez, J
Conejero, RA
Segota, E
Weitzel, JN
Thelander, M
Peterlongo, P
Radice, P
Pensotti, V
Dolcetti, R
Bonanni, B
Peissel, B
Zaffaroni, D
Scuvera, G
Manoukian, S
Varesco, L
Capone, GL
Papi, L
Ottini, L
Yannoukakos, D
Konstantopoulou, I
Garber, J
Hamann, U
Donaldson, A
Brady, A
Brewer, C
Foo, C
Evans, DG
Frost, D
Eccles, D
Douglas, F
Cook, J
Adlard, J
Barwell, J
Walker, L
Izatt, L
Side, LE
Kennedy, MJ
Tischkowitz, M
Rogers, MT
Porteous, ME
Morrison, PJ
Platte, R
Eeles, R
Davidson, R
Hodgson, S
Cole, T
Godwin, AK
Isaacs, C
Claes, K
De Leeneer, K
Meindl, A
Gehrig, A
Wappenschmidt, B
Sutter, C
Engel, C
Niederacher, D
Steinemann, D
Plendl, H
Kast, K
Rhiem, K
Ditsch, N
Arnold, N
Varon-Mateeva, R
Schmutzler, RK
Preisler-Adams, S
Markov, NB
Wang-Gohrke, S
de Pauw, A
Lefol, C
Lasset, C
Leroux, D
Rouleau, E
Damiola, F
Dreyfus, H
Barjhoux, L
Golmard, L
Uhrhammer, N
Bonadona, V
Sornin, V
Bignon, YJ
Carter, J
Van Le, L
Piedmonte, M
DiSilvestro, PA
de la Hoya, M
Caldes, T
Nevanlinna, H
Aittomaki, K
Jager, A
van den Ouweland, AMW
Kets, CM
Aalfs, CM
van Leeuwen, FE
Hogervorst, FBL
Meijers-Heijboer, HEJ
Oosterwijk, JC
van Roozendaal, KEP
Rookus, MA
Devilee, P
van der Luijt, RB
Olah, E
Diez, O
Teule, A
Lazaro, C
Blanco, I
Del Valle, J
Jakubowska, A
Sukiennicki, G
Gronwald, J
Lubinski, J
Durda, K
Jaworska-Bieniek, K
Agnarsson, BA
Maugard, C
Amadori, A
Montagna, M
Teixeira, MR
Spurdle, AB
Foulkes, W
Olswold, C
Lindor, NM
Pankratz, VS
Szabo, CI
Lincoln, A
Jacobs, L
Corines, M
Robson, M
Vijai, J
Berger, A
Fink-Retter, A
Singer, CF
Rappaport, C
Kaulich, DG
Pfeiler, G
Tea, MK
Greene, MH
Mai, PL
Rennert, G
Imyanitov, EN
Mulligan, AM
Glendon, G
Andrulis, IL
Tchatchou, S
Toland, AE
Pedersen, IS
Thomassen, M
Kruse, TA
Jensen, UB
Caligo, MA
Friedman, E
Zidan, J
Laitman, Y
Lindblom, A
Melin, B
Arver, B
Loman, N
Rosenquist, R
Olopade, OI
Nussbaum, RL
Ramus, SJ
Nathanson, KL
Domchek, SM
Rebbeck, TR
Arun, BK
Mitchell, G
Karlan, BY
Lester, J
Orsulic, S
Stoppa-Lyonnet, D
Thomas, G
Simard, J
Couch, FJ
Offit, K
Easton, DF
Chenevix-Trench, G
Antoniou, AC
Mazoyer, S
Phelan, CM
Sinilnikova, OM
Cox, DG
AF Blein, Sophie
Bardel, Claire
Danjean, Vincent
McGuffog, Lesley
Healey, Sue
Barrowdale, Daniel
Lee, Andrew
Dennis, Joe
Kuchenbaecker, Karoline B.
Soucy, Penny
Terry, Mary Beth
Chung, Wendy K.
Goldgar, David E.
Buys, Saundra S.
Janavicius, Ramunas
Tihomirova, Laima
Tung, Nadine
Dorfling, Cecilia M.
van Rensburg, Elizabeth J.
Neuhausen, Susan L.
Ding, Yuan Chun
Gerdes, Anne-Marie
Ejlertsen, Bent
Nielsen, Finn C.
Hansen, Thomas V. O.
Osorio, Ana
Benitez, Javier
Andres Conejero, Raquel
Segota, Ena
Weitzel, Jeffrey N.
Thelander, Margo
Peterlongo, Paolo
Radice, Paolo
Pensotti, Valeria
Dolcetti, Riccardo
Bonanni, Bernardo
Peissel, Bernard
Zaffaroni, Daniela
Scuvera, Giulietta
Manoukian, Siranoush
Varesco, Liliana
Capone, Gabriele L.
Papi, Laura
Ottini, Laura
Yannoukakos, Drakoulis
Konstantopoulou, Irene
Garber, Judy
Hamann, Ute
Donaldson, Alan
Brady, Angela
Brewer, Carole
Foo, Claire
Evans, D. Gareth
Frost, Debra
Eccles, Diana
Douglas, Fiona
Cook, Jackie
Adlard, Julian
Barwell, Julian
Walker, Lisa
Izatt, Louise
Side, Lucy E.
Kennedy, M. John
Tischkowitz, Marc
Rogers, Mark T.
Porteous, Mary E.
Morrison, Patrick J.
Platte, Radka
Eeles, Ros
Davidson, Rosemarie
Hodgson, Shirley
Cole, Trevor
Godwin, Andrew K.
Isaacs, Claudine
Claes, Kathleen
De Leeneer, Kim
Meindl, Alfons
Gehrig, Andrea
Wappenschmidt, Barbara
Sutter, Christian
Engel, Christoph
Niederacher, Dieter
Steinemann, Doris
Plendl, Hansjoerg
Kast, Karin
Rhiem, Kerstin
Ditsch, Nina
Arnold, Norbert
Varon-Mateeva, Raymonda
Schmutzler, Rita K.
Preisler-Adams, Sabine
Markov, Nadja Bogdanova
Wang-Gohrke, Shan
de Pauw, Antoine
Lefol, Cedrick
Lasset, Christine
Leroux, Dominique
Rouleau, Etienne
Damiola, Francesca
Dreyfus, Helene
Barjhoux, Laure
Golmard, Lisa
Uhrhammer, Nancy
Bonadona, Valerie
Sornin, Valerie
Bignon, Yves-Jean
Carter, Jonathan
Van Le, Linda
Piedmonte, Marion
DiSilvestro, Paul A.
de la Hoya, Miguel
Caldes, Trinidad
Nevanlinna, Heli
Aittomaki, Kristiina
Jager, Agnes
van den Ouweland, Ans M. W.
Kets, Carolien M.
Aalfs, Cora M.
van Leeuwen, Flora E.
Hogervorst, Frans B. L.
Meijers-Heijboer, Hanne E. J.
Oosterwijk, Jan C.
van Roozendaal, Kees E. P.
Rookus, Matti A.
Devilee, Peter
van der Luijt, Rob B.
Olah, Edith
Diez, Orland
Teule, Alex
Lazaro, Conxi
Blanco, Ignacio
Del Valle, Jesus
Jakubowska, Anna
Sukiennicki, Grzegorz
Gronwald, Jacek
Lubinski, Jan
Durda, Katarzyna
Jaworska-Bieniek, Katarzyna
Agnarsson, Bjarni A.
Maugard, Christine
Amadori, Alberto
Montagna, Marco
Teixeira, Manuel R.
Spurdle, Amanda B.
Foulkes, William
Olswold, Curtis
Lindor, Noralane M.
Pankratz, Vernon S.
Szabo, Csilla I.
Lincoln, Anne
Jacobs, Lauren
Corines, Marina
Robson, Mark
Vijai, Joseph
Berger, Andreas
Fink-Retter, Anneliese
Singer, Christian F.
Rappaport, Christine
Kaulich, Daphne Geschwantler
Pfeiler, Georg
Tea, Muy-Kheng
Greene, Mark H.
Mai, Phuong L.
Rennert, Gad
Imyanitov, Evgeny N.
Mulligan, Anna Marie
Glendon, Gord
Andrulis, Irene L.
Tchatchou, Sandrine
Toland, Amanda Ewart
Pedersen, Inge Sokilde
Thomassen, Mads
Kruse, Torben A.
Jensen, Uffe Birk
Caligo, Maria A.
Friedman, Eitan
Zidan, Jamal
Laitman, Yael
Lindblom, Annika
Melin, Beatrice
Arver, Brita
Loman, Niklas
Rosenquist, Richard
Olopade, Olufunmilayo I.
Nussbaum, Robert L.
Ramus, Susan J.
Nathanson, Katherine L.
Domchek, Susan M.
Rebbeck, Timothy R.
Arun, Banu K.
Mitchell, Gillian
Karlan, Beth Y.
Lester, Jenny
Orsulic, Sandra
Stoppa-Lyonnet, Dominique
Thomas, Gilles
Simard, Jacques
Couch, Fergus J.
Offit, Kenneth
Easton, Douglas F.
Chenevix-Trench, Georgia
Antoniou, Antonis C.
Mazoyer, Sylvie
Phelan, Catherine M.
Sinilnikova, Olga M.
Cox, David G.
CA Breast Canc Family Registry
EMBRACE
GEMO Study Collaborators
HEBON
TI An original phylogenetic approach identified mitochondrial haplogroup
T1a1 as inversely associated with breast cancer risk in BRCA2 mutation
carriers
SO BREAST CANCER RESEARCH
LA English
DT Article
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; GENETIC MODIFIERS; OXIDATIVE STRESS;
DNA HAPLOGROUPS; SUSCEPTIBILITY; OVARIAN; CONSORTIUM; VARIANTS;
MULTIPLE; DISEASES
AB Introduction: Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers.
Methods: We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals.
Results: We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk.
Conclusions: This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects.
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RP Cox, DG (reprint author), Univ Lyon 1, Ctr Rech Cancerol Lyon, CNRS, INSERM U1052,UMR5286, F-69365 Lyon, France.
EM david.cox@lyon.unicancer.fr
RI del Valle, Jesus/I-2527-2015; montagna, marco/E-2225-2012; Jansen van
Rensburg, Elizabeth (Lizette)/B-9104-2011; Dolcetti,
Riccardo/O-3832-2015; Teixeira, Manuel/E-4885-2011; Andrulis,
Irene/E-7267-2013; Cox, David/A-2023-2009; Gronwald, Jacek/A-4576-2017;
manoukian, siranoush/E-7132-2017; Peissel, Bernard/E-8187-2017;
OI Evans, Gareth/0000-0002-8482-5784; Blanco, Ignacio/0000-0002-7414-7481;
Ramus, Susan/0000-0003-0005-7798; Barrowdale,
Daniel/0000-0003-1661-3939; del Valle, Jesus/0000-0003-3607-7045; Papi,
Laura/0000-0003-4552-9517; Joseph, Vijai/0000-0002-7933-151X; Tommasi,
Stefania/0000-0002-2157-2978; Yannoukakos,
Drakoulis/0000-0001-7509-3510; VENAT-BOUVET,
Laurence/0000-0002-0716-2550; montagna, marco/0000-0002-4929-2150;
Dolcetti, Riccardo/0000-0003-1625-9853; Teixeira,
Manuel/0000-0002-4896-5982; Cox, David/0000-0002-2152-9259; Gronwald,
Jacek/0000-0002-3643-2871; manoukian, siranoush/0000-0002-6034-7562;
Peissel, Bernard/0000-0001-9233-3571; Robson, Mark/0000-0002-3109-1692;
benitez, javier/0000-0002-0923-7202; Eeles, Rosalind/0000-0002-3698-6241
FU European Commission Seventh Framework Program [223175:
HEALTH-F2-2009-223175]; Cancer Research UK [C12292/A11174, C1287/A10118,
C1287/A11990, C5047/A8385]; National Health and Medical Research Council
(NHMRC) program; National Health and Medical Research Council (NHMRC);
American Cancer Society Early Detection Professorship
[SIOP-06-258-01-COUN]; Intramural Research Program of the National
Cancer Institute, National Institutes of Health; National Cancer
Institute, National Institutes of Health [UM1 CA164920]; Lithuania
(BFBOCC-LT): Research Council of Lithuania [LIG-07/2012]; LSC
[10.0010.08]; European Social Fund
[2009/0220/1DP/1.1.1.2.0/09/APIA/VIAA/016]; Liepaja City Council,
Liepaja, Latvia; Breast Cancer Research Foundation; Cancer Association
of South Africa (CANSA); Morris and Horowitz Families Professorship in
Cancer Etiology and Outcomes Research; NEYE Foundation; Spanish
Association against Cancer (Asociacion Espanola Contra el Cancer)
[AECC08]; Thematic Network Cooperative Research in Cancer (Red Tematica
Investigacion Cooperativa en Cancer (RTICC), Centro de Investigacion
Cancer, Salamanca, Spain) [RTICC 06/0020/1060]; Spanish Ministry of
Science and Innovation [FIS PI08 1120]; Fondo de Investigacion Sanitaria
(FIS) [SAF2010-20493]; Fundacion Mutua Madrilena (FMMA); City of Hope
Clinical Cancer Genetics Community Network and the Hereditary Cancer
Research Registry (COH-CCGCRN); National Cancer Institute and the Office
of the Director, National Institutes of Health [RC4CA153828]; Italian
citizens; Fondazione IRCCS Istituto Nazionale Tumori; Italian
Association for Cancer Research (AIRC); European Union (European Social
Fund (ESF); Greek national funds through the "Education and Lifelong
Learning" operational program of the National Strategic Reference
Framework (NSRF) - Research Funding Program of the General Secretariat
for Research and Technology: ARISTEIA; "Heracleitus II: Investing in
knowledge society through the European Social Fund"; Deutsches
Krebsforschungszentrum (DKFZ); National Institute for Health Research
(NIHR) grant to the Biomedical Research Centre, Manchester, UK; NIHR
grant to the Biomedical Research Centre at The Institute of Cancer
Research and The Royal Marsden NHS Foundation Trust, London; University
of Kansas Cancer Center [P30 CA168524]; Kansas Bioscience Authority
Eminent Scholar Program; Chancellors Distinguished Chair in Biomedical
Sciences Professorship; German Cancer Aid [109076]; Center for Molecular
Medicine Cologne (CMMC); Ligue National Contre le Cancer; Association
"Le cancer du sein, parlons-en!" Award; Canadian Institutes of Health
Research for the CIHR Team in Familial Risks of Breast Cancer program;
GOA [BOF10/GOA/019]; Ghent University Hospital; National Cancer
Institute grants to the GOG Administrative Office and Tissue Bank [CA
27469]; GOG Statistical and Data Center [CA 37517]; GOG's Cancer
Prevention and Control Committee [CA 101165]; Instituto de Salud Carlos
III (ISCIII), Madrid, Spain [RD12/00369/0006, 12/00539]; European
Regional Development Fund (Fonds europeen de developpement regional
(FEDER)) funds; Helsinki University Central Hospital Research Fund;
Academy of Finland [266528]; Finnish Cancer Society; Sigrid Juselius
Foundation; Dutch Cancer Society [NKI1998-1854, NKI2004-3088,
NKI2007-3756]; Netherlands Organization of Scientific Research [NWO
91109024]; Pink Ribbon grant [110005]; Biobanking and Molecular Resource
Infrastructure (BBMRI) [NWO 184.021.007/CP46]; Hungarian Research and
Technological Innovation Fund (KTIA)/Hungarian Scientific Research Fund
(Orszagos Tudomanyos Kutatasi Alapprogramok (OTKA)) [KTIA-OTKA CK-80745,
KTIA-OTKA K-112228]; Institut Catala d'Oncologia (ICO): contract grant
sponsor: Asociacion Espanola Contra el Cancer; Spanish Health Research
Foundation; Ramon Areces Foundation; Instituto de Salud Carlos III
(ISCIII); Catalan Health Institute; Autonomous Government of Catalonia;
International Hereditary Cancer Center (Department of Genetics and
Pathology, Pomeranian Medical University, Szczecin, Poland)
[PBZ_KBN_122/P05/2004]; Icelandic Association "Walking for Breast Cancer
Research"; Landspitali University Hospital Research Fund; Canadian
Institutes of Health Research (CIHR) for the "CIHR Team in Familial
Risks of Breast Cancer" program, Canadian Breast Cancer Research
Alliance [019511]; Ministry of Economic Development, Innovation and
Export Trade [PSR-SIIRI-701]; Ministero della Salute and a "5 x 1,000"
Istituto Oncologico Veneto grant; Liga Portuguesa Contra o Cancro;
National Breast Cancer Foundation; Queensland Cancer Fund; Cancer
Councils of New South Wales, Victoria, Tasmania and South Australia;
Cancer Foundation of Western Australia; National Institutes of Health
(NIH) through the National Cancer Institute (NCI) [CA 116167, CA 128978,
CA 176785]; NCI Specialized Program of Research Excellence (SPORE) in
Breast Cancer [CA116201]; US Department of Defense Ovarian Cancer Idea
award [W81XWH-10-1-0341]; Ministry of Health of the Czech Republic to
Masaryk Memorial Cancer Institute [MMCI 00209805]; European Regional
Development Fund; State Budget of the Czech Republic (RECAMO) [CZ.
1.05/2.1.00/03.0101]; Charles University in Prague project [UNCE204024];
Robert and Kate Niehaus Clinical Cancer Genetics Initiative; Intramural
Research Program of the National Cancer Institute; Westat, Inc,
Rockville, MD, USA [N02-CP-11019-50, N02-CP-65504]; Clalit Health
Services in Israel; Israel Cancer Association; Breast Cancer Research
Foundation (BCRF), New York, NY, USA; Russian Federation for Basic
Research [11-04-00227, 12-04-00928, 12-04-01490]; Federal Agency for
Science and Innovations, Russia [02.740.11.0780]; Ohio State University
Comprehensive Cancer Center; Istituto Toscano Tumori (ITT); Israeli
Inherited Breast Cancer Consortium; Swedish Breast Cancer; Swedish
Cancer Society; Ralph and Marion Falk Medical Research Trust;
Entertainment Industry Fund National Women's Cancer Research Alliance;
University of California, Los Angeles Jonsson Comprehensive Cancer
Center Foundation: Breast Cancer Research Foundation; University of
California, San Francisco Cancer Risk Program and Helen Diller Family
Comprehensive Cancer Center; Cancer Research UK; University of
Pennsylvania: National Institutes of Health (NIH) [R01 CA102776, R01
CA083855]; Susan G Komen for the Cure, Basser Center for BRCA; Victorian
Familial Cancer Trials Group (VFCTG): Victorian Cancer Agency, Cancer
Australia, National Breast Cancer Foundation; [5U01 CA113916]; [R01
CA140323]; [ISCIIIRETIC RD06/0020/1051]; [PI09/02483]; [PI10/01422];
[PI10/00748]; [PI13/00285]; [PI13/00189 2009SGR290]; [PI13/00189
2009SGR283]; [CA125183]; [R01 CA142996]; [1U01CA161032]
FX Higher-level funding: The COGS project is funded through a European
Commission Seventh Framework Program grant (agreement number 223175:
HEALTH-F2-2009-223175). The CIMBA data management and data analysis were
supported by Cancer Research UK grants C12292/A11174 and C1287/A10118.
SH is supported by a National Health and Medical Research Council
(NHMRC) program grant (to GCT).; Individual researcher support: ACA is a
Cancer Research UK Senior Cancer Research Fellow (C12292/A11174). DFE is
a Principal Research Fellow of Cancer Research UK. GC, MCS and IC are
supported by the National Health and Medical Research Council (NHMRC).
BK holds an American Cancer Society Early Detection Professorship
(SIOP-06-258-01-COUN). MHG and PLM were supported by funding from the
Intramural Research Program of the National Cancer Institute, National
Institutes of Health. OIO is an American Cancer Society Clinical
Research Professor. JS is Chairholder of the Canada Research Chair in
Oncogenetics.; Funding of constituent studies: The Breast Cancer Family
Registry (BCFR) was supported by grant UM1 CA164920 from the National
Cancer Institute, National Institutes of Health. The content of this
article does not necessarily reflect the views or policies of the
National Cancer Institute or any of the collaborating centers in the
BCFR, nor does mention of trade names, commercial products or
organizations imply endorsement by the US Government or the BCFR. The
Baltic Familial Breast Ovarian Cancer Consortium (BFBOCC) is partly
supported by Lithuania (BFBOCC-LT): Research Council of Lithuania grant
LIG-07/2012; BFBOCC-LV (Latvia) is partly supported by LSC grant
10.0010.08 and in part by a grant from the European Social Fund number
2009/0220/1DP/1.1.1.2.0/09/APIA/VIAA/016 and the Liepaja City Council,
Liepaja, Latvia; Beth Israel Deaconess Medical Center Cancer Center is
supported by the Breast Cancer Research Foundation; BRCA-gene mutations
and breast cancer in South African women (BMBSA) was supported by grants
from the Cancer Association of South Africa (CANSA) to Elizabeth J van
Rensburg; SLN (Beckman Research Institute, City of Hope, Duarte, CA,
USA) was partially supported by the Morris and Horowitz Families
Professorship in Cancer Etiology and Outcomes Research; the Copenhagen
Breast Cancer Study (CBCS) was supported by the NEYE Foundation; the
Spanish National Cancer Research Center (Centro Nacional de
Investigaciones Oncologicas (CNIO)) was partially supported by the
Spanish Association against Cancer (Asociacion Espanola Contra el Cancer
AECC08), Thematic Network Cooperative Research in Cancer (Red Tematica
Investigacion Cooperativa en Cancer (RTICC), Centro de Investigacion
Cancer, Salamanca, Spain) RTICC 06/0020/1060, Spanish Ministry of
Science and Innovation grants FIS PI08 1120 (Fondo de Investigacion
Sanitaria (FIS)) and SAF2010-20493, and the Fundacion Mutua Madrilena
(FMMA); the City of Hope Clinical Cancer Genetics Community Network and
the Hereditary Cancer Research Registry (COH-CCGCRN), supported in part
by award number RC4CA153828 (Principal Investigator: JNW) from the
National Cancer Institute and the Office of the Director, National
Institutes of Health. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institutes of Health.; CONsorzio Studi ITaliani sui Tumori
Ereditari Alla Mammella, Italy (CONSIT Team): Funds from Italian
citizens who allocated the "5 x 1,000" share of their tax payment in
support of the Fondazione IRCCS Istituto Nazionale Tumori, according to
Italian laws (Istituto Nazionale dei Tumori (INT) institutional
strategic project "5 x 1,000") (to SM); the Italian Association for
Cancer Research (AIRC) (to LO); National Centre for Scientific Research
"Demokritos" has been cofinanced by the European Union (European Social
Fund (ESF)) and Greek national funds through the "Education and Lifelong
Learning" operational program of the National Strategic Reference
Framework (NSRF) - Research Funding Program of the General Secretariat
for Research and Technology: ARISTEIA; "Heracleitus II: Investing in
knowledge society through the European Social Fund"; the DKFZ study was
supported by the Deutsches Krebsforschungszentrum (DKFZ);
Epidemiological Study of BRCA1 and BRCA2 Mutation Carriers (EMBRACE) is
supported by Cancer Research UK grants C1287/A10118 and C1287/A11990;
DGE and FL are supported by a National Institute for Health Research
(NIHR) grant to the Biomedical Research Centre, Manchester, UK; the
investigators at The Institute of Cancer Research and The Royal Marsden
NHS Foundation Trust are supported by an NIHR grant to the Biomedical
Research Centre at The Institute of Cancer Research and The Royal
Marsden NHS Foundation Trust, London; RE and EB are supported by Cancer
Research UK grant C5047/A8385; Kansas University Medical Center: The
authors acknowledge support from The University of Kansas Cancer Center
(P30 CA168524) and the Kansas Bioscience Authority Eminent Scholar
Program; AKG was funded by grants 5U01 CA113916 and R01 CA140323 and by
the Chancellors Distinguished Chair in Biomedical Sciences
Professorship; The German Consortium of Hereditary Breast and Ovarian
Cancer (GC-HBOC) is supported by German Cancer Aid (grant 109076 (to
RKS) and by the Center for Molecular Medicine Cologne (CMMC); GC-HBOC is
deeply grateful to Dr Sabine Preisler-Adam for providing information and
samples; the GEMO Study was supported by the Ligue National Contre le
Cancer; the Association "Le cancer du sein, parlons-en!" Award; and the
Canadian Institutes of Health Research for the CIHR Team in Familial
Risks of Breast Cancer program; G-FAST: KDL is supported by GOA grant
BOF10/GOA/019 (Ghent University) and spearhead financing of Ghent
University Hospital; the Gynecologic Oncology Group (GOG) was supported
by National Cancer Institute grants to the GOG Administrative Office and
Tissue Bank (grant CA 27469), the GOG Statistical and Data Center (grant
CA 37517) and GOG's Cancer Prevention and Control Committee (grant CA
101165); HCSC was supported by grants RD12/00369/0006 and 12/00539 from
Instituto de Salud Carlos III (ISCIII), Madrid, Spain, partially
supported by European Regional Development Fund (Fonds europeen de
developpement regional (FEDER)) funds; the Helsinki Breast Cancer Study
(HEBCS) was financially supported by the Helsinki University Central
Hospital Research Fund, Academy of Finland (266528), the Finnish Cancer
Society and the Sigrid Juselius Foundation; HEBON is supported by the
Dutch Cancer Society grants NKI1998-1854, NKI2004-3088 and NKI2007-3756,
the Netherlands Organization of Scientific Research grant NWO 91109024,
the Pink Ribbon grant 110005 and Biobanking and Molecular Resource
Infrastructure (BBMRI) grant NWO 184.021.; 007/CP46; HEBON thanks the
registration teams of the Comprehensive Cancer Centre Netherlands and
Comprehensive Centre South (together the Netherlands Cancer Registry)
and PALGA (Dutch Pathology Registry) for part of the data collection;
the High Risk Breast Cancer Program (HRBCP) is supported by the Hong
Kong Hereditary Breast Cancer Family Registry and the Dr Ellen Li
Charitable Foundation, Hong Kong; the Hungarian Breast and Ovarian
Cancer Study (HUNBOCS) was supported by Hungarian Research and
Technological Innovation Fund (KTIA)/Hungarian Scientific Research Fund
(Orszagos Tudomanyos Kutatasi Alapprogramok (OTKA)) research grants
KTIA-OTKA CK-80745 and KTIA-OTKA K-112228; Institut Catala d'Oncologia
(ICO): contract grant sponsor: Asociacion Espanola Contra el Cancer;
Spanish Health Research Foundation; Ramon Areces Foundation; Instituto
de Salud Carlos III (ISCIII); Catalan Health Institute; and Autonomous
Government of Catalonia; contract grant numbers ISCIIIRETIC
RD06/0020/1051, PI09/02483, PI10/01422, PI10/00748, PI13/00285,
PI13/00189 2009SGR290 and PI13/00189 2009SGR283; the International
Hereditary Cancer Center (Department of Genetics and Pathology,
Pomeranian Medical University, Szczecin, Poland) was supported by grant
PBZ_KBN_122/P05/2004; Landspitali - The National University Hospital of
Iceland was supported by the Icelandic Association "Walking for Breast
Cancer Research" and by the Landspitali University Hospital Research
Fund; the Interdisciplinary Health Research Internal Team Breast Cancer
Susceptibility Study (INHERIT) was supported by the Canadian Institutes
of Health Research (CIHR) for the "CIHR Team in Familial Risks of Breast
Cancer" program, Canadian Breast Cancer Research Alliance grant 019511
and Ministry of Economic Development, Innovation and Export Trade grant
PSR-SIIRI-701; the Istituto Oncologico Veneto Hereditary Breast and
Ovarian Cancer Study (IOVHBOCS) is supported by the Ministero della
Salute and a "5 x 1,000" Istituto Oncologico Veneto grant; the
Portuguese Oncology Institute-Porto Breast Cancer Study (IPOBCS) was
supported in part by Liga Portuguesa Contra o Cancro; kConFab is
supported by a grant from the National Breast Cancer Foundation and
previously by the National Health and Medical Research Council (NHMRC),
the Queensland Cancer Fund, the Cancer Councils of New South Wales,
Victoria, Tasmania and South Australia, and the Cancer Foundation of
Western Australia; the Mayo Clinic is supported by National Institutes
of Health (NIH) grants CA 116167, CA 128978 and CA 176785 through the
National Cancer Institute (NCI), an NCI Specialized Program of Research
Excellence (SPORE) in Breast Cancer (CA116201), a US Department of
Defense Ovarian Cancer Idea award (W81XWH-10-1-0341), a grant from the
Breast Cancer Research Foundation, a generous gift from the David F and
Margaret T Grohne Family Foundation and the Ting Tsung and Wei Fong Chao
Foundation; McGill University Jewish General Hospital Weekend to End
Breast Cancer, Quebec Ministry of Economic Development, Innovation and
Export Trade; Modifier Study of Quantitative Effects on Disease
(ModSQuaD) was supported by the Ministry of Health of the Czech Republic
to Masaryk Memorial Cancer Institute (MH CZ - DRO) (MMCI 00209805) and
by the European Regional Development Fund and the State Budget of the
Czech Republic (RECAMO, CZ. 1.05/2.1.00/03.; 0101) (to LF), and by
Charles University in Prague project UNCE204024 (MZ); Memorial Sloan
Kettering Cancer Center (MSKCC) is supported by grants from the Breast
Cancer Research Foundation and Robert and Kate Niehaus Clinical Cancer
Genetics Initiative; National Cancer Institute, National Institutes of
Health: The research of MHG and PLM was supported by the Intramural
Research Program of the National Cancer Institute and by support
services contracts N02-CP-11019-50 and N02-CP-65504 with Westat, Inc,
Rockville, MD, USA; the National Israeli Cancer Control Center (NICCC)
is supported by Clalit Health Services in Israel; some of its activities
are supported by the Israel Cancer Association and the Breast Cancer
Research Foundation (BCRF), New York, NY, USA; NN Petrov Institute of
Oncology has been supported by the Russian Federation for Basic Research
(grants 11-04-00227, 12-04-00928 and 12-04-01490) and the Federal Agency
for Science and Innovations, Russia (contract 02.740.11.0780); The Ohio
State University Clinical Cancer Genetics (OSUCCG) is supported by The
Ohio State University Comprehensive Cancer Center; the Pisa Breast
Cancer Study (PBCS) was supported by Istituto Toscano Tumori (ITT)
grants 2011-2013; Sheba Medical Center was partially funded through a
grant from the Israel Cancer Association and funding for the Israeli
Inherited Breast Cancer Consortium; the Swedish Breast Cancer Study
collaborators are supported by the Swedish Cancer Society; The
University of Chicago is supported by NCI Specialized Program of
Research Excellence (SPORE) in Breast Cancer (CA125183), R01 CA142996
and 1U01CA161032 and by the Ralph and Marion Falk Medical Research
Trust, the Entertainment Industry Fund National Women's Cancer Research
Alliance and the Breast Cancer Research Foundation; University of
California, Los Angeles Jonsson Comprehensive Cancer Center Foundation:
Breast Cancer Research Foundation; University of California, San
Francisco Cancer Risk Program and Helen Diller Family Comprehensive
Cancer Center; UK Familial Ovarian Cancer Registry (UKFOCR) was
supported by a project grant from Cancer Research UK (to Paul DP
Pharoah); the University of Pennsylvania: National Institutes of Health
(NIH) grants R01 CA102776 and R01 CA083855; the Breast Cancer Research
Foundation; the Susan G Komen for the Cure, Basser Center for BRCA;
Victorian Familial Cancer Trials Group (VFCTG): Victorian Cancer Agency,
Cancer Australia, National Breast Cancer Foundation; The Women's Cancer
Program (WCP) at the Samuel Oschin Comprehensive Cancer Institute,
Cedars-Sinai Medical Center, is funded by the American Cancer Society
Early Detection Professorship (SIOP-06-258-01-COUN).
NR 54
TC 3
Z9 3
U1 7
U2 33
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1465-542X
EI 1465-5411
J9 BREAST CANCER RES
JI Breast Cancer Res.
PD APR 25
PY 2015
VL 17
AR 61
DI 10.1186/s13058-015-0567-2
PG 15
WC Oncology
SC Oncology
GA CL2KV
UT WOS:000356773600001
PM 25925750
ER
PT J
AU Guo, B
Fang, ZZ
Yang, L
Xiao, L
Xia, YL
Gonzalez, FJ
Zhu, LL
Cao, YF
Ge, GB
Yang, L
Sun, HZ
AF Guo, Bin
Fang, Zhongze
Yang, Lu
Xiao, Ling
Xia, Yangliu
Gonzalez, Frank J.
Zhu, Liangliang
Cao, Yunfeng
Ge, Guangbo
Yang, Ling
Sun, Hongzhi
TI Tissue and species differences in the glucuronidation of glabridin with
UDP-glucuronosyltransferases
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Article
DE Glabridin; Glucuronidation; UDP-glucuronosyltransferases; Species
differences
ID TANDEM MASS-SPECTROMETRY; MESSENGER-RNA EXPRESSION; ISOFLAVAN GLABRIDIN;
CYNOMOLGUS MONKEY; 1A ISOFORMS; INHIBITION; ENZYMES; LIVER; SELECTIVITY;
ABSORPTION
AB Glabridin (GA) has gained wide application in the cosmetics and food industry. This study was performed to investigate its metabolic inactivation and elimination by glucuronidation by use of liver and intestine microsomes from humans (HLM and HIM) and rats (RLM and RIM), and liver microsomes from cynomolgus monkeys and beagle dogs (CyLM and DLM). Both hydroxyl groups at the C2 and C4 positions of the B ring are conjugated to generate two mono-glucuronides (M1 and M2). HIM, RIM and RLM showed the most robust activity in catalyzing M2 formation with intrinsic clearance values (Cl-int) above 2000 mu L/min/mg, with little measurable M1 formation activity. DLM displayed considerable activity both in M1 and M2 formation, with Cl-int values of 71 and 214 mu L/min/mg, respectively, while HLM and CyLM exhibited low activities in catalyzing M1 and M2 formation, with Cl-int values all below 20 mu L/min/mg. It is revealed that UGT1A1, 1A3, 1A9, 2B7, 2B15 and extrahepatic UGT1A8 and 1A10 are involved in GA glucuronidation. Nearly all UGTs preferred M2 formation except for UGT1A1. Notably, UGT1A8 displayed the highest activity with a Cl-int value more than 5-fold higher than the other isoforms. Chemical inhibition studies, using selective inhibitors of UGT1A1, 1A9, 2B7 and 1A8, further revealed that UGT1A8 contributed significantly to intestinal GA glucuronidation in humans. In summary, this in vitro study demonstrated large species differences in GA glucuronidation by liver and intestinal microsomes, and that intestinal UGTs are important for the pathway in humans. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Guo, Bin; Sun, Hongzhi] Liaoning Med Univ, Affiliated Hosp 1, Jinzhou, Peoples R China.
[Fang, Zhongze] Tianjin Med Univ, Sch Publ Hlth, Dept Toxicol, Tianjin, Peoples R China.
[Guo, Bin; Fang, Zhongze; Yang, Lu; Cao, Yunfeng] Chinese Acad Sci, Dalian Inst Chem Phys, Joint Ctr Translat Med, Dalian, Peoples R China.
[Guo, Bin; Fang, Zhongze; Yang, Lu; Cao, Yunfeng] Liaoning Med Univ, Affiliated Hosp 1, Dalian, Peoples R China.
[Xiao, Ling; Zhu, Liangliang] Anqing Normal Univ, Sch Life Sci, Ctr Drug & Food Safety Evaluat, Anqing 246011, Peoples R China.
[Xia, Yangliu; Ge, Guangbo; Yang, Ling] Chinese Acad Sci, Dalian Inst Chem Phys, Lab Pharmaceut Resource Discovery, Dalian, Peoples R China.
[Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Cao, Yunfeng] Shanghai Inst Planned Parenthood Res, Shanghai Engineer & Technol Res Ctr Reprod Hlth D, Key Lab Contracept & Devices Res NPFPC, Shanghai, Peoples R China.
RP Zhu, LL (reprint author), Anqing Normal Univ, Sch Life Sci, Ctr Drug & Food Safety Evaluat, 128 Linghu South Rd, Anqing 246011, Peoples R China.
EM binguo_ln@163.com; zhull_better@163.com
FU Startup Project of Doctorial Scientific Research; Anqing Normal
University [K05000130011]; Natural Science Foundation of Anhui
Educational Commission [AQKJ2014B007]; 973 Program [2013CB531800]
FX The authors thank the Startup Project of Doctorial Scientific Research,
Anqing Normal University (K05000130011), Natural Science Foundation of
Anhui Educational Commission (AQKJ2014B007) and the 973 Program
(2013CB531800) for their support of this work.
NR 29
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PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0009-2797
EI 1872-7786
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD APR 25
PY 2015
VL 231
BP 90
EP 97
DI 10.1016/j.cbi.2015.03.001
PG 8
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA CH0VS
UT WOS:000353741100011
PM 25765239
ER
PT J
AU Spong, C
AF Spong, Cathy
TI Project placenta
SO NEW SCIENTIST
LA English
DT Editorial Material
C1 US NIH, Human Placenta Project, Bethesda, MD 20892 USA.
RP Spong, C (reprint author), US NIH, Human Placenta Project, Bethesda, MD 20892 USA.
NR 0
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U1 0
U2 0
PU REED BUSINESS INFORMATION LTD
PI SUTTON
PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND
SN 0262-4079
J9 NEW SCI
JI New Sci.
PD APR 25
PY 2015
VL 226
IS 3018
BP 29
EP 29
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CH2PQ
UT WOS:000353867500015
ER
PT J
AU Yutin, N
Kapitonov, VV
Koonin, EV
AF Yutin, Natalya
Kapitonov, Vladimir V.
Koonin, Eugene V.
TI A new family of hybrid virophages from an animal gut metagenome
SO BIOLOGY DIRECT
LA English
DT Article
ID DNA VIRUSES; EVOLUTION; TRANSPOSONS; EUKARYOTES; ORIGIN; RECOMBINATION;
TRANSPOVIRONS; ENVIRONMENT; SUGGESTS; SPUTNIK
AB Search of metagenomics sequence databases for homologs of virophage capsid proteins resulted in the discovery of a new family of virophages in the sheep rumen metagenome. The genomes of the rumen virophages (RVP) encode a typical virophage major capsid protein, ATPase and protease combined with a Polinton-type, protein primed family B DNA polymerase. The RVP genomes appear to be linear molecules, with terminal inverted repeats. Thus, the RVP seem to represent virophage-Polinton hybrids that are likely capable of formation of infectious virions. Virion proteins of mimiviruses were detected in the same metagenomes as the RVP suggesting that the virophages of the new family parasitize on giant viruses that infect protist inhabitants of the rumen.
C1 [Yutin, Natalya; Kapitonov, Vladimir V.; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
FU US Department of Health and Human Services
FX The authors' research is supported by intramural funds of the US
Department of Health and Human Services (to the National Library of
Medicine).
NR 36
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U1 0
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD APR 25
PY 2015
VL 10
AR 19
DI 10.1186/s13062-015-0054-9
PG 9
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA CG8EG
UT WOS:000353539400002
PM 25909276
ER
PT J
AU Gonzalez-Calixto, C
Cazares-Raga, FE
Cortes-Martinez, L
del Angel, RM
Medina-Ramirez, F
Mosso, C
Ocadiz-Ruiz, R
Valenzuela, JG
Rodriguez, MH
Hernandez-Hernandez, FD
AF Gonzalez-Calixto, Cecilia
Cazares-Raga, Febe E.
Cortes-Martinez, Leticia
Maria del Angel, Rosa
Medina-Ramirez, Fernando
Mosso, Clemente
Ocadiz-Ruiz, Ramon
Valenzuela, Jesus G.
Henry Rodriguez, Mario
de la Cruz Hernandez-Hernandez, Fidel
TI AealRACK1 expression and localization in response to stress in C6/36 HT
mosquito cells
SO JOURNAL OF PROTEOMICS
LA English
DT Article
DE C6/36 HT cells; Receptor for Activated C; Kinase (RACK1); Scaffold
protein; Stress conditions; Aedes mosquito
ID O-GLCNAC MODIFICATION; PROTEIN-KINASE-C; G-BETA-GAMMA; AEDES-ALBOPICTUS;
DENGUE-VIRUS; SCAFFOLD PROTEIN; RACK1 FUNCTION; CRYO-EM; RECEPTOR;
ARABIDOPSIS
AB The Receptor for Activated C kinase 1 (RACK1), a scaffold protein member of the tryptophanaspartate (WD) repeat family, folds in a seven-bladed 3-propeller structure that permits the association of proteins to form active complexes. Mosquitoes of the genus Aedes sp., are vectors of virus producing important diseases such as: dengue, chilcungunya and yellow fever. Based on the highly conserved gene sequence of AeaeRACK1 of the mosquito Aedes aegypti we characterized the mRNA and protein of the homologous AealRACK1 from the Ae. alloopictusderived cell line C6/36 HT. Two protein species differing in MW/pI values were observed at 35 kDa/8.0 and 36 IrDa/6.5. The behavior of AealRACK1 was studied inducing stress with serum deprivation and the glucocorticoid dexamethasone. Both stressors induced increase of the expression of AealRACK1 mRNA and proteins. In serum-deprived cells AealRACK1 protein was located cortically near the plasma membrane in contrast to dexamethasone-treated cells where the protein formed a dotted pattern in the cytoplasm. In addition, 33 protein partners were identified by immunoprecipitation and mass spectrometry. Most of the identified proteins were ribosomal, involved in signaling pathways and stress responses. Our results suggest that AealRACK1 in C6/36 FIT cells respond to stress increasing its synthesis and producing phosphorylated activated form.
Biological significance
Insect cells adapt to numerous environmental stressors, including chemicals and invasion of pathogenic microorganisms among others, coordinating cellular and organismal responses. Individual cells sense the environment using receptors that trigger signaling pathways that regulate expression of specific effector proteins and/or cellular responses as movement or secretion. In the coordination of responses to stress, scaffold proteins are pivotal molecules that recruit other proteins forming active complexes. The Receptor for Activated C Kinase 1 (RACK1) is the best studied member of the conserved tryptophan-aspartate (WD) repeat family. RACK1 folds in a seven-bladed p-propeller structure and it could be activated during stress, participating in different signaling pathways. The presence and activities of RACK1 in mosquitoes had not been documented before, in this work the molecule is demonstrated in an Aedes albopictus-derived cell line and its reaction to stress is observed under the effect of serum deprivation and the presence of glucocorticoid analog dexamethasone, a chemical used to cause stress in vitro. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Gonzalez-Calixto, Cecilia; Cazares-Raga, Febe E.; Cortes-Martinez, Leticia; Maria del Angel, Rosa; Medina-Ramirez, Fernando; Mosso, Clemente; Ocadiz-Ruiz, Ramon; de la Cruz Hernandez-Hernandez, Fidel] IPN, Ctr Invest & Estudios Avanzados, Dept Infectom & Patogenesis Mol, Mexico City 07360, DF, Mexico.
[Valenzuela, Jesus G.] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Henry Rodriguez, Mario] Inst Nacl Salud Publ, Ctr Invest Sobre Enfermedades Infecciosas, Cuernavaca, Morelos, Mexico.
RP Hernandez-Hernandez, FD (reprint author), IPN, Ctr Invest & Estudios Avanzados, Dept Infectom & Patogenesis Mol, Av Inst Politecn Nacl 2508, Mexico City 07360, DF, Mexico.
EM cruzcruz@cinvestav.mx
RI Hernandez-Hernandez, Fidel/I-5193-2012;
OI Hernandez-Hernandez, Fidel/0000-0002-7276-7513; del Angel,
Rosa/0000-0002-6785-2035
FU CONACyT, Mexico [202753]; CONACYT [83866, 180514]; ICyTDF
[PIFUTP09-298]; Fundacion Miguel Aleman A. C. [19]; Universidad Simon
Bolivar Mexico
FX We thank J. Garcia Jimenez and J. M. Ceballos Ramirez, for their
technical assistance; to Abel Trujillo Ocampo M.Sc. and Javier Cezares
Apatiga M.Sc by their advice, Departamento de InfectOmica y Patogenesis
Molecular, CINVESTAV-IPN, Mexico. Cecilia Gonzalez Calixto received a
PhD scholarship from CONACyT, Mexico (No. 202753). We are grateful for
the financial support from CONACYT (Projects No. 83866 and No. 180514),
ICyTDF (PIFUTP09-298), Fundacion Miguel Aleman A. C. (Grant 2012 #19)
and Universidad Simon Bolivar Mexico (Grant 2012 to FCHH). Funding
agencies did not participate in any part of the study design, writing of
the report or the decision to submit the paper for publication.
NR 78
TC 1
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U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
EI 1876-7737
J9 J PROTEOMICS
JI J. Proteomics
PD APR 24
PY 2015
VL 119
BP 45
EP 60
DI 10.1016/j.jprot.2014.11.019
PG 16
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA CH9GN
UT WOS:000354344100005
PM 25555378
ER
PT J
AU Brown, P
Ritchie, D
Ironside, J
Abee, C
Kreil, T
Gibson, S
AF Brown, Paul
Ritchie, Diane
Ironside, James
Abee, Christian
Kreil, Thomas
Gibson, Susan
TI Blood transmission of prion infectivity in the squirrel monkey: The
Baxter study
SO PRION
LA English
DT Meeting Abstract
C1 [Brown, Paul] NIH, Bethesda, MD 20892 USA.
[Ritchie, Diane; Ironside, James] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Abee, Christian] Univ Texas, Bastrop, TX USA.
[Kreil, Thomas] Baxter Biosci, Vienna, Austria.
[Gibson, Susan] Univ S Alabama, Mobile, AL 36688 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
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PY 2015
VL 9
SU 1
MA P.164
BP S98
EP S98
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900182
ER
PT J
AU Brown, P
Farrell, M
AF Brown, Paul
Farrell, Michael
TI A practical approach to avoiding iatrogenic CJD from invasive
instruments
SO PRION
LA English
DT Meeting Abstract
C1 [Brown, Paul] NIH, Bethesda, MD 20892 USA.
[Farrell, Michael] Beaumont Hosp, Dublin, Ireland.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.163
BP S98
EP S98
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900181
ER
PT J
AU Chesebro, B
Striebel, J
Rangel, A
Phillips, K
Hughson, A
Caughey, B
Race, B
AF Chesebro, Bruce
Striebel, James
Rangel, Alejandra
Phillips, Katie
Hughson, Andrew
Caughey, Byron
Race, Brent
TI Role of brain interstitial fluid flow in very early generation and
spread of PrPres after microinjection of prion infectivity in C57BL
mouse brain
SO PRION
LA English
DT Meeting Abstract
C1 [Chesebro, Bruce; Striebel, James; Rangel, Alejandra; Phillips, Katie; Hughson, Andrew; Caughey, Byron; Race, Brent] NIAID, Rocky Mt Lab, Hamilton, MT 59840 USA.
NR 0
TC 0
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U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA O.03
BP S2
EP S2
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900004
ER
PT J
AU Edskes, H
Wickner, R
AF Edskes, Herman
Wickner, Reed
TI Sporadic distribution of prion-forming ability of Sup35p and Ure2p from
yeasts and fungi
SO PRION
LA English
DT Meeting Abstract
C1 [Edskes, Herman; Wickner, Reed] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.41
BP S33
EP S33
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900059
ER
PT J
AU Greene, L
Yim, YI
Park, BC
Yadavalli, R
Zhao, XH
Eisenberg, E
AF Greene, Lois
Yim, Yang-in
Park, Bum-chan
Yadavalli, Rajgopal
Zhao, Xiaohong
Eisenberg, Evan
TI The multivesicular body is the major internal site of prion conversion
SO PRION
LA English
DT Meeting Abstract
C1 [Greene, Lois; Yim, Yang-in; Park, Bum-chan; Yadavalli, Rajgopal; Zhao, Xiaohong; Eisenberg, Evan] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.117
BP S72
EP S73
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900135
ER
PT J
AU Groveman, BR
Orru, CD
Hughson, AG
Zanusso, G
Pocchiari, M
Coulthart, MB
Caughey, B
AF Groveman, Bradley R.
Orru, Christina D.
Hughson, Andrew G.
Zanusso, Gianluigi
Pocchiari, Maurizio
Coulthart, Michael B.
Caughey, Byron
TI An improved test for the detection of Creutzfeldt-Jakob Disease from
human CSF using new RT-QuIC conditions
SO PRION
LA English
DT Meeting Abstract
C1 [Groveman, Bradley R.; Orru, Christina D.; Hughson, Andrew G.; Caughey, Byron] NIAID, Lab Persistent Viral Dis, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Zanusso, Gianluigi] Univ Verona, Dept Neurol & Movement Sci, I-37100 Verona, Italy.
[Pocchiari, Maurizio] Ist Super Sanita, Dept Cell Biol & Neurosci, I-00161 Rome, Italy.
[Coulthart, Michael B.] Publ Hlth Agcy Canada, Canadian CJD Surveillance Syst, Ottawa, ON, Canada.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.23
BP S23
EP S23
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900041
ER
PT J
AU Hughson, A
Orru, C
Groveman, B
Campbell, K
Caughey, B
AF Hughson, Andrew
Orru, Christina
Groveman, Bradley
Campbell, Katrina
Caughey, Byron
TI Factors that improve RT-QuIC detection of prion seeding activity
SO PRION
LA English
DT Meeting Abstract
C1 [Hughson, Andrew; Orru, Christina; Groveman, Bradley; Campbell, Katrina; Caughey, Byron] NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.56
BP S40
EP S41
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900074
ER
PT J
AU Kraus, A
Groveman, BR
Anson, KJ
Raymond, L
Dorward, DW
Hughson, A
Caughey, B
AF Kraus, Allison
Groveman, Bradley R.
Anson, Kelsie J.
Raymond, Lynne
Dorward, David W.
Hughson, Andrew
Caughey, Byron
TI Ultrastructural and biochemical analyses of prion protein amyloids and
the role of lysine and proline residues in amyloid formation
SO PRION
LA English
DT Meeting Abstract
C1 [Kraus, Allison; Groveman, Bradley R.; Anson, Kelsie J.; Raymond, Lynne; Dorward, David W.; Hughson, Andrew; Caughey, Byron] NIH, Rocky Mt Labs, Hamilton, MT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.126
BP S77
EP S77
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900144
ER
PT J
AU Manca, M
Zanusso, G
Caughey, B
AF Manca, Matteo
Zanusso, Gianluigi
Caughey, Byron
TI Detection of sCJD prions in human saliva by RT-QuIC
SO PRION
LA English
DT Meeting Abstract
C1 [Manca, Matteo; Caughey, Byron] NIAID, Lab Persistent Viral Dis, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Zanusso, Gianluigi] Univ Verona, Dept Neurol & Movement Sci, I-37100 Verona, Italy.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.13
BP S17
EP S17
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900031
ER
PT J
AU Moore, R
Head, M
Ironside, J
Zanusso, G
Choi, YP
Priola, S
AF Moore, Roger
Head, Mark
Ironside, James
Zanusso, Gianluigi
Choi, Young Pyo
Priola, Suzette
TI Variable relative contribution of methionine and valine at residue 129
to protease resistant prion protein in heterozygous cases of
Creutzfeldt-Jakob disease
SO PRION
LA English
DT Meeting Abstract
C1 [Moore, Roger; Priola, Suzette] NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Head, Mark; Ironside, James] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Zanusso, Gianluigi] Univ Verona, I-37100 Verona, Italy.
[Choi, Young Pyo] Korea Brain Res Inst, Daegu, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.96
BP S61
EP S62
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900114
ER
PT J
AU Orru, CD
Groveman, BR
Raymond, LD
Hughson, AG
Nonno, R
Zou, WQ
Ghetti, B
Gambetti, P
Caughey, B
AF Orru, Christina D.
Groveman, Bradley R.
Raymond, Lynne D.
Hughson, Andrew G.
Nonno, Romolo
Zou, Wenquan
Ghetti, Bernardino
Gambetti, Pierluigi
Caughey, Byron
TI An apparently universal substrate for RT-QuIC-based detection and
discrimination of prion strains
SO PRION
LA English
DT Meeting Abstract
C1 [Orru, Christina D.; Groveman, Bradley R.; Raymond, Lynne D.; Hughson, Andrew G.; Caughey, Byron] NIAID, Lab Persistent Viral Dis, Rocky Mt Labs, NIH, Hamilton, MT USA.
[Nonno, Romolo] Ist Super Sanita, Dept Vet Publ Hlth & Food Safety, I-00161 Rome, Italy.
[Zou, Wenquan; Gambetti, Pierluigi] Indiana Univ Sch Med, Dept Pathol & Lab Med, Indianapolis, IN 46202 USA.
[Ghetti, Bernardino] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.47
BP S36
EP S36
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900065
ER
PT J
AU Race, B
Phillips, K
Meade-White, K
Striebel, J
Chesebro, B
AF Race, Brent
Phillips, Katie
Meade-White, Kimberly
Striebel, James
Chesebro, Bruce
TI Increased infectivity of anchorless mouse scrapie prions in transgenic
mice overexpressing human prion protein
SO PRION
LA English
DT Meeting Abstract
C1 [Race, Brent; Phillips, Katie; Meade-White, Kimberly; Striebel, James; Chesebro, Bruce] NIAID, Rocky Mt Labs, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1933-6896
EI 1933-690X
J9 PRION
JI Prion
PD APR 24
PY 2015
VL 9
SU 1
MA P.94
BP S60
EP S61
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA CI0RG
UT WOS:000354444900112
ER
EF